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hepatitis]]></video:title><video:description><![CDATA[So an autoimmune disease is this special sort of disease where your own immune cells have gone rogue and start to attack your own cells, right? 

Hepatitis happens to mean inflammation of the liver, so it’s reasonable to say that autoimmune hepatitis is this resulting inflammation of the liver tissue because they’re being attacked by your own immune cells.

Like many autoimmune diseases, the root cause of autoimmune hepatitis is ultimately not super clear, but some researchers think it’s a combination of environmental triggers and genetic predisposition. 

It tends to occur most often in young women, and the female to male ratio is around 4:1. 

Also though, an important piece of the genetic puzzle is the human leukocyte antigen system, shortened to HLA, which is this location of genes on chromosome 6 that regulate our immune functions. 

Specifically, these genes control the proteins that are encoded and used on the cell’s surface to present foreign molecules to the immune system, so although they present antigens, they’re also a form of antigen themselves, but they aren’t the same type of antigen as one on an infectious molecule, but actually alloantigens that vary from person to person and are our specific “self-proteins”. 

Usually, our thymus makes sure the T cells that attack these self proteins aren’t allowed to survive, in autoimmune disease, there may be some abnormality associated with specific self-proteins that lets the T cells attack. 

Based on studying people with autoimmune hepatitis, they often have HLA- DR3 and DR4, which are both MHC class II surface receptors.

The DR part refers to its location on the chromosome, for example, depending on the location, you could have HLA-A, HLA-B, HLA-C or HLA D, and HLA-D has three subregions: P, Q, R, so this one is HLA-DR. 

So there seems to be some sort of connection between these particular “self-proteins” and mounting an attack against your own liver. 

Autoimmune hepatitis also tends to be asso]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2vB_dNHCT0CH01A3uMpHUStVSXS_0A9j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis]]></video:title><video:description><![CDATA[Hepatitis, meaning like this inflammation, of the liver, most commonly comes about because of a virus. 

These viruses tend to target the cells in the liver, and when they get in and infect these cells, they tend to cause them to present these weird and abnormal proteins via their MHC class 1 molecules, and at the same time, you’ve also got these immune cells infiltrating the liver and trying to figure out what’s going on, and so the CD8 positive T cells recognize these abnormal proteins as a sign that the cells are pretty much toast, and the hepatocytes go through cytotoxic killing by the T cells and apoptosis. 

Hepatocytes undergoing apoptosis are sometimes referred to as Councilman bodies, shown on histology here, and this typically takes place in the portal tracts and lobules of the liver. 

This cytotoxic killing of hepatocytes is the main mechanism behind inflammation of the liver, and eventual liver damage in viral hepatitis! 

As someone’s hepatitis progresses, we’ll see a couple classic symptoms related to your immune system mounting an attack, like fever, malaise, and nausea.

Additionally though, patients might have hepatomegaly, where their liver is abnormally large from inflammation, which might cause some pain. 

Also, as more and more damage is done to the liver, the amount of transaminases in their blood will increase. 

Your liver has these transaminase enzymes so it can do its job of breaking down various amino acids.

Typically the serum amino transaminase, or the amount in your blood, is pretty low, but when your hepatocytes start getting damaged they start leaking these into the blood, so a common sign is a greater amount of both alanine aminotransferase, or ALT, and aspartate aminotransferase, or AST, typically even though both are elevated, ALT will be greater than AST in viral hepatitis and will also be the last of the two liver enzymes to return to normal. 

Also, elevated levels of atypical lymphocytes are common to see with vira]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Wilson_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t34GsryRQh6HpQjraUROGnnuRR2qCLFI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Wilson disease]]></video:title><video:description><![CDATA[One essential mineral that our body needs to get through the diet is copper, and typically we take in about 1 to 2 mg per day from the food we eat, things like whole grains, beans, nuts and potatoes; but really our body only needs about 0.75 mg / day, so that extra copper is excreted.

About 90% of the excess copper is excreted into the bile, where it eventually ends up as fecal copper, and the other 10% is excreted in the urine. 

In Wilson disease, there’s genetic defect that results in the excess copper being kept in the body and deposited in various tissues...where it’s not supposed to be, and just like iron, free copper reacts with hydrogen peroxide in the body to form the hydroxyl radical, a reactive oxygen species that’s pretty good at damaging tissue, so over time those tissues are seriously damaged by free radical generation.

Now your liver cells, or hepatocytes, play a really important role in helping the body get rid of excess copper. 

So usually the copper from the diet is absorbed in the small intestine via enterocytes, and passed off into the portal vein to the liver. 

Once it’s in the liver it’s sent to a special transport protein called ATP7B, which has a couple super important jobs.

The first job, is that it binds copper to apoceruloplasmin, which is the major copper-carrying protein in the blood and is responsible for carrying 95% of the copper in blood. 

After it binds copper it’s then just called ceruloplasmin, and this guy can haul 6 molecules of copper at once. 

ATP7B’s other job is to gather up the rest of the copper into vesicles to be exocytosed into into the bile canaliculi, where it goes into the bile and is eventually excreted.

With Wilson disease, there’s an autosomal recessive defect in this ATP7B transport protein. As you could probably guess, that means it can’t incorporate the copper into ceruloplasmin or excrete it into the bile. 

Since it’s not doing either of these things anymore, the copper builds up inside the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aortic_dissection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6YP2_RL1QmWcuffZKWYBz3uyQwC1sYZD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aortic dissection]]></video:title><video:description><![CDATA[An aortic dissection is where part of the tunica intima (which is the endothelial, or the innermost layer of a blood vessel) of the aorta is ripped off. What happens is a tear in the tunica intima of the aorta forms, and the high-pressured blood flowing through the aorta begins to tunnel between the tunica intima and the tunica media, separating the two layers. This is widely accepted as an unideal situation.

Now as the high-pressured blood continues to shear more and more of the tunica intima off the tunica media, blood starts to pool between the two layers, increasing the outside diameter of the blood vessel. The area where blood collects between the tunica intima and the media is called a false lumen, and the true lumen is the regular lumen of the blood vessel.

Since high pressure is a cause of aortic dissection, it’s no surprise that the aorta is the prime target for this problem. So what causes aortic dissections? Well, chronic hypertension is the major cause, whether the hypertension is caused by stress or from increased blood plasma volume like in pregnancy. Blood vessel coarctation, which is the narrowing of a blood vessel, also can cause  dissection. 

Aortic dissections most often happen in the first 10 cm of the the aorta closest to the heart. In order for an aortic dissection to occur, an underlying condition usually has to exist that weakens the aorta’s wall. Connective tissue disorders like Marfan’s and Ehlers-Danlos syndrome can cause a dissection, as well as a decreased blood flow to the vasa vasorum. Aneurysms can be a cause of aortic dissection as well, and incidentally dissection can also cause aneurysms because again, the dissection weakens the blood vessel wall.

In other words, weak walls can lead to outpouching of the blood vessel or a break in the tunica intima, and both of these weaken the walls further.

Aortic dissections cause a whole wack load of other problems too. A lot of complications are related to where the blood in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Syndrome_of_inappropriate_antidiuretic_hormone_secretion_(SIADH)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wb_jRpGGQ_avpVWIuLcxQ307S4qnnWW0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Syndrome of inappropriate antidiuretic hormone secretion (SIADH)]]></video:title><video:description><![CDATA[How does your body know when to retain fluids and when to get rid of them?

It’s not like you just think to yourself “I’ve had too much water, better get rid of some.” (If you do, and it works, call us). 

Your body uses chemicals called hormones to send widespread messages, kind of like how the P.A. system at school tells everyone to ignore the smoke billowing out of the science wing. 

The antidiuretic hormone, abbreviated as ADH, is the hormone that controls water retention in the body. 

It also constricts blood vessels, and incidentally the vasoconstrictor drug called vasopressin is just ADH. Cool! But that’s not what we’re talking about right now. 

Anyways, the more ADH floating around in your blood, the more fluid you retain. 

The less ADH in your blood, the more fluid you excrete.

The nephrons in the kidneys are the structures that physically control how much water is excreted from your body. 

Nephrons are mostly a series of tubes attached end-to-end that type fluids and wastes towards the bladder. 

These tubes though also allow fluids and electrolytes to move through the tube walls and back into the blood if needed. 

ADH affects the last two-thirds of these tubes, called the distal convoluted tubule and the collecting ducts. 

These tubes focus almost exclusively on reabsorbing water back into the blood.

The wall of these tubes are unsurprisingly made up of cells, a common trait of living things, but these cells have proteins called aquaporins. 

Aquaporins allow water to move quickly in and out of the cells. 

The more ADH floating around in the blood, the more aquaporins are available to... ahem...facilitate water movement through the cell (yo, wata, come over here for a sec). 

So when ADH is low, most of the water flows through the distal convoluted tubule and the collecting duct, giving us diluted urine. 

When ADH is high, aquaporins grab much of the water passing through the these tubes and throws them back into the blood.

When I dr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Appendicitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qSduAcNYQGCOtrQSOQstdX4vSmWCoZVY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Appendicitis]]></video:title><video:description><![CDATA[The appendix is the little one-ended tube that’s attached to the cecum of the large intestine, sometimes it’s called the vermiform appendix, where vermiform means “worm-shaped”, so, that should paint a pretty clear picture of what it looks like. 

This odd, yet kinda cute little worm-like structure’s function is actually unknown, though some theories suggest it might be a “safe-house” for the gut flora, and some evidence seems to suggests it plays a part in the lymphatic and immune system; other, arguably more cynical viewpoints maintain that it’s just a useless vestigial organ from our ancestors. 

Whatever the case, the fact remains, it’s pretty talented at getting inflamed and causing abdominal pain, a condition known as appendicitis, as much as 10% of the population develops appendicitis, and it’s the most common surgical emergency of the abdomen. 

Since the appendix is a hollow tube, the most common cause of inflammation is something getting stuck in or obstructing that tube, like a fecalith, a hardened lump of fecal matter that finds its way into the the lumen of the appendix and wedges itself there. 

It could also be other things though, like seeds that weren’t digested, or even pinworm infections, which are intestinal parasites. 

Another cause of obstruction, especially in children and adolescents, is lymphoid follicle growth, also known as lymphoid hyperplasia. 

Lymphoid follicles are dense collections of lymphocytes that get to their maximum size in the appendix during adolescence. Sometimes this growth can literally obstruct the tube. 

Also, when exposed to viral infections like adenovirus, measles, or even after immunizations, the immune system ramps up and these follicles can grow as well. 

Whatever the obstruction is, now this appendix is plugged up, right? 

Well, the intestinal lumen, including the appendix, is always secreting mucus and fluids from its mucosa to keep pathogens from entering the bloodstream and also to keep the tissue]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Primary_biliary_cirrhosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UEXG8rJNSaqBgT2jltYz-4c4QfCRNMGq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Primary biliary cholangitis]]></video:title><video:description><![CDATA[Primary biliary cholangitis and cirrhosis, or PBC, is an autoimmune disease where the T cells attack the cells that line the smaller-sized bile ducts in the liver. 

As the cells are damaged or destroyed by immune attack, they start letting bile leak through their tight junctions and into the interstitial space, where it can get into the blood and the other liver cells. 

This can cause inflammation and symptoms that are similar to cholestasis and obstructive jaundice, both of which there’s some disturbance in bile flow. 

At first it presents as chronic inflammation, which is where it gets the name cholang-itis, for inflammation of the bile ducts, but advanced stages of the disease leads to cirrhosis as more cells are destroyed both from the autoimmune attack and infiltration of bile.

As with a lot of autoimmune diseases, the exact reason why T-cells start attacking these bile duct cells is unknown, and it’s likely related to genetic predisposition in combination with environmental triggers, and is associated with other autoimmune diseases like autoimmune hepatitis and Sjogren’s syndrome. 

PBC tends to affect women at a much higher rate than men, about a 9:1 female to male ratio. 

For some reason that has yet to be completely figured out, in almost all cases of PBC, your body creates antibodies to mitochondria, specifically a mitochondrial protein called PDC-E2; for that reason, one of the most notable markers in PBC are these antibodies to mitochondrial proteins (or AMAs) in the patient’s blood, as many as 95% of patients with PBC have AMAs in their blood. 

Why though, are the bile duct cells specifically targeted? Don’t all cells have mitochondria? Shouldn’t these AMA’s be targeting all cells then? 

One theory is based on a concept called molecular mimicry, where the antigens that bring about this autoimmune response are really similar to another protein, but different enough so that the immune system gets confused and thinks it’s a foreign version]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Biliary_atresia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P3I4jCMASkGzGrzg0HzK4OdhQImcJktP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Biliary atresia]]></video:title><video:description><![CDATA[Atresia refers to the obstruction or absence of a lumen or passageway, biliary has to do with the bile, bile ducts, or gallbladder, so biliary atresia is when there’s some sort of blockage, deformity, or even total absence of a bile duct.

Biliary atresia specifically refers to newborns or young infants, and it can be a congenital defect, meaning something that happens during fetal development, but more commonly it’s some sort of inflammation that happens soon after birth that leads to destruction of the bile ducts. 

There isn’t a definitive cause of biliary atresia; but it’s generally thought that some viral or toxic substance might induce the inflammation.

Some genetic mutations have also been suggested—like a mutation in the CFC1 gene which is involved in development of the left-right embryonic axis. Mutations with this gene have been linked to other congenital defects as well. 

At any rate, the mechanisms and pathogenesis are still pretty foggy, and it likely depends on a combinations of genetic and environmental factors. 

Newborns with biliary atresia usually develop jaundice. 

Since there’s some destruction or deformity of the bile ducts, eventually there’s an obstruction to bile flow right? ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Primary_sclerosing_cholangitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G48w8CnETPaluT4mviTOeoqtSnqUIpil/_.jpg</video:thumbnail_loc><video:title><![CDATA[Primary sclerosing cholangitis]]></video:title><video:description><![CDATA[The name “primary sclerosing cholangitis” or PSC, is actually pretty straightforward, primary refers to it not being known to have been caused by anything else, in other words it isn’t secondary to something else. 

Sclerosing means hardening of the tissue and cholangitis is inflammation of the bile ducts. 

So with PSC we have this fibrosis and inflammation of both the intra- and extra-hepatic ducts, so inside and outside the liver. 

As these cells around the bile ducts become inflamed, die, and harden due to fibrosis, you get this like tightening of the ducts in some areas where there’s been serious fibrosis, and then dilation in other areas that aren’t as affected, and this leads to the classic PSC finding of this sort of “beaded” appearance of the bile ducts. 

These areas of fibrosis in the bile ducts can also be seen on histology, and looks a bit like an onion skin since you’ve got these concentric rings of fibrosis around the bile duct, so sometimes it’s referred to as “onion-skin fibrosis”.

Again, with PSC, we don’t really know what causes it right? One clue though is that it’s been known to be associated with ulcerative colitis which is an autoimmune disease and crohn’s disease which is immune-system related; knowing that, PSC’s thought to possibly be an autoimmune disorder itself involving the immune system’s T cells attacking and destroying bile duct epithelial cells.

Why they might start doing this, though, is not very well known, and likely happens in people with certain genetic predispositions when they’re exposed to some specific stimuli in their environment. 

Certain genetic factors have been linked to developing PSC; studies have shown that patients with PSC tend to have in common specific human leukocyte antigens, or HLAs. 

HLAs are these specific markers on cells that tell your body whether these cells are your own cells or someone else’s cells, and sometimes, for reasons that are usually not well known, the body’s immune system mig]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mycobacterium_tuberculosis_(Tuberculosis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_RMKpLhMTleDbhhWC5Az5RKJRP29ennB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mycobacterium tuberculosis (Tuberculosis)]]></video:title><video:description><![CDATA[It’s estimated that about two billion people worldwide are infected with mycobacterium tuberculosis, often just shortened to tuberculosis or simply ‘TB’. Two billion is a ton of people, but even though they’re infected, that doesn’t mean that all those people have symptoms, the vast majority, about 90-95%,  aren’t even aware that they’re infected. And this is because usually the immune system can contain it such that it isn’t able to multiply, and often remains latent, or dormant, as opposed to active, which usually causes symptoms and can be spread to others. If the host’s immune system becomes debilitated at some point down the road, like with AIDS or some other illness, or as a person grows older, it can be allowed to reactivate, or basically wake up and become very serious, especially if it spreads throughout the body.

Mycobacteria are an interesting bunch, they’re slender, rod-shaped, and need oxygen to survive, in other words, they’re “strict aerobes”. They’ve got an unusually waxy cell wall, which is mainly a result of the production of mycolic acid. Because of this waxy cell wall, they’re “acid-fast”, meaning that they can hold on to a dye in spite of being exposed to alcohol, leaving it bright red colored when a Ziehl–Neelsen stain is used.  The wall also makes them incredibly hardy, and allows them to resist weak disinfectants and survive on dry surfaces for months at a time.

Now Mycobacterium tuberculosis is usually transmitted via inhalation, which is how they gain entry into the lungs. Now, we breathe in all sorts of virus and bacteria all the time, but we’ve got defenses that take care of most of them. For one, air that we breathe in is turbulent in the upper airways, and drives most bacteria against mucus which is then cleared pretty quickly. Ultimately, though, TB can avoid the mucus traps and make its way to the deep airways and alveoli where we have macrophages that eat up foreign cells, digest, and destroy them. With TB, they recognize]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/HIV_(AIDS)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wOIW4cwPT9uGDvhw532VvIU_T9O4Vzon/_.jpg</video:thumbnail_loc><video:title><![CDATA[HIV (AIDS)]]></video:title><video:description><![CDATA[HIV, or human immunodeficiency virus, is a virus that targets cells in the immune system. 

Over time, the immune system begins to fail which is called immunodeficiency, and this increases the risk of infections and tumors that a healthy immune system would usually be able to fend off. 

These complications are referred to as AIDS, or acquired immunodeficiency syndrome. 

Now there are two distinct types of HIV—HIV-1 and HIV-2. 

HIV-1 is the more commonly associated with AIDS in the US and worldwide, HIV-2 is more rare, and typically restricted to areas in western Africa and southern Asia. 

HIV-2 is so uncommon that “HIV” almost always refers to HIV-1. 

Alright HIV targets CD4+ cells, meaning cells that have this specific molecule called CD4 on their membrane. Macrophages, T-helper cells, and dendritic cells are all involved in the immune response and all have CD4 molecules; therefore they can be targeted by HIV. 

The CD4 molecule helps these cells attach to and communicate with other immune cells, which is particularly important when the cells are launching attacks against foreign pathogens.

So this little molecule is pretty important for our immune system, but it’s also extremely important for HIV. HIV targets and attaches to the CD4 molecule via a protein called gp120 found on its envelope. 

HIV then again uses gp120 to attach to another receptor, called a co-receptor. 

HIV needs to bind to both the CD4 molecule and a coreceptor to get inside the cell. 

The most common co-receptors that HIV uses are the CXCR4 co-receptor, which is found mainly on T-cells, or the CCR5 co-receptor which is found on T-cells, macrophages, monocytes, and dendritic cells. 

These coreceptors are so important that some people with homogeneous genetic mutations in their CCR5 actually have resistance or immunity to HIV, since HIV can’t attach and get into the cell. 

In fact, even heterozygous mutations which lead to fewer co-receptors on the cells, can make it harder fo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Celiac_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0s39GfdzTZSTgE9bCmcIO1YlQp6_47Zz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Celiac disease]]></video:title><video:description><![CDATA[It’s becoming more and more common to see things like “gluten-free pizza” or “gluten-free buns” and other gluten-free items at restaurants, grocery stores, or other food-based businesses. This is partly because there’s this increasing recognition, awareness, and diagnosis of a disease called Celiac Disease, in the past called celiac sprue. As many as 1 in 100 people have Celiac disease although many remain undiagnosed. 

Now, Celiac disease is currently understood as an immune system-mediated disorder, where the gluten in food triggers the body’s immune cells to attack the cells in the small intestine as well as produce auto-antibodies against tissue transglutaminase also found in the small intestine as well as other tissues like the heart or the liver. 

Gluten’s found in common wheats and grains, including wheat, rye and barley. If we take a look at wheat, you’ve got your individual wheat kernels, and then inside each kernel there is the endosperm, which has a bunch of nutrients for the seed’s embryo, mostly protein and starch, and some vitamins. The type of protein here is gluten, the main culprit in celiac disease. 

Well, really the main culprit behind celiac disease is gliadin, an umbrella term given to a group of gluten peptides that share a 33 amino-acid sequence which triggers an immune response. So, if somebody with celiac disease eats a wheat-based pizza, it’s broken down in the stomach into gluten peptides ...and a whole lot of other stuff.

That other stuff is no challenge for digestion - gluten peptides, like the gliadin in wheat, however, are high in proline and glutamine, two amino acids which make it a tough little bugger to digest.

So when the undigested gluten proteins, like gliadin, get to the small intestine, they meet the intestinal mucosa, which is lined with a layer of intestinal epithelial cells. Gluten proteins can then get across the gut epithelial cells, either between them, or through the cell, from the apical to the basolater]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ventricular_fibrillation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IxmZQa6LT0CMeIcAsJNoSlpPTjq6f81_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ventricular fibrillation]]></video:title><video:description><![CDATA[Ventricular refers to the bottom chambers of the heart, the right and left ventricles, rather than the top chambers, the right and left atria. Fibrillation means quivering from uncoordinated muscle fiber contraction. So, ventricular fibrillation, sometimes called v-fib or VF, means that the heart’s muscle fibers start quivering because they’re not contracting at the same time.

Normally, an electrical signal spreads fast enough that all the muscle fibers in the ventricles contract at almost the same time, which essentially acts like a single, coordinated contraction. If they don’t all contract at about the same time, not much gets accomplished. It’s kind of like a rowboat; it works best when everyone rows at the same time, right?

Well, with VF, all the rowers stop rowing together, and just row whenever they want; the rowboat just moves in circles, and eventually sinks. 

Just like a rowboat, if the heart’s not squeezing anymore, and it’s just squirming around “like a bag of worms” — a common description of what it looks like — then you can probably guess that this situation is extremely dangerous. Because your body, and especially your brain, isn’t getting fresh oxygen, ventricular fibrillation can lead to death within minutes of onset, which is called sudden cardiac death.

Now, the exact mechanisms leading up to VF aren’t always super clear because it’s hard to know what’s happening in the heart immediately before VF. Most often, however, the heart cells become stressed or damaged in such a way that different areas of tissue are structurally and electrically changed, and thus have different properties; this known as tissue heterogeneity. When they’re homogenous, or the same, they all behave in the same ways and can depolarize and contract at nearly the same time. 

When the tissues have different electrical properties, they aren’t as good as working together, and are more prone to abnormal behavior and depolarizing on their own. In general, tissue heter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ventricular_tachycardia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RAVXxOSYRpGL5LsMLbPdCGlKQcuvcXk4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ventricular tachycardia]]></video:title><video:description><![CDATA[Ventricular refers to the bottom chambers of the heart, the right and left ventricles, as opposed to the top chambers, the right and left atria. Tachycardia refers to a fast heart rate. Typically, a tachycardic, or fast, heart rate is considered anything above 100 beats per minute, or bpm. However, ventricular tachycardia is different than a fast heart rate from exercising, which is called sinus tachycardia. 

Normally, the electrical signals that generate each heartbeat start in the right atrium at the sinus node, which is also known as the sinoatrial node, or the SA node. If the rate goes over 100 bpm and originates in the SA node, it’s considered sinus tachycardia, which is totally normal.

However, heartbeats can become abnormal if the electrical signals don’t start in the SA node, but start in the ventricles instead. Premature Ventricular Contractions, or PVCs, are single beats originating from the lower chambers. Any time there are more than three beats like this in a row, then it’s defined as ventricular tachycardia. Ventricular tachycardia, sometimes called V-tach, or VT, can cause the heart rate to rise above 100 beats per minute, which can be extremely dangerous and lead to sudden cardiac death.

Hold on, how can that happen? It’s not like while we exercise we’re risking sudden cardiac death, right? Well, even though we say tachycardia is anything above 100 beats per minute, most patients with ventricular tachycardia experience heart rates as high as 250 beats per minute. 250 beats per minute mean that the heart is beating over four times per second.  When the chambers are pumping that fast, they don’t have enough time to even fill with blood, so the heart is furiously pumping out only tablespoons of blood to your body, and most importantly, to your brain, which is just not enough. If this happens, a person can have symptoms from not having enough perfusion to their tissues, such as chest pain, fainting, dizziness, or shortness of breath. It can ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diverticulosis_and_diverticulitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DCTfJmWcQBaRdoFxV8Evda8ER0S95Lnm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diverticulosis and diverticulitis]]></video:title><video:description><![CDATA[Diverticula, or a single diverticulum, is this pouch that forms along the walls of a hollow structure in the body, kind of like a cave. 

Usually we talk about these caves or pouches in the context of the large intestine, so it’d be a colonic diverticula, but it can also happen in the small intestine as well as other hollow structures in the body. 

The walls of the large intestine are made up of several layers, starting with the inner layer, the mucosa, then the submucosa, then the muscle layer, and finally serosa.

Sometimes these little out-pouches include all the layers, from mucosa to serosa, and these are true diverticula, and sometimes only the mucosa and submucosa poke through the muscle layer, and these would be called pseudo or false diverticula, where the muscle layer isn’t included and the mucosa and submucosa are covered only by serosa. 

Most of the time, diverticula in the large intestine are false diverticula. 

It’s thought that the formation of colonic diverticula is a result of high pressures that literally push the walls such that they bubble out and form these pouches. 

Now remember that the large intestine has this smooth muscle layer, right? And it’s able to contract using that muscle layer, just like any other muscle we contract, except that we can’t consciously control these because it’s smooth muscle rather than skeletal muscle. 

This smooth muscle contraction accomplishes a couple things, like mixing ingested food and moving digested food toward the end of the line.

Whenever it contracts, though, higher pressures are generated inside the lumen, since it’s sort of like being squeezed and compressing the air inside, and normally you’d imagine that the higher pressure would be equally felt throughout the lumen, right? 

Well, it’s thought that the contractions in patients with diverticula are exaggerated or abnormal in some way, which causes an unequal distribution of pressure with some specific areas having really high pressures]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epilepsy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PgKmaI5XTyWlTxorXDso1Q_iS2_edPGr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Seizures and epilepsy]]></video:title><video:description><![CDATA[A seizure refers to a one-time event caused by abnormal, excessive, and synchronous electrical activity in the brain that can result in autonomic, sensory, and motor symptoms. When seizures specifically involve motor activity, like jerking, we call them convulsions. Most seizures last less than 5 minutes, but if the seizure continues for 5 minutes or more, it’s called status epilepticus.    

Keep in mind that seizures are a symptom, not a diagnosis, meaning they can occur due to various underlying causes, such as trauma, infections, and metabolic imbalances. However, when seizures arise without a clear cause, they are considered unprovoked. And if someone experiences two or more unprovoked seizures, at least twenty-four hours apart, think epilepsy. 

Normally, the brain and its neurons rely on a balance between excitatory and inhibitory neurotransmitters. Think of excitatory neurotransmitters like green traffic lights that speed things up, encouraging the neuron to pass electrical impulses to the next one. On the other hand, inhibitory neurotransmitters act like red traffic lights that slow traffic down, stopping the further propagation of electrical impulses. 

Now, whether there’s too much excitation or not enough inhibition, neurons can begin firing impulses simultaneously. This leads to abnormal, excessive, and synchronous electrical activity in the brain, which results in a seizure. 

Now, there are various causes of seizures, and you can remember the most important ones using the mnemonic “VITTAMINS”. “V” stands for Vascular conditions, like strokes and intracranial hemorrhage, and “I” covers Infection, including meningitis, encephalitis, and brain abscess. Next, the first “T” refers to head Trauma, while the second “T” refers to Toxins, such as cocaine or amphetamine overdose, but also alcohol withdrawal. “A” is for Autoimmune conditions, such as CNS vasculitis and lupus; and “M” is for Metabolic conditions, including hepatic- and uremic encep]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alzheimer_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fCiVKOBaS6OQAGXWuU-WjC_ARauAsIoY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alzheimer disease]]></video:title><video:description><![CDATA[Dementia isn’t technically a disease, but more of a way to describe a set of symptoms like poor memory and difficulty learning new information, which can make it really hard to function independently. 

Usually dementia’s caused by some sort of damage to the cells in the brain, which can be caused by a variety of diseases. Alzheimer’s disease, now referred to as Alzheimer disease, is the most common cause of dementia.

Alzheimer disease is considered a neurodegenerative disease, meaning it causes the degeneration, or loss, of neurons in the brain, particularly in the cortex. This, as you might expect, leads to the symptoms characteristic of dementia.

Although the cause of Alzheimer disease isn’t completely understood, two major players that are often cited in its progression are plaques and tangles. 

Alright, so here we’ve got the cell membrane of a neuron in the brain. In the membrane, you’ve got this molecule called amyloid precursor protein, or APP, one end of this guy’s in the cell, and the other end’s outside the cell. It’s thought that this guy helps the neuron grow and repair itself after an injury. 

Since APP’s a protein, just like other proteins, it gets used and over time it gets broken down and recycled. 

Normally, it gets chopped up by an enzyme called alpha secretase and it’s buddy, gamma secretase. 

This chopped up peptide is soluble and goes away, and everything’s all good. 

If another enzyme, beta secretase, teams up with gamma secretase instead, then we’ve got a problem, and this leftover fragment isn’t soluble, and creates a monomer called amyloid beta. 

These monomers tend to be chemically “sticky”, and bond together just outside the neurons, and form what are called beta-amyloid plaques—these clumps of lots of these monomers. 

These plaques can potentially get between the neurons, which can get in the way of neuron-to-neuron signaling. 

If the brain cells can’t signal and relay information, then brain functions like memory can ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autism_spectrum_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wr5ScujNRQqi4OQz_EpGBz0iSECKba4c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autism spectrum disorder]]></video:title><video:description><![CDATA[Even though everyone develops at slightly different paces, almost everyone hits the same general developmental milestones and learns the same sets of skills on about the same timeline.

These skills progress as the brain develops, and they include: language and communication; social interaction; cognitive skills, like problem solving; and physical milestones, like walking, crawling, and fine motor skills. 

If one of these skills doesn’t develop as scheduled, it may, depending on the severity of the delay, be described as a type of neurodevelopmental disorder, neuro referring to the brain.

When certain skills related to socializing and communicating don’t proceed as expected, this can result in isolation. 

This is where the name autism originated: auto means “self,” and so autism refers to a condition where somebody might be removed from social interaction and communication, leaving them alone or isolated.

Before 2013, the DSM-4 (which has since been updated to the DSM-5), described autism as one of several pervasive developmental disorders, a category that also includes Asperger’s syndrome, childhood disintegrative disorder, and those pervasive developmental disorders that are not otherwise specified, or PDD-NOS for short. 

Asperger’s syndrome was used to describe children who appeared to have characteristics of autism, like difficulties with social interactions or non-verbal communication, but didn’t generally have significant delays in language or cognitive development.

Therefore, Asperger’s syndrome was sometimes referred to as a “high-functioning” form of autism. 

Childhood disintegrative disorder was used to describe the late onset of developmental delays. 

These children developed typically at first, but then they seemed to lose their acquired social and communication skills sometime between ages two and ten. 

“Pervasive developmental disorder: not otherwise” specified is essentially a catch-all category in which patients meet some, but not ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cerebral_palsy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pXZa4jhkQRa-AdK-yb3AjduMT_miIDL1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cerebral palsy]]></video:title><video:description><![CDATA[It’s pretty well-established that your brain’s really important. It’s like, if your body was a computer, your brain’s the mainframe. It controls everything, whether you’re aware of it or not. Cerebral palsy means “brain condition causing paralysis”; so essentially, cerebral palsy refers to damage to the brain that causes loss of muscle control, like for example if the cerebellum was damaged, patients might have issues with fine motor skills like writing or typing. 

That being said, though, cerebral palsy’s a broad umbrella term to basically cover a wide variety of issues, since ultimately the muscles affected and severity depends on which part of the mainframe’s been affected, right? Cerebral palsy is considered a neurodevelopmental condition, meaning that something happens to an area of the brain during its initial development, which is an extremely sensitive period. If that area doesn’t develop right, then it can’t carry out whatever function it’s supposed to control. 

But what’s this vague “something” that can happen, though? Well, it’s “something” because there’s such a wide variety of causes. The majority of cerebral palsy cases are thought to happen before birth, or prenatally, which typically means the underlying cause is really hard to pin down. Exposure to radiation or infection during fetal development can cause cerebral palsy. Hypoxia to the developing fetus been linked as well, in this case the developing brain doesn’t get enough oxygen, potentially from problems like the placenta not being able to supply enough oxygen and nutrients. Cerebral palsy doesn’t have to happen prenatally, though, and some postnatal causes are things like head trauma, or again an infection or a period of oxygen deprivation. Although most cases are likely due to some trauma or injury, a very small proportion of cases are due to a genetic mutation. Even though the brain damage or injury or abnormality is permanent, one super important point to remember about cerebral ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Down_syndrome_(Trisomy_21)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xD6ThEGXRiGFBY8umcKdLBsNTwektX6x/_.jpg</video:thumbnail_loc><video:title><![CDATA[Down syndrome (Trisomy 21)]]></video:title><video:description><![CDATA[Down syndrome or trisomy 21 is a genetic condition associated with a partial or complete copy of the 21st chromosome. Down syndrome is named after a British doctor John Langdon Down, who first described this condition as “mongolism” because the physical features of these individuals were similar to the physical characteristics of people from Blumenbach’s Mongolian race. Since the name was inaccurate and pejorative, in the 1970s, the name was changed to Down syndrome. 

As you’re probably well-aware, our DNA is like this humongous blueprint of information on how to make a human. Usually this massive document is packaged up nicely into a storage bin called a chromosome. Actually, usually we have 46 chromosomes that we use to neatly organize all our information, depending on how you define organize. Each of the 46 chromosomes is actually part of a pair of chromosomes, since you get one from each parent, so 23 pairs.  

If you wanted to make another human, first you’d have to find someone that feels the same way, and then you both contribute half of your chromosomes, so one from each pair, right? Fifty-fifty. Now, what if someone contributes one too many? Say Dad contributes 23 and Mom contributes 24, is that possible? Yes, and it’s the basis of one of the most common chromosomal disorders—Down Syndrome. Someone with Down syndrome has 47 chromosomes instead of 46, specifically they have an extra copy of chromosome 21, so instead of two, they have three, so Down Syndrome’s also known as trisomy 21, in other words, “three chromosome 21s”.  

Alright, so in order to package up half the chromosomes into either a sperm cell or an egg cell, you actually start with a single cell that has 46 chromosomes, let’s just say we’re making an egg cell for the mother, I’m just going to show one pair of chromosomes, but remember that all 23 pairs do this. So the process of meiosis starts, which is what produces our sex cells, and the chromosomes replicate, and so now they’re so]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Attention_deficit_hyperactivity_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z9HCrwFYTFqIXjqodgIjVZkyTayzvoGL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Attention deficit hyperactivity disorder]]></video:title><video:description><![CDATA[What most people know—or think they know—about attention deficit disorder, or ADD, is that it’s used to describe somebody who can’t stay focused…and when they REALLY can’t focus, they have attention deficit hyperactivity disorder, or ADHD. This continuum from one to the next isn’t quite how it works, though. 

ADD and ADHD are actually synonymous, as in, they’re the same. ADD is an outdated term used prior to 1987, after which it evolved into ADHD to encompass more of the symptoms that people with ADHD often experience, which in addition to being inattentive, includes both hyperactivity and impulsiveness. So somebody might be diagnosed with ADHD because they have symptoms related to not being able to pay attention, but they also might be diagnosed with ADHD if they have symptoms relating to being overly active and impulsive. They might also have ADHD if they have symptoms of both.

According to the diagnostic and statistical manual for mental disorders, the Fifth Edition, text revision, the most recent update being in 2022, ADHD is split into these 3 subtypes: inattentive, hyperactive-impulsive, or both. 

Inattentive and hyperactive-impulsive each have a set of 9 symptoms. For example, someone with the inattentive subtype might make careless mistakes, or not listen, or be easily distracted; and someone with the hyperactivity and impulsive subtype might fidget, or squirm around, or get up from their chair often. 

Now, you might be thinking that everyone fidgets now and then, right? Well a diagnosis is given when someone has 6 of the 9 symptoms for either subtype for at least 6 months occurring in more than one setting. Most commonly though, children have symptoms of both subtypes and therefore have the combined subtype. 

Since ADHD is considered a neurodevelopmental disorder, the symptoms also have to have started between age 6 and 12, and the behavior can’t be appropriate for their age or developmental level.

Alright, but what causes someone to be hype]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Schizophrenia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7HPmr2P9S-yz58Sy8EEd-S36RvSn0TcE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Schizophrenia]]></video:title><video:description><![CDATA[Schizo means split, and phrenia, in this case refers to the mind. 

Even though schizophrenia can be interpreted to mean “splitting of the mind”, it does not refer to a split personality, like some media sources might portray, but rather schizophrenia describes a scattered or fragmented pattern of thinking. 

Schizophrenia’s actually a syndrome, meaning there’re all sorts of symptoms that might be associated with it and different patients might experience different symptoms, although the symptoms can be broadly categorized into three major areas: positive symptoms, negative symptoms, and cognitive symptoms.

Alright taking a step back, most human symptoms from any illness are extreme versions of a normal physiologic process (for example everyone has a heartbeat and tachycardia is a fast heartbeat,  everyone has a normal body temperature, but during a fever that temperature is higher). 

In schizophrenia, patients have positive symptoms which aren’t positive in the sense that they’re helpful, but positive in the sense that they’re some new feature that doesn’t have some “normal” or physiologic counterpart. 

These are the psychotic symptoms, so delusions, hallucinations, disorganized speech, and disorganized or catatonic behavior; none of which occur physiologically. 

Delusions are false beliefs that the patient might feel very strongly about, so much so that they won’t change their mind, even if you give them evidence against it. 

There are all sorts of different delusions, like, for example, a delusion of control, where somebody thinks that some outside force or person or thing is controlling their actions. 

They could also be delusions of reference, where someone might think that insignificant remarks are directed at them, like a newscaster is speaking directly to them through the TV. 

Hallucinations are a second type of positive symptom, and can be any kind of sensation that’s not actually there, including visual but also including auditory sensatio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_leukemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OXM3sWD7QJqVincJ6WFnthMgTgS2-bKo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute leukemia]]></video:title><video:description><![CDATA[With acute leukemia, leuk- refers to white blood cells, and -emia refers to the blood, so in acute leukemia, there’s uncontrolled proliferation of partially developed white blood cells, also called blast cells, which build up in the blood over a short period of time.

Although leukemia means cancer white blood cells, it can also be used to refer to cancer of any of the blood cells, including red blood cells and platelets.

Acute leukemia can be broadly classified into acute myeloid leukemia, or AML; and acute lymphoblastic leukemia, ALL.

AML is more common in old age, where as ALL is more common in children. In both cases, accumulation of blast cells interferes with the development and function of healthy white blood cells, platelets, and red blood cells.

Now, every blood cell starts its life in the bone marrow as a hematopoietic stem cell. Hematopoietic stem cells are multipotent -- meaning that they can give rise to both myeloblasts, which are precursors of myeloid blood cells, and lymphoblasts, which are precursors of lymphoid blood cells.

These lymphoblasts can be pre-B cells, which develop into B lymphocytes; or pre-T cells, which develop into T lymphocytes.

If a hematopoietic stem cell develops into a myeloid cell, it’ll mature into an erythrocyte -- or a red blood cell, a thrombocyte -- or a platelet, or a leukocyte -- or a white blood cell, like a monocyte or granulocyte.

Granulocytes are cells with tiny granules inside of them -- they include neutrophils, basophils, and eosinophils.

If a hematopoietic stem cell develops into a lymphoid cell, on the other hand, it’ll mature into some other kind of leukocyte: a T cell, a B cell, or a natural killer cell, which are referred to as lymphocytes.

Once the various blood cells form, they leave the bone marrow, and travel around the blood, or settle down in tissues and organs like the lymph nodes and spleen.

Acute leukemia is caused by a mutation in the precursor blood cells in the bone marrow. In t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Phobias</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ANOSs6GRSvGbOXtQ3lasZo0HQHWw-Ubm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Phobias]]></video:title><video:description><![CDATA[Everybody, whether they like to admit it or not, has fears and gets anxious about certain things, whether it be a spider crawling on the ground or speaking in front of large groups of people. 

In most cases though, people cope with those fears and confront them. 

A phobia is the most extreme type of fear. 

Someone with a phobia will go to great lengths to avoid being exposed to the fear or perceived danger, even if there’s no actual risk or danger, and people often feel powerless against it. 

Phobias are considered the most common psychiatric disorder, affecting almost 10% of the population. 

Phobias are extreme, often unreasonable and irrational fears of something, which could literally be anything, like: pyrophobia, the fear of fire;  alektorophobia, the fear of chickens; triskaidekaphobia, the fear of the number 13; phobophobia, the fear of developing phobias; or even pinaciphobia, the fear of lists.

Unreasonable or irrational fears get in the way of daily routines, work, and relationships, because patients with phobias often do whatever they can to avoid the anxiety and terrifying feelings associated with the phobia.

For example, most people don’t necessarily enjoy the company of spiders, but they also don’t let this fear affect their social or daily life; like, even though I know there are spiders in the woods, I wouldn’t avoid a camping trip on account of the spiders. 

Even if they love camping, somebody with arachnophobia—a fear of spiders—might refuse to go because they know there’s a possibility of seeing a spider in close quarters.

In this case the fear’s clearly interfering with their social life and relationship with friends, meaning it’s a phobia. 

An irrational fear of an object or situation like this is called a specific phobia. 

The DSM-5 splits these specific phobias into five categories: fear of animals, like arachnophobia or alektorophobia; fear of the natural environment, like thalassophobia (fear of the ocean) or nyctophobia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Panic_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KPEp586rQNKTV8JrFcANybbDS-CMiQef/_.jpg</video:thumbnail_loc><video:title><![CDATA[Panic disorder]]></video:title><video:description><![CDATA[At some point you’ve probably heard someone say or joke about “having a panic attack,” but panic attacks are very real situations where someone experiences a sudden period of intense fear or discomfort, believing that something bad’s going to happen and that there’s some imminent threat or danger. 

These feelings are often so intense that they’re accompanied by physiological symptoms like heart palpitations, dizziness, or shortness of breath. 

These symptoms peak within the first 10-20 minutes, but some might last hours. 

Sometimes patients having a panic attack might feel as though they’re having a heart attack or some other life-threatening illness. 

Panic attacks can happen even in familiar places where there are no real threats, which makes them unpredictable, which can further increase anxiety about when the next panic attack is going to happen. 

The DSM-5 outlines the specific criteria required for diagnosis of a panic attack. 

Patients need to experience the abrupt onset of at least four of the following 13 symptoms: pounding heart or fast heart rate; chest pain or discomfort; sweating; trembling; shortness of breath; nausea; dizziness; chills; numbness; feelings of choking; feelings of being detached from oneself; fear of losing control; and fear of dying.

Admittedly, some of these symptoms might naturally occur together, so they can be very hard to tease apart. 

For example, it would be unusual for a person who’s sweating, feeling dizzy, and feeling chills to also not be trembling. 

It’s also important to note that some of these are physical symptoms whereas others are mental, like specific thoughts and ideations. 

Panic attacks can happen in the context of several mental disorders including depressive disorders, posttraumatic stress disorder, and substance abuse disorders. 

They can also, however, happen in the context of a panic disorder, which is basically identified in someone who has panic attacks that are recurrent—meaning 2 or mo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Generalized_anxiety_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IAWxXFzfTvmgHzcQZLoIDZDhRzS07TqW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Generalized anxiety disorder]]></video:title><video:description><![CDATA[Generalized anxiety disorder, or GAD for short, is a mental health condition characterized by prolonged and excessive anxiety about everyday situations, such as finances, relationships, or day-to-day tasks. This anxiety is often out of proportion to the actual situation and can cause significant distress in daily functioning.  

Imagine you have a big presentation coming up at school. You’ve been preparing for days, your slides look amazing, and you’ve practiced your delivery more times than you can count. But when you finally stand in front of the class to speak, your brain’s fear circuit suddenly kicks in.  

The amygdala, which is an almond-shaped structure buried deep in the temporal lobe,  

recognizes this situation as a potential threat and sends excitatory signals to the hypothalamus. The hypothalamus then activates the sympathetic nervous system, setting off a chain of reactions in the body, including a fast heartbeat, rapid breathing, sweating, muscle tension, and a dry mouth.  

Meanwhile, the locus coeruleus in the brainstem releases norepinephrine, which floods the amygdala, activating beta-adrenergic receptors and pushing it into a state of hyperarousal. Additionally, adrenal glands start pumping out corticosteroids, which are stress hormones that can increase activity in fear-related circuits, making you more sensitive to stressful situations.  

All these changes represent a typical anxiety response. It is uncomfortable but temporary and appropriate to the situation. 

Once it’s all over and the room fills with applause, that wave of anxiety finally starts to fade. Your brain begins to wind down, and this is when the ventromedial prefrontal cortex comes into play. This part of the cortex directly inhibits the amygdala using the inhibitory neurotransmitter called GABA, quieting its activity and calming the anxiety response. At the same time, the ventromedial prefrontal cortex stimulates the raphe nuclei to release serotonin, which helps]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Crohn_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6x8ZtFrJRturByxIwQiqljvZRhKXlhk1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Crohn disease]]></video:title><video:description><![CDATA[Crohn’s disease, now more frequently referred to as Crohn disease, is an inflammatory bowel disease that, well, causes inflammation of the bowel. 

Unlike its cousin, ulcerative colitis, which only affects the large intestine, Crohn disease causes inflammation and tissue destruction anywhere along the gastrointestinal tract, from the mouth to the anus. 

Although ulcerative colitis is classified and treated as an autoimmune disease, Crohn disease isn’t technically classified as an autoimmune disease, but rather an immune-related disorder...what does that mean exactly?

Well, with “auto” immune, we think that your own cells and proteins trigger the immune system to start attacking itself.

In Crohn disease, the immune system is thought to be triggered by some foreign pathogen in the gastrointestinal tract. 

Several pathogens have been implicated, like Mycobacterium paratuberculosis as well Pseudomona and Listeria species. 

So the immune system’s reacting to foreign pathogens...isn’t that what it’s supposed to be doing? Well, yes and no; yes because it’s targeting a foreign invader, no because the inflammatory response is large and uncontrolled and leads to destruction of the cells in the gastrointestinal tract.

So what’s thought to happen is one of these pathogens activates the immune system by antigen presentation, meaning one of the gastrointestinal cells is like “here, I think this is an infectious molecule”, and that’s fine, because it is. 

At that point T helper cells, or Th1 cells swoop in and release cytokines—which are cell signaling molecules—like interferon-gamma, and tumor necrosis factor alpha, which further stimulate the inflammatory response.

The cytokines attract Inflammatory cells like macrophages which start releasing even more inflammatory substances like proteases, platelet activating factor, and free radicals, all which contribute to inflammation. 

Although not definitively understood, it’s thought that for patients with Crohn dise]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatocellular_carcinoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3awueHfeQoeSEAH2xXI8HCwfS42KSZnF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatocellular carcinoma]]></video:title><video:description><![CDATA[As opposed to benign hepatic tumors, malignant hepatic tumors are cancerous, very severe, and are actually now the third leading cause of cancer deaths worldwide. 

With these malignant liver cells or hepatocytes, just like malignant cells in other cancers, they develop some mutation that causes them to replicate at way higher rates and form these masses of cells that continue to grow and potentially spread to other tissues.

This would be a primary hepatic tumor, since it starts in the liver. It’s totally possible, though, for liver tumor to develop as a metastasis from another primary cancer, in which case it would not be hepatocellular carcinoma, but a carcinoma from somewhere else, and this is actually more common than primary liver tumors themselves. 

The most common sources of the tumor cells that got to the liver but started somewhere else are the colon, pancreas, lung and breast. 

What exactly causes the mutation in the hepatocyte though?

Well the mechanism isn’t fully understood and can probably be caused by a lot of different things, most importantly though, things that put the liver in a constant cycle of damage and repair are the biggest culprits.

If the liver cells are constantly being forced to repair, this raises the chances of genetic mistakes or mutations, potentially leading to carcinogenesis or development of cancer cells. 

Examples might be any disease that leads to cirrhosis and scarring of the liver tissue, which can include alcoholic hepatitis and cirrhosis, hereditary hemochromatosis, primary biliary cirrhosis, alpha-1 antitrypsin deficiency, and others.

The most common risk factor, the ones that have been linked the most with hepatocellular carcinoma are the hepatitis B and hepatitis C viruses, both of which can become chronic or long-lasting. 

In this case, these cells are at greater risk because of the constant state of infection and immune cell attack, leading to constant damage and repair. 

HBV is particularly problemat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_cholecystitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BW0yulRnQG28Zt5tQYgNZSgXRKatxYP_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute cholecystitis]]></video:title><video:description><![CDATA[Acute cholecystitis, or inflammation of the gallbladder, usually comes about because of a gallstone being lodged in the cystic duct. The cystic duct is the one that leaves the gallbladder and connects to the common bile duct. 

So let’s say this person’s gallbladder’s got a few gallstones in it, and they go to eat a hamburger, the small intestine secretes cholecystokinin, sometimes shortened to CCK, into the blood where it makes it’s way to the gallbladder, and signals it to squeeze out some bile to give it a hand with digestion of that hamburger. The gallbladder contracts and one of these stones gets lodged right in the cystic duct, which blocks bile flow...now what? Well this person probably start experiencing some pain, specifically midepigastric pain, which happens because the gallbladder’s trying to squeeze on a blocked duct...and just like if you squeezed a partly filled balloon with the end blocked off, it physically stretches out and irritates the nerves in the gallbladder and duct. This can also lead to nausea and vomiting, which can last for long periods of time. And as the gallbladder squeezes more and more, the stone might get even more stuck, and at this point the bile, being stuck in the same place, or in a state of stasis, becomes a kind of chemical irritant, and causes the mucosa in the walls to start secreting mucus and inflammatory enzymes, which results in some inflammation, distention and pressure buildup. 

At this point, there might also start to be some bacterial growth, most commonly E coli which is all over the gut, but also Enterococci, Bacterioides fragilis, and Clostridium, which can also be found there. As it sort of balloons up, the pain might start to shift to the right upper quadrant, and it’ll be this kind of dull, achy pain that can even radiate up to the right scapula and shoulders. After a while, bacteria starts invading into the gallbladder wall and eventually through the wall, causing peritonitis, inflammation of the p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Delirium</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yu6-wm9tQvWrLHkdRzmTasotRQ_ErMEZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Delirium]]></video:title><video:description><![CDATA[Delirium is a common and very serious neuropsychiatric syndrome. 

Typically it affects older patients with multiple medical problems, in fact up to half of all elderly patients in the hospital will have an episode of delirium at some point, but being said it can affect anyone - even children, even though that’s much less common. 

So, what is delirium exactly? Well let’s look at a quick example. Let’s say there is an elderly man with diabetes and heart disease, who comes into the hospital with pneumonia. 

He might be slowly recovering, even about to go home, and then one evening things change all of the sudden. He might get really hyperactive, and by that I mean that he may get agitated or aggressive with the staff, mumble or say things incoherently, and have disorganized thoughts or even delusions, perhaps talking about things that haven’t happened or happened years ago. He might even hear or see things like hallucinations, and not know where he is or what he’s doing there. 

We would call this an episode of delirium, and it can be really scary for him or someone who is taking care of him, especially the first time it happens because it can come out of the blue. 

These are the symptoms of what we call hyperactive delirium. 

But there’s also hypoactive delirium which is like the flip side of the coin. 

As an example, you might have a woman with a history of chronic constipation who has recently come out of back surgery. 

If she has hypoactive delirium she might feel suddenly sluggish and drowsy, less reactive and sullen, and might look withdrawn, perhaps because she’s scared of having hallucinations. 

These symptoms of both hyperactive and hypoactive delirium can start pretty suddenly and can happen off and on over the course of a few hours to a few days, with some patients having what they call mix state delirium where they are sometimes having hyperactive symptoms and sometimes having hypoactive symptoms. 

As you might guess, delirium symptoms ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Borrelia_burgdorferi_(Lyme_disease)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1FR0_4NvTaKsDXE7QWPfbeUEQQC1R7y1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Borrelia burgdorferi (Lyme disease)]]></video:title><video:description><![CDATA[Lyme disease, or Lyme borreliosis, is an infectious, blood-borne bacterial disease that is transmitted by ticks.

It’s caused by Borrelia burgdorferi species.

Now, the genus Borrelia contains several species.

Lyme disease in people is caused primarily by Borrelia burgdorferi in North America and by B. afzelii, B. garinii, and B. burgdorferi in Europe and Asia.

In domestic animals, only B burgdorferi is confirmed to cause Lyme disease..

Borrelia are spirochetes, which means spiral-shaped bacteria.

They have outer surface proteins, abbreviated as Osp, which play a role in virulence; and sets of flagella that run between the cell wall and outer membrane, which they use to spin or twist to move in a wave-like motion.

Hard-shelled, Ixodes ticks, or deer ticks, are the vector for B. Burgdorferi, meaning they are the intermediate organism that spreads the bacteria.

In the northeast and Midwest USA, I. scapularis, the black-legged deer tick is the main vector; while on the Pacific coast, it’s I. pacificus, the western black-legged tick.

In Europe and Asia I ricinus and I. persulcatus are the primary vectors.

Ticks like environments with moderate humidity and temperature so they’re often found in wooded areas, thick brush, marshes, and tall grass.

The ticks are small, and even adults are only about 3 mm long, so they can be hard to notice.

Now Ixodes ticks feed on the blood from hosts throughout their life stages of larva, nymph, and adult.

When they hatch as larvae, they are uninfected.

When they feed on infected hosts as larvae or nymphs, they can pick up the B. burgdorferi bacteria.

In the younger stages of their life, they often feed on smaller animals like rodents, birds and even lizards.

When they grow into adults, they move on to larger mammals like dogs, cats, or horses.

A tick infected with B. Burgdorferi can transmit the bacteria to humans and animals through their saliva during feeding.

In the first few hours after attachment, the bacter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vascular_tumors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fp72qNSDTu2DNKerhCY4vhfvSF69mS3s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vascular tumors]]></video:title><video:description><![CDATA[Vascular tumors are tumors of the blood vessels, and there actually a lot of different types, so this is just a quick overview of three types of tumors: Kaposi sarcoma, hemangioma, and angiosarcoma. Kaposi sarcoma is a malignant vascular tumor that is linked with an infection of the human herpesvirus 8 (otherwise known as HHV-8). And it’s a cancer of the blood vessel endothelial cells. This virus is thought to get inside of the cells, and cause the cells to replicate uncontrollably. This type of cancer is seen in people who have suppressed immune systems. That’s why it’s one of the common diseases you’re at risk of getting if you have AIDS, and is a complication of organ transplant patients.

The most common symptoms of Kaposi sarcoma affect the skin, causing purple and red lesions. These lesions look somewhat like a bruise, but unlike a bruise they don’t blanch, or turn pale,  when pressed. That’s because a Kaposi sarcoma has blood filled blood vessels whereas bruises are caused by blood leaking outside of blood vessels into the skin. Initially these lesions start off flat, but over time they may become raised and more painful. In people who have a compromised immune systems, the disease can also cause lesions in other tissues like the mouth, the nose, the throat, the lymph nodes, the lungs, and the gastrointestinal tract.

You can sometimes treat affected skin by surgically removing it or freezing it using cryotherapy, however treating the disease in immunocompromised patients is a little more difficult. If someone’s immune system is compromised because of drugs such as corticosteroids, it might be necessary to adjust immunosuppressants and allow the immune system to recover. It’s a lot harder to treat the disease in an AIDS patient whose immune system is severely compromised, so antiretroviral therapy is commonly used by patients to restore immunity. Radiation and chemotherapy are also treatment options.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ventricular_septal_defect</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7ruE6B3aRyioL0txO2C8GiLqTFOv5gGC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ventricular septal defect]]></video:title><video:description><![CDATA[If you look at the heart, you’ve got the right and left atrium up top, and the right and left ventricles down low. Each of these pairs is separated by a wall, called a septum. A ventricular septal defect is when this lower wall—the ventricular septum—has a gap in it after development. 

The septum is formed during development as this muscular ridge of tissue grows upward from the apex, or the tip, and then fuses with a thinner membranous region coming down from the endocardial cushions. Voila—two separate chambers. If these don’t fuse though, then a gap is left between the two chambers; in other words, a ventricular septal defect, or VSD. The majority of cases are caused by a defect in the membranous portion of the septum.

Among babies, VSDs are actually the most common congenital defect overall, but 30 to 50% of VSDs can spontaneously close during childhood, which makes ventricular defects less common with adults. VSDs are associated with fetal alcohol syndrome and Down syndrome, and are often associated with other cardiac deformities as well. 

Alright so now let’s check out what happens with blood flow, now that there’s this opening between the two ventricles. I’m going to actually switch to this super duper simplified heart instead, just because it’s easier to show what’s going on with blood flow. Alright, so deoxygenated blood comes from the body to the right atrium, and then flows down into the right ventricle, where now it can either be pumped out to the lungs, as normal, or pop over to the left ventricle. Since the pressure on the left side of the heart is actually higher than on the right, and blood likes to flow from high pressure to low pressure, it actually prefers to just keep going on to the lungs. When oxygenated blood comes back from the lungs to the left atrium, and then the left ventricle, now again, it’s got two choices: it can either be pumped out to the body, or flow over to the right ventricle through the gap. Since now it’s in the l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atrial_septal_defect</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q25dcwvsQmarvAEZyfkrx0M4Tj6usErP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atrial septal defect]]></video:title><video:description><![CDATA[With atrial septal defects, “atrial” refers to the heart’s two upper chambers, called the atria; “septal” refers to the septum, which is the wall that separates them; while “defect” means there’s an opening that shouldn’t be there. So, an atrial septal defect is a congenital heart defect characterized by an abnormal gap in the wall separating the atria.  

To understand how this opening forms, we need to review how the atrial septum forms during fetal development. Early during heart development, the atria start as a single chamber called the common atrium. Around the fourth week of development, a thin wall called the septum primum begins to grow downward from the roof of the common atrium, gradually dividing it into right and left atria.  

As the septum primum grows, it leaves a small opening at the bottom called the ostium primum or “first opening”. But, as the septum primum continues to grow, the ostium primum becomes narrower. And before the septum primum reaches the endocardial cushions and completely closes the ostium primum, another opening called the ostium secundum, or “second opening”, appears in the upper area of the septum.  

Then, just next to the septum primum, the heart grows a thicker wall called the septum secundum that grows downward and covers the ostium secundum like a curtain. This leaves a small gap called the foramen ovale. You can think of the septum primum and septum secundum as a pair of double doors that don’t quite line up perfectly, allowing blood to slip through the space between them. This arrangement creates a one-way passage, with the septum primum acting like a flap valve, allowing blood to flow from the right atrium to the left atrium, but not the other way around.   

This atrial communication is essential during fetal development because the fetus isn’t using its lungs yet. In the fetus, the lungs are collapsed and filled with fluid, so the pulmonary vessels are squeezed tight. Because of this high resistance in the pu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coarctation_of_the_aorta</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5EngCRyiTviQA6e84tiW5uYYR3af5Idr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coarctation of the aorta]]></video:title><video:description><![CDATA[Coarctation is a fancy way of saying “narrowing,” so a coarctation of the aorta means a narrowing of the aorta. If we look at the heart, we’ve got the right and left atria, the right and left ventricles, the pulmonary artery leaving the right ventricle to go to the lungs, and the aorta leaving the left ventricle to go to the body. 

There are two forms of aortic coarctation to be familiar with: an “infant” form and an “adult” form. With the infant form, which accounts for about 70% of cases, the coarctation comes after the aortic arch, which branches off to the upper extremities and to the head, and before the ductus arteriosus. Now, you might be thinking, “Hey, what’s this ductus arteriosus thing doing here?” Well, typically this guy only exists during fetal development and closes after birth, but with infantile coarctation, the ductus arteriosus is usually still open, or patent, so there’s a patent ductus arteriosus. In fact, sometimes this form is also called preductal coarctation.

So, if we draw out a more simplified version of the heart, we’ve got deoxygenated blood coming into the right atrium that flows into the right ventricle. Now, as it’s pumped out of the pulmonary artery, it’s got two choices, right? One option is to go through the patent ductus arteriosus and continue down the aorta; the other option is to continue down the way it’s going. Well, since it’s higher pressure over here on the left side, you might think that the blood would say “thanks, but no thanks,” and keep going down the lower pressure pulmonary artery. Instead, this aortic coarctation adds a little twist. Since the spot right before the ductus arteriosus is narrower, blood flowing from the left side has a harder time going through, so actually there’s high pressure upstream of the coarctation, but low pressure downstream. So, what happens is that blood decides to go this way, through the patent ductus arteriosus and into the lower pressure area in the systemic circulation, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mitral_valve_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4K0pi_EOSneqBKZIdvQYChu1RGOF_ZNG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mitral valve disease]]></video:title><video:description><![CDATA[The mitral valve has two leaflets: the anterior leaflet and the posterior leaflet. Together, they separate the left atrium from the left ventricle. During systole the valve closes, which means blood cannot do anything but be ejected out of the aortic valve and into circulation. 

If the mitral valve doesn’t completely shut, blood can leak back into the left atrium; this is called mitral valve regurgitation. During diastole, the mitral valve opens and lets blood fill into the ventricle. If the mitral valve doesn’t open enough, it gets harder to fill the left ventricle; this is called mitral valve stenosis.

Let’s start with mitral valve regurgitation. The leading cause of mitral valve regurgitation, and the most common of all valvular conditions, is mitral valve prolapse. When the left ventricle contracts during systole, a ton of pressure is generated so that the blood can be pumped out of the aortic valve; therefore, a lot of pressure pushes on that closed mitral valve. Normally, the papillary muscles and connective tissue, called chordae tendineae or heart strings, keep the valve from prolapsing, or falling back into the atrium. 

With mitral valve prolapse, the connective tissue of the leaflets and surrounding tissue are weakened; this is called myxomatous degeneration. Why this happens isn’t well understood, but it is sometimes associated with connective tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome. Myxomatous degeneration results in a larger valve leaflet area and elongation of the chordae tendineae, which can sometimes rupture; this rupture typically happens to the chordae tendineae on the posterior leaflet, and can cause the posterior leaflet to fold up into the left atrium.

Patients with a mitral valve prolapse are usually asymptomatic, but often have a classic heart murmur that includes a mid-systolic click, which is sometimes followed by a systolic murmur. 

The click is a result of the leaflet folding into the atrium and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Transposition_of_the_great_vessels</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7JW2MGF-Q8eBv8D_9JMrHy4EQh6uDrzP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Transposition of the great vessels]]></video:title><video:description><![CDATA[Normally, the heart is set up so that the left ventricle pumps oxygenated blood out to the body through the aorta; deoxygenated blood comes back to the right atrium, flows into the right ventricle, and is pumped to the lungs through the pulmonary artery. From the pulmonary artery, it comes back to the left atrium, flows into the left ventricle, and the whole process restarts. The “great arteries,” are the two main arteries taking blood away from the heart: the aorta and pulmonary artery. “Transposing” means that two things switch places with each other. So, transposition of the great arteries, or TGA, is when these two arteries swap locations. 

Normally, blood flows through all of these chambers and blood vessels in a big circuit, but if you switch these two main arteries, you switch from one big circuit to two smaller circuits. On the left side, blood is now pumped from the left ventricle, to the pulmonary artery, and to the lungs; it then comes back to the left atrium and left ventricle, and restarts the circuit. On the right side, blood is pumped out of the right ventricle through the aorta, and then goes to the body; blood comes back the the right atrium and right ventricle, and restarts the circuit. Blood on the right side therefore never gets oxygenated, and blood on the left side never gets deoxygenated. This isn’t good. This situation is actually called complete TGA, or sometimes dextro-TGA or d-TGA; dextro means “right,” because, in this case, the aorta is in front of and primarily to the right of the pulmonary artery.

All right, when the fetus in still in the mother’s uterus, babies with d-TGA don’t have any symptoms because they aren’t using their lungs yet. Instead, they rely on blood from the mother and a few shunts for blood flow, including: the foramen ovale, a gap between the atria; the ductus arteriosus, a vessel connecting the aorta and pulmonary artery; and the ductus venosus, a vessel connecting the umbilical cord to the inferior vena]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemochromatosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LhjLDV4WQ-OF7kwL78p8syrRT5W7KLFz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemochromatosis]]></video:title><video:description><![CDATA[Hemochromatosis is a metabolic disorder where the body absorbs too much iron from the food you eat. 

This accumulation of iron leads to elevated iron in the blood and poisoning of tissues in the liver, pancreas, heart, pituitary gland, joints and skin. 

The root -chromat- actually refers to color or the darkening of the skin that happens when iron is deposited into it. 

If we take a close look at our red blood cells, we’ll notice that they’re loaded with millions of copies of the same exact protein called hemoglobin, which binds to oxygen and turns our blood cells into little oxygen transporters, and basically allow us to move oxygen to all the tissues in our body. 

If we take an even closer look at those hemoglobin proteins, we’ll find that they’re made of four heme molecules, which have, right in the middle, iron. 

This iron molecule is what binds to oxygen, so without iron, we probably wouldn’t fare too well, right? Right. 

Normally, you actually lose a small amount of iron every day, about 1 mg, some in the sweat, some in shedded skin cells, and some in shedded cells in the gastrointestinal tract. 

Most of us, through the diet, take in 10-20 mg of iron every day, and absorb about 10% of that, so 1-2 mg, which is perfect! 

People with hemochromatosis, though, absorb an unusually high amount of iron, sometimes as much as 4 mg per day, even though you probably only need about 1 mg to even out your losses, right? 

You’d think that absorbing more of something is good, but in this case, a net gain of about 3 mg a day comes out to about 1 g per year of excess iron in your body, leading to more than 20 g by age 40! 

Most of this iron you hold on to is deposited in your organs, most notably the liver, but also in your pancreas, your heart, joints, skin, and pituitary gland. 

This process of depositing iron into organs is called hemosiderosis. But hey, a little hemosiderosis over the course of a lifetime never hurt anyone, right? Wrong!

Unfortunately]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Systemic_lupus_erythematosus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/26a7Dhz_TCybV0S7znZ6CZn8SY2gkdWV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Systemic lupus erythematosus]]></video:title><video:description><![CDATA[Alright, “systemic lupus erythematosus,” k we totally got this. “Systemic” is easy, and refers to affecting multiple organs in the body. 

“Erythematosus” means reddening of the skin, alright alright. 

“Lupus” is latin for “wolf”. So affects multiple organs wolf...reddening of the skin? 

Not exactly, the modern use of lupus usually refers to a variety of diseases that affect the skin...which was possibly originally used since these diseases resemble a wolf bite on the patients’ skin. 

Is that true? Who knows. At any rate, systemic lupus erythematosus, or SLE, sometimes just lupus, is a disease that’s systemic, and affects a wide variety of organs, but notably often causes red lesions on the skin.

But how does lupus affect all these organs? Well usually the immune system protects the body’s tissues from invaders, but lupus is an autoimmune disease, which means that immune cells start attacking the very tissues their supposed to protect. 

With lupus, essentially any tissue or organ can be targeted. 

And just like a ton of other autoimmune diseases though, it’s not completely clear why it develops, and like most diseases it’s the result of both genetics and the environment. 

Alright so let’s go over a specific scenario to show how this plays out.

Let’s say this guy has susceptibility genes—genes that make him susceptible to getting lupus, and he’s exposed to UV radiation in sunlight, which we know is an environmental risk factor for lupus. 

Well, given enough UV rays, think like sunburn, the cell’s DNA can become so badly damaged, that the cell undergoes programmed cell death, or apoptosis, and it dies. 

This produces all these little apoptotic bodies, and exposes the insides of the cell, including parts of the nucleus, like DNA, histones, and other proteins, to the rest of the body. 

Well those susceptibility genes specifically have an effect on this person’s immune system such that their immune cells are more likely to think that these are foreig]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Wolff-Parkinson-White_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4i2Kf3mDS1uSwsJgb6VAClJ0TMSOF1-M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Wolff-Parkinson-White syndrome]]></video:title><video:description><![CDATA[Wolff-Parkinson-White pattern, or WPW, is a type of heart arrhythmia caused by an accessory pathway, or an extra electrical conduction pathway, connecting the atria and ventricles, or the upper and lower chambers of the heart.

Normally, an electrical signal starts at the sinoatrial node, or SA node, in the right atrium. It then propagates out through both atria, including bachmann’s bundle in the left atrium, and contracts both atria. Then, it’s delayed just a little bit as it goes through the atrioventricular node, or AV node, before it passes through the Bundle of His and to the Purkinje fibers of the left and right ventricles, causing them to contract as well. 

On an electrocardiogram, the P-wave corresponds to atrial contraction, the PR interval corresponds to the slight delay through the AV node, and the QRS complex corresponds to ventricular contraction.

Now, in a normal electrical conduction system, the AV node is the only place where the signal can get through to the ventricles from the atria. It’s kind of like there’s a gatekeeper that has to stop the signal and make sure everything’s good before letting it pass, so there’s always a slight delay here. People with WPW essentially have a secret, backdoor entrance. Because this entrance is secret, it doesn’t have a gatekeeper; therefore, there’s no delay as the signal moves through it. This secret backdoor entrance is a tiny bundle of cardiac tissue that conducts electrical signals really well, called the Bundle of Kent. Using the Bundle of Kent means the ventricles start to contract a little bit early, which is called pre-excitation. If the Bundle is on the left side of the heart, it’s called “type A pre-excitation.” If it’s on the right side, it’s called “type B pre-excitation.” Type A, on the left side, is a lot more common. 

All right, even though one signal sneaks through early, the other signal waiting at the AV node eventually makes its way through, and the two signals essentially combine ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atrial_fibrillation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KYfNs3BVSNa6zmgjjqkMlUx1S__ds1qx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atrial fibrillation]]></video:title><video:description><![CDATA[The heart has four chambers: two upper chambers, the right and left atrium; and two lower chambers, the right and left ventricles. Fibrillation describes when the muscle fibers are all contracting at different times, so the end result is a quivering, or twitching movement. 

Normally, an electrical signal is sent out from the sinus node in the right atrium. The signal then propagates out through both atria super fast, which allows them to depolarize at about the same time, so that you end up with a nice, coordinated contraction of the atria. That signal then moves down to the ventricles and causes them to contract shortly after. 

With Atrial fibrillation, or A-fib or AF, signals move around the atria in a completely disorganized way that tends to override the sinus node. Instead of one big contraction, you get all these mini contractions that make it look like the atria are just quivering. 

On an  electrocardiogram, or ECG, normally the “P wave” corresponds to the atrial contraction. The “QRS complex,” which is the ventricular contraction, follows shortly after. During AF, all these small areas contract at different times so that you end up with an electrocardiogram that looks like scribbles, where each little peak corresponds to one spot in the atria twitching. Sometimes, a signal from one of these areas makes it down to the ventricles and cause ventricular contraction; these QRS complexes are interspersed at irregular intervals though, and usually at fairly high rates between 100 and 175 beats per minute. 

In the normal heartbeat, a well-coordinated atrial contraction contributes a small amount of blood that’s called the “atrial kick.” People with AF lose this atrial kick; however, this loss isn’t life-threatening.

Okay, but how or why does this happen in the atrium? Why do the cells start depolarizing in a totally uncoordinated way? Well, the answer isn’t super cut-and-dry. There are a ton of risk factors that predispose someone to developing AF, an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Truncus_arteriosus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fv8kOo7dRzWpB_0WLY6dVVRGS-mNBFCn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Persistent truncus arteriosus]]></video:title><video:description><![CDATA[The truncus arteriosus is a big structure that’s present during fetal development; later in development, it divides to form two separate arteries: the aorta and pulmonary artery. Once it’s fully developed, the aorta comes from the left ventricle, and the pulmonary artery comes from the right ventricle. 

A persistent truncus arteriosus describes when this developmental structure doesn’t divide into the two separate arteries. Instead, the baby’s left with one giant artery that branches off from both the right and the left ventricles that then splits off into the aorta and the pulmonary artery. Sometimes, this condition is simply referred to as truncus arteriosus, or TA. The cause of TA is unknown; however, a lot of cases seem to be associated with 22q11.2 deletion syndrome, also known as DiGeorge Syndrome.

Let’s switch to a more simplified view of the heart. All right, so usually deoxygenated blood comes in from the body and travels to the right atrium; then, it goes to the right ventricle and is pumped through the pulmonary artery to the lungs to be re-oxygenated. Next, freshly oxygenated blood passes from the lungs to the left atrium, goes to the left ventricle, and gets pumped through the aorta to the body. Then that circuit repeats, right?  

If these two great arteries, the aorta and the pulmonary artery, don’t divide, you essentially have this massive artery coming from both ventricles. However, notice that this one big artery does eventually split into the aorta and pulmonary artery. Even though they eventually split off, before they do, it’s just one single vessel; thus, the oxygenated and deoxygenated blood mix. When deoxygenated blood mixes into the systemic circulation, it’ll often present as cyanosis, a bluish-purple discoloration of the skin, which can be seen in a baby within the first days after birth.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_cholecystitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0Dav1YpzSECFYgtEh-PDImcrQ4iQWq0E/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic cholecystitis]]></video:title><video:description><![CDATA[With acute cholecystitis, a gallstone gets lodged in the cystic duct, or maybe in the common bile duct, and then causes acute inflammation, pain, and possibly, but not usually, infection; almost all cases of acute cholecystitis though, about 90%, clear up after about a month and the gallstone dislodges. 

It’s possible though, that gallstones get stuck again, and then dislodge, and then get stuck again, and dislodge, and so on. 

So over time, you can imagine the gall bladder walls taking a serious beating, and as those epithelial cells go through this cycle of inflammation over and over again, patients are essentially in this constant state of inflammation, also known as chronic cholecystitis. 

After a while, they can begin to show signs of cellular damage and the epithelial cells can possibly even die off. 

Some patients might not even have had cases of acute cholecystitis where the gallstone gets lodged in the ducts, and sometimes they just have gallstones that cause this constant state of irritation and mild inflammation just by being in the gallbladder. 

Gallstones can be made up of bilirubin, called pigment gallstones, or cholesterol, called cholesterol stones, or maybe they’re made up of both both, and when they roll around and are in contact with the epithelial cells, they can cause inflammation. 

One study found that cholesterol stones in particular might have a more potent ability to stimulate inflammation of the gallbladder epithelial cells.

Whatever the case, chronic inflammation can take its toll, and changes in the gallbladder wall structure can start to take place.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Reye_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/izhestzhSdW7Z-u-JHGX_onnQsCeK4tn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Reye syndrome]]></video:title><video:description><![CDATA[Here’s an example label taken from a pretty common bottle of aspirin, notice that the first warning is “Reye’s syndrome”, and it says that “children or teenagers who are recovering from chicken-pox or flu-like symptoms should not use this product.” Why’s that? 

Reye’s syndrome is characterized by encephalopathy, where encephalo refers to the brain and pathy means that the tissue or organ isn’t quite functioning properly, so there’s some change in the way the brain’s functioning. 

Reye’s syndrome’s also characterized by liver failure. 

This disease is extremely rare, but when it does happen it typically happens in children between the ages of 4 and 12, following an infection like the flu or chicken-pox and is highly associated with the use of aspirin during the infection. 

Since this association was found, the incidence of Reye’s syndrome has dropped significantly, and has led to the requirement of the warning seen on the label for aspirin.

Why though, does Reye’s syndrome seem to happen most often when aspirin is taken during an infection in children? 

Ultimately the answer to this question is still unknown, what is known is that in patients with Reye’s syndrome the mitochondria inside their liver cells, or hepatocytes, become damaged. 

Mitochondria do a few super important things for our cells, right? Including oxidative phosphorylation and fatty-acid beta-oxidation, both of which help provide energy as ATP to the cell. 

So mitochondria are the energy producers of the cell, right? 

And when the cells can’t generate ATP they can eventually die because they have lose their main source of energy.

Since the liver cells seem to be the main cells targeted in Reye’s disease, the liver becomes one of the main organs affected.

Still, the question of how mitochondria, specifically in hepatocytes, become damaged remains mostly a mystery. 

It’s known that salicylates like aspirin are able to uncouple oxidative phosphorylation, which might help to explain ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Zika_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iEzHkFbJSBKY_wvfNcP8_QsdRXSsf5bm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Zika virus]]></video:title><video:description><![CDATA[There are a lot of viruses out there that can infect humans, but two things that can get really alarming is when a virus spreads quickly and when it causes serious harm. 

Zika virus has the potential to do both of these things, which is why it’s gotten a lot of attention. 

Given this, it makes sense to understand a bit about Zika virus and the disease it causes.

Zika virus is an arbovirus, meaning it’s transmitted via certain arthropods, specifically mosquitos, so it’s a mosquito-borne virus. 

Mosquito-borne doesn’t mean that the virus is “born” in the mosquito, though, but it’s “borne”, with an ‘e’, which means carried or transported. 

Sometimes we call organisms like this “vectors”, where all they do is transport the virus. 

So with Zika virus, just like other mosquito-borne viruses like dengue fever, yellow fever, Japanese encephalitis, and West Nile virus, the mosquito acts as a vector that transmits the virus from one person to the next. 

These viruses are all in the genus flavivirus.

In order to mature her offspring, female mosquitoes need a blood-meal, which they get from unsuspecting hosts. 

Mosquitoes find their blood-meals using chemical compounds that we and other organisms give off, like carbon dioxide, ammonia, lactic acid, and octenol.

So when a mosquito that also happens to be carrying the virus finds her meal and digs in, the virus infects the human host and starts to multiply or reproduce within the human. 

With most flaviviruses though, the virus isn’t able to replicate enough in the human host to actually be able to reinfect another mosquito, and so the human is considered a dead-end-host. 

However, the Zika virus, along with yellow and dengue fever, is well enough adapted to human hosts such that they can multiply to a point where it can re-infect another unsuspecting mosquito, which can then go on to infect more people. 

This window lasts for the first week of infection, during which the Zika virus can be found in the bloo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arteriovenous_malformation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9uW4XhxNTDOavlkUlpUU47TJQU62jyCo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arteriovenous malformation]]></video:title><video:description><![CDATA[Arterio refers to the arteries, which are the the blood vessels that take blood away from the heart. Venous refers to the veins, which carry blood toward the heart. Mal means “badly,” so an arteriovenous malformation, or AVM, is some sort of “bad” or abnormal formation between the arteries and veins. 

Typically, oxygen-rich blood is carried to the body’s tissues via arteries. Large arteries split into smaller and smaller arteries, and feed into capillary beds, where cells exchange oxygen for carbon dioxide. The capillaries then feed into larger and larger veins, which carry deoxygenated blood away from the tissues. Normally, arterial blood is under a high-pressure system, and as it goes through smaller and smaller vessels, and ultimately into the capillary bed, pressure in the vessels becomes significantly lower, and blood drains into the lower pressure systemic veins. So, this capillary bed dampens the arterial flow a bit. 

With AVM, this whole capillary bed isn’t there, and a group of arteries directly link up with a group of veins instead. The vessels in the AVM can start to tangle up and are called a nidus, which is Latin for “nest.” When a single artery and a single vein link up abnormally like this, it’s called an arteriovenous fistula. 

In AVM, the arteries and the veins are both under high systolic blood pressures because there are no capillaries to dampen the pressure, which means that the AVM can expand in size over time and can put pressure on the surrounding tissue. This pressure on surrounding capillaries can pinch them shut and prevent that functional tissue from getting blood flow. Also, the high pressure causes the arteries supplying blood to dilate and the veins to thicken and undergo fibrosis. Vessel walls are also prone to forming aneurysms, which are these balloon-like protrusions. Because the vessel walls are weakened and stretched out, they are also at risk for ripping and tearing. 

Although AVMs can form anywhere in the body, the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atrial_flutter</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TLyeLp1uRxmPPIwVAk71wAL6TY2B0K0c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atrial flutter]]></video:title><video:description><![CDATA[The heart has four chambers, two upper chambers—the left and right atrium, or together the atria, and two lower chambers—the left and right ventricles. 

Atrial flutter is used to describe when the atria contract at really high rates—about 300 beats per minute, but sometimes as high as 400 beats per minute. Why flutter? 

Well there’s a wave of muscle contraction that flows through the atria that looks like its flapping or fluttering, hence the name.

Normally, an electrical signal is sent out from the sinus node in the right atrium, but then propagates out through both atria super fast, causing the atria to contract. 

Usually, that signal moves in one direction from the atria to the ventricles through the AV node, it then moves down to the ventricles, and causes them to contract shortly after. 

After each ventricular contraction, the ventricle has to wait for another signal from the sinus node. With atrial flutter, a reentrant rhythm starts in either the right or left atrium. 

Reentrant signals loop back on themselves, overriding the sinus node and setting up an endless cycle that causes the atria to contract again and again and again—at really fast rates.

There are actually two types, type 1 or typical atrial flutter is more common and is caused by a single reentrant circuit that moves around the annulus, or the ring of the tricuspid valve of the right atrium, usually in a counterclockwise direction when viewed looking up through the tricuspid valve. 

Ok so imagine you’re this eyeball looking up through the valve, you’ll see the superior vena cava or SVC, the inferior vena cava or IVC, and the coronary sinus, or CS. 

In this case, a stretch of tissue along the pathway called the cavotricuspid isthmus propagates the signal more slowly than the surrounding tissue. 

Tissue that was just activated can’t be activated again until a certain amount of time has passed, which is called the refractory period; so that slow propagation gives the tissue enough ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Type_I_hypersensitivity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3BzV4wpdSCSh2UvZSF5OHW5ZQQ_BCzy1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Type I hypersensitivity]]></video:title><video:description><![CDATA[Having a hypersensitivity means that someone’s immune system has reacted to something in such a way that it ends up damaging them, as opposed to protecting them. 

There are four different types of hypersensitivities, and in the first type or type one, the reactions rely on Immunoglobulin E, or IgE antibody, which is a specific type of antibody - the other major ones being IgG, IgA, IgM, and IgD. 

So because IgE is involved with type one hypersensitivity reactions they are also called IgE-mediated hypersensitivities.

This type of reaction is also sometimes called immediate hypersensitivities, because the reaction happens super fast—on the order of minutes.

So most allergic reactions are IgE-mediated, and therefore most allergies are type I hypersensitivity reactions. 

“Allergy” comes from the Greek Allos which roughly means “other” and ergon which means “reactivity”. 

Essentially, allergies are reactions to molecules from outside your own body that most people don’t react to—and these are specific molecules from things you might breathe or take in like foods, animal dander, bee stings, mold, drugs or medications, and pollen. 

You can also mount an allergic reaction to things you come in contact with on your skin like latex, lotions, and soaps. 

These specific molecules are also called antigens, and when they cause an allergic reaction, they’re called allergens. 

An allergic reaction happens in two steps, a first exposure, or sensitization, and then a subsequent exposure, which is when it gets a lot more serious. 

People that react to these allergens usually have a genetic predisposition to having over-reactions to unknown molecules or allergens. 

This means that these people have certain genes that cause their T-helper cells to be more hypersensitive to certain antigens. 

Since the production of these T-helper cells is genetically linked, allergies to things tend to run in families.

So let’s say this person breathes in some ragweed pollen, that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Restrictive_cardiomyopathy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BMoPPOWqReKTrXrxYZpIhGrjRoSbdSdg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Restrictive cardiomyopathy]]></video:title><video:description><![CDATA[Cardiomyopathy translates to “heart muscle disease,” so cardiomyopathy is a broad term used to describe a variety of issues that result from disease of the myocardium, or heart muscle. 

When cardiomyopathy develops as a way to compensate for some other underlying disease like hypertension or valve diseases, it’s called secondary cardiomyopathy, but when it develops all by itself it’s called a primary cardiomyopathy.

Restrictive cardiomyopathy is where the heart muscle is restricted, meaning it becomes stiffer and less compliant. The muscles and size of the ventricles, though, stay about the same or maybe they only get slightly enlarged.

Normally, when blood fills the ventricles, they’re compliant so they stretch out and allow more blood to fill in. When blood fills into restricted ventricles, though, they aren’t allowed to expand. So stiffer, less compliant ventricles means that the ventricles can’t stretch, and less blood fills into the ventricle, which means the heart’s starts to fail to pump out enough blood to the body. So restrictive cardiomyopathy causes heart failure, and since filling happens during diastole, we say this is a type of diastolic heart failure.

Now several mechanisms can lead to stiffer heart muscles and restrictive cardiomyopathies. One of these is amyloidosis. Amyloids are proteins that have been misfolded, and once misfolded they become insoluble and can deposit in various tissues and organs, making them less compliant. 

Familial amyloid cardiomyopathy is a genetic disorder where mutant transthyretin protein, or TTR, is misfolded and prone to depositing in the heart tissue. TTR’s a protein that usually circulates in the blood and helps transport thryoxine and retinol. And mutations in TTR are more common in African Americans. Similarly, senile cardiac amyloidosis is where, over time, wild-type, or normal TTR deposits in the heart, and this is typically seen in the elderly.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lactose_intolerance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/02UeqXYgSQCwDRd66T-UYF4RQv2b48HA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lactose intolerance]]></video:title><video:description><![CDATA[The three most common forms of sugar are glucose, fructose, and galactose, and these are all types of monosaccharides, meaning they’re made of just one sugar molecule, molecules like this are called carbohydrates, because they’re made up of carbon, hydrogen, and oxygen, usually with a hydrogen-oxygen ratio of 2:1. 

If you link two of these guys together, you get a  disaccharide because “di” means two, and this is also a carbohydrate. 

Now our body uses these sugar molecules for energy, right? 

For us humans, glucose is our gasoline, our energy source, we’ll take galactose and fructose...but ultimately we need to use glucose, so almost all the fructose and galactose we ingest is converted to glucose, and then we use that glucose for energy. 

Alright, but usually carbohydrates aren’t in monosaccharide form when we ingest them, and a lot of what we take in are in the disaccharide form, and one notorious disaccharide that tends to cause serious gastrointestinal distress for a lot of people, is lactose. 

Lactose is a disaccharide that’s made up of a glucose molecule and a galactose molecule. 

For us to use it as energy, though, we have to first break it down to those two monosaccharides.

In the milk of most mammals, lactose is generally the major carbohydrate, so when you have a glass of milk, and it gets through your stomach to the small intestine, that lactose gets chopped into glucose and galactose by an enzyme that’s fittingly called lactase. 

The gene responsible for production of the lactase enzyme is expressed exclusively in the enterocytes lining the small intestine, which are cells that help absorb nutrients from stuff that we eat. 

Once produced, the enzyme makes it’s way to the cell’s surface along the cell’s microvilli, these little tentacles that help increase surface area and absorb nutrients. 

K, once lactose gets chopped by lactase, we’re good to go, and we absorb the glucose and galactose and all is well. 

Now, as mammals, we’re wire]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rheumatic_heart_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nQ3A3K7lQ_a9VE6xfjLH4hzsRqOFwwpN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rheumatic heart disease]]></video:title><video:description><![CDATA[“Rheumatism” is used to describe inflammation in the joints, muscles, and the fibrous tissue, so rheumatic fever is a type of inflammatory disease that can damage the heart tissue, and lead to rheumatic heart disease. 

Rheumatic fever develops after streptococcal pharyngitis, inflammation of the throat due to Streptococcus pyogenes where pyogenes literally means “makes pus”. The bacteria is sometimes referred to as “Group A beta hemolytic” streptococcus, and the infection itself is most often just called Strep throat. This particular group of streptococcus has an antigen that lumps it into a group called “group A”, and it also produces an enzyme called streptolysin, that completely lyses nearby red blood cells, or causes them to rupture—rupturing red blood cells is called hemolysis, right? And when those red blood cells rupture and are destroyed, it’s called beta-hemolysis—as opposed to alpha-hemolysis, where cells aren’t actually destroyed, they’re just damaged or bruised.

Some of these strep bacteria have a protein on their cell wall called “M protein”, and this particular protein is highly antigenic, meaning that the immune system sees it and recognizes it as a foreign molecule, and mounts an immune response, which rightfully so, produces antibodies against these proteins. Those antibodies, though, are thought to cross-react with proteins on some of our body’s own cells, like cells in the myocardium (or heart muscle) and heart valves, but also cells in the joints, the skin and the brain.

This phenomenon, where antibodies accidentally target proteins on our own cells because they look like the proteins on foreign cells, is called molecular mimicry, and is an example of what’s called a type 2 hypersensitivity reaction. Once bound to cardiac tissue, the antibodies activate nearby immune cells, which causes a cytokine-mediated inflammatory response and tissue destruction.

Obviously though, not everyone that gets strep throat gets rheumatic fever, right?]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoarthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9EIdPyO4RzyFOFZEoUYRqSN8Sa2NZvId/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteoarthritis]]></video:title><video:description><![CDATA[Osteo- means “bone”, and -arth- refers to “arthron” which means joint, and -itis means “inflammation”, so osteoarthritis is a disease involving inflammation of the bone and joint cartilage. 

It was once thought that the “itis” part of osteoarthritis was a misnomer, and that inflammation didn’t play a role in its development, and that it was mostly a degenerative disease resulting from simple “wear and tear”. 

Nowadays, it’s thought that inflammation does indeed play an important role in the development of osteoarthritis.

Alright, so a healthy joint consists of two bones, each with its own layer of articular cartilage, which is a type of connective tissue that allows the two bones to glide against each other essentially without friction.

With Osteoarthritis, we’re really talking about one particular kind of joint which is a synovial joint.  

Along with articular cartilage, another important component of synovial joints, and where they get their name from, is the synovium, which along with the surface of the articular cartilage, forms the inner lining of the joint space. 

The synovium’s composed of loose connective tissue, blood vessels, lymphatic vessels, and on the surface—”Type A” cells that clear cellular debris and “Type B” cells that produce components of synovial fluid, which helps lubricate the two articular surfaces. 

One of the main issues in osteoarthritis is the progressive loss of this articular cartilage, which means there’s not much separating the two bones anymore, which adds a significant amount of friction between them, which then generates inflammation, and triggers pain through the nerve endings in this joint space. 

Maintaining healthy articular cartilage is the chondrocyte’s job, a specialized cell responsible for maintaining everything cartilage-related.

The chondrocytes produce and are embedded within a strong gel or extracellular matrix which contains type II collagen, a protein that provides structural support, as well as p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heart_failure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vyvPhLxoSOC_1X1C43fFjU1uQS2qGYcj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heart failure]]></video:title><video:description><![CDATA[Heart failure’s used to describe a point at which the heart can’t supply enough blood to meet the body’s demands. 

This can happen in two ways, either the heart’s ventricles can’t pump blood hard enough during systole, called systolic heart failure, or not enough blood fills into the ventricles during diastole, called diastolic heart failure.

In both cases, blood backs up into the lungs, causing congestion or fluid buildup, which is why it’s also often known as congestive heart failure, or just CHF. 

Congestive heart failure affects millions of people around the world and since it means that the body’s needs are not being met, it can ultimately lead to death. 

Part of the reason why so many people are affected by heart failure, is that there are a wide variety of heart diseases like ischemia and valvular disease that can impair the heart’s ability to pump out blood and—over time—can ultimately cause the heart to fail.

Alright, first up is systolic heart failure, kind of a mathematical way to think this one is that the heart needs to squeeze out a certain volume of blood each minute, called cardiac output, which can be rephrased as the heart rate (or the number of beats in a minute) multiplied by the stroke volume (the volume of blood squeezed out with each heart beat). 

The heart rate is pretty intuitive, but the stroke volume’s a little tricky. 

For example, in an adult the heart might beat 70 times per minute and the the left ventricle might squeeze out 70ml per beat, so 70 x 70 equals a cardiac output of 4900 ml per minute, which is almost 5 liters per minute. 

So notice that not all the blood was pumped out right?

And the stroke volume is only a fraction of the total volume. 

The total volume might be closer to 110 ml, and 70ml is the fraction that got ejected out with each beat, the other 40ml kind of lingers in the left ventricle until the next beat, right? 

In this example, the ejection fraction would be 70ml divided by 110 ml or about 64]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocarditis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ing4ONyZTFu8-4m6KDwHQfi8QRS8N1AX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocarditis]]></video:title><video:description><![CDATA[Endocarditis means “inflammation of the inner layer of the heart.” The heart’s wall is made up of three layers: the epicardium, the outermost layer; the myocardium; and then the endocardium, which is the layer that gets inflamed.

It turns out that most cases of endocarditis are due to a microbial infection of the endocardium, usually involving the endocardium lining the cardiac valves. Why the valves? Well, it turns out that the valves have tiny blood vessels that nourish them, even though they’re flopping around in blood all day long. This means that an infection can potentially result from a damaged valve, because it would allow microbes to escape the tiny blood vessels and invade the valve tissue, or on the flip side, microbes in the blood might enter the tiny vessels within the valve. 

Either way, a microbe has to first get into the bloodstream, and that might happen if a person: has an open wound or an abscess; a dental or surgical procedure; or, an injection with an infected needle or infected substance, from using illegal drugs. 

Most often, the valves on the left side — the mitral valve and the aortic valve — are affected, sometimes due to predisposing conditions, such as mitral valve prolapse and bicuspid aortic valves, but it really depends on the circumstances. Risk factors for either valve include having prosthetic valves, congenital cardiac defect involving the valves, damage to the valves from rheumatic heart disease, and intravenous drug use, which typically affects the tricuspid valve.

Now, the first step that happens in endocarditis is that the endothelial lining of the valve gets damaged. There are a number of ways this can happen, such as previous inflammation or injury. This damage exposes the underlying collagen and tissue factor, causing platelets and fibrin to adhere, which forms this tiny thrombosis or blood clot. This is called Nonbacterial Thrombotic Endocarditis, or NBTE. It’s nonbacterial because it happens even before the b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DiGeorge_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vTaoNfz7QvmxQbclKnTCs_ACROanL3Lm/_.jpg</video:thumbnail_loc><video:title><![CDATA[DiGeorge syndrome]]></video:title><video:description><![CDATA[The name DiGeorge syndrome isn’t the most descriptive name, which is why it’s often also referred to as 22q11.2 deletion syndrome, which is actually pretty descriptive, and describes a condition in which a small portion of chromosome 22 is deleted, which causes a bunch of developmental abnormalities and complications.

Alright so our chromosomes are composed of genes, right? 

Which are essentially instructions for everything from development to day-to-day survival, and these genes are spread out across 23 pairs of chromosomes. 

22q11.2 is like an address, so 22 stands for chromosome 22, with q designating the long arm of the chromosome, then it’s on region 1, band 1, and sub-band 2. 

This portion of dna, 22q11.2, spans about 30 genes and 1.5 to 3 million base pairs, which classifies it as a microdeletion since it’s less than 5 million base pairs. 

Even though this region is relatively small, it encodes for some really important genes, one of which is the TBX1 gene, which is thought to play a big role in the disease.

The TBX1 gene is involved in normal development of the pharyngeal pouches, specifically pouch 3 and 4, which are fetal structures that develop into parts of the head and neck. 

The third pharyngeal pouch goes on to develop into the thymus and the inferior parathyroid gland, the fourth pouch goes on to develop into the superior parathyroid gland. 

So with a 22q11.2 deletion and therefore no TBX1 gene, the thymus and parathyroid gland both end up underdeveloped, called hypoplasia. 

T lymphocytes or T cells are immune cells that’re super important for the adaptive immune response, and are produced in the bone marrow but mature in the thymus. 

If someone has thymic hypoplasia and thymic dysfunction, the T cells don’t mature, and so these people often have a deficiency in mature T cells. 

It turns out, though, that most people with DiGeorge syndrome have mild to moderate thymic dysfunction, called partial DiGeorge syndrome, which means that the immunodeficiency isn’t life-threatening. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Type_II_hypersensitivity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BoLkqBtrTnWrp9fi3U7pOKACSHuCXCwI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Type II hypersensitivity]]></video:title><video:description><![CDATA[Having a hypersensitivity means that the immune system is reacting to something in a way that damages the body rather than protecting it. 

There are four different types of hypersensitivities, and the second type or type II hypersensitivity is sometimes called cytotoxic hypersensitivity because a lot of disorders caused by this hypersensitivity involve antibody mediated destruction of healthy cells. 

These disorders tend to be tissue specific meaning that the antibodies are generally specific to one type of tissue or organ. 

There are other antibody-mediated hypersensitivities that are systemic, and these are generally Type III hypersensitivities. 

Our immune system is setup to fight anything that is considered “non-self” right? Anything that’s not “self”, or you. 

This works in large part because of a process called central tolerance which is when developing immune cells that are self-reactive get destroyed or inactivated, whereas immune cells that aren’t are allowed to survive.

This happens while they are still in their primary lymphoid organs, which is the thymus for T cells and the bone marrow for B cells.

This process, though, is not perfect and some self-reactive B and T cells will escape. 

These escaped self-reactive cells can then attack healthy tissue and result in autoimmune disease.  

In type II hypersensitivity these escaped self-reactive B cells become activated and produce IgM or, with the help of CD4 positive T helper cells, IgG antibodies that attach to antigens on host cells. 

There are two type of antigens involved with type II hypersensitivity: intrinsic meaning an antigen the host cell normally makes or extrinsic which is an antigen from an infection or even some medications, like penicillin that gets attached to the host cell.  

Alright so let’s say a drug, like penicillin, binds to a red blood cell - well it becomes an extrinsic antigen. 

An IgG or more rarely an IgM antibody that is penicillin specific might bind to the p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Type_III_hypersensitivity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SWNxNPyTQ3e8L8t8RLBrroEQSwabBAJ7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Type III hypersensitivity]]></video:title><video:description><![CDATA[Having a hypersensitivity means that someone’s immune system has reacted to something in a way that ends up damaging them, as opposed to protecting them. 

There are four different hypersensitivities and the third type or type III hypersensitivity reaction happens when antigen-antibody complexes deposit in blood vessel walls, causing  inflammation and tissue damage.

Alright so first off, type III hypersensitivity reactions are mediated by immune complexes. Immune complexes, aka antigen-antibody complexes are made of two parts—the antigen and the antibody. 

Antibodies, sometimes called immunoglobulins, are produced by plasma cells, which are basically fully matured and differentiated B cells. 

Initially these cells make IgM - which can be secreted or bound to the plasma cell surface where it acts as a B cell receptor. 

When a B cell undergoes cross-linking of two surface bound IgMs, it then takes up the antigen and presents a piece of it to T helper cells via t cell receptor to the MHC- class II molecule presenting the piece of antigen, along with costimulatory molecule CD4. 

The B cell’s CD40 also binds to the T cell’s CD40 ligand, and then the t cell releases cytokines, which results in b cell activation and class switching, or isotype switching, where it changes the type of antibodies it makes.

In type III hypersensitivity reactions, typically B cells will switch from making IgM to making IgG antibodies. 

Now remember that all antibodies are specific, right? Meaning that they recognize specific molecules called antigens, the second part of immune complexes.  

Antigens can come in all sorts of flavors, some float around in the blood by themselves, and are soluble, but some are bound to cell surfaces. 

Immune complexes are formed when antibodies bind to soluble antigens. 

Antibodies can also target antigens on cell surfaces, but these are not considered immune complexes. 

This is the first major distinction between type II hypersensitivity react]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Type_IV_hypersensitivity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zLWy0MGyQiePWNPQz6y_5yZPSUaqo01d/_.jpg</video:thumbnail_loc><video:title><![CDATA[Type IV hypersensitivity]]></video:title><video:description><![CDATA[Having a hypersensitivity means that someone’s immune system has reacted to something in such a way that it ends up damaging them, as opposed to protecting them. 

There are four different types of hypersensitivities, and in the fourth type or type 4, the reactions are caused by T lymphocytes, or T cells, and so type IV is also sometimes known as T-cell-mediated hypersensitivity.

T cells are called T cells because they mature in the thymus. 

The two types of T cells that cause damage to tissues in type IV hypersensitivity are CD8+ T cells also known as killer T cells or cytotoxic T cells, as well as CD4+ T cells also known as helper T cells. 

CD8+ killer T cells do exactly what their name implies - they kill things. 

They are like silent assassins of the immune system that go after very specific targets. 

In contrast, CD4+ T cells locally release cytokines, which are small proteins that can stimulate or inhibit other cells. 

So CD4+ T cells act like little army generals coordinating immune cells around them. 

But both CD8+ and CD4+ cells start off as naive cells because their T cell receptor or TCR has not yet bound to their target antigen - which is that specific molecule it can bind to.

Alright so let’s play out a scenario. Let’s say someone’s skin brushes up against poison ivy, and gets the molecule urushiol all over.

That molecule’s small enough to quickly make it’s way through the epidermis to the dermis, which is where it might combine with small proteins, it then might get picked up by a langerhans cell also known as a dendritic cell, which is a type of antigen-presenting immune cell. 

The dendritic cell then takes it to the nearest lymph node - the draining lymph node, where it presents the antigen on its surface using a MHC class II molecule, which is basically a serving platter for CD4+ T cells to come check out. 

If a TH cell recognizes the antigen, it binds to the MHC class II molecule using its T cell receptor, as well as CD4, which]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_venous_insufficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5MgvsMCyTm6euazm2pGVqgQXRvSqwoK4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic venous insufficiency]]></video:title><video:description><![CDATA[Varicose veins are veins that have become enlarged and twisted, and this most commonly happens in the veins of the leg.

How do they form? Well - the arterial circulation, going away from the heart, is a high pressure system, meaning the movement of blood is dependent on high pressures that essentially push it through the arteries, on the order of 120 mmHg. 

The venous circulation going back to the heart, on the other hand, is a low-pressure system with a central venous pressure around 5mm Hg. 

This means that the movement of blood has to rely heavily on what’s called the skeletal muscle pump, which is just a way of saying that it relies on the contraction of surrounding skeletal muscles, which compresses the vein and propels blood through the vessels. 

But let’s think about the veins in the legs when you’re standing, now to get to the heart the blood has to go up, right, which is working against gravity. 

So if your calf muscles contract and squeeze the blood inside, some blood gets propelled downward, while some gets propelled upward, but then gravity pushes that upward-moving blood back down, and it doesn’t seem like much gets accomplished...and it wouldn’t, but that’s not the whole story—most veins also have one-way valves. 

These valves only let blood move in one direction, toward the heart. 

So now, as the skeletal muscles contract, it squeezes the veins, and this lower valve stays closed to prevent blood from going downward, while the upper valve lets blood through, but even though gravity wants to push it back down, that blood isn’t allowed to fall back down through the upper valve, right?

For some people, the downward gravitational pull on blood causes the walls of the leg veins to stretch apart over time, which tends to also pull apart those valves.

If these valves fail to close properly, they can allow blood to leak backward and pool in the veins, which can lead to more valves stretching out and failing. 

The veins have now become varic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atrioventricular_nodal_reentrant_tachycardia_(AVNRT)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cB_dxlT5TPmknc8rcCkVb7ddRuSvN_EL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atrioventricular nodal reentrant tachycardia (AVNRT)]]></video:title><video:description><![CDATA[The atria are the heart’s upper chambers; the ventricles are the lower chambers. Reentrant tachycardias are fast heart rates caused by electrical signals that loop back on themselves.

Normally, an electrical signal starts at the sinoatrial or SA node in the right atrium and propagates out through both atria, including bachmann’s bundle in the left atrium, and then contracts both atria. It’s then delayed just a little bit as it goes through the atrioventricular, or AV node, before it passes through the Bundle of His and on to the Purkinje fibers of the left and right ventricles, causing them to contract as well.

Usually, the only place where a signal can go from the atria to the ventricles is at the AV node, and once that signal gets to the purkinje fibers, it stops and the heart tissue waits for another signal from the SA node. With an atrioventricular reentrant tachycardia, or AVRT, the electrical signal actually uses a separate accessory pathway to get back up from the ventricles to the atria, which causes the atria to contract before the SA node sends out another signal. The signal then moves back down the AV node to the ventricles and purkinje fibers, contracts the ventricles, and goes back up that accessory pathway. This cycle repeats, which is why AVRT can result in rates as high as 200-300 bpm. This type of tachycardia is known as a supraventricular tachycardia because the signal causing the fast rate originates above the ventricles. The most common type of AVRT is Wolff-Parkinson-White syndrome, where the accessory pathway is called the Bundle of Kent. This type of reentry is known as an anatomical reentrant circuit because the accessory pathway is a fixed, anatomically-defined pathway. 

Another type of reentrant circuit is atrioventricular nodal reentrant tachycardia, or AVNRT. AVNRT, just like AVRT, is a type of supraventricular tachycardia; however, with AVNRT it’s in or near the AV node, which similarly contracts the ventricle and the atria ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Major_depressive_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4_bddpThSu6Y47lVR4lFZHsCRfiJHdLM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Major depressive disorder]]></video:title><video:description><![CDATA[Clinical depression, which is sometimes called major depressive disorder or unipolar depression, is a serious mental disorder characterized by by persistent sadness and a loss of interest in the activities of daily life, like working, studying, participating in hobbies, eating, and sleeping. 

Clinical depression has a lifetime incidence of up to 20% in women and 12% in men, making it one of the most common reasons people seek out mental health services. 

In addition to being relatively common, clinical depression is very serious because it essentially leads to an overall feeling that life isn’t enjoyable. 

We don’t exactly know what specifically causes clinical depression, but  it’s probably the result of a combination of genetic factors, biological factors, environmental factors, and psychological factors. 

It’s been shown that people with family members who have depression are three times more likely to have it themselves, especially if they’re closely related.

Medications that address the biological factors of depression focus specifically on neurotransmitters. 

Neurotransmitters are signaling molecules in the brain that are released by one neuron and received by the receptors of another neuron. 

Through this process, a message is transmitted from one neuron to the next. 

The body’s ability to regulate how many of these neurotransmitters are sent between neurons at any given time is thought to play an important role in the development of depression’s symptoms. 

That’s because neurotransmitters are likely involved in regulating a lot of brain functions, including mood, attention, sleep, appetite, and cognition. 

The three main neurotransmitters that treatment for depression focuses on are serotonin, norepinephrine, and dopamine. 

That’s because medications that increase the amount of these neurotransmitters in the synaptic cleft — this space between the neurons — are shown to be effective antidepressants. 

This finding led researchers to deve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prerenal_azotemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/doCGeT50ThCKsUqAH8uR-R-UTM_9Nqmt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prerenal azotemia]]></video:title><video:description><![CDATA[Acute kidney injury, or AKI, is when the kidney isn’t functioning at 100% and that decrease in function develops relatively quickly, typically over a few days. Actually, AKI used to be known as acute renal failure, or ARF, but AKI is a broader term that also includes subtle decreases in kidney function. 

AKI can essentially be split into three types, prerenal AKI meaning the cause of kidney injury’s coming before the kidneys, postrenal AKI—meaning after the kidneys, or intrarenal AKI—meaning within the kidneys. 

Now the kidney’s job is to regulate what’s in the blood, so they might remove waste, or make sure electrolyte levels are steady, or regulate the overall amount of water, and even make hormones - the kidneys do a lot of stuff! 

Blood gets into the kidney through the renal artery, into tiny clumps of arterioles called glomeruli where it’s initially filtered, with the filtrate, the stuff filtered out, moving into the renal tubule. 

Sometimes fluid or electrolytes can move back from the filtrate into the blood - called reabsorption, and sometimes more fluid or electrolytes can move from the blood to the fitrate - called secretion. 

Along with fluid and electrolytes, though, waste-containing compounds are also filtered, like urea and creatinine, although some urea is actually reabsorbed back into the blood, whereas only a little bit of creatinine is reabsorbed. In fact, in the blood, the normal ratio of blood urea nitrogen, or BUN, to creatinine is between 5 and 20 to 1—meaning the blood carries 5 to 20 molecules of urea for every one molecule of creatinine, and this is a pretty good diagnostic for looking at kidney function!

Ultimately the filtrate is turned into urine and is excreted from the kidney through the ureter, into the bladder, and peed away. Meanwhile, the filtered blood drains into the renal vein. 

Alright so prerenal kidney injury is due to a decreased blood flow into the kidneys. 

So if you’ve got your body fluid, with fluid in ci]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_azotemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BIAW2jLBSnS55UXjazxAAmAhQCGDPncm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal azotemia]]></video:title><video:description><![CDATA[Acute kidney injury, or AKI, is when the kidney isn’t functioning at 100% and that decrease in function develops relatively quickly, typically over a few days. Actually, AKI used to be known as acute renal failure, or ARF, but AKI is a broader term that also includes subtle decreases in kidney function. 

AKI can essentially be split into three types, prerenal AKI meaning the cause of kidney injury’s coming before the kidneys, postrenal AKI—meaning after the kidneys, or intrarenal AKI—meaning within the kidneys. 

Now the kidney’s job is to regulate what’s in the blood, so they might remove waste, or make sure electrolyte levels are steady, or regulate the overall amount of water, and even make hormones - the kidneys do a lot of stuff! 

Blood gets into the kidney through the renal artery, into tiny clumps of arterioles called glomeruli where it’s initially filtered, with the filtrate, the stuff filtered out, moving into the renal tubule. 

Sometimes fluid or electrolytes can move back from the filtrate into the blood - called reabsorption, and sometimes more fluid or electrolytes can move from the blood to the fitrate - called secretion. 

Along with fluid and electrolytes, though, waste-containing compounds are also filtered, like urea and creatinine, although some urea is actually reabsorbed back into the blood, whereas only a little bit of creatinine is reabsorbed. 

In fact, in the blood, the normal ratio of blood urea nitrogen, or BUN, to creatinine is between 5 and 20 to 1—meaning the blood carries 5 to 20 molecules of urea for every one molecule of creatinine, and this is a pretty good diagnostic for looking at kidney function! 

Ultimately the filtrate is turned into urine and is excreted from the kidney through the ureter, into the bladder, and peed away. Meanwhile, the filtered blood drains into the renal vein. 

Typically intrarenal AKI’s due to damage to the tubules, the glomerulus, or the interstitium—the space between tubules. Starting with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Jaundice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QiMAJDz-QCK-g_gVJui_YXFeTa2OT2wd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Jaundice]]></video:title><video:description><![CDATA[Jaundice, which doesn’t have the most intuitive name, comes from the french jaunice, meaning yellowing. 

It’s also sometimes referred to as icterus though, the origin of which is even less intuitive, coming from the thought that jaundice could once be cured by looking at a yellow bird, the more you know! 

Anyways, as you’ve probably gathered, jaundice involves someone taking on yellow pigments, specifically in the skin and eyes. 

The yellowing pigment is caused by a compound called bilirubin, a component of bile and the main cause of bruises being yellow, and after its metabolism, the yellow-ness of urine and brown-ness of feces.

So since bilirubin’s our main culprit of yellow-ness, it’s super important to know where it comes from. 

As red blood cells near the end of their lifespan—which is about 120 days—they’re eaten up or phagocytosed by macrophages in the reticuloendothelial system, aka the macrophage system, where the spleen plays the largest part, but it’s also made of parts of the lymph nodes. 

K so first the macrophage eats up the blood cell, and hemoglobin is broken up into heme and globin, the globin is further broken into amino acids. 

The heme on the other hand is split into iron and protoporphyrin, protoporphyrin is then converted into unconjugated bilirubin, or UCB. 

Unconjugated bilirubin is the form of bilirubin that’s lipid-soluble, meaning it’s not water-soluble, sometimes it’s also known as indirect bilirubin. 

Albumin in the blood then binds to UCB and gives it a lift over to the liver where it’s taken up by hepatocytes, where it’s conjugated by an enzyme called uridine glucuronyl transferase (UGT), making it now water soluble. 

At this point the conjugated bilirubin is secreted out the bile canaliculi where it drains into the bile ducts and sent to the gallbladder for storage as bile. 

Now when you eat a donut or something, your gallbladder secretes the bile and CB, it moves through the common bile duct to the duodenum of th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_agenesis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c_Uz8LTzTCmDtgTrl1zXBoFeQMGKI2At/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal agenesis]]></video:title><video:description><![CDATA[Alright, so renal agenesis—genesis is the origin or formation of something, and the prefix a means not, and renal refers to the kidneys, so renal agenesis is when the kidneys don’t form. Since there are two kidneys, renal agenesis can refer to just one kidney not developing, called unilateral renal agenesis, or URA, or neither kidney developing, called bilateral renal agenesis, or BRA.

Alright so during fetal development, first off, you’ve got this structure called the mesonephric duct which is involved in development of urinary and reproductive organs, and during the 5th week of gestation, a little guy called the ureteric bud starts pushing its way into another structure called the metanephric blastema, and together, these two little embryologic structures go on to develop into a kidney. At about the 7th week, nephrogenesis, or formation of the kidneys, starts under the influence of that ureteric bud. 

By about 20 weeks, the ureteric bud has formed the ureters, the renal calyces, collecting ducts, and collecting tubules, while the metanephric blastema develops into the nephron itself, which includes the epithelial cells and the podocytes of the Bowman’s capsule.

In the third trimester and throughout infancy, the kidneys continue to grow and mature.

With renal agenesis, the ureteric bud fails to induce development of the metanephric blastema, and so either one or both kidneys don’t develop. Although not completely known, it’s thought that this is a result of a combination of genetic as well as in utero environmental factors like toxins and infections. 

Newborns with unilateral renal agenesis are usually asymptomatic if the other kidney’s otherwise healthy. Now that one kidney’s doing all the filtering, though, over time unilateral renal agenesis can lead to hypertrophy, or growth of the kidney, which later in life can increase the risk of hypertension as well as renal failure.

Alright so let’s move to bilateral agenesis, which is where there are no k]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hirschsprung_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oPB22yOWSZGJ34_2cdw8Lw18TsagAf8C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hirschsprung disease]]></video:title><video:description><![CDATA[Hirschsprung disease is also known as congenital aganglionic megacolon, so Hirschsprung’s is a disease that’s present since birth, in which a ganglion, or cluster of nerves is missing, which ultimately leads to a blocked colon, causing it to enlarge.

Alright, so the intestines move waste through the bowels via peristalsis, which is this series of coordinated wave-like muscle contractions that helps move feces in one direction, and this is essentially automatic, happening without you even having to think about it. 

The type of muscle that causes these contractions is smooth muscle, as opposed to skeletal muscle or cardiac muscle.

In the gut, there’s a layer of smooth muscle just under the submucosa, which sits under the mucosa, which is the innermost layer of the gut nearest to the lumen. 

On the other side of the smooth muscle layer is the serosa. 

Now if we look closer at the smooth muscle layer, it’s actually composed of the circular muscle layer, arranged in circular rings which contract and constrict the gut behind the feces, which keeps it from moving backward, while the longitudinal muscle layer, arranged along the length of the gut, relaxes which lengthens and therefore pulls things forward.

Also though, within these layers are two plexuses, or networks of nerves, which are made up of ganglia—which are clusters of individual nerves, which help coordinate muscle contraction and relaxation. 

First there’s the myenteric plexus, also known as Auerbach’s plexus, which when activated, primarily causes smooth muscle relaxation. 

The myenteric plexus connects with the second plexus—the submucous plexus, or also known as Meissner’s plexus, which is buried in the submucosa and is responsible for helping to control blood flow and epithelial cell absorption and secretion. 

These groups of nerves are clearly super important for normal bowel function. 

For people with Hirschsprung’s disease, both these plexuses are gone—they’re completely absent in some]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bulimia_nervosa</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nF5OqeA4QkaY7X0zit2apw5-TPKozc7E/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bulimia nervosa]]></video:title><video:description><![CDATA[Bulimia nervosa, or simply bulimia, is a condition characterized by rapid, out-of-control binge eating beyond the point of fullness or comfort, followed by compensatory behaviors to prevent weight gain. These include self-induced vomiting, fasting, excessive exercise, or misuse of laxatives or diuretics. To fit the diagnosis, cycles of binge eating and inappropriate compensatory behaviors must repeat consistently at least once a week for 3 months, though they can occur several times per day.  

Bulimia usually begins in adolescence or young adulthood, usually in individuals with low self-esteem who focus heavily on their body shape and weight when evaluating themselves. Often, they experience poor emotional regulation, as well as traits of impulsivity, perfectionism, or compulsivity, which contribute to the condition.  

Now, in bulimia nervosa, you can think of binge eating as an unhealthy way of coping with stress and overwhelming emotions. After binge eating, individuals use inappropriate compensatory behaviors to &amp;quot;fix&amp;quot; what they&amp;#39;ve done and prevent weight gain. Most commonly, they turn to self-induced vomiting, which is also known as purging.  

Additionally, they may try to control their weight in other ways, like taking stimulants, following calorie restrictive diets, fasting, or exercising too much. However, when a person reduces calorie intake, they trigger feelings of hunger, increasing the likelihood of additional binge eating episodes, which in turn trigger compensatory behaviors and further caloric restriction. In other words, instead of “fixing” the problem, these behaviors only keep the cycle going. 

Now, it’s important not to confuse bulimia nervosa with another eating disorder—anorexia nervosa. The main distinction between the two is that people with anorexia nervosa have an intense fear of gaining weight, so they end up restricting their energy intake to the point of significant weight loss. Eventually, this l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multicystic_dysplastic_kidney</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/de1xBR1wTauJ5RmLkr33ONMSTs_7k8LM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multicystic dysplastic kidney]]></video:title><video:description><![CDATA[Multicystic dysplastic kidney or MCDK is a congenital disease where one or both kidneys don’t form quite right, specifically causing them to not drain urine properly, which results in urine building up in the kidneys and forming multiple fluid-filled sacs called cysts.

Alright so during fetal development, first off you’ve got this structure called the mesonephric duct which is involved in development of urinary and reproductive organs, and during the 5th week of gestation, a little guy called the ureteric bud starts pushing its way into another structure called the metanephric blastema, and together, these two little embryologic structures go on to develop into a kidney. 

At about the 7th week, nephrogenesis, or formation of the kidneys, starts under the influence of that ureteric bud. 

By about 20 weeks, the ureteric bud has formed the ureters, the renal calyces, collecting ducts, and collecting tubules, while the metanephric blastema develops into the nephron itself, which includes the epithelial cells and the podocytes of Bowman’s capsule.

In the third trimester and throughout infancy, the kidneys continue to grow and mature.

Although not completely known, it’s thought that MCDK is a result of some sort of abnormal induction of the metanephric blastema by the ureteric bud. 

This failure might be the fault of the mesonephric duct not forming right, or the ureteric bud not forming right, or both. 

Regardless of the cause of failure, the ureteric bud is supposed to go on to form the ureters as well as the rest of the tubules that branch out to collect urine. 

So as blood starts coming in to be filtered, and urine starts getting produced, a failure to properly develop into these urine-collecting tubules means that the urine has nowhere to go, and so it builds up in the kidneys and forms these fluid-filled cysts that are composed of abnormal connective tissue—especially cartilage—that actually replaces normal kidney tissue and decreases the kidney’s ability to function. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cluster_B_personality_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oQIu6fxqTgyDm9KY35TcD8WVSxmrebtQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cluster B personality disorders]]></video:title><video:description><![CDATA[If you were asked to describe a friend’s personality, you might describe them as generally being a creative type, or easy-going but nervous in groups. 

Basically, you’re trying to summarize the personal traits that make them who they are—either how they think or how they act. 

Sometimes these thought patterns or behaviors which make up a person’s personality can actually be harmful in the sense that they interfere with their day-to-day functioning in their personal life, at work, or in social settings. 

If this were the case, we would say that the individual has a personality disorder. 

The DSM-5, or the diagnostic and statistical manual for mental disorders, the 5th edition, lists ten personality disorders that are split into three different ‘clusters’, referred to as clusters A, B, and C. 

These used to be under the category “Axis 2” but that way of organizing isn’t really used anymore.

Cluster B includes antisocial personality disorder, borderline personality disorder, histrionic personality disorder, and narcissistic personality disorder. 

All four of these have a genetic relationship with mood disorders- like depression and bipolar disorder, as well as substance use disorders. 

Okay, so antisocial personality disorder—this sounds like they don’t get along well with others, but in fact, it’s the opposite, they can be really charming and often use that to manipulate others for their personal gain. 

These individuals disregard moral values and societal norms, have little empathy, and poor impulse control. 

This combination makes them willing to hurt others if it helps them, making them prone to aggressive and unlawful behavior, at times earning the label sociopath or psychopath. 

In fact, individuals with this disorder tend to be overrepresented in prison populations and have higher rates of substance use. 

These individuals typically fail to show remorse or guilt and rarely accept responsibility for any of the harm that they cause others. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cluster_A_personality_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DyvOWDm8TASrW88_wezzDwwgS8uF4ity/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cluster A personality disorders]]></video:title><video:description><![CDATA[If you were asked to describe a friend’s personality, you might describe them as generally being a creative type, or easy-going but nervous in groups. 

Basically, you’re trying to summarize the personal traits that make them who they are—either how they think or how they act. 

Sometimes these thought patterns or behaviors which make up a person’s personality can actually be harmful in the sense that they interfere with their day-to-day functioning in their personal life, at work, or in social settings. 

If this were the case, we would say that the individual has a personality disorder. 

The DSM5, or the diagnostic and statistical manual for mental disorders lists ten personality disorders that are split into three different ‘clusters’- referred to as clusters A, B, and C. 

These used to be under the category “Axis 2” but that way of organizing isn’t used anymore.

Alright so cluster A personality disorders are characterized by “odd and eccentric thinking or behavior” such as believing in aliens or the Tooth Fairy at an adult age. 

They include paranoid personality disorder, schizoid personality disorder, and schizotypal personality disorder, each with its own specific thought patterns and behaviors. 

Paranoid personality disorder describes someone who is accusatory or generally distrustful and suspiciousness of other people without really having a reason to do so, and assumes that others will disappoint them, manipulate them, or talk about them behind their back.

Because of this, they think excessively about making sure that they have the loyalty of their friends and family. 

These beliefs are so strong that they wind up affecting the way individuals act. 

These people react severely if they feel that they have been lied to, or slighted in any way, which can result in their holding grudges for long periods of time. 

In many ways, this behavior can totally affect the individual’s work, family life and the way they relate to those around]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cystic_fibrosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/miLHpGk_QZG8QBl-cPR3UFzIT5Gj6zAE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cystic fibrosis]]></video:title><video:description><![CDATA[You’re probably aware that cystic fibrosis, or CF, is a genetic disorder that affects the lungs, but that’s only part of the story. 

In fact, the name “cystic fibrosis,” refers to the disease’s effects on the pancreas, where it can lead to cysts, which are fluid-filled sacs wrapped in a membrane and fibrosis—excess deposition of connective tissue that can replace or infiltrate normal tissue in an organ. 

CF is an autosomal recessive disorder involving the CFTR gene, which stands for “cystic fibrosis transmembrane conductance regulator,” and this gene codes for the CFTR protein. 

CF develops when there’s a mutation in the CFTR gene, but because it’s autosomal recessive, you need to inherit two mutated CFTR genes, one from mom and one from dad. 

Now if mom and dad both have one copy of the mutated gene and one normal gene, they’re considered carriers and don’t have the disease. 

Inheriting CF is more common in people of European descent. 

The CFTR protein is a channel protein that pumps chloride ions into various secretions, those chloride ions help draw water into the secretions, which ends up thinning them out.

The most common mutation is the “∆F508” mutation. 

Delta means a deletion, and the F (which can also be written as “Phe”) is short for phenylalanine, and the 508 is the five hundred and 8th amino acid in the CFTR protein. 

So, the ∆F508 mutation is where the 508th amino acid out of 1480, phenylalanine, is deleted and missing. 

This CFTR protein with the ∆F508 mutation gets misfolded and can’t migrate from the endoplasmic reticulum to the cell membrane, meaning there’s a lack of CFTR protein on the epithelial surface, and this means that it can’t pump chloride ions out, which means water doesn’t get drawn in, and the secretions are left overly thick.

In a newborn, thick secretions can affect the baby’s meconium, or first stool, or, which can get so thick and sticky that it might get stuck in the baby’s intestines and not come out, and this]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Post-traumatic_stress_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jHK9NQS_RciBMADlVPUo58CiTg6JJ7tt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Post-traumatic stress disorder]]></video:title><video:description><![CDATA[Post-traumatic stress disorder, also called PTSD, happens when some memory of a past traumatic event—like war or sexual assault—causes recurrent mental and physical distress. 

Now the Diagnostic and Statistical Manual 5th edition or the DSM 5 categorizes PTSD as a “trauma-and-stressor-related-disorder” that happens when the symptoms of an acute stress response persist for over a month. 

The main symptoms are psychological ones, for example someone might re-experience their trauma through nightmares, flashbacks, and intrusive thoughts, but these can lead to behavioral changes as well. 

Somebody might start to avoid environments and situations that remind them of their trauma and feel a sense of hypervigilance where they are constantly on guard or hyperarousal where they have this exaggerated startle response to the smallest of triggers. 

Not surprisingly, all of these thoughts and behaviours can lead to trouble sleeping and general irritability, which can lead to angry outbursts. 

Interestingly, this pattern is different for young children who are less likely to show distress, but instead they might use play to express their memories, sometimes acting out scenes that trouble them. 

Whether or not someone develops PTSD in response to trauma is determined by a number of different factors. 

For example, it’s clear that interpersonal trauma, like rape or violent muggings, are more likely to result in PTSD than accidents or environmental disasters.

In addition, people that go through extreme trauma as children are more likely to develop PTSD in response to other traumas faced in their adult life. 

Having said that, if someone manages to develop effective coping strategies for trauma including having a social support network, then that can help with future traumas as well. 

As far as causes go, there are some clues about biological factors related to development of PTSD. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cleidocranial_dysplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gO42df1EQe_0vhY_XOjApkvORiSWT8OU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cleidocranial dysplasia]]></video:title><video:description><![CDATA[In the Netflix series “Stranger Things”, the character Dustin’s missing a few teeth, and he says [“I’ve told you a million times! My teeth are coming in! It’s called cleidocranial dysplasia!”], he’s then asked to [“do the arm thing...CRACK—GROANS”]. 

Both Dustin and his real-life counterpart—Gaten Matarazzo—have a rare genetic condition—cleidocranial dysplasia or sometimes cleidocranial dysostosis. 

“Cleido-” means “clavicle”, which is the collarbone, and “-cranial” refers to the skull, “dys-” means abnormal, and “-plasia” means formation. 

So people with cleidocranial dysplasia usually have underdeveloped or missing collarbones, which gives them a wide range of shoulder movement, as well as abnormalities in other bones, especially the skull bones including the jaw, which can result in delayed eruption of the teeth.

Now cleidocranial dysplasia, or CCD, is a rare congenital disorder—meaning present since birth—and it’s caused by a mutation in a gene on chromosome 6, located at 6p21, which means chromosome 6, the short arm, or P, region 2, band 1. 

The gene’s called CBFA1 or RUNX2, so let’s just go with RUNX2. 

RUNX2 mutations are inherited in an autosomal dominant pattern, meaning if one parent has the disorder and one doesn’t, 50% of their offspring will inherit the disorder and 50% won’t. 

Those that inherit the disorder end up with one chromosome that has the mutation and one normal chromosome in every cell, and having just one chromosome with the mutation is enough to cause the disorder. 

Sometimes, though, the mutation might be sporadic, meaning it wasn’t inherited from the parents, but it’s a new mutation that just pops up in one of the children.

This RUNX2 gene encodes for a specific RUNX2 protein that acts as a transcription factor. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Minimal_change_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4sOW7SpRR-G5GPXPizOfBENXSKidg1vS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Minimal change disease]]></video:title><video:description><![CDATA[Minimal-change disease, sometimes called nil disease, affects the millions of the kidney’s glomeruli, which are the specific parts of the kidney where small molecules are first filtered out of blood and into the urine. 

Specifically, it’s a type of nephrotic syndrome, in fact, the most common nephrotic syndrome seen in children.

But what exactly is nephrotic syndrome? Well usually the glomerulus only lets small molecules—like sodium and water—move from the blood into the kidney nephron where it eventually make its way into the urine. 

But with nephrotic syndromes, the glomeruli are damaged and they become more permeable, so they start letting plasma proteins come across from the blood to the nephron and then into the urine, which causes proteinuria—typically greater than 3.5 grams per day. 

An important protein in the blood is albumin, and so when it starts leaving the blood, people get hypoalbuminemia—low albumin in the blood. 

With less protein in the blood the oncotic pressure falls, which lowers the overall osmotic pressure, which drives water out of the blood vessels and into the tissues, called edema. 

Finally, it’s thought that as a result of either losing albumin or losing some protein or proteins that inhibit the synthesis of lipids—or fat—you get increased levels of lipids in the blood, called hyperlipidemia. 

Just like the proteins, these lipids can also get into the urine, causing lipiduria. 

And those are the hallmarks of nephrotic syndrome—proteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.

Okay, so minimal change disease is a type of nephrotic syndrome—got it, but how exactly do those glomeruli start letting plasma proteins like albumin through? 

Well, usually, in the glomerulus, you’ve got your endothelial cells lining the capillaries, then the basement membrane, and then the podocytes, which are the cells that have these long tentacle-like projections, called foot processes, and this is also why they’re called podocytes since podo refers to the foot. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cluster_C_personality_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ikm9sj1bQ86byb95KZvz2Cr7RIabnwof/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cluster C personality disorders]]></video:title><video:description><![CDATA[If you were asked to describe a friend’s personality, you might describe them as a creative type, or easy-going but nervous in groups. 

Basically, you’re trying to summarize the personality traits that make them who they are—either how they think or how they act. 

Sometimes these thought patterns or behaviors which make up a person’s personality can actually be harmful in the sense that they interfere with their day-to-day functioning in their personal life, at work, or in social settings. 

If this were the case, we would say that the individual has a personality disorder. 

The DSM-5 lists ten personality disorders that are split into three different “clusters”: A, B, and C. 

These used to be under the umbrella of “Axis 2” but that way of organizing isn’t really used anymore.

Cluster C personality disorders include avoidant personality disorder, obsessive compulsive personality disorder, and dependent personality disorder. 

As you can probably guess, they all have a genetic association with anxiety disorders. 

Let’s start with avoidant personality disorder. 

Individuals with this disorder tend to be shy, timid, and socially inhibited, with extremely low self-esteem, seeing themselves as incapable, inadequate, and undesirable. 

These individuals often want close relationships with others, but rarely take social risks, and avoid social situations, which makes it hard for them to meet new people.

People with this disorder can be hypersensitive to rejection and negative feedback, becoming even more withdrawn when that happens. 

There is overlap between avoidant personality disorders and social phobias, but one key difference is that social phobias tend to be focused on anxiety of specific situations like public speaking or dancing in public, while avoidant personality disorder is defined by an anxiety of social situations more generally.

Next we’ve got obsessive compulsive personality disorder (OCPD), which is where individuals are obsessed with o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Measles_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9u-epNkETPScopZLcXwbCDpbRwyjXd2s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Measles virus]]></video:title><video:description><![CDATA[Measles is one of the most contagious infectious diseases, and remains a leading cause of death particularly among young children, especially in areas with low rates of vaccination. 

Measles is also called rubeola, which can easily get confused with German measles which is also called rubella—similar sounding names but very different viruses.

Regular measles is caused by the measles virus, seriously, the species is the “measles virus”, of the genus Morbillivirus and family Paramyxoviridae. 

The reason why this guy’s so contagious is that it’s airborne, and spreads via tiny liquid particles that get flung into the air when someone sneezes or coughs, and can live for up to two hours in that airspace or nearby surfaces.

If someone breathes in that air or touches a surface and then touches their eyes, their eyes, or their mouths, they can become infected. 

Measles is so contagious that if one person has it, 90% of nearby non-immune people will also become infected.

Once the measles virus gets onto the mucosa of an unsuspecting person, it quickly starts to infect the epithelial cells in the trachea or bronchi. 

Measles virus uses a protein on its surface called hemagglutinin, or just H protein, to bind to a target receptor on the host cell, which could be CD46, which is expressed on all nucleated human cells, CD150, aka signaling lymphocyte activation molecule or SLAM, which is found on immune cells like B or T cells, and antigen-presenting cells, or nectin-4, a cellular adhesion molecule.

Once bound, the fusion, or F protein helps the virus fuse with the membrane and ultimately get inside the cell. 

Now this virus is a single-stranded RNA virus, and it’s also a negative sense, meaning it first has to be transcribed by RNA polymerase into a positive-sense mRNA strand. 

After that it’s ready to be translated into viral proteins, wrapped in the cell’s lipid envelope, and sent out of the cell as a newly made virus. 

Within days, the measles virus spread]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Focal_segmental_glomerulosclerosis_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vcr3iwEYQUuTudkHMVkSWdk-QZGxyWkC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Focal segmental glomerulosclerosis (NORD)]]></video:title><video:description><![CDATA[Focal segmental glomerulosclerosis, or sometimes focal glomerular sclerosis, or just sometimes FSGS, is a type of kidney disease that affects the kidney’s glomeruli, which is where small molecules are first filtered out of blood and into the urine. 

From the name, you have glomerulosclerosis, which indicates sclerosis, or scar tissue, forming  in the glomeruli. 

Segmental means that only a segment, or part of the glomeruli is affected, and focal means that among all those glomeruli in the kidney, only some are affected. 

Those glomeruli that are affected, though, allow proteins to filter through into the urine, and ultimately people with FSGS develop nephrotic syndrome. 

But what exactly is nephrotic syndrome? Well usually the glomerulus only lets small molecules, like sodium and water, move from the blood into the kidney nephron, where it eventually makes its way into the urine. But with nephrotic syndromes, the glomeruli are damaged and they become more permeable, so they start letting plasma proteins come across from the blood to the nephron and then into the urine, which causes proteinuria, typically greater than 3.5 grams per day.

An important protein in the blood is albumin, and so when it starts leaving the blood, people get hypoalbuminemia—low albumin in the blood. 

With less protein in the blood the oncotic pressure falls, which lowers the overall osmotic pressure, which drives water out of the blood vessels and into the tissues, called edema. 

Finally, it’s thought that as a result of either losing albumin or losing some protein or proteins that inhibit the synthesis of lipids, or fat, you get increased levels of lipids in the blood, called hyperlipidemia. 

Just like the proteins, these lipids can also get into the urine, causing lipiduria. 

And those are the hallmarks of nephrotic syndrome—proteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.

So focal segmental glomerulosclerosis is a type of nephrotic syndrome, that’s he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Huntington_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pUVvQtvcRFag3uNl0vzLCQIST42pV6GL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Huntington disease]]></video:title><video:description><![CDATA[Huntington disease, or HD, is a rare neurodegenerative disease that involves a repeated sequence of DNA that causes an abnormal protein to form, leading to abnormal movements and cognitive problems. 

Huntington disease is an autosomal dominant genetic disorder, which means that one affected copy of a gene is enough to cause disease. Affected people are typically present in each generation, because an affected person (male or female) has a 50% chance of passing on the affected gene to a child, which causes that child to have the disease. 

In most people, a gene called huntingtin or HTT on chromosome 4, contains a triplet repeat, where the nucleotides C, A, and G are repeated 10-35 times in a row. In people with Huntington disease, this repeat goes on for 36 or more times in a row. CAG codes for the amino acid glutamine, so people with Huntington disease patients will have 36 or more glutamines in a row in the huntingtin protein. So, in addition to being a triplet repeat disorder, HD is, more specifically, a “polyglutamine” disease. 

The specific way in which extra glutamines cause HD symptoms isn’t fully worked out, but some clues are that the mutated protein aggregates within the neuronal cells of the caudate and putamen of the basal ganglia causing neuronal cell death. Cell death might be related to excitotoxicity – which is excessive signaling of these neurons, which leads to high intracellular calcium.

The expanded CAG repeats not only affect the huntingtin protein – they affect DNA replication itself. When copying the HTT gene, DNA polymerase can basically lose track of which CAG it’s on and accidently add extra CAGs. Since as a zygote develops into a fetus and eventually into a full adult, by the time sperm and eggs are created, several dozen cell divisions, each with a round of DNA replication have taken place, and so there have already been ample opportunities for repeat expansion, and the more repeats that’re added, the more unstable it gets.

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Membranoproliferative_glomerulonephritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cEKpxVZXQV213-vPoOJi5ZXTTTa-zx_2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Membranoproliferative glomerulonephritis]]></video:title><video:description><![CDATA[Membranoproliferative glomerulonephritis, or MPGN, is a kidney disease triggered by immune deposits which end up in the walls of the glomerulus, which are the tufts of capillaries where blood is filtered. 

These deposits lead to inflammation and result in structural changes to the glomerulus, that cause a decrease in kidney function, which commonly presents as a nephrotic syndrome.

But what exactly is nephrotic syndrome? Well usually the glomerulus only lets small molecules, like sodium and water, move from the blood into the kidney nephron, where it eventually makes its way into the urine. But with nephrotic syndromes, the glomeruli are damaged and they become more permeable, so they start letting plasma proteins come across from the blood to the nephron and then into the urine, which causes proteinuria, typically greater than 3.5 grams per day.

An important protein in the blood is albumin, and so when it starts leaving the blood, people get hypoalbuminemia—low albumin in the blood. 

With less protein in the blood the oncotic pressure falls, which lowers the overall osmotic pressure, which drives water out of the blood vessels and into the tissues, called edema. 

Finally, it’s thought that as a result of either losing albumin or losing some protein or proteins that inhibit the synthesis of lipids, or fat, you get increased levels of lipids in the blood, called hyperlipidemia. 

Just like the proteins, these lipids can also get into the urine, causing lipiduria.

And those are the hallmarks of nephrotic syndrome—proteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.

Okay so membranoproliferative glomerulonephritis is a type of nephrotic syndrome, got it. But how exactly do these glomeruli start letting plasma proteins like albumin through? Well, with MPGN, there are actually three types, so let’s go through one by one. 

Type I MPGN is the most common form, and it usually starts one of two ways. The first way involves circulating immune ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Narcolepsy_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FZO4woicSkiPDFFw812m9lyUTHORAW4f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Narcolepsy (NORD)]]></video:title><video:description><![CDATA[At one time or another you’ve probably had to force yourself to stay awake, maybe while driving or when you’re in a looong lecture. In these situations, you were exerting control over your sleep-wake cycles. Narcolepsy is a disorder in which the ability to regulate sleep-wake cycles is impaired, so the normal boundaries between sleeping and being awake are weak, leading to frequent lapses into sleep and the occurrence of elements of sleep while a person is awake. 

In a deep part of the brain called the hypothalamus, there is a special group of neurons that help stabilize wakefulness and sleep. These neurons produce the neurotransmitters orexin A and B, also called hypocretin 1 and hypocretin 2, which connect to key sites in the brainstem and elsewhere that regulate wake and sleep states. Specifically, orexins have an excitatory effect, which helps stabilize wakefulness across the day, and sleep throughout the night. 

In individuals with the classic form of narcolepsy, an autoimmune process kills off nearly all the orexin-producing neurons during adolescence, resulting in five key symptoms: daily sleepiness despite adequate sleep at night; episodes of muscle weakness known as cataplexy; an inability to move at the start or end of sleep; vivid hallucinations at the start or end of sleep; and fragmented sleep.  

Sleepiness is usually the most challenging symptom. People with narcolepsy can doze off with little warning, usually when sitting down, like in a class or while working at a computer, but they generally don’t sleep more than healthy people in a given 24 hour period. Most individuals with narcolepsy find that a short, 15-minute nap substantially improves their alertness for a few hours, which suggests that the sleepiness of narcolepsy is caused by a problem with the brain circuits that normally promote full alertness, rather than poor quality or insufficient sleep. Normally when a healthy person goes to bed, they go through a sleep cycle lasting an ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Achondroplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zPuGx_YgR5KGyCKMEsRS6oJYS_CSd-k8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Achondroplasia]]></video:title><video:description><![CDATA[In HBO’s adaptation of Game of Thrones, the character Tyrion Lannister is treated poorly by his father and siblings because he is born with dwarfism.

In a classic scene in the show, he says [“I’m guilty of being a dwarf! [father says: You’re not on trial for being a dwarf] Oh! Yes I am, I’ve been on trial for that my entire life]. 

Both Tyrion and his real-life counterpart—Peter Dinklage—have achondroplasia, an autosomal dominant genetic condition which is the most common cause of dwarfism and results from a heterozygous mutation in a gene called FGFR3, or fibroblast growth factor receptor 3, on chromosome 4, which codes for FGFR3 protein. 

When FGFR3 protein binds fibroblast growth factors, or FGFs, it slows down the growth of certain bones. 

The mutation causing achondroplasia is almost always the 380th amino acid, which is glycine, getting swapped out for arginine in the FGFR3 protein, and this swap causes the FGFR3 receptor to be constitutively active, which means constantly, active. 

In other words, the mutation makes the receptor behave as though it’s binding an FGF even when it’s not, which sends a strong signal to inhibit bone growth.

More specifically, FGFR3 that is “always on” causes chondrocytes at the growth plate to proliferate slowly and become disorganized. 

So, because of this it mostly affects endochondral bone formation, which is the process of bone forming right on previously-laid-down cartilage matrix, which causes the bone to elongate. 

With the mutation though, this elongation is inhibited, which means long bones like the humerus and phalanges are affected. 

Alright so the mutation affects endochondral bone formation, but bones that are products of intramembranous bone formation are way less affected. 

This is where bone grows without an existing cartilage matrix. 

This includes flat bones like the skull and ribs. Also an intramembranous process is appositional growth, which is the process of widening of long bones, so that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testing_effect</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aQyLc8W7QR_N2glhqSAMPYqARf6Vl48a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Testing effect]]></video:title><video:description><![CDATA[Let’s say you have a big exam coming up and you need to review the material—what would be the best way for you to study? 

Well you might think that you should re-read the textbook or look over your notes, but it turns out that one of the most effective ways to study is by testing yourself on the material. 

In other words, the mere act of answering questions will strengthen memory—a  phenomenon that is called the Testing Effect, or sometimes test-enhanced learning or retrieval practice.

This phenomenon happens for a number of reasons. 

One is that active learning is better than passive learning. 

When we read a textbook chapter or re-read our notes, we are engaging with the material in a relatively passive way. 

We like to think that we are information sponges—that we absorb the knowledge as it passes by our eyes—but it turns out that real learning happens when we actively engage with the material—for example, when we think about how it relates to other material we’ve learned or are learning. 

Actively thinking about the material increases the likelihood that we will recall the information when we need it later on—like on an exam.

In fact, the more actively you can engage with the material—the better.

Research has shown that you should take the time to test yourself in ways that force you to struggle with the material, rather than just focusing on plain recall. 

The benefits of testing are largest when the questions are complex and you really need to work to come up with the answer.

Another reason has to do with the dynamics of recalling.  

In order to answer a question on a test you have to search through your memory and retrieve the answer, right? 

Well, it turns out that—at least in one respect—your memory is more like a muscle than like a filing cabinet.  

When you first rode a bike you probably fell a lot, and your movements were rough and wobbly, but with practice, the movements become easier and smoother. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bruxism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I-yDaYXpQa_UXQmUz34uWTr3Q3Osssdl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bruxism]]></video:title><video:description><![CDATA[When people are stressed they sometimes clench their jaw and grind their teeth. 

This is called bruxism. Bruxism can happen day or night, with episodes sometimes lasting a few days, but other times going on for months. 

Usually, it’s long-term teeth-grinding that can really cause problems.

Grinding the top and bottom teeth together can lead to something called dental abfraction. 

This loss of tooth structure and general dental attrition occurs as the biting surfaces of each tooth are flattened out. 

Over time, this can wear away the protective outer surface of the tooth, called the enamel, revealing the much more sensitive dentin below, leading to tooth hypersensitivity and increased risk of cavities.

In its most severe forms, bruxism can even cause teeth to fracture, loosen, or even fall out, and the constant grinding can also cause damage to existing dental work like crowns and fillings. 

Occasionally people with bruxism bite their tongue as well, which can lead to a crenated or scalloped tongue marked by tooth-shaped indentations. 

People with bruxism sometimes have canker sores from chewing their lips and inner cheeks, too.

Bruxism can also lead to temporomandibular joint disorder, or TMJ, which involves the temporalis, masseter, and pterygoid muscles; these muscles help with chewing by working together to move the mandible or jawbone. 

Clenching these muscles over and over can be tiring and painful, particularly in the preauricular area right in front of the ear, causing headaches around the temples. 

Bruxism can also lead to inflammation of the periodontal ligaments, the tiny ligaments that attach each tooth to the bony socket they’re nestled in, which can make chewing quite painful. 

Finally the repeated clenching can cause the chewing muscles to hypertrophy or grow, which worsens the grinding action by making it more powerful and therefore more painful.

Bruxism is an unconscious behavior.

When it happens at night it’s called “sleep br]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Membranous_nephropathy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/61jz223rSVy4dfLV345lITw-Ro6-N4KS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Membranous nephropathy]]></video:title><video:description><![CDATA[Membranous glomerulonephritis, also known as membranous nephropathy, is where the glomerular basement membrane, or GBM, which lines the glomeruli in the kidney, becomes inflamed and damaged, which results in increased permeability and proteins being able to filter through into the urine, causing nephrotic syndrome. 

But what exactly is nephrotic syndrome? Well usually the glomerulus only lets small molecules, like sodium and water, move from the blood into the kidney nephron, where it eventually makes its way into the urine. But with nephrotic syndromes, the glomeruli are damaged and they become more permeable, so they start letting plasma proteins come across from the blood to the nephron and then into the urine, which causes proteinuria, typically greater than 3.5 grams per day. 

An important protein in the blood is albumin, and so when it starts leaving the blood, people get hypoalbuminemia—low albumin in the blood. 

With less protein in the blood the oncotic pressure falls, which lowers the overall osmotic pressure, which drives water out of the blood vessels and into the tissues, called edema. 

Finally, it’s thought that as a result of either losing albumin or losing some protein or proteins that inhibit the synthesis of lipids, or fat, you get increased levels of lipid in the blood, called hyperlipidemia. 

Just like the proteins, these lipids can also get into the urine, causing hyperlipiduria.

And those are the hallmarks of nephrotic syndrome—proteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.

Alright, so with membranous glomerulonephritis, the basement membrane becomes damaged which causes nephrotic syndrome. How does this happen, though? Well, ultimately this damage is caused by immune complexes—complexes composed of an antigen with an antibody bound to it. 

One way these complexes can form is as a result of autoantibodies directly targeting the glomerular basement membrane. 

Two major antigen targets that’ve been identifi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Poststreptococcal_glomerulonephritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KNqPqDjQQBKIYvDrSalAeYb2RkKa_Cx6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Poststreptococcal glomerulonephritis]]></video:title><video:description><![CDATA[Poststreptococcal glomerulonephritis or PSGN is where the kidneys’ glomeruli, which is the location where small molecules are first filtered out of blood and into the urine, become inflamed after an infection by streptococcal bacteria.

Most commonly, PSGN starts with an infection by strains of group A beta-hemolytic streptococci bacteria, and this particular group of streptococcus has a specific antigen on its surface that lumps it into a group called “group A”. 

This group A streptococci also produces an enzyme called streptolysin, and when the bacteria is grown on a petri dish of blood, the enzyme completely lyses red blood cells that are near the bacterial colony—called beta-hemolysis. 

Beta-hemolysis is where they’re completely destroyed—as opposed to alpha-hemolysis, where cells aren’t actually destroyed, but they’re just damaged or bruised. 

Additionally, these strains are considered nephritogenic strains because they carry the M-protein virulence factor, a protein that essentially helps them get around host defenses. 

An infection by a nephritogenic strain of group A beta-hemolytic streptococcus bacteria initiates a type III hypersensitivity reaction, where immune complexes are formed, composed of antigens and antibodies, often IgG or IgM, that end up being carried in the bloodstream to the glomerulus and become trapped. 

Specifically these deposits end up in the glomerular basement membrane or GBM, and most of the time they’re subepithelial, meaning between the epithelial cells, or podocytes, and the basement membrane. 

It’s also possible the antigens from the bacteria are first trapped in the glomeruli, and then antibodies bind in the glomerulus itself. 

Either way, these complexes initiate an inflammatory reaction in the glomerulus, which involves activation and deposition of C3 complement, inflammatory cytokines, oxidants, and proteases that all damage the podocytes. 

This damage ends up allowing larger molecules to filter into the urin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postrenal_azotemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/48lRrutVQ0a3snZhSz557DH9SNu9TKfK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postrenal azotemia]]></video:title><video:description><![CDATA[Acute kidney injury, or AKI, is when the kidney isn’t functioning at 100% and that decrease in function develops relatively quickly, typically over a few days. Actually, AKI used to be known as acute renal failure, or ARF, but AKI is a broader term that also includes subtle decreases in kidney function. 

AKI can essentially be split into three types, prerenal AKI meaning the cause of kidney injury’s coming before the kidneys, postrenal AKI—meaning after the kidneys, or intrarenal AKI—meaning within the kidneys. 

Now the kidney’s job is to regulate what’s in the blood, so they might remove waste, or make sure electrolyte levels are steady, or regulate the overall amount of water, and even make hormones - the kidneys do a lot of stuff! 

Blood gets into the kidney through the renal artery, into tiny clumps of arterioles called glomeruli where it’s initially filtered, with the filtrate, the stuff filtered out, moving into the renal tubule. Sometimes fluid or electrolytes can move back from the filtrate into the blood - called reabsorption, and sometimes more fluid or electrolytes can move from the blood to the fitrate - called secretion. 

Along with fluid and electrolytes, though, waste-containing compounds are also filtered, like urea and creatinine, although some urea is actually reabsorbed back into the blood, whereas only a little bit of creatinine is reabsorbed. In fact, in the blood, the normal ratio of blood urea nitrogen, or BUN, to creatinine is between 5 and 20 to 1—meaning the blood carries 5 to 20 molecules of urea for every one molecule of creatinine, and this is a pretty good diagnostic for looking at kidney function!

Ultimately the filtrate is turned into urine and is excreted from the kidney through the ureter, into the bladder, and peed away. Meanwhile, the filtered blood drains into the renal vein. 

Alright, so with postrenal AKI, there’s some obstruction to the outflow from the kidneys. 

Reduced flow can be a result of something compr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disruptive,_impulse_control,_and_conduct_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m8MCOpbaQNCDEXPpTJ0cBmdxQlig5677/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disruptive, impulse control, and conduct disorders]]></video:title><video:description><![CDATA[The Diagnostic and Statistical Manual of Mental Disorders, the 5th edition, or DSM 5, has a relatively new category called “Disruptive, Impulse Control, and Conduct Disorders” or DIC for short, which were previously organized into different sections. This category includes a number of disorders like oppositional defiant disorder, conduct disorder, antisocial personality disorder, intermittent explosive disorder, as well as other impulse control disorders like the compulsive desire to start fires, or pyromania, and the compulsive desire to steal things, or kleptomania. The common thread that runs through all of these is that they all involve impulsive behaviors, or a lack of self-control. These disorders tend to start in childhood or adolescence, and persist into adulthood.    

Oppositional defiant disorder, or ODD, is defined by defiant behavior that’s both persistent and willful, and can be thought of in terms of emotional, behavioral, and cognitive patterns. People with ODD have emotional dysregulation which can lead them to feel irritable and resentful towards others. These emotions can lead to behaviors like frequent arguments, angry outbursts, and refusing to go along with the requests of authority figures - like teachers. People with ODD might even deliberately annoy their family or friends, purposefully defying anyone who tries to control their behavior. Cognitively, these people often fall into a pattern of vindictiveness and spitefulness, believing that others are to blame for their own behaviors. In order to meet the criteria for ODD, these emotional, behavioral, and cognitive patterns must be ongoing for at least 6 months, and must interfere with family, school, and other social interactions. 

Conduct disorder has a lot of overlap with oppositional defiant disorder with one key additional feature - aggressive behavior towards people and animals. For example, people with conduct disorder might violently destroy property, steal things, or hurt p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rapidly_progressive_glomerulonephritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eTtWBt72Q_i1JoDBuhiHsPVwRtK_XsaU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rapidly progressive glomerulonephritis]]></video:title><video:description><![CDATA[Crescentic glomerulonephritis, which is sometimes called rapidly progressive glomerulonephritis, is a type of nephritic syndrome, meaning it involves inflammation of the kidney’s glomeruli. 

This inflammation ultimately causes a proliferation of cells in the Bowman’s space, which forms a crescent shape and this change leads to renal failure relatively quickly—within weeks to months.

The development of crescents in Bowman’s space can happen in several ways. 

In some cases it’s the idiopathic, meaning there’s no identifiable cause. 

When the cause is identifiable, though, it can be split into several types. 

Type I is caused by anti-glomerular basement membrane, or GBM, antibodies, antibodies that target the GBM. 

Type I is associated with Goodpasture syndrome, which also involves pulmonary hemorrhages.

Type II is immune-complex-mediated, meaning caused by immune complexes, composed of antigens and antibodies. 

This might be the case with poststreptococcal glomerulonephritis, systemic lupus erythematosus, IgA nephropathy, and Henoch-Schonlein purpura. 

And finally type III is known as pauci-immune, meaning little or no anti-GBM antibodies or immune-complex deposits. 

In these cases, often anti-neutrophilic cytoplasmic antibodies or ANCAs are in the blood, which are autoantibodies against the body’s own neutrophils. 

Furthermore, you can break it down into the type of ANCA. C-ANCAs, or cytoplasmic ANCAs, are associated with Wegener granulomatosis. 

P-ANCAs or perinuclear ANCAs on the other hand are associated with microscopic polyangiitis and Churg-Strauss syndrome, the latter of which can be distinguished by having granulomatous inflammation, which is when immune cells attempt to wall off a substance perceived as foreign, asthma, and eosinophilia

Whatever the underlying cause is, the common feature is severe glomerular injury and the development of a crescent shape. 

Typically, as a result of cell-mediated immunity as well as macrophage involvement, the glomerular basement membrane breaks. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nephroblastoma_(Wilms_tumor)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_ytJgI8uSS2FDWWfgQF1VaX3Q3a76zhH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nephroblastoma (Wilms tumor)]]></video:title><video:description><![CDATA[Wilms’ tumor, or nephroblastoma, is a type of kidney tumor composed of metanephric blastemal cells, cells involved in kidney development, and is the most common malignant kidney tumor in children; only rarely is it seen in adults.

Wilms’ tumor is thought to be caused by mutations in genes responsible for normal genitourinary development, which includes the kidneys as well as the gonads, typically the genes are located around 11p13—which means chromosome 11, the short arm p, region 1, band 3. 

One gene critical for normal kidney and gonad development is WT1 (or Wilms’ Tumor 1), which a tumor suppressor gene. 

Mutations that result in a “loss of function” of WT1, like deletions, for example, seem to lead to the development of tumor cells seen with Wilms’ tumor. 

Wilms’ tumors as a result of WT1 mutations are sometimes part of a developmental syndrome, meaning other abnormalities are present as well, likely because of deletion or mutation of other genes in addition to WT1. 

For example, in WAGR syndrome, a mutation in the 11p13 region causes deletion of both WT1 and the PAX6 genes, among others, which leads to Wilms’ tumor and Genitourinary malformations as a result of WT1 deletion, as well as Aniridia (which is absence of iris) and intellectual disability (which is formerly referred to as mental Retardation), as a result of PAX6 deletion.

Another syndrome associated with WT1 mutations is Denys-Drash syndrome, which is characterized by Wilms tumor, early-onset nephrotic syndrome, and male pseudohermaphroditism.

Another gene, WT2, also located on chromosome 11, seems to also be involved with other Wilms’ tumor-containing syndromes, like Beckwith-Wiedemann syndrome, which includes Wilms’ tumor, macroglossia, organomegaly, and hemihypertrophy.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_bronchitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-C3CTQwdQQ_cw786l3SlbiYwSa6AvfhK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic bronchitis]]></video:title><video:description><![CDATA[Bronchitis means inflammation of the bronchial tubes in the lung, and it’s said to be chronic when it causes a productive cough—which means produces mucus—for at least 3 months each year for 2 or more years.

Chronic bronchitis is actually lumped under the umbrella of chronic obstructive pulmonary disease (or COPD), along with emphysema. 

These two are different in that chronic bronchitis is defined by clinical features, like a productive cough, whereas emphysema is defined by structural changes—specifically enlargement of the air spaces. 

That being said, they often coexist, probably because they share the same major risk factor — smoking. 

Other risk factors for chronic bronchitis include exposure to air pollutants like sulfur and nitrogen dioxide, exposure to dust and silica, as well as genetic factors like having a family history of chronic bronchitis. 

With COPD, the airways become obstructed, and the lungs don’t empty properly, and that leaves air trapped inside the lungs. 

For that reason, the maximum amount of air people with COPD can breath out in a single breath, known as the FVC, or forced vital capacity, is lower. 

This reduction is especially noticeable in the first second of air breathed out in a single breath, called FEV1—forced expiratory volume (in one second), which typically is reduced even more than the FVC. 

A useful metric therefore is the FEV1 to FVC ratio, which, since the FEV1 goes down even more than FVC, causes the FEV1 to FVC ratio to go down as well. 

Alright so say normally your FVC is 5 L, and your FEV1 is 4 L, your FEV1 to FVC ratio would end up being 80%. 

Now, someone with COPD’s FVC might be 4 L instead, which is lower than normal, but the volume of air that he or she can expire in the first second is only 2 L, so not only are both these values lower, but their ratio is lower as well—and this is a hallmark of COPD.

All that had to do with air breathed out right? Conversely, for air going in, the TLC, or total lu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Horseshoe_kidney</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/abVXxMgcTGOPEcVC7x59_ZSBRHyosepd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Horseshoe kidney]]></video:title><video:description><![CDATA[Horseshoe kidney, or sometimes renal fusion, is a congenital disorder where the two kidneys fuse together into one during fetal development, resulting in one large horseshoe-shaped kidney.

Normally during fetal development, the future kidneys develop in the pelvis as a structure called the metanephrose before finally migrating upward into the abdomen and becoming everyone’s favorite organ duo. 

For people with horseshoe kidney, their kidneys fused together at some point during development, and there are two main working theories on how this might happen. 

The first is mechanical fusion, which happens during the metanephros stage, which is around about the 5th week of gestation. 

At this point, the two kidneys are still in the pelvis, and are therefore pretty close together, so close that it’s thought that some flexion or growth of the developing spine and pelvic organs essentially pushes them together, causing the lower or inferior poles of the kidneys to touch and fuse together, forming what’s called a fibrous isthmus, fibrous because it’s composed of connective tissue. 

The other theory involves a teratogenic event. Teratogenic meaning something that disrupts fetal development in some way. 

In this case it’s thought that the posterior nephrogenic cells, which are the cells that help to form part of the kidney, migrate and rendezvous in the wrong spot, and therefore again form an isthmus connecting the two kidneys, but this time since the isthmus is composed of kidney cells as opposed to connective tissue, it’s called a parenchymal isthmus.

Whichever one happens, now you’ve got this single, horseshoe-shaped kidney in the pelvis. 

During the 7th and 8th weeks, it tries to migrate up into the abdomen, but it literally hits a bit of a roadblock and hooks around the inferior mesenteric artery, which keeps it lower in the abdomen than normal.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Body_focused_repetitive_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BusQr6p9SXeZp5jy7KiODSJjTSKH4OLy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Body focused repetitive disorders]]></video:title><video:description><![CDATA[Body-focused repetitive disorders is an umbrella term in the DSM-5 for disorders where individuals compulsively damage their physical appearance. 

These used to be classified as impulse-control disorders, but now belong in the family of obsessive-compulsive disorders. 

Two of the more well-known ones are trichotillomania, which is a hair-pulling disorder, and excoriation, which is a skin-picking disorder. 

Obsessive-compulsive disorders are usually defined by psychological obsessions—thoughts, urges, and images that are unwanted, intrusive, and recurrent—as well as behavioral compulsions exhibited physically in response to the obsessions. 

For body-focused repetitive disorders, though, the self-damaging behavior isn’t usually related to a conscious psychological obsession, but occurs instead when a person feels stressed, anxious, or even bored. 

Once a person starts engaging in the self-damaging behavior, there’s usually a strong urge to keep doing it over and over again. 

This can happen in multiple short episodes throughout the day, or during single long sessions that can last for hours at a time. 

People with body-focused repetitive disorders aren’t always fully aware of their behavior while engaged in the compulsion, making it difficult to stop. 

These behaviors are distinct from intentional behaviors aimed at improving physical appearance, like plucking one’s eyebrows. 

They’re also not attributable to problems stemming from disorders like substance abuse, like, for example, the skin-picking associated with amphetamine or cocaine use.

Body-focused repetitive disorders don’t include compulsions resulting from other mental disorders, like picking at skin during a tactile hallucination, when someone thinks bugs are crawling under their skin. 

They’re unrelated to behaviours made in response to irritating stimuli from other illnesses, like scratching at an itchy scabies rash. 

Finally, body-focused repetitive disorders aren’t related to side-e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spina_bifida</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y4mlNkVcSBaYrWGReW-x8a-rQE_OdfxI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spina bifida]]></video:title><video:description><![CDATA[With spina bifida, “spina” refers to the spine, while bifida means “split”. So, spina bifida literally means “split spine”. It occurs during embryonal development when the posterior part of the spine doesn’t fully close, leaving behind various degrees of defects, usually in the lumbosacral region of the spine. 

To understand spina bifida, we need to zoom in on the embryo during its earliest weeks of development. At this stage, the embryo has three main layers. The ectoderm on the outside, the mesoderm in the middle, and the endoderm on the inside. Around the third week of development, the ectoderm forms a flat sheet of cells known as the neural plate. Soon after, the plate begins to fold inward along the midline, creating a neural groove with raised folds on each side. By the fourth week, these folds move closer and fuse, forming the neural tube. The top part of this tube, called the cranial end, will become the brain, while the bottom part, known as the caudal end, will develop into the spinal cord.  

Also, the ectoderm will give rise to three protective layers called the meninges, which wrap around the brain and spinal cord, cushioning them with cerebrospinal fluid.  But that’s not all. Thanks to the mesoderm, the body organizes to form structures like muscles, bones, and the overall skeletal framework. This adds another layer of protection because the mesoderm forms the vertebral column that surrounds and protects the spinal cord. 

The vertebral column is divided into five regions, each with its own set of vertebrae. The cervical region has 7 vertebrae, labeled C1 to C7; the thoracic region has 12, named T1 to T12; and the lumbar region includes 5, from L1 to L5. Below these, the sacral region consists of 5 fused vertebrae, S1 to S5, and the coccygeal region has 4 fused vertebrae, Co1 to Co4. Now, each vertebra has two main parts. The vertebral body at the front and the vertebral arch at the back. Together, they form a central opening called the vert]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parkinson_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M4GdGRpMREuEQz6Uxa8XmOjSTiCnBTdo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parkinson disease]]></video:title><video:description><![CDATA[Parkinson’s disease, which is sometimes called Parkinson disease, Parkinson’s, or PD, is a movement disorder where the dopamine-producing neurons in the substantia nigra of the brain undergo degeneration.

Parkinson’s is one of the most common neurological disorders. It’s a progressive, adult-onset disease, and it gets more common with age. Most of the time, there’s no known cause. But in a few cases, there might be a genetic cause, like mutations in the PINK1, parkin, or alpha synuclein genes, and in rare cases, Parkinsonian symptoms may be caused by MPTP, a toxic impurity that can be found in the recreational drug MPPP or desmethylprodine, which is a synthetic opioid.

In other people, one or more risk factors, rather than a single outright cause, might contribute to Parkinson’s, for example pesticide exposure or DNA variants in genes like LRRK2.

No matter what the cause is, Parkinson’s derives from the death of dopamine-producing, or dopaminergic, neurons in the substantia nigra.
The name substantia nigra means “black substance,” since it is darker than other brain regions when you look at a slice of the brain on an autopsy.

We usually refer to the substantia nigra as if it’s in a single location, but there are actually two of these regions in the brain, one on each side of the midbrain. The substantia nigra is a part of the basal ganglia, a collection of brain regions that control movement through their connections with the motor cortex.

In Parkinson’s, these darkened areas of substantia nigra gradually disappear. Under a microscope, Lewy bodies, which are eosinophilic, round inclusions made of alpha-synuclein protein are present in the affected substantia nigra neurons before they die. The function of alpha-synuclein is unknown, as well as the significance of Lewy bodies, and they are both found in other diseases like Lewy body dementia and multiple system atrophy.

The substantia nigra actually can be split into two sub-regions. 

First, there’s t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gallstone_ileus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_imbIIn4R06txMa_sx5QdeLpT264pyJR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gallstone ileus]]></video:title><video:description><![CDATA[Gallstones are hard stones found in the gallbladder, and gallstone ileus is when a gallstone becomes lodged in the small bowel.

Risk factors for developing gallstones include things like female sex, obesity, pregnancy, and age, sometimes remembered by the 4 F’s—female, fat, fertile, and forty. 

Sometimes those gallstones can get lodged in the cystic duct for long periods of time, and in that case, the bile inside the gallbladder tends to stagnate, and since the blockage doesn’t allow it to be squeezed out periodically to help with digestion, that stagnant bile which tends to irritate the gallbladder mucosa in the walls, and causes it to start secreting mucus and inflammatory enzymes, which results in some inflammation, distention and pressure build up—a condition known as cholecystitis, or inflammation of the gallbladder. 

If the gallstone dislodges, the inflammation can clear up.

On rare occasion, a large stone (typically over two and a half centimeters) can cause ongoing or repeated inflammation of the gallbladder, which can make the wall of the gallbladder a bit edematous or swollen and slightly more sticky.

As a result, the gallbladder wall can actually adhere to a nearby structure, most commonly at the duodenum, but occasionally to the stomach, colon, and jejunum.

Eventually these repeated bouts of inflammation might cause the gallbladder wall to thin out and erode away completely, forming a fistula—which is essentially a passageway between the gall bladder and the organ that it’s stuck to. 

If the other organ is the small intestine, then this is called a cholecystoenteric fistula, and the fistula becomes a direct route for gallstones to enter the bowel. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Transitional_cell_carcinoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ygxszTFcSu6GlvJ4kAEwnxpKR4WdotqK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Transitional cell carcinoma]]></video:title><video:description><![CDATA[The most common form of cancer in the lower urinary tract—or the bladder and the urethra— is transitional cell carcinoma (or TCC), and to be more specific, urothelial cell carcinoma (or UCC). 

While this cancer can affect tissues in the upper urinary tract, such as the renal pelvis and the ureter, it most commonly arises in the urothelium of the bladder. 

The urothelium (or uroepithelium)  is a specific type of transitional cell epithelium that lines the inner surface of much of the urinary tract. This tissue is composed of 3–7 cell layers, and it forms a tight barrier which holds urine without allowing toxins to move across the epithelium and back into the body. 

That barrier function is largely accomplished by large umbrella cells that line the inner or luminal surface of the urothelium, and are held together by high resistance tight junctions, and are lined with a unique protein/lipid complex, called a plaque, along their apical membrane. 

Now when you think about the bladder, it’s going to cyclically change shape during the course of its normal function. 

For example, after you chug a tall mango lassi, your bladder will become completely filled up only to be emptied again when you rush to the restroom. Therefore, the urothelium has to be able to maintain its impermeable properties during these normal changes in bladder shape. Most of this is allowed for by the unfolding of the mucosal surface when the bladder fills up.

When the bladder is empty, this surface is highly wrinkled with rugae which then smooths out as the bladder becomes distended. In addition to this, these umbrella cells of the urothelium, have the ability to stretch with an expanding bladder. In fact, the term “transition” of transitional epithelium refers to this ability to go  through transitions of shape.

Cancers that affect the urothelium usually arise through two distinct mechanisms. One way for a urothelial cell carcinoma to arise  is through a mutation in the tumor sup]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Emphysema</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2V5u7FAGSZO3KFz_Mc1h960BQwKbT-QE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Emphysema]]></video:title><video:description><![CDATA[Emphysema means “inflate or swell”, which makes sense because in the lungs of people with emphysema, the alveolar air sacs, which are the thin walled air spaces at the ends of the airways where oxygen and carbon dioxide are exchanged, become damaged or destroyed. 

The alveoli permanently enlarge and lose elasticity, and as a result, individuals with emphysema typically have difficulty with exhaling, which depends heavily on the ability of lungs to recoil like elastic bands.

Emphysema’s actually lumped under the umbrella of chronic obstructive pulmonary disease (or COPD), along with chronic bronchitis. 

The two differ in that chronic bronchitis is defined by clinical features, like the productive cough, whereas emphysema is defined by structural changes, mainly enlargement of the air spaces. 

That being said, they almost always coexist, probably because they share the same major cause—smoking.

With COPD, the airways become obstructed, the lungs don’t empty properly, and that leaves air trapped inside the lungs. 

For that reason, the maximum amount of air people with COPD can breath out in a single breath, known as the FVC, or forced vital capacity, is lower. 

This reduction is especially noticeable in the first second of air breathed out in a single breath, called FEV1—forced expiratory volume (in one second), which typically is reduced even more than the FVC. 

A useful metric therefore is the FEV1 to FVC ratio, which, since the FEV1 goes down even more than FVC, causes the FEV1 to FVC ratio to go down as well. 

Alright so say normally your FVC is 5 L, and your FEV1 is 4 L, your FEV1 to FVC ratio would end up being 80%. 

Now, someone with COPD’s FVC might be 4 L instead, which is lower than normal, but the volume of air that he or she can expire in the first second is only 2 L, so not only are both these values lower, but their ratio is lower as well—and this is a hallmark of COPD.

All that had to do with air breathed out right? Conversely, for a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ascending_cholangitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DA5ZK3qKQJa28ybYpSDzQaiWSj_sgaT3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ascending cholangitis]]></video:title><video:description><![CDATA[With ascending cholangitis, “cholang-” refers to the bile ducts and “-itis” refers to inflammation which is usually caused by a bacterial infection. 

These bacteria are normally found in the intestines and work their way up the bile ducts from the duodenum of the small intestine, so that’s why it’s known as ascending cholangitis, also sometimes acute cholangitis because it can happen over a relatively short period of time. 

Normally bacteria from the gut has a pretty tough time ascending up the bile ducts, and this is because bile flows down from the gallbladder, along with some pancreatic juice from the pancreas, into the duodenum, and this tends to flush out any bacteria trying to sneak their way up. 

In ascending cholangitis this flow of bile is often blocked, and one common reason is choledocholithiasis, which refers to gallstones in the common bile duct. 

In choledocholithiasis, gallstones form in the gallbladder and occasionally slip out, travel through the cystic bile duct, and then lodge into the common bile duct, obstructing the normal flow of bile. 

These gallstones are typically made up of bile components, and risk factors for developing them include things like female sex, obesity, pregnancy, and age, sometimes remembered by the 4 F’s—female, fat, fertile, and forty. Other, less common causes include things that cause stricture, or narrowing of the bile ducts—like a nearby cancerous growth, which can compress the duct as the tumor slowly enlarges, or injury experienced during a laparoscopic procedure.

Once the flow of bile is blocked, bacteria can slowly make their way up the ducts and colonize the biliary system without the risk of being washed away. 

Most commonly the bacterial species involved are a mixture of enteric organisms including common ones like E coli, Klebsiella species, and Enterococcus species. 

These bacteria can migrate up to the blockage and continue to infect the stagnant bile as well as the surrounding tissue. 

Als]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_pyelonephritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dhAGZ71jQZWo5SFxX3klqqkCR6GiD5B5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic pyelonephritis]]></video:title><video:description><![CDATA[With chronic pyelonephritis, pyelo- means pelvis, and -neph- refers to the kidney, so in this case it’s the renal pelvis, which is the funnel-like structure of the kidney that drains urine into the ureter, and -itis means inflammation. This inflammation is usually caused by bacterial infection of the kidney, which is called acute pyelonephritis. 

When somebody has recurrent episodes of acute pyelonephritis, the kidney becomes visibly scarred, at which point it’s referred to as chronic pyelonephritis.

Now a urinary tract infection, or UTI, is any infection of the urinary tract, which includes the upper portion of the tract—the kidneys and the ureters, and the lower portion of the tract—the bladder and urethra.

So acute and chronic pyelonephritis are types of upper urinary tract infection.

Now, an episode of acute pyelonephritis often clears up without much complication. Certain people, though, are predisposed to having recurring bouts of acute pyelonephritis, which eventually leads to chronic pyelonephritis and permanent scarring of the renal tissue.

The most common risk factor for recurrent acute pyelonephritis and therefore chronic pyelonephritis, is vesicoureteral reflux, or VUR, which is where urine is allowed to move backward up the urinary tract, which can happen if the vesicoureteral orifice fails.

The vesicoureteral orifice is the one-way valve that allows urine to flow from each ureter into the bladder, but not in the reverse direction. 

VUR can be the result of a primary congenital defect or it can be caused by bladder outlet obstruction, which increases pressure in the bladder and distorts the valve. 

That being said, chronic obstruction is its own independent risk factor for chronic pyelonephritis. 

Obstructions in the urinary tract causes urinary stasis, meaning it tends to cause urine to stand still, which makes it easier for bacteria to adhere to and colonize the tissue, making lower UTIs more likely and therefore upper UTIs more lik]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Irritable_bowel_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/noIJGYWLRBiVdwjvjjHHjA71QwSMosvg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Irritable bowel syndrome]]></video:title><video:description><![CDATA[Irritable Bowel Syndrome, or IBS, describes a pattern of recurrent bouts of abdominal pain and abnormal bowel motility causing things like constipation or diarrhea, or a mixture of the two, and often times the abdominal pain improves after a bowel movement. 

Although it sounds similar, IBS is different from inflammatory bowel disease or IBD, which involves some of the same IBS symptoms, but also includes inflammation, ulcers, or other damage to the bowel, whereas IBS does not involve these, and instead can be thought of as a functional disorder. 

Right now, the underlying biological mechanisms that produce the symptoms of irritable bowel syndrome aren’t well understood, so most research is focused on these key symptoms: abdominal pain and abnormal bowel motility. 

With regard to abdominal pain, a lot of people with irritable bowel syndrome have “visceral hypersensitivity,” which means that the sensory nerve endings in the intestinal wall have an abnormally strong response to stimuli like stretching during and after after a meal.

This visceral hypersensitivity might explain why people with the disease experience recurrent abdominal pain.  

With regard to abnormal bowel motility, the underlying mechanism is a little less clear. 

One clue is that eating foods that contain short chain carbohydrates such as lactose and fructose often trigger the symptoms. 

One possible explanation is that unabsorbed short-chain carbohydrates act as solutes that draw water across the gastrointestinal wall and into the lumen. 

In addition to triggering visceral hypersensitivity which causes pain, that excess water can also cause smooth muscle lining the intestines to spasm, and create diarrhea if the excess water’s not reabsorbed back into the body. 

To make matters worse, the unabsorbed short-chain carbohydrates are often metabolized by gastrointestinal bacterial flora which produce gas that could trigger more bloating, spasm, or pain.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/IgA_nephropathy_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/81Uy-NL4S8OSZn1pBHfwE2Z2SpW5smdQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[IgA nephropathy (NORD)]]></video:title><video:description><![CDATA[IgA nephropathy is a disease associated with the kidneys, which are two bean-shaped organs in our body that filter out toxic waste products and excess water from blood and excrete them in the urine. Now, inside each kidney there are clusters of capillaries, that is, tiny blood vessels, called glomeruli, which act like filters of the kidney to let water and the harmful wastes through while keeping important things like red blood cells and proteins in.

IgA nephropathy is caused by an abnormal form of IgA, a type of immunoglobulin, also called an antibody.  Normally, this is  a type of protein that helps the body fight against bacteria and other foreign organisms. When the IgA has an abnormal structure, it can accumulate in the kidneys, causing inflammation and damage.

Now, because of the glomerular injury, red blood cells leak into the urine, causing hematuria. The amount of blood sometimes is enough to cause  reddish or blackish discoloration of the urine. Protein leaking into the urine causes proteinuria and may make the urine appear foamy. Frequently, IgA nephropathy presents in children or young adults as either microscopic or visible hematuria, meaning that it can be seen under a microscope or with the naked eye, and it typically develops during an infection involving the mucosal lining, like infections of the gastrointestinal or respiratory tract. In these sorts of infections, the production of the abnormal IgA antibody gets ramped up, leading to more accumulation in the glomerulus, causing inflammation and injury. With each mucosal infection, the glomeruli undergo more injury, so over time, sometimes decades, individuals may progress to renal failure. Renal failure means decreased kidney function which may cause less formation of urine and building up of excess water in the circulation. This leads to high blood pressure which can damage other organs like the brain and heart. In addition, the protein lost in the urine normally helps water stay in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gallbladder_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sgw55HafTmqEVr82Kw4M-L8OTAmvqPty/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gallbladder carcinoma]]></video:title><video:description><![CDATA[When tissues are inflamed and irritated, they usually regenerate by cell division and laying down new protein. Tissues are mostly cells and protein after all. 

Now each time a cell divides, there’s a chance that something will go wrong - a mistake will happen, and a normal gene will mutate. 

If this happens with genes involved in cell replication itself, then you might have a cell that continues to divide out of control.

This is why tissues that are constantly subject to irritation and inflammation (especially tissues that are not used to it and typically don’t have as much cell division happening) are more likely to develop tumors, and the gallbladder’s no exception. 

About three-quarters of patients that develop gallbladder cancer have cholesterol gallstones, and having gallstones in general is thought to increase the risk of gallbladder cancer significantly. Why is that though? 

Well gallstones are known to induce inflammation of the glandular tissue along the gallbladder walls, also known as cholecystitis. 

Over time, this constant state of inflammation and cell turnover increases the risk of a genetic mistakes and mutations, potentially leading to a carcinogenesis, or cancer formation.

If these cells do become carcinogenic, they proliferate and start forming a mass of these defective tumor cells in the glandular tissue of the gallbladder, which is why we can call it gallbladder adeno-carcinoma, or cancer of the glandular tissue. 

With chronic inflammation of the gallbladder, the risk for carcinogenesis increases more and more over time, and that chronic inflammation of the gallbladder leads to calcification and fibrosis, a condition known as porcelain gallbladder. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_pancreatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uQGsOcxTSrqln02LGzbuixFuTNmz2z8y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic pancreatitis]]></video:title><video:description><![CDATA[Chronic pancreatitis is persistent, chronic inflammation of the pancreas often due to repeated bouts of acute pancreatitis. 

While a history of acute pancreatitis might lead to chronic pancreatitis these diseases have distinct histopathologies. 

Acute pancreatitis is inflammation caused by destruction of the pancreas by its own digestive enzymes—a process called  autodigestion, and is generally reversible. 

Chronic pancreatitis is inflammation due to irreversible changes to the pancreatic structure, like fibrosis, atrophy and calcification.

The pancreas is a long, skinny gland the length of a dollar bill and is located in the upper abdomen, or the epigastric region, behind the stomach. It plays endocrine roles—for example, alpha and beta cells make hormones like insulin and glucagon that are secreted into the bloodstream, but it also plays exocrine roles— for example, acinar cells make digestive enzymes that are secreted into the duodenum to help digest food.

These pancreatic digestive enzymes break down macromolecules like carbohydrates, lipids and proteins found in food, but these macromolecules are also found in the cells of the pancreas. 

To protect the pancreas, the acinar cells manufacture inactive forms of the enzymes called proenzymes, or zymogens. 

These zymogens are normally activated by  proteases which cleave off a polypeptide chain, which is kind of like pulling the pin on a grenade.

For additional security, the zymogens are kept away from sensitive tissues in storage vesicles called zymogen granules, and are packaged with protease inhibitors that prevent enzymes from doing damage if they become prematurely active. 

To digest a meal, these zymogens are released into the pancreatic duct, and delivered to the small intestine where they are activated by the protease trypsin. 

Trypsin is a pancreatic digestive enzyme that is produced as the zymogen trypsinogen. 

Normally, trypsinogen isn’t activated until it is cleaved by protease enter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_hemorrhage</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dagI_-6rRAiEXW2NMJuhsQCgRkyyapn8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postpartum hemorrhage]]></video:title><video:description><![CDATA[Postpartum hemorrhage is a significant loss of blood after giving birth, and it’s the number one reason for maternal morbidity and maternal death around the world. 

Specifically it’s defined as losing more than 500ml of blood after a vaginal delivery or more than 1000ml after a cesarean section delivery. 

Of course, deliveries can be messy and it’s impossible to measure the precise amount of blood that’s lost, and there’s the possibility of internal bleeding. 

So additional criteria to consider for postpartum hemorrhage include a decrease of 10% or more in hematocrit from baseline, as well as changes in the mother’s heart rate, blood pressure, and oxygen saturations —all of which suggest a significant blood loss. 

Significant bleeding in the first 24 hours after delivery is called primary postpartum hemorrhage, and after that it’s called secondary, or late, postpartum hemorrhage. 

The most common causes of postpartum hemorrhage can be lumped into four groups which can easily be remembered as the “4 Ts”: Tone, Trauma, Tissue, and Thrombin. 

Tone refers to a lack of uterine tone, also known as uterine atony—basically a soft, spongy, boggy uterus, and this is the main cause of postpartum hemorrhage, generally resulting in a slow and steady loss of blood. 

Now, the uterus is a muscular organ wrapped by three layers of smooth muscle called the myometrium, which contracts during labor to dilate and efface the cervix and ultimately push out the fetus and placenta.

After delivery, the myometrium continues to contract and this squeezes down on the placental arteries at the point where they are attached to the uterine wall, which clamps them shut, and therefore reduces uterine bleeding. 

The contractions continue for a few weeks after the delivery. 

With uterine atony, though, the uterus fails to contract after birth, and those placental arteries don’t clamp down, which leads to excessive bleeding and postpartum hemorrhage.

Uterine atony can be caused by ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polycystic_kidney_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hoUcBwp0TqK3u5kklHvIYp9VQ9Otk80K/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polycystic kidney disease]]></video:title><video:description><![CDATA[Polycystic kidney disease, or PKD, is a genetic disease in which the kidneys become filled with hundreds of cysts, or fluid-filled sacs, causing them to be larger than normal and to quit functioning over time.

These cysts develop in the outer layer—the cortex, as well as the inner layer—the medulla—of both kidneys. 

These cysts, which are lined with renal tubular epithelium, fill up with fluid and get larger and larger over time, making the kidneys much larger than normal. 

The blood vessels that feed neighboring healthy nephrons can get compressed by growing cysts, which literally starves them of oxygen. 

Poorly perfused kidneys respond by activating the renin-angiotensin-aldosterone system, which facilitates fluid retention and leads to hypertension. 

Also, expanding cysts can compress the collecting system, causing urinary stasis, and in some cases this can lead to kidney stones. 

Additionally, destruction of the normal renal architecture can cause symptoms like flank pain and hematuria, or blood in the urine. 

Over time, as enough nephrons are affected, it leads to renal insufficiency and eventually renal failure. 

Now the first type of PKD is autosomal dominant PKD or ADPKD, which used to be called adult PKD, since symptoms usually manifest in adulthood. 

The first gene responsible for ADPKD is PKD1, which when mutated causes the more severe and earlier onset variety, and PKD2, which when mutated causes less severe disease and is also later in onset. PKD1 and PKD2 code for the polycystin 1 and polycystin 2 proteins, respectively, which are components of the primary cilium. 

Now, the primary cilium is an appendage that sticks out from most cells in the body and receives developmentally important signals. 

More specifically, in the nephron, as the urinary filtrate flows by and cause it to bend, polycystin 1 and polycystin 2 respond by allowing calcium influx, which activates pathways in the cell that inhibit cell proliferation. 

If either co]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aphthous_ulcers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uuvk5NwvReSmOT8RKSdoIllFTKungyob/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aphthous ulcers]]></video:title><video:description><![CDATA[Aphthous ulcers, often called canker sores, are painful inflammatory lesions or spots on the inside of the mouth.

Most often, people develop minor aphthous ulcers, which is where the lesions are a few millimeters across, round or oval in shape, and disappear within a week. 

There are also two other unusual variations, however, major aphthous ulcers and herpetiform ulcers, which are much more severe and debilitating.

The underlying cause of this inflammatory disease is not well understood. One theory suggests tissue specific autoimmunity, where a localized cell-mediated immune reaction happens in the oral mucosa creating an accumulation of T-cells, specifically T helper cells Th1 cells, and macrophages, as well as chemokines like interferon-gamma and tumor necrosis factor. 

Aphthous ulcers typically arise, either singly, or a few at a time, on the inside of the lips and cheeks or under the tongue. 

Initially there is a small raised bump of inflammation in your mouth, and as it heals it turns into an ulcer covered by a fibrous membrane “cap” that looks yellowish-white or gray with well defined margins. 

The ulcer is typically surrounded by a characteristic red halo due to inflammation in neighbouring blood vessels. 

Aphthous ulcers are usually mildly painful and annoying, with individual lesions measuring a few millimeters across and healing within 7 to 10 days without scarring. And these usually recur 3-4 times per year. 

There are some variations on this general pattern. Some individuals have recurrent aphthous ulcers which is where the recurrence is more frequent - sometimes each month, and this starts during childhood and resolves around age 40. 

Another variation is major aphthous ulcers which describes lesions that measure over one centimeter in size and are generally more painful, last longer, and recur frequently.

Major aphthous ulcers can take between 10 days to over a month to heal, and can also leave a scar. 

Finally there are herpetifo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gout</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KgAdT1uBRFi66ucj2HxcG5-KS-OY2To0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gout]]></video:title><video:description><![CDATA[Gout is an inflammatory disease in which monosodium urate crystals deposit into a joint, making it red, hot, tender  and swollen within hours. 

When this happens, it’s called a gouty attack. 

The underlying cause is hyperuricemia—too much uric acid in the blood, which results in the formation of sharp, needle-like crystals, in areas with slow blood flow like the joints and the kidney tubules. 

Over time, repeated gouty attacks can cause destruction of the joint tissue which results in arthritis. 

To understand where the uric acid comes from, let’s start with purines, which, together with pyrimidines, are nature’s most common nitrogen-containing heterocycles. 

A heterocycle being any molecular ring or cycle with different types of atoms. 

Purines, as well as pyrimidines, are key components of nucleic acids like DNA and RNA, and when cells, along with the nucleic acids in those cells, are broken down throughout the body, those purines are converted into uric acid—a molecule that can be filtered out of the blood and excreted in the urine. 

Uric acid has limited solubility in body fluids, though. Hyperuricemia occurs when levels of uric acid exceed the rate of its solubility, which is about 6.8mg/dL. 

At a physiologic pH of about 7.4, uric acid loses a proton and becomes a urate ion, which then binds sodium and forms monosodium urate crystals.

These crystals can form as a result of increased consumption of purines, like from consuming purine-rich foods like shellfish, anchovies, red meat or organ meat.

Also, though, they can result from increased production of purines, for example high-fructose corn syrup containing beverages could contribute to the formation of uric acid by increasing purine synthesis.

Another way crystals could form is from decreased clearance of uric acid, which can result from dehydration from not drinking enough water or from consumption of alcoholic beverages, both of allowing uric acid to precipitate out. 

Regularly eating t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sickle_cell_disease_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9NRYbR1TTheJ7z58uBFUD8ORRAafI9qW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sickle cell disease (NORD)]]></video:title><video:description><![CDATA[Sickle cell disease, also called sickle cell anemia or just “sickle cell,” is a genetic disease where red blood cells can take the shape of a crescent, or sickle, and that change allows them to more easily be destroyed, causing anemia among other things. 

Sickle cell disease is caused by defective hemoglobin, which is the oxygen-carrying protein in red blood cells. Hemoglobin is actually made up of four peptide chains, each bound to a heme group. 

Different hemoglobins have different combinations of these chains. Hemoglobin A (or HbA), made up of two α-globin and two β-globin peptide chains, is the primary hemoglobin affected in sickle cell. 

Specifically, the β-globin chains end up misshapen. This is because of a mutation in the beta globin gene, or HBB gene. 

Sickle cell is an autosomal recessive disease, so a mutation in both copies of the beta globin gene is needed to get the disease; if the person has just one copy of the mutation and one normal HBB gene, then they’re a sickle cell carrier, also called sickle trait. 

Having sickle trait doesn’t cause health problems unless the person is exposed to extreme conditions like high altitude or dehydration, where some sickle cell disease-like symptoms can crop up. 

What it does do is decrease the severity of infection by Plasmodium falciparum malaria, so in parts of the world with a high malaria burden, like Africa and pockets of southern Asia, those with sickle trait actually have an evolutionary advantage. 

This phenomenon is called heterozygote advantage, and it&amp;#39;s unfortunate consequence is a high rate of sickle cell disease in people from these parts of the world. 

Almost always, the sickle cell mutation is a nonconservative missense mutation that results in the 6th amino acid of beta globin being a valine instead of glutamic acid. 

A nonconservative substitution means that the new amino acid—valine, which is hydrophobic—has different properties that the one it replaced—glutamic acid, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myasthenia_gravis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sbIVJTHlRO_ltbxr3Exv5C0fR222YMAR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myasthenia gravis]]></video:title><video:description><![CDATA[Myasthenia gravis comes from the Greek word ‘myasthenia’, meaning muscle weakness; and the Latin word ‘gravis’, meaning severe. So, myasthenia gravis is an autoimmune condition that causes serious muscle weakness. 

First, let&amp;#39;s focus on physiology and how muscles normally work. Whether you’re reaching for a slice of pizza or sinking that perfect shot in basketball, it all starts in the brain. The upper motor neuron of the cerebral cortex fires an action potential down the spinal cord to activate lower motor neurons. Next, lower motor neurons pick up these signals and pass them along their axons toward terminal branches and axon terminals, all the way to skeletal muscle fibers.  

This communication site between the lower motor neuron and the skeletal muscle fiber is known as the neuromuscular junction, which consists of three main parts. First, there’s the presynaptic membrane, which is the axon terminal of the lower motor neuron packed with acetylcholine vesicles. Acetylcholine is actually the neurotransmitter that enables muscle contraction. Next, there’s the postsynaptic membrane, which is the membrane of the skeletal muscle fiber, rich in nicotinic acetylcholine receptors.  

Finally, this tiny space between two membranes is called the synaptic cleft and contains the enzyme acetylcholine esterase. 

Now, the arrival of the action potential at the axon terminal triggers the opening of voltage-gated calcium channels in the presynaptic membrane, allowing calcium ions to rush in. This triggers the acetylcholine vesicles to fuse with the presynaptic membrane and release acetylcholine into the synaptic cleft. Once inside the cleft, acetylcholine moves across to bind nicotinic acetylcholine receptors on the postsynaptic membrane. Eventually, this binding triggers the muscle cell to depolarize, setting off a chain of intracellular events that lead to contraction. Once the contraction is over, acetylcholine is broken down by acetylcholine esteras]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Resting_membrane_potential</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KbPMoToaRUSmvqRAutMt4vBtTgCFauTj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Resting membrane potential]]></video:title><video:description><![CDATA[Each cell in the human body is wrapped in a membrane that separates the inner environment and outer environment, and positively and negatively charged ions aren’t equally distributed on both sides of the membrane. 

Fundamentally, it’s these differences in concentration and charge as well as permeability across the membrane that establishes the cell’s resting membrane potential.

Generally speaking there is a higher concentration of Na+ or sodium, Cl- or chloride, and Ca2+ or calcium on the outside of a cell, and a higher concentration of (K+) or potassium and (A-), which is just what we just write for negatively charged anions, on the inside of a cell. 

These anions include a variety of amino acids and proteins that are produced by the cell. 

Let’s start with the sodium-potassium pump which uses ATP to move three sodium ions out of the cell for every 2 potassium ions that it moves into the cell, this is the workhorse of the cell and it helps establish the concentration gradient for potassium and sodium. 

Let’s focus on potassium, which has a concentration of 150 mMol/L on the inside of the cell and about 5 mMol/L on the outside of the cell. 

With so much potassium within the cell relative to outside the cell, there will be fairly strong concentration gradient moving potassium ions out of the cell. 

Although these ions can’t simply diffuse through the phospholipid bilayer membrane, it turns out that potassium can get across the membrane using potassium leak channels and inward rectifier channels that are scattered throughout the membrane. 

So using those channels, the concentration gradient pushes potassium out of the cell, and that potassium brings with it some positive charge and leaves behind unpaired anions which carry negative charge because they aren’t able to go through the leak channels. 

Over time as more potassium ions leave the cell, a negative charge builds up within the cell and this starts to attract positively charged potassium ions b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spaced_repetition</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ds9dQ8osTjOMTyxNmHvpaoOWRQGN1Uyl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spaced repetition]]></video:title><video:description><![CDATA[Like most students, you’ve probably crammed the night before an exam. 

And after it, you probably did OK or maybe you even did well, but did you remember any of what you learned after the exam?

One evidence-based way to better remember what you’ve learned is through Spaced Repetition, or spacing out your learning and practice of new knowledge or skills.

Although this might seem novel, this is hardly a new concept; it was first described in 1885 by a German psychologist named Herman Ebbinghaus. Here’s how it works. 

Say you plot your retention, or how much you remember of something, vs. time. 

Now you learn that something on day 0. 

Without reviewing it, the “forgetting curve” will look like an exponentially decaying curve, which is kind of scary! 

If you review (or better yet actively retrieve) the material at increasingly spaced intervals after learning it, then the forgetting curve starts to flatten out and you’ll get a lot better longer-term retention. 

Now, the goal here is to review the material at the right time. 

It turns out that the best time to revisit information that you are trying to learn is right around the time you would naturally forget it. Since forgetting typically follows this exponential curve, the trick becomes timing your study sessions around it.

Practically, this means having more widely spaced intervals between study times for the material that you are more familiar with, and shorter intervals between study sessions for material that you are less familiar with. 

While this strategy would be effective for all fields of study, it is especially important for students in the medical field, who have to retain key knowledge and skills in order to care for their patients.  

Kind of frighteningly, one study found that without spaced repetition, after one year medical students forgot up to 33% of their basic science knowledge, and after two years, more than 50%! 

But when students and residents applied spaced repetition strate]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tropical_sprue</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NUJArmOuR8K0G54ngS6fXtc0TfO54sbR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tropical sprue]]></video:title><video:description><![CDATA[Tropical sprue is a gastrointestinal disease that results in malabsorption of nutrients and water. 

Just like the other “sprue” diseases, like celiac sprue which is more often known as celiac disease, in tropical sprue the villi of the small intestine become flattened, but the exact cause isn’t known. 

The biggest clue is that tropical sprue seems to mostly affect individuals living in the the tropical regions of the world, like the Caribbean, India, and Southeast Asia.

The most widely accepted theory is that an acute intestinal infection, which could be bacterial, viral, or protozoal, initially damages the intestinal lining, and this causes the first bit of inflammation. 

In response, the intestinal cells secrete enteroglucagon, which is a hormone that decreases intestinal motility. 

Decreased motility means that food’s allowed to linger in the intestines for longer than usual. 

More food means more resources, so this sets the stage for a change in the normal bacterial flora, which leads to bacterial overgrowth. 

Bacterial overgrowth refers to the idea that some organisms begin to overpopulate and therefore dominate the bacterial ecosystem of the intestines. 

In tropical sprue, Klebsiella, E. coli, and Enterobacter end up becoming those dominant bacteria. These guys release toxic byproducts as they ferment the food that lingers in the gut, and these toxins can damage the intestinal lining, leading to more inflammation.

Over time, all of this chronic inflammation leads to villous atrophy, which is flattening of the villi that line the small intestine. 

Villi are important because they provide the surface area and digestive enzymes necessary for nutrient absorption. 

Flattening of the villi reduces this surface area, which means less nutrients and water can be absorbed across the intestinal wall, which leads to malabsorption. 

This (1) means more food is left behind for the bacteria, which leads to more intestinal wall injury and inflammation, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sialadenitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nZON_tvPQe6jO67DcQWXdkldQoid_q24/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sialadenitis]]></video:title><video:description><![CDATA[“Sial” refers to saliva, “aden” refers to a gland, and “itis” is inflammation, so acute sialadenitis is the sudden inflammation of any of the salivary glands, the major ones being the parotid, submandibular and sublingual gland. 

Sialadenitis usually affects a single parotid gland rather than both, and is most common among individuals in their 50s and 60s but can happen at any age, even in a newborn. 

Acute sialadenitis is most often caused by the bacteria Staphylococcus aureus, but may also be caused by Streptococcus viridans, or by Haemophilus influenzae, as well as viruses like mumps and HIV. 

When it’s a bacterial infection, it often starts up after a salivary duct is plugged up by a salivary stone. 

Salivary glands secrete saliva through tiny ducts in the mouth, to help lubricate the inside of the mouth and also moisten and soften food. 

The antibacterial properties of saliva and the quick flow through the salivary duct both help to prevent infections from developing. 

But there are various factors that reduce the rate of salivary flow, like dehydration, illness, and certain medications. These factors can allow deposits to settle in the walls of the salivary duct, physically blocking the path and further slowing down the flow of saliva. 

This can allow tiny areas of stagnation where more deposits of calcium, phosphorous, and other electrolytes can precipitate out, ultimately forming small concretions called microsialoliths, or tiny salivary stones.

Over time, these can grow into sialoliths which are larger salivary stones.

Salivary stones block up the duct, which allows bacteria to move from the mouth up and around the blockage and into the salivary duct. 

And this results in inflammation and tissue swelling which can further compress the salivary duct, and worsen the problem.

Acute sialadenitis causes pain and swelling as well as redness of the skin overlying the affected gland. 

Because the salivary gland is affected, it also means that ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Behcet's_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6rfBE1MeQMWKR1L-FvP23NgLTryeQPFq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Behcet&apos;s disease]]></video:title><video:description><![CDATA[Behcet disease, is a rare disorder and most of the symptoms are thought to be a result of an autoimmune process involving the blood vessels, so it’s a type of vasculitis. 

Among the family of disorders that cause vasculitis, Behcet’s is fairly unique because it causes inflammation in blood vessels of all sizes—small, medium, and large ones—on both the arterial and venous side of the circulation. 

The underlying cause of Behcet’s is unknown, but there are a number of clues. 

The biggest clue is that the human leukocyte antigen, or HLA, genes seem to play a role, and this is based on the fact that having a specific type—the HLA-B51 type—predisposes individuals to having Behcet disease. 

HLA genes encode proteins found on the surface of immune cells, and play a key role in regulation of those cells, and since the disease is a result of an autoimmune process, it makes sense that the HLA-B51 proteins could be involved. 

Another, clue is that an individual’s response to viral and bacterial infections might be involved. 

For example, some individuals with Behcet’s generate relatively high levels of antibodies to Helicobacter pylori which may go on to damage blood vessel walls. 

And this is an example of molecular mimicry where an antibody to a foreign pathogen starts to cross-react and damage the person’s own tissue. 

Individuals with Behcet’s also seem to have a weakened innate immune system, a higher proportion of autoreactive T cells, and activated neutrophils which destroy healthy tissue, as well as altered levels of T helper cells and cytokines. 

In summary, these clues span genetic and environmental factors as well as both the innate and adaptive immune system. 

When looking at the blood vessels in particular, the classic finding is seeing lymphocytes in the walls of capillaries, veins, and arteries of all sizes, making them inflamed and boggy. 

Sometimes the inflammation can get so severe that the tissue around the vessel starts to die off compl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/atopic_dermatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iZDr5iU1QDe8lUFJ8lADgU87Q_am5fP6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atopic dermatitis]]></video:title><video:description><![CDATA[With atopic dermatitis, dermatitis refers to skin inflammation, while “atopic” comes from the Greek word “atopia” meaning “out of place”. This phrase reflects the idea that in atopic dermatitis, the immune system overreacts to everyday, harmless substances, such as dust and pollen, as if they were dangerous, subsequently triggering inflammation and an extremely itchy rash. Atopic dermatitis, also known as atopic eczema, is a chronic, relapsing skin condition that’s particularly common among young children, but it can also persist well into adulthood. 

Now, the skin is the body’s natural barrier that protects you from environmental substances and microbes. The outer layer of your skin called the epidermis, has four layers stacked up like a protective team. At the bottom is the stratum basale, followed by the stratum spinosum, then the stratum granulosum. The outermost layer and the front line of the skin barrier is the stratum corneum. Think of it as a brick wall. In this wall, bricks represent dead, flattened skin cells called corneocytes, which lock in moisture and keep allergens, irritants, and microbes out. But even the strongest wall needs reinforcement, and that’s where filaggrin comes in. This special protein works like rebar inside the wall. It links neighboring cells, flattens them out, and gives the skin its strength and flexibility. 

At the heart of atopic dermatitis is a complex interaction between genetics, environmental factors, and the immune system.  

On the genetic side, many individuals have mutations in the gene that encodes filaggrin. Without enough functional filaggrin, the wall loses its strength and cracks open leaving our body vulnerable. In other words, the skin loses its ability to retain moisture and keep out harmful substances.   

Moreover, this compromised skin barrier opens the door to environmental triggers and allergens, such as dust mites and pollen. But here’s the thing. The immune system is always on alert, with antige]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuron_action_potential</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PLfHsBaqQ0Gugh4Jpf7bb4u6SHazOihJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuron action potential]]></video:title><video:description><![CDATA[Neurons are the cells that make up our nervous system, and they’re made up of three main parts. 

The dendrites, which are little branches off of the neuron that receive signals from other neurons, the soma, or cell body, which has all of the neuron’s main organelles like the nucleus, and the axon which is intermittently wrapped in fatty myelin. 

Those dendrites receive signals from other neurons via neurotransmitters, which when they bind to receptors on the dendrite act as a chemical signal. 

That binding opens ion channels that allow charged ions to flow in and out of the cell, converting the chemical signal into an electrical signal. 

Since a single neuron can have a ton of dendrites receiving input, if the combined effect of multiple dendrites changes the overall charge of the cell enough, then it triggers an action potential, which is an electrical signal that races down the axon up to 100 meters per second, triggering the release of neurotransmitter on the other end and further relaying the signal. 

So neurons use neurotransmitters as a signal to communicate with each other, but they use the action potential to propagate that signal within the cell.

Some of these neurons can be very long, especially ones that go from the spinal cord to the toes, so the movement of this electrical signal within the cell is super important!

But why does the cell have an electric charge in the first place? Well, it’s based on the different concentrations of ions on the inside versus the outside of the cell. 

Generally speaking, there are more Na+ or sodium ions, Cl- or chloride ions, and Ca2+ or calcium ions on the outside, and more K+ or potassium ion and A- which we just use for negatively charged anions, on the inside of the cell. 

Overall, the distribution of these ions gives the cell a net negative charge of close to -65 millivolts relative to the outside environment, and this is called the neuron’s resting membrane potential. 

When a neurotransmitter bin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preeclampsia_&amp;_eclampsia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X3PX7g2XQPSPIc7i4BR-Al-yQzOyLMI7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preeclampsia &amp; eclampsia]]></video:title><video:description><![CDATA[Preeclampsia is a disorder that only happens in pregnant women, and it happens after 20 weeks’ gestation, and in some cases develops up to 6 weeks after delivery. 

Preeclampsia causes new-onset hypertension and proteinuria, which is a marker of kidney damage, and can also cause damage to other organs like the brain and liver. 

There can be a wide range of symptoms. For some women there may be no symptoms or only mild ones, whereas for others, it can turn into a life-threatening illness. 

If a woman with preeclampsia develops seizures, she is then said to have eclampsia.

Preeclampsia tends to occur more often during a first pregnancy, in pregnancies with multiple gestations, or in mothers 35 years or older. 

Other risk factors include having hypertension, diabetes, obesity, or a family history of preeclampsia. 

Alright, but why do these changes happen in preeclampsia and eclampsia? 

Well, the exact cause is unclear, but a key pathophysiologic feature though is the development of an abnormal placenta. 

Normally, during pregnancy, the spiral arteries dilate to 5-10 times their normal size and develop into large uteroplacental arteries that can deliver large quantities of blood to the developing fetus. 

In preeclampsia, these uteroplacental arteries become fibrous causing them to narrow, which means less blood gets to the placenta. 

A poorly perfused placenta can lead to intrauterine growth restriction and even fetal death in severe cases. 

This hypoperfused placenta starts releasing pro-inflammatory proteins. 

These then get into the mother’s circulation and cause the endothelial cells that line her blood vessels to become dysfunctional. 

Endothelial cell dysfunction causes vasoconstriction—narrowing of the blood vessels—and also affects the kidneys in a way that makes them retain more salt, both of which result in hypertension. 

When diagnosing preeclampsia, hypertension is defined as a systolic blood pressure of 140 mmHg or greater or diastoli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stages_of_labor</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v5Hmq3NNRqO1M_CZ4Fu8Ob3mTSe5sgfI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stages of labor]]></video:title><video:description><![CDATA[Learning medicine is hard work. Osmosis makes it easy. It takes your lectures and notes to create a personalized study plan with exclusive videos, practice questions and flashcards and so much more. Try it free today!

Labor, also called parturition, describes the hard work of delivering a baby!

It specifically refers to the process which starts with uterine contractions which cause cervical changes which allow the fetus to be delivered vaginally, and ends with delivery of the placenta.

Labor typically begins at some point when the fetus is considered full term—between 37 and 42 weeks’ gestation.

In the third trimester, before labor starts, a woman might have a plug of mucus and blood fall out of the opening to the cervix, sometimes called a “bloody show”.

Other times the amniotic sac might rupture, sometimes called “water breaking”.

Either of these can trigger the onset of labor and so-called true labor contractions.

These guys have to be distinguished from the milder and ineffective false labor contractions, also called Braxton Hicks contractions (or sometimes called practice contractions).

Once they start, true labor contractions progress in frequency, duration, and intensity, and they can feel like waves that build up to a peak intensity and then gradually decrease.

The contractions pull on the thick tissues of the cervix, causing it to efface or get thinner and also dilate or open up, so then the fetus can leave the uterus and enter the world.

From the moment true contractions begin to the baby’s delivery usually takes about 12 to 18 hours for a first-time pregnancy, and about half that time for subsequent pregnancies.

Although, as any mother knows, this time can vary a lot!

Even though labor is a continuous process, it can be broken down into three stages.

Additionally, this first stage is subdivided into two phases.

The first phase is the early phase or latent phase, and usually lasts up to 20 hours, or until the cervix dilates to 6 cen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tourette_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/89xuJFx0RS2qrlpSbUKzHdmcRNuTbpKE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tourette syndrome]]></video:title><video:description><![CDATA[There are three major types of tic disorders listed in the DSM-5: Tourette syndrome, which is the most well-known; persistent motor or vocal tic disorder; and finally, provisional tic disorder. 

Individuals with these disorders all suffer from tics, which are quick, nonrhythmic movements or vocalizations that occur over and over, and aren’t side effects of some other condition like Huntington’s disease or substance abuse. 

For example, individuals might feel the urge to spontaneously and repeatedly clap their hands, make a facial grimace, grunt, or even perform hidden movements like moving the tongue around inside the mouth. 

Although these actions and gestures might be appropriate in some situations, the fact that they are repeated even in inappropriate situations is why they are considered abnormal. 

In addition to having a tic, three additional criteria are used to help differentiate between the three types of tic disorders. 

Criteria A is the number of motor or vocal tics, criteria B is the duration of the tic disorder, and criteria C is the age of the person when they started having tics.

For a diagnosis of Tourette syndrome (also called Tourette’s), an individual must have multiple motor tics and at least one vocal tic; however, these do not have to happen at the same time. 

The important thing here is that both motor and verbal tics are present. 

The frequency of individual tics might change over time, but they need to persist for at least one year. 

Finally, the tics must have started before the age of 18—in fact, they most often appear between the ages of 4 and 6. 

Of the three types of tic disorders, Tourette’s is considered to be the most severe.

For a diagnosis of persistent motor or vocal tic disorder, also called chronic tic disorder, an individual must have either a single or multiple motor tics or vocal tics—but not both.

As with Tourette’s, the tics have to persist for at least a year and must have started before the age of 18.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eustachian_tube_dysfunction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_47a3h_WTxu5d9qjrGt9VyyCQqyvvD1T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eustachian tube dysfunction]]></video:title><video:description><![CDATA[The ear can be broken into three sections. 

The first is the outer ear which is the part you see called the pinna as well as the ear canal.

Next is the middle ear, which is a tiny chamber that houses the tiny ear bones—the malleus, incus, and stapes. 

And finally there’s the inner ear, which contains very special tissue structures called the cochlea which converts sound waves into electrical impulses for the brain and the semicircular canals which help with balance. 

Between the outer and middle ear is an eardrum, also called the tympanic membrane, so no air passes between the two areas.

But the middle ear does have another possible outlet, called the eustachian tube which acts like a valve connecting the middle ear to the nasopharynx.

This tube has three main functions—equalizing pressure across the tympanic membrane, protecting the middle ear from reflux of fluids going up from the nasopharynx, and clearing out middle ear secretions.

Eustachian tube dysfunction describes situations when one or all of these functions aren’t happening normally.

In an adult, the eustachian tube is a roughly 4 centimeter long part-bone, part-cartilage canal that’s surrounded by four key muscles: the tensor veli palatini, the levator veli palatini, the salpingopharyngeus, and the tensor tympani, and it’s those first two that help a lot with opening up the tube. 

Actions like chewing, swallowing, and yawning all pull on those muscles to help open up the eustachian tube. 

The first and most common type of eustachian tube dysfunction relates to a problem equalizing pressure across the tympanic membrane, and a classic example is on an airplane.

As the plane rises, the air pressure decreases. 

Since the middle ear chamber is a closed environment, it’s pressure stays relatively high and the tympanic membrane can begin to bulge a bit into the outer ear.

That increased middle ear pressure pushes a tiny bubble of air down the eustachian tube and into the nasopharynx where]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Herpes_simplex_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NEbcG99VSaiFmPvXJ-WtupRnQf6_Bc3T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Herpes simplex virus]]></video:title><video:description><![CDATA[Most of the time, when herpes simplex virus or HSV infects a person, there are no symptoms. 

In fact, it also usually moves from one person to another in the absence of symptoms, so it can therefore it can move through a population silently. 

Once in a while, though, it can cause symptoms, and typically those are in the form of skin and mucous membrane lesions which can be divided into infections “above the waist”—mostly involving the mouth and tongue, and those “below the waist”—involving the genitals. 

There are two types of herpes simplex viruses—HSV1 and HSV2—both of which are part of a larger family of enveloped double-stranded DNA viruses: the herpesviridae family. 

Generally speaking, HSV1 tends to cause infections above the waist and HSV2 tends to cause infections below the waist, but there’s a lot of crossover because both viruses can cause both types of infections. 

Although herpes is most contagious when there are virus-filled lesions present, it can also spread by asymptomatic shedding which means that herpes viruses can be in saliva or genital secretions even when there are no signs of a cold sore or genital lesion. 

Typically, when herpes virus lands on a new host, in other words a person that’s never had herpes before, it dives into small cracks in the skin or mucosa and binds to epithelial cell receptors, which triggers those cells to internalize the virus. 

Once inside, the virus starts up the lytic cycle, which is where its DNA gets transcribed and translated by cellular enzymes which help to form viral proteins which are packaged into new herpes viruses which can leave to go off and infect neighbouring epithelial cells. 

HSV1 and HSV2 also infect nearby sensory neurons, and travel up their axon to the neuron’s cell body to start up the latent cycle. 

The sensory neurons of the face have their cell bodies in the trigeminal nuclei and those around the genitalia are located in the sacral nuclei.

So that’s ultimately where the herp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pyloric_stenosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AzIDF7WQTwezRhjWaRG250J2ThuZ83gt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pyloric stenosis]]></video:title><video:description><![CDATA[With hypertrophic pyloric stenosis, hypertrophy refers to an increase in size, pyloric refers to the pylorus which is the tissue between the stomach and the duodenum, and stenosis means narrowing, so hypertrophic pyloric stenosis, or HPS, is a congenital condition where a baby’s pylorus grows in size such that it narrows the tiny opening between the stomach and the duodenum. 

The pylorus itself has two parts to it, the pyloric antrum, which connects to the body of the stomach, and the pyloric canal, which connects to the duodenum. 

At the end of the pyloric canal you’ve got the pyloric sphincter, which is a ring of smooth muscle that contracts and acts like a valve, letting food pass down into the duodenum, but not go back up into the stomach.

In HPS, babies are born with a normal pylorus, but within a few weeks after birth, the smooth muscle of the pyloric antrum begins to undergo hypertrophy and hyperplasia, meaning an increase in the size of each cell as well as an increase in the overall number of cells, respectively. 

This causes the pyloric antrum to nearly double in size. 

This thick and muscular antrum obstructs the pathway of food, which makes it harder for food to leave the stomach and enter the small intestine. 

Clinically the enlarged pylorus can be felt as an “olive” in the right upper quadrant or epigastric region of the abdomen, which is just above the umbilicus. 

Also, there’s normally contraction and relaxation of the smooth muscle lining the stomach, a process called peristalsis.

Obstruction from HPS can cause the stomach smooth muscle to have to work much harder to push food through, and sometimes there can even be hypertrophy of those muscles, which can result in peristalsis that can be felt or seen. 

If food can’t pass through the pylorus, it quickly starts to build up to the point where it has nowhere to go, which can lead to vomiting. 

This usually happens around 2-6 weeks, and can get more intense over time, until it ultim]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intestinal_atresia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3rAjMPzET5GtJpzrrLDbaKq0RamjnQOc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intestinal atresia]]></video:title><video:description><![CDATA[With intestinal atresia, atresia refers to a passageway that’s closed or gone completely, so intestinal atresia is when a malformation during fetal development results an absent portion of the small or large intestine.

If instead the passageway was just narrowed, then it’s referred to as intestinal stenosis—oftentimes these are both just lumped together as intestinal atresia and stenosis.

The specific type of intestinal atresia is named depending on what section of the intestines is affected. 

Duodenal atresia or stenosis is where the first section—the duodenum—is affected.

The underlying cause of duodenal atresia isn’t known, although it’s commonly associated with trisomy 21, also known as Down syndrome, suggesting that it’s likely due to genetic defects affecting normal development.

Although it isn’t known why intestinal atresia develops isn’t known, it is fairly well known how it develops.

Normally, early on in development, the gut’s a hollow tube. 

But by around 6 weeks gestation, the epithelium of the duodenum proliferates and it ends up plugging up the lumen making it a completely solid stick of tissue. 

After that, the cells in the middle undergo apoptosis, or programmed cell death, and by 9 weeks gestation, the tube’s hollow again, called recanalization. 

This entire process is called vacuolation.

In duodenal atresia, this vacuolation process fails, and the duodenum doesn’t recanalize properly, resulting in atresia or stenosis of the duodenum.

Non-duodenal intestinal atresias or stenoses, like those affecting the jejunum or ileum, or even affected the large intestine like the colon, are generally not a result of recanalization, and instead are more likely to result from ischemic injury, meaning lack of bloodflow, to the developing gut. 

Now, the jejunum, ileum, and large intestine rely on blood supply from the superior mesenteric artery, while only part of the duodenum does. 

So for example, looking at the jejunum, if the vessels suppl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscular_dystrophy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aAo593OwQrKYAWfl-wp6iFT6Sqqcujgs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscular dystrophy]]></video:title><video:description><![CDATA[With muscular dystrophy, “dys” means bad or difficult, and “troph” means nourish; so muscular dystrophy basically refers to the muscle appearing poorly nourished because of degeneration, which leads to muscle weakness. 

Under a microscope, a biopsy of the tissue shows changes in the muscle itself but not in the nerve or neuromuscular junction; this distinguishes muscular dystrophy from other problems that cause muscle weakness as a result of nerve damage, like neuropathies. 

Muscular dystrophy is actually a group of disorders, all of which are caused by genetic mutations. 

Within that group, dystrophinopathies are the most common, which includes Duchenne muscular dystrophy, or DMD, and Becker muscular dystrophy, both of which result from mutations in the dystrophin gene. 

In addition to those two, genetic mutations in other genes are responsible for several dozen other muscular dystrophies, some of which code for proteins that form a protein complex with dystrophin protein. 

These other muscular dystrophies, therefore end up causing a lot of the same symptoms as the dystrophinopathies.

Now, the fact that both Duchenne and Becker muscular dystrophy result from mutations in the same dystrophin gene means that they are “allelic disorders,” and when a mutation occurs in dystrophin that’s severe enough to result in no protein at all, for example a nonsense or a frameshift mutation, the result is Duchenne muscular dystrophy, which ends up being the more severe of the two, with symptoms usually presenting by age 5. 

On the other hand, mutations that allow for a misshapen protein to form, like missense mutations, lead to Becker muscular dystrophy which is basically a milder form of Duchenne muscular dystrophy that presents later on, usually between age 10 to 20.

Alright so the dystrophin gene is a huge gene on the X-chromosome, that has 79 exons and is over 2 million base pairs in length. 

By comparison, most genes have only about 10 exons and are 50 thou]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kidney_stones</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3X2H1O85TRenyTwk4uJ9UlAZSmylxdGN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kidney stones]]></video:title><video:description><![CDATA[With nephrolithiasis, “nephro-” refers to the kidneys, and “-lithiasis” means stone, so nephrolithiasis means kidney stones, sometimes also referred to as renal calculi or urolithiasis.

Kidney stones form when solutes in the urine precipitate out and crystalize, and although these most commonly form in the kidneys themselves, they can also form in the ureters, the bladder, or the urethra. 

Now, urine’s a combination of water, which acts as a solvent, and all sorts of particles, or solutes. 

In general, when certain solutes become too concentrated in the solvent, they become supersaturated. 

Urinary supersaturation of certain solutes results in precipitation out of the solution and formation of crystals. 

Those crystals then act as a nidus, or place where more solutes can deposit and over time it builds up a crystalline structure. 

This can happen if there’s an increase in the solute, or a decrease in the solvent, as would be the case with dehydration. 

In addition, there are substances like magnesium and citrate that inhibit crystal growth and aggregation, preventing kidney stones from forming in the first place. 

In the majority of cases, the inorganic precipitate is calcium oxalate, formed by a positively charged calcium ion binding to a negatively charged oxalate ion, which results in a black or dark brown colored stone that is radio-opaque on an Xray, meaning that it shows up as a white spot. 

Sometimes, instead of oxalate, the calcium binds a negatively charged phosphate group to form calcium phosphate stones which are dirty white in color and also radiopaque on an X-ray. 

Calcium oxalate crystals are more likely to form in acidic urine, whereas calcium phosphate crystals are more likely to form in alkaline urine. 

The exact reason why these stones form is usually unknown, but there are some known risk factors like hypercalcemia and hypercalciuria, having too much calcium in the blood and urine, respectively. 

Hypercalcemia can result from]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prader-Willi_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iwtgb1w9TFO_MeoOfSGcNRUfQJqBItNd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prader-Willi syndrome]]></video:title><video:description><![CDATA[Prader-Willi syndrome is a genetic disorder that, in infancy, causes poor feeding and low muscle tone, and then in childhood, causes overeating, intellectual disability, and low sex hormones starting in childhood. 

Prader-Willi syndrome happens when a handful of genes on chromosome 15 aren’t transcribed into messenger RNA and therefore aren’t expressed. 

Among these are SNRPN which stands for Small Nuclear Ribonucleoprotein Polypeptide N and a cluster of snoRNAs, which stands for small nucleolar RNAs, and these genes all have  protein products that modify other RNAs. 

Now, normally, the copies of the genes contributed by the mother, or maternally derived genes, to this region, are silenced, or turned off, and only the genes from dad, or paternally-derived genes, get expressed. 

This special genetic process is called imprinting, where only one copy of the gene gets expressed, not both. 

And this differs from most genes in the genome, where both the maternal and paternal copies are expressed.

So those maternal copies in this region are imprinted and therefore silenced. 

And this silencing of the maternal copies is an epigenetic process. 

In the word “epigenetic”, “epi” means outside of, and “genetic” refers to the DNA sequences of A’s, C’s, G’s, and T’s. 

So epigenetic silencing of a gene means turning it off while keeping the DNA sequence itself the same. 

The Prader-Willi genes get turned off when methyl groups get attached to the DNA, a process that happens way back when the mother was making an egg. 

Even after fertilization of the egg and all of the cell divisions it takes to make a person, that epigenetic mark remains, kind of like a reminder to keep those maternally-derived copies of the genes turned off. 

Unfortunately, though, this means that if paternal copies of the genes don’t get expressed, then there aren’t any backup copies being expressed, and so no copies get expressed! 

And this is what happens in  Prader-Willi syndrome!

Now, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastroschisis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rSo75tIYRHWp7uP1qLAQpiTsQ9uFYkpc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastroschisis]]></video:title><video:description><![CDATA[With gastroschisis, gastro- refers to the gastrointestinal tract, and -schisis refers to separation; so in gastroschisis, the anterior abdominal wall fails to close and remains open or separated throughout fetal development, and this results in a newborn’s abdominal organs, often the intestines, protruding out and being exposed to the outside environment.  

Now, during the fourth week of fetal development, the embryo starts to change shape from a flat, three-layer disc to something closer to a cylinder, called embryonic folding.

Looking at the embryo in the horizontal plane, the two lateral folds eventually come together and close off at the midline, except for one tiny spot where the umbilical cord connects the fetus to the placenta.

That opening later becomes the umbilicus, also known as the belly button. 

This folding allows for the formation of the gut within the abdominal cavity.

With gastroschisis, those lateral folds don’t close all the way, essentially leaving an opening in the abdominal wall. 

The hole almost always extends through the rectus muscle to the right of the umbilicus, although it’s not really known why it tends to be on the right side.

Whatever the reason is, this opening allows the developing organs to protrude through into the amniotic sac. 

Exposing the abdominal organs to amniotic fluid can sometimes cause the intestines to get irritated and inflamed, which can lead to malabsorption issues. 

Following delivery in gastroschisis, the bowels are exposed and they’re not covered by a peritoneal layer. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Volvulus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rbHODRd9T8KDhjKT5sfQBQ-cSLyQfl6b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Volvulus]]></video:title><video:description><![CDATA[The term volvulus actually comes from the Latin word volvere, which means “to roll”. 

So a volvulus is an obstruction caused by a loop of the intestine that rolls or twists around itself and its surrounding mesentery, which is the tissue that attaches the intestine to the back wall of the abdomen. 

The three most common types of volvulus are a sigmoid volvulus, which happens in the the last part of the large intestine, leading to the rectum; a cecal volvulus, which happens in the beginning of the large intestine, and a midgut volvulus, which happens in the small intestine.

Now, a sigmoid volvulus is the most common type of volvulus, and it can happen in a variety of settings.

One classic one being pregnancy, because the growing fetus can cause displacement and twisting of the colon. 

It can also develop, though, in middle-aged and elderly individuals. 

This can sometimes happen as a result of chronic constipation, where a big load of stool can act like a pivot point around which the rest of the colon can twist. 

Hirschsprung disease, a disease of the large intestine that causes severe constipation or intestinal obstruction, therefore raises the risk for developing sigmoid volvulus. 

In addition, there are also abdominal adhesions, where internal scar tissue creates a physical attachment between two parts of the abdomen, which again serves as a pivot point around which the colon can twist.  

A cecal volvulus is usually found in young adults, and usually happens in individuals who didn’t develop their abdominal mesentery normally during fetal development.

Since some mesentery contacts may be missing in these individuals, the colon can flop around freely and any large object—like a baby in pregnancy or a load of stool in someone constipated—can act as a pivot point in the cecum and cause the colon to twist.

Midgut volvulus is most commonly found in babies and small children and is the result of abnormal intestinal development in fetuses. 

In norma]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disseminated_intravascular_coagulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VWiC_rfUTqyq6SbvKvER_X9_Sz_tkRtu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disseminated intravascular coagulation]]></video:title><video:description><![CDATA[Disseminated intravascular coagulation, or DIC, describes a situation in which the process of hemostasis, which is when after blood vessel wall injury, liquid blood rapidly becomes a gel, called coagulation or clotting, starts to run out of control. 

When this happens, lots and lots of blood clots start to form in blood vessels serving various organs, leading to organ ischemia. 

DIC, though, is also called a consumption coagulopathy, because all this clotting consumes platelets and clotting factors. 

Without enough platelets circulating in the blood, other parts of the body begin to bleed with even the slightest damage to the blood vessel walls. So paradoxically, patients have too much and too little clotting.

Normally, after a cut and damage to the endothelium, or inner lining of blood vessel walls, there’s an immediate vasoconstriction or narrowing of the blood vessel which limits the amount of blood flow. 

After that, some platelets adhere to the damaged vessel wall, and become activated and then recruit additional platelets to form a plug. 

The formation of the platelet plug is called primary hemostasis. 

After that, the coagulation cascade is activated. First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver, and usually these are inactive and just floating around in the blood. 

The coagulation cascade starts when one of these proteins gets proteolytically cleaved. 

This active protein then proteolytically cleaves and activates the next clotting factor, and so on. 

This cascade has a huge degree of amplification and takes only a few minutes from injury to clot formation. 

The final step is activation of the protein fibrinogen to fibrin, which deposits and polymerizes to form a mesh around the platelets. 

So these steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis and results in a hard clot at the site of the injury. 

Now, as so]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intussusception</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fNypkyLjSOedPfBXoSEudamtTsy9ZYpI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intussusception]]></video:title><video:description><![CDATA[Intussusception is a condition that occurs when a part of the intestine folds into another section of intestines, resulting in obstruction. 

This is commonly referred to as telescoping, because it’s similar to how one part of a collapsible telescope retracts into another part.

Intussusception is the most common cause of intestinal obstruction in infants and young children, with about two-thirds of them happening among infants under one year of age, though adults can occasionally have intussusception too. 

Now, intussusception usually happens in the ileocecal region of the intestines, which is where the ileum of the small intestine and cecum of the large intestine meet, and almost all intussusceptions happen when the ileum folds, or telescopes, into the cecum. 

In adults, telescoping is usually caused by an abnormal growth in the intestine, like a polyp or a tumor, which serves as a lead point or leading edge. 

What happens is that the normal wave-like contractions of the intestine, called peristalsis, grab this leading edge and pull it into the part of the bowel ahead of it. 

In babies the leading edge is most often caused by lymphoid hyperplasia, or the enlargement of lymphoid tissue. 

There are a ton of tiny lymph nodes sprinkled throughout the intestines called Peyer’s patches, and they’re particularly common in the ileum. 

When a child gets some sort of viral infection in the gastrointestinal tract, usually caused by rotavirus or norovirus, the Peyer’s patches enlarge to help fight off the infection, and sometimes become a lead point that drags the ileum into the cecum, causing intussusception.

Intussusception can also be caused by a Meckel’s diverticulum, which is an abnormal outpouching of gastrointestinal tissue, that sticks out of the ileum and into the peritoneal cavity. 

Occasionally, the diverticulum can invert and stick back into the intestine, allowing it to serve as a lead point that again drags the ileum into the cecum.

Altho]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blended_learning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wx9EoOzTSKSLqb2VLaeuvm67SMus3sJa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blended learning]]></video:title><video:description><![CDATA[Blended learning is a way of teaching that combines online resources with in-person instruction to create a more personalized learning environment. 

With blended learning, instructors often make some or all of the content available to the students outside of class-time. 

Taking this to the extreme, students could consume all of the traditional lecture material at home at their own pace, and during class time students could complete work assignments traditionally given as homework during class, as well as other activities like team-based or project-based learning. 

This describes the flipped classroom model, because it flips what students do at home and in the classroom. 

Typically when a teacher creates a lecture they have to make an educated guess about the knowledge level of their audience, as they have limited information about what each student knows or remembers. 

If a lecture is too difficult, then most of the students will be lost. 

If it’s too easy, then most of the students will be bored. 

So teachers typically end up lecturing to the mythical middle of the class, and hoping for the best. 

By placing didactic content online, students can move at their own pace. 

Those who are familiar with the material can go through it quickly—even watching it at an increased speed! 

While others who aren’t as familiar with it can pause to take notes, rewatch it, or call up other resources to help them understand a concept being explained. 

An additional benefit for all students is that they can choose to engage with the material when they’re most alert, which satisfies both the early bird and the night owl. 

And those students who have disabilities can take the breaks that they need without having to worry about missing out or distracting others. 

Putting work assignments back in the classroom also has a number of benefits from a learning science perspective. 

A lot of students describe the frustration of feeling like they understand a concept in c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Carpal_tunnel_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Gkt_sV33Q8i2958aHYAZkiHLTvSZoDsV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Carpal tunnel syndrome]]></video:title><video:description><![CDATA[Carpal tunnel syndrome is a nerve entrapment disorder that results from compression of the median nerve which winds its way through the wrist through a narrow passageway called the carpal tunnel. 

This compression typically causes pain, numbness, and tingling in the thumb, index finger, middle finger, and the thumb side of the ring finger, which are the areas of skin innervated by the median nerve. 

Now taking a cross section of the wrist, we’ll see a bony arch known as a carpal arch on the dorsal side of the hand which forms the floor of the carpal tunnel, and a sheath of connective tissue called the flexor retinaculum or transverse carpal ligament, which is on the palmar side of the hand forms the roof of the carpal tunnel.

Also there are nine flexor tendons, which go to the fingers and thumb, as well as one nerve—the median nerve—which travels down the forearm and go through the carpal tunnel. 

The skin  of the hand served by the median nerve includes the thumb, the index finger, and middle finger, as well as half of the ring finger that’s on the thumb side. 

The other side of the ring finger and pinky are served by the ulnar nerve, and the back of the hand’s served by the radial nerve, only the median nerve goes through the carpal tunnel.

Carpal tunnel syndrome is caused by compression of the median nerve, and that typically happens as a result of inflammation of the nearby tendons and tissues, which creates local edema or swelling which increases the amount of fluid in a very tight space, and essentially puts pressure on the median nerve. 

Initially that pressure can cause a dull ache or discomfort in any of the areas of the hand that are innervated by the median nerve. 

Eventually this discomfort can lead to sharp, pins-and-needles-like pain, called paresthesia, which can extend up the forearm.

People might also have muscle weakness which can cause clumsiness with tasks like holding small objects, turning doorknobs and keys, or fine motor ta]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Placenta_previa</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E5gTAWUsTjabN5FxsZ5vWEzvRTmwPz8p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Placenta previa]]></video:title><video:description><![CDATA[Placenta previa means “placenta first,” because the placenta is the first thing within the uterine cavity. 

In this condition, the placenta implants in the lower uterus, close to or even covering the uterine opening, called the internal cervical os, and it can therefore easily bleed, which usually happens after 20 weeks of gestation.

Normally the placenta implants in the upper uterus, and it&amp;#39;s unclear why it implants in the lower uterus. 

One hypothesis is that the placenta implants lower down when the endometrium in the upper uterus is not well vascularized. 

In fact, endometrial damage from things like a previous cesarean section, an abortion (which could be induced or spontaneous), uterine surgery, and multiparity or multiple pregnancies can decrease vascularization and increase the risk of placenta previa. 

In other cases, risk factors for placenta previa include having multiple placentas or a placenta with a larger than normal surface area, which can both happen with twins or triplets, as well as maternal age of 35 years or more, intrauterine fibroids, and maternal smoking.

Placenta previa is classified by how close the placenta is to the cervical os, it can be complete where the placenta completely covers the cervical os; partial where the placenta partially covers the cervical os; or marginal where the edge of the placenta extends to within 2 cm of the cervical os.

As the pregnancy progresses, the lower uterine segment grows, and if the placenta’s in the lower uterus, this growth disrupts the placental blood vessels, which can cause bleeding. 

This usually a sudden onset of painless bright red bleeding that typically happens after 20 weeks gestation. 

The amount of bleeding can vary, and it can be intermittent or continuous, sometimes increasing during labor because of uterine contractions and cervical dilation. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemophilia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yCNdJaFYT3iHqsAa4boBswz1SraxT-rI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemophilia]]></video:title><video:description><![CDATA[The word “hemophilia” is a combination of the Greek words for “blood” and “love”, a way of saying that people with hemophilia “love to bleed”, or rather that it’s hard to stop bleeding. This is because the process called hemostasis, literally meaning to stop the flow of blood, is impaired.

Normally, after a cut and damage to the endothelium, or the inner lining of blood vessel walls, there’s an immediate vasoconstriction or narrowing of the blood vessel which limits the amount of blood flow. After that some platelets adhere to the damaged vessel wall, and become activated and then recruit additional platelets to form a plug. The formation of the platelet plug is called primary hemostasis. 

After that, the coagulation cascade is activated. First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver, and usually these are inactive and just floating around the blood. The coagulation cascade starts when one of these proteins gets proteolytically cleaved. This active protein then proteolytically cleaves and activates the next clotting factor, and so on. This cascade has a great degree of amplification and takes only a few minutes from injury to clot formation. The final step is activation of the protein fibrinogen to fibrin, which deposits and polymerizes to form a mesh around the platelets. So these steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis and results in a hard clot at the site of the injury.

In most cases of hemophilia there is a decrease in the amount or function of one or more of the clotting factors which makes secondary hemostasis less effective and allows more bleeding to happen.

Now, that coagulation cascade can get started in two ways. The first way is called the extrinsic pathway, which starts when tissue factor gets exposed by the injury of the endothelium. Tissue factor turns inactive factor VII into activated factor VIIa (a for]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-urothelial_bladder_cancers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ftqy0SZCS4mTb5uRSGWXIwRNRvuJfo3B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-urothelial bladder cancers]]></video:title><video:description><![CDATA[There are two types of bladder cancers—urothelial and non-urothelial types. 

The urothelium is special type of transitional cell epithelium that forms a stretchy, protective barrier in the bladder. The majority of primary bladder tumors are urothelial cell carcinomas also known as transitional cell carcinomas that obviously originate from the urothelium. 

Somewhat confusingly, non-urothelial tumors, like squamous cell carcinomas and adenocarcinomas, also often arise from the urothelium layer but are distinguished by the way that their cells differentiate. 

For example, the normal bladder surface is not normally lined with squamous epithelium, yet the cells in the urothelium can change shape and take on a flat, pancake-like appearance of squamous cells. This non-cancerous change is called squamous cell metaplasia. 

If these cells begin to grow unchecked they can turn into a squamous cell carcinoma. These tumors typically pop up in multiple locations, and show extensive keratinization, which is where the cytoplasm of the cells is filled with keratin, the same tough material in hair and nails. 

Squamous cell carcinomas typically arise in response to chronic irritation like from recurrent urinary tract infections, and long-standing kidney stones. 

Another cause, common in some parts of the world, is an infection with Schistosoma haematobium - a type of flatworm. In this infection, the infective larvae linger in the water and then burrow into human skin when given the opportunity, and travel to the liver to mature into adult flukes. From there young flukes migrate to the urinary bladder veins to sexually reproduce and lay eggs in the bladder wall. These eggs can get urinated out, but they also cause chronic inflammation in the bladder wall which is how they lead to squamous cell carcinomas.

Primary adenocarcinomas of the bladder are more rare, but unlike squamous cell carcinomas, they frequently metastasize. These are usually solitary, and derive from gl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Omphalocele</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fcIht7jiSzmu6-f_tGt6EHl0Qb_8to9p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Omphalocele]]></video:title><video:description><![CDATA[With an omphalocele, omphalo- refers to the naval, also known as the bellybutton—or more formally the umbilicus—which is the attachment site of the umbilical cord, and -cele relates to hernia or swelling. 

Omphalocele, therefore, is when some of the bowels herniate out into the umbilical cord.

During the fourth week of fetal development, the embryo starts to change shape from a flat, three-layer disc to something more shaped like a cylinder, a process called embryonic folding. 

In the horizontal plane, the two lateral folds eventually come together and close off at the midline, except for at the umbilicus, where the umbilical cord connects the fetus to the placenta. 

This folding allows for the formation of the gut within the abdominal cavity.

During around the sixth week of development, the liver and intestines grow really quickly, and because the abdominal cavity’s still pretty small, there’s limited space, which causes the midgut to herniate through the umbilical ring into the umbilical cord, and this happens normally. 

At about week 10, though, the abdominal cavity typically has grown enough to allow the midgut to come back from the umbilical cord.

With omphalocele, the midgut—along with potentially other organs from the abdominal cavity—fail to return back to the abdominal cavity, and therefore stay in the umbilical cord all the way through fetal development and even after birth. 

Now, since the intestines and potentially other organs aren’t meant to be in the umbilical cord, there can be complications like the abdominal cavity not growing to its normal size, as well as pinched blood vessels and loss of blood flow to an organ. 

So with an omphalocele, after birth the abdominal organs protrude out of the body, but are contained within the umbilical cord, meaning the organs are sealed by a peritoneal layer. 

In contrast, a related defect called gastroschisis involves the abdominal contents herniating out of the abdominal cavity as well, but it]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Opioid_dependence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0dmZ9ckBRJuWPrlHw6MnmqJoRtiNVIQJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Opioid dependence]]></video:title><video:description><![CDATA[Worldwide, opioids are the most common cause of drug-related deaths.The number of individuals using opioids has drastically increased over time, with an uptick in heroin use, and an even bigger uptick in prescription opioid use, and a large number of people using both. Because of the potential for opioid use disorder and overdose, opioids are regulated substances in many countries.  

As a class, opioids share one thing in common—they bind to opioid receptors in the brain, spinal cord, and gastrointestinal tract. Some are endogenous, meaning that they are produced naturally by the body, like endorphins, which are named for “endogenous morphine” due to their similar effects on the body. But others are exogenous, meaning that they come from outside the body, like heroin and morphine, which come from the opium poppy—a flowering plant that oozes a milky white liquid—while others like fentanyl are synthesized in the laboratory.  

To understand how opioids work, let’s zoom in on a region of the spinal cord that has opioid receptors. Normally, in the absence of endorphins, nociceptive fibers carry pain signals from the body to the dorsal, or posterior, horn of the spinal cord.  

Here they release neurotransmitters,  

like glutamate, substance P and calcitonin gene-related peptide. These neurotransmitters cause pain signals to be transmitted to the brain via ascending pain pathways. 

Now, let’s say someone goes to play a rigorous game of badminton. Exercise releases endorphins which activate the three major opioid receptors located on neurons, called the mu, kappa, and delta receptors.  

As endorphins or other opioids bind to these receptors on the presynaptic terminals of nociceptive fibers, they inhibit the opening of calcium channels, preventing calcium influx, and thereby blocking the release of pain-causing neurotransmitters like glutamate, substance P and calcitonin gene-related peptide. At the same time, endorphins also bind to postsynaptic neurons, op]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Posterior_urethral_valves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F4iCB_QUSZWjwnh8OwdYuD-aT72FnD1n/_.jpg</video:thumbnail_loc><video:title><![CDATA[Posterior urethral valves]]></video:title><video:description><![CDATA[Posterior urethral valve, or PUV, is a congenital disorder in boys where the posterior urethra, which is the section of the urethra nearest the bladder, is obstructed by membranous folds, or flaps of tissue. These flaps of tissue are collectively referred to as a congenital obstructive posterior urethral membrane, or COPUM. 

This blockage means urine can’t easily flow out, which leads to a backup of urine which can cause kidney problems, as well as less amniotic fluid which can cause respiratory problems.

Although the cause of PUV isn’t completely understood, it’s thought that normal development of the male urethra is disrupted between weeks 9 and 14 of gestation. 

Normal development involves the Wolffian duct integrating with the posterior urethra, which results in thin mucosal folds called plicae colliculi. 

It’s thought that PUV might result from abnormal integration of the wolffian duct, resulting in large plicae colliculi that fuse anteriorly, making it more difficult for urine to flow through.

When that urine can’t easily flow out because of increased resistance from an obstruction,  the intravesical pressure, or bladder pressure, starts to creep up. 

Holding urine under higher pressure leads to bladder wall hypertrophy and collagen deposition, both of which thicken the bladder wall. This thickening makes the bladder less compliant, meaning that small increases in urine volume causes large increases in bladder pressure, which makes the problem even worse. 

That high-pressure urine has nowhere to go but up to the ureters and eventually to the kidneys, causing hydronephrosis, which is the swelling of a kidney due to a buildup of urine. 

In PUV, since the bladder outlet is obstructed, the hydronephrosis is bilateral, meaning it affects both kidneys. 

Severe obstruction in utero can also lead to oligohydramnios, which is a low volume of amniotic fluid, since normally a significant proportion of amniotic fluid comes from fetal urine, and also, th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alcohol-induced_liver_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kM_cb9TcS1uKiFfbawQFF5EmQIaRCCZh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alcohol-associated liver disease]]></video:title><video:description><![CDATA[Alright, so when you drink alcohol, what happens? Well, okay, what happens to the alcohol? Well that’s mainly your liver’s job, right? 

Basically, once the alcohol gets to your stomach, most of it’s sent to your liver for processing. 

In very small amounts, alcohol is more or less harmless, but in excess, it can lead to serious liver complications, and is the leading cause of liver disease in western nations. 

Once in the liver cells or hepatocytes, it can take one of three pathways, one of which involves an enzyme called alcohol dehydrogenase or simply ADH, and this happens in the cytosol of the cell, another involves a catalase inside organelles called peroxisomes, and a third involves being converted by the enzyme cytochrome P450 2E1, sometimes just shortened to CYP2E1. 

All three of these pathways lead to the conversion of alcohol to acetaldehyde. 

Once the ADH enzyme is used to convert the alcohol, it needs another compound called NAD+, which is then converted into NADH. 

As NADH levels increase, and NAD+ levels decrease, this has two effects, higher NADH levels tell the cell to start producing more fatty acids, and lower NAD+ levels result in less fatty acid oxidation, both of which lead to more fat production in the liver. 

Now excessive fat in the liver is also known as fatty change or fatty liver, where it gets large, heavy, greasy, and tender, but typically at this point, patients don’t have symptoms like fever or high levels of neutrophils in the blood. 

The liver also often takes on a more yellowish color, which is due to all these fat deposits, and we can see that on histology. 

All these circles are deposits of fat that contribute to fatty liver disease, and sometimes this buildup of fat in the liver is referred to as steatosis. 

Treating fatty liver disease usually involves simply stopping the alcohol consumption. 

K so that’s fatty liver, but that’s not the only thing that excessive alcohol consumption can cause, right? 

Looking]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alport_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4VyaeKj2TkmmQzNGdW-7mho0RZSJvZcG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alport syndrome]]></video:title><video:description><![CDATA[Collagens are a family of proteins that are collectively the most abundant protein in the body, and can be found throughout the various connective tissues. 

Each member of the family is named with a Roman numeral, and if mutated or absent, can lead to problems in the tissues where that particular collagen is found. 

Alport syndrome occurs as a result of mutations in Type IV collagen, which is particularly important in the glomerulus of the kidney, the eye, and the cochlea, and that’s why the symptoms of Alport syndrome are specific to those tissues.

Type IV collagen is a sheet-like structure found in all basement membranes and serves to support cells and form barrier. 

The three basement membrane layers are the lamina lucida, lamina densa (where type IV collagen is), and lamina reticularis. 

Now within the kidneys, there are glomeruli, which filter the blood and that together with a tubule forms a nephron. 

These glomeruli happen to have a basement membranes, called the glomerular basement membrane, or GBM, and that GBM, along with the fenestrated, meaning has pores, capillary endothelium and the podocyte slit diaphragm, forms a selective filter, meaning that water and certain other plasma components can escape the capillary, forming the filtrate that will become urine, but red blood cells and most proteins stay in the glomerular capillary. 

In Alport syndrome, kidney function is normal through early childhood, but over time, the missing or nonfunctional type IV collagen causes the GBM to become thin and overly porous. 

This allows red blood cells to pass right through from the capillary to the urinary filtrate leading to microscopic hematuria, which is where red blood cells are seen in the urine under a microscope, and this might eventually lead to gross hematuria, where the red blood cells can be seen with the naked eye. 

Over time, excessive amounts of protein start to get through the filter, resulting in proteinuria, or protein in the urine. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bipolar_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8ZBkEHo0TqOnGzf8N7aHMajkRuaMky98/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bipolar and related disorders]]></video:title><video:description><![CDATA[Maybe you’ve heard the term “bipolar” used flippantly to describe someone who’s moody, or who has mood swings, but the colloquial use of the term is really different from clinically diagnosed bipolar disorder. Bipolar disorder, which used to be called manic depression, is a serious mental disorder that causes a person to have dramatic shifts in emotions, mood, and energy levels: moving from extreme lows to extreme highs. But these shifts don’t happen moment to moment—they usually happen over several days or weeks. Now, bipolar and related disorders include several different conditions, but the most important ones are bipolar I disorder, bipolar II disorder, and cyclothymic disorder. 

Now, let’s cover some important clinical features associated with these conditions. The first one is a major depressive episode, which is characterized by the low moods that are identical to those in a related disorder: major depressive disorder, also known as unipolar depression. During major depressive episodes, individuals  can feel hopeless and discouraged, lack energy and mental focus, and can have physical symptoms like eating and sleeping too much or too little.  

But along with these lows, the thing that sets bipolar disorders apart from unipolar depression is that individuals can have periods of high moods, which are called manic episodes or hypomanic episodes, depending on their level of severity.  

Manic episodes are described as an abnormally elevated mood that lasts for at least one week or requires hospitalization. In a manic state, people can feel energetic, overly happy or optimistic, euphoric with really high self-esteem, or even unusually irritable.  

And on the surface, these might seem like very positive characteristics, but when an individual is in a full manic episode, these symptoms can reach a dangerous extreme. A person experiencing mania might invest all of their money in a risky business venture or behave recklessly.  

Individuals might tal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypoxia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GpKN561xTl_FXuTXyNeZSheGTriOxYKC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypoxia]]></video:title><video:description><![CDATA[So by this point, you’re probably aware that your body needs oxygen to survive, right? 

In fact, every cell in your body needs that precious oxygen. 

Those cells use the oxygen to produce energy in the form of ATP, or adenosine triphosphate, a super super important molecule, sometimes even called “the molecular unit of currency”.

The cells use it to basically pay the molecules inside the cell to do their specific jobs. 

It’s like one big factory with a bunch of workers that all have specific jobs needed to run the factory, and they only take ATP as payment.

Now the mitochondrion of the cell takes in oxygen and makes ATP to pay the workers, through a process called oxidative phosphorylation, the mitochondrion’s like the factory’s payroll department, right?

When the cell doesn’t get enough oxygen, and so payroll can’t produce the ATP that they need to pay the workers to do their jobs, the whole cellular factory can be damaged or even die, and we call that process hypoxia, where hypo means “less than normal” and oxia means “oxygenation”. 

When the oxygen comes in, typically it goes straight to payroll, specifically to the inner mitochondrial membrane where oxidative phosphorylation takes place. 

Oxygen’s used in one of the last steps, and serves as an electron acceptor, and this allows the process to finish and produce ATP. 

So without oxygen, we can’t finish oxidative phosphorylation and produce ATP.

But why does the whole factory fall apart when payroll stops making ATP? Why don’t they just pause for a bit? Take a little break? 

Well, when certain workers stop doing their jobs...things get a little out of hand. 

One super important worker is the sodium potassium pump on the cell’s membrane, pretty much like the bouncer that makes sure there isn’t too much sodium diffusing into the cell, basically by pumping it back out every time it diffuses in and maintaining a concentration gradient, this process also keeps too many water molecules from passiv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gallstones</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IqDyl2_IQgOBm6UWWP4X7falR_mfwdAu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gallstones]]></video:title><video:description><![CDATA[Gallstones are hard deposits, or simply stones, that form inside the gallbladder. This condition is also known by the Greek name, cholelithiasis. &amp;quot;Chole&amp;quot; means bile, &amp;quot;lith&amp;quot; comes from the word lithos, meaning stone, and &amp;quot;-iasis&amp;quot; refers to an abnormal condition in the body. Put it all together, and cholelithiasis means having bile stones.  

Now, picture yourself enjoying a creamy plate of Greek moussaka. As those fats move through your digestive system, they finally reach the small intestine. But fats are difficult to process, and that’s where the small, pear-shaped organ gallbladder steps in.  

The gallbladder acts as a storage tank for bile produced by the liver. The liver carefully blends this digestive smoothie with just the right mix of bile salts, phospholipids, cholesterol, and bilirubin. 

The liver starts the recipe by converting cholesterol into bile acids, such as cholic acid. Then it mixes these bile acids with amino acids like taurine to create water-soluble bile salts that flow smoothly into the bile.  

But not all cholesterol takes this path. Some slip directly into bile as free cholesterol, where it mixes with bile salts and phospholipids like lecithin. These ingredients act like tiny detergents, wrapping around cholesterol molecules to keep them from crystallizing and clumping.  

Another key ingredient in bile is bilirubin, which comes from the natural breakdown of red blood cells. When red blood cells reach the end of their life, they release hemoglobin, which is further broken down into heme and globin. The body converts heme into biliverdin and biliverdin to unconjugated bilirubin. However, unconjugated bilirubin isn’t water-soluble, so it binds to albumin to hitch a ride to the liver. In the liver, the body transforms unconjugated bilirubin into water-soluble conjugated bilirubin ready for excretion into bile. 

The liver produces bile continuously, sending it either direct]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breastfeeding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pfK1TKHrQd62sHkeDXcvHUxRRICNYR9l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breastfeeding]]></video:title><video:description><![CDATA[Breast milk is pretty amazing; it has all of the nutrients that a baby needs in the first six months of life. The benefits for the baby are impressive - they include lower rates of allergies, ear and lung infections, obesity, and sudden infant death, as well as healthier weight gain, and other long-term outcomes. That’s compared to infants given cow-milk formula. Moms can benefit from breastfeeding, too. It reduces uterine bleeding, burns calories, and decreases the risk of breast, ovarian, and uterine cancer, as well as osteoporosis, arthritis, type II diabetes, and heart disease. Finally, breastfeeding is free and offers mothers and babies a valuable opportunity to bond from the very first skin-to-skin contact—which should start minutes after birth.

To understand breastfeeding, let’s start with the breasts themselves. Breast tissue develops during puberty, and is made up of adipose or fat tissue, as well as glandular tissue that makes the milk, and lactiferous ducts which serve as passageways which guide the milk to the nipple. 

Zooming in on the glandular tissue, there is the alveolus, which is a modified sweat gland made up of alveolar cells which actually make the breast milk. Wrapping around the alveolus are special myoepithelial cells that squeeze down and push the milk out of the alveolus, down the lactiferous ducts, and out one of the pores on the nipple, at which point it enters the baby’s mouth. When the breasts are full of milk they can get heavy, and there are suspensory ligaments called Cooper’s ligaments which help to hold them up against the chest wall. 

During pregnancy the placenta releases human placental lactogen and progesterone, and the anterior pituitary gland releases prolactin, and all three of these hormones stimulate the growth of more glandular tissue and prepare the alveolar cells to produce milk. However, even though the breasts are capable of making milk by mid-pregnancy, the high levels of progesterone associated with pre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hydronephrosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gmc_HbyURbq-e1vLoz-ZqGrORt6gLev4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hydronephrosis]]></video:title><video:description><![CDATA[With hydronephrosis, -hydro means water, -nephro means kidneys, and -osis refers to a disease state, so hydronephrosis refers a disease or condition where excessive amounts of water, in the form of urine, causes the kidneys to dilate. 

Now, normally, inside the kidneys, urine forms in the nephron and then drains through the papilla which is an inverted cone shaped pyramid, that, like a shower head, pours urine into the calyces, which comes from the latin -calix which means large cup, like a Roman chalice.  

From there it enters the renal pelvis which funnels the urine into the ureter.

If there’s an obstruction to this normal flow of urine, then it can cause urinary pressures to increase and push out on the walls of these structures making them dilate. This might happen because of something within the urinary tract,for example, a kidney stone, or from external compression, for example, when a fetus pushes up against the urinary tract during pregnancy. 

Typically the dilation starts closest to the site of the problem and then slowly continues back up towards the kidneys. 

Now, if there’s dilation of just the ureter, it’s called hydroureter, but if there’s dilation of the ureter, renal pelvis, and the calyces, it’s called hydroureteronephrosis or more commonly just hydronephrosis. 

The causes of hydronephrosis differ by age group. 

Hydronephrosis in the fetus is called antenatal hydronephrosis, and sometimes the cause here is unknown, and it develops and disappears on its own, so it may be a variation of normal development. But if hydronephrosis progresses through fetal development into the third trimester, then there may be an actual underlying pathology. For example, there’s congenital ureteropelvic junction obstruction, which is where the ureteropelvic junction—which connects the ureter to the kidney—fails to canalize during development, which can obstruct the flow of urine.

Another cause is vesicoureteral reflux which is where urine is allowed to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Placental_abruption</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O3yOzSMVRsO7d2CDNGcQGk_ASrCh-c_h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Placental abruption]]></video:title><video:description><![CDATA[Placental abruption is the premature separation of all or even just a part of the placenta from the uterine wall, resulting in hemorrhage, or bleeding. 

This usually happens after about 20 weeks of gestation, and affects about 1% of pregnancies worldwide. 

The placenta forms where the embryo attaches to the uterine wall and it’s a unique organ because it develops from both the mom and the fetus, and it’s job is to permit gas and nutrient exchange between them. 

The word “placenta” literally means “flat cake.” So picture it as a cake with two layers, the maternal layer and a fetal layer. 

The maternal layer, the decidua basalis, is literally a flattened out bag of blood with uterine arteries delivering blood in and uterine veins pulling blood out. 

But unlike other parts of the circulatory system where blood stays within narrow blood vessels, the decidua basalis is a huge pool of blood.

The fetal layer of the placenta on the other hand is called the chorion, which is a tissue that has fingerlike projections called chorionic villi which contain tiny fetal arterioles and venules. 

These villi push into the decidua basilis, like tiny fingers reaching into a warm pool of oxygen-rich maternal blood. 

Gases and nutrients move back and forth between the decidua basalis and the fetal veins, by diffusing through the tissue layer of the thin chorionic villi. 

Placental abruption happens when there is a separation of the uterine wall and decidua basalis.

This separation is usually caused by degeneration of the uterine arteries that supply blood to the placenta typically from chronic problems like smoking or hypertension. 

These diseased vessels rupture, causing hemorrhage and separation of the placenta.

If the separation is near the margin of the placenta, it can cause vaginal bleeding, but if the separation is more central, there might be a pocket of blood that stays concealed between the decidua basalis and the uterine wall.  

Placental abruption can be]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperkalemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fcgiIOuNQdqaKwMuwoarushETU2BcXnH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperkalemia]]></video:title><video:description><![CDATA[With hyperkalemia, hyper- means over and -kal- refers to potassium, and -emia refers to the blood, so hyperkalemia means higher than normal potassium levels in the blood, generally over 5.5 mEq/L.

Now, total body potassium can essentially be split into two components—intracellular and extracellular potassium, or potassium inside and outside cells, respectively.

The extracellular component includes both the intravascular space, which is the space within the blood and lymphatic vessels and the interstitial space, the space between cells where you typically find fibrous proteins and long chains of carbohydrates which are called glycosaminoglycans.

Now, the vast majority, around 98%, of all of the body’s potassium is intracellular, or inside of the cells.

In fact, the concentration of potassium inside the cells is about 150 mEq/L whereas outside the cells it’s only about 4.5 mEq/L.

Keep in mind that these potassium ions carry a charge, so the difference in concentration also leads to a difference in charge, which establishes an overall electrochemical gradient across the cell membrane. This is called the internal potassium balance.

This balance is maintained by the sodium-potassium pump, which pumps 2 potassium ions in for every 3 sodium ions out, as well as potassium leak channels and inward rectifier channels that are scattered throughout the membrane.

This concentration gradient is extremely important for setting the resting membrane potential of excitable cell membranes, which is needed for normal contraction of smooth, cardiac, and skeletal muscle.

Also, though, in addition to this internal potassium balance, there’s also an external potassium balance, which refers to the potassium you get externally through the diet every day.

On a daily basis the amount of potassium that typically gets taken in usually ranges between 50 mEq/L to 150 mEq/L, which is way higher than the extracellular potassium concentration of 4.5 mEq/L, so your body has to figur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypokalemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/06fxE5eOSRemwguAXnDGaw27THWBQVUz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypokalemia]]></video:title><video:description><![CDATA[With hypokalemia, hypo- means under and -kal- refers to potassium, and -emia refers to the blood, so hypokalemia means lower than normal potassium levels in the blood, generally under 3.5 mEq/L.

Now, total body potassium can essentially be split into two components—intracellular and extracellular potassium, or potassium inside and outside cells, respectively. 

The extracellular component includes both the intravascular space, which is the space within the blood and lymphatic vessels and the interstitial space—the space between cells where you typically find fibrous proteins and long chains of carbohydrates which are called glycosaminoglycans. 

Now, the vast majority, around 98%, of all of the body’s potassium is intracellular, or inside of the cells. 

In fact, the concentration of potassium inside the cells is about 150 mEq/L whereas outside the cells it’s only about 4.5 mEq/L. 

Keep in mind that these potassium ions carry a charge, so the difference in concentration also leads to a difference in charge, which establishes an overall electrochemical gradient across the cell membrane. 

And this is called the internal potassium balance. This balance is maintained by the sodium-potassium pump, which pumps 2 potassium ions in for every 3 sodium ions out, as well as potassium leak channels and inward rectifier channels that are scattered throughout the membrane. 

This concentration gradient is extremely important for setting the resting membrane potential of excitable cell membranes, which is needed for normal contraction of smooth, cardiac, and skeletal muscle.

Also, though, in addition to this internal potassium balance, there’s also an external potassium balance, which refers to the potassium you get externally through the diet every day. 

On a daily basis the amount of potassium that typically gets taken in, usually ranges between 50 mEq/L to 150 mEq/L, which is way higher than the extracellular potassium concentration of 4.5 mEq/L, so your body has]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Learning_disability</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/81cq3z3LScSW5aNP3115SLi5R12gaX0v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Learning disability]]></video:title><video:description><![CDATA[The DSM-5 defines specific learning disorders as a set of disorders that relate to having difficulty learning and developing certain skills for at least 6 months. 

First, there’s dyslexia, which is difficulty with reading, then there’s dysgraphia, which is difficulty with writing, and finally there’s dyscalculia, which is difficulty with mathematics. 

People can have difficulty with just one of those activities, but they can also have problems in all three areas. 

These disorders are considered specific learning disorders because they don’t stem from another condition like an intellectual disorder or a global developmental delay, and they aren’t due to an obvious environmental cause like not being taught how to read, write, or do math. 

Learning disorders are usually diagnosed during the school-aged years, when a child’s skill can be assessed and is found to fall significantly below the average of other children in their age group. 

Dyslexia affects both oral and written communication throughout an individual’s life. 

People with dyslexia often have trouble identifying letters or words, and this can result in slow, inaccurate, and effortful reading. 

This often becomes obvious when a person with dyslexia is reading aloud, because they might have to hesitate or guess at words, and they might end up reading without normal intonation or expression.

Dyslexia can also cause difficulty with spelling because a person might add or omit letters by mistake. 

Having to go through all of this extra effort with reading means that people with dyslexia might also have a hard time understanding what they’ve read, missing the deeper meaning of a passage, forgetting the correct sequence of events, or being unable to make inferences about what they’ve read. 

Dysgraphia describes having trouble with writing: specifically, poor spelling and difficulty with grammar. 

People with dysgraphia often have poor handwriting, even though they don’t have trouble with other fi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypospadias_and_epispadias</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yideCJAhQ7WCWujAgvckQOxaSJCQ8oMT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypospadias and epispadias]]></video:title><video:description><![CDATA[With hypospadias and epispadias, the prefix -hypo means below, - epi means above, and the suffix -spadias refers to a slit or opening.

So instead of having an opening at the tip of the urethra, hypospadias refers to an abnormal opening on the bottom of the urethra and epispadias refers to an abnormal opening on the top of the urethra, and both of these can happen in boys and girls, but are way, way more common in boys. 

During genital development in the fetus, there&amp;#39;s a point in the 8th week of gestation, when both boys and girls have a similar bit of tissue called the genital tubercle which normally grows in the cranial direction, meaning that it grows towards the head.

After that point, in boys, the genital tubercle responds to the hormone dihydrotestosterone and stretches out a bit into a primitive phallus. 

As it grows in length, an area of tissue on the underside called the urethral plate invaginates to form a urethral groove which is lined with epithelial cells. 

In the 14th week of gestation, the two urethral folds on the sides pinch off the groove to make it close, and form the penile urethra. 

In the 17th week of gestation, the ectodermal cells of the glans penis or head of the penis also undergo a process of canalization, and the urethral canal connects with the penile canal, and that means that the urethra eventually meets the outside world at the tip of the penis.

In a boy, hypospadias happens when the urethral folds along the penile urethra don’t meet up and close properly.

And that leaves an opening somewhere along the bottom of the penile shaft and urine can leak out at that spot, instead of going out the tip of the penis like it should. 

Anatomically, hypospadias can happen in three areas: glanular, which is near the head of the penis, midshaft, which is the middle of the penis, and penoscrotal—where the penis and scrotum come together. 

Generally, the  least severe hypospadias are glanular and most severe are penoscrotal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alcohol_use_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xutOQk2wTeWGeDNexCCaNR-iQxuniRaS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alcohol use disorder]]></video:title><video:description><![CDATA[Alcohol is one of the most widely used psychoactive substances in the world, and has been a part of different cultures for hundreds of years. 

Drinking alcohol can have serious harmful consequences, it’s been linked to various cancers, gastrointestinal diseases, and metabolic problems. 

Over time, regular use of alcohol can lead to alcohol dependence and bouts of withdrawal, and this can take a serious physical and emotional toll on a person’s life. 

Alcoholic drinks contain the chemical ethanol, which is a tiny molecule that reduces the activity of various inhibitory and excitatory neurotransmitter pathways in the brain. 

Inhibitory neurotransmitters make neurons in the central nervous system less likely to fire an action potential, and the brain’s major inhibitory neurotransmitter—gamma-aminobutyric acid or GABA—acts as an “off” switch and restricts brain activity. 

Ethanol is a GABA agonist, so when it binds to GABA receptors it makes that inhibitory signal even stronger. 

Ethanol also activates opioid receptors and induces the release of endogenous morphine—known as endorphins. 

The opioids then bind to receptors on dopaminergic neurons in the nucleus accumbens, which trigger the release of dopamine and serotonin in that part of the brain. 

Ethanol also acts as a glutamate antagonist. 

In other words, ethanol blocks glutamate, which is an excitatory neurotransmitter, from binding to glutamate receptors, making it less likely that those neurons will fire. 

The combined effect that ethanol has on these neurotransmitters varies by the location in the brain. 

For example, in the nucleus accumbens and the amygdala, which are the reward centers of the brain, ethanol produces pleasant or rewarding feelings like euphoria. 

This is important because if a person believes that drinking leads to euphoria, they are more likely to drink again. 

In the cerebral cortex, the thought-processing center of the brain, ethanol slows everything down, making it d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Potter_sequence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zPe1poMlRwuDnuLxd_TtwKi2S_uuh1zg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Potter sequence]]></video:title><video:description><![CDATA[Potter sequence is a rare disorder that is sometimes called oligohydramnios sequence—a term that helps define it because oligo- means low and -hydramnios means amniotic fluid. 

So in Potter sequence there’s basically very little amniotic fluid and this makes the uterus a pretty hostile place for the fetus to grow. 

Typically, around the 20th week of gestation, the kidneys, ureters, and urethra develop and start producing and excreting urine, and this urine becomes the major source of amniotic fluid. 

Various conditions like renal agenesis, which is when one or both kidneys are missing, or atresia of the ureter or urethra, which is where those parts of the urinary tract are obstructed, can lead to an inability to produce or excrete urine and therefore leads to oligohydramnios. 

Other common causes can include amniotic rupture, which is the leakage of amniotic fluid, or uteroplacental insufficiency,  which is where there’s low blood flow from the placenta meaning the fetal organs—which includes the fetal kidneys—see less blood flow, which in turn leads to decreased urine production.

When there’s very little amniotic fluid, a couple of things happen as a result. First, amniotic fluid is crucial for the development of the fetal lungs, by both helping the airways physically stretch out as well as contributing amino acids like proline, which helps with the formation of connective tissue and collagen in the lung. 

With less amniotic fluid, though, there’s pulmonary hypoplasia. Hypo meaning under, and -plasia means formation, so the lungs basically remain underdeveloped. 

Not only that though, with less amniotic fluid, there’s less space in the amniotic sac, and so the fetus is literally compressed into a smaller space, which causes developmental abnormalities like a flattened face, wrinkly skin, widely separated eyes with epicanthal folds, low-set ears, as well as limb abnormalities like clubbed feet. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Angiomyolipoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V2WwyU9yR1qGE5G8SxmqTKLdQAyQOfdi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Angiomyolipoma]]></video:title><video:description><![CDATA[Angiomyolipomas are the most common benign tumors found in the kidneys, although they can be found in other tissues like the liver and on rare occasions in some reproductive structures. 

If we break down the word we see that they are tumors that are comprised of blood vessels (angio), smooth muscle (myo), and adipose or fat tissue (lipo). 

Angiomyolipomas are often described as hamartomas, which means that they are focal, abnormal growth of cells which are normally found at that site, but are disorganized. 

It’s a bit like a house with a front door that can’t be reached, it’s the right part for the structure, but it’s not organized in the right way. 

Angiomyolipomas also belong to the perivascular epithelioid cell tumor family, or PEComa family, meaning that they are made of epithelial-like cells that are found around blood vessels. 

Now, it’s worth mentioning that normally there are no perivascular epithelioid cells that exist; the name just refers to the way that the tumor cells look under the microscope. 

The actual cell type from which PEComas, including angiomyolipomas arise, is not known.

The majority of angiomyolipomas will pop up sporadically - which means they are not a part of a syndrome - as isolated lesions. 

Interestingly, the tumors develop more often in the right kidney than in the left. 

However, these tumors are also strongly associated with tuberous sclerosis which is a genetic disease that causes benign tumors to develop in various parts of the body. 

Individuals with tuberous sclerosis often have multiple angiomyolipomas along the surface of both kidneys, and they can be larger in size than the sporadic ones.

Regardless of whether the angiomyolipoma occurs sporadically or as a consequence of tuberous sclerosis, there is usually an underlying mutation in one of the tuberous sclerosis genes - TSC1 or TSC2 - which code for the tuberous sclerosis complex proteins hamartin and tuberin, respectively. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Plasmodium_species_(Malaria)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qJW6m6B0R7SgUgwslyuWuRA-RZKL_wcS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Plasmodium species (Malaria)]]></video:title><video:description><![CDATA[Malaria is an infection that can be caused by a few different types of Plasmodium species, which are single-celled parasites that get spread around by mosquitoes. 

Once the plasmodium gets into the bloodstream, it starts to infect and destroy mainly liver cells and red blood cells, which causes a variety of symptoms and sometimes even death. 

Malaria is a serious global health problem that affects millions of people, particularly young children under the age of 5, pregnant women, patients with other health conditions like HIV and AIDS, and travelers who have had no prior exposure to malaria. 

Tropical and subtropical regions are hit the hardest, together the most affected regions form the malaria belt, which is a broad band around the equator that includes much of latin america, sub-saharan africa, south asia, and southeast asia. 

There are hundreds of types of Plasmodium species, but only five cause malarial disease in humans, and those are Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, Plasmodium ovale, and Plasmodium knowlesi. 

Plasmodium vivax uses a specific erythrocyte surface receptor called the Duffy antigen. 

And some individuals, particularly those with sickle-cell anemia lack this receptor, meaning that Plasmodium vivax cannot get into their cells. 

In other words, having sickle cell anemia is genetically related to having relative protection from Plasmodium vivax. 

Other diseases, like thalassemia and G6PD deficiency make the parasite-infected erythrocyte more susceptible to dying from oxidative stress. 

So despite the obvious downside to having any of these diseases, they do offer an upside when it comes to warding off a malaria infection. 

In fact, because malaria has historically circulated in Africa, the genes underlying these diseases are thought to have conferred a natural selection advantage and therefore become more common in the genetic pool. 

Now, malaria begins when a plasmodium-infected female Ano]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Somatic_symptom_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NsSzLXtWTvWTasYdLN7D1jzQT7iwJXEX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Somatic symptom disorder]]></video:title><video:description><![CDATA[Somatic symptom disorder, which used to be called somatization or somatoform disorder, involves physical symptoms that aren’t explained by any known physical or mental disorder; in other words, their origins are unknown. 

That said, individuals aren’t “faking” their symptoms; these symptoms are very real and often made worse by the fact that they cannot be scientifically explained. 

This is pretty different from situations where an individual with a factitious disorder might fake an illness or injury in order to get attention.

A diagnosis of somatic symptom disorder requires that individuals experience some set of unexplained physical symptoms, called somatic symptoms, for a period of at least 6 months.

The symptoms experienced by individuals with this disorder can be incredibly varied, encompassing anything from pain to gastrointestinal problems to sexual symptoms. 

Although the somatic symptoms being experienced are chronic, the exact location, kind, and severity of the symptoms typically changes over time. 

The one symptom that does often persist over time is chronic pain, and because it’s persistent and has no clear underlying cause, it can be particularly hard to treat.

Somatic symptom disorder often leads to cognitive symptoms as well, with people having persistent thoughts and feelings about their symptoms, like worry and anxiety, and sometimes in particularly bad cases, catastrophic thoughts about death. 

More often than not, it’s these cognitive symptoms felt in response to the physical symptoms, rather than the physical symptoms themselves, that are used as the basis for a diagnosis of somatic symptom disorder.

In fact, clinicians rate the severity of somatic symptom disorder based on the person’s experience with these cognitive symptoms, rather than the physical ones.

The condition is considered mild if there’s only one cognitive symptom, like ruminating a lot on the symptoms. 

It would be considered moderate if there are two or more cognitive symptoms, like rumination and anxiety. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Warthin_tumor</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BvHZDLfAQNeFQzXw4ypfn-9TTDKjH1fH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Warthin tumor]]></video:title><video:description><![CDATA[Warthin’s tumor, or Warthin tumor, is a benign slow-growing tumor of the parotid gland named for Dr. Aldred Scott Warthin, who was the first pathologist to described it. 

Normally, the parotid gland has glandular cells that make enzymes that help to break down food, as well as tiny ducts lined by epithelial cells that carry those enzymes towards the mouth. 

Warthin tumor’s other name, papillary cystadenoma lymphomatosum, is long and technical but describes the disease pretty well. 

Cystadenoma refers to the fact that the ducts grow in size and fill up with serous fluid and cellular debris which forms a large cyst. 

Papillary refers to the fact that the layer of epithelial cells start to fold into the duct which forms a finger-like projection, called a papilla. 

Finally, lymphomatosum refers to the fact that the epithelium layer gets infiltrated by lymphocytes which organize themselves into what look like germinal centers, which is something you’d would expect to find if you looked at the cross section of a lymph node. 

Looking at histology, we can see the papilla, the lymphocytes, and the cystic space where the serous fluid and cellular debris are.

Now, Warthin’s tumor isn’t malignant, meaning that it doesn’t break through the basement membrane layer of the tissue, although there is a connective tissue capsule usually forms around the growing tumor, which clearly demarcates it from the rest of the parotid gland. 

Also, the parotid gland start to not function normally, since the ducts turn into cysts and normal epithelial cells stop functioning. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_sclerosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zPXHtFZ5RMGTSlKC2Zxo5DxORu_8yi0O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple sclerosis]]></video:title><video:description><![CDATA[Multiple sclerosis is a demyelinating disease of the central nervous system, which includes the brain and the spinal cord. 

Myelin is the protective sheath that surrounds the axons of neurons, allowing them to quickly send electrical impulses. 

This myelin is produced by oligodendrocytes, which are a group of cells that support neurons. 

In multiple sclerosis, demyelination happens when the immune system inappropriately attacks and destroys the myelin, which makes communication between neurons break down, ultimately leading to all sorts of sensory, motor, and cognitive problems. 

Now, the brain, including the neurons in the brain, is protected by things in the blood by the blood brain barrier, which only lets certain molecules and cells through from the blood. 

For immune cells like T and B cells that means having the right ligand or surface molecule to get through the blood brain barrier, this is kind of like having the a VIP pass to get into an exclusive club.

Once a T cell makes its way in it can get activated by something it encounters - in the case of multiple sclerosis, it’s activated by myelin. 

Once the T-cell gets activated, it changes the blood brain barrier cells to express more receptors, and this allows immune cells to more easily bind and get in, it’s kind of like bribing the bouncer to let in a lot of people. 

Now, multiple sclerosis is a type IV hypersensitivity reaction, or cell-mediated hypersensitivity. And this means that those myelin specific T-cells release cytokines like IL-1, IL-6, TNF-alpha, and interferon-gamma, and together dilate the blood vessels which allows more immune cells to get in, as well as directly cause damage to the oligodendrocytes. 

The cytokines also attract B-cells and macrophages as part of the inflammatory reaction. 

Those B-cells begin to make antibodies that mark the myelin sheath proteins, and then the macrophages use those antibody markers to engulf and destroy the oligodendrocytes.

Without oligo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bladder_exstrophy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C2_S_byNQ-WaBJLK3HxfFUwvSE_P9Cz2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bladder exstrophy]]></video:title><video:description><![CDATA[Bladder exstrophy is a congenital abnormality that results in an “inside-out” bladder, where the bladder protrudes out of the  abdomen, leaving the inside of the bladder exposed to the outside environment. 	

Normally, in the first trimester, endoderm in the hindgut expands to form the cloaca, which is a temporary structure that connects the urinary, digestive, and reproductive tracts. Separately, the ectoderm forms the anterior abdominal wall. 

At around eight weeks of development three important things happen. First, the anterior abdominal wall matures and forms the muscles and connective tissue of the lower abdomen. 

Second, the cloaca splits to form the urogenital sinus and rectum, the urogenital sinus later goes on to become the urinary and genital ducts, as well as the urinary bladder. 

And third, the cloacal membrane opens up to the outside of the body, creating openings for the urogenital tract and anus.

All right, so bladder exstrophy occurs when the developing bladder and urethra herniate anteriorly and this causes some problems. First, it prevents the normal development of the lower abdominal wall which leaves it open. 

Second, it prevents fusion of the pelvis leaving a wide split at the symphysis pubis. 

Also, most cases of bladder exstrophy involve epispadias, which is where the urethra exits the top of the penis, but the opposite is not true, not all cases of epispadias involve bladder exstrophy. 

One way to kind of think about the final result is to imagine the bladder and urethra, and making a cut through the top of the urethra and bladder, and also imagine that cut goes up through the symphysis pubis as well as the abdominal wall. 

After that, imagine pushing on the bladder from the bottom until it’s inside out, and this is essentially is what the final defect in bladder exstrophy looks like, and that bladder pushes through the abdominal wall into the outside world.

In addition to this, bladder exstrophy causes other changes as we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_cortical_necrosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ozVt9bfLQzqCKiHpiQ8646Q8SHam7JLH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal cortical necrosis]]></video:title><video:description><![CDATA[Renal cortical necrosis, sometimes called diffuse cortical necrosis, can be explained by the name. Renal refers to the kidneys, cortical refers to the outer layer, and necrosis refers to tissue death, so renal cortical necrosis describes the outer layer of the kidney dying—usually because of ischemia or a lack of blood flow.

Normally, around 20% of the blood leaving the heart goes into the renal arteries and through cortical radial arteries to reach the renal cortex, which is where the glomeruli of the nephrons are located. And that’s a lot of blood, especially given that the kidneys are relatively smallish organs when you put them next to the brain and liver.

Literally millions of glomeruli in the kidneys work to filter that large volume of blood, and they do so at a rate called the glomerular filtration rate. 

It’s also worth noticing that those cortical radial arteries are end arteries, meaning that they rarely anastomose with adjacent branches, and are, therefore, more susceptible to infarction—since a single blocked artery is all it takes to cause ischemia because the tissue cannot be saved by neighboring arteries. 

Some causes of reduced blood flow or a complete blockage are thrombi, which are blood clots that fill the blood vessels, and vasospasm, which is the narrowing of the blood vessel. 

Interestingly, renal cortical necrosis has been associated with pregnancy complications, like placental abruption—which is when the placental lining is separated from the uterus—as well as prolonged intrauterine fetal death—which is when the fetus dies and then remains dead inside the uterus—and infected abortion—which is when there&amp;#39;s an infection of the remnants of the placenta or fetus. 

All of these are obviously terrible complications, and they relate back to renal cortical necrosis because they can progress to septic shock or disseminated intravascular coagulation, both conditions that can lead to the widespread formation of blood clots.	

So]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Primary_adrenal_insufficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MfU7nSbBSJ6scmGoBvaELhNkQPWMD3_P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Primary adrenal insufficiency]]></video:title><video:description><![CDATA[Primary adrenal insufficiency occurs when the adrenal glands fail to produce key hormones like glucocorticoids and mineralocorticoids.  

It can be acute, also known as adrenal crisis, and chronic, which is referred to as Addison disease. 

Now, each of the two adrenal glands sits on top of a kidney and has two main parts:  

The inner part, the medulla, produces the hormones epinephrine and norepinephrine.  

On the flip side, the outer part, the cortex, has three layers.  

The outermost layer, the zona glomerulosa, produces mineralocorticoids, such as aldosterone. With mineralocorticoids, “mineralo-” refers to minerals, because these hormones help regulate sodium and potassium levels. 

The middle layer, the zona fasciculata, produces glucocorticoids, like cortisol. With glucocorticoids, “gluco-” refers to glucose, because they help increase blood glucose levels.  

The innermost layer, the zona reticularis, produces androgens, such as dehydroepiandrosterone, which is a precursor of testosterone.  

Now, the inner and middle layers of the cortex are mainly under the control of the hypothalamus-pituitary-adrenal axis.  

The hypothalamus releases corticotropin-releasing hormone, which stimulates the corticotrophs in the anterior pituitary gland. Corticotrophs then produce pro-opiomelanocortin or POMC.  

Next, corticotrophs cleave this protein into melanocyte-stimulating hormone and adrenocorticotropic hormone or ACTH.  

Melanocyte-stimulating hormone stimulates the melanocytes in the skin to release melanin, which can darken skin pigmentation.  

On the flip side, ACTH travels through the bloodstream to the adrenal glands, where it stimulates the zona reticularis to release androgens and the zona fasciculata to release cortisol, which plays a big role in metabolism.  

On one hand, cortisol signals the liver to convert amino acids into glucose; on the other, it reduces glucose uptake in peripheral tissues. Together, these actions raise blood sugar leve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_incontinence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PB2X_qfZTDGXamQcduryLdafS5_uzmIV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary incontinence]]></video:title><video:description><![CDATA[Urinary incontinence is a problem where the process of urination, also called micturition, happens involuntarily, meaning that a person might urinate without intending to. 

Urinary incontinence is particularly problematic because it affects a person’s personal hygiene as well as their social life in a way that can be very limiting. 

Normally, urine is held in the bladder, which receives urine from two ureters coming down from the kidneys and then that urine leaves the bladder through the urethra. As urine flows from the kidney, through the ureters and into the bladder, the bladder starts to expand into the abdomen. 

The bladder is able to expand and contract because it’s wrapped in a muscular layer, called the detrusor muscle, and within that, lining the bladder itself is a layer of transitional epithelium containing “umbrella cells”. These umbrella cells get their name because they physically stretch out as the bladder fills, just like an umbrella opening up in slow-motion. In a grown adult, the bladder can expand to hold about 750ml, slightly less in women than men because the uterus takes up space which crowds out the bladder a little bit.

Alright, so when the urine is collecting in the bladder, there are basically two “doors” that are shut, holding that urine in. The first door is the internal sphincter muscle, which is made of smooth muscle and is under involuntary control, meaning that it opens and closes automatically. Typically, that internal sphincter muscle opens up when the bladder is about half full. 

The second door is the external sphincter muscle, and it’s made of skeletal muscle and is under voluntary control, meaning that it opens and closes when a person wants it to. This is the reason that it’s possible to stop urine mid-stream by tightening up that muscle, which is called doing kegel exercises. 

Once urine has passed through the external sphincter muscle, it exits the body—in women the exit is immediate and in men the ur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lupus_nephritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i6fcRElCS2iZuiVlevOoHeqVT_q4Qs0s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lupus nephritis]]></video:title><video:description><![CDATA[The term ‘lupus’ refers to systemic lupus erythematosus, ‘nephritis’ refers to the ‘nephron,’ the Greek word for kidney, and ‘itis’ means inflammation, so lupus nephritis refers to inflammation of the kidney that results from having systemic lupus erythematosus. 

Lupus is an autoimmune disease in which the immune system attacks various parts of the body, including the skin, joints, lungs, heart, central nervous system, and, of course, the kidneys. 

In fact, about half of all individuals with lupus develop some form of lupus nephritis.

In lupus, what happens is that some cells have their DNA so badly damaged, that the cell undergoes programmed cell death, or apoptosis, and it dies. This produces all these little apoptotic bodies, and exposes the insides of the cell, including parts of the nucleus, like DNA, histones, and other proteins, to the rest of the body. 

Now in lupus the immune system is more likely to think that cellular parts are foreign, or antigens, and since they’re from the nucleus, their referred to as nuclear antigens, and immune cells try to attack them.

Not only that though, individuals with lupus have less effective clearance, essentially they aren’t as good at getting rid of the apoptotic bodies and so they end up having more nuclear antigens floating around. 

So as a result of all of this, B cells start producing antibodies against these pieces of nucleus, which are called antinuclear antibodies. 

These antinuclear antibodies bind to nuclear antigens, forming antigen-antibody complexes, which drift away in the blood and deposit in various places including the kidneys. 

These immune complexes can then initiate an inflammatory reaction, which is known as a type III hypersensitivity reaction. 

Lupus nephritis is classified into various types depending on the exact site of these immune complexes and subsequent inflammatory reaction. The most common site of deposition is just underneath the capillary wall, also known as the endothel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-alcoholic_fatty_liver_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hWEa58-OSvO66jSEGjJ3e0DwQFm_7JXq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-alcoholic fatty liver disease]]></video:title><video:description><![CDATA[Nonalcoholic fatty liver disease is actually a spectrum of disease, going from least to most severe—steatosis, steatohepatitis, fibrosis, and finally cirrhosis.

Nonalcoholic fatty liver disease results from fat deposition in the liver, which is unrelated to alcohol or viral causes. 

Typically, it affects individuals with metabolic syndrome, which includes a combination of three of the following five diagnoses: obesity, hypertension, diabetes, hypertriglyceridemia, and hyperlipidemia. 

Given how common metabolic syndrome has become, it’s not surprising that the rate of nonalcoholic fatty liver disease has also increased dramatically. 

It’s a massive problem growing in lock-step with expanding waistlines, affecting about three quarters of all obese individuals, including many children. 

Although the exact mechanism of nonalcoholic fatty liver disease isn’t clear, insulin resistance seems to play an important role. 

Over time, insulin receptors on various tissues including the liver become less responsive to insulin, and as a result the liver goes into a mode where it increases fat storage and decreases fatty acid oxidation. 

That means decreased secretion of lipids into the bloodstream, in the form of lipoproteins, and increased synthesis and uptake of free fatty acids from the blood, a process called steatosis. 

Steatosis causes fat droplets to form within hepatocytes, some of which become large enough to cause the hepatocytes to swell up with fat and push the nuclei to the edge of the cell. 

You can see this on a histopathology slide of the liver. 

All of these white circles are large deposits of fat. 

Zooming out and looking at the liver, you see widespread steatosis which makes the liver appear large, soft, yellow, and greasy. 

Over time, that fat in the hepatocytes is vulnerable to degradation. 

Unsaturated fatty acids, or fatty acids that have at least one double bond in their carbon chain, have hydrogen atoms that are especially vulnerabl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vesicoureteral_reflux</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BZVIkYLfRmutGOUQI-rt8FlMQLabbTlF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vesicoureteral reflux]]></video:title><video:description><![CDATA[Vesico refers to bladder and ureteral refers to the ureter - so vesicoureteral reflux means that urine is refluxing or getting backed up. 

Normally, urine flows in one direction - it starts in the kidneys, goes down into the bladder and when the bladder is full, urine flows out of the body through the urethra. 

In vesicoureteral reflux, there is some obstruction in that path which causes pressure to build up and a current of urine actually pushes backward from the bladder into the ureters and kidneys. 

There are two types of vesicoureteral reflux, or VUR. Primary vesicoureteral reflux is the most common type and happens when a child is born with a defect at the ureterovesical junction, which is the spot where the ureter enters the bladder, which also acts as a valve preventing urine from pushing back from the bladder into the ureter. 

Normally about two centimeters of the ureter sticks into the bladder wall, allowing urine to flow into the bladder, but as the bladder fills up and stretches, it also stretches that section of the ureter and presses it against the top of the bladder, causing the ureter to close shut. 

If the tube isn’t long enough though, that small piece of the ureter doesn’t stretch very much, and it stays open even when the bladder fills with urine. In that situation, as the bladder pressure builds with more urine, it starts to go back up the ureters.

In secondary vesicoureteral reflux, there’s an obstruction at some point in the urinary tract and it causes an increase in pressure, causing urine to follow the path of least resistance which often means flowing backward into the ureters or kidneys.

Secondary vesicoureteral reflux is most commonly caused by recurrent urinary tract infections, which can cause inflammation in the ureters making them swell up and close. 

Another cause that is often diagnosed in babies is called posterior urethral valve disorder, which is when an abnormal membrane develops in the posterior part of the ure]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperaldosteronism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZocG92r6T5eA-daMwrDwxTBySTS-Xb-u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperaldosteronism]]></video:title><video:description><![CDATA[With hyperaldosteronism, &amp;quot;hyper&amp;quot; means too much, and &amp;quot;aldosteronism&amp;quot; refers to the hormone aldosterone, which is made by the adrenal glands. So, hyperaldosteronism is a condition where the adrenal glands produce too much aldosterone. 

Now, each of the two adrenal glands sits on top of a kidney and has two main parts.  

The inner part, the medulla, produces the hormones epinephrine and norepinephrine.  

On the flip side, the outer part, the cortex, has three layers. The innermost layer, the zona reticularis, produces androgens, such as dehydroepiandrosterone, which is a precursor of testosterone. The middle layer, the zona fasciculata, produces glucocorticoids, like cortisol. With glucocorticoids, “gluco-” refers to glucose, because they help increase blood glucose levels. The outermost layer, the zona glomerulosa, produces mineralocorticoids, such as aldosterone. With mineralocorticoids, “mineralo-” refers to minerals, because these hormones help regulate sodium and potassium levels. Now, the zona glomerulosa is controlled by the renin-angiotensin-aldosterone system. 

When blood pressure or sodium levels drop, the juxtaglomerular cells in the kidneys release renin into the bloodstream. In the bloodstream, renin cleaves angiotensinogen into angiotensin I, which is later converted by angiotensin-converting enzyme or ACE, into angiotensin II.  

Angiotensin II raises blood pressure through two mechanisms.  

First, it triggers vasoconstriction of small arterioles, subsequently increasing peripheral vascular resistance. Second, angiotensin II stimulates the zona glomerulosa to release aldosterone.  

Once in the bloodstream, aldosterone travels to the kidneys, more specifically, to the distal tubules and collecting ducts of the nephron.  

Here, aldosterone squeezes into principal cells and stimulates mineralocorticoid receptors. When aldosterone activates mineralocorticoid receptors, the sodium-potassium pumps kick ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spinal_muscular_atrophy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jcm3qLQKRWyxMeU3xMM-h9WNRyWXIixE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spinal muscular atrophy]]></video:title><video:description><![CDATA[Spinal muscular atrophy, or SMA, is a genetic disorder where nerve cells in the spinal cord die prematurely, and this causes the muscles that would normally be controlled by those nerves to atrophy, or wither away, which causes weakness.

When the brain wants a muscle to contract, it sends a signal through an upper motor neuron, which takes the impulse from the brain to the spinal cord, and then through a lower motor neuron, which goes from the spinal cord to the neuromuscular junction, which is where the lower motor neuron touches the muscle cell. 

The lower motor neurons which cause voluntary contraction of skeletal muscle are called alpha motor neurons, and these alpha motor neurons are the ones that die in SMA. Their cell bodies are located in the anterior horn, or front part, of the spinal cord, and their axons project from the spinal cord all the way to the muscles they innervate. A group of these neurons is called a motor nerve.

If a lower motor neuron dies or if the entire nerve is injured, the motor unit, which includes the neuron and the muscle fibers it innervates, stops working. 

Depending on how many muscle fibers stop contracting, there can be overall muscle weakness or in an extreme situation, a flaccid, or low-tone paralysis. 

This denervated muscle also atrophies over time, a classic example of “use it or lose it”. This contrasts with the increased muscle tone and spasticity that develops after an upper motor neuron is damaged. 

When a lot of these muscle fibers are affected, fasciculations can happen which are, spontaneous, involuntary muscle contractions. 

Alpha motor neurons also carry the signal for muscle contraction in deep tendon reflexes, like the knee-jerk reflex, and they diminish or disappear when alpha motor neurons are damaged. 

Now, it turns out that there are a few types and subtypes of SMA. 

Type 1a, congenital SMA, is the most severe of all and it starts even before birth, when mothers may notice decreased fetal mo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Factitious_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zp4ZLDuPSVyirEtp3mRdTOfFSD_lVJGg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Factitious disorder]]></video:title><video:description><![CDATA[Factitious disorder, which is sometimes called Munchausen syndrome, is where an individual fabricates or exaggerates physical or psychological symptoms because they enjoy being in the “sick role”. 

These symptoms are sometimes faked but may also be induced; for example, a person with factitious disorder might purposefully ingest something to induce vomiting. 

Factitious disorder is listed in the DSM-5 as a somatic symptom disorder. 

But unlike other disorders in that group, individuals don’t experience any symptoms, nor are they concerned that they will develop any symptoms. 

Factitious disorder can happen as a single episode, but generally individuals have recurrent hospitalizations and are very knowledgeable about the symptoms they are trying to pass off as real. 

Individuals with factitious disorder are generally motivated by the attention and sympathy that they receive when pretending to be sick. 

These motivations are often subconscious, which is to say that individuals often don’t even realize why they fabricate their symptoms. 

Importantly, individuals with this disorder are usually not faking their symptoms for money, time off of work, access to medications, or any other obvious external reward; if this were the case, it’d be a psychological condition known as malingering. 

A related diagnosis is “factitious disorder imposed on another” which is also called factitious disorder by proxy or Munchausen syndrome by proxy. 

In this form of the disorder, one person deliberately makes a second person ill without that person’s knowledge. 

Once again, the motivation is to vicariously experience the sick role, rather than to cause harm to that second person out of malice. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/WAGR_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vQ2qYpmvQDibQbqxC6pcN0A0QFWR6tXV/_.jpg</video:thumbnail_loc><video:title><![CDATA[WAGR syndrome]]></video:title><video:description><![CDATA[WAGR syndrome stands for Wilms’ tumor, aniridia, genitourinary anomalies, and mental retardation, which is now called intellectual disability, and this is a genetic disorder that’s caused when a part of chromosome 11 is missing, or deleted. 

Not everyone with WAGR has all of the symptoms, for example only about a half of the individuals have Wilms’ tumor. 

On the flip side, some have additional symptoms, too, like progressive kidney failure, growth retardation, small head size, and obesity.

The most specific feature of WAGR syndrome is aniridia, which is the complete or partial absence of the iris, the colored part of the eye. And this is an easily noticeable feature, and it’s present at birth, so it’s usually the first thing to raise suspicion of WAGR syndrome. 

Now, a normal iris controls how much light enters the eye, and it constricts the pupil when there’s a lot of light around to keep the vision sharp. With aniridia, too much light gets into the eye, which leads to blurry vision and photophobia, which is discomfort when the eyes are exposed to light. 

Additional eye features in WAGR syndrome can include cataracts, which is a clouded lens, glaucoma, or increased pressure in the eye, and nystagmus—abnormal rhythmic eye movements of the eye.

Wilms’ tumor, also called nephroblastoma, is generally a malignant kidney tumor that affects children. 

Wilms’ tumor’s composed of metanephric blastema, which is a cell type that’s seen in the developing kidney, stromal cells which are part of the connective tissue, and epithelial cells which self-organize into primitive glomeruli and tubules.

Children with Wilms’ tumor often develop a large flank mass, as well as hematuria, which is blood in the urine, and hypertension. 

Now, that hypertension is a result of increased renin secretion; which either comes from the tumor itself or from healthy kidney tissue that secretes renin because it’s physically compressed by the tumor. 

It’s worth noting that Wilms’ tu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_artery_stenosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wjmSHuATS421x8H5OmclyZjOTT24Ugvm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal artery stenosis]]></video:title><video:description><![CDATA[With renal artery stenosis, ‘stenosis’ means narrowing, which refers to a progressive narrowing of the renal artery,  which carries blood to the kidney. This means that the blood downstream of the narrowed spot that goes to the kidney is at lower pressure, which gets sensed by the kidney.

Since an important role of the kidney is to sense and help the maintain a normal blood pressure, the kidney then tries to raise blood pressure throughout the body.  

Inside the kidney, there are millions of nephrons, each of which help to filter the blood and then fine-tune the composition of blood by carefully reabsorbing and secreting electrolytes as fluid passes through various parts of the nephron. 

Blood approaches the nephron via the afferent arteriole. You can remember it as ‘A’ for approach, and then forms a tangle of capillaries called the glomerulus, before exiting via the efferent arteriole - “e” for exit. That efferent arteriole goes on to split into another set of capillaries - the vasa recta - which surround the nephron, and then blood leaves via the venule. 

So there are two capillary beds per nephron, usually we think of it going arteriole - capillary - venule, but in the nephron it goes arteriole - capillary - arteriole - capillary - and finally venule. 

So nephrons have the general shape of the letter “U”, with the beginning and end portions getting pretty close to each other.

The reason that this matters, is that over here, lining the inside of the afferent arteriole are endothelial cells. 

Wrapped around them are juxtaglomerular cells which are super special smooth muscle cells that contract down like normal smooth muscle cells, but also have the ability to release a hormone called renin in response to low blood pressure.

Over here, close to the distal convoluted tubule, there is another special group of cells that line the tubule called macula densa cells which are sodium-chloride-sensing cells that detect the sodium concentration in the tubul]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholestatic_liver_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0U0pWBk3SmybXd-G_046mtp-QU2dWBYY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholestatic liver disease]]></video:title><video:description><![CDATA[For healthy humans, bile usually flows from the liver and into the small intestine, and this is a super important part of digestion and absorption of nutrients.

When there isn’t enough bile flowing between these two, we can say that there’s some sort of cholestasis going on, because chole- means bile and -stasis means inactivity.

This reduction in bile flow can basically be split into two types, hepatocellular cholestasis, where for some reason the hepatocytes aren’t making enough bile, and obstructive cholestasis, where something’s physically blocking bile flow. 

For hepatocellular cholestasis, which would be considered a form of intra-hepatic cholestasis since it’s happening inside the liver, a really important culprit is the hormone estrogen. 

Estrogen is thought to basically cause the hepatocytes to not be able to pump out bile acids, usually in the form of cholic acid, which is produced when hepatocytes break down cholesterol.

And in this case, hepatocytes literally can’t pump out the cholic acid, because it’s been found that estrogen inhibits the export pump that usually moves the bile acid from the hepatocyte to the bile canaliculi, which leads to the bile ductules and eventually the common hepatic duct. 

But bile acids are just one component of bile, right? Wouldn’t the bile still be made, just without the bile acids? 

Well, production and secretion of bile acids is a major driving force for the synthesis of bile in the hepatocytes, so when the cells can’t transport the bile acids and so they build up inside the cells, and this is basically a signal to down-regulate bile acid synthesis and excretion of bile altogether, which decreases the total amount of bile production. 

When excretion of bile components like conjugated bilirubin are down, but they’re still being conjugated, they also build up along with the bile acids, and eventually, it’s thought that they diffuse or are exocytosed into the interstitial space, where it can access the blo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neurogenic_bladder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hOBlXkTjQb_7CbtYP-iniYZOTCi-ILs_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neurogenic bladder]]></video:title><video:description><![CDATA[With neurogenic bladder, neurogenic means arising from the nervous system, so neurogenic bladder is typically some difficulty emptying the bladder normally, as a result of either damage to the peripheral nerves, brain, or spinal cord. 

Normally, urine is held in the bladder, which receives urine from two ureters coming down from the kidneys and then that urine leaves the bladder through the urethra.

As urine flows from the kidney, through the ureters and into the bladder, the bladder starts to expand into the abdomen. The bladder is able to expand and contract because it’s wrapped in a muscular layer, called the detrusor muscle, and within that, lining the bladder itself is a layer of transitional epithelium containing “umbrella cells”. These umbrella cells get their name because they physically stretch out as the bladder fills, just like an umbrella opening in slow-motion. 

In a grown adult, the bladder can expand to hold about 750ml, slightly less in women than men because the uterus takes up space which crowds out the bladder a bit. 

Okay - so when the urine is collecting in the bladder, there are basically two “doors” that are shut, holding that urine in. The first door is the internal sphincter muscle, which is made of smooth muscle and is under involuntary control, meaning that it opens and closes automatically. Typically, the internal sphincter muscle opens up when the bladder is about half full.

Now the second door is the external sphincter muscle, and it’s made of skeletal muscle and is under voluntary control, meaning that it opens and closes when a person wants it to. This is the reason that it’s possible to stop urine mid-stream by tightening up that muscle, which is called doing kegel exercises. Once urine has passed through the external sphincter muscle, it exits the body, in women the exit is immediate and in men the urine flows through the penis before it exits.

So, when specialized nerves called stretch receptors in the bladder wall ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Goodpasture_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X9oAJ1YgSw2a_oHThQ5NrFmUQe6AHYFi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Goodpasture syndrome]]></video:title><video:description><![CDATA[Goodpasture syndrome is an autoimmune disease that primarily affects two organs - the lungs and the kidneys. 

It causes inflammation and eventually bleeding in the lungs which leads to ‘hemoptysis’ or coughing up of blood, and hematuria or blood in the urine, a pattern first recognized by the pathologist - Dr. Ernest Goodpasture. 

To understand Goodpasture syndrome, let’s start by thinking about the basement membrane which is a thin, sheet-like layer of tissue made of protein that keeps the epithelium stuck firmly to actual organ - a bit like double-sided tape which keeps gift wrapping paper stuck to the gift. 

The basement membrane is made up of various proteins, but the major one is collagen, and since basement membrane exists throughout every organ system, it’s no wonder that collagen is the most abundant protein in the human body. 

As far as proteins go, collagen is a pretty awesome looking one, with a triple-helix structure composed of three separate chains that are intertwined like braided hair. 

Each of the chains can be one of six types, named α1 through α6, and the most common form of collagen found in the basement membrane is collagen type IV, which is made by mixing and matching these six α-chains. 

One version of type IV collagen combines the α3, α4, and α5 chains. Another combines two α1’s and an α2. A third version has two α5’s and an α6. And so on. 

So it turns out that the α3/α4/α5 variant is most common in the glomerular basement membrane of the kidneys and the alveolar basement membrane of the lungs.  

In Goodpasture syndrome, autoantibodies bind to a specific part of the α3 chain that is usually hidden deep within the folded chains. 

This is an example of a type II hypersensitivity reaction, because once these autoantibodies, usually IgG but rarely IgM or IgA, bind to the the α3 chain, they activate the complement system. The complement system is a series of small proteins present in the blood that act like an enzymatic cascade ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abscesses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ptPIHLJdQoyxPSiL7Qj4k7uOT8qWo-Y5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abscesses]]></video:title><video:description><![CDATA[Everyone who has ever had a pimple has had an abscess, even though they’re tiny, they’re still abscesses. 

An abscess forms when normal tissue, like skin for example, is split apart and that new space is invaded by nearby pathogens like bacteria. 

And there are roughly ten bacterial cells for every one human cell and they cover every surface of the human body.

So any cut or break in the skin or closed off area within the body is an invitation for bacteria to dive in and multiply. 

When that happens the immune system typically responds and a battle ensues with the result being pus - a mixture of bacteria, immune cells, and dead tissue.

So, in response to an injury, the tissue releases small chemicals in the local area called cytokines, like tumor necrosis factor, interleukin-1, interleukin-6 and interleukin-17, and chemokines which attract nearby white blood cells which are part of the immune system. It’s kinda like yelling for help and being heard by the nearby police. 

In addition to attracting immune cells, the cytokines also dilate nearby capillaries - which brings more blood to the site, and make the capillaries more leaky, so that the white blood cells that do show up, can slip out of the blood and get into the tissue more easily. 

Often times, the first immune cells at the scene are neutrophils, which release chemicals and enzymes that kill bacteria and dissolve pieces of of dead cells, creating a pool of dead material. 

This is a specific type of acute inflammatory response called suppurative inflammation, which simply means that pus is created in the process. 

From a macroscopic view, this is sometimes referred to a liquefactive necrosis, because the area of dead tissue turns to liquid. 

As those immune cells get to a point where they can’t withstand the environment, they die too, and become part of that pool. 

Initially the debris might be intermixed with healthy tissue, but over time it can coalesce into a single area - a process that ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Influenza_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SnxLu-ZJTkeS8IuVtG0na9uiT1WaPguU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Influenza virus]]></video:title><video:description><![CDATA[Influenza, the virus that causes the flu, is one of the most common infectious diseases. 

Now, there are three types of influenza that infect humans, called type A, type B, and type C, each one with slightly different genome and proteins. 

Influenza belongs to the virus family Orthomyxoviridae - and type A and B have genomes that are made up of eight RNA segments, whereas type C, has a seven-segment RNA genome, with each segment containing a few genes. 

Now, type A, the most common type of influenza virus, can be further subdivided based on two of the glycoproteins on its protective envelope surface; H protein, or Hemagglutinin,  and N protein, or neuraminidase. 

Hemagglutinin and Neuraminidase can vary a bit in their structure, so different versions are identified by a number. 

For example, type A subtype H3N2, sometimes just called H3N2, has hemagglutinin number 3 and neuraminidase number 2 on its surface. 

H3N2 and H1N1 are the most common type A subtypes to infect humans, but they both also infect various animals.  

To give the full name of a virus, we use the type, the original host that it came from, the location where the virus was first identified, which is usually a city, the strain number, the year of origin, and—for type A influenza—the subtype named by the H and N glycoproteins. 

For example, an H1N1 type A flu virus of duck origin from the province of Alberta, Canada, that is the 35th strain discovered in 1976 would be called A/duck/Alberta/35/76 (H1N1).

Type B influenza is less common, it only infects humans and doesn&amp;#39;t mutate as often as type A.

Type B influenza only has a few types of H and N glycoproteins on its surface. 

Therefore the naming pattern is similar to type A influenza without the H and N subtype included at the end or the host type, since it only infects humans. 

For example, a type B virus found in Yamagata, Japan, which is the 16th strain discovered in 1988 would be called B]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetic_nephropathy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_zW5y6YkS_Kjai6KKVZ9SIP0QmGVaqnP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetic nephropathy]]></video:title><video:description><![CDATA[Diabetic nephropathy refers to the kidney damage caused by both type I and type II diabetes. 

Because of the growing number of people affected by diabetes, diabetic nephropathy is currently the leading cause of end-stage renal disease in most developed countries around the world. 

Each kidney has millions of nephrons, each of which is served by a tiny capillary bed called a glomerulus. 

The tiny arteriole that approaches the glomerulus is called the afferent arteriole - a for approaching, and the arteriole that exits the glomerulus is called the efferent arteriole - e for exits. 

The glomeruli are a tiny cluster of capillaries that are physically supported by mesangial cells. 

So when blood is filtered it moves through the endothelium lining the capillary, then through the basement membrane, and then through the epithelium lining the nephron, and finally into the nephron itself - at which point its called filtrate. 

The endothelium has pores that keep cells from entering the filtrate, and the basement membrane is negatively charged and repels other negatively charged molecules and proteins, like the protein albumin. 

The epithelium has of special cell type called a podocyte which looks like an octopus because it has foot processes that wrap around the basement membrane, leaving tiny gaps between its octopus-like projections called filtration slits.

In diabetes mellitus, there’s an excess of glucose in the blood, because it can’t get into cells, and when blood gets filtered through the kidneys, some of that excess glucose starts to spill into the urine, called glycosuria. 

In addition, when there’s a lot of glucose in the blood, it also starts sticking to proteins in the blood — a process called non-enzymatic glycation because no enzymes are involved. 

Because glucose can get through the endothelium, this process of glycation can also involve the basement membrane of small blood vessels making it thicken. The process particularly affects the effer]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemolytic-uremic_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LrhVFzhfQu_q0kz4e2daVdguRmu04154/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemolytic-uremic syndrome]]></video:title><video:description><![CDATA[‘Hemo’ refers to the blood, ‘lytic’ refers to breaking down, and ‘uremic’ refers to increased urea levels in the blood. 

And this helps explain hemolytic uremic syndrome because the two main effects are destruction of red blood cells and the declining function of the kidney causing uremia - both of which result from tiny blood clots that form in tiny blood vessels - predominantly in the kidneys.

Classically, especially in children, hemolytic uremic syndrome is triggered by a bout of bloody diarrhea. 

When that happens, it’s called diarrhea-positive or D positive hemolytic syndrome, sometimes shortened to HUS or simply typical HUS. 

Escherichia coli or E. coli is usually the culprit, and  children often pick it up through contaminated food or drink, like contaminated beef or unpasteurised milk from an infected cow. 

The particular strain of E.coli responsible for hemolytic uremic syndrome is known as enterohemorrhagic E. coli or EHEC, serotype O157:H7. 

These numbers and letters refer to the specific antigens on the surface of the bacteria. 

‘157’ refers to the O-antigen present in the lipopolysaccharide cell wall and ‘7’ refers to the H-antigen located on the flagella of the bacteria. 

Other strains of E. coli as well as other bacteria can also cause hemolytic uremic syndrome, but E. coli O157:H7 is the most common culprit.

After entering the digestive tract, E. coli O157:H7 attaches to the intestinal wall and secretes a toxin called Shiga-like toxin. 

The toxin gets its name due to its structural similarity with shiga toxin produced by Shigella dysenteriae, another bacteria that causes bloody diarrhea and subsequent hemolytic uremic syndrome. 

So that toxin gets absorbed by intestinal blood vessels and is then picked up by immune cells like eosinophils, basophils and neutrophils.

From there, the toxin is carried on the surface of these cells to the site of blood filtration - which is the glomerular capillaries of the kidney. 

Endothelial]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medullary_sponge_kidney</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ivWxHNqMTfesr-vulzCAWzRhRZ2X3c1X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medullary sponge kidney]]></video:title><video:description><![CDATA[Medullary sponge kidney, also known as cacchi-ricci disease is a congenital disease where the medullary part of the kidney, which is deeper inside the kidney, gets loaded with fluid-filled cysts which gives the kidney the appearance of a sponge. 

Now, the kidney can be divided into the cortex which is the outer layer and the medulla which is the layer below that. 

Kidneys contain millions of tiny nephrons which filter the blood - each of which is like a little tube receiving blood on one end in the cortex.

From there, the nephron dips into the medulla, and then goes back out into the cortex, and finally dips back into the medulla a second time to connect to the collecting ducts which gather up all of the urine. Not every nephron has this exact structure, but a lot of them do. 

From there, the urine drains through the papilla which is an inverted cone shaped pyramid, that, like a shower head, pours urine into the calyces, which comes from the latin -calix which means large cup, kinda like a Roman chalice. 

From there it enters the renal pelvis which funnels the urine into the ureter, then to the bladder, and then finally leaves the body out the urethra.

Now, medullary sponge kidney has to do with the development of the kidney. So during fetal development, first off you’ve got this structure called the mesonephric duct which is involved in development of urinary and reproductive organs, and during the 5th week of gestation, a little guy called the ureteric bud starts pushing its way into another structure called the metanephric blastema, and together, these two little embryologic structures go on to develop into a kidney. 

At about the 7th week, nephrogenesis, or formation of the kidneys, starts under the influence of that ureteric bud. 

By about 20 weeks, the ureteric bud has formed the ureters, the renal calyces, collecting ducts, and collecting tubules, while the metanephric blastema develops into the nephron itself, which includes the epithelial ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypermagnesemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oHUJnfmqRfqgqMSxUY67YOD9QPSyHqTp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypermagnesemia]]></video:title><video:description><![CDATA[‘Hyper-’ means ‘over’ and ‘-magnes-’ refers to magnesium, and -emia refers to the blood, so hypermagnesemia means higher than normal magnesium levels in the blood, and symptoms typically develop at a level over 4 mEq/L.

An average adult has about 25 grams of magnesium in their body. 

About half is stored in the bones, and most of the other half is found within cells.

In fact, magnesium is a really common  positively charged ion found within the cell, second only to king potassium.

A very tiny fraction, roughly 1% of the total magnesium in the body, is in the extracellular space which includes both the intravascular space - the blood and lymphatic vessels, and the interstitial space - the space between cells. 

About 20% of the magnesium in the extracellular space, which would be about 0.2% of the total magnesium, is bound to negatively charged proteins like albumin, but the other 80% or 0.8% of the total magnesium, can be filtered into the kidneys. 

So in the kidney, that magnesium gets filtered into the nephron, andi about 30% gets reabsorbed at the proximal convoluted tubule, 60% gets reabsorbed in the ascending loop of Henle, and 5% get reabsorbed at the distal convoluted tubule. 

That leaves only 5% to get excreted by the kidneys.

So, in order for there to be too much magnesium in the blood, this normal balance has to be disturbed. 

The most common reason is when those nephrons in the kidneys can’t excrete magnesium properly - which can happen in renal failure, when the kidneys typically aren’t able to excrete anything properly. 

Another cause of hypermagnesemia is ingesting more magnesium  than the kidneys can excrete. 

Sometimes this can be due to an intravenous infusion of magnesium that isn’t prepared correctly.

Other times it can be due to a magnesium containing medication like magnesium hydroxide which can be used to treat symptoms like constipation and heartburn.

If these medications are taken in excess over a long period of time, it]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypomagnesemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1sQRHd14SBW5CXQUxxUEPnluTvqedDia/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypomagnesemia]]></video:title><video:description><![CDATA[With hypomagnesemia, ‘hypo-’ means ‘lower’ and ‘-magnes-’ refers to magnesium, and -emia refers to the blood, so hypomagnesemia means lower than normal magnesium levels in the blood, and symptoms typically develop at a level below 1 mEq/L.

An average adult has about 25 grams of magnesium in their body. About half is stored in the bones, and most of the other half is found within cells. 

In fact, magnesium is a really common  positively charged ion found within the cell, second only to potassium.

A very tiny fraction, roughly 1% of the total magnesium in the body, is in the extracellular space which includes both the intravascular space - the blood vessels and lymphatic vessels, and the interstitial space - the space between cells. 

About 20% of the magnesium in the extracellular space, which would be about 0.2% of the total magnesium, is bound to negatively charged proteins like albumin, but the other 80% or 0.8% of the total magnesium, can be filtered into the kidneys. 

So inside the kidney, that magnesium gets filtered into the nephron, and about 30% gets reabsorbed at the proximal convoluted tubule, 60% gets reabsorbed in the ascending loop of Henle, and 5% get reabsorbed at the distal convoluted tubule. And that leaves only 5% to get excreted by the kidneys.

Magnesium levels can fall in a few situations. One scenario is when the nephron fails to reabsorb the magnesium that’s filtered out of the blood, which would mean more would be excreted in the urine instead of kept in the blood. 

Magnesium reabsorption is mostly a passive process where the positively charged magnesium ion follows the electrochemical gradient and moves from the positively charged lumen into the cells lining the lumen which usually have a negative charge. 

Now, loop and thiazide diuretics can disrupt that process, because they both make the lumen less positively charged, and this diminishes magnesium’s electrochemical gradient and causing more of the ions to stick around in t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperphosphatemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pOmhDLeAQ7SBml_tIFaxxv1QTHyA1Hmi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperphosphatemia]]></video:title><video:description><![CDATA[With hyperphosphatemia, hyper- means over, -phosphat- refers to phosphate, and -emia refers to the blood, so hyperphosphatemia means having a high phosphate level in the blood, typically above 4.5 mg/dL.

Now, phosphate is made up of one central phosphorus atom surrounded by four oxygen atoms in a tetrahedral arrangement, kind of like a mini pyramid, and has a charge of minus 3 and is written PO43-. 

In the body, about 85% of the phosphate is stored in the bones, where it combines with calcium to make a tough compound called hydroxyapatite which is the stuff that makes bones hard. 

Of the remaining phosphate, a tiny amount is extracellular, or outside the cells like in the blood, so this is the bit that gets measured, and the majority is intracellular, or inside cells, where it does all sorts of things. 

It’s responsible for phosphorylation, where it binds to fats and proteins. 

It forms the high energy  bonds of adenosine triphosphate or ATP, which is the most common energy currency in the cell. 

It’s part of the DNA and RNA backbone that links individual nucleotides together, and it’s also part of cellular signaling molecules like cyclic-adenosine monophosphate or cAMP. Bottom line is that phosphate is really important.

Now, because most of phosphate is locked up with calcium in the bones, the levels of phosphate are heavily tied with the levels of ionized calcium in the body. 

If calcium levels fall, the four parathyroid glands buried within the thyroid gland release parathyroid hormone which frees up both calcium and phosphate ions from the bones. 

It does this by stimulating osteoclasts, the cells that break bone down, to release hydrogen ions which dissolves the hard, mineralized hydroxyapatite. 

As soon as the positively-charged calcium and negatively-charged phosphate are released from the bones, they grab onto each other again, meaning that the ionized calcium level doesn’t really go up very much at all. 

These two make their way to the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sudden_infant_death_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WJIBGUy9RbyTWpVSQPM3NQfpQ6CWjUVp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sudden infant death syndrome]]></video:title><video:description><![CDATA[Sudden infant death syndrome, or SIDS, which is also known as cot death, crib death, is the sudden and unexplainable death of an infant during their first year of life. 

Because of the seemingly random nature of the condition, there are a number of risk factors that seem to correlate with getting SIDS, but there’s no clear mechanism or cause that’s been identified. 

SIDS is considered a diagnosis of exclusion, meaning all other causes have to be ruled out before an infant death is given that label. 

The most well-known risk factors have to do with how an infant sleeps; to lower the risk of SIDS the recommendation is to make sure that babies sleep alone in a crib, on their backs and without blankets. 

The risk of SIDS is higher among boys rather than girls, as well as infants between two and four months old, and among formula-fed babies, and those born prematurely or with low birth weight. 

Risk factors that relate to a mother include receiving little or no prenatal care, being a teenage mother, and smoking during the pregnancy. 

Alcohol consumption is also thought to be a risk factor because there are more cases of SIDS during weekends, the New Year, and other times of year when drinking is included in celebrations. 

The fact that far more boys die of SIDS than girls shows that there is a level of genetic susceptibility at play, but the exact specifics are unclear. 

A minority of SIDS-related deaths show a correlation with genetically inherited channelopathies, which are defects in ion channels that affect a variety of tissues, including the heart. 

Another possible genetic link is the higher incidence of SIDS in babies with gene mutations involved in the autonomic nervous system. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypercalcemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eduApVl4Tn6HpoFl9qopkyRbS8mCy0as/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypercalcemia]]></video:title><video:description><![CDATA[With hypercalcemia, hyper -means over and -calc- refers to calcium, and -emia refers to the blood, so hypercalcemia means higher than normal calcium levels in the blood, generally over  10.5 mg/dL. 

Now, calcium exists as an ion with a double positive charge - Ca2+ - and it’s the most abundant metal in the human body. 

So I know what you’re thinking - yeah, we’re all pretty much cyborgs,- Cool, huh? 

So about 99% of that calcium is in our bones in the form of calcium phosphate, also called hydroxyapatite. 

The last 1% is split so that the majority, about 0.99% is extracellular - which means in the blood and in the interstitial space between cells, and 0.01% is intracellular or inside cells. 

High levels of intracellular calcium causes cells to die. 

In fact, that’s exactly what happens during apoptosis, also known as programmed cell death. 

For that reason, cells end up spending a lot of energy just keeping their intracellular calcium levels low. 

Now, calcium gets into the cell through two types of channels, or cell doors, within the cell membrane. 

The first type are ligand-gated channels, which are what most cells use to let calcium in, and are primarily controlled by hormones or neurotransmitters. 

The second type are voltage-gated channels, which are mostly found in muscle and nerve cells and are primarily controlled by changes in the electrical membrane potential. 

So calcium flows in through these channels, and to prevent calcium levels from rising too high, cells kick excess calcium right back out with ATP-dependent calcium pumps as well as Na+-Ca2+ exchangers. 

In addition, most of the intracellular calcium is stored within organelles like the mitochondria and smooth endoplasmic reticulum and is released selectively just when it&amp;#39;s needed.

Now, the majority of the extracellular calcium is split almost equally between two groups - calcium that is diffusible and calcium that is not diffusible. 

Diffusible calcium is s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypocalcemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rzcCi3IuQ9WFMPr8IlLcP5TjTY_9jgo9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypocalcemia]]></video:title><video:description><![CDATA[With hypocalcemia, -hypo means below, calc- refers to calcium, and -emia refers to the blood, so hypocalcemia means lower than normal calcium levels in the blood, generally less than 8.5 mg/dL. 

Now, calcium exists as an ion with a double positive charge - Ca2+ - and it’s the most abundant metal in the human body. So I know what you’re thinking - yeah, we’re all pretty much cyborgs. 

Anyways, about 99% of that calcium is in our bones in the form of calcium phosphate, also called hydroxyapatite. 

The last 1% is split so that the majority, about 0.99% is extracellular - which means in the blood and in the interstitial space between cells, whereas 0.01% is intracellular. 

High levels of intracellular calcium causes cells to die. In fact, that’s exactly what happens during apoptosis, also known as programmed cell death. For that reason, cells end up using a ton of energy just keeping their intracellular calcium levels low. 

Now, calcium gets into the cell through two types of channels, or cell doors, within the cell membrane. The first type are ligand-gated channels, which are what most cells use to let calcium in, and are primarily controlled by hormones or neurotransmitters. 

The second type are voltage-gated channels, which are mostly found in muscle and nerve cells and are primarily controlled by changes in the electrical membrane potential.

So calcium flows in through these channels, and to prevent calcium levels from getting too high, cells kick excess calcium right back out with ATP-dependent calcium pumps as well as sodium calcium exchangers. 

In addition, most of the intracellular calcium is stored within organelles like the mitochondria and smooth endoplasmic reticulum and is released selectively just when it&amp;#39;s needed.

Now, the majority of the extracellular calcium, the calcium in the blood and interstitium, is split almost equally between two groups - calcium that is diffusible and calcium that is not diffusible. 

Diffus]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_cell_carcinoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I98JYT3hTDKaA4Bmq8byGrKZRIayOsq8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal cell carcinoma]]></video:title><video:description><![CDATA[Renal cell carcinomas (or RCC’s) are the most common type of malignant kidney cancer in adults, generally affecting older men.

Unfortunately, RCC is often considered a “silent” cancer because symptoms don’t typically get noticed until the tumor has grown pretty large.

Renal cell carcinomas form from epithelial cells in the proximal convoluted tubule of the kidney; this is the section of the nephron that is usually located in the renal cortex—the outer rim of the kidney. 

The most common type of renal cell carcinoma is composed of polygonal epithelial cells, which have funny angular shapes with at least four sides and are filled with clear cytoplasm full of  carbohydrates and lipids. It’s those lipids that give the tumors their yellow color.

At a genetic level, renal cell carcinomas have been linked to mutations on the short arm of chromosome 3, or 3p. An easy way to remember this is that RCC has three letters and it’s linked to chromosome 3. 

One of the main genes involved in renal cell carcinomas is the VHL gene, which codes for the von Hippel-Lindau tumor suppressor protein, or pVHL which is normally expressed in all tissues.

Mutations in pVHL can allow IGF-1, the type 1 insulin-like growth factor, pathway to go into overdrive. This does two things. 

First, there is dysregulated cell growth, and second it upregulates specific transcription factors called hypoxia-inducible factors, which in turn help generate more vascular endothelial growth factor or VEGF, as well as VEGF receptor, leading to growth of new blood  vessels, or angiogenesis. Dysregulated cellular growth and angiogenesis are a recipe for tumor formation.

Renal cell carcinomas can arise sporadically or they can be a part of an inherited syndrome. Sporadic tumors are usually solitary tumors in the upper pole of the kidney, and most often happen among older men that smoke cigarettes.

Inherited syndromes, like von Hippel-Lindau disease, can also give rise to renal cell carcinomas, and i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fwZd2wWlTTGrY1P3HhOoOUesTtWesPed/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pregnancy]]></video:title><video:description><![CDATA[Pregnancy is an amazing process that affects almost every body system. 

Throughout the pregnancy, estrogen and progesterone levels steadily rise, and it leads to a number of anatomic and physiologic changes that occur throughout the body.

Everything starts with ovulation, so let’s call that day 0. 

On that day, in the ovary, an ovarian follicle – which is an egg or oocyte plus its surrounding tissues– matures and ovulation occurs which is when the egg gets ejected while the surrounding structure becomes the corpus luteum and quickly starts making estrogen and progesterone. 

Normally, the egg gets fertilized by a sperm within 12-24 hours to form a zygote, so let’s say that fertilization happens a day later on day 1. 

Almost right away, cells start to divide over and over, until there’s a ball of cells called the blastocyst on day 4. 

The blastocyst typically floats around inside the uterus for another day before it finds a specific spot to implant on day 5. 

Around this time, the corpus luteum makes a lot more progesterone relative to estrogen, and the low estrogen to progesterone ratio is necessary for implantation. 

At this early stage, there are two parts to the blastocyst - an inner set of cells that go on to become the fetus, and an outer set of cells called the trophoblast that burrow into the endometrium on day 6 and eventually develop into the fetal part of the placenta. 

That trophoblast cells start to produce a hormone called human chorionic gonadotropin or HCG around day 8, and this is important for two reasons. 

One - it’s the hormone that lets the corpus luteum know that there has been a successful implantation into the endometrium, and that it should continue to make estrogen and progesterone. 

And it’s the continued presence of estrogen and progesterone that suppresses other ovarian follicles from maturing. 

Two - HCG is the hormone that most pregnancy tests are able to detect, causing the little sign to form which can happen as e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Angelman_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iPxZTd7dSF2OZuoN5JeyR7tORGy8NCn5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Angelman syndrome]]></video:title><video:description><![CDATA[Angelman syndrome is a genetic disorder that causes intellectual and developmental delay, seizures, frequent laughter, and ataxia, or poor control of voluntary movements.

Now, it happens when a gene on chromosome 15 called UBE3A is not expressed, or transcribed into messenger RNA. 

UBE3A stands for ubiquitin-protein ligase E3A, and the protein it codes for is called E6AP or E6-associated protein. 

The job of E6AP is to go around tagging, or attaching, a tiny protein called ubiquitin to other proteins, a process called ubiquitination. 

Once that happens, the ubiquitinated protein is degraded by the proteasome, a part of the cell’s recycling machinery. 

It’s kind of painting an orange U on a tree so that a lumberjack knows to chop it down. 

So E6 associated protein has an important job, and it turns out that the region of chromosome 15 around UBE3A is imprinted, imprinting refers to gene expression that’s dependent on the parent of origin of a gene. 

This means that either the maternally derived or paternally derived copy of the gene is silenced. 

This differs from most genes in the genome, where both the maternal and paternal copies are expressed. 

Normally, in the brain, only the maternally derived copy of UBE3A is expressed, while the paternal copy is silenced, unfortunately this process of imprinting leaves the maternal copy of UBE3A vulnerable. 

So with the paternal copy of the gene imprinted, and epigenetically silenced, you’ve only got the maternal copy left. 

So this means that if anything happens to the maternal copy, the result is Angelman syndrome.

There are a few different types of mutations that can cause Angelman syndrome. 

The most common one is a deletion of a couple million base pairs of DNA on the maternal copy of chromosome 15 which includes UBE3A.

Sometimes the deletion overlaps a nearby gene called OCA2, which codes for a pigment that gives color to eye, hair, and skin. 

As a result of this, these Angelman syndrome patient]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_pressure,_blood_flow,_and_resistance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xU-8fqzOQ9eAuQ3TcsvpgpF5SP_ie382/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood pressure, blood flow, and resistance]]></video:title><video:description><![CDATA[Pressure is a force over an area, so with blood pressure, we’re measuring the force that the blood exerts on the surface area of the walls of the blood vessels. Differences in blood pressure throughout the body keep blood flowing from high-pressure areas, like the arteries, to low-pressure areas, like the veins. When we say “blood flow,” we’re referring to the volume of blood that flows through a vessel or an organ over some period of time. Now, the amount of blood flow from one end of a blood vessel to another is affected by the blood pressure, and by the resistance, which comes from the vessels themselves. Vasoconstriction, where the vessels constrict, decreases blood flow, and vasodilation, where the blood vessels expand, increases blood flow. 

Now, blood flow is not the same thing as the velocity of blood. Blood flow is the volume of blood that moves by a point over some period of time. So let’s say this chunk of blood has a volume of 83 cm^3, and it took 1 second for this much to flow past the blue circle—this is the blood flow, represented by the variable capital Q. 

Now, velocity on the other hand, is the distance traveled in a certain amount of time. So maybe in the same one second, a red blood cell at the very edge here traveled a distance of 27 cm, then it’d be moving 27 cm/s, represented by lowercase v. Even though these aren’t equal, they are related, and the last piece is area, specifically the cross-sectional area of the blood vessel, which in reality is the same as the blood cross section like this. So, based on units, since area’s going to be expressed in cm^2, we see that flow rate equals area times velocity! Alright, so for example, let’s say we want to calculate blood velocity, and we have a person’s cardiac output of 5L/min, which is average for an adult, and the diameter of their aorta, which is 2cm.

First off, using the equation for the area of a circle, (D/2)^2 x pi, we get (2 / 2)^2 x pi = 3.14 cm^2. Next, since cardiac output is]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Laryngomalacia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vNTqErASQe23uHFZtdkXoV25Q3SKJ8Zc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Laryngomalacia]]></video:title><video:description><![CDATA[“Laryngo” refers to the larynx and “malacia” refers to a body tissue that is soft, so laryngomalacia is a developmental condition where the larynx doesn’t form correctly and ends up being soft and floppy. 

Normally, the epiglottis, a flap of cartilage located just above the vocal cords, makes a firm arc over the airway. 

It’s connected to the larynx by cartilaginous structures called aryepiglottic folds. 

In children born with laryngomalacia, the aryepiglottic folds are shorter than normal, so they pull the normally arc-shaped epiglottis down into a distinctive omega shape. 

Weak laryngeal muscle tone is thought to cause the condition, but the exact mechanism isn’t well understood. 

The cartilaginous tissues are also softer than normal, so they flop into the airway. 

That means that when the child breathes, that floppy structure gets sucked into the airway, causing stridor which is a high-pitched, whistling sound during breathing. 

In some cases the obstruction of the airway can be so bad that it can make breathing difficult. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypophosphatemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XU43naMDQ9q19VC0zrSfZ_55STSBJDJu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypophosphatemia]]></video:title><video:description><![CDATA[Hypo- means under, phosphat- refers to phosphate, and -emia refers to the blood, so hypophosphatemia means having a low phosphate level in the blood, typically below 2.5mg/dL. 

Phosphate is made up of one central phosphorus atom surrounded by four oxygen atoms in a tetrahedral arrangement, like a mini pyramid, and has a charge of minus 3 and is written PO43-. 

In the body, about 85% of the phosphate is stored in the bones, where it combines with calcium to make a tough compound called hydroxyapatite which is the stuff that makes bones hard.

Of the remaining phosphate, a tiny amount is extracellular, or outside cells like in the blood, so this is the bit that gets measured, and the majority is intracellular, or inside cells, where it does all sorts of things.

It’s responsible for phosphorylation, where it binds to fats and proteins. 

It forms the high energy  bonds of adenosine triphosphate or ATP, which is the most common energy currency in the cell. 

It’s part of the DNA and RNA backbone that links individual nucleotides together, and is also part of cellular signaling molecules like cyclic-adenosine monophosphate or cAMP. 

Bottom line - phosphate is super important.

Because most of the phosphate is locked up with calcium in the bones, the levels of phosphate are heavily tied with the levels of ionized calcium in the body.

If calcium levels fall, the four parathyroid glands buried within the thyroid gland release parathyroid hormone which frees up both calcium and phosphate ions from the bones. 

It does this by stimulating osteoclasts, the cells that break bone down, to release hydrogen ions which dissolves the hard, mineralized hydroxyapatite. 

As soon as the positively-charged calcium and negatively-charged phosphate are released from the bones, they grab onto each other again like a pair of star-crossed lovers, meaning that the ionized calcium level doesn’t really go up very much at all. 

Now, these two make their way to the nephron of the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colorectal_polyps</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kIjmEnE5TjWRJgDD0-23PbklRpuLHlvV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colorectal polyps]]></video:title><video:description><![CDATA[A colorectal polyp is a small clump of epithelial cells that form a small bump or overgrowth of tissue along the lining of the colon or rectum. 

The cells lining the colon and rectum are constantly dividing, and typically when there’s an overgrowth of tissue it’s benign, but some can become malignant, meaning that the dividing cells can start invading nearby tissues over time. 

There are various types of colorectal polyps. 

The most common ones are adenomatous polyps, also called colonic adenomas. 

They form when there is a mutation in the adenomatous polyposis coli gene or APC gene, which is a tumor suppressor gene that regulates cell growth. 

When the APC gene is mutated, the epithelial cells start to quickly divide forming polyps. 

But even though they are dividing, these polyps only become malignant - meaning they only invade nearby tissues if there are additional mutations in other tumor suppressor genes like the p53 gene or in proto-oncogenes like K-Ras. 

Some people with a genetic condition called familial adenomatous polyposis syndrome or FAP are born with a mutation in their APC gene, and they end up developing hundreds or even thousands of polyps in their colon. 

These people often need to have their entire colon surgically removed because having so many polyps increases the chance that one cell among all of those polyps will develop another mutation and become malignant.

Adenomatous polyps can also be classified histologically based on their growth pattern as being tubular where the growth has little holes within it looking at a cross section of tissue or a tube if you imagine it in three dimensions or villous where the growth looks like a little tree with branches.

Some adenomatous polyps look like a mix of the two with tubes and tree-like structures and are called tubulovillous.

This description is helpful because it turns out that a growth with a more villous growth pattern is more likely to become malignant, and therefore needs mo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Allergic_rhinitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HVsKJSBmSeq7PmngSDTyBaXHQA_XGB1y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Allergic rhinitis]]></video:title><video:description><![CDATA[“Rhin” refers to the nose and “itis” refers to inflammation, so rhinitis is nasal inflammation. 

Allergic rhinitis is also called hay fever, and it’s typically caused by allergens like hay, as well as pollen, dust, animal hair, or mold spores. 

When the main trigger is pollinating plants, allergic rhinitis will flare up at specific times of the year.

Allergic rhinitis is a type 1 hypersensitivity reaction, which is a type of allergic reaction that starts with exposure to an environmental allergen. 

So - let’s say that a bit of pollen enters the nose. It can get picked up by a dendritic cell which is a type of immune cell that gobbles up foreign particles and presents it to a nearby lymphocyte called a T cell. 

If the T cell gets activated, it kicks into action, producing cytokines which helps to get other immune cells involved. 

The exact type of T cell determines the type of immune response, and in allergic rhinitis there’s a bit of a T cell imbalance.

There are too many T cells that, when activated, stimulate B cells, another group of lymphocytes, to produce IgE antibodies. 

Those IgE antibodies get released into the bloodstream and bind to mast cells, which are immune cells in the tissue that carry within themselves a load histamine. 

Once bound by IgE the mast cells are “primed”, meaning if pollen enters the body again in the future, those mast cells degranulate and release their histamine into the local tissue. 

The histamine causes blood capillaries to dilate and become leaky which brings more fluid and immune cells to the area where the mast cells are located.

Because the eyes and nose are portals of entry for infections, there are lots of mast cells around those areas for extra protection. 

The IgE-primed mast cells release their histamine, which causes nearby capillaries to dilate - flooding the facial tissues with fluid.

Interestingly, there’s evidence that early exposure to allergens might protect against type 1 hypersensitivity. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_kidney_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VlkpAtIFTG_u6_d3W9SgC2MgRIWLTsoH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic kidney disease]]></video:title><video:description><![CDATA[Chronic kidney disease is a broad term that includes subtle decreases in kidney function that develop over a minimum of three months. 

In contrast, acute kidney injury refers to any deterioration in kidney function that happens in less than three months. 

Now the kidney’s job is to regulate what’s in the blood, so they might remove waste, or make sure electrolyte levels are steady, or regulate the overall amount of water, and even make hormones - the kidneys do a lot of stuff! 

Blood gets into the kidney through the renal artery, and once inside it goes gets into tiny clumps of arterioles called glomeruli where it’s initially filtered, and the filtrate which is the stuff that gets filtered out, moves into the renal tubule. 

The rate at which this filtration takes place is known as glomerular filtration rate or GFR. In a normal healthy person, this is somewhere around 100-120 milliliter of fluid filtered per minute per 1.73 m2 of body surface area. The value is slightly less in women than men and it decreases slowly in all of us as we grow older.   

One of the most common causes of chronic kidney disease is hypertension. 

In hypertension, the walls of arteries supplying the kidney begin to thicken in order to withstand the pressure, and that results in a narrow lumen. A narrow lumen means less blood and oxygen gets delivered to the kidney, resulting in ischemic injury to the nephron’s glomerulus. 

Immune cells like macrophages and fat-laden macrophages called foam cells slip into the damage glomerulus and start secreting growth factors like Transforming Growth Factor ß1 or TGF-ß1.

These growth factors cause the mesangial cells to regress back to their more immature stem cell state known as mesangioblasts and secrete extracellular structural matrix. This excessive extracellular matrix leads to glomerulosclerosis, hardening and scarr, and diminishes the nephron’s ability to filter the blood - over time leading to chronic kidney disease. 

The most com]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lymphatic_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2gEPQ176Q0iz9X8MlUXjJ3vISaOZ7f4X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lymphatic system anatomy and physiology]]></video:title><video:description><![CDATA[“Lymph” means “clear water” in Latin, and it describes the fluid that flows through the lymphatic vessels and lymph nodes which make up the lymphatic system. The three major roles of the lymphatic system - the reason we need it in the first place - are that it returns fluid from the tissues back to the heart, it helps large molecules like hormones and lipids enter the blood, and it helps with immune surveillance to keep infections from running amok.

So, let’s take a closer look at lymph and where it comes from. The blood in the arteries is under a lot of pressure because it needs to reach every little nook and cranny of the body. The arteries branch out into narrower and narrower arteries, and then arterioles, and finally gets to the capillaries - which have walls that are only one cell thick and are slightly porous. Red blood cells are too big to fit through capillary pores, but small proteins like albumin and fluid can make it through. Every day 20 liters of fluid water and protein - seep out of the capillaries and becomes part of the interstitial fluid between cells. About 17 liters gets quickly reabsorbed right back into the capillaries,
but that leaves 3 liters of fluid behind in the tissues each day. This 3 liters of fluid needs to find a way back into the blood so that the body’s interstitial fluid volume and blood volume both stay constant over time. That’s where the lymphatic vessels, or lymphatics, come in: they collect excess interstitial fluid and return it to the blood. Once the interstitial fluid is in the lymphatic vessels, it’s called lymph. 

Now - you may be wondering how there can be 20 liters of fluid seeping out each day if the blood volume is only 5 liters, but remember that the 5 liters is constantly in motion and that it gets recycled over and over in a single day. 

Unlike the circulatory system, the lymphatic system isn’t a closed loop because fluid and proteins make their way into the microscopic lymphatic capillaries, and all o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Laminar_flow_and_Reynolds_number</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6NF2hzoaRzeja9NPfyF9QnaFSKi-_EKT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Laminar flow and Reynolds number]]></video:title><video:description><![CDATA[Laminar means smooth, and so laminar blood flow is blood that’s flowing smoothly through the vessels. Turbulent flow, on the other hand, is when the blood’s not flowing smoothly, and we can figure out if blood is likely to be laminar or turbulent by finding its Reynolds number or Re, which is named after Osborne Reynolds, a Victorian scientist who not only studied fluid dynamics, but is a man who knows how to rock a beard and bowtie.

If everything’s moving like it should and the blood flow is laminar, the linear velocity of the blood  -- how fast it’s moving in a straight line -- is greatest in the center of the blood vessel, and lowest near the walls of the vessel, dropping to zero at the wall. 

Sometimes, though, blood flow is disrupted, like if it has to pass by a crusty old atherosclerotic plaque along the wall, which reduces the diameter of the blood vessel at that point and causes turbulence. There are a number of factors help predict turbulence, they include the density of the blood, usually denoted by the greek letter rho, the viscosity denoted by the greek letter nu. You can kind of think of a fluid’s viscosity as it’s thickness, like for example the viscosity of honey is greater than that of water. Alright, then there’s velocity of blood flow (v), and the diameter of the blood vessel (d).These values can all be used to come up with a single value—the reynold’s number, often denoted Re, and the equation looks like this: 

NR = pdv/

Generally speaking, if the Reynolds number is low - below 2000, then blood flow will be laminar - think “low” and “laminar”, and if the Reynolds number is above 3000 it’ll be turbulent. A Reynolds number between 2000 and 3000 is somewhere in between. As a real-life example, a person with anemia has a low red blood cell count, and in general has a lower hematocrit, the ratio of red blood cells to total blood volume. This essentially means the blood’s less thick or viscous, which means based on our equation, if viscosi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Resistance_to_blood_flow</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iokH08X2QVGjlLY8NKvTKhLZTT_1iJ0p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Resistance to blood flow]]></video:title><video:description><![CDATA[Blood flow refers to the volume of blood travelling through a blood vessel, an organ, or the entire body over a period of time, and it can be measured as liters per minute. As blood flows, it encounters various factors that resist flow and movement of blood, known as the vascular resistance.

The first factor to contribute to vascular resistance is blood viscosity, where you can think of viscosity as the fluid’s thickness, or how sticky it is. The relationship is directly proportional, which can be represented as resistance ∝ η which is the greek letter eta and represents viscosity. So this means that as viscosity goes up, the harder it is for the liquid’s molecules to slide past each other, and the resistance goes up. Think about a heaping stack o’ pancakes, then picture some maple syrup. Even on flipping the syrup upside down it doesn’t really come out right away and resists moving right away; slowly it gloops out and doesn’t splash but just coats those pancakes in a delicious film of sugary goodness, oh right. Now, with another stack, grab some orange juice and pour...it immediately comes out and pretty goes everywhere. This is because the juice is less viscous than the syrup, so there’s going to be less resistance to movement. Because blood is full of large proteins and cells, it’s pretty viscous and moves much more slowly than just plain water, or orange juice. Blood viscosity doesn’t change much over time, but certain conditions like polycythemia, where the person has too many red blood cells, can increase viscosity, and conditions like anemia, where the person doesn’t have enough red blood cells, can decrease viscosity.

A second factor that affects resistance is total blood vessel length. Just like with viscosity, the relationship is directly proportional, and this can be represented as resistance ∝ L, so, simply put, shorter vessels have less resistance and longer vessels have more resistance because there’s more friction resisting flow. This mean]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tobacco_dependence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q5nMVjT0QhiPd8XkMLWeLdXYR-S4wfZk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tobacco use disorder]]></video:title><video:description><![CDATA[There are over a billion people who smoke tobacco around the world, which makes it one of the most popular psychoactive substances used in society. 

The majority of tobacco users smoke cigarettes, but some smoke cigars or pipes, chew tobacco, or practice snuffing, which is where ground-up tobacco leaves are pushed up the nose. 

Given the popularity of tobacco as well as its negative health consequences, it’s considered one of the leading causes of preventable death and disease worldwide. 

Cigarette smoke contains over 4,000 toxic chemicals. 

These toxins cause endothelial cell damage which creates inflammation along the inner lining of arteries. 

The inflammation increases the risk of having a myocardial infarction (or heart attack), a stroke, and peripheral vascular disease which causes severe pain in the lower legs. 

The toxins in cigarette smoke can also cause pulmonary problems when they’re deposited into the lungs, as they damage the lung tissue and increase the likelihood of developing a lung infection. 

Finally, cigarette smoke contains many different carcinogens including ammonia, formaldehyde, and carbon monoxide, all of which are associated with cancers of the mouth, throat, lung, bladder, pancreas, and uterus. 

Combining these effects, a heavy smoker who smokes two packs of cigarettes each day for 20 years loses about 14 years of life. 

Despite the negative consequences of smoking, most people continue to smoke because tobacco contains nicotine, a tiny, fat-soluble molecule that creates pleasurable psychoactive effects and is extremely addictive. 

Nicotine is considered “responsible” for the high rates of tobacco dependence and addiction, while the 4,000 other chemicals and compounds are “responsible” for the negative health effects associated with smoking. 

When a cigarette is lit, some of the nicotine is destroyed by the heat, and some gets into the smoke that’s then inhaled. 

As a result, smokers are able to “self-titrate” their n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nasal_polyps</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QFu5YsfiRZOyy3DL8haYFKHMTf2vk0pq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nasal polyps]]></video:title><video:description><![CDATA[A nasal polyp is a clump of epithelial cells that forms a small bump or overgrowth of tissue along the lining the nasal cavity, the inside of the nose. 

The nasal cavity is made up of three regions. 

The first, is the nasal vestibule which is the area just inside the nostrils. 

Beyond that, is the respiratory region which delivers air to the sinuses and lungs, and above it is the olfactory region, which is involved in smelling. 

Lining the respiratory region are epithelial cells that create mucus to moisten the air and trap pathogens. 

There are also air-filled spaces within the skull that are on either side of the the nose called paranasal sinuses which are lined by the same layer of epithelial cells as the respiratory region. 

The paranasal sinuses are named for the bones that house the sinus: the sphenoid, located next to the eyes; the ethmoid, between the eyes; the frontal, above the eyes behind the forehead; and the maxillary, behind the cheeks and below the eyes. 

Each of the sinuses normally produce mucus, which drain into the respiratory region. 

Holes at the back of the respiratory region, called choanae act like funnels to direct the mucus into the throat to be swallowed.

Nasal polyps develop when epithelial cells that line the respiratory region simply overgrow - a process called hyperplasia. 

Most of the time, one or more nasal polyps forms in the maxillary or ethmoid sinus. 

Nasal polyps can get large - the size of a pea, but they are usually non-cancerous, meaning they don’t break through the basement membrane of the epithelium. 

Unfortunately, they often obstruct air flow as well as mucus drainage which allows pathogens to linger in the sinuses and cause infections. 

Recurrent infections causes mucosal swelling as immune cells infiltrate the tissue and create an inflammatory response. 

The swelling makes airway obstruction and mucus drainage even worse. 

The reason that the epithelial cells start to grow into a polyp isn’t ent]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mumps_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q0UfniCES76t2LNyXqxyhIwfS9aNraBJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mumps virus]]></video:title><video:description><![CDATA[Mumps is a disease caused by the mumps virus, which is a member of the paramyxoviridae family.

This is actually a large family of viruses which includes measles virus and parainfluenza viruses, and all of these tend to affect children the most.

Mumps only affects humans and is spread by tiny respiratory droplets that are small enough to be carried short distances in the air, so mumps virus is extremely contagious and anyone near a person with mumps is at risk for getting the disease as well.

The mumps virus has a single strand of RNA and a viral polymerase enzyme surrounded by a phospholipid bilayer envelope studded with viral proteins hemagglutinin-neuraminidase, or HN protein, and fusion or F protein.

The HN protein allows the virus to stick to a potential host cell, and cut itself loose if necessary, and the F-protein which fuses the viral and cell membranes together allowing the mumps virus to enter the cell.

Once mumps enters a cell, the single stranded RNA, which is negative sense, gets transcribed by the viral polymerase enzyme, into a complementary positive sense strand of mRNA, which can then be translated by the host cell ribosomes into new copies of the envelope proteins and the viral polymerase, which get assembled into new viruses.

What also ends up happening with these, though, is that those HN and F-proteins on the cell surface now bind other cells, so they actually end up bind epithelial cells to one another, which forms a clump of connected cells called a multinucleated giant cell or a syncytium.

Mumps enters the body and first infects the epithelial cells of the nasopharynx, where it starts replicating and causing local damage to the tissue.

From there, it can cause viremia or virus in the blood, and reach various organs and tissues.

The mumps virus has tropism, or preference for, the parotid salivary glands, and the most classic finding in mumps is swelling of parotid salivary glands either on one side or on both sides, sometime]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatic_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2bmr_IwAT_iQqs-55jirr7xxT7uQejhG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatic cancer]]></video:title><video:description><![CDATA[Pancreatic carcinoma describes the pancreas having cancerous cells arise. 

Now a healthy pancreas has two types of glands, exocrine glands which sends digestive enzymes off to the small intestine, and endocrine glands which help regulate metabolism in the body, for example, maintaining normal blood sugar. 

Over 95% of pancreatic tumors develop in the pancreas’s exocrine tissues, and of these, tumors arising in the epithelial cells lining the pancreatic ducts account for the vast majority of cases.

This type of pancreatic cancer is known as pancreatic adenocarcinoma due to the cells glandular-like (“adeno”) appearance under the microscope, often pancreatic adenocarcinoma is used interchangeably with pancreatic carcinoma. 

These tumors typically form in the head or neck of the pancreas, but in some cases tumors form in the tail. 

Around 5% of exocrine pancreatic carcinomas are caused by malignancies in the acinar cells, which are the cells that produce the digestive enzymes like trypsinogen, and around 1% are cystadenocarcinomas, or malignant cysts. 

There are also other types of pancreatic cancer, but those are even more rare. 

Generally, pancreatic carcinoma is caused by genetic mutations in the ductal epithelial cells, and these mutations might activate oncogenes which promote cancer or inactivate tumor suppressor genes. 

Either way, this can lead to uncontrolled cell growth caused by the disruptions of the cell signalling pathways that regulate cell survival and growth, as well as multiple immune system responses like inflammation and stress responses. 

Although it’s not exactly clear how the genetic mutations that trigger pancreatic carcinoma develop, there are some well known modifiable risk factors like smoking which increases the risk by two to five-fold, obesity, as well as eating a diet high in red meat. 

There are also some non-modifiable risk factors like being male, being African American, and being over 65 years old.

Also, certain ot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glaucoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uzl-EFuiRGaI-wlwvXr6RopGTGiyCPDC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glaucoma]]></video:title><video:description><![CDATA[Glaucoma is actually a group of eye diseases that are usually due to intraocular hypertension, or increased pressure in the eye, which damages the optic nerve and if left untreated can lead to blindness. 

Taking a closer look at this cross section of the eye, you can see that it’s split up into different chambers: The anterior chamber includes the area from the cornea to the iris, the posterior chamber is this really narrow space between the iris and the lens.

And then this larger vitreous chamber includes the space between the lens and the back of the eye. 

Not to be too confusing, but both the anterior and posterior chambers are located in the anterior segment of the eye, while the vitreous chamber is part of the posterior segment of the eye. 

Typically all of the chambers in the eye are filled with fluid. 

The chambers in the anterior section are filled with a liquid called aqueous humor, and the posterior section is filled with vitreous humor. 

The aqueous humor is a transparent, watery fluid that is secreted by the ciliary epithelium, which in addition to secreting aqueous humor and providing nutrients to the lens and cornea, it provides structural support and helps to keep the shape of the eye.

So that fluid’s secreted into the posterior chamber, and then flows through a narrow space between the front of the lens and the back of the iris through the pupil to the anterior chamber.

From there the fluid flows out of the eye through the trabecular meshwork, which is a spongy tissue that acts like a drain, and this allows the fluid to go down into a circular channel called the canal of Schlemm and finally into aqueous veins that are part of the episcleral venous system—the veins around the sclera of the eye. 

In glaucoma, part of this aqueous humor drainage pathway becomes partially or completely blocked, so that fluid can’t easily drain out.

This causes the pressure within the fixed space of the anterior chamber to quickly build up causing intr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_pancreatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9Dv4jy8RTZesx1e8lMagdvUkS8ScAZkc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute pancreatitis]]></video:title><video:description><![CDATA[Acute pancreatitis is the sudden inflammation and hemorrhaging of the pancreas due to destruction by its own digestive enzymes—a process fittingly called autodigestion. 

Most of the time the disease is actually relatively mild, but it can easily become severe, so it&amp;#39;s critical to diagnose and treat it quickly. 

The pancreas is a long, skinny gland the length of a dollar bill and is located in the upper abdomen, or the epigastric region, behind the stomach.

It plays endocrine roles—for example, alpha and beta cells make hormones like insulin and glucagon that are secreted into the bloodstream, but it also plays exocrine roles— for example, acinar cells make digestive enzymes that are secreted into the duodenum to help digest food. 

These pancreatic digestive enzymes break down macromolecules like carbohydrates, lipids and proteins found in food, but these macromolecules are also found in the cells of the pancreas. 

To protect the pancreas, the acinar cells manufacture inactive forms of the enzymes called proenzymes, or zymogens. 

These zymogens are normally activated by  proteases which cleave off a polypeptide chain, which is kind of like pulling the pin on a grenade. 

For additional security, the zymogens are kept away from sensitive tissues in storage vesicles called zymogen granules, and are packaged with protease inhibitors that prevent enzymes from doing damage if they become prematurely active. 

To digest a meal, these zymogens are released into the pancreatic duct, and delivered to the small intestine where they are activated by the protease trypsin.

Trypsin is a pancreatic digestive enzyme that is produced as the zymogen trypsinogen. 

Normally, trypsinogen isn’t activated until it is cleaved by protease enteropeptidase which is found in the duodenum. But if trypsinogen and these zymogens become activated too early, then it can cause acute pancreatitis, and this might happen as a result of any injury to the acinar cells, or anythi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/X-linked_agammaglobulinemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5nvp9oBMSl_gahppR3IvCfc9RROG7f9E/_.jpg</video:thumbnail_loc><video:title><![CDATA[X-linked agammaglobulinemia]]></video:title><video:description><![CDATA[With X-linked agammaglobulinemia, or XLA for short, gamma globulin is another name for immunoglobulin, which is another name for antibodies, a- means without, and -emia refers to the blood. 

So this is a disease where there aren’t any antibodies in the blood, and X-linked means that it’s caused by a gene mutation on the X chromosome.

Now, normally, immunoglobulins are secreted into the blood by plasma cells, which are fully matured or differentiated B cells, a type of immune cell. 

Way before that ever happens, though, those B cells start out in the bone marrow as pluripotent stem cells, pluripotent meaning that they can develop into a number of different types of cells.

But to become a B cell, first that pluripotent stem cell differentiates into a lymphoid precursor cell, then a pro-B cell, then a pre-B cell, then an immature B cell which migrates from the bone marrow to the spleen, where it becomes a mature or naive B cell, which after being exposed to the right antigen, moves into the blood or lymph and becomes an antibody-secreting plasma cell.

In XLA, this maturation process stops at the pre-B cell stage. 

Why does it do that? Well, by the immature B cell stage, it has a B cell receptor, which is a membrane-bound antibody, specifically an immunoglobulin M or IgM. 

But in the Pre- and Pro-B cell stages, this B cell receptor’s still being assembled, once it’s finished, it’s made up of heavy chain and light chain protein subunits, and the heavy chains are put together first. 

Since it hasn’t been fully assembled yet, this IgM’s known as a pre-B cell receptor. 

Now, an enzyme called bruton’s tyrosine kinase is super important for both the development and normal functioning of the B cell receptor. 

With XLA, though, there’s a mutation in the BTK gene which makes the BTK enzyme ineffective. 

And because of this ineffective BTK enzyme, the B cell maturation process gets stopped at this Pre-B cell stage, meaning no B cells leave the bone marrow, so]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medullary_cystic_kidney_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/96VYt-MOSHOwS46Sywx7CxRxRBmf8AWM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medullary cystic kidney disease]]></video:title><video:description><![CDATA[Nephronophthisis, which means “nephron wasting”, and medullary cystic kidney disease, which refers to fluid-filled sacs in the medulla, are two kidney diseases that share some similar features: they’re both genetic, they both affect the nephrons, and both can lead to kidney cysts and renal failure over time.

To help understand these diseases, let’s first take a zoomed-in look at a nephron and talk about how it works. Alright so the outer layer of the kidney is called the cortex, and this is where the glomeruli live, which is where blood is initially filtered into the nephron, as well as the proximal convoluted tubule, where some of the filtered substances are reabsorbed back into the body. 

The filtered substances, or filtrate, that don’t get reabsorbed then moves down through the medulla via the descending and then ascending parts of the loop of Henle. 

The filtrate then goes back to the cortex briefly in the distal convoluted tubule, and then returns back to the medulla in the collecting duct. 

Zooming back out a bit, the collecting ducts in each region of the kidney - called a renal pyramid, converge on the renal papilla, which dumps fully formed urine into a minor calyx. 

From there the urine goes into the major calyx, and soon after, it goes into the ureter and the bladder. 

And finally, zooming back in, surrounding each nephron’s tubule is the tubular interstitium, a hypertonic environment optimized to help resorb water and other substances from the tubules. 

Alright so in nephronophthisis, which presents in childhood, the tubules atrophy and the interstitium gets infiltrated by macrophages and becomes fibrotic. 

Inflammation of the tubules and the interstitium qualifies nephronophthisis as a tubulointerstitial nephritis, but don’t confuse this with nephritic syndrome, which is where red blood cells and protein escape in the urine as a result of damage to the glomerulus.

In nephronophthisis, the affected tubules lose their ability to concent]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Insomnia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rsu4VIZcRuyhhfX7gV-H5Ji6SC_shuCu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Insomnia]]></video:title><video:description><![CDATA[The word insomnia comes from Latin, where the prefix “in” means “without” and “somnia” refers to “sleep”. In other words, insomnia is a sleep disorder characterized by difficulty falling asleep, staying asleep, or waking up too early, and not being able to fall back asleep. So, insomnia is not just about a bad night here or there. It’s when this sleep disturbance sticks around and affects your day-to-day life. 

Each night, after long hours of preparing for exams, you fall asleep to get some well-deserved rest. But, for that to happen, there needs to be a delicate balance between two systems in the brain.  

First, we have the sleep-promoting centers located in the ventrolateral preoptic nucleus and the median preoptic area. These regions release sleep-promoting substances, like GABA, serotonin, adenosine, melatonin, and prostaglandin D2.  

On the flip side, we have the wake-promoting centers, also known as the arousal centers. These include the reticular activating system, the tuberomammillary nucleus, the dorsal raphe, and the locus coeruleus. These regions release stimulating substances, such as catecholamines, orexin, and histamine. 

As you begin to fall asleep, the sleep-promoting centers send inhibitory signals to the arousal centers, gradually quieting brain activity and easing you into sleep.  

After a good rest, the process reverses.  

The arousal centers slowly reactivate and start sending inhibitory signals to the sleep centers, helping you wake up and stay alert during the day.  

This push-pull system is the basis of the sleep-wake cycle, and you can think of it as a light switch. When it’s on, the arousal centers are active, keeping you awake. When it’s off, the sleep-promoting centers take over, allowing you to fall asleep. 

Now, the activity of the sleep and arousal centers is controlled by two key processes. First, there&amp;#39;s the wake-dependent sleep drive, which is mainly driven by adenosine. As we stay awake, adenosine gradual]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anorexia_nervosa</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lsLZKy9ISEWaBC6YXVKah4TMTBaBy4mm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anorexia nervosa]]></video:title><video:description><![CDATA[Anorexia nervosa, which is often just called anorexia, is a disorder characterized by very low weight (typically less than 85% of normal body weight), a constant fixation on avoiding putting on even the slightest amount of weight, and having a distorted view of one’s own body weight or shape, often believing that one is overweight, while actually being underweight.

There are two main types of anorexia. One form of the disorder is the restricting type, where people reduce the amount of food they eat in order to lose weight. 

Another form of the disorder is the binge-and-purge type, where individuals eat large amounts of food in one sitting and then purge that food by vomiting or taking laxatives. 

This second type can be confused with another eating disorder, bulimia nervosa, but the main distinction between these two disorders has to do with an individual’s weight. 

Individuals with bulimia are usually normal weight or overweight, whereas individuals with anorexia are underweight. 

Because of this, people can potentially start out with bulimia, and then develop anorexia over time.

Anorexia can be further split by levels of severity. 

A body mass index (or BMI) between 18.5 and 24.9 is considered healthy. 

People diagnosed with anorexia have a BMI below this threshold:  a BMI between 17 and 18.5 is considered mildly anorexic, a BMI of 16-17 is considered moderately anorexic, a BMI of 15-16 is severely anorexic, and a BMI of less than 15 is considered extremely anorexic.

In addition to having a low BMI, individuals with anorexia are typically fearful of weight gain, and often have a psychological obsession with the caloric and fat content of food. 

This leads to food-restrictive behaviors, purging, over-exercise, and frequent weight checks. 

People with anorexia might perform specific food rituals, like cutting food into small pieces, or eating foods in a specific order. 

They might refuse to ever eat in front of people, or cook elaborate meals f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lung_volumes_and_capacities</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FsLOumP7Sjq9FFY-PjF6CwQ_ToOfkx1O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lung volumes and capacities]]></video:title><video:description><![CDATA[The main job of the lungs is gas exchange, pulling oxygen into the body and getting rid of carbon dioxide.

Normally, during an inhale - the diaphragm contracts to pull downward, and chest muscles contract to pull open the chest to suck in air like a vacuum cleaner, and then during an exhale - the muscles relax, allowing the lungs to spring back to their normal size pushing that air out.  

Now, we can use a spirometer to measure the volume of air that moves in and out of the lungs with each breath using an instrument called a spirometer; the test is called spirometry. 

At this point there are more sophisticated electronic spirometers, but a classic example is having an air chamber submerged in water that the person can breathe into.

As they take air in, the chamber moves down into the water, which moves a pencil that traces as it moves, then when they breathe out, the chamber moves up and the pen moves down. 

So, if this is a healthy adult woman, as  she breathes the spirometer makes a wave-like tracing on the paper. 

The plot you end up with therefore has volume of air on the vertical axis, and the horizontal axis shows time. 

During normal, quiet breathing the volume of air moving in and out with each breath is represented by the height of the wave and it’s called the tidal volume; it’s typically around 0.5 L or 500 ml. 

After a few cycles, we might ask the woman to inhale the maximum volume of air that she can, and then exhale the maximum volume of air that she can. The volume of air that she maximally inhales above the tidal volume is known as the inspiratory reserve volume, and it’s typically around 3 liters. This is sort of a like a massive backup capacity that you don’t typically use, but might need to in a specific situation like if you’re going for a dive in the ocean. 

Similarly, the expiratory reserve volume is the volume of air that she maximally exhales below the tidal volume, and it’s typically around 1.2 liters. 

Now, even after she]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Superior_vena_cava_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3z5X-t9KRLOI7XSzLovDm-eNQmKSuI12/_.jpg</video:thumbnail_loc><video:title><![CDATA[Superior vena cava syndrome]]></video:title><video:description><![CDATA[Superior vena cava syndrome occurs when blood flow through the superior vena cava is obstructed either from within due to a blood clot or from external compression. 

The superior vena cava is a short and wide vein on the right side of the chest that drains blood from the head, upper body and both arms, and delivers all of that blood to the right atrium of the heart. 

The superior vena cava can get obstructed a few different ways, and the most common way is via a nearby tumor, through mass effect, where inflammation and swelling pushes up against the superior vena cava. 

Alternatively, though, there can be direct tumor invasion into the superior vena cava which is when tumor cells penetrate and grow directly into the superior vena cava. But this is only possible if the tumor is located on the right side near the superior vena cava. 

The most common type of cancer that does this is a lung cancer, and when it’s located in the apex of the right lung near the superior vena cava, it’s given the name Pancoast tumor - after Dr. Henry Pancoast who first described them.

Also in that area, though, you’ve got a bunch of lymph nodes, and another possible cause of SVC syndrome a tumor of the lymph nodes, which would could lead to compression of the SVC. 

This could be lymphomas – or primary cancers of the lymph node - cause superior vena cava syndrome, or secondary and have spread from somewhere else, like the lungs. 

Apart from tumors, the superior vena cava can also get obstructed if a blood clot or thrombosis forms within it. This most often develops in individuals who have a long-term device like an indwelling central venous catheter.

Regardless of the cause, when the superior vena cava gets obstructed, behind the obstruction you’ll get an increase in venous pressure. 

When this happens, blood starts to get re-routed through different blood vessels, essentially draining into the inferior vena cava, which also drains into the right atrium. 

These are now ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ag6gZ9z3SN2VV3FHMMvod9f2Tym3ubpe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular system anatomy and physiology]]></video:title><video:description><![CDATA[The circulatory system is also called the cardiovascular system, where “cardi” refers to the heart, and “vascular” refers to the blood vessels. So, these are the two key parts: the heart, which pumps blood, and the blood vessels, which carry blood to the body and return it back to the heart again. Ultimately, this is how nutrients like O2, or oxygen, get pushed out to the organs and tissues that need it, and how waste like CO2, or carbon dioxide, which is the main byproduct of cellular respiration, gets removed.

The heart is about the size of a person’s fist, which makes sense: a bigger person has a bigger fist and, therefore, a bigger heart.And it’s shaped like a cone, and sits slightly shifted over to the left side, in the mediastinum, which is the middle of the chest cavity, or thorax.It sits on top of the diaphragm, which is the main muscle that helps with breathing, behind the sternum, or breastbone, in front of the vertebral column, squished in between the two lungs, and protected by the ribs. 

If you look more closely, you can see that the heart sits inside a sac of fluid that has two walls, called the serous pericardium. The outer layer is called the parietal layer. It gets stuck tightly to another layer called the fibrous pericardium, which is made of tough, dense connective tissue, which holds the heart in place and prevents it from overfilling with blood. The inner layer is called the visceral layer, and it gets stuck tightly to the heart itself, forming the epicardium, or the outer layer of the heart. The cells of the serous pericardium, both the parietal and visceral layer -- secrete a protein-rich fluid that fills the space between those layers and serves as a lubricant for the heart, allowing it to move around a bit with each heartbeat without feeling too much friction. 

So, moving from the outside to the inside of the heart, after the epicardium, there’s the myocardium, which is the muscular middle layer. This forms the bulk of the heart]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3rtnO4okQySUBrKE79NPmyfhR1_y3K0Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory system anatomy and physiology]]></video:title><video:description><![CDATA[The main job of the lungs is gas exchange, pulling oxygen into the body and getting rid of carbon dioxide. Normally, during an inhale - the diaphragm contracts to pull downward and chest muscles contract to pull open the chest, which helps suck in air like a vacuum , and then during an exhale - the muscles relax, allowing the lungs to spring back to their normal size pushing that air out.

When you breathe in, air flows through the nostrils and enters the nasal cavity which is lined by cells that release mucus. That mucus is salty, sticky, and contains lysozymes, which are enzymes that help kill bacteria. Nose hairs at the entrance of the nasal cavity get coated with that mucus and are able to trap large particles of dust and pollen as well as bacteria, forming tiny clumps of boogers. 

The nasal cavity is connected to four paranasal sinuses which are air-filled spaces inside the bones that surround the nose. There’s the frontal, ethmoid, sphenoid, and maxillary sinus. The paranasal sinuses help the inspired air to circulate for a bit so it has time to get warm and moist. The paranasal sinuses also act like tiny echo-chambers that help amplify the sound of your voice, which is why you sound so different when they’re clogged with  mucus during a cold!

So the relatively clean, warm, and moist air goes from the nasal cavity into the pharynx or throat, the region connecting the two is called the nasopharynx, and the part connecting the pharynx to the oral cavity is called - you guessed it - the oropharynx. The soft palate, the softer portion of the roof of your mouth behind the hard part that you can feel with your tongue, and the pendulum-like uvula hanging at its end move together to form a flap or valve that closes the nasopharynx off when you eat to prevent food from going up into the nasopharynx. Finally, there’s the laryngopharynx, the part of the pharynx that’s continuous with the larynx or the voice box.

Up to this point, food and air share a common ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sleep_apnea</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/26aKTedvREergQ6fnZX3hwO0TzmYGpZE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sleep apnea]]></video:title><video:description><![CDATA[Sleep apnea is a sleep disorder which causes irregular breathing and snoring patterns that can ultimately cause apnea, which is where a person momentarily stops breathing altogether. The inability to get restful sleep can also lead to severe exhaustion.

Individuals can have obstructive sleep apnea, central sleep apnea, or features of both. Obstructive sleep apnea is the most common form, and it develops when there’s a blockage of the airways. Now, air has to go from the nose through the nasopharynx into the laryngopharynx, through the larynx and then into the trachea. Somewhere along that path, there might be a blockage in the flow of air.

Allergies might cause swelling in the tissues in the nasopharynx, or there might be swollen adenoid glands or tonsils because of an infection. There might be a severe overbite which pulls the jaw back and blocks the airway. In individuals that are overweight, there could be too much weight in the soft tissues of the neck, which can weigh down the airway especially when a person is lying down.

These problems are most obvious at night because hormonal changes at night cause the muscles around the airway to become slightly less stiff while sleeping. This means that they are less able to keep the airway open, making it more likely to get a bit squashed or obstructed.

Central sleep apnea, on the other hand, refers to the fact that the problem is “central” or related to the central nervous system. This is where the brain intermittently stops making an effort to breathe for 10 to 30 seconds. The apnea can persist for several seconds even after waking up, triggering feelings of panic and further disrupting the sleep cycle.

Central sleep apnea starts with an initial episode of hyperpnea, which is when the brain directs the lungs to start hyperventilating during sleep by increasing the respiratory rate. This rapid breathing causes hypocapnia, a drop in the blood’s carbon dioxide levels. 

When the carbon dioxide falls below a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pleural_effusion</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G0SzXlDmSQS7nR6FO3kq0bgbT9G1Bvpf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pleural effusion]]></video:title><video:description><![CDATA[“Pleural” refers to the space between the chest cavity and the lungs, and “effusion” refers to a collection of fluid, so a pleural effusion is when a disease process causes fluid to start to collect in the pleural space, which can sometimes restrict lung expansion.

The pleural cavity or pleural space lies between the parietal pleura which is stuck to the chest wall and the visceral pleura which is stuck to the lungs. 

Because the lungs fit snugly inside the chest cavity, the visceral and parietal pleura lie right next to each other, and the very very thin space between them contains a layer of fluid that acts as lubrication to allow the lungs to slide back and forth as they expand and contract. 

This pleural fluid is similar to interstitial fluid and is made slippery by proteins like albumin. 

It’s so similar to interstitial fluid because it--essentially--is interstitial fluid. 

There is always a tiny bit of plasma that leaks out of capillaries and gets into the interstitial space, and since these capillaries are so close to the edge of the pleural space, that fluid makes its way into that space and collects there. 

If there were no way out of the pleural space, then it would fill up with fluid, but fortunately, there are lymphatic vessels in the pleura then drain the fluid away and deliver it back into the circulatory system. 

A pleural effusion is when there’s excess fluid in the pleural space either because too much pleural fluid is produced by the body, which can be due to either a transudative or exudative effusion or because the lymphatics can’t effectively drain away the fluid, called a lymphatic effusion. 

A transudative pleural effusion occurs when too much fluid starts to leave the capillaries either because of increased hydrostatic pressure or decreased oncotic pressure in the blood vessels. 

Hydrostatic pressure is what we normally think of as blood pressure; it is the force that blood exerts on the walls of the blood vessel, and can b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Premature_atrial_contraction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Bod0J9E6T0ukO93csL9K2mzDSGqIt32K/_.jpg</video:thumbnail_loc><video:title><![CDATA[Premature atrial contraction]]></video:title><video:description><![CDATA[The heart has two upper chambers, which are called the atria, and a premature atrial contraction, or PAC, is when the atria contract earlier than normal in the cardiac cycle. 

So normally, the sinoatrial, or SA, node sends an electrical signal called a depolarization that propagates out through the walls of the heart and causes both upper chambers to contract. Then, that signal moves to the atrioventricular, or AV, node, where it’s delayed for a split second. Then, the signal travels down into the ventricles, or lower chambers, where it moves down the bundle of His into the left and right bundle branches and into each ventricle’s Purkinje fibers, causing them to contract as well. This trip is called a depolarization wave, and in a healthy heart, it makes sure that the upper chambers contract before the lower chambers contract. On an electrocardiogram, or ECG, which measures the electrical activity of the heart via electrodes that are placed on the skin, the atrial depolarization and its contraction are seen as a P-wave, the ventricular contraction is seen as a QRS complex, and the ventricular repolarization and its relaxation are seen as a T-wave. 

If an atrial cell outside of the SA node initiates a depolarization, that’s called an atrial ectopic focus. Now, this could be initiated by a cell that’s part of the conduction system, or it could just be initiated by another cardiac muscle cell. This typically happens when atrial cells are irritated and stressed by electrolyte imbalances, drugs like cocaine or methamphetamines, ischemic damage like a heart attack, or anything that increases sympathetic activity, like anxiety. Another type of atrial ectopic focus is a reentrant loop, which is when there’s some tissue that doesn’t depolarize properly, which could happen in scar tissue after a heart attack. As a result of this damage, the depolarization wave ends up circling around and around that tissue. A reentrant loop basically starts sending out depolarizat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_development_days_1-4</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2fM47MhMQZuivwzqTkB15feBQHy7fuEA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human development days 1-4]]></video:title><video:description><![CDATA[Human development begins with fertilization, which is the moment when a sperm cell and an oocyte (or egg cell) fuse to form a zygote, the seed of what will eventually grow into a human baby. 

During sex, semen containing about 200 million spermatozoa (or sperm) enters the vagina. 

This seminal fluid is alkaline, which means it’s capable of neutralizing acidic vaginal fluids. 

The sperm quickly make their way through the cervix and uterus and swim into the fallopian tubes, which are also called the uterine tubes. 

Eventually, these millions of sperm enter the ampulla of the uterine tube and then the infundibulum, an opening which flowers out next to the ovary. 

By this point, most of the 200 million sperm that entered the body during sex have died for numerous reasons: some got stuck in the vaginal mucus, others ended up lost in the cervix, and the rest were killed and absorbed by the white blood cells. 

About a thousand lucky survivors are left to wait in the uterine tube for the egg to arrive.

As the sperm wait, they start to rub up against the walls of the uterine tube, and that helps them remove the protective glycoprotein coat and plasma membrane covering the acrosome, a cap-like structure covering what you might think of as the sperm’s head. This process is called capacitation.

Once these protective outer layers are gone, the sperm are able to secrete an enzyme called hyaluronidase which can break down hyaluronic acid, a major component of the extracellular matrix protecting the egg. 

Now, the egg is the largest cell in the human body, big and round, the size of a grain of sand. 

As you’ll soon see, it’s kind of like an onion, as it’s made up of many layers. 

The sperm trying to enter and fertilize this big egg are the smallest cells in the human body—about 1/30th the size of the egg—and they’re long and thin. 

The most intrepid sperm make their way past the extracellular matrix surrounding the egg to a deeper layer called the corona radia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_development_days_4-7</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oT_j2mrzSBSfmu0SfjVzsZVhTa__vHQh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human development days 4-7]]></video:title><video:description><![CDATA[During fertilization, the sperm and egg fuse to form a new diploid cell called a zygote. 

The zygote’s cells divide, forming a new, multicellular cluster called a blastocyst, which travels to the uterus where it implants itself on the inner surface of the uterine wall.

A few hours after syngamy, when the sperm and egg have fused into a zygote, the new diploid cell undergoes a process called cleavage, dividing into a new pair of cells called blastomeres. 

The blastomeres keep splitting, becoming a loose clump of four cells, then eight cells, and finally a more structured, mulberry-shaped 16-cell cluster called a morula, with inner and outer cell masses. 

The morula’s cells are held in a vaguely spherical arrangement by the zona pellucida.

The morula gradually develops an outer cell mass of trophoblast cells and an interior cell cluster with a fluid-filled cavity at the core, which is called the blastocoel. 

As soon as the blastocoel forms, the morula is no more: it’s now a water balloon-shaped arrangement of cells called a blastocyst.

The cells making up the inner cell wall of the blastocyst are collectively called the embryoblast, because they will go on to form the fetus. 

The embryoblast cells cluster together at one end of the blastocyst in an area called the embryonic pole. 

Meanwhile, the trophoblast cells flatten out into a barrier around the blastocyst called the epithelial wall. 

Fully-formed, the blastocyst hatches from the zona pellucida around the end of day four, and is now ready to attach itself to the wall of the uterus. 

Trophoblast cells help the blastocyst implant into the wall of the uterus by releasing L-selectin molecules on their surface. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Klinefelter_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tjDt8Z5zQZqiCx28oysSv5dFSOiMU14I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Klinefelter syndrome]]></video:title><video:description><![CDATA[Klinefelter syndrome, named after Dr. Harry Klinefelter who first identified it, is a chromosomal problem where a person with an XY genotype - biologically a male - inherits at least one extra X-chromosome, and sometimes a few extra ones. 

Having an extra X chromosome makes the testicular cells generate less testosterone, which is the hormone responsible for primary sex characteristics like development of the sex organs as well as secondary sex characteristics like height and body shape. 

It’s worth mentioning up front, that we’re using the term male here, rather than boy or man, to talk about the biological category of a person’s sex rather than a person’s gender identity.

Now, in puberty, in both males and females, the hypothalamus starts to release more gonadotropin releasing hormone, which gets the pituitary gland to release luteinizing hormone and follicle-stimulating hormone.

In males, these hormones affect the Leydig cells and the Sertoli cells. 

The Leydig cells are in the interstitium of the testes, and in response to luteinizing hormone they convert cholesterol into testosterone. 

The testosterone along with follicle-stimulating hormone, then stimulate Sertoli cells in the seminiferous tubules of the testes to make more sperm. 

To main balance or homeostasis, testosterone reduces gonadotropin releasing hormone and luteinizing hormone, and Sertoli cells release the hormone inhibin which inhibits release of follicle-stimulating hormone.        

In Klinefelter syndrome, this hormone balance is altered. 

The extra X-chromosome interrupts the normal function of the Sertoli and Leydig cells. 

Starting at puberty and continuing throughout life, Sertoli and Leydig cells don’t produce inhibin or testosterone, respectively. 

This means that levels of luteinizing hormone and follicle stimulating hormone increase. 

Less testosterone also suppresses testes maturation and sperm production as well as development of secondary male characteristics.

I]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Compliance_of_blood_vessels</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PIELgn5ZQnmg1bSFFkQ1AhKQTZKK3bvU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Compliance of blood vessels]]></video:title><video:description><![CDATA[Compliance, which is sometimes called capacitance or distensibility, refers to the ability of a vessel to respond to an increase in pressure by to distending or swell and increase the volume of blood it can hold, or with decreased pressure, a decrease in volume. The way that this applies to blood vessels is to remember that they are stretchable tubes like rubber hoses rather than lead pipes. So if the pressure increases, the walls of the tube can actually stretch out a bit to accommodate a larger volume, and exactly how much they stretch out depends on their compliance.

We can calculate a given blood vessel’s compliance, C, by dividing the volume of blood, V, in mL by the amount of pressure (P) in mmHg, that the blood is experiencing. And so we measure compliance in mL / mm Hg.

So we can plot out volume as a function of pressure, where the slope, volume over pressure, is the compliance. The veins have high compliance, meaning they’re high-volume, low pressure vessels, and even a small increase in pressure expands the volume a loti. The arteries, on the other hand have low compliance, and are low-volume, high pressure vessels, meaning with same amount of pressure, their volume doesn’t expand as much. Furthermore, a hardened artery would be even less compliant, and is like a lead pipe, in other words it takes an incredible amount of pressure to change the volume even a tiny bit.

With that in mind, since veins are more compliant, the majority of the blood in the body at any given time is in the veins, whereas less blood is in the thicker, less compliant arteries at any given time. Now, when the arteries harden due to arteriosclerosis, they become even less compliant over time, which means they can’t hold as much blood volume at the same pressure. That volume of blood is going to wind up in the veins. In this situation, blood simply moves away from the even higher pressure arteries to the area of lowest pressure, typically where the compliance is highest, l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Erythropoietin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2kyji924Sumk6f5YEgQBNJvsQYGtKnnq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Erythropoietin]]></video:title><video:description><![CDATA[With erythropoietin, ‘-poietin’ means ‘to make’ and ‘erythro-’ refers to red blood cells, so erythropoietin is a hormone that stimulates the production of erythrocytes or red blood cells in the bone marrow. Erythropoietin, or EPO, is produced in the kidneys, and to a lesser extent in the liver, and travels through the blood to the bone marrow where it stimulates immature cells to transform into mature red blood cells.

Every cell in the body uses oxygen for cellular respiration. As we breathe, oxygen diffuses into the bloodstream where it binds hemoglobin within the red blood cells and gets carried off to various parts of the body. Red blood cells live for about 120 days, so there is a constant need to produce new red blood cells.

Now, in the bone marrow, there are proerythroblasts, which are primitive or immature red blood cells. The kidneys produce a constant level of erythropoietin, which gets released into the blood and makes its way to the bone marrow, where it binds to erythropoietin receptors on the immature red blood cells and causes them to erythrocytes, or mature into red blood cells, usually this production of erythropoietin is constant, so the production of mature red blood cells is constant. If there’s ever decreased oxygen delivery to the tissues, then one thing the body can do is ramp up production of oxygen delivery vehicles, in other words red blood cells. In this situation, the kidney cells ramp up production of erythropoietin, therefore ramping up production of mature red blood cells. Interestingly, erythropoietin prevents immature red blood cells from killing themselves by apoptosis, meaning that without erythropoietin, developing red blood cells die via apoptosis.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_tubular_acidosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eCtieSwaQ2qWmyoy_2YF-UrPQvyZUo6_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal tubular acidosis]]></video:title><video:description><![CDATA[With renal tubular acidosis, renal refers to the kidney, tubular refers to the main tube-portion of the nephron, and acidosis refers to having too many protons or increased acidity in blood, so renal tubular acidosis or RTA describes increased acidity in the blood because the renal tubules can’t get rid of protons. 

The kidneys contain millions of nephrons, each of which has a renal corpuscle, and a renal tubule that ends in a collecting duct. 

The renal corpuscle filters large amounts of solutes that go from the blood into the filtrate and eventually the urine, and the renal tubule and collecting duct are responsible for fine tuning the reabsorption and secretion of solutes to adjust the amount that ultimately gets retained by or removed from the body.

Broadly speaking, renal tubular acidosis can develop in either the proximal convoluted tubule, sometimes called just the proximal tubule, or the distal convoluted tubule, or distal tubule, and the nearby collecting duct. 

The proximal tubule is lined by brush border cells which have two surfaces. One is the apical surface that faces the tubular lumen and is lined with microvilli, which are tiny little projections that increase the cell’s surface area to help with solute reabsorption. 

The other is the basolateral surface, which faces the peritubular capillaries, which run alongside the nephron. 

Now - when a molecule of bicarbonate approaches the apical surface of the brush border cell it binds to hydrogen to form carbonic acid. 

At that point, an enzyme called carbonic anhydrase type 4 which lurks in tubule among the microvilli like a shark, swims along and splits the carbonic acid into water and carbon dioxide. The overall equation looks like this: 

H+ + HCO3- &amp;lt;-&amp;gt; H2CO3 &amp;lt;-&amp;gt; H2O + CO2

The water and carbon dioxide happily diffuse across the membrane into the cells where carbonic anhydrase type 2 facilitates the reverse reaction - combining them to form carbonic acid,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testosterone</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EAdobHSURH_f06S4ns2OPjGRQoGHpKnW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Testosterone]]></video:title><video:description><![CDATA[When someone mentions testosterone, it might conjure up images of a burly alpha male.

That’s because testosterone, the primary male hormone, is an androgen, andro meaning male and gen meaning “to produce”, which means testosterone helps generate the characteristics associated with male sexuality. 

The effects of testosterone are first seen in the fetus. 

During the first six weeks of development, the reproductive tissues of males and females are identical, 

but in week seven, genes in the sex-determining region of the Y chromosome initiate the development of testicles. 

Once they form, the fetal testicles secrete testosterone which guides development of the male urogenital tract and external genitalia, 

as well as testicular descent through the inguinal canal which happens in the last two months of fetal development. 

The fetal ovaries also secrete testosterone but at much lower levels, and this largely explains the differences in fetal development between boys and girls. 

In puberty, the hypothalamic-pituitary axis takes center stage in regulating testosterone levels and gonadal function - which are the testes in young men. 

The hypothalamus secretes gonadotropin-releasing hormone which moves through the bridge between the hypothalamus and the pituitary gland, called the hypothalamo-hypophyseal portal system, and gets to the anterior lobe of the pituitary. 

In response, the anterior pituitary secretes luteinizing hormone and follicle-stimulating hormone - two gonadotropic hormones which get secreted into the blood and reach the gonads. 

Leydig cells, slowly turn cholesterol into testosterone through a number of steps, and the first step of this process is stimulated by luteinizing hormone. 

Two important intermediate molecules in that process are dehydroepiandrosterone, also called DHEA, and the molecule that it gets converted into - androstenedione.

The testes have the enzyme 17β-hydroxysteroid dehydrogenase, which takes androstenedione and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Memory_palaces</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dAuqpHO_ThaVGweRX9BM4H0ERceQXL0r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Memory palaces]]></video:title><video:description><![CDATA[A memory palace is a type of memory technique where you imagine a physical location to help you remember more abstract information. 

The reason that memory palaces work is that our brains are better at remembering images and locations, as opposed to abstract things like names and numbers.

Let’s start with an example to show you how this works. Let’s say that you’re trying to remember the six drugs or drug classes that are known to cause pancreatitis, or inflammation of the pancreas.

The list is diuretics, corticosteroids, alcohol, azathioprine, didanosine, and valproic acid. 

First, you have to ask yourself - is this something worth remembering and is the learning objective clear? 

Clinically, it’s really helpful to have these six drugs or drug classes in your working memory so that you can spot them on a medication list and think about them as a potential cause of pancreatitis. 

So if you decide it’s worth remembering a list like this using a memory palace, you’ve got to start with picking a place that you’re familiar with, like a bedroom. 

But it can be any place you know - like the gym, a store, or someplace you’ve seen or imagined like in a TV show like the Office.

Next, you can start identifying specific spots called loci in that place. 

It’s nice to pick really distinct spots - and in this case we can pick out six spots since there are six things to remember - let’s pick the bed, the window, the doorway, the dresser, the rug, and the ceiling light. 

Next, you have to create images for each term you’re trying to remember. You can try a few approaches here. 

First you might go with “sounds like”, for example “papule” sounds like papa and mule, so you can imagine an excited new dad riding around on his baby mule. 

Another trick is to go with “looks like”, for example, a parietal cell looks like a fried egg. 

Finally, you might try “seems like”, for example, taking sedative medication and feeling drowsy seems like what a bear might feel whil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_twins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uD22ZVhiQ5G35ZXgUtUkwaSfTxqLxk7f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of twins]]></video:title><video:description><![CDATA[In most pregnancies a single embryo develops in the uterus, but in some cases, two embryos develop together. These are called twins. 

Most twins are fraternal or dizygotic twins, meaning that they originate from two separate eggs that are fertilized individually. 

A minority are identical or monozygotic twins, meaning that they originate from a single zygote that quickly splits into two separate groups of cells. 

Fraternal twins are from two separate eggs that are fertilized by different sperm, so they have completely separate genetic makeups. 

They don’t look any more or less alike than regular siblings, although the resemblance can still be very close—you may be surprised to learn that Mary-Kate and Ashley Olsen, for example, are fraternal twins, not identical twins. 

Fraternal twinning occurs at a rate of about 10 per 1000 births worldwide. 

Most of the time, fraternal twinning happens when the ovaries release two eggs simultaneously, which is called hyperovulation, instead of releasing one egg at a time. 

Research suggests that some mothers of fraternal twins may produce an overabundance of a hormone called follicle-stimulating hormone, or FSH, which stimulates the growth of ovarian follicles. 

People who become pregnant with fraternal twins tend to be taller and heavier on average, with shorter, more frequent menstrual cycles, all of which are characteristic of having high levels of follicle-stimulating hormone. 

Because follicle-stimulating hormone levels gradually rise with age, fraternal twin pregnancies become increasingly likely in people aged 35 or older, and this also helps explain why parents who have given birth to fraternal twins once are more likely to do so again. 

The likelihood of having fraternal twins resulting from hyperovulation is thought to have a genetic component, but no specific gene has been identified yet. 

Identical twins are less common than fraternal twins, occurring at a rate of about 4 per 1000 births worldwide]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Electrical_conduction_in_the_heart</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tl8mfCE5T3WhmCVnehdTgtTGT2OyGqPL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac conduction system]]></video:title><video:description><![CDATA[So, electrical conduction in the heart refers to the electrical signals that go from cell to cell in the heart. This happens in the form of  action potentials, which get sent out by the pacemaker cells in the heart. 

The pacemaker cells, also called conducting cells, are a relatively tiny group -- only about 1% of the heart cells -- but they’re a pretty influential minority. 

They’re special ability is that they are autorhythmic, which means that they are able to continually generate new action potentials that go out to the rest of the heart -- the other 99%. 

This is different from how it works in skeletal muscle cells, which get their action potential signals directly from neurons. 

The cells that receive the cardiac action potential from the pacemaker cells are called myocytes - they make up the myocardium, which is the muscular middle layer of the heart. 

Myocytes are also called contractile cells because they contract and that’s how the heart pumps blood. 

Action potentials are initiated by depolarization, which is the opposite of polarization. In this case polarization is when there are more positive ions outside the cell than inside. 

This difference in charge is called the membrane potential and is negative since there are more positive ions outside the cell. 

So, depolarization is when the membrane potential gets smaller making a cell slightly more positive than it normally would be - imagine a negative, gloomy cell enjoying a moment of joy. 

If one cell after another depolarizes, then there’s a depolarization wave which is just like a crowd of people doing the wave at a football stadium.

So, there’s a group of pacemaker cells in the sinoatrial node or SA node, which is a small sinus or cavity tucked up into the right atrium. During each heartbeat, one pacemaker cell out of the group will automatically depolarize first. 

In fact, each heart beat might be led by a different cell in the group, but eventually at least one of them will]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pressures_in_the_cardiovascular_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zGgNS_F6RYunsSKMKjza08QYQVSIEhS_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pressures in the cardiovascular system]]></video:title><video:description><![CDATA[When we talk about pressures in the cardiovascular system, we’re talking about blood pressure. Pressures in different parts of the cardiovascular system aren’t equal and these differences in pressures keep the blood moving from high pressure areas leaving the heart like the arteries to low pressure areas like the veins. 

Actually, the pressure curve looks a little more like this, and fluctuates in the arteries depending on part of the cardiac cycle it’s in, with these peaks being systole, and these low points being diastole -That being said, this original line is the average of these fluctuations, or the mean arterial pressure. Now, since systole takes up about a third of a single cardiac cycle, and diastole takes up the remaining 2/3 of the cycle, we can calculate the mean arterial pressure at any time by the equation:

                            MAP = (⅓) SBP + (⅔) DBP

Which after distributing we get:

                            MAP = DBP + (⅓) PP

Now, looking at these fluctuations on the arterial side, there’s a couple important things to notice. First of all, on the downswing of the curve, there’s a sharp sharp pressure drop followed by a rise again forming what’s called the dicrotic notch or incisura. As blood is ejected out into the aorta, pressure rises quickly, and then as a tiny amount of blood flows back into the ventricle, and causes the valve to snap shut and the pressure to fall. That snapping shut of the valve causes it to recoil back, which causes a brief increase in pressure of aorta, and then finally the pressure falls as the aorta settles and the heart relaxes.

A second interesting thing to notice is that the pulse pressure in the large arteries downstream of the aorta is larger than those in the aorta themselves!That’s because the pressure from blood travels a bit faster than blood itself. To understand that idea - think of the molecules and cells in the blood like Newton’s cradle, and while they move together, they bump into each ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Surface_epithelial-stromal_tumor</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1NoxOEXkSGiP79YMh2iTtc5aQ5OSwz45/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovarian surface epithelial tumors]]></video:title><video:description><![CDATA[Epithelial refers to the surface lining, and ovarian refers to ovary, of which women have two that sit along either side of the uterus so epithelial ovarian cancer, is a cancer that forms along the surface of an ovary. 

Now, each ovary contains multiple follicles. 

And, each follicle is made up of a germ cell, also known as an oocyte, which is the immature egg. 

Between the follicles is the stromal or connective tissue cells, and lining the ovary is a layer of epithelial cells. 

Ovarian tumors are generally grouped based on these three types of cells in the ovaries, and the majority of ovarian cancers are epithelial kind. 

Now, if an epithelial cell starts to divide uncontrollably, it can either be a benign tumor which means that it does not invade nearby tissue or spread to other parts of the body, or it can be a malignant tumor which means that it might invade or spread to other tissues. 

Compared with benign tumor cells, a distinguishing feature of malignant tumor cells have slightly less organized nuclei. 

A third class of tumors are called borderline tumors because they have features that are intermediate between the other benign and malignant tumors.

Epithelial ovarian cancers can be subdivided into four types: serous, mucinous, endometrioid and transitional. 

Serous and mucinous tumors arise from epithelial cells that line the outside of ovaries, whereas even though the tumors are found in the epithelium, the endometrioid and transitional cell tumors arise from other cell types. 

Serous tumors have fluid-filled cysts, typically a single cyst, and can be benign, malignant, or borderline. 

Benign serous tumors are called serous cystadenomas, and are the most common type, and often develop on both ovaries, and typically affect premenopausal women. 

Mucinous tumors, on the other hand, have mucus-filled cysts that often involve large multiloculated cysts, but can also be benign, malignant, or borderline. 

Benign mucinous tumors are called mu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Free_radicals_and_cellular_injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4Y9UDJGaSJa83CGN5PkYX2ABTwm-yq_6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Free radicals and cellular injury]]></video:title><video:description><![CDATA[Electrons in an atom are present in spaces called orbitals, and each orbital can fit different pairs of electrons. 

Now free radicals are molecules with only one electron, or an unpaired electron, in their outer orbital. 

Free radicals have a habit of stealing electrons from any molecule they come across to make themselves stable and it’s what causes all the trouble and potentially can cause cellular injury.

Now, a free radical is formed when any molecule gains or loses an electron. 

In the body, free radicals can be generated physiologically, which means as a part of normal metabolic processes; or pathologically, which is due to some disease.  

A major physiological source of free radicals is cellular respiration, which is also called oxidative phosphorylation. 

Oxidative phosphorylation is the process of making ATP by donating electrons to complexes embedded within the inner mitochondrial membrane. 

Together, they form the electron transport chain, which pass electrons from complex to complex, and finally to oxygen, creating a proton gradient that will be used to make ATP. 

The final step of this process involves a molecule called cytochrome c oxidase, sometimes known as complex IV, which transfers electrons to oxygen. 

Normally, when oxygen gets four electrons, it gets converted into water. 

But when oxygen doesn’t get all four electrons, then it will have unpaired electrons in its orbital, giving rise to free radicals. 

Since these are formed from oxygen, they’re collectively called reactive oxygen species, or simply ROS. 

Okay so if oxygen is given one electron, it becomes superoxide (O2−) If it gets two electrons, it becomes hydrogen peroxide, or H2O2, and then 3 electrons, it’s the hydroxyl radical (OH.).

There are also pathological conditions where free radicals can be generated. 

First, they can be produced during inflammation by phagocytes like macrophages and neutrophils. 

When a pathogen invades the body, the phagocyte gobbles up]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sex_cord-gonadal_stromal_tumor</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/weyuUMspT0qCrVUTszT_Q4mgQzu6csFw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovarian sex-cord stromal tumors]]></video:title><video:description><![CDATA[With sex cord-stromal ovarian cancer, Ovarian refers to “ovary”, of which women have two that sit along either side of the uterus. The term sex cord refers to an embryonic structures that develop into ovarian follicles and stromal cells are the connective tissue of any organ. So a sex cord-stromal ovarian cancer is a type of tumor that develops from either ovarian follicle cells or connective tissue cells.

Each ovary has multiple follicles. Each follicle is made up of an oocyte, which is an immature egg, surrounded by two types of cells - theca cells and granulosa cells. Granulosa and theca cells work together to support follicle development. Luteinizing hormone stimulates theca cells to generate androgens and follicle stimulating hormone stimulates granulosa cells to convert those androgens to estradiol using the enzyme aromatase. A large increase in estradiol triggers ovulation.

During ovulation, the oocyte pops out of the ovary, causing a bit of damage to the surface. Fibrocytes detect that damage and differentiate into fibroblasts and lay down collagen to help repair the damage. 

If any of those cells starts to divide uncontrollably, it can either form a benign tumor which means that it doesn’t invade nearby tissue or spread to other parts of the body, or it can be a malignant tumor which means that it can invade nearby tissue and spread to other parts of the body. Compared with benign tumor cells, malignant tumor cells have key features like not having a clearly defined border or like having slightly less organized nuclei.

The first main type of sex-cord stromal tumor is a granulosa-theca cell tumor. And these are the most common malignant stromal tumors and they’re associated with middle-aged women. These tumors often end up producing way too much estradiol, and this can cause very specific hormone associated symptoms like uterine bleeding, breast tenderness, and early puberty in young girls. Under the microscope, these tumors classically develop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Writing_great_questions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P2L05Ea5QOOhVQN40IZKKI2XQKGHIGWF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Writing great questions]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Writing great questions through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bordetella_pertussis_(Whooping_cough)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Voo-r7y9RtaloFQSPOioWeR3RYaQJ1iM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bordetella pertussis (Whooping cough)]]></video:title><video:description><![CDATA[Pertussis is a contagious infection caused by the bacteria Bordetella pertussis, which causes violent coughing spells, called paroxysms, which make it difficult to breathe. 

When it is finally possible to breathe in, air is drawn in through partially closed, swollen airways and that creates a whooping noise which gives pertussis its other name, whooping cough.

Bordetella pertussis is a gram negative coccobacilli - meaning that it looks like a short pink rod on a gram stain. 

It transmits from one person to another through a sneeze or cough, when that happens thousands of bacteria-filled droplets spray out about two meters or six feet away. 

These droplets can land in the mouths or noses of nearby people, or get directly inhaled into the lungs. 

The bacteria can also survive for several days on dry surfaces, so it’s also possible to get the bacteria by touching a surface, like a contaminated doorknob, and then touching your own eyes, nose, or mouth. 

Bordetella pertussis releases toxins which are proteins that help the bacteria in various ways to attach to and damage the respiratory epithelial cells. 

It starts with three toxins: Filamentous hemagglutinin, pertactin, and agglutinogen - all of which help to anchor Bordetella pertussis to the epithelia where it remains during an infection. 

Next there’s the tracheal cytotoxin which paralyzes the cilia that are the little hairy projections on the epithelial cells so they can’t sweep back and forth anymore. 

Normally these cilia sweep away mucus and any bacteria stuck in the mucus, so paralyzing the cilia allows pertussis to stay snugly attached to the epithelia. 

This also means that mucus starts building up which triggers a violent cough reflex to clear the airway starting up those coughing fits. 

Another toxin is pertussis toxin which also helps with anchoring pertussis to the epithelia as well. 

In addition to this, though, pertussis toxin causes an increase in the absolute lymphocyte level in t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neonatal_hepatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NLNn9RTSRsels2opYs_f4dwdTFG4tIX7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neonatal hepatitis]]></video:title><video:description><![CDATA[Neonatal hepatitis is this inflammation of the liver tissue in newborns, usually between 1 and 2 months after birth. 

A minority of cases, about 20%, are known to be caused by a virus that infected the infant before birth, through the mother, or maybe shortly after birth.

Several viruses that have been known to cause neonatal hepatitis are rubella, cytomegalovirus, and hepatitis viruses A, B and C. 

The other 80% of cases are said to be idiopathic, meaning we don’t really know what the underlying cause was, a lot of times viruses are suspected, but it could also be due to other genetic disorders, cholestasis where bile flow is impaired, or metabolic liver disorders like alpha-1 antitrypsin deficiency. 

This last one’s an inherited disease in which the alpha-1 antitrypsin or AAT protein that’s produced in the liver is not quite produced right, and is essentially the wrong shape. 

When this happens, it can’t get out of the liver cells, ultimately building up and causing liver cell death, inflammation of liver tissue, and hepatitis.

A newborn or infant with neonatal hepatitis will often have jaundice, causing yellowed skin and eyes due to the blockage or inflammation of the bile ducts. 

When these are blocked, bilirubin, a yellow pigmented component of bile, builds up in the blood and starts to get into tissues, causing yellowed skin and eyes. 

Bile’s an essential part of fat digestion and absorption of fat soluble vitamins like vitamin A, D, E, and K, so children with neonatal hepatitis and jaundice may fail to gain weight and grow normally due to lack of adequate nutrition. 

Bile also functions in removing toxins from the body, like bilirubin but also things like drug metabolites, so if bile flow is reduced, these might deposit and build up in the skin and lead to itching and rashes. 

Bilirubin might also be filtered into the urine through the kidneys, causing darker colored urine. 

Since hepatitis is an inflammation of the liver, patients may al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutcracker_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2JxIp2q-SXe-cj312dlUXjULQvmsW1w0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutcracker syndrome]]></video:title><video:description><![CDATA[Renal nutcracker syndrome is when the left renal vein, which drains blood from the left kidney, gets squeezed between two large arteries: the superior mesenteric artery and abdominal aorta. It’s kind of like the renal vein is the nut and the two arteries are the nutcracker.  

Now, blood heading toward the lower body exits the left ventricle, swoops around the aortic arch, and then flows downward through the descending aorta, a large, muscular blood vessel about as thick as a thumb. The descending aorta runs along the back of the abdominal wall next to the spine, where it’s called the abdominal aorta, until it splits into the common iliac arteries. The abdominal aorta gives rise to many smaller arteries, including three unpaired arteries: the celiac artery, the superior mesenteric artery, and the inferior mesenteric artery. All three of these arteries branch off the anterior wall and supply blood to the digestive tract.

The renal vein carries blood returning from the kidney to the heart, passing between the aorta and the superior mesenteric artery. The angle formed between these two vessels is called the aortomesenteric angle. It’s usually around 45 degrees, with the renal vein cushioned by a bit of fat in the mesentery. If that aortomesenteric angle is reduced, the arteries begin to pinch the left renal vein like a nutcracker, preventing blood from returning back to the heart. This leads to a backup of blood in the left kidney, causing renal hypertension. Over time, the high pressures can cause small breaks in the renal blood vessels, and a bit of blood can even get into the urine. Also, because the left testicular vein drains into the left renal vein, blood can end up pooling in the left testicle as well. 

In young people, reduction of the aortomesenteric angle can happen due to normal growth as well as changes in body proportions. As a result, sometimes the angle can widen just as easily as it can narrow. In adults, the most common cause is extreme we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Germ_cell_ovarian_tumor</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aWH1vrrKQm_xhTwPaUbsBvo3QrycYbdI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovarian germ cell tumors]]></video:title><video:description><![CDATA[With germ cell ovarian cancer, germ cell refers to the precursor cells that develop into eggs, ovarian refers to ovary which is where the germ cells live, of which there are two that sit on either side of the uterus. 

So, a germ cell ovarian cancer refers to situations where these precursor germ cells become cancerous and form tumors.

During fetal development, the entire body derives from three layers, called germ layers, the ectoderm, mesoderm, and endoderm. 

These germ layers are made of germ cells, and the germ cells migrate out and differentiate into all of the different types of tissues, for example some ectodermal germ cells become cells of the brain and spinal cord, some mesodermal form bone and muscle, and some endodermal cells become cells in the gastrointestinal tract. 

Some very special germ cells, however, remain as germ cells - meaning that they don’t differentiate, they remain pluripotent, meaning that unlike the cells that differentiate these germ cells retain their ability to turn into other cell types. They’re like ancient little shape-shifters. 

Normally, during development these germ cells head to the ovary in women or testicle in men where they remain for decades, eventually developing into eggs or sperm, respectively. 

Now, if those germ cells in the ovaries start to divide uncontrollably, it can either form a benign tumor which means that it does not invade nearby tissue or spread to other parts of the body, or it can be a malignant tumor which means that it can both invade and spread to other tissues. 

Compared with benign tumor cells, malignant tumor cells have key features like not having a clearly defined border or like a slightly less organized nuclei.

There are four types of germ cell tumors and each type is named after the type of cell that these pluripotent germ cells develop into. 

The first, are teratomas, terato means monster and oma is a tumor. 

So teratomas are monster tumors, and they are called that because th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyponatremia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MLA63swyRuCsFqa3A_tmWGAFT_Wce9LF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyponatremia]]></video:title><video:description><![CDATA[With hyponatremia, hypo- means under or low, and -natrium is latin for sodium, often written as Na plus, and -emia  refers to the blood, so hyponatremia means a lower than normal concentration of sodium in the blood, generally below 135 mEq/L.

The concentration of sodium depends on both sodium and water levels in the body. 

About 60% of our body weight comes from just water, and it basically sits in two places or fluid compartments—one third of it is in the extracellular fluid, meaning outside the cells, and two thirds of it is in the intracellular fluid, or inside cells. 

The extracellular fluid includes the fluid in blood vessels, lymphatic vessels, and the interstitial space, which is the space between cells that is filled with proteins and carbohydrates. 

Normally, the two compartments have the same osmolarity -- total solute concentration -- and that allows water to move freely between the two spaces. 

But the exact composition of solutes differs quite a bit. 

The most common cation in the extracellular compartment is sodium, whereas in the intracellular compartment it’s potassium and magnesium. 

The most common anion in the extracellular compartment is chloride, whereas in the intracellular compartment it’s phosphate and negatively charged proteins. 

Of all of these, sodium is the ion the moves back and forth across cell membranes, and subtle changes in sodium concentration tilts the osmolarity balance in one direction or another and that moves water. 

This is why we say “wherever salt goes, water flows”. 

That being said, hyponatremia, or low concentration of sodium in the extracellular fluid and therefore the blood, can be caused by either losing more sodium than water, or gaining more water than sodium. 

Broadly speaking, hyponatremia can be divided into three categories based on water volume status. 

The first is hypervolemic hyponatremia where there’s an enormous increase in total body water with a less significant increase in total ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ECG_rate_and_rhythm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QrUUtn-XSiGHiokRaXXnQI3lS8GKCTZy/_.jpg</video:thumbnail_loc><video:title><![CDATA[ECG rate and rhythm]]></video:title><video:description><![CDATA[An electrocardiogram - an ECG - or the dutch and german version of the word - elektrokardiogram or EKG, is a tool used to visualize “gram” the electricity “electro” that flows through the heart “cardio”. 

An ECG tracing specifically shows how the depolarization wave moves during each heartbeat - which is a wave of positive charge - looks from the perspective of different sets of electrodes.

This particular set of electrodes is called lead II, with one electrode on the right arm and the other on the left leg, so essentially when the wave’s moving toward the left leg electrode, you get a positive deflection, like this big positive deflection correspond to the wave moving down the septum. 

To read an ECG there are a few key elements to keep in mind, one of them includes figuring out the rate and rhythm. There are a couple ways of figuring out the heart rate on an ECG. 

The first one is called the “box method” because you count the number of boxes between heartbeats. Each small box represents 0.04 seconds, and each big box is five small boxes, so each big box is 0.2 seconds. 

To do that, you can count the number of small boxes between R waves since R waves are tall and pointy and easy to see in lead 2 of an ECG strip. 

You can find an R wave that has a peak that falls at the beginning of a box, and then count up how many boxes until the same point on the next R wave.

Let’s say that there are 4 big boxes and 1.5 small boxes between two R waves, meaning there are 4 x 5 + 1.5 = 21.5 small boxes, and that means there’s 0.04 seconds x 21.5 or .86 seconds between heartbeats. 

Now, to get something a little more meaningful we can take the inverse which is 1 over 0.86 beats per second, or 1.16 beats per second.  

Now there’re 60 seconds in a minute, so multiplying that by 60 we end up with 70 beats per minute—the heart rate! 

Now, if the distance between two R waves is exactly 1 big box, then the heart rate would be 300 beats per minute—really fast. If R wav]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomic_and_physiologic_dead_space</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9v0wyi1ITNO9fsVZJ-piCDdQT5icqkBD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomic and physiologic dead space]]></video:title><video:description><![CDATA[The main job of the lungs is gas exchange, pulling oxygen into the body and getting rid of carbon dioxide.

Normally, during an inhale - the diaphragm and chest muscles contract to pull open the chest and that sucks in air like a vacuum cleaner, and then during an exhale - the muscles relax, allowing the lungs to spring back to their normal size pushing that air out.  

But as it turns out, not all the air that we breathe in, ends up participating in gas exchange. 

As we inhale, air enters the nasal cavity or the oral cavity and travels down the trachea and then splits into the two mainstem bronchi and enters the two lungs.

Within  the lungs, the bronchi divide into progressively smaller and smaller bronchioles until air gets down to tiny thin-walled air-sacs called alveoli which are surrounded by tiny capillaries. This is the site of gas exchange.

So, the part of the respiratory tree prior to these alveoli, starting from the nose, or the mouth, right up to the tiny terminal tiny bronchioles without these alveoli, merely acts to conduct or transport air to the alveoli. This part is known as the conducting zone and it does not take part in gas exchange. 

The volume of air contained in this conducting zone is known as anatomic dead space. 

‘Dead’ sounds kind of ominous but it basically reflects the fact that this air is as good as dead to the body, because you can’t extract oxygen from it. 

‘Anatomic’ means that this dead space is inbuilt within the anatomy of the respiratory system and doesn’t really change; no matter what we do, we cannot ever use this air for gas exchange.

Alright, so now let’s simplify all this—so this ball represents all the alveoli, and this portion represents all of the conducting zone, in other words the anatomic dead space. So how much air is part of this anatomic dead space? 

A normal person, when breathing quietly without any active effort, takes in about 500 ml or half a liter of air - this is the tidal volume, represente]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_valve_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I_Jpg92mSMWHxxOfLYPCCwxWSri131gN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary valve disease]]></video:title><video:description><![CDATA[The pulmonary valve is typically made up of three leaflets, the anterior, the left, and the right, and it opens during systole to allow blood to be ejected to the lungs. During diastole, it closes to allow the heart to fill with blood and get ready for another systole. If the pulmonary valve doesn’t open all the way, it makes it harder for the heart to pump blood out to the lungs, and this is called pulmonary stenosis. If the pulmonary valve doesn’t close all the way, then blood leaks back into the right ventricle, and this is called pulmonary valve regurgitation or pulmonary insufficiency.

Pulmonary valve stenosis is often congenital, meaning that at birth, the leaflets are irregularly shaped or not fully developed. Pulmonic valve stenosis is often associated with congenital heart conditions like Tetralogy of Fallot, which affects all four chamber of the heart, as well as a genetic condition called Noonan&amp;#39;s syndrome. In other cases, pulmonary valve stenosis can be caused by mechanical stress over time, which damages endothelial cells around the valves. This damage causes fibrosis and calcification, which harden the valve and make it more difficult for the valve to open all the way. 

Because pulmonary valve stenosis makes it harder for the valve to open when the right ventricle tries to eject blood, the valve resists for a second before finally snapping open, and this causes a characteristic “ejection click.” Because the blood has to flow through a narrow opening, we get increased turbulence, which creates a noise called a murmur. This murmur gets louder as more blood flows past the opening, and then it gets quieter as the amount of blood flowing through the valve decreases because There’s less in the ventricle. This sound is described as a crescendo-decrescendo murmur. 

Since it’s more difficult to open this hardened valve and push blood past it, the right ventricle has to generate really high pressures. To achieve those pressures it thickens ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tricuspid_valve_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rjP395YMQyO1OojU26BGIITBSLOFmFRG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tricuspid valve disease]]></video:title><video:description><![CDATA[The tricuspid valve has three leaflets: the anterior, posterior and medial or septal leaflets. Together, these separate the right atrium from the right ventricle. During systole, or muscle contraction, the tricuspid valve closes, and during diastole, or heart relaxation, the tricuspid valve opens and lets blood fill the right ventricle. Tricuspid valve regurgitation happens when the tricuspid valve doesn’t close completely and blood leaks back from the right ventricle into the right atrium. Tricuspid valve stenosis happens if the tricuspid valve can’t open completely, making it difficult to fill the right ventricle.

Let’s start with tricuspid valve regurgitation. Often, regurgitation is due to pulmonary hypertension which causes an increase in right ventricular pressure. This pressure then dilates the tricuspid valve, allowing blood to go backward. Another well-known cause of regurgitation is rheumatic heart disease, an autoimmune reaction that involves the valve leaflets and causes inflammation. This chronic inflammation leads to leaflet fibrosis, which makes it so that they don’t form a nice seal and instead let blood leak through. Still another cause of tricuspid regurgitation is damage to the papillary muscles from a heart attack. If these papillary muscles die, they can’t anchor the chordae tendineae, which then allows the tricuspid valve to flop back and allows blood to flow backward from the right ventricle into the right atrium. There are also congenital causes for this condition, like Ebstein’s anomaly, which is when a person is born with leaflets that are located too low, i.e., in the ventricle rather than between the atria and the ventricle, and this makes it hard for the leaflets to form a nice seal.

In all of these situations, blood flows back into the right atrium during systole. This movement of blood can be heard as a holosystolic murmur, because it’s possible to hear blood flowing through the valve for the duration of systole. Another po]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombophlebitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WLWI9wvEREGpC-Qh1fqf3MfSS7iJCvtQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombophlebitis]]></video:title><video:description><![CDATA[Thrombophlebitis can be broken down into “thrombo” or thrombus which refers to a blood clot,  “phleb” which refers to a vein, and “itis” which refers to inflammation. So thrombophlebitis is a blood clot that gets lodged in a vein and causes inflammation.

Normally, the process starts with damage to the endothelium, or inner lining of the blood vessel walls, after which there’s an immediate vasoconstriction or narrowing of the blood vessel which limits the amount of blood flow. After that, some platelets adhere to the damaged vessel wall, and become activated by collagen and tissue factor, which are proteins that are normally kept separated from the blood by an intact endothelium. These platelets then recruit additional platelets to form a platelet plug. The formation of the platelet plug is called primary hemostasis. 

After that, the coagulation cascade is activated. First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver, and usually these are inactive and just floating around in the blood. The coagulation cascade starts when one of these proteins gets proteolytically cleaved. This active protein then proteolytically cleaves and activates the next clotting factor, and so on. The final step is activation of the protein fibrinogen to fibrin, which deposits and polymerizes to form a mesh around the platelets. So these steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis and results in a hard clot at the site of the injury. 

This cascade has a huge degree of amplification and takes only a few minutes from injury to clot formation. So the activation of the cascade is carefully controlled by anticoagulation proteins that target and inactivate key clotting factors. For example, antithrombin inactivates Factors IXa, Xa, XIa, XIIa, VIIa and thrombin while protein C inactivates Factors Va and VIIIa. 

As the clot grows in size, it limits the amount of bl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_pulmonary_airway_malformation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BEV6g_D1RyykUYAT0BaK-qOoQROarPWB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital pulmonary airway malformation]]></video:title><video:description><![CDATA[A congenital pulmonary airway malformation, abbreviated CPAM, is a lung malformation that usually affects a single lobe of one of the lungs, and forms during fetal development. 

The old name for CPAMs was congenital cystic adenomatoid malformation, because they have both “cysts” and “glands” in them, but are terribly malformed and disorganized. 

CPAM cysts are continuous with the airways, so they’re filled with fluid in utero, and become filled with air after birth.

The cause of CPAMs isn’t known. 

It isn’t even known whether they’re a developmental failure or if they’re a type of hamartoma, which is a benign overgrowth of tissue. 

Sometimes, the growing CPAM can prevent normal healthy lung tissue from developing - causing pulmonary hypoplasia - which is underdevelopment of the lungs. 

Also, a CPAM can push on the heart or large veins, causing blood to back up throughout the fetus’s veins. 

When that happens, fluid can start to leak into the fetal tissues, a condition called fetal hydrops. 

Whether or not any of this happens largely depends on the size and location of the CPAM. 

CPAMs can arise from different spots along the tracheobronchial tree, and that’s how they’re sub-typed. 

The five subtypes are named 0 through 4, with type 0 arising from the most proximal airways – the trachea and proximal bronchioles, and type 4 developing all the way down in the alveolus. 

Type 0 CPAMs develop at the trachea or proximal bronchus with small cysts, but are pretty rare. 

Type 1 CPAMs, which develop in the distal bronchi and proximal bronchioles, are the most common, and have one or more large cysts, with tissue like cartilage in between the cysts. 

Type 2’s come from the terminal bronchioles and have smaller cysts. 

Type 3s arise almost all the way down to the alveolus, and have cysts that are so small that they look like a solid mass. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Premature_ventricular_contraction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aZYZtGefQUSSU0ZYdpUw8R80QCOQGDVE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Premature ventricular contraction]]></video:title><video:description><![CDATA[The heart has two lower chambers, called the ventricles, so a premature ventricular contraction is when the ventricles contract earlier than normal in the cardiac cycle. This happens because an abnormal contraction signal, called a depolarization, originates from somewhere in the ventricles rather than coming from the pacemaker cells.

So, if we simplify this heart a little bit, normally, the sinoatrial node or SA node sends an electrical signal that propagates out through the walls of the heart and contracts both upper chambers. Then that signal moves to the atrioventricular node or AV node, where the signal is delayed for a split second, and then it goes down into the ventricles or lower chambers where it moves down the bundle of His and into the left and right bundle branches and into each ventricle’s Purkinje fibers, causing them to contract as well. So, in a healthy heart the upper chambers contract first, then shortly after, the lower chambers contract. On an electrocardiogram or ECG, which measures the electrical activity of the heart via electrodes that are placed on the skin, the atrial depolarization, and therefore its contraction, is seen as a p-wave; the ventricular contraction is seen as a QRS complex; and the ventricular repolarization, and therefore its relaxation, is seen as a T-wave. 

This empty space here is called the PR segment, and it corresponds to the pause in the AV node, and this one is called the ST segment, and it corresponds to the interval between ventricular depolarization and repolarization, and this one is called the TP segment, which represents the heart’s quiet time when the cells are finished repolarizing and are ready for another signal. 

Now, if we just look at the QRS complex, which normally lasts less than 100 milliseconds or 2-and-a-half little boxes, it’s usually made up of three smaller waves, also called deflections. If the first wave after the p-wave is downwards, or negative, it’s called a Q wave - which you c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Superior_mesenteric_artery_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ojU1fj_6RR_h9s5kSK-h2YpiQY6dVz1V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Superior mesenteric artery syndrome]]></video:title><video:description><![CDATA[Superior mesenteric artery syndrome is when the first part of the small intestine—which is the duodenum—gets squeezed between two large arteries: the abdominal aorta and the superior mesenteric artery.

So, when the duodenum gets squashed, food can’t easily pass by, and it leads to intestinal obstruction. 

Normally, blood heading toward the lower parts of the body exits the heart, swoops through the aortic arch, and then flows downward through the descending aorta, which is a large, muscular blood vessel about as wide as a thumb. 

The descending aorta runs along the back of the abdominal wall in front of the spine, and that part is called the abdominal aorta.

The abdominal aorta then forks into the common iliac arteries near the fourth lumbar vertebra, or L4. 

Along the way, it gives rise to a number of paired arteries like the renal arteries, as well as three unpaired arteries—the celiac trunk, the superior mesenteric artery, and the inferior mesenteric artery—all of which come off of the anterior or front wall of the aorta and supply blood to the stomach and intestines.

Usually, the angle between the aorta and the superior mesenteric artery as it branches off—the aortomesenteric angle—is around 45 degrees. 

It turns out that the duodenum, which is the C-shaped first section of the small intestines - passes through this little archway.

More specifically, it’s the third or transverse section of the duodenum, and as it passes through it’s cushioned by the mesenteric fat pad which is a collection of fat that protects the duodenum from getting crushed by the two arteries. 

In superior mesenteric artery syndrome the mesenteric fat pad starts to thin out which reduces the aortomesenteric angle, allowing the aorta and the superior mesenteric artery to pinch down on the transverse duodenum. This blocks food from passing from the duodenum to the jejunum, and the backup of food leads to intestinal obstruction. 

There are a few reasons why this might happen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_syncytial_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kgY0FvIfTlSukLv9MPvQneQKRcGeYG11/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory syncytial virus]]></video:title><video:description><![CDATA[Bronchiol refers to the small airways of the lungs, and itis means inflammation, so bronchiolitis describes inflammation of the small airways in the lungs. 

It’s most often caused by infection from the respiratory syncytial virus, or RSV. 

It mostly affects young children, and actually causes illness in nearly every child at some point in their life. 

Respiratory syncytial virus is a virus that causes the cells lining the respiratory tract to merge; they form a large multinucleated “cell” called a syncytia.

Respiratory syncytial virus is part of the Pneumoviridae family. 

It’s transmitted when an infected person sneezes or coughs, which spreads thousands of droplets containing the virus into the surrounding area up to about two meters, or six feet, away. 

These droplets can then land in the mouths or noses of people nearby, or be inhaled into their lungs. 

The virus can also survive on surfaces for a few hours, so it’s possible to get the virus by touching an infected surface, like a contaminated doorknob, and then touch your own eyes, nose, or mouth. 

Upon entering the body, the virus encounters the epithelial cells lining the nasopharynx, which is the part of your throat nearest your nose. 

It creates some local damage, and then works its way down the respiratory tree; it’s kind of like a secret agent rappelling down a rope of mucus.

The virus travels down past the trachea and main bronchi to eventually reach the bronchioles, its primary target. 

Respiratory syncytial virus is an enveloped virus with a linear negative-sense strand of RNA. 

This means that once the virus enters its RNA into a respiratory epithelial cell, that strand has to be converted into a complementary sense strand in order to be translated. 

The cell is forced to use its energy and organelles to make viral proteins; it basically turns into a virus factory. 

The new viruses invade neighboring cells, creating multinucleated syncytia out of some cells while destroying othe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sheehan_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o_WqSp-1QfWEMsL96DXHqPpBQ-itRxA-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sheehan syndrome]]></video:title><video:description><![CDATA[Sheehan syndrome, also known as postpartum pituitary gland necrosis, was first described in the 1930s by British doctor and pathologist Harold Sheehan. In postpartum pituitary gland necrosis, “postpartum” means after childbirth; “pituitary gland” refers to a small, powerful gland that helps control hormones during pregnancy and beyond; while “necrosis” means cell death. So, in postpartum pituitary gland necrosis, parts or sometimes the entire pituitary gland can be damaged after childbirth, usually due to severe blood loss during or after delivery. 

The pituitary gland sits in a small space at the base of the brain called the sella turcica, and it acts as the body&amp;#39;s hormone control center. The front part, called the anterior pituitary gland, produces growth hormone, which helps the body grow; prolactin, which stimulates mammary glands to produce milk; as well as follicle-stimulating hormone and luteinizing hormone, which control menstrual cycle and fertility. Additionally, the anterior part produces thyroid-stimulating hormone, which keeps the metabolism running flawlessly, and adrenocorticotropic hormone, which stimulates the adrenal glands to produce cortisol. On the other hand, the back part, called the posterior pituitary gland, stores and releases two main hormones. One is the antidiuretic hormone, which controls the water balance in the body, and the second is oxytocin, which plays a key role in labor and contractions of the womb during childbirth. 

During pregnancy, the pituitary gland works overtime to support the body through pregnancy and get it ready for childbirth and breastfeeding. One specific group of cells in the anterior pituitary, called lactotrophs, starts to grow in size and increase in number. These cells are responsible for prolactin production. As the lactotrophs grow and become more active, the pituitary gland grows, demanding more energy and resources. But here’s the catch. Even though the lactotrophs are growing, workin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ectoderm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x8_Eji6GSj2tdRtlpeAWY5MZR6_GtMXk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ectoderm]]></video:title><video:description><![CDATA[When the embryo is a week old, it has two layers of cells: a dorsal epiblast layer and a ventral hypoblast layer. 

During week 3 of development the embryo undergoes gastrulation where the cells in the epiblast layer form a three-layered trilaminar disc with an ectoderm, mesoderm and endoderm layer.

So, imagine the embryo is like a strawberry birthday cake with the ectoderm as the candles, the mesoderm as the lime frosting, and the delicious sponge cake as the endoderm. 

We can even put three candles on this cake to help you remember that gastrulation happens during week 3.

During gastrulation, some mesodermal cells start to differentiate and they form a structure called the notochord, a rod of cells that release different genetic transcription factors that help embryonic cells develop into the body’s various organs and structures. 

The notochord also kickstarts a process called neurulation, stimulating the cells in the nearby ectoderm layer to thicken and form a layer of cells called the neural plate. 

As it forms, the neural plate starts to fold, and it dips down to form a neural groove with edges called neural folds. 

As the groove continues to deepen, ventral to the ectoderm layer, the neural folds comes together and pinch off from the surface of the ectoderm layer, forming the neural tube. 

The neural tube now sits between the mesoderm and the ectoderm. 

On the dorsal side of the neural tube where the neural folds fuse, there are special cells called neural crest cells that migrate out and form a new layer of cells between the ectoderm and neural tube.

Neural crest cells are like little explorers: they migrate throughout the developing fetus to form a variety of tissues including the peripheral nervous system, melanocytes in the skin, specific parts of the facial bones, chromaffin cells of the adrenal glands, and parafollicular C cells in the thyroid.

In fact, neural crest cells are responsible for so many of the body’s organs and tissues th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ECG_intervals</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/056251j7SrKLfODh1rPAr3RZQRmc2DCY/_.jpg</video:thumbnail_loc><video:title><![CDATA[ECG intervals]]></video:title><video:description><![CDATA[An electrocardiogram is also known as an ECG; the Dutch and German version of the word, elektrokardiogram, is shortened to EKG. It is a tool used to visualize, or “gram,” the electricity, or “electro,” that flows through the heart, or “cardio.” Specifically, an ECG tracing shows how the depolarization wave, which is a wave of positive charge, moves during each heartbeat by providing the perspectives of different sets of electrodes. This particular set of electrodes is called lead II; one electrode is placed on the right arm and the other on the left leg. Essentially, when the wave’s moving toward the left leg electrode, you get a positive deflection. This big, positive deflection corresponds to the wave moving down the septum. When reading an ECG, there are a few key elements to keep in mind; one of them is looking at the intervals.

In a typical waveform, there’s a p-wave, QRS complex, and t-wave. In addition, there are certain intervals, including the PR interval, the QRS complex itself, and the QT interval. 

The PR interval spans from the beginning of the p-wave to the beginning of the QRS complex, and it represents the time from the beginning of atrial depolarization to the beginning of ventricular depolarization. It’s normally 0.12-0.20 seconds, which is three to five little boxes, since each little box is 0.04 seconds. Therefore, the PR interval shown is about four boxes or 0.16 seconds. 

Any deviation in the normal depolarization pathway from the SA node to the ventricles can change the PR interval. For example, consider if the atria are depolarized by an ectopic atrial focus, such as an irritable atrial cell outside of the SA node. If it was farther away from the AV node, it’d result in a longer PR interval, because the signal has to travel a greater distance. Alternatively, if it was really close to the AV node, the PR interval might be super short. Another example is first degree heart block, which is when the electrical signal travels more slo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ECG_cardiac_hypertrophy_and_enlargement</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A5sQg2b_QI_Ar1LvDcFCevWVSNSiQSCC/_.jpg</video:thumbnail_loc><video:title><![CDATA[ECG cardiac hypertrophy and enlargement]]></video:title><video:description><![CDATA[An electrocardiogram - an ECG - or the dutch and german version of the word - elektrokardiogram or EKG, is a tool used to visualize “gram” the electricity “electro” that flows through the heart “cardio”. 

An ECG tracing specifically shows how the depolarization wave moves during each heartbeat - which is a wave of positive charge - looks from the perspective of different sets of electrodes. 

This particular set of electrodes is called lead II, with one electrode on the right arm and the other on the left leg, so essentially when the wave’s moving toward the left leg electrode, you get a positive deflection, like this big positive deflection correspond to the wave moving down the septum. 

There are lots of things to look for when reading an ECG, one of them includes figuring out if part of the heart has undergone hypertrophy or enlargement.

Hypertrophy means that a heart’s muscular wall has increased in thickness while dilation refers to an increase in the volume of the chamber. 

The term enlargement is generally used when both hypertrophy and dilation occur together, and this is what typically happens in the atria. 

In contrast, the ventricles often undergo hypertrophy without dilation. An ECG can show evidence of hypertrophy and enlargement in all of the heart’s four chambers - so let’s go through them one by one. 

Normally, atrial depolarization produces a pretty normal looking - symmetric P wave. In right atrial enlargement, all of that extra right atrial muscle tissue results in a large P wave in leads V1 and V2, often over 1.5 mm, as well as in the inferior leads - leads II, III, and aVF, often over 2.5 mm. 

One reason why right atrial enlargement develops is that there can be a stenotic or narrowed tricuspid valve that makes it more difficult for the atria to eject blood into the ventricles, and in response, the right atrium enlarges. 

In left atrial enlargement, the left atrium has extra muscle tissue and that results in a P wave with two p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cocaine_dependence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xEr_O1ZMR0KEWzXKdjAO7DVuQhafrYtE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cocaine dependence]]></video:title><video:description><![CDATA[Cocaine, sometimes called coke, is a powerful psychoactive stimulant that alters how the brain functions—specifically, how we perceive our surroundings. 

Cocaine comes from the leaves of the South American coca plant, and has been used for over a thousand years. 

In modern times, it’s become a popular “party drug” because cocaine reduces inhibitions and creates a feeling of euphoria or pleasure; this feeling lasts between fifteen and ninety minutes, depending on how the drug’s it’s administered. 

Around 18 million people worldwide use cocaine, and because of its strong potential for addiction and overdose, the drug is heavily regulated in many countries. 

To understand how cocaine works, let’s zoom into one of the synapses of the brain. 

Normally, electrical signals, or action potentials, travel down the axon to the axon terminal, where they trigger the release of chemical messengers called neurotransmitters from synaptic vesicles into the synapse.

The neurotransmitters travel across the synapse and bind to receptors on the postsynaptic neuron, where they give the cell a message. 

After the neurotransmitters have done their job, they unbind from the receptors, and can just diffuse away, get degraded by enzymes, or get picked up by proteins and returned to their release site in a process called reuptake.

Cocaine increases the release of certain neurotransmitters, but it’s biggest effect is blocking reuptake receptors on presynaptic axon terminals. 

Both of these actions keep neurotransmitters like dopamine, norepinephrine, and serotonin in the synapse longer, increasing their effects. 

For example, increased concentrations of dopamine in the brain’s reward pathway (which includes the nucleus accumbens, ventral tegmentum, and prefrontal cortex) produce intense feelings of euphoria, pleasure, and the emotional “high” associated with cocaine. 

This physical “high” or feeling of hyper-stimulation is caused by increased norepinephrine concentrations t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypernatremia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MDG8YADmQeajjlLzBmWMv14jR66br81a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypernatremia]]></video:title><video:description><![CDATA[With hypernatremia, hyper- means high, and -natrium is latin for sodium, often shortened to Na+, and -emia  refers to the blood, so hypernatremia means a higher than normal concentration of sodium in the blood, generally above 145 mEq/L.

The concentration of sodium depends on both sodium and water levels in the body. 

About 60% of our body weight comes from just water, and it basically sits in two places or fluid compartments—it either outside the cells in the extracellular fluid or inside the cells in the intracellular fluid.

The extracellular fluid includes the fluid in blood vessels, lymphatic vessels, and the interstitial space, which is the space between cells that is filled with proteins and carbohydrates. 

One third of the water in the body is in the extracellular compartment, wheres two thirds of it is in the intracellular compartment. 

Normally, the two compartments have the same osmolarity -- total solute concentration -- and that allows water to move freely between the two spaces.But the exact composition of solutes differs quite a bit. 

The most common cation in the extracellular compartment is sodium, whereas in the intracellular compartment it’s potassium and magnesium. 

The most common anion in the extracellular compartment is chloride, whereas in the intracellular compartment it’s phosphate and negatively charged proteins.

Of all of these, sodium is the ion the flits back and forth across cell membranes, and subtle changes in sodium concentration tilts the osmolarity balance in one direction or another and that moves water. This is why we say “wherever salt goes, water flows”. 

So with hypernatremia, someone can have a high concentration of sodium in the extracellular fluid and therefore the blood, by either losing more water than sodium, or gaining more sodium than water. Either way this increases the sodium concentration in the extracellular fluid, draws water out of the cells. 

When hypernatremia develops over a long period of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ECG_QRS_transition</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jE0hI_FjSDiA7eZpazbMu8I6RrG9Ujjw/_.jpg</video:thumbnail_loc><video:title><![CDATA[ECG QRS transition]]></video:title><video:description><![CDATA[An electrocardiogram is also known as an ECG; the Dutch and German version of the word, elektrokardiogram, is shortened to EKG. It is a tool used to visualize, or “gram,” the electricity, or “electro,” that flows through the heart, or “cardio.” Specifically, an ECG tracing shows how the depolarization wave, which is a wave of positive charge, moves during each heartbeat by providing the perspectives of different sets of electrodes. This particular set of electrodes is called lead II; one electrode is placed on the right arm and the other on the left leg. Essentially, when the wave’s moving toward the left leg electrode, you get a positive deflection. This big, positive deflection corresponds to the wave moving down the septum. To read an ECG, there are a few key elements to keep in mind; one is to figure out the QRS transition.

The chest leads will have a mostly positive deflection, if a depolarization wave is moving towards them. The QRS transition zone refers to where the QRS complex switches from being mostly negative to mostly positive, from the point of view of the chest leads, V1 through V6, which “view” the heart through the horizontal plane. The QRS transition usually happens in lead V3 or V4, depending on factors such as chest lead placement and the exact anatomy of a person’s heart. So, the QRS transition tells us when the overall QRS vector is aligned in the direction of the chest leads; it’s a way of understanding what’s happening to the QRS axis in the horizontal plane. 

If something alters the heart’s overall QRS vector, then the QRS transition zone can shift to the right, towards V1 and V2, or to the left, towards V5 and V6. For example, a myocardial infarction leads to the formation of scar tissue that can’t depolarize. Generally speaking, the QRS transition zone will shift away from a region of scar tissue, because it no longer contributes to the overall QRS vector. Consider the following: a blockage in the left circumflex artery can cau]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_placenta</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MmQ10bb7TwuqvAQFAD8Baj0JTNyghTRT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the placenta]]></video:title><video:description><![CDATA[The placenta is an organ that’s co-created by the fetus and the mother during development. 

Deoxygenated fetal blood gets to the placenta through two umbilical arteries, and the blood picks up oxygen and glucose while dropping off carbon dioxide.

Oxygenated fetal blood then heads back towards the heart through a large umbilical vein. 

That umbilical vein and the two umbilical arteries collectively form the vessels of the umbilical cord. 

Development of these structures goes back to the first week of development, when the fetus is just a little ball of cells called a blastocyst. 

Going forward, we’ll refer to this blastocyst as the fetus just to avoid changing names.

By day 7 or 8, the fetus implants on the surface of the endometrial wall or decidua; the point of contact is called the decidua basalis. 

To snuggle deeper into the decidua basalis, trophoblast cells from the outer layer of the fetus assemble into two layers of cells called the cytotrophoblast and the syncytiotrophoblast. 

The cytotrophoblast is an inner layer of mononucleated cells, and the syncytiotrophoblast is an outer layer of multinucleated cells with no distinct cell boundaries. 

Syncytiotrophoblast cells don’t undergo cell division which means that their population of cells would be doomed to simply die out over time without the help of the cytotrophoblast. 

To replenish the number of syncytiotrophoblast cells, there’s a steady flow of cytotrophoblast cells that fuse with the syncytiotrophoblast cells, literally merging with them and forming an expanding syncytium. 

It’s a bit like maintaining the population in a retirement community where individuals aren’t raising youngsters and occasionally pass away, by attracting a steady inflow of new retirees. 

The multinucleated syncytiotrophoblast grows larger and moves like an octopus deeper into the decidua basalis. 

Around day 14 of development, cells of the syncytiotrophoblast start to form little protrusions called primary vil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ECG_normal_sinus_rhythm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RHYN3WYOQ0WAqbayj06p-68ASWilhsqM/_.jpg</video:thumbnail_loc><video:title><![CDATA[ECG normal sinus rhythm]]></video:title><video:description><![CDATA[An electrocardiogram, or ECG, or elektrokardiogramm or EKG in German, is a tool that allows us to visualize the heart&amp;#39;s electrical activity. A 12-lead ECG uses multiple electrodes placed around the body, which are combined in specific ways to create electrical views of the heart, called leads. There are six chest leads, six limb leads, and each one captures the heart’s activity from a different angle. With each heartbeat, the ECG records the electrical signals, including depolarization, which is the activation of the heart muscle, and repolarization, which is the recovery phase. Now, to read an ECG, there are a few key elements to keep in mind, and one of the most important ones is determining whether the tracing shows normal sinus rhythm. 

But before we proceed with what a normal sinus rhythm is, let’s look at a single heartbeat from the viewpoint of lead II. First, here’s a quick note about the ECG paper. The horizontal axis represents time, where each small box counts 0.04 seconds, while each bigger box counts 0.2 seconds. The vertical axis represents voltage. Each small box measures 1 millimeter, which equals 0.1 millivolts. At 0 millivolts, we have the baseline voltage, which is also known as the isoelectric line. And any movement away from this line reflects electrical activity.    

Normally, the heart&amp;#39;s natural pacemaker, called the sinoatrial, or SA node, initiates each heartbeat. The SA node spontaneously depolarizes, sending an electrical signal across both atria. First, the right atrium depolarizes, then the left atrium follows. On the ECG, this atrial depolarization shows up as a positive deflection known as the P wave. Normally, the P wave is less than 0.12 seconds wide and less than 2.5 millimeters tall.   

Once the atria depolarize, the signal reaches the atrioventricular or AV node, which is located between the atria and ventricles. The AV node briefly slows the signal down, giving the atria just enough time to fully co]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Action_potentials_in_pacemaker_cells</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1l3dmCbFQuen7kWMLQVh0_lARii_Ks5b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Action potentials in pacemaker cells]]></video:title><video:description><![CDATA[Action potentials are the really rapid electrical changes that occur across the membrane of certain cells, and often propagates from one cell to an adjacent cell. Cells in the heart communicate this way. That signal’s gotta start somewhere, so some of these cells, called pacemaker cells, have the responsibility of  setting the rhythm and the pace of the heartbeat. They’ve got this really important job, but they’re a relatively tiny group -- only about 1% of the heart cells -- and they’re able to continually generate new action potentials that get conducted to the rest of the heart -- the other 99% -- and that’s what tells the heart pump. Now, pacemaker cells also listen to which usually come from neighboring pacemaker cells. But if those don’t come, then a pacemaker cell will simply launch its own and that action potential will then spread around. This is called automaticity, and that’s easy to remember because it’s got “automatic” right in it. 

So let’s start by mapping out those pacemaker cells. The first clump of pacemaker cells is tucked up here into the corner of the right atria, and that’s the sinoatrial node, which sometimes gets called the SA node. We’ve also got pacemaker cells in internodal tracts between nodes, in the atrioventricular, or AV node, the Bundle of His, and the Purkinje fibers, and that’s our electrical conduction system.

And all around these pacemaker cells are heart muscle cells or cardiomyocytes and they pick up the action potential too, but that happens just a tiny bit more slowly -- we can think of these bands of pacemaker cells as highways that carry the action potential to its destination super fast, and then the muscle cells are like little side roads where it’s slower. That’s important because we want all of the myocytes to pick up that action potential and contract at the same time. We call this whole system a functional syncytium, which means that the mechanical, chemical, and electrical connections between these cells ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myocarditis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iHk6nQn8Sky5kwMhxFsS603mTLWeLGm-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myocarditis]]></video:title><video:description><![CDATA[With myocarditis, myo- means muscle, card- means heart, and -itis means inflammation. So, myocarditis is inflammation of the myocardium, which is the muscular middle layer of the heart wall, which contracts and relaxes so the heart can pump blood all around the body.

Inflammation in the myocardium layer causes swelling, which damages the heart muscle cells’ ability to contract. That means that less blood gets pumped out of the heart with each heartbeat. If myocarditis is severe enough, it can lead to heart failure, which is when the heart can’t keep up with the demands of the body. Once the inflammation resolves, the heart contraction typically returns to normal, but occasionally, when the inflammation is really severe, it can cause fibrosis, or scar tissue, in the myocardium. Scar tissue doesn’t contract normally, so if that happens, it can cause long term problems with heart contraction.

In North America, viral infections, specifically Coxsackievirus B infections, are the main cause of myocarditis. Viral infections can trigger lymphocytic myocarditis, which is when lymphocytes - the B and T cells of the immune system - and water make their way into the  interstitial space - the space in between heart muscle cells. There are plenty of other infectious causes as well, though. One of these is trypanosoma cruzi, a single-cell protozoan that causes Chagas disease throughout South America. In Chagas disease, under a microscope, it’s possible to see groups of amastigotes within the heart muscle cells, which are trypanosomes that are in the intracellular stage. As a result, the heart muscle cells necrose or die. There’s  also Trichinella, a roundworm that moves from the intestines into various parts of the body, causing a variety of problems, including myocarditis. Myocarditis can also be seen in Lyme disease which is caused by the bacteria Borrelia burgdorferi, which is spread by deer ticks. Finally, in immunocompromised individuals, there’s Toxoplasma gondii]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cirrhosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XVY1czA_T5iE8uFhtdvULhdmRE2b6pZq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cirrhosis]]></video:title><video:description><![CDATA[When cells are injured or damaged and die off, usually that dead tissue that was previously full of living cells becomes fibrotic, meaning it becomes thickened with heaps and heaps of protein and forms scar tissue.

So when your liver is constantly forced to process alcohol like in alcoholic liver disease, or subject to a viral attack for a long time like in HBV, or anything else that causes a long-term or chronic state of liver cell or hepatocyte destruction and inflammation, your liver can become seriously scarred and damaged to the point where it’s no longer reversible, at which point it becomes fibrotic and in the liver we call this process cirrhosis. 

Because it’s usually irreversible, cirrhosis is often referred to as “end-stage” or “late-stage” liver damage.

When liver cells are injured, they start to come together and form what are called regenerative nodules. You can think of these as colonies of living liver cells. These are one of the classic signs of cirrhosis and are why a cirrhotic liver is more bumpy as opposed to a smooth, healthy liver. 

Also with cirrhotic liver tissue, you’ll see that in between these clumps of cells or nodules, is fibrotic tissue and collagen. 

Here’s a classic histology image of cirrhotic tissue, this clump of cells in the middle is the regenerative nodule, and these blue stains surrounding it are the bands of protein from the process of fibrosis. 

If we zoom out a bit and look at it with the naked eye, we’ll again see these nodules, which have fibrotic protein bands in between. 

How do these bands of fibrotic tissue form though? Well fibrosis is a process mediated by special cells called stellate cells, that sit between the sinusoid and hepatocyte, known as the perisinusoidal space. 

Here’s a pretty basic layout of the basic functional unit of the liver, you’ve got the portal vein and hepatic artery that combine into a sinusoid, which then goes into the central vein, and these are all lined with hepatocytes.

A]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ECG_cardiac_infarction_and_ischemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9nnabGUNR3WVFVhJFYHlHHbJQB2h_zvo/_.jpg</video:thumbnail_loc><video:title><![CDATA[ECG cardiac infarction and ischemia]]></video:title><video:description><![CDATA[An electrocardiogram - an ECG - or the dutch and german version of the word - elektrokardiogram or EKG, is a tool used to visualize “gram” the electricity “electro” that flows through the heart “cardio”. 

An ECG tracing specifically shows how the depolarization wave moves during each heartbeat - which is a wave of positive charge - looks from the perspective of different sets of electrodes. 

This particular set of electrodes is called lead II, with one electrode on the right arm and the other on the left leg, so essentially when the wave’s moving toward the left leg electrode, you get a positive deflection, like this big positive deflection correspond to the wave moving down the septum. 

To read an ECG there are a few key elements to keep in mind, one of them includes figuring out if part of the heart has is suffering from ischemia or has undergone an infarction.

The term ischemia means that blood flow to a tissue has decreased, which results in hypoxia, or insufficient oxygen in that tissue, whereas infarction goes one step further and means that blood flow has been completely cut off, resulting in necrosis, or cellular death. That typically happens if blood flow has been cut off for about 20 minutes. 

In the heart, ischemia and infarction can be transmural, affecting the entire thickness of the myocardium, or subendocardial, affecting just the innermost part of the myocardium - the part just beneath the endocardium. 

Out of all four chambers of the heart, the ECG is most sensitive to transmural or subendocardial ischemia or infarction in the left ventricle because that’s the chamber with the thickest walls and therefore has the most cardiac tissue. 

Alright, let’s start with subendocardial ischemia, which might happen when there’s incomplete blockage - let’s say 70% - in a coronary artery. 

In that situation, at rest there’s enough blood flowing through to meet the demand of the myocardium, but during exercise there’s not enough to meet the incre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroglossal_duct_cyst</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/a5NMyK0IRt2oauQMft7uLBeoSpmJZfW6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroglossal duct cyst]]></video:title><video:description><![CDATA[A thyroglossal duct cyst, sometimes just called a thyroglossal cyst, is a congenital disorder where the thyroglossal duct, which is a tiny canal connecting the thyroid gland with the tongue during fetal development, grows in size and fills up with mucus, which forms a cyst.

Now, normally during fetal development, a tiny depression, called the foramen cecum, forms at a spot between the front two-thirds and the back one-third of the tongue.

The tissue underlying the foramen cecum is different than the rest of the tongue, and it’s cells develop into the thyroid gland.

Through development, the thyroid gland tissue migrates downward as it grows, but it still stays connected by a tiny canal called the thyroglossal duct. 

The thyroid gland descends down past the base of the tongue and the hyoid bone, which is a small bone present below the chin, before finally settles down in front of the trachea, in the neck. 

The walls of the thyroglossal duct are lined by lymphoid cells, as well as epithelial cells which secrete mucus into the cavity.

Normally, once the thyroid gland has reached its final resting position, it stretches out a bit and the walls of the thyroglossal duct stick to each other, obliterating the canal. 

Over time the thyroglossal duct starts to disintegrate and by the third month of fetal development, the duct is usually gone. 

In some people, though, the thyroglossal duct doesn’t close completely, and instead parts of it widen to form pockets, or cysts.

The cysts get filled with mucus secreted by the epithelial cells in its walls.

These mucus filled thyroglossal duct cysts stick around as the fetus develops, and then they can cause a few problems. 

For example, when there’s an infection of the respiratory tract, it can easily spread to the thyroglossal duct cyst since there are lymphoid, aka immune cells in the walls of the cyst. 

Local inflammation also stimulates the epithelial cells of the thyroglossal duct cyst to increase their secre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Idiopathic_pulmonary_fibrosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ScM5tkKbQJWpvj9T7JzJS_wdR6m-YQGn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Idiopathic pulmonary fibrosis]]></video:title><video:description><![CDATA[Idiopathic pulmonary fibrosis can be broken down into idiopathic which means a disease without a known cause or mechanism, pulmonary which refers to the lungs, and fibrosis which refers to excess collagen in connective tissue, or interstitial tissue between cells, usually after tissue damage. 

So idiopathic pulmonary fibrosis is the ongoing repair process of having excess collagen or scar tissue in the interstitial tissue of the lung. 

What triggers the repair process is unknown, but it’s a chronic process that leads to a progressive loss of lung tissue. 

Normally, gas exchange happens between the alveoli which carry air and capillaries which carry blood. 

The alveoli are lined by type I and type II alveolar epithelial cells, also called type I and type II pneumocytes. 

Type I pneumocytes make up the majority of cells - they’re simple squamous cells that form a nearly continuous barrier between the air and underlying connective tissue. 

Type II pneumocytes are studded throughout the type I - they’re shaped like cubes, have microvilli to sweep away invading particles, and secrete surfactant, an oily mixture of proteins, phospholipids, and neutral lipids which prevent the alveoli from collapsing during exhalation. 

Type II pneumocytes also have the ability to divide to make more type II pneumocytes and can also divide and become type I pneumocytes as well. 

Now, between the type I and type II pneumocytes and the capillaries is interstitial tissue of the lung, which has macrophages and fibroblasts. 

When the alveolar lining is damaged, type I pneumocytes release transforming growth factor beta1, which gets the type II pneumocytes to stimulate fibroblasts to proliferate and develop into myofibroblasts, which are fibroblasts with some smooth muscle cell properties. 

The myofibroblasts secrete reticular fibers, a type of collagen which provides structural strength, as well as elastic fibers, which provide the rubber-band like elasticity of the lungs. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Premature_ovarian_failure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FG32IyVISkeGZfKpHNh5oRy2QLqLbVBP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Premature ovarian failure]]></video:title><video:description><![CDATA[In premature ovarian failure, which is also called primary ovarian insufficiency, the ovaries stop functioning normally, and this means that they stop ovulating, or releasing egg cells, and they also stop producing hormones, mainly estrogen and progesterone, and this all happens before a woman is 40 years old. It’s considered a “primary” problem because the problem is with the ovaries themselves, rather than glands or hormones that act on the ovaries.

Normally, the hypothalamus, which is located at the base of the brain, secretes gonadotropin-releasing hormone, or GnRH. GnRH makes the nearby pituitary gland secrete two hormones of its own, called gonadotropins. These are follicle stimulating hormone, or FSH, and luteinizing hormone, or LH. These hormones travel to the follicles within the ovaries. The follicles are small clusters of granulosa and theca cells that protect the developing egg cell.

FSH acts on the granulosa cells, making the follicles grow and mature, as well as secrete estrogen, while LH stimulates theca cells to secrete progesterone and small amounts of androstenedione, which is a precursor of testosterone. All three of these hormones belong to a class of steroids, or lipid-soluble hormones.

At birth, a woman has millions of follicles, each ready and excited to do its job. During puberty, the monthly menstrual and ovarian cycles begin, which is when the endometrium, or inner lining of the uterus, goes through cyclic changes in response to the ovarian hormones.

During the ovarian cycle, the ovarian hormones also help a handful of follicles to start growing. Eventually, there’s ovulation which is when a single follicle fully matures and ruptures, releasing its egg cell, while the other follicles degenerate and die off.

Over time, many ovarian follicles degenerate, and the ones that remain become less and less sensitive to gonadotropin stimulation. This goes on until menopause, when there are no remaining follicles responding to gonadotro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Benign_liver_tumors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FMXKd9RjRkemKnqFUkMjhrtmRV_zqOsh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Benign liver tumors]]></video:title><video:description><![CDATA[Benign tumors are masses of cells that can’t invade neighboring tissues or organs, and therefore are usually defined as non-cancerous. 

Benign liver tumors are actually pretty common, and typically don&amp;#39;t cause any serious complications, and there are three major types: cavernous hemangiomas, focal nodular hyperplasias, and hepatocellular adenomas. 

Cavernous hemangiomas are the most common form and are these masses or swelling of the endothelial cells in blood vessels of the liver that, when we check it out on histology, they form these huge vascular spaces that sort of look like a system of caves. 

In other words, instead of blood flowing through a tube, the blood goes into a giant cavern with endothelial cells randomly sprinkled throughout. 

Although these vascular spaces look huge on histology, most patients have relatively small lesions, usually less than about 1.5 cm, and therefore don’t have any symptoms; in more rare cases, with larger lesions, patients may develop symptoms and in very rare cases, experience rupture and intraperitoneal bleeding. 

Finding and diagnosing these hemangiomas can be done through several imaging techniques like ultrasound, CT scans, and MRI.

The second most common type of benign liver tumor is a focal nodular hyperplasia, or FNH. 

These are like these localized (focal) aggregates (nodular) of rapidly reproducing liver cells (hyperplasia). 

FNH is actually the most common non-blood vessel-related benign tumor in the liver and are seen slightly more in women than men, but can happen at any age. 

Basically this is a loosely used term to describe when nodules or aggregations of seemingly benign hepatocytes are found in the liver. 

Ultimately, we don’t really know why these form, but it’s thought that they could be a response to vascular injury of some kind that leads the hepatocytes to ramp up reproduction and form these aggregates of cells. 

Another reason it’s thought to be a result of vascular injury is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ECG_axis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UdXRKQimRfO5SUVXRClZuJvES5Ke_4rl/_.jpg</video:thumbnail_loc><video:title><![CDATA[ECG axis]]></video:title><video:description><![CDATA[An electrocardiogram - an ECG - or the Dutch and German version of the word - EKG, is a tool used to visualize the electricity that flows through the heart  And the way it looks depends on the set of electrodes you’re using. This particular set of electrodes is called lead II, for example, with one electrode on the right arm and the other on the left leg, so essentially when the wave’s moving toward the left leg electrode, you get a positive deflection, like this big positive deflection corresponding to the wave moving down into the left and right ventricles. To read an ECG there are a few key elements to keep in mind, one of them includes figuring out the axis. 

The axis of an ECG is the average direction of electrical movement through the heart during a depolarization. More specifically, axis usually refers to the mean QRS vector, which is the size and direction of the depolarization wave as it moves through the ventricles. Normally, the QRS axis aims downward and to the left in relation to the body.

So, if we simplify this heart a bit, normally, the sinoatrial (or SA) node sends an electrical signal that propagates out through the walls of the heart and contracts both upper chambers, then that signal moves to the atrioventricular or AV node, where the signal is delayed for a split second, and then goes down into the ventricles or lower chambers where it moves down the bundle of His into the left and right bundle branches and into each ventricle’s Purkinje fibers, causing the ventricles to contract as well. So, in a healthy heart, the upper chambers contract first, then shortly after, the lower chambers contract.

On an ECG, the atrial depolarization and contraction is seen as a p-wave, the ventricular depolarization and contraction is seen as a QRS complex, and the ventricular repolarization, and therefore its relaxation, is seen as a T-wave. A general principle to keep in mind is that a depolarization is caused by the movement of positive charge, so ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_storm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gyjkfT7VQue0x-5zONRwjgJzSy2sZp6-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid storm]]></video:title><video:description><![CDATA[Thyrotoxic crisis, more commonly called thyroid storm, is a severe, acute complication of hyperthyroidism. 

In hyperthyroidism, there’s an excess of thyroid hormone, and in thyroid storm the symptoms and physiologic effects of having excessive thyroid hormones are suddenly magnified.

Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary. 

The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH. 

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”. 

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. 

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4. 

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body. 

Once inside the cell T4 is mostly converted into T3, and it can exert its effect.

T3 speeds up the basal metabolic rate. 

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy. 

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response. 

Thyroid hormone is important - and the occasional increase is like getting a boost to fight off a hungry predator or to stay warm during a snowstorm! 

Now, hyperthyroidi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pituitary_adenoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CeTCMU0qQ2aUfh3oox4_3q-lRdSStQ-c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pituitary adenoma]]></video:title><video:description><![CDATA[Pituitary adenoma can be broken down - “adeno” refers to a gland and “oma” refers to a tumor, so pituitary adenoma is a tumor that develops in the hormone-producing cells of the pituitary gland.

Normally, the pituitary is a pea-sized gland, hanging by a stalk from the base of the brain. 

It sits just behind the eyes near the optic chiasm, which is where the optic nerves cross. 

The anterior pituitary, which is the front of the pituitary gland, contains a few different types of cells, each of which secretes a different hormone. 

The largest group of cells are the somatotropes which secrete growth hormone, or GH for short, which goes on to promote tissue and organ growth. 

The second largest cell group are the corticotrophs which secrete adrenocorticotropic hormone, or ACTH for short. 

ACTH stimulates the adrenal glands to secrete cortisol, a hormone that controls the stress response and metabolic regulation. 

A smaller cell group are the lactotrophs which secrete prolactin. 

Prolactin stimulates breast milk production, and also inhibits ovulation, which is when an egg cell is released from the ovary, and inhibits spermatogenesis, which is the development of sperm cells. 

There are also thyrotrophs which are cells that secrete thyroid stimulating hormone, or TSH which goes on to stimulate the thyroid gland. 

And finally, there are also gonadotrophs which secrete two gonadotropic hormones - luteinizing hormone, or LH, and follicle-stimulating hormone, or FSH, both of which go on to stimulate the ovaries or testes.

In pituitary adenomas, one of these cells mutates and becomes neoplastic, meaning that it starts dividing uncontrollably and over time it forms a tumor. 

But these cells don’t invade neighboring tissues, so this is considered a benign tumor rather than a malignant one. 

Pituitary adenomas can be classified by their size, adenomas smaller than 1cm are called microadenomas, and those larger than 1cm are called macroadenomas. 

Macroadenom]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physician_compensation_in_the_United_States</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bc1kzjMiReep3Q0pOLNbrFAoRM24tvmR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physician compensation in the United States]]></video:title><video:description><![CDATA[The way that physicians get paid in the United States has changed quite a bit over the years. 

For example, a long time ago, doctors got paid directly by patients - which was no different than how you might pay a mechanic today. 

It was a fee-for-service system, which meant that the more a doctor did for you, the more you paid. But unlike a car, folks can’t walk away from bad health, and that’s where the private insurance company stepped in.  

And for those without private insurance there were government funded insurance options - like Medicare, which covers the elderly, and the Children&amp;#39;s Health Insurance Program, or CHIP, which covers children. 

Doctors who took care of patients with Medicare or CHIP got paid a set amount according to a fee schedule. 

For example, taking out a child’s tonsils might have earned a doctor $200, but actually collecting that money meant navigating a few different systems and filling out forms. 

Doctors had to use the physician quality reporting system, known as PQRS, to document how they cared for a patient, and then they had to use the value-based modifier system to show that the quality of care was aligned with the cost of care. 

Finally, doctors had to make sure that they were appropriately documenting everything into the electronic health records, or EHRs, according to the meaningful use system.

Having three completely different systems made it hard for a doctor to get paid because each system had it’s own reporting system, and not only that, there was a combined 9% penalty among all three programs for “low-performing” doctors, which are those who didn’t meet program standards. 

It would be like working hard for two weeks, and then having to fill out three completely different forms about what you did and why you did it, so that three different groups could pay you a small part of your overall paycheck, and then getting paid less, for not completing the forms the right way. 

Needless to say, doctors wer]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mesoderm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Lx6lVYOsQ9WrNdO5snfzEi1WRXOaF3yP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mesoderm]]></video:title><video:description><![CDATA[When the embryo is one week old, it has two layers of cells: a dorsal or outer epiblast layer and a ventral or inner hypoblast layer. 

During week 3 of development the embryo undergoes gastrulation where the cells in the epiblast layer form a three layered trilaminar disc with an ectoderm, mesoderm and endoderm layer. 

So, imagine the embryo like a birthday cake with the ectoderm as the candles, the mesoderm as the frosting, and the delicious cake as the endoderm. We can put three candles on this cake to help you remember gastrulation happens during week 3.

Around day 17, a group of mesoderm cells form a solid rod of cells - kind of like the shaft of an arrow - and this structure is called the notochord.

The notochord is a transient embryonic structure, meaning that it doesn’t exist as a structure in the adult, in fact, the only remnant adults have of the notochord is that it contributes to the nucleus pulposus - which is the jelly-like center of the intervertebral discs. 

Nevertheless, the notochord is extremely important during early development for a couple of reasons. 

First, the notochord is a solid structure and it helps influence how the embryo folds early on. 

Second, the cells of the notochord secrete a protein called Sonic HedgeHog or Shh for short, which diffuses out through the trilaminar disc. 

The closer a cell is to the notochord, the higher the concentration of Shh, so it’s a way for all of the cells to know where they are in three-dimensional space. This helps the surrounding tissues differentiate and develop in the right way. 

On day 20, mesoderm cells around the notochord differentiate into three specialized types of mesoderm called the paraxial mesoderm, intermediate mesoderm, and lateral plate mesoderm, each of which goes on to make different tissues and organs.

The paraxial mesoderm is the closest to the notochord and it quickly starts to segment into paired blocks of tissue called somites, one with each somite in the pair s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_respiratory_distress_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bhWPjMdBR2idAwP0f0OERRLDTJORjbzc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute respiratory distress syndrome]]></video:title><video:description><![CDATA[Acute Respiratory Distress Syndrome, or ARDS, is exactly what it sounds like. 

‘Acute’ means that it happens rapidly. 

‘Respiratory distress’ means that a person becomes unable to breathe and oxygenate their blood, and  ‘syndrome’ means that it is a group of symptoms that may be caused by any number of underlying conditions. 

In ARDS, the alveoli and the capillaries that surround them - the site of  gas exchange in the lungs - are damaged by an inflammatory process like pneumonia or sepsis.

Air enters the lungs through a series of airways that branch and narrow until they end in clusters of alveoli, which look kinda like a bunch of grapes. 

The alveoli are covered in nets of capillaries that allow gas exchange into and out of the blood. 

Gas exchange happens efficiently between alveoli and capillaries because each of their walls is only one cell thick! 

Capillaries are lined with a single layer of endothelial cells and alveoli are lined with a single layer of epithelial cells. 

These cell layers are fused to one another by the basement membrane and surrounding the alveoli and blood vessels is connective tissue made up of mostly proteins and water - in a space called the interstitial space.

The alveolar epithelial cells—called pneumocytes—come in two types. 

The vast majority are type I pneumocytes, which are thin and have a large surface area, a shape that allows oxygen and carbon dioxide to pass through them easily. 

There are also type II pneumocytes scattered around which are smaller and thicker, and are important because they make surfactant, an oily secretion that coats the alveoli. 

The alveoli are so tiny that their walls end up being really close together. 

Surface tension from water molecules lining the alveolar walls can easily attract one another, and pull the walls together, making the alveoli collapse. 

Surfactant contains various phospholipids and is a bit like a droplet of oil that coats the inside of the alveoli, blocking the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_development_week_2</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OxK0X1xdTwqmKug71YLxshZBR-GdvhxC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human development week 2]]></video:title><video:description><![CDATA[During the second week of human development, the blastocyst attaches to the wall of the uterus.

The cells in the blastocyst’s outer layer are called trophoblast cells, and they penetrate into the uterus, establishing a connection between the blastocyst and the mother.

The cells in the blastocyst’s inner layer are called embryoblast cells, and they turn into a new, flat, two-layered structure which eventually gives rise to all of the organs and tissues of the body.

By day 7 or 8, the blastocyst implants on the surface of the endometrial wall, or decidua; the area where it implants is called the decidua basalis.

To snuggle deeper into the decidua basalis, trophoblast cells from the outer layer of the blastocyst assemble into two layers of cells.

One layer is called the cytotrophoblast, which consists of mononucleated cells, and the other is called the syncytiotrophoblast, which consists of a multinucleated cluster of cells.

Slowly, the syncytiotrophoblast expands into the decidua basalis.

By day 9, the syncytiotrophoblast has pushed deeper into the decidua basalis, and by day 11, the blastocyst is almost completely buried within it—like a seed getting pushed into soil.

Around day 12, the decidua undergoes the decidual reaction.

High levels of progesterone cause the decidual cells to enlarge, and they become coated in a sugar-rich, fatty fluid the syncytiotrophoblast can absorb to sustain its growth; this fluid also helps sustain the embryo early on.

Initially, the decidual reaction only occurs at the decidua basalis, the site of implantation, but eventually it spreads throughout the entirety of the decidua.

Around day 14 of development, syncytiotrophoblast cells start to form little protrusions called primary villi—each one looks a bit like a tree.

These primary villi trees form all the way around the fetus, and cells start to clear out from between the primary villi, leaving behind empty spaces called lacunae.

While this is all happening, arter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ECG_basics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Age5LcS9QwS-v1EXOJZqD6YpTsWFRVCP/_.jpg</video:thumbnail_loc><video:title><![CDATA[ECG basics]]></video:title><video:description><![CDATA[An electrocardiogram is also known as an ECG; the Dutch and German version of the word, elektrokardiogram, is shortened to EKG. It is a tool used to visualize, or “gram,” the electricity, or “electro,” that flows through the heart, or “cardio.” Specifically, a 12-lead ECG tracing shows how the depolarization wave, which is a wave of positive charge, moves during each heartbeat, by providing the perspectives of different sets of electrodes. This particular set of electrodes is called lead II; one electrode is placed on the right arm and the other on the left leg. Essentially, when the wave’s moving toward the left leg electrode, you get a positive deflection. This big, positive deflection corresponds to the wave moving down the septum. 

To understand the basics, let’s start with an example of how we can look at the heart with only one pair of electrodes: a positive and a negative one. These electrodes detect the charge on the outside of the cell. Remember, at rest, cells are negatively charged relative to the slightly positive outside environment; let’s make these cells red. When they depolarize, the cells become positively charged, and leave a slightly negative charge in the outside environment; let’s make these cells green. Now, if we freeze this “wave of depolarization” as it’s moving through the cells, half of the cells are negative, or depolarized, and half are positive and resting; therefore, there’s a difference of charge across this set of cells. You can think of the charge difference as being a dipole, because there are two electrical poles. We can draw this dipole out as an arrow, or vector, pointing towards the positive charge. Remember, the electrodes detect charge on the outside of the cell, so this points toward where the positive charge is, outside. 

Now, if there’s a dipole vector pointing toward the positive electrode, then the ECG tracing shows it as a positive deflection; the bigger the dipole is, the bigger the deflection is. If we unp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ischemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7FccpJdZQRWmH4IYPTx3BORWR5qD8rQG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ischemia]]></video:title><video:description><![CDATA[Hypoxia, or lack of oxygen in cells and tissue, can happen in a number of ways, and ischemia’s one of them. 

Ischo- means “restraint” or “suppression”, and -emia refers to the blood, so ischemia must mean some kind of suppression or reduction of blood flow to an organ or tissue. 

And blood carries oxygen right? So when there’s a reduction in blood flow to cells, that also means there’s a reduction of oxygen to those cells, and this is due to lowered blood flow in the blood vessels.

This lowered flow could be from something blocking the blood from the inside, or it could be something compressing the blood vessel from the outside. 

An example of something blocking the blood vessel from the inside is a thrombus, also known as a blood clot, these are solid clumps of platelets and fibrin that obstruct blood flow. 

Ischemia resulting from something outside the blood vessel is traumatic injury, which can cause inflammation and swelling that physically applies external pressure to the blood vessel, compresses it, and restricts blood flow. 

Alright, so let’s say this is your artery, and it’s like the one-way highway leading all these red-blood-cells into the city, which is like a major organ in the middle here, so maybe this is organ-apolis. 

These red blood cells are super pumped for their day where they can drive around the capillaries, like the smaller city streets, and supply the city with fresh oxygen and pick up waste. 

And this organ-apolis is made up of thousands of cells, like homes, that use up the oxygen and create waste that needs to be picked up, the deoxygenated blood cells drain out through different small streets which are the veins and go back towards the heart. 

So one way this organ-city could become ischemic, is if there’s some obstruction to arterial flow into the tissue. Now only a few red-blood-cells can get in at a time. 

You might imagine that organ-apolis sees a lot less blood and a lot less oxygen, and becomes ischemic!

A super]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypoprolactinemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qo64Cq4gRICsUxDMGnbv-hXxQkWTNBvv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypoprolactinemia]]></video:title><video:description><![CDATA[With  hypoprolactinemia, hypo- means below, -prolactin refers to the hormone produced by the pituitary gland, and -emia refers to the blood, so hypoprolactinemia means lower than normal prolactin levels in the blood.

Normally, at the base of the brain, there’s a small pea-sized gland called the pituitary gland. 

The anterior pituitary - which is the front of the pituitary gland - has a number of different cells, each of which secrete a different hormone. 

One group, the lactotroph cells, secrete prolactin. 

In men, prolactin decreases testosterone production. 

In women, during pregnancy, elevated levels of estrogen stimulate the lactotroph cells to produce large amounts of prolactin which stimulates alveolar cells in the breasts. 

In response to prolactin, the alveolar cells divide and enlarge - and once a baby is born, lactogenesis starts - which means that milk is produced. 

Apart from milk production, high levels of prolactin also inhibit the release of gonadotropin releasing hormone from the hypothalamus, which results in decreased luteinizing and follicle stimulating hormone levels, which in turn, decreases estrogen levels. 

In women, this can stop ovulation and menstruation, which is why women typically don’t have a menstrual period while breastfeeding. 

In women that are not pregnant or breastfeeding, as well as in men, prolactin levels are usually kept in check by the hypothalamus in two ways. 

The first way is the most important, and it’s when the hypothalamus secretes a constant stream of dopamine which in this setting is called prolactin inhibiting factor. 

Dopamine binds to specific receptors on the lactotroph cells and inhibit the release of prolactin. 

The second way is less significant, and it’s when the hypothalamus secretes thyrotropin releasing hormone, also called prolactin releasing hormone, which can stimulate prolactin release. 

If the level of prolactin rises for any reason, then it signals the hypothalamus to release mo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ventilation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TWQLTHDHRJ_BLvP7htFzhVxeSt_kfawe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ventilation]]></video:title><video:description><![CDATA[The main job of the lungs is gas exchange, pulling oxygen into the body and getting rid of carbon dioxide. 

Normally, during an inhale - the diaphragm and chest muscles contract to pull open the chest and suck in air like a vacuum cleaner, and then during an exhale - the muscles relax, allowing the lungs to spring back to their normal size pushing that air out. 

Ventilation rates measure the volumes of air moving in and out of the lungs, over a period of time.

During normal quiet breathing, each breath of air that enters and leaves the lungs is about half a liter, which is called the tidal volume. 

The respiratory rate is the number breath a person takes per minute. In an adult this is normally around 15 breath per minute at rest.

So the minute ventilation is the amount of air moved in and out of the lungs in a minute. So minute ventilation is given by

		Minute Ventilation = (Tidal Volume) X (Respiratory Rate)

In a normal healthy adult, this means 500 ml per breath times 15 breaths per minute, or about 7.5 litres per minute. 

However, not all the air that we breathe in reaches the alveoli, where gas exchange actually takes place.

Some air is trapped in the airways - an area called the anatomical dead space. 

Also, some of the alveoli may be defective and can’t even participate in gas exchange. 

When you add the volume of air lost in these malfunctioning alveoli to the anatomical dead space, you get the physiological dead space. 

So to calculate alveolar ventilation, it’s the tidal volume minus the physiologic dead space and that volume gets multiplied by the respiratory rate:

  Alveolar ventilation = [(Tidal volume) - (Physiological dead space)] X (Respiratory Rate)

In a normal healthy person, almost all the alveoli are functioning properly, and the physiological dead space is about equal to the anatomic dead space which is about 150 ml. 

So the alveolar ventilation comes to about (500 - 150) ml  or 350 ml per breath, times 15 breaths per mi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharyngeal_arches,_pouches,_and_clefts</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GGH9rYb4RraYNDsIpk7y-1wfTemTMJQM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharyngeal arches, pouches, and clefts]]></video:title><video:description><![CDATA[Early in development, the embryo is a flat, disc-shaped organism made up of three layers of pluripotent cells called germ layers: an inner layer, called endoderm, a central layer, called mesoderm, and an outer layer, called ectoderm. 

These three specialized cell layers give rise to all the organs and tissues in the body.

By week 4 of development, the embryo takes on a more recognizably human form—but to be honest, it still looks more like a shrimp than a baby. 

At the cranial (head) end of this little shrimp-like creature, a set of structures called the pharyngeal apparatus begins to develop, consisting of pharyngeal arches, clefts, and pouches.

The pharyngeal apparatus starts forming around weeks 4 and 5, when six little bars of mesoderm, the pharyngeal arches, sprout from the primitive pharynx. 

The pharyngeal arches develop in a craniocaudal fashion—meaning they form at the head and continue developing towards the tail end of the fetus. 

These paired, symmetrical bumps are numbered from 1 to 6—it’s important to note that the fifth arch either never forms, or it quickly regresses, so it doesn’t develop into any structures. 

Between the five pharyngeal arches, four pharyngeal clefts form and cover the external part of the corresponding arch with ectoderm cells, while four pharyngeal pouches line the internal part of their corresponding arches with endoderm.

The components of the pharyngeal apparatus develop into various head and neck structures, and sometimes multiple arches join together to give rise to a single structure. 

Each pharyngeal arch, with its associated pouch and cleft, carries its own cranial nerve that innervates the structures that develop from that arch.

The first pharyngeal arch is mainly associated with everything we need to chew. 

Structures from this arch are innervated by the trigeminal nerve–more specifically, its mandibular branch. 

In terms of bones, it gives rise to the maxilla (which forms the upper jaw) and the man]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchiectasis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4UM_nRP9REu4MTIjPGO76yCQTXa_IqCM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchiectasis]]></video:title><video:description><![CDATA[With bronchiectasis, “bronchi” refers to bronchi and bronchioles, which are small airways in the lungs, while “-ectasis” means dilation. So, in bronchiectasis, chronic inflammation in the lungs damages the smooth muscle cells and elastic tissue that support these small airways, resulting in their permanent dilation. 

When you take a breath, your diaphragm moves down, creating negative pressure within your chest. This gentle vacuum in the chest pulls air in through your nose or mouth down the trachea. From here, the air travels through the primary bronchi, into the secondary bronchi, then tertiary bronchi, and finally into the bronchioles, which lead directly to the alveoli, where the gas exchange occurs.  

Now, the walls of our airways consist of smooth muscle cells and elastic tissue that help the airways open and return to their shape as we breathe. These walls are lined with epithelial cells, which have tiny brush-like projections called cilia, and goblet cells, which produce sticky mucus. The mucus traps dust, bacteria, and other unwanted particles, and the cilia move together in coordinated waves, pushing the mucus and trapped particles toward the throat so we can clear them out of the lungs. This system is called the mucociliary escalator. This way, we can either swallow or cough out foreign particles that end up in our airways. 

Now, bronchiectasis can develop due to chronic respiratory infections or lung obstructions. These are closely related and tend to trigger each other, setting off a cycle that slowly damages the airways over time. 

First, let’s look at how chronic, recurrent respiratory infections can lead to bronchiectasis. When a pathogen reaches the small airways in the lungs, epithelial cells respond by releasing pro-inflammatory cytokines, which signal neutrophils to join the action. As neutrophils fight the pathogen, they use powerful weapons, like elastase and reactive oxygen species. These substances are great at killing pathogens]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_development_week_3</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8SW2eqy9QpG5a32LVwwOO_vcTmW3ki2T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human development week 3]]></video:title><video:description><![CDATA[During week 3 of human development, the blastocyst is fully embedded in the endometrial tissues, or decidua, and it undergoes a process called gastrulation, which starts around day 14.

During gastrulation, the cells of the blastocyst become reorganized significantly, and by the time the process is finished, it’s no longer a blastocyst at all—it’s a gastrula!

Gastrulation begins with the formation of the primitive groove (sometimes called the primitive streak), a narrow depression that runs down the center of the epiblast layer. 

When viewed from above, the groove starts near the tail or caudal end of the embryo, and grows towards the head, or cranial end. 

This groove defines the cranial-caudal axis, and the two sides of the groove represent the first instance of bilateral symmetry in the embryo—a left and right side to the body. 

Closer to the midline (where the groove is located) is considered medial, and closer to the edges is lateral. 

If you view the groove from the side, then you can see that the groove forms on the dorsal, or back, side of the embryo, which makes the dorsal-ventral axis more obvious. 

The round bilaminar disc also elongates, and starts to resemble a guitar pick, narrow at the caudal end and wide at the cranial end.

At the cranial end of the primitive groove, a small mound of tissue develops called the primitive node, and a tiny dimple forms within it, called the primitive pit. 

The primitive groove, primitive node, and primitive pit together form the primitive streak. Try saying that 3 times quickly...

Okay, so as the primitive streak forms in the epiblast layer, some epiblast cells start to migrate towards the primitive groove, move down into the bottom of the groove, and then actually dive right into it. It’s a bit like a child diving into a ball pit at a funhouse.

The epiblast cells that slip through the primitive groove begin to differentiate to form new cell layers. 

Some epiblast cells dive deep and form the embryo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_leukemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WDFJ0I1HRGyb7TgKM7g_TKECTzKdRug7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic leukemia]]></video:title><video:description><![CDATA[With chronic leukemia, “leuk” refers to white blood cells, and “emia” refers to the blood; so in chronic leukemia there are lots of partially developed white blood cells in the blood over a long period of time. 

These partially developed white blood cells interfere with the development and function of healthy white blood cells, platelets, and red blood cells.

Now, every blood cell starts its life in the bone marrow as a hematopoietic stem cell. 

Hematopoietic stem cells are multipotent -- meaning that they can give rise to both myeloid or lymphoid blood cells.

If a hematopoietic stem cell develops into a myeloid cell, it’ll mature into an erythrocyte -- or a red blood cell, a thrombocyte -- or a platelet, or a leukocyte -- or a white blood cell, like a monocyte or granulocyte. 

Granulocytes are cells with tiny granules inside of them -- they include neutrophils, basophils, and eosinophils. 

If a hematopoietic stem cell develops into a lymphoid cell, on the other hand, it’ll mature into some other kind of leukocyte: a T cell, a B cell, or a natural killer cell, which are referred to as lymphocytes. 

Once the various blood cells form, they leave the bone marrow, and travel around the blood, or settle down in tissues and organs like the lymph nodes and spleen. 

Chromosomal abnormality in hematopoietic stem cells that are destined to become leukocytes is the most common cause of chronic leukemia. 

Some examples of abnormalities include a chromosomal deletion, where part of a chromosome is missing, a trisomy, where there’s one extra chromosome, and a translocation, where two chromosomes break and swap parts with one another. 

Now there are two types of chronic leukemia. 

The first is chronic myeloid leukemia, CML, which is caused by a particular chromosomal translocation that affects granulocytes. 

The second is chronic lymphocytic leukemia, CLL, which is caused by a variety of chromosomal mutations that affect lymphocytes, in particular B cells. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hedgehog_signaling_pathway</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xnGLnqy7SoeBoxuvDpvJxAedQa6vDLKr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hedgehog signaling pathway]]></video:title><video:description><![CDATA[The hedgehog signalling pathway is a pathway based on three specific proteins called the hedgehog proteins. 

The most well-studied of these proteins is the Sonic hedgehog protein, or SHH, which plays a key role in structuring the general shape of the body, called patterning. 

During the third week of development, a solid rod of mesoderm called the notochord forms at the midline of the embryo. 

The notochord is extremely important during early development because it helps influence how the embryo folds. 

It also guides how the various tissues differentiate and develop so that the embryo ends up with two arms, two legs, and one head, instead of some other combination.

Groups of proteins in the notochord secrete proteins that guide this process. 

These include Desert hedgehog protein (DHH), Indian hedgehog protein (IHH), and Sonic Hedgehog protein (SHH). 

Desert and Indian Hedgehog protein were named first, and Sonic was named a bit later—if you played video games in the ‘90s, you’ll know that it’s named after the fast-moving rodent, Sonic the Hedgehog!

The Hedgehog proteins are ligands, meaning they’re molecules that move from one cell over to another and facilitate communication—like letters that one cell might send to another cell around the corner. 

Early in development, the notochord sends all three Hedgehog proteins out to undifferentiated cells throughout the entire embryo. 

When Sonic Hedgehog protein gets released, it slowly diffuses through the interstitial liquid and binds to a receptor called patched (ptc), which can be found on the cell membranes of embryonic cells. 

The patched receptor inhibits the embryonic cell from differentiating, but Sonic Hedgehog protein inhibits patched, meaning it inhibits the inhibitor! 

Without the inhibition usually imposed by patched, the embryonic cell starts to activate specific genes that allow it to differentiate. 

But every embryonic cell doesn’t differentiate in the same way—some might activate g]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endoderm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_prrH6rXQOawJsqhhfPxM_IfSrCohIQV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endoderm]]></video:title><video:description><![CDATA[The endoderm is the innermost germ layer, which makes it easy to remember the body parts it gives rise to: stuff inside our bodies, specifically, spaces and cavitations like the gut tube and body cavities that house our internal organs. 

Endoderm also forms things like the lining of the ear canals, the trachea and respiratory tract, and parts of the bladder and urethra. 

During week 4 of development, the embryo folds in two directions. 

In the longitudinal plane, the embryo folds slightly at the cranial and caudal ends, so it looks less like a pancake and more like a little shrimp. 

This is the very beginning of its curling into the fetal position. 

This folding shapes part of the yolk sac into a gut tube, with the remainder of the yolk sac remaining connected not at the cranial or caudal end, but just in the middle.

Now let’s switch to the transverse plane, looking at a spot near the middle of our embryo where you can see the yolk sac. 

In the transverse plane, the lateral plate mesoderm splits into a dorsal layer called the parietal (or somatic) mesoderm layer, and a ventral layer called the visceral (or splanchnic) mesoderm layer. 

The parietal layer of mesoderm follows the ectoderm and forms the chest wall and abdominal body wall of the embryo. 

The visceral layer of mesoderm follows the endoderm and forms the gut tube.

More specifically, the endoderm becomes the epithelial cell lining of the gastrointestinal tract while the visceral layer of mesoderm becomes the muscular wall. 

The mesoderm also gives rise to serous membranes that become the visceral and parietal pleura. 

Two layers of the visceral pleura come together to form the mesentery, a flap of tissue that suspends the gut tube in the abdominal cavity. 

Interestingly, the mesentery was only recently officially classified as a body organ! 

Meanwhile, the ectoderm and parietal layer of mesoderm fold around the dorsal side of the embryo, with the two sides meeting up and seamlessly c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_digestive_system_and_body_cavities</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z1Y_9ksITTqeAd5SywVQUrEtTdCoCFNl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the digestive system and body cavities]]></video:title><video:description><![CDATA[During the third week of development, the embryo is a flat, three-layered disc, and each layer contains germ cells that give rise to the organs and tissues of the body. 

The ventral, or bottom, germ layer is called the endoderm, and it forms the lining of the gut tube and the respiratory system. 

The middle germ layer is called the mesoderm, and it forms connective tissues like muscles and bones. 

And the dorsal, or top, germ layer is called the ectoderm, and it gives rise to the sensory organs like the skin, the eyes, and the central nervous system. 

The mesoderm differentiates into the paraxial mesoderm, intermediate mesoderm, and lateral plate mesoderm, and, at around day 19, a space forms in the lateral plate mesoderm.  

This space, called the intraembryonic coelom, or cavity, separates the lateral plate mesoderm into dorsal and ventral layers.  

The dorsal layer is the parietal mesoderm layer, and its cells adhere to cells from the overlying ectoderm and wrap around the amnion. 

The ventral layer is called the visceral mesoderm layer, and its cells adhere to cells from the underlying endoderm, which covers the yolk sac.  

The parietal mesoderm gives rise to the serous membranes that line the different cavities in the body, and the visceral mesoderm becomes the serous membrane that covers the lungs, heart, and abdominal organs. 

These membranes are really important because they prevent the organs from getting injured as they rub up against each other or against the body wall. 

During the fourth week of development, the embryo undergoes structural changes, transitioning from a trilaminar disc into a more cylindrical shape. 

The combined visceral mesoderm and endoderm layer, which lines the yolk sac, folds rostrally and caudally, creating a primitive gut tube out of the yolk sac and leaving the remainder of the yolk sac in the middle section of the gut. 

While that’s happening, the combined parietal mesoderm and ectoderm folds down with the a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_fetal_membranes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i6PyCUUcQNiZw4XpsLgxdwoTRPSHr79T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the fetal membranes]]></video:title><video:description><![CDATA[The fetal membranes, sometimes called extraembryonic membranes, are tissues that form in the uterus during the first few weeks of development and develop along with the growing embryo. 

These are the amnion, the yolk sac, the chorion, and the allantois, and each of these membranes starts out as a thin sheet of tissue that surrounds a fluid filled cavity.

The first membranes to form are the amnion and the yolk sac. 

At the beginning of week 2, the embryo is not quite an embryo yet—it’s just a blastocyst, and the blastocyst is partially embedded into the endometrium of the mother. 

The blastocyst has two parts: an outer cell mass called the trophoblast and an inner cell mass called the embryoblast. 

The trophoblast is divided into the cytotrophoblast, which forms the wall of the blastocyst, and the syncytiotrophoblast, which is outside the wall and invades into the uterus.

The embryoblast is a bilaminar disc with a dorsal epiblast layer and a ventral hypoblast layer. 

During day 8, a tiny space called the amniotic cavity forms between the epiblast and cytotrophoblast. 

The epiblast cells migrate to form a thin membrane called the amnion that surrounds the amniotic cavity, separating it from the cytotrophoblast.

During day 9, hypoblast cells begin to migrate to form a thin membrane lining the rest of the blastocoel, forming the walls of the yolk sac. 

The yolk sac fills with fluid, called vitelline fluid, which washes across the embryo, nourishing it during this early stage. 

So basically, by the middle of the second week, the two-layered embryonic disc is sandwiched between the amniotic cavity and the yolk sac.

By day 10, some epiblast cells differentiate into extraembryonic mesoderm, and they settle between the amniotic cavity and the cytotrophoblast, eventually creating a thick layer of extraembryonic mesoderm tissue between the two. 

Then, over time, a space starts to form within this thick layer of extraembryonic mesoderm. 

The cells migrat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fibromyalgia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/26eQZO7HTSuDqanNy7BNo9f2SGq3OJnT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fibromyalgia]]></video:title><video:description><![CDATA[The term fibromyalgia can be broken down. Fibro-  refers to fibrous tissue, -my- refers to muscle and -algia refers to pain. 

Fibromyalgia is a chronic condition, which occurs more often in women, that causes widespread muscle pain, extreme tenderness in various parts of the body, and sleep disturbances.

Normally, if a person cuts their finger, a specific type of sensory neuron called a nociceptor or pain receptor, converts that stimulus into an electrical signal. 

These are the first neurons and they’re primarily found in the skin, joints, or the walls of organs. 

The electrical signal goes from the dendrite of the nociceptor into its peripheral axon branch and heads up the hand and arm towards its cell body. 

The cell body is located in the dorsal root ganglion which is a cluster of nerve cell bodies located in a dorsal root of the spinal nerve. 

The dorsal root ganglia contains the cell bodies of many sensory neurons that receive information. 

So in this case, the cell body would receive the electrical signal, and if it’s strong enough, it would start to release substance P, which is a small chemical involved in pain perception. 

Substance P would go down the other axon branch of the nociceptor and would get released from the neuron’s terminal button. 

Substance P then binds to receptors on a second neuron which has its cell body located in the dorsal horn of the spinal cord, which makes up the back portion of the spinal cord that receives sensory information. 

There is also a separate group of neurons called inhibitory neurons in the spinal cord that dampen or reduce the pain response, counteracting the effect of nociceptors. 

These inhibitory neurons release neurotransmitters such as serotonin and norepinephrine and they also act on the second neuron in the spinal cord to inhibit the pain signal. 

If the signal from the nociceptors is greater than the signal from the inhibitory neurons, then it triggers the second neuron in the spinal cord]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Zollinger-Ellison_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w8tCp9sjSluJdBVNHSx1dxcqTjS942KE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Zollinger-Ellison syndrome]]></video:title><video:description><![CDATA[Zollinger-Ellison syndrome, named after Dr. Zollinger and Dr. Ellison - the two surgeons who first described it, is a rare endocrine disorder where there’s actually three interrelated pathologies. 

First, there’s a gastrinoma, which is a gastrin-secreting tumor. 

Second, the gastrinoma leads to increased gastric acid secretion from parietal cells. 

Third, the excess gastric acid causes peptic ulcers. 

Normally, the inner wall of the entire gastrointestinal tract is lined with mucosa, which consists of three cell layers. 

The innermost layer is the epithelial layer and it absorbs and secretes mucus and digestive enzymes. 

The middle layer is the lamina propria and it contains blood and lymph vessels. 

The outermost layer of the mucosa is the muscularis mucosa, and it is a layer of smooth muscle that contracts and helps with the breakdown of food. 

In the stomach, there are four regions - the cardia, the fundus, the body, and the pyloric antrum. 

There’s also a pyloric sphincter, or valve, at the end of the stomach which closes while eating, keeping food inside for the stomach to digest. 

The epithelial layer in different parts of the stomach contains different proportions of gastric glands which secrete a variety of substances. 

Having said that, the cardia contains mostly foveolar cells that secrete mucus which is mostly made up of water and glycoproteins.

The fundus and the body have mostly parietal cells that secrete hydrochloric acid and chief cells that secrete pepsinogen, an enzyme that digests protein.

Finally, the antrum has mostly G cells that secrete gastrin in response to food entering the stomach. 

These G cells are also found in the duodenum and the pancreas, which is an accessory organ of the gastrointestinal tract. 

Gastrin stimulates the parietal cells to secrete hydrochloric acid, and also stimulates the growth of glands in the epithelial layer.

In addition, the duodenum contains Brunner glands which secrete mucus rich in bi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypothyroidism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DQn1jZIURfG3wJ2Ix3kwf90YQ9OBK1vx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypothyroidism]]></video:title><video:description><![CDATA[In hypothyroidism, ‘hypo&amp;#39; refers to having too little, and ‘thyroid’ refers to thyroid hormone, so hypothyroidism refers to a condition where there’s a lack of thyroid hormones.

Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.

The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH.

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins.

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body.

Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the cell’s basal metabolic rate.

So as an example, the cell might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy.

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.

Thyroid hormone is important - and the occasional increase can be really useful when you need a boost to get through the final rounds of a sporting competition or when you’re trying to stay warm during a snowstorm!

Now, hypothyroidism can happen a few different ways - ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cushing_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LlZ3RTQES9mZZhkEaRrbF5pzSSu1wHSI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cushing syndrome]]></video:title><video:description><![CDATA[Cushing syndrome, named after the famous neurosurgeon, Harvey Cushing who first described it, is an endocrine disorder with elevated cortisol levels in the blood. In some cases, Cushing syndrome results from a pituitary adenoma making excess ACTH, and in those situations it’s called Cushing disease. 

Normally, the hypothalamus, which is located at the base of the brain, secretes corticotropin-releasing hormone, known as CRH, which stimulates the pituitary gland to secrete adrenocorticotropic hormone, known as ACTH. ACTH, then, travels to the pair of adrenal glands, on top of each kidney, where it specifically targets cells in the adrenal cortex.

The adrenal cortex is the outer part of the adrenal gland and is subdivided into three layers- the zona glomerulosa, the zona fasciculata, and the zona reticularis. Zona fasciculata is the middle zone and also the widest zone and it takes up the majority of the volume of the whole adrenal gland. 

The ACTH specifically stimulates cells in this zone to secrete cortisol, which belongs to a class of steroids, or lipid-soluble hormones, called glucocorticoids. Glucocorticoids are not soluble in water, so most cortisol in the blood is bound to a special carrier protein, called cortisol-binding globulin, and only about 5% is unbound or free. In fact, only this small fraction of free cortisol is biologically active, and its levels are carefully controlled. Excess free cortisol is filtered in kidneys and dumped into the urine. 

Free cortisol in the blood is involved in a number of things and it’s part of the circadian rhythm. Cortisol levels peak in the morning, when the body knows we need to “get up and go” and then drop in the evening, when we’re preparing for sleep. In times of stress, the body needs to have plenty of energy substrates around, so cortisol increases gluconeogenesis, which is the synthesis of new glucose molecules, proteolysis, which is the breakdown of protein and lipolysis, which is the breakdow]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NBJY0ZXjTymtDVuvUXquYwwkRCyycLcL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock]]></video:title><video:description><![CDATA[So, when we talk about ischemia, we’re usually talking about this lack of blood flow to a specific area of tissue. For example, with a heart attack, a coronary artery in the heart that supplies the left ventricle with blood gets blocked, so that localized area of heart tissue doesn’t get enough blood and oxygen; that damage is localized to that left ventricle. Shock is like ischemia, but on a global scale. In other words, it’s a circulatory failure of the whole body; blood flow to tissues is dangerously low, which leads to cellular injury, possibly damages multiple organs, and can even lead to multiple organ failure if not treated immediately. 

Okay, so with shock, the body’s tissues aren’t getting enough oxygen via the blood, right? Normally, blood perfuses through tissue and delivers oxygen because there’s enough pressure in the circulatory system to push it through; so, blood pressure majorly affects the amount of blood perfusing through tissues. 

Now, blood pressure is determined by two components: the resistance to blood flow in the blood vessels, which is affected by things like vessel length, blood viscosity, and vessel diameter; and the cardiac output, which is the volume of blood pumped by the heart through the body per minute. You can break that down into heart rate, or the number of beats per minute, multiplied by stroke volume, or the amount pumped out each beat. The stroke volume is found by taking the total volume of blood left over after contraction, which is called the end-systolic volume, and subtracting it from the total volume in the heart after filling, or the end-diastolic volume.

All right, keeping all this in mind, shock can be caused by many different things, but we can categorize the different types of shock into the three main categories with some subcategories. The first category is called hypovolemic shock. Hypo means “low,” vol refers to “volume,” and emia refers to the blood; thus, hypovolemic shock is shock induced by a lo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_edema</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SDV-jeJfQiyVpnhXN2KSL09eQXSgh1FE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary edema]]></video:title><video:description><![CDATA[Pulmonary edema refers to the buildup of fluid in the lungs including the airways like the alveoli - which are the tiny air sacs - as well as in the interstitium, which is the lung tissue that’s sandwiched between the alveoli and the capillaries. 

This space is mostly full of proteins, and when it starts filling up with fluid, it can make it hard for oxygen to cross over from the alveoli into the capillary, leaving the body hypoxic - or deprived of oxygen. 

To understand pulmonary edema, let’s first talk about the three main factors that determine how fluid moves between the capillaries and interstitial fluid, which are the hydrostatic pressure, oncotic pressure and capillary permeability. 

Hydrostatic pressure refers to the pressure felt by fluid in a confined space, pushing the fluid out of that space.

In the interstitial space, it’s the same thing as the blood pressure in the pulmonary capillaries, and because the pulmonary circulation is a low pressure system, the hydrostatic pressure is pretty low. But it’s still higher than the hydrostatic pressure exerted by the interstitial fluid of the lungs - which is almost zero. 

So, to be clear, if hydrostatic pressure was the only factor involved, a lot of fluid would be continuously leaking out of the pulmonary capillaries into the lung’s interstitial space. 

The next factor, though, is oncotic pressure; which is a type of osmotic pressure exerted by cells and proteins that can’t cross the capillary membrane and therefore tend to attract fluid. 

The oncotic pressure is higher in the pulmonary capillaries than in the interstitial fluid, so it opposes the hydrostatic pressure. 

Finally, there’s capillary permeability or leakiness which affects how easily fluid is actually able to get through. 

When taking these three factors together, the net result is that a very small amount of fluid leaks into the interstitial space, and that fluid is normally whisked away by the lymphatic channels in the lungs, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peptic_ulcer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lSQPaKLqSLWH9mzzxatiNXn5Rci3GNbZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peptic ulcer]]></video:title><video:description><![CDATA[Peptic refers to the stomach, and an ulcer is a sore or break in a membrane, so peptic ulcer disease describes having one or more sores in the stomach - called gastric ulcers - or duodenum - called duodenal ulcers- which are actually more common.

Normally, the inner wall of the entire gastrointestinal tract is lined with mucosa, which has three cell layers.

The innermost layer is the epithelial layer and it absorbs and secretes mucus and digestive enzymes.

The middle layer is the lamina propria and it contains blood and lymph vessels. 

Then there’s the outermost layer which is the muscularis mucosa, and it’s a layer of smooth muscle that contracts and helps break down food. 

In the stomach, there are four regions - the cardia, the fundus, the body, and the antrum. 

So the epithelial layer in different parts of the stomach contains different proportions of gastric glands which secrete various substances. 

Having said that, the cardia contains mostly foveolar cells that secrete mucus which is a mix of water and glycoproteins. 

The fundus and the body have mostly parietal cells that secrete hydrochloric acid and chief cells that secrete pepsinogen, an enzyme that digests protein.

Finally, the antrum has mostly G cells that secrete gastrin in response to food entering the stomach. These G cells are also found in the duodenum and the pancreas, which is an accessory organ of the gastrointestinal tract. 

Gastrin stimulates the parietal cells to secrete hydrochloric acid, and more broadly stimulates the growth of glands throughout the stomach. 

In addition, the duodenum contains Brunner glands which secrete mucus rich in bicarbonate ions. 

In fact, with all of the digestive enzymes and hydrochloric acid floating around, the stomach and duodenal mucosa would get digested if not for the mucus coating the walls and bicarbonate ions secreted by the duodenum which neutralizes the acid.

In addition, the blood flowing to the stomach and duodenum brings in ev]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acromegaly</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aOjiGZ7dQ3adcizN2suXZBDTQHGpIGjq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acromegaly]]></video:title><video:description><![CDATA[Acromegaly can be broken down into “acro” which refers to extremity and “megaly” which refers to enlargement.

So acromegaly is a hormonal disorder in adults where there is an excess of growth hormone or somatotropin, and causes continued growth of the extremities in adults, leading to large hands, feet and face. 

As examples, the French wrestler André the Giant who played Fezzik in the movie The Princess Bride and actor Richard Kiel who played Jaws in the James Bond movies both had acromegaly. 

In children, excess growth hormone causes a different disorder, called gigantism, because their long bones haven’t stopped growing yet. 

So let’s talk about how growth hormone is made. 

Normally, the hypothalamus which is at the base of the brain, secretes growth hormone-releasing hormone in bursts throughout the day - every couple hours, and this can increase based on things like low blood glucose levels, lack of food, increased exercise, increased sleep, and increased stress like trauma. 

The growth hormone-releasing hormone goes into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary which is smaller in size than a pea. 

The growth hormone-releasing hormone binds to a surface protein on somatotroph cells of the anterior pituitary gland, and in response, they release growth hormone.

The body uses three main ways to help limit the amount of growth hormone that gets made. 

First, too much growth-hormone-releasing hormone signals the hypothalamus to stop making more.

Second, when growth hormone reaches tissues like the liver, bones, and muscles, they make somatomedins, which are small protein hormones. 

These somatomedins signal the anterior pituitary to stop producing growth hormone. 

Third, growth hormone and somatomedins together signal to the hypothalamus to produce somatostatin, another hormone, whose role is also to signal the anterior pituitary to stop producing growth hormone.

Now,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypoparathyroidism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/a5g-wzQaTQOg2EGv8DKVWtP2RdmpEpMM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypoparathyroidism]]></video:title><video:description><![CDATA[With hypoparathyroidism, “hypo” refers to under, and “parathyroid” refers to the parathyroid glands, so hypoparathyroidism refers to a condition where there is an underproduction of parathyroid hormone.

Parathyroid hormone comes from the parathyroid glands which are buried within the thyroid gland, and their main job is to keep blood calcium levels stable.

Now, the majority of the extracellular calcium, the calcium in the blood and interstitium, is split almost equally between two groups - calcium that is diffusible and calcium that is not diffusible. 

Diffusible calcium is small enough to diffuse across cell membranes and is separated into two subcategories. 

The first is free-ionized calcium, which is involved in all sorts of cellular processes like neuronal action potentials, contraction of skeletal, smooth, and cardiac muscle, hormone secretion, and blood coagulation, all of which are tightly regulated by enzymes and hormones. 

The second category is complexed calcium, which is where the positively charged calcium is ionically linked to tiny negatively charged molecules like oxalate, which is a small anion that are normally found in our blood in small amounts. 

The complexed calcium forms a molecule that’s electrically neutral but unlike free-ionized calcium it’s not useful for cellular processes. 

Both of these are called diffusible because they’re small enough to diffuse across cell membranes.

Finally there’s the non-diffusible calcium which is bound to negatively charged proteins like albumin. 

The resulting protein-calcium complex is too large and charged to cross membranes, leaving this calcium also uninvolved in cellular processes.

Changes in the body’s levels of extracellular calcium are detected by a surface receptor in parathyroid cells that’s called the calcium-sensing receptor. 

These changes affect the amount of parathyroid hormone that’s released by the parathyroid gland. 

The parathyroid hormone gets the bones to release ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hodgkin_lymphoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OT0OcG6MSA6xSW2AIA-oTie2SJmFuqaQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hodgkin lymphoma]]></video:title><video:description><![CDATA[The term Hodgkin lymphoma -can be broken down. Lymph- refers to lymphocytes and oma- refers to a tumor. 

So, Hodgkin lymphoma is a tumor derived from lymphocytes - specifically B-cells which mainly reside in lymph nodes. 

In case you’re wondering, the disease gets its name from the English physician Thomas Hodgkin, who first described these tumors.

B-cell development begins in the bone marrow, which is a primary lymphoid organ. 

That’s where young precursor B-cells mature into naive B-cells. 

The naive B cells then leave the bone marrow and circulate in the blood and eventually settle down in lymph nodes. 

Humans have hundreds of lymph nodes, scattered throughout the body, and they’re considered secondary lymphoid organs. 

Each lymph node has B-cells which group together in follicles in the cortex or outer part of the lymph node, along with T-cells in the paracortex just below the cortex. 

B-cells differentiate into plasma cells, which are found in the medulla or center of the lymph nodes.

Plasma cells release antibodies or immunoglobulins. 

Antibodies bind to pathogens like viruses and bacteria, to help destroy or remove them. 

Various immune cells, including B-cells have surface proteins or markers that are called CD, short for cluster of differentiation, along with a number - like CD19 or CD21. 

In fact, the combination of surface proteins that are on an immune cell works a bit like an ID card. 

Now, a B cell is activated when it encounters an antigen that binds just perfectly to its surface immunoglobulin. 

Some of these activated B-cells mature directly into plasma cells and produce IgM antibodies. 

Other activated B-cells go to the center of a primary follicle in the lymph node and they differentiate into B-cells called centroblasts and start to quickly proliferate or divide.

These proliferating centroblasts form a germinal center, located in the center of the follicle of the lymph node. 

These centroblasts have a rear]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Graves_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7-syY0yaSWGoNvO0RNk7qymWTO6J03Cj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Graves disease]]></video:title><video:description><![CDATA[First described by Irish surgeon Robert James Graves, Graves disease is an autoimmune disorder that causes hyperthyroidism. 

In hyperthyroidism, ‘hyper’ refers to having too much, and ‘thyroid’ refers to thyroid hormone, so Graves disease refers to a condition where there’s excess thyroid hormones.

Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary. 

The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH. 

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”. 

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. 

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4. 

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body. 

Once inside the cell T­4 is mostly converted into T3, and it can exert its effect. 

T3 speeds up the basal metabolic rate. 

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. 

It’s as if the cells are in a bit of frenzy. 

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response. 

Thyroid hormone is important - and the occasional increase is like getting a boost to fight off a hungry predator or to stay warm during a snowstorm! 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Toxic_multinodular_goiter</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kIRxTqZrQ_mD8AZQWoyC6S_YRUS3bNE8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Toxic multinodular goiter]]></video:title><video:description><![CDATA[In toxic multinodular goiter, also called Plummer’s disease, ‘toxic’ refers to something harmful, ‘nodular’ refers to little lumps or nodules of tissue, and ‘goiter’ refers to a large thyroid gland.

So toxic multinodular goiter is a condition where the thyroid gland enlarges and is filled with lots of little nodules of tissue - each of which produce so much thyroid hormone that it becomes harmful to the body. 

Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.

The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH.

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells.

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins.

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body.

Once inside the cell T­4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate.

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats.

It’s as if the cells are in a bit of frenzy.

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.

Thyroid hormone is important - and the occasional ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arterial_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4XDBX0TlRNmL66mvxZSoUzQnSmWRZ4G3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arterial disease]]></video:title><video:description><![CDATA[So these three words look the same: Arteriosclerosis, Atherosclerosis, and Arteriolosclerosis. 

Arteriosclerosis is a general umbrella term describing diseases where the wall of the artery becomes thicker, harder, and less elastic than normal. 

You can figure that out right from the name: “arterio” which is Greek for artery, and sclerosis which is Greek for “hardening”.

Now the word arteriolosclerosis is any sort of hardening of small arteries in arterioles.

This is also pretty easy to remember since the “olo” in the middle of the word indicates small arterioles.

And then finally, atherosclerosis is the hardening of any artery (even though it’s usually medium- to large-sized arteries) which is caused by the buildup of plaque.

These plaques are called atheromatous plaques and happen in the innermost wall of the blood vessel called the tunica intima or endothelium. Okay now that we’ve differentiated been all three of those words, let’s first take a look at atherosclerosis.

So the blood vessel endothelium is made up of a single layer of cells and does two jobs: First,it protects the rest of the blood vessel wall from the blood, like a coat of varnish on your wood furniture and then, secondly, it secretes proteins on its surface to prevent the blood from clotting, because blood just inherently likes to clot whenever it gets the chance.

Now, Your endothelium can become damaged in lots of different ways. Low density lipoproteins, chemicals from smoking cigarettes, and high blood pressure all wreak havoc on the endothelium because these irritants break down the endothelium.

The damaged endothelium allow low-density lipoproteins to enter the endothelial wall. 

The white blood cells called monocyte follow the low-density lipoproteins and break them down through oxidation. 

Okay, so you might think macrophages eating the embedded low-density lipoproteins is a good thing, but if there is a lot of low-density lipoprotein, then the macrophage will eat so muc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperthyroidism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nrGqlGQxTmSYx5NBle_XFv8ZSceAXWKl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperthyroidism]]></video:title><video:description><![CDATA[In hyperthyroidism, ‘hyper’ refers to having too much, and ‘thyroid’ refers to thyroid hormone, so hyperthyroidism refers to a condition where there’s excess thyroid hormones. 

The condition is also called thyrotoxicosis, and is generally due to overproduction from the thyroid gland.

Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary. 

The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH. 

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”. 

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. 

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4. 

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body. 

Once inside the cell T­4 is mostly converted into T3, where it can exert its effect. T3 speeds up the cell’s basal metabolic rate. 

So as an example, the cell might produce more proteins and burn up more energy in the form of sugars and fats. 

It’s as if the cells are in a bit of frenzy. 

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response. 

Thyroid hormone is important - and the occasional increase can be really useful when you need a boost to get through the final rounds of a sporting competi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kallmann_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Uy3IpNg8SC_0YOm13qessri3QxmZYsMe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kallmann syndrome]]></video:title><video:description><![CDATA[Kallmann syndrome is an endocrine disorder caused by a decrease in sex hormones, either testosterone in males or estrogen and progesterone in females. That decrease leads to a failure to start or complete puberty. 

The syndrome is named after Dr. Franz Kallmann, the geneticist who first described it.

Normally, during fetal development there’s a region of the brain called the olfactory placode. Two groups of neurons emerge from that region. 

The first group contains olfactory neurons that eventually help with sensing smells. 

These neurons migrate down from the olfactory placode and get embedded in the cribriform plate, which is a bone plate that separates the nasal cavity from the brain, forming the olfactory bulb.

The second group contains neurons that release gonadotropin-releasing hormone. 

And these neurons migrate through the cribriform plate, and settle in the hypothalamus. 

The hypothalamic-pituitary-gonadal axis is a system of hormone signaling between the hypothalamus, pituitary gland, and gonads, either the testes or ovaries, to control sexual development and reproduction. 

Gonadotropin-releasing hormone is released into the hypophyseal portal system, which is a network of capillaries connecting the hypothalamus to the hypophysis, or pituitary. 

When gonadotropin-releasing hormone reaches the pituitary gland, it stimulates cells in the anterior pituitary, called gonadotrophs, to release gonadotropin hormones, luteinizing hormone and follicle-stimulating hormone into the blood. 

These gonadotropin hormones then stimulate the gonads to produce sex specific hormones. 

These are estrogen and progesterone in women and testosterone in men. 

Early on in male development, testosterone helps the external sex organs to differentiate into male genitals and causes the testes to descend from the abdomen into the scrotal sac.

During puberty, the Leydig cells of the testes respond to the luteinizing hormone by converting more cholesterol into testo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/5-alpha-reductase_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ymAKLdo2TUmt39fiLoOId9KDQva5fBtG/_.jpg</video:thumbnail_loc><video:title><![CDATA[5-alpha-reductase deficiency]]></video:title><video:description><![CDATA[5α- reductase deficiency is a genetic disorder in which a protein called 5α reductase is defective or absent. 

That’s an enzyme that converts the male hormone testosterone to its more potent form, called dihydrotestosterone.

One of the most important roles of dihydrotestosterone is to help male external genitalia develop in a male fetus. 

Okay, normally, very early on in fetal life, male and female internal sex organs and external genitalia are undifferentiated and look identical.

Within the first few months of development, testes develop in the male fetus. 

The testes start producing testosterone - a male steroid hormone that belongs to a class of hormones called androgens. 

The testosterone gets released into the blood and a tiny fraction of it gets converted by 5α- reductase, which is mainly made in the skin of the genital area, into dihydrotestosterone. 

Over time, dihydrotestosterone levels start rising and it affects undifferentiated genital structures.

Looking closely at these structures, at the top there’s the genital tubercle, which is a small projection. 

Just below that, there&amp;#39;s the urethral groove, which is the external opening of the urogenital sinus or the future urethra and bladder and is surrounded by the urethral folds and the labioscrotal swellings.

Now, once dihydrotestosterone reaches these structures, it makes the genital tubercle elongate into the phallus which will eventually be the penis.

The elongating genital tubercle pulls up the urethral folds which fuse in the midline, forming the spongy or penile urethra. 

The tips of the urethral folds remain unfused and that forms the external urethral opening at the distal tip of the penis. 

The labioscrotal swellings also fuse proximally to form the scrotum, which eventually houses the testes. 

In females, the gonads develop into ovaries, which produce very low levels of androgens, so the genital tubercle remains small, forming the clitoris and the urethral folds and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Small_bowel_ischemia_and_infarction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pKEK0Sh8RGq2YGO2nh9QX2SATq2XrfGK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Small bowel ischemia and infarction]]></video:title><video:description><![CDATA[Small bowel refers to the small intestine and infarction is when ischemia, which is an inadequate blood supply, causes necrosis, or tissue death. 

So, a small bowel infarction happens when there’s a reduced blood supply to the small intestine causing parts of the intestinal wall to necrose or die which can be life threatening. 

Now, the small intestine is made of several layers. 

The innermost layer is the mucosal layer and it’s composed of a few of its own layers. 

The first layer is the epithelial lining and it faces the lumen; next is the lamina propria, which is rich with blood and lymph vessels; and finally the muscularis mucosae, which has smooth muscle. 

Deep to this mucosal layer is the submucosal layer, which has connective tissue with proteins like collagen and elastin, as well as glands, and additional blood vessels. 

The submucosal layer also contains the Meissner plexus which is a part of the enteric nervous system. 

Below the submucosal layer is the muscularis propria which is basically two layers of smooth muscle with the myenteric plexus, another part of the enteric nervous system, sandwiched between them. 

These muscles are particularly important in helping to move food through the bowel. 

Finally, there’s the serosal layer which is the outermost layer of the small intestines that faces the abdominal cavity. 

The superior mesenteric artery is the main supplier of blood to the small intestine.

Branches of the artery spread through the mesentery - called mesenteric arteries - and penetrate the serosa layer and travel to the submucosa where they branch further into arterioles.

Because the small intestine has a high demand for oxygen and nutrients to sustain digestion, it is highly susceptible to tissue injury from ischemia. 

To reduce the risk of that happening, the mesenteric arteries branch and reconnect at points forming collateral circulation. 

That’s protective because if blood flow is reduced in one pathway, then the tissu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pituitary_apoplexy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hQQCNRhFRx_NCcAdacjB12Q8RXCBd_dO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pituitary apoplexy]]></video:title><video:description><![CDATA[With pituitary apoplexy, pituitary refers to a tiny gland at the base of the brain, and apoplexy refers to bleeding or loss of blood flow to an organ.

So, pituitary apoplexy is a disorder where there is either severe bleeding, or loss of blood flow to the pituitary gland, resulting in cell death and sudden loss of function. 

Normally, the pituitary is a pea-sized gland, hanging by a stalk from the base of the brain. 

It sits just behind the eyes near the optic chiasm, which is where the optic nerves cross. 

The anterior pituitary, which is the front of the pituitary gland, contains a few different types of cells, each of which secretes a different hormone. 

The largest group of cells are the somatotropes which secrete growth hormone, which goes on to promote tissue and organ growth.

The second largest cell group are the corticotrophs which secrete adrenocorticotropic hormone, or ACTH, which stimulates the adrenal glands to secrete cortisol, a hormone that controls the stress response, blood pressure, and metabolic regulation.

A smaller cell group are the lactotrophs which secrete prolactin. 

Prolactin stimulates breast milk production, and also inhibits ovulation, which is when an egg cell is released from the ovary, and inhibits spermatogenesis, which is the development of sperm cells. 

There are also thyrotrophs which are cells that secrete thyroid stimulating hormone, or TSH, that stimulate the thyroid gland. 

And finally, there are the gonadotrophs which secrete two gonadotropic hormones - luteinizing hormone, or LH, and follicle-stimulating hormone, or FSH, both of which go on to stimulate the ovaries or testes. 

The posterior pituitary, which is the back of the pituitary gland releases the antidiuretic hormone, or ADH, which is made by a part of the brain called hypothalamus.

ADH acts on the kidneys to decrease the amount of water lost in the urine. 

The pituitary gland gets blood through two arteries - the superior hypophyseal artery, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Social_anxiety_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6e0BtPqVSuqE06H8wbv2J3CFTGq6vHMs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Social anxiety disorder]]></video:title><video:description><![CDATA[Say it’s your first day at a new job. Maybe you’re nervous or jittery. You want to make a good impression. 

Those feelings are pretty normal, and may actually help you be more alert and careful. 

But after a few weeks, once you’re used to the job, and you know your coworkers, that nervousness usually diminishes, right? 

Well, for some people that initial anxiety is really high, and stays really high over time. 

For those people, the fear of being judged negatively by new people might be so daunting that it affects their ability to do their job well. 

In fact, the idea of having to be somewhere where they may be scrutinized by others might make them not want the job or avoid looking for work in the first place. 

This describes social anxiety disorder. 

It’s unclear what causes social anxiety disorder, but it’s thought to be a combination of genetic and environmental factors; first degree relatives of people with anxiety disorders have between two and six times the risk of having some form of social anxiety, and people who have experienced neglect or abuse are also more likely to develop social anxiety.

The DSM-5 defines social anxiety disorder as the fear of acting in a certain way that could be negatively evaluated by others. 

Social anxiety disorder causes intense distress that significantly interferes with someone’s normal routine, occupational or academic functioning, or with their social activities and relationships. 

What’s more is that this fear or anxiety is persistent, lasting for 6 or more months.

The main cause for distress in individuals with social anxiety disorder is the fear that their behavior will be judged negatively by others. 

For example, one person might get really anxious while making small talk with acquaintances, or meeting new people. 

Another person might get performance anxiety, and not feel able to give a presentation, or give a toast at a friend’s wedding. 

With the exception of some cases in which the individual ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alveolar_gas_equation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KDwI5QFsRliSeQIO24Us7PnrQaOgQm0J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alveolar gas equation]]></video:title><video:description><![CDATA[The main job of the lungs is gas exchange, pulling oxygen into the body and getting rid of carbon dioxide.

Normally, during an inhale - the diaphragm and chest muscles contract to pull open the chest and that sucks in air like a vacuum cleaner, and then during an exhale - the muscles relax, allowing the lungs to spring back to their normal size pushing that air out.

When we breathe in, oxygen-filled air from the environment enters through the nostrils, goes through the airways, and finally reaches the alveoli, the tiny air-filled sacs in the lungs where oxygen finally moves into the blood. 

The amount of oxygen in the alveolus equals whatever enters from the airways minus whatever moves into the blood, and that relationship is the alveolar gas equation.

The total pressure of the air in the alveoli is equal to the atmospheric pressure outside, Patm. 

But unlike atmospheric air, the air inside the alveoli gets saturated with water vapor after travelling through the moist airways. 

The partial pressure of water vapor is Pvapor. 

So in the alveoli, the total pressure, which is equal to the atmospheric pressure, is equal to the pressure of water vapor plus the pressure of the mixture of gases. 

So, rearranging, the total alveolar pressure exerted from all of the gases except water vapor is equal to (Patm- Pvapor). 

Now, let&amp;#39;s take this mixture of gas particles, red being oxygen and blue being CO2, the partial pressure of one of the gases is proportional to the fractional concentration of the gas in that mixture, which is a fancy way of saying the fraction of that gas molecule to all the gas molecules, so in this case CO2 would have a fractional concentration of 0.3, since it accounts for 30% of the gas molecules, and O2 would be .7, since it accounts for the remaining 70%. 

The reason these are proportional to the partial pressure is that more molecules are more likely to bounce around and hit the container. 

With our example, we see way mor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_hormone_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/URnYQWRTSheMET9RXN_vSGPoREuDwOjO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth hormone deficiency]]></video:title><video:description><![CDATA[Growth hormone deficiency is a condition that occurs when the pituitary gland fails to release enough growth hormone. 

Growth hormone, also known as somatotropin, helps promote overall growth of the body, muscle mass development, protein synthesis, and carbohydrate and lipid metabolism. 

So a deficiency in growth hormone, which can occur in kids and adults, results in problems in all of these areas.

Growth hormone is released by the pituitary which is a pea sized gland that is connected by a stalk to a part of the brain called the hypothalamus. 

The hypothalamus secretes growth hormone releasing hormone which travels through a network of capillaries called the hypophyseal portal system. 

Releasing hormone eventually reaches the anterior pituitary and triggers it to secrete growth hormone. 

Growth hormone then travels via the blood to various target tissues in the body to stimulate growth. This is called the hypothalamic pituitary axis. 

Normally, growth hormone is released in a pulsatile manner, throughout the day and peaks one hour after you fall asleep, but it is also secreted in response to various forms of internal and external stimuli. 

For example, the hypothalamus senses when there’s hypoglycemia, or low blood sugar, and in response it secretes growth hormone releasing hormone. 

Exercise causes the adrenal glands to secrete epinephrine and that stimulates the hypothalamus to react in the same way. 

Estrogen and testosterone which are produced in high levels during puberty, stimulate the hypothalamus to release growth hormone releasing hormone as well.    

The hypothalamic pituitary axis, however, is also regulated by three negative feedback loops which can prevent the release of additional growth hormone. 

First off, high levels of growth hormone and growth hormone releasing hormone in the blood can signal the hypothalamus to stop secreting more growth hormone releasing hormone. 

Second, it also signals the hypothalamus to produce ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperparathyroidism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JE72LfM8Seynq08FMYZBC6DOQ_Om07yj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperparathyroidism]]></video:title><video:description><![CDATA[With hyperparathyroidism, “hyper” refers to over, and “parathyroid” refers to the parathyroid glands, so hyperparathyroidism refers to a condition where there is an overproduction of parathyroid hormone. 

Parathyroid hormone comes from the parathyroid glands which are buried within the thyroid gland, and their main job is to keep blood calcium levels stable.

Now, the majority of the extracellular calcium, the calcium in the blood and interstitium, is split almost equally between two groups - calcium that is diffusible and calcium that is not diffusible. 

Diffusible calcium is small enough to diffuse across cell membranes and is separated into two subcategories. 

The first is free-ionized calcium, which is involved in all sorts of cellular processes like neuronal action potentials, contraction of skeletal, smooth, and cardiac muscle, hormone secretion, and blood coagulation, all of which are tightly regulated by enzymes and hormones. 

The second category is complexed calcium, which is where the positively charged calcium is ionically linked to tiny negatively charged molecules like oxalate, which is a small anion that are normally found in our blood in small amounts. 

The complexed calcium forms a molecule that’s electrically neutral but unlike free-ionized calcium it’s not useful for cellular processes. 

Both of these are called diffusible because they’re small enough to diffuse across cell membranes.

Finally there’s the non-diffusible calcium which is bound to negatively charged proteins like albumin. 

The resulting protein-calcium complex is too large and charged to cross membranes, leaving this calcium also uninvolved in cellular processes.

Changes in the body’s levels of extracellular calcium are detected by a surface receptor in parathyroid cells that’s called the calcium-sensing receptor. 

These changes affect the amount of parathyroid hormone that’s released by the parathyroid gland. 

The parathyroid hormone gets the bones to releas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_hypertension</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aLj_nhmnSTC_v4qxHe6F7n3kRS6u-_rb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary hypertension]]></video:title><video:description><![CDATA[Pulmonary hypertension refers to increased blood pressure in the pulmonary circulation, more specifically a mean pulmonary arterial pressure that is greater than 25 mmHg.

The pulmonary circulation starts with the right ventricle. 

From there - blood is pumped into the large pulmonary trunk, which splits to form the two pulmonary arteries – one for each lung. 

The pulmonary arteries divide into smaller arteries known as pulmonary arterioles and then eventually into pulmonary capillaries which surround the alveoli - which are the millions of tiny air sacs where gas exchange happens. 

At that point, oxygen enters the blood and carbon dioxide enters the alveoli. 

The pulmonary capillaries drain into small veins that join to form the two pulmonary veins exiting each lung, and these pulmonary veins complete the circuit by delivering oxygen-rich blood into the left atrium. 

The blood pressure in the pulmonary circulation is normally much lower than the systemic blood pressure. 

The normal pulmonary artery pressure is about 25/10 mmHg with a mean arterial pressure of 15 mmHg. 

Pulmonary hypertension most commonly develops as a result of left heart disease. 

Here the pulmonary blood vessels are normal and undamaged, but the left side of the heart is unable to pump efficiently – for example because of heart failure or valvular dysfunction. 

This causes a backup of blood in the pulmonary veins and capillary beds, which can increase the pressure in the pulmonary artery. 

Another cause of pulmonary hypertension is chronic lung disease, which typically causes hypoxic vasoconstriction. 

That’s when some area in the lung is diseased and is unable to deliver oxygen to the blood. 

To help adapt to this, the pulmonary arterioles in that area, start to constrict - and this effectively shuttles blood away from those damaged areas of the lung, and towards healthy lung tissue. But if the problem is widespread, like in individuals with emphysema, the mechanism can ba]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stroke_volume,_ejection_fraction,_and_cardiac_output</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EWlTrl4mRJifFjfiGT1t4J__RBuxe_br/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stroke volume, ejection fraction, and cardiac output]]></video:title><video:description><![CDATA[The main job of the heart is to pump oxygenated blood with nutrients through the arteries to the body’s tissues and receive back deoxygenated blood full of waste products through the veins.

Now, let’s zoom into the left ventricle. There’s a moment when the left ventricle is fully relaxed. It occurs at the end of filling or diastole, also called the end-diastolic point, and the volume of blood within the left ventricle is called the end-diastolic volume, and it’s about 120 milliliters. Then the left ventricle contracts, forcing blood through the aorta and into the whole arterial system. After that is another moment when the left ventricle is fully contracted. It occurs at the end of contraction or systole, also called the end-systolic point, and the volume of blood within the left ventricle is called end-systolic volume, and it’s about 50 milliliters. So, end-diastolic volume minus end-systolic volume, gives us the stroke volume, which is the volume of blood that the left ventricle ejects with every heartbeat, or stroke. In this case, the stroke volume is 120 minus 50, which equals 70 milliliters.

Stroke volume is a useful measurement, but it can vary based on the size of a person. For example, a stroke volume of 50 milliliters might be absolutely fine for a small person with a small heart volume, but may be low for a large person with a bigger heart volume. So another helpful measurement is the ejection fraction, which is the stroke volume divided by the end-diastolic volume, Ejection fraction = Stroke Volume / End- Diastolic Volume. In a normal individual that’s 70/120, or about 58%, but it can fluctuate between 50 and 65% and still be considered normal. In other words, at least half of the blood volume in the left ventricle should get pumped out during each heartbeat. In hearts that have a low contractility - a low force of contraction - the ejection fraction can fall below 50%. 

Every minute, though, our heart beats many times, so if we multiply the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meningitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rYeEmnLRTSOWYItNIpXyreshQ_2UZA9l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meningitis]]></video:title><video:description><![CDATA[With meningitis, mening- refers to the meninges which are three protective membranes that cover the brain and spinal cord, and -itis refers to inflammation; so meningitis is an inflammation of the meninges. 

More specifically, it refers to the inflammation of the two inner layers which are called the leptomeninges. 

The outer layer of the meninges is the dura mater, the middle layer is the arachnoid mater, and the inner layer is the pia mater. 

These last two, the arachnoid and pia maters, are the leptomeninges. 

Between the leptomeninges there’s the subarachnoid space, which houses cerebrospinal fluid, or CSF. 

CSF is a clear, watery liquid which is pumped around the spinal cord and brain, cushioning them from impact and bathing them in nutrients. 

In one microliter or cubic millimeter, there are normally a few white blood cells, up to 5. 

If we look at a bigger sample, like say a decilitre, then around 70% of those will be lymphocytes, 30% monocytes, and just a few polymorphonuclear cells -- PMNs -- like neutrophils. 

That same volume will contain some proteins, as well, about 15-50 mg as well as some glucose, about 45-100 mg, which is close to two thirds of the glucose we’d find in the same volume of blood. 

The CSF is held under a little bit of pressure, below 200 mm of H2O, which is just under 15 mm of mercury -- which is less than a fifth of the mean arterial pressure. 

Now at any given moment, there’s about 150 ml of CSF in the body. 

This is constantly replenished, with around 500 ml of new CSF produced everyday and the excess, or 500 minus 150 mL or 350 mL, is absorbed into the blood. 

But for any nutrients to enter and leave the CSF, and the brain itself for the matter, they have to go through the tightly regulated by the blood-brain barrier. 

The blood brain barrier is the special name given to the blood vessels in the brain. That’s because the endothelial cells in the blood vessels are so tightly-bound to one another that they prev]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Angiosarcomas</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iZ4wasBFSIOR_qlUkjiIMQ1aTjiGHfPr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Angiosarcomas]]></video:title><video:description><![CDATA[In angiosarcoma, -sarcoma refers to a malignant tumor, and angio- refers to a blood vessel or a lymphatic vessel. So angiosarcoma is a cancer of either a blood vessel, in which case it’s called a hemangiosarcoma, or a cancer of a lymphatic vessel, in which case it’s called a lymphangiosarcoma. Both arise from the inner lining of the vessel wall, known as endothelium. 

Angiosarcomas form when endothelial cells suddenly start proliferating abnormally. If these masses grow inside the blood vessel lumen, they can obstruct the blood flow, and that interferes with the oxygen and nutrient supply to various tissues, and can eventually result in tissue ischemia. If lymph flow is obstructed, lymph fluid backs up in the tissues, causing lymphedema. 

Cancer cells from hemangiosarcomas and lymphangiosarcomas can also invade the vessel wall, destroying it and making it burst, leading to bleeding or lymph fluid outflow in the surrounding tissue. In general, these cancer cells multiply rapidly and can be easily carried by blood flow or lymphatic flow to far-off sites within the body, particularly the lungs, where they form a new, metastatic tumor or tumors. Because of this, angiosarcoma is considered to be a particularly aggressive type of cancer. 

Angiosarcomas can occur anywhere in the body, but most often develop within the skin, bone, soft tissue, breast, or liver, and often spread from those locations to the lungs. Angiosarcoma of the skin usually shows up on the head or neck as a raised, purplish skin area that looks like a bruise that doesn’t heal; it may bleed, be painful, or be accompanied by swelling of the skin surrounding the affected area. Angiosarcoma of the bone is usually multifocal, meaning it affects multiple sites within the same bone, or involves multiple bones of the same limb. 

The exact causes of angiosarcoma remain unknown. One risk factor is chronic lymphedema in some part of the body, like the arms or legs, that goes on for several years. Thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Androgen_insensitivity_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dEHsqwb_Rfmgb-45Vl55wozTQi6Hwav-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Androgen insensitivity syndrome]]></video:title><video:description><![CDATA[Androgen insensitivity syndrome is a genetic disorder, in which a person with an XY genotype - genetically a male – is “insensitive” or doesn’t respond to androgens, which are male sex hormones. 

Androgens are responsible for primary sex characteristics like development of the penis and testes as well as secondary sex characteristics like height and body shape, so in androgen insensitivity syndrome all of these can be affected.

Okay, normally, very early on in fetal life, male and female genital tissues are undifferentiated and look identical. 

During the 7th or 8th week, the fetal gonads develop either into testes or ovaries.

In males, a gene on the Y chromosome, called the sex-determining region Y gene, or SRY gene for short, helps the fetal gonads turn into the testes.  

By the end of week 8, the testes start producing androgens, the main one being testosterone. 

A small fraction of testosterone, gets converted by the enzyme 5α- reductase into its more potent form, called dihydrotestosterone, which is mostly responsible for development of male external genitalia. 

Looking closely at these structures, at the top there’s the genital tubercle, which is a small projection. 

Just below that, there&amp;#39;s the urethral groove, which is the external opening of the urogenital sinus or the future urethra and bladder and is surrounded by the urethral folds and the labioscrotal swellings. 

Now, once dihydrotestosterone reaches the undifferentiated external genital structures, it makes the genital tubercle elongate into the phallus that eventually becomes part of the penis. 

The elongating genital tubercle pulls up the urethral folds which fuse in the midline, forming the spongy or penile urethra. 

Only the tips of these folds remain unfused to form the external urethral opening at the distal part of the penis.

The labioscrotal swellings also grow toward each other fuse medially to form the scrotum, which is the sac skin that contain the testes. 

In]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Marfan_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OBz-bTrFTv6AXWRY-vNLsilqRpChQ8C4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Marfan syndrome]]></video:title><video:description><![CDATA[Marfan syndrome is a genetic disorder that results in defective connective tissue, which can affect a person’s skeleton, heart, blood vessels, eyes, and lungs.

Normally, the interstitial space of various body tissues is full of microfibrils - which are strong rope-like structures that provide tissue integrity and form connective tissue. 

Each microfibril is made of cellulose as well as glycoproteins including the protein fibrillin. In some structures microfibrils form a scaffold for additional proteins like elastin. 

Elastin fibers are highly cross-linked, and that gives them a rubber-band-like quality, which allows tissues to stretch and then spring back to their original shape. 

Tissues that have elastin fibers are the arteries, skin, and lungs, and tissues that have microfibrils but no overlying layer of elastin are like tendons and the ciliary zonules that hold the eye lens in place. 

These tissues are less stretchable, but still have considerable tensile strength. 

In addition to being part of microfibrils, fibrillin also regulates tissue growth.

Fibrillin sequesters or removes transforming growth factor beta, or TGF-β, which stimulates tissue growth, so fibrillin therefore lowers how much TGF-β is available to stimulate growth. 

Marfan syndrome is caused by mutations in a gene called FBN1, or fibrillin 1, on chromosome 15. 

It’s autosomal dominant, which means that even if there’s a normal copy of the gene, a single mutated copy of the gene – in other words a heterozygous mutation – is sufficient to cause the disease. 

The FBN1 gene encodes Fibrillin-1 protein, one of three fibrillin subtypes.

In Marfan syndrome, fibrillin-1 is either less abundant or it is dysfunctional. As a result, there are fewer functioning microfibrils in the extracellular matrix, and that means there’s less tissue integrity and elasticity. 

Connective tissue is found throughout the body, so this can affect nearly every body system. 

Additionally, TGF-β doesn’t get]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cor_pulmonale</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GaAJzq3PTJC1a-cbALZfs4jcQuGhPvGA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cor pulmonale]]></video:title><video:description><![CDATA[With cor pulmonale, cor is Latin for heart and pulmonale is Latin for lungs. 

Cor pulmonale, then, is a relationship between the two, it’s when a disorder of the lungs causes dysfunction of the heart.

Normally, de-oxygenated venous blood from the body goes into the right atrium of the heart. 

From there, it goes into the right ventricle and gets pumped into the lungs where it is reoxygenated as it goes through the pulmonary circulation.

The pulmonary circulation is a low-resistance system with pressures ranging between 10 mmHg and 14 mmHg. 

After going through the lungs, oxygenated blood goes into the left atrium, and then into the left ventricle, and finally gets pumped back out to the body. 

When the heart can’t pump enough blood to meet the body’s demands, it’s initially called heart dysfunction and can worsen to the point where it’s called heart failure. 

This can happen in two ways, either it’s systolic heart failure, where the ventricles can’t pump blood hard enough during systole, or diastolic heart failure, where not enough blood fills the ventricles during diastole, called diastolic heart failure. 

Heart failure can affect the right ventricle, the left ventricle, or both ventricles, so someone might have, right-sided heart failure, left-sided heart failure, or both which is called biventricular heart failure. 

Cor pulmonale is when a lung disorder causes right-sided heart dysfunction that can develop into right-sided heart failure. 

Lung disorders make it harder to oxygenate the blood, which can lead to hypoxia, or low oxygen levels. 

In response, this triggers a process called hypoxic pulmonary vasoconstriction. 

Let’s say you have a couple pulmonary arterioles here, meaning they’re in the lungs, and the alveoli of the lungs here, and oxygen exchange between the two. 

If one of these alveoli is poorly ventilated, the corresponding arteriole vasoconstricts to divert blood away from it. 

This works pretty well, but when lots of alveol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physiologic_pH_and_buffers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tUp7AYPoRVWPOCcnYGBJxKbQS7CJ8k1X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physiologic pH and buffers]]></video:title><video:description><![CDATA[Physiologic pH is a way of quantifying the balance between acids and bases in the body. In fact, the pH depends on the concentration of hydrogen ions and can be described with this equation. 

The cells and enzymes in our tissues and organs work best when the concentration of hydrogen ions is 40 x 10-9 Eq/L, otherwise known as 40 nEq/L. Small changes to that number matter a lot, and because it can get annoying working with such small numbers, scientists converted this concentration into a logarithmic function and expressed it as pH. In this case, a hydrogen ion concentration of 40 x 10^-9 Eq/L, works out to a pH of 7.4. Now, there are two important aspects to remember when using this logarithmic function. First, as hydrogen concentrations increase, the pH decreases, because of the negative sign in front of the log. Second, since it’s a logarithmic function, pH and the hydrogen ion concentration don’t have a linear relationship. For example, an increase in pH from 7.4 to 7.6 means a decrease in the hydrogen concentration of 15 nEq/L. Whereas a decrease in pH from 7.4 to 7.2 means an increase in the hydrogen concentration of 23 nEq/L. That’s why the graph of hydrogen ion concentration versus pH has a curve to it, rather than being a straight line. For simplicity sake, when the body’s pH drops below 7.4 it’s considered acidemia, and when it goes above 7.4, it’s considered alkalemia. So due to this logarithmic relationship, a change in pH in the acidic range, pH &amp;lt; 7.4, will show a larger change in hydrogen concentrations than if the same change occurred in pH in the alkaline range, pH &amp;gt; 7.4. 

Maintaining a pH between 7.37 and 7.42 is essential for the human body. This is accomplished with buffers. In everyday language a &amp;quot;buffer,&amp;quot; is something that acts like a protective cushion or shield, and the same is true of physiologic buffers - they shield the pH from rising or falling too quickly. The reason the body needs buffers is]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brugada_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hdetQ9TnQ8uz1s6ND8TMQ253R-aue2y8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brugada syndrome]]></video:title><video:description><![CDATA[Brugada syndrome is named after two Spanish brothers, Pedro and Josep Brugada, who recognized a specific pattern of ventricular fibrillation on the electrocardiogram or ECG, of previously healthy individuals who had a sudden death! They identified this as Brugada syndrome and found that some cases could be traced back to a specific genetic cause.

Many individuals with Brugada syndrome don’t have an identifiable genetic cause, but in some individuals, there is one. The most well-known cause is a mutation in the gene SCN5A. The SCN5A mutation is inherited in an autosomal dominant pattern, meaning a single mutation is enough to cause the disease. 

The gene codes for sodium ion channels in the cell membranes of cardiac muscle cells, and a faulty sodium ion channel affects the heart cell’s ability to conduct an action potential. So the mutation results in some regions of the heart having abnormal repolarization. In some cases, the heart might have a normal rhythm but then develop into a Brugada syndrome in the presence of certain medications like sodium channel blockers.

On an electrocardiogram, Brugada syndrome typically has ST elevations (which are often a sign of ventricular strain), as well as a right bundle branch block, which indicates that the ventricles aren’t depolarizing normally. As a result, these regions become susceptible to a reentrant loop, which is when a depolarization signal starts going around and around in a loop, causing ventricular tachycardia and sometimes ventricular fibrillation. 

Ventricular fibrillation, sometimes called v-fib, means the heart’s muscle fibers start quivering because they’re not contracting at the same time. Normally, an electrical signal spreads fast enough so that all of the muscle fibers in the ventricles contract almost at the same time, which essentially looks like a single, coordinated contraction. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ankylosing_spondylitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IhmqUJN4TBmWlCnMy0Rcu7SoQIunwjTM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ankylosing spondylitis]]></video:title><video:description><![CDATA[Ankylosing spondylitis can be broken down - Ankylosing means stiffening, spondylo- refers to the vertebra, and -itis refers to inflammation. 

So ankylosing spondylitis is a chronic inflammatory disease that affects the vertebral joints and makes the spine really stiff, but can also cause inflammation in other parts of the body like the eyes and blood vessels.  

Ankylosing spondylitis, also called Bechterew disease, is part of a group of diseases called seronegative spondyloarthropathies. 

Spondyloarthropathies are all autoimmune diseases that affect the joints, and they’re seronegative, which refers to the fact that rheumatoid factor, which is an autoantibody, is not found in the blood.

Alright, so in the healthy adult, the vertebral column is made up of 33 bones. 

From top to bottom, the first seven bones are the cervical vertebrae, the next twelve are the thoracic vertebra and the next five, are the lumbar vertebrae. 

Below that is a bone called the sacrum, which is attached to the pelvic bone on either side, called the ilium, and where they meet is the sacroiliac joint. 

Below the sacrum is a tiny bone called the coccyx or tailbone. 

There are two types of joints between the vertebra. 

Between each of the vertebral bodies is an intervertebral disc which is made of type I and type II collagen and has two parts, the annulus fibrosis, an outer fibrous ring, and the nucleus pulposus, an inner jelly-like substance. 

This disc forms a joint between each vertebra, and it allows slight movement and acts as a shock absorber. 

In addition to the intervertebral discs, each vertebra has joints called facet joints with the vertebra above and the vertebra below, one on each side. 

These joints are synovial, meaning they have a joint capsule and a small amount of synovial fluid in between. 

When you stretch your back the capsule in these joints stretches too and decreases the pressure in the joint space, which makes any gas suddenly come out of solution, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Plasma_anion_gap</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iY6-qThfS4e1AV-RNqbb2Sd6Sqe-iI2s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Plasma anion gap]]></video:title><video:description><![CDATA[Plasma anion gap is a measurement of the balance between positively charged ions called cations and negatively charged ions called anions, within the plasma. 

Its normal range is typically between 3 and 11 mEq/L, while anything  below 3 mEq/L is considered abnormally low, and above 11 mEq/L is usually considered abnormally high, and.

Every single moment, trillions of cations and anions are floating around inside our blood vessels. For them to happily and stably coexist, the plasma has to be kept electrically neutral. 

That means that the sum of all positive charge from cations has to equal the sum of all negative charge from anions. 

The vast majority of cations are sodium Na+ ions, followed by potassium K+ ions, then calcium Ca2+ ions, then magnesium Mg2+ ions, and finally various positively charged proteins. 

The majority of anions are chloride Cl− ions, followed by bicarbonate HCO3− ions, then phosphate PO43- ions, then sulfate SO42- ions, and finally some organic acids and negatively charged plasma proteins, like albumin.

So, to prove that there’s electroneutrality, let’s say we try to measure the concentration of the cations and anions in our plasma. 

Unfortunately, not all of the ions are easy or convenient to measure. Specifically, among cations, usually just sodium Na+ is measured, which is typically around 137 mEq/L and among anions, chloride Cl− is measured, which is about 104 mEq/L, and  bicarbonate HCO3− is measured, which is around 24 mEq/L. 

So just counting up these three ions, there’s a difference, or “gap” between the sodium Na+ concentration and the sum of bicarbonate HCO3− and chloride Cl− concentrations in the plasma, which is 137 minus 128 (104 plus 24) or 9 mEq/L.

This is known as the anion gap, or in other words, how many more cations are there than anions.

Now just a few moments ago, we said that cations equal anions, so why does this gap even exist? Well, it’s because sodium Na+ accounts for the vast majority of cations i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Restrictive_lung_diseases</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VAJXD3dITiWWVi13Xn-tYXHxRa6G5L1m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Restrictive lung diseases]]></video:title><video:description><![CDATA[Restrictive lung diseases are just as they sound, restrictive. 

There are two types of restrictive lung diseases, interstitial and extra-pulmonary. 

For the interstitial type, it refers to the lung tissue itself being damaged.

Imagine a lung being hard and stiff like tough rubber, that lung tissue won’t easily allow air to enter during inhalation, thereby reducing the lung volume.

In the extra-pulmonary type, the structures around the lung are damaged and that prevents chest expansion. 

Think about how hard it would be to take a breath when you have someone sitting on your chest. 

During inhalation, both the diaphragm and intercostal muscles located in between your ribs contract to pull the ribs up and out and expand the chest cavity. This creates a vacuum which pulls the lungs open. 

The air reaches the alveoli and this is where the majority of gas exchange occurs in the lungs. 

Between the alveoli, there’s connective tissue made up of proteins like elastin fibers, which give the lungs their rubber-band like properties, and collagen, which gives the lungs their firmness and their overall shape. 

During exhalation, both the diaphragm and the intercostal muscles relax to allow the chest wall to fall and return the chest cavity back to normal. 

At the same time, the elastin and collagen fibers in the interstitium allow the lung to spring back and push the air back out. 

There are a number of ways to measure the volume of air as it is inhaled and exhaled from the lungs. 

For example, total lung capacity is the total amount of air that the lungs can hold. 

Tidal volume is the volume of air inhaled during normal inhalation and the functional residual capacity is the total amount of air left in the lungs after a normal exhalation. 

There’s also the forced vital capacity, or FVC, which is the maximum amount of air exhaled after a full inhalation, and the forced expiratory volume in one second, or FEV1, which is the amount of air forcibly breathed ou]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_acidosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U6V07f3sRUeTOrUlWGSUhSfOQ3_a6oym/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory acidosis]]></video:title><video:description><![CDATA[With respiratory acidosis, “acidosis” refers to a process that lowers blood pH below 7.35, and “respiratory” refers to the fact that it’s a failure of the respiratory system carrying out its normal pH- balancing job.

Normally, during an inhalation, the diaphragm and chest wall muscles contract to pull open the chest and that sucks in air like a vacuum cleaner. Then, during an exhalation, the muscles relax, allowing the elastin in the lungs to recoil, pulling the lungs back to their normal size and pushing that air out. 

Ultimately, the lungs need to pull oxygen into the body and get rid of carbon dioxide CO2. CO2 binds to water H2O in the blood and forms H2CO3 carbonic acid, which then dissociates into hydrogen H+ and bicarbonate ions HCO3-. 

So, in order to prevent pH fluctuations, the CO2 concentration, or the partial pressure of CO2, called PCO2, needs to be kept within a fairly narrow range. 

For this reason, lungs maintain the ventilation rate they need to get rid of CO2 at the same rate that it’s created by the tissues. 

If PCO2 levels starts to rise and pH starts to fall, chemoreceptors that are located in the walls of the carotid arteries and in the wall of the aortic arch start to fire more, and that notifies the respiratory centers in the brainstem that they need to increase the respiratory rate and the depth of breathing.

As the respiratory rate and depth of each breath increase, the minute ventilation increases - that’s the volume of air that moves in and out of the lungs in a minute. 

The increased ventilation helps move more carbon dioxide CO2 out of the body, reducing the PCO2 in the body, which raises the pH.

In respiratory acidosis, the normal mechanism of ventilation is disturbed, and minute ventilation becomes inadequate to balance the pH.

This could be due to a number of problems. Sometimes, the problem is not in the lungs themselves, but in the respiratory centers of the brainstem. 

After a stroke or a medication overdose, li]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_granulomatous_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1OjOxxBhRdWt7xNraSpRHBgjS-_jl_KW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic granulomatous disease]]></video:title><video:description><![CDATA[With chronic granulomatous disease, granulomatous refers to the development of small nodules called granulomas. 

Granulomas are collections of immune cells, especially phagocytes, which cluster together when they can&amp;#39;t kill invading pathogens, like bacteria or fungi.

So chronic granulomatous disease is an immunodeficiency where phagocytes are unable to kill pathogens, and instead they form granulomas throughout the body.

Normally, when a pathogen invades the body, phagocytes, like neutrophils and macrophages, are the first on the scene. 

When a phagocyte detects a pathogen, it stretches itself out as if it had two little arms. 

These arms wrap around the pathogen and seal themselves back up, forming a vesicle inside the phagocyte called a phagosome. 

Because the phagosome is lined by what was previously part of the phagocyte&amp;#39;s surface membrane, whatever structures were previously surface-bound, like this protein complex called NADPH oxidase, end up inside the phagosome. 

The phagocyte also has other organelles, like lysosomes, which are full of digestive enzymes that can destroy a pathogen.

When a lysosome fuses with a phagosome, it forms a phagolysosome, and lysosomal enzymes start to destroy the pathogen. 

The lysosomal enzymes also activate NADPH oxidase, which came from the phagosome, causing NADPH to undergo oxidation, and lose one of its electrons.

Nearby oxygen molecules can grab these electrons to become reduced and form superoxide ions, or O2- ions. 

Another enzyme, superoxide dismutase, can take these ions and combine them with hydrogen ions to form hydrogen peroxide, or H2O2. 

This process of producing superoxide ions and hydrogen peroxide is called the respiratory burst. 

These ions and molecules destroy pathogens by damaging their cell membranes and proteins.

In chronic granulomatous disease, there’s a mutation in the genes that code for NADPH oxidase, so the enzyme is less functional.

One common mutation ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_umbilical_cord</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bE0zrcCrQcyTV3TzZa0HdNqUSjaDLwyD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the umbilical cord]]></video:title><video:description><![CDATA[During development, the fetus is connected to the placenta via the umbilical cord, a long, flexible stalk that has two small arteries and a large vein. 

Deoxygenated fetal blood flows through the umbilical arteries to the placenta where it picks up oxygen and glucose while dropping off carbon dioxide.

Oxygenated blood then heads back towards the fetus’s heart through the umbilical vein.

When the baby is born the umbilical cord is no longer needed, so it’s cut off, leaving the navel or belly button. 

In week 2 of development, the blastocyst has two parts—an inner part called the embryoblast, and an outer part called the trophoblast, which develops into the cytotrophoblast and syncytiotrophoblast. 

The embryoblast has two layers called the epiblast, which contains the amniotic fluid, and the hypoblast, which contains the yolk sac filled with vitelline fluid that can nourish the embryo. 

Cells from the epiblast layer start to differentiate into extraembryonic mesoderm cells, so-named because they are outside of the developing embryo. 

These are some of the earliest mesoderm cells, and they start to form even while the embryoblast itself is a bilaminar disc. 

These mesoderm cells line the inside of the cytotrophoblast and syncytiotrophoblast and form the chorion. 

As development progresses, a space called the chorionic cavity develops between the embryoblast and the chorion, and these two structures are connected by a short band of extraembryonic mesoderm called the body stalk. 

The body stalk contains the umbilical vessels and is the first of three structures that make up the umbilical cord. 

In week 3 of development, the embryo folds in two directions. 

In the longitudinal plane, there is a cranial and caudal fold, so that the embryo now looks less like a pancake and more like a little shrimp. 

The folding process shapes part of the yolk sac into a gut tube, with the rest of the yolk sac remaining connected not at the cranial or caudal end, but ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_alkalosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Nc-woYxPS-uE1GSzpDaCtMnVRiqb9PYG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory alkalosis]]></video:title><video:description><![CDATA[With respiratory alkalosis, “alkalosis” refers to a process that causes alkali accumulation or acid loss, and “respiratory” refers to the fact that it’s a failure of the respiratory system carrying out its normal pH- balancing job. 

Normally, during an inhalation, the diaphragm and chest wall muscles contract to pull open the chest and that sucks in air like a vacuum cleaner. Then, during an exhalation, the muscles relax, allowing the elastin in the lungs to recoil, pulling the lungs back to their normal size and pushing that air out. Ultimately, the lungs need to pull oxygen into the body and get rid of carbon dioxide CO2. CO2 binds to water H2O in the blood and forms H2CO3 carbonic acid, which then dissociates into hydrogen H+ and bicarbonate ions HCO3-. So, in order to prevent pH fluctuations, the CO2 concentration, or the partial pressure of CO2, called PCO2, needs to be kept within a fairly narrow range. For this reason, lungs maintain the ventilation rate they need to get rid of CO2 at the same rate that it’s created by the tissues. If PCO2 levels start to fall and pH starts to rise, peripheral chemoreceptors that are located in the walls of the carotid arteries and in the wall of the aortic arch start to fire less, and that notifies the respiratory centers in the brainstem that they need to decrease the respiratory rate and depth of breathing. As the respiratory rate decreases and breaths become more shallow, the minute ventilation decreases - that’s the volume of air that moves in and out of the lungs in a minute. The decreased ventilation, means less carbon dioxide CO2 moves out of the body, increasing the PCO2 in the body, which lowers the pH. 

In respiratory alkalosis, the normal mechanism of ventilation gets disturbed, and the minute ventilation goes higher than what’s needed to balance the pH. For ventilation to increase, the respiratory centers have to start firing more than usual. This increased firing may be a normal compensatory response]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_excitation-contraction_coupling</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Bu1wqk6bRmua0XAPOIiHkqx1SliWSvbg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac excitation-contraction coupling]]></video:title><video:description><![CDATA[Cardiac excitation-contraction coupling is the relationship between electrical signals in the form of action potentials, and mechanical changes in the heart muscle cells, called cardiomyocytes, that causes them to contract. 

Let’s start by looking at the structure of a cardiomyocyte. Cardiomyocytes have branches, and have intercalated disks along their edges which have small holes called gap junctions that allow ions to flow from one cardiomyocyte to the next. When a cardiomyocyte depolarizes, ions like calcium move from that cell into a neighboring cell, and these ions trigger depolarization to happen in that cell. This is what makes cardiomyocytes part of a “functional syncytium,” they’re like a little community of cells intimately working together. In addition, cardiomyocytes stay physically attached to one another through proteins called desmosomes, which are like staples that hold the cells together when they’re contracting. Another feature of cardiomyocytes are passageways called transverse tubules, or T-tubules. T-tubules are extensions of the outside environment. They increase the surface area of the cardiomyocyte and they look like the letter T, so it’s easy to remember their name. Think of a large walk-through aquarium: you can walk through tunnels and look at the sea creatures all around you, but you’re not in the water with them. Finally, there’s the sarcoplasmic reticulum, which is an organelle that stores intracellular calcium, the calcium that is sequestered inside the cell. 

When a depolarization wavefront hits a cardiomyocyte, a few calcium ions flow through gap junctions, and if a threshold membrane potential is reached, then sodium channels start to open up. If there’s a depolarization, then ions start to move across the cell membrane, and that’s where the T-tubules play a key role. During the part of the cardiomyocyte action potential when calcium ions flow into the cell, the presence of T-tubules helps bring calcium deep into the cel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polymyositis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f6oEItynR3CAPK4SlRmc55W4TEi-UdRa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polymyositis]]></video:title><video:description><![CDATA[In polymyositis, “myos-“ refers to the muscles, “poly-“ means many, and “-itis” refers to inflammation, so polymyositis is an inflammatory disorder which involves many muscle groups around the body.  

Polymyositis is an immune- mediated disease, meaning that the immune system attacks the muscles in our own body. 

Normally, the cells of the immune system are ready to spot and destroy anything foreign that could cause the body harm. 

To help with this, most cells in the body have a set of proteins that combine together to form something called a major histocompatibility complex, or MHC, class I molecule that sits on the surface of their cell membrane. 

These surface proteins act kind of like a serving platter, presenting molecules from within the cell for the immune system to continually sample. 

Normally though the molecule’s just a sample from the cell, and the immune system recognizes it as harmless, and this is known as a self-antigen, and there’s no response. 

But when a cell is actually invaded by a pathogen like a virus, viral antigens are presented on the MHC class I molecule, and that sparks a different immune response. 

A type of T-lymphocyte, called a CD8+ T-cell, also known as a cytotoxic T-cell, uses its T-cell receptors to bind to the antigen presented by the MHC class I molecule. 

If the cytotoxic T-cell binds strongly, than the antigen is recognized as foreign, and the cytotoxic T-cell secretes a whole lot of perforin and granzymes. 

Perforin forms big holes in the infected cell and that allows the granzymes to enter the cell. 

Once inside, the granzymes induce apoptosis, or programmed cell death. 

As if that weren’t enough, the cytotoxic T-cells have a protein called Fas ligand on their surface, and it binds to a molecule called Fas on the surface of the infected cell. 

When these two combine, it triggers a cascade of signaling events inside the target cell that also leads to apoptosis. 

Meanwhile, B- lymphocytes that react to t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pneumonia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RFEWubI-RKqhYmBYJxr3zh61TSGin80a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pneumonia]]></video:title><video:description><![CDATA[Pneumonia is an infection in the lung tissue caused by microbes, and the result is inflammation. 

The inflammation brings water into the lung tissue, and that extra water can make it harder to breathe.

During inhalation, air reaches your lungs by traveling down your trachea, then it continues through the bronchi and the bronchioles and ends up in the alveoli. 

The alveoli are tiny air sacs that look like tiny clumps of grapes, that are wrapped up in a net of capillaries. This is where the majority of gas exchange happens in the lungs. 

Oxygen leaves the air in the alveoli and crosses into the bloodstream while carbon dioxide leaves the bloodstream and is then exhaled out of the body. 

Now, now in addition to air, you’re constantly breathing in other stuff, like microbes. But we’re usually good at protecting ourselves.

For example, we have mechanical techniques like coughing, a mucociliary escalator that lines the entire airway and moves out larger bacteria, and macrophages that are nestled deep inside the alveoli and ready to destroy anything that lands there. 

But sometimes, a particularly nasty microbe might succeed in colonizing the bronchioles or alveoli, and when that happens - Congratulations! You’ve got pneumonia. 

Those microbes typically multiply and cross over from the airways into the lung tissue, creating an inflammatory response. 

The tissue quickly fills with white blood cells as well as proteins, fluid, and even red blood cells if a nearby capillary gets damaged in the process.

Now, there are lots of different pneumonia-causing microbes. 

Usually it’s caused by viruses and bacteria, but it can also be caused by fungi and a special class of bacteria called mycobacteria.

In adults, the most common viral cause of pneumonia is influenza, sometimes just called the flu. 

In adults, bacterial causes include streptococcus pneumoniae, haemophilus influenzae, and staphylococcus aureus. 

There are also more unusual bacteria like mycoplasm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cannabis_dependence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SWVFYG6ETQepDf9SRhJujmHyQ0qNPBD1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cannabis dependence]]></video:title><video:description><![CDATA[Cannabis, or marijuana, is one of the most popular psychoactive substances worldwide, especially among teenagers. 

Although the specifics of cannabis’ addictive qualities are still very much under debate, cannabis dependence disorder is officially classified in the DSM-5 and prolonged, heavy use of cannabis has been shown to cause some level of dependency.

Cannabis comes from the flowers of Cannabis sativa plants, which has oils with concentrations of tiny, fat-soluble, psychoactive molecules called cannabinoids. 

The three main cannabinoids, tetrahydrocannabinol (also called THC), cannabidiol (also called CBD), and cannabinol (also called CBN), are each associated with unique psychoactive effects.

For example, THC is associated with high-grade recreational marijuana, and produces effects, like euphoria, analgesia, mild hallucinations, and an increased appetite. 

Cannabidiol on the other hand does not have psychoactive effects and is commonly included in medical marijuana because it has a variety of effects including being analgesic, anti-inflammatory, anti-seizure, appetite stimulating, and anxiety-reducing.

To understand how cannabis works, let’s zoom in on a synapse of the brain to see how a stimulus response is induced generally, without drugs. 

Normally, electrical signals, or action potentials, travel down the axon to the axon terminal, triggering the release of chemical messengers called neurotransmitters from synaptic vesicles into the synapse. 

The neurotransmitters travel across the synapse and bind to receptors on the postsynaptic neuron, where they give the cell a message. 

After the neurotransmitters have done their job, they unbind from the receptors and can simply diffuse away, be degraded by enzymes, or be picked up by proteins and returned to their release site in a process called reuptake.

When cannabis is consumed, the cannabinoid compounds it contains bind to cannabinoid receptors which are found in the central and peripheral ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dissociative_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/95y2rQv7Q7S6ty7z5xxfY-T-R7qNlbOZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dissociative disorders]]></video:title><video:description><![CDATA[Maybe you’ve had the experience of driving on “autopilot.” One minute you got in your car, and the next minute you’ve arrived at your destination, but you can’t actually remember the details of the drive. This is an example of normal, everyday dissociation, a term that describes a mental state of disconnection from what is going around you.

Normally this day-dreamy state doesn’t last very long, and most people can snap out of it if something or someone requires their attention. 

But for some people, dissociation is more pervasive, and can’t be turned off so easily. 

In fact, the feeling of disconnection may become so intense and happen so often that it stops a person from functioning in their daily life. When this is the case, we say the person has a dissociative disorder. 

Dissociative disorders are a group of disorders that cause an impaired awareness of one’s own actions, thoughts, physical sensations, and even identity, which is a sense of who you are. Dissociative disorders tend to stem from trauma, usually early childhood abuse or neglect, and are thought to be a way of adapting to negative feelings and experiences.  

Dissociative disorders are divided into three main types: depersonalization/derealization disorder, dissociative amnesia, and dissociative identity disorder. Each of these disorders fall along a spectrum of severity, with depersonalization/derealization disorder being the least severe of the dissociative disorders, dissociative amnesia falling somewhere in the middle, and dissociative identity disorder being the most severe. Typically, individuals with more severe dissociative disorders may have elements of less severe ones as well. 

With v, depersonalization refers to a feeling of detachment from oneself, your own person, while derealization refers to a feeling that the world around you is not fully real. 

Those with the disorder often feel as if they are watching themselves from the outside, maybe watching a movie about their l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Seasonal_affective_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vxYs9v3-Rsmgbsk1eTnE8fC1QzGf7ZLW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Major depressive disorder with seasonal pattern]]></video:title><video:description><![CDATA[Recently, the DSM-5 changed the name of “seasonal affective disorder,” or SAD, to “depressive disorder with seasonal pattern.” 

The new name isn’t quite as catchy as “SAD,” but it does describe the condition more precisely. 

That’s because depressive disorder with seasonal pattern is not really a distinct disease, but rather depression that worsens at the same time each year, usually in the late fall and winter. 

So let’s first review depression. Depression, or major depression, is a serious condition where someone loses their sense of life being enjoyable; this feeling of malaise affects every aspect of their day-to-day life, whether they’re working, studying, eating, or sleeping. 

The causes of depression aren’t fully known, but it’s thought to involve a deficiency of monoamine neurotransmitters in the brain, like dopamine, norepinephrine, and especially serotonin.

In depressive disorder with seasonal pattern, there’s a strong relationship with the circadian rhythm, the internal clock that keeps your body in tune with the rising and setting of the sun. 

At the base of the brain there’s a region called the hypothalamus, and within it are a group of neurons located in a specific spot called the suprachiasmatic nucleus or SCN.

The neurons in the SCN get information about light from optic nerves, and use that information to run the circadian rhythm. 

The SCN relays that information to the pineal gland, a tiny, cone-shaped structure near the hypothalamus. 

And when it’s dark out, the pineal gland releases the hormone melatonin, which is chemically related to serotonin.

Melatonin lowers your heart rate and body temperature, helping you go to sleep. 

When it’s light outside, the pineal gland stops releasing melatonin, and that has the opposite effect by raising your heart rate and body temperature, keeping you awake. 

A risk factor for developing depressive disorder with seasonal pattern is having a sleep phase delay, which is when a person’s body p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pneumothorax</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/axu_n_xkSs_HhVvDL8yIFFLiQQSZKEFM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pneumothorax]]></video:title><video:description><![CDATA[With pneumothorax, pneumo refers to air and thorax means chest, so a pneumothorax is when there is air in the chest; more specifically air in the space between the lungs and chest wall – called the pleural space.

The pleural space lies between the parietal pleura, which is stuck to the chest wall, and the visceral pleura, which is stuck to the lungs. 

The pleural space normally contains a lubricating fluid that helps reduce friction as the lungs expand and contract. 

Pressure within the pleural space is established by two main opposing forces. 

One is the muscle tension of the diaphragm and chest wall which contract and expand the thoracic cavity outwards, and the other is the elastic recoil of the lungs, which try to pull the lungs inward. 

The two pull on each other creating a balance between the forces that creates a slight vacuum in the pleural space. 

It results in the pleural space having a pressure of -5 centimeters of water relative to the pressure of 0 centimeters of water in both the thoracic cavity and the lungs.

A pneumothorax forms when the seal of the pleural space is punctured and air moves in from the outside, making the pressure in the pleural space equalize to 0 centimeters of water. 

Since the negative pleural pressure is lost, the two opposing forces no longer pull on one another. 

As a result, the lungs simply pull inwards and collapse, and the chest wall simply springs outward a bit. 

A collapsed lung limits how well it can exchange air, and can lead to a reduction in oxygen being brought into the body, and a build-up of carbon dioxide in the body because it can’t easily get released. 

There are many types of pneumothorax. 

The first is a spontaneous pneumothorax which typically occurs when a bullae, which is an air pocket, forms on the surface of the lungs and breaks. 

Bullae form when the alveoli, which are the terminal ends of the lung where gas exchange occurs, develop a tiny leak and air slowly seeps into the surroun]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertension</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BWnlepajQQKEYJR8kiseK7N8QOyFO016/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertension]]></video:title><video:description><![CDATA[Over a billion people around the world have hypertension, or high blood pressure, so that pretty much means it’s pretty common. 

Let’s start by defining it. Typically, it’s represented by two numbers: the top number is the systolic blood pressure, which is the arterial pressure when the heart’s contracting; and the lower number is the diastolic blood pressure, which is the arterial pressure when the heart’s relaxing or refilling. Most of the time, blood pressure is taken in the brachial artery in your upper arm, because if the pressure is high there, it’s probably high throughout all of the arteries.

The guidelines for categorizing blood pressure have recently changed to reflect a growing body of evidence that shows that even moderately high blood pressures can significantly increase your risk for developing heart disease. Now, ‘normal’ systolic blood pressure is defined as less than 120 mmHg, and a normal diastolic pressure is less than 80 mmHg. Elevated systolic blood pressure is considered between 120 and 129 mmHg and less than 80 mmHg on the diastolic side. Stage 1 hypertension is between 130 and 139 mmHg on the systolic side, and between 80 and 89 mmHg on the diastolic side. Stage 2 hypertension is defined as anything that is 140 mmHg or higher on the Systolic side and 90 mmHg or higher on the diastolic side.

Typically, both systolic and diastolic pressures tend to climb or fall together, but that’s not always the case. Sometimes, you can have systolic or diastolic hypertension, when one number is normal and the other is really high. This is referred to as isolated systolic hypertension or isolated diastolic hypertension. 

High blood pressure is a serious problem for the blood vessels because it causes wear and tear on the endothelial cells that line the inside of the blood vessels. Just like a garden hose that’s always under high pressure, in the long term, blood vessels can develop tiny cracks and tears that can lead to serious problems, like my]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polycystic_ovary_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PwsyhTqySHCx66Ekv2T_6ROrRimnAoBH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polycystic ovary syndrome]]></video:title><video:description><![CDATA[In polycystic ovary syndrome, “poly” means many, and “cystic” refers to cysts. 

So you might think that having many ovarian cysts is a crucial part of polycystic ovary syndrome. 

But while some people with polycystic ovarian syndrome do have ovarian cysts, ovarian cysts are no longer a necessary characteristic of the condition. 

Instead, polycystic ovary syndrome is a dysfunction in the hypothalamic-pituitary-ovarian axis, which are the hormones that regulate the menstrual cycle. 

A normal menstrual cycle can be divided into two phases: the follicular phase, which takes place before ovulation, and the luteal phase, which takes place after ovulation. 

During the follicular phase, the hypothalamus secretes gonadotropin-releasing hormone, or GnRH. 

GnRH makes the anterior pituitary gland secrete two other hormones, called gonadotropins, in roughly equal amounts, which it releases in pulses. 

One of these gonadotropins is the luteinizing hormone, or LH. 

The other is the follicle-stimulating hormone, or FSH. 

LH and FSH travel to the follicles in the ovaries. 

The follicles are small clusters of theca and granulosa cells that protect the developing oocyte, or egg. 

The theca cells develop LH receptors which allow them to bind LH, and in response they secrete a hormone called androstenedione. 

Granulosa cells develop FSH receptors, which allow them to bind to FSH and produce an enzyme called aromatase, which converts the androstenedione into 17β-estradiol - a member of the estrogen family. 

As follicles grow, the level of 17β-estradiol in the blood increases, and it acts as a negative feedback signal – that is, it tells the pituitary to secrete less FSH. 

Less FSH in the blood means there’s only enough to stimulate one follicle. 

The follicle that has the most FSH receptors grows the quickest, and becomes the dominant follicle. 

At this point, about midway through the follicular phase, the granulosa cells also begin to develop LH receptors. 

As]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypersensitivity_pneumonitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qMc6rTVzRfq9RKDSm00QhYG_SC26u4BJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypersensitivity pneumonitis]]></video:title><video:description><![CDATA[Hypersensitivity refers to an abnormal and excessive immune reaction, and pneumonitis refers to an inflammation of the lungs. 

So, hypersensitivity pneumonitis is when a person’s immune system reacts excessively to something that’s inhaled, causing lung inflammation. 

The lungs are made up of a collection of branching tubes called bronchioles that get smaller and smaller until they end in little air-filled sacs called alveoli. 

The alveoli are like clusters of grapes, and they’re covered by nets of tiny capillaries - and that’s where gas exchange occurs. 

Between the airways and the blood vessels there’s lung tissue - called interstitium, which is full of proteins and structural cells . 

Hypersensitivity pneumonitis can be caused by a variety of organic antigens, from coffee bean dust, to moldy sugarcane, to bacterial spores in the mist from hot tubs. The resulting disease is often named for the profession at risk. 

For instance, the most common type is Farmer’s lung, which is caused by breathing in the spores of actinomycetes that live in moist, newly harvested hay. 

Sugarcane farmers might also get bagassosis, from inhaling actinomycete spores in moldy bagasse, or sugarcane fiber. 

Malt worker’s lung is from Aspergillus spores from moldy barley. 

Humidifier or air conditioner lung is caused by inhaling the spores of actinomycetes that grow in the warm water reservoirs of these machines. 

Pigeon breeders lung is caused by breathing in proteins from bird poop or feathers, but other animal proteins, such as those from fur, can also cause the disease. 

When a person inhales an organic antigen, it travels down the trachea, into the bronchi and ends up in the lungs where they settle in the alveolus. There, it gets picked up by an alveolar macrophage which takes it to the nearest lymph node,

Inside the lymph node the macrophage it presents the antigen on its surface using a MHC class II molecule, which is basically a serving platter for CD4+ T cells]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Precocious_puberty</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oZKxhKPtQRqbr6UvUyvICFKMRhGLxSTl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Precocious puberty]]></video:title><video:description><![CDATA[Puberty is the time in an individual’s life when they physically become sexually mature and able to have children. Precocious refers to puberty occurring at an earlier age than the average age among an individual’s peers. Generally, puberty is considered precocious if it begins before the age of 8 in females and the age of 9 in males. 

The hypothalamic-pituitary-gonadal axis is a system of hormone signaling between the hypothalamus, pituitary gland, and gonads, either the testes or ovaries, to control sexual development and reproduction. Gonadotropin-releasing hormone is released by the hypothalamus into the hypophyseal portal system, which is a network of capillaries connecting the hypothalamus to the hypophysis, or pituitary.  When gonadotropin-releasing hormone reach the pituitary gland, it stimulates cells in the anterior pituitary, called gonadotrophs, to release gonadotropin hormones: luteinizing hormone and follicle-stimulating hormone into the blood. These gonadotropin hormones then stimulate the gonads to produce specific steroids, sex hormones.  

Beginning at puberty, the Leydig cells of the testes respond to the luteinizing hormone by converting more cholesterol into testosterone. In addition, the Sertoli cells of the testes respond to follicle-stimulating hormone by producing more sperm. The major sex specific hormones in women are estrogen and progesterone, and they are produced by the ovarian follicles that are scattered on the ovaries. Each ovarian follicle is made up of a ring of granulosa and theca cells surrounding a primary oocyte at its core. Beginning at puberty, theca cells respond to luteinizing hormone by producing androstenedione, an androgen. Then, the granulosa cells respond to follicle stimulating hormone by converting the androstenedione into estrogen and progesterone. 

Waves of estrogen and progesterone regulate monthly changes to the ovary stroma to promote egg maturation and ovulation, and changes to the uterine wall]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amnesia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eCBgFEScSj_bBe5uT6szlMRSTbaZVd5m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amnesia]]></video:title><video:description><![CDATA[In the movie The Bourne Identity, CIA assassin Jason Bourne tells his new acquaintance Marie Kreutz about washing up on shore, unconscious, with two bullets in his back. 

He tells her that he can’t remember anything that happened before regaining consciousness, saying: “No, I’m serious. I don’t know who I am, I don’t know where I’m going, none of it.” 

Jason Bourne has amnesia which refers to lacking memory.

Now, memory can be divided into two main types.

The first is implicit memory, also known as procedural memory. 

Procedural memory refers to replicating the sorts of skills you can perform automatically, without thinking much about it. 

For example, walking, riding a bike, or texting—anything that has become a habit. 

The second type of memory is explicit memory, also known as declarative memory. Declarative memory refers to retaining and recalling facts—the sort of stuff you need to win a trivia contest. 

These memories do take some degree of conscious effort to retrieve; when trying to remember things like, “How many countries start with the letter J?”, most of us need to stop and focus. 

You can think of procedural memory as “remembering how,” and declarative memory as “remembering what.” 

When we talk about amnesia, we really mean that some part of a person’s declarative memory, the “remembering what” part, has been affected.

Jason Bourne may not remember who he is, but he has no problem remembering how to speak foreign languages or how to fight. 

Now, the process of forming declarative memory can be broken down into four stages, each involving specific parts of the brain. 

The first stage is encoding, which occurs in the prefrontal cortex. 

Encoding begins as soon as you first sense something. 

Say you’re tasting a strawberry. Encoding would involve classifying the strawberry according to sweetness, size, color and texture. 

Think of encoding as a process of breaking down an experience into manageable parts for the rest of the brain]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-Hodgkin_lymphoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JnCWbqM8TDams9bB0e4UAVoRT1_egwcz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-Hodgkin lymphoma]]></video:title><video:description><![CDATA[The term non-Hodgkin lymphoma, sometimes called NHL, can be broken down. Lymph- refers to lymphocytes and oma- refers to a tumor. 

“Non-Hodgkin” refers to the absence of a key cell that’s seen in Hodgkin lymphoma, the  Reed-Sternberg cell.  

So, non-Hodgkin lymphoma is a tumor derived from lymphocytes - specifically B-cells and T-cells, which mainly live in the lymph nodes and move through the blood and lymphatic system. 

Now, B-cell development begins in the bone marrow, which is a primary lymphoid organ. That’s where young precursor B-cells mature into naive B-cells. 

The naive B cells then leave the bone marrow and circulate in the blood and eventually settle down in lymph nodes. 

Humans have hundreds of lymph nodes, scattered throughout the body, and they’re considered secondary lymphoid organs. 

Each lymph node has B-cells which group together in follicles in the cortex or outer part of the lymph node, along with T-cells in the paracortex just below the cortex. 

B-cells differentiate into plasma cells, which are found in the medulla or center of the lymph node. 

Plasma cells release antibodies or immunoglobulins. 

Antibodies bind to pathogens like viruses and bacteria, to help destroy or remove them. 

Various immune cells, including B-cells have surface proteins or markers that are called CD, short for cluster of differentiation, along with a number - like CD19 or CD21.

In fact, the combination of surface proteins that are on an immune cell works a bit like an ID card. 

Now, a B cell is activated when it encounters an antigen that binds just perfectly to its surface immunoglobulin. 

Some of these activated B-cells mature directly into plasma cells and produce IgM antibodies.

Other activated B-cells go to the center of a primary follicle in the lymph node and they differentiate into B-cells called centroblasts and start to proliferate or divide.

These proliferating centroblasts form a germinal center, located in the center of the follicl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Reactive_arthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vPjxyoSkQtygYXi0XCVqN8sUQCalMuEx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Reactive arthritis]]></video:title><video:description><![CDATA[Reactive arthritis, formerly known as Reiter’s syndrome, is inflammation of a joint which usually develops after an infection, and that infection is typically a sexually transmitted disease or gastroenteritis. Reactive arthritis is part of a group of diseases called seronegative spondyloarthropathies. Spondyloarthropathies are autoimmune, inflammatory joint diseases, and they’re seronegative, which refers to the fact that an auto-antibody called rheumatoid factor is absent from the blood.

Normally, the immune cells are ready to spot and destroy anything foreign that could cause the body harm. To help with this, most cells in the body have a set of proteins that combine together to form something called a major histocompatibility complex, or MHC, and this is a molecule that sits on the surface of their cell membrane. There are two kinds of MHC molecules, class I and class II. Class I molecules are found on most cells in the body, and they present molecules from within the cell for the immune system to continually sample. Normally the molecule’s just a sample from inside the cell, also known as a self-antigen. When immune cells pass by, they recognize this self-antigen as harmless so there’s no response. 

MHC class II molecules are found specifically on phagocytic cells like macrophages which destroy and digest foreign pathogens like bacteria. Once a macrophage destroys a bacterium, it presents a piece of that bacterium on its MHC class II receptor, and the macrophage then makes its way to the lymph node to find some T-lymphocytes. A type of T-lymphocyte, called a CD4+ T-cell, also known as a helper T-cell, uses its T-cell receptors to bind to the foreign antigen presented by the MHC class II molecule. If the helper T-cell binds strongly, the antigen is recognized as foreign, and the helper T-cell switches on the corresponding B-cell, so it can start producing a whole lot of antibodies. These antibodies bind to the specific pathogen, and typically prevent ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Puberty_and_Tanner_staging</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/voW2dbjGSryfjinGa2vCskraQ02PtqkV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Puberty and Tanner staging]]></video:title><video:description><![CDATA[A long time ago, in an uterus far, far away, there was a sexually undifferentiated embryo, that could develop into either a male or a female according to its sex chromosomes. 

During that time, most of its organs and systems took shape and started functioning. 

But one system - the reproductive system - developed and then waited for a trigger to kick into action.

Even though we’re born with differentiated, male or female, sex organs, it’s not until puberty that they fully mature. That’s when an individual becomes capable of reproduction.

Sexual maturation is under the control of the hypothalamic-pituitary-gonadal axis. 

The hypothalamic-pituitary-gonadal axis is a system of hormone signaling between the hypothalamus, pituitary gland, and gonads, either the testes or ovaries, to control sexual development and reproduction. 

Gonadotropin-releasing hormone, or GnRH is released into the hypophyseal portal system, which is a network of capillaries connecting the hypothalamus to the hypophysis - or pituitary. 

When gonadotropin-releasing hormone reach the anterior lobe of the pituitary gland, it stimulates cells called gonadotrophs, to release gonadotropin hormones: luteinizing hormone, or LH, and follicle-stimulating hormone, or FSH, into the blood. 

These gonadotropin hormones then stimulate the gonads to produce sex specific hormones - which are estrogen and progesterone in females, and testosterone in males. 

Now, the amount of hormone that gets produced by this axis varies over a person’s lifetime, and that affects the development of the sex organs, as well as the appearance of secondary sexual characteristics.

GnRH secretion begins during week 4 of intrauterine life - and the pituitary starts secreting FSH and LH between weeks 10 and 12 - but after a mid-pregnancy peak, levels of these hormones drop.

Once the baby is born, secretion of GnRH, FSH and LH continues, but the levels remain low throughout childhood, with the FSH level being higher tha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Migraine</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ROJaESknR12AtxQsvgViz2OlTiGhrlzw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Migraine]]></video:title><video:description><![CDATA[Migraine is a primary type of headache, meaning it happens on its own, not because of something like a head injury or tumor. The word “migraine” comes from Greek and means “half of the skull” because the pulsating pain often affects just one side of the head. 

Now, let’s take a moment to talk about pain. Imagine you’re trying to hit a nail with a hammer but accidentally smack your thumb instead. Special nerve cells called pain receptors immediately detect the hit and convert it into an electrical signal that travels up your spinal cord to your brain, which interprets the signal as pain. Interestingly, the brain itself doesn’t have pain receptors, so it doesn’t actually feel pain. So, when you have a headache, it’s not the brain that hurts, it’s the structures around it, like the venous sinuses and the meninges, especially the dura mater. 

Now, the innervation of these structures comes from the trigeminal ganglion, which sends C fibers and A-delta fibers along the trigeminal nerve, particularly the ophthalmic branch. Together, these fibers form part of the trigeminovascular system, which connects the trigeminal nerve to the blood vessels and meninges.  

When this system is activated, the C fibers release calcitonin gene-related peptide, or CGRP, a key chemical involved in pain signaling and inflammation. Interestingly, CGRP receptors are located on A-delta fibers, allowing local cross-talk between these fibers.  

When CGRP binds to receptors on nearby A-delta fibers, it makes them more responsive to stimuli, enhancing the transmission of pain signals. 

While the exact cause of migraine remains a mystery, we think that the trigeminovascular system and CGRP play a major role. During a migraine episode, C fibers release CGRP, stimulating CGRP receptors on A-delta fibers and vascular smooth muscle cells of the dura mater. Eventually, this leads to vasodilation and promotes neurogenic inflammation, contributing to migraine pain.  

Also, migraines tend to r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acoustic_neuroma_(schwannoma)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BwS5L2gFRO_yvgL0dDEP_WsiRDurnYm5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acoustic neuroma (schwannoma)]]></video:title><video:description><![CDATA[Schwannoma, sometimes called neurilemmoma, is a tumor that develops from Schwann cells. 

Schwann cells belong to a category of cells called glial cells, which surround and support the neurons of the nervous system, and get their name from Theodor Schwann, a nineteenth-century physicist who first discovered them. 

Neurons are made up of three main parts. 

The dendrites, which are little branches off of the neuron that receive signals, which is essentially an electrical impulse, from other neurons; the soma, or cell body, which has all of the neuron’s main organelles like the nucleus; and the long axon, which transmits the signal to the next neuron in the series. 

In the peripheral nervous system, Schwann cells synthesize a fatty substance made of lipoproteins called myelin, which forms insulating sheaths at along parts of the axon. 

The myelin sheath plays an important role in conducting electrical impulses or action potentials.

Action potentials propagate along the axon when sodium ions move into the cell through ion channels.

In sections with a myelin sheath, there are no ion channels, but sections in between, called nodes of Ranvier, have a ton of ion channels. 

The action potential therefore doesn’t have to move along each section of the neuron, but rather from node to node, resulting in super fast saltatory conduction. 

Also, the Schwann cells express a gene called neurofibromin 2, or NF2, which encodes a protein called merlin. 

In schwann cells, merlin acts as a tumor suppressor, meaning it prevents the Schwann cells from dividing uncontrollably. 

And that’s exactly what happens with a schwannoma, the schwann cells start dividing uncontrollably.

No one knows what causes most schwannomas from developing. The majority of schwannomas are solitary tumors of Schwann cells which are found around peripheral nerves. 

They are usually benign meaning that the cells don’t invade surrounding tissue structures, and schwannomas therefore don’t metastas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pressure-volume_loops</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jw3_rfMKRneTG4Pd8AKo91Q4RuKQFbCD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pressure-volume loops]]></video:title><video:description><![CDATA[Pressure- volume loops are graphs, where the pressure inside the left ventricle is on the y axis and the volume of the left ventricle is on the x axis. Each loop represents one cardiac cycle, including both ventricular systole and diastole, or more simply, one heartbeat.

Alright, let’s start at the lower right hand corner. This is the end-diastolic point, and it’s the point in the cardiac cycle when diastole is over. The mitral valve, or the “communicating door” between the left atrium and left ventricle has just closed. And as it closed, it made a loud, long sound, kind of like a “lup”. That’s known as the first heart sound, or S1. So, at this point, the left ventricle is filled with the maximum volume of blood, known as end- diastolic volume, which is normally about 120 milliliters. You can imagine the ventricle as a relaxed sack of muscle that’s full of blood, so pressure is low. After that, the left ventricle contracts, and that marks the beginning of systole. This makes the pressure shoot up, but since both mitral and aortic valves are closed, blood can neither enter nor leave the ventricle, the volume doesn’t change. This phase is called isovolumetric contraction and it lasts for about 0.05 seconds. Eventually the pressure inside the left ventricle reaches approximately 75 mmHg, becoming just higher than the pressure inside the aorta, forcing the aortic valve to pop open. This pressure reflects the pressure in the aorta right at the beginning of ejection phase, or the lowest that the blood pressure in the aorta is going to be and is known as the diastolic blood pressure, or DBP for short.

Okay, now, once the ejection phase starts, it lasts for about 0.25 seconds. That’s when blood is ejected out of the left ventricle and into the aorta, decreasing left ventricular volume. The left ventricle continues to contract, so ventricular pressure keeps rises further. Meanwhile, blood is rushing through the aorta, so its pressure increases, as well. In fact, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ataxia-telangiectasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v0ojQ1G7RMql-OOS8kJ2Tk2qQ7Ck94u3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ataxia-telangiectasia]]></video:title><video:description><![CDATA[With ataxia telangiectasia, ataxia refers to poor coordination and telangiectasia refers to dilated blood vessels, which are the two key symptoms of this disease. 

Ataxia telangiectasia develops when a genetic mutation causes the lack of a protein called ataxia telangiectasia mutated serine-threonine kinase, or just ATM for short, which normally fixes up damaged DNA.

DNA of every cell gets damaged over and over again from various environmental factors like radiation and chemical toxins. 

Now, one of the most severe types DNA damage is a double-strand break, where both strands of the DNA’s double helix are severed, damaging the genetic information that was stored there. To help with this sort of repair, there’s a protein called ATM.  

ATM is primarily located in the cell&amp;#39;s nucleus, and you can sort of think of ATM as like a manager of the DNA’s repair.

It’s protein kinase, which means that it uses it’s managing skills to activate other proteins through phosphorylation, which is the addition of a phosphoryl or -PO32−  group. 

So at the site of the double strand break, ATM phosphorylates proteins like the tumor suppressor protein p53, that stop the cell from reproducing. 

ATM also phosphorylates additional proteins which will either fix the DNA or kill the faulty cell through a process of apoptosis - controlled cell death. This way we don&amp;#39;t end up with a bunch of defective cells trying to reproduce. 

That&amp;#39;s the main role of ATM, but it also plays a role in the development of immune cells, especially T lymphocytes. 

T lymphocytes need to be able to recognize a wide variety of antigens, and to do this, they purposefully create double strand breaks in their DNA during development. That way parts of their DNA can get rearranged, and code for new and unique antigen receptors. 

Once again, ATM helps to fix these breaks - and that keeps the T-cells functioning normally. 

In ataxia telangiectasia, there&amp;#39;s an au]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_endocrine_neoplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gTZ6XUG5QLWZqvFNnlR9ARwYRpiCaF-U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple endocrine neoplasia]]></video:title><video:description><![CDATA[The multiple endocrine neoplasias, or MEN for short, are a group of inherited diseases which cause tumors to grow in the endocrine glands of the body. 

The endocrine glands affected in multiple endocrine neoplasia are the pituitary gland, the thyroid gland, the parathyroid glands, the adrenal glands and the pancreas.

So in multiple endocrine neoplasias there are tumors that form in these glands that lead to overproduction of hormones. 

Let’s start by going through the glands that are affected and what they do. 

The pituitary gland is a pea-sized gland found at the base of the brain that makes hormones to control many of the other endocrine glands in the body. 

These hormones include thyroid stimulating hormone which acts on the thyroid to make thyroid hormone, adrenal corticotropic hormone that acts on the adrenal glands to make cortisol, follicle stimulating hormone and luteinizing hormone which acts on the ovaries and testes to make estrogen in women and testosterone in men. 

So it’s like the king of the endocrine glands telling them how much hormone to produce. 

The pituitary also makes growth hormone which makes you grow, prolactin which stimulates milk production in women, oxytocin which triggers milk release, antidiuretic hormone which help the kidneys reabsorb water, and melanocyte stimulating hormone helps the melanocytes create more melanin or pigment. 

Next, in the neck is the thyroid gland which makes thyroid hormones that control the metabolic rate, as well as calcitonin, a hormone that decreases calcium levels. 

Within the thyroid gland, are buried four parathyroid glands which make parathyroid hormone which increases calcium levels.

Lower down, there are the adrenal glands which sit just above each kidney and produce epinephrine and norepinephrine which are fight or flight hormones that increase cardiac output, dilate the pupils, and increase blood flow to the muscles.

Finally, there’s the pancreas which makes insulin to help lower]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_renal_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wg0wwitqTiqzMaj9_Wa3ns_YS8uWHR4u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the renal system]]></video:title><video:description><![CDATA[The renal system starts developing during week 4 of intrauterine life. 

At this point, the embryo is made up of three primitive germ layers: the ectoderm, the mesoderm and the endoderm. 

The mesoderm also has three parts: the paraxial mesoderm, which flanks the embryo’s future vertebral column; the intermediate mesoderm, which is just lateral to the paraxial mesoderm; and the lateral plate mesoderm, which is the most lateral of all.  

The intermediate mesoderm on either side of the embryo condenses to form a cylindrical structure called the urogenital ridge. 

This ridge runs parallel to the embryo’s future vertebral column, and it gives rise to both the urinary and genital systems. 

The portion of the urogenital ridge called the nephrogenic cord develops into the urinary structures. 

Now, during the development of the urinary system, there are three sets of structures that emerge from the nephrogenic cord, and they form in a craniocaudal fashion—from head to tail-end. 

The first structure to emerge from the nephrogenic cord is the pronephros, which appears in the neck region of the embryo at the beginning of week 4. 

The pronephros consists of the pronephric duct and the nephrotomes in front of it. 

The pronephric duct is basically a pipe that runs down the length of the nephrogenic cord, and the nephrotomes are small chunks of tissue that break off from the nephrogenic cord. 

However, the pronephros doesn’t produce urine, and regresses by the end of week 4. 

Before the pronephros completely disappears, a second set of structures called the mesonephros appears in the thoracic and upper lumbar region of the nephrogenic cord. 

The mesonephros has a mesonephric duct and mesonephric tubules in front of it. 

The mesonephric duct develops off of the pronephric duct, making it longer so that it reaches all the way to the cloaca, which is the last part of the primitive digestive tract. 

So for a short while, the urinary and digestive system share a c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Changes_in_pressure-volume_loops</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n3TRSQnURkeXLgxWGspXzxZvQNyyRXNW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Changes in pressure-volume loops]]></video:title><video:description><![CDATA[Pressure- volume loops are graphs, where the pressure inside the left ventricle is on the y axis and the volume of the left ventricle is on the x axis. Each loop represents one cardiac cycle, including both ventricular systole and diastole, or more simply, one heartbeat.

The lower right hand corner is the end-diastolic point, and it’s the point in the cardiac cycle when diastole is over. Αt this point, the mitral valve is closed and the left ventricle is filled with the maximum volume of blood, known as end-diastolic volume. After that, the left ventricle contracts, and systole begins. This makes the pressure shoot up, but since both mitral and aortic valves are closed, the left ventricular volume doesn’t change. This phase is isovolumetric contraction. Eventually the pressure inside the left ventricle exceeds aortic pressure, forcing the aortic valve to pop open, and that starts the ejection phase. Blood leaves the left ventricle and goes into the aorta, decreasing left ventricular volume. The left ventricle continues to contract, so ventricular pressure keeps rises further, but then falls slightly and finally the aortic valve shuts when aortic pressure exceeds the left ventricular pressure. That point, called the end-systolic point, marks the end of systole. At this point, left ventricular pressure is called end-systolic pressure, and left ventricular volume is called end-systolic volume. The difference between end-diastolic volume and end-systolic volume, is the stroke volume. After that, the left ventricular muscle starts relaxing, so left ventricular pressure falls. However, all valves are closed, so the volume remains constant. This phase is isovolumetric relaxation. Eventually, the pressure drops below left atrial pressure, and that allows the mitral valve to open and blood to flow from the left atrium flows into the left ventricle. As the left ventricle fills with blood, its volume rises back to its end-diastolic volume, and the pressure increases]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Estrogen_and_progesterone</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-R2QHIVNTQqxmUBvoEkguD4cSciE7cgn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Estrogen and progesterone]]></video:title><video:description><![CDATA[Estrogen and progesterone are the female sex hormones, and they’re produced mainly by the ovaries - the female gonads. 

The female body can synthesize 3 types of estrogens: estradiol, estrone and estriol. 

Of the three, the ovaries synthesize estradiol, which is the most biologically active of them all, and accounts for the majority of sex-specific changes that begin in puberty - like monthly ovulation and menstruation as well as the development of the secondary sex characteristics. 

Small amounts of estrogen are also produced by the adrenal cortex and fat cells in adipose tissue, and the placenta secretes these hormones during pregnancy, as well. 

But during the reproductive period, it’s the ovaries that produce the majority of estrogen and progesterone in the female body. 

Before puberty, the hypothalamus secretes small amounts of a hormone called gonadotropin-releasing hormone, or GnRH. 

That GnRH travels to the nearby pituitary, which secretes two hormones of its own - follicle stimulating hormone, or FSH, and luteinizing hormone, or LH. 

Once puberty hits, the hypothalamus starts to secrete GnRH in pulses, sometimes more and sometimes less, and FSH and LH make the ovarian follicles develop and secrete hormones. 

The ovarian follicles are scattered throughout the ovaries, and each ovarian follicle is made up of a ring of follicular cells surrounding a primary oocyte at its core.  

As the ovarian follicles develop, the follicular cells differentiate into theca cells and granulosa cells, which both play a role in the synthesis of progesterone and estrogen. 

How much of these hormones is secreted is directly related to the phases of the female menstrual cycle. 

The menstrual cycle lasts 28 days on average, and it’s centered around a surge of FSH and LH happening on day 14 - which makes ovulation possible. 

The variations in FSH and LH levels result in fluctuating levels of estrogen and progesterone that vary according to the phases of the mens]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_tamponade</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FmPYr5i0TomY9ttIHlSCpgaBQhyd8rAc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac tamponade]]></video:title><video:description><![CDATA[The name “cardiac tamponade” can be broken down: “tamponade” refers to pressure which obstructs blood flow, and “cardiac” refers to the heart. So in cardiac tamponade there’s a buildup of fluid in the pericardium, and that fluid puts pressure on the outside of the heart. As a result, the heart is unable to pump normally and blood flow is obstructed.  

Normally, the heart sits inside a two-layered pouch or cavity called the pericardium. The outer layer is the fibrous pericardium, which helps keep the heart in place within the chest cavity. The inner layer of the pouch is the serous pericardium, which includes the pericardial cavity; it’s filled with a small amount of fluid that lets the heart slip around as it beats. The cells of the serous pericardium secrete and reabsorb the fluid, so usually there’s no more than 50 milliliters of fluid in the pericardial cavity at any time—that’s about as much as would fit into a shot glass.

A pericardial effusion happens when this normally protective fluid begins to pool in the pericardial space. It can develop into cardiac tamponade depending on how much fluid there is and how quickly that fluid accumulates. 

A rapid accumulation of fluid can occur as a result of trauma to the chest. For example, a stab wound can puncture a blood vessel and fill the pericardium with blood. Even blunt trauma like a steering wheel getting pushed into your chest during a car crash can lead to tamponade, because the force of the impact causes the rupture of lots of small blood vessels. Cardiac tamponade can also happen a few days after a myocardial infarction, because the weak, infarcted ventricular wall ruptures when it’s exposed to the high ventricular pressures. It’s a bit like how jeans might tear at the spot where the denim is worn away and already quite weak. A rare cause is heart surgery, where, once again, a weakened muscle can rupture and cause cardiac tamponade days after the operation. Yet another cause is aortic dissection, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gigantism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sl2a1NY-RSGG7y4JQiKGDVDDRFKg1epG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gigantism]]></video:title><video:description><![CDATA[With gigantism, “gigant” refers to giant, so gigantism is a rare hormonal disorder in children and adolescents where there is an excess of growth hormone, and it causes rapid and excessive growth of long bones, like the tibia and humerus. 

As an example, the French wrestler André the Giant who played Fezzik in the movie The Princess Bride had gigantism. 

In adults, excess growth hormone causes a different disorder, called acromegaly, because their long bones have stopped growing.

Let’s start with how growth hormone, or somatotropin, is made. 

Normally, the hypothalamus which is at the base of the brain, secretes growth hormone-releasing hormone in bursts throughout the day - every couple hours, and this can increase based on things like low blood glucose levels, lack of food, increased exercise, increased sleep, and increased stress like trauma.

The growth hormone-releasing hormone goes into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary which is smaller in size than a pea. 

The growth hormone-releasing hormone binds to a surface protein on somatotroph and mammosomatotroph cells of the anterior pituitary gland, and in response, they release growth hormone. 

Now, growth hormone affects lots of tissues directly and indirectly throughout the body. 

Direct effects occur in certain tissues where growth hormone stimulates cellular metabolism and leads to organ growth. 

The liver releases more glucose into the blood, the body retains nitrogen leading to more muscle growth, and osteoblasts get stimulated which causes the bones to thicken. 

Another direct effect of growth hormone is to increase insulin resistance - making it harder for cells to take in glucose - which leads to an increase in blood insulin levels.

Because it is like what happens in individuals with diabetes, this effect of growth hormone is called diabetogenic. 

An important indirect effect, is that growth hormone stim]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mesothelioma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eiAxXfH6Qh2giLK0Mq-BE2n5Tq2i9vu_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mesothelioma]]></video:title><video:description><![CDATA[Mesothelioma is an aggressive cancer that attacks the mesothelium, which is a thin membrane made of epithelial cells that lines all of the body’s organs as well as body spaces like the thoracic cavity and abdominal cavity. 

Mesothelioma most often develops in the lining of the lungs and pleural cavity, and is well known for its association with the carcinogen asbestos.

In fact, the late Hollywood actor Steve McQueen is well-known for having developed mesothelioma after years of asbestos exposure while in the military.

The vast majority of mesothelioma cases stem from asbestos exposure. 

Asbestos is a mineral that was widely used as construction material in everything from paint to insulation to roofing tiles because it has strong fibers that were resistant to fire and served as good insulation. 

Asbestos fibers are jagged in shape, and extremely tiny - about 500 times finer than a human hair. 

If those tiny asbestos fibers get inhaled over time, they make their way into the interstitial space of the lungs and then slowly make their way over to the epithelial cells of the visceral or parietal pleura - both of which are layers of mesothelium. 

The microscopic, jagged asbestos fibers are so small that they can get tangled up with the cell’s chromosomes. 

At that point, they can damage the DNA causing a variety of mutations, which ultimately allow those epithelial cells to divide uncontrollably, turning into a tumor. 

Over time, small cancerous growths called mesothelial plaques start to cover the visceral pleura over the lungs and the parietal pleural under the chest wall. 

Interestingly, these growths start to express a lot of calretinin, a calcium-binding protein, involved in regulating calcium levels within the cell - this is something that helps to distinguish mesotheliomas from other types of tumors.

In addition to affecting the lungs and pleural lining, asbestos fibers can also end up in the stomach if saliva containing the material or mucus from the airways is swallowed.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Riedel_thyroiditis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hm4k32W4SWuXi9VhUnBbv7_BQAWnnfnE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Riedel thyroiditis]]></video:title><video:description><![CDATA[With Riedel’s thyroiditis, thyroid- refers to the thyroid gland, and -itis means inflammation. So, Riedel’s thyroiditis is a condition where there is inflammation of the thyroid gland, which slowly causes fibrous tissue to replace the normal thyroid tissue. The condition is named after the German surgeon - Dr. Bernhard Moritz Carl Ludwig Riedel - who first described it.

Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, known as ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary gland. The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, thyrotropin, or simply TSH. 

TSH stimulates the thyroid gland, which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”. If we zoom into the thyroid gland, we’ll find thousands of follicles, which are small, hollow spheres whose walls are lined with follicular cells and are separated by a small amount of connective tissue. Follicular cells convert thyroglobulin, a protein found in follicles into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins, but only a small amount of T3 and T4 will travel unbound in the blood and these two hormones get picked up by nearly every cell in the body.

Once inside the cell, T4 is mostly converted into T3, and then it can exert its effect. T3 speeds up the basal metabolic rate. So as an example, they might produce more proteins and burn up more energy in the form of fats and sugars. It’s as if the cells are in a bit of a frenzy.

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.

Th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Delayed_puberty</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iKeOejgFSfKQDvOE1K3fPLG6TNqi5n1z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Delayed puberty]]></video:title><video:description><![CDATA[Puberty is the time in an individual’s life when they physically become sexually mature and able to have children. Generally speaking, it’s considered delayed if puberty hasn’t started for a female by age 13 and for a male by age 14.

The hypothalamic (HYpo-tha-lamb-ic)-pituitary-gonadal (Go-nad-al) axis is a system of hormonal signaling between the hypothalamus, pituitary gland, and gonads, the gonads are either the testes or the ovaries, and this will control sexual development and reproduction. Gonadotropin (Go-nad-ah-tro-pin) -releasing hormone is released into the hypophyseal (high-poth-ah-see-al) portal system, which is a network of capillaries connecting the hypothalamus to the hypophysis (high-pof-o-sis), or pituitary.  When gonadotropin(Go-nad-ah-tro-pin) -releasing hormone reach the pituitary gland, it stimulates cells in the anterior pituitary, called gonadotrophs (Go-nad-a-trofs), to release gonadotropin hormones: luteinizing hormone and follicle-stimulating hormone which then enter the blood. These gonadotropin hormones then stimulate the gonads to produce sex specific hormones. These are estrogen and progesterone in females and testosterone is the major sex specific hormone in males. 

Early on in male development, testosterone helps the external sex organs to differentiate into male genitals and causes the testes to descend from the abdomen into the scrotal sac. Beginning at puberty, the Leydig cells of the testes respond to the luteinizing hormone by converting more cholesterol into testosterone. In addition, the Sertoli cells of the testes respond to follicle-stimulating hormone by producing more sperm. The major sex specific hormones in women are estrogen and progesterone, and they are produced by the ovarian follicles that are scattered on the ovaries. Each ovarian follicle is made up of a ring of granulosa and theca cells surrounding a primary oocyte at its core. Beginning at puberty, theca cells respond to luteinizing hormone by produc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Candida</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TPJ8py5GTCaS-gjxdFXgTHGqSJGusalD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Candida]]></video:title><video:description><![CDATA[Candida is a yeast, not the maple syrup-loving country in North America - although Candida can be found in Canada as well! 

Candida sometimes causes a mild yeast infection, but in some situations, can get into the bloodstream and cause severe illness.

Now, there are various types of Candida species, and over twenty of them cause disease in humans - C. albicans, C. parapsilosis, C. tropicalis, C. glabrata, C. krusei, C. auris, the list goes on.

Of these, the most common one is C. albicans. Candida is found throughout the body; it likes warm, moist environments like the mouth, the diaper region of babies, and in women it can be found in the vagina. 

Now, it’s normal for microbes - bacteria, fungi, and viruses - to live all over the body, but each microbe is slightly different in terms of whether it’s colonizing the body - in other words just living and not causing any problems, or whether it’s infecting the body, causing some degree of tissue damage or destruction. 

An important factor is exactly how much of a microbe is present. 

Candida is considered an opportunistic microbe. 

When the amount of Candida is relatively low, it&amp;#39;s harmless. 

But if a person’s immune system is weakened or if there’s less competition for the Candida, then the amount of Candida can increase - and that’s called Candida overgrowth. 

Now, Candida can exist in multiple forms - it’s a bit like a chameleon. 

Sometimes the cells can appear round or oval and these are called yeast cells, other times it can appear like hyphae where it looks like long thin filaments - kind of like a segmented cactus plant. 

It can also take an in-between appearance called pseudohyphae. 

Each of these morphologies or “looks” reflect the same Candida cells that are expressing different protein profiles, and they give the cells different properties. 

When the Candida is in “yeast mode” it’s better at moving from one part of the body to another, whereas when it’s in “filamentous mode” it’]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rheumatoid_arthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QWQXkLJJRYKSvcCae9XOoc-1RKqNbcX8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rheumatoid arthritis]]></video:title><video:description><![CDATA[In rheumatoid arthritis, “arthr-“ refers to joints, “-itis” means inflammation, and “rheumatoid” comes from rheumatism, which more broadly refers to a musculoskeletal illness. 

So, rheumatoid arthritis is a chronic, inflammatory disorder that mostly affects the joints, but can also involve other organ systems like the skin and lungs as well.

Alright, so a healthy joint typically has two bones covered with articular cartilage at the ends. 

Articular cartilage is a type of connective tissue that acts like a protective cushion - a lubricated surface for bones to smoothly glide against. 

One type of joint, like the knee joint is called a synovial joint. 

A synovial joint connects two bones with a fibrous joint capsule that is continuous with the periosteum or outer layer of both bones. 

The fibrous capsule is lined with a synovial membrane that has cells that produce synovial fluid and remove debris. 

The synovial fluid is normally a viscous fluid like the jelly-like part of a chicken egg and it helps lubricate the joint. 

To help serve these synovial cells, the synovial membrane also has blood vessels and lymphatics running through it.

Together, the synovial membrane and the articular cartilage form the inner lining of the joint space.  

Rheumatoid arthritis is an autoimmune process that is typically triggered by an interaction between a genetic factor and the environment. 

For example, a person with a certain gene for an immune protein like human leukocyte antigen, or HLA- DR1 and HLA–DR4, might develop rheumatoid arthritis after getting exposed to something in the environment like cigarette smoke or a specific pathogen like a bacteria that lives in the intestines. 

These environmental factors can cause modification of our own antigens, such as IgG antibodies or other proteins like type II collagen or vimentin.

Τype II collagen and vimentin can get modified through a process called citrullination. 

That’s when  the amino acid arginine found in ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_respiratory_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mLqm4IbFTcKfxyRRkj88CVufTNOEG0UF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the respiratory system]]></video:title><video:description><![CDATA[The respiratory system starts developing during week 4 of intrauterine life, and it begins when a lung bud sprouts out of the primitive digestive tract. 

The lung bud is an outgrowth of the foregut portion of the digestive tract, and it turns into lower respiratory tract structures such as the larynx, trachea, and lungs. 

Around week 4, the embryo has developed all three embryonic germ layers, and of the three, respiratory tract structures arise from the endoderm and mesoderm. 

The larynx starts developing at the beginning of week 4, as nothing more than a slit between the fourth and the sixth pharyngeal arches. 

The pharyngeal arches are paired, symmetrical embryonic structures that sprout from the foregut and arch towards the embryo’s front midline. 

They consist of a mesoderm core and that mesoderm is made up mostly of mesenchyme—a soupy, fetal tissue that eventually turns into circulatory tissue, lymphatic tissue, and musculoskeletal tissue. 

The arches are covered on the outside by the pharyngeal cleft, which is made of ectoderm, and lined on the inside with the pharyngeal pouch, which is made of endoderm. 

In fish, these arches develop into gills, but in our case they serve as a foundation for many important structures around the head and neck. 

The endoderm of the 4th and 6th pharyngeal arches forms the laryngeal epithelium and glands, and the mesoderm forms the laryngeal cartilages, while the arches themselves carry the laryngeal branches of the vagus nerve to these structures. 

All in all, these two arches give us our ability to talk. Doesn’t beat breathing under water, but still pretty cool, right? 

In week 5, a laryngeal orifice forms, which is a T-shaped opening that leads to the larynx. 

The epithelium inside the larynx turns into laryngeal ventricles, which give rise to the vocal cords.

In week 6, the epiglottis forms, and in week 12 the laryngeal opening has its adult shape, as well as thyroid, cricoid, and arytenoid cartilages. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Euthyroid_sick_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xiaBOp9XSEqhFCu89d5lyUQ4TxmtSE-b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Euthyroid sick syndrome]]></video:title><video:description><![CDATA[The term euthyroid sick syndrome, also known as nonthyroidal illness syndrome, can be broken down. Eu- refers to good and -thyroid refers to the thyroid gland which produces thyroid hormones. 

So, euthyroid sick syndrome is a state where the thyroid gland is functioning normally, but the thyroid hormones are at abnormal levels. 

Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, known as ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary. 

The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, thyrotropin or simply TSH. 

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”. 

If we zoom into the thyroid gland, we’ll find thousands of follicles, which are small hollow spheres whose walls are lined with follicular cells, and are separated by a small amount of connective tissue. 

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4. 

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body. 

Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate.

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy. 

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response. 

Thyroid hormone is important - and the occasiona]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Menstrual_cycle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LB-BZoDKRC_cXKNjLiGYkP8LTL6W4KuV/_.png</video:thumbnail_loc><video:title><![CDATA[Menstrual cycle]]></video:title><video:description><![CDATA[The menstrual cycle refers to the regular changes in the activity of the ovaries and the endometrium that make reproduction possible. 

The endometrium is the layer of tissue lining the inside of the uterus. 

This lining consists of a functional layer, which is subject to hormonal changes and is shed during menstruation, and a thin basal layer which feeds the overlying functional layer. 

The menstrual cycle actually consists of two interconnected and synchronized processes: the ovarian cycle, which centers on the development of the ovarian follicles and ovulation, and the uterine or endometrial cycle, which centers on the way in which the functional endometrium thickens and sheds in response to ovarian activity. 

Menarche, which refers to the onset of the first menstrual period, usually occurs during early adolescence as part of puberty. 

Following menarche, the menstrual cycle recurs on a monthly basis, pausing only during pregnancy, until a person reaches menopause, when her ovarian function declines and she stops having menstrual periods. 

The monthly menstrual cycle can vary in duration from 20 to 35 days, with an average of 28 days. 

Each menstrual cycle begins on the first day of menstruation, and this is referred to as day one of the cycle. 

Ovulation, or the release of the oocyte from the ovary, usually occurs 14 days before the first day of menstruation (i.e., 14 days before the next cycle begins). 

So, for an average 28-day menstrual cycle, this means that there are usually 14 days leading up to ovulation (i.e., the preovulatory phase) and 14 days following ovulation (i.e., the postovulatory phase). 

During these two phases, the ovaries and the endometrium each undergo their own set of changes, which are separate but related. 

As a result, each phase of the menstrual cycle has two different names to describe these two different parallel processes. 

For the ovary, the two weeks leading up to ovulation is called the ovarian follicular ph]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuroblastoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K9FyAQI4TduSzuc65YJ6TMY9RRqCho6I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuroblastoma]]></video:title><video:description><![CDATA[Neuroblastoma is a type of tumor composed of “neuroblasts,” specifically neural crest cells, which are cells involved in the development of the sympathetic nervous system. 

Neuroblastoma is the most common cancer in infants, and it’s only rarely seen in children over five years old. 

When a fetus is in its 5th week of development, special cells called neural crest cells start migrating along the spine. 

In the thoracic region of the spine, neural crest cells differentiate into the neurons of the sympathetic chain, lying on either side of the entire spinal cord.

In the lumbar region, neural crest cells differentiate into the cells of the adrenal medulla, the inner part of the adrenal gland that sits atop the kidneys. 

Together, the sympathetic chain and adrenal medulla form the sympathetic nervous system, connecting the brain and central nervous system to various organs including the heart and blood vessels. 

So, when you’re under some sort of stress, like playing a competitive sport like badminton, the sympathetic nervous system kicks into action. 

The sympathetic neurons releases norepinephrine, also called noradrenaline, and the cells of the adrenal medulla release norepinephrine and epinephrine, also called adrenaline. 

These hormones bind to receptors in various tissues like the blood vessels, the heart, and the lungs, redirecting blood flow to your muscles, make your heart pump faster, and expanding the airways in your lungs, all of which can help you make the winning hit. 

After the game is over, and the hormones are no longer needed, epinephrine and norepinephrine break down into metabolites like homovanillic acid or HMA, and vanillylmandelic acid, or VMA. 

In neuroblastoma, some neural crest cells in the sympathetic chain or adrenal medulla don’t differentiate properly during fetal development, and these cells ultimately go on to form a tumor, which most often form in the adrenal medulla, but can also develop in other areas of the sympath]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_conduction_velocity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uNmAlsGrT8OukPrMgJsUWOXQTp2_x-1j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac conduction velocity]]></video:title><video:description><![CDATA[Cardiac conduction velocity is the velocity at which a depolarization wave moves through the myocardium, the muscular middle layer of the heart, and it’s measured in meters per second. 

The depolarization wave travels through the sinoatrial node, or SA node, through both atria, down the atrioventricular or AV node, through the Bundle of His and the Purkinje fibers, and finally to all of the parts of the ventricles, all in about 220 milliseconds, which is less than a quarter of a second!

If we zoom in on the myocardium, the depolarization waves move across neighboring cells. It moves from one cell to the next when ions like calcium and sodium slip through gap junctions and trigger voltage-gated sodium channels in that cell over to open up, allowing a rush of more sodium into the cell and causing an action potential to occur. 

That then results in more sodium and calcium leaking through to the next cell, triggering an action potential, which goes on to the next, and so on. 

Ultimately these cellular processes determine how fast or slow a depolarization wave will move across different types of tissues. 

More sodium channels and gap junctions speed up the depolarization wave, Fewer gap junctions and fewer sodium channels slow down the depolarization wave.

Alright so let’s break down the conduction velocities in the different parts of the heart, starting at the SA node,i the depolarization wave moves through the myocytes in the atria at about 1 meter per second, then goes through the AV node really slowly, roughly between 0.01 and 0.05 meters per second. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Waterhouse-Friderichsen_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sqF8ZPjISTK0Q_Vx-og2n2a_RjSLtTVW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Waterhouse-Friderichsen syndrome]]></video:title><video:description><![CDATA[Waterhouse-Friderichsen syndrome occurs when the blood vessels in the adrenal gland rupture during a severe bacterial infection, turning the adrenal glands into sacks of blood. 

This results in adrenal crisis, or acute adrenal insufficiency, which is when the adrenal gland suddenly stops producing hormones.

The syndrome is named after two physicians - Waterhouse and Friderichsen who separately described the syndrome back in the early 1900’s.

Now, there are two adrenal glands, one above each kidney, and each one has an inner layer called the medulla and an outer layer called the cortex. 

The adrenal cortex is subdivided into three more layers, the zona glomerulosa, zona fasciculata, and the zona reticularis. 

The adrenal cortex secretes hormones under the control of adrenocorticotropic hormone, released by pituitary gland. 

The outermost layer is the zona glomerulosa, which makes the hormone aldosterone.

Aldosterone acts on the nephrons of the kidney, and decrease potassium levels, increase sodium levels, and increase blood volume and blood pressure. 

The middle layer is the zona fasciculata, which makes the hormone cortisol, as well as other glucocorticoids. 

The main job of glucocorticoid is to increase blood glucose levels, especially when there’s emotional and physical stress. 

Finally, the innermost layer is the zona reticularis, which makes a group of sex hormones called androgens.

In men, androgen stimulates development of male reproductive tissues and secondary sex characteristics like facial hair and a large Adam’s apple. 

In women, androgen causes a growth spurt, and growth of underarm and pubic hair during puberty. 

The adrenal gland gets blood through three main arteries- the superior, middle, and inferior suprarenal arteries. 

All three divide into branches that supply the adrenal cortex and the adrenal medulla. 

After delivering oxygen to those tissues, the blood starts to collect again in the medullary vein and eventually into ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Buffering_and_Henderson-Hasselbalch_equation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LhZTcYIkS_OhBFPk_4gx81t_TqCfj_qK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Buffering and Henderson-Hasselbalch equation]]></video:title><video:description><![CDATA[Every single moment, there are trillions of biochemical reactions occurring throughout the human body that are mediated by enzymes. Enzymes are types of proteins, and they’re generally sensitive to even slight changes in the environment - in particular things like the hydrogen ion concentration.

For this reason, the blood pH which corresponds to the hydrogen ion concentration needs to stay in a very narrow range---between 7.37 and 7.42. 

If the blood pH rises or falls by more than a few tenths of a unit, it can lead to death. 

Now, acids and bases are generated by cells all the time. So, the body has a few mechanisms to deal with these molecules and keep blood pH within normal range. 

The first scientist who studied one of these mechanisms was Robert Pitts. 

Pitts injected 150 mEq of hydrochloric acid HCl into his dog. 

He calculated this his dog’s body contained a total 11.4 liters of water, so separately, Pitts put 150mEq of hydrochloric acid HCl in a volume of 11.4 liters of water. 

The dog’s blood pH dropped from 7.44 to 7.14, which is very low, but not fatal. 

In the water, the pH dropped from 7 to 1.84, and that would have killed the dog instantly. 

Based on this, Pitts concluded that his dog had a buffer contained in its body fluids, and the dog concluded that he could no longer trust Pitts to take care of him.

Physiologic buffers shield the pH from rising or falling too quickly. 

The reason the body needs buffers is that acids - molecules that readily give up their hydrogen ion - are being generated by the body all the time.

So the body needs a way to handle the extra hydrogen ions that are released without having a major shift in the overall pH.

To accomplish this, buffers are usually a weak acid with its conjugate base form, or a weak base with its conjugate acid form. 

The weak acid could be symbolized as HA, where A represents molecules like fluorine or acetate. And the fact that it’s weak means that it has a “weak” effect on pH, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Metabolic_acidosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8Gt4G6ahT6ukr7PHRgYspvX2SkOPIkVP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Metabolic acidosis]]></video:title><video:description><![CDATA[With metabolic acidosis, “acidosis” refers to a process that lowers blood pH below 7.35, and “metabolic” refers to the fact that it’s a problem caused by a decrease in the bicarbonate HCO3− concentration in the blood.

Normally, blood pH depends on the balance or ratio between the concentration of bases, mainly bicarbonate HCO3−, which increases the pH, and acids, mainly carbon dioxide CO2, which decrease the pH. 

The blood pH needs to be constantly between 7.35 and 7.45, and in addition the blood needs to remain electrically neutral, which means that the total cations, or positively charged particles, equals the total anions, or negatively charged particles. 

Now, not all of the ions are easy or convenient to measure, so typically the dominant cation, sodium Na+, which is typically around 137 mEq/L and the two dominant anions, chloride Cl−, which is about 104 mEq/L, and  bicarbonate HCO3−, which is around 24 mEq/L, are measured. 

The rest are unmeasured. So just counting up these three ions, there’s usually a difference, or “gap” between the sodium Na+ concentration and the sum of bicarbonate HCO3− and chloride Cl− concentrations in the plasma, which is 137 minus 128 (104 plus 24) or 9 mEq/L. 

This is known as the anion gap, and normally it ranges between 3 and 11 mEq/L. The anion gap largely represents unmeasured anions like organic acids and negatively charged plasma proteins, like albumin. 

So, basically, metabolic acidosis arises  either from the buildup of acid in our blood, which could be because it’s produced or ingested in increased amounts, or because the body can’t get rid of it, or from excessive bicarbonate HCO3− loss from the kidneys or gastrointestinal tract. 

The main problem with all of this is that they lead to a primary decrease in the concentration of bicarbonate HCO3− in the blood. 

They can be broken down to two categories, based on whether the anion gap is high or normal. So, the first category of metabolic acidosis is a high ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Subacute_granulomatous_thyroiditis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Xnon9KnlS7iyDihvWHNnJoaJSBWH0GJS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Subacute granulomatous thyroiditis]]></video:title><video:description><![CDATA[Subacute granulomatous thyroiditis, also known as De Quervain’s thyroiditis, belongs to a group of disorders featuring inflammation “-itis” of the thyroid gland. 

This inflammation is “granulomatous”, meaning there are aggregations of immune cells, mainly activated macrophages, that form tiny nodules within the thyroid gland. 

Subacute implies that it’s somewhere between acute and chronic, typically developing after an acute event, like a viral infection.

Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, known as ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary. 

The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, thyrotropin or simply TSH.  

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.

If we zoom into the thyroid gland, we’ll find thousands of follicles, which are small hollow spheres whose walls are lined with follicular cells, and are separated by a small amount of connective tissue. 

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body. 

Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate.

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy.

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sinusitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HtRKKyEkSz2zwkZ7fcPf5vdhQW6VC3BF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sinusitis]]></video:title><video:description><![CDATA[Sinusitis is inflammation of the paranasal sinuses - which are pairs of air spaces that surround the nose in the front of the face. 

Usually, acute sinusitis can last up to four weeks, subacute sinusitis lasts between 1 to 3 months, and chronic sinusitis lasts more than 3 months. 

When you breathe in, air flows through the nostrils and enters the nasal cavity, which is lined by goblet cells that release mucus. 

That mucus is salty, sticky, and contains lysozymes, which are enzymes that help kill bacteria. 

Nose hairs at the entrance of the nasal cavity get coated with that mucus and are able to trap large particles of dust and pollen as well as bacteria, forming tiny clumps of boogers. 

The nasal cavity is connected to four paired paranasal sinuses, named according to the bones in which they lie. 

The largest are the maxillary sinuses, found right below the eyes. 

Then we have the ethmoidal and sphenoidal sinuses behind the eyes. 

Finally, the frontal sinuses are in the forehead, right above the eyes.

The paranasal sinuses act like tiny echo-chambers that help amplify the sound of your voice, which is why you sound so different when they’re clogged with  mucus during a cold! 

They also allow the inspired air to circulate for a bit so it has time to get warm and moist. 

Like the rest of the respiratory tract, the walls of the paranasal sinuses are made up of a mucosal epithelium. 

The mucosal epithelium contains goblet cells, which produce mucus to trap small foreign particles, as well as columnar cells, which have cilia, which are tiny little hair like projections that move mucus, draining into the nasal passages.

One of these passages is also called a nasal meatus, and there are three; the superior, middle, and inferior meatus which help drain mucus. 

The sphenoidal sinus drains to the spheno-ethmoidal recess, which is a small space in the nasal cavity right above the superior meatus. 

The ethmoid sinus can be divided into posterior, which ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Carcinoid_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lEdooVE0TqCrOmgJjizQwHsRSNawjUfT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Carcinoid syndrome]]></video:title><video:description><![CDATA[Carcinoid syndrome refers to a constellation of symptoms like diarrhea, shortness of breath and flushing, which arise when a specific type of tumor called a neuroendocrine tumor begins secreting hormones. 

Neuroendocrine tumors were also called “carcinoid tumors” in the past, because of their association with carcinoid syndrome. 

Neuroendocrine cells are found in tissues throughout the body, particularly in the epithelial layer of gastrointestinal organs and the lungs. They receive signals from nerve cells and, in response, they release hormones into the blood. 

Neuroendocrine cells release a variety of hormones including amines, like serotonin and histamine; polypeptides, like bradykinin, a vasodilator; and prostaglandins which are also powerful vasodilators. The production of these hormones can also be regulated by other hormones. 

For example, somatostatin is a hormone that’s made by cells in the hypothalamus as well as the gastrointestinal tract, and it travels through the blood and binds to receptors on the surface of neuroendocrine cells. 

Binding of somatostatin inhibits the release of a number of hormones from neuroendocrine cells, including serotonin. 

Now, when serotonin does get released from neuroendocrine cells, it enters the liver through the portal vein. 

In the liver, some of the serotonin is metabolized to 5-hydroxyindoleacetic acid which is eliminated from the body through the urine. 

The remaining serotonin is not metabolized, and this portion remains in the systemic circulation where it has various effects. 

In the gastrointestinal tract, serotonin increases motility and peristalsis; in the vasculature, platelets take up the serotonin and later use it to constrict blood vessels, particularly after injury; and in the connective tissue of the heart, it stimulates fibroblasts which make lots of collagen.  

A cell can become cancerous when DNA mutations cause abnormal cellular functions, like uncontrolled, unregulated cellular div]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Menopause</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8laSieh4R9qH3xJ4bJwY_p4HRESzUOjq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Menopause]]></video:title><video:description><![CDATA[In females, the reproductive period, or fertility period refers to the years of monthly menstrual cycles between the first menstrual period, which happens at puberty and then the permanent stopping of menstrual cycles - which is called menopause. Menopause usually sets in around age 50, and it’s preceded by a couple of years of hormonal and physical changes and this is called perimenopause. To be more specific, a woman’s entered menopause when an entire year has passed since her last menstrual period.  

During the reproductive period, the ovaries have basically got a ton of ovarian follicles scattered inside them. And each ovarian follicle is made up of a ring of granulosa and theca cells surrounding a primary oocyte the core. And during each menstrual cycle, one of these follicles ruptures at ovulation, and it releases the oocyte out into the fallopian tube - where it can be fertilized by a sperm, or it can just carry on down its path and you don’t get pregnant. So the weird thing is, even though females are born with millions of follicles, only about 400 of them are actually mature enough to release their oocyte throughout the lifetime.

Anyway, all of this process is ultimately controlled by the hypothalamus, which is all the way away from the gonads up in the brain. And the hypothalamus secretes gonadotropin releasing hormone, or GnRH, which travels to the nearby pituitary gland and makes it secrete two hormones of its own - follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH. FSH and LH then make the ovarian follicles secrete sex hormones. So, the theca cells make androstenedione, a sex hormone precursor that the granulosa cells convert into estradiol - a member of the estrogen family - and progesterone. 

The menstrual cycle on average lasts about 28 days, and for the first two weeks, which are called the follicular phase, the granulosa cells make more estrogen sends a negative feedback signal to the pituitary which inhibits the pro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prolactinoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Mki1Fsl2R_2472upq3sEjiK4SIeV8TYE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prolactinoma]]></video:title><video:description><![CDATA[With prolactinoma, prolactin refers to the endocrine hormone secreted by the pituitary gland and -oma refers to a tumor. 

So a prolactinoma is a benign tumor, or adenoma, of the pituitary gland that secretes excess prolactin. 

Normally, the pituitary is a pea-sized gland, hanging by a stalk from the base of the brain. 

It sits just behind the eyes near something called the optic chiasm, which is where the optic nerves cross. 

The anterior pituitary, which is the front of the pituitary gland, contains a few different types of cells, and each of which secretes a different hormone. 

One group of cells in the anterior pituitary are called lactotrophs and they secrete prolactin.

Prolactin stimulates breast milk production. 

Another group of cells are the gonadotrophs and they secrete two gonadotropic hormones - luteinizing hormone, or LH, and follicle-stimulating hormone, or FSH, both of which stimulate the ovaries in women which make estrogen and stimulate the testes in men which make testosterone. 

Prolactin release is controlled by something called the hypothalamus, which is a structure at the base of the brain just above the pituitary gland. 

It makes two key hormones, thyrotropin-releasing hormone which increases prolactin release, and  dopamine, which inhibits the prolactin release and actually overrides the stimulatory effect of thyrotropin-releasing hormone. 

That’s why dopamine is known as prolactin-inhibiting factor, and why it’s constantly released to prevent prolactin release in anyone that’s not pregnant. 

High levels of prolactin in the blood sends a negative feedback signal to the hypothalamus, making it release more dopamine which then decreases prolactin levels. 

High levels of prolactin can also signal the hypothalamus to decrease the secretion of gonadotropin releasing hormone or GnRH.

Gonadotropin releasing hormone acts on the anterior pituitary to make follicle stimulating hormone and luteinizing hormone or FSH and LH. 

Now, d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tubular_reabsorption_of_glucose</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6Lvfola0TIOgn3P4SKtmDRreQEyEiFPH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tubular reabsorption of glucose]]></video:title><video:description><![CDATA[Glucose is found in almost every food we eat, like bread, potatoes, or fruit. Once it’s absorbed by the body, it’s converted into a source of energy.

The body needs the plasma glucose levels to remain within a pretty narrow range, between 70 mg/dl to 110 mg/dl, when you’ve had nothing to eat and less than 140 mg/dl after a meal.

Now, the entire blood volume is about 5 liters, and the plasma volume is about 3 liters of that. 

The kidneys filter the entire plasma volume 60 times a day, which means that means our kidneys filter approximately 180 liters of plasma each day! 

If each liter of plasma contains about 1 g of glucose, this means about 180 g of glucose get filtered by the kidneys per single day. That’s the filtration rate of glucose. 

If you had a blood glucose concentration of 1.5 g of glucose per L, you’d end up with a filtration rate of glucose of 270 g / day. Essentially, the higher the plasma glucose concentration, the more glucose will get filtered. 

If we wanted to illustrate that in a graph, with plasma glucose concentration on the x axis and glucose filtration rate on the y axis, we would see that as the plasma glucose concentration increases, the filtered load of glucose increases linearly. 

Now, looking at the kidney, specifically inside the kidney, there are two main parts, the outer cortex and the inner medulla.

If we zoom in, there are millions of tiny functional units called nephrons which go from the outer cortex down into the medulla and back out into the cortex again. 

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins. 

When glucose enters the glomerulus, some of it gets filtered into the renal tubule. 

Zooming in on one of these renal tubules, each one is lined by brush border cells which have two surfaces. 

One is the apical surface which faces the tubular lumen and is lined with microvilli, which are tiny little projections that increase the cell’s surface area to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Temporomandibular_joint_dysfunction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uP8wwXY2SLO5zCObw-j482tRR3iS0zvI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Temporomandibular joint dysfunction]]></video:title><video:description><![CDATA[Temporomandibular disorders are a group of disorders that all involve the temporomandibular joint, which is located between the temporal bone of the skull and mandible, or jawbone; as well as the muscles and associated structures that are involved in chewing and speech.

Normally, between the temporal bone and the mandible is a synovial cavity, which is wrapped in fibrocartilage and filled with synovial fluid, which is a protein rich fluid that reduces friction between the sliding bones. 

The synovial cavity is divided into an upper and lower compartment by an articular disc within the synovial fluid. 

The lower compartment is bound, inferiorly, by the condylar head of the mandible. 

The lower compartment allows the mandible to rotate, which lets the mouth open and close. 

The upper compartment is bound, superiorly, by two regions of the temporal bone: the mandibular fossa, in the middle and back, and articular tubercle, in the front.

Separating these two compartments is the articular disc. 

The upper compartment allows the condylar head to move forward and rotate. 

The movements of the temporomandibular joint are coordinated by numerous muscles, including: the temporalis, which is a fan-shaped muscle on both sides of the cranium; the masseter, which connects to the mandible and the zygomatic arch of the temporal bone; the medial pterygoid, which connects to the mandible and medial aspect of the lateral pterygoid plate; and the lateral pterygoid, found at the condylar process. 

These muscles are innervated by branches of the trigeminal nerve. 

Now, the causes of temporomandibular disorders can be categorized as intra-articular, within the joint, or extra-articular, involving the surrounding musculature. 

Intra-articular causes, are called temporomandibular joint disorders, and they include things like abnormalities of the bones in the joint, inflammation in the joint from conditions like osteoarthritis or rheumatoid arthritis; disorders of the ar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_gastrointestinal_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wELKLXGLQ2OY8vodsEFES6yWT76pqwYp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the gastrointestinal system]]></video:title><video:description><![CDATA[During week 3, the embryo is a flat disc made up of three germ layers: the endoderm, the mesoderm, and the ectoderm. 

From the endoderm, which you can think of as being the belly side of this three-layered embryo pancake, a fluid filled bubble called the yolk sac forms and grows alongside the developing embryo. 

The digestive system starts forming when the embryo folds along its vertical and horizontal axes—so it rolls up on itself, and turns into a tubular structure that looks a bit like a little shrimp.

Folding also pinches the yolk sac, sort of like squeezing a balloon through a ring, so a part of it goes inside the embryo and forms the primitive gut tube.

The primitive gut tube is initially sealed off at both ends—the buccopharyngeal membrane at the top separates the tube from the primitive mouth, and the cloacal membrane at the bottom separates it from the primitive anus. 

This tube is divided into three parts, based on the arterial blood supply. 

The first portion is the foregut, and it’s nourished by the celiac artery. 

The middle portion, the midgut, is nourished by the superior mesenteric artery.

For a short while, the midgut communicates with the yolk sac through the vitelline duct, which is eventually incorporated into the umbilical cord.

Finally, there’s the last portion, the hindgut, which is nourished by the inferior mesenteric artery. 

The hindgut ends with the cloaca, which is the primitive common drainage site for the urinary, genital, and digestive systems.

The foregut gives rise to the superior part of the digestive tube—up to and including the first half of the duodenum, as well as the liver, the gallbladder, and the pancreas. 

At the very top of the foregut, starting at the buccopharyngeal membrane, there’s the primitive pharynx, which is initially just five sets of symmetrical pharyngeal arches. 

These pharyngeal arches turn into various bones, muscles, and cartilages of the head and neck, and the last two arches give ris]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_reproductive_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hkQzX45CTxK7cDP_qRY2jnZcSnul1-_W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the reproductive system]]></video:title><video:description><![CDATA[Reproductive system development is the series of events that an embryo goes through to sexual differentiate into a male or female with regard to the gonads, genital ducts, and external genitalia. 

The process starts at conception - when the gametes, the sperm and oocyte, fuse into a single cell that has either XX sex chromosomes in a female or XY sex chromosomes in a male - establishing the genetic sex of the embryo. 

Through the first 5 weeks of development however, sexual development is basically identical for both sexes. 

At that point, the embryo is made up of three primitive germ layers: the ectoderm, the mesoderm and the endoderm. 

The mesoderm also has three parts: the paraaxial mesoderm, flanking the embryo’s future vertebral column, the intermediate mesoderm which is just lateral to it, and the lateral plate mesoderm which is the most lateral of all.   

The intermediate mesoderm on both sides of the embryo condenses into two cylindrical structures called the urogenital ridges.

Each urogenital ridge runs parallel to the embryo’s future vertebral column, and organizes into a cylinder of mesoderm called the nephrogenic cord. 

Most of the nephrogenic cord goes on to form urinary structures, but a strip of it in the middle gives rise to the gonads in males and females. 

This portion that gives rise to the gonads is called the genital or sometimes gonadal ridge. 

The genital ridge has a mesoderm core and is covered with epithelium.

Gonad development, interestingly enough, starts in a tissue outside the embryo called the yolk sac -  which is lined with endoderm cells, and connects to the embryo through the vitelline duct. 

Early in development, some endoderm cells from the wall of the yolk sac differentiate into primordial germ cells, and they begin to migrate - physically move - along the vitelline duct, to the primitive digestive tract, and finally to the dorsal mesentery - a sheet of tissue that anchors the digestive tract to the posterior ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_muscular_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ur7rTqhdRYmlY0HLnWpaBEgbR9m774wx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the muscular system]]></video:title><video:description><![CDATA[The muscular system starts taking shape when the embryo is just a flat little pancake made up of two layers: the epiblast on the dorsal, or back, side, and the hypoblast on the ventral, or front, side. 

A line called the primitive streak appears on the epiblast “back” of this two-layered creature.

Cells migrate along the primitive streak during gastrulation, leading to a now three-layered embryo pancake, with each layer containing germ cells that form organs and tissues of the body. 

The ventral, or bottom, germ layer is called endoderm, the dorsal, or top, germ layer is called ectoderm, and the layer in between these two is called mesoderm. 

Collectively, these germ cells produce all of the organs and tissues in the body. 

During week 3, the embryo transitions from a flat organism to a more tubular creature by folding along its longitudinal and lateral axes. 

At the same time, a solid rod of mesoderm called the notochord forms on the midline of the embryo. 

Above the notochord, the ectoderm invaginates to form the neural tube, an early precursor of the central nervous system.

This is the embryo’s first symmetry axis, and the mesoderm on either side of the neural tube differentiates into three distinct portions: immediately flanking the neural tube there’s the paraxial mesoderm; next, there’s the intermediate mesoderm; and finally, the lateral plate mesoderm.

Between the cells of the lateral plate mesoderm, small gaps appear and coalesce to form the intraembryonic coelom, a cavity inside the embryo’s body. 

This cavity separates the lateral plate mesoderm into two layers: a parietal layer that’s in contact with the ectoderm, and a visceral layer that’s in contact with the endoderm. 

The paraxial and lateral plate mesoderm will become the skeletal muscles in our body. 

Before the mesoderm cells develop into skeletal muscle, they first organize into cell blocks called somites. 

Somites arise in pairs from a combination of paraxial mesoderm cells]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Constitutional_growth_delay</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WdaNoccpQrKLsp7uZ_vUzvbITwuGgsgG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Constitutional growth delay]]></video:title><video:description><![CDATA[Constitutional growth delay is a normal variation of development where there’s a temporary delay in growth that occurs during early childhood and puberty. 

You can think of it as a slowed rate of maturation, which happens normally in some people. 

It’s the most common cause of short stature and pubertal delay in children and adolescents, but by adulthood, people with constitutional growth delay generally end up with normal adult heights. 

Generally speaking, there are two hormonal systems that control growth - the growth hormone axis and the hypothalamic-pituitary-gonadal axis. 

The growth hormone axis starts with the hypothalamus which is at the base of the brain.

The hypothalamus secretes growth hormone-releasing hormone and that stimulates the anterior pituitary gland to produce growth hormone. 

Now, growth hormone affects lots of tissues - in particular it makes the body retains nitrogen leading to more muscle growth, and osteoblasts get stimulated which causes the bones to thicken. 

Growth hormone also stimulates certain tissues like the liver, skeletal muscles, bones, and kidneys to produce somatomedin C, also called insulin-like growth factor 1. 

Insulin-like growth factor 1 promotes cellular metabolism, prevents cell death, and helps cell divide and differentiate throughout the body. 

It’s also the key hormone that stimulates the growth in length of long bones. 

Now, sexual maturation is under the control of the hypothalamic-pituitary-gonadal axis. 

This axis also starts with the hypothalamus which releases Gonadotropin-releasing hormone, or GnRH which stimulates the anterior pituitary to produce the gonadotropin hormones: luteinizing hormone, or LH, and follicle-stimulating hormone, or FSH.

LH and FSH stimulate the gonads to produce sex specific hormones - which are estrogen and progesterone in females, and testosterone in males. 

Now, the amount of hormone that gets produced by this axis varies over a person’s lifetime, and that affe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Upper_respiratory_tract_infection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/btWh5URiS6aMR7kP54FQRdHcSeWoJJ0r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Upper respiratory tract infection]]></video:title><video:description><![CDATA[An upper respiratory tract infection is any infection that involves the nasal cavity, paranasal sinuses, pharynx, or larynx, and it’s most often caused by an invading pathogen like a virus.

When you breathe in, air flows through the nostrils and enters the nasal cavity, which is lined by cells that release mucus.

That mucus is salty, sticky, and contains lysozymes, which are enzymes that help kill bacteria. 

Nose hairs at the entrance of the nasal cavity get coated with that mucus and are able to trap large particles of dust and pollen as well as bacteria, forming tiny clumps of boogers. 

The nasal cavity is connected to four sinuses which are air- filled spaces inside the bones that surround the nose, there’s the frontal, ethmoid, sphenoid, and maxillary sinus. 

The paranasal sinuses help the inspired air to circulate for a bit so it has time to get warm and moist. 

The paranasal sinuses also act like tiny echo-chambers that help amplify the sound of your voice, which is why you sound so different when they’re clogged with  mucus during a cold! 

So the relatively clean, warm, and moist air goes from the nasal cavity into the pharynx or throat. 

At each side of the back of the throat, there is the pair of tonsils, which are small are clumps of lymphoid tissue that act as the body&amp;#39;s first line of defense that swallow viruses and bacteria that enter through the mouth or nose. 

The lower part of the pharynx is continuous with the larynx or the voice box. 

Αt the top of the larynx sits a spoon- shaped flap of cartilage called the epiglottis which acts like a lid that seals the airway off when you’re eating, so that the food can only go one way - down the esophagus and towards the stomach. 

Now, once air makes its way into the larynx, it can continue its journey through the trachea, or windpipe, towards the lungs.

Now, in addition to air, you’re constantly breathing in other stuff like viruses or bacteria. 

For example, when an infected pe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Metabolic_alkalosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ktAt7BpMT_KkzDuF8Qzsp1A_QSO8XR67/_.jpg</video:thumbnail_loc><video:title><![CDATA[Metabolic alkalosis]]></video:title><video:description><![CDATA[With metabolic alkalosis, “alkalosis” refers to a process that raises blood pH above 7.45, and “metabolic” refers to the fact that it’s caused by an increase in the concentration of bicarbonate HCO3− in the blood.

Normally, blood pH depends on the balance or ratio between the concentration of bases, mainly bicarbonate HCO3−, which increases the pH, and acids, which decrease the pH. 

The blood pH needs to be constantly between 7.35 and 7.45. 

Now, metabolic alkalosis can typically happen from two main causes - loss of hydrogen H+ ions and gain of HCO3− bicarbonate ions, or, most often, a combination of these two. 

Loss of hydrogen H+ ions can occur either from the gastrointestinal tract or from the kidneys. 

The first case most commonly happens during vomiting, because the gastric secretions are very acidic, meaning that they have lots of hydrogen H+ ions. 

On top of that, normally, as gastric secretions flow into the pancreas, they’re met with HCO3− bicarbonate secretions which neutralize the acid so that the various pancreatic enzymes like trypsin and chymotrypsin, can work effectively. 

So during vomiting, not only is the stomach acid lost, but in addition the pancreas doesn’t secrete HCO3− bicarbonate into the intestines, and so it builds up in the blood instead. 

Another way that hydrogen H+ ions can be lost is through the urine, in the context of having too much of the hormone aldosterone. 

This can happen, when there’s an adrenal tumor that secretes excess aldosterone. 

The aldosterone makes the α- intercalated cells of the distal convoluted tubule and collecting duct dump out hydrogen H+ ions and reabsorb more bicarbonate HCO3− ions. 

The result is that the urine becomes more acidic and the blood becomes more basic. 

Now, the second cause - a primary gain of HCO3− bicarbonate ions - is usually caused by an increased reabsorption of HCO3− bicarbonate ions from the kidneys. 

There are various things that could stimulate the kidneys to do ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Horner_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gl68rhZdRzaL0EnVgmmQWRGaRNeW2qdI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Horner syndrome]]></video:title><video:description><![CDATA[Horner’s syndrome, named after the ophthalmologist Johann Friedrich Horner, is caused by a problem with the sympathetic nerve supply to one side of the face. 

This disruption results in miosis, which is constricted pupil; ptosis, a droopy eyelid; and anhidrosis, a failure to sweat.

Broadly speaking, the autonomic nervous system is a part of the nervous system that controls involuntary body functions like the heart rate, blood pressure and digestion. 

The autonomic nervous system can be subdivided into the sympathetic and parasympathetic nervous system, which have opposite effects. 

The sympathetic nervous system controls functions like increasing heart rate, blood pressure, and slowing digestion. All of this maximizes blood flow to the muscles, and can help you either run away from a threat or fight it which is why it’s also called the fight-or-flight response. 

The parasympathetic nervous system has the opposite effect; it slows heart rate, decreases blood pressure, and stimulates digestion - the effects can be summarized as &amp;#39;rest and digest&amp;#39;.

Now, with regard to the face and eye, there’s an oculosympathetic pathway with three groups of neurons called first-order, second-order and third-order neurons.

The body of the first-order neuron is located in the hypothalamus, and it’s axon extends down into the spinal cord, where it synapses with the second-order neuron.

The body of the second-order neuron is located in the cervical region of the spinal cord, and it’s axon exits the spinal cord and enters the sympathetic chain, which is a structure full of sympathetic ganglions or nerve cell bodies, and it runs along both sides of the spine. 

The sympathetic chain looks similar to a string of pearls where the ganglions are the pearls and the nerve fibers make up the string. 

The first three ganglia within the sympathetic chain are called the superior, middle, and inferior cervical ganglion. 

The axon of the second-order neuron run]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bacterial_epiglottitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GGBZZd2aTqCI71e-4zN1py5KQMWvs1yJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bacterial epiglottitis]]></video:title><video:description><![CDATA[With Epiglottitis, “itis” means inflammation and epiglottis is a flap of elastic cartilage that sits at the top of the larynx or voice box. The epiglottis keeps food and liquid going down the esophagus and prevents it from going down the trachea by accident. So bacterial epiglottitis is when bacteria infect this flap of tissue and cause it to get swollen. This can be life threatening because it can flop down and block the trachea, making it impossible to breathe. This infection is actually thought  to have been the cause of death for George Washington, America’s first president.     

Now, the larynx is located in the bottom portion of the neck, just below where the pharynx splits into the trachea and the esophagus. The larynx is also called the voice box because it contains the vocal cords, which are two folds of mucous membrane that can open and close like curtains.  Just like the rest of the respiratory tract, the walls of the larynx are made up of mucosal epithelium. 

The epiglottis extends from the base of the tongue and anchors to the anterior rim of the thyroid cartilage, which is just in front of the larynx. The lateral borders of the epiglottis connect to the aryepiglottic folds, which have ligamentous and muscular fibers. This allows the epiglottis to act like a lid on a box and serve as the guardian of the airways. During swallowing, the epiglottis covers the larynx, preventing food and liquids from entering the airway; and during breathing, the epiglottis opens the larynx, allowing air to flow in and out.

Epiglottitis happens when the epiglottis, aryepiglottic folds, and other adjacent tissues become infected. Most commonly, epiglottitis is caused by Haemophilus influenzae, a gram negative rod bacterium, but in settings where Haemophilus influenzae type b vaccine is used commonly, other bacteria like Group A Streptococcus can also cause the infection. These bacteria are spread person-to-person by direct contact or through respiratory droplets]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Deep_vein_thrombosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-VBr6WbuSe27SK-kYbEC1hduTQqT46pQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Deep vein thrombosis]]></video:title><video:description><![CDATA[“Deep vein” refers to the veins that typically run between muscles as they travel back towards the heart, as opposed to superficial veins that you can see on the surface, and “thrombosis” refers to a blood clot. So a deep vein thrombosis or DVT is a blood clot in one of those deep veins. 

Normally, blood makes it back to the heart from the tissues and organs via a network of veins that merge over and over. Superficial veins drain blood into deep veins, which rely on the skeletal muscle pump to move blood forward. The way it works is that the surrounding skeletal muscles compress the vein and propel blood forward, and the veins prevent blood from moving backwards by using one-way valves. 

Ultimately, all of the blood ends up in the superior or inferior vena cava and then dumps into the right atrium. From there, the blood goes into the right ventricle and before being pumped into the pulmonary artery and eventually into the lungs. Deep vein thrombosis most commonly develops in the lower legs, below the knee, although blood clots can form in both superficial and deep veins and in other parts of the body as well. 

Normally, the process starts with damage to the endothelium or inner lining of blood vessel walls, after which there’s an immediate vasoconstriction or narrowing of the blood vessel, limiting the amount of blood flow. After that, some platelets adhere to the damaged vessel wall, and become activated by collagen and tissue factor, proteins that are normally kept separate from the blood by the intact endothelium. These platelets then recruit additional platelets, forming a plug. The formation of the platelet plug is called primary hemostasis. 

After that, the coagulation cascade is activated. First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver; usually these are inactive and just float around in the blood. The coagulation cascade starts when one of these proteins gets proteolytically cleaved]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fragile_X_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/51AzjLC4ToeFt71yWhHHNQ3DSIGHXitB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fragile X syndrome]]></video:title><video:description><![CDATA[With Fragile X syndrome, sometimes just called Fragile X, the “X” refers to the X chromosome, where the disease gene is located. 

The “fragile” refers to the fact that under a microscope, the X chromosome looks fragile or broken at the site of the mutation.  

That’s because the chromatin which makes up the chromosome gets really condensed at that point. 

Fragile X is a genetic disease that affects various organ systems.

Now, the gene for Fragile X is called FMR1, which stands for Fragile X mental retardation 1. 

Mental retardation is the old term for intellectual disability, which is one of the key features of Fragile X syndrome. 

The FMR1 gene has a triplet repeat, or trinucleotide repeat, which means that a group of three DNA nucleotides is repeated multiple times in a row.  

In FMR1, it’s the nucleotides cytosine, guanine, and guanine, or CGG.  

These CGGs are found in the 5’ untranslated region of FMR1. 

A 5’ untranslated region is the part of DNA at the beginning of the gene that’s made into mRNA but not protein, and helps modulate gene expression. 

Just upstream from the 5’ untranslated region is FMR1‘s promoter, the region that causes the gene to be transcribed to mRNA, which is usually turned on.  

Expressed FMR1 mRNA gets translated into Fragile X mental retardation protein, or FMRP, and it helps in development of the brain and other tissues. 

In Fragile X syndrome, there is a repeat expansion, meaning there’s an increased number of CGG repeats in the gene. 

This repeat expansion is caused by slipped mispairing, which is where the enzyme DNA polymerase gets confused when copying a repetitive sequence. 

DNA polymerase loses its place among the FMR1 triplet repeats and goes back to recopy what it already just copied. 

This is like getting lost in a video and watch the same part over and over. 

But since DNA polymerase is making copies, the effect is an increase, or expansion, of the number of repeats. 

The normal number of CGG tripl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypopituitarism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pRUot0A0S7CBXWVD-sPoJUbgQ0a2jjfg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypopituitarism]]></video:title><video:description><![CDATA[With hypopituitarism, “hypo” means under and “pituitarism” refers to the pituitary gland which normally secretes various endocrine hormones. 

So hypopituitarism is the underproduction of hormones released by the pituitary gland, and the symptoms depend on which hormones are actually undersecreted.

If all of the pituitary hormones are affected, it’s called panhypopituitarism. 

The pituitary is a pea-sized gland, hanging by a stalk from the base of the brain. 

It sits just behind the eyes near the optic chiasm, which is where the optic nerves cross and the gland rests in a very small depression of the skull known as the sella turcica. 

The pituitary gland produces and secretes hormones when it receives signals from another part of the brain called the hypothalamus. 

Together, they form the hypothalamic-pituitary axis which regulates the release of all the major endocrine hormones.

The pituitary itself has two distinct parts: the anterior pituitary and the posterior pituitary. 

The anterior pituitary, which is the front of the pituitary gland, contains a few different types of cells, each of which secretes a different hormone.

The largest group of cells are the somatotropes which secrete growth hormone, which goes on to promote tissue and organ growth. 

The second largest cell group are the corticotrophs which secrete adrenocorticotropic hormone, or ACTH, which stimulates the adrenal glands to secrete cortisol, a hormone that controls the stress response, blood pressure, and metabolic regulation. 

A smaller cell group are the lactotrophs which secrete prolactin. 

Prolactin stimulates breast milk production, and also inhibits ovulation, which is when an egg cell is released from the ovary, and inhibits spermatogenesis, which is the development of sperm cells. 

There are also thyrotrophs which are cells that secrete thyroid stimulating hormone, or TSH, that stimulate the thyroid gland. 

And finally, there are the gonadotrophs which secrete tw]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_thyroiditis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/42nGAikuTdeH7lyZfYvQD4zbSJ_ptkbz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postpartum thyroiditis]]></video:title><video:description><![CDATA[With postpartum thyroiditis, postpartum means &amp;quot;after birth&amp;quot;, thyroid refers to the thyroid gland, and -itis means inflammation, so postpartum thyroiditis is an inflammation of the thyroid gland that women experience after giving birth.

Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, or ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary gland. 

The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, thyrotropin, or simply TSH. 

TSH stimulates the thyroid gland, which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.

If we zoom into the thyroid gland, we’ll find thousands of follicles, which contain a sticky substance called colloid, which sits within follicular cells.

Follicular cells convert the protein thyroglobulin into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.

Once released from the thyroid gland, these hormones enter the blood and the majority is bound to circulating plasma proteins, with only a small amount of T3 and T4 traveling unbound in the blood.

Ultimately, these two hormones get picked up by nearly every cell in the body.

Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate. 

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy. 

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response. 

Thyroid hormone is important - and the occasional increase can be really useful when you need a boost to get through the final rounds of a sporting competition o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_role_of_the_kidney_in_acid-base_balance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EapuASmDQb69TQQ5qoZVRUUQR5uZFyGw/_.jpg</video:thumbnail_loc><video:title><![CDATA[The role of the kidney in acid-base balance]]></video:title><video:description><![CDATA[The kidneys have two main ways to maintain acid-base balance - their cells reabsorb bicarbonate HCO3− from the urine back to the blood and they secrete hydrogen H+ ions into the urine. 

By adjusting the amounts reabsorbed and secreted, they balance the bloodstream’s pH. 

Our kidneys filter blood continuously by distributing the blood that comes into the kidney to millions of tiny functional units called nephrons.

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins.

When blood passes through a glomerulus, about one-fifth of the plasma leaves the glomerular capillaries and goes into the renal tubule. 

Reabsorption of the good stuff---water and electrolytes---and leaving behind the bad stuff---waste products and acid--- is the job of the the renal tubular system. 

The renal tubule is a structure with several segments: the proximal convoluted tubule, the U- shaped loop of Henle with a thin descending and a thick ascending limb, and the distal convoluted tubule, which winds and twists back up again, before emptying into the collecting duct, which collects the final urine. 

Each of these tubules is lined by brush border cells which have two surfaces. 

One is the apical surface that faces the tubular lumen and is lined with microvilli, which are tiny little projections that increase the cell’s surface area to help with solute reabsorption. 

The other is the basolateral surface, which faces the peritubular capillaries, which run alongside the nephron. 

So with bicarbonate reabsorption, as the filtrate leaves the glomerulus, it first goes through the proximal convoluted tubule. 

Now at first, this filtrate contains the same concentration of electrolytes as the plasma it came from. But when a molecule of bicarbonate approaches the apical surface of the brush border cell it binds to hydrogen H+ secreted by the brush border cell in exchange for a sodium ion from the tubule to form carbonic acid. 

At that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Body_fluid_compartments</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rJnq6aSoRZuvoa6eFsoZMF7lQia0Nq_4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Body fluid compartments]]></video:title><video:description><![CDATA[Water is the key to life, and it takes up a big proportion of our body weight, typically around 60 percent! The precise amount of water depends on a person’s body composition. 

Since fat doesn’t store any water, a person’s water content is inversely proportional to a person’s fat content. 

So a really muscular and lean person would have a relatively high proportion of their body weight made up of water. 

Additionally, females tend to have more fat than males and so on average tend to have lower proportion of their body weight made up of water. 

Total body water can be subdivided into two major compartments, intracellular fluid which is fluid inside cells, and extracellular fluid which is fluid outside of cell like in the blood and in the interstitial tissue between cells. 

Assuming that the total body water is about 60% of their body weight, roughly 2/3 of that, or 40% is intracellular fluid, and the other 1/3 or 20% is extracellular fluid. This is also known as the 60-40-20 rule.   

Intracellular fluid is important for dissolving cations which are molecules with a positive charge, and anions which are molecules with a negative charge. 

The major intracellular cations are potassium (K+) and magnesium (Mg2+), whereas the major anions are proteins and organic phosphates like ATP. 

Fluid compartments always maintain the same concentration of positive charges as negative ones in order to stay electrically neutral - that’s called the principle of macroscopic electroneutrality. So for example, the K+ in the intracellular fluid is balanced out by negatively charged proteins and organic phosphates. 

The extracellular fluid can be subdivided further into interstitial fluid, which is the fluid that can be found surrounding the cell, and plasma, which is the aqueous portion of blood. 

The major cation in extracellular fluid, both in the interstitial fluid and in the plasma, is sodium (Na+) and the major anions are chloride (Cl-) and bicarbonate (HCO3-). 

N]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_axial_skeleton</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jyTnowWIQBmPcoXGDCCx_ak1S-eOusPA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the axial skeleton]]></video:title><video:description><![CDATA[The fetal skeleton starts developing soon after gastrulation, which is when the trilaminar disc with ectoderm, mesoderm and endoderm layers are formed. 

There are two parts to the skeleton - the axial skeleton, which includes the bones in the skull, the vertebrae, the rib cage, and the sternum, and the appendicular skeleton, comprising of the pelvic and shoulder girdle, as well as the bones in the limbs. 

The bones in the axial skeleton mostly derive from the mesoderm layer, except for some bones in the skull which come from the ectoderm. 

All the bones in the appendicular skeleton derive from the mesoderm. 

During week 3, the embryo transitions from a flat organism to a more tubular creature, by folding along its longitudinal and lateral axes. 

At the same time, a solid rod of mesoderm called the notochord forms on the midline of the embryo. 

Above the notochord, the ectoderm invaginates to form the neural tube - an early precursor for the central nervous system. 

This is the embryo’s first symmetry axis, and the mesoderm on either side of the neural tube differentiate in 3 distinct portions: immediately flanking the neural tube, there’s the paraxial mesoderm. 

Next, there’s the intermediate mesoderm, and finally, the lateral plate mesoderm.

The intermediate mesoderm gives rise to the urinary and genital systems, while the paraxial mesoderm and lateral plate mesoderm work together to give rise to most of bones and muscles in our body.

The first step in skeletal development is when paraxial mesoderm segments into blocks of mesodermal tissue called somites, which are made up of lots of cube-shaped cells. 

Next, the somites divide into three different cell populations: the sclerotome, which forms the vertebrae, the rib cage, and the lower part of the occipital bone, the dermatome, which forms the skin of the back, and the myotome, which forms the back, limb and intercostal muscles. 

Meanwhile, lateral plate mesoderm splits into parietal mesoderm ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_and_physiology_of_the_male_reproductive_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NmVROJgVTZaBxQmiMYchCr3WSHO18m6u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy and physiology of the male reproductive system]]></video:title><video:description><![CDATA[The male reproductive system includes internal and external organs and structures that help with reproduction. 

The external male sex organs are the penis, and below it, the scrotum. 

Inside the scrotum, there are the two testicles, or testes - the male gonads. 

Inside the body, there’s a system of ducts through which sperm travel during ejaculation, as well as the male accessory sex glands, which secrete nourishing fluids for the travelling sperm. 

Now, the testes are two organs the size of small plums, that are located in a skin and muscle pouch called the scrotum. 

This pouch has a line called the scrotal raphe running down the middle, which separates it in two chambers - one for each testis.

The scrotum hangs outside of the body but has several layers of muscles and fascia that keep the testis temperature about 3 degrees lower than body temperature, which is perfect for sperm production.

When it’s cold outside, the scrotal skin wrinkles and the scrotum elevates to bring the testes closer to the body to warm up. 

When it’s warm outside, the scrotal skin loosens up and the scrotum lowers the testes away from the body, and heat is released through sweating. 

The testes themselves are covered on the outside by the tunica albuginea - a white, fibrous layer. 

If we slice a testis open and look inside - sorry for the cringe moment, guys - we can see that the tunica albuginea, sends fibrous projections called septa towards the center of the testis.

These septa partition each testis into about 250 lobules, and each lobule contains at least one and up to four seminiferous tubules, which is where sperm is synthesized. 

The seminiferous tubules come together and form a single straight tubule that exits the lobule, and enters a small network of tubules called the rete testis. 

The rete testis are a small network of ducts that split up and come together again - like catacombs, and these are located in the center of the testes - a region called the media]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_cardiovascular_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UEPl8K_uT7KBVHNTvFxI4gLvQAmi0BVn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the cardiovascular system]]></video:title><video:description><![CDATA[The cardiovascular system starts developing at the beginning of week 3 of intrauterine life. 

At that point, the embryo is a flat little pancake made up of two layers: the epiblast on the dorsal, or back, side, and the hypoblast on the ventral, or front, side. 

A line called the primitive streak appears on the epiblast back of this two-layered creature. 

Cells migrate along the primitive streak during gastrulation, resulting in a three-layered embryo pancake, with each layer containing germ cells that form organs and tissues of the body. 

The ventral, or bottom, germ layer is called endoderm, the dorsal, or top, germ layer is called ectoderm, and the layer in between these two is called mesoderm. 

The heart derives from a part of the mesoderm called the visceral mesoderm.

Let’s look at this three-week-old creature from above. Mesoderm cells go through the primitive streak and make their way up to the embryo’s head, forming an area that’s called the primary heart field, a horseshoe-shaped area that has two limbs, with one on either side of the future brain. 

This region lies on a blanket of endoderm cells that secrete vascular endothelial growth factor, which is called VEGF for short. 

VEGF signals the cells in the limbs of the horseshoe to self-organize into two heart tubes. 

A primitive pericardial cavity also appears lateral to each endocardial tube.  

At its inferior end, each endocardial tube connects to a vitelline vein, which comes from an extraembryonic tissue called the yolk sac and through which blood enters the endocardial tube. 

Blood exits each endocardial tube at its superior end through a dorsal aorta, which then continues down the embryo’s back.  

During lateral folding, the flat embryo goes from a trilaminar disc to a more cylindrical shape. 

The lateral borders of the embryo reach out towards each other and meet anteriorly at the midline, forming a cylindrical shape. 

This process makes the two endocardial tubes fuse into one]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urea_recycling</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C3QeP1QTR-2lIJnNtFo0szOTSUWRcUzn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urea recycling]]></video:title><video:description><![CDATA[If we take a cross-section of the kidney, there are two main parts, the outer cortex and the inner medulla. 

If we zoom in, there are millions of tiny functional units called nephrons which go from the outer cortex down into the medulla and back out into the cortex again. 

These nephrons perform the major function of the kidney, which is to clear harmful substances from the body by filtering the blood. 

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins. 

The stuff that gets filtered into the tubule is called the filtrate, and the rest of it leaves the glomerulus through the efferent arteriole. 

Interestingly, the blood that leaves these glomeruli does not enter into venules. Instead the efferent arterioles divide into capillaries a second time. 

These peritubular capillaries then reunite and at that point the blood enters venules and eventually drains back into the venous system. 

Now, The renal tubule is a structure with several segments: the proximal convoluted tubule, the U- shaped loop of Henle with a descending and ascending limb and the distal convoluted tubule, which winds and twists back up again, before emptying into the collecting duct, which collects the final urine. 

Now, zooming in on this nephron’s tubule, each one’s lined by brush border cells which have two surfaces. 

One is the apical surface which faces the tubular lumen and is lined with microvilli, which are tiny little projections that increase the cell’s surface area to help with solute reabsorption. 

The other is the basolateral surface, which faces the peritubular capillaries, which run alongside the nephron.

The urine osmolarity is the concentration of urine, and is measured in Osmoles per liter,which is the solute particles that exist in a liter of urine. 

To concentrate urine, or increase its osmolarity, nephrons rely on the corticopapillary gradient, which is a concentration gradient that spans from the cortex to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dental_caries_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pBlocJ9GRz2XEdZV6U1HdlxlTvuM2Eu3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dental caries disease]]></video:title><video:description><![CDATA[Dental caries disease, also called tooth decay, refers to demineralization or weakening of the teeth, and the end result of caries disease is a caries lesion. 

An advanced caries lesion can progress to a point where the tooth surface forms a cavitation or a hole, which is the physical evidence of tooth breakdown. 

Let&amp;#39;s start by building a model of a tooth and its surrounding structures.

In the mouth, the bone beneath the bottom row of teeth is the mandible, and the bone above the top row of teeth is the maxilla. 

Both bones have an alveolus, or socket, for each tooth. 

The socket is lined on the inside by a periodontal ligament.

Protecting the alveolus on the outside, is a layer of soft, supportive tissue called the gingiva, or gums, that sits on top of the bone and covers the root surface from the bone to the cementoenamel junction - where the cementum and enamel come together.

The tooth itself can be roughly divided into a few parts. 

The first part is the root, and it sits within the alveolus. 

The root is covered by cementum, which is a bonelike substance that the periodontal ligament’s fibers attach to. 

Next, there’s the neck, which is the transition between the root portion covered by bone and the crown. 

The crown is the visible part of the tooth that protrudes from the gingiva, and it’s covered in enamel, which has such a high mineral content that it’s the hardest substance in the human body. 

When the teeth are developing, enamel is made before the tooth erupts into the mouth by a group of cells called the ameloblasts that die once the tooth erupts - meaning that the teeth lose the ability to make more enamel forever. 

Now, let’s fill the tooth in from the inside out. 

Blood vessels and nerves come from the jaw bones, and enter the center of the root through a narrow passage, called the apical foramen. 

From there, they enter the soft center of the tooth, called the pulp, where they provide nutrition and sensation. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sarcoidosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kgZdLydpTjW9H0dzqM3NLoUnSiKH4WB0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sarcoidosis]]></video:title><video:description><![CDATA[With sarcoidosis, sarcoid refers to the flesh and osis means disorder - and the reason we called it that, is that sarcoidosis is an immunologic disorder that results in lots of small nodules forming throughout the body. The disease is actually poorly understood though we know it’s most common among African American females.

Normally, the trusty cells of the immune system are ready to spot and destroy any foreign pathogens that could cause the body harm. To help with this mission, there’s a category of cells in the body called antigen-presenting cells, and these include macrophages, B-cells, and dendritic cells.

The most common member of the antigen presenting cell club is the dendritic cell which is named after its long beautiful branch-like arms called dendrites. When a dendritic cell comes into contact with a pathogen, it latches onto it and with its dendrites pulls and engulfs it. The pathogen is then broken down and the dendritic cell presents a piece of it, called an antigen, on something called a major histocompatibility complex class II molecule, or MHC-class II for short.

The dendritic cell then carries the antigen to the lymph node to find some naive helper T-cells which are T-cells that have never seen an antigen before. Eventually, it runs into a naive helper T-cell with a T-cell receptor that recognizes and binds to the antigen. Then, Cytokines get released by the dendritic cell and this helps to activate the helper T-cell which then begins to divide or proliferate.

The new T-cells then leave the comfort of their lymph node to fulfill their destiny in the great fight against infection. These brave T-cells start secreting proinflammatory cytokines, or signaling molecules, and they then recruit more immune cells like additional T-cells and macrophages.

In sarcoidosis though, this process unfolds over and over throughout the body without the presence of a specific pathogen that the body is trying to destroy. In other words, the immune system ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Frontotemporal_dementia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/thtrJ-eWTaS7aasaZnNDeh7UQxGY9pds/_.jpg</video:thumbnail_loc><video:title><![CDATA[Frontotemporal dementia]]></video:title><video:description><![CDATA[Frontotemporal dementia, or FTD for short, refers to a degeneration of the frontal and temporal lobes of the brain. FTD is often mistakenly called Pick disease, or Pick’s disease. However, this is only a specific subtype of frontotemporal dementia, characterized by the presence of Pick bodies, which are tangles of abnormal nerve cell proteins called tau proteins.

Now, if we take a step back and take a look at the brain - it can be divided into four lobes: the frontal, temporal, parietal, and occipital lobes. Within each lobe is a dense network of neurons, which allows neurons to communicate with one another. Like most cells, neurons have a cytoskeleton made up of filaments and microtubules that give the cell its structure. Microtubules help neurons move molecules along the length of the cell, kind of like a railway track. And just like in a railway track, the individual units of a microtubule, called tubulins are tied together with a protein called tau. Tau comes in six different shapes and sizes, or isoforms, and one of the key features of these isoforms is how many times a particular sequence of 29 amino acids gets repeated. For three of those isoforms, it&amp;#39;s repeated three times -- they&amp;#39;re called the 3R isoforms -- and for the other three, it&amp;#39;s repeated four times -- they&amp;#39;re called the 4R isoforms.

Although it&amp;#39;s not completely understood why, in frontotemporal dementia, abnormal protein inclusions form in the cytoplasm or nuclei of neurons. These inclusions are often made up of tau proteins. Specifically, in the case of Pick disease, 3R isoforms of the tau protein get hyperphosphorylated, meaning that phosphate groups keep binding onto the proteins until no more will fit. These hyperphosphorylated tau proteins change shape and stop being able to tie together the tubulins in the neuron&amp;#39;s cytoskeleton. What&amp;#39;s more, the hyperphosphorylated tau proteins start clumping t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Using_an_inhaler:_Information_for_patients_and_families</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NViQ3RpURteZYh9CncUNbNDESvqcS2Ek/_.jpg</video:thumbnail_loc><video:title><![CDATA[Using an inhaler: Information for patients and families]]></video:title><video:description><![CDATA[Inhalers are small devices that deliver medications like bronchodilators and anti-inflammatory drugs to the lungs.

Zooming in a little bit, bronchodilators open up the airways, allowing more air to flow into the lungs, and anti-inflammatory drugs reduce inflammation and swelling in the lungs.

The first major class of inhalers is a metered dose inhaler. 

Metered dose inhalers have a metal canister with an actuator, otherwise known as a plastic covering, as well as a mouthpiece. 

They’re often used with a valved holding chamber or a spacer. 

Now, when you’re using a metered dose inhaler for the first time, you should first prime it by removing the cap and shaking it for 5 to 10 seconds. 

Then aim the mouthpiece at the floor, and press the top of the canister to puff out the medication. 

You may need to re-shake the inhaler and dispense the medication a few more times, depending on the medication.

Now when you’re ready to use the inhaler start by shaking it for 5 to 10 seconds.

If you’re using a spacer, you can insert the mouthpiece of the inhaler into the spacer. 

Then exhale fully and place your mouth around the mouthpiece of the inhaler or spacer. 

Be sure to part your teeth and tuck your tongue out of the way to clear a path for unobstructed airflow, and aim the inhaler at the back of your throat. 

Inhale and then press the top of the canister as you take a deep, slow breath through your mouth for 3 to 5 seconds. 

Next, hold your breath as long as you comfortably can, up to 10 seconds, then remove the inhaler and exhale. 

If you need a second puff of medication, or have been instructed to take a second puff of medication, you should wait about 30 seconds, then repeat the process. 

After you’re done, if the medication is a type of steroid, rinse your mouth with water. 

Swish, gargle, and spit—don’t swallow the water. This prevents any excess medication from remaining on the inside of your mouth. 

Another type of inhaler is a dry powder inh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ischemic_stroke</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CRIQbT6tQYyozPLBbEMUfKcWQFalRtmj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ischemic stroke]]></video:title><video:description><![CDATA[There are two main types of stroke: an ischemic stroke which is when there’s a blocked artery that reduces blood flow to the brain and a hemorrhagic stroke which is when an artery in the brain breaks, creating a pool of blood that damages the brain. 

Of the two, ischemic strokes are much more common, and the amount of damage they cause is related to the parts of the brain that are affected and how long the brain suffers from reduced blood flow. 

Now if symptoms self-resolve within 24 hours, it’s called a transient ischemic attack and there are usually minimal long-term problems.

OK - let’s start with some basic brain anatomy. The brain has a few regions - the most obvious is the cerebrum, which is divided into two cerebral hemispheres, each of which has a cortex - an outer region - divided into four lobes including the frontal lobe, parietal lobe, temporal lobe, and the occipital lobe. 

There are also a number of additional structures - including the cerebellum, which is down below, as well as the brainstem which connects to the spinal cord.

The right cerebrum controls muscles on the left side of your body and vice versa. 

The frontal lobe controls movement, and executive function, which is our ability to make decisions. 

The parietal lobe processes sensory information, which lets us locate exactly where we are physically and guides movements in a three dimensional space. 

The temporal lobe plays a role in hearing, smell, and memory, as well as visual recognition of faces and languages. 

Finally there’s the occipital lobe which is primarily responsible for vision. 

The cerebellum helps with muscle coordination and balance.

And finally there’s the brainstem plays a vital role in functions like heart rate, blood pressure, breathing, gastrointestinal function, and consciousness. 

The brain receives blood from the left and right internal carotid arteries, as well as the left and right vertebral arteries, which come together to form the basilar arte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Treponema_pallidum_(Syphilis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xaPpelBPQGCvcOtw2ZQHQWdVSzmDTr__/_.jpg</video:thumbnail_loc><video:title><![CDATA[Treponema pallidum (Syphilis)]]></video:title><video:description><![CDATA[Treponema pallidum can be considered a gram-negative bacterium even though its cell envelope differs from other gram-negative bacteria.

You might know T. pallidum because it causes syphilis, a sexually transmitted disease that affects the skin and mucous membranes of the external genitalia, and also sometimes the mouth.

Treponema pallidum is an obligate parasite bacteria, meaning it can&amp;#39;t survive outside a living body. To be more specific, outside of a human being&amp;#39;s body. They belong to a group of bacteria called spirochetes, which are long and thin, and contain endoflagella, which are a band of protein filaments that coil within the spirochetes, and give them a spiral shape - kind of like a curly fry, but a little less appetizing. The endoflagella also help the spirochetes to move around by spinning or twisting, a bit like a drill that’s slowly boring into a piece of wood.

People that have syphilis can transmit the disease to others, in one of two ways. The first way is called acquired syphilis and that’s when Treponema pallidum enters the body through bodily fluids. That can happen when there are tiny cuts, or breaks in the skin or mucous membranes of the external genitalia or mouth and when there’s sexual contact - including oral, anal, and vaginal sex.

It can also happen when people share contaminated needles, or when they have direct contact with a skin lesion on an infected person, because the lesion is covered in this fluid which is rich in spirochetes. The second way is called congenital syphilis and that’s when a pregnant person has syphilis and Treponema pallidum infects a baby either in the uterus or while the baby exits through the vagina at birth.

In acquired syphilis, there are three stages to the infection. The first stage is called primary syphilis or the early localized stage, and it usually starts 1 to 3 weeks after the T. pallidum lands on the skin or mucous membrane.

During this stage, the spirochetes destroy the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Serum_sickness</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P2CWH0TOTUuKU2RI8yPaDxRyReickEbQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Serum sickness]]></video:title><video:description><![CDATA[Let&amp;#39;s imagine for a minute that you found yourself in the somewhat unfavorable position of having been bitten by a venomous snake.

Now, to treat that, you might get injected with anti-venom, which is the serum, or just the liquid part of blood and it’s had the coagulation proteins removed, and it comes from another animal, like a mouse, and that mouse has already encountered that particular venom and so it’s developed antibodies against it. These antibodies can bind to the venom molecules and render them harmless.

Now normally that&amp;#39;s the end of that, but in serum sickness, your immune system actually mounts an attack against the foreign serum. It’s just like attacking a friendly police officer that’s trying to help you out. Serum sickness is a type III hypersensitivity reaction, which means that it’s mediated by immune complexes, which are combinations of antibodies and soluble antigens, in this case the antigens are the foreign antibodies in the serum.

Now normally, antibodies, which are sometimes called immunoglobulins, are produced by plasma cells, which are fully mature and differentiated B cells. B cells have multiple IgM antibodies on their surface and they act like receptors. When an antigen binds to two of these receptors it’s called cross-linking. This triggers the B cell to take in the antigen, break it all apart, and present a piece on the surface on a protein called MHC class II, which stands for major histocompatibility complex class II. Nearby T helper cells can then bind to the MHC class II protein via their T cell receptor, this happens along with costimulatory molecule CD4.

The B cell’s CD40 also binds to the T cell’s CD40 ligand, and that causes the T cell to release cytokines, which then results in B cell activation and class switching, or isotype switching. This means that it changes from producing IgM antibodies to producing IgG antibodies instead.

After class switching, B cells become plasma cells and they focus]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fetal_circulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j-b0_vnWRnu1Ob2hcY1E6_vAQTi-7BiV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fetal circulation]]></video:title><video:description><![CDATA[In the adult, oxygenated blood is sent from the left atrium to the left ventricle and then out the aorta to arteries in the rest of the body. Blood then returns through veins to the right atrium and goes into the right ventricle, which pumps it to the lungs in order to drop off carbon dioxide and pick up oxygen. 

In the fetus, the lungs are not mature enough to do that, so oxygenation happens in the placenta, and four key adaptations or structures make this possible. 

These are the umbilical veins and arteries in the umbilical cord, the ductus venosus, the foramen ovale, and the ductus arteriosus. 

So imagine you’re an oxygen rich red blood cell that has to get from the placenta to the fetal tissues. Blood from the placenta is highly oxygenated blood, so let’s color that red. 

From the placenta, blood heads through the umbilical vein, the first adaptation of fetal circulation, that carries oxygenated blood toward the liver. 

When the umbilical vein reaches the liver, it dumps blood into the portal vein. The blood in the portal vein goes out to every lobule of the liver, and becomes deoxygenated so we’ll color it blue, although in reality it’s more of a dark, dark red color.  

This deoxygenated blood enters the hepatic vein, which then drains into the inferior vena cava, which is one of two enormous veins that carries deoxygenated blood from the lower half of the body to the right atrium. 

Now, from the umbilical vein, a vessel called the ductus venosus forms and connects to the inferior vena cava. This bypasses the liver circulation, and represents the second adaptation of fetal circulation..  

From there, the red oxygenated blood from the placenta mixes with the blue deoxygenated blood from the lower body, so red and blue make purple, and that purple blood is joined by the blood from the hepatic vein before it all flows into the right atrium. 

Meanwhile, deoxygenated blood from the upper body flows through the other enormous vein, the superior ve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renin-angiotensin-aldosterone_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Lj3OlxAaSz_zi7o4F5i-aeOVTOyFlhMR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renin-angiotensin-aldosterone system]]></video:title><video:description><![CDATA[The main job of the cardiovascular system is to keep the blood moving, and to help facilitate that - blood pressure and more importantly is kept under tight control.

A major way the body does that is through a set of hormones that make up the renin- angiotensin- aldosterone system.

But, first things first.

Everything starts in the kidney.

Now, within each kidney, blood from the renal artery flows into smaller and smaller arteries, eventually reaching the tiniest of arterioles called the afferent arterioles.

After the afferent arteriole, blood moves into a tiny capillary bed called the glomerulus.

The glomerulus is part of the functional unit of the kidney, called the nephron.

There&amp;#39;s about 1 million nephrons in each kidney, and each of them consists of a renal corpuscle - made up of the glomerulus and the Bowman’s capsule surrounding it - and a renal tubule.

The renal corpuscle is where blood filtration starts. 

Interestingly, once the blood leaves the glomerulus, it does not enter into venules.

Instead the glomerulus funnels blood into efferent arterioles which divide into capillaries a second time.

These capillaries are called peritubular capillaries - because they are arranged around the renal tubule.

Now, the renal tubule is made up of a proximal convoluted tubule, the nephron loop - also known as the loop of Henle - which has an ascending and a descending limb - and finally the distal convoluted tubule.

As filtrate makes its way through the renal tubule, waste and molecules like ions and water are exchanged between the tubule until, finally, urine is formed.

At the same time, the peritubular capillaries reunite to form larger and larger venous vessels.

The veins follow the path of the arteries, but in reverse - so they keep uniting until they finally form the large renal vein, which exits the kidney and drains into the inferior vena cava.

Okay - now if we zoom into the wall of the afferent arterioles, we’ll find a very special]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Regulation_of_renal_blood_flow</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JwGjRvePRN2C9K7AMiOVjAz7QAqxEBhP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Regulation of renal blood flow]]></video:title><video:description><![CDATA[The kidneys’ main job is to filter the blood to remove the waste - so it shouldn’t be surprising that they receive about a quarter of the blood that the heart pumps with each beat. 

On average, the heart pumps out almost 5 liters of blood every minute, so one-quarter of that - or 1.25 liters - flows into the renal artery every minute. 

Blood from the renal artery flows into smaller and smaller arteries, eventually reaching the tiniest of arterioles called the afferent arterioles. 

After the afferent arteriole, blood moves into a tiny capillary bed called the glomerulus. 

The glomerulus is part of the functional unit of the kidney, called the nephron. 

There’s about 1 million nephrons in each kidney, and each of them consists of a renal corpuscle - made up of the glomerulus and the Bowman’s capsule surrounding it -  and a renal tubule. 

Interestingly, once the blood leaves the glomerulus, it does not enter into venules. 

Instead the glomerulus funnels blood into efferent arterioles which divide into capillaries a second time. 

These capillaries are called peritubular capillaries - because they are arranged around the renal tubule. 

Now, blood filtration starts in the glomerulus, where an urine precursor called filtrate is formed. 

The amount of blood filtered into the nephrons by all of the glomeruli each minute is called the glomerular filtration rate, and it’s actually just a small fraction of the blood that gets to the kidneys, because the glomerulus doesn’t allow red blood cells and proteins to pass through and be excreted into urine. 

So right from the start, what passes through the glomerulus is mostly plasma - which normally makes up about 55% of blood. 

What is more, the glomerulus only filters about 20% of that plasma in one go. 

So when all is said and done, of those around 1.25 liters that the heart pumps out every minute, glomerular filtration rate is normally around 125 milliliters. This filtrate then enters the renal tubule. 

The]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glomerular_filtration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BL93lAmaSpmHZFmvTK9e-YabTNOfzLr6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glomerular filtration]]></video:title><video:description><![CDATA[The workhorses of the urinary system are the kidneys which are the twin, bean-shaped organs in your body that clear harmful substances by filtering blood - like a water purification plant that helps clean the drinking water for a city. 

Blood filtration happens inside the over a million nephrons scattered inside each kidney, and each nephron is made up of a renal corpuscle and a renal tubule. 

So let’s zoom in on the renal corpuscle, which is where blood filtration starts. 

The renal corpuscle is made up of the glomerulus - a tiny bed of capillaries - and the Bowman’s capsule surrounding the glomerulus.

Between the glomerulus and Bowman’s capsule there’s a space called Bowman’s space. 

Blood gets to the glomerulus through the afferent arteriole, but interestingly enough, once the blood leaves the glomerulus, it doesn’t enter into venules. 

Instead the glomerulus funnels blood into efferent arterioles which divide into capillaries a second time. 

These capillaries are called peritubular capillaries - because they are arranged around the renal tubule. 

Now, the first step in blood filtration happens at the glomerular filtration barrier. 

The glomerular filtration barrier is made up of three layers and together they separate the blood inside the glomerular capillaries from the fluid inside Bowman’s capsule. 

They work like a sieve, allowing water and some solutes in the plasma like sodium, to pass into Bowman’s space, while keeping red blood cells and plasma proteins in the blood.

Starting from the capillary lumen, the first layer of the glomerular filtration barrier is the endothelium, made up of glomerular capillary endothelial cells. 

These cells have fenestrations, which are like pores in the cell themselves, tiny spots where the cytoplasm isn’t filled in so that solutes and proteins can pass right through. But the fenestration are tiny so they block red blood cells from passing through. 

Blood minus red blood cells is plasma - so plasma gets]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acid-base_map_and_compensatory_mechanisms</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H7GZojfGT7iBoZlehx850NzbTCyP9R8h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acid-base map and compensatory mechanisms]]></video:title><video:description><![CDATA[Every single moment, there are trillions of biochemical reactions going on inside our bodies. These reactions are mediated by enzymes, and for these enzymes to function properly, the pH of our body fluids needs be within a tightly regulated range. 

This pH depends on the ratio of the concentration of bases, mainly HCO3−, and acids, mainly CO2, and it’s calculated by a lengthy, complicated equation, known as the Henderson-Hasselbalch equation, where pH = 6.1 + log HCO3− concentration / 0.03 partial pressure of CO2.

If we focus on the pH of our arterial blood, we can design a diagram, or acid- base map, with the concentration of HCO3− on the x axis, and the partial pressure of CO2, or PCO2, on the y axis. 

Using the Henderson-Hasselbalch equation, we can plot a line called an isohydric line that starts at the origin. 

The term isohydric means that along these points, they all share the same or “iso-“ concentration of hydrogenated ions or same pH - “hydric”. 

For example, let’s say HCO3− concentration is 24 mEq/L and PCO2 is 40 mmHg. According to the Henderson- Hasselbalch equation, this would give us a pH of 7.4. Now, we’ d have the same pH of 7.4 if there was a HCO3− concentration of 36 mEq/L and PCO2 of 60 mmHg, or with a HCO3− concentration of 12 mEq/L and a PCO2 of 20 mmHg. 

In fact, we can draw out two more isohydric lines - this time for a pH of 7.35, and another for a pH of 7.45. A normal pH is between 7.35 and 7.45, so you can see that there are a lot of combinations of HCO3− concentration and PCO2 that are between these two lines that would result in a normal pH. 

In fact, because it’s so important for the body to stay between these lines, the body has designed several mechanisms to maintain homeostasis or balance. 

One mechanism involves the lungs, specifically the rate and depth of breathing which controls the amount of CO2 that’s breathed out. 

And another mechanism involves the kidneys, which, slowly can carefully control the amount of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pheochromocytoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JRleHsCQQ7GqOYQmJnPJI6rwSla4FxsP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pheochromocytoma]]></video:title><video:description><![CDATA[In pheochromocytoma, pheo- means dark, chromo- refers to color, cyto- refers to a cell and -oma means tumor. So a pheochromocytoma is a rare adrenal gland tumor where the cells darken when they form tumors.

Now, there are two adrenal glands, one above each kidney, and each one has an outer layer called the cortex and an inner layer called the medulla. 

In the medulla, there are cells called chromaffin cells and their job is to make hormones called catecholamines. The catecholamines include epinephrine and norepinephrine - the fight or flight hormones. 

Normally, the chromaffin cells in the adrenal gland secrete epinephrine and norepinephrine into the blood when something scary happens - like someone saying BOOM! 

The epinephrine and norepinephrine bind to alpha and beta receptors in various tissues throughout our body and cause an increase in cardiac output, increased blood pressure, dilated pupils, increased blood flow to skeletal muscles, and increased blood sugar. 

Pheochromocytomas are tumors that form when these chromaffin cells start to divide uncontrollably. 

They typically form in one of the adrenal glands, but rarely can be in both and sometimes can even develop in other parts of the body where chromaffin cells are found like the carotid arteries in the neck, the bladder, and the abdominal aorta. 

Most pheochromocytomas arise sporadically, but some are associated with an inherited syndrome. 

One of these is multiple endocrine neoplasias type 2A and type 2B, where pheochromocytoma is caused by a mutation in the RET gene, which is a protooncogene that encodes for proteins that promote cell growth and division. 

When the RET gene mutates, it becomes an oncogene that causes the cells to divide constantly. 

Another disease associated with pheochromocytomas is Von Hippel-Lindau disease, which develops when there’s a mutation in the VHL gene which codes for the von Hippel-Lindau tumor suppressor protein. 

Tumor suppressor proteins normally inh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmoregulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xFZPmT22QT64G6byTBP8GjCARGKxAvEq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osmoregulation]]></video:title><video:description><![CDATA[Osmoregulation refers to the regulation of body fluid solute concentrations. 

Solute concentrations are measured in osmolarity, usually mOsm/L, which is the number of osmoles within a litre of solution. 

Now remember that an osmole refers to the individual ions within a solution. For example, a solution of 1 mmol/L of a salt like NaCl which can split apart in water to become Na+ and Cl- will have both Na+ and Cl- contribute to the osmolarity. So 1 mmol/L of NaCl is 2 mOsm/L.

In a normal body, blood plasma osmolarity is very tightly regulated and kept at around 290 to 300 mOsm/L. 

The main components of this osmolarity is made up of ions like sodium, glucose, and urea. 

To get the actual osmolarity of the body, a calculation like this one can be used: = 2[Na+] + [Glucose]/18 + [ BUN ]/2.8, where [Glucose] and [BUN] are measured in mg/dL. 

Both glucose and BUN can be converted from mg/dl to mOsm/L by dividing them by 18 and 2.8 respectively.

Let’s say that it&amp;#39;s a super sunny day out and you forget to bring water with you. Well first, as you walk around, you’re constantly losing water through sweat as well as water vapor from your mouth and nose as you breathe out - these are insensible water losses. Without drinking water, you can quickly get dehydrated. 

This causes your plasma osmolarity to increase, because the fluid levels in your blood drop, but the total number of solute particles in remains roughly the same. 

Two things now begin to happen simultaneously. First, a region in the brain called the anterior hypothalamus has a cluster of neurons called supraoptic nuclei, which have osmoreceptors that sense even tiny changes in osmolarity, as small as 1 mOsm/L. These neurons are always sampling the blood that passes by. 

With increases in plasma osmolarity, water will flow out of the cell causing it to contract. 

Increases in osmolarity past the normal set point of 290 to 300 mOsm/L stimulates the hypothalamus to produce antidiuretic hor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lewy_body_dementia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A55RgOLZTTmfWOEDEBrs-M91QZi3gwYR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dementia with Lewy bodies]]></video:title><video:description><![CDATA[Lewy body dementia is a type of dementia, where individuals lose their memory and have difficulty learning new information. 

Lewy bodies refers to protein deposits found inside neurons, and they’re named after Frederic Lewy, the neurologist who discovered them. 

Lewy body dementia is a neurodegenerative disease, meaning that it worsens over time, and it’s the disease that afflicted comedian and actor Robin Williams.

The brain is made up of billions of neurons that communicate with each other by releasing neurotransmitters.

Most neurons in the cerebral cortex are called cholinergic neurons because they produce acetylcholine. 

In contrast, neurons in a section of the midbrain called the substantia nigra are in charge of initiating movement and other motor functions. 

These neurons are called dopaminergic because they produce dopamine.

The underlying cause of Lewy body dementia isn’t well understood. 

Normally, neurons contain a protein called alpha synuclein, and in Lewy body dementia, this protein gets misfolded within the neurons. 

The misfolded alpha-synuclein aggregates to form Lewy bodies that deposit inside neurons, particularly in the cortex and the substantia nigra. 

Under a microscope, Lewy bodies look like dark, eosinophilic inclusions inside the affected neurons. 

As the disease progresses, more and more neurons accumulate Lewy bodies and die. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_insipidus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xAvbJkxsQEy75kAi32IBU409Q-C_6Nfn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes insipidus]]></video:title><video:description><![CDATA[With diabetes insipidus, “diabetes” means an increased passing of urine, and “insipidus” means tasteless; so diabetes insipidus is a condition characterized by the production of large quantities of dilute and tasteless urine. 

The tasteless urine of diabetes insipidus distinguishes it from diabetes mellitus which describes sweet tasting urine- and, yes, urine was really tasted at one point in time to make that distinction!

Now, in the brain there’s a region called the hypothalamus.

Inside the hypothalamus are osmoreceptors, which can sense the osmolality of the blood, or how concentrated it is.

Osmolality is the concentration of dissolved particles in the blood plasma, or the liquid portion of blood.

There are a number of dissolved particles in the blood plasma, but the major ones are glucose, sodium, and blood urea nitrogen, and a normal osmolality is between 285 and 295 milli Osmoles per kilogram. 

During periods of dehydration there is an increase in concentration of these particles in the blood and osmolality increases.

The osmoreceptors in the hypothalamus detect the increased osmolality and that triggers the sensation of thirst, which tells us to drink more water. The water then gets absorbed and dilutes the blood, bringing the osmolality back to normal. 

In addition to osmoreceptors, the hypothalamus also contains a cluster of neurons that are found in a specific spot called the supraoptic nucleus.

These neurons produce a hormone called antidiuretic hormone, or ADH. ADH is also called vasopressin because it causes smooth muscle around the blood vessels to contract, which increases blood resistance and raises blood pressure. 

When the osmoreceptors detect high osmolality, they signal the supraoptic nucleus to send ADH down the supraoptico-hypophyseal tract, which runs through the infundibulum or pituitary stalk, and into the posterior pituitary gland, where it is then released into the blood. 

ADH travels to the kidneys, specifically to th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Frank-Starling_relationship</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d_bYI-tMSe2geCHVR0z9M4p9Rxy3aO5S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Frank-Starling relationship]]></video:title><video:description><![CDATA[More than a century ago, two physiologists, Otto Frank and Ernest Starling discovered that as the heart gets filled up with more blood during diastole, it contracts harder and pumps out more blood during systole. So they came up with the Frank Starling Law to explain this relationship.

To understand this relationship, let’s zoom into the wall of the ventricles. The bulk of these walls is made up of short, branched cardiac muscle cells packed one next to the other. Zooming in further, if we look inside the muscle cells, we see bundles of myofibrils, or long chains of sarcomeres. The sarcomere is the smallest structure in the muscle that is capable of contracting so it&amp;#39;s considered the basic contractile unit of the muscle. The sarcomere has two Z discs that form its boundary and a M line in the middle.  Attached to the Z disc are thin filaments made of actin protein. These actin filaments have structural polarity which means both ends of the filament look different.  We can think of it like an arrow with the pointed end being the “minus end,” pointing towards the M line, and the tail end being the “plus end,” attached to the Z disc. Just like an arrow, the actin filament can only move in one direction: the direction it’s pointed at.  Attached to the M line are the myosin filaments which are thick bundles of myosin proteins with two globular heads. During a muscle contraction, the myosin heads grabs onto the actin filaments, and pull them towards the M line which brings the two Z discs closer together.  

Overall, the amount of tension developed, or the force of muscle contraction during systole, depends on the number of myosin heads that bind to actin. And this number directly depends on the length of the overlapping section between actin and myosin filaments. The length of the overlapping section depends on the overall length of the sarcomere. And the length of the sarcomere depends on how much blood fills the ventricle during diastole - beca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Familial_adenomatous_polyposis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VQA86vxDT-uaONEsfUC7WYQnRL_EHjc6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Familial adenomatous polyposis]]></video:title><video:description><![CDATA[With familial adenomatous polyposis, or simply FAP, familial refers to the fact that the disease runs in the family, and adenomatous polyposis refers to the fact that people affected develop multiple polyps that arise from the glands in the large intestine, which includes the colon and the rectum. 

Now, the walls of the gastrointestinal tract are composed of four layers. 

The outermost layer is called serosa. 

Then there’s the muscular layer, which contracts in a synchronized way to move food through the bowel.

Then there is the submucosa, which consists of a dense layer of tissue through which blood vessels, lymphatics, and nerves run and branch into the mucosa and the muscular layer. 

Finally, the inner lining of the intestine is called the mucosa; it surrounds the lumen of the gastrointestinal tract, and comes into direct contact with digested food. 

The mucosa is organized as invaginations called the intestinal glands or colonic crypts, lined with large cells that are specialized in absorption.

Familial adenomatous polyposis is caused by an autosomal dominant mutation in the adenomatous polyposis coli gene or APC gene on chromosome 5q, which is a tumor suppressor gene. 

Tumor suppressor genes stop cells from dividing uncontrollably. 

But if the gene is mutated and the cell is without a functioning APC, the intestinal gland cells are more likely to accumulate mutations and start dividing faster than usual - ultimately giving rise to polyps, which are benign outgrowths of intestinal gland tissue. 

Even though for any single polyp the chance that it evolves into cancer is generally quite low, polyps might accumulate additional mutations in other genes like the p53 gene (another tumor suppressor) or K-ras gene (a proto-oncogene), and with enough mutations, a cell might become completely unregulated and might start invading nearby tissue and become malignant. 

Polyps can be classified by their gross appearance. 

Some are flat, which means that t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aqueductal_stenosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b9kjIx4FSGipf0JNpJPOnKxAQaqiAWPc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aqueductal stenosis]]></video:title><video:description><![CDATA[With aqueductal stenosis, aqueductal refers to a channel in the brain that allows fluid to flow through, and stenosis refers to a narrowing. 

So aqueductal stenosis is a problem where a channel in the brain’s ventricular system gets narrowed, and that makes it hard for cerebrospinal fluid to flow through.

Let&amp;#39;s start with some relevant anatomy. 

The brain has four interconnected cavities in the brain called ventricles, and each one contains a structure called a choroid plexus. 

The choroid plexus is made up of ependymal cells which produce cerebrospinal fluid - a fluid that helps provide buoyancy and protection, as well as metabolic fuel for the brain. 

Highest up, are two C-shaped lateral ventricles that lie deep in each cerebral hemisphere.

The two lateral ventricles drain their cerebrospinal fluid into the third ventricle, which is a narrow, funnel-shaped, cavity at the center of the brain. 

The third ventricle makes a bit more cerebrospinal fluid and then sends all of the cerebrospinal fluid to the fourth ventricle via the cerebral aqueduct. 

The fourth ventricle is a tent-shaped cavity located between the brainstem and the cerebellum. 

After the fourth ventricle, the cerebrospinal fluid enters the subarachnoid space, which is the space between the two inner linings of the brain - the arachnoid and pia mater. 

Cerebral aqueduct stenosis develops when there’s a blockage of the cerebral aqueduct between the third and fourth ventricle, and most of the time this blockage is caused by a tumor. 

Most often it’s a pineal gland tumor, which sits just dorsal to the aqueduct at the level of the midbrain. 

Cerebral aqueduct stenosis can also be a congenital problem like if the channel itself is malformed, with lots of abnormal branching that have dead-ends. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dandy-Walker_malformation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k6wCNYXvRBmIjCuPryNQqbOHRwuQNWOZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dandy-Walker malformation]]></video:title><video:description><![CDATA[Dandy-Walker malformation, first described by  Dr. Walter Dandy and Dr. Arthur Walker, is a congenital brain defect where there’s a cystic malformation in the cerebellum that blocks cerebrospinal fluid from exiting the brain. 

This results in increased intracranial pressure and can affect the cerebellum’s ability to control motor skills like walking.

The cerebellum, or &amp;quot;little brain&amp;quot;, sits just below the main part of the brain and it’s divided at the midline into two hemispheres by a short worm-like structure called the vermis. 

The cerebellum is contained within the back of the skull, in an area known as the posterior fossa, and it sits above the foramen magnum, an opening at the base of the skull through which the spinal cord enters. 

The cerebellum controls balance and posture, and helps to initiate as well as fine-tune voluntary motor activity - think about the fancy finger work of a piano player or the vocal cords of a singer - that’s the cerebellum in action. 

Now, within the brain there are also four interconnected cavities called ventricles, each of which create and help circulate cerebrospinal fluid. 

Highest up, are two C-shaped lateral ventricles that lie deep in each cerebral hemisphere.

The two lateral ventricles drain their cerebrospinal fluid into the third ventricle, which is a narrow, funnel-shaped, cavity at the center of the brain. 

The third ventricle makes a bit more cerebrospinal fluid and then sends all of the cerebrospinal fluid to the fourth ventricle via the cerebral aqueduct. 

The fourth ventricle is a tent-shaped cavity located between the brainstem and the cerebellum and is continuous with the central canal. 

After the fourth ventricle, the cerebrospinal fluid enters the subarachnoid space, which is the space between the two inner linings of the brain - the arachnoid and pia mater. 

In a Dandy-Walker malformation, there are three main defects. 

First, there’s a cyst in the fourth ventricle which ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyper_IgM_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EPL3Xk8YR-arjwdkjqCwdOg-Qx_U1eAs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyper IgM syndrome]]></video:title><video:description><![CDATA[Hyper IgM syndrome is a problem where B cells are unable to undergo antibody class-switching, meaning that they can produce IgM antibodies, or immunoglobulins, but struggle to produce other types of antibodies, and that leaves individuals at risk for certain infections.

Let’s take a look at how B cells end up secreting different types of antibodies. Each B cell is born in the bone marrow from a stem cell and develops its own B cell receptor, which sits on the cell surface. The B cell receptor consists of two parts - a protein called CD79 that communicates with the rest of the cell and a membrane bound IgM or IgD antibody that can bind to an antigen. An antigen is any substance recognized by that particular antibody. 

Each antibody has two identical light chains and two identical heavy chains that combine into a Y shape. So this Y-shaped antibody’s got two arms with identical tips, which is called the variable region. This variable region contains an antigen binding domain that’s unique to that antibody.  

Below the variable region, or toward the point where the arms meet, is the constant region where every member of an antibody class is identical – so all IgM antibodies have the same constant region, but IgM and IgA constant regions are different.

And there are five classes of antibodies in total: IgM, IgG, IgA, IgE, and IgD class antibodies. And each antibody class has a slightly different job. For example, IgMs are part of B cell receptors, and are the first free-floating antibodies produced in an immune response. They’re secreted as a pentamer, meaning there are five antibodies connected together, which provides many binding sites for grabbing antigens and taking them out of the blood. Each antibody has complement protein binding sites on the heavy chains, so these IgM pentamers are also great at activating complement proteins, which help destroy and remove pathogens. 

IgG antibodies stick to the surface of bacteria and viruses – and that prevents ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Raynaud_phenomenon</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w4Z-gKUFQjG4RXXiUAkLCtb-Szux25Ep/_.jpg</video:thumbnail_loc><video:title><![CDATA[Raynaud phenomenon]]></video:title><video:description><![CDATA[Raynaud phenomenon is a phenomenon where there’s vasoconstriction of arteries near the skin that make a body part, often the fingers, turn white, then blue, and then red in response to a trigger like cold weather. 

The phenomenon is named after Auguste Gabriel Maurice Raynaud, a French physician, who first described it. 

To clear up some potentially confusing terminology, it’s called Raynaud disease or primary Raynaud phenomenon where the condition occurs alone and is not associated with any other disease, and it’s called Raynaud syndrome or secondary Raynaud phenomenon when it is associated with diseases like systemic lupus erythematosus or scleroderma.

Normally blood flows from large arteries into medium-sized or muscular arteries, and then into small arterioles which carry the blood to capillary beds.

All arterial vessels have three layers: from inside moving out, there’s the endothelium, then the media layer which contains smooth muscle, and finally the adventitia layer which has loose connective tissue and nerves. 

Some nerve fibers in the skin function as thermoreceptors, which sense changes in temperature.

When stimulated, they cause the nerve to fire, sending signals up through the spinal cord to the hypothalamus, which is at the base of the brain.

The hypothalamus serves as the body’s thermostat because it coordinates the brain’s response to temperature changes. 

The hypothalamus is what triggers the thought – “Hey, it’s pretty cold here. Maybe I should find a friendly llama to snuggle with for warmth.”

The hypothalamus also coordinates changes in the sympathetic and parasympathetic nervous system.

For example, normally, there’s a lot of heat energy in the blood, that gets lost to the environment. 

When the sympathetic nervous system gets stimulated it causes contraction of smooth muscle that wraps around arterioles causing vasoconstriction and a reduction of blood flow to the skin. 

That shunts blood away from the skin and towards the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Charcot-Marie-Tooth_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AE9lPCCPShyzu9VjNQj6gB6lRWG-KQno/_.jpg</video:thumbnail_loc><video:title><![CDATA[Charcot-Marie-Tooth disease]]></video:title><video:description><![CDATA[Charcot-Marie-Tooth disease is named after three neurologists - Jean-Martin Charcot, Pierre Marie and Howard Henry Tooth.

The disease is actually not a single disease, but a group of related diseases that are progressive hereditary disorders of peripheral nervous system. 

Said differently, these disorders are inherited, worsen over time, and affect both sensory and motor nerve cells.

Broadly speaking, the nervous system consists of two parts, the central nervous system, and the peripheral nervous system.

The central nervous system consists of the brain and the spinal cord, and the peripheral nervous system includes the nerves that fan out from the central nervous system and connect it with the skin, muscles, organs, and exocrine glands. 

Now, zooming in to a neuron, each one is made up of three main parts. 

The dendrites, which are little branches that receive signals from other neurons, the soma or cell body, which has all of the neuron’s main organelles, and the axon, which transmits the signal to the next neuron in the series. 

Myelin is the protective sheath that surrounds the axons of the peripheral neurons, allowing them to quickly send electrical impulses. 

And this myelin is produced by Schwann cells, which are a group of cells that support neurons.

There are multiple forms of Charcot-Marie-Tooth disease and all of them are related to the defective production of proteins in either the myelin sheath or the neuron’s axon. 

Regardless of the part of the neuron that’s affected, signals fail to reach their target tissues, and this can affect both sensory and motor peripheral neurons. 

The most common forms of Charcot-Marie-Tooth disease are CMT1 and CMT2, both of which are autosomal dominant diseases. 

CM T1 is caused by mutations in the PMP22 and MPZ genes, which encode proteins that are part of the myelin sheath made by the Schwann cells. 

Loss of myelin slows down transmission of electrical impulses through the nerves. 

Over time, Schwa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vasculitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JJDCst7XTM_LGOj-C6BjhYqrSViXWue2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vasculitis]]></video:title><video:description><![CDATA[With vasculitis, you have “inflammation”, of the “blood vessels”, and even though this can happen in arteries or veins, we’re going to focus on vasculitis in arteries because it’s way more common. 

Vasculitides—plural for vasculitis—are categorized by the size of the blood vessels they affect, so we have small-vessel, medium-vessel, and large-vessel vasculitis. 

Typically vasculitis is due to an autoimmune disease, where the immune system confuses a part of normal body as a foreign invader, and there are a couple of ways this might happen.

Sometimes the body confuses the innermost layer of the blood vessel, which is the endothelial layer, with a foreign pathogen and directly attacks it. 

To be a little bit more specific, the white blood cells of the immune system mix up the normal antigens on the endothelial cells with the antigens of foreign invaders like bacteria simply because they look similar—and this is called molecular mimicry. 

This autoimmune confusion is thought to be the cause several types of medium-vessel and large-vessel vasculitides. 

Other times the immune system attacks healthy cells that are near the vascular endothelium, and the endothelial cells are only getting indirectly damaged. 

This is the situation in many small-vessel vasculitides, where the immune system attacks white blood cell enzymes or other non-endothelial cell targets. 

Once the endothelium is damaged either directly or indirectly, almost all vasculitis diseases progress in a similar way. 

The damaged endothelium exposes the underlying collagen and tissue factor, and these exposed materials increase the chance of blood coagulation. 

The blood vessel walls themselves get weaker as they’re more damaged, making aneurysms more likely. 

And finally as the vessel wall heals, it becomes harder and stiffer because fibrin is deposited into the vessel walls as part of the healing process.

And actually, that’s vasculitis in a nutshell. 

The different types of vasculitis ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oxytocin_and_prolactin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RAakK0Q-Qc6XbmZP0LKcPMt4RzWpgK4j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oxytocin and prolactin]]></video:title><video:description><![CDATA[Oxytocin and prolactin are two hormones that are mostly involved in the production and release of milk from the breasts during the nursing period. Prolactin - pro meaning “for” and “lactin” referring to milk - it stimulates the production of milk. 

Oxytocin, on the other hand, makes the smooth muscle cells around the glands in the breasts contract so that they release the milk.

Oxytocin also helps the muscle in the uterus contract during labor. Both of these hormones are synthesized all the way up in the brain, by two interconnected structures – the hypothalamus and the pituitary gland.

So, basically, the hypothalamus is a part of the brain made up of several nuclei – or clusters of neurons.

Two of these nuclei, the paraventricular and supraoptic nuclei, contain neurons that secrete oxytocin, as well as other hormones like vasopressin, or antidiuretic hormone, which is involved in regulating the amount of water in our body. 

When oxytocin is produced, it travels down the axons of these neurons, and reaches the posterior lobe of the pituitary gland. 

Down the length of these axons, there are small dilations called Herring bodies – which store the oxytocin until it’s released in the blood. 

Outside of pregnancy, oxytocin levels are low, but production increases just a bit during an orgasm - so here’s the reason for that lovely “afterglow”.  

Prolactin, on the other hand, is synthesized by special cells called lactotrophs, which are in the anterior lobe of the pituitary. 

In women that are not pregnant or breastfeeding, and in men, prolactin levels are usually kept in check by the hypothalamus in two ways. 

The first way is the most important, and it’s when the hypothalamus secretes a constant stream of dopamine - which is also called prolactin inhibiting factor. 

Dopamine binds to specific receptors on the lactotrophs and inhibits the release of prolactin. 

The second way is when the hypothalamus secretes thyrotropin releasing hormone, also calle]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Measuring_renal_plasma_flow_and_renal_blood_flow</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IcEJ1TnjR5KNf21T9PQPispJQIW37luT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Measuring renal plasma flow and renal blood flow]]></video:title><video:description><![CDATA[Renal blood flow refers to the amount of blood that the kidneys receive over a period of time. 

Blood gets to the kidneys through the renal artery.

Blood from the renal artery flows into smaller and smaller arteries, eventually forming the tiniest of arterioles called the afferent arterioles. 

After the afferent arteriole, blood moves into a tiny capillary bed called the glomerulus. The glomerulus is part of the functional unit of the kidney, called the nephron.

There’s about 1 million nephrons in each kidney, and each of them consists of a renal corpuscle - made up of the glomerulus and the Bowman’s capsule surrounding it -  and a renal tubule.  

Interestingly, once the blood leaves the glomerulus, it does not enter into venules. Instead the glomerulus funnels blood into efferent arterioles which divide into capillaries a second time. These capillaries are called peritubular capillaries - because they are arranged around the renal tubule. 

Now, blood filtration starts in the glomerulus, where an urine precursor called filtrate is formed. 

The amount of blood filtered into the nephrons by all of the glomeruli each minute is called the glomerular filtration rate, and it’s actually just a small fraction of the blood that gets to the kidneys, because the glomerulus doesn’t allow red blood cells and proteins to pass through and be excreted into urine. 

So right from the start, what passes through the glomerulus is mostly plasma - which normally makes up about 55% of blood. What is more, the glomerulus only filters about 20% of that plasma in one go. So when all is said and done, of those around 1.25 liters that the heart pumps out every minute, glomerular filtration rate is normally around 125 milliliters. That plasma-derived filtrate then enters the renal tubule.

The renal tubule is made up of a proximal convoluted tubule, the nephron loop - also known as the loop of Henle - which has an ascending and a descending limb - and finally the distal convol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_adrenal_hyperplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UdwOgUgkQt61jT2KPt3R9ZF5T-uoVmzZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital adrenal hyperplasia]]></video:title><video:description><![CDATA[With congenital adrenal hyperplasia, congenital means present from birth, adrenals refer to the two adrenal glands that sit above the kidney, and hyperplasia refers to increased cell proliferation which leads to tissue growth. 

So congenital adrenal hyperplasia is a disease where there are enlarged adrenal glands that are present at birth, and the reason for the adrenal enlargement is that there’s a deficiency in an enzyme involved with steroid production.

Now, each adrenal gland one has an inner layer called the medulla and an outer layer called the cortex which is subdivided into three more layers, the zona glomerulosa, zona fasciculata, and the zona reticularis. 

The outermost layer is the zona glomerulosa, and it’s full of cells that make the hormone aldosterone. 

The first step in aldosterone production is when an enzyme called cholesterol desmolase turns cholesterol into pregnenolone. 

Pregnenolone is the precursor to all of the adrenal cortex hormones, sometimes called the steroid hormones. 

Next, pregnenolone is turned into progesterone by the enzyme 3 beta-hydroxysteroid dehydrogenase. 

Then, progesterone is turned into 11 deoxycorticosterone by the enzyme 21 hydroxylase. 

11 deoxycorticosterone then gets turned into corticosterone by the enzyme 11 beta-hydroxylase. 

And finally, corticosterone is turned into aldosterone by the enzyme aldosterone synthase. 

Whew! That’s like going through the washing machine twice. 

So the final result is aldosterone which is part of a hormone family called the renin-angiotensin-aldosterone system. 

Aldosterone signals the kidney to reabsorb more Na+ into the blood and excrete more potassium. 

When Na+ is reabsorbed, water also moves into the blood, which increases blood volume and blood pressure. 

The middle layer of the adrenal cortex is the zona fasciculata, and the cells there make the hormone cortisol. 

This process starts when pregnenolone and progesterone move into the zona fasciculata. 

The]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amyloidosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kR6o6VWBTGqbV-Xc-MigxLF3Qwa6p0_C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amyloidosis]]></video:title><video:description><![CDATA[In amyloidosis, “amyloid” refers to starch-like, and it goes back to an observation made by the German scientist Rudolf Virchow, who saw mysterious deposits in the tissue that stained blue with iodine, just like plant starch. 

As it turns out, amyloids are actually just proteins that take on an abnormal shape, which makes them stick together and settle in tissues. 

And amyloidosis is the name for the disease that develops as a result of the tissue damage from these protein deposits.

Normally, our cells produce thousands of proteins each and every moment, and these proteins need to fold into a particular shape in order to do their jobs properly. 

If a protein folds incorrectly, it’s normally spotted right away and destroyed by proteases, which are enzymes that chop up larger proteins into tiny bits.

In amyloidosis, there are a few different ways that protein folding can go wrong. 

One way is when normal proteins are produced in enormous amounts, and just a small fraction of them fold incorrectly. 

A second option is that abnormal proteins with incorrect amino acid sequences are produced in normal amounts, and they fold incorrectly. 

Either way, the misfolded proteins, called amyloids start to build up. 

Sometimes there’s simply too many of them for the protease to handle, and other times, the way that they’re folded makes them tough to break down - a bit like a pistachio that doesn’t have an opening for your fingers to work with. Nightmare. 

When the amyloid proteins get excreted out of the cell, they tend to clump together forming a rigid, insoluble structure called a β-sheet - like a folded sheet of paper. 

These β- sheets then deposit in the extracellular space of tissues and cause damage.

So amyloidosis is a process where there are extra protein deposits, and there are many different proteins and diseases that follow that same underlying process. 

In general, amyloidosis can be systemic, meaning that those protein deposits occur in multiple]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Action_potentials_in_myocytes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8i7nQBTISP6xr_b8RMD8CoqRTASi7Srl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Action potentials in myocytes]]></video:title><video:description><![CDATA[Action potentials are the really fast electrical changes that happen across the membrane of certain cells, and often propagate from one cell to an adjacent cell. And cells in the heart communicate this way. Now, that signal’s gotta start somewhere, so some of these cells, called pacemaker cells, have the responsibility of setting the rhythm and pace of the heartbeat. So they’ve got this really important job, but they’re a relatively tiny group, and make up only about 1% of the heart cells. But they’re able to continually generate new action potentials that get conducted to the rest of the heart, or the other 99%, and so these are what tell the heart to pump. The cells that receive that signal are called myocytes because they make up the myocardium, which is the muscular middle layer of the heart. Myocytes are also called contractile cells because they contract to allow the heart to pump blood. Myocytes are different from skeletal muscle cells though, which get their action potential signals directly from neurons. Cardiac myocytes receive signal from pacemaker cells causing them to contract.

Now let’s focus on a single myocyte cell going through a single action potential. The action potential of a myocyte is broken into five phases. Often they’re shown on a graph of membrane potential vs. time. We’re going to start with Phase 4, because why not.

In phase 4, or the resting phase, our little myocyte friend is at rest, hanging out with an overall charge or membrane potential of -90 mV. Now, the interesting thing is that it has gap junctions which are openings between two myocytes. So when the myocyte’s neighbour depolarizes, some ions - mainly calcium ions - start leaking through the gap junctions and that makes the membrane potential go up to about -70 mV. -70mV is called the threshold potential and it marks the start of phase 0.

Phase 0 is known as the depolarization phase. Basically, some voltage gated sodium channels open up when they sense that the mem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lymphedema</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d0Zkk4IsSJuZtRccygtqKsNdRI_YqJjF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lymphedema]]></video:title><video:description><![CDATA[Lymph is the fluid circulating in the lymphatic system, and edema refers to fluid buildup in the body’s tissues; therefore, lymphedema is a buildup of lymph somewhere in the body’s tissues.Typically, this happens as a result of some obstruction in the lymphatic system.

All right, let’s back up and briefly talk about this lymph stuff. Oxygenated blood gets sent from the heart to your tissues via arteries, which get smaller and smaller until they feed the capillary beds. The capillary beds then provide nutrients to your cells and pick up waste. Now, deoxygenated blood then feeds back into larger and larger veins, and goes back to the heart. Pressure on the arterial side is a lot higher than on the venous side, so as blood comes into the capillary bed from the smaller arteries, called arterioles, the plasma — the colorless, fluid part of blood — is literally forced out into the interstitial space, or the space between cells. The majority of that fluid is reabsorbed on the venous side, but typically there’s more forced into the tissue through the arterial side than is taken out by the venous side.

Here’s where the lymphatic system comes into play. All of that excess fluid gets pulled into the afferent lymphatic capillaries, which are closed-ended vessels found throughout the body, including, scientists discovered in 2015,  in the brain. These lymphatic capillaries have larger openings than the venous capillaries, which means that in addition to the interstitial fluid, they can accept larger proteins, cellular debris, and even bacteria, which get squeezed out of the arterial side, but are too large to get back into the venous capillaries. Once all of that stuff is in the lymphatic system, it’s called lymph. Also, those afferent lymphatic vessels have one-way valves that, along with smooth muscle contraction, keep the lymph moving along toward the lymph nodes, which have immune cells that once again help filter the fluid, getting rid of potential microbial thr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bundle_branch_block</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ql-eVp5QTUeKLC-xQIcGOvRiRwCFtaX2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bundle branch block]]></video:title><video:description><![CDATA[Each heartbeat starts with the heart’s pacemaker cells in the sinoatrial node, sometimes called the SA node, in the right atrium. The SA node sends out an electrical signal that propagates out and contracts both upper chambers. The signal then moves through the atrioventricular node, or AV node, down into the lower chambers. Here it reaches the bundle of His and splits into the left and right bundle branches, which serve the left and the right ventricles. The signal then goes on to each ventricles’ Purkinje fibers, which leads to ventricular contraction.

Now, a “bundle branch block” describes when that electrical signal gets completely blocked or held up along one of the bundle branches. In most cases, this block, or delay, is caused by fibrosis, or scarring, that either occurs acutely or chronically. Acute causes can be things like ischemia, heart attack, or myocarditis, the inflammation of the heart tissue. Chronic conditions might lead to fibrosis of the heart tissue, because they all can cause slow and steady remodeling of the heart muscle; these include: hypertension, coronary artery disease, and cardiomyopathies.If the block happens on the right side, it’s referred to as a right bundle branch block. With this type, the electrical signal starts at the SA node, contracts the atria, moves through the AV node, splits at the bundle of His, and then moves down the left bundle branch, but is blocked on the right bundle branch. This causes the left ventricle to contract first. The signal then spreads from the purkinje fibers of the left ventricle over to the right ventricle, which causes the right ventricle to contract after the left has contracted. So, with right bundle branch block, the right ventricle contracts late. If the block happened to be on the left side instead, which is called a left bundle branch block, the signal would be delayed on that side, and so the right ventricle would contract first, and then the left ventricle would contract late.

No]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Friedreich_ataxia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UNwh-uG3RE_aq7_-qC1lTMH1RLKpRCfp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Friedreich ataxia]]></video:title><video:description><![CDATA[Friedreich’s ataxia is a disorder where there is impaired mitochondrial function that results in damage to various organ systems. In particular, the nervous system gets damaged which causes ataxia, where the muscles cannot be moved in a coordinated way. The disorder also affects other organs like the heart and pancreas. The disease gets its name from the German physician Nikolaus Friedreich who first described the disease over 150 years ago.

So, normally on chromosome 9, there’s a gene called the FXN gene that encodes a mitochondrial protein called frataxin. The normal amount of frataxin varies by tissue, with some tissues like the nervous system, pancreas, and heart, containing lots of it. Frataxin helps put together cofactors called iron-sulfur clusters. It is a combination of iron and sulfur that form part of enzymes with many functions such as electron transfer, a key part of mitochondrial ATP production. 

Friedreich’s ataxia is caused by a mutation in the FXN gene where there is an abnormal repetition of a GAA sequence within that gene. This is called a triplet repeat, or trinucleotide repeat, which means that a group of three DNA nucleotides is repeated multiple times in a row, in this case guanine, adenine, and adenine. Normally, the GAA sequence is repeated 7 to 34 times within the FXN gene. But, in Friedreich’s ataxia there is repeat expansion where there are 100 to 1700 times as many copies, with most individuals having repeats ranging from 600 to 1200 times. 

Now, Friedreich’s ataxia is inherited as an autosomal recessive condition. It’s passed on by parents who are “carriers” because they have one expanded FXN gene and one normal FXN gene, but don’t have any symptoms of Friedreich ataxia.  They end up passing on their expanded FXN genes to their kid. Inheriting both copies of the FXN gene with an expanded GAA repeat is the most common way to get Friedreich’s ataxia. 

The repeat expansion causes gene silencing which is when the FXN gene is n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Retropharyngeal_and_peritonsillar_abscesses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z1nYdAYBShqyWHPsKbKm8hqfSA_Vy_vf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Retropharyngeal and peritonsillar abscesses]]></video:title><video:description><![CDATA[With a retropharyngeal and peritonsillar abscess, an abscess is a collection of pus, and retropharyngeal and peritonsillar describe where the abscess is found. 

A retropharyngeal abscess develops behind the pharynx - in the tissue that lies just behind the back of the throat. 

A peritonsillar abscess develops around the tonsils, particularly the palatine tonsils which are at the back of the throat. 

Let’s start by better defining the locations of these spaces. 

The retropharyngeal space is the region between the pharynx and vertebrae and is bound posteriorly, closer to the vertebrae, by the alar fascia and anteriorly, closer to the pharynx, by the buccopharyngeal fascia. 

These fascial layers are thin fibrous layers that coat muscles, tendons, and bones muscle, and between them in the retropharyngeal space are lymph nodes. 

These lymph nodes are like surveillance stations that bring in lymphatic fluid from the throat and other nearby tissue. 

If there are pathogens in that lymphatic tissue, immune cells in the lymph node can respond and try to destroy the invading pathogens. 

Next, is the peritonsillar region which refers to the palatine tonsils.

The palatine tonsils are on either side of the oropharynx and are attached to the soft palate at the back of the oral cavity. They’re basically dense collections of lymphatic tissue wrapped within a fibrous capsule - like tiny lymph burritos, that help defend against pathogens in the food and air. 

When pathogens like bacteria invade tissues in the mouth they’re brought to nearby lymph nodes. 

When the retropharyngeal lymph nodes or palatine lymph nodes receive a pathogen, it activates an immune response. 

Often times, the first immune cells at the scene are neutrophils, which release chemicals and enzymes that kill bacteria and dissolve pieces of of dead cells, creating a pool of dead material. 

This is a specific type of acute inflammatory response called suppurative inflammation, which simply means]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Excitability_and_refractory_periods</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RuJMpeN3QrCd_nNgvkcyptpKRGWz5vi6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Excitability and refractory periods]]></video:title><video:description><![CDATA[Cardiac excitability refers to the amount of inward current needed by myocytes or myocardial cells, cells in the muscular middle layer of the heart, to depolarize or generate an action potential. Whether or not it depolarizes depends on if its voltage-gated «sodium ion channels are excitable or not. 

A more excitable cell might have more of its Na+ ion channels in the ready state, and even if there were a relatively weak current of Na+ ions flowing in, the cell might still depolarize easily. On the other hand, a less excitable cell might have most of it’s Na+ ion channels inactivated, where they won’t open in response to stimuli, represented by this little ball stuck in the opening, and only a few of them are ready, and it would require a strong current of Na+ ions to flow in before it depolarized. 

So let’s say this is a myocyte in one of the ventricles,, And this is a graph of membrane potential over time. First, a few positive ions like sodium and calcium travel through gap junctions and enter into the cell, raising the membrane potential to a threshold level—typically around 70 mV. At that point, the voltage gated Na+ channels open up, and lots of Na+ ions rush into the cell, causing depolarization. Right after depolarizing, at about +20 mV, the channels become inactivated, making those channels unavailable for another depolarization. After the upstroke, there’s the plateau, and then as the cell repolarizes the sodium channels start to recover, and even though they’re closed, they’re still excitable, and eventually the cell repolarizes back to it’s usual state around -90mV..

During most of the action potential, the myocardial cell is unable to depolarize again, and this is called the absolute refractory period. In other words, during the absolute refractory period, pretty much all the myocyte’s sodium channels are inactivated, so , so even if a bunch of inward current comes from the neighboring cell, it literally can’t depolarize.There are many Na+ ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rett_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DiduG7wdT9ijP3A8p5g3rDnpRduYB5ML/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rett syndrome]]></video:title><video:description><![CDATA[Rett syndrome is a rare neurological disorder that mostly in young girls and causes severe impairments in their ability to talk, walk, eat, and even breathe. 

A classic feature is that children often make repetitive hand movements - like flapping their hands or clasping their hands together tightly. 

The disease was named after Dr. Andreas Rett, a pediatrician who discovered the syndrome in the 1960s.

To begin, the brain is composed of billions of interconnected neurons, each of which is made of up dendrites, that receive signals from other neurons, the soma, or cell body, which has all of the neuron’s main organelles, and the axon which sends signals to other neurons. 

In Rett syndrome there’s an X-linked autosomal dominant mutation of the Methyl-CpG-binding protein 2 gene, or MECP2 gene, which codes for MeCP2 protein. 

The mutation in the MECP2 gene usually occurs sporadically, meaning that it’s usually not inherited from a parent. 

It’s thought that the MeCP2 protein helps to silence or turn off other genes. 

Males have only one X chromosome, so if there’s a mutation in the MECP2 gene, then they cannot make functional MeCP2 protein, and that might be why males with the mutation typically die in utero or shortly after birth. 

Very rarely a male with Klinefelter syndrome, where there’s an XXY set of chromosomes, might develop Rett syndrome. 

Females have 2 X chromosomes, however, so one mutated MECP2 gene can be compensated for by a normal MeCP2 gene on the other X chromosome. 

The genes that are regulated by MeCP2 proteins are particularly important for brain development, specifically to help establish neuronal connections. 

So in young girls, when they’re first born, the low levels of MeCP2 proteins are sufficient for normal brain development. But as the brain grows more complex, the level of MeCP2 becomes insufficient and the brain fails to develop normally. 

In addition to neurologic effects, Rett syndrome is also associated with prolonged]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Poliovirus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ELggtG4-Q3qOhjo0_h1GTrFnRC_fDqRQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Poliovirus]]></video:title><video:description><![CDATA[In poliomyelitis, also called polio, “polio” refers to the poliovirus, which is an enterovirus that invades the intestines, “myel” refers to the spinal cord which is affected in the disease, and -itis refers to inflammation. 

So poliomyelitis is an enteroviral disease first enters the body through the intestines, but then spreads and causes nerve injury in the spinal cord.  

Former US president Franklin D. Roosevelt contracted polio when he was a baby, and it left him wheelchair-bound.  

Broadly speaking, the nervous system consists of two parts. 

The central nervous system consists of the brain and the spinal cord. 

So the peripheral nervous system includes the nerves that fan out from the central nervous system to reach the skin, muscles, and organs. 

Now looking at the cross-section of the brain, there’s gray matter at the periphery of the brain. This is called the cerebral cortex and it consists of nerve cell bodies. 

Just inside the gray matter of the brain, is the white matter, and it consists of nerve axons. 

In contrast, if you look at the cross-section of the spinal cord, the white matter is on the outside and the gray matter is on the inside, and overall it kinda looks like a butterfly. 

If we draw a horizontal line through the spinal cord, the front half is the anterior or ventral half, and the back half is the posterior or dorsal half. 

And the butterfly wings are sometimes referred to as horns; so we have two dorsal horns that contain cell bodies for sensory neurons and two ventral horns that contain cell bodies for motor neurons. 

So for example, if you step on a lego in your living room, the sensation of discomfort is carried from the nerves in your foot, through the peripheral nervous system to reach the dorsal horn in the spinal cord. 

It then travels up the spinal cord to the brain, letting you know that there’s tissue damage. 

In response, your brain sends a message through the upper motor neurons, which are part of the cere]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dermatomyositis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ertXGl_iQaa2yho6lgacfKKbRKK7qV3x/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dermatomyositis]]></video:title><video:description><![CDATA[In dermatomyositis, “-itis” refers to inflammation, “myos-“ to the muscles and “dermato-“ to the skin, so dermatomyositis is an inflammatory disorder which involves both the skin and the muscles. 

Dermatomyositis is considered to be an autoimmune disease, meaning that the immune system has gone rogue and started attacking its own muscles and skin. 

Okay, normally, the cells of the immune system are always hanging around, ready and excited to spot and fight against anything foreign that could cause harm inside the body.  

B- lymphocytes produce antibodies against a specific part of these foreign pathogens, called antigen. 

The tips of these antibodies strongly binds to this antigen, while the base of the antibody, called the constant region, gets recognized by complement proteins.  

These complement proteins are a group of small proteins made by the liver that work together. 

One complement protein cuts or cleaves the next one, activating it and creating an enzymatic cascade. 

This process gets started with C1, the first of the complement proteins, which binds to the Fc, or the constant region of two antibody attached to the pathogen. 

C1 then cleaves C2 and C4. 

Portions of the C2 and C4 binds to the antigen and form an enzymatic complex that cleaves C3 into two portions, C3a and C3b. 

C3b joins the enzymatic complex and then the complex is able to cleave C5 into two portions, C5a and C5b portion.  

C5a and C3a float off into the blood where they attract other cells of the immune system to the affected area. 

Meanwhile, C5b, C6, C7, C8 and multiple C9 proteins, come together on the surface of the pathogen to form the membrane attack complex or MAC. 

The MAC attacks pathogenic cells, such as bacteria, by creating a channel in the cell membrane. 

Because cells have more solutes in them than the outside environment, water flows into the cell by the process of osmosis, and that causes the cell to swell up and burst, which is called cell lysis. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Central_pontine_myelinolysis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DNsTvUNKRgmVrsBOdXvrr4gCQW_M0CsE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Central pontine myelinolysis]]></video:title><video:description><![CDATA[In central pontine myelinolysis, pontine refers to the pons of the brainstem, myelin refers to the fatty layer of insulation that wraps around neurons, and -lysis refers to destruction. 

So, central pontine myelinolysis is the destruction of the myelin sheath around nerve cells that are in the pons. 

The main cause of destruction is rapid osmotic changes, meaning that a lot of water leaves the cells, and dries them out, causing them to die. 

So the other name for central pontine myelinolysis is osmotic demyelination syndrome.

Taking a look at the brain, the pons is part of the brainstem and it’s nestled between the midbrain and the medulla oblongata. 

The pons itself has control centers that help manage the respiration rate and the depth of breathing while we’re awake and when we sleep. So if you try to take a deep breath right now - that’s your pons in action!

Neuron clusters or nuclei for cranial nerves V: trigeminal, VI: abducens, VII: facial, and VIII: vestibulocochlear are also housed in the pons. 

Cranial nerve V allows you to feel things on your face and controls the muscles that help you chew, bite, and swallow. 

Cranial nerve VI allows your eyes to move side to side. 

Cranial nerve VII helps with facial expressions - like making a weird face, and cranial nerve VIII helps with hearing. 

All of these nerves are made up of lots of individual neurons which capture signals from their dendrites, and pass those signals along through their axons. 

In addition to the neurons, there are also supporting cells called oligodendrocytes and astrocytes. 

Oligodendrocytes physically wrap their fatty myelin-rich cell membranes around neuronal axons that are nearby to help action potentials move more quickly through them. 

And astrocytes help repair damaged neurons.

Neurons and oligodendrocytes are very sensitive to changes in the amount of water and electrolytes in themselves and their environment.In other words, in the intracellular and extracellular]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fats_and_lipids</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yEvDMJiaRmawhP9UO6lCGkeDSd6n3d-B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fats and lipids]]></video:title><video:description><![CDATA[Fats are an essential part of a healthy diet. They contribute to the taste and texture of foods, like the smoothness of guacamole and the flakiness of a croissant. Fats are also a major source of energy and a critical component of cells and tissues, and they also help absorb essential vitamins, and can be converted into other molecules like prostaglandins which help cells communicate with each other. 

Fats have a three-carbon backbone called glycerol, as well as fatty acid chains. The fatty acid chain is basically a string of carbon and hydrogen atoms. When an “OH” group from the glycerol molecule binds to a Hydrogen from the fatty acid, an “H20” or a water molecule - gets released, and the two molecules link up. 

If this happens once, the result is a monoglyceride. If it happens twice, it’s a diglyceride, and three times makes a triglyceride. 

Now, there are various types of fatty acid chains, and one way to categorize them is by their length, in other words, how many carbons they have. Short chain fatty acids have 2 to 5 carbons, medium chain fatty acids have 6 to 12 carbons, and long chain fatty acids have 13 or more carbons.

Fatty acid chains are also categorized by the bonds connecting the carbons in the chain. A single bond is just one bond between the carbon atoms, and when a fatty acid chain has only single bonds, it’s called a saturated fatty acid - because it has as many hydrogen atoms as possible or it’s saturated with them. 

Triglycerides with saturated fatty acids are nice and straight so they pack together really well, and as a result they’re usually solid at room temperature. And the longer the saturated fatty acid chain, the more likely it will be solid at room temperature.

Carbons can also have double bonds between them though, and when a fatty acid has one or more double bonds, it’s called an unsaturated fatty acid because it’s not saturated with hydrogen atoms - for every double bond there are two fewer hydrogen atoms. Also, a doub]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Normal_heart_sounds</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RenN1BKYSK2LbRitMo6q1Jg8S6WZ2Lhe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Normal heart sounds]]></video:title><video:description><![CDATA[If you put a stethoscope over the chest, you’ll usually hear something that sounds like lub dub, lub dub, lub dub, which repeats over and over again, with each cardiac cycle, or heartbeat.

Now, the question is, where does this sound come from? Normally, blood is constantly moving through the four chambers of the heart- coming through the veins into the right atrium, going to the right ventricle, then shooting off via the pulmonary arteries to the lungs and coming back from the pulmonary veins into the left atrium and the left ventricle, to be pumped into the aorta. So, in every step, some valves have to open and others have to close. Valves are just “communicating doors” that, when open, allow blood to pass through, and when closed, hold blood within a chamber. So, in total, our heart has four valves- two atrioventricular valves, which separate the atria from the ventricles and are the mitral valve, on the left side, and the tricuspid valve, on the right side, and two semilunar valves, which separate the ventricles from the large arteries coming off of them and are the pulmonary valve, on the right side, and the aortic valve, on the left side. And when these valves are closing, just like a door slamming shut, they are going to make a sound that is transmitted in the direction of the blood flow.

Now the heart is positioned in such a way that the sound of the closing of each of these valves is projected onto a small area on the chest wall. If you place a stethoscope between the second and third rib, known as the right second intercostal space, just next to the upper border of the sternum, you’ll hear the aortic valve closing. Then, if you place a stethoscope in the left second intercostal space, at the left upper sternal border, you can hear the pulmonary valve closing. Making our way down, between the fourth and fifth rib, next to the left lower border of the sternum, is where you can best hear the tricuspid valve closing. Finally, let’s move down to betw]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bell_palsy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sxFGLYyDS0uYxzpfmBqkmntqQ8GA26hO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bell palsy]]></video:title><video:description><![CDATA[Bell palsy, named after the Scottish doctor Charles Bell, who first described the condition, is the most common type of facial nerve palsy. Facial palsy occurs when there’s damage to the facial nerve, also known as the seventh cranial nerve, which results in weakness and paralysis on one side of the face. This can happen due to various conditions, including stroke or tumors, but if the underlying cause remains unknown, we call it Bell palsy. 

Remember when you were a kid and felt crushed because your family was watching a movie instead of your favorite cartoon? That grumpy face you made, that’s your facial nerve telling your muscles what to do. 

The ultimate control of facial muscles comes from the left and right upper motor neurons in the primary motor cortex of the precentral gyrus.  

First, let’s talk about the lower right half of the face. The upper motor neuron from the left side of the brain travels down to the brainstem, crosses over the midline, and connects to a lower motor neuron in the facial nucleus. From here, the lower motor neuron sends signals through the right facial nerve to the lower right half of the face. So, when it comes to the lower part of your face, each side of your brain handles the opposite lower side. 

But the upper half of the face is like “Nah, I want backup and signals from both sides of the brain.” In this case, the upper motor neuron from the left side of the brain extends to the lower motor neuron on the opposite side. But, at the same time, the upper motor neuron from the right side sends backup to the lower motor neuron on the same side. So, when it comes to the upper half of the face, both sides of your brain team up to get the job done. 

Now, let&amp;#39;s focus on the facial nerve, which emerges from the pontomedullary junction of the brainstem. Next, it enters the petrous part of the temporal bone, where it travels through a narrow Z-shaped canal called the facial canal. After passing through the canal, it ex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gingivitis_and_periodontitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T5Odr-jRSKq-kI9Q_FTEp_3WQYmr8KRZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gingivitis and periodontitis]]></video:title><video:description><![CDATA[With gingivitis, gingiva refers to the gums, and -itis refers to inflammation, so gingivitis is inflammation of the gums. 

With periodontitis, peri- means around, and odon-, refers to the tooth, so it’s inflammation and destruction of the supporting structures around the teeth. 

Broadly speaking, the two are on a spectrum starting with simple gingivitis on one end, and if the process doesn’t get treated, it can develop into more severe disease - periodontitis, which is on the other end of the spectrum.

Let&amp;#39;s start by building a model of a tooth and its surrounding structures.

In the mouth, the bone beneath the bottom row of teeth is the mandible, and the bone above the top row of teeth is the maxilla. 

Both bones have an alveolus, or socket, for each tooth.

The socket is lined on the inside by a periodontal ligament. 

Protecting the alveolus on the outside, is a layer of soft, supportive tissue called the gingiva, or gums, that sits on top of the bone. 

The tooth itself can be roughly divided into two parts. 

The first part is the root, and it sits within the alveolus. 

The root is covered by a bonelike substance called cementum, and that’s what the periodontal ligament’s fibers attach to. 

Next, there’s a short zone called the neck, which is the transition between the root and the crown. 

The crown is the visible part of the tooth that protrudes from the gingiva, and it’s covered in enamel.

Enamel has such a high mineral content that it’s the hardest substance in the human body. 

The portion of gingiva that sticks up and is not anchored to the tooth is sometimes called the free gingiva, and the space between the free gingiva and the crown is called the gingival crevice or gingival sulcus. 

A watery substance called gingival crevicular fluid flows into this space in small amounts. 

Gingival crevicular fluid contains various immune proteins and cells like neutrophils, complement proteins, and antibodies. 

Within the mouth there are]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tubular_secretion_of_PAH</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XuWEYu2JSSW-fFDvz_pho1qvT_mP49KP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tubular secretion of PAH]]></video:title><video:description><![CDATA[If we take a cross-section of the kidney, there are two main parts, the outer cortex and the inner medulla. 

If we zoom in, there are millions of tiny functional units called nephrons which go from the outer cortex down into the medulla and back out into the cortex again. 

These nephrons perform the major function of the kidney, which is to clear harmful substances from the body by filtering the blood. 

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins. 

Interestingly, once the blood leaves these glomeruli it does not enter into venules. Instead the glomerulus funnels blood into efferent arterioles which divide into capillaries a second time. 

These peritubular capillaries then reunite and at that point the blood enters venules and eventually drains back into the venous system. 

Now, when blood gets filtered, some fluid remains in the glomerulus, and some fluid goes into the renal tubule. 

The renal tubule is a structure with several segments: the proximal convoluted tubule, the U- shaped loop of Henle with a descending and ascending limb and the distal convoluted tubule, which winds and twists back up again, before emptying into the collecting duct, which collects the final urine. 

Now, zooming in on this nephron’s tubule, each one’s lined by brush border cells which have two surfaces. One is the apical surface which faces the tubular lumen and is lined with microvilli, which are tiny little projections that increase the cell’s surface area to help with solute reabsorption. 

The other is the basolateral surface, which faces the peritubular capillaries, which run alongside the nephron.

Alright, now, one substance that’s filtered out of the glomerulus and into the tubule is para-aminohippuric acid, or PAH for short. 

Actually, PAH is an organic acid, and about 90% is bound to plasma proteins. So, really, only the unbound 10% can pass through the glomerular capillaries. 

Essentially, the high]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Innate_immune_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oemk50XPTMCOhCg67DGSu9MkQmKz_RzU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Innate immune system]]></video:title><video:description><![CDATA[Your immune system is like the military - with two main branches, the innate immune response and the adaptive immune response.

Key features of the innate immune response are that the cells are non-specific, meaning that they don’t distinguish one invader from another invader, the response is really fast - occurring within minutes to hours, and that there’s no memory associated with innate responses.

In other words, the innate response will respond to the same pathogen in the exact same way no matter how many times it sees the pathogen. 

The innate immune response includes things that you may not even think of as being part of the immune system. 

Things like chemical barriers, like lysozymes in the tears and a low pH in the stomach, as well as physical barriers like the epithelium in the skin and gut, and the cilia which line the airways to keep invaders out. 

Now if a pathogen happens to get in, then the immune system kicks in and it usually begins with the macrophage - which is the garbage truck of the body. 

Macrophages eat up dead and dying cells, so that the tissue doesn’t become cluttered with them, and that makes room for new cells. They also eat invading pathogens. 

Since macrophages live in the tissue they begin recognizing pathogens within minutes of an infection. 

And the way that a macrophage figures out if something is a healthy host cell or a pathogen is by the molecules that a cell or pathogen has on it’s surface.

This is because cells of the innate immune response don’t distinguish one invader from another invader. 

You see - pathogens have molecules that humans don’t have and they’re called pathogen associated molecular patterns or PAMPs. 

PAMPs include bacterial wall components like peptidoglycan, lipopolysaccharide or LPS, and lipoteichoic acid, fungal wall components like mannan, and flagella proteins which can be found on some parasites and bacteria.

For intracellular pathogens, like viruses, PAMPs might include the viral RN]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_hormone_and_somatostatin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0eaNedtOQaiFlpfyAKVtaJcZT6Cg8HZn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth hormone and somatostatin]]></video:title><video:description><![CDATA[Growth hormone, also known as somatotropin, is a hormone which helps regulate the rate of growth in the body. 

Secretion of growth hormone is dependent on the hypothalamic-pituitary axis. 

The hypothalamus, which is a part of the brain, secretes growth hormone-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior, or front part of the pituitary gland.

In the anterior pituitary, there are many different types of cells, each responsible for producing a type of hormone.

The growth hormone-releasing hormone binds to a surface protein on one of these cells, called somatotroph cells, and stimulates them to release of growth hormone. 

Normally, growth hormone releasing hormone is released in a pulsatile manner, throughout the day and peaks one hour after you fall asleep, but it is also secreted in response to various forms of internal and external stimuli. 

For example, the hypothalamus senses when there’s hypoglycemia, or low blood sugar, and in response it secretes growth hormone releasing hormone. 

Exercise causes the adrenal glands to secrete epinephrine and that stimulates the hypothalamus to secrete growth hormone releasing hormone as well. 

Also, during puberty, increased levels of estrogen and testosterone stimulate the hypothalamus to release growth hormone releasing hormone, which is responsible for the growth spurt. 

Now there are a few negative feedback loops that generally control the release of growth hormone.

First, increased levels of growth-hormone-releasing hormone in the blood signals the hypothalamus to stop making more.

Second, when growth hormone reaches tissues like the liver, muscles, and bones, they make somatomedins, which are hormones that signal the anterior pituitary to stop producing growth hormone. 

Third, growth hormone and somatomedins together signal to the hypothalamus to produce somatostatin, which is also called the growth hormone inhibitin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epidural_hematoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8_HpIR6SS9aCiZt3NM3kFmrxTtWfbhQY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epidural hematoma]]></video:title><video:description><![CDATA[Epidural hemorrhage can be broken down. &amp;quot;Epi&amp;quot; means above, &amp;quot;dural&amp;quot; refers to the outermost protective layer of the brain, which is called dura mater and and “hemorrhage” refers to bleeding. 

So, an  epidural  hemorrhage is when there’s bleeding above the dura mater.

OK - let’s start with some basic brain anatomy. The brain is protected by the meninges, which are 3 thin layers  of tissue which cover the brain and spinal cord. 

The inner layer of the meninges is the pia mater, the middle layer is the arachnoid mater, and the outer layer is the dura mater.

The pia and arachnoid maters, are also called leptomeninges. 

Between the leptomeninges, there’s the subarachnoid space, which houses cerebrospinal fluid, or CSF.

CSF is a clear, watery liquid which is pumped around the spinal cord and brain, cushioning them from impact and bathing them in nutrients. 

The outer membrane, the dura mater consists of two layers. 

The internal layer of the dura mater lies above the arachnoid mater - the two are separated by the subdural space. 

The external layer of the dura mater adheres to the inner surface of the skull.

These two layers of the dura mater travel together, but at certain spots, the internal layer of the dura mater separates from the external one to form the meningeal folds. 

The meningeal folds help divide the sections of the brain like the falx cerebri which separates the two hemispheres of the cerebrum, and the tentorium, which covers the cerebellum and separates it from the cerebrum. 

Between the external layer of the dura mater and the inner surface of the skull, there are arteries that supply meninges. 

The most common cause of epidural hemorrhage is a head trauma which might happen after tripping and falling in a bathtub. 

The meningeal arteries are protected by the skull but can be damaged by a serious head trauma. 

The most common site is at the pterion which is the spot where the frontal, parietal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Proximal_convoluted_tubule</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cff0TbyeT0OPOKPH9-EdOZDnTqKamuSU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Proximal convoluted tubule]]></video:title><video:description><![CDATA[If we take a cross-section of the kidney, there are two main parts, the outer cortex and the inner medulla. 

If we zoom in, there are millions of tiny tubes called nephrons which go from the outer cortex down into the medulla and back out into the cortex again. 

Nephrons filter out harmful substances in the blood so that we can excrete them into the urine. 

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins. These capillaries have very thin walls and they act like a coffee filter. 

Red blood cells and proteins are large and stay in the capillaries whereas blood plasma and smaller particles get filtered out.

This filtrate, called tubular fluid, collects in a cup shaped structure containing the glomerulus called the Bowman&amp;#39;s capsule.

Together, the glomerulus and the Bowman’s capsule make up the renal corpuscle. 

The Bowman’s capsule is connected to the renal tubule which has a few segments: the proximal convoluted tubule, the U- shaped loop of Henle with a descending and ascending limb, and the distal convoluted tubule which empties into the collecting duct, which collects the urine. 

So the proximal convoluted tubule comes right after the glomerulus and it’s where most of the reabsorption happens in the kidney. It’s called “convoluted” because it has a twisting path. 

Zooming in on the proximal convoluted tubule, it’s lined by tubule cells which are also known as brush border cells. 

On one side is the apical surface which faces the tubular lumen and is lined with microvilli. 

Microvilli are tiny projections that increase the cell’s surface area to help it reabsorb more solutes or water. 

On the other side is the basolateral surface, which faces the interstitium or the space between the tubule and the peritubular capillaries. 

The peritubular capillaries run alongside the nephron and return solutes and water that were reabsorbed into the interstitium back into the circulation. 

Var]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/wound-healing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P2TzkKcWSN29Rm40XpIBCDvERBasUYxL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Wound healing]]></video:title><video:description><![CDATA[Wound healing, is the process where the body repairs damaged tissue after any traumatic injuries--anything from a paper cut to a stab wound. 

Acute wounds heal up quickly over days to weeks, whereas chronic wounds like bed sores, foot ulcers, or infections, can persist for months.

Now, some tissues regenerate more easily than others, and the regenerative capacity of tissue is classified as labile, stable, and permanent. 

Labile tissues like skin, connective tissue, and small and large intestine heal extremely well, because they contain stem cells, which are undifferentiated cells that can divide and renew the cells that have died. 

Stable tissue, like the liver, recover from injury by having mature differentiated cells divide or regenerate via hyperplasia. 

Permanent tissues like skeletal muscle, cartilage, neurons, and cardiac tissue have a weak regenerative capacity, because they lack these stem cells and cannot replicate via hyperplasia. 

Typically, injured permanent tissues are replaced by scar tissue or fibrosis--ultimately resulting in loss of function of the tissue. 

Now when it comes to the skin - which is often the most visible tissue that’s damaged, wound healing occurs by primary, secondary, and tertiary intention. 

Healing by primary intention is when the wound edges come together--like what happens when two wound margins are stitched or sutured together. 

When this happens, stem cells in the epidermis, or uppermost layer of skin are brought close together and can regenerate the damaged tissue near the surface of skin--leaving a minimal scar. 

Healing by secondary intention occurs when the wound edges are too far from one another--this can be consequence of significant tissue loss or if there’s an object embedded in the wound that prevents the edges from coming together. 

Examples of healing by secondary intention include tooth extraction sockets or severe burn injuries. 

Since the stem cells in these wounds do not approximate,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_components</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mh9APp3YSf_vvBhVV00bn3ZhQDOvvMVy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood components]]></video:title><video:description><![CDATA[The word “blood” evokes lots of thoughts - from tiny paper cuts to major injuries - spilling the red liquid is almost never a good thing. That’s because

blood helps us move nutrients and waste around the body, regulate our pH level, and helps prevent infections. 

In fact, some components of blood help prevent the loss of blood during an injury.

The components of blood can be separated out by simply spinning the blood in a centrifuge-- a machine that whips a vial of blood in a circle over and over, really quickly. A bit like what happens to clothes in a washing machine. 

When blood is centrifuged, the heaviest blood components moving to the bottom, and the lightest ones moving to the top. 

Overall, three distinct layers form: the erythrocytes or red blood cells at the bottom, the buffy coat--which contains platelets and immune cells in the middle, and plasma at the top.

So starting at the bottom of the tube, there’s the large layer that takes up approximately 45% of the total blood volume made up of erythrocytes. This value is called the hematocrit.

A decreased hematocrit means that there are too few erythrocytes, either because they’re not being made or because they are being destroyed. 

On the other hand, an increased hematocrit can be due to dehydration, because if there’s less liquid in the blood, then the portion taken up by erythrocytes would rise. 

Alternatively, there might simply be too many erythrocytes being made, which can happen in some diseases. 

Now, the main function of erythrocytes is to carry oxygen to tissues and bring carbon dioxide to the lungs so it can be expired. 

Erythrocytes are shaped liked thin biconcave discs--meaning they have a depressed center which makes them flexible enough to fit through even the smallest blood vessels. 

This shape also increases their surface area which helps them conduct gas exchange efficiently. 

Erythrocytes lack organelles like the nucleus, which creates even more room for hemoglobin prot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscular_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/INUCfTsPSF69mWa3BOE84_EYQEyAMsMG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscular system anatomy and physiology]]></video:title><video:description><![CDATA[The muscular system is made up of three types of muscle tissue: skeletal, smooth, and cardiac muscle tissue.

They differ in terms of their location, cell structure, and innervation. But they also share some characteristics: they’re all excitable, meaning that the cells react to a stimulus, they all contract--meaning that the cells will shorten, they all have extensibility--meaning that the cells can be stretched, and they’re all elastic--meaning that they can recoil or bounce back to their original length. 

Let’s start with skeletal muscles. Skeletal muscles usually attach to bones, but in some cases, they attach to the skin, like the muscles in our face that control facial expression. 

Skeletal muscles are voluntary muscles, meaning that they can be controlled consciously, but some skeletal muscles are also controlled subconsciously. 

Your diaphragm, for example, you can contract consciously when you take a big breath, but it also continues to contract and relax without conscious effort when you’re fast asleep or thinking about other things.

Skeletal muscles help you maintain your posture and stabilize joints, and because skeletal muscles use up a lot of energy as they contract and relax, they also generate a lot of heat as a byproduct. That’s why we shiver to stay warm when it’s really cold.

Now let’s take a look at the biceps brachii, a skeletal muscle in your upper arm. Like most muscles there’s the belly of the muscle and the muscle tendons. 

The muscle belly is the part that contracts and it’s wrapped in a layer of connective tissue called the epimysium. 

Now let’s take a look at the cross-section of the muscle belly, there are thin layers of connective tissue called the perimysium that separate the muscle into fascicles.

Each muscle fascicle consists of a bundle of muscle fibers, and each muscle fiber is a muscle cell, or myocyte.

Every myocyte is surrounded by a smaller connective tissue sheath called the endomysium. 

Together, the endom]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nervous_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mlWV7bQORcOFedtNU7cpIV_pSdWWYkuN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nervous system anatomy and physiology]]></video:title><video:description><![CDATA[The nervous system is involved in nearly everything we do - from how we see, to how we walk and talk. 

The nervous system is divided into the central nervous system, so the brain and the spinal cord, and the peripheral nervous system, which is further divided into the somatic and the autonomic nervous systems. 

Broadly speaking, the nervous system can be split into an afferent and an efferent division. 

The afferent division brings sensory information from the outside into the central nervous system, and includes visual receptors, auditory receptors, chemoreceptors, and somatosensory or touch receptors. 

On the other hand, the efferent division brings motor information from the central nervous system to the periphery, ultimately resulting in contraction of skeletal muscles to trigger movement through the somatic nervous system, as well as contraction of the smooth muscles to trigger activity of the internal organs through the autonomic nervous system.

The nervous system is made up of two main types of cells: neurons and glial cells.

Neurons are the main cells of the nervous system. They’re composed of a cell body, which contains all the cell’s organelles, and when there’s a group of neuron cell bodies that are next to each other in the central nervous system, the whole thing is called a nucleus, while a group of neuron cell bodies that are located outside of the central nervous system is called a ganglion. 

Neurons have nerve fibers that extend out from the neuron cell body- these are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons. 

Where two neurons come together is called a synapse, and that’s where one end of an axon releases neurotransmitters, further relaying the signal to the dendrites or directly to the cell body of the next neuron in the series.

To trigger the release of neurotransmitters, neurons use an electrical signal that races down the axon, known as the action potential. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pericarditis_and_pericardial_effusion</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wEDf06DQR72ipfhsLEIJGpKqQFGQ2k0D/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pericarditis and pericardial effusion]]></video:title><video:description><![CDATA[With pericarditis, “peri” means “around,” card means “the heart”, and itis means “inflamed”. So pericarditis means the pericardial layer of tissue that covers the heart has inflammation. Acute pericarditis generally lasts just a few weeks, whereas chronic pericarditis lasts longer, usually more than 6 months. People who develop pericarditis are also at risk of also developing a pericardial effusion - that’s when the inflammation causes fluid to accumulate around the heart.

The pericardium is a pouch or cavity that the heart sits inside of. The outer layer of this pouch is the fibrous pericardium and it helps keep the heart in place within the chest cavity. The inner layer of the pouch is the serous pericardium that includes the pericardial cavity, and is filled with a small amount of fluid that lets the heart slip around as it beats. The cells of the serous pericardium secrete and reabsorb the fluid, so usually there’s no more than 50 milliliters of fluid in the pericardial cavity at one time -  that’s about as much as a shot glass.

Now, the cause of acute pericarditis is usually idiopathic, meaning that we don’t know what causes it. When the cause is identified, it’s usually a viral infection, like Coxsackie B virus. Another cause is Dressler syndrome which occurs several weeks after a myocardial infarction, or heart attack. Basically, when heart cells die in a myocardial infarction, it leads to massive inflammation that also involves the serous pericardium. Another cause of pericarditis, called uremic pericarditis, is when blood levels of urea, a nitrogen waste product, get really high usually due to kidney problems. The high levels of urea irritate the serous pericardium, making it secrete a thick pericardial fluid that’s full of fibrin strands and white blood cells. This gives the wall of the serous pericardium a “buttered bread” appearance.

Pericarditis can also be seen in autoimmune diseases, like rheumatoid arthritis, scleroderma, or systemic lup]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Trypanosoma_cruzi_(Chagas_disease)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1rzdOaPDSPuJHMBFjPI4clPeQHu_RMvX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Trypanosoma cruzi (Chagas disease)]]></video:title><video:description><![CDATA[Chagas Disease, also called American trypanosomiasis, is a parasitic disease common in Central and South America, caused by a protozoan called Trypanosoma cruzi or T. cruzi for short. 

T. cruzi is transmitted through the feces of the insect triatominae. 

Triatominae is a type of reduviid bug also called the kissing bug because it typically bites people on the face as they sleep at night - one heck of a good night kiss, huh? 

The disease gets its name from Carlos Chagas, the physician who first described it.  

The life cycle of T. cruzi starts with the epimastigote T. cruzi which sits in the lumen of the Reduviid bug’s midgut. 

–Mastigote refers to the whip-like structure called a flagellum which protrudes from the center of the T. cruzi and helps it move around.

While in the midgut, the epimastigote multiplies through binary fission. 

Over time, the epimastigote transforms into a trypomastigote and at that point it loses its ability to divide, but the trade-off is that it gains the ability to invade human cells. 

In fact “trypo” means to bore or punch into.

Reduviid bugs feed off the blood of humans, and they prefer biting a person’s face, which is why they’re also called kissing bugs.

But unlike a normal kiss, the reduviid bug then defecates at the bite site, and if the reduviid bug is infected with T. cruzi, the feces can contain trypomastigotes. 

These trypomastigotes can then infect human skin cells at the bite location; or at mucous membranes, particularly the conjunctiva of the eyes. 

That can happen if a person unknowingly transfers the trypomastigotes by rubbing the bite site on their face and then touching their eyes. 

Once the trypomastigote invades a human cell, it transforms into an amastigote meaning that it loses its flagellum. 

The amastigotes multiply intracellularly, again through binary fission, and then transform into blood trypomastigotes which can move through the blood and lymph to other tissues. 

The blood trypoma]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Laryngitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3bTSJkdHSxeU6vZkeYiYgwDST5Oc63cO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Laryngitis]]></video:title><video:description><![CDATA[With laryngitis, “laryng-” refers to the larynx and “-itis” refers to inflammation. 

So, laryngitis is inflammation of the larynx, something that especially affects children. 

It’s further classified into acute if it lasts less than three weeks, and chronic if it lasts more than three weeks.

The larynx is located in the upper portion of the neck, just below where the pharynx splits into the trachea and the esophagus. 

The larynx is also called the voice box because it contains the vocal cords, which are two folds of mucous membrane that can open and close like curtains. 

When they are closed, air pressure builds up below them, causing them to vibrate and produce sound when we speak. 

Like the rest of the respiratory tract, the walls of the larynx are made up of mucosal epithelium. 

The mucosal epithelium contains goblet cells, which produce mucus to trap small foreign particles as well as columnar cells, which have cilia, which are tiny little hair like projections that moves mucus up the respiratory tract so it can be coughed out.

Acute laryngitis is most common and it’s usually due to an upper respiratory tract infection, most often due to a virus. 

These viruses are the same ones that cause the common cold like rhinovirus, coronavirus, influenza virus, respiratory syncytial virus- or RSV for short, and parainfluenza virus.

Bacterial infections are another cause of acute laryngitis, and sometimes they can develop during or right after a viral infection - that’s called a superinfection. 

Common bacterial causes include Group A streptococcus, Streptococcus pneumoniae, or Haemophilus influenzae. 

These bacteria, and particularly Haemophilus influenzae, have a special preference for the superior portion of the larynx and the epiglottis, causing epiglottitis. 

In acute laryngitis, the goblet cells to over secrete mucus leading to congestion of the airway, and immune cells like neutrophils and macrophages release chemicals that cause pain and swel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Asthma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/scsgYrh0Tr6D-mOc5iEwZBZsR9GO84Cv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Asthma]]></video:title><video:description><![CDATA[Asthma is a chronic respiratory condition characterized by recurrent episodes of airway inflammation and obstruction, known as asthma attacks, which result in breathing difficulties, such as dry cough, wheezing, and shortness of breath. 

When you take a breath, the air travels through your nose or mouth down the trachea. From here, it moves into the primary bronchi, which branch into smaller secondary bronchi, then tertiary bronchi, and finally into the bronchioles. Bronchioles lead directly to tiny alveoli, where the gas exchange occurs.    

Now, the airway walls contain smooth muscle cells and elastic tissue that help them open and return to their shape as we breathe.  

The lining of the airways includes epithelial cells with tiny brush-like projections called cilia and goblet cells that produce sticky mucus. The mucus traps dust and other unwanted particles; while the cilia move together in coordinated waves, pushing the mucus and trapped particles toward the throat. This system, known as the mucociliary escalator, allows us to either swallow or cough out foreign particles. And if the mucus traps a pathogen, immune cells in our airways step in to eliminate the threat. 

Now, asthma develops when the immune system in the airways becomes hypersensitive and overreacts to triggers that should be harmless. Based on the underlying cause, asthma can be classified as atopic- and non-atopic asthma. 

Atopic asthma, also known as allergic asthma, is the most common type of asthma. It usually begins when someone breathes in allergens like pollen or dust mites. Instead of ignoring these harmless substances, the immune system identifies them as threats. As a result, antigen-presenting cells in the respiratory mucosa capture the allergen through a process called phagocytosis and break it down. Next, they present some of its fragments, known as antigens, on their surface. It’s their way of signaling to the immune system: “We have an intruder!” Using these antigens,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatic_neuroendocrine_neoplasms</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Lvrmrgr-STSLXI73sCHtxiKYT8Wy2agT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatic neuroendocrine neoplasms]]></video:title><video:description><![CDATA[With pancreatic neuroendocrine neoplasms, neuroendocrine refers to pancreatic cells which release hormones in response to signals from the nerves, and neoplasm refers to a cancer. 

So, pancreatic neuroendocrine neoplasm is a cancer of neuroendocrine cells that are within the pancreas. 

They can also be called pancreatic neuroendocrine tumors, or just panNETs for short. 

In addition to endocrine cells, the pancreas also has exocrine cells, which make up a majority of the gland. 

Most pancreatic cancers arise from exocrine cells and they’re called adenocarcinomas, whereas only a minority arise from panNETs.

The pancreas is a long, skinny gland the length of a dollar bill which sits to the left of the duodenum and behind the stomach, in the upper abdomen, or the epigastric region. 

It plays two main roles - there’s the exocrine part of the pancreas which has acinar cells that make digestive enzymes that are secreted into the duodenum to help digest food. 

There’s also the endocrine part of the pancreas which has a few different types of islet cells, or neuroendocrine cells, each of which make different hormones.

These neuroendocrine cells are present in clusters, or islands, called islets of Langerhans. 

The largest group of cells are the beta (β) cells which secrete insulin. 

Insulin mainly lowers the blood glucose levels by transporting glucose into the cells, and also pushes potassium into cells, which decreases potassium in the blood. 

Another group are the alpha (α) cells which secrete glucagon, a hormone that does exactly the opposite of insulin, it raises the blood glucose levels by getting the liver to generate glucose from amino acids and lipids, and to break down glycogen into glucose. 

There are also Delta cells which secrete somatostatin, which decreases the release of other hormones, including insulin, glucagon, and serotonin. 

There are also pancreatic polypeptide cells, which secrete pancreatic polypeptide, which stimulates the rel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/smsGaCyCQJa3_LrH9GOGCLWLT3iwZ6Qy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid cancer]]></video:title><video:description><![CDATA[The thyroid gland is an endocrine gland in the neck that produces thyroid hormones.

If the cells of the thyroid gland start to divide uncontrollably, then that’s considered a thyroid cancer.

Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, or ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary. 

The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, thyrotropin or simply TSH. 

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”. 

The entire gland is covered in a thin, tough membrane called the fibrous capsule.  

If we zoom into the thyroid gland, we’ll find thousands of follicles, which are small hollow spheres whose walls are lined with follicular cells, and are separated by a small amount of connective tissue.

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4. 

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body. 

Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate.

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy. 

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response. 

Thyroid hormone is important - and the occasional increase is like getting a boo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholinergic_receptors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qc9hpOPCSk2QY-GFyn5yyEGZQX_zRet-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholinergic receptors]]></video:title><video:description><![CDATA[Cholinergic receptors are receptors on the surface of cells that get activated when they bind a type of neurotransmitter called acetylcholine. 

There are two types of cholinergic receptors, called nicotinic and muscarinic receptors - named after the drugs that work on them. 

The nervous system is divided into the central nervous system, so the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs.

The peripheral nervous system is divided into the somatic nervous system, which controls skeletal muscles, and the autonomic nervous system, which is further divided into the sympathetic and the parasympathetic, and controls internal organs.

Neurons are the main cells of the nervous system. They’re composed of a cell body, which contains all the organelles, and nerve fibers, which are projections that extend out from the neuron cell body. 

Nerve fibers are dendrites that receive signals from other neurons, and axons that send signals along to other neurons. 

Where two neurons come together is called a synapse; that’s where an axon releases neurotransmitters that bind to receptors present on the cell membrane of the dendrites or the cell body of the next neuron in the series. 

Now the autonomic nervous system - so both sympathetic and parasympathetic - is made up of a relay that includes two neurons: preganglionic neurons, which have their cell bodies in nuclei throughout the spinal cord, and postganglionic neurons, which have their cells bodies in ganglia out of the spinal cord.

Axons of preganglionic neurons exit the spinal cord to reach the ganglia and synapse with postganglionic neurons. Then, the axons of postganglionic neurons exit the ganglia to reach the organs and synapse with the target organ cells. 

Let’s zoom into the synapses. In the sympathetic nervous system, preganglionic and postganglionic neurons release different neurotransmitters. 

Preg]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cell_cycle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wr_LgW8LTZCFf9fLPlkqmCimSquWq5dr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cell cycle]]></video:title><video:description><![CDATA[The cell cycle refers to the events that somatic cells - which includes all of the cells in our bodies except the reproductive cells - go through from the moment they’re formed until the moment they divide in two identical daughter cells. 

This cycle varies in length depending on the type of cell - for rapidly dividing cells, like skin cells, it takes less than a day, whereas for other cells, like liver cells, the cell cycle can last years. 

The cell cycle has two phases: interphase, and mitosis. 

Interphase the longest part of the cell cycle, and it’s a state of preparation, during which the cell carries out its cell functions, grows and replicates its DNA to prepare for mitosis - or cellular division. 

After a parent cell divides, each of the two daughter cells enter interphase again. 

Now, interphase can further be broken down in three subphases: G1, S, and G2. G1 stands for “gap” or “growth” 1, and it’s the longest phase of the cell cycle. 

During G1, the cell mostly grows and the organelles take care of regular cellular business - like the synthesizing proteins and producing energy. 

Inside the cell nucleus, there’s our DNA, organized as chromosomes - and during G1, each chromosome is made up of a single, thin spaghetti of DNA, called a chromatid.

At the end of G1, there’s a cell cycle control point called the G1 checkpoint - where the cell checks to see if the DNA is not damaged, and it synthesized the right proteins in the correct amount. 

If it turns out that there is any reason for the cell not to divide - such as DNA damage, things can go one of two ways: the cell can either enter a non-dividing state, called the G0 phase, where the DNA repair mechanisms try to fix the problem, or the cell can self-destruct in a process called apoptosis. 

Now, if the cell does get the go-ahead at the G1 checkpoint, it enters the S phase. S stands for “synthesis”, because during this phase, DNA is replicated, so that each daughter cell receives identical]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Normal_pressure_hydrocephalus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BDb7lOLCSByv0CWjp3vbF9QXRvOuSn7J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Normal pressure hydrocephalus]]></video:title><video:description><![CDATA[In normal pressure hydrocephalus, hydrocephalus can be broken down into “hydro” which means water and “cephalus” which means head. 

Hydrocephalus, which is also termed as “water on the brain”, is an excessive buildup of cerebrospinal fluid within the brain. 

Even though the pressure on lumbar puncture is expected to be increased, in this case, it’s normal, which is why it’s termed as “normal pressure” hydrocephalus.

Let&amp;#39;s start with some relevant anatomy. The brain has four interconnected cavities in the brain called ventricles, and each one contains a structure called a choroid plexus. 

The choroid plexus is made up of ependymal cells which produces cerebrospinal fluid - a fluid that helps provide buoyancy and protection, as well as metabolic fuel for the brain. 

Highest up, are two C-shaped lateral ventricles that lie deep in each cerebral hemisphere. 

The two lateral ventricles drain their cerebrospinal fluid into the third ventricle, which is a narrow, funnel-shaped, cavity at the center of the brain. 

The third ventricle makes a bit more cerebrospinal fluid and then sends all of the cerebrospinal fluid to the fourth ventricle via the cerebral aqueduct. 

The fourth ventricle is a tent-shaped cavity located between the brainstem and the cerebellum. 

After the fourth ventricle, the cerebrospinal fluid enters the subarachnoid space, which is the space between the two inner linings of the brain - the arachnoid and pia mater. 

Now, the arachnoid mater protrudes into the outermost covering, called dura mater, at various points. 

It looks a bit like little fingers poking through, and these protrusions are called arachnoid granulations. 

Cerebrospinal fluid makes its way through these arachnoid granulations and gets into the dural sinus which is filled with venous blood and is on the other side of the arachnoid granulation. 

The pressure within the subarachnoid space is higher than the pressure in the dural sinus, so CSF flows through the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oxygen_binding_capacity_and_oxygen_content</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4A2IwaZeQuCKhJvS1jtoeuvkSd2SZQtL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oxygen binding capacity and oxygen content]]></video:title><video:description><![CDATA[Oxygen content is the amount of oxygen in a certain volume of blood, typically 100mL. 

Oxygen binding capacity is the maximum amount of oxygen that can be bound to hemoglobin, abbreviated as Hb, which is the main protein found inside of red blood cells, which is a main component of blood.

As it turns out, there are two major ways for oxygen to move around in the blood. 

The majority of oxygen is bound to hemoglobin inside red blood cells, and a small amount is dissolved directly in the blood plasma. 

So the oxygen content of blood is the sum of these two, oxygen content equals hemoglobin-bound oxygen plus dissolved oxygen.

Now, if you just wanted to calculate dissolved oxygen, you’d do that by multiplying the partial pressure of oxygen, measured in mmHg, with the solubility of oxygen.

And the solubility of oxygen is the amount of oxygen that can be dissolved in 100mL of blood, and it has a constant value of 0.003 mL of O2, per mmHg per 100mL of blood. 

So the equation becomes dissolved oxygen equals partial pressure of oxygen in mm of mercury times 0.003. 

So if we plug in a physiologic arterial pressure of O2 of 100 mmHg, we get 0.3 ml of oxygen in 100ml of blood. 

Now, that’s not enough oxygen to meet the metabolic demands of the body. So that’s where hemoglobin comes to the rescue.

The oxygen binding capacity of hemoglobin, is the maximum amount of oxygen in milliliters that 1 gram of hemoglobin can bind, multiplied by the number of grams of hemoglobin in 100mL of blood.

Each hemoglobin molecule can carry up to four molecules of O2, that’s one oxygen molecule for each of the four hemoglobin subunits. 

Now, because each red blood cell carries a few hundred million hemoglobin proteins, that means that each red blood cell carries over a billion O2 molecules. 

So that for each gram of hemoglobin there’s 1.34 mL O2 carried around.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_embolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ach5MPj6T_GhAzLSrgEEbBdeR0O873cU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary embolism]]></video:title><video:description><![CDATA[A pulmonary embolism happens when an embolus, which is a type of blockage, suddenly gets lodged inside a pulmonary artery. 

Depending on which pulmonary artery or arteries are affected by the blockage, that can seriously decrease the amount of oxygenated blood that gets out to the body. 

Normally, blood makes it back to the heart from all of the tissues and organs through a network of veins that merge over and over. 

Superficial veins drain blood into deep veins, which rely on the skeletal muscle pump to move blood forward. The way it works is that the surrounding skeletal muscles compress the vein and propel blood forward, and the veins prevent blood from moving backwards by using one-way valves. 

Ultimately, all of the blood ends up in the superior or inferior vena cava and dumps into the right atrium. 

From there the blood goes into the right ventricle and gets pumped into pulmonary artery and eventually into the lungs. 

The pulmonary artery splits at a spot called the pulmonary saddle, which looks like a bit like a horse saddle, and then the right and left pulmonary arteries enter their respective lungs. 

Subsequent branches off the pulmonary artery lead to smaller and smaller arteries, then arterioles, and finally capillaries that form nets around the alveoli, which is where gas exchange occurs.  

When a pulmonary embolism happens, a blockage in any of the arteries leads to a decrease in blood flow to lung tissue downstream. 

The majority of the time, this blockage is caused by a broken off piece of a blood clot commonly associated with deep vein thrombosis. 

A deep vein thrombosis most commonly develops in the lower legs, below the knee, although a blood clot can form in both superficial and deep veins and also in other parts of the body as well.

Normally, the process starts with damage to the endothelium, or inner lining of blood vessel walls, after which there’s an immediate vasoconstriction or narrowing of the blood vessel which limits ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mendelian_genetics_and_punnett_squares</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h1rDArLNSKmxgM-PiEtHg7foSFipgeii/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mendelian genetics and punnett squares]]></video:title><video:description><![CDATA[Genetics is the science that studies inheritance, or the way parents transmit certain traits to their descendants. 

And Mendelian genetics, refers to Gregor Mendel—an Austrian monk—who studied inheritance by experimenting on pea plants.

He cross-pollinated the flowers of different plants together, took the seeds the developed from the pairing, planted those seeds, and took careful notes on the types of peas that resulted in the subsequent generations. As a monk he was just trying to find his inner peas (peace)! 

Now in addition to having lots and lots of peas in his garden, he helped to formulate two important laws; the law of segregation and the law of independent assortment. 

So to start out - Mendel took plants with violet flowers and plants with white flowers and crossbreed them.

This original group of flowers are called the P generation, as in “parent,” and then when he obtained some peas, he planted them and got more plants and the flowers in this offspring generation was called F1, or filial one. 

It turned out that the F1 generation consisted of all violet flowers, so he called the violet trait “dominant,” while the white trait which appeared to be lost in the F1 generation, was called “recessive.” 

Next, Mendel let the violet flowers in the F1 generation cross-pollinate amongst themselves, and when they formed peas - he planted them again. 

He got more plants and the flowers from that second generation of plants he called filial two or F2. 

It turned out that some of the plants in this F2 generation had white flowers whereas other plants had purple flowers! In fact, the ratio was about 3 violet flowering plants for every 1 white flowering plant. 

Based on this experiment, Mendel drew a few conclusions. 

First, since the F1 violet flowers had some offspring plants that produced violet flowers and other offspring plants that produced white flowers, it meant that the F1 plants must have contained both of these elements. 

The inheritable e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hydration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0mipm1RFQBu5v1VZH04bXeCYTLC85gki/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hydration]]></video:title><video:description><![CDATA[Water is essential for human life, (shocking I know) but it’s why human civilizations historically sprouted up along the banks of rivers, lakes, and oceans.

Water is the main substance in our bodies, making up more than 50% of a person’s body weight, and it’s directly involved in every biochemical reaction in each cell in our body. 

Ultimately maintaining the right balance of water is what keeps us alive.

Water is a V-shaped molecule made up of two hydrogen atoms that bind to a single oxygen atom, and it’s commonly referred to by its chemical composition of H20. 

The bond between hydrogen and oxygen is a way of representing the fact that the two atoms share a single electron that zips around in the space between them. The space where it moves around is called an electron cloud and it’s a bit lopsided, since the sharing isn’t completely balanced. 

Because the electron spends a bit more time on the side nearest the oxygen, the oxygen has a partial negative charge and the hydrogens have a partial positive charge. That’s called a dipole, with the hydrogen end of the bond having a slight positive charge, and the oxygen end having a slight negative charge.

In fact, it’s this dipole that really explains the magic of water, because it allows the slightly positive hydrogens to line up with slightly negative oxygen atoms from other water molecules. That attraction between water molecules is called a hydrogen bond, and ultimately it’s the reason that water molecules huddle up together.

Think about the dew droplets that form on leaves early in the morning, that bead is huddled up because of millions of hydrogen bonds within it. 

Also, having lots of slightly positive hydrogens and slightly negative oxygens is what allows water to be a great solvent for other molecules like sugar and salt which can easily dissolve right into it.

Total body water can be subdivided into two major compartments, intracellular fluid which is fluid inside cells, and extracellular fl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Carbohydrates_and_sugars</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q8Y9EeEyT0CDhq_GEA75AgovTd6UOJ5_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Carbohydrates and sugars]]></video:title><video:description><![CDATA[Carbohydrates include both simple sugars which are little ring-shaped molecules made of carbon, hydrogen and oxygen - either alone or in pairs, as well as more complex carbohydrates, which are formed when these the rings link up together to make long chains. 

Carbohydrates provide us with calories or energy, and simple sugars in particular play many roles in our diet - they sweeten lemonade, balance out an acidic miso soup, fuel yeast in rising dough and alcohol, and help preserve jams and jellies. 

We have an innate liking for sweetness, which simple sugars provide.

Historically, simple sugars were available in more modest quantities than they are today, and eating too many calories from sugar can become a problem. 

Unhealthy diets, including those with too many calories from simple sugars, are associated with an increased risk for diseases like obesity, diabetes mellitus, and cardiovascular disease, but the good news is that a healthy diet can reduce that risk as well.

Sugars are found naturally in plants like fruits, vegetables, and grains, as well as animal products like milk and cheese. 

Added sugars are the sugars that get added to foods like cereals, ketchup, energy bars, and even salad dressings. 

To be clear, even if the sugar being added comes from a natural source like sugar cane or honey, it’s still considered an added sugar. In fact, a variety of ingredients listed on food labels may be sources of added sugars, some of which you’re likely familiar with.

Sugar actually refers to a family of molecules called saccharides - monosaccharides where “mono” means one, so one sugar molecule, disaccharides where “di” means two, so two sugar molecules linked together, oligosaccharides where “oligo” means a few, so it’s three to nine sugar molecules linked together, and polysaccharides where “poly” means many, so it’s ten or more sugar molecules linked together.

Glucose is the most important member of the sugar family and it’s a monosaccharide. It]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Subarachnoid_hemorrhage</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MkgV17Y3QGOCQAkV10CMBNh5TZmhsA8L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Subarachnoid hemorrhage]]></video:title><video:description><![CDATA[There are two main types of stroke: a hemorrhagic stroke, which occurs when an artery ruptures and bleeds within the brain, and an ischemic stroke, which occurs when an artery gets blocked.

Hemorrhagic strokes can be further split into two types, an intracerebral hemorrhage which is when bleeding occurs within the cerebrum, and a subarachnoid hemorrhage which is when  bleeding occurs between the pia mater and arachnoid mater of the meninges - the inner and middle layers that wrap around the brain.

We’ll focus on subarachnoid hemorrhage, which can quickly lead to death if they’re left untreated. 

Subarachnoid hemorrhages can lead to a pool of blood under the arachnoid mater that increases the intracranial pressure and prevents more blood from flowing into the brain.

Ok - let’s start with three protective layers of the brain called meninges.

The inner layer of the meninges is the pia mater, the middle layer is the arachnoid mater, and the outer layer is the dura mater.  

Between the arachnoid mater and the pia mater is the subarachnoid space, which houses cerebrospinal fluid, or CSF. 

CSF is a clear, watery liquid which is pumped around the spinal cord and brain, cushioning them from impact and bathing them in nutrients. 

This space is also where the arteries that supplies the brain travel, and it is the location of the blood brain barrier where CSF and the vascular system can exchange nutrients.  

The brain has a few regions - the most obvious is the cerebrum, which is divided into two cerebral hemispheres, each of which has a cortex - an outer region - divided into four lobes including the frontal lobe, parietal lobe, temporal lobe, and the occipital lobe. 

There are also a number of additional structures - including the cerebellum, which is down below, as well as the brainstem which connects to the spinal cord. 

The right cerebrum controls muscles on the left side of your body and vice versa. 

The frontal lobe controls movement, and executive ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_the_immune_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AsaccAI8Qb2DqK-vxR2oYGKgQEu72BJY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to the immune system]]></video:title><video:description><![CDATA[Despite being surrounded by harmful microorganisms, toxins, and the threat of our own cells turning into tumor cells, humans manage to survive; thanks largely to our immune system. The immune system is made up of organs, tissues, cells, and molecules that all work together to generate an immune response that protects us from microorganisms, removes toxins, and destroys tumor cells - hopefully, though, not all at once! The immune response can identify a threat, mount an attack, eliminate a pathogen, and develop mechanisms to remember the offender in case you encounter it again - all within 10 days. In some cases, like if the pathogen is particularly stubborn or if the immune system starts attacking something it shouldn’t like your own tissue, it can last much longer, for months to years, and that leads to chronic inflammation. 

Your immune system is like the military - with two main branches, the innate immune response and the adaptive immune response. The innate immune response includes cells that are non-specific, meaning that although they distinguish an invader from a human cell, they don’t distinguish one invader from another invader. The innate response is also feverishly fast - working within minutes to hours. Get it? “Feverishly” - that’s ‘cause it’s responsible for causing fevers. The trade-off for that speed is that there’s no memory associated with innate responses. In other words, the innate response will respond to the same pathogen in the exact same way no matter how many times it sees the pathogen. The innate immune response includes things that you might not even think of as being part of the immune system. Things like chemical barriers, like lysozymes in the tears and a low pH in the stomach, as well as physical barriers like the epithelium in the skin and gut, and the cilia that line the airways to keep invaders out. 

In contrast, the adaptive immune response is highly specific for each invader. The cells of the adaptive immune resp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Evolution_and_natural_selection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r6AVrjc4SNWrEZVvfIaSA0QqTtKJRcl_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Evolution and natural selection]]></video:title><video:description><![CDATA[Evolution is the process by which populations change over time. 

Definitions matter - so population refers to a group of organisms within a species that live in the same place, and a species is a group with similar characteristics and are able to breed with one another. 

Sometimes there are so many changes that accumulate in a population over time, that it leads to a whole new species, one that’s different from the original species. 

This is the process that leads to an incredible variety of living beings in the world —biodiversity— that can come from a common ancestor. 

Charles Darwin revolutionized the world of biology when he proposed natural selection as the mechanism by which evolution happens - based on his observations. 

First off, he saw that each population contains individuals with traits that are different from one another. 

Secondly, he noticed that some individuals survived and reproduced while other individuals did not. 

Finally, he noticed that some individuals had traits which seemed to confer a better chance of surviving and reproducing — and he called this fitness. 

This laid the framework for natural selection, which states that individuals with different traits have differential rates of survival and reproduction. 

And in this way, a population slowly changes over time, favoring organisms with reproductive advantages over time.

As an example, in 18th century England, most of the trees were covered by lichens - which are a combination of fungi and bacteria - that made the tree trunks look white. 

And around those trees, there were peppered moths - just chilling and hanging around. 

Some of them were white and others were black. 

Now this lichen started making it easy for birds to see the black moths, whereas the white moths were camouflaged pretty well on the tree trunks. 

As a result, the black moths got eaten up, while more of the white moths would survive and reproduce — this is called differential reproduction. 

After ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/hair-skin-and-nails</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8oySvOcrRa6ibVQqiEbXXbIXS_CMo6cE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hair, skin and nails]]></video:title><video:description><![CDATA[Hair, skin glands (including oil and sweat glands), and nails are all considered skin appendages, and they help with regulating body temperature and protection from the environment. 

These appendages are found in a layer of skin called the dermis which is a layer sandwiched between two other layers called the epidermis and hypodermis. 

The epidermis is the thin outermost layer of skin, the dermis is the thicker layer that lies below that, and the hypodermis is the lowest layer that’s made of fat and connective tissue and anchors the skin to the underlying muscle. 

Hair is found on nearly every part of skin except the palms of the hands, soles of the feet, and the lips. 

Every strand of hair is composed of the shaft, root, and bulb that sits in a pouch like structure called the hair follicle. 

The hair follicle is epidermal tissue that dips down into the dermis, and is associated with other structures like apocrine glands, sebaceous glands, the arrector pili muscle, and nerve receptors. 

Inside the bulb lies the hair matrix which serves as the active site of hair growth and gives hair its color. 

It contains two different cell types - follicular keratinocytes and melanocytes, and these cells receive blood from a small cluster of capillaries called the papilla. 

Similar to the epidermal keratinocytes in the skin, follicular keratinocytes in the hair replicate rapidly and die in a process called keratinization. During this process, keratinocytes produce keratin. 

Keratin is a long filamentous protein that comes in many different forms depending on the type of keratinocytes producing it, but it is generally divided into soft and hard keratin; where soft keratin is produced by skin and hard keratin is produced by hair and nails. 

Hard keratin is much denser than the soft keratin produced by epidermal keratinocytes in the epidermis, which gives hair and nails their durability.

During keratinization, the hard keratin fills up the entire cell, causing t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complement_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JJ8L3kJgRfKAZQa_UMhGv6LuTyOoRl48/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complement system]]></video:title><video:description><![CDATA[The complement system refers to a group of plasma proteins called the complement proteins, which are produced in the liver, and act collectively to help destroy pathogens. Think of them like a little militia that “complement” the work of antibodies. 

There are actually three complement pathways: The classical pathway - called that because it was discovered first, the alternative pathway which was found second and is always at work, and the Lectin binding pathway - which was found third and when folks got more descriptive with their naming. 

So let’s start with the proteins that make up the classical pathway - C1, C2, C3, C4, C5, C6, C7, C8, and C9. Pretty easy right? 

Now these were numbered, in the order they were discovered, but not the order in which they function. 

Generally speaking, each complement protein is normally inactive, and it becomes activated when it’s cleaved - in other words when some part of it breaks free. A bit like how a fire extinguisher isn’t “active” until a pin is pulled out. 

Now in the classical pathway things start out with C1.

C1 has three component C1q, C1r, and C1s. 

It has six C1q subunits, which are able to bind to the Fc portion of an antibody when it is bound to antigen.

Each C1q can bind to 1 antibody-antigen complex, so technically each C1 molecule can bind 6 antibodies. 

Both the C1r and C1s subunits are both enzymes called serine proteases. 

C1q has zero enzymatic activity and typically the serine proteases C1s and C1r are hidden so they cannot perform their enzymatic activity. 

This is all tied together in a calcium bow, so when there is a lack of calcium, C1 is also lacking. 

When 2 or more of the C1q portions bind to the Fc receptors of 2 or more antibodies that are bound to antigen it causes a conformational change of the C1 molecule which twists, exposing the C1s and C1r serine protease sites. A bit like taking the safety cover off of a pair of scissors. 

This allows C1r to to cleave C1s activating ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cell-cell_junctions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DsOPbPMHT1u_Qe2kwqjojRVLQjeHvJ81/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cell-cell junctions]]></video:title><video:description><![CDATA[Cell-cell junctions are protein structures that physically connect cells to one another. 

Cell-cell junctions facilitate for cellular communication, boost tissue structure, help with transport of materials between cells, or create an impermeable barrier for certain substances. 

Cell-cell junctions are only found between immobile cells of organs and tissues-- so mobile cells like sperm and macrophages don’t have these structures. 

Cell-cell junctions are most abundant in epithelial tissue, which is found in skin and the innermost layer of the gastrointestinal tract. 

However, these structures are also found in other organs like the heart, kidneys, and liver. 

The three types of cell-cell junctions are adherens junctions, tight junctions, and gap junctions. 

Adherens junctions are formed by groups of proteins that anchor cells together side by side and prevent their separation - making them “adhere” to one another. 

Adherens junctions have three major components. 

The first component are long filamentous proteins called actin filaments that are part of the cytoskeleton and help give a cell its shape. 

The second component is protein plaques, which are protein structures within the cytoplasm that are anchored to the plasma membrane that bind to the actin filaments. 

Third, are transmembrane proteins called cadherins which attach to the protein plaques on one side and transverse the plasma membrane and connect to cadherins of an adjacent cell, linking the two together. 

In this way, adherens junctions create a continuous network of interconnected cells via actin, which ultimately ties all these cells together to prevent their separation and provides extra strength. 

This is particularly important in tissues that are exposed to constant shearing or abrasive forces like the skin or gastrointestinal tract. 

It’s a bit like the reinforcing steel bar or rebar that sits within cement blocks to give a wall extra strength. 

Now, tight junctions, also kno]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myocardial_infarction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k8PyWwsGQR2rFr4xxCuF0RtDTGyGYWc_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myocardial infarction]]></video:title><video:description><![CDATA[According to the world health organization, cardiovascular disease is the leading cause of death worldwide, as well as in the US. Of those, a large proportion are caused by heart attacks, also known as acute myocardial infarctions, or just myocardial infarctions, sometimes just called MI. 

The word infarction means that some area of tissue has died due to a lack of blood flow, and therefore a lack of oxygen. “Myo” refers to the muscle, and “cardial” refers to the heart tissue. So with a heart attack, or MI, you have death of heart muscle cells because of a lack in blood flow, a process called necrosis. Now the heart’s main job is to pump blood to your body’s tissues right? Well, the heart also needs blood, and so it also pumps blood to itself, using the coronary circulation. The coronary circulation is this system of small arteries and veins that help keep the heart cells supplied with fresh oxygen. Heart attacks happen when these small arteries become blocked and stop supplying blood to the heart tissue, and if this happens for long enough, heart tissue dies.

Almost all heart attacks are ultimately a result of endothelial cell dysfunction, which relates to anything that irritates or inflames the slippery inner lining of the artery—the tunica intima. One classic irritant are the toxins found in tobacco which float around in the blood and damage these cells. That damage then becomes a site for atherosclerosis, a type of coronary artery disease where deposits of fat, cholesterol, proteins, calcium, and white blood cells build up and start to block blood flow to the heart tissue. This mound of stuff has two parts to it, the soft cheesy-textured interior and the hard outer shell which is called the fibrous cap. Collectively this whole thing’s ominously called plaque. Usually, though, it takes years for plaque to build up, and this slow blockage only partially blocks the coronary arteries, and so even though less blood makes it to heart tissue, there’s still ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Febrile_seizure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qbeZQyDtSlaocSCc9_yg89J8TruVMQL-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Febrile seizure]]></video:title><video:description><![CDATA[Febrile seizures are seizures that happen with a fever, and they typically occur in young children between six months and five years of age.

Now, neurons are the main cells of the nervous system. They’re composed of a cell body, which has all the cell’s organelles, and nerve fibers, which are projections that extend out from the neuron cell body. 

Nerve fibers are either dendrites that receive signals from other neurons, or axons that send signals signals called action potentials along to other neurons. 

Where two neurons come together is called a synapse, and that’s where one end of an axon sends neurotransmitters to the dendrites or directly to the cell body of the next neuron in the series. 

Some neurotransmitters bind to the receptors and tell the cell to open up the ion channels and relay an electrical message and these are called excitatory neurotransmitters. 

But there are others which can close the ion channels and prevent an electrical message from going through and these are called inhibitory neurotransmitters. 

The main excitatory neurotransmitter in the brain is glutamate. 

Glutamate binds to NMDA receptors which tell the cell to open up calcium ions channels. Since calcium has a positive charge, it makes the inside of the cell more positive and that helps triggers an action potential.

On the flip side, the main inhibitory neurotransmitter in the brain is GABA. 

GABA binds to GABA receptors, which tell the cell to open up chloride ion channels. 

Since chloride has a negative charge, it makes the inside of a cell more negative and that inhibits an action potential. 

During a seizure, large groups of neurons become active synchronously, meaning all at the same time. 

And in a febrile seizure, the trigger for that neuronal activity is a fever. 

So that makes you wonder, why? Well, we actually don&amp;#39;t know for sure, but there are some possible explanations. The first is that a fever, raises the core body temperature and it ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eQRDg54sR2G8DtBJmFISqZfWS0yqmHyV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal system anatomy and physiology]]></video:title><video:description><![CDATA[The gastrointestinal tract consists of a long tube, where food travels through, which runs from the mouth to the anus, as well as a number of accessory organs that sprout off the sides of that tube.

The gastrointestinal tract is made up of the mouth, pharynx, esophagus, stomach, small intestine, large intestine, and finally the anal canal. 

The accessory organs include the teeth, tongue, salivary glands, the liver, gallbladder, and the pancreas.

The main job of the gastrointestinal system is ingestion - taking in food, digestion - breaking it down into nutrients, absorption - pulling these nutrients into the bloodstream, and finally, excretion - getting rid of waste. 

All right, so let’s say we eat a slice of pizza. The pizza goes in our oral cavity where we use our teeth to masticate, or chew the food up into small fragments. 

These fragments get tasted and rolled around by the tongue, which is basically a huge muscle that lines the floor of the mouth. 

The roof of the mouth, which separates it from the nasal cavity, is made up by the anterior hard palate, which provides a hard surface for the tongue to mash food against and the posterior soft palate, which moves together, along with the pendulum- like uvula to form a flap or valve that helps makes sure food flows down instead of going up into the nose. 

At the same time, the three sets of salivary glands - the sublingual, below the tongue, the submandibular, below the mandible, and the parotid gland, which is near the ear all secrete saliva to lubricate the food. 

The saliva helps to make the food compact down into a soft, warm ball, called a “bolus”.

Saliva also contains salivary amylase, an enzyme that breaks long carbohydrates down into smaller sugars. 

Once that bolus of food gets swallowed through the pharynx it goes into the esophagus. Right at that moment, there’s a spoon-shaped flap of cartilage called the epiglottis which acts like a lid and seals the airway off so that the food d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intracerebral_hemorrhage</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2z0c8wGxQV6rrzJs0L4g3UA-Rr_I-2rb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intracerebral hemorrhage]]></video:title><video:description><![CDATA[There are two main types of stroke: a hemorrhagic stroke, which occurs when an artery ruptures and bleeds within the brain, and an ischemic stroke, which occurs when an artery gets blocked. 

Hemorrhagic strokes can be further split into two types, an intracerebral hemorrhage which is when bleeding occurs within the cerebrum, and a subarachnoid hemorrhage which is when bleeding occurs between the pia mater and arachnoid mater of the meninges - the inner and middle layers that wrap around the brain. 

We’ll be focusing on intracerebral hemorrhages which are more common. 

An intracerebral hemorrhage that involves just the brain tissue is called an intraparenchymal hemorrhage, whereas if the blood extends into the ventricles of the brain which store cerebrospinal fluid, it’s called an intraventricular hemorrhage. 

OK - let’s start with some basic brain anatomy. The brain has a few regions - the most obvious is the cerebrum, which is divided into two cerebral hemispheres, each of which has a cortex - an outer region - divided into four lobes including the frontal lobe, parietal lobe, temporal lobe, and the occipital lobe. 

There are also a number of additional structures - including the cerebellum, which is down below, as well as the brainstem which connects to the spinal cord. 

The right cerebrum controls muscles on the left side of your body and vice versa.

The frontal lobe controls movement, and executive function, which is our ability to make decisions. 

The parietal lobe processes sensory information, which lets us locate exactly where we are physically and guides movements in a three-dimensional space. 

The temporal lobe plays a role in hearing, smell, and memory, as well as visual recognition of faces and languages. 

Finally, there’s the occipital lobe which is primarily responsible for vision. 

Within the cortex are deeper structures like the internal capsule, which is like a highway that allows information to flow through neurons that are goi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Basal_ganglia:_Direct_and_indirect_pathway_of_movement</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lsdrJmC0RNiMTPykjaF2GBqATl2Rg6Gs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Basal ganglia: Direct and indirect pathway of movement]]></video:title><video:description><![CDATA[The basal ganglia or basal nuclei is a structure located deep within the brain, and it’s made up of a group of nuclei - so millions of nerve cell bodies. 

Put simply, the cerebral cortex decides how it wants to move the body and sends that input to the basal ganglia, and then the basal ganglia’s job is to help execute a smooth movement. 

The basal ganglia are actually two pairs of deep structures - one on the left side and one on the right side of the brain. 

Each pair consists of the globus pallidus, which has the internal globus pallidus and the external globus pallidus, and the striatum - which includes the caudate nucleus and the putamen. 

The basal ganglia is linked to other brain structures, like the ventral anterior nuclei and ventral lateral nuclei of the thalamus, as well as the substantia nigra of the midbrain.

The basal ganglia can help start, stop, and control desired movements, while also inhibiting undesired movements. 

As an example, when you walk, you have to move one leg at a time - so the basal ganglia help one leg to step forward, while inhibiting the other leg, so that it’s stationary - and that prevents you from falling! 

Additionally, the basal ganglia is involved in perception. 

Let’s take a look at this picture as an example. You can either see a rabbit - with its two long ears - or a duck, with its beak. And you can choose which animal to see, but you can’t see both simultaneously, because the basal ganglia stimulates the vision of one, while it inhibits the vision of the other one. For this reason, the brain can only perceive one image at a time.

For the basal ganglia to work, nearly the entire cerebral cortex projects onto the striatum. 

The striatum then projects onto the thalamus, and from there neurons head back to the cerebral cortex through two pathways: the direct pathway - which is excitatory - and the indirect pathway, which is inhibitory.

So the direct pathway and indirect pathway have to be carefully balanced]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/skin-anatomy-and-physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HZgJNKE0RTymJsMriaehzmVQTFCmccPB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skin anatomy and physiology]]></video:title><video:description><![CDATA[The skin makes up around 16%  of total body weight, making it the largest organ in the body - although it’s hard to imagine it as a single organ. The skin along with its accessory structures--like oil and sweat glands--makes up the integumentary system. The integumentary system protects the body from infections, helps regulate body temperature, and contains nerve receptors that detect pain, sensation, and pressure.

Now, the skin is divided into three layers--the epidermis, dermis, and hypodermis. The epidermis forms the thin outermost layer of skin.  Underneath, is the thicker dermis layer that contains the nerves and blood vessels. And finally, there’s the hypodermis which is made of fat and connective tissue that anchors the skin to the underlying muscle.

The epidermis itself is made of multiple layers of developing keratinocytes - which are flat pancake-shaped cells that are named for the keratin protein that they’re filled with. Keratin is a fibrous protein that allows keratinocytes to protect themselves from getting destroyed when you rub your hands through the sand at the beach. Keratinocytes also make and secrete glycolipids, glyco meaning part sugar and lipid meaning part fat. Glycolipids help to prevent water from easily seeping into and out of the body. Keratinocytes start their life at the lowest layer of the epidermis called the  stratum basale, or basal layer, which is made of a single layer of stem cells that continually divide and produce new keratinocytes. These new keratinocytes then migrate upwards to form the other layers of the epidermis. The stratum basale also contains another group of cells - melanocytes, which secrete a protein pigment, or coloring substance, called melanin. Melanin is actually a broad term that constitutes several types of melanin found in people of differing skin color. These subtypes of melanin range in color from black to reddish yellow and their relative quantity define a person’s skin color. When keratinocyt]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuromuscular_junction_and_motor_unit</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m9L6tUyuRkyf9Wi5gTEZ_I1wQ-KiPdxQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuromuscular junction and motor unit]]></video:title><video:description><![CDATA[In order for a skeletal muscle to contract, your brain sends a signal, in the form of an action potential in an upper motor neuron. 

The upper motor neuron is part of the cerebral cortex, and it activates a lower motor neuron, which is located in the anterior horn of the spinal cord.

From here, the action potential is sent through an axon down to its ending branches, called axon terminals, to muscle fibers which they innervate. 

The place where an axon terminal meets the muscle fiber is the neuromuscular junction. 

The neuromuscular junction has three main parts: a presynaptic membrane, which is the membrane of an axon terminal; a postsynaptic membrane, which is the membrane of a skeletal muscle fiber and is also called a motor end-plate; and a synaptic cleft, which is the gap between the presynaptic and postsynaptic membrane.

When an action potential reaches the axon terminal, it stimulates voltage-gated calcium channels in the membrane to open and extracellular calcium ions flow into the lower motor neuron.

Inside the axon terminal are synaptic vesicles that contain neurotransmitters called acetylcholine. 

The calcium that enters the axon terminal binds to the vesicles, which allows them to fuse with the cell membrane of the axon terminal, releasing the acetylcholine into the synaptic cleft.

The acetylcholine then diffuses over to the motor end plate on the muscle fiber - and because it’s a short distance, that diffusion happens really quickly. 

Here, two acetylcholine molecules will bind to one ligand-gated ion channel, also called nicotinic receptor. 

When that happens, these ligand-gated ion channels, which are selective for positively charged ions, open up. 

When they open, lots of sodium ions rush into the skeletal muscle fiber, and a few potassium ions leak out of the cell. 

But overall there’s an increase in positive charge on the inside of the muscle fiber and therefore on the inside of the membrane, relative to the outside of the mem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Somatosensory_pathways</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nc-jtX4FQ8W2dOqDfsnPV1RWSvySQ8oR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Somatosensory pathways]]></video:title><video:description><![CDATA[Broadly speaking, the nervous system can be split into an afferent or sensory division and an efferent or motor division. 

The afferent division brings sensory information from the outside world into the brain.

Sensory information may involve special senses - so vision, hearing, taste, and smell - as well as general somatic senses, so the somatosensory system, which is involved in the sense of touch, proprioception, pain, and temperature. These sensations are transduced by sensory receptors, which are present in the cell membrane of highly specialized cells found all over the body. 

According to the stimulus they respond to, sensory receptors are classified as mechanoreceptors for touch and proprioception, nociceptors for pain, and thermoreceptors for temperature.

Now, neurons are the main cells of the nervous system. They’re composed of a cell body, which contains all the cell’s organelles, and nerve fibers, which are projections that extend out from the neuron cell body. These are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons. 

Where two neurons come together is called a synapse, and that’s where one end of an axon sends neurotransmitters to the dendrites or directly to the cell body of the next neuron in the series. 

To trigger the release of neurotransmitters, neurons use an electrical signal that races down the axon, known as the action potential. 

To help speed up that electrical signal, some axons are intermittently wrapped by a fatty protective sheath called myelin, which comes from glial cells like oligodendrocytes in the central nervous system, and Schwann cells in the peripheral nervous system. 

Since the axons in the somatosensory system can be very long, the fact that myelin helps speed up action potentials is super important! But myelin requires energy to generate and takes up space, so not all fibers are myelinated. 

Somatosensory fibers are classified as non myelinated f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colorectal_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/afiDudYqSZ_gipJLHkKHqSYuS_m2HJ84/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colorectal cancer]]></video:title><video:description><![CDATA[Colorectal carcinoma, also known as colon cancer, is when malignant or cancerous cells arise in the large intestines, which includes the colon and rectum. 

It is the most common type of cancer of the gastrointestinal tract, and a major cause of death and disease around the world. 

The large intestine is found in the abdominal cavity, which can be thought of as having two spaces - the intraperitoneal space and the retroperitoneal space. 

The intraperitoneal space contains the first part of the duodenum, all of the small intestines, the transverse colon, sigmoid colon, and the rectum; the retroperitoneal space contains the distal duodenum, ascending colon, descending colon, and anal canal. 

So the large intestines essentially weave back and forth between the intraperitoneal and retroperitoneal spaces. 

Now, the walls of the gastrointestinal tract are composed of four layers. The outermost layer is the called serosa for the intraperitoneal parts, and the adventitia for the retroperitoneal parts.

Next is the muscular layer, which contracts to move food through the bowel. 

After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. 

And finally, there’s the inner lining of the intestine called the mucosa; which surrounds the lumen of the gastrointestinal tract, and comes into direct contact with digested food. 

The mucosa has invaginations called intestinal glands or colonic crypts, and it’s lined with large cells that are specialized in absorption.

Most colorectal carcinomas are adenocarcinomas, meaning that they arise from the cells lining the intestinal glands. 

Most cases of colorectal tumors happen because of sporadic mutations, but a small number are caused by known genetic mutations that run in a person’s family. 

An example of this is the adenomatous polyposis coli gene, or APC gene, which is a tumor suppressor gene. 

Normally, the APC protein identifies when a cell is accumula]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vascular_dementia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CTJezStiQbm_zw37gGd-wVImT16_jRDe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vascular dementia]]></video:title><video:description><![CDATA[With vascular dementia, vascular refers to the blood flow to the brain, and dementia refers to problems like poor memory, difficulty communicating, and difficulty learning new information. 

Vascular dementia is also known as multi-infarct dementia, and it’s a progressive loss of brain function caused by long term poor blood flow to the brain, typically because of a series of strokes. 

OK, let’s start with some basic brain anatomy. The brain has a few regions - the most obvious is the cerebrum, which is divided into two cerebral hemispheres, each of which is divided into four lobes: the frontal, parietal, temporal, and occipital lobe.

The frontal lobe controls movement, and  our personalities, it also handles our ability to count and spell, and make decisions. 

The parietal lobe processes sensory information, which lets us locate exactly where we are physically and guides movements in a three dimensional space. 

The temporal lobe plays a role in hearing, smell, and memory, as well as visual recognition of faces and languages. 

Finally there’s the occipital lobe which is primarily responsible for processing visual information.

All the cells in the body need oxygen - and that’s particularly relevant for neurons, which can only function in aerobic conditions, meaning with constant supply of oxygen. 

Neurons also don’t have long term energy stores, so they need a constant supply of glucose to keep working.

Each time the heart beats, about a quarter of the blood pumped out goes directly to your brain, via the internal carotid arteries and the vertebral arteries in the neck.

Once they reach the base of the brain, these arteries join to form a ring, called the circle of Willis, which then branches off into smaller and smaller arteries, the smallest being the perforating arteries, that eventually supply the entire brain with oxygen and glucose. 

Vascular dementia develops in some individuals, when atherosclerosis starts to form in the arteries. 

That’s ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kidney_countercurrent_multiplication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9TN4zXpwRTWsIl-bMAWzeH2-TpKY7Sr2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kidney countercurrent multiplication]]></video:title><video:description><![CDATA[If we take a cross-section of the kidney, there are two main parts, the outer cortex and the inner medulla. 

If we zoom in, there are millions of tiny functional units called nephrons which go from the outer cortex down into the medulla and back out into the cortex again.

These nephrons perform the major function of the kidney, which is to clear harmful substances from the body by filtering the blood. 

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins. 

The stuff that gets filtered into the tubule is called the filtrate, and the rest of it leaves the glomerulus through the efferent arteriole. 

Interestingly, the blood that leaves these glomeruli does not enter into venules. Instead the efferent arterioles divide into capillaries a second time. These peritubular capillaries then reunite and at that point the blood enters venules and eventually drains back into the venous system.

Now, The renal tubule is a structure with several segments: the proximal convoluted tubule, the U- shaped loop of Henle with a descending and ascending limb and the distal convoluted tubule, which winds and twists back up again, before emptying into the collecting duct, which collects the final urine. 

Now, zooming in on this nephron’s tubule, each one’si lined by brush border cells which have two surfaces. One is the apical surface which faces the tubular lumen and is lined with microvilli, which are tiny little projections that increase the cell’s surface area to help with solute reabsorption. 

The other is the basolateral surface, which faces the peritubular capillaries, which run alongside the nephron.

The urine osmolarity is the concentration of urine, and is measured in Osmoles per liter, which is the solute particles that exist in a liter of urine. 

To concentrate urine, or increase its osmolarity, nephrons rely on the corticopapillary gradient, which is a concentration gradient that spans from the cortex to the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lower_urinary_tract_infection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WObMMVtgTOeRcp4iHVAF-aPSSZ_r4YXc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lower urinary tract infection]]></video:title><video:description><![CDATA[With cystitis, cyst- refers to the bladder, and -itis refers to inflammation, therefore cystitis describes an inflamed bladder, which is usually the result of a bacterial infection, but also can result from fungal infections, chemical irritants, foreign bodies like kidney stones, as well as trauma. 

Now a urinary tract infection, or UTI, is any infection of the urinary tract, which includes the upper portion of the tract—the kidneys and ureters, and the lower portion of the tract—the bladder and urethra. 

So cystitis, when it’s caused by an infection, is a type of lower UTI.

Lower UTIs are almost always caused by an ascending infection, where bacteria typically moves from the rectal area to the urethra and then migrate up the urethra and into the bladder. 

Having said that, on rare occasions, a descending infection can happen as well where bacteria starts in the blood or lymph and then goes to the kidney and makes its way down to the bladder and urethra. 

Normally, urine is sterile, meaning bacteria doesn’t live there; the composition of urine, which has a high urea concentration and low pH, helps keep bacteria from setting up camp. 

Also, though, the unidirectional flow in the act of urinating also helps to keep bacteria from invading the urethra and bladder. 

Some bacteria, though, are better surviving in and resisting these conditions, and can stick to and colonize the bladder mucosa. 

E. coli accounts for the vast majority of UTIs, also though, other gram negative bacteria that can infect the bladder include Klebsiella, Proteus, Enterobacter, and Citrobacter species. 

On the other hand, gram positive bacteria can also cause problems, like Enterococcus species, and Staphylococcus saprophyticus, which is actually the second most common cause after E. coli and particularly affects young, sexually active women.

That said, as far as risk factors go, sexual intercourse is a major risk factor, because bacteria can be introduced into the urethra, and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lung_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hip-T9q1TA6htuJlgq5eHtBeRsaFI-6m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lung cancer]]></video:title><video:description><![CDATA[Lung cancer, or lung carcinoma, is the uncontrolled division of epithelial cells which line the respiratory tract. There are two main categories of lung cancer: small cell and non-small cell which depend on the type of epithelial cell that’s dividing. Both types can be fatal, especially if the cancerous cells aggressively spread and establish secondary sites of cancer in other tissues. The major cause of lung cancer is smoking tobacco products, and has contributed to the deaths of millions of people, including famous individuals like Walt Disney and Claude Monet.

Now, air enters the respiratory tract through either the nose or mouth, and flows down the trachea, which divides into the right and left bronchi. Each bronchus enters its respective lung at the hilum, or the root of the lung. The bronchi then divides into lobar bronchi, which divide into segmental bronchi, and then into subsegmental bronchi which further branch to form conducting bronchioles, and then respiratory bronchioles which end with small sacs called alveoli that are surrounded by capillaries, which is where gas exchange happens. 

Lining these airways are several types of epithelial cells which serve multiple functions. These include ciliated cells that have hairlike projections called cilia that work to sweep foreign particles and pathogens back to the throat to be swallowed. Another type called Goblet cells, which are called that because they look like goblets, secrete mucin to moisten the airways and trap foreign pathogens. There are also basal cells that are thought to be able to differentiate into other cells in the epithelium, club cells that act to protect the bronchiolar epithelium, and neuroendocrine cells that secrete hormones into the blood in response to neuronal signals.  

Cells can become mutated because of environmental or genetic factors. A mutated cell becomes cancerous when it starts to divide uncontrollably. As cancer cells start piling up on each other, they become a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperprolactinemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2IuzuuIWTFe8nb0ED_Nn-vOCT-W-jOTO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperprolactinemia]]></video:title><video:description><![CDATA[With hyperprolactinemia, hyper- means above, -prolactin refers to the hormone produced by the pituitary gland, and -emia refers to the blood, so hyperprolactinemia means higher than normal prolactin levels in the blood.

Normally, at the base of the brain, there’s a small pea-sized gland called the pituitary gland. 

The anterior pituitary - the front of the pituitary gland - has a number of different cells, each of which secretes a different hormone. 

One group, the lactotroph cells, secrete prolactin. In men, excess prolactin decreases testosterone production. 

In women, during pregnancy, elevated levels of estrogen stimulate the lactotrophs to produce large amounts of prolactin which stimulates alveolar cells in the breasts. 

In response to prolactin, the alveolar cells divide and enlarge - and once a baby is born, lactogenesis begins - which means that milk is produced. 

Apart from milk production, high levels of prolactin also inhibit the release of gonadotropin releasing hormone from the hypothalamus, which results in decreased luteinizing and follicle stimulating hormone levels, which in turn, decreases estrogen levels. 

In women, this can stop ovulation and menstruation, which is why women typically don’t have a menstrual period while breastfeeding. In women that are not pregnant or breastfeeding, and in men, prolactin levels are usually kept in check by the hypothalamus in two ways. 

The first way is the most important, and it’s when the hypothalamus secretes a constant stream of dopamine which is also called prolactin inhibiting factor. 

Dopamine binds to specific receptors on the lactotrophs and inhibits the release of prolactin. The second way is when the hypothalamus secretes thyrotropin releasing hormone, also called prolactin releasing hormone, which can stimulate prolactin release. 

If the level of prolactin rises for any reason, then it signals the hypothalamus to release more dopamine, eventually decreasing its own production, a p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nuclear_structure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7HSaY0ZcRt2RW_6tdEQQqsPpQ0WvQ3_b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nuclear structure]]></video:title><video:description><![CDATA[The nucleus is a cellular organelle, found in eukaryotic cells that contains most of the cell’s genetic material in the form of DNA. 

DNA contains the genes, which are, essentially, blueprints for various proteins that the cell needs to live. 

Most cells in the human body have a single nucleus. 

But some cells, like red blood cells, have no nuclei, whereas some like skeletal muscle and liver cells have more than one nucleus.

Now, the nucleus is surrounded by the nuclear envelope. 

Inside the nucleus, there is the nucleoplasm - a liquid environment very similar to the cell&amp;#39;s cytoplasm.

Suspended in the nucleoplasm, there’s chromatin, which is the densely packed DNA, and also the nucleolus - which makes ribosomes, which, in turn, help build proteins.

Let’s start with the nuclear envelope, which has an inner and the outer membrane - both of which are made of phospholipid bilayers. 

The outer membrane has lots of anchoring proteins that allow the nucleus to remain suspended within the cytoplasm - like a puppet on strings. 

The inner membrane is covered by the nuclear lamina - which is a network of lamin proteins.

These lamin proteins are thin filamentous proteins that create a dense protein web within the nucleus - a bit like dense spider web.

The nuclear lamina provides something for the chromatin to drape itself over, a bit like caterpillars hanging out all over those spiderwebs. 

The nuclear envelope is selectively permeable - meaning, it allows some things to pass through, while preventing others. 

There are also relatively large nuclear pores, and each pore has a nuclear pore complex lining it on the inside, made out of proteins called nucleoporins, and it kinda resembles a basketball hoop with a net. 

So large molecules like nucleic acids and proteins aren’t able to come and go easily, but small water soluble molecules have no trouble. 

The main role of the nucleus is to house the DNA - it is, essentially, a central genetic librar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Platelet_plug_formation_(primary_hemostasis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/233KGyJmRY_1aQ14hrJ7lltVSC2u3RMq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Platelet plug formation (primary hemostasis)]]></video:title><video:description><![CDATA[Platelet plug formation, also called primary hemostasis, is the first of two steps needed for hemostasis. 

Hemostasis is how the body prevents blood loss a blood vessel is injured and broken. 

Without hemostasis even a minor injury would be life-threatening - imagine dying from a nosebleed! During primary hemostasis, platelets clump up together and form a plug around the site of injury. 

Then in the second stage, called secondary hemostasis, the platelet plug is reinforced by a protein mesh made up of fibrin. 

You can think of it like a brick wall where the platelets make up the bricks and the fibrin makes up the mortar that goes between the bricks. 

So going back to primary hemostasis, the clumping up of platelets - this step can be further divided into five steps: endothelial injury, exposure, adhesion, activation, and aggregation.

Let&amp;#39;s imagine that you accidently slice a tiny artery in your finger while cutting fruit, ouch! When this happens, the knife cuts several layers of the artery. 

The innermost layer of the artery is the endothelium, and it’s made up of endothelial cells. 

Just outside of this layer are several layers of smooth muscle cells, which control the size of the lumen, or the inner diameter of the vessel by contraction and relaxation.

Outside of the smooth muscle there’s a layer of protein - specifically elastic fibers which give the blood vessel the ability to expand and contract.

Outside of the elastic fibers, there’s connective tissue made up of collagen, which is the major structural protein in humans. 

This fibrous layer protects the vessel and anchors it to the surrounding tissues.  

So, the first thing that happens when the knife cuts your finger is endothelial injury.

When that happens, nerves that are attached to endothelial cells and the smooth muscle cells detect the injury and triggers a reflexive contraction of the smooth muscles near the injury site called vascular spasm. 

This makes the vessel ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenergic_receptors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AfcWtSBISuay_Po_-jZdqE5ZRDWPrt3T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenergic receptors]]></video:title><video:description><![CDATA[Adrenergic receptors are receptors on the surface of cells that get activated when they bind a type of neurotransmitter called a catecholamine. 

Catecholamines are involved in the stimulation of our organs by the sympathetic nervous system; they help to trigger the fight or flight response.

The nervous system is divided into the central nervous system, so the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. 

The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles, and the autonomic nervous system, which is further divided into the sympathetic and the parasympathetic, and controls the involuntary movement of the smooth muscles and glands of our organs. 

The sympathetic and parasympathetic nervous systems have opposite effects on the body. 

The sympathetic nervous system controls functions like increasing the heart rate and blood pressure, as well as slowing digestion. All of this maximizes blood flow to the muscles and brain, and can help you either run away from a threat or fight it, which is why it’s also called the fight or flight response. 

The parasympathetic nervous system instead slows the heart rate and stimulates digestion - the effects can be summarized as &amp;#39;rest and digest&amp;#39;.

Now, neurons are the main cells of the nervous system. They’re composed of a cell body, which contains all the cell’s organelles, and nerve fibers, which are projections that extend out from the neuron cell body. Nerve fibers are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons. 

Where two neurons come together is called a synapse, and that’s where one end of an axon releases neurotransmitters that bind to receptors present on the cell membrane of the dendrites or the cell body of the next neuron in the series.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Baroreceptors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z93mo7nJROeaG3hFmkHzO8a1Rwya2NQo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Baroreceptors]]></video:title><video:description><![CDATA[“Baro-“ means pressure or stretch, so baroreceptors are special nerve cells or receptors that sense blood pressure, by the way that the walls of the blood vessels stretch. That information is sent from the baroreceptors to the brain to help keep blood pressure balanced.

Alright, baroreceptors are actually groups of nerve endings located within the blood vessel walls. and they can be classified into two types based on their location: the arterial ones and the cardiopulmonary ones. The arterial baroreceptors can be found on the wall of the aortic arch as well as on the wall of the carotid sinus, which is basically a bulge of the internal carotid artery just above its split from the common carotid artery in the neck. In the aortic arch, these nerve endings join up to form the vagus, or tenth (X) cranial nerve, and in the carotid sinus, they form the glossopharyngeal, or ninth (IX) cranial nerve. Both of these cranial nerves travel up towards the brainstem, carrying information about the stretch they sense in the arteries. They synapse at the nucleus tractus solitarius in the medulla oblongata of the brainstem, which then relays the information to the cardiovascular centers. The cardiovascular centers are areas in the lower one-third of the pons and medulla oblongata of the brainstem, responsible for the autonomic or involuntary control of the cardiac and vascular function. They do that by coordinating the sympathetic and parasympathetic branches of the autonomic nervous system. There are two main cardiovascular centers - the first is the vasomotor control center, which controls the diameter of the blood vessels, using the sympathetic nerve fibers to cause vasoconstriction. The second is the cardiac control center, which is further divided into the cardiac accelerator and cardiac decelerator centers. The cardiac accelerator center speeds up the heart rate and increases cardiac contractility through the sympathetic outflow tract, while the cardiac decelerator ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cellular_structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cnCfGPqRTLejN-df_ldjoQ-HRnWjC0jX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cellular structure and function]]></video:title><video:description><![CDATA[The cell is the basic unit that makes up every living organism. 

It’s the smallest form of life that can replicate on its own, but cells in our body differ quite a lot from one another. 

The human body alone has over 200 distinct cell types - from long skinny neurons that can get over 1 meter long to macrophages that gobble up pathogens to myocytes that contract to let you to flex your muscles. 

But despite their differences, they share lots of similar features. 

So let’s imagine the average cell as a small apartment. First, we want some walls to distinction between what’s “outside” and what’s “inside.” These walls are the cell membrane or plasma membrane, and they’re made out of a double layer of phospholipid molecules. 

Phospholipids have a “head” made out of negatively charged phosphate, which is hydrophilic - meaning it likes water. 

Phospholipids also have a “tail” made out of two fatty acids, which are hydrophobic - meaning, they avoid water.

In water, phospholipids form a bilayer - where the hydrophobic tails are oriented inwards, where there is no water, and the hydrophilic heads oriented outwards, in contact with water molecules.

So the plasma membrane forms a wall with water on both sides. 

This wall is semipermeable - meaning it allows some things through, like oxygen or carbon dioxide - but doesn’t allow other things through, like glucose and sugars. 

Fortunately, we have the “doors” and “windows” on this apartment, and they’re made of special protein channels that are, essentially, tiny tunnels through the phospholipid bilayer.

These channels allow water and specific ions like sodium and potassium to come in and out of the cell.  

Now, like any well built apartment, our cell has a sturdy framework called the cytoskeleton. 

The cytoskeleton is made out of proteins like microfilaments, microtubules, and intermediate filaments, which all provide structural stability. 

The cytoskeleton is also very dynamic, allowing the cell to chang]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Regulation_of_pulmonary_blood_flow</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5Pize4P6TBKnXLpBrqOr6pkjTpqrhd9v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Regulation of pulmonary blood flow]]></video:title><video:description><![CDATA[Okay - so pulmonary circulation starts with the right ventricle. 

From there - blood is pumped into the large pulmonary trunk, which splits to form the two pulmonary arteries – one for each lung.

The pulmonary arteries divide into smaller arteries known as pulmonary arterioles and then eventually into pulmonary capillaries which surround the alveoli - which are the millions of tiny air sacs where gas exchange happens.

At that point, oxygen enters the blood and carbon dioxide enters the alveoli. 

The pulmonary capillaries drain into small veins that join to form the two pulmonary veins exiting each lung, and these pulmonary veins complete the circuit by delivering oxygen-rich blood into the left atrium.

Pulmonary blood flow (Q) is the volume of blood usually in milliliters, that’s being pumped out of the right ventricle over time, usually in 1 minute. 

Said differently, pulmonary blood flow is the cardiac output of the right ventricle. 

And cardiac output is the stroke volume, the volume of blood pumped per beat from the right ventricle of heart, expressed as mL per heartbeat; multiplied by the heart rate in beats per minute.

Now pulmonary blood flow is directly proportional to the difference in pressure between the pulmonary artery and the left atrium, or the delta P; and inversely proportional to the resistance of the pulmonary vasculature (R).

The blood pressure and resistance in the pulmonary circulation is normally much lower than the systemic blood pressure. 

The normal pulmonary artery pressure is about 25/10 mmHg with a mean arterial pressure of 15 mmHg. 

If pulmonary blood flow needs to change in response to a situation or vasoactive substance, it’s done by changing the resistance of the vasculature, particularly the arterioles, which is related to the diameter of the blood vessels. 

Specifically, a decrease in the diameter of the arterioles causes an increase in resistance, and that leads to a decrease in blood flow. 

On the other han]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mean,_median,_and_mode</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Kw1_E44TQ06cKRhUAMiqP5O3SEmkbcym/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mean, median, and mode]]></video:title><video:description><![CDATA[In statistics, it’s often helpful to know the central point of a set of data, because it gives a pretty good idea about the whole data set. It’s like a one number summary of the data. 

What’s the number of words on a page in a book? About 250. Of course it depends on the book, but that’s the one number summary.

The mean, median and mode are the most commonly used ways to measure this central point. 

Let’s start with the mean, which is also called the average. 

You can calculate the mean by adding up each value in a data set and then dividing by the total number of data points. 

Let’s look at an example. Let’s say 7 students took a test on biostatistics and out of 100 possible points, one student got 17, another got 19, two got 20, two more got 61 and the last student got 62. 

The mean score would be the total number of points they all got added up together divided by the number of students, which is 7. 

So that’s: 17+19+20+20+61+61+62 = 260 = 37.14

To show this as a formula, we can say that the mean, written as X with a bar over it, is the total sum of the individual data points X1, X2, ......., Xn, divided by n, which is the number of data points.

A mean test score of 37.14, quickly tells us that overall, these students didn’t do well on this test. 

But, the problem with the mean, is that it can be influenced by an extreme value called an outlier. 

Let’s say that another student comes along and get a perfect 100 out of 100 on the test. 

That means that the average is now: 17+19+20+20+61+61+62+100 = 360 divided by 8, which is 45. 

This one number summary isn’t a very good summary because the only reason that it is so high is due to this one high-scoring student. 

In this case, 100 is an outlier, and any data set with an outlier is called skewed data.

To calculate the central point when there may be outliers, you can use the median. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parasympathetic_nervous_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6hrhiqXTT86sju8OYFlsLI6SS82M8Fvy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parasympathetic nervous system]]></video:title><video:description><![CDATA[The nervous system is divided into the central nervous system, so the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. 

The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles, and the autonomic nervous system, which is further divided into the sympathetic and the parasympathetic, and controls the involuntary movement of the smooth muscles and glands of our organs. 

The sympathetic and parasympathetic nervous systems have opposite effects on the body.

The sympathetic nervous system controls functions like increasing the heart rate and blood pressure, as well as slowing digestion. All of this maximizes blood flow to the muscles and brain, and can help you either run away from a threat or fight it, which is why it’s also called the fight-or-flight response.

The parasympathetic nervous system instead slows the heart rate and stimulates digestion - the effects can be summarized as &amp;#39;rest and digest&amp;#39;.

Now, neurons are the main cells of the nervous system. They’re composed of a cell body, which contains all the cell’s organelles, and nerve fibers, which are projections that extend out from the neuron cell body. These are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons. 

Where two neurons come together is called a synapse, and that’s where one end of an axon sends neurotransmitters to the dendrites or directly to the cell body of the next neuron in the series. 

Now the autonomic nervous system - so both the sympathetic and parasympathetic nervous system - is made up of a relay that includes two neurons. And when there’s a group of neuron cell bodies located next to each other in the central nervous system, the whole thing is called a nucleus, while a group of neuron cell bodies located outside the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/B-cell_development</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dkDXT7UXTbm5C1m_p8-ta9v9QmGBZpBo/_.jpg</video:thumbnail_loc><video:title><![CDATA[B-cell development]]></video:title><video:description><![CDATA[Your immune system is like the military - with two main branches, the innate immune response and the adaptive immune response.

The innate immune response is immediate and non-specific, meaning that although it can distinguish an invader from a human cell, it doesn’t distinguish one invader from another invader. 

In contrast, the adaptive immune response is highly specific for each invader, and that’s because the cells of the adaptive immune response have receptors that differentiate friendly bacteria and potentially deadly ones from their unique parts - called antigens.

This adaptive immune response takes days to weeks to become activated, but is also responsible for immunologic memory. 

Now, the key cells of the adaptive immune response are the lymphocytes- the B and T cells -which are generated during lymphopoiesis. 

Lymphopoiesis has three goals - first, to generate a diverse set of lymphocytes - each with a unique antigen receptor, second, to get rid of lymphocytes that have receptors that are self-reactive meaning that they’ll bind to healthy tissue, and third, to allow lymphocytes that aren’t self-reactive to continue maturing in secondary lymphoid tissue. 

Normally, hematopoietic stem cells, within the bone marrow mature into a common lymphoid progenitor cell, which then becomes either a B-cell or a T-cell. 

To become a B cell, it has to develop into an immature B-cell in the bone marrow and then complete its maturation into an antibody secreting B cell, called a plasma cell, in the lymph nodes and spleen. 

To become a T cell, it has to migrate to the thymus and become a thymocyte, where it completes its development into a mature T cell. 

So, “B” for bone marrow and “T” for thymus. 

Throughout B cell development, the developing cells are interacting closely with the stromal cells of the bone marrow, which are largely composed of mesenchymal stem cells. 

Mesenchymal cells are multipotent and can differentiate into various cells including m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Loop_of_Henle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZdAJVaQaSMiEhd5otqkyE73sQ6_iXxjs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Loop of Henle]]></video:title><video:description><![CDATA[If we take a cross-section of the kidney, there are two main parts, the outer cortex and the inner medulla. 

If we zoom in, there are millions of tiny tubes called nephrons which go from the outer cortex down into the medulla and back out into the cortex again. 

Nephrons filter out harmful substances in the blood so that we can excrete them into the urine. 

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins.

These capillaries have very thin walls and they act like a coffee filter. Red blood cells and proteins are large and stay in the capillaries whereas blood plasma and smaller particles get filtered out. 

This filtrate, called tubular fluid, collects in a cup shaped structure containing the glomerulus called the Bowman&amp;#39;s capsule.

Together, the glomerulus and the Bowman’s capsule make up the renal corpuscle. 

The Bowman’s capsule is connected to the renal tubule which has a few segments: the proximal convoluted tubule, the U- shaped loop of Henle with a thin descending, a thin ascending limb and a thick ascending limb, and finally the distal convoluted tubule which empties into the collecting duct, which collects the urine.

Zooming in on the U shaped loop of Henle, it’s lined by epithelial cells. 

On one side is the apical surface which faces the tubular lumen, and on the other side is the basolateral surface, which faces the interstitium between the tubule and the peritubular capillaries. 

The peritubular capillaries run alongside the nephron, and the capillaries that run along the loop of henle are called vasa recta. 

Solutes and water that are reabsorbed into the interstitium go into the vasa recta and re-enter circulation. 

Now, when tubular fluid leaves the proximal tubule, it has an osmolarity of around 300 mOsm/L  which is the same as the osmolarity of the interstitial fluid around the tubule. 

The tubular fluid mainly contains water, sodium, potassium, chloride, calcium, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cranial_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oAo9jmJgTpaRC1ffalStp3vrR6mAFmhn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cranial nerves]]></video:title><video:description><![CDATA[The cranial nerves consist of 12 pairs of nerves originating directly from the brain and brainstem. They supply both motor and sensory information from the brain to other parts of the body, primarily supplying the region of the head and neck.  

The nervous system is divided into the central nervous system, so the brain and the spinal cord, and the peripheral nervous system, which is further divided into the somatic and the autonomic nervous systems. Broadly speaking, the nervous system is split into an afferent and an efferent division. The afferent division brings sensory information - like vision, smell, touch, and proprioception - from the outside world into the brain. On the other hand, the efferent division brings motor information from the brain to the periphery, ultimately resulting in contraction of skeletal muscles to trigger movement through the somatic nervous system, as well as the contraction of the smooth muscles to trigger activity of the glands and organs through the autonomic nervous system. 

Now, neurons are the main cells of the nervous system. And they’re composed of a cell body, which contains all of the cell’s organelles, and when there’s a group of neuron cell bodies found in the central nervous system, the whole thing is called a nucleus, while a group of neuron cell bodies that are located outside of the central nervous system is called a ganglion. Neurons also have nerve fibers that extend out from the neuron cell body - these are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons. Where two neurons come together is called a synapse, and that’s where one end of an axon releases neurotransmitters, further relaying the signal to the dendrites or directly to the cell body of the next neuron in the series.

Now, the peripheral nervous system consists of nerves, which are enclosed bundles of axons that connect the central nervous system to every other part of the body. Some ner]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Distal_convoluted_tubule</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R8amt8GDQDuXkaKbmetYc49rQ6OLfBsp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Distal convoluted tubule]]></video:title><video:description><![CDATA[If we take a cross-section of the kidney, there are two main parts, the outer cortex and the inner medulla. 

If we zoom in, there are millions of tiny tubes called nephrons which go from the outer cortex down into the medulla and back out into the cortex again. 

Nephrons filter out harmful substances in the blood so that we can excrete them into the urine. 

Each nephron is made up of the glomerulus, or a tiny clump of capillaries, where blood filtration begins. These capillaries have very thin walls and they act like a coffee filter. Red blood cells and proteins are large and stay in the capillaries whereas blood plasma and smaller particles get filtered out. 

This filtrate, called tubular fluid, collects in a cup shaped structure containing the glomerulus called the Bowman&amp;#39;s capsule.

Together, the glomerulus and the Bowman’s capsule make up the renal corpuscle. 

The Bowman’s capsule is connected to the renal tubule which has a few segments: the proximal convoluted tubule, the U- shaped loop of Henle with a descending and ascending limb, and the distal convoluted tubule which empties into the collecting duct, which collects the urine.

Zooming in on the distal convoluted tubule, it’s lined by tubule cells which are similar to the one found in the proximal tubule but they don’t have microvilli. 

On one side is the apical surface which faces the tubular lumen. On the other side is the basolateral surface, which faces the interstitium or the space between the tubule and the peritubular capillaries. 

The peritubular capillaries run alongside the nephron and return solutes and water that were reabsorbed into the interstitium back into the circulation.  

The distal convoluted tubule is split up functionally into the early distal convoluted tubule and the late distal convoluted tubule which is very similar to the collecting ducts. 

The early distal convoluted tubule is impermeable to water, and the tubular fluid contains more sodium than the tu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sliding_filament_model_of_muscle_contraction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wbk_ubz7SzyOCZjs8Z5rhl7VRPWC5yXn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sliding filament model of muscle contraction]]></video:title><video:description><![CDATA[In order for a skeletal muscle to contract, your brain sends a signal, from an upper motor neuron down the spinal cord where it synapses with the cell bodies of lower motor neurons located in the anterior horn of the spinal cord.

From here, the signal travels through the lower motor neuron’s axon and until it reaches the axon terminal which is next to a muscle fiber. 

At the site where an axon terminal meets the muscle fiber, called the neuromuscular junction, it releases small membrane-enclosed synaptic vesicles filled with acetylcholine.

Acetylcholine is a neurotransmitter that tells the muscle to contract.

Now before we continue with the actual events that happen during the contraction, let’s focus on one muscle cell a myocyte and its functional units called sarcomeres. 

A myocyte is a long cylindrical cell with multiple nuclei located just below the sarcolemma, which is the cell membrane. 

The sarcolemma is unique because it makes these tiny tunnels called T-tubules that project downwards from the surface towards the center of the muscle fiber. 

The cytoplasm of a myocyte is called sarcoplasm, and the myocyte has a special type of smooth endoplasmic reticulum which is called sarcoplasmic reticulum. 

The sarcoplasmic reticulum stores lots of calcium and runs parallel to the T tubules. 

Now, the sarcoplasm is filled with stacks of long filaments called myofibrils and each myofibril consists of contractile proteins and regulatory proteins. 

Contractile proteins include thick myosin and thin actin filaments. 

The thick myosin filament is made up of hundreds of myosin proteins, and each myosin protein has a tail and two myosin heads - it looks a bit like two golf clubs with their handles twisted around one another.

Multiple myosin proteins join their tails together to form the central part of the thick filament.

In comparison, the thin actin filaments are made up of small, globular proteins called G-actin.

Each G-actin has an active site where]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Taste_and_the_tongue</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xDLtj3pLQReekWl35NNEjOEfSYWlNaSb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Taste and the tongue]]></video:title><video:description><![CDATA[The tongue is a muscular organ in the mouth, and it’s used for many things like speech, chewing and swallowing food, and most important of all, tasting delicious foods, which is called gustation.

The surface of the entire tongue is covered by a mucus membrane called the mucosa, and below that there’s a combination of intrinsic and extrinsic muscles which are all innervated by the hypoglossal nerve which is cranial nerve 12. 

Intrinsic muscles start and end within the tongue, and help change its shape, whereas extrinsic muscles attach to structures outside the tongue and help guide its movement. 

Now, on the tongue, there’s a V shaped groove called the sulcus terminalis that runs across the posterior portion of the tongue dividing it into an posterior ⅓ and anterior ⅔. 

The posterior ⅓ of the tongue is covered in bumps made of lymphoid tissue called lingual papillae which contains B and T cells that help fight off pathogen that enters the mouth. 

The anterior ⅔ which is covered in smaller lumps called papillae that help increase the surface area and give it a rough texture that helps food particles stick to the tongue. 

There are four different types of papillae and they’re found in different regions of the tongue. The most numerous type are the thread-like, filiform papillae which are scattered all over the anterior ⅔ of the dorsal surface of the tongue.

The filiform papillae are in charge of the sensation of touch on the tongue but not taste. 

Next are the mushroom-shaped fungiform papillae which are most common at the tip of the tongue. 

Then there are the leaf-like foliate papillae, which are most common on the sides of the tongue. 

And finally there are 8-12 very large round circumvallate papillae, which are located at the back of the anterior ⅔ of the tongue, just in front of the sulcus terminalis. 

The fungiform, foliate, and circumvallate papillae contain multiple taste buds, and each taste bud contains specialized epithelial cells called]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sympathetic_nervous_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2Vz4nEm2SGmLFMis6VXvkCqPSk6Dv51u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sympathetic nervous system]]></video:title><video:description><![CDATA[The nervous system is divided into the central nervous system, so the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. 

The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles, and the autonomic nervous system, which is further divided into the sympathetic and the parasympathetic, and controls the involuntary movement of the smooth muscles and glands of our organs.

The sympathetic and parasympathetic nervous systems have opposite effects on the body. 

The sympathetic nervous system controls functions like increasing the heart rate and blood pressure, as well as slowing digestion. All of this maximizes blood flow to the muscles and brain, and can help you either run away from a threat or fight it, which is why it’s also called the fight-or-flight response.

The parasympathetic nervous system instead slows the heart rate and stimulates digestion - the effects can be summarized as &amp;#39;rest and digest&amp;#39;.

Now, neurons are the main cells of the nervous system. They’re composed of a cell body, which contains all the cell’s organelles, and nerve fibers, which are projections that extend out from the neuron cell body. 

Nerve fibers are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons. 

Where two neurons come together is called a synapse, and that’s where one end of an axon sends neurotransmitters to the dendrites or directly to the cell body of the next neuron in the series. 

Now the autonomic nervous system - so both the sympathetic and parasympathetic nervous system - is made up of a relay that includes two neurons. And when there’s a group of neuron cell bodies that are next to each other in the central nervous system, the whole thing is called a nucleus, while a group of neuron cell bodies that are l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Somatosensory_receptors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e1xvcTeRRvqC4oxu_BSYaKYrQFCyqLY4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Somatosensory receptors]]></video:title><video:description><![CDATA[Broadly speaking, the nervous system can be split into an afferent or sensory division and an efferent or motor division.

The afferent division brings sensory information from the outside world into the brain. 

Sensory information involves special senses - like vision, hearing, taste, and smell - as well as general somatic senses which make up the somatosensory system, which is involved in the sense of touch, proprioception, pain, and temperature. These sensations are felt by sensory neurons all over the body. 

These sensory neurons have receptors that are classified according to the stimulus they respond to - there are mechanoreceptors for touch and proprioception, nociceptors for pain, and thermoreceptors for temperature.

Now, neurons are the main cells of the nervous system. They’re composed of a cell body, which contains all the cell’s organelles, and nerve fibers, which are projections that extend out from the neuron cell body. These are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons. 

Where two neurons come together is called a synapse, and that’s where one end of an axon sends neurotransmitters to the dendrites or directly to the cell body of the next neuron in the series. 

The somatosensory pathways are made up of a relay of four neurons. 

The first neuron is called the first order neuron or sensory neuron, which has the sensory receptors and converts stimuli from the outside world into an impulse that can be passed through a synapse to the next neuron in series.

Next is the second order neuron, and it may have its cell body in the spinal cord or up in the brainstem. 

The second order neuron then takes the impulse to the third order neuron, which has its cell body in the thalamus. 

Finally, the third order neuron takes the impulse to the fourth order neuron, which has its cell body further up in the sensory cortex of the brain.

Now let’s zoom into first order or sensory neurons]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Relative_and_absolute_risk</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/armN_pr6Ro_4H81XVvqdhs3aTZ_542GP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Relative and absolute risk]]></video:title><video:description><![CDATA[Risk is the probability of an event occurring - for example let’s say that we’re talking about the risk of being struck by lightning. 

You might want to know - your chance of being struck by lightning - that would be the absolute risk. You might also want to know your chance of getting struck by lightning if you’re sipping hot chocolate under a blanket in your bed, versus your chance if you’re out flying a kite in a storm. 

Now, let’s say that the kite-fliers are at higher risk then the chocolate-sippers of getting struck by lightning. 

Well - you may want to know how many times higher is the risk - the risk ratio, or how much higher is the risk - the risk difference. 

So let’s use some numbers to make this concrete. Say we have 400 people in the lightening study - imagine the incentives you’d need to get folks to sign up for that study. 

So, let’s say that 200 of the people are sent out to fly a kite in a terrible storm, while the other 200 are sent indoors with a cup of hot chocolate and a blanket. 

Now let’s say that 50 of the kite-fliers are struck by lighting. 

Based on that data, the absolute risk of being struck by lightning if you’re out flying a kite is the number of lightning strikes, which is 50, divided by the number of people in the group, which is 200. 

So, 50/200 or 0.25 is answer - a 25% risk. 

Absolute risk = Number of events in a group / individuals in that group

While all that is happening, let’s say that 10 unfortunate chocolate-sipper also gets struck by lightning while sitting under a blanket. 

Based on that data, the absolute risk of being struck by lightning if you’re sipping chocolate inside is the number of lightning strikes, which is 10, divided by the number of people in the group, which is 200. 

So, 10/200 or 0.05 is answer - a 5% risk. 

If you want to compare these two risks, you could say that the relative risk or risk ratio, is the risk in one group, let’s call that group A, divided by the risk in another group,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aneurysms</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dGYqgf4nQzGJJufkl20m47KtQfiExt5b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aneurysms]]></video:title><video:description><![CDATA[The word “aneurysm” comes from the Greek word aneurysma, meaning “dilation.” This  makes sense because aneurysms are defined as abnormal dilations in a blood vessel. A bulge in a blood vessel is officially labelled as an aneurysm when the diameter of the bulge is approximately one and a half times larger than the normal diameter of the blood vessel.

Aneurysms can happen to any blood vessel in your body, including the aorta, the femoral artery, the iliac artery, the popliteal artery, and the cerebral arteries. They can also happen in your veins too, but those are less common as blood pressure in veins is much, much lower than in the arteries. 

There are two major categories of aneurysms: true aneurysms and pseudoaneurysms. In true aneurysms, all the layers of the blood vessel wall dilate together. True aneurysms that balloon out symmetrically on all sides of the blood vessel are called fusiform aneurysms, whereas asymmetrically shaped aneurysms balloon out on  one side of the blood vessel. This asymmetrical shape usually happens because for some reason one side of the blood vessel wall experiences higher blood pressure than the rest of the vessel wall, or because the wall was weaker on one side to begin with. Asymmetrical true aneurysms can be called either “saccular” or “berry” aneurysms. 

Pseudoaneurysms, on the other hand, are like false aneurysms because they are not actually aneurysms at all. They are caused by a small hole in your blood vessel which allows blood to leak out of the vessel and form a pool of blood that looks like a fusiform or berry aneurysm depending on where the hole is and its size. The blood pools because the surrounding tissues act as walls that contain the blood in one spot.

Arterial aneurysms occur most commonly in the aorta with about 60% of true aortic aneurysms happening in the abdominal section of the aorta, and the other 40% happening in the thoracic section. Of all the abdominal aortic aneurysms, you can find about 95% ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Surviving_and_thriving_in_first_year</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PdO0d4-aTNi56QEWZv1QDpBGTnu15x7q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Surviving and thriving in first year]]></video:title><video:description><![CDATA[Hey, Congrats! You got accepted to medical school! Nice! 

So now that you’re in - how do you succeed? 

They say that learning in med school is “like drinking from a fire hose” - it can be overwhelming. 

But don’t worry! There are four basic ways to make sure that you’re in control - you can work on your study skills, create healthy habits, manage your money, and avoid getting overloaded with your options. 

Let’s start with study skills.

In short, how you study is just as important as what you study. 

You might have made it through college by cramming the night before a test, but that’s not going to get you through med school successfully. 

Unlike different subjects in undergrad, in med school the information builds upon itself - meaning that just because you finish a class, you can’t forget what you learned. 

So there are some proven learning strategies that you should take advantage of - like interleaving, where you mix up the order of what you learn. 

As well as spaced repetition, where you study material over different periods of time depending on how well you know that information. 

Both of these strategies help you retain information and maximize the effectiveness of your study time. 

It so happens that the Osmosis learning platform incorporates these strategies to make them an automatic part of how you study. 

Now, in addition, some students love studying in groups initially, and then splitting off to work alone, whereas others like to do the opposite. 

The key here is to figure out what works for each class, and be willing to experiment until you feel like you have an approach that works. 

Alright, so next, you should make sure you develop healthy habits. 

Days will get busy when you are in medical school, so it’s important to get plenty of sleep, exercise, and eat healthy food to keep you performing at your best. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_and_physiology_of_the_eye</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rWdk74IkTWCnE977gfOfnW8JR9ubupUZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy and physiology of the eye]]></video:title><video:description><![CDATA[Our eyes allow us to visualize the world around us. They do this by converting light waves into neural signals so that our brains can process them. 

The eye itself is shaped like a sphere that is elongated horizontally, as opposed to being perfectly round, and only the anterior one-sixth of the eye is visible. The rest of the eye is contained within the orbit, or eye socket, of the skull.

Now, the eye consists of three layers: the outermost fibrous layer, the middle vascular layer, and the inner neural layer.

The outer fibrous layer contains two main structures: the sclera and the cornea. 

The sclera makes up the majority of the outer layer and is the white portion of the eye. It’s like a tough, fibrous covering that protects the more delicate structures within the eye and it also acts as an anchoring point for the extrinsic eye muscles to attach to. 

The sclera is like a wall that’s built around the eye, that only has a tiny opening at the back to let the optic nerve through. 

As the sclera approaches the anterior portion of the eye it reaches a transition point known as the corneal limbus where it becomes the cornea. 

The cornea itself  is a transparent, dome shaped clear layer that covers the iris and the pupil. It allows light to enter the eye, and its curved shape helps focus light on the retina in the back of the eye. 

At the periphery of the cornea, there are stratified squamous epithelial cells which continually divide and regenerate the cornea, and they help to heal after a corneal injury or abrasion. 

The cornea doesn’t contain blood vessels and therefore immune cells can&amp;#39;t access the cornea. As a result, it’s one of the few parts of the body that is considered &amp;quot;immune privileged&amp;quot; since it can be transplanted without the fear of an immune response and organ rejection.

Moving inwardly from the fibrous layer, the next layer of the eye is the middle vascular layer, which is also called the u]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_and_physiology_of_the_female_reproductive_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nEa5_FcjT3yx3yWH-tljcZl4QVudxRZR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy and physiology of the female reproductive system]]></video:title><video:description><![CDATA[The female reproductive system includes all of the internal and external organs that help with reproduction. The internal sex organs are the ovaries, which are the female gonads, the fallopian tubes, two muscular tubes that connect the ovaries to the uterus, and the uterus, which is the strong muscular sack that a fetus can develop in. The neck of the uterus is called the cervix, and it protrudes into the vagina. At the opening of the vagina are the external sex organs, and these are usually just called the genitals and they’re in the vulva region. They include the labia, the clitoris, and the mons pubis. 

The ovaries are a pair of white-ish organs about the size of walnuts. They’re held in place, slightly above and on either side of the uterus and fallopian tubes by ligaments. Specifically, there’s the broad ligament, the ovarian ligament, and the suspensory ligament. And the suspensory ligament is particularly important because the ovarian artery, ovarian vein, and ovarian nerve plexus pass through it to reach the ovary. If you slice the ovary open and look at it (don’t try this at home) there’s an outer layer called the cortex, which has ovarian follicles scattered throughout it, and an inner layer called the medulla, which contains most of the blood vessels and nerves. 

At birth, the ovarian cortex has around two million follicles - that’s roughly the population of Paris - and they’re called primordial follicles. Each primordial follicle has a single immature sex cell called the primary oocyte at the core, and a layer of follicular cells surrounds this. The primary oocyte has 46 chromosomes, but eventually it has to turn into a gamete with only 23 chromosomes. To do this, the primary oocytes have to complete meiosis 1, and in a person’s lifetime only about 400 successfully do that. This process of oocyte development follows that of follicular development, which can be broken into three stages. 

The first stage lasts from infancy to puberty, and duri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Translation_of_mRNA</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BUlresjHQ3m0vGfYYwAyNPZtQra2MKt-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Translation of mRNA]]></video:title><video:description><![CDATA[Deep within the cell’s nucleus, there’s our DNA. DNA is made up of genes, and each gene is basically a specific part of the DNA that codes for a protein. 

And genes become proteins in two steps: transcription and translation. 

Transcription is the first step in creating a protein, during which a specific gene is “read” and copied on an individual mRNA, or messenger RNA molecule - which is like a blueprint with instructions on what protein to build. 

Translation is the second step, and it’s when organelles called ribosomes assemble the protein from amino acids lying around in the cytoplasm.  

Each mRNA has a “direction” - running from the 5’ end towards the 3’ end. 

mRNA is a chain of four types of nucleotides - which are the individual “letters” or “building blocks” of mRNA. 

Nucleotides are made out of a ribose, which is a 5-carbon sugar, a phosphate, and one of the four nucleobases - guanine, uracil, adenine, and cytosine - or, commonly, G, U, A, C for short. 

These nucleotides are the actual information carried within the RNA - each 3 letters is one amino acid. 

In total, these four nucleotides can be arranged into a total of 64 combinations.

The freshly made mRNA floats out of the nucleus through a pore, and hooks up with an idle ribosome to begin getting translated into a protein. 

Right away, there’s a process called initiation which is where the ribosome grabs the mRNA. 

Groups of 3 “letters” are called codons, and each codon codes for one amino acid, or gives a certain signal, such as start or stop. 

So, for the ribosome to start, it needs to find a start codon. That is usually a sequence of A U G - which simultaneously codes for amino acid methionine. So most proteins actually begin with methionine! 

When the ribosome runs into this, it knows that from here on, every subsequent codon represents one amino acid in the protein. 

Now while each codon codes for a single amino acid; each amino acid can be coded for by one or more codons. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Selective_permeability_of_the_cell_membrane</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2hhFUbF8QBWBJzIn3-pv4kEbQ2mexMDX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Selective permeability of the cell membrane]]></video:title><video:description><![CDATA[The cell membrane is there to define what’s on the inside of a cell - the intracellular space - versus what’s on the outside of a cell - the extracellular space.

And it helps regulate what comes in or out of the cell, which is called selective permeability.

Movement across the cell membrane can occur by passive transport, which requires no energy, and active transport, which requires energy in the form of adenosine triphosphate, or ATP for short.

There are three types of passive transport - diffusion, facilitated diffusion, and osmosis.

Diffusion helps small, non-polar molecules, like oxygen and carbon dioxide, move across the membrane, from an area of high concentration to low concentration.

The difference in concentrations is known as the concentration gradient, and diffusion can occur as long as this gradient exists, and stops once there are equal concentrations of the molecule on both sides.

Facilitated diffusion helps larger molecules and polar molecules move across the membrane.

Facilitated diffusion uses transport proteins like channels and carrier proteins.

Channels are not very specific, and they can open or close to allow water and small polar molecules, like ions, that are dissolved in it to pass through.

These channels open in response to certain stimuli - for example, the voltage gated calcium channels respond when the electrical charges on the two sides of the cell membrane change.

Normally, there are more negative ions inside the cell than outside, so the inside of the cell membrane is negatively charged, and the outside is positively charged.

When positive ions make their way inside the cell through one form of transport or another, the cell starts to depolarize gradually - so step by step, the membrane becomes more positive on the inside, and more negative on the outside.

This change in the distribution of electrical charges makes the voltage gated calcium channels open and allow water, a lot of calcium ions, and a few sodium i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocytosis_and_exocytosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c4w0Wy0yReS9sRinL5ifL5MzRlK8POK2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocytosis and exocytosis]]></video:title><video:description><![CDATA[Cells transport material in and out across their cell membrane, which is a barrier made up of a double layer of lipids with embedded protein and carbohydrate components. 

Some molecules can diffuse across the membrane, or be transported across with the help of membrane-bound proteins.

For transport of larger cargo, cells use endocytosis and exocytosis to transport material in and out of the cell, respectively.

And there are roughly five categories of molecules that try to get across the cell membrane. 

Small non-polar molecules, like oxygen or carbon dioxide, are able to diffuse rapidly through the cell membrane. 

Small, polar molecules, like water, can cross as well, but very slowly. 

Large, nonpolar molecules like Vitamin A, are also very slow to cross the cell membrane. 

And large, polar molecules, like glucose, as well as highly polar, charged ions like Na+, K+, Cl-, or molecules that possess a charge, like amino acids are highly unlikely to get across a cell membrane on their own. 

So many of these molecules - some common ones being water, glucose, and ions, pass through the membrane using transport proteins. 

Examples of transport proteins include channels, like aquaporins - a water channel and chloride channels which let chloride ions get across membranes, or carriers - such as the glucose transporter. 

However, when the cell needs to transport a lot of molecules, or a very big molecule, it resorts to bulk transport, which comes in two flavors: endocytosis and exocytosis. 

Endocytosis is a process that cells use to engulf extracellular material. 

And exocytosis is the opposite process, during which cells expel material into the extracellular space. 

Both endocytosis and exocytosis need energy in the form of adenosine triphosphate or ATP, used in the movement of the substances in and out of the cell. 

There are three types of endocytosis - phagocytosis, pinocytosis and receptor-mediated endocytosis. 

Phagocytosis - where phago- means t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Biliary_colic</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VyWJVwdUSqC3L4n-jkbIuZbrQ2SCgeFr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Biliary colic]]></video:title><video:description><![CDATA[“Colic” refers to severe abdominal pain, and “biliary” refers to the bile ducts; biliary colic happens when gallstones get lodged in the bile ducts, which causes temporary severe abdominal pain. 

Sometimes this is also called a “gallbladder attack” because it can come on pretty quick.

When you eat foods that’re high in fat, like delicious french fries, they make their way to the small intestine, and the fatty acids in the fries stimulate cells which are the enteroendocrine cells or hormone secreting cells of the intestine. 

These cells secrete cholecystokinin (also called CCK) into the bloodstream, and those hormones make their way to the gallbladder and tell it to squeeze. 

Meanwhile CCK relaxes the sphincter of Oddi so that the bile can make its way to the duodenum. 

Now, bile’s a fat emulsifier, essentially helping to break fats or lipids into small “micelles”, and then pancreatic lipase gets in there and helps with break it down into even smaller molecules, which can then be absorbed by the villi of the small intestine.

Now, some people develop gallstones, which are hard stones that form in the gallbladder and are made up of the components of bile.

Risk factors for developing gallstones include things like female sex, obesity, pregnancy, and age, sometimes remembered by the 4 F’s—female, fat, fertile, and forty. 

Now, after having a meal, that gallbladder might contract and eject the gallstone into the cystic duct, where it gets lodged. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/VDJ_rearrangement</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rktCYrCNRbGUketiWUHgHFm4SBOyu3g5/_.jpg</video:thumbnail_loc><video:title><![CDATA[VDJ rearrangement]]></video:title><video:description><![CDATA[The adaptive immune response is highly specific for each invader, and that’s because the cells of the adaptive immune response have receptors that differentiate friendly bacteria and potentially deadly pathogens from their unique parts - called antigens. 

The key cells of the adaptive immune response are the lymphocytes- the B and T cells. 

And the antigen receptors for T cells and B cells have a lot of things in common, one of which is that they share the same mechanism - called VDJ rearrangement - to generate a massively diverse set of receptors. 

VDJ stands for variability, diversity, and joining, respectively, and VDJ rearrangement has 4 key characteristics that help ensure that each antigen receptor is unique. 

First, each individual inherits multiple V, D, and J gene segments; second, the V, D, and J gene segments randomly recombine - meaning that any V can pair with any D and any J; third, there’s recombinational inaccuracy - meaning that this process is purposefully error prone - which leads to additional variation; and fourth, there’s random reassortment of two chains - meaning that this process involves two different chains that come together to make the receptor. 

First, let’s look at our antigen receptors. The B cell receptor, or BCR,  is essentially an antibody, except that it has a transmembrane part that goes through the membrane and attaches the receptor to the surface of a B cell. 

Just like antibodies, the B cell receptor has a heavy chain and a light chain. 

One region or fragment of the B cell receptor binds the antigen and it’s called the fragment - antigen binding or Fab region. 

There are two Fab regions on every B cell receptor. 

Then there’s the constant region or fragment called the fragment - constant or Fc region, which is the part that determines what class of B cell receptor it will be - for example, IgM or IgD, and whether or not it will remain a membrane bound B cell receptor or if it will get secreted as a free flo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cell_membrane</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/edBkkievQ0KWbO6z3ttr3FsdTUCh-Dk1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cell membrane]]></video:title><video:description><![CDATA[The cell membrane is an important structural element of the building block of life - the cell. 

Its main role is to define what’s inside - the intracellular space -  and what’s outside - the extracellular space. 

It also regulates what comes in or out of the cell - that’s called selective permeability. 

The cell membrane is basically made up of a bilayer of phospholipid molecules. 

Phospholipids are amphiphilic molecules, meaning “both-loving”. 

Now, the phospholipid is made out of three things - their head, which is made out of negatively charged phosphate, a tail - made out of two fatty acids, and a skeleton made out of glycerol, that brings everything together. 

Their  “head” is hydrophilic - meaning it likes water. Meanwhile, their “tail” is lipophilic - meaning, it loves fats. 

These lipophilic parts also exclude water - so they’re not just lipophilic, they’re also hydrophobic. 

In water, phospholipids form a bilayer - where the hydrophobic tails are oriented inwards, where there are no water molecules, and the hydrophilic heads oriented outwards, in contact with water molecules. 

So the plasma membrane forms a wall with water on both sides. 

The cell membrane is also semipermeable. 

That means that the membrane allows some molecules to pass through, but not others - and it’s mostly based on the molecule’s size, polarity, and charge. 

There are roughly five categories. Small and nonpolar molecules, like oxygen or carbon dioxide will diffuse through the membrane quickly. 

Small, polar molecules, like water, will be able to pass through, but it happens relatively slowly. 

That’s because even though the middle of the phospholipid bilayer is hydrophobic, the occasional molecule of water can sort of slip through because it’s such a small molecule. 

Now, large and nonpolar molecules, such as retinol - also known as Vitamin A1 - can also cross the cell membrane thanks to them being non-polar - but once again, the crossing is really slow, becau]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_and_physiology_of_the_ear</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O_XfkdOBQeSaf0SXziVid_ekS7i3bGw1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy and physiology of the ear]]></video:title><video:description><![CDATA[Our ears help us hear and balance ourselves in space, and they have three parts. 

The first part is the outer ear which is the part you see and hang earrings on, called the pinna, as well as the ear canal.

The second part is the middle ear, which is a tiny chamber that houses even tinier ear bones—the malleus, incus, and stapes. 

The third part is the inner ear, which contains the cochlea, a special structure that converts sound waves into electrical impulses for the brain, as well as the semicircular canals which help with balance.  

Let’s start with the external ear. The pinna, also called the auricle, is made up of cartilage that gives our ears their various shapes and sizes, and it also has a fleshy bit at the bottom- called  the ear lobe, or lobule.

The pinna directs sound waves towards the opening of the ear canal. 

The ear canal, or the external acoustic meatus, is a short, curved tube that burrows through the temporal bone for about 1 inch - or 2 and a half centimeters - and ends at the tympanic membrane. 

On the inside, the ear canal is covered by skin, along with hair follicles and ceruminous glands - which secrete cerumen, or the sticky, yellow-ish, earwax. 

Cerumen helps prevents foreign objects or tiny insects from getting in and damaging the tympanic membrane. That’s a creepy thought.

The tympanic membrane is also called the eardrum, and it’s a thin, translucent membrane that separates the external ear from the middle ear. It’s shaped a bit like a cone, protruding slightly into the middle ear. 

When sound waves reach the eardrum, it vibrates and transmits those vibrations to the tiny bones in the middle ear.

Now, the middle ear is an air-filled cavity inside the temporal bone, shaped like tiny chamber with 4 walls, a floor and a roof. 

The eardrum makes up the lateral wall of this cavity - and opposite from it there is the medial, or internal wall, that separates the middle ear from the inner ear. 

The internal wall has two windo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/MHC_class_I_and_MHC_class_II_molecules</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6yc_bKFdSCynemqnCoFHQV0sT02v9jaB/_.jpg</video:thumbnail_loc><video:title><![CDATA[MHC class I and MHC class II molecules]]></video:title><video:description><![CDATA[Your immune system has an innate immune response which is immediate and nonspecific, as well as an adaptive immune response which is delayed and specific. The adaptive immune response is carried out by lots of unique B cells and T cells, which are highly specific for pathogens based on their unique parts - called antigens. Now, focusing on just T cells - they can only bind antigens, which are typically short peptides, when these antigens are displayed on a Major Histocompatibility Complex or MHC molecule, which is sort of like a silver platter that is on the surface of a cell.  

The MHC molecules are also called human leukocyte antigens and these proteins are encoded for by MHC genes, which are found on chromosome 6. There are actually two groups of genes. One group of genes encodes the MHC class I molecule, which is bound by the CD8 molecule on the surface of cytotoxic T cells. Another group of genes encodes the MHC class II molecule, which is bound by the CD4 molecule on the surface of helper T cells. MHC class I genes encode the proteins HLA-A, HLA-B, and HLA-C, which is easy to remember as for MHC 1 it is always 1 letter. MHC class II genes encode the proteins HLA-DP, DQ, and DR which is also easy to remember because for MHC class 2 there are always 2 letters. And these genes are called histocompatibility because they are really important in determining whether or not a transplant is compatible or gets rejected. But their role isn’t just to wreak havoc on transplants! They’re critically important in making sure that different types of T cells recognize and react to antigens of microbes they are best designed to combat. And even though they’re called human leukocyte antigens, they’re not just found in leukocytes or white blood cells.  

HLA proteins that code for MHC class I molecules are found on all nucleated cells throughout the body, even platelets which are fragments of nucleated cells! In fact, the only cells that don’t have them are mature ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oxygen-hemoglobin_dissociation_curve</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z0q80kAYSVmC7b61PvbdmKM-QFWxXWCt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oxygen-hemoglobin dissociation curve]]></video:title><video:description><![CDATA[The oxygen-hemoglobin dissociation curve shows how the hemoglobin saturation with oxygen (SO2,), is related to the partial pressure of oxygen in the blood (PO2).

Hemoglobin is the main protein within red blood cells, and it’s made of four globin subunits, each containing a heme group capable of binding one molecule of O2. 

So each hemoglobin protein can bind 4 molecules of oxygen. But each hemoglobin isn’t always 100% saturated or bound by oxygen. 

A hemoglobin molecule might have no oxygen bound, and be 0% saturated, called deoxyhemoglobin, and it will take on a tense state shape, or T-state; or it might have one oxygen bound and three open spots, meaning that particular protein would be 25% saturated; or two filled spots and two open spots—50%; or 3 spots filled and one spot open—75%, or all spots filled and 100% saturated. 

All of these states - where oxygen is bound to hemoglobin - are called oxyhemoglobin, changing to its relaxed state, or R-state with each O2 molecule that binds. 

And since there are millions of hemoglobin molecules in a single cell and millions of red blood cells, the hemoglobin saturation of oxygen is the average saturation among all of these proteins. 

Now it turns out that hemoglobin absorbs different wavelengths of light as it gets more and more oxygenated. 

A technique called pulse oximetry uses this property of hemoglobin to figure out the average oxygen saturation across millions of hemoglobin proteins. 

The main factor that influences oxygen saturation is the partial pressure of oxygen in the blood, measured in millimeters of mercury (mm Hg). 

So for example, at a partial pressure of 25mmHg, hemoglobin proteins might be 50% saturated, called P50; and at a partial pressure of 100mmHg, they might be 98% saturated, meaning most are fully saturated. 

And when these points are plotted, the curve takes on a sigmoidal shape.

In practical terms, this sigmoidal shape means that hemoglobin has an increasing affinity for O2 ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hashimoto_thyroiditis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/49Xcq3AFQm__m2Tnf2rmLrbfTzCuYcdC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hashimoto thyroiditis]]></video:title><video:description><![CDATA[Hashimoto’s thyroiditis, named after the Japanese physician Hakaru Hashimoto who first described it, belongs to a group of disorders where there’s some form of inflammation “-itis” of the thyroid gland. 

It’s basically an autoimmune destruction of the thyroid gland, which typically progresses gradually to hypothyroidism, or state of too low “hypo-“ thyroid hormones.

In fact, Hashimoto’s thyroiditis is the most common cause of hypothyroidism in areas of the world where dietary iodine, the basic structural element of thyroid hormones, is sufficient.

Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, or ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary. 

The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, thyrotropin or simply TSH.  

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”. 

If we zoom into the thyroid gland, we’ll find thousands of follicles, which are small hollow spheres whose walls are lined with follicular cells, and are separated by a small amount of connective tissue.

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4. 

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body. 

Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate.

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy. 

T3 increases cardiac output, stimulates]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atrophy,_aplasia,_and_hypoplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2lfnmJ02QCOHt_C6-CAtwBJSRoKSqvdX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atrophy, aplasia, and hypoplasia]]></video:title><video:description><![CDATA[Growing is an important part of living. 

In fact, everything from an individual muscle cell, to a baby blue whale - strives to grow, in order to live and perhaps replicate or reproduce. 

Sometimes, however, growth fails to occur, or even reverts back, and we call that atrophy, aplasia, or hypoplasia, depending on the situation. 

Let’s break down these words. Atrophy, “a” means “no”, and “trophy”, means nourishment. So, atrophy means “no nourishment”. 

Aplasia, “a” means “no” and “plasia” means development. So aplasia means “no development”, and “hypo” means “under” so hypoplasia is “under formation”. 

In a nutshell, atrophy is the reduction in size of a cell, organ, or tissue, after it has attained its normal, matured growth.

This happens either through decrease in cell number or decrease in cell size. 

Decrease in cell number most commonly happens due to apoptosis, which is controlled type of cell death - a bit like cellular suicide. 

An example would be weight loss. In the first few weeks to months of eating healthy and losing weight, the fat cells or adipocytes get smaller but are ready to fill up again with fat.

Over months to years of eating healthy, however, the adipocytes undergo apoptosis - and at that point it’s a bit more difficult to gain back the weight. 

Decrease in cell size, however, is a bit more complex.

Usually, the first step is the loss of nerve or hormonal supply, both of which provide nourishment to cells. 

Then there’s something called the ubiquitin proteasome pathway.

You see, cells have a cytoskeleton, which is a framework of various filaments that keep the cell propped up. 

As cells start getting less nourishment, those filaments get “tagged” for demolition with a protein called ubiquitin. 

Ubiquitin proteins start to attach to one another - a process known as polyubiquitination. 

And then an intracellular protein complex called a proteasome comes in to destroy all polyubiquitinated filaments, causing the cell to d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fatty_acid_synthesis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/stuCy_jfQXuCjkyPqZUjs54yT6Swp7cC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fatty acid synthesis]]></video:title><video:description><![CDATA[In addition to carbohydrates and proteins, lipids are the third main macromolecule we consume in our diet. 

Fatty foods include red meat, dairy products, and even peanut butter. 

And lipids come in many forms, including cholesterol, glycerol, phospholipids, and fatty acids. 

Of these, fatty acids are the simplest form of lipids - they’re basically just long chains of carbon and hydrogen, that are grouped by length into short, medium, long and very long chain fatty acids.

Fatty acids can also combine with glycerol to make triacylglycerides, which is made of 3 fatty acids attached to a glycerol molecule, and is the main storage form of fat in our body. 

Now, short and medium-chain fatty acids are primarily obtained from the diet, but the liver and fat cells can synthesize long chain fatty acids. 

This occurs by combining lots of 2-carbon molecules, called acetyl-coenzyme A or acetyl-CoA, into a single 16-carbon, long chain fatty acid called palmitoyl-coenzyme A, or palmitoyl-CoA.

Palmitoyl-CoA can then serve as a precursor to even longer chain fatty acids. 

To make palmitoyl-CoA, acetyl-CoA provides the carbon atoms, and nicotinamide adenine dinucleotide phosphate, or NADPH provides the hydrogen atoms.

As it turns out, most of the acetyl-CoA used to make fatty acids comes from carbohydrate metabolism - specifically glucose, which is a 6-carbon sugar molecule. 

After eating a glucose-rich dinner, like cake and cookies, glucose levels in the blood rise quickly.

In response, the pancreas secretes insulin, a hormone which makes our cells take in and process a lot more glucose. 

Inside the cells, glucose can enter glycolysis where it’s broken down into two 3-carbon pyruvate molecules, and that yields a bit of energy in the form of adenosine triphosphate - or ATP. 

Pyruvate then moves into the mitochondria, and is converted to acetyl-CoA by an enzyme called pyruvate dehydrogenase. 

Inside the mitochondria, acetyl CoA enters the citric acid cycle by c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chiari_malformation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dwbtstifT4WL-hrMCg1DhnPmSsSaZwZB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chiari malformation]]></video:title><video:description><![CDATA[Chiari malformations are a group of conditions where the cerebellum of the brain extends down into the spinal canal and results in the blockage of the normal flow of cerebrospinal fluid.

The cerebellum, or &amp;quot;little brain&amp;quot;, is divided into two hemispheres which are separated by a narrow worm-like structure in the middle called the vermis. 

Directly beneath the hemispheres are two smaller lobes called cerebellar tonsils. 

Normally, the cerebellum and cerebellar tonsils sit right above the foramen magnum which is the opening at the base of the skull through which the spinal cord passes through.  

The cerebellum is contained within the posterior fossa or floor of the back of the skull, which also contains the medulla oblongata. 

The cerebellum controls balance, posture, and helps to initiate as well as fine-tune voluntary motor activity - think about the fancy finger work of a piano player or the vocal cords of a singer - that’s the cerebellum in action.

The medulla, on the other hand, controls autonomic functions such as breathing and blood pressure, as well as reflexes such as coughing, vomiting, gagging, and swallowing.

Now, there’s also a set of four interconnected cavities in the brain called ventricles, each of which create and circulate cerebrospinal fluid. 

Highest up, are two C-shaped lateral ventricles that lie deep in each cerebral hemisphere. 

The two lateral ventricles drain their cerebrospinal fluid into the third ventricle, which is a narrow, funnel-shaped, cavity at the center of the brain. 

The third ventricle makes a bit more cerebrospinal fluid and then sends all of the cerebrospinal fluid to the fourth ventricle via the cerebral aqueduct.

The fourth ventricle is a tent-shaped cavity located between the brainstem and the cerebellum and is continuous with the central canal. 

After the fourth ventricle, the cerebrospinal fluid enters the subarachnoid space, which is the space between the two inner linings of the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Metaplasia_and_dysplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f3TpG5jmRNqT9SCvkeRsE7LfT_Owy0Uw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Metaplasia and dysplasia]]></video:title><video:description><![CDATA[Do you remember your first day in elementary school? Everything and everyone was new and nothing was impossible. 

But as you went through your education, you got further and further differentiated from your original classmates. That’s analogous to what happens to a cell that undergoes cellular differentiation. 

An undifferentiated stem cell can become pretty much any tissue, influenced by both genes and the environment. Now sometimes, environmental stresses can alter that developmental path. 

In metaplasia what happens is that a mature, differentiated cell type is replaced by another mature, differentiated cell type. 

Often, this happens because there’s an environmental stressor, that the new cell type is better suited to handle. One example, is switching from breathing clean air to inhaling tobacco smoke each day. 

Our airways are lined with columnar respiratory epithelial cells, which generally work well with air breathing, but not so well when faced with an irritant, such as tobacco smoke. 

In response to the toxins in the smoke, already differentiated, mature columnar respiratory epithelial cells are replaced by stem cells undergoing differentiation into sandbag-shaped squamous epithelial cells, which become stratified - meaning that they form layers on top of another. 

This replacement of already differentiated, mature cells into another type of cell is known as metaplasia. 

Another example is our esophagus, which is lined with a nonkeratinizing squamous epithelium. These cells are adapted to withstand the passage of food going down to our stomach. 

However, in case of gastroesophageal reflux disease, acid from the stomach makes its way up into the esophagus on a regular basis. Esophagus cells are not well-suited for chronic contact with acid and can get damaged. 

Normally, when there’s occasional damage, stem cells differentiate into new squamous epithelial cells to replace the damaged ones. 

But when there’s regular exposure to acid, stem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenocorticotropic_hormone</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S9vBT0H7RSOUm_8LERSMldnLRbiOXHjP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenocorticotropic hormone]]></video:title><video:description><![CDATA[Adrenocorticotropic hormone, also known as adrenocorticotropin, corticotropin, or simply ACTH, is a peptide hormone that helps regulate the release of hormones by the adrenal glands which sit above the kidneys. Secretion of ACTH is dependent on the hypothalamic-pituitary axis. 

The hypothalamus, which is at the base of the brain, secretes corticotropin releasing hormone, or CRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior part of the pituitary gland. 

In the anterior pituitary, there are many different types of cells, each responsible for producing a type of hormone. 

The corticotropin releasing hormone binds to a surface protein of one of these cell types, called corticotroph cells, and stimulates them to release ACTH. 

Inside corticotroph cells, ACTH is synthesized from a large precursor molecule called pre- proopiomelanocortin, or pre- POMC. 

Pre- proopiomelanocortin has a short tail called a leader or signal peptide which is cleaved off to form proopiomelanocortin, or POMC, and POMC is then split into multiple peptide hormones, and one of them is ACTH. 

ACTH is then stored inside granules within the corticotroph cells, where it waits until it’s released into the blood. 

Normally, ACTH is released in a pulsatile manner throughout the day and peaks in the morning around 6am but it is also secreted in response to various forms of stressful stimuli. 

For example, the hypothalamus senses when there’s hypoglycemia or low blood sugar, and in response it secretes more corticotropin releasing hormone. 

Another example, is during an infection, where pro-inflammatory cytokines, act on the hypothalamus and anterior pituitary to cause ACTH secretion.

Now, when ACTH is released it travels to the adrenal glands, which sit above each kidneys and binds to the ACTH receptor, also called melanocortin receptor 2, located in the membrane of  their target cells which are adrenocortical cells. 

Ea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anaphylaxis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W78z1h0nTmCpJbhqVnmtENHTSTyyqbiC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anaphylaxis]]></video:title><video:description><![CDATA[Anaphylaxis comes from the greek word “ana-“ which roughly means against and “phylaxis” which means protection, implying that someone’s immune system has reacted to something in such a way that ends up damaging them, instead of protecting them. 

It’s basically a severe type of allergic reaction that affects multiple organ systems and it’s potentially life-threatening.

Normally, the immune system recognizes and acts against pathogens that can cause disease. 

These pathogens have specific molecules on their surface, called antigens, and they help trigger an immune response. 

In some individuals, though, the immune system overreacts and starts targeting harmless molecules that don’t cause any problems for most people. 

These include molecules found in foods like peanuts and shellfish, medications like antibiotics, and in the venom of insect bites. 

In most cases, there might be a mild to moderate allergy, but sometimes things get really serious, involving two or more organ systems, and at that point it’s called anaphylaxis. 

Anaphylaxis, just like any allergic response, happens in two steps, a first exposure, or sensitization, and then a subsequent exposure, which is when it actually gets a lot worse. 

So, let’s say a person is stung by a bee from a nearby beehive, for the first time in their life. 

When the bee pierces the skin with its stinger, its venom gets into the skin. 

Part of that venom molecule can get picked up by a dendritic cell, which is a type of immune cell. 

The dendritic cell gobbles up the foreign particle and presents it to a nearby lymphocyte, called a T cell. 

If the T cell is activated, it starts to produce cytokines, which stimulate B cells, another group of lymphocytes, which produce IgE antibodies. 

These IgE antibodies get released into the bloodstream and bind to the surface of mast cells and basophils, which are immune cells that are full of granules that contain proinflammatory molecules.  

Okay now, let’s say that ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Insulins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pSKA2lEQSYOX1_zQFlkhJkt0RAKv45FY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Insulins]]></video:title><video:description><![CDATA[Insulin is a type of peptide hormone that reduces the amount of glucose in the blood. It is produced in the pancreas by beta cells. These cells are found within clusters of endocrine cells called the Islets of Langerhans, which are distributed across the pancreas. If the body is unable to produce enough insulin, then insulin therapy is used to keep the blood glucose low. 

Insulin’s main function is to facilitate the transport of glucose from the blood  into the various insulin-responsive tissues like muscle cells and adipose tissue. This hormone binds to insulin receptors on the surface of the cell membrane. Now, these receptors have two alpha and two beta subunits. Alpha subunits are located outside of the cell and they bind insulin; while two beta subunits are located within the cell and they have tyrosine kinase activity which carries signals into the cell. Once stimulated, insulin receptors cause intracellular storage vesicles, which contain glucose transport proteins called GLUT4, to fuse with the cell membrane.  Next, the GLUT4 proteins embed themselves into the membrane and allow glucose to move into the cell. 

As a result, insulin promotes glucose uptake and glycogenesis, which is the conversion of glucose to glycogen. Glycogenesis is the process that takes place in the liver and skeletal muscles. When glycogen storage capacity is reached, insulin promotes glycolysis, which is the breakdown of glucose to pyruvate. It also stimulates lipogenesis, the synthesis of fatty acids and triglycerides in the liver and adipose tissue; and amino acid uptake and protein synthesis in skeletal muscles. 

Finally, insulin activates Na+/K+- ATPase pumps and shifts potassium into intracellular space, thereby decreasing potassium levels in the blood. On the flip side, insulin inhibits glycogenolysis, which stands for the breakdown of glycogen; and gluconeogenesis, which is glucose production from lactic acids and noncarbohydrate molecules. Finally, insulin inh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glucagon</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ee8JaEXARlqjbqqFDSn5WrHXQwO2_4oG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glucagon]]></video:title><video:description><![CDATA[Glucagon is a hormone that’s involved in raising the blood glucose levels or glycemia while fasting. Glucagon is produced by some small islands of cells in the pancreas called the Langerhans islets. 

The pancreas lies in the upper left part of the abdomen, right behind the stomach. 

The vast majority of the pancreas is made up of exocrine glands in charge of secreting digestive enzymes into the small intestine to help digestion.

But about 1 to 2% of the mass of the pancreas is made up of the islets of Langerhans, which are endocrine glands made up by five different cell types, each of which secretes a specific hormone.

The most abundant are the beta cells, which produce insulin. 

But you can also find alpha cells that secrete glucagon, delta cells that secrete somatostatin, gamma cells that secrete pancreatic polypeptide, and finally epsilon cells that secrete ghrelin  

Let’s focus on alpha cells. 

Alpha cells are in charge of producing glucagon, which is a peptide hormone encoded by the GCG gene on chromosome 2. 

Glucagon is first synthesized as a single polypeptide called preproglucagon. 

Preproglucagon has a short tail called a leader or signal peptide which is cleaved off to form proglucagon, and proglucagon is then further cleaved to form glucagon.

This mature glucagon is stored inside granules within the alpha cells where it waits until it’s released into the blood. 

The most important glucagon regulator is glucose.

Apha cells are sensitive to glucose concentrations in blood, and when blood glucose levels are low - for instance during fasting or after intense physical activity - alpha cells secrete glucagon into the blood to help increase those levels. 

Glucagon secretion is also stimulated by adrenaline from the sympathetic nervous system, which is activated during stressful situations with high energy consumption. 

Glucagon secretion is also stimulated by cholecystokinin which is secreted by intestinal cells to stimulate digestion and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thymic_aplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6-atmDn4QdaUXtPG8eESfIk_QRa-la4w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thymic aplasia]]></video:title><video:description><![CDATA[In thymic hypoplasia, thymic refers to the thymus which is an immune organ that sits between the lungs, hypo- refers to under, and -plasia refers to development.

So, thymic hypoplasia is a condition where the thymus is underdeveloped and has a reduced number of cells. 

By week 4 of development, the embryo takes on a more recognizably “human” form—but to be honest, it still looks more like a shrimp than a baby. 

At the head end of this little shrimp-like creature, a set of structures called the pharyngeal apparatus begins to develop, consisting of pharyngeal arches, clefts, and pouches. 

The components of the pharyngeal apparatus develop into various head and neck structures, and sometimes multiple arches join together to give rise to a single structure. 

Now, the epithelial tissue of the embryo’s third and fourth pouch turns into the inferior parathyroid glands and superior parathyroid glands, while the epithelial tissue that lines the ventral region of the third pouch forms the thymus. 

Both glands then go on to break off from the pharyngeal wall and eventually attach to the posterior side of the thyroid. 

The thymus now free, migrates down the middle of the pharynx, until it ends up in its final position in the front of the thorax where it fuses with its counterpart from the opposite side.  

During childhood, the thymus occupies considerable room behind the sternum, in a part of the chest known as the mediastinum, a space in the chest between the lungs that also contains the heart.

But when people become older, it atrophies and is replaced by fatty tissue. 

It&amp;#39;s here in the thymus, where certain immune cells from the bone marrow mature into T lymphocytes or T cells, where the T stands for Thymus. 

Once mature, these T cells help defend the body against infections by activating other cells of the immune system and checking the body’s cells for viral infection or abnormalities like cancer.

In thymic hypoplasia, a small portion of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abnormal_heart_sounds</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Oco5l4WGSBemVaNtAdMl6Wq4SayDRLit/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abnormal heart sounds]]></video:title><video:description><![CDATA[If you put a stethoscope over the chest, you’ll usually hear something that sounds like lub dub, lub dub, lub dub, which repeats over and over again, with each cardiac cycle, or heartbeat.

In total, our heart has four valves- two atrioventricular valves, between the atria and the ventricles, which are the tricuspid valve, on the Left  side, and the mitral valve, on the left side, and two semilunar valves, between the ventricles and the large arteries coming off of them, which are the pulmonary valve, on the right side, and the aortic valve, on the left side. Normally, in every heartbeat, some valves open, allowing blood to pass through and others close to hold blood within a chamber. The sound of the closing of each of these valves is projected onto the chest wall. The two normal heart sounds are S1, which is basically the tricuspid and mitral valve closing, and S2 which is the aortic and pulmonic valve closing. Between S1 and S2, we have systole, which is when ventricles are contracting and pushing blood out, and between S2 and S1 of the next heart cycle, we have diastole which is when blood is filling the relaxed ventricles. Together, S1 and S2 form the “lub dub” of the heart beat.

Alright, now in addition to S1 and S2, there are two other &amp;quot;extra&amp;quot; sounds that are sometimes heard in the cardiac cycle, called S3 and S4. S3 and S4 are heard in different parts of diastole. In early diastole, which is right after S2, the atrioventricular valves are open and blood is flowing from the atria into the ventricles. If there’s a lot of blood coming in, the ventricles fill up quickly, and fluid waves bounce off of the walls of the ventricles which makes them vibrate, creating a third heart sound, or S3. S3 sounds kind of like “lub-dub-ta”. In trained athletes and also in pregnancy this is totally normal and just means that the ventricles are handling extra blood volume. But an S3 can also be a sign of volume overload, like in congestiv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peutz-Jeghers_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wBT-52jCSEOFje99-N3rCxIISEuHGVQa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peutz-Jeghers syndrome]]></video:title><video:description><![CDATA[Peutz-Jeghers syndrome, named after Dr. Jan Peutz, who first described it, and Dr. Harold Joseph Jeghers, who later reported on it, is a rare autosomal dominant condition in which individuals develop polyps throughout their gastrointestinal tract, as well as dark spots called melanotic macules in their mouth, lips, genitalia, palms, and soles. 

The large intestine is found in the abdominal cavity, which can be thought of as having two spaces - the intraperitoneal space and the retroperitoneal space. 

The intraperitoneal space contains the first part of the duodenum, all of the small intestines, the transverse colon, sigmoid colon, and the rectum; the retroperitoneal space contains the distal duodenum, ascending colon, descending colon, and anal canal. 

So the large intestines essentially weave back and forth between the intraperitoneal and retroperitoneal spaces.

Now, the walls of the gastrointestinal tract are composed of four layers. 

The outermost layer is the called serosa for the intraperitoneal parts, and the adventitia for the retroperitoneal parts. 

Next is the muscular layer, which contracts to move food through the bowel.

After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves.

And finally, there’s the inner lining of the intestine called the mucosa; which surrounds the lumen of the gastrointestinal tract, and comes into direct contact with digested food. 

The mucosa has invaginations called intestinal glands or colonic crypts, and it’s lined with large cells that are specialized in absorption.

Peutz-Jeghers syndrome is caused by a mutation of the STK11 gene, which is a tumor suppressor gene that codes for a protein called STK11. 

So without a functioning STK11 gene, the gastrointestinal cells are more likely to accumulate mutations and start dividing faster than usual - ultimately giving rise to polyps. 

These polyps are benign outgrowths that arise along the gastroin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inclusion_body_myopathy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uskbOidNQv_EejzybmBtnTR9TSKc0W34/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inclusion body myopathy]]></video:title><video:description><![CDATA[In inclusion body myopathy, “myopathy” refers to muscle disease and “inclusion body” refers to the presence of inclusions, or vacuoles, formed by clumps of protein that collect within the muscle fibers. 

There’s a sporadic form, sporadic meaning that it strikes at random, which is the most common and is also called inclusion body myositis - because it causes muscle inflammation. 

There’s also a rare hereditary form, that causes no muscle inflammation.

Normally, the cells of the immune system are ready to spot and destroy anything foreign that could cause the body harm.

To help with this, most cells in the body have a set of proteins that come together to form a major histocompatibility complex, or MHC, class I proteins which sits on the surface of their cell membrane. 

These surface proteins act kind of like a serving platter, presenting molecules from within the cell for the immune system, so that it can have a way of performing ongoing surveillance. 

Normally the MHC class I proteins serves up a normal harmless molecule from the cell - a self-antigen, and there’s no response. 

But if a cell is invaded by a pathogen like a virus, then viral proteins are served upon on the MHC class I proteins.

When these viral antigens are displayed on the cell surface, it sparks an immune response.

Specifically, a type of T-lymphocyte, called a CD8+ T-cell or a cytotoxic T-cell, will bind to the antigen presented by the MHC class I proteins. 

If the cytotoxic T-cell binds strongly, than the antigen is recognized as foreign, and the cytotoxic T-cell secretes inflammatory molecules and enzymes - like perforin and granzymes. 

Perforin is able to form holes in the infected cell and that allows the granzymes to enter the cell. 

Once inside, the granzymes induce apoptosis, or programmed cell death - which destroys the cell. 

And as if that weren’t enough, the cytotoxic T-cells have a protein called Fas ligand on their surface. 

Fas ligand binds to a protein calle]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Isolated_primary_immunoglobulin_M_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j9qZp8KAQHKADoMrA4D4xvjhQ2eWXNvI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Isolated primary immunoglobulin M deficiency]]></video:title><video:description><![CDATA[In isolated primary immunoglobulin M deficiency, there’s a decrease in the number of IgM antibodies in the blood, while the levels of other types of antibodies remain normal.

Let’s take a look at how B cells end up secreting different types of antibodies. 

Each B cell is born in the bone marrow from a stem cell and develops its own B cell receptor, which sits on the cell surface. 

The B cell receptor consists of two parts - a protein called CD79 that communicates with the rest of the cell and a membrane bound IgM or IgD antibody that can bind to an antigen.

An antigen is any substance recognized by that particular antibody. 

Each antibody has two identical light chains and two identical heavy chains that combine into a Y shape. 

So this Y-shaped antibody’s got two arms with identical tips, which is called the variable region. 

This variable region contains an antigen binding domain that’s unique to that antibody. 

Below the variable region, or toward the point where the arms meet, is the constant region where every member of an antibody class is identical – so all IgM antibodies have the same constant regions, but IgM and IgA constant regions are different. 

And there are five classes of antibodies in total: IgM, IgG, IgA, IgE, and IgD class antibodies, and each one has a slightly different job. 

For example, IgMs are part of B cell receptors, and are the first free-floating antibodies produced in an immune response. 

They’re secreted as a pentamer, meaning there are five antibodies connected together, which provides many binding sites for grabbing antigens and taking them out of the blood. 

Each antibody has complement protein binding sites on the heavy chains, so these IgM pentamers are also great at activating complement proteins, which help destroy and remove pathogens. 

IgG antibodies stick to the surface of bacteria and viruses – and that prevents them from adhering to and infecting cells. 

IgG also allows macrophages and neutrophils to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_mellitus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H_cRLu14TGGfpxLc-oBM1x3qSY6lRKcb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes mellitus]]></video:title><video:description><![CDATA[In diabetes mellitus, your body has trouble moving glucose, which is a type of sugar, from your blood into your cells.

This leads to high levels of glucose in your blood and not enough of it in your cells, and remember that your cells need glucose as a source of energy, so not letting the glucose enter means that the cells starve for energy despite having glucose right on their doorstep.

In general, the body controls how much glucose is in the blood relative to how much gets into the cells with two hormones: insulin and glucagon.

Insulin is used to reduce blood glucose levels, and glucagon is used to increase blood glucose levels.

Both of these hormones are produced by clusters of cells in the pancreas called islets of Langerhans.

Insulin is secreted by beta cells in the center of the islets, and glucagon is secreted by alpha cells in the periphery of the islets.

Insulin reduces the amount of glucose in the blood by binding to insulin receptors embedded in the cell membrane of various insulin-responsive tissues like muscle cells and adipose tissue.

When activated, the insulin receptors cause vesicles containing glucose transporters that are inside the cell to fuse with the cell membrane, allowing glucose to be transported into the cell.

Glucagon does exactly the opposite, it raises the blood glucose levels by getting the liver to generate new molecules of glucose from other molecules and also break down glycogen into glucose so that it can all get dumped into the blood.

Diabetes mellitus is diagnosed when the blood glucose levels get too high, and this is seen among 10% of the world population.

There are two types of diabetes - Type 1 and Type 2, and the main difference between them is the underlying mechanism that causes the blood glucose levels to rise.

About 10% of people with diabetes have Type 1, and the remaining 90% of people with diabetes have Type 2.

Let’s start with Type 1 diabetes mellitus, sometimes just called type 1 diabetes. In t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Problem-based_learning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/spypJVUHR0SG4FnyMCteyrUQQFCBrKPq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Problem-based learning]]></video:title><video:description><![CDATA[Problem-based learning, or PBL for short, is an educational approach that’s collaborative and built around solving a complex real-life “problem” or scenario that you might come across in a professional setting. 

Now, in traditional teaching, there’s teacher who stands in front of a big group of students and gives a lecture while the students scramble to listen, understand, and remember everything the teacher is saying. 

It can be hard to keep track all of that new information, let alone really absorb it. 

In contrast, problem-based learning is designed to teach students how to teach themselves while becoming master problem solvers along the way! 

The classroom looks like this: a handful of students work in small groups exploring real-life scenarios with the guidance of a tutor. 

Problem-based learning is often used in medical education where students work through clinical cases based on real life patients. 

As an example, let’s say that our problem-based learning case describes a 72-year-old man who has chest pain.

The student-doctors start thinking about this problem by brainstorming a list of follow up questions. 

Where exactly is the pain? When did it start? Are there any other symptoms? What is the past medical, drug, and family history? Could the patient have a heart, gastrointestinal, lung or even musculoskeletal problem? 

Over the course of the session, the case might include lab data, pictures, videos or even a real life patient actor who will answer their questions. 

Together, the students figure out what they already know and where they may have gaps in their knowledge. 

Many questions start threads of information that lead to more questions and more threads and it can quickly evolve into a giant tangled spider web of knowledge and questions! 

All of the information and these questions are tracked by a student scribe either on a whiteboard or a shared document online. 

Many groups also create concept maps to organize their thoughts, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antidiuretic_hormone</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XGRQxmwVTdm8cR6H11YBBQ7QRxmRDOKB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antidiuretic hormone]]></video:title><video:description><![CDATA[Antidiuretic hormone, or ADH, is a peptide hormone that is anti- or against -diuresis which is excessive urine production.

Antidiuretic hormone is also called vasopressin because it causes vasoconstriction - constriction of blood vessels. 

So antidiuretic hormone prevents making too much urine, which leads to water retention, and vasoconstriction, and together these two actions help increase the blood pressure. 

Now, the brain has two interconnected structures: the hypothalamus and the pituitary gland. These two structures are connected by the pituitary stalk. 

The hypothalamus is a part of the brain  that contains several nuclei, or clusters of neurons. And two of these nuclei, the paraventricular and supraoptic nuclei, contain neurons that secrete ADH. 

When ADH is produced, it travels down the axons of these neurons, and these axons have small dilations called Herring bodies, which is where ADH is stored.

When the body needs more ADH, the stored hormone is released and continues down the axon through the pituitary stalk.

From there it’s released into the posterior pituitary gland which is interstitial tissue near capillary beds, so that the ADH can easily enter the bloodstream. 

Let’s say that it&amp;#39;s a super sunny day out and you forget to bring water with you. Well first, as you walk around, you’re constantly losing water through sweat as well as water vapor from your mouth and nose as you breathe out - these are insensible water losses. Without drinking water, you can quickly get dehydrated. This causes your plasma osmolarity to increase, because the fluid levels in your blood drop, but the total number of solute particles remains roughly the same.

Now, two things now begin to happen simultaneously. First, a region in the brain called the anterior hypothalamus has a cluster of neurons called supraoptic nuclei, which have osmoreceptors that sense even tiny changes in osmolarity, as small as 1 mOsm/L. These neurons are always sampling th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leukocyte_adhesion_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PYvGuTGHQ0KBxPwMsV1Ga69eSzem--sD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leukocyte adhesion deficiency]]></video:title><video:description><![CDATA[Leukocyte adhesion deficiency is a rare inherited immunodeficiency which develops because a group of immune cells called phagocytes fail to bind to the blood vessel wall, and therefore cannot get to the site of inflammation or tissue injury.

Normally, phagocytes, which are mostly neutrophils, circulate in the blood waiting for a signal that something’s wrong somewhere in the body. 

As soon as this signal comes, in the form of cytokines which are pro-inflammatory molecules, they try to speed over to the affected tissue.

But to get there, they first have to pass through the endothelial cells that line the blood vessel wall. 

Getting through the endothelial cells is known as extravasation and involves multiple steps. 

First, the endothelium expresses molecules called selectins, which binds to sialyl-Lewis X, a carbohydrate that’s found on the surface of phagocytes, making them slow down and roll along the vessel wall. 

Second, is a step called adhesion. 

That’s basically a tight interaction between cellular adhesion molecules on the surface of endothelial cells, and integrins on the surface of the phagocytes. 

Third, phagocytes manage to transmigrate or squeeze around the endothelial junctions, which are the sites of connection between two adjacent endothelial cells. 

Fourth, the phagocytes use the concentration gradient of the cytokine signals to move towards the area of inflammation. 

This process is critical for destroying invading pathogens, in particular bacteria and fungi. 

In fact, after a long battle with bacterial or fungal cells, phagocytes, especially neutrophils, die and can form a collection of pus, which can accumulate in a closed tissue space, developing into an abscess. 

The process of extravasation is also essential for wound healing, where phagocytes help remove dead and damaged cells. 

In addition to typical settings of wound healing, this function of phagocytes is required soon after birth. 

That’s because once the umbilical ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_hormones</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FUPW8OwMSv_fo8qBcYEEdiZUS8ySXFiN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid hormones]]></video:title><video:description><![CDATA[Thyroid hormones are triiodothyronine or T3, and thyroxine, also called T4 or tetraiodothyronine. 

They’re two tyrosine-based iodine-containing hormones that help regulate our body’s metabolism. 

T3 and T4 are produced by the thyroid gland, which is located in the neck and consists of two lobes that look like two thumbs hooked together in the shape of a “V”. 

If we zoom into the thyroid gland, we’ll find thousands of follicles, which are small hollow spheres whose walls are lined with follicular cells or thyrocytes, and are separated by a small amount of connective tissue. 

Follicular cells are bipolar cells - with an apical side that surrounds a central cavity or lumen filled with the colloid, which is a fluid that contains the precursor hormone thyroglobulin. 

Thyroglobulin is a large glycoprotein that is synthesized by the follicular cells and then it is secreted into the lumen of the follicle to be stored in the colloid. 

The basolateral side of follicular cells is in contact with blood vessels. 

The basolateral membrane contains a sodium-iodide symporter, which pumps two sodium ions into the cell down their electrochemical gradient, in order to bring one iodide ion into the cell from blood. 

Iodide is then pumped into the colloid through an ion transporter called pendrin, which exchanges iodide for chloride, since they’re both negatively charged. 

Once iodide is in the colloid, it undergoes oxidation with the enzyme thyroperoxidase, which changes it into an iodine atom. 

It’s then attached to tyrosine amino acid residues which are found throughout thyroglobulin. 

This process is called iodination. 

Some tyrosine residues are bound by only one iodine, whereas others are bound by two iodine atoms, yielding monoiodotyrosine or MIT, and diiodotyrosine or DIT, respectively. 

These molecules are then linked together by thyroperoxidase. 

Linking one MIT with one DIT creates T3, while linking two DIT molecules creates T4 - and both T3 and T4 rem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Transcription_of_DNA</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-2lk2oacS8mqrEnEs6TcIJ2cSx__-e_o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Transcription of DNA]]></video:title><video:description><![CDATA[Deep within the cell’s nucleus, there’s our DNA. DNA is made up of genes, and each gene is basically a specific part of the DNA that codes for a protein. 

And genes become proteins in two steps: transcription and translation. 

Transcription is the first step in creating a protein, during which a specific gene is “read” and copied on an individual mRNA, or messenger RNA molecule - which is like a blueprint with instructions on what protein to build. 

Now, DNA has two strands, which wrap one around the other to form the characteristic “double helix”. 

Each single strand of DNA is composed of four types of nucleotides - which are the individual “letters” or “building blocks” of DNA. 

Nucleotides of DNA are made out of a sugar - deoxyribose, a phosphate, and one of the four nucleobases - adenine, cytosine, guanine, and thymine - or, commonly, A, C, G, T for short.

The nucleotides on one strand pair up through hydrogen bonds with nucleotides on the opposing strand, to create the double-stranded DNA : specifically, A bonds with T, and C bonds with G, so they’re called complementary bases.  

Now, with these two strands - one strand is called the coding, or the sense strand, and the other strand is called the template, or the anti-sense strand. 

The coding strand has a coding sequence of nucleotides that serves as a master blueprint for our protein. 

It’s a what-you-see-is-what-you-get kind of thing. 

The template strand, on the other hand, has a sequence of nucleotides that is complementary to the sequence on the coding strand. 

In addition, the two DNA strands also have a “direction” - the coding strand runs from the 5’ end towards the 3’ end, while the template strand runs from the 3’ to the  5’ end.

A bit like two snakes coiled up together but facing different directions. 

So, if the coding strand looks like this:

5’ end - A A T C C A G T A - 3’ end

The template strand will look like this:

3’ end - T T A G G T C A T - 5’ end 

*Disclaimer: no c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Role_of_Vitamin_K_in_coagulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vGP_Kqt7SvW64tADIH9Tg_FRSwKMFtbU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Role of Vitamin K in coagulation]]></video:title><video:description><![CDATA[Vitamin K helps to regulate the process of blood coagulation by assisting in the conversion of certain coagulation factors into their mature forms. Without vitamin K, our bodies would be unable to control clot formation. Imagine being unable to form blood clots effectively--that would mean that we would lose all of our blood volume from something as simple as a pinprick! To prevent this extreme scenario - vitamin K must be ingested, metabolized, and utilized to create mature coagulation factors.

Now, to understand the regulation of clot formation, we first need to talk briefly about hemostasis, in which hemo refers to the blood, and stasis means to halt or stop. Hemostasis is divided into two phases: primary and secondary hemostasis. Primary hemostasis involves the formation of a platelet plug around the site of an injured blood vessel, and secondary hemostasis  reinforces the platelet plug with the creation of a protein mesh called fibrin. To get to fibrin, a set of coagulation factors, each of which are enzymes, need to be activated. These enzymes are activated via a process called proteolysis- which is where a portion of the protein is clipped off. In total, there are twelve coagulation factors numbered factors I-XIII, there’s no factor VI.  Most of these factors are produced by liver cells, and it turns out that producing coagulation factors II, VII, IX, and X requires an enzyme that uses vitamin K. 

Vitamin K is found in abundance in green leafy foods—things like spinach, kale, and chard which all have high concentrations of vitamin K. It’s a fat-soluble vitamin, along with vitamins A, D, and E, meaning that it can be stored in fat cells instead of being excreted by the kidneys. Vitamin K is also synthesized by bacteria in our gastrointestinal tract as a byproduct of their metabolism, which further contributes to overall intake.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chemoreceptors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dylakoWHRvinLBOToETo8O6jTNK8zqdw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chemoreceptors]]></video:title><video:description><![CDATA[“Chemo-“ refers to the chemical composition of the blood, so chemoreceptors are special nerve cells or receptors that sense changes in the chemical composition of the blood. That information is sent from the chemoreceptors to the brain to help keep the cardiovascular and respiratory systems balanced. 

Alright, according to their location, chemoreceptors can be classified into two types: peripheral and central ones. Now, the peripheral chemoreceptors are so named because they live outside the brain. They are actually tiny bodies, or clusters of nerve cells and include the aortic body which sits along wall of the aortic arch, and the carotid body which is located at the point where each common carotid artery splits in the internal &amp;amp; external carotid arteries, running alongside the neck. Both the aortic and carotid bodies are bathed in arterial blood- and they carefully monitor changes in the concentration or partial pressure of oxygen, PO2 for short, but also in the partial pressure of carbon dioxide, PCO2 for short, as well as the concentration of hydrogen ions, which determines blood pH. The aortic body sends this information along to the vagus, or tenth (X) cranial nerve, and the carotid body sends this information along to the glossopharyngeal, or ninth (IX) cranial nerve. These two large nerves travel up towards the respiratory centers which are in the brainstem. The respiratory centers are groups of neurons, located in the pons and medulla oblongata, that are responsible for the autonomic or involuntary control of breathing. The respiratory centers also communicate with the cardiovascular centers. 
The cardiovascular centers are areas in the lower one-third of the pons and medulla oblongata of the brainstem, responsible for the autonomic or involuntary control of the cardiac and vascular function. They do that by coordinating the sympathetic and parasympathetic branches of the autonomic nervous system. There are two main cardiovascular center]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_disseminated_encephalomyelitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fHeexxJySc21PZ3juVtTRBjzTo2G7Ns7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute disseminated encephalomyelitis]]></video:title><video:description><![CDATA[In acute disseminated encephalomyelitis or ADEM, acute means that the disease evolves rapidly, disseminated refers to the fact that there are multiple sites involved, encephalo- refers to the brain, myelo- refers to the spinal cord, and -itis refers to inflammation.

So acute disseminated encephalomyelitis is an autoimmune disease of the central nervous system, where there’s sudden inflammation and demyelination at multiple sites of the brain and spinal cord. 

The central nervous system consists of the brain and the spinal cord. 

Grossly, the central nervous system can be divided into two main areas: the grey matter, which is made up of neuron cell bodies, and the white matter, which is made up of projections from the neuron cell bodies known as axons and dendrites. 

The dendrites receive electrical impulses from other neurons; the neuron cell body has all of the neuron’s main organelles like the nucleus; and finally the axons transmit electrical impulses to the dendrites of the next neuron in the series. 

Some axons are surrounded by a fatty protective sheath called myelin that helps increase the speed at which electrical impulses are sent. 

This myelin is produced by oligodendrocytes, which are a group of cells that support neurons. 

Now, the brain is protected by harmful things in the blood by the blood brain barrier, which only lets certain molecules and cells through. For immune cells like T and B cells that means having the right ligand or surface molecule to get through the blood brain barrier, this is kind of like having a VIP pass to get into an exclusive club. 

Once a T cell makes its way in, it can get activated by something it encounters.

Once the T-cell gets activated, it changes the blood brain barrier cells to express more receptors, and this allows immune cells to more easily bind and get in, kind of like bribing the bouncer to let a lot of people in. 

In the case of acute disseminated encephalomyelitis, T-cells are activated by my]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lac_operon</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/adteVFA2Rr_wxX9lUxofh5XgT4aYHnxF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lac operon]]></video:title><video:description><![CDATA[With the lac operon, lac refers to lactose, which is a sugar found in milk, and an operon is a portion of DNA where genes with related functions are grouped together and are controlled by the same promoter. 

In the case of the lac operon, the proteins the lac operon produces are all required for transporting lactose into the cell and metabolising it in Escherichia coli as well as other bacteria. 

Although glucose is the preferred carbon source for most bacteria, the lac operon allows these bacteria to use lactose when glucose isn’t available. 

Gene regulation of the lac operon is well studied, and that’s why it has become a classic example of gene regulation in bacteria.

Now before getting into the details of the lac operon and how it functions, let’s review gene expression. 

DNA is made up of genes, and each gene is basically a specific part of the DNA that codes for a protein. 

Genes become proteins in two steps: transcription and translation. 

In transcription a segment of DNA is copied into RNA, specifically messenger or mRNA, by the enzyme RNA polymerase. 

RNA polymerase unwinds the DNA double helix to produce the complementary mRNA, which is like a blueprint on what protein to build. 

Then there’s translation which is where organelles called ribosomes assemble and utilize the mRNA produced during transcription to create proteins from amino acids lying around in the cytoplasm.  

Now, the lac operon is a part of E coli’s DNA and it includes structural genes, like lacZ, lacY, and lacA, as well as regulatory genes like the promoter and operator. 

The structural genes lacZYA code for the proteins that ultimately allow E coli to transport and metabolize lactose. 

LacZ, produces the enzyme beta galactosidase, also called lactase, which break down lactose into glucose and galactose. 

LacY produces beta-galactosidase permease, which allows lactose to enter, or permeate into the cell, and lacA encodes beta-galactoside transacetylase, and its funct]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/T-cell_development</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rlE-1lWqTaWax7ocraSmnThsRCCMIvbM/_.jpg</video:thumbnail_loc><video:title><![CDATA[T-cell development]]></video:title><video:description><![CDATA[Your immune system is like the military - with two main branches, the innate immune response and the adaptive immune response. The innate immune response is immediate and non-specific, meaning that although it can distinguish an invader from a human cell, it doesn’t distinguish one invader from another invader. In contrast, the adaptive immune response is highly specific for each invader, and that’s because the cells of the adaptive immune response have receptors that differentiate one pathogen from another by their unique parts - called antigens. This adaptive immune response takes days to weeks to become activated, during which time the innate immune system provides protection. The second important feature of the adaptive immune response is that it has memory, which means that once a response against an antigen is triggered, subsequent responses will be faster and stronger. This, of course, is why vaccines are so effective – once you get a vaccine containing a part of a pathogen, the next time you see that same pathogen, you will remember the previous encounter (from the vaccine) and you will kill it. 

Now, the key cells of the adaptive immune response are the lymphocytes - the B and T cells - which are generated during lymphopoiesis. Lymphopoiesis has two main goals - to generate a diverse set of lymphocytes, each with a unique antigen receptor, and to get rid of lymphocytes that have receptors that are self-reactive, meaning that they could attack one’s own healthy tissue. Normally, hematopoietic stem cells within the bone marrow mature into a common lymphoid progenitor cell, which then becomes either a B-cell or a T cell. To become a B cell, it has to develop into an immature B-cell in the bone marrow and then complete its maturation in the spleen. To become a T cell, it has to migrate to the thymus and become a thymocyte, where it completes its development into a mature T cell. So, “B” for bone marrow and “T” for thymus. 

In T cell development, the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_clearance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W_89RX7oRFSiUlOceNZ7K03iT32PY8gA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal clearance]]></video:title><video:description><![CDATA[In order for the body to function properly, it needs a way to get rid of toxins and other waste materials. That’s where the kidneys come in. Their main function is to filter the blood and remove any unwanted substances from the body. Now, the first step in blood filtration happens at the glomerulus - a tiny bed of capillaries surrounded by the Bowman’s capsule. The glomerular filtration barrier is made up of three layers and together they separate the blood inside the glomerular capillaries from the fluid inside Bowman’s capsule. They work like a sieve, allowing water and some solutes in the plasma like sodium, to pass into Bowman’s space, while keeping negatively charged particles like proteins, or large particles like red blood cells in the blood. The filtered fluid, now called pre-urine, leaves the Bowman’s space and travels through the nephron.

The nephron is the basic unit of the kidney, and is essentially one long tube bent into a “U” shape.  Different sections of this tube either reabsorb substances back into systemic circulation or actively secrete them into the nephron to be excreted in urine. 

Renal clearance of a substance refers to how quickly a particular substance is removed from the plasma by the kidney and excreted in urine. So something with a high renal clearance means that it will be quickly removed from the blood, and vice versa. There’s a formula to calculate renal clearance for some substance X. 

In this formula, C stands for the renal clearance which is the volume of blood plasma that’s cleared of that substance over time in minutes. C equals the concentration of the substance in urine [U]x multiplied by the urine flow rate (V) which is the amount of urine excreted over time in minutes. All of that’s divided by the plasma concentration of the substance [P]x. So, if the urine concentration is high but the plasma concentration is low, then that must mean that a lot of the substance was removed from the blood, leading to a high renal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Slow_twitch_and_fast_twitch_muscle_fibers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BimqS72SSWmTB9SRVC6ws-RBSYChxKV8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Slow twitch and fast twitch muscle fibers]]></video:title><video:description><![CDATA[Skeletal muscle fibers are divided into two main types: slow-twitch, which are also called slow oxidative fibers, and fast-twitch muscle fibers. 

Fast-twitch muscle fibers are further subdivided into fast oxidative and fast glycolytic fibers. This classification is based on the speed of contraction and the metabolic pathway that’s used to make ATP, a molecule that stores energy for muscle contraction. 

Most muscles possess a mix of slow-twitch and fast-twitch fibers, but the predominant one determines the primary function of the muscle.

Alright, now let’s take a look at a muscle cell, or myocyte - and specifically it’s sarcoplasm, which is the cytoplasm of a muscle cell. 

The sarcoplasm is filled with stacks of long filaments called myofibrils. 

Each myofibril has thick myosin and thin actin filaments that don’t extend through the entire length of the muscle fiber, instead they’re arranged into shorter segments called sarcomeres. 

The myosin filaments have these small club-like extensions, which are called myosin heads. 

The thin actin filament look like a pearl necklace that’s gently twisted. Each pearl represents one G-actin protein, which has an active site where the myosin head binds to during contraction. 

Now, before myosin can bind actin, myosin needs to power up. Part of the myosin head is an ATPase, meaning that it can cleave an ATP molecule to ADP and phosphate ion and release some energy. The energy is used to cock the myosin head backwards, into its high energy position. 

Next, the myosin head binds to the active site, and this triggers the release of the stored energy in the myosin head. When that happens, the myosin head launches pulling the thin filament along with it. This is called the power stroke. 

The combined power strokes of all the myosin heads lead to sliding of the thin filament along the thick filament, and this results in the contraction of the skeletal muscle fiber. 

Now, the speed of contraction depends on how quickl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ulcerative_colitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9fCNHdJwQNuCt_PIdhgCJ8tAR1_bvkzI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ulcerative colitis]]></video:title><video:description><![CDATA[Inflammatory bowel disease can cause inflammation in the small and large intestine, in other words...inflammation of the bowel. 

Colitis refers specifically to inflammation in the colon, or the large intestine. Ulcerative colitis is a type of inflammatory bowel disease that tends to form ulcers along the inner-surface or lumen of the large intestine, including both the colon and the rectum. 

These ulcers are spots in the mucosa where the tissue has eroded away and left behind open sores or breaks in the membrane. 

Sometimes there is a flare which means that new damage has occurred, and then there are periods of remission when the tissue starts to heal up.

Ulcerative colitis is actually the most common type of inflammatory bowel disease, not that there are that many, but this one causes inflammation and ulcers in the mucosa and submucosa of the large intestine only, which is an important point that sets it apart from Crohn disease, another inflammatory bowel disease. 

Now although certain environmental factors like diet and stress were once thought to be the culprit behind these ulcers forming in the gut, now it’s thought that these are more secondary, meaning they seem to make symptoms worse, but ulcerative colitis is now ultimately thought to be autoimmune in origin. 

In fact, cytotoxic T cells from the immune system are often found in the epithelium lining the colon, so the thought is that inflammation and ulceration in the large intestine is caused by T cells destroying the cells lining the walls of the large intestine, leaving behind these eroded areas or ulcers.

It’s unclear what exactly these T cells are meant to be targeting though. 

Some patients have p-ANCAs in their blood, or perinuclear antineutrophilic cytoplasmic antibodies, which are a kind of antibodies that target antigens in the body’s own neutrophils. 

Although not completely understood, some theories suggest this may be partly due to an immune reaction to gut bacteria that have ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lambert-Eaton_myasthenic_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xPZgtY0zTIOjPItWeS7h8seWTLKVtOVf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lambert-Eaton myasthenic syndrome]]></video:title><video:description><![CDATA[With Lambert-Eaton myasthenic syndrome, or LEMS for short, “myasthenia” refers to muscle weakness, and Lambert-Eaton refers to Edward Lambert and Lealdes Eaton, the two physicians who first described the condition. So, Lambert-Eaton myasthenic syndrome is a rare autoimmune condition that attacks the peripheral nervous system, causing muscle weakness, weak or absent reflexes, and autonomic dysfunction. 

First, let&amp;#39;s focus on physiology and how muscles normally work. Whether you’re reaching for a slice of pizza or sinking that perfect shot in basketball, it all starts in the brain. The upper motor neuron of the cerebral cortex fires an action potential down the spinal cord to activate lower motor neurons. Next, lower motor neurons pick up these signals and pass them along their axons toward terminal branches and axon terminals, all the way to skeletal muscle fibers. 

This communication site between the lower motor neuron and the skeletal muscle fiber is known as the neuromuscular junction, which consists of three main parts. First, there’s the presynaptic membrane, which is the axon terminal of the lower motor neuron packed with acetylcholine vesicles. Acetylcholine is actually the neurotransmitter that enables muscle contraction. Next, there’s the postsynaptic membrane, which is the membrane of the skeletal muscle fiber, rich in nicotinic acetylcholine receptors.  

Finally, this tiny space between two membranes is called the synaptic cleft and contains the enzyme acetylcholine esterase. 

Now, when the action potential reaches the axon terminal, it opens voltage-gated calcium channels called P/Q type channels. Next, calcium rushes in through these channels, triggering the acetylcholine vesicles to fuse with the presynaptic membrane and release acetylcholine into the synaptic cleft. Once inside the cleft, acetylcholine moves across to bind nicotinic acetylcholine receptors on the postsynaptic membrane. Eventually, this binding triggers the muscle]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocrine_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XUmOFJf_SviJGFovP3PprGvhSMyFxIgV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocrine system anatomy and physiology]]></video:title><video:description><![CDATA[The endocrine system is made up of various endocrine glands that each secrete hormones into the bloodstream. 

When hormones reach their target cell, they bind to a receptor on the cell’s membrane or within that cell, and in response the target cell changes what it’s doing.  

So at the end of the day, the endocrine system helps establish homeostasis - a sense of balance even when there are changes in the external environment. 

Now, structurally, hormones can be either steroids or non-steroids. 

Steroid hormones are made from cholesterol, and they’re made by the adrenal glands, which sit above each kidney, and the gonads - either the testes or ovaries. 

Steroid hormones are hydrophobic or non-polar - meaning that they hate watery environments, so they travel through the bloodstream bound to transport proteins to reach their target cells. 

But because steroid hormones are relatively small, and non-polar, they are also able to diffuse right across phospholipid membrane of target cells. Once inside the cell, they bind to a receptor that goes on to activate certain genes in the nucleus. 

Non-steroid hormones, on the other hand, are either peptides or proteins - so chains of amino-acids, or they can derive from a single amino acid. 

Peptidic hormones, like insulin and glucagon, are hydrophilic - meaning they love coursing through our blood. 

However, when they reach the cell membrane of a target cell, they can’t pass through the phospholipid bilayer. Instead, they bind to cell surface receptor proteins. 

Once the receptors bind to a non-steroid hormone, they change shape, and that activates various proteins and enzymes that go on to create changes in gene expression within the cell. 

So ultimately, once the non-steroid hormone binds to the receptor, there’s a change in the cell even though the hormone never actually enters the cell. 

Finally, there are amino-acid hormones that derive from the amino acid, tyrosine, which are the thyroid hormones, as we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parathyroid_hormone</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YU9tRX3fQt_gDNl3P8Uo9IHTQ_W542Y8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parathyroid hormone]]></video:title><video:description><![CDATA[The body’s blood calcium level stays stable thanks to three hormones: parathyroid hormone, vitamin D, and calcitonin. 

Parathyroid hormone and vitamin D help increase calcium levels, whereas calcitonin helps lower them. Let’s focus on the role of parathyroid hormone.

The majority of the extracellular calcium, the calcium in the blood and interstitium, is split almost equally into calcium that’s diffusible and calcium that’s not diffusible.

Diffusible calcium is small enough to diffuse across cell membranes and there are two subcategories.

The first is free-ionized calcium, which is involved in all sorts of cellular processes like neuronal action potentials, contraction of skeletal, smooth, and cardiac muscle, hormone secretion, and blood coagulation, all of which are tightly regulated by enzymes and hormones. 

The second category is complexed calcium, which is where the positively charged calcium is ionically linked to tiny negatively charged molecules like oxalate and phosphate, which are small anions, that are found in our blood. 

The complexed calcium forms a molecule that’s electrically neutral but unlike free-ionized calcium it’s not useful for cellular processes. 

Finally there’s the non-diffusible calcium which is bound to large negatively charged proteins like albumin. 

The resulting protein-calcium complex is too large and charged to cross membranes, so the non-diffusible calcium is also uninvolved in cellular processes.  

Now blood calcium is regulated mainly by parathyroid hormone.  

Parathyroid hormone, or PTH, comes from the parathyroid glands, which are 4 pea sized glands buried within the posterior part of the thyroid gland.

Inside the parathyroid glands are parathyroid or chief cells which synthesize a protein called preproPTH in their endoplasmic reticulum. 

This long protein chain is 115 amino acid long and contains the parathyroid hormone segment, but also a “pre” segment  and a “pro” segment. 

In the endoplasmic reticulum a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Types_of_data</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JkZqZqeJQzWBJUN2qZiwQpw8RJaKM8Ev/_.jpg</video:thumbnail_loc><video:title><![CDATA[Types of data]]></video:title><video:description><![CDATA[Data are like a set of facts that are measured and recorded, and then summarized to help us make conclusions. 

Data can either be quantitative or in numbers, like a person’s age, measured in number of years they’ve been alive or it can be qualitative, which is non-numerical, like someone’s blood type {A, B, AB, or O}. 

So, data are classified into two main groups - quantitative or numeric data and qualitative or categorical data. 

Let’s start with categorical data, which involves assigning subjects to a category, ie. “red” vs “blue” or “high” vs. “low”.  

Categorical data can be further broken down into nominal and ordinal data.

Nominal data is based on categories that cannot be logically ordered. 

For example, blood types - A, B, AB and O are nominal data; There is no logical order or magnitude in blood type.

A is not higher than AB, and O is not less than B - they are just different, like apples and oranges. 

Now you could say that type AB blood has more antigens than type O blood or that apples are firmer than oranges, but then we’re looking at different data - antigen number and firmness, and not simply the blood type or fruit type. 

Other attributes like sex, type of religion, or ethnic background are all examples of nominal data. 

These attributes are measured in categories, instead of numbers. 

Therefore, they don’t have any magnitude; that’s why when you summarize nominal data, you have to use proportions.

For example, take a group of 20 classmates: 10 are Blood Type A’s, 5 are Blood Type B’s, and 5 are Blood Type O’s. 

You can say that 50% are A, 25% are Type B, and 25% are Type O. 

And while you can’t calculate a mean or median, you can identify the “mode”, which is the most frequently appearing value of this data: Blood Type A.

Ordinal data are also measured in categories, but unlike nominal data, ordinal data come with a logical order attached. 

For example, let’s say you want to measure happiness, and you send 100 people a surv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ventilation-perfusion_ratios_and_V/Q_mismatch</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/95kjtd7kRSykmbWqjxJ4PY_jSeGBvSxp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ventilation-perfusion ratios and V/Q mismatch]]></video:title><video:description><![CDATA[Alveolar ventilation (V) is the amount of air that reaches alveoli in the lungs, measured in liters/minute (L/min); and perfusion (Q) is the pulmonary blood flow, or cardiac output, that reaches the arteries, and specifically the capillaries, surrounding the alveoli, also measured in L/min. 

When the lungs are upright and at rest, ventilation is about 4 L/min and perfusion is about 5 L/min, giving a ratio of 0.8.

Now, the lungs can be divided into three distinct zones. 

Zone 1 is the top of the lungs, or the apexes; zone 2 is the middle of the lungs; and zone 3 is the bottom, or bases, of the lungs. 

In an upright position, gravity dramatically affects both ventilation and perfusion across all three zones, and overall the V/Q ratio progressively decreases from zone 1 to zone 2 and finally to zone 3.

In zone 1, the flow of air and blood is the lowest with ventilation of around 0.25 L/min, and perfusion of around 0.07 L/min; generating a V/Q ratio of 3.6. 

In zone 2, ventilation is equal to perfusion; generating a V/Q ratio of about 1.  

In zone 3, the flow of air and blood is the highest with ventilation of around 0.8 L/min, and perfusion of around 1.3 L/min; generating a V/Q ratio of 0.6. 

So the V/Q ratio varies depending on which part of the lung is involved, but the overall ratio is an average of the three zones and works out to be 0.8.

Now, the ratio of V to Q influences how efficiently gases,  specifically O2 and CO2 , are exchanged in the lungs. 

In healthy lungs with a V/Q ratio of 0.8, the alveolar partial pressure of O2 (PAO2), is about 100 mmHg or millimeters of mercury; and the alveolar partial pressure of CO2 (PACO2) is about 40 mmHg. 

Meanwhile, the arterial partial pressure of O2 (PaO2) is around 95 mmHg - slightly lower than what’s on the alveolar side; and the arterial partial pressure of CO2 (PaCO2) is about 40 mmHg - the same as what’s on the alveolar side. 

But these partial pressures are also an average over the the three lu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cytoskeleton_and_intracellular_motility</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2lKELKrFQKuubDvZPVNFotjSQKet9dF5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cytoskeleton and intracellular motility]]></video:title><video:description><![CDATA[The cell is the basic unit of life, that can replicate on its own. 

The human body alone has over 200 different cell types - from long skinny neurons that can grow over 1 meter long to myocytes or heart muscle cells that contract to let you to flex your muscles. 

But despite their differences, they share many features, including the cytoskeleton.

The cytoskeleton is a network of proteins within the cell. 

The cytoskeleton gives each cell its shape and anchors organelles in place - keeping everything sturdy - a bit like the frame for a house. 

But it’s also a dynamic network, which can change shape when the cell wants to move, contract, divide, or pull in or push out molecules. Imagine if your house could do that - perhaps it would get up and walk away during an earthquake! 

So the cytoskeleton is pretty special and it’s made up of three proteins: actin filaments, intermediate filaments, and microtubules. 

Actin filaments are the thinnest of the three proteins, so they’re also called microfilaments. 

They’re made up of two strands of actin proteins arranged in a long twisting chain like a twisted necklace. 

The actin filaments connect to one another to form a network - like a spider&amp;#39;s web - that’s located just below the cell membrane. 

The actin filaments slide closer together and further apart, allowing the cell to change shape during muscle contraction. 

Not surprisingly, muscle cells have plenty of actin, as well as another protein called myosin. 

Myosin filaments bind to actin filaments, and that’s what allows the actin to slide closer together and further apart.

And ultimately, that makes the muscle cells shrink and stretch during muscle contraction and relaxation. 

Similarly, sometimes these networks change their shape and that allows cells to move. 

White blood cells like neutrophils use extensions called pseudopodia, or false feet, to crawl in and out of blood vessels - a process called diapedesis. 

The way that works is tha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hardy-Weinberg_equilibrium</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DvOJKSSQShW97oZI9ieyynTDRqubYbRu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hardy-Weinberg equilibrium]]></video:title><video:description><![CDATA[Two scientists - G. H. Hardy and Wilhelm Weinberg - helped to bridge two major concepts - Mendelian genetics and natural selection. 

Mendelian genetics state that traits are inherited from one generation to the next through genes, which come in two different versions called alleles. 

Alleles can be dominant or recessive, the difference being that it only takes one dominant allele to express a dominant trait, but there need to be two recessive alleles in order to express a recessive trait. 

Natural selection, on the other hand, states that organisms that have traits which make them better adapted for their environment are more likely to pass on their genes to their descendents. 

Hardy and Weinberg realized that dominant and recessive alleles offer variation in a population and that natural selection would act upon that variation, altering the overall frequency of those traits. 

So they took the altering factor - natural selection - off the table and came up with the Hardy-Weinberg principle, or equilibrium, which is a hypothetical state of balance in a population, where the frequency of dominant and recessive alleles remains the same from one generation to the next.

So for a population to achieve this balance there have to be no factors altering its genetic composition. 

One altering factor is natural selection. 

Other factors are mutations - where alleles actually change and become a new variety of a certain trait - and migration - where new and maybe different alleles enter or leave the population causing its composition to change. 

Finally, a determining factor is the size of the population - a smaller lot has a greater risk of losing alleles from one generation to the next because some organisms don’t get to reproduce - a process called genetic drift. 

If none of these factors affect a population, the genetic pool remains constant. 

Now let’s say we have a population with a genetic pool that’s large and stable over time. 

And let’s assume th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibody_classes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kk86BQx_RKqu5m_FOlCy3PZyTHSF5Qv0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibody classes]]></video:title><video:description><![CDATA[The immune response is highly specific for each invader, and that’s because the cells of the adaptive immune response have unique receptors that are able to differentiate friendly bacteria from potentially deadly pathogens from their unique parts - called antigens. 

The key cells of the adaptive immune response are the lymphocytes - the B and T cells. 

B cells develop in the bone marrow where they undergo a process called VDJ rearrangement to generate a massively diverse set of B cell receptors.

The B cell receptor is essentially an antibody except that has a transmembrane part that goes through the membrane attaching the receptor to the surface of the B cell. 

The B cell receptor, has two heavy chains and two light chains, and the region or fragment of the B cell receptor that binds the antigen is called the fragment-antigen binding or Fab region. 

The Fab region is where the ends of the heavy and light chains meet, and there are two Fab fragments on each B cell receptor. 

The remainder of the heavy chain makes up the constant region or constant fragment region, also called Fc. 

The two heavy chains are linked to one another by disulfide bonds and each heavy chain is also linked to a light chain by a disulfide bond.

Each B cell receptor, has two identical heavy and light chains, resulting in two identical antigen binding sites.

As the B cell develops into a plasma cell, the B cell receptor gets secreted as an antibody with the exact same antigen specificity. 

However, the heavy chain actually changes as the B cell develops. 

There are 5 major types of heavy chains which encode the isotypes or classes of immunoglobulins: IgM, IgD, IgG, IgA, and IgE. 

These five are encoded by heavy chain genes which are referred to by the greek letters mu, delta, gamma, alpha, and epsilon. 

Each of these immunoglobulins has a different function, shape, and consequently valence.

The valence of an antibody is the amount antigen binding or Fab fragments it has. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aortic_valve_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZmjjzVqoQCOIBkBQbJUJAorfSEa_n-jk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aortic valve disease]]></video:title><video:description><![CDATA[The aortic valve is typically made up of three leaflets: the left, the right, and the posterior leaflet and it opens during systole to allow blood to be ejected to the body. During diastole, it closes to allow the heart to fill with blood and get ready for another systole. If the aortic valve doesn’t open all the way, it gets harder to pump out to the body and this is called aortic stenosis. If it doesn’t close all the way, then blood leaks back into the left ventricle called aortic valve regurgitation or aortic insufficiency.

Usually, the aortic valve opens to about 3-4 cm2, but with stenosis it can become less than 1 cm2. This is usually caused by mechanical stress over time, which damages endothelial cells around the valves, causing fibrosis and calcification, which hardens the valve and makes it more difficult to open completely. This type usually shows up in late adulthood, with patients over 60 years old.

Similarly, patients that have a bicuspid valve — with two leaflets — as opposed to a tricuspid — with three — are more at risk of fibrosis and calcification because the mechanical stress that’s usually distributed between three leaflets is now being split by two leaflets and therefore, they see more stress per leaflet. Another important cause of aortic stenosis is chronic rheumatic fever, which can cause repeated inflammation and repair, leading to fibrosis. In this case, the leaflets can actually fuse together — called commissural fusion — which is an important distinction from the type caused by mechanical stress over time.

When the valve fuses together or hardens, it doesn’t open as easily, right? And so as the left ventricle contracts, it creates this high pressure that eventually pushes on the valve until it finally snaps open, causing a characteristic “ejection click.” Since the blood has to flow through a narrow opening, there’s turbulence which creates noise, or a murmur, which gets initially louder as more blood flows past the opening, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancoast_tumor</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VgipMCL1RciMF27nSGMOm9I0QO2FUyw5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancoast tumor]]></video:title><video:description><![CDATA[Pancoast tumors get their name from Dr. Henry Pancoast, who was the first radiologist to describe them. 

So to be clear, these tumors are classified based on their location in the lung apices - the tops of the lungs - rather than on the type of lung cancer they emerge from. 

The reason that Pancoast tumors are given special consideration is that this location allows them to interfere with nerves and blood vessels, which leads to problems that are unique from tumors in other locations.

Lung tumors are divided into small cell and non-small cell cancers based on the way they look under a microscope and how they behave. 

Generally speaking, small cell lung tumors are made up of small cells which divide rapidly and spread quickly, and non-small cell lung cancers, which should probably be called large cell lung cancers, have large cells that divide and spread slowly. 

As it turns out, the majority of Pancoast tumors are non-small cell lung tumors, but a few are small cell lung tumors. 

Most of the time, the signs and symptoms of Pancoast tumors result from the tumor creating local inflammation and swelling and pushing up against nearby nerves or blood vessels – which disrupts their function; a phenomenon known as mass effect. 

In some instances, there is tumor invasion, which is when tumor cells penetrate and grow directly into surrounding structures. 

Now, at the first thoracic nerve root or T1, you’ve got sympathetic nerves that supply the head, neck and eyes. 

This point is super close to the lung apices and so susceptible to compression or even invasion from a nearby Pancoast tumor. 

Normally, these sympathetic nerves help to dilate the pupil, raise the eyelid, and help stimulate the sweat glands. 

If a pancoast tumor pushes on or invades these sympathetic nerves, it can cause miosis - a small or constricted pupil, ptosis - a droopy eyelid, and anhidrosis - a failure to sweat, all on the ipsilateral, or same side, of the face as the nerve. 

Toget]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preparing_for_the_MCAT</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3JYUdXNJQQ2dbl05yoNqwcjGR0Gbbknq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preparing for the MCAT]]></video:title><video:description><![CDATA[If you’ve decided to apply to medical school in the United States or Canada, you’ll likely need to take the Medical College Admission Test, or MCAT for short. 

The MCAT is a multiple choice, computer-based exam that’s designed to test your critical thinking and problem solving skills.

The MCAT is administered by the Association of American Medical Colleges, or AAMC, and their overall goal is to make sure that you have a good foundational understanding of both the scientific and cultural complexities of medicine. 

Okay - so the MCAT itself has four sections: Chemical and Physical Foundations of Biological Systems or Chem/Phys for short, Critical analysis and Reasoning Skills or CARS for short, Biological and Biochemical Foundations of Living Systems or Bio/Biochem for short, and lastly Psychological, Social, and Biological Foundations of Behavior or Psych/Soc for short. 

The first, third, and fourth sections have 59 questions each with a time limit of  95 minutes per section. 

Each section has 10 passages with 4 to 6 questions per passage. 

There are also 15 independent questions that are not associated with a passage. 

In the second section, the Critical Analysis and Reasoning Skills section, or CARS section, there are 53 questions that you have to answer in 90 minutes.

This section has 9 passages with 5 to 7 questions per passage. 

In total, the exam lasts about seven and a half hours, if you include the time for breaks. 

So let’s go section by section. Let’s start with the chem/phys section which consists of 30% general chemistry, 25% biochemistry, 25% physics, 15% organic chemistry, and 5% biology.

Topics in this section include Newtonian mechanics, electrostatics and electrodynamics, waves and optics, atomic structure, molecular structure and interactions, solutions and acid/base chemistry, electrochemistry, separation and purification techniques, thermodynamics and kinetics, and the structure, function, and reactivity of biologically-releva]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tqVpVC-hToSdqZFOXuVsHKJrTWCZ3mt9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osmosis]]></video:title><video:description><![CDATA[Osmosis is a group of people that take complicated medical topics and teach them in an organized and effective way so that the information seeps into your brain and leads to longer retention… oh wait, not that Osmosis? 

Well, then, simply put, osmosis is how water molecules move across a semipermeable membrane that separates two solutions.  

It can be thought of as passive diffusion of water and it requires no energy. 

When water molecules move like this, they end up equalizing the concentrations of the solutions on either side of the membrane. 

This is possible because a semipermeable membrane, like the cell membrane for example, is kinda like a sieve with pores that let small molecules like water across, but not larger molecules or ions like sodium and chloride. 

So let’s say that we’re looking at a lab beaker that is filled with a salt water solution, and we separate it in two compartments - A and B -  with a semipermeable membrane in the middle. 

Now, first off - the salt which is sodium chloride will separates out into sodium ions and chloride ions once it’s in the water. 

And since the concentration of sodium and chloride ions is the same on either side of the membrane, we say that A and B are isotonic to each other. 

Now, inside the two compartments, water molecules and sodium and chloride ions are moving around and bouncing off each other. 

It’s a bit like two big dance parties happening in two adjacent warehouses that are connected by doors that are semipermeable - meaning that the water molecules can get through but not the larger sodium and chloride ions. 

Now some of the water molecules may go through one of these doors to go from party A to party B, and some water molecules might go the other direction from party B to party A. 

But the truth is that the water molecules aren’t particularly drawn to either compartment, because crossing the membrane to go one way is just as easy as crossing the membrane to go the other way. 

We call t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DNA_structure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Df_NSOGFQIemmYtlB2BL3A9QSgWLCqfs/_.jpg</video:thumbnail_loc><video:title><![CDATA[DNA structure]]></video:title><video:description><![CDATA[Buried deep within the nucleus, lies our genetic information, called DNA - which stands for deoxyribonucleic acid. 

DNA is made up of two strands that are coiled around one another in a double helix. 

Each of the two strands that make up DNA is a polynucleotide chain - so it’s a string of nucleotides one after another. 

Nucleotides are organic molecules that are made up of a 5-carbon sugar, a phosphate group and a nitrogenous base - also called a nucleobase - or, simply, a “base”. 

For DNA, the 5-carbon sugar is deoxyribose. Deoxyribose looks like a pentagon, and the tips of the pentagon are 4 carbons and an oxygen molecule. 

The 5th carbon is outside the ring, and it binds to the phosphate group. 

The sugar and phosphate elements are the same for the 4 nucleotides that make up DNA - the difference comes from the nucleobase, which is attached to the first carbon of the sugar. 

There are four nucleobases that make up and give DNA nucleotides their name - adenine, or A, thymine, or T, cytosine, or C and guanine, or G. 

Structurally, these bases can be either purines or pyrimidines - the purines, guanine and adenine, are made up of 2 heterocyclic rings. 

The pyrimidines, cytosine and thymine, are made up of a single ring. 

You can remember this with “CUT PYe (pie)” - because cytosine and thymine along with uracil, which is a nucleotide found in RNA, are all Pyrimidines.  

The nucleotides bind to one another using their sugar and phosphate groups. 

The phosphate group on the 5th carbon of the sugar of one nucleotide - also called the 5’ carbon - forms a covalent bond with the 3rd carbon on the sugar of the next nucleotide - also called the 3’ carbon. 

This gives each DNA strand a sugar-phosphate backbone, as well as a “direction” - one of the strands runs from the 5’ end towards the 3’ end, while the other one runs from 3’ to 5’. 

This makes DNA an “antiparallel” molecule - it’s a bit like two snakes coiled up together but facing different direct]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cortisol</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C4qh5l7RSoOg4wW6P8sdEtllQvq7ayfO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cortisol]]></video:title><video:description><![CDATA[Cortisol is a steroid hormone that helps regulate the metabolic and immune pathways of our body. Cortisol belongs to the glucocorticoid class of hormones produced by a pair of adrenal glands which are located above each kidney. 

Each gland is made up of an inner medulla, which secretes catecholamines, and an outer cortex. The adrenal cortex itself is divided into three zones, each one secreting a different steroid hormone. 

The outermost zone is the zona glomerulosa, which secretes mineralocorticoids. Next, there’s the zona fasciculata, which secretes glucocorticoids, cortisol being the most important one. And finally, there’s the zona reticularis that secretes androgens. 

Cortisol production is controlled by the hypothalamus-pituitary axis. The hypothalamus, which is at the base of the brain, secretes corticotropin releasing hormone which is sensed by the anterior, or front part of the pituitary gland. 

In the anterior pituitary, the corticotropin releasing hormone binds to a surface protein on a group of pituitary cells, called corticotroph cells, and stimulates them to release adrenocorticotropic hormone, or ACTH, into the bloodstream. 

Adrenocorticotropic hormone then travels to the adrenal glands, binds to receptors on the cells of the adrenal cortex, and makes them take up cholesterol from the blood. 

The cells of the zona fasciculata contain the enzymes needed to convert cholesterol into cortisol. Cortisol is structurally derived from cholesterol, which is a lipid molecule, and can slip in and out of cells relatively easily. 

As a result, cortisol isn’t stored - it gets secreted as it’s being produced. Normally, cortisol secretion is pulsatile throughout the day, peaking in the morning around 6am. 

But cortisol is also secreted in response to various stressful stimuli - including hypoglycemia or low blood sugar, infections, caffeine, sleep deprivation, and psychological stress - like getting in a fight with your best friend.

Once it’s made,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Independent_assortment_of_genes_and_linkage</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YGoPf3cfSz_H3KndstOMqcO0TYqZddJc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Independent assortment of genes and linkage]]></video:title><video:description><![CDATA[Inheritance is possible because of chromosomes. 

These chromosomes come in pairs - one from mom and one from dad - so they’re called homologous chromosomes. 

Each chromosome has genes, which are segments of DNA that carry genetic information for a specific trait.

And different versions of the same gene are called alleles. 

As an example, brown eye color and blue eye color are both alleles for the eye color gene.

And each parent offers one allele of a gene. 

Now, these alleles can be either dominant often represented with a capital letter, or recessive, represented with the corresponding lowercase letter, the difference being that it only takes one dominant allele for its traits to be expressed, whereas it takes two recessive alleles for its traits to be expressed. 

Human somatic cells - that is, all of the cells aside from the sperm and eggs, which are called gametes - have 23 pairs of chromosomes; 22 somatic pairs and one sexual pair - adding up to 46 chromosomes in total. 

These chromosomes, along with the alleles they carry, segregate during meiosis -  which is the process of making new gametes. 

Gametes only carry half the genetic information of the parent - so 23 chromosomes. 

Once the male and female gametes merge during fertilization, their alleles combine to make the genotype —or genetic information— of the new organism. 

For every gene, alleles can combine to give rise to three possible genotypes, homozygous dominant - or  AA, heterozygous - or Aa - and homozygous recessive - or aa. 

This determines all of a person’s features —or phenotype— such as eye color, hair color, or even whether or not they’re color blind.

Now, independent assortment means that no matter which alleles an organism inherits for one gene that codes for a trait like eye color, it won’t affect the alleles it inherits for another gene that codes for a different trait, like hair color. 

Let’s start with a simple example. Let’s represent the eye color gene with the l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_motility</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LboK_hVOTw2m9n4H_tNFYPCSQhy47tq1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal motility]]></video:title><video:description><![CDATA[When we eat, food enters the mouth where it is chewed up by the teeth into a smaller, soft mass called the food bolus.

The bolus is then pushed by the tongue into the pharynx and continuous to travel down through the esophagus, squeezed by an involuntary movement called peristalsis, until it reaches the stomach.

So, the esophagus is a muscular tube that runs vertically downwards and carries food from the pharynx to the stomach. In an adult it’s about 25 cm long and can be divided into three regions. 

First is the cervical region, where it connects with the pharynx behind the trachea. 

Separating the pharynx and the cervical region of the esophagus is the upper esophageal sphincter, which is a muscular ring that contracts and relaxes to control the entrance of food into the esophagus.

Below the cervical region is the thoracic region, that begins at the level of the suprasternal notch and ends when the esophagus goes through the diaphragm via an opening called the esophageal hiatus. 

And finally there&amp;#39;s the abdominal region, which starts at the esophageal hiatus and ends where the esophagus connects to the stomach. 

Separating the abdominal region and the stomach is the lower esophageal sphincter, also known as the gastroesophageal sphincter, which relaxes to let food into the stomach. 

Now, because most of the esophagus is located inside the thorax, the intraesophageal pressure is equal to the intrathoracic pressure, and both of these pressures are lower than abdominal pressure. This means that food in the esophagus gets pulled towards the area with lower pressure - a bit like how dirt gets pulled into a vacuum. 

So, the upper and lower esophageal sphincters have to stay contracted to prevent air from entering the digestive tract and altering this pressure gradient. 

In addition, the lower esophageal sphincter also prevents stomach acids from entering the esophagus.

The esophagus receives most of its nerve supply from two sources - ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sturge-Weber_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5wrTVaC6QqiAANBwa3eQ8G1uT6a18z-4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sturge-Weber syndrome]]></video:title><video:description><![CDATA[Sturge-Weber syndrome is a congenital neurocutaneous disorder named after William Sturge and Frederick Weber, the first physicians to describe it. 

Neurocutaneous because it affects the brain and the skin. 

In fact, Sturge-Weber syndrome is also called encephalotrigeminal angiomatosis; encephalo- refers to the brain, trigeminal refers to the trigeminal or fifth cranial nerve, and angiomatosis refers to a vascular malformation. 

That’s because in Sturge-Weber syndrome there are too many capillaries in the meninges covering the brain, as well as in some areas of the face that are innervated by the trigeminal nerve, like the forehead and upper eyelid. 

Finally, in Sturge-Weber syndrome there’s often a congenital mark - a birthmark - called a port-wine stain. 

When the embryo is one week old, it has two layers of cells: a dorsal or outer epiblast layer and a ventral or inner hypoblast layer. 

During week 3 of development the embryo undergoes gastrulation where the cells in the epiblast layer form a three layered trilaminar disc with an ectoderm, mesoderm and endoderm layer. 

The ectoderm is the dorsal most germ layer, and through a process called neurulation forms the neural tube. 

From the neural tube, neural crest cells migrate to help form the central and peripheral nervous systems, as well as the cornea of the eyes and the epidermis layer of the fetal skin. 

During week 6 of development, as the cephalic portion of the neural tube grows, a network of tiny blood vessels called a vascular plexus develops, to better supply that neural tissue. 

There’s a gene called the GNAQ gene which codes for a guanine nucleotide-binding protein, and that protein is involved in development of the vascular plexus. 

Normally, around week 9 of development, the GNAQ gene stops getting expressed, and that leads to regression of the vascular plexus.

In Sturge-Weber syndrome a sporadic mutation occurs in the GNAQ gene during embryonic development, and that keeps the GNA]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fatty_acid_oxidation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DPEp2W4pR2GGmJdCoQ2miNvRSi_rwAn3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fatty acid oxidation]]></video:title><video:description><![CDATA[Our bodies are capable of surviving without food for long periods of time, at least 3-4 weeks with hydration! 

The reason we can do that is that we can store our dietary fuels, and then break them down when needed to make energy in the form of adenosine triphosphate, or ATP. 

Fat is one of the most important ways we store energy and the term “burning fat”, actually refers to fatty acid oxidation. 

In fact, if two individuals were stranded in the Andes mountains with no food, the person with more fat content would survive longer - yet another reason to avoid working out.

What makes fat such a great source of energy are fatty acids, which are the simplest form of fats, composed of long chains of carbon and hydrogens. 

The transfer of electrons in the form of hydrogen from these fatty acids to certain molecules, can then be used to generate ATP. 

Fatty acid oxidation primarily takes place in the mitochondria of heart, skeletal muscle, and liver cells. 

Before we can oxidize fat, it needs to be moved from storage sites to the cells that can use it. Fat is stored in adipocytes or fat cells as triglycerides, which are 3 fatty acids attached to a glycerol molecule. 

Triglycerides can be broken down by the enzyme hormone sensitive lipase, into free fatty acids and glycerol. So if you’re starving in the Andes, first your blood glucose level falls. 

In response, the pancreas secretes a hormone called glucagon which increases the activity of hormone sensitive lipase, and increases the breakdown of triglycerides. 

Now, the free fatty acids can leave the fat cell, and enter the bloodstream, where they bind to a protein called albumin. 

Albumin carries the fatty acids to target cells, like liver cells, that are capable of fatty acid oxidation. First, the free fatty acid dissociates from albumin and diffuses into the cell. 

Once inside the cell, a cytosolic enzyme called fatty acyl-CoA synthetase adds a coenzyme A molecule to the end of the fatty acid, turnin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Calcitonin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z6NG9yj4RsWlPs4zIC5aG5RJRjKeH4Uo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Calcitonin]]></video:title><video:description><![CDATA[The body’s blood calcium level stays stable thanks to three hormones: parathyroid hormone, vitamin D, and calcitonin. 

Parathyroid hormone and vitamin D help increase calcium levels, whereas calcitonin helps lower them. Let’s focus on the role of calcitonin.

The majority of the extracellular calcium, the calcium in the blood and interstitium, is split almost equally into calcium that’s diffusible and calcium that’s not diffusible.

Diffusible calcium is small enough to diffuse across cell membranes and there are two subcategories. 

The first is free-ionized calcium, which is involved in all sorts of cellular processes like neuronal action potentials, contraction of skeletal, smooth, and cardiac muscle, hormone secretion, and blood coagulation, all of which are tightly regulated by enzymes and hormones. 

The second category is complexed calcium, which is where the positively charged calcium is ionically linked to tiny negatively charged molecules like oxalate and phosphate, which are small anions, that are found in our blood. 

The complexed calcium forms a molecule that’s electrically neutral but unlike free-ionized calcium it’s not useful for cellular processes. 

Finally there’s the non-diffusible calcium which is bound to large negatively charged proteins like albumin. 

The resulting protein-calcium complex is too large and charged to cross membranes, so the non-diffusible calcium is also uninvolved in cellular processes.  

Now, calcitonin is a polypeptide hormone involved in regulating blood calcium levels.

Calcitonin comes from the parafollicular cells, or C cells, of the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”. 

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. 

C cells are adjacent to follicles, more precisely in the connective tissue that separates the follicles.

C cells synthesize preprocalcitonin, a pept]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Zones_of_pulmonary_blood_flow</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/etjHOLjiQ4a1aLX7ToTC3TDcQLyZ4D06/_.jpg</video:thumbnail_loc><video:title><![CDATA[Zones of pulmonary blood flow]]></video:title><video:description><![CDATA[Air from the environment enters through the nostrils, goes through the airways, and finally reaches the alveoli, the tiny air-filled sacs in the lungs. 

Here, gas is exchanged between the alveoli and blood flowing through the capillaries that surround each alveolus. 

And blood flows from the higher pressured arteriole (Pa) to the lower pressured venule (Pv). 

Now, PA, which is the pressure within the alveoli of the lungs is relatively constant throughout the lungs. 

At the end of expiration, it’s equal to atmospheric pressure, which is 0 centimeters of water (0 cmH2O) And although Pa is always greater than Pv , their values change at different vertical levels within the lungs. 

Consider the fact that some blood vessels are more vertical while others are more horizontal. The horizontal ones are unaffected by gravity, but the more vertical ones are affected by gravity. 

The analogy would be a cylinder filled with water - the cylinder represents a blood vessel and the water would be the blood. 

As you add more and more water, the height (H) of the water increases. And when the column is completely filled, the pressure (P) from the water that’s exerted on the bottom of the cylinder, or the hydrostatic pressure, is equal to the density of water (p) multiplied by gravitational acceleration (g), multiplied by the height of the column of water above it.

Blood in vertical blood vessels in upright lungs have similar hydrostatic effects. 

At the apex of the lung, Pa and Pv are relatively low, at the base of the lung, Pa and Pv are relatively high, and in the middle of the lung, Pa and Pv are somewhere in between.

Now because PA is constant, the relationship of Pa and Pv with respect to PA changes. And it’s the relationship between these three that determines the zones of the lungs.    

In zone 3, at the base of the lungs, Pa is higher than Pv, and both are higher than PA.

In zone 3, blood flows through the capillaries because of the pressure difference be]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Carbon_dioxide_transport_in_blood</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CFjeAfMvQeeMLM0MTPDaAt4aT3SMsvUA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Carbon dioxide transport in blood]]></video:title><video:description><![CDATA[Carbon dioxide is made as a waste product by cells, and blood helps to transport that carbon dioxide from the tissues to the lungs - where we can breathe it out. Now, to facilitate this - blood has   three important mechanisms to move carbon dioxide around.  

First, a small amount of carbon dioxide is dissolved in the plasma - which is the liquid portion of blood. Now, to calculate the concentration of dissolved carbon dioxide, you can multiply the partial pressure of carbon dioxide, measured in millimeters of mercury, with the solubility of carbon dioxide. 

The solubility of carbon dioxide is the amount of carbon dioxide that can be dissolved in blood, and it turns out that in a 100 mL of blood, 0.07 mL of carbon dioxide is dissolved per millimeter of mercury of carbon dioxide. 

In venous blood, the equation becomes dissolved carbon dioxide equals the venous partial pressure of carbon dioxide in millimeters of mercury times 0.07mL carbon dioxide, per millimeters of mercury, per 100 mL blood. 

And, if we plug in the partial pressure of carbon dioxide in the veins, which is about 45 millimeters of mercury, we get 3.15 mL of carbon dioxide in 100 mL of blood. 

This works out to be about 5% of the total carbon dioxide transported by the blood, but it can go up to 10%. Now another 10-20%         is transported a second way: carbon dioxide binds directly to the terminal amino acids of each of the four globin chains in a hemoglobin protein. Hemoglobin is the most abundant protein in the red blood cells, and each hemoglobin, can hold on to 4 molecules of carbon dioxide. When hemoglobin is bound to carbon dioxide it’s called carbaminohemoglobin.  

Now, as carbaminohemoglobin alters the shape of the hemoglobin molecule slight and it decreases hemoglobin’s affinity for oxygen, and this is called the Bohr Effect. It leads to slightly more oxygen becoming unbound and getting dropped off in tissues full of carbon dioxide. This causes a shift to the right in the o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Movement_of_water_between_body_compartments</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kHPXqja4StyAiuOMvoXopjIMQyi7hBQM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Movement of water between body compartments]]></video:title><video:description><![CDATA[Water is the key to life - It has very unique properties like being an amazing solvent, which means that it’s easy for solutes to dissolve into water. 

As a result, water can carry essential nutrients to our cells as well as toxins or waste products away from our cells to be excreted out of our system. 

Total body water can be subdivided into two major compartments, intracellular fluid (ICF) and extracellular fluid (ECF).

On average total body water in a person is about 60% of their body weight. 

From the total body water, 2/3 of that, or 40% of body weight is intracellular fluid. The other 1/3 or 20% of body weight is extracellular fluid. This is also known as the 60-40-20 rule. 

Intracellular fluid is the fluid which is inside the cell and extracellular fluid is the fluid outside of the cell.

Extracellular fluid can be further subdivided into interstitial fluid, which is the fluid surrounding the cell and plasma which is the fluid that circulates within blood vessels. 

Extracellular fluid is the first to be lost and makes up fluids like gut fluids, sweat and other secretions.

The extracellular fluid is made up of different solutes, the major cation being sodium (Na+) and the major anions being chloride (Cl-) and bicarbonate (HCO3-). 

Each compartment has a specific solute concentration measured in mOsm/L or osmolarity, which is the number of osmoles within a liter of solution.

Now remember that an osmole refers to the individual ions within a solution. So for example, NaCl splits apart in water to become Na+ and Cl-, so a solution of 1 mmol/L of NaCl is actually 2 mOsm/L. Normally, osmolarity in the intracellular fluid and extracellular fluid is equal. 

If either side ever has a few more solutes, than water will flow in that direction to lower the concentration slightly and maintain the balance. This process is called osmosis. 

Now, some solutes like NaHCO3 (sodium bicarbonate) as well as large sugars like mannitol, are too large to cross cel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ketone_body_metabolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F635ntGHSoqEQpXOXY4EZCxATFCDpc_t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ketone body metabolism]]></video:title><video:description><![CDATA[In life, it’s helpful to have a plan B in case plan A doesn’t work out. 

In terms of energy, the body’s plan A is to generate energy from carbohydrates, fats, and proteins - basically in that order. 

But if these main fuels aren’t readily available, then plan B is to use an alternative fuel source - ketone bodies. 

Ketone bodies are a group of carbon-containing molecules produced by liver mitochondria using a 2-carbon molecule called acetyl-CoA. 

The liver makes ketone bodies in physiologic states like prolonged fasting or exercise, as well as in pathological states like type 1 diabetes mellitus or alcoholism. 

Ketone bodies can be released into the circulation and get picked up by the majority of cells. 

Inside the cells, they’re reconverted back into acetyl-CoA, at which point they can then enter the mitochondria and produce ATP. 

The 3 primary ketone bodies are acetoacetate, beta-hydroxybutyrate, and acetone. 

Alright, so let’s say you decide to go on a 5-day fast. 

About 12 hours into your fast, your blood glucose levels start to dip. 

In response, glucagon is secreted from the pancreas and stimulates hepatic glycogenolysis - meaning that the liver begins to break down glycogen into glucose and release that glucose into the blood. 

About 24 hours into your fast, your liver begins running out of glycogen, so it starts the process of gluconeogenesis which is where it makes new glucose molecules from substrates like amino acids.

Then, around 1 to 3 days into your fast, your body begins to run out of the necessary substrates to make new glucose. 

So, it switches to breaking down fatty acids for energy.

Fatty acids are mobilized from fat stores and are broken down to acetyl CoA through beta oxidation in the mitochondria of most cells - except for brain cells. 

See, thing is, fatty acids can’t cross the blood-brain barrier, so brain cells can only use glucose for energy - or, when there’s no glucose they use ketone bodies. 

This makes sense f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epigenetics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eqESy5OaQVm0bxy6Psd_yaddSp6tPPMt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epigenetics]]></video:title><video:description><![CDATA[Epigenetics is a process of gene regulation - turning genes on and off. 

Think about it - you have about 37 trillion cells, and over 200 different types of cells in your body. 

For example, there are muscle cells, for looking great at the beach as well as neurons that tell your muscles to flex when it’s time to show off. 

And both muscle cells and neurons have the same origin and genetic material - meaning, 46 chromosomes, with each chromosome made up of a single DNA molecule. 

Along that chromosome are sequences of DNA that code for genes, with thousands of genes on each one. 

It makes sense that there would have to be a process to control all of those genes.

Now, it turns out, that DNA is a very long molecule - over 2 meters when fully stretched. 

So to save space, DNA is wrapped around special proteins called histones. 

Now - histones actually come in groups of 8 - 4 stacks of 2, like poker chips - and the DNA molecule wraps around each group of 8 histones twice, forming a nucleosome. 

Different sections of DNA - meaning, different genes - wrap around different stacks of histones. 

Finally, the nucleosomes are packed together even more tightly - resulting in chromatin which looks like threads of cotton-candy within the nucleus.

Now - a cell type boils down to what a cell does - and, in turn, what a cell type does boils down to the kind of proteins it makes to carry out its role. 

Proteins are made based on genes - so our collection of genes, or genotype is actually like an incredible wardrobe - it contains something for every occasion. 

And different cell types wear different attires. 

For example, our muscle cells are usually doing the hard work of contracting and relaxing all day, so they would require the equivalent of athletic gear to do their job. 

Posh neurons, on the other hand, might prefer a tuxedo to tend to their synapses in. 

So, the muscle cell needs only certain parts of that wardrobe and the neuron needs a very different p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_shunts</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6ND68bxUQaWLelf2TiTZwtw8Q8yb-2hP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary shunts]]></video:title><video:description><![CDATA[Pulmonary circulation starts with oxygen (O2) poor and carbon dioxide (CO2) rich blood in the right atrium that flows into the right ventricle.

From there - blood is pumped into the large pulmonary trunk, which splits to form the two pulmonary arteries – one for each lung. 

The pulmonary arteries divide into smaller arteries known as pulmonary arterioles and then eventually into pulmonary capillaries which surround the alveoli - which are the millions of tiny air sacs where gas exchange happens. 

At that point, O2 enters the blood and CO2 enters the alveoli. 

The pulmonary capillaries drain into small veins known as pulmonary venules that flow into two pulmonary veins exiting each lung, and these pulmonary veins complete the circuit by delivering O2-rich and CO2-poor blood into the left atrium, which flows into the left ventricle and then into the aorta where it enters systemic circulation.

Normally, about 2% of the blood follows a slightly different path. It’s diverted, or shunted, so that it bypasses the pulmonary capillaries, and this is called a physiologic shunt. 

There are two main ways this happens. First, when blood goes out to the heart muscle itself - it returns through tiny veins called thebesian veins. 

Rather than draining into the venous system and going into the right atrium, these veins sometimes dump that blood into the closest chamber of the heart. 

So, for example, if blood that goes out the aorta and through the coronary arteries to the muscle in the left ventricle of the heart, then the deoxygenated blood might then drain directly into the left ventricle chamber of the heart. At that point it would mix with the rest of the oxygenated blood and get squeezed right back out through the aorta. 

So - this blood basically bypasses the pulmonary circulation. 

Second, the conducting airways of the lungs, like the bronchi, receive systemic arterial blood from the bronchial arteries. 

But the deoxygenated blood can flow, or anastomose]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Angina_pectoris</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_2b-3YYsQeeXeECyHP-HknHNQ8qbNZfC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Angina pectoris]]></video:title><video:description><![CDATA[Angina comes from the latin angere, which means to strangle, and pectoris comes from pectus, meaning chest—so angina pectoris loosely translates to “strangling of the chest”, which actually makes a lot of sense, because angina pectoris is caused by reduced blood flow which causes ischemia to the heart muscle, or lack of oxygen to the heart, almost like the heart’s being strangled which causes terrible chest pain.

Stable angina or chronic angina is the most common type of angina and it usually happens when the patient has greater than or equal to 70% stenosis, meaning 70% of the artery is blocked by plaque buildup. 

This small opening that blood flows through might be enough to supply the heart during rest, but if the body demands more blood and oxygen, like during exercise or stressful situations, the heart has to work harder, and therefore needs more blood and oxygen itself. 

It’s during these time of exertion or emotional stress that people with stable angina have chest pain, since the blood flow isn’t meeting the metabolic demands of the heart muscle, or myocardium. 

But the pain usually goes away with rest. 

In the majority of cases, the underlying cause of stable angina is atherosclerosis of one or more the coronary arteries—arteries supplying blood to the heart muscles. 

Other heart conditions that might lead to stable angina are ones that cause a thickened heart muscle wall, which would require more oxygen. 

This increase in muscle size can be due to hypertrophic cardiomyopathy from a genetic cause, or as a result from the heart having to pump against higher pressures, as is the case in aortic stenosis, which is a narrowing of the aortic valve, or hypertension. 

These larger, thicker heart muscles require more oxygen, and if the patients can’t meet increasing demands, they feel pain in the form of angina.

Whatever the case, the heart needs blood, and if we look at the heart wall, there’s three layers—the outermost layer, the epicardium, the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atrioventricular_block</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w7-GRwM-TEiheMRsfcULVREET_iN_0eo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atrioventricular block]]></video:title><video:description><![CDATA[Each heartbeat starts with the heart’s pacemaker cells in the sinoatrial node, sometimes just called the SA node, in the right atrium. The SA node sends an electrical signal that propagates out through the walls of the heart and contracts both upper chambers, then moves through the atrioventricular node, or AV node, where the signal stops for a split second. Next, the signal goes down into the lower chambers, where it moves down the bundle of His, into the left and right bundle branches, and into each ventricles’ Purkinje fibers, causing them to contract as well. So, in a healthy heart, the upper chambers contract first, and then shortly after, the lower chambers contract. 

On an ECG, the atrial contraction is seen as a “P wave,” and the ventricular contraction is seen as the “QRS complex.” The interval from the start of the P wave to the start of the QRS complex is called the “PR interval,” and is normally between 120 and 200 milliseconds, or 3-5 tiny boxes on the graph paper that it’s usually printed out on, since each box is 40 milliseconds or 0.04 seconds. Heart block describes a type of arrhythmia, or abnormal rhythm, that happens when the electrical signal gets delayed or blocked entirely at some point along the conduction system.

These blocks and delays usually happen because of some sort of damage or fibrosis to the electrical conduction system, the pathways that conduct the electrical signal. Lev’s disease, or Lenegre-lev syndrome, describes the large proportion of cases that are idiopathic and described as progressive cardiac conduction defects. This means it’s not clear exactly what causes it, but over time fibrosis, or scarring, develops in the conduction system which can delay or stop electrical conduction. This is usually a result of the aging process in the heart, and happens most often in the elderly, although some hereditary forms have been identified and can happen in younger people. However, another large proportion of cases are a resu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperplasia_and_hypertrophy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dkPza0nuRDmC-78IrtcO_DuZQnyFW8k1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperplasia and hypertrophy]]></video:title><video:description><![CDATA[Imagine a lumberjack.  At first she can handle cutting down a few trees a day, but suddenly her boss wants her to chop down an entire forest by the end of the week! Now she’s stressed out from the increased demand! 

Our body is the same; when the demand placed on an organ or tissue is more than it can handle, its called “stress,” and the body can adapt through either hyperplasia or hypertrophy.  

Hyperplasia refers to the process where cells in an organ or tissue increase in number, so its like hiring a bigger pack of lumberjacks. 

Hypertrophy is when these cells in an organ or tissue increase in size, like if the lumberjack gets really tough so that she can cut down twice as many trees. 

So hyperplasia, bigger pack, and hypertrophy, tough lumberjack!

So, a tissue or organ might get stressed by physiological processes or from disease processes. 

An example of physiologic hypertrophy is lifting a 10 pound sack of potatoes which puts a bigger functional demand on your skeletal muscles. 

In response, the muscle cells produce more proteins or myofilaments and get larger in size, allowing the biceps as a whole to generate more force. As a result your muscles also become bigger and tougher. 

An example of pathologic hypertrophy is when the heart undergoes hypertrophy to deal with high blood pressure or hypertension. 

In hypertension, the heart has to pump blood against a high resistance and cardiac myocytes once again adapt by increasing the synthesis of myofilaments causing individual cells to get bigger. 

In both cases there’s hypertrophy, but the triggers are quite different.

Now, in hyperplasia there’s an increase in the number of cells - a larger pack. 

And that can only happen in organs with stem cells that can undergo cellular differentiation to become a mature cell in that organ, like cells in the intestines for example. 

So hyperplasia doesn’t occur in relatively permanent tissues without stem cells- like cardiac, nerve, and adult skeletal ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/B-cell_activation,_differentiation,_and_contraction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m3ZEsec_SnOhC71W1ZZ7gkffQ7yzKR8P/_.jpg</video:thumbnail_loc><video:title><![CDATA[B-cell activation, differentiation, and contraction]]></video:title><video:description><![CDATA[The adaptive immune response is highly specific for each invader. The cells of the adaptive immune response have receptors that differentiate one pathogen from another by their unique parts - called antigens.  The key cells of the adaptive immune response are the lymphocytes - the B and T cells. B cells develop in the bone marrow where they undergo a process called VDJ rearrangement to generate a massively diverse set of B cell receptors. 

The B cell receptor is essentially an antibody except that it has a transmembrane part that goes through the membrane attaching the receptor to the surface of the B cell. The B cell receptor has two heavy chains and two light chains, and the region or fragment of the B cell receptor that binds the antigen is called the fragment-antigen binding or Fab region.  

The Fab region is where the ends of the heavy and light chains meet, and there are two Fab fragments on each B cell receptor. The remainder of the heavy chain makes up the fragment-crystalline region, also called Fc, which crystallizes in solution and is also constant or identical in every antibody of a particular type.  

The two heavy chains are linked to one another by disulfide bonds, and each heavy chain is also linked to a light chain by a disulfide bond. Each B cell receptor has two identical heavy and light chains, resulting in two identical antigen binding sites. As the B cell develops into a plasma cell, the B cell receptor gets secreted as an antibody with the exact same antigen specificity. However, the heavy chain actually changes as the B cell develops.  

There are 5 major types of heavy chains which encode the isotypes or classes of immunoglobulins: IgM, IgD, IgG, IgA, and IgE. These five are encoded by heavy chain genes which are referred to by the Greek letters mu, delta, gamma, alpha, and epsilon.  

When a B cell is first developing it initially expresses the mu heavy chain, and as a result all of the B cell receptors are IgMs that are on the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_groups_and_transfusions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MXZToVwMROqO3FhlofM5wdWNTCSjkz1o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood groups and transfusions]]></video:title><video:description><![CDATA[A blood transfusion is the procedure where a person receives blood, or elements of blood usually through an intravenous infusion - meaning through a vein. 

Now - if you take blood and spin it in a centrifuge, the heaviest blood components move to the bottom, and the lightest ones move to the top. 

Overall, three distinct layers form: the erythrocytes or red blood cells at the bottom, the buffy coat--which contains platelets and immune cells in the middle, and plasma at the top. 

Now, in rare situations, like in traumatic injuries, someone might receive a whole blood transfusion, but more commonly a person is given one of the components of the blood. 

For example, a person with anemia could just receive packed red blood cells, a person with clotting factor deficiency could get fresh frozen plasma which contains the coagulation factors, or someone with platelet deficiency might receive platelets.

Now, most blood transfusions are homologous transfusions, where the blood comes from an anonymous donor. 

Sometimes the transfused blood is autologous, meaning the blood was taken out of the person at a prior time, like when they plan to have surgery in the near future.  

In both cases, once the blood is taken, it’s mixed with sodium citrate which prevents the blood from coagulating, and then refrigerated or frozen for storage, or separated into its components by centrifuge.

Now, before whole blood or packed red blood cells can be transfused, it’s important to know the blood typing of both the donor and the recipient of the blood. 

Every person has a unique blood group based on two classification systems: the ABO system and the Rh system. 

Both systems are based on the presence or absence of glycoproteins, which are proteins attached to a sugar molecule, found on the surface of red blood cells. 

Now, if blood that has any of these glycoproteins is given to a person that has immune cells that have never seen those glycoproteins before, then the glycoprotei]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case-control_study</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0elJjjV5Slu2sjuzUVR6_yxzQzWPjK72/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case-control study]]></video:title><video:description><![CDATA[Case-control studies are a type of study design that compares the history of two groups of people - those that have a certain outcome, called cases, and those that don’t have a certain outcome, called controls; to see if they’ve been exposed to different things. 

For example, a case-control study might find that the odds of using tanning beds is higher for people with skin cancer, the cases, compared to people without skin cancer, the controls.   

Because case-control studies look at the past exposures of people with and without the outcome, this type of study is called retrospective, retro meaning past. 

The opposite would be to start with people who either have the exposure or don’t have the exposure, and then follow them over time to see if they develop an outcome in the future. 

That would be a prospective study. 

But, following people over time can take a lot of time and cost money. 

By comparison, case-control studies are often quicker and cheaper, since they use data that’s already collected or is relatively easy to collect, like medical records, employment records, or individual interviews and surveys. 

For example, researchers might interview a group individuals with skin cancer and a group of individuals without skin cancer to see how many times they used tanning beds in the past five years, then compare the results. 

This is particularly true when it comes to rare diseases, but the definition of “rare” varies around the world. 

For example, in the United States, 1 in 1,500 people is considered rare, but in Japan, 1 in 2,500 people is considered rare. 

Either way, it’s easier to recruit individuals with rare diseases into a study, rather than start with a group of healthy individuals and wait to see who develops a rare disease in the future. 

For example, in the United States, you’d have to follow a group of 30,000 healthy individuals over time, to identify 20 people who develop a rare disease. 

Case-control studies are also useful in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholesterol_metabolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8n8w1xA4QXGRq44ij893uKCBRKO13TD3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholesterol metabolism]]></video:title><video:description><![CDATA[Cholesterol is a lipid molecule that helps maintain the structure of cell membranes, and is a precursor to steroid hormones, bile acids, and vitamin D.

As it turns out, we make most of our cholesterol ourselves, but some comes through the diet. 

Cholesterol synthesis, also called the mevalonate pathway, happens in the smooth endoplasmic reticulum of a cell. 

It begins with 2 acetyl-CoA molecules getting joined together by the enzyme acetyl-CoA acyl-transferase. 

The result is a 4-carbon molecule called acetoacetyl-CoA and then a free CoA molecule. 

Next, the enzyme HMG-CoA synthase combines acetoacetyl-CoA and acetyl-CoA to form a 6-carbon molecule called 3-hydroxy-3-methylglutaryl CoA, or HMG-CoA - so 3 acetyls and the an free CoA molecule.

Then, an enzyme called HMG-CoA reductase reduces HMG-CoA into mevalonate, by removing a CoA-SH and a water molecule. 

This step with HMG-CoA reductase is the rate-limiting step of cholesterol synthesis. 

In other words, the rate of this reaction determines the overall rate of cholesterol synthesis - it’s like the slowest step in the assembly line for a factory.

Now, cholesterol synthesis is regulated by a trio of proteins - sterol regulatory element binding protein - or SREBP and two others that just go by SCAP and INSIG-1. 

Let’s say that cholesterol levels drop because there’s less cholesterol coming into the cell from the diet. 

In that situation, INSIG-1 falls off of SREBP, like pulling a pin from a grenade, and the SREBP-SCAP complex then gets cleaved by cellular enzymes. 

The cleaved SREBP floats into the nucleus, and binds to the sterol regulatory element on the DNA. 

When it binds, it increases expression of the genes encoding HMG-CoA reductase. 

That leads to more HMG-CoA reductase, which speeds up endogenous cholesterol synthesis. 

Once HMG-CoA reductase has made the 6 carbon mevalonate, it then undergoes a number of additional enzyme-mediated transformations before it becomes cholesterol. 

Fi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9uyqcOeDQQW4t47EkVVuhL9BT16FZjHh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia: Clinical]]></video:title><video:description><![CDATA[Anemia is a blood disorder where the body doesn’t have enough healthy red blood cells or hemoglobin, resulting in poorly oxygenated tissues throughout the body. This condition takes many forms, ranging from mild to severe depending on the cause. 

Anemia in males is a hemoglobin below 13.5 g/dL or a hematocrit less than 41%, and in females it’s a hemoglobin below 12.0 g/dL or a hematocrit less than 36%, but those numbers can differ based on which guidelines you’re using. Also, people with chronic respiratory diseases like emphysema or medical problems like malnutrition may have symptoms of anemia even at normal levels of hemoglobin and hematocrit. In addition, those living at altitude can have high levels of hemoglobin and hematocrit to help deal with the lower oxygen levels. So it’s good to keep in mind that these guidelines aren’t appropriate for everyone. Now, the most common signs and symptoms of anemia are dyspnea with exertion and at rest, fatigue, pallor, and a hyperdynamic state like bounding pulses and palpitations.

If someone is anemic, the first thing to look at is the mean corpuscular volume or MCV. An MCV of less than 80 femtoliters is low, so microcytic, between 80 and 100 femtoliters is normal, so normocytic, and above 100 femtoliters is high, so macrocytic. Of course, some individuals might have a few types or causes of anemia mixed together, and that’s where things get more complicated. Most microcytic and macrocytic anemias are caused by a problem in producing either red blood cells or hemoglobin, and in those situations we can measure the reticulocyte production index (RPI) or corrected reticulocyte count (CRC). This number is the percentage of red blood cells that are reticulocytes, or immature, and is normally between 0.5 and 2.5%. A person with anemia and less than 2% RPI means that their body is not capable of producing enough red blood cells. In certain normocytic anemias that are caused by the loss or destruction of red ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qIuGWuTOTseW5Hdc0LsxbgrLSPu2CFYN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammation]]></video:title><video:description><![CDATA[Inflammation classically describes four key signs - each of which have a latin derivation. Calor or heat, dolor or pain, rubor or redness, and tumor or swelling. Sometimes these four signs combine to cause a fifth sign, which is functio laesa or temporary loss of function due to pain or swelling. Okay - so inflammation usually starts with some stimuli, like a pathogen. Now, even though pathogens are a common cause of infection which can lead to inflammation, inflammation can be caused by other things as well like toxins and trauma. For example, after an intense workout, your muscles may feel sore - that’s due to inflammation trying to repair your overused muscle fibers. Ultimately, the goal of inflammation is to respond to the stimuli and restore balance. Oftentimes that includes eliminating the cause of tissue injury, clearing out necrotic or dead cells, and starting tissue repair. Broadly speaking, inflammation can be triggered by external and internal factors.  

External factors can be non-microbial or microbial. Non-microbial factors include allergens, irritants, and toxic compounds. Now, the two main microbial factors that trigger inflammation are virulence factors and pathogen associated molecular patterns or PAMPs. Virulence factors are molecules that help pathogens colonize tissues and cause infection. PAMPs are small molecules with conserved patterns that are shared across many different pathogens, including bacterial wall components like peptidoglycan, lipopolysaccharide or LPS, and lipoteichoic acid, and fungal wall components like mannan. For intracellular pathogens, like viruses, PAMPs might include the viral RNA or DNA. Our immune system recognizes virulence factors and PAMPs as foreign substances, and can trigger an inflammatory response against them.  

Now, in terms of internal factors, it turns out that there’s an endogenous equivalent to PAMPs, called damage associated molecular patterns or DAMPs. DAMPs are intracellular proteins that g]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prions_(Spongiform_encephalopathy)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eOs1C8NYToKaflF-yu6zaPCxTO_EAqSB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prions (Spongiform encephalopathy)]]></video:title><video:description><![CDATA[Spongiform encephalopathy can be broken down. Spongiform means sponge like, encephalo- refers to the brain, and -path refers to a disease process. 

So spongiform encephalopathy is a disease where the brain tissue degenerates and healthy tissue gets replaced by clusters of tiny liquid filled, thin-walled cavities called cysts, making the brain look like a sponge. 

The underlying cause of spongiform encephalopathy is the accumulation of misfolded proteins called prions.

First, let’s review a bit. Proteins are made up of a long string of amino acids, and the exact sequence of these amino acids is called the primary structure. 

These long chains of amino acids can fold to form different shapes, like an α-helix which is a right-handed coiled strand and a ß pleated-sheet which is when the chain folds so that segments line up alongside one another. 

Each protein can contain multiple α-helices or ß pleated-sheets. 

Now, there’s a protein called Prion protein, or Prp, which is encoded by the PrNP gene. 

This protein is 253 amino acid long and is made up of mostly α-helices.  

It’s most commonly found on the cell membrane of neurons. 

Although the function of Prp is unknown, it’s thought that it might play a role in synapses between neurons and the uptake of copper into the cell. 

When a prion protein is misfolded, it changes from mostly having α-helices to having a lot of ß pleated-sheets. 

This new abnormal protein is called a “prion”. 

When the misfolded protein enters the cells of the nervous system and interact with the normal prion protein, it acts as a template and induces misfolding in the normal prion proteins. 

These prions are also highly resistant to being broken down by proteases, which are the enzymes that break down abnormal proteins. 

As a result, these misfolded prion proteins cannot be easily broken down, they cause normally folded proteins to misfold and become like them, and they have an affinity for the brain - they’re basically li]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chewing_and_swallowing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kOY-WSZ-TdK0lC44g6gflbhrQ0CT3OVr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chewing and swallowing]]></video:title><video:description><![CDATA[Some people eat to live, others live to eat. For both groups - the first step of digestion is chewing, or mastication. 

This is where food gets moistened by saliva, and is broken down into smaller bits that are easy to swallow and pass through the esophagus. 

It’s also the step that helps smear the food out over the tongue so that it can be fully tasted.

The journey of food starts in the oral cavity, which is the first part of the digestive tract.

The oral cavity is like an empty room, there’s the roof, which is formed by the hard and soft palate, the floor, which is formed by the tongue and the mylohyoid muscles, the lateral walls formed by the inside of the cheeks, and there’s the front which gets sealed off by the lips and teeth. 

A layer of epithelial cells line the inside of the mouth and form the first line of defense against pathogens. 

The surface of the epithelial cells is kept moist by mucus secreted by salivary glands.

The major salivary glands are actually located outside the oral cavity. 

These are the parotid glands, found in front of each ear, the submandibular or submaxillary glands, found under the mandible and the sublingual glands that sit beneath the tongue, under the floor of the mouth. 

Now, even though the salivary glands are not located inside the mouth, they have ducts that travel to the oral cavity so they can secrete saliva into it. 

The secretion of saliva is mainly controlled by the parasympathetic nervous system through cranial nerves. 

The parotid glands are innervated by the glossopharyngeal nerve, or cranial nerve nine, while the submandibular and sublingual glands are innervated by the facial nerve, or cranial nerve seven. 

Saliva is mostly made of water, but it has other important components like salivary amylase, which is a digestive enzyme that breaks down starch, and mineral salts like sodium bicarbonate that help maintain a pH of 6.5 to 7.5 inside the mouth. 

It also contains mucus which protects the oral]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Optic_pathways_and_visual_fields</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FZiYmRgHTsG8mF7NzHg1kAbTTLW7PTD4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Optic pathways and visual fields]]></video:title><video:description><![CDATA[When light enters the eye, it hits a light sensitive neural layer of tissue near the back of the eye called the retina. 

That’s where phototransduction occurs, which is the process by which light waves are converted into electrical signals. 

Afterwards, these electrical signals are sent to the brain for visual processing. 

So, let’s start by taking a look at the optic pathway and understanding visual fields. 

You can think of a visual field as everything that can be seen with a single eye, so we have a left visual field for the left eye, and a right visual field for the right eye. 

These visual fields overlap and produce a binocular visual field, but for now, let’s just look at the left visual field. 

The left visual field can be divided into two halves. 

The half that’s closer to your nose is the nasal visual field, and the half that’s closer to your ear is the temporal visual field. 

Similarly, the retina in each eye has a nasal and temporal region as well. 

When light enters the eye, the temporal field of vision is projected to the opposite side, onto the medial nasal retina, and the nasal field of vision gets projected to the opposite side, onto the lateral temporal retina. 

The visual fields are further divided into the superior and inferior visual fields, so the visual fields are actually divided into quadrants. 

The superior visual field projects to the inferior retina, and the inferior visual field projects to the superior retina. 

So, the visual information that appears in the right upper quadrant is actually project to the left lower retina. 

When light hits the retina it triggers visual receptor cells in the retina, called rods and cones, to send an electrical signal.

The rods and cones synapse with bipolar cells which in turn synapse with ganglion cells. 

These ganglion cells have long axons that travel through the retina layer to the back of the eye where they come together to form a single optic nerve, or cranial nerve II, that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Somatic_hypermutation_and_affinity_maturation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yQI1FOA_T8ykglo84sFpQnlHRo_j9_O_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Somatic hypermutation and affinity maturation]]></video:title><video:description><![CDATA[The immune response is highly specific for each invader, and that’s because the cells of the adaptive immune response have receptors that differentiate one pathogen from another by their unique parts - called antigens. The key cells of the adaptive immune response are the lymphocytes - the B and T cells which have unique antigen receptors known as the B cell receptor or BCR and T cell receptor or TCR respectively. Both B cells and T cells undergo a process called VDJ rearrangement to generate a massively diverse set of receptors. B cells can further enhance the diversity of their BCR repertoire using a process called somatic hypermutation, and the result is that the cells that emerge will have a stronger and more specific response to the antigen - and this is called affinity maturation.  

Now remember, that the B cell receptor is essentially an antibody except that it’s attached to the surface of the B cell. And each B cell receptor or antibody has two general parts- the variable region which binds antigen and the constant region which determines the specific antibody class - IgM, IgG, IgA, IgD, or IgE. 

First, let’s start with the activation of B cells, which occurs when a foreign antigen binds and cross-links adjacent BCRs, thereby triggering a cascade of events that help B cells proliferate and differentiate. 

Once activated, the B cell internalizes the antigen and presents a piece of it on a major histocompatibility complex class II molecule, or MHC-class II for short. At some point, along comes a CD4+ helper T cell that binds to the presented antigen.  

When this interaction occurs, the T cell expresses a protein called CD40 ligand on its surface, which binds the CD40 receptor on the B cell. This triggers a series of events that eventually result in the activation of the enzyme called Activation Induced cytidine deaminase or AID for short. This enzyme is only found in B cells and allows them to make cuts in the DNA, causing the B cell to class-swi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hunger_and_satiety</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TqGSdwEgQk_p5YCGWI1cyGQ0TaWoERk1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hunger and satiety]]></video:title><video:description><![CDATA[The hypothalamus is a small part of your brain that lies just above the pituitary gland. It controls various body functions like hunger, thirst, body temperature and hormones released by the pituitary gland. The three parts of the hypothalamus that regulate food intake are called the ventromedial nuclei, the lateral hypothalamic area, and the arcuate nucleus. The ventromedial nuclei is the satiety center, and when stimulated, it causes the sensation of fullness. On the other hand, the lateral hypothalamic area is the feeding center and when stimulated, it causes the sensation of hunger. Finally there’s the arcuate nucleus which is like a switchboard that receives various signals from the gastrointestinal tract. This nucleus sends neuron fibers to regulate the feeding center and the satiety center. 

Alright, let’s say you forgot to buy lunch, and it’s the late afternoon. Two things happen to trigger your hunger. First, mechanoreceptors in your stomach detect that your stomach is empty, so they fire slowly through the vagus nerve to a cluster of neurons in the medulla called the solitary nucleus. The solitary nucleus then sends nerve fibers to the arcuate nucleus in the hypothalamus. The arcuate nucleus then activates the feeding center through orexigenic neurons, and inhibits the satiety center through anorexigenic neurons. Orexigenic refers to something that stimulates the appetite, and anorexigenic refers to something that inhibits the appetite. In addition to this, the decreased firing of the mechanoreceptors and low blood glucose levels triggers P/D1 also known as ghrelin cells, or Gr cells for short, in the lining of the stomach to secrete the hormone ghrelin into the blood. Ghrelin is the hunger hormone and it travels directly to the arcuate nucleus, further causing it to stimulate the feeding center and inhibiting the satiety center.

Now, let’s say you decide to eat a tasty enchilada. The enchilada stretches out your stomach and that increases the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Enteric_nervous_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dBALKn6hTlaqFSsf1s2Bzj5BSmqjTEeq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Enteric nervous system]]></video:title><video:description><![CDATA[The gastrointestinal tract has intrinsic and extrinsic innervation. 

The intrinsic component is the enteric nervous system and the extrinsic component is the sympathetic and parasympathetic innervation which come from the central nervous system. 

The enteric nervous system can function independently to control digestive activities, which is why it’s sometimes called the second brain. 

So the parasympathetic input basically enhances digestion, and sympathetic input inhibits digestion.

From the esophagus to the anus, the walls of the gastrointestinal tract are lined by the same four layers of tissue. 

The outermost layer is either the adventitia, a thick fibrous connective tissue, or the serosa, a slippery serous membrane. 

Next is the muscularis externa, a smooth muscle layer, which contracts automatically, without you even having to think about it. If we look closer at this muscle layer, it’s actually composed of an inner circular muscle layer, arranged in circular rings which contract and constrict the tract behind the food, which keeps it from moving backward, while the outer longitudinal muscle layer, arranged along the length of the tract, relaxes and lengthens and therefore pulls things forward. Together, they perform what’s called peristalsis, which is a series of coordinated wave-like muscle contractions that helps squeeze the food bolus in one direction.

In specific places along the tract, like the esophageal sphincter, the circular layer thickens, forming sphincters that keep food from passing from one part of the gastrointestinal tract to the next. 

Next is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. 

Finally, there’s the inner lining of the intestine called the mucosa which secretes mucus and digestive enzymes because this is the layer that comes into direct contact with food.

The enteric nervous system is found within the walls of the entire gastrointestinal tract and i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cartilage_structure_and_growth</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pfImK_dUS3GLSYT-MIlQ97sAQQ2xlXPd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cartilage structure and growth]]></video:title><video:description><![CDATA[Cartilage is a strong, flexible type of connective tissue that makes up part of your nose, your ear, and provides cushioning between your joints.

Its job is to support and connect various parts of your body, like the costal cartilage that connects your ribs to your sternum or breastbone. 

Usually, there’s a layer of connective tissue that wraps around cartilage called the perichondrium. 

The perichondrium has an outer layer that contains fibrous connective tissue and blood vessels, and it has an inner layer that contains chondroblasts.

Chondroblasts secrete the proteins that make up the extracellular matrix of the cartilage - which has a gel-like consistency. 

Eventually, these chondroblasts get trapped inside the very matrix that they create, in small holes called lacunae. When that happens chondroblasts turn into chondrocytes.

Chondrocytes don’t make much extracellular matrix, instead they maintain and repair the extracellular matrix. 

The extracellular matrix is composed of protein fibers like collagen which gives it strength and elastin which gives it flexibility.

And these protein fibers are embedded in a viscous gel, made of water and proteoglycan aggregates which are large molecules that look a bit like a centipede. 

A long chain of hyaluronic acid molecules called a hyaluronan makes up the body of this proteoglycan aggregate, and hundreds of proteoglycans make up the legs.

These proteoglycan legs are basically proteins attached to long chains of sugars called glycosaminoglycan or GAGs. 

Now, cartilage has two patterns of growth, appositional growth and interstitial growth. 

Appositional growth occurs when chondroblasts secrete new matrix along existing surfaces and this causes the cartilage to expand and widen. 

In interstitial growth, chondrocytes secrete new matrix within the cartilage and this causes it to grow in length. 

Both types of growth can be seen in the growing bones of children and teenagers before they reach adulthood. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Necrosis_and_apoptosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NR93wmkQTDmYrmUa8HKitgQJQiShEqXF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Necrosis and apoptosis]]></video:title><video:description><![CDATA[Generally speaking, cells have two ways to die. One way is by apoptosis, which is a form of programmed cell death. The second way is by necrosis, which is when cells die due to injury or disease. Overall, apoptosis occurs much more often than necrosis. One example is when old skin cells undergo apoptosis and get replaced by new skin cells. Another example is in our hands and feet during fetal development. Initially, human hands and feet look like duck’s feet, with webs of skin connecting the fingers. But the cells in the webbing undergo apoptosis, and that allows us to form individual digits that allow us to pick our nose and play the piano. In contrast, necrosis occurs less frequently. An example of necrosis is when a blood vessel that feeds an area of the body, say the big toe, becomes blocked and can’t deliver oxygen and nutrients to the cells like usual, it causes ischemia, and the cells die. As a result, the tissues of the toe will turn a nasty shade of black, signaling necrosis.  

In apoptosis, there are two activating mechanisms - the intrinsic pathway, also called the mitochondrial pathway, and the extrinsic pathway, also called the death receptor pathway.  

The intrinsic pathway occurs when a cell is exposed to stress like radiation, hypoxia, or low oxygen, a high intracellular concentration of calcium ions, or oxidative stress, which is where reactive molecules with unpaired electrons called free radicals steal electrons from nearby molecules.  

These stressors cause two intracellular proteins, Bax and Bak, to move from the cytosol to the mitochondria. Once in the mitochondria, Bax and Bak pierce the outer mitochondrial membrane making it porous and leaky. This allows two additional proteins, called SMACS and cytochrome C, to spill into the cytosol. SMACS binds to proteins that normally inhibit apoptosis and deactivates them. Meanwhile, cytochrome C binds to both ATP - the main form of intracellular energy - as well as an enzyme called Ap]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_tumors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j0utR6YsST_qv0rtGjW_MaUMSsCf5LvR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac tumors]]></video:title><video:description><![CDATA[Cardiac tumors are abnormal growths of cells that form a mass in the heart. If the cell growth has the potential to invade and spread to other tissues — a process called metastasis — it’s a malignant tumor, more commonly known as a cancer. If it is not able to invade other tissues, it’s referred to as a benign tumor.

Now, the vast majority of tumors of the heart are actually secondary, meaning that a tumor developed somewhere  else in the body, metastasized, and spread to the heart. 

Even though these secondary tumors can come from anywhere, they’re most commonly metastases from lung cancer, lymphoma or lymphatic system cancer, breast cancer, leukemia or blood cell cancer, melanoma or skin cancer, hepatocellular carcinoma or liver cancer, and colon cancer, in this order. Cancer most commonly metastasizes through the lymphatic system to the pericardium, the membrane around the heart. When the pericardium is involved, it often leads to pericarditis, or inflammation of the pericardium, and pericardial effusion, an accumulation of fluid in the pericardial cavity. Metastases to the myocardium are less common, but arise more commonly when cancer spreads via the blood. 

Primary cardiac tumors, on the other hand, are actually extremely rare. The most common type of primary tumors in adults — when they do happen — are myxomas. Myxomas are benign tumors that arise from the mesenchymal connective tissue inside the heart, as opposed to the actual myocytes, or heart cells, because the heart of an adult is fully developed and its cells, or myocytes, are permanent and don’t proliferate. 

These masses are gelatinous in consistency, as a result of an abundance of ground substance on histology, and pedunculated, meaning attached to a peduncle, or a stalk of tissue.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Extracellular_matrix</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PIzEmqMLTPeNNSClWDBmrDf-Snq4kVzG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Extracellular matrix]]></video:title><video:description><![CDATA[Cells live within an environment called the extracellular matrix, and it’s a bit like how homes have yards and streets that surround them. 

Also, just like how lots of homes form a community, lots of cells form a tissue.

And there are different types of tissues - epithelial, connective, muscular, and nervous tissue. 

Each tissue has an extracellular matrix that’s got a unique composition that’s adapted for each tissue’s unique needs. 

Having said that, all of the different types of extracellular matrix are made up of three major molecules - adhesive proteins, structural proteins, and proteoglycans.

First, there’s adhesive proteins, which help to stick the individual cells together and organizes the tissue into a neat structure.

Now, adhesive proteins - like integrins and cadherins - are found on the cell’s surface and they’re like molecular velcro. 

Cells use adhesive proteins to anchor themselves to other cells and to molecules in the extracellular matrix. 

Adhesive proteins also help communicate messages from the extracellular matrix to the cell. 

For example, signals relayed by integrins can help a cell decide when it’s time to grow, divide, differentiate, or even die - like in apoptosis.

Next, there are structural proteins which give our tissues their tensile and compressive strength. 

Some examples are collagens, elastins, and keratins. 

Collagen is the most common type of structural protein in the human body, mostly because it resists tension and it can also stretch. 

When collagen is made and released into the extracellular space, it’s in the form of a precursor called procollagen. 

Procollagen is a protein made up of three polypeptide strands, each coiled into a left-handed helix, and then all three are twisted together into a right-handed triple helix or &amp;quot;superhelix&amp;quot; with three loose strands at each end.

Once procollagen is in the extracellular space, it encounters a tiny band of enzymes called collagen peptidase]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clot_retraction_and_fibrinolysis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yXg9tEGtQzSkambGH7ohglOmTwmiDuuN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clot retraction and fibrinolysis]]></video:title><video:description><![CDATA[In hemostasis, hemo referring to blood, and stasis meaning to stop—so hemostasis is the process where blood flow is stopped after there’s damage to a blood vessel.

Primary hemostasis involves the formation of a platelet plug at the site of an injured blood vessel, and secondary hemostasis involves the coagulation cascade which is where a protein net called a fibrin mesh forms over the platelet plug to reinforce it - forming a blood clot.

Now, anticoagulation occurs during primary and secondary hemostasis and helps regulate clot formation, whereas clot retraction and fibrinolysis occur after primary and secondary hemostasis are complete, and help a clot contract and degrade.

Anticoagulation prevents clots from growing too large and blocking blood flow to tissues supplied by the vessel. It also prevents clots from getting so big that small parts of the growing clot break off in the form of emboli. Depending on the location of the primary blood clot, these emboli may then cause a disruption in blood flow to organs like the heart or brain.

Now, the most important point of clot regulation is when a coagulation factor called thrombin is produced. Thrombin, or factor II, is a very important clotting factor, because it has multiple pro-coagulative functions. Think of thrombin as the accelerator on a car--the pedal that takes secondary hemostasis from 20 miles per hour to 100 miles per hour!

First, thrombin binds to receptors on platelets causing them to activate. Activated platelets change their shape to form tentacle-like arms that allow them to stick to other platelets. Second, thrombin activates two cofactors; factor V used in the common pathway, and factor VIII used in the intrinsic pathway.

Third, thrombin proteolytically cleaves fibrinogen or factor I, into fibrin or factor Ia which binds with other fibrin proteins to form a fibrin mesh. And finally, thrombin proteolytically cleaves stabilizing factor or factor XIII into factor XIIIa.

Factor XIIIa com]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Synthesis_of_adrenocortical_hormones</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jUAsbJNhTY_DP9g4Sv9r0K3lRHWYpZY9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Synthesis of adrenocortical hormones]]></video:title><video:description><![CDATA[The adrenal glands are two glands that sit like a hat, one on top of each kidney. Each one has an inner layer called the medulla and an outer layer called the cortex. 

The adrenal cortex is subdivided into three more layers, the zona glomerulosa, zona fasciculata, and the zona reticularis, which secrete steroid hormones under the control of adrenocorticotropic hormone, or ACTH.

Adrenocorticotropic hormone is released by the anterior pituitary gland and binds to receptors on adrenal cortex cells in all three layers, and makes them take up cholesterol from the blood. 

ACTH also stimulates an enzyme called cholesterol desmolase inside these cells, which converts cholesterol to pregnenolone, which is the precursor to all of the adrenal cortex hormones.

The outermost layer is the zona glomerulosa, and it’s full of cells that make the hormone aldosterone. 

The first step in aldosterone production is when an enzyme called 3 beta- hydroxysteroid dehydrogenase, (or 3 beta- HSD) turns pregnenolone into progesterone. 

Next, progesterone is turned into 11 deoxycorticosterone (or 11- DOC) by the enzyme 21 hydroxylase. 11 deoxycorticosterone then gets turned into corticosterone by the enzyme 11 beta-hydroxylase. 

And finally, corticosterone is turned into aldosterone by the enzyme aldosterone synthase. Whew! That’s like going through the washing machine twice. 

Aldosterone synthase is stimulated by the hormone angiotensin II, which is produced in the lungs in response to decreased blood volume and blood pressure.

So the final result is aldosterone which belongs to a group of hormones called mineralocorticoids, which help regulate the body’s sodium concentration.

Aldosterone binds to receptors on the cells that line the distal tubules and collecting ducts in the kidney, and increases the expression of sodium/potassium ion pumps, which are on the basolateral surface of the cells - the side facing the blood. 

These ion pumps drive potassium from the blood into t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastric_motility</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YwentOQWRZOhjSwSsT8dx7r-QQ_4TlNT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastric motility]]></video:title><video:description><![CDATA[When we eat food, it’s first chewed up in the mouth and mixes with saliva to form a mushy mass called a bolus, and then it travels down a muscular tube called the esophagus.

Next, it enters the stomach through the lower esophageal sphincter, which is a ring of muscle surrounding an opening. 

The stomach has three main parts: the fundus, the body and the antrum. 

The body is further divided into a proximal portion and a distal portion.  

The fundus, and proximal body make up the orad region, or top half of the stomach.

The distal body and the antrum make up the caudad region or bottom half of the stomach. 

Once the food bolus is partially digested in the stomach, it’s called chyme and it passes through the pyloric sphincter and into the duodenum, which is the first part of the small intestine. 

The pancreas is connected to the duodenum through the pancreatic duct, and it secretes many digestive enzymes to further break down food. 

All these part play a role in gastric motility which is the contraction of the stomach to break up food and move it into the intestine. 

Like other parts of the gastrointestinal tract, the stomach has 4 layers. 

Starting from the innermost layer to the outermost layer, these layers are the mucosa, submucosa, muscularis externa, and serosa. 

The mucosa and muscularis externa layers are modified in the stomach.  

The mucosa contains various glands filled with different cells that secrete the components of gastric juice. 

In the body of the stomach, there are parietal cells that secrete hydrochloric acid or HCl, a strong acid that helps to break down protein, and chief cells that secrete pepsinogen, an inactive enzyme. 

When pepsinogen is exposed to HCl it activates to becomes pepsin - an enzyme that helps break down proteins. 

In the antrum, there are mucous cells which secrete mucus which protects the stomach lining from the acidic environment. There are also G cells which secrete a hormone called gastrin. 

Unlike t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coagulation_(secondary_hemostasis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cKeMwbkLQSCQUWAzRUtE9cmRTCaK3Y6G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coagulation (secondary hemostasis)]]></video:title><video:description><![CDATA[Hemostasis can be broken down into hemo referring to blood or bleeding and stasis meaning to stop - so together it means stopping bleeding. Hemostasis has two phases: primary and secondary hemostasis. 

In primary hemostasis, platelets aggregate to form a plug at the site of an injured blood vessel. While these platelets are aggregating, coagulation, or secondary hemostasis starts. 

This is where numerous enzymes that are always floating around in the blood called clotting factors get proteolytically activated, meaning that activation happens when a small piece is chopped off - a bit like pulling the pin out of a grenade. 

These factors activate one another, eventually leading to the activation of fibrin or factor Ia. That results in a fibrin mesh which forms around the platelet plug to reinforce it and hold it together.  

Without primary and secondary hemostasis, our body would suffer massive blood loss from even the most minor injuries--imagine losing all of your blood volume from something as simple as a pinprick! 

So let’s get into the details of secondary hemostasis. The process of forming the fibrin mesh begins via two pathways --the extrinsic and intrinsic pathways. 

The intrinsic pathway is called intrinsic because all of the factors required to activate it are intrinsic, or found within the blood. 

Conversely, the extrinsic pathway is called extrinsic because it’s activated by tissue factor found extrinsically, or outside of the blood. 

Both pathways can become activated independently and ultimately culminate in the activation of factor X, which then proceeds to activate the rest of the coagulation cascade via the common pathway. 

Let&amp;#39;s start with the extrinsic pathway. It starts when trauma damages the blood vessel, and exposes the cells under the endothelial layer, like smooth muscle cells, which have tissue factor or factor III in their membrane. 

Now, it turns out that there’s an enzyme called factor VII floating ar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Range,_variance,_and_standard_deviation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cfFdQyz1RimxXposPyEB2Zw1QdK4CgAc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Range, variance, and standard deviation]]></video:title><video:description><![CDATA[To understand a set of data - having a single number like the mean or median gives us a one number summary, but understanding how the data is distributed is also very important - and that’s where the range, variance, and standard deviation can be helpful. 

For example, let’s say we are looking at the weight of 10 people and we divided them into groups A and B. 

weight of group A(in kg)                                                          weight of group B(in kg) 
40    45      50     55      60                                                     10      30     50     70      90 .

Mean = (40+45+50+55+60)/5= 50kg		  	          Mean = (10+30+50+70+90)/5= 50kg

Now, if you calculate the mean weight of group A and group B, you will find both of them have the same value of 50 kg, but the weights of individuals in group A are much more centered around the mean than in group B.

So let’s start by looking at the range, which is the difference between the highest and lowest value in a dataset.

In group A, we have (60-40)=20 kg, whereas in group B we have (90-10)=80 kg. 

So far so good. But now, let’s say we have decided to include another group called group C.    

Weight of Group C (in kg) 10    45    50    55     90. 
Mean = (10+45+50+55+90)/5= 50 kg
Range 90-10 = 80kg

So even when we change two data points, group C still has the same mean and range as group B since it depends only on the highest and lowest values, thus it provides no information about how the rest of the data points are distributed. 

In this situation, it’s clear that we need a better idea of how all of the values are distributed and to do that we can look at the variance. 

To calculate the variance, which is written out as σ2, we take each data point (x), subtract it from the mean (x-bar), and then we square this value so we don’t end up with a negative number. 

Next, we add up the squared values and divide that result with the total number of data points (n).

So, let’s use this fo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/T-cell_activation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zY8WbCuAQnOJLSXuY7cL778FT-Gt6okZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[T-cell activation]]></video:title><video:description><![CDATA[The immune response is highly specific for each invader, and that’s because the cells of the adaptive immune response have receptors that can differentiate friendly bacteria from potentially deadly pathogens from their unique parts - called antigens.

The key cells of the adaptive immune response are the lymphocytes - the B and T cells.

T cells develop in the thymus where they undergo a process called VDJ rearrangement to generate a massively diverse set of T cell receptors, or TCRs.

There are two types of T cells which are identified based on molecules they express on their surface.

Helper T cells express CD4 on their surface, and their main function is to support other immune cells.

Cytotoxic T cells express CD8 on their surface, and their main function is to kill infected or cancerous cells.

A T cell starts out naive and then gets primed or activated - at which point it differentiates into an effector T cell and proliferates. Activation of both helper and cytotoxic T cells requires two signals.

After that the cytokines present around the cell determine the type of T cell it will become. The first signal occurs when a T cell receptor binds to an antigen.

Now, a T cell receptor can only recognize antigens that are peptides, rather than carbohydrates or lipids.

And the T cell receptor also needs to have a peptide presented on a major histocompatibility complex, also known as MHC.

MHC molecules act like serving platters present the antigen to T cells.There are two types of MHC molecules that work with the two types of T  cells.

MHC class I molecules present antigen to CD8+ T cells and MHC class II molecules present antigen to CD4+ T cells.

MHC class II molecules are found on the surface of an antigen presenting cell like a macrophage or dendritic cells while MHC class I molecules are found on all nucleated cells throughout the body.

The antigen presented on the MHC molecule must be the right size and shape to bind strongly to the T cell receptor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatic_secretion</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yc8hQJzTRtiglT4xqj55q_rzTQ_v_FZ3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatic secretion]]></video:title><video:description><![CDATA[The pancreas is a long, skinny gland the length of a dollar bill and is located in the upper abdomen, or the epigastric region, behind the stomach. It has endocrine functions meaning it secretes hormones into the blood that eventually act upon other target tissues. 

For example, alpha and beta cells in the pancreas make hormones like insulin and glucagon that are secreted into the bloodstream to regulate blood sugar levels. 

However, approximately 90% of the pancreas is dedicated to its exocrine functions. 

The exocrine pancreas secretes enzymes and fluids that help neutralize and digest food within the intestines.

The exocrine pancreas can be divided into lobules, each of which contain lots of functional units called an acinus. 

An acinus is a cluster of acinar cells that all work together to make digestive enzymes. 

In fact, the word “acinus” means “berry” which describes the berry-like appearance of these cell clusters. 

Each acinus secretes digestive enzymes which flow into small intercalated ducts that are lined by ductal cells. 

These ductal cells secrete bicarbonate and fluids that make up the liquid portion of pancreatic fluid, and ultimately help to neutralize the acidic stomach contents as they enter the intestines. 

The intercalated ducts merge together forming an intralobular duct which join with other interlobular duct, and finally drain into the main pancreatic duct. 

The main pancreatic duct travels through the length of the pancreas and drains into the duodenum. 

Now let’s look at the enzymes made by the acinar cells. The main enzymes include pancreatic amylase which breaks down carbohydrates; trypsin and chymotrypsin, which break down proteins; and lipase which break down lipids. 

Now as it turns out, macromolecules like carbohydrates, proteins, and lipids are also found in the cells of the pancreas. 

Thus, in order protect the pancreas from destroying itself, the acinar cells manufacture inactive forms of the enzymes called p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nucleotide_metabolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/POmeIOJsTC6EaCDOy8yOYs-oQCy4z73_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nucleotide metabolism]]></video:title><video:description><![CDATA[Nucleotides are the building blocks of nucleic acids - deoxyribonucleic acid, or DNA - and ribonucleic acid, or RNA. The most basic structure of the nucleotide can be broken down into three subunits - a five carbon sugar, a phosphate group, and a nitrogenous base, also known as nucleobase.

So, the five carbon sugar is either deoxyribose or ribose - and depending on which is used, the final product is either deoxyribonucleic acid, or ribonucleic acid. The nucleobases can be either pyrimidines or purines. There are 3 pyrimidine bases, and they are all made up of a single heterocyclic ring - cytosine, or C, thymine, or T - which is DNA-specific, or T, and uracil, or U, which is RNA-specific. There are two purine bases, adenine, or A, and guanine, or G, and they’re made up of two rings. Now if we link up just the sugar and the nucleobase, we’ve got ourselves a nucleoside. To make a nucleotide, all we’ve got to do is add a phosphate group to the 5th carbon of the sugar on a nucleoside. 

So, nucleosides have slightly different names - in RNA, ribose plus adenine makes adenosine, guanine makes guanosine, cytosine makes cytidine, and uracil makes uridine. So, adding a phosphate, the “full name” of RNA nucleotides would actually be adenosine monophosphate, or AMP, guanosine monophosphate, or GMP, cytidine monophosphate, or CMP and uridine monophosphate - or UMP. For DNA, we’re using deoxyribose instead of ribose, so the nucleosides would be deoxyadenosine, deoxyguanosine, deoxycytidine and deoxythymidine - and similarly, with addition of phosphate group, the nucleotide would be called, for example, deoxyguanosine monophosphate, or dGMP. We know, all of this sounds complicated. Don’t shoot the messenger. 

There are two ways our cells can make nucleotides - one is to make from scratch, also known as de novo synthesis, and the other is the salvage pathway, that recycles nucleotides that are already semi-degraded. Let’s begin with the ribose-containing nucleotide sy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skeletal_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7yoeqDD3Sv6NDxLYVjh5xsiyTbCxjxce/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skeletal system anatomy and physiology]]></video:title><video:description><![CDATA[We all have 206 bones, and together they make up the skeleton which gives the body structure, protects important organs like the brain and heart, and allows muscles to facilitate movement.  

Without bones you’d be a shapeless, immobile blob. 

Normally, the skeleton can be broken down into the axial and the appendicular skeleton. 

The axial skeleton consists of bones located along the vertical axis of your body. It contains 80 bones; 22 bones that make up the skull, 33 vertebrae, 24 ribs, and the sternum. 

The appendicular skeleton consists of bones in your limbs as well as the bones that attach the limb bones to the axial skeleton, like the pelvis and the scapulae. 

The appendicular skeleton is made up of around 126 bones; 4 bones in both shoulders, 6 bones in the arms, 54 bones in the hands, 2 hip bones that form the pelvic girdle, 8 bones in the legs, and 52 bones in the feet.

Now there are 5 types of bones based on their shape - long bones, short bones, flat bones, sesamoid bones, and irregular bones. 

Long bones are longer than they are wide, and they’re in the limbs and include the humerus, radius, and ulna in the arms; as well as the metacarpals and phalanges of the hand and fingers. 

Long bones also include the femur, tibia, and fibula in the leg as well as metatarsals and phalanges of the feet and toes. 

During childhood and adolescence, long bones continues to grow and are the bones that are responsible for your height.

Unlike long bones, the short bones have a similar length and width, and that gives them a round or cube-like appearance. They include the carpal bones of the wrist and tarsal bones of the ankle and their main functions are to support the hand and foot.

Flat bones are thin bones, and some of them are curved. They include bones of the skull, the two shoulder blades or scapulae, sternum, and ribs. Their main job is to serve as armor plating that protects vital organs like the brain, heart, and lungs.

Sesamoid bones, are em]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscle_contraction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uy3kcqWxToqJs17yAhGxwkGXSJOI03dX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscle contraction]]></video:title><video:description><![CDATA[Even when you’re sitting perfectly still, when meditating for example, your muscles are still contracting a bit to stabilize joints and bones. And this force that the muscles apply at rest is called muscle tone.

On the other hand, when you pick up a 10 pound sack of potatoes, the force generated by the muscle contraction is much higher than the normal muscle tone in your biceps. 

The pulling force transmitted through the muscle fiber is called the muscle tension. 

Now let’s dive into some basics of muscle physiology, starting with a single muscle cell or muscle fiber. Within the muscle fiber is the sarcoplasm, which is the cytoplasm of a muscle fiber. 

The sarcoplasm is filled with stacks of long filaments called myofibrils. 

And each myofibril consists of contractile proteins called thin actin and thick myosin filaments. 

These filaments don’t extend through the entire length of the muscle fiber - instead they’re arranged into shorter segments called sarcomeres. Alright, now let’s zoom into a sarcomere. 

At the center of the sarcomere is the M line made of myomesin proteins, where the thick filaments attach. 

At the borders of the sarcomere are the two Z-discs made of alpha actin proteins, where the thin filaments attach. 

For every thick filament, there are two thin filaments-one above and one below and the two types of filaments overlap. 

The region with only thin filaments is called the I band and it appears light.

The region with thick filaments is called an A band and it appears dark. 

Now, most of the A band has overlap between the thick and thin filaments, but there’s an area towards the center called the H zone where there are only thick filament, so it appears slightly lighter. 

When the muscle contracts, the thick filaments pull the thin filaments above and below it towards the M line. 

The Z discs attached to the thin filament also gets pulled towards the M line, and the whole sarcomere gets shorter. 

Now, the A band does not cha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inheritance_patterns</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mJguEUDuQGO-lz6wSkatrPu6ThWH86jQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inheritance patterns]]></video:title><video:description><![CDATA[Inheritance patterns are the different ways in which traits are passed from one generation to another. 

Inheritance relies on homologous chromosomes, which come in pairs - one from mom and one from dad. Each chromosome has genes, which are regions of DNA that carry information for a specific trait.

And different versions of the same gene are called alleles. 

As an example, brown eye color and blue eye color are both alleles for the eye color gene. 

Each parent offers one allele of a gene, which can be either dominant represented with a capital letter, like big A, or recessive, represented with a lowercase letter, like little a. 

It only takes one dominant allele for its trait to be expressed, whereas it takes two recessive alleles for its trait to be expressed. 

Human somatic cells - so, all of the cells aside from the gametes - have 23 pairs of chromosomes; 22 somatic pairs and one sexual pair - adding up to 46 chromosomes in total. 

For the sex chromosomes, a genetic female has two X chromosomes, while a genetic male has an X and Y chromosome. 

All 46 of these chromosomes, along with the alleles they carry, segregate during meiosis -  which is the process of making gametes. 

Gametes only carry half the genetic information of the parent - so 23 chromosomes. Females require an egg and a sperm that are both “22, X”, whereas males require an egg that’s “22,X” and a sperm that’s “22,Y”. 

Once the male and female gametes merge during fertilization, their alleles combine to give rise to one of three possible genotypes of the offspring, homozygous dominant - or AA -, heterozygous - or Aa - , and homozygous recessive - or aa. 

This genotype determines a person’s features —or phenotype— such as hair color, or whether or not they have a genetic disease.

Genetic diseases develop when a gene doesn’t work well because of a mutation that affects one of the two alleles, and if the person has children these mutations can be inherited. 

To get a quick picture]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sjogren_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yY1KCIJ3Qkm9hCFZkll9O3GWTKW6Guks/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sjogren syndrome]]></video:title><video:description><![CDATA[Sjogren&amp;#39;s syndrome, named after Dr. Henrik Sjogren who first identified it, is a common autoimmune disorder, typically occurring in women.

In Sjogren’s syndrome, the body’s immune cells go rogue and start attacking various exocrine glands, which are glands that pour their secretions into a duct; most commonly the salivary glands and the lacrimal, or tear, glands.

Normally, the cells of the immune system are ready to spot and destroy anything foreign pathogens that could cause the body harm. 

Immune cells called antigen-presenting cells, which include macrophages and dendritic cells, latch onto pathogens and engulf them - literally swallowing them up. 

Pieces of the pathogen called antigens are then presented on a major histocompatibility complex class II molecule, or MHC-class II molecule - which is like a serving platter for antigens. An antigen presenting cell then searches for a T cell that can bind to the antigen. 

Once found, binding to the antigen helps activate this T cell, which then releases proinflammatory cytokines, or signaling molecules, that recruit more immune cells - ultimately leading to inflammation. 

The exact cause for Sjogren&amp;#39;s syndrome is unknown, but it seems to be related to both genetic and environmental factors. 

Genetic factors include genes which code for specific types of MHC class II molecules, called human leukocyte antigen, or HLA genes. Specifically HLA- DRW52, HLA- DQA1, or HLA- DQB1. 

Environmental factors include an infection of exocrine glands like the salivary and lacrimal glands. Infections can damage the cells of the salivary gland, and expose their cell components, including their DNA, RNA, and histones to circulating immune cells. 

These cell components get picked up by antigen-presenting cells, and presented to T-cells. In individuals with Sjogren&amp;#39;s syndrome, a T cell gets inappropriately activated by these nuclear components, and considers them to be foreign nuclear antigens. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Liver_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O5NRfMRESVS4nsGDDiPHJ8wMQl6XuAhd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Liver anatomy and physiology]]></video:title><video:description><![CDATA[Your liver lies just below your diaphragm in the right upper quadrant of your abdominal cavity. And it does a wide range of things - from helping to manage the body’s metabolism, detoxification, and bile production. 

The surface of the liver is covered by a serous membrane called the visceral peritoneum. 

The visceral peritoneum folds over on itself, and it suspends the liver from the abdominal wall and the diaphragm. 

There are five of these peritoneal folds and they’re referred to as ligaments. 

There’s the falciform ligament, which attaches the liver to the anterior wall of the abdominal cavity. 

There’s the round ligament of the liver, which is a fibrous cord found in the free margin of the falciform ligament.

There’s the coronary ligament, which attaches the liver to the inferior surface of the diaphragm. 

There’s the right triangular ligament, which is a small triangular fold which attaches the right lateral surface of the liver to the diaphragm.

And lastly there’s the left triangular ligament, which attaches the upper left surface of the liver to the diaphragm.

Now, viewed from above, the liver is divided by the falciform ligament into two main lobes: the larger right lobe and the smaller left lobe. 

When viewed from below, the liver has two additional lobes between the right and left lobe--the posterior caudate lobe and the anterior quadrate lobe. These two lobes are separated by the porta hepatis, which literally means “the gate to the liver”. 

Now the porta hepatis contains the hepatic artery, the hepatic portal vein, and the common hepatic duct. 

The hepatic artery delivers oxygen-rich arterial blood from the heart to the liver, while the hepatic portal vein delivers nutrient-rich venous blood from the gastrointestinal tract, but also from the spleen, and pancreas. 

Lastly, the common hepatic duct drains bile from the liver into the gallbladder. 

Now let’s take a closer look inside a section of the liver, which shows the functional]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Randomized_control_trial</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VMcQzqd2SnGGlyfL3D9qzplhQVCua_1N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Randomized control trial]]></video:title><video:description><![CDATA[Randomized controlled trials or RCTs are a type of study design that’s often used to figure out if there’s a causal relationship between an exposure and an outcome. 

For example, let’s say we want to find out if a newly discovered drug, let’s call it Drug A, can prevent migraines for up to a year. 

In this example, Drug A is the exposure and having a migraine is the outcome. 

In the most basic randomized controlled trial, the sample population might be randomly split into two treatment groups, an exposure group that receives Drug A, and a control group that receives a placebo. 

The placebo looks and tastes like Drug A but is completely harmless and ineffective - like a tiny capsule filled with water. 

After both groups get their treatments, researchers would compare the number of individuals in each group who got migraines over the next year.

Typically, the goal of a randomized controlled trial is to figure out if the intervention can help some target population - usually that’s just people in the general population. 

That means that it’s important to perform the trial on individuals that accurately represent the general population. 

In other words, the sample population should be similar to the general population. 

For example, if researchers want to find out if Drug A helps prevent migraines in women, then women are the target population. 

And the randomized control trial should be done on women rather than being done on men. 

Furthermore, if the goal is to use Drug A for women around the world, then the sample population shouldn’t just include women living in Vancouver, British Columbia. 

Instead it should include women of all ages, races, and socioeconomic statuses from around the world.

If the sample population and that target population are really similar, then the randomized controlled trial has high external validity, meaning that any conclusions made about the sample population can be applied to the target population, which is good ne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amino_acid_metabolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k9yPZS_LQJiPESrxiyJRJI5rSN2IU-qA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amino acid metabolism]]></video:title><video:description><![CDATA[Amino acids are the building blocks of proteins. 

And just like how you can make lots of words with a finite alphabet, it’s possible to make lots of proteins with just 20 amino acids! 

Each amino acid has nitrogen-containing amine group, and a carboxylic acid - hence the name amino acid! 

Each amino acid also has a unique side chain that’s kind of like the amino acid’s fingerprint.

10 of the 20 amino acids are essential, meaning that you obtain them from dietary sources rich in protein, such as meats or tofu. 

The other 10 amino acids are non-essential, which means that they can be made in our body, so you don’t have to get them from your diet. 

So let’s say you had a nice big bowl of lentils rich in protein.

Protein would get broken down into amino acids, and those amino acids would make their way into various cells to serve as building blocks in protein synthesis. 

And the cell has to try to make use of these amino acids, because ammonia which is the nitrogen-containing amine group in amino acids, can become toxic to the cell if it gets freed up and starts to build up in the cell.

Ultimately, to get rid of it, ammonia must first be removed from the amino acid and then sent to the liver where it can get metabolized into a less toxic molecule called urea. 

To do that, a group of enzymes called transaminases or aminotransferases transfer that nitrogen containing amino group from amino acids to ketoacids, like alpha-ketoglutarate. 

These reactions are called transamination reactions and they’re reversible reactions, meaning that the reaction can go in either direction using the same enzyme. 

And generally speaking, transamination reactions requires pyridoxine, or vitamin B6, as a cofactor to help move things along. 

So let’s take an example of a transamination reaction with the amino acid alanine in a muscle cell.

First, the enzyme alanine transaminase, or ALT, switches the amino group on alanine with the oxygen group on alpha-ketoglutarate, re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/B-_and_T-cell_memory</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/khUegKHYS9WofgU4auOOIrfYS-_C2DrT/_.jpg</video:thumbnail_loc><video:title><![CDATA[B- and T-cell memory]]></video:title><video:description><![CDATA[Your immune system is like the military - with two main branches, the innate immune response and the adaptive immune response. 

Key features of the innate immune response are that the cells are non-specific, meaning that they don’t distinguish one invader from another invader, the response is really fast - occurring within minutes to hours, and there’s no memory associated with innate responses. 

The adaptive response, which is mediated by lymphocytes like B and T cells - is the opposite of the innate immune response. 

B and T cells have unique receptors - the B cell receptor and T cell receptor - that differentiate pathogens from each other using their unique parts - called antigens. 

These receptors are developed while the T cell or B cell is developing in the bone marrow for B cells or thymus for T cells.

Once the cell has a unique antigen-specific receptor expressed on its surface it begins traveling through the lymphatic system - passing through lymph nodes in search for the one antigen that fits the receptor perfectly. 

If they encounter that antigen, a signal gets delivered to the cell’s nucleus that lead to clonal expansion. 

That’s where a single T cell or B cell replicates over and over - creating an army of clones that can combat the pathogen.

Once the immune response is complete, many of these cells die by apoptosis restoring the immune response to its original size - with one major change. 

Some of the B and T cells become memory cells, which are basically a pool of lymphocytes that are all set to combat the pathogen, if they encounter it again!

Immunologic memory is sometimes referred to as a secondary or anamnestic response, and it’s different from the primary response. 

During the primary response a small number of naive B and T cells require activation before they can respond to the pathogen. 

And activating those B and T cells requires a relatively high pathogen burden and can take days to weeks. 

And the innate response is r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fibrous,_cartilage,_and_synovial_joints</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GLOXLxi_QFOK7a3eLB_cY69OTIq1IfbN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fibrous, cartilage, and synovial joints]]></video:title><video:description><![CDATA[Your body is made of around 206 bones, which are connected together by about 360 joints. 

These joints can be classified into three main groups based on their structure and how they move. 

Fibrous joints which generally don’t move at all, cartilaginous joints which allow some movement, and synovial joints which are freely movable.

Let’s begin with the fibrous joints, which are also called synarthrosis or fixed joints. 

In fibrous joints, bones are connected by ligaments and they fall into three main categories based on their location.

First, we have sutures, which are the joints between the bones of the skull. 

Skull bones are supported by their interlocking design and short ligaments that connect adjacent bones together. 

Adult sutures are stiff and completely fixed. But in the fetus and the babies, the sutures are more widely spaced and therefore partially movable. 

During labor, there’s a process called molding where the baby’s skull bones slightly overlap, temporarily reducing the baby’s head diameter, so that it can pass through a mother’s pelvis. 

Second, there’s the syndesmosis which is the joint between the radius and ulna in the forearm. Along their shafts, they are attached by long bands of ligaments called the interosseous membrane. 

Unlike the interlocking sutures, syndesmoses are slightly mobile throughout life. 

The third category of fibrous joints is a gomphosis, which is a joint between the roots of a tooth and its socket within the jawbone - either the maxilla or mandible. 

A tooth is anchored in its socket by periodontal ligaments, which allow light movements to lessen the impact, like when you are chewing on corn nuts.

Next are the cartilaginous joints, which are joints surrounded by hyaline cartilage which can stretch to allow some movement. 

One type of cartilaginous joint is a synchondrosis, and an example of a synchondrosis is the costochondral joint where a bit of cartilage attaches the rib to the sternum. 

The e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bile_secretion_and_enterohepatic_circulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q1L9aHN-QXKSQByIx25TyOtlR8KCjjCQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bile secretion and enterohepatic circulation]]></video:title><video:description><![CDATA[Bile is a greenish liquid that’s made by the liver and is stored in the gallbladder. 

Bile is a bit like an alkaline soup and it’s ingredients include a variety of organic molecules. 

Bile does a number of things including helping with digestion, absorption of fats, and excretion of various molecules.  

Normally, lipids are insoluble in water, so that’s why bile is needed to help emulsify and solubilize them. 

The organic composition of bile is mainly made up of bile salts and phospholipids, with cholesterol, and bile pigments called bilirubin, making up only a small percentage. 

Bile is first manufactured in the liver by cells called hepatocytes. 

Hepatocytes use an enzyme called 7-alpha-hydroxylase to convert cholesterol into two primary bile acids, called cholic acid and chenodeoxycholic acid. 

In the intestines, some of these primary bile acids get dehydroxylated, giving rise to secondary bile acids - deoxycholic acid and lithocholic acid. 

The liver can conjugate, or attach the amino acids glycine or taurine to all four of these bile acids and this ultimately gives rise to 8 different forms of bile salts. And it’s these bile salts that are the main component of bile. 

So bile is made in the liver and flows into the intestines. 

The journey starts when bile flows into the left and right hepatic ducts which eventually merge to form the common hepatic duct. 

The common hepatic duct then leads to the cystic duct which brings the bile to the gallbladder. 

The gallbladder is a small pear-shaped hollow organ located beneath the liver, and this is where bile is stored and becomes more concentrated. 

Approximately 30 minutes after consuming a meal, the food is broken down into a slurry called chyme, and that chyme begins to enter the first part of the small intestine - the duodenum. When that happens, I-cells, which are in the mucosal lining of the intestine secrete a hormone called cholecystokinin, or CCK, into the bloodstream. 

Cholecystokinin ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bone_remodeling_and_repair</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EBHj4Gw8Q2yc2y2zChhrsQMySBC8N_1O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bone remodeling and repair]]></video:title><video:description><![CDATA[Bone remodeling is when old, brittle bone tissue is removed or resorbed and gets replaced by new bone tissue. Remodeling also occurs when reshaping your bones after a fracture or when repairing micro-cracks which form during ordinary activities, especially when your bones are under stress, like after lifting heavy weights.

Now the surface of the bones is covered by this layer called the periosteum, except at the articular cartilages, which are the parts involved in the joints. The periosteum consists of an outer fibrous layer which protects the bones and provides attachment for the tendons and the ligaments, and it also has an inner cellular layer which houses progenitor stem cells. These progenitor stem cells develop into both osteoblasts which secrete the bone matrix, and chondroblasts - which produce cartilage.

Now let’s look at the femur - the longest bone in the body.  The two ends of the bone that form the joints are called epiphysis, while the shaft of the bone is called the diaphysis.  Looking at the diaphysis, it has an external part; the cortical bone, which consists of many tiny cylinders known as osteons. 

Each osteon is made of many lamellae, which are these concentric layers made of an organic part - mostly collagen, and an inorganic part called hydroxyapatite, which is mostly calcium phosphate. In the center of every osteon is a Haversian canal, which contains the blood supply and innervation for the bone cells. In the center of the bone, is the medullary canal - a hollow space lined by a honeycomb-looking structure called the spongy or cancellous bone. The medullary canal contains the bone marrow, which is the site of blood cell production. 

Now, the epiphysis is made of a lot of spongy bone. And when you look closer at the spongy bone, it’s made of crosslinking tiny roads called trabeculae, which make your bones resistant to mechanical stress, so that they can bear weights without caving in. And just like the medullary cavity, the spac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vitamin_D</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t13qETTWSwOpFaWmRw5XaOATTI6XY50I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vitamin D]]></video:title><video:description><![CDATA[The blood calcium level stays stable thanks to three hormones: Vitamin D, parathyroid hormone, and calcitonin.

We’ll focus on Vitamin D, which along with parathyroid hormone, helps increase calcium levels, whereas calcitonin helps lower them. 

The majority of the extracellular calcium, the calcium in the blood and interstitium, is split almost equally into calcium that’s diffusible and calcium that’s not diffusible.

Diffusible calcium is small enough to diffuse across cell membranes and there are two subcategories.

The first is free-ionized calcium, which is involved in all sorts of cellular processes like neuronal action potentials, contraction of skeletal, smooth, and cardiac muscle, hormone secretion, and blood coagulation, all of which are tightly regulated by enzymes and hormones.

The second category is complexed calcium, which is where the positively charged calcium is ionically linked to tiny negatively charged molecules like oxalate and phosphate, which are small anions, that are found in our blood. 

The complexed calcium forms a molecule that’s electrically neutral but unlike free-ionized calcium it’s not useful for cellular processes. 

Finally there’s the non-diffusible calcium which is bound to large negatively charged proteins like albumin. 

The resulting protein-calcium complex is too large and charged to cross membranes, so the non-diffusible calcium is also uninvolved in cellular processes.  

Now, after parathyroid hormone, the metabolically active form of vitamin D, also called calcitriol, is the second most important hormone involved in regulating blood calcium.

Vitamin D is a steroid hormone, which means that it’s made from cholesterol and it’s fat-soluble. 

Active vitamin D starts out as one of two metabolically inactive molecules. 

Either vitamin D2, or ergocalciferol, which comes from plant sources in our diet, and vitamin D3, or cholecalciferol, which can either come from animal products in our diet, but can also be made i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DNA_mutations</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9glFaRkdRHGkaGVb32-iTX8TTBGBpA2I/_.jpg</video:thumbnail_loc><video:title><![CDATA[DNA mutations]]></video:title><video:description><![CDATA[Our DNA is like a library - found in the nucleus of our cells - with thousands of books. 

Some of these books - called genes - are extremely important, because they carry the recipes for every single protein found in the cell. 

These genes are scattered among 23 pairs of chromosomes - which are like the bookcases of the library. 

Chromosomes come in homologous pairs because - one comes from mom and one comes from dad. 

Each chromosome of the pair carries different versions of the same genes, called alleles. 

Now, on the molecular level, DNA is made up of two strands of nucleotides, so each gene is just a segment of this nucleotide sequence. 

There are four types of nucleotides: adenine, guanine, thymine, and cytosine - or A, G, T, C. 

Gene expression includes transcription and translation. 

Transcription is where the enzyme RNA polymerase uses the gene as a template to create a molecule that can leave the nucleus. 

This molecule is called messenger RNA or mRNA and it has the same nucleotide sequence as the gene, with one tweak: it has uracil nucleotides - or U - instead of thymine.

This mRNA molecule - or message - is encoded so that any 3 nucleotides equate to a specific codon which codes for an amino acid or is a stop codon which signals that the protein is complete. 

In translation, specialized proteins in the cytoplasm - called ribosomes - use the mRNA template to recognize the specific codons, and match them with the corresponding amino acids that will make up the protein. 

Now there are 64 different codons, and each of them codes for a single amino acid - but there are only 20 amino acids. 

That’s because some amino acids are encoded by more than one nucleotide triplet. 

Now - a mutation, put simply, is an alteration in the nucleotide sequence of one or more genes - but can sometimes affect large chunks of chromosomes.

These mutations can affect the chromosomes in somatic cells - meaning any cell in our body other than the gametes - or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Transverse_myelitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IL5v0CTwSoi6mIJFl-Qf9rpgRW6omtqQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Transverse myelitis]]></video:title><video:description><![CDATA[The name of the disorder transverse myelitis can be broken down. Transverse means extending completely across something - in this case, it refers to going across the spinal cord, and myelitis means inflammation of myelin which is the fatty substance surrounding nerves. 

So, in transverse myelitis there’s inflammation that damages the myelin as well as the rest of the neuron across a section of the spinal cord. 

Now, neurons are the main cells of the nervous system. They’re composed of a cell body, which contains all the cell’s organelles, and nerve fibers, which are projections that extend out from the neuron cell body. 

Nerve fibers are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons.

Where two neurons come together is called a synapse, and that’s where one end of an axon sends neurotransmitters to the dendrites or directly to the cell body of the next neuron in the series. 

The axons are intermittently wrapped in a fatty substance called myelin.

Myelin is extremely important to neurons, because it helps to allow an action potential to propagate much faster. 

An action potential is an electrical signal that races down the axon, triggering the release of neurotransmitters or a chemical signal, on the other end. 

Without myelin this signal propagation is very slow and inefficient. 

Since some of these neurons can be very long, especially ones that go from the spinal cord to the toes, the fact that myelin helps speed up action potentials is super important! 

Now, the spinal cord is composed of both grey and white matter. 

Grey matter consists of cell bodies. It’s in the middle of the spinal cord and is shaped like a butterfly. 

Surrounding the grey matter is white matter, which consists of the myelinated axons of various neurons. 

The neurons in the spinal cord form different neural tracts that carry information to and from the brain. 

There are three main tracts to remember. The corti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Juvenile_polyposis_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uCBl2AhFRXCEDxuEsHSDupE-SrmrDLMZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Juvenile polyposis syndrome]]></video:title><video:description><![CDATA[In juvenile polyposis syndrome, young children develop multiple polyps throughout the gastrointestinal tract, especially in the large intestine, and unfortunately some of those polyps can develop into colon cancer at some point in their life.

The large intestine is found in the abdominal cavity, which can be thought of as having two spaces - the intraperitoneal space and the retroperitoneal space. 

The intraperitoneal space contains the first part of the duodenum, all of the small intestines, the transverse colon, sigmoid colon, and the rectum; the retroperitoneal space contains the distal duodenum, ascending colon, descending colon, and anal canal. 

So the large intestines essentially weave back and forth between the intraperitoneal and retroperitoneal spaces.

Now, the walls of the gastrointestinal tract are composed of four layers. 

The outermost layer is the serosa for the intraperitoneal parts, and the adventitia for the retroperitoneal parts.

Next is the muscular layer, which contracts to move food through the bowel.

After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. 

And finally, there’s the inner lining of the intestine called the mucosa; which surrounds the lumen of the gastrointestinal tract, and comes into direct contact with digested food. 

The mucosa has invaginations called intestinal glands or colonic crypts, and it’s lined with large cells that are specialized in absorption.

In juvenile polyposis syndrome there’s an autosomal dominant mutation in the SMAD4 gene, which encodes a protein that’s part of a pathway that induces apoptosis or programmed cell death. 

Without a functioning SMAD4 gene, the gastrointestinal cells that mutate are more likely to escape having to undergo apoptosis, and instead they simply divide faster than usual - ultimately giving rise to polyps, which are benign outgrowths that arise along the gastrointestinal tract, mostly in the colon]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dilated_cardiomyopathy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3qoxjnwnTtmH3Te7LXN_Ces-QReCezmF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dilated cardiomyopathy]]></video:title><video:description><![CDATA[Cardiomyopathy translates to “heart muscle disease,” so cardiomyopathy is a broad term used to describe a variety of issues that result from disease of the myocardium, or heart muscle. 

When cardiomyopathy develops as a way to compensate for some other underlying disease, such as hypertension or valve diseases, it’s called secondary cardiomyopathy. When it develops all by itself, it’s called primary cardiomyopathy.

Now, the most common type is dilated cardiomyopathy, which can cause all four chambers of the heart to dilate, or get bigger. Specifically, new sarcomeres, or muscle units, in the walls are added in series, and the chambers grow larger, which leaves the walls relatively thin compared to the large chamber size, with less muscle to use for contraction.

In other words, they have really weak contractions, which means less blood is pumped out each contraction. This also means that there’s a lower stroke volume, and if the heart’s failing to pump out as much blood to both the body from the left ventricle, and the lungs from the right ventricle, patients develop biventricular congestive heart failure. Since contraction happens during systole, we say this is a type of systolic heart failure. 

Also, when the chambers get larger, they tend to stretch out the valves that separate the atria and ventricles. When they are stretched, the valves can’t close all the way, so they start to regurgitate blood back into the atria. This is called mitral valve regurgitation on the left side, and tricuspid valve regurgitation on the right. Mitral valve regurgitation might be heard on auscultation as a holosystolic murmur, meaning that it happens throughout systole.

Additionally, you might also hear an S3 heart sound on auscultation, which is the result of blood rushing and slamming into the dilated ventricular wall during diastole.

Another complication can be arrhythmias, because stretching out the muscle walls can irritate the cells in the conduction system, whic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gel_electrophoresis_and_genetic_testing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Mb_kcvGjTs2Ad6022skTO2I9Rm238o2B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gel electrophoresis and genetic testing]]></video:title><video:description><![CDATA[DNA is a huge molecule consisting of a long sequence of 4 nucleotides - adenine, or A, cytosine, or C, thymine, or T and guanine, or G.

What’s more, we have 46 of these DNA molecules - compressed in our 46 chromosomes - and each of them is packed with thousands of genes that code for our various traits - like hair color, eye color, and even whether or not we have a genetic disease.

Now, sometimes genetic diseases can be caused by a mutations in a single gene - and to identify such a particular needle in the DNA haystack, we can use a tool called gel electrophoresis.

With gel electrophoresis, first, DNA is chopped up into smaller fragments using restriction enzymes - which are enzymes that break the DNA at specific nucleotide sequences. Then the DNA fragments are poured into a well within a piece of agarose gel.

The gel looks solid but it’s actually only semi-solid - and on a microscopic level it looks like catacombs filled with water.

There’s a negative charge placed at the end with the wells, and a positive charge placed at the far end of the gel.

And an electric current is passed through the gel and that pulls the negatively charged DNA fragments through the gel catacombs - towards the positive end.

The key is that the smaller fragments are more nimble and can move more quickly through the gel than the larger fragments.

Now, ideally, if we’re looking for a mutation and we had an easy way to spot it - then life would be easy! Unfortunately, finding a mutation is sometimes a bit trickier.

But this is where restriction enzymes come in so handy. Let’s say that we used a restriction enzyme called EcoRI to digest the DNA.

EcoRI binds to every G A A T T C sequence of DNA, and breaks the DNA between the G and the first A. So if we have a DNA sequence like this, then there would be three G A A T T C sites where the restriction enzyme EcoRI would break the DNA, and the resulting fragments will look like this. 

If this DNA is then put into a well on a ge]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cell-mediated_immunity_of_natural_killer_and_CD8_cells</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7sv39PBMS-GMpHKnu2oVPtCaSRqwCq3N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cell-mediated immunity of natural killer and CD8 cells]]></video:title><video:description><![CDATA[The key cells of the adaptive immune response are the lymphocytes - the B and T cells. 

And there are two types of T cells. 

Helper T cells which express CD4 on their surface, and cytotoxic T cells which express CD8 on their surface.

Helper T cells primarily support other immune cells, whereas cytotoxic T cells kill cells that are infected with a pathogen or are cancerous. 

Cytotoxic T cells, along with natural killer cells, are part of cell mediated immunity. 

Cell mediated immunity refers to the part of the immune response that’s based on cellular interactions, and cannot be transferred through serum from one person to another. 

That makes sense since both natural killer and cytotoxic T cells need to interact directly with a target cell in order to destroy it.

Now, when a T cell is initially formed it’s considered naive. 

Later when that T cell encounters an antigen in the lymph node- it gets activated or primed - and turns into an effector T cell. 

This process of priming requires two signals. 

The first signal is the antigen itself, which is usually presented on an MHC molecule on the surface of an antigen presenting cell like a macrophage or dendritic cell. 

Cytotoxic T cells respond to intracellular antigens - like viruses, intracellular bacteria, and tumor antigens. 

The naive cytotoxic T cell needs a high level of stimulation to become activated and it relies on a process called cross-presentation to reach that level.

In cross-presentation macrophages or dendritic cells take up the antigen and then present it to the cytotoxic T cell. 

These antigens typically come from extracellular pathogens or from tumor cells or virally infected cells. 

The first signal is that the antigen has to bind perfectly to the T cell receptor or TCR. 

The second signal is called costimulation - and it’s when a ligand called CD28 on the surface of a T cell binds to a ligand called B7 on the antigen presenting cell. 

This region, which includes the T cell ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Photoreception</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wm__AXP9Re_8dpKcb_8Vy2pETwWNrFGc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Photoreception]]></video:title><video:description><![CDATA[Photoreception is the process that describes how photoreceptors like rods and cones absorb light waves that enter the eye and convert them into electrical signals which are then sent to the brain for visual processing. 

Photoreceptors are located in the retina, which is a light sensitive neural layer of tissue at the back of the eye. 

The retina itself is composed of ten of its own distinct layers. 

Moving from the deepest layer of the retina, from posterior to anterior, the layers are as follows: the pigment epithelium, the photoreceptor layer, the outer limiting membrane, the outer nuclear layer, the outer plexiform layer, the inner nuclear layer, the inner plexiform layer, the ganglion cell layer, the nerve fiber layer, and finally the inner limiting membrane. 

Since the inner limiting membrane and nerve fiber layer are the most anterior portions of the retina, you would think that as light enters the eye it would hit these layers first. 

However, light actually travels right past all the retinal layers until it  comes into contact with the deepest layer of the retina, the pigmented layer. 

So let’s trace the pathway of a visual impulse as it travels from the pigmented layer, all the way through to the nerve fiber layer and eventually to the brain. 

The first layer, the pigmented layer is only a single-cell thick and is the layer closest to the choroid, the vascular portion of the eye just posterior to the retina. 

The pigmented layer contains epithelial cells which absorb light so it doesn’t scatter within the eye.

The second layer, the photoreceptor layer contains photoreceptors. 

Photoreceptors are specialized neurons that detect light and when they hyperpolarize, they send visual impulses in the form of electrical signals to the brain. 

The third layer is the outer limiting membrane which sits at the base of the photoreceptor cells and provides mechanical support to the retina, helping it to maintain its structure. 

The fourth layer of t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cytokines</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o2MmVhqnSxqgfg1Sgh62lMpeQhCIgPZv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cytokines]]></video:title><video:description><![CDATA[Cytokines are tiny proteins that are secreted by both immune and non-immune cells to communicate with one another. Cytokines bind to receptors and trigger a response in the receiving cell. Oftentimes, cytokines promote activation, proliferation, and differentiation of immune cells, but they can do other things like help increase the body temperature - causing a fever.

Now, cytokines signal to other cells mainly through autocrine and paracrine signaling; but to a lesser extent, endocrine signaling can also be employed. Now, autocrine means the cell producing the cytokine is also the cell responding to the cytokine. An example is Interleukin-2, or IL-2 which is secreted by CD4+ T helper cells. IL-2 promotes the proliferation of T lymphocytes - including the CD4+ T helper cell that produced it. Paracrine means that the cytokine is produced by one cell and that it affects cells in the near vicinity. Once again, an example is IL-2  because it helps nearby CD8+ cytotoxic T cells proliferate. That’s important because the CD8+ cytotoxic T cells aren’t good at making their own IL-2. Finally, there’s endocrine, which is when the cytokine affects a cell that’s far away, perhaps in a different organ. An example would be the inflammatory triad of Interleukin 1-beta or IL-1beta, Interleukin-6 or IL-6, and Tumor Necrosis Factor-alpha, or TNF-alpha. These cytokines are produced by macrophages and dendritic cells. During acute inflammation,  these cytokines travel to the liver and the brain. In response, the liver produces acute phase reactants like C-reactive protein and Mannose Binding Lectin, and the brain increases the body’s temperature, triggering a fever. At the same time, IL-1beta and TNF-alpha also help to recruit other immune cells to the site of injury, enhancing the inflammatory response. 

Overall, there are 5 main classes of cytokines. The first and most varied group are the Interleukins, which are numbered in the order they were identified, so the numbers d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Subdural_hematoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gm500QT4S3ymDf71r6gwEJ-6SwujM63e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Subdural hematoma]]></video:title><video:description><![CDATA[Subdural hemorrhage can be broken down. Sub means below, “dural” which refers to the outermost protective layer of the brain, which is called dura mater, and “hemorrhage” refers to bleeding. So, a subdural hemorrhage is when there’s bleeding below the dura mater. 

OK - let’s start with some basic brain anatomy. The brain is protected by 3 thin layers  of tissue called the meninges which covers the brain and spinal cord. 

The inner layer of the meninges is the pia mater, the middle layer is the arachnoid mater, and the outer layer is the dura mater. The pia and arachnoid maters, are also called leptomeninges. 

Between the leptomeninges, there’s the subarachnoid space, which houses cerebrospinal fluid, or CSF. 

CSF is a clear, watery liquid which is pumped around the spinal cord and brain, cushioning them from impact and bathing them in nutrients. The outer membrane, the dura mater consists of two layers. 

The internal layer of the dura mater lies above the arachnoid mater - the two are separated by the subdural space.  The external layer of the dura mater adheres to the inner surface of the skull. 

These two layers of the dura mater travel together, but at certain spots, the internal layer of the dura mater separates from the external one to form the meningeal folds. 

The meningeal folds help divide the sections of the brain like the falx cerebri which separates the two hemispheres of the cerebrum, and the tentorium, which covers the cerebellum and separates it from the cerebrum. The subdural space plays a major role in venous blood drainage in the brain. 

The surface of the brain is supplied by numerous arteries in the subarachnoid space that provides oxygen rich blood to the brain. 

After the brain tissue has taken up the oxygen and nutrients, the blood drains into superficial cerebral veins, or bridging veins, that also sit in the subarachnoid space.

These veins travel through the arachnoid mater, pass through the subdural space and penetrate t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ectopic_pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7jdKwuSsRPmnv9a1a5Pfw2vfQRiHR9uJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ectopic pregnancy]]></video:title><video:description><![CDATA[In ectopic pregnancy, ectopic means “out of place,” so an ectopic pregnancy means that a pregnancy occurs somewhere other than in the uterine cavity.

In order for an ectopic pregnancy to take place, a couple of things need to happen differently from the normal process of a pregnancy. 

First, following ovulation, the egg must be fertilized and come to rest somewhere other than the endometrium of the uterine cavity.

Next, when it arrives at this destination, it must implant on a surface with a rich enough blood supply to support a developing embryo. 

Ectopic pregnancies have been known to occur on various surfaces, including the ovaries, intestines, and most commonly, in the ampulla of the Fallopian tube. 

After implantation, the embryo begins developing and growing just like it would in a normal pregnancy. 

Over time, a few different things can happen. Sometimes the tissue can no longer provide a sufficient blood supply for the embryo, leading to its death. 

On the other hand, if the tissue can supply the embryo with sufficient blood, then hormones from the corpus luteum and placenta can lead to a missed menstrual period and other body changes like nausea and fullness of breasts, which are typically seen in early pregnancy.

If the ectopic pregnancy occurs in the ampulla of the fallopian tube, it eventually runs out of space. 

Slowly the ectopic pregnancy stretches the nerve fibers within the wall of the fallopian tube, causing lower abdominal pain. 

Eventually, the expansion causes damage to the wall of the ampulla, potentially rupturing the fallopian tube. 

A ruptured ectopic can also lead to massive hemorrhaging into the abdominal cavity, and the blood can irritate the peritoneum which can cause referred pain to the shoulder. 

Occasionally, there can be light vaginal bleeding as well. 

The combination of internal bleeding, severe pain, and damage to the fallopian tube make an ectopic pregnancy a medical emergency.

The cause of an ectopic pre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glycogen_metabolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sRV0ain_QI6z_T9_WGqXQfuSRuiCS2fs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glycogen metabolism]]></video:title><video:description><![CDATA[Glucose is a 6-carbon molecule that’s used to make energy, in the form of adenosine triphosphate, or ATP. 

Glucose is such an important energy source, that our body stores excess glucose in skeletal muscle cells and liver cells in the form of glycogen. 

Glycogen is basically an enormous molecule or polymer, that’s made up of glucose molecules linked together by glycosidic bonds.

You can think of glycogen having a main chain, and there being multiple branches sprouting off of it. 

These branches allow glycogen to be compact and capable of rapid addition and removal of glucose. 

It’s a bit like growing a plum tree in a tiny house with a short ceiling. 

The short ceiling limits the tree’s vertical growth, but the tree’s able to branch off, so that it can still grow and produce many plums in a tight space. 

Now let’s say that you just wrapped up a delicious lunch - you had tacos! Glucose is absorbed from the intestine and our blood sugar goes up. The pancreas responds to high blood sugar by secreting insulin. 

Insulin acts on glucose transporters on the cell membrane, which are called GLUTs - and makes them bring more glucose into all the cells in our body. 

Inside the cell, an enzyme called hexokinase adds a phosphate group to it’s 6th carbon, creating glucose 6 phosphate.

Then, glucose-6-phosphate is broken down during glycolysis, making ATP as a byproduct. 

Over time, ATP levels start to rise and that inhibits certain enzymes in glycolysis. 

When that happens, the extra glucose-6 phosphate can be used to make glycogen. And that usually takes place in the liver and muscle cells. 

There are four main steps in glycogen synthesis. 

First is attaching a uridine diphosphate, or UDP molecule to glucose. 

Second, is attaching the glucose part of the UDP-glucose molecule to a glycogen primer called glycogenin, forming a short linear glycogen chain, which serves as a primer. 

Third, is adding more glucose molecules to that primer - a bit like forming ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oncogenes_and_tumor_suppressor_genes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JiQ2j_xiR26mEpLcLK-XLLcHSHGI6SUM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oncogenes and tumor suppressor genes]]></video:title><video:description><![CDATA[Oncogenes and tumor suppressor genes are classes of genes that code for various proteins that are involved in the progression of the cell cycle. 

Oncogenes are actually mutated versions of proto-oncogenes, which are normal genes in charge of positive regulation of the cell-cycle. 

So the protein products of proto-oncogenes stimulate cell growth and division - they’re like a gas pedal in a car.

Tumor suppressor genes, on the other hand, are in charge of negative regulation of the cell cycle, so their protein products stop its progression and promote apoptosis or cell death. 

Tumor suppressor genes are involved in DNA repair mechanisms and inhibiting transcription factors that try to push the cell along in the cell cycle - so they’re like the brake pedal in a car.

Now, the cell cycle is the series of events that a cell goes through as it changes from being one cell into two daughter cells. 

The cell cycle has two phases: interphase and mitosis. Interphase is comprised of the G1 phase, during which the cell grows and performs its cell functions, the S phase, during which DNA is replicated, and the G2 phase, during which the cell grows again before entering mitosis. 

At the end of G1 and G2, there are cell cycle control points called the G1 and G2 checkpoints, where the cell checks to see if there’s any DNA damage.

The main control point is the G1 checkpoint. 

If it turns out that there is DNA damage, then the cell can either enter a non-dividing state called the G0 phase, where the DNA repair mechanisms try to fix the problem, or the cell can self-destruct in a process called apoptosis. 

Now, if the cell does get the go-ahead at the G1 checkpoint, it enters the S phase. 

And then if the cell gets past the G2 checkpoint, it enters mitosis, and it divides in two identical daughter cells. 

However, once cells differentiate and become mature cells - like liver cells for example - they don’t necessarily go through the cell cycle over and over again. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polymerase_chain_reaction_(PCR)_and_reverse-transcriptase_PCR_(RT-PCR)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hv2bFDZnT_qqfIpRMSGYK34lSOm-1IYx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polymerase chain reaction (PCR) and reverse-transcriptase PCR (RT-PCR)]]></video:title><video:description><![CDATA[Our DNA contains loads of information, neatly stacked to insanely small sizes, able to fit within a cell nucleus. 

A single DNA molecule has two strands, which wrap one around one another to form a double helix. 

Each single strand of DNA is composed of a sequence of four types of nucleotides - which are the individual letters or building blocks of DNA. 

Nucleotides of DNA are made up of a sugar - deoxyribose, a phosphate, and one of the four nucleobases - adenine, cytosine, guanine, and thymine - or A, C, G, T for short. 

The nucleotides on one strand form hydrogen bonds to complementary nucleotides on the other strand; specifically, A bonds with T via two hydrogen bonds, and C bonds with G, via three hydrogen bonds. 

Additionally, the two DNA strands also have a “direction” - meaning, one of them runs from the 3’ end to the 5’ end, while the other one runs from the 5’ end to the 3’ end. 

Kinda like two snakes coiled up together, but facing in different directions. Every single protein of our body is encoded through combinations of just four nucleotides. 

When there are errors in our genetic information, diseases occur. And let’s be honest, we were always interested in knowing what was written in our DNA.

Polymerase chain reaction, or PCR for short, is a technique used in molecular biology to amplify a segment of DNA. Let’s take a step back. A single copy of DNA is not very much DNA. 

So to work with DNA, we basically make lots and lots of lots of copies of it, so that it’s easier to analyze. For example, if we want to visualize it, we can use a technique called gel electrophoresis. 

PCR is based on DNA replication, a process that our cells normally use to duplicate their genetic material before dividing in two identical daughter cells. 

So first of all, we’re going to need a machine called a thermal cycler - that’s where the PCR magic happens. 

You can think of it like a cauldron filled with a solution, where genetic wizards add the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Electron_transport_chain_and_oxidative_phosphorylation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IQfI6uYXQ5SAsnhBKWWpI2YlQDChQ_i_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Electron transport chain and oxidative phosphorylation]]></video:title><video:description><![CDATA[Your heart is constantly working. Whether you’re swimming or taking a nap, your heart is always on the go. 

The main form of energy that keeps our heart cells, and really all of our body cells, going is adenosine triphosphate, or ATP. 

In most cells, the main ATP producing factory is the mitochondria, which has an inner and an outer membrane, and it’s along the inner membrane where a process called oxidative phosphorylation occurs. 

“Oxidative” refers to oxidation - which is when a molecule donates its electron, and “phosphorylation” which refers to the addition of a phosphate group to adenosine diphosphate, or ADP, to form ATP. 

So oxidative phosphorylation is the process of making ATP by donating electrons to complexes embedded within the inner mitochondrial membrane. 

These complexes are proteins or lipids coupled with metals like iron and copper that facilitate the movement of electrons. 

Together, they form the electron transport chain. 

During the electron transport chain, electrons are passed on from complex to complex, and finally to oxygen, creating a proton gradient that will be used to make ATP. 

The electron transport chain begins with two key molecules that want to donate their electrons: nicotinamide adenine dinucleotide, or NADH, and flavin adenine dinucleotide, or FADH2, both of which get oxidized in the electron transport chain.

NADH and FADH2 are primarily generated in the citric acid cycle which occurs in the mitochondria, but it can also come directly from glycolysis - which is the breakdown of glucose in the cytoplasm, or fatty acid oxidation, which is the breakdown of fats in the mitochondria.

Enzymes called dehydrogenases help generate the electron-rich NADH and FADH2.  

And when those molecules are coming from the cytoplasm they can only enter the mitochondria using a specific shuttle.

When using the malate-aspartate shuttle, electrons enter the electron transport chain as NADH. 

When using the glycerol-3-phosphate shut]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Citric_acid_cycle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QoVlcgDZTKWACmj1FnC8DyBRTZa4evQJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Citric acid cycle]]></video:title><video:description><![CDATA[For cells to perform any function, any work, they must have energy. 

You can’t go jogging or lifting weights if you’re tired, because a cell won’t work without the help of chemical energy. 

The main energy currency in the cells is adenosine triphosphate, or ATP, but any nucleoside triphosphate, like guanosine triphosphate, GTP, will do. 

For cells to make ATP, a process generating electricity has to take place in our mitochondria. 

Electricity is power! 

And thanks to this electricity, ATP is made. 

Now to create electricity, electron rich molecules must deliver electrons to a chain of complexes, the electron transport chain, which move them to a final acceptor, a molecule of oxygen. 

And there are two electron donor molecules: nicotinamide adenine dinucleotide, or NADH, and flavin adenine dinucleotide, or FADH2. 

But of course, the cell has to produce NADH and FADH2 in the first place, and they’re produced by critical enzymes called dehydrogenases. 

Dehydrogenases are the main enzymes found in the citric acid cycle or Kreb’s cycle. 

In fact, the citric acid cycle is a set of 8 enzymatic reactions that start with a molecule called acetyl-CoA, and four of the enzymes, half of them, are dehydrogenases. 

And in this process, AcetylCoA gets converted into carbon dioxide.

Acetyl-CoA comes from various sources depending on whether you’ve just eaten or are starving. 

Let’s say that you’re hungry and a bit angry - so you’re feeling hangry. 

That’s when stress hormones like glucagon, epinephrine, and cortisol start to rise. 

In this hangry state, fatty acids from triglycerides become the primary source of acetyl-CoA. 

Now, let’s say you have a bowl of delicious French onion soup, everything changes - insulin is plentiful and you have plenty of acetyl-CoA from breaking down glucose, fructose, and galactose -with glucose playing the biggest role. 

Now, alcohol is also a source of Acetyl-CoA in the liver where it’s metabolized.    

In addition, prote]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Enzyme_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2aghAUqXR9WWqFgy-NfiBRQvR9y8cc4F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Enzyme function]]></video:title><video:description><![CDATA[Enzymes are proteins that play a major role in the biochemical reactions happening every moment inside our bodies - everything from digesting a bowl of ramen noodles to flexing your muscles in front of a mirror. 

Enzymes act as catalysts - meaning that they speed up the rate at which these biochemical reactions happen. 

So instead of waiting months to years for a reaction to happen, it can happen in seconds - which is essential for life to happen. 

Imagine trying to digest a single bowl of ramen for a year - you’d die of hunger before you could do it! 

Every biochemical reaction has a substrate and a product - so let’s put them on this graph called a reaction coordinate diagram. 

The X axis shows how a reaction progresses, while the Y axis shows the energy level at the different points along the reaction. 

In the beginning, we’ve got the substrate -  let’s call it A - with a fair amount of free energy. 

At the end of it, there’s the product - or B, which ranks lower energy-wise. 

The energy of the product minus the energy of the substrate is called the energy of the reaction, also known as Gibbs free energy, or ΔG. 

Because lower energy states are preferred, a reaction spontaneously occurs when the product has a lower free energy than the substrate - so a negative ΔG. 

So let’s say we’re looking at one such spontaneously occurring reaction, but between going from the substrate to the product there’s an intermediate transition step that has a really high energy state. 

The amount of extra energy the substrate requires to get to the transition state - so the height of the upslope - is called the activation energy - or a ΔG‡ plus plus. 

As soon as it enters the transition state, the molecule is highly unstable - and wants to go to a more stable lower-energy molecule 

It either goes back to being a substrate or to being a product. 

If it’s a substrate once again, it can go back up to the transition state if there’s enough activation energy once m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glycolysis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7ZOxhqm5TPW-P-MyrDZje5WcSvSVOf4h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glycolysis]]></video:title><video:description><![CDATA[Let’s say that you just ate a big slice of pizza with onions, mushrooms, bell peppers, and jalapenos. To pull energy out of the glucose in that pizza or really any food, requires glycolysis. 

Glycolysis is a series of enzymatic reactions in which glucose, a 6 carbon sugar molecule, is broken down into two 3 carbon pyruvate molecules. 

And as glucose gets processed, energy is produced in the form of adenosine triphosphate, or ATP. 

Now, glycolysis happens in the cytoplasm of cells, and no special organelles or even oxygen are needed to turn glucose into ATP. 

Therefore, all cells can use glucose to make energy; and it’s possible to do glycolysis even when oxygen levels are low.

Glycolysis can be divided into two phases: an energy-consuming phase, and an energy-producing phase. 

It’s like a business investment - the cell needs to spend some energy before it can start making energy, and like any good investment the cell gets more energy back than it puts in. 

The energy-consuming phase requires ATP, and the energy-producing phase generates ATP, as well as other molecules like reduced nicotinamide adenine dinucleotide, or NADH, which can be used to make ATP. 

We can keep track of all of this using an energy counter.

Going back to that delicious pizza, first, glucose from those ingredients has to first get from the small intestine into the bloodstream. 

In response to high blood glucose, the pancreatic beta-cells secrete insulin. 

Now, to get inside the cells, glucose utilizes glucose transporters, or GLUT, which are on the cell membrane. 

In fact, some GLUTs like GLUT2 in the liver and pancreatic beta-cells are particularly responsive to glucose in the presence of insulin.

Once glucose gets inside the cell, it’s prevented from diffusing across the cell membrane back into the circulation by enzymes called kinases which phosphorylate the glucose.

Adding a phosphate group changes the shape of the glucose molecule, which means it can’t easily diffuse]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gluconeogenesis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JeE_k7wVTZ_F-a-ls2JsQXNKSzirgiHb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gluconeogenesis]]></video:title><video:description><![CDATA[Carbohydrates are made of sugar molecules, and the most important one is the 6-carbon sugar, glucose. It’s important to keep a steady amount of glucose in the blood, because cells use it to produce energy - in the form of adenosine triphosphate, or ATP. One of the ways you can do this is by eating carbohydrate-rich foods like pasta. But in between meals, when fasting, the body maintains glucose levels using gluconeogenesis.

Gluconeogenesis is a metabolic pathway that uses enzymatic reactions to make glucose from other molecules, like amino acids, lactate, and glycerol. Gluconeogenesis primarily takes place in liver cells, but it can also happen in the epithelial cells of the kidney and the intestines. Specifically, it takes place in the cytoplasm, mitochondria, and endoplasmic reticulum of cells found in these tissues. 

Okay, so let’s say you’re going hiking in the woods, and you fuel up on some pasta before you leave. Now, during the hike, you get lost and end up stranded with no food. Initially, the glucose in your pasta is broken down by a series of enzymatic reactions to make pyruvate, producing ATP in the process. This is called glycolysis, and it keeps you going for a couple of hours. Some of the extra glucose is stored in the liver cells in the form of glycogen, which is a bunch of glucose molecules stringed together. When you’re fasting, you still need glucose, in particular for your red blood cells and your brain. And you might need it to find your way out of the woods. So, it’s up to your liver to maintain adequate blood glucose levels while fasting. There are two pathways that can contribute glucose: glycogenolysis and gluconeogenesis. So with glycogenolysis, the liver breaks down glycogen into individual glucose molecules, but that only helps for 12 to 24 hours of fasting, because glycogen stores are finite. In contrast, gluconeogenesis makes glucose from scratch, so it can keep on going in the event that you fast for more than a day.  Actual]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cell_signaling_pathways</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GiGy8bkiRjOIUBn1UU2Fi_59S8O3SIUi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cell signaling pathways]]></video:title><video:description><![CDATA[To make a multicellular organism, cells must be able to communicate with one another, and to do it cells often send out tiny chemical signals that act on the receptors on other cells. 

Signals can be classified according to the distance between the signaling cell and the target cell. 

Autocrine signals are produced by a cell and go to its own receptors, so the cell sends a signal to itself.

Paracrine signals are produced by a cell and go to target cells that are nearby. 

And endocrine signals are produced by a cell and go to target cells that are further away. 

Examples of these include hormones that are secreted into the bloodstream, as well as cytokines that can be released at the site of injury and act on the brain to cause a fever.

Signaling molecules or ligands can be hydrophobic, meaning that they tend to repel water, or hydrophilic, meaning that they tend to stay in water. 

Hydrophobic signalling molecules can’t freely float in the extracellular space, so they’re brought to the target cells by carrier proteins. 

Hydrophobic molecules can diffuse across the cell membrane and bind to receptor proteins inside the target cell - either in the cytoplasm or in the nucleus. 

Most signal molecules are hydrophilic, so they can freely float in the extracellular space to reach the target cells, but are then unable to cross the cell membrane. 

So to pass on the signal, hydrophilic molecules bind to receptors on the cell surface. 

These receptors are transmembrane proteins, with an extracellular end that binds to the ligand, and an intracellular end that triggers a signaling pathway inside the cell. 

We can think of the cell signaling pathway in three stages.

The first stage is reception, which is when the target cell’s receptor binds to a ligand. It’s like a key fitting into a lock. 

Then there’s transduction, which means that the receptor protein changes in some way and that activates intracellular molecules - the second messengers. 

The third st]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertrophic_cardiomyopathy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kdoLHL_2RcS4JoFufpuzCcJ9TyWuBPcI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertrophic cardiomyopathy]]></video:title><video:description><![CDATA[Cardiomyopathy means “heart muscle disease,” so cardiomyopathy is a broad term used to describe a variety of issues that result from disease of the myocardium, or heart muscle. 

When cardiomyopathy develops as a way to compensate for some other underlying disease, like hypertension or valve diseases, it’s called secondary cardiomyopathy; when it develops all by itself, it’s called primary cardiomyopathy.

Now, hypertrophic cardiomyopathy is when the walls get thick, heavy, and hypercontractile; essentially, the muscles grow a lot larger because new sarcomeres are being added parallel to existing ones. 

Usually, the left ventricle is affected, and in most cases, this muscle growth is asymmetrical, meaning that the interventricular septum grows larger relative to the free wall. 

These larger muscles do two things: the walls take up more room, so less blood is able to fill the ventricle; and they become more stiff and less compliant, so they can’t stretch out as much, again, leading to less filling. When the ventricles don’t fill as much, they don’t pump out as much blood, and so stroke volume goes down. Thus, the heart can fail to pump enough blood to the body; this is called heart failure. Because this is due to a dysfunction in filling, which happens during diastole, this is a type of diastolic heart failure. 

In some patients, the muscle growth of the interventricular septum essentially gets in the way of the left ventricular outflow tract during systole, or ventricular contraction. This increases blood velocity through the smaller opening, and pulls the anterior leaflet of the mitral valve toward the septum. This is called the venturi effect, which further obstructs the left ventricular outflow tract. For this reason, hypertrophic cardiomyopathy is sometimes called hypertrophic obstructive cardiomyopathy. 

An obstructed left ventricular outflow tract means blood is forced through a tiny opening, which tends to cause a crescendo-decrescendo murmur. A]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brown-Sequard_Syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_sattEA4QLWLPSlXF7ciWMwJQPewXWNk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brown-Sequard Syndrome]]></video:title><video:description><![CDATA[Brown-Séquard syndrome, first described by the physiologist Charles-Édouard Brown-Séquard, is a condition associated with hemisection or damage to one half of the spinal cord. The hemisection damages neural tracts in the spinal cord that carry information to and from the brain. This results in a loss of sensations like pain, temperature, touch, as well as paralysis or loss of muscle function in some parts of the body.

Now, if you look at the cross-section of the spinal cord, the white matter is on the outside and the gray matter is on the inside, and overall it looks like a butterfly. If we draw a horizontal line through the spinal cord, the front half is the anterior or ventral half, and the back half is the posterior or dorsal half. And the butterfly wings are sometimes referred to as horns; so we have two dorsal horns that contain cell bodies of sensory neurons and two ventral horns that contain cell bodies of motor neurons.  The white matter consists of myelinated axons which are separated into tracts that carry information to and from the brain. Think of them like highways for neural signals, where some highways carry sensory information to the brain and some carry motor information from the brain to the muscles.

There are a few main tracts to remember. First, there’s the spinothalamic tract which is an ascending pathway and it’s divided into two parts. The lateral tract carries sensory information for pain and temperature, while the anterior tract carries information for pressure and crude touch--or the sense one has been touched, without being able to localize where they were touched. Second, there are two ascending dorsal column tracts- the fasciculus gracilis which carries sensory information from the lower trunk and legs, and the fasciculus cuneatus which carries sensory information from the upper trunk and arms. These tracts both carry sensations like vibration; fine touch, which is where you can localize where you were touched; and propriocep]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Miscarriage</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_anEt3EFQPSWU5vNnhKd8poXTD27WI7h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Miscarriage]]></video:title><video:description><![CDATA[A miscarriage, or spontaneous abortion, is defined as a pregnancy loss that occurs without outside intervention before the 20th week of pregnancy. 

Pregnancy is so complex that there are many different ways for the process to get off course and for a miscarriage to occur. 

For example, if there’s a chromosomal abnormality in the sperm or egg then the resulting zygote will have a problem. 

One of these problems is called aneuploidy, which is when there are missing chromosomes or additional chromosomes. 

For example, if there’s one member of a chromosome pair missing, that results in 45 chromosomes total, instead of the normal 46, it’s called a monosomy.

And if there’s one extra chromosome joining a pair, that results in 47 chromosomes total, and it’s called a trisomy. 

Some types of aneuploidy are viable like Turner’s syndrome or Down syndrome, whereas many are not and lead to a miscarriage. 

Another abnormality is polyploidy, and that’s when a zygote receives more than one set of 23 chromosomes from either the sperm or egg, resulting in three sets, totaling 69 chromosomes, or even four sets, totaling 92 chromosomes. 

Polyploidy is generally not viable and leads to a miscarriage. 

One more abnormality is a translocation. 

It can either be balanced, where two nonhomologous chromosomes essentially trade equal amounts of DNA, or unbalanced, where the chromosomes exchange unequal amounts of DNA, resulting in either too many or too few copies of certain genes on the involved chromosomes. 

Now even if a parent carries a balanced translocation, the sperm or egg may end up with an unbalanced translocation, and the zygote won’t have a normal number of genes. 

Some translocations are viable, whereas many are not, and can lead to a miscarriage.

Now, let’s say that there are a normal number of chromosomes present, and that the zygote becomes a blastocyst and tries to implant, there are still many ways in which a miscarriage can occur. 

First if the blasto]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cohort_study</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1DzA2HTcSVSf3SBslWWzO7pZTq2QznLg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cohort study]]></video:title><video:description><![CDATA[A group of people who share a common characteristic is called a cohort. 

For example, people born in the year 1981 make up a birth cohort, and people who work in construction make up an occupational cohort. 

Now, cohort studies or longitudinal studies are a type of study design that follows a cohort of people over time to figure out if there’s an association between an exposure and an outcome. 

Typically, cohort studies look at individuals in a cohort who have a certain exposure, as well as individuals in a cohort who have not had that exposure, to compare their rates of a certain outcome in the future. 

For example, let’s say we want to figure out if there’s a relationship between smoking cigarettes and developing lung cancer. 

To do this, we could follow 100,000 individuals that smoke cigarettes, the exposed group, and 100,000 individuals that don’t smoke cigarettes, the non-exposed group, for ten years. 

After ten years, let’s say that 82 of the 100,000 people - 0.082% - who smoked developed lung cancer, and only 3 of the 100,000 people - 0.003% - who didn’t smoke developed lung cancer. 

We can then compare the groups by dividing the probability of lung cancer for people who smoked - 0.00082 - by the probability of lung cancer for people who didn’t smoke - 0.00003 - and determine that people that smoked had 27 times the risk of developing lung cancer during that ten period. 

As it turns out, smoking is the number one risk factor of most types of lung cancer, and people who smoke are 15 to 30 times more likely to develop lung cancer than people who don’t smoke.

Now, there are two main types of cohort studies. 

The first type is called prospective cohort or concurrent cohort, because individuals are followed forward in time. 

An example would be if in 2018 a group of smokers and a group of non-smokers are recruited for the study. 

Then the two groups are followed for ten years, until 2028, and the number of people who develop lung cancer is co]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amino_acids_and_protein_folding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QBIjwoeGSs6VcLr9sw6CIzwnTsit1A0s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amino acids and protein folding]]></video:title><video:description><![CDATA[Proteins are vital for the normal function of a cell.

Essentially, a protein is, at its simplest, a very long chain of individual units, called amino acids, bound to each other by peptide bonds to form an amino acid chain. 

They sorta resemble a string of beads, and they get twisted and folded into a final protein shape. 

To make a protein, we need to get to know two things - the “ingredients”, which are the amino acids, and the “recipe” - or how the finished amino acid chain folds into the protein.

Humans use 20 amino acids in our day-to-day protein making. 

Let’s get to know them a bit better. So, we have: alanine (Ala), arginine (Arg), asparagine (Asn), aspartic acid (Asp), cysteine (Cys), glutamic acid (Glu), glutamine (Gln), glycine (Gly), histidine (His), isoleucine (Ile), leucine (Leu), lysine (Lys), methionine (Met), phenylalanine (Phe), proline (Pro), serine (Ser), threonine (Thr), tryptophan (Trp), tyrosine (Tyr), valine (Val). Phew, that’s 20. 

One way to divide them, is into the ones that we make ourselves, and the ones that we cannot. 

There are 5 amino acids that are dispensable - alanine, aspartic acid, asparagine, glutamic acid, and serine - because we can make them de novo ourselves at any time, and in good quantity.

Then, there’s 6 of them that we call conditionally essential because we can make them most of the time, but not always - arginine, cysteine, glutamine, glycine, proline, and tyrosine.  

Finally, there are 9 of them that we cannot make ourselves - His, Ile, Leu, Lys, Met, Phe, Thr, Trp, and Val, and as a result we have to obtain them from our diet. We call these the essential amino acids. 

Okay, so, the amino acid. Just from the name, you can tell they’ve got an amine group, or “NH2”, and also an acid, in this case a carboxylic acid group “COOH”. 

The amine and carboxylic acid groups are both bound to the same carbon, called the alpha carbon. 

Now, at a physiologic pH of 7.4, the amine group has a positive electrica]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticoagulants:_Warfarin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ed8SJHVGQIyT6fyE3H-8_S75T4KFC-00/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticoagulants: Warfarin]]></video:title><video:description><![CDATA[Anticoagulant medications are used to prevent blood clots from forming. These medications work by interfering with the normal function of plasma proteins called coagulation factors, which take part in secondary hemostasis. But let’s focus specifically on the anticoagulant warfarin, which works by preventing the synthesis of coagulation factors II, VII, IX and X, and anticoagulation proteins C and S. Now, to understand the regulation of clot formation we first need to talk briefly about hemostasis-- in which hemo refers to the blood, and stasis means to halt or stop. Hemostasis is divided into two phases: primary and secondary hemostasis. 

Primary hemostasis involves the formation of a platelet plug around the site of an injured blood vessel, and secondary hemostasis  reinforces the platelet plug with the creation of a protein mesh called fibrin. To get to fibrin, a set of coagulation factors each of which or enzymes need to be activated. These enzymes are activated via a process called proteolysis- which is where a portion of the protein is clipped off. In total, there are twelve coagulation factors numbered factors I-XII, but there’s no factor VI.  Most of these factors are produced by liver cells, and it turns out that producing coagulation factors II, VII, IX, and X requires an enzyme that uses vitamin K. 

Now, when vitamin K is absorbed from the digestive tract and travels to the liver, it’s in its dietary form and it’s called vitamin K quinone. An enzyme, called quinone reductase, takes electrons from NADPH, and donates them to vitamin K quinone, converting it into the reduced form which is called vitamin K hydroquinone. Then, vitamin K hydroquinone acts as a cofactor by donating its electrons to an enzyme called gamma glutamyl carboxylase, which converts the non-functional forms of coagulation factors II, VII, IX, and X into their functional forms. Gamma glutamyl carboxylase adds a carboxyl group, which is a chemical group made up of one carbo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heart_failure:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pGOshllbTzmb9esjat6We3iOSpyQmjIR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heart failure: Clinical]]></video:title><video:description><![CDATA[Heart failure is when the heart can’t supply enough blood to meet the body’s demands. 

A variety of heart diseases like ischemia and valvular disease can impair the heart’s ability to pump out blood, and over time can lead to heart failure.

This can happen in two ways, either the heart’s ventricles can’t pump blood hard enough during systole, called systolic heart failure, or not enough blood fills into the ventricles during diastole, called diastolic heart failure. 

In both cases, blood backs up, causing congestion or fluid buildup, which is why it’s also often called congestive heart failure.

All right, so the heart needs to squeeze out a certain volume of blood each minute, called cardiac output, which is the heart rate - or the number of beats in a minute - multiplied by the stroke volume – or the volume of blood squeezed out with each heartbeat.

Then the ejection fraction is the portion of blood that’s pumped out of the left ventricle- in other words the stroke volume divided by the total left ventricular volume.

The ejection fraction is normally around 50 to 70%, between 40 to 50% is borderline, and anything below 40% is systolic heart failure or heart failure with reduced ejection fraction.

There’s also diastolic heart failure, or heart failure with preserved ejection fraction.

That’s where the heart has very thick ventricular walls so that the chamber doesn’t get an adequate load of blood, so the heart is squeezing hard enough but not filling up enough. 

In this case, the stroke volume is low, but the ejection fraction is normal.

All right, so heart failure can affect the right ventricle, the left ventricle, or both ventricles, so biventricular heart failure, which defines where the failure is happening - and then there’s systolic or diastolic failure, which defines why the failure is happening. 

With left ventricular or left sided heart failure, blood gets backed up into the lungs, and that causes pulmonary hypertension and pulmonary ed]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypoplastic_left_heart_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5t98vHmdRvSO7bdmLgAf0RUwT6eytMza/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypoplastic left heart syndrome]]></video:title><video:description><![CDATA[Hypo means “beneath” or “under,” and plasia means “molding” or “formation,” so hypoplastic means “under form” or in this case, “underdeveloped.” Therefore, hypoplastic left heart syndrome means that the left side of the heart doesn’t fully develop. 

Hypoplastic left heart syndrome, or HLHS, is a congenital heart defect that affects the left side of the heart; it specifically affects the left ventricle and ascending aorta. Also, the aortic valve and mitral valve might be either too small to allow enough blood to flow through, or they might be absent altogether, which is called atresia. The exact mechanism that causes HLHS isn’t known, but one popular theory is that there might be some other primary congenital heart defect that reduces the blood flow through the LV and outflow tract during fetal development, so that part of the heart does not grow and develop normally. This said, HLHS is also often associated with other congenital heart defects, and in particular, with an atrial septal defect, which is an opening between the left and right atria. In fact, not only do these babies usually have this defect, they essentially need it to survive after birth. This is in addition to a patent ductus arteriosus, or PDA, a blood vessel that connects the aorta to the pulmonary artery, which usually closes within a few days after birth. 

Let’s switch to a more simplified version of the heart to see what happens with blood flow. So, right here you have the atrial septal defect connecting the left and right atria, and the ductus arteriosus, which connects the aorta to the pulmonary artery. This is a really underdeveloped left ventricle and a smallish aortic and mitral valve. 

All right, so now let’s take out this septal defect and PDA. What happens? Well, deoxygenated blood comes from the body and goes into the right atrium, then goes to the right ventricle, gets pumped to the lungs, and then oxygenated blood comes back to the left atrium. At this point, blood has a su]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cerebellum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/77nyyoo0RD274JjOYdiyuZ56S7Ov6II9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cerebellum]]></video:title><video:description><![CDATA[Cerebellum literally means little brain - and it looks like a miniature version of the brain, or cerebrum. 

The cerebellum coordinates movements, controls posture, balance and fine motor movement, and is involved in motor learning - like learning how to ride a bicycle.

The cerebellum sits in the posterior part of the skull called the posterior cranial fossa. 

Above it are the occipital and temporal lobes of the brain. It’s separated from the brain by a fibrous membrane called the tentorium cerebelli - a fold of dura matter which is one of the layers called meninges that covers the brain and spinal cord. 

The cerebellum lies posterior to the brainstem and is attached to it by a stalk of tissue divided into three parts - the superior, middle, and inferior peduncles. 

These peduncles contain nerve axons going back and forth between the cerebellum and the brain, the internal ear, and the spinal cord via the brainstem. 

The cerebellum consists of two hemispheres separated by a narrow, ridge in the middle called the vermis. 

Now if we look at a cross-section, we can see three lobes. 

We have the anterior lobe superiorly, and it is separated from the posterior lobe by the primary fissure. 

At the tip of the posterior lobe is a very tiny lobe called the flocculonodular lobe and these two are separated by the posterolateral fissure.  

The outer layer of the cerebellum is called the cortex and it’s folded into many tiny wrinkles called folia. These are much smaller than the wrinkles found on the cerebrum, and this allows it to have a larger surface area when unfolded even though it occupies only 10% of the brain volume. 

The cortex of the cerebellum consists of three layers: The innermost, granular layer which contains the cell bodies of the granular cells, the Purkinje layer which contains the cell bodies of the Purkinje cells, and the molecular layer were various neurons synapse with each other. 

Under the cortex, lies the white matter, also referred t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacodynamics:_Drug-receptor_interactions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SuDxkPqhTQeGk77QhsGo_vF9Ra2RmFP4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacodynamics: Drug-receptor interactions]]></video:title><video:description><![CDATA[Pharmacodynamics refers to the mechanisms and effects of medications within the body. Or more simply, it’s what medications do to the body and how they do it.

In order to have an effect, most medications have to reach their target cells and bind to a receptor. Receptors are specialized proteins both inside the cell and on the cell membrane that can bind to a ligand and get triggered to alter their shape or activity. This gives rise to a signal cascade of intracellular molecules, known as the second messengers, which, ultimately, results in some change in the cell’s function. 

Intracellular receptors are typically located in the cytoplasm or nucleus of the cell and recognize small, hydrophobic, meaning water- hating,  ligands. These include molecules like steroids, which are happy to diffuse across the phospholipid membrane. Once bound to their ligand, the receptor- ligand complex attaches to specific DNA sequences that activate or inhibit specific genes.  

On the cell membrane are cell-surface receptors, which are embedded into the plasma membrane and bind to ligands too large or hydrophilic to pass through. Based on their structure and properties, cell- surface receptors fall into three main types: ligand-gated ion channels, enzyme coupled receptors, and G-protein coupled receptors.

Starting with ligand-gated ion channels, also known as the ionotropic receptors, these form channels or pores that are generally closed. Once they bind a specific ligand, they open up and allow ions like chloride, calcium, sodium, and potassium to passively flow through the membrane, down their gradient, and trigger the signaling pathway.

Next are enzyme-coupled receptors, which are usually single-pass transmembrane proteins, meaning that they have only one transmembrane segment.  The extracellular end of these receptors binds to medications, and their intracellular end has enzyme activity. The enzymatic domain is usually a protein kinase known as the tyrosine kinase, whi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pentose_phosphate_pathway</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pufgCMHUR-2NZtuGeNcyWMEoQs6c2Y35/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pentose phosphate pathway]]></video:title><video:description><![CDATA[Let’s say you just ate a carbohydrate loaded meal, like a bowl of rice. 

A few hours after you’re done, those carbohydrates are broken down in the small intestine into their simplest chemical form; monosaccharides, the most important of which is glucose - a 6-carbon molecule that’s in the shape of a ring. 

Glucose moves from the small intestine into the bloodstream, and blood glucose levels rise, which causes the pancreas to secretes a hormone called insulin. 

Insulin makes more glucose enter cells through specific transporters called GLUTs. 

Once glucose is in the cell, an enzyme called hexokinase attaches a phosphate group to its sixth carbon, creating glucose-6-phosphate. 

From there, the cell has the option to take glucose through a metabolic pathway called glycolysis; which is the breakdown of glucose in order to generate ATP. 

But if the cell doesn’t need ATP, glucose can be used to make some other useful products by entering an alternative metabolic pathway called the pentose phosphate pathway. 

The pentose phosphate pathway is named for the products it ultimately generates; pentose refers to a five-carbon sugar called ribose, and phosphate refers to a molecule called nicotinamide adenine dinucleotide phosphate, or NADPH. 

So the pentose phosphate pathway is an alternative pathway that glucose can enter when cells need to make more ribose and NADPH. 

Ribose can be used to make nucleotides, which are the building blocks of our DNA and RNA. 

And NADPH is rich in electrons, and can be used in various anabolic pathways. 

Anabolic pathways are ones that synthesize molecules like fatty acids, from scratch, and require an electron donor - such as NADPH. 

Like glycolysis, the pentose phosphate pathway happens exclusively in the cytoplasm and it doesn’t require any special organelles which means that all of our cells can use this pathway.

The pentose phosphate pathway can be divided into two phases: an irreversible oxidative phase that ultimatel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Selective_immunoglobulin_A_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8arDIvjyR-6TuTgMpn5UzEa7SR_Mq8kS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Selective immunoglobulin A deficiency]]></video:title><video:description><![CDATA[Selective immunoglobulin A deficiency is a condition where there’s a lack of immunoglobulin or antibody A, called IgA for short. It’s called “selective” because all the other antibody classes, IgM, IgG, IgE and IgD are produced normally. IgA is in charge of protecting the mucosal surfaces of the body against foreign invaders, so without it, there’s a higher risk of mucosal infections.

Now, B cells make antibodies, and normally, B cells are “born” in the bone marrow, which is the spongy tissue inside some bones of the body. This is where they develop their B cell receptors on their surface which eventually can get released - and when they’re freely floating in the blood they’re called antibodies.

Antibodies are Y- shaped protein molecules, formed by two heavy and two light chains, each of which has a variable region, at one end, and a constant region (C region) at the other end. Variable regions are unique to each B cell and they are designed to bind to a very specific antigen, whereas C regions determine the antibody class.

Initially all of the B cells have IgM and IgD class antibodies on their surface, with each B cell recognizing and binding to its own unique antigen. Mature B cells leave the bone marrow and migrate to peripheral lymphoid organs, like the spleen, lymph nodes or mucosa-associated lymphoid tissue, which is also called MALT. 

MALT is composed of clusters of lymphoid tissue scattered under the mucous membranes lining the mouth, airways, and digestive tract. This is a really strategic position, because a variety of antigens are constantly being picked up and filtered from these body tissues. As a result, B cells are likely to encounter an antigen they recognize. A bit like spending time at a train station during rush hour to look for someone that catches your eye.

If two of a B cell’s receptors bind to the same antigen, they can cross-link - meaning that two adjacent receptors on the B cell surface can get pulled close together. When tha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_biostatistics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0S5vn6j-Q-uOi42sJy1ZqkgoR2SQnjom/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to biostatistics]]></video:title><video:description><![CDATA[Let’s say you want to figure out if people with high body mass index, or BMI, are at a higher risk of hypertension - or high blood pressure. 

Let’s say that you decide to go out and find 100 people with hypertension and 100 people without hypertension and find out the BMI of each person in each group. 

You might also collect other information about the individuals in each group, like how old they are, if they smoke cigarettes, or if they drink alcohol, since all of these factors can influence a person’s risk of hypertension. 

All of these different pieces of information - called variables - can be put together into a single document or file, called a data set.

A data set usually includes independent variables which are thought to influence or change dependent variables.

In our example, the body mass index would be the independent variable and hypertension would be the dependent variable.

The process of collecting, organizing, and analyzing variables in a data set is called statistics, and when the data were collected from living things - like humans, aardvarks, algae, or bacteria - it’s called biostatistics, bio meaning life. 

Now, there are two main types of biostatistics.

The first type is descriptive statistics, which is used to describe or summarize information about each individual variable in the data set. 

Descriptive statistics can be used to find the mean - the average number calculated from a particular variable, the median - the middle number in a variable, and the mode - the number that occurs the most in the variable.

The descriptive statistics of each variable can be calculated for the whole sample - all 200 people - or in each group separately - the 100 people in the group with hypertension or the other 100 people in the group without hypertension. 

For example, we might find that the mean body mass index of all people in the study is 24.5, or that the mean body mass index is 28 for the group with hypertension and 21 for the group]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kawasaki_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZvWb7OcxS3ut2IGrSOT02t_eQ06pTjZr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kawasaki disease]]></video:title><video:description><![CDATA[Kawasaki disease isn’t at all related to the motorcycle and engine company, other than the fact that they were both founded or first described in Japan. Kawasaki disease is a vasculitis or an inflammation of the blood vessels, that mostly affects the coronary arteries but can also affect any large- or medium-sized arteries as well. With Kawasaki disease, the immune system attacks the arteries. Ultimately, it’s not quite known why this happens though, some theories suggest it has some infectious cause, though autoimmune reactions and genetic predisposition probably play a part as well.

Whatever the case, when the endothelial cells in the blood vessels are attacked, they become damaged which exposes the underlying collagen and tissue factor found in the middle layer of the blood vessel, or the tunica media.

And this leads to a few serious problems: First, these exposed materials increase the chance of blood coagulation. When blood coagulates it forms clots that can block blood flow in the coronary arteries, leading to ischemia of the heart muscle.

Secondly, damaged endothelial cells in coronary arteries mean weak artery walls, which can lead to coronary aneurysms. These aneurysms form because fibrin is deposited into the blood vessel wall as part of the healing process. Fibrin makes the vessel stiffer, less elastic, and unable to gently stretch with high arterial pressures; instead, the arteries develop permanent bulges that we call aneurysms. Aneurysms 8mm or larger are at the most risk of rupturing, which reduces blood flow to the heart, causing ischemia and potentially myocardial infarction, or heart attack. 

And third, in some cases, the fibrosis doesn’t lead to aneurysms, but instead, the fibrosis of the blood vessel walls make the vessel walls thicker, which reduces the lumen diameter and restricts blood flow. If blood flow’s restricted or reduced, the heart again might become ischemic, leading to a heart attack.

Kawasaki disease is most commonly ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Wiskott-Aldrich_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YhFgu27YSmiOf5WATTcJKJemQq6XVHNS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Wiskott-Aldrich syndrome]]></video:title><video:description><![CDATA[Wiskott-Aldrich syndrome is also called eczema-thrombocytopenia-immunodeficiency syndrome. 

So, one by one, there’s eczema, also called atopic dermatitis, which is characterized by dry red patches arising on the skin. 

There’s a type of thrombocytopenia called microthrombocytopenia because not only are there very few platelets, but the platelets are also small in size. 

And there’s a problem with the immune system that leads to repeated infections.

All of the hematopoietic cells, which are cells in the bone marrow, produce Wiskott-Aldrich syndrome protein, or WASp for short.

There’s also a gene - called the WIPF1 gene, which encodes a protein called WAS/WASL-interacting protein family member 1, which helps stabilize Wiskott-Aldrich protein. 

So WASp, aside from having a really long name that shortens down to the name of a scary flying insect - helps to reorganize the cell’s cytoskeleton, and therefore its overall shape. 

The cytoskeleton can change by either adding to or removing actin proteins from the end of an actin chain. 

The chain grows longer in the direction that a cell wants to move and shortens on the side that a cell wants to move away from. 

This helps with various cellular activities like phagocytosis and cellular division. 

Platelets specifically rely on this functionality, because they originate from large precursor cells called megakaryocytes. 

This megakaryocyte has many long arms - like a squid - and the cytoskeleton changes shape so that these arms can detach to form cellular fragments called platelets. 

The platelets then go off to form clots at damaged sites in the blood vessels, to stop bleeding. 

Another cell type are the T-cells, which are a type of immune cell, also rely on the cytoskeleton being able to change shape.

When they encounter a pathogen, T-cells form pseudopods or false legs that reach out and synapse or communicate with other cells. 

Think of it like they’re shaking hands to exchange information.

Helper]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sample_size</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8ZX1S7KJTfW3I8FiHzRU4JxaT5_95tj0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sample size]]></video:title><video:description><![CDATA[Typically, the goal of a study is to explore the relationship between an exposure and an outcome in a target population.

For example, let’s say we want to find out if Medication A, can lower blood pressure better than Medication B, which is the current treatment, in people with hypertension - or high blood pressure - who live in Perth, Australia.

But the population of Perth is around 2 million people, and almost a third of the population has hypertension, so that makes our target population nearly 670 thousand people.

It would take way too much money and time to include them all in the study, so instead, we have to select just a sample of them - which becomes our sample population. 

And the sample population should be selected by randomization, so that we have a high chance of including people of ages, races, and socioeconomic statuses that reflect the target population.

But how many people do we choose? 

Choosing too many costs more time and money, and choosing too few means that they may not adequately represent the target population. 

For example, let’s say we choose 20 people as our sample population for our study, 10 are given Medication A and 10 are given Medication B, and we check their blood pressures after five years. 

In the Medication A group, 5 people have a lower blood pressure, and in the Medication B group, 2 people have a lower blood pressure. 

This gives us an overall relative risk of 2.5, meaning that Medication A is 2.5 times more effective than Medication B in the sample population. 

But that doesn’t necessarily mean that Medication A will be 2.5 times more effective among all of the hypertensive people in Perth. 

For example, maybe the sample contained all women, and Medication A happens to work really well just in women - in which case we may be overestimating this effect.

Or what if it works really well in women, but even better in men - in which case we’re underestimating the effect. 

To figure out the perfect sample si]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Selection_bias</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vUbWUzbyS1uK6d1B3_oktoHqSdC0T2RR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Selection bias]]></video:title><video:description><![CDATA[Selection bias is a type of bias or error that can occur when researchers choose who will be included in a study. 

Studies with selection bias might end up having results that can’t be applied to the population outside the study - so lacking external validity. 

They may also result in an inaccurate representation of the relationship between an exposure and an outcome - so lacking internal validity.  

Typically, the goal of a study is to figure out if an exposure is associated with an outcome in a target population. 

So ideally a study should be done on a sample population of individuals that is similar to that target population in every meaningful way, which would give the study high external validity. 

For example, if you want to figure out how smoking impacts the risk of lung cancer in Portland, Oregon, then people living in Portland are your target population. 

Ideally, your sample population would include individuals from Portland. 

And in addition, the sample population should include people of ages, races, and socioeconomic statuses that reflect the target population as well, because these are all factors that are likely to affect the risk of lung cancer. 

If your study only recruits students from one of the local high schools, then your sample population probably won’t represent your target population, since the average age in your study will be younger than the average age in Portland, which is 36 years old.

Now, to make the sample population represent the target population, one tool that can be used is randomization, meaning that individuals get selected to enter the study through a process of chance.

To show how that works, let’s say the researchers put the names of every person in Portland into a brown paper bag, which would have to be pretty big, since there would be over 600,000 names in that bag - probably with a number of repeats.

Then let’s say that you choose a thousand names out of the bag to include in the study - either by si]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mitosis_and_meiosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rzgiKvYpQGiqVA--sVhBnS3jRMGgRoam/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mitosis and meiosis]]></video:title><video:description><![CDATA[Pretty much everything alive - from a humble bacteria, to a baby blue whale, has two main goals - to grow and to reproduce. 

Our cells are no different. They grow and they reproduce. 

But the reproduction part can be done in two distinct ways - mitosis, or meiosis. 

Mitosis gives rise to daughter cells that are almost identical to the parent cell in terms of their genetic information. 

Whereas in meiosis the daughter cells or gametes, sperm in males and eggs in females, get only half of the genetic information of the parent cell. 

These gametes can then pair with completely different gametes to form a cell that’s quite different from the parent cell. 

This newly formed cell can then do mitosis to form an entirely new organism.

Mitosis is one part of the cell cycle. 

Most of the cell cycle is taken by interphase - which is usual cellular day-to-day activities, including growth, protein synthesis, making new organelles, and so on. 

Interphase has three phases: G1, S and G2.

The first phase is called G1. 

During G1, the cell gets bigger in preparation for cell division. 

At this point the 46 chromosomes look like spaghetti and are called chromatin fibers. 

Each chromatin fiber is made of a single copy of the genetic material - called a chromatid. 

The second phase is the S phase. 

During S phase, each chromatid is copied and pasted so there are still 46 chromosomes, but each chromosomes now has two sister chromatids. 

The two chromatids are joined together in a region called the centromere - adding up to 92 chromatids total. 

The third phase is G2. 

During G2, the cell does some more growing before finally entering mitosis. 

Some cells, like neurons, enter what’s called the G0 phase - where they basically continue to live but don’t divide. 

But most cells do enter mitosis after G2, and mitosis can be divided into four distinct phases: prophase, metaphase, anaphase, and telophase - and you can remember them as PMAT - a mat that you pee on. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Auditory_transduction_and_pathways</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V7zXM2q_SWm7n3UeM9sLKlkVS3iTVOIN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Auditory transduction and pathways]]></video:title><video:description><![CDATA[In auditory transduction, auditory refers to hearing, and transduction is the process by which the ear converts sound waves into electric impulses and sends them to the brain so we can interpret them as sound. And the ear itself is made up of three parts: the outer ear, the middle ear and the inner ear, and all three play a role in hearing.

You can think of the ear like a house, with a porch, a living room and a short corridor that leads to two bedrooms at the end. The porch would be the outer ear, made up of the pinna and the external auditory canal. The middle and inner ear, would be the actual “house”, carved inside the temporal bone. The middle ear is like a living room, furnished with the tiny ear bones - called the malleus, incus, and stapes - that articulate or touch one another. The inner ear is the rest of the house, made up of a corridor and two rooms -  where the corridor is the vestibule, and the two rooms are: the cochlea, which is anterior to the vestibule - so towards the front of our head -  and the semicircular canals - posterior to the vestibule, so towards the back.

Now, the outer, middle and inner ear are functionally connected to one another, which is crucial for hearing. Between the outer and middle ear there is the tympanic membrane - or eardrum - and between the middle and inner ear there are two windows: the oval window, above, and the round window, below. So, when you hear the wind rustling through the leaves, the resulting sound waves are directed by the pinna into the external auditory canal, and they reach the eardrum, making it vibrate. The malleus is attached to the eardrum, so the vibrations are transmitted along the tiny bones - from the malleus to the incus, and then from the incus to the stapes. The foot of the stapes rests on the oval window - and since the oval window is about 20 times smaller than the eardrum, the sound waves are amplified as they vibrate their way across the tiny bones. From the oval window, the vib]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ecologic_study</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XFJGsqb7QSWGfbdI14GCv8CoRF2awLLS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ecologic study]]></video:title><video:description><![CDATA[An ecological study is a study design that uses group-level or aggregate-level data to figure out if there is a potential association between two variables. 

For example, let’s say you want to figure out if women that eat more fat have a higher risk of breast cancer. 

Perhaps you have information about the average dietary fat intake per capita as well as breast cancer rates in 10 different countries. 

You could plot this information on a graph with dietary fat intake on the x-axis and yearly incidence of breast cancer - which is the number of new cases of breast cancer in a year, per 100,000 women - on the y-axis. 

In Japan, the dietary fat intake per capita is around 650 calories, and the incidence of breast cancer is 50 cases per 100,000 women. 

On the flip side, in the United States the dietary fat intake per capita is around 1400 calories, and the incidence of breast cancer is 235 cases per 100,000 women. 

The rest of the countries - Switzerland, Denmark, France, Norway, Australia, Spain, Hong Kong, and Romania - have an average fat intake and breast cancer rates somewhere between Japan and the U.S. 

Generally, we can see that the more fat a country consumes, the higher the rate of breast cancer is for that country, and at this point we might conclude that eating more fat leads to breast cancer. 

The problem with this conclusion is that we only have information from the whole country, and we don’t have information about each individual within that country. 

In fact, we might get very different results from a study that uses individual-level data!

For example, let’s say you conduct a cohort study using individual-level data from all 10 countries. 

Cohort studies look at individuals in a group who have a certain exposure, as well as individuals in a cohort who have not had that exposure, to compare their rates of a certain outcome in the future. 

So, you could follow 500,000 individuals that have a high fat diet, the exposed group, and 500,00]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DNA_replication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mFQ0XlTwSXiI5J1V-xfk6kHCSzy2fyFK/_.jpg</video:thumbnail_loc><video:title><![CDATA[DNA replication]]></video:title><video:description><![CDATA[At a quick glance, the life of a cell - it’s cell cycle - is pretty routine.

It’s either actively dividing, or preparing to divide into two daughter cells. 

The cell cycle itself has an interphase, made up of subphases G1, S and G2, during which the cell is preparing for division, and mitosis, during which the cell actively divides. 

During the S phase, the cell performs DNA replication - which is when its 46 chromosomes are duplicated so that each daughter cell can get its own copy of the genetic material.  

A single chromosome is made up a single DNA molecule that has two strands, which wrap one around one another to form a double helix.

Each single strand of DNA is composed of a sequence of four types of nucleotides - which are the individual letters or building blocks of DNA.

Nucleotides of DNA are made up of a sugar - deoxyribose, a phosphate, and one of the four nucleobases - adenine, cytosine, guanine, and thymine - or, commonly, A, C, G, T for short. 

The nucleotides on one strand form hydrogen bonds to complementary nucleotides on the other strand; specifically, A bonds with T via two hydrogen bonds, and C bonds with G, via three hydrogen bonds. 

Additionally, the two DNA strands also have a “direction” - meaning, one of them runs from the 3’ end to the 5’ end, while the other one runs from the 5’ end to the 3’ end. 

Kinda like two snakes coiled up together, but facing in different directions. 

DNA replication can be described as semiconservative. 

That means that each strand of the double helix acts as a “template”, based on which a new, complementary strand will form. 

Eventually the original chromosome will split into two exact copies, each made of one of original strands, and one of the newly made ones. 

Overall, DNA replication has 3 steps: initiation, elongation, and termination.

Initiation kicks off when a group of proteins get together to form the pre-replication complex.

This pre-replication complex looks for specific nucle]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prostate_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hZdLy4DRRaOj-Zkum91gRxY6R2_Y4Su_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prostate cancer]]></video:title><video:description><![CDATA[Prostate cancer, usually refers to prostate adenocarcinoma, where adeno- means gland and carcinoma refers to uncontrolled growth of cells - so prostate cancer is a tumor or growth that originates in the prostate gland. 

Only males are born with a prostate, so this condition only affects males and not females. 

Typically, when there’s a prostate cancer it’s considered malignant, meaning that the tumor cells can metastasize, or invade and destroy surrounding tissues as well as tissues throughout the body.

The prostate is a small gland, about the size and shape of a walnut, that sits under the bladder and in front of the rectum. 

The urethra which is the tube through which urine leaves the bladder, goes through the prostate before reaching the penis. 

And that part of the urethra is called the prostatic urethra. 

The prostate is covered by a capsule of tough connective tissue and smooth muscle.

Beneath this layer, the prostate can be divided into a few zones.  

The peripheral zone, which is the outermost posterior section, is the largest of the zone and contain about 70% of the prostate’s glandular tissue. 

Moving inward, the next section is the central zone which contains about 25% of the glandular tissue as well as the ejaculatory ducts that join with the prostatic urethra. 

Last, is the transitional zone, which contains around 5% of the glandular tissue as well as a portion of the prostatic urethra. 

The transitional zone gets its name because it contains transitional cells which are also found in the bladder. 

The transitional zone undergoes hyperplasia, or an increase in the number of cells, in a large percentage of older men, and that often leads to compression of the urethra. 

This is called benign prostatic hyperplasia and is often considered a normal part of aging.  

At the microscopic level, each of the tiny glands that make up the prostate is surrounded by a basement membrane made largely of collagen. 

Sitting within that basement me]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Interleaved_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qPmWrijoQJuS5eBWHvvOa6QUQ4KRYU1V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Interleaved practice]]></video:title><video:description><![CDATA[Interleaving is a study strategy where you mix up the order of the topics that you’re studying, instead of reviewing them in blocks.

For example, let’s say you have an exam coming up and you want to make a study schedule to help you make the best use of your time. 

One approach is called blocking or massed practice, that’s where you set aside big blocks of time dedicated to each topic you’re studying. 

Like spending time studying for topic A, then topic B, before moving on to topic C. 

In other words, you practice a topic until you achieve proficiency or comfort and then you move onto the next one. 

It sort of looks like this:

[AAA] [BBB] [CCC]  

But research shows that the best way to learn material is to actually mix, or interleave, your studying. 

So, if you want to learn concepts A, B, and C, then you should mix up what you’re studying, so that it looks like this:

[ABC] [ABC] [ABC]

So if you’re reviewing the various classes of medications that treat hypertension. 

Instead of reviewing all of the ACE-inhibitors, followed by the diuretics, followed by calcium channel blockers, you should mix things up. 

If you spend a bit of time reviewing ACE-inhibitors, then calcium channel blockers, then back to ACE-inhibitors again, then go to diuretics, then back to calcium channel blockers, then back to diuretics - you’ll learn faster and remember it for longer. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Contracting_the_immune_response_and_peripheral_tolerance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SRIfweGcSxiwXi02dLYFSiJPSxqAF8Yd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Contracting the immune response and peripheral tolerance]]></video:title><video:description><![CDATA[The adaptive immune system, specifically the T- and B-cells, is the part of the immune system that is immunologically tolerant or unresponsive to self-antigens. Immunological tolerance can develop through two mechanisms- central and peripheral. Central tolerance mechanisms eliminate self-reactive lymphocytes during their initial development in the bone marrow and thymus. Peripheral tolerance mechanisms eliminate self-reactive lymphocytes that escape the radar of central mechanisms; in the peripheral tissues and secondary lymphoid organs. Failure of these mechanisms can result in autoimmune diseases like systemic lupus erythematosus.

The major peripheral tolerance mechanisms include T regulatory cells, clonal anergy, and peripheral deletion.

Now, the immune response is like a community of cells that fight together. Antigen-presenting cells, like dendritic cells, pick up antigens floating around in the body and serve them to naive T-cells, partially stimulating their activation. When the antigen is foreign, it strongly induces the expression of co-stimulatory proteins like the B7 on the antigen-presenting cell surface. B7 binds to the CD28 receptor on the naive T-cell and provides the additional stimulation needed to completely activate them, and also helps in their differentiation into specific types like effector or memory T-cells. 

The CD4+ helper T cells are one of the most important immune cells. They secrete cytokines and provide signals that promote B-cell differentiation into plasma cells, class switching, and antibody production. CD4+ helper T cells also secrete cytokines that recruit phagocytes and help them kill more effectively. That’s why many of the peripheral tolerance mechanisms are aimed at shutting down CD4+ helper T cells. 

Let’s start with T regulatory cells, which are able to inhibit the responses of all other immune cells. It’s thought that when a T cell responds a little too strongly to a self-antigen but not strong enough to be ki]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polymyalgia_rheumatica</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A8pgBfhXSCiUrZHHXGbLPoVHQHeBTyZx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polymyalgia rheumatica]]></video:title><video:description><![CDATA[With polymyalgia rheumatica, “poly-“ means many, “mya-” means muscles, and “-algia” means pain.

“Rheumatica” comes from rheumatism, which broadly refers to conditions that affect the joints and connective tissue.

So, polymyalgia rheumatica is a disorder that causes muscle pain and joint stiffness.

It is considered to be an immune- mediated disease, meaning that the immune system attacks our own body.

It is important to note that although “myalgia” means muscle pain, the muscles are usually spared and it&amp;#39;s the tissue around the joints that mostly gets inflamed.

Normally, the cells of the immune system are always hanging around, ready and excited to spot and fight against anything foreign that could cause harm inside the body.

One particular type of immune cell - the dendritic cell - is a type of antigen-presenting cell, meaning that it grabs a pathogen for example a bacteria, destroys it, and presents a part of that bacteria, called an antigen, to other immune cells.

Dendritic cells take their name from the fact that they have branch like arms called dendrites which help them grab antigen.

Dendritic cells take their captured antigen and move over to a nearby lymph node, where they present the antigen to a helper T-cell.

Dendritic cells “present” the antigen on a protein called a major histocompatibility complex, or MHC, class II molecule which is on their cell surface.

MHC class II molecules are like a serving platter, which hold the antigen as it gets presented to the helper T-cells.

Once these antigens are recognized as foreign, T-helper cells get activated and start secreting a lot of proinflammatory cytokines, or signalling molecules, that recruit more immune cells, such as macrophages, to the site of inflammation.

At the same time, other cytokines, called interleukins, trigger B-cells to secrete antibodies against the targeted antigens.

These antibodies block pathogens from causing harm, and also “tag” them so that other immune ce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adaptive_learning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ChHJ50pMQ6W7AabpK6Wm_VwKQWGQR52q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adaptive learning]]></video:title><video:description><![CDATA[Adaptive learning is where the material that a student receives, “adapts,” or changes, based on their individual performance, often in real-time. 

Adaptive learning is often automated and driven by technology. 

In medicine, this approach can help facilitate learning with real-world problems - like a clinical issue affecting a patient. 

To show how this works, let’s say there’s a medical student named Lindsay, who is part of a team of residents and nurses, and she’s taking care of a man who’s been in a car crash and has a serious head injury. 

Lindsay can learn an incredible amount from caring for this patient - everything from the specifics of the medical case to issues around teamwork and communication with his family. 

The first step for approaching this case is for Lindsay and her entire team to do a gap identification - to figure out what Lindsay already knows and to figure out where the gaps are. 

To do that, Lindsay has to answer key questions. Like, what do I know about head trauma? What is the family most concerned about? And what are the complications that I need to be aware of? 

Each of these questions could lead Lindsay in a different direction and could take her hours to read about - oftentimes leading to more questions - like going down the rabbit hole!  

But even if she doesn’t go out and answer every last one, just having a questioning attitude helps sharpen her mind and makes her a better clinician.

After making a list of questions, the next challenge is figuring out how to prioritize which ones to tackle. 

This is where Lindsay can use her best judgment and then get feedback from more senior folks on her team to get their guidance as well.

So, let’s assume that Lindsay does both of those things, and that she decides to learn more about or increased ICP, or intracranial pressure, - since that seems to be the main issue for her patient. 

At this point comes the planning phase. Lindsay now has to figure out which resources she wan]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Syringomyelia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cqSBI6OVRFucR9OWKSebk9knQsioodBe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Syringomyelia]]></video:title><video:description><![CDATA[In syringomyelia, syrinx means cyst or cavity, and myelia means a condition of the spinal cord. So, syringomyelia is a cystic enlargement of the spinal cord, and it typically starts medially and enlarges outwards, eventually damaging the spinothalamic tract, which is a part of the spinal cord that sends sensory signals about pain, pressure, temperature, and touch to the brain.

Now, the spinal cord itself is composed of both grey and white matter. Grey matter is found within medial portion of the spinal cord and is shaped like a butterfly. This is where the cell bodies of different neurons can be found. In the center of the grey matter there’s a small cavity the central canal which is filled with cerebrospinal fluid. Cerebrospinal fluid helps provide nutrients and mechanical support to the brain and spinal cord. Surrounding the grey matter is white matter, which consists of the axons of various neurons. The spinal cord has different neural tracts that carrying sensory information to and from the brain. The corticospinal tract is a descending pathway which carries motor information from the brain to various muscles. The dorsal column, located in the posterior portion of the spinal cord, is responsible for sensing pressure, vibration, fine touch, and proprioception, or the awareness of one’s body position in space. Then there’s the spinothalamic tract, which is divided into two distinct tracts - the lateral spinothalamic tract which is responsible for sensing pain, pressure, and temperature, as well as the anterior spinothalamic tract which senses crude touch. The spinothalamic tract carries all of this sensory information from the spine up to the thalamus of the brain where the information is processed. This happens through three neurons that synapse with one another. First, a primary neuron carries sensory information, such as pain, from the skin to the dorsal horn of the spinal cord, where it synapses with a secondary neuron. The secondary neuro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Odds_ratio</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gKpct4nuTyWCenAm--EjD9u6ToyF0ZRD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Odds ratio]]></video:title><video:description><![CDATA[In statistics, the words probability and odds are often confused with each other, because they help measure the same thing - the chance that an outcome will occur - and in both cases, we need to know the same two things - the number of times an outcome actually happened, or didn’t happen, and the total number of times an outcome could have happened. 

The probability is the number of times an outcome happened divided by the number of times the outcome could have happened, and is often represented by a capital P. 

For example, let’s say we want to figure out the probability of having a heart attack for people with hypertension - or high blood pressure.

To do this, we could carry out a cohort study which is where we start with two exposure groups and follow them over time to see if they develop a certain outcome. 

We could recruit 100 people with hypertension, The exposed group - and 100 people without hypertension - the non-exposed group - and organize our results in a 2 by 2 table, and keep track of how many of them have heart attacks in the next year. 

The two outcomes - heart attack or no heart attack - labeled on the top, and the two exposure groups - hypertension or no hypertension - on the side, and each of the cells inside the box labeled as a, b, c, or d. 

Now, let’s say there are 9 people that have heart attacks in the group with hypertension - cell a - and 3 people that have heart attacks in the group without hypertension - cell c.

That means that there are 100 minus 9, or 91, people that didn’t have heart attacks in the group with hypertension - cell b - and 100 minus 3, or 97, people that didn’t have heart attacks in the group without hypertension - cell d. 

To calculate the relative risk, we need the probability of having a heart attack in the group with hypertension - so cell a, 9, divided by cell a plus cell b or 100, which gives us 0.09. 

We also need the probability of having a heart attack in the group that doesn’t have hypertensio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Type_I_and_type_II_errors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GrjwFFA6QAuzT6otLpVVCVxNTRuCqJXL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Type I and type II errors]]></video:title><video:description><![CDATA[Let’s say that you’re trying to figure out if a certain medication, Medication A, lowers blood pressure better than the currently prescribed medication, Medication B. So you find 100 people with high blood pressure and give 50 of them Medication A and 50 of them Medication B, and after 6 months see which group has lower mean or average blood pressure. 

For this study we would make two hypotheses. 

The first hypothesis is called the null hypothesis, and it basically says there’s no difference between two variables that you care about. 

For example, our null hypothesis would state that there’s no difference between the mean blood pressure after the 6 month study period, for the group that takes Medication A compared to the mean blood pressure for the group that takes Medication B. 

In other words, that there’s no relationship between medication type and blood pressure. 

On the other hand, the alternate hypothesis would state that there is a difference between the mean blood pressure for the group that takes Medication A compared to the mean blood pressure for the group that takes Medication B. 

Again, in other words, that there is a relationship between medication type and blood pressure. 

In theory, there are four possible conclusions that can come from this study, and we can organize them in a 2 by 2 table, where the true relationship between medication and blood pressure is on top, and the study conclusions are on the side. 

When a study doesn’t see a relationship between medication and blood pressure, represented here as an arrow with a red cross, and there really isn’t one, then this is called a true negative.

When the study finds that there is a relationship, represented on our table by a green arrow, between medication and blood pressure, and there really is one, then this is a true positive. 

Similarly, when the study concludes that there is a relationship between medication and blood pressure but there really is no difference - this is a f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leukemia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lnuerepXSQu5RocWnrugIrgPS86tS7QJ/_.png</video:thumbnail_loc><video:title><![CDATA[Leukemia: Clinical]]></video:title><video:description><![CDATA[Leukemia is a cancer of bone marrow progenitor cells that spreads into the bloodstream, and it typically causes the white blood cell count to exceed 11 x 10^9 cells/liter. 

This is in contrast to lymphoma, which is a malignancy of white blood cells that arises from the lymph nodes. 

Leukemia can be classified based on cellular lineage - so it’s myeloid for granulocytes, which include basophils, eosinophils, neutrophils and mast cells, and lymphoid for lymphocytes, which include T-cells, B-cells, and natural killer cells. 

If the maturational process is blocked at an early stage of cell differentiation, so that the cancerous cells are immature blast cells with tiny nuclei and lots of cytoplasm, it’s called acute leukemia. 

If the block happens at a later stage, the cancerous cells are slightly more mature with large nuclei and little cytoplasm, and it’s called chronic leukemia.

Immature cells tend to be less capable of doing their intended job, so they often cause more problems then slightly more mature cells. 

Acute leukemia patients tend to have more symptoms like fatigue and bone pain, while, chronic leukemia patients are often asymptomatic and go unnoticed until a routine complete blood count or CBC is done, which often shows a white blood cell count that may be as high as 100 x 10^9 cells/liter.

So overall, there’s acute myeloid leukemia or AML, acute lymphoid leukemia or ALL, chronic myeloid leukemia or CML, and chronic lymphoid leukemia or CLL. 

If leukemia is suspected based on symptoms like frequent infections, easy bleeding, fatigue, and weight loss, then a workup typically includes a CBC, looking for high white blood cell count. 

If the majority of the white blood cells are neutrophils, the likely diagnosis is AML or CML. 

If the majority of cells are lymphocytes, then the likely diagnosis is CLL if chronic, and ALL if acute. 

Additionally, a peripheral blood smear is done to look for the malignant cells and their level of ma]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/tetralogy-of-fallot</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eSNG1WtISW2IApW2CKrY9XdGSjqjy5hA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tetralogy of Fallot]]></video:title><video:description><![CDATA[Tetralogy of Fallot or TOF is a congenital heart condition where patients have four heart abnormalities.

Okay so now let’s go through these four findings in TOF one-by-one. The first abnormality is stenosis, or narrowing of the right ventricular outflow tract into the pulmonary artery. And this could either be narrowing of the valve itself, or narrowing of the infundibulum, the area right below the valve. Either way, this makes it harder for deoxygenated blood to get to the pulmonary circulation.

In response—and this also happens to be the second feature—the myocardium of the right ventricle hypertrophies, or gets really thick, in order to contract harder and push blood past the stenosis.

This causes their heart to look “boot-shaped” on an x-ray.

The third feature is that patients have a large ventricular septal defect, this gap between the ventricles that allows shunting of blood between them. 

Now, in a patient with an isolated ventricular septal defect (meaning those that don’t have TOF), oxygenated blood is shunted from the left side to the right side because the pressure on the left is higher than the pressure on the right. For patients with TOF, though, the right ventricular outflow obstruction might block the normal blood flow so much that the pressure in the right ventricle has to be really high to get past it. Well the high right-sided pressures means that the left side of the heart actually becomes the path of least resistance and deoxygenated blood shunts from the right side to the left side.

The fourth and final feature is that the aorta overrides the ventricular septal defect. This one is super variable, sometimes the aorta’s way over here sitting on top of the septal defect and sometimes it’s more on the left ventricular side. Either way, if deoxygenated blood is shunted from right-to-left, then it flows over to the left ventricle and immediately out to the body.

When you think about it—the critical feature of these four is the degree ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peripheral_artery_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hvj3er6QSjKdxO_jCvX_08AHQYuG7_GL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peripheral artery disease]]></video:title><video:description><![CDATA[Vascular refers to the blood vessels, and peripheral means the outer limits or edge of something, which in peripheral vascular disease refers to any vessels that aren’t supplying the heart or the brain, like ones in the legs, arms, or other organs. Peripheral vascular disease happens when one of these arteries becomes narrowed, which reduces blood flow; this often affects the limbs.

Peripheral vascular disease, or PVD, usually involves the arteries, so sometimes it’s also referred to as peripheral artery disease or PAD. PVD is usually caused by a blockage, called organic PVD, that is most commonly created by atherosclerosis. Atherosclerosis is a buildup of lipids and fibrous material just under the inner lining of the blood vessel, called the tunica intima. When plaque builds up, it narrows the artery, which reduces perfusion to whatever tissue it tends to supply; this buildup usually happens over the course of many years. However, the vessel could be blocked by an embolus, which can happen suddenly if a blood clot from some upstream artery lodges in a peripheral artery; this clot would obviously stop blood flow from getting to the tissue the vessel supplies. 

Besides organic PVDs, there are also functional PVDs. With functional PVDs, blood vessels stop blood flow by changing diameter, such as with vasospasms, where the vessel constricts and blood flow is reduced. This type of PVD is usually short term, and can come and go.

The arteries supplying the legs are the most commonly affected vessels in peripheral vascular disease. When less blood gets to the muscle tissue in the legs, the tissue receives less oxygen and becomes ischemic. Ischemic cells release adenosine, a type of signaling molecule, which is thought to affect nerves in these areas; this is felt as pain. This pain in the legs is often referred to as claudication. Sometimes, even though blood flow is narrowed with PVD, when a person is at rest, there’s enough of blood to meet the tissue’s dema]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticoagulants:_Heparin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V9psuAfoSjGBlyoMD4QvFskkQSa7zeqZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticoagulants: Heparin]]></video:title><video:description><![CDATA[Anticoagulant medications are used to prevent blood clots from forming. These medications work by interfering with the normal function of plasma proteins called coagulation factors, which take part in secondary hemostasis-- where hemo refers to blood, and stasis meaning to halt or stop. In this video we’re going to focus on heparin, which works by indirectly inhibiting  two clotting factors called thrombin and factor Xa by binding to and enhancing the activity of an anticoagulant protein called antithrombin III. 

Now, before we discuss heparin in detail, we need to talk about the coagulation cascade, which is where heparin exerts its effect. The coagulation cascade begins via two pathways --the extrinsic and intrinsic pathways. The intrinsic pathway starts when circulating factor XII comes into contact with the surface of activated platelets or collagen. Activated factor XII, then activates factor XI, which activates factor IX which activates factor X. Factor Xa starts the common pathway where it activates factor II, or thrombin, which activates factor I that builds the fibrin mesh. When factor II gets activated it also activates 4 other factors: V, VIII, IX, and XIII. Factor V gets activated and acts as a cofactor for X, factor VIII acts as a cofactor for factor IX, and factor XIII helps factor I, or fibrin, form crosslinks. In the extrinsic pathway, exposed tissue factor activates factor VII, which activates factor X and starts the common pathway.

Now, the most important point of clot regulation is when a coagulation factor called thrombin is produced. Thrombin, or activated factor II, is a very important clotting factor, because it has multiple pro-coagulative functions. Think of thrombin as the accelerator on a car--the pedal that takes secondary hemostasis from 20 miles per hour to 100 miles per hour! First, thrombin binds to receptors on platelets causing them to activate. Activated platelets change their shape to form tentacle-like arms that allow]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oral_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DxD0BYRuRJifu31pg83455tgSDSP9mtv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oral cancer]]></video:title><video:description><![CDATA[Oral cancer describes cancers that originate in the oral cavity. 

The oral cavity includes the lips, the gingiva, or gums, the floor of the mouth, the buccal mucosa which is the soft lining of the inner lips and cheeks, the anterior or front two-thirds of the tongue, the hard palate which is the tough front part of the roof of the mouth, and the retromolar trigone which is the mucosa right behind the last molars on the bottom row of teeth. 

Behind the oral cavity is the oropharynx. 

The oropharynx includes the soft palate which is the soft part of the roof of the mouth right behind the hard palate, the tonsils, the walls of the throat, and the posterior or back one-third of the tongue. 

The oral cavity and oropharynx are lined by epithelium - and there are a few different types.

The first type of epithelium is called keratinized stratified squamous epithelium. 

These epithelial cells produce keratin, a protein that makes the layer tough, and protects against normal wear and tear from food and drinks.

Beneath the epithelium, there’s another layer called the basement membrane made of tough connective tissue, and below that is the lamina propria which yet more connective tissue that houses blood vessels, lymphatics, nerves, and immune cells. 

The oral surfaces covered in keratinized epithelium include the hard palate, the dorsal surface, or top, of the tongue, and the gingiva.

A second type of epithelium is non-keratinized stratified squamous epithelium, and it contains cells that don’t produce much keratin, making this layer less tough. 

The oral surfaces covered by non-keratinized stratified squamous epithelium include the buccal mucosa, the floor of the mouth, the lateral and ventral, or bottom, surfaces of the tongue, the soft palate, and the retromolar trigone.

Now the mucosal tissue in the oral cavity can undergo several premalignant pathological changes.

The first one of these is leukoplakia, where leuko- means white and -plakia means a fla]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nitrogen_and_urea_cycle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/B8UEJGxWTbCRrWo2QHWWcEG3Q2at6o9f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nitrogen and urea cycle]]></video:title><video:description><![CDATA[The human body generates a lot of waste products, and fortunately, our kidney is capable of getting rid of most of them.

However, there is one arch nemesis that the kidney can’t deal with on its own. So, the liver comes to the rescue. The villain is ammonia.

Ammonia is the major toxin that results from the metabolism of amino acids. 

Amino acids are made of a nitrogen group, a carbon skeleton, and a side chain that is unique to each amino acid. 

When amino acids are metabolized, the nitrogen is formed into ammonia, and ammonia is toxic to the cells. 

So the ammonia is shuttle over to the liver and sent through the urea cycle, which is a series of enzymatic reactions that convert ammonia into urea. 

The urea cycle takes place within the mitochondria, so that it doesn’t affect proteins and organelles in our cytoplasm. 

Urea can then easily be dealt with by the kidney. 

It’s a bit like how a mama bird might mash up a worm so that it’s easier for a baby bird to digest. 

In this case the liver is the mama bird, and the kidney is the baby bird.

Alright, so first, ammonia needs to get to the liver.

And it has to be done carefully because it’s toxic. 

So, much like a prisoner, it needs to be carried in the circulation by a police officer, to its prison, which is the liver mitochondria. 

There are two ways this can happen. The first way is used throughout by cells throughout the body. 

The enzyme glutamine synthetase adds ammonia to the amino acid glutamate forming glutamine. 

Glutamine can move into the blood, and essentially transport ammonia around the block, until it gets to a liver cell. 

Once inside the mitochondria of a liver cell, an enzyme called glutaminase cleaves glutamine back into glutamate and ammonia, and the ammonia can then enter the urea cycle. 

The second way to move ammonia around is done mostly by skeletal muscle cells. 

In skeletal muscle cells, the enzyme glutamate dehydrogenase incorporates ammonia into the molecule alpha-]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Confounding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HqNpJXIOTnSdXwh2Rg3OJGaLSQu-mmEh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Confounding]]></video:title><video:description><![CDATA[A confounder is a variable in a study that distorts the true relationship between an exposure and an outcome, so it looks like the exposure and the outcome are either more associated or less associated than they really are. 

For example, let’s say you hear on the news that drinking coffee is associated with developing heart disease, and - because you drink a lot of coffee - you decide to conduct a study to see if this is true. 

First, you recruit 100 people that drink coffee and 100 people that don’t drink coffee, follow them for ten years, and then compare the number of people who developed heart disease in each group.

First, off you must really love coffee and be fairly wealthy to spend ten years studying it at the drop of a hat.

Now, let’s say that the proportion of people who develop heart disease in the coffee drinking group is  - 50 out of 100, or 50% - and proportion of people who develop heart disease in the non-coffee drinking group - is 20 out of 100, or 20%. 

Comparing 50% and 20%, you get a relative risk of 2.5, meaning the risk of developing heart disease for people that drink coffee is 2.5 times the risk for people that don’t drink coffee. 

The association between coffee drinking and heart disease can be represented by an arrow pointing from the exposure to the outcome.

The arrow represents a potential causal relationship - in other words, coffee drinking potentially causes the development of heart disease. 

But does drinking coffee really cause heart disease? Maybe, or maybe there’s a mysterious third variable - like smoking - that’s confounding the relationship, or making it look like there’s an association when there really isn’t one. 

To be considered a confounder, two conditions have to be met. 

The first condition is that a variable has to be associated with the exposure - meaning that the variable is seen to occur significantly more frequently among one group than the other. 

So in this case, people that smoke would have to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lesch-Nyhan_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XPuKmaf1TcSTVlPyd7PEZYD7Q6OC50fx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lesch-Nyhan syndrome]]></video:title><video:description><![CDATA[Lesch-Nyhan syndrome is a rare genetic condition which leads to excess uric acid in the blood, and it causes kidney, joint, neurological, and behavioral problems.

Normally, each cell contains both DNA and RNA, and diving deeper, each nucleotide can be broken down into a sugar, a deoxyribose in DNA or a ribose in RNA, one to three phosphate groups, and a nucleobase, which can be either a pyrimidine or a purine.

There are three pyrimidine bases– cytosine, thymine and uracil and two purine bases, adenine and guanine. 

So, the name of a ribose-containing, monophosphatic nucleotide, based on guanine, would be guanosine monophosphate, or GMP for short, whereas one based on adenine, would be adenosine monophosphate, or AMP, for short.

Now, there are two ways our cells can make nucleotides - one is to make from scratch, also known as de novo synthesis, and the other is the salvage pathway, which recycles nucleotides that are already semi-degraded. 

Let’s focus on the purine salvage pathway. 

In the case of GMP, the enzyme purine nucleoside phosphorylase, first removes the ribose and the phosphate from it, turning it into guanine. 

Next, another enzyme called guanase removes an amine group turning guanine into xanthine. 

Finally, xanthine is oxidized into uric acid by the enzyme xanthine oxidase. 

On the other hand, for AMP to become uric acid, first the enzyme AMP deaminase removes an amine group from it, turning it into IMP. 

Then purine nucleoside phosphorylase comes in and removes the phosphate and the ribose from IMP, making hypoxanthine. 

Hypoxanthine is then oxidized twice by xanthine oxidase - first to become xanthine, and then finally, to uric acid. 

Uric acid can then be filtered out of the blood and excreted in the urine. 

Now those intermediate molecules in purine degradation, guanine and hypoxanthine, can be restored into fresh new nucleic acids, through what is known as a salvage pathway. 

There’s an enzyme called hypoxanthine-guanine ph]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Incidence_and_prevalence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XBIM6aYuTGqMY7WdyeKP5iBMTbO1nKtW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Incidence and prevalence]]></video:title><video:description><![CDATA[Prevalence and incidence are two ways to measure the number of people who have a certain disease in a population. 

Prevalence includes all individuals with a disease, or all cases, regardless of when they developed it, divided by the total population. 

Whereas incidence includes the new cases of a disease - meaning anyone who develops a disease, over some period of time, divided by the population of individuals that can get that disease.

And both of these have to take into account the population at risk. 

Sometimes incidence and prevalence are reported as a proportion of a population like 5 per 1000, or 5 per 100, 000 if it’s a rare disease. 

Let’s use a quick analogy to show the relationship between incidence and prevalence. 

Imagine a bucket of green marbles - with each marble representing a sick person. 

New green marbles keep falling into the bucket - these are the new cases.

We can count up how many green marbles enter the bucket in a year, and that would be the incidence.

Now some marbles also fall out of the bucket - perhaps some cases recover from the disease while other cases die.

Either way, they don’t have the disease anymore and are no longer cases in our bucket.

We can count up the number of green marbles in the bucket and that would be our prevalence. 

So the prevalence really depends on the incidence of new cases, the recovery rate of the cases, and the death rate of the cases. 

So for prevalence we have all cases of a disease over the population at risk.

If it’s done at some specific moment, like the day that a survey is being done, then it’s called point prevalence. 

And occasionally, if it’s done over a period of time, like over a month or year, then it’s called period prevalence. 

Now when we have new cases of a disease in a certain period of time, it’s called incidence rate. 

This can’t be done at a specific moment, since we need some time window to capture the new cases, and sometimes it’s hard to follow up with everyo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brachial_plexus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KSzKug6MSGOLscd2ysCOCVoXS8CaOmky/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brachial plexus]]></video:title><video:description><![CDATA[The brachial plexus may look difficult to draw, but here’s a shorthand way to  draw the brachial plexus really fast. 

Now that the nerves are all drawn, let’s begin labeling the brachial plexus, starting with the cervical and thoracic nerves - C5, C6, C7, C8, &amp;amp; T1. 

The brachial plexus is also divided into roots, trunks, divisions, cords, and terminal branches. 

The order can be remembered using the acronym “Remember To Drink Cold Beer.” 

Then to remember the terminal branches, you can use the word “MARMU.” Which stands for the musculocutaneous, AXILLARY, radial, median, and ulnar nerves respectively. 

Next, we can start labeling the collateral nerves starting with those that branch off the roots. 

The dorsal scapular nerve branches off of the C5 root, and the long thoracic nerve arises from the C5, C6, and C7 roots. 

The superior trunk has two collateral branches, the suprascapular and subclavius nerves. 

And the cords have a total of 7 collateral branches. 

The lateral cord gives rise to the lateral pectoral nerve. 

The POSTERIOR cord gives rise to the upper, middle, and lower subscapular nerves. 

And the medial cord gives rise to the medial pectoral, medial cutaneous nerve of the arm, and the medial cutaneous nerve of the forearm.

The nervous system is divided into the central nervous system, which includes the brain and spinal cord, and the peripheral nervous system, which is further divided into the somatic and the autonomic nervous systems.

Broadly speaking, the nervous system is split into an afferent and an EFFERENT division. 

The afferent division brings sensory information from the outside into the central nervous system, and includes visual receptors, auditory receptors, and touch receptors.

On the other hand, the EFFERENT division brings motor information from the central nervous system to the periphery, ultimately resulting in contraction of skeletal muscles to trigger movement through the somatic nervous system, as wel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lymphoma:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wXAvFL3HReqXv0xUuigHRSxGSBei3qco/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lymphoma: Clinical]]></video:title><video:description><![CDATA[Lymphoma is a malignancy of lymphocytes - that is B-cells, T-cells, and natural killer cells - that usually involves the lymph nodes, or other lymphoid structures like the tonsils and the spleen. 

Lymphoma is considered the most common hematologic malignancy in adults. 

If there’s an enlarged lymph node, so lymphadenopathy, it’s important to see if it’s tender and if it’s mobile.

In reactive lymphadenopathy due to an infection, the lymph node is typically tender and mobile.

If the lymph node is due to lymphoma or from a metastasis from another malignancy, the lymph node is typically non-tender and non-mobile or fixed. 

In malignancy, lymphadenopathy can also be accompanied by “B” symptoms, which are caused by cytokine release, and include a fever, drenching sweats, and an unintentional 10% weight loss within six months. 

If malignancy is suspected, an excisional lymph node biopsy should be done to assess the tissue architecture of the lymph node, because the hallmark of lymphoma is a disruption of this lymph node architecture. This is done by completely removing the entire lymph node surgically. 

A fine needle aspiration, or FNA of the lymph node is inadequate for making the diagnosis, because an FNA is just poking a needle into the lymph node, and aspirating or pulling out lymphocytes. And any individual lymphocyte in lymphoma could look completely normal. 

If the excisional biopsy confirms that there’s a lymphoma it’s generally classified as a Hodgkin lymphoma or non-Hodgkin lymphoma based on the presence or absence of Reed-Sternberg cells. 

Reed-Sternberg cells have a bilobed nucleus and a surrounding clear space! 

Once the diagnosis of Hodgkin lymphoma or non-Hodgkin lymphoma is made, the next step is to do staging using positron emission tomography combined with a computed tomography, or PET/CT scan of the chest, abdomen, and pelvis. This is done by giving the patient an intravenous bolus of radiolabeled glucose, called fluorodeoxyglucose, o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tuberous_sclerosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VkEMoUB_TeaFjUeyi4uQ7yFdTgmsdhdR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tuberous sclerosis]]></video:title><video:description><![CDATA[Tuberous sclerosis is a genetic condition that causes growths to form in various body organs. Most commonly affecting the brain, skin, kidneys, lungs, and eyes.

Normally, there are two genes called TSC1 and TSC2 that help control the growth and division of cells in the body. 

TSC1 encodes the protein hamartin and TSC2 encodes the protein tuberin. 

Both of these proteins, are tumor suppressors, meaning they help slow down cell growth and prevent tumors. 

They do this by combining to form a hamartin-tuberin protein complex, which binds to and inhibits another protein called mechanistic target of rapamycin, or mTOR. 

mTOR activity speeds up the cell cycle and increases cell proliferation mainly thanks to its effect on protein synthesis. 

So when mTOR is switched off by the hamartin-tuberin protein complex, it slows growth and division of cells throughout the body.

Individuals with tuberous sclerosis have a mutation in either the gene TSC1 or TSC2, and these mutations have an autosomal dominant inheritance pattern. 

The mutations lead to an altered hamartin-tuberin protein complex that’s unable to switch off mTOR. 

Because of that, benign tumors and growths called hamartomas form throughout the body. 

Hamartomas are kind of like tumors, but they’re made of a variety of cell types from the tissue where they arise, rather than a single cell type.

In fact, if we think of the tissue like a sheet of fabric, a hamartoma is like a knot in the sheet. 

Benign tumors and hamartomas can form in any tissue, but the brain and the skin are usually affected the most, along with the kidneys, lungs and eyes.

On top of that the lifetime risk of cancer is increased in individuals with tuberous sclerosis.

That’s because the rapidly dividing cells can develop additional mutations that eventually make these growths expand beyond the basement membrane and invade neighboring tissues.

In the brain, the most common growths are glioneural hamartomas, also known as a corti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Concussion_and_traumatic_brain_injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UCb6RwuuS86itHjdFS0qA2yDSR2NKv-N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Concussion and traumatic brain injury]]></video:title><video:description><![CDATA[Concussion, also called a mild traumatic brain injury, usually starts with a hit to the head.

But what makes it a concussion is that the hit results in diffuse brain injury--meaning a large part of the brain is affected rather than a small specific area. 

Also, concussions don’t cause obvious brain trauma that can be seen on imaging--like bleeding. 

Most concussions are the result of injuries from things like motor vehicle accidents, falling down the stairs, recreational activities - like getting hit in boxing or getting tackled in a football game, or even violence in the home. 

Now, the brain is made up of neurons--the functional cells of the nervous system. 

Neurons are made up of three main parts. The dendrites, which are little branches off of the neuron that receive signals from other neurons, the soma, or cell body, which has all of the neuron’s main organelles like the nucleus, and the axon which is intermittently wrapped in fatty myelin. 

When an electrical impulse called an action potential flows through a neuron, it causes the release of stored neurotransmitters into the gap between two neurons called the synapse. 

This first neuron is called the presynaptic neuron. 

And the next neuron, called the postsynaptic neuron, has receptors for the neurotransmitters on its dendrites which trigger the opening of ion channels in the postsynaptic neuron. 

When the neurotransmitter glutamate binds to a postsynaptic neuron, it causes ion channels to open, and positively charged ions like sodium, potassium, and calcium enter the cell. 

This is called an excitatory postsynaptic potential, or EPSP, because more positive charge inside the cell causes a depolarization to happen. 

If the overall charge of the cell increases enough, it triggers an action potential, which is an electrical signal that races down the axon at speeds of up to 100 meters per second, triggering the release of more neurotransmitter at the next synapse.  

In contrast to glut]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Olfactory_transduction_and_pathways</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yrsC8O6zQeOdUnInbCAa-gWKTtm9YldP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Olfactory transduction and pathways]]></video:title><video:description><![CDATA[The sensation of smell, also called olfaction, is carried out by the olfactory nerve or cranial nerve I, and it comes from specialized sensory neurons located in the roof of the nasal cavity, within the nose.

The nasal cavity is made up of three regions. The first, is the nasal vestibule which is the area just inside the nostrils. 

The second is the respiratory region, which is just above the nasal vestibule and is separated by three shelf-like bony structures; the superior, middle and inferior nasal conchae.

Lining the respiratory region is a layer of epithelial cells that create mucus to moisten the air and trap pathogens. 

The third, is the olfactory region which is at the top of the nasal cavity and is involved in smelling. 

Lining the olfactory region is a layer of special epithelial cells which form the olfactory epithelium. 

The olfactory epithelium consists of olfactory receptor cells which are chemoreceptors that respond to molecules, called odorants. 

The olfactory epithelium also contains columnar epithelial cells which support those olfactory receptor cells. 

Below the olfactory epithelium is a layer of connective tissue called the lamina propria. 

The lamina propria contains olfactory glands or Bowman’s glands which produce nasal mucus that protects the surface of the olfactory epithelium. 

Below the lamina propria is the roof of the olfactory region which is formed by the cribriform plate of the ethmoid bone.

Now, if we zoom in a bit, we can see that the olfactory receptor cells are bipolar neurons, meaning that they have two projections outside the olfactory epithelium. 

One projection carries their dendrites to the bottom of the epithelium and gives off hair-like structures called the olfactory hairs, or cilia. 

These cilia protrude beyond the nasal mucosa so that they can come into contact with odorants trapped by the mucus. 

The other projection is an axon that joins up with axons of other receptors to form tiny olfactory ne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Test_precision_and_accuracy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/a4Cls67rT5mMhlOsV_L6q1PUTwmUza-d/_.jpg</video:thumbnail_loc><video:title><![CDATA[Test precision and accuracy]]></video:title><video:description><![CDATA[Let’s say you want to figure out if eating more daily servings of vegetables will decrease a person’s body mass index (BMI), which is a number calculated by dividing a person’s weight in kilograms by their height in meters squared. 

The first step to figuring this out is to collect data about each person in the study, and this is typically done using some type of measurement tool. 

For example, we might use a scale to measure a person’s weight, a measuring rod to measure a person’s height, and design a survey to find out how many daily servings of vegetables a person eats. 

Now, it’s important to collect high quality data in a study, which means the information collected in the study should accurately reflect what’s really happening. 

For example, if a person eats 5 servings of vegetables per day, the data should reflect that they eat 5 servings, instead of 2 servings. 

Data quality is determined by the tools used to collect the information, and ideally, these tools have high validity - or accuracy - and high reliability - or repeatability.

A tool with high validity will provide a measurement that’s very close to the true or known value for the thing being measured. 

Let’s say we’re going to measure a woman’s weight using two different scales. 

One scale is a family heirloom that was passed down over multiple generations - so it’s pretty old - and the other scale was a gift from your friend who’s a doctor - so it’s really modern and sophisticated. 

The old scale provides a measurement of 80 kilograms, and the modern scale provides a very different measurement of 66 kilograms. 

In reality, this woman weighs 65 kilograms, so, since the modern scale provides a measurement that is closer to the woman’s true weight, the modern scale has higher validity.

Using tools with high validity is important for getting correct results in descriptive or inferential statistics.

For example, if we used the old scale for all the people in the group with hypertensi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscle_spindles_and_golgi_tendon_organs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lkWCGQOORyOtS1dT5Zs0uoNvSGWUacne/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscle spindles and golgi tendon organs]]></video:title><video:description><![CDATA[In order to do the forward bend position during your yoga class, your nervous system has to do a number of things. 

First, an upper motor neuron from your brain - specifically your cerebral cortex - has to send a signal down to a lower motor neuron that’s in the anterior horn of the spinal cord. 

This lower motor neuron is also called an alpha motor neuron, and it relays an action potential through an axon that goes to muscles in your legs, which enable you to extend them. 

Now, when you stretch or flex your muscles, proprioceptors that detect the position and movement of the muscles initiate reflexes that prevent you from damaging the muscles from overstretching or over contracting.

These proprioceptors are scattered throughout your skeletal muscles, and operate on a subconscious level so you never even notice them.

Now a muscle looks like it’s made of a bundle of muscle fibers with extrafusal muscle fibers on the outside and intrafusal muscle fibers on the inside. 

Extrafusal muscle fibers provide most of the force during a muscle contraction, and are innervated by lower motor neurons which are also called alpha motor neurons. 

Extrafusal muscle fibers attach to bones with tendons which are a specific type of connective tissue. 

These tendons have proprioceptors called golgi tendon organs which lie at the ends of these extrafusal fibers. 

Now, if we pull apart the extrafusal fibers, there’s another proprioceptor called the muscle spindle that lies within the extrafusal fibers. 

Each muscle spindle contains multiple intrafusal muscle fibers. 

Just like extrafusal muscle fibers, intrafusal muscle fibers have contractile proteins like actin and myosin. However these contractile proteins don’t extend through the entire length of intrafusal muscle; instead they’re only present at each end of a intrafusal muscle fiber. 

Therefore, the central region of a intrafusal muscle doesn’t contract, even though the ends do. 

The central portion of the intra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DNA_damage_and_repair</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g6Wv5aKBQp6kfaVeWMXGAtRGQfGvQcBv/_.jpg</video:thumbnail_loc><video:title><![CDATA[DNA damage and repair]]></video:title><video:description><![CDATA[Our DNA is like a library - found in the nucleus of our cells - with thousands of books. 

Some of these books - called genes - are extremely important, because they carry the recipes for every single protein found in the cell. 

Now, on a molecular level, DNA is made up of two strands of nucleotides, so each gene is just a segment of this nucleotide sequence. 

Nucleotides of DNA are made out of a sugar - deoxyribose, a phosphate, and one of the four nucleobases - adenine, cytosine, guanine, and thymine - or, A, C, G, T for short. 

The nucleotides on one strand pair up using hydrogen bonds with nucleotides on the opposing strand, to create the double-stranded DNA: specifically, A bonds with T, and C bonds with G, so they’re called complementary bases. 

Now, the goal of DNA is to store information and pass it onto their daughter cells, and to use this information to create proteins. 

To do this, there are two critical processes - DNA replication and gene expression.

DNA replication occurs during the cell cycle - more specifically, during the S phase of interphase. 

So, the cell cycle is made up of interphase - when the cell prepares for division - and mitosis - or the actual splitting of the cell in two daughter cell. 

Interphase has 3 subphases - G1, S and G2, and during the S subphase, the cell replicates its DNA, so that the two daughter cells get the exact same DNA during mitosis. 

If we zoom onto the double- stranded DNA, we can see that during DNA replication, the two DNA strands are separated by an enzyme called DNA helicase. 

Then another enzyme, DNA polymerase, uses each of the single strands as a template and adds complementary nucleotides to it. 

Gene expression, on the other hand, is the process of decoding the information stored in the DNA in order for the cell to make proteins, and it includes transcription and translation. 

Transcription is where RNA polymerase copies the nucleotide sequence of the gene and creates a mess]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pyramidal_and_extrapyramidal_tracts</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cBktlhMUS76gZx66JluEygWXQraW2WS8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pyramidal and extrapyramidal tracts]]></video:title><video:description><![CDATA[In order for you to flex your bicep in the mirror, your brain and brainstem has to send a motor signal through the spinal cord to the muscles in the body. 

These motor signals are carried through two tracts, the pyramidal and extrapyramidal tracts. 

Neurons in the pyramidal tract are composed of upper motor neurons that directly innervate lower motor neurons in the anterior horn of the spinal cord. 

Neurons in the extrapyramidal tract do not directly innervate lower motor neurons, but instead help coordinate muscle movement by indirectly activating or inhibiting groups of lower motor neurons through interneurons. 

These groups of lower motor neurons usually innervate multiple muscles that share the same function, usually either flexors or extensors. 

The pyramidal pathway is the primary pathway that carries out motor commands for voluntary movement. And it can be broken down into two main tracts, the corticospinal tract and the corticobulbar tract. 

The corticospinal tract originates in the motor cortex where the cell bodies of the upper motor neurons are located. 

The axons of these neurons travel together as fibers through the internal capsule to reach the brainstem where they form the medullary pyramids on the ventral surface of the brainstem.  

At the level of the medulla, these fibers divide, and 90% of them form the lateral corticospinal tract which cross over to the opposite side of the medulla at the pyramidal decussation, while the remaining 10% of them form the anterior corticospinal tract which does not cross over just yet, and both tracts then travel through the spinal cord. 

Neurons from the lateral corticospinal tract synapse on lower motor neurons in the anterior horn, while the neurons in the anterior corticospinal tract cross over in the spinal cord first before they synapse on the lower motor neurons in the anterior horn. 

The upper motor neurons activate the lower motor neurons which leave the spinal cord and innervate the diff]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Positive_and_negative_predictive_value</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xcl-d1doR5Ss97cBcE10gdQ7SciWHcwc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Positive and negative predictive value]]></video:title><video:description><![CDATA[Imagine that a person gets the results of a colon cancer screening test.

There are two possible scenarios - either the result is positive, indicating that they have colon cancer, or the result is negative, indicating they don’t have colon cancer. 

At this point, the person may ask themselves, how worried should I be that it was a positive test result? Or, how reassured should I be that it was a negative test result? 

Each test has a positive predictive value, or PPV, which is the probability that people with a positive test result truly have the outcome, and a negative predictive value, or NPV, which is the probability that people with a negative test result truly don’t have the outcome. 

Let’s take an example to show how it’s possible to measure a test’s predictive value. 

Let’s say that we recruit 1000 people - 100 people with colon cancer and 900 people without colon cancer - and then we give them all the same screening test. 

That way we can see how many people with positive results actually have colon cancer and how many people with negative results actually don’t have colon cancer. 

We can organize the results using a 2 by 2 table, where the true disease status of the individual is on the top of the box, and the results of the screening test are on the side, and each of the cells is labeled a, b, c, or d. 

A true positive would be a person who gets a positive test result and has colon cancer. 

A true negative would be a person who gets a negative test result and doesn’t have colon cancer. 

A false positive would be a person who gets a positive test result even though they don’t have colon cancer. 

And a false negative would be a person who gets a negative test result even though they have colon cancer. 

To calculate the positive predictive value, we divide the number of true positives by the total number of people who tested positive - so cell a divided by the sum of cell a and b.

A test with a perfect positive predictive value would hav]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Interaction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ksd2ljcmT6eVPci_S9M997YNTCqPiYsF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Interaction]]></video:title><video:description><![CDATA[The word “interaction” can refer to biological interaction - which is where two exposures like radon gas and toxins in cigarettes work together to influence an outcome - like lung cancer. 

But the word “interaction” can also refer to statistical interaction, also called effect modification, which is the statistical methodology used to find out if there’s a biological interaction. 

Most diseases are caused by multiple exposures that work together, like our example of radon gas and smoking cigarettes leading to lung cancer. 

Radon is a radioactive gas that gets released from the decay of elements like uranium and radium in rocks and soil. 

It can be found in dust particles in the air, so most people breathe in a low level of radon every day. 

Unfortunately, radon causes mutations in DNA and people who breathe in high levels of radon have an increased risk of lung cancer. 

Similarly, people who smoke cigarettes have a higher risk of lung cancer because of tobacco contains various toxins that also mutate the DNA. 

In addition, cigarette smoke harms the cilia in the lungs. Those are the little hairlike structures that normally clear out things like mucus, dust particles, and chemicals. 

Damaged cilia is a big problem for people who are exposed to high levels of radon, because the lungs can’t get rid of radon-containing dust. 

This is an example of biological interaction, because even though radon and smoking can both separately cause lung cancer, they also work together to amplify the risk. 

Statistical interaction can help us figure out how much the risk increases for people who are exposed to both factors compared to people who are exposed to one factor or the other. 

Statistical interaction can be assessed by  comparing the effect of one exposure on the outcome in each strata or level of the other exposure.

For example, you could figure out how smoking affects the risk of lung cancer among people exposed to high levels of radon, and how it affect]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vaccinations</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oHnSGMy0SYKu66FD6R52WoFCRBmF_R1M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vaccinations]]></video:title><video:description><![CDATA[When you get an infection, you develop adaptive immunity. 

In other words, you generate memory T and B cells, so that if you encounter the same antigen again, they can quickly replicate and respond.

Most of the time we think of immunologic memory developing after natural infection. But memory T and B cells also develop after vaccination.

Vaccination is the process of generating a protective adaptive immune responses against microbes by exposure to nonpathogenic forms or components of microbes. 

That’s the key - getting long term active protection to a harmful microbe, from something that’s not harmful. 

Vaccination also helps up to establish herd immunity. 

Herd immunity is the concept that if enough people in the population - or herd - are vaccinated the entire population, even those who are unvaccinated, develop a higher resistance to that infection. 

The amount of people within a herd that need to be vaccinated to maintain herd immune status differs from pathogen to pathogen. 

When too few people in a herd are vaccinated, there are more people in the population that are able to get the illness and spread it. 

Vaccination is an active process of developing immunity. 

This is different from passive immunity which is where a person gets antibodies that are made by another person or animal like a horse or mouse or by cells in a lab. 

A common form of this is when antibodies are pooled from the community and is given intravenously - it’s called intravenous immunoglobulin or IV-Ig. 

Passive immunity last for only as long as the antibodies last - usually weeks to months. 

The antibodies that an infant receives from their mother in utero or during breastfeeding are examples of passive immunity. 

IgG antibodies in the blood cross the placenta initially protecting the baby to some pathogens that mom has already made antibodies to. 

These IgG maternal antibodies will be degraded around six months of age. 

IgA antibodies are plentiful in breast milk]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nernst_equation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v8__ojf9SYmIpVkaPU92bbnITdeHeGfc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nernst equation]]></video:title><video:description><![CDATA[The Nernst equation helps explain how a Galvanic cell works - so let’s start by drawing out a galvanic cell. 

A galvanic cell has two electrodes - so for our example, let’s say there’s one solid zinc electrode and that it’s in a 1.0 molar solution of zinc-two-plus ions, and that there’s a solid copper electrode and it’s in a 1.0 molar solution of copper-two-plus ions.

Now, copper ions turn their solution a blue color, whereas zinc ions don’t color their solution - so it’s colorless.

Since the concentration of both copper and zinc ion solutions is 1.0 molar and if we assume that the temperature is 25 degrees celsius, then we’re under standard conditions. 

Now, in our galvanic cell, the two electrodes are connected by a wire with an open switch and there’s also a salt bridge between the two compartments. 

The salt bridge allows electrical charge to travel between the two solutions. 

To get the galvanic cell started, we need to close the switch, so that electrons or electrical current can flow through the wire. 

Now, if we want to calculate the cell potential, or cell voltage, for this zinc-copper cell, we need to use the Nernst equation.  

So here’s the Nernst equation, E refers to the instantaneous voltage of the galvanic cell, or the voltage at a specific moment in time. 

Enaught or Ezero is a constant called the “standard voltage,” and it’s simply based on the two metals that we’re using in our galvanic cell. 

We can look up this number for zinc and copper, and we find that it has a value of +1.10 volts. 

N refers to the number of moles of electrons that are transferred during the redox reaction. 

Q is the reaction quotient, which is the ratio of the concentration of reactants to the concentration of products in our galvanic cell. 

When we calculate this, we only include the concentration of the ions, and we leave out the pure solids like the zinc and copper electrodes. This tells us the progress of the reaction. 

Now, we can look ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cell-mediated_immunity_of_CD4_cells</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Cu9oJ-twSWKb0zmaiykAIwd6QBW-sLGe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cell-mediated immunity of CD4 cells]]></video:title><video:description><![CDATA[The key cells of the adaptive immune response are the lymphocytes - the B and T cells. And there are two types of T cells. T helper cells which express CD4 on their surface, and cytotoxic T cells which express CD8 on their surface. Helper T cells primarily support other immune cells, whereas cytotoxic T cells kill cells that are infected with a pathogen or are cancerous.  Cell mediated immunity refers to the part of the immune response that’s based on cellular interactions, and cannot be transferred through serum from one person to another. That makes sense since CD4 helper T cells interact with other immune cells to stimulate them. 

Now, when a T cell is initially formed it’s considered naive. This naive T cell is a bit like a student in school that isn’t ready to choose a career path. Later when that T cell encounters an antigen - it gets activated or primed - and turns into an effector T cell. This process of priming requires two signals. The first signal is the antigen itself, which is usually presented on an MHC molecule on the surface of an antigen presenting cell like a macrophage or dendritic cell. This antigen has to bind perfectly to the T cell receptor. The second signal is called costimulation - and it’s when a ligand called CD28 on the surface of a T cell binds to a ligand called B7 on the antigen presenting cell. This region, which includes the T cell receptor which binds to the MHC-Antigen and CD4; and CD28 which bind with B7, is called the immune synapse. Once the T cell receives both of these signals, a number of changes occur within the cell that transforms the naive T cell into an activated T cell. An activated T cell is one that’s ready to become an effector T cell and the developmental path it chooses often depends on the cytokines in the environment. Going back to the student analogy, an activated student is one that’s gotten the signals it needs to graduate from college and is finally prepared to choose a career path. 

Now, within ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vestibulo-ocular_reflex_and_nystagmus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bgDdvtHCSPmE7i8yrwJx0rvvS_mYQyvC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vestibulo-ocular reflex and nystagmus]]></video:title><video:description><![CDATA[Vestibulo- refers to the vestibular apparatus which is in the inner ear, that helps maintain our balance, and ocular refers to the eyes. 

So the vestibulo-ocular reflex is a reflex that starts in the vestibular apparatus, in response to head movement, and ends with movement of the eyes. 

The inner ear, sometimes called the labyrinth, is a marvelous bit of engineering. On the outside, it has a tough bony shell - the bony labyrinth; and inside the bony labyrinth, there’s the membranous labyrinth. 

The bony and membranous labyrinth help form all three parts of the inner ear.

The first is the vestibule, which is like a hallway that leads up to two other parts or rooms - the cochlea, towards the front of our head, that deals with hearing, and a second room towards the back of our head, that contains three semicircular canals - an anterior, a posterior and a lateral one -  which play a role in balance. 

Along with the semicircular canals, there are also two other balance-related structures in the vestibule - the utricle and the saccule. 

Together, the semicircular canals, the utricle, and the saccule make up the vestibular apparatus, and each of these structures have special balance receptors called hair cells - which function like motion sensors, picking up different kinds of movement. 

Hair cells in the semicircular canals detect changes in our dynamic equilibrium, like when we rotate our head, while those in the utricle and saccule detect changes in our head position in relation to horizontal or vertical acceleration - like when we feel pushed towards the back of the seat in a speeding car, or when we go up or down an elevator. 

Now let’s switch gears and look at the eyes - pun intended! The eyes normally focus on an image that’s projected on the fovea - which is the central part of the retina. But, our head is almost always moving - from bopping ever so slightly when we walk, to turning when we want to take a sneak peek at a cute person walking by. S]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sensitivity_and_specificity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rBJyX1HFT0a--Z_2B8RNWiu0QZKkiP2v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sensitivity and specificity]]></video:title><video:description><![CDATA[Let’s say a new screening test is developed to figure out if people have diabetes before they start showing symptoms. Before using the test, we have to make sure that the test works - in other words, can the test correctly identify if a person has diabetes or not? This is the test’s validity, and it has two components - sensitivity and specificity. 

A test with high sensitivity will correctly identify most people who have the condition, and a test with high specificity will correctly identify most people who don’t have the disease.

So let’s say that we recruit a 1000 people - 100 people who have diabetes and 900 people who don’t to put our diabetes test to the test! 

We can organize the results using a 2 by 2 table, where the true disease status, positive or negative, of the individual is on the top of the box and the results of the screening test, positive or negative, are on the side, and each of the cells is labeled a, b, c, or d. In this situation, a positive test indicates that a person has diabetes. 

So let’s look at this table closer, a person who gets a positive test result and has positive disease status, so has diabetes, is called a true positive.

A person who gets a negative test result and a negative disease status, so doesn’t have diabetes, would be a true negative. 

A person who gets a positive test result even though they don’t have diabetes, would be a false positive. 

And lastly a person who gets a negative test result even though they have diabetes, would be a false negative. 

To calculate sensitivity, we divide the number of true positives by the total number of people who have diabetes - so cell a divided by the sum of cell a and cell c. 

A test with perfect sensitivity would have 100 true positives in cell a, because the test would correctly identify everyone who has diabetes, and zero false negatives in cell c. 

To calculate specificity, we divide the number of true negatives by the total number of people who do not have dia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Paired_t-test</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cTrQl_nwRhydyK_VSIA5OesfQneWzp9x/_.jpg</video:thumbnail_loc><video:title><![CDATA[Paired t-test]]></video:title><video:description><![CDATA[The Student’s t-test or simply, the t-test, is a type of parametric statistical test used to determine if there’s a significant difference between the means or averages of two groups.

And significance is normally defined by a p-value of less than 0.05 or 5%. 

Now when doing any parametric test, there are three key assumptions that we have to make about the population.

First, the sample population must have been recruited randomly. 

Choosing names randomly ensures that the people included in the study will have similar characteristics to the target population. 

This is important because that ensures that the results of the t-test can be applied to the target population - meaning it has good external validity! 

The second assumption is that each individual in the sample was recruited independently from other individuals in the sample.

In other words, no individuals influenced whether or not any other individual was included in the study.

For example, if two friends decided to get their blood pressures measured on the same day, and they were both included in the study, these two individuals would not be independent of each other and the second assumption would not be met.

Like random sampling, independent recruitment of individuals is important because it ensures that the sample population approximates the target population.

The third assumption is that the sample size is large enough to approximate the target population, which usually means having more than 20 people. 

If it’s impossible to get a large sample size, then the sample population must follow a normal bell-shaped distribution for the characteristic being studied because that’s what we would expect to see in the target population.

Okay, now let’s say you want to figure out if a certain medication lowers systolic blood pressure. 

So, you measure 25 people’s systolic blood pressures and find that the mean systolic blood pressure for the whole group is 138 mmHg.

Then, you give them the m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronary_artery_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uy5YPAxdT02OlZRjF4e5gOqyTUePQ6vA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronary artery disease: Clinical]]></video:title><video:description><![CDATA[Coronary artery disease can lead to myocardial ischemia which is when the myocardium isn’t getting a sufficient blood supply; so there isn’t enough oxygen to meet the heart’s demands. 

And coronary artery disease is characterized by a type of chest pain called angina pectoris, which can be due to either vasospastic disease and atherosclerotic disease. 

Vasospastic disease, also called Prinzmetal angina, is when for unclear reasons there’s transient vasoconstriction of a coronary artery, leading to transient ischemia. 

These attacks generally occur at rest, during the night or early morning, and occur in clusters. 

Atherosclerotic disease is when a coronary artery narrows due to build up of atherosclerotic plaque, and it can be further divided into stable angina, unstable angina, and myocardial infarction.

Unstable angina and myocardial infarction are collectively called acute coronary syndrome.

Patients with stable angina don’t feel pain at rest, but they do feel chest pain during intense physical exercise, because that’s when the myocardium has increased oxygen demand, which leads to transient or demand ischemia. 

The chest pain stops when the exercise stops, so these patients often just rest rather than going to the emergency department or ED. 

Now, angina is considered unstable if it presents at rest, or if it becomes more frequent, lasts longer, or occurs with less exertion than previous episodes of angina. 

In unstable angina there’s prolonged myocardial ischemia, but there’s no myocardial cell death yet, so it’s not a myocardial infarction. 

But if it’s not taken care of promptly, the ischemia can get prolonged and can lead to myocardial infarction, which is life-threatening.

When a patient comes into the ED with acute chest pain, a number of things have to be done within 10 minutes to confirm or exclude a myocardial ischemia. 

The differential diagnosis includes gastroesophageal reflux, pulmonary embolism, aortic dissection, a pneumonia,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertension:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rfj7HkXFQfG2npDNWW49MLMJRL6KnD-O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertension: Clinical]]></video:title><video:description><![CDATA[Hypertension, or high blood pressure, affects over a billion people around the world. 

Now, ‘normal’ systolic blood pressure is defined as less than 120 mmHg, and normal diastolic pressure is less than 80 mmHg. 

Elevated blood pressure is when systolic blood pressure is between 120 and 129 mmHg and less than 80 mmHg on the diastolic side.

Stage 1 hypertension is between 130 and 139 mmHg on the systolic side, and between 80 and 89 mmHg on the diastolic side.

Stage 2 hypertension is defined as anything that is 140 mmHg or higher on the Systolic side and 90 mmHg or higher on the diastolic side. 

Typically, both systolic and diastolic pressures tend to rise or fall together, but that’s not always the case. 

Sometimes, you can have systolic or diastolic hypertension, when one number is normal and the other is really high. This is referred to as isolated systolic hypertension or isolated diastolic hypertension. 

There are two main types of blood pressure measurements - office blood pressure, which is taken in a clinic, emergency department, or hospital, and an out-of-office blood pressure. 

The out-of-office blood pressure is either a home blood pressure, which is taken by the patient at home, or an ambulatory blood pressure monitoring or ABPM, which involves 24-hour monitoring of blood pressure as the patients live their normal daily life, and while they sleep, to see if the blood pressure falls at night compared to during the day. It uses a small digital blood pressure machine that is attached to a belt around the body and it’s connected to a cuff around the upper arm. 

Ambulatory blood pressure monitoring is the best way to diagnose hypertension, but it’s not always feasible, so it’s usually done when office and home blood pressure measurements are really discordant from one another. 

Now, the first step for an office blood pressure, is to make sure that the patient has rested for at least five minutes and is positioned properly - sitting with their]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Plasma_cell_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4EvBVdv1Q2aIdeIB4ro-bHa6RuahJBbI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Plasma cell disorders: Clinical]]></video:title><video:description><![CDATA[Plasma cell disorders are a group of hematological malignancies that primarily occur in the elderly, and are characterized by unregulated proliferation of plasma cells in the bone marrow. 

They include multiple myeloma, monoclonal gammopathy of unknown significance or MGUS, and Waldenström’s macroglobulinemia. 

Each of them produces a monoclonal or M-protein, which is a unique protein of a single type, like a protein “clone”. 

In multiple myeloma the most common M-protein that’s produced is IgG, followed by IgA - and these M-proteins have both a heavy and light chain. 

More rarely, the myeloma cells only make the kappa or lambda light chain of the immunoglobulin, and in that situation, the resulting protein is called the Bence-Jones protein. 

The clinical presentation of multiple myeloma can be summarized by the mnemonic CRAB, where “C” is for hypercalcemia resulting from increased osteoclast activity due to the release of osteoclast activating factor from the plasma cells. 

“R” is for renal disease, which is generally due to the light chains depositing and obstructing the renal tubules - this is called light chain cast nephropathy or myeloma kidney. 

Renal disease can also be due to type two renal tubular acidosis, secondary amyloidosis, or even hypercalcemia. 

“A” is for anemia, which causes fatigue and shortness of breath, and is often due to infiltration of the bone marrow by the plasma cells. 

And finally, “B” is for bone pain, which is due to increased osteoclast activity causing lytic bone lesions. 

Other manifestations include spinal cord compression if the tumor infiltrates from the vertebrae, and infections, because the immunoglobulins produced by the malignant plasma cells are not useful in fighting infections. 

A workup for multiple myeloma includes a CBC, which often shows normocytic normochromic anemia, and a peripheral smear, which can show a rouleaux formation due to IgG proteins attaching to red blood cell membranes, and then co]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psoriatic_arthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AMb-FHP2QfyNNeul4kWe0Q-_RQSDsrrX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psoriatic arthritis]]></video:title><video:description><![CDATA[In psoriatic arthritis, arthritis means joint inflammation, and psoriatic refers to psoriasis, which is an autoimmune disease characterized by red scaly patches in the skin. 

So psoriatic arthritis is a type of joint inflammation that happens in individuals with psoriasis. 

Psoriatic arthritis is also one disease in a group of diseases called seronegative spondyloarthropathies. 

Spondyloarthropathies are autoimmune diseases that affect the joints, and they’re seronegative, meaning that there aren’t any specific autoantibodies linked to them.

Normally, immune cells are ready to spot and destroy anything foreign that could cause the body harm. 

To help with this, most cells express the gene HLA-B27, which encodes a protein that forms a major histocompatibility complex, or MHC, class I molecule that sits on the surface of the cell membrane. 

This MHC class I molecule acts like a serving platter, presenting molecules from within the cell for the immune system to sample. 

A CD8+ T-cell, also called a cytotoxic T-cell, uses its T-cell receptor to bind to the antigen presented by the MHC class I molecule. 

Normally, the antigen that’s presented is from the cell, and the immune system recognizes it as a harmless self-antigen, which leads to no response. 

Now, many individuals with psoriatic arthritis have a specific version of the gene HLA-B27, which somehow leads to an autoimmune process. 

In these individuals, the immune system attacks self-antigens specifically ones in the joints. 

Exactly what causes this is unclear, but it&amp;#39;s clear that the gene is not enough to trigger psoriatic arthritis. 

Often, an environmental trigger like physical trauma or an infection seems to play a role as well. 

Ultimately, once the self-antigens are seen as foreign, T cells release cytokines which increases inflammation, and stimulates other immune cells to release Tumor Necrosis Factor or TNF, IL-12, and IL-23. 

This triggers keratinocytes and fibroblasts to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brain_herniation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A3cP-PDCQLeX0srtaVX6Pfl7RCyFfFnP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brain herniation]]></video:title><video:description><![CDATA[Brain herniation is what it’s called when some brain tissue moves outside of the skull, or moves across or into a structure with the skull. 

Brain herniation typically happens in response to increased intracranial pressure, which refers to a high pressure within the skull. 

An intracranial pressure above 15 mmHg is considered high.

OK - let’s start with some basic brain anatomy. The brain has a few regions - the most obvious is the cerebrum, which is divided into two cerebral hemispheres, each of which has a cortex - an outer region - divided into four lobes including the frontal lobe, parietal lobe, temporal lobe, and the occipital lobe. 

There are also a number of additional structures - including the cerebellum, which is down below, as well as the brainstem which connects to the spinal cord. 

Now zooming in, the brain and spinal cord is covered by the meninges, which are three protective layers of the brain. 

The inner layer of the meninges is the pia mater, the middle layer is the arachnoid mater, and the outer layer is the dura mater.

These first two, the pia and arachnoid maters, form the subarachnoid space, which houses the cerebrospinal fluid, or CSF. 

CSF is a clear, watery liquid which is pumped around the spinal cord and brain, cushioning them from impact and bathing them in nutrients. 

The outer membrane is the dura mater, which forms the meningeal folds, such as falx cerebri and tentorium.

The falx cerebri is a meningeal fold that goes down into the longitudinal fissure that separates the hemispheres of the brain.

The free edge of the falx cerebri is in close contact with the central part of the brain called corpus callosum, which connects the left and right hemisphere.

There’s also the tentorium which is a meningeal fold located in the back of our skull, that separates the cerebrum from the cerebellum. 

The free edge of the tentorium is in close contact with the brainstem, which is the region that connects the brain and the spina]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiphospholipid_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MC99TYukQAezRiRFz9dTmuwTSWCup9Xn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiphospholipid syndrome]]></video:title><video:description><![CDATA[In antiphospholipid syndrome, individuals produce antiphospholipid antibodies, which attack the phospholipids in the cell membrane of their own cells, or attack proteins that are bound to those phospholipids.

So antiphospholipid syndrome, or APS, is an autoimmune disease. 

Antiphospholipid syndrome can be primary or secondary. Primary antiphospholipid syndrome occurs by itself, whereas secondary antiphospholipid syndrome occurs with other autoimmune diseases, especially systemic lupus erythematosus. 

And just like most autoimmune diseases, antiphospholipid syndrome is more common in young females. 

The exact cause of antiphospholipid syndrome isn’t known, but there are some known genetic and environmental factors.

For instance, the HLA-DR7 gene encodes a specific type of a protein called major histocompatibility complex or MHC class II, which sits on the surface of the B cell.

These surface proteins help activate B cells so that they can start producing antibodies. 

Now, having a mutated HLA-DR7 gene predisposes individuals to activate B cell production of antiphospholipid antibodies. 

But the presence of the mutated HLA-DR7 gene alone isn’t enough to develop antiphospholipid syndrome - an environmental trigger must also be present. 

There’s a variety of potential triggers - some common ones include infections - like syphilis, hepatitis C, HIV, and malaria - drugs, like some cardiovascular drugs - including procainamide, quinidine, propranolol, and hydralazine - or antipsychotic drugs like phenytoin and chlorpromazine.

The main antiphospholipid antibody is anti-beta2-glycoprotein I, which targets the protein beta2-glycoprotein I, also called apolipoprotein H. 

This protein binds to phospholipids and inhibits agglutination which is when platelets clump together to form blood clots. 

So when anti-beta2-glycoprotein I binds beta2-glycoprotein I, it’s not free to do its job, and that leads to clot formation. 

Another antiphospholipid antibody is a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Staphylococcus_aureus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GFXmalryR6yl22hq9PPcq8PwRKSCdWXG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Staphylococcus aureus]]></video:title><video:description><![CDATA[Staphylococcus aureus, sometimes called staph aureus, is coccal, or round-shaped, and grows in clusters. 

In fact, its name, broken down, means “golden cluster of grapes”. 

It sorta starts making sense if you look at it under a microscope - it tends to grow in sticky clusters, and it stains purple when Gram-stained due to its peptidoglycan cell wall, so it’s Gram positive and it resembles grapes. 

As for its “golden” color, when it’s grown on blood agar plates, the colonies have a distinctive golden-yellow color.

Staphylococcus aureus are Gram positive and facultative anaerobes, meaning that they can survive in aerobic and anaerobic environments. 

They’re non-motile and don’t form spores. 

Staphylococci produce an enzyme called catalase which converts hydrogen peroxide to water and oxygen. 

Other common cocci, such as streptococci and enterococci, are catalase negative so they don’t have this ability and we can use a few drops of hydrogen peroxide to differentiate them. 

Catalase positive bacteria will foam up, while in catalase negative bacteria, nothing happens.

Now, a couple of other staphylococci species, like Staph epidermidis and Staph saprophyticus are also catalase positive, so to distinguish between them we can look for another enzyme that’s made by Staph aureus, called coagulase. 

Coagulase converts fibrinogen into fibrin. 

So let’s say that we stir up some Staph aureus bacteria in a liquid “emulsion”, and then add a few drops of plasma which contains fibrinogen. The coagulase positive staph aureus will convert the soluble fibrinogen to sticky fibrin, which then visibly clumps up, whereas coagulase negative bacteria won’t.   

Staph aureus is extremely common and about a quarter of the population is colonized by it, usually in their nostrils, groin, armpits, and other parts of their skin. 

But, most of the time it’s a normal part of our skin flora, and doesn’t cause trouble. 

The skin flora is a complex ecosystem of different bacteri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_system_anatomy_and_physiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qof9m4doQ4mgG0RXNFnUuStwThyxCqhf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal system anatomy and physiology]]></video:title><video:description><![CDATA[The workhorses of the urinary system are the kidneys which are the twin, bean-shaped organs in your body that clear harmful substances by filtering your blood. They’re like a water purification plant that helps clean the drinking water for a city. They also regulate blood pH, volume, pressure, osmolality as well as produce hormones. 

The kidneys are located between the T12 and L3 vertebrae, and they’re partially protected by ribs 11 and 12--which are the floating ribs. The kidneys are roughly the size of a fist and are retroperitoneal, meaning they sit behind the peritoneal membrane alongside the vertebral column. The right kidney is pushed down by the liver so it sits slightly lower than the left kidney. 

In the middle of each kidney there is an indentation that forms the renal hilum. This is the entry and exit point for the ureter, renal artery and renal vein, lymphatics, and nerves going into and coming out of the kidney. 

The kidney is surrounded by three layers of tissue. On the outside is the renal fascia which is a thin layer of dense connective tissue that anchors the kidney to its surroundings. The middle layer, or the adipose capsule, is a fatty layer that protects the kidney from trauma. And the deepest layer, called the renal capsule, is a smooth, transparent sheet of dense connective tissue that gives the kidney its distinctive shape. 

If you take a cross-section of the kidney, there are two main parts. The inner portion is the renal medulla and the outside rim is the renal cortex. The medulla is made up of 10 to 18 renal pyramids with the base of the pyramids facing the renal cortex and the tips of the pyramids, called renal papilla—or nipples, pointing towards the center of the kidney. The renal papilla project into minor calyces which join together to form major calyces which funnel into the renal pelvis. Urine collects in the renal pelvis and then heads out of the kidney through the ureter. 

The renal cortex can be divided into an out]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myotonic_dystrophy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C2X5K5gxQfWOYws-6B_DuDCNSHCMeOQe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myotonic dystrophy]]></video:title><video:description><![CDATA[With myotonic dystrophy, “myo” means muscle, “tonic” means spasm, “dys” means bad, and “troph” means nourish; so myotonic dystrophy refers to the muscle appearing poorly nourished and weak, and being contracted, without being able to relax.

Myotonic dystrophy is actually a group of disorders, all of which are caused by autosomal dominant genetic mutations. 

This means that one affected copy of a gene is enough to cause disease. 

Affected people are typically present in each generation, because an affected person (male or female) has a 50% chance of passing on the affected gene to a child, which causes that child to have the disease.

There are two major types of myotonic dystrophy: type 1, or DM1 for short, also known as Steinert’s disease and type 2, or DM2 for short. 

In myotonic dystrophy type 1, the affected gene is on the long arm of chromosome 19 and is called DMPK. 

The DMPK gene has a trinucleotide repeat, which means that a group of three DNA nucleotides is repeated multiple times in a row.  

In DMPK, it’s the nucleotides cytosine, thymine, and guanine, or CTG.  

These CTGs are found in the 3’ untranslated region of DMPK. 

The 3’ untranslated region is at the end of the DMPK gene that’s made into mRNA but not protein, and it helps modulate gene expression. 

Expressed DMPK mRNA gets translated into a protein called myotonic dystrophy protein kinase, and it helps in the communication between muscle cells, but also heart and brain cells. 

In the muscle, this kinase shuts off a muscle protein called myosin phosphatase, which is involved in muscle tensing or contraction and relaxation.

In myotonic dystrophy type 2, the affected gene is located on the long arm of chromosome 3 and is called CNBP.  

Instead of a trinucleotide repeat, the CNBP gene contains a tetranucleotide repeat where the nucleotides cytosine, cytosine, thymine, and guanine, or CCTG are repeated multiple times in a row. 

These CCTGs are found in the first intron of CMBP, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Wernicke-Korsakoff_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/00FPln9tQ8W_2RAR8Wj2yTNBQLi2INO9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Wernicke-Korsakoff syndrome]]></video:title><video:description><![CDATA[Wernicke Korsakoff syndrome is named after Carl Wernicke and Sergei Korsakoff, the physicians who discovered the condition in the late 1800s. Wernicke Korsakoff syndrome is caused by Vitamin B1 or thiamine deficiency and it refers to a spectrum of disease. Wernicke&amp;#39;s encephalopathy is the acute, reversible stage of the syndrome, and if left untreated it can later lead to Korsakoff syndrome, which is chronic and irreversible.

Thiamine is typically stored in the liver and absorbed in the jejunum and ileum, and then moves throughout the body, where it’s involved in numerous cellular processes that require thiamine. The enzyme thiamine pyrophosphate synthetase transfers a pyrophosphate group from ATP to thiamine, turning it into the coenzyme thiamine pyrophosphate - which is the metabolically active form of thiamine. Now, as a coenzyme, thiamine pyrophosphate functions to assist other enzymes such as pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase carry out reactions, particularly regarding glucose metabolism. Furthermore, within the brain, thiamine pyrophosphate helps metabolize lipids and carbohydrates as well as maintain normal amino acid and neurotransmitter levels. In some neurons, thiamine even helps with propagation of a neural impulses down the axon.

Given it’s multifaceted  role, a deficiency of thiamine can have serious consequences. Specifically, thiamine deficiency impairs glucose metabolism and this leads to a decrease in cellular energy. One of the major causes of thiamine deficiency, and therefore Wernicke Korsakoff syndrome, is alcohol abuse. Alcohol leads to decreased thiamine levels in various ways. First, alcohol interferes with the conversion of thiamine to its active form, thiamine pyrophosphate by blocking the phosphorylation of thiamine. Second, thiamine is normally absorbed through the first portion of the small intestine called the duodenum. However, ethanol prevents this absorptio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neurofibromatosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y_lZPvyYRsO1ucHeHMKZmbu5Sf2iNQaY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neurofibromatosis]]></video:title><video:description><![CDATA[With neurofibromatoses, neuro refers to the nerves, fibro- refers to fibrous tissue, and -oma means growth, or tumor. 

So neurofibromatosis refers to fibrous tumors originating from the nervous system. 

The body’s central nervous system is made up of the brain and the spinal cord, which are surrounded by three protective layers called the meninges. 

Part of the central nervous system are the cranial nerves, which originate in the brainstem and innervate the head and neck, and the spinal nerves, which originate in the spinal cord, and supply the rest of the body. 

Each nerve is surrounded by a nerve sheath, which is produced by cells called fibroblasts. 

Inside, each nerve there are several fascicles, and each fascicle, in turn, is made up of several axons. 

The axons are the long projections of neurons, that carry the information as electrical signals running up and down their length. 

Along the axon there are cells called Schwann cells, which produce  a myelin cover for the axon. 

The myelin helps electrical signals travel along the axon faster. 

Now, neurofibromatoses are genetic diseases which cause non-cancerous growths to form in the body’s nerve tissue, and there are two types - type I and type II. 

They’re caused by inheriting faulty copies of either the NF1 or NF2 gene, which are found on chromosomes 17 and 22, respectively. 

Just remember, NF1 goes with chromosome 17 and NF2 goes with chromosome 22. 

Both of these have an autosomal dominant inheritance pattern, so a child only needs one faulty copy from either parent to get the disease. 

Normally, these are tumor suppressor genes, which means they stop cells from dividing uncontrollably. 

So when there’s a mutation in the gene, it leads to uncontrolled growth of fibromas which are growths that have multiple cell types including neurons, Schwann cells, and other supporting connective tissue. 

Neurofibromatosis type I, is also called von Recklinghausen’s syndrome typically affects the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Long_QT_syndrome_and_Torsade_de_pointes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/grpKA5mCRE_z_zRTv4j2NSv0Rg6tuuDx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Long QT syndrome and Torsade de pointes]]></video:title><video:description><![CDATA[On a normal ECG, you’ve got the P, Q, R, S, and T waves. 

The QT interval spans from the start of the Q to the end of the T wave. 

Long QT syndrome, or LQTS, is when somebody’s QT interval is longer than normal, which should typically be less than half of a cardiac cycle. 

In fact, for a heart rate of 60 beats per minute, the QT interval’s generally considered to be abnormally long when it’s greater than 440 milliseconds in males or 460 milliseconds in females. 

If you measure someone’s QT interval at a different rate though, say 90 beats per minute and it was 400 milliseconds, you can’t really use that to compare that to these value at 60 beats per minute, since the QT interval changes depending on the rate. 

As rate increases, the QT interval decreases. 

So what we have to do is find the corrected QT interval, or QTc, at the different rate so that you can compare it to the QT interval at 60 beats per minute. 

Even though there are several formulas you can use, the Bazett’s formula is probably the simplest, where the corrected QT interval equals the QT interval in milliseconds divided by the square root of the R to R interval in seconds divided by 1 second. 

As a bit of a side-note, usually this formula is expressed without the “divide by 1 second” bit, but the astute observer will notice that the units won’t work out if you do that. 

Interestingly, the original formula did include dividing by 1 second to get the units to work out, but for some reason in a paper way back when that step wasn’t included, and basically the version without the 1 second, the sort of unit-incorrect version, has been used ever since! 

Anyways, let’s do a quick example of a male with a 400 milliseconds QT interval at a rate of 90 beats per minute. 

Comparing to the values at 60 beats per minute, 400 milliseconds wouldn’t be considered a long QT, right? 

If we use our handy formula, though, we’ll plug in 400 for QT and 90 beats per minute or .66 seconds per beat. 

So ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dental_abscess</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JFHQM1nqQY2dq8s_W6pzw4t8RVKDN50_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dental abscess]]></video:title><video:description><![CDATA[Everyone who has ever had a pimple has had an abscess, even though they’re tiny, they’re still abscesses. 

An abscess forms when normal tissue, like the gingiva or gums and teeth for example, is split apart and that new space is invaded by nearby pathogens like bacteria. 

In a healthy mouth, normal or commensal bacteria thrive but don’t cause disease. 

However, any cut or break in the mucosa is an invitation for bacteria to dive in and multiply, causing an infection. 

When that happens, the immune system typically responds and a battle ensues with the result being pus - a mixture of bacteria, immune cells, and dead tissue.

So, in response to an injury, cells release small chemicals called cytokines, like tumor necrosis factor, interleukin-1, interleukin-6, interleukin-8, and interleukin-17, and these attract nearby immune cells. 

It’s kinda like yelling for help and being heard by the nearby police. 

In addition, the cytokines also dilate nearby capillaries and make them leaky - which brings more blood to the site, and allows immune cells that do show up, to easily slip out of the blood and into the tissue. 

The first immune cells at the scene are neutrophils, and they release chemicals and enzymes that kill themselves and the bacteria they swallow up, creating a pool of dead bacteria and cells. 

This is a specific type of acute inflammatory response called suppurative inflammation, which simply means that pus is created in the process.

From a macroscopic view, this is sometimes referred to a liquefactive necrosis, because the area of dead tissue turns to liquid. 

Initially the dead tissue is intermixed with healthy tissue, but over time it can coalesce into a single area. 

And around this pool of pus, a wall of fibrinogen - starts to harden into a barrier. 

Occasionally sheets of fibrin form septations, creating loculations or pockets of pus within the abscess itself...kinda like an abscess within an abscess... 

Even though the pus is largel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Syncope:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5TtSzOJUQLedLYrGv-pqldqKSX_1Vi1q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Syncope: Clinical]]></video:title><video:description><![CDATA[Syncope, or fainting, is when a person loses consciousness and muscle strength. It usually comes on quickly, doesn’t last long, and there’s usually a spontaneous recovery requiring no resuscitation. 

It’s caused by a decrease in blood flow to the brain, usually due to low blood pressure. 

There’s also presyncope, which is near loss of consciousness with lightheadedness, muscular weakness, blurred vision, and feeling faint without actually fainting. 

Presyncope can lead to syncope, so you can think of it as a spectrum of the disease. 

Recognizing symptoms of presyncope may allow to act fast and prevent evolution of the episode into a full faint. 

The immediate treatment of an individuals with syncope or presyncope starts with laying the individual supine, with legs elevated if possible to help venous return to the heart and restore adequate brain perfusion. 

Then, you should assess vital signs, namely a pulse and evidence of respiration, to distinguish cardiac arrest from syncope, and call for additional help if needed. 

Finally, you should attempt to arouse the individual without trying to raise them up until they’re ready.

Ok so once the individual has regained consciousness, the next step is to identify the cause. 

Neurocardiogenic, vasovagal, and reflex syncope are the most common causes of syncope, and this is a benign condition triggered by parasympathetic activation resulting in vagus nerve discharge. 

This discharge may in turn be triggered by urination, defecation, coughing, prolonged standing, or a stressful event like seeing blood and needles. 

Carotid sinus hypersensitivity is a variant of neurocardiogenic syncope. 

That’s when mild external pressure on the carotid bodies in the neck is enough to induce this reflex response. 

It can be triggered by a tight collar, shaving, or head turning. Most patients with neurocardiogenic syncope experience a prodrome, which is a period of symptoms lasting at least a few seconds just prior t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/acne-vulgaris</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dSEsyuI2TpG5dEz7qIHpqBneSaa1sUc3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acne vulgaris]]></video:title><video:description><![CDATA[With acne vulgaris, acne means “eruption” and vulgaris, means “common”. So acne vulgaris is a common skin eruption that occurs when hair follicles, or pores, get blocked by particles like dead skin cells or oil. Once hair follicles are blocked, it forms small raised, red bumps on the skin. Acne is particularly common among teenagers because of the skin changes that occur during puberty. Acne can be categorized into different types based on specific characteristics. For example, mild acne usually consists of whiteheads and blackheads, moderate acne, usually consists of pustules, and severe acne, usually consists of cysts and nodules. 

Now, the skin is divided into three main layers--the epidermis, dermis, and hypodermis. The epidermis forms the thin outermost layer of skin, and has 5 sublayers: the stratum corneum as the outermost layer followed by the stratum granulosum, the stratum spinosum, and the stratum basale. In the palms and feet, which are areas with thicker skin, there is a fifth layer called the stratum lucidum which is around one cell layer thick. Underneath the layers of the epidermis is the dermis, and it’s mainly made up of connective tissue but also contains nerve endings, hair follicles, sweat glands, sebaceous glands, lymphatic vessels and blood vessels. Focusing on the hair follicles, each one contains a strand of hair, composed of the shaft, root, and bulb that sits in the follicle. The hair follicle is epidermal tissue that dips down into the dermis, and is associated with other structures like apocrine glands, sebaceous glands, the arrector pili muscle, and nerve receptors. Now, sebaceous glands, or oil glands, are located in the dermis layer of the skin and are connected to hair follicles. Each sebaceous glands secrete an oily substance called sebum into a nearby hair follicle or through pores that extend directly to the skin surface. Sebum is a substance made of different fatty acids and waxy esters to help transport nutrients and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vestibular_transduction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/geweW1UJS32pMlWqXLTV5NqbSySZIcp1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vestibular transduction]]></video:title><video:description><![CDATA[With vestibular transduction, “vestibular” refers to balance, and transduction refers to the process by which the ear converts specific head movements into electric impulses, so that we can interpret where we are in space. 

The ear is made up of three parts: the outer ear, the middle ear, and the inner ear.  

The first part is the outer ear which is the part you see and hang earrings on, called the pinna, as well as the ear canal. 

The second part is the middle ear, which is a tiny chamber that houses even tinier ear bones—the malleus, incus, and stapes. 

The outer and middle ear only play a role in hearing - however, the third part, the inner ear, deals with both hearing and balance. 

On the outside, the inner ear has a tough bony shell - the bony labyrinth; and inside the bony labyrinth, there is the membranous labyrinth. 

Now, both of these sections are filled with fluid - the bony labyrinth contains a fluid called perilymph, while the membranous labyrinth contains endolymph. 

The bony and membranous labyrinth make up the structure of all three parts of the inner ear. 

The first is the vestibule, which is like a hallway that leads up to two other parts or rooms - the cochlea, towards the front of our head, that deals with hearing, and a second room containing the three semicircular canals, towards the back. 

The semicircular canals, along with two other structures - the utricle and saccule, which are located in the vestibule - make up the vestibular apparatus, that helps us detect changes in our static and dynamic equilibrium.

Our static equilibrium is a job for the utricle and saccule - also known as the otolith organs. They contain endolymph, as well as special balance receptors that detect changes in our head position in relation to horizontal or vertical acceleration. 

Now, inside the utricle, there’s a region called the macula - which looks like like a bean-shaped shaggy rug lying on the floor. 

The macula is where our balance receptors]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Limited_systemic_sclerosis_(CREST_syndrome)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rnnANa7ISFC6nFDNso6FMPJnQ8ylSYme/_.jpg</video:thumbnail_loc><video:title><![CDATA[Limited systemic sclerosis (CREST syndrome)]]></video:title><video:description><![CDATA[CREST syndrome, also known as limited cutaneous systemic sclerosis, is an autoimmune condition, and its name is an acronym that stands for calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasias. 

Calcinosis is the deposition of calcium in the skin, Raynaud’s is spasm of the arteries in the fingers, esophageal dysmotility refers to difficulty swallowing, sclerodactyly is tightening of the skin over the fingers, and telangiectasias are small dilated blood vessels on the skin surface. 

So, normally, when there’s an infection in the body, macrophages will eat some of the invading organisms and break them down. 

In addition to destroying the pathogen, they also present a fragment of the pathogen, called an antigen, to naive T cells. 

When the naive T-cells bind to this presented antigen, they mature into T-helper cells, also called CD4+ T-cells, and go on to help and recruit more immune cells. 

The T-helper cells release cytokines, which increase the activity of macrophages and attract nearby neutrophils.

They also release cytokines, like TGF-β, that tells fibroblasts to repair damaged tissue after the infection by laying down collagen.

The cause of CREST syndrome isn’t known exactly, but individuals in the first two years of the disease have a higher than normal number of T-helper cells in the skin on their hands and face, particularly near small blood vessels. 

The T-helper cells release cytokines to attract other immune cells, like macrophages and neutrophils, which cause a lot of inflammation in the skin. 

There is so much inflammation that the tissue dies, in a process called necrosis.

When the cells die, calcium in the cytosol binds to fragments of cell membrane and builds up in the skin, which is called calcinosis. 

It’s not clear why it happens, but individuals with CREST often experience Raynaud’s phenomenon, which is an episodic, dramatic vasoconstriction of arterial blood vessels in the hands. 

It’s n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cross_sectional_study</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2Qwn0QVIQjicG0B9fCZRH-uzQwu8WDk4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cross sectional study]]></video:title><video:description><![CDATA[A cross- sectional study is a study design where an exposure and an outcome are measured at the same time.

For example, let’s say you want to figure out if people who are obese – which means having a body mass index or BMI of 30 or higher - have higher serum cholesterol levels compared to people who are not obese – having a body mass index below 30. 

To do this, you might look at the medical records of 100 people to see who has high cholesterol levels and who has low cholesterol levels and compare that to how many people in each group are obese or not obese.

You can think about a cross-sectional study like a snapshot of the population at a certain point in time. 

Since you can only collect the information you see in that one moment, you don’t know what happens before or after the snapshot was taken. 

So, we can only collect information on prevalence – the proportion of exposures or outcomes that already exist at a certain time – and not incidence – the proportion of new exposures or outcomes that occur in a certain time period.

In terms of prevalence, there’s an outcome prevalence and an exposure prevalence. 

The outcome prevalence is the proportion of people who have an outcome in the exposed group and the non-exposed group. 

In a cross-sectional study this can be organized in a 2 by 2 table, with the exposure – obesity or no obesity – on the side and the outcome – high or low cholesterol levels – on the top, and each box is labeled a, b, c, or d. 

Cell a includes individuals who have high cholesterol and who are obese; cell b includes individuals who have low cholesterol and who are obese; cell c includes individuals who have high cholesterol and who are not obese; and cell d includes individuals who have low cholesterol and who are not obese.

We can calculate an outcome prevalence to figure out if high cholesterol – the outcome – is more prevalent for people who are obese or not obese – the exposure. 

Let’s say that there are 50 people in cel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Graft-versus-host_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qN4FynOrS3WDOiRl_MGGoFE1TaSILh2g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Graft-versus-host disease]]></video:title><video:description><![CDATA[With “graft-versus-host disease”, “graft” refers to a section of transplanted, or donated tissue, like bone marrow or peripheral blood, and “host” refers to the tissues of the person receiving the transplant. 

In graft versus host disease, immune cells in the donated tissue attack the recipient’s body cells.

Normally, the immune system’s job is to fight against anything foreign that might cause harm, without harming the body’s own cells.

To make that work, the immune system cells are trained, from early on, to distinguish non-self or foreign, from self. 

Recognizing whether a cell is non-self or self involves a set of genes called histocompatibility genes, which make up the major histocompatibility complex, or MHC proteins. 

These MHC proteins also go by the name human leukocyte antigens, or HLA. 

The histocompatibility genes actually code for two classes of proteins, MHC class I and MHC class II.  

MHC class I molecules are found on all nucleated cells throughout the body, while MHC class II molecules are only expressed on antigen presenting cells like monocytes, macrophages, dendritic cells, and B cells.

But because the genes coding for them are so variable in the population, two different individuals will have major differences in the antigens expressed on their cells, even siblings - unless, of course, they’re identical twins.

When there’s a tissue transplantation, the transplant usually comes from a genetically different individual, and it’s called an allograft. 

If there are immune cells within that allograft, they will see the MHC proteins that coat every cell of the recipient body as “non-self”. 

In fact, that’s why transplantation donors are really carefully selected, to make sure that they share as many of the same HLA antigens with the host as possible. 

But even between HLA-identical individuals, other antigens, called minor histocompatibility antigens, can be recognized as foreign and trigger an immune response between the donor an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kluver-Bucy_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/krSQg7bUTOOEQdUHV2bp7GTWSmWw6TAR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kluver-Bucy syndrome]]></video:title><video:description><![CDATA[Klüver-Bucy syndrome is neurobehavioral condition first observed in the 1930s by Heinrich Klüver and neurosurgeon Paul Bucy.  

They discovered that monkeys that had bilateral temporal lobe lobectomies developed dramatic behavior changes in their memory, as well as their social and sexual behaviors. 

In retrospect, it’s not surprising that having a significant portion of the brain removed caused behavior changes in monkeys - the biggest one was probably anger at Klüver and Bucy for putting them through that!

The temporal lobe is one of the four major lobes of the brain. 

It has a variety of functions which are involved in sensory processing. 

The ventral, or anterior, part of the temporal lobe helps process visual information, such as the recognition of objects and faces. 

Whereas, the medial, or middle portion, of the temporal lobe, along with the hippocampus, is responsible for the formation of new memories. 

The temporal lobe also houses the primary auditory cortex, which is needed for speech comprehension. 

Other important structures found within the temporal lobe include the olfactory cortex, which processes the sensation of smell, and the amygdala, which processes emotions. 

The amygdala also plays a role in the reward center of the brain which motivates and reinforces behaviors that elicit positive feelings. 

In Klüver-Bucy syndrome there’s a bilateral lesion of the temporal lobe. 

The most common cause of such a brain lesion is herpes simplex encephalitis - a viral infection that particularly affects the temporal lobes. 

Other causes of Klüver-Bucy syndrome include trauma, stroke, Alzheimer&amp;#39;s disease, and Niemann Pick disease, which is a rare metabolic condition that affects various organs of the body, including the brain. 

The damage affects the amygdala which is a part of the brain that regulates emotions and reinforces behaviors related to food and sex. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_products_and_transfusion:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vl_kOkOlRful0542dkuCFJG1T_ClyO4S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood products and transfusion: Clinical]]></video:title><video:description><![CDATA[Blood transfusions are life-saving treatment options, to the point where informed consent is not necessarily required if it has to be done in an emergency to save a person’s life. 

Additionally, blood banks have developed a sophisticated variety of blood products to ensure that they’re free of infection and compatible with a recipient’s blood type. 

To understand them all, let’s review the normal components of blood. When blood is spun down in a centrifuge, the layers separate out. 

The first layer is the cellular component, which accounts for 45% of blood, and includes red blood cells, or RBCs, white blood cells, or WBCs, and platelets.

Second is the acellular component, also called plasma, which accounts for 55% of blood. 

Plasma is composed of everything that isn’t a cell, including proteins like albumin, electrolytes like sodium, molecules like glucose, coagulation factors like factor 8, and lipoproteins like low-density lipoprotein, or LDL. 

Now, the main blood products that can be transfused are packed red blood cells, or PRBCs, which are RBCs that had most of their surrounding plasma removed, fresh frozen plasma, or FFP, which is made of all the coagulation factors together, platelets, prothrombin complex concentrates, or PCCs, which are composed of factors 2,7,9 and 10, cryoprecipitate, which is made of fibrinogen, von willebrand factor, and factors 8 and 13 and finally pure coagulation factor concentrates, like pure factor 8. 

Alright, so acutely bleeding or anemic patients can require PRBC transfusions. 

To do that, a sample of their blood is taken, and the bank performs a “type and screen”.

Type refers to looking at the recipient’s RBCs surface antigens, which include their ABO, Rh or D-antigens and checking if they’re compatible with the donor’s RBCs.

Screen refers to looking for antibodies in the recipient’s plasma, and if they’re present, then making sure that the donor RBCs don’t have antigens that would get bound by those antibodi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alpha_1-antitrypsin_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GMmqMvVqSrmOmlw3eKWuZFrzTSG_W6Rd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alpha 1-antitrypsin deficiency]]></video:title><video:description><![CDATA[Alpha-1 antitrypsin deficiency is a genetic disorder in which a protein called alpha-1 antitrypsin is defective or absent, and it causes lung and liver disease. 

Trypsins are a type of protease, which is an enzyme that can break down other proteins. 

So this antitrypsin protein is a protease inhibitor, and inactivates trypsins, thereby preventing protein breakdown. 

The “alpha-1” is just a holdover from when the protein was discovered – a letter and number combination given before its role was known. 

Now, in the lungs, if we zoom in on a tiny alveolus—where gas exchange happens—if there’s some sort of infection or other cause of inflammation, immune cells like neutrophils arrive on the scene. 

Neutrophils make an enzyme called neutrophil elastase, a protease capable of breaking down elastin, which is an extracellular matrix protein that gives elasticity and strength to lung tissues. 

So while these little guys can help fight off infection by breaking down proteins of the bacteria, it can also go on to break down that precious elastin. 

Fortunately, the liver makes alpha-1 antitrypsin which gets released into the blood and sent to the lungs, where it inhibits neutrophil elastase just like it inhibits trypsin, inactivating it before it can break down the protein elastin. 

Without alpha-1 antitrypsin, the opposite happens - neutrophil elastase goes unchecked, and it damages the walls of the alveoli, and without that elastin, the alveoli loses its elasticity and structural integrity. 

Zooming out a bit and looking at the acinus, which is a bunch of alveoli, it just turns into one big cavity. This destruction and enlargement of the air spaces is called emphysema. 

It turns out that emphysema can develop in a couple different ways, and alpha-1 antitrypsin deficiency causes pan-acinar emphysema, meaning the whole acinus is affected, and it also tends to affect the lungs’ lower lobes the most. 

Another effect of unchecked inflammation in alpha-1 antitr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osgood-Schlatter_disease_(traction_apophysitis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gRLlxY_hQa6jAc6o762EIew2Ta_tvA19/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osgood-Schlatter disease (traction apophysitis)]]></video:title><video:description><![CDATA[Osgood-Schlatter disease is an inflammation of the patellar tendon, right at the point where it inserts on the tibial tuberosity, resulting in painful swelling just below the knee. It’s named after two orthopedic surgeons; the American Robert Osgood, and the Swiss Carl Schlatter. Now, just to be clear what we’re talking about, the patellar tendon is sometimes also called the patellar ligament, but tendon is more common.   

So, focusing in on the knee, the proximal epiphysis of the tibia, which is the upper end of the tibia that contributes to the knee joint, has a bony prominence called the tibial tuberosity. This is considered an apophysis, meaning that it’s a bony prominence that serves as a site for tendon attachment. The tibial tuberosity specifically serves as the attachment site for the patellar tendon, which is an extension of the quadriceps muscle tendon. When the quadriceps muscle contracts, the patellar tendon tightens, extending the knee. At birth, the proximal epiphysis consists of cartilage, but it contains an ossification center inside. This ossification center begins to ossify or turn to bone between the age of nine and fifteen and becomes a bony tuberosity around the age of eighteen.  

Osgood-Schlatter disease typically develops between the age of ten and fifteen when the tuberosity hasn’t ossified yet and therefore isn’t hard enough to resist traction of the patellar tendon. So, this is why the disease is very common in young adolescents who play sports requiring the quadriceps muscles to contract repetitively, causing the patellar tendon to excessively strain on the not-yet-ossified tibial tuberosity. This results in inflammation of the tendon at the point it inserts to the tuberosity, what is known as traction apophysitis. When the traction is too excessive, it can cause the ossification center inside the tuberosity to crack into tiny bone fragments. Eventually, that results in a more prominent tuberosity or a callus during the healing]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Normal_distribution_and_z-scores</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PvOBUOZ-Q52-3iWIC5WS9-2wR6uKTtL9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Normal distribution and z-scores]]></video:title><video:description><![CDATA[Let’s say you ask 1000 men for their weight, and then you plot their answers on a histogram, which is a plot that shows the distribution of any measurement or data. 

Let’s say that the average weight is 170 pounds or about 77 kilograms, and that it turns out that the majority of men weighed that amount, whereas fewer men weighed a little bit higher or a little bit lower than the average, and even fewer men weighed much higher or much lower than the average. 

If we draw a curve over the top of our histogram, we get the normal distribution curve, which is also called the bell curve, because it’s shaped like a bell. 

The bell curve is symmetrical, with half the data on the left of the average and half the data on the right side of the average.

The area under the bell curve is equal to 1, or 100%, with the highest percentage of data in the middle section and the lowest percentage of data in the outer tails of the curve. 

Typically, for population data, the average point in a bell curve is labeled with the greek letter mu, and mu refers to the mean, median, and mode, because when data are normally distributed, the mean, median, and mode are all equal to each other. 

The standard deviation is a measure of how spread out the data are from the average, and for population data it’s represented by the greek letter sigma.

For example, let’s say the standard deviation of weight for our sample of men is 29 pounds, or 13 kilograms. 

In a normal distribution, 68 percent of the data are within one standard deviation.

That means that 68 percent of men will weigh somewhere between 170 minus 29, or 141 pounds, and 170 plus 29, or 199 pounds. 

Also, 95 percent of the data are found within two standard deviations - so, since 29 times 2 is 58, then 95 percent of men will weigh somewhere between 170 minus 58, or 112 pounds, and 170 plus 58, or 228 pounds. 

Finally, 99.7 percent the data are found within three standard deviations, and since 29 times 3 is 87, 99.7% of m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leukodystrophy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MaAVQc8VSwWR676TYQOci9egQqS3G0Ue/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leukodystrophy]]></video:title><video:description><![CDATA[Leukodystrophy can be broken down. Leuko- means “white”, -dys means “abnormal” and -troph means “growth”. 

So, leukodystrophy means degeneration of the white matter of the brain, and that’s the part of the cerebral cortex that’s filled with myelinated axons. 

Myelin refers to the electrical insulation sheath around axons which allows neurons to quickly send electrical impulses to one another. 

Leukodystrophy is a dysmyelinating disease, meaning the structure of the myelin is abnormal, and it’s usually due to a genetic mutation. 

In contrast, in a demyelinating diseases, previously normal myelin is damaged, like in multiple sclerosis where the immune cells attack the myelin. 

There are many different kinds of leukodystrophy, but the most common ones are Krabbe disease, metachromatic leukodystrophy, and adrenoleukodystrophy. 

The cerebral cortex is the largest region of the brain and it’s responsible for sensory and motor functions. 

The cerebral cortex has an outer grey area and an inner white area. 

The grey area, referred to as grey matter, houses neuron cell bodies. 

And the white area, referred to as white matter, houses myelinated axons. 

It is lighter because of the high fat content in myelin.

Neurons are the key cells that transmit neural impulses to one another through synapses. 

Each neuron has dendrites, a cell body, and an axon. 

Dendrites are the branches that first receive a neural impulse at a synapse with another neuron. 

The neural impulse passes through the cell body and goes through an axon, which projects information away from the cell body to another cell. 

Glial cells are support cells for neurons and they produce myelin to coat the axons.

Myelin is a specialized membrane which helps insulate the axon to make neural impulses travel faster. 

Glial cells in the central nervous system, are called oligodendrocytes, and glial cells in the peripheral nervous system are called Schwann cells. 

Now the myelin is composed of cer]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mortality_rates_and_case-fatality</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IztJqN5cSRW9g4M9AvlpCHOESPqv8EOh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mortality rates and case-fatality]]></video:title><video:description><![CDATA[Let’s say we want to figure out the risk of dying for people who live in a certain population, like the population of France in 2015, which was around 66.6 million people. 

The first way we could do this is by calculating the all-cause mortality rate or death rate. 

That’s the total number of deaths from all causes in 1 year divided by the total number of people at risk in the population at mid-year, and typically that’s the number of people at risk of death in the entire population. 

For example, in 2015, there were approximately 620,000 deaths. 

So, the all-cause mortality rate in France was 620,000 divided by 66.6 million, or 0.0093.

We can express the mortality rate in a few different ways. 

First, we could say that the absolute risk of dying from all causes in France in 2015 was 0.0093. 

Alternatively, we might express it as a percentage, by multiplying it by 100 - so 0.0093 times 100 equals 0.93%. 

Most often though, we express mortality rate in terms of number of deaths per 100,000 people. 

So, we multiply the mortality rate - 0.0093 - by 100,000, which is 930. 

This means that, in France, there were 930 deaths per 100,000 people in 2015. 

Mortality rates can be calculated for any time period, like 1 month, 1 year, or 10 years, but it’s important to specify which time period is used in the calculation, since the rate might be different for different time periods. 

For example, a natural disaster - like an earthquake or forest fire - might increase the number of deaths in a certain time period. 

Sometimes we’re interested in the mortality rate in a certain subpopulation, like only women or only people who are older than 65 years. 

In those situations, we use a specific rate - like an age-specific rate or a gender-specific rate - which is calculated by dividing the number of deaths from all causes in one year by the number of people at risk of death in the subpopulation at mid-year.

For example, there were around 33.9 million women in F]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Legg-Calve-Perthes_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EZvFZOrqSYm-3CbidCs5kLzGRWyzasWe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Legg-Calve-Perthes disease]]></video:title><video:description><![CDATA[Legg–Calvé–Perthes disease is a childhood hip disorder that occurs when the blood supply to the head of the femur gets disrupted and leads to death or necrosis of the tissue. 

The disease was named after three doctors; Arthur Legg, Jacques Calvé, and Georg Perthes.

The hip joint is a ball and socket type, because the ball-shaped head of the femur sits and rotates inside the cup-shaped socket called the acetabulum. 

This gives the hip joint the ability to move nearly in all directions, as long as the ball can smoothly rotate inside the socket. 

Now, the head of the femur is supplied by branches of 3 arteries, the medial and lateral femoral circumflex arteries, as well as the artery of ligamentum teres. 

The arteries send branches that climb up the neck of the femur to supply the head of the femur, providing the tissue with the nutrition it needs to grow and maintain its spherical shape.

In Legg–Calvé–Perthes disease, for some children, the blood supply to the femoral head becomes interrupted for some reason - and it’s not known why exactly. 

The result is that the tissue begins to die off - a process called avascular necrosis. 

Over time, there’s new blood vessel formation into the necrotized bone and that allows the dead tissue to get removed by immune cells called macrophages. 

That process causes the head of the femur to lose mass, leaving it weak and prone to fractures.

When this happens, the head of the femur becomes misshapen and can no longer smoothly rotate inside the concave acetabulum, which results in reduced range of motion.

Now, over time, Legg–Calvé–Perthes disease typically self-resolves and the bone is able to heal - once again it’s not known exactly why or how this happens.

When bone remodeling occurs, new bone replaces the necrosed bone, and the spherical shape of the head of the femur gets restored and properly fits in the acetabulum again. 

With time, there’s normal functioning of the joint once more. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Standard_error_of_the_mean_(Central_limit_theorem)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CgcY-UQFQqmVbmEd9ooOEFMFRzGSPVit/_.jpg</video:thumbnail_loc><video:title><![CDATA[Standard error of the mean (Central limit theorem)]]></video:title><video:description><![CDATA[Let’s say you ask 1000 men for their weights and then plot those weights on a histogram, which is a type of plot that shows the distribution of measurements or data. 

So let’s say that the majority of men weighed the same as the average - which in this case might be 170 pounds, or around 77 kilograms - while fewer men weighed a little bit higher or a little bit lower than the average, and even fewer men weighed much higher or much lower than the average.

If we draw a curve over the top of our histogram, we get the normal distribution curve, which is also called the bell curve, because it’s shaped like a bell. 

The bell curve is symmetrical, with half the data on the left of the average and half the data on the right side of the average. 

The area under the bell curve is equal to 1, or 100%, with the highest percentage of data in the middle section and the lowest percentage of data in the outer tails of the curve. 

Typically, for population data, the average point in a bell curve is labeled with the greek letter mu, and mu refers to the mean, median, and mode, because when data are normally distributed, the mean, median, and mode are all equal to each other. 

The standard deviation is a measure of how spread out the data are from the average, and for population data it’s represented by the lowercase greek letter sigma. 

For example, let’s say the standard deviation of weight for our sample of men is 29 pounds, or 13 kilograms. 

In a normal distribution, 68 percent of the data are found within one standard deviation. 

That means that 68 percent of men will weigh somewhere between 170 minus 29, or 141 pounds, and 170 plus 29, or 199 pounds.

Also, 95 percent of the data are found within two standard deviations - so, since 29 times 2 is 58, then 95 percent of men will weigh somewhere between 170 minus 58, or 112 pounds, and 170 plus 58, or 228 pounds. 

Finally, 99.7 percent the data are found within three standard deviations, and since 29 times 3 is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disease_causality</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uvS-k0jHRKaMO7el1kAogxerTuCg1o7J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disease causality]]></video:title><video:description><![CDATA[One of the main goals of epidemiology is to identify causal relationships between outcomes - like death, diseases, or injuries  - and exposures - like smoking cigarettes, eating junk food, or drinking alcohol. 

For example, nowadays, it’s widely known that smoking cigarettes causes lung cancer, or in other words, that smoking cigarettes leads to the development of lung cancer in many people. But how did we figure this out? 

In the mid- 1950’s, an epidemiologist named Sir Austin Bradford Hill came up with nine guidelines for determining whether or not two things are causally related, and these are called the Bradford Hill Criteria. 

The first criterion refers to the strength of association, and says that two things are more likely to be causally related if the strength of association between them is large. 

For example, for people who smoke, the relative risk of lung cancer is around 25, meaning people that smoke have 25 times the risk of developing lung cancer compared to people that don’t smoke. 

On the flip side, the relative risk of breast cancer for people who smoke is only about 1.5, which is much lower than the relative risk of lung cancer. 

So, smoking is much more likely to cause lung cancer than it is to cause breast cancer.

The second criterion states that causal relationships are dose- dependent, meaning a person who has higher amounts of exposure will also have a higher risk of developing the outcome.

For example, the relative risk of lung cancer for people who smoke 10 cigarettes per day might be 8, the relative risk of lung cancer for people who smoke 15 cigarettes per day might be 13, and the relative risk of lung cancer for people who smoke 20 cigarettes per day might be 22. 

On the other hand, if a person decreases or stops their exposure, their risk of the outcome also decreases. 

For example, in people who stop smoking, the risk of dying from lung cancer decreases by half. 

In a causal relationship, the exposure has to precede]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complement_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ys1gZrotTXivh4mVFDhakBHPSQOa1ghQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complement deficiency]]></video:title><video:description><![CDATA[With complement deficiency, there’s a deficiency in one or more of the complement proteins, which are part of the immune system. 

Complement deficiencies can either be acquired or inherited, and often result in a weaker immune response to infections.

So let’s start with the proteins that make up the classical pathway - C1, C2, C3, C4, C5, C6, C7, C8, and C9. 

And parts of these proteins are designated with lower case letters like “a” or “b”. Pretty easy right? 

Now these were numbered, in the order they were discovered, but not the order in which they function. 

Generally speaking, each complement protein is normally inactive, and it becomes activated when it’s cleaved - in other words when some part of it breaks free. 

A bit like how a fire extinguisher isn’t “active” until a pin is pulled out. 

The complement system helps with three important immune processes: inflammation, phagocytosis, and the creation of membrane attack complexes or MACs. 

Inflammation is when chemicals and cells collect to protect a damaged or infected area; phagocytosis is when certain white blood cells called phagocytes engulf and digest antigens; and membrane attack complexes are structures which dig into antigen surfaces and lyse them, or rupture and kill them.

There are actually three complement pathways: The classical pathway - called that because it was discovered first, the alternative pathway which was found second and is always at work, and the Lectin binding pathway - which was found third and when folks got more descriptive with their naming.

So all three pathways start out a bit differently, but end the same way - with a membrane attack complex which is a protein complex that creates a hole in a bacterial cell membrane - effectively destroying mainly gram negative bacteria. 

The various complement fragments contribute to these three pathways, but also play other additional roles as well.

For example, C3b serves as an opsonin - which means that it helps immune]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Direct_standardization</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uawyelJ_TeOWH3atBbcCqkhyS5qe5M4P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Direct standardization]]></video:title><video:description><![CDATA[In epidemiology, we often want to compare the mortality rates, or the frequency of deaths, and morbidity rates, or the frequency of a certain disease, in different populations. 

Typically, we do this by calculating the crude mortality rate for each population, which is the number of deaths that occur within a certain timespan, like a year, divided by the total number of people in the population. 

For example, let’s say we want to compare the crude mortality rates in two cities - City 1, which has a population of 23,000 people, and City 2, which has a population of 26,000 people. 

In one year, there were 68 deaths in City 1, and 122 deaths in City 2. 

So the crude mortality rate in City 1 is 68 deaths divided by 23,000 people, or 0.003. 

This means that there were 3 deaths for every 1,000 people that year in City 1. 

The crude mortality rate for City 2 is 122 divided by 26,000, which equals 0.005, or 5 deaths per 1,000 people.

We can use a mortality ratio, or a ratio of two mortality rates, to compare the crude mortality rate of City 1 to the mortality rate of City 2, and we get a ratio of 3 to 5. 

And if we divide both sides by the bigger number, 5, we get a mortality ratio of 0.6 to 1, which means that, in one year, City 1 had a mortality rate 40% lower than City 2. 

That may convince some folks to pack their bags and move to City 1! 

Sometimes though, calculating the crude mortality ratio doesn’t provide an accurate picture of the two populations, and this is usually because the populations have different distributions of certain characteristics, like age, sex, or race. 

For example, let’s say City 1 and City 2 have different age distributions, so City 1 has an older population with a large percentage of people over the age of 40, whereas City 2 has a younger population with only a small percentage of people over the age of 40. 

Typically, mortality rates tend to be higher in older populations and lower in younger populations. 

So, we can sp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Indirect_standardization</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J4NEg4zlTBS0u2sGGTx-F5IeToeprkD9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Indirect standardization]]></video:title><video:description><![CDATA[In epidemiology, we often want to compare the mortality rates, or the frequency of deaths, and the morbidity rates, or the frequency of a certain disease, in different populations. 

Typically, we do this by calculating the crude mortality rate for each population, which is the number of deaths in that occur within a certain timespan, like a year, divided by the total number of people in the population. 

For example, let’s say we want to compare the crude mortality rates in two cities - City 1, which has a population of 23,000 people, and City 2, which has a population of 26,000 people. 

In one year, there were 68 deaths in City 1, and 105 deaths in City 2. So the crude mortality rate in City 1 is 68 deaths divided by 23,000 people, or 0.003. This means that there were 3 deaths for every 1,000 people that year in City 1. 

The crude mortality rate for City 2 is 105 divided by 26,000, which equals 0.004, or 4 deaths per 1,000 people. 

We can use a mortality ratio, or a ratio of two mortality rates, to compare the crude mortality rate of City 1 to the mortality rate of City 2, and we get a ratio of 3 to 4. And if we divide both sides by the bigger number, 4, we get a mortality ratio of 0.75 to 1, which means that, in one year, City 1 had a mortality rate 25% lower than City 2. That may convince some folks to pack their bags and move to City 1! 

Sometimes though, calculating the crude mortality ratio doesn’t provide an accurate picture of the two populations, and this is usually because the populations have different distributions of certain characteristics, like age, sex, or race. 

For example, let’s say City 1 and City 2 have different age distributions, so City 1 has an older population with a large percentage of people over the age of 40, whereas City 2 has a younger population with only a small percentage of people over the age of 40. 

Typically, mortality rates tend to be higher in older populations and lower in younger populations. So, we can spe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hematopoietic_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PPVxjtw3RDuZwTngKpNYA11YR0Ku2td6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hematopoietic medications]]></video:title><video:description><![CDATA[Hematopoietic medications increase the amount of blood cells. 

Ηema refers to blood and poiesis means to make. 

Specifically, hematopoietic medications increase the production of erythrocytes or red blood cells, leukocytes or white blood cells, and platelets, which are small clot forming fragments of a larger cell called a megakaryocyte.

Now, before we discuss these medications in detail, let&amp;#39;s take a step back and talk about the physiology of hematopoiesis, which can result in the production of over one hundred billion new cells every single day! 

Hematopoiesis occurs in the bones of the body, but primarily in the bones of the pelvis, ribs, and sternum. 

This process starts in the bone marrow, the innermost portion of bone, where the hematopoietic stem cells reside. 

These serve as progenitor cells for all the different cell types found in the blood. 

First, hematopoietic stem cells, also called hemocytoblasts, can become lymphoid progenitors or myeloid progenitors. 

The lymphoid progenitors can develop into lymphoblasts, which can then differentiate into T-lymphocytes, B-lymphocytes, or natural killer cells. 

The myeloid progenitors can differentiate into erythrocytes, megakaryocytes, or myeloblasts, which can then become immune cells like monocytes, neutrophils, basophils, and eosinophils. 

Now, in order for a hematopoietic stem cell to reach its final, mature form, the cell needs to receive the appropriate signals in the form of specific growth chemicals, called growth factors or stimulating factors. 

While there are a multitude of these factors that cause differentiation of these cells, we’re only going to discuss the most important ones related to hematopoietic medications.

First, GM-CSF, or granulocyte macrophage colony stimulating factor, and G-CSF, or granulocyte colony stimulating factor, are glycoproteins released in response to infection by the endothelium, which is the inner lining of blood vessels, and immune cells such a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombocytopenia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ibR-2VEFRb_BEWQWwqzOtmr0SjSXYd2v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombocytopenia: Clinical]]></video:title><video:description><![CDATA[Say you get one of those annoyingly painful paper cuts, which damages your blood vessel endothelium, causing you to bleed. Normally, the first responders to endothelial damage are platelets, which quickly plug the site of injury - that’s primary hemostasis. 

Later, coagulation factors come in to strengthen that platelet plug - that’s secondary hemostasis. 

Now, a low number of those first responder platelets is thrombocytopenia, and it’s defined as a platelet count below 150,000 cells per microliter, with the normal range being between 150,000 and 450,000. 

Thrombocytopenia is mild if the platelet count is between 100,000 and 150,000, moderate if it’s between 50,000 and 100,000, and severe if it’s less than 50,000. 

Generally, the lower the platelet count, the higher the risk of bleeding or bruising. 

Spontaneous bleeds starting to happen when the platelet count falls below 30,000, with spontaneous intracranial bleeds developing when the platelet count falls below 10,000. 

Low platelets cause mucocutaneous bleeding, which includes petechiae - which are pinpoint superficial skin bleeds, anterior epistaxis - which are usually mild nosebleeds, immediate bleeding after surgical procedures, like tooth extraction, or bleeding from mucocutaneous surfaces, like gingival, gastrointestinal, or vaginal bleeding. 

Finally, most surgical procedures can be performed as long as the platelet count is above 50,000. 

One quick thing to look for is hemodilution and it happens when the platelet concentration falls as a result of large volume transfusions of platelet-free products, like packed red blood cells or intravenous fluids. This can happen in trauma patients who lose a lot of blood.

Another thing to keep in mind is pseudothrombocytopenia - meaning that it’s a lab error. 

When a blood sample is collected from a patient, an anticoagulant called ethylene-diamine-tetraacetic acid, or EDTA is often added to prevent the blood from clotting. 

But the platelets of s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Paget_disease_of_bone</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LI9ZE8bKSUuVVI2_TPTfuU0cTHKkbX2e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Paget disease of bone]]></video:title><video:description><![CDATA[Paget disease of bone is a disorder in which there’s a lot of bone remodeling that happens in some regions of the bone. 

Typically there’s excessive bone resorption followed by excessive bone growth, and it leads to skeletal deformities and potential fractures. 

Normally, bones undergo a continuous process of bone remodeling. 

Old brittle bone tissue gets reabsorbed by multinucleated bone cells called osteoclasts, which have 5 to 20 nuclei per cell. 

The resorbed bone tissue gets replaced by a new one made by another type of bone cell called an osteoblast.

At the cellular level, the process begins when osteoblasts release receptor activator of nuclear factor κβ ligand, or RANKL for short, which is a substance that binds to RANK receptors on the surface of osteoclast. 

When RANKL binds to the RANK receptor, it activates the osteoclasts, and they start secreting lysosomal enzymes like collagenase as well as hydrochloric acid. 

Together they digest the collagen protein and dissolve the minerals that make up the bone matrix. 

Once there’s been sufficient bone demineralization, the osteoblasts secrete another substance called Osteoprotegerin, or OPG for short, which binds RANKL and prevents it from activating the RANK receptors. This causes the osteoclasts to stop demineralizing the bones.

Once that happens, the osteoblasts start secreting a substance called osteoid seam, which is mainly made up of collagen and acts like a scaffold upon which calcium and phosphate can get deposited. And that’s how new bone begins to get formed again.

The exact cause of Paget disease of bone is unclear, but it can get triggered by infections like the measles virus, and is linked to genetic mutations like the SQSTM1 mutation, which encodes a protein involved in regulating osteoclasts. 

When Paget disease of bone occurs, it can affect a single bone or the whole skeletal system. 

Most often, it involves the skull, lumbar vertebrae, the pelvis, and the femur.

Now, there]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DALY_and_QALY</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VPb6nDCNTJ2jtfauLA9ROly7R9K9ewdG/_.jpg</video:thumbnail_loc><video:title><![CDATA[DALY and QALY]]></video:title><video:description><![CDATA[Disability-adjusted life years or DALYs are a measurement of disease burden, which is the impact of a health problem on an individual or in a population. 

Typically, disability-adjusted life years are used to compare the burden of two diseases, like type II diabetes - which is a chronic condition where the body doesn’t produce enough insulin - and malaria - which is an infectious disease spread by mosquitoes that causes a person to have flu-like symptoms. 

These two diseases are usually hard to compare because they affect different populations, have different short-term and long-term complications, and are managed completely differently. 

So, to compare the two diseases, you could calculate the disability-adjusted life years for both diabetes and malaria, and the disease with the highest disability-adjusted life years has the highest disease burden. 

Disability-adjusted life years are particularly useful for helping determine how resources should be allocated to a specific health issue. 

For example, if you have 100 thousand dollars to donate, do you want to spend it towards helping people with type II diabetes in Canada or helping people with malaria in India?

So let’s try to calculate the disability-adjusted life years for diabetes in Canada, and that requires knowing two things.

First, you need to know the years of life lost to premature death, or YLL. 

The years of life lost is calculated by multiplying the number of deaths that were the result of the disease (N), and the standard life expectancy at the age of death (L). 

The standard life expectancy is just the average life expectancy in a population minus the age of the person who died. 

For example, the average life expectancy in Canada is 82 years old, so the standard life expectancy of a person at age 60 is 22 years, because 82 minus 60 is 22. And if we’re only talking about 1 person who died, the number of deaths is 1. 

So the years of life lost for a 60-year-old person that died from ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Septic_arthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/19ppLjCxTsefArVdNk9ei7JWTVGfnJ7l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Septic arthritis]]></video:title><video:description><![CDATA[Septic arthritis, also called infectious arthritis, refers to any joint inflammation caused by a microbe - and usually it results from a bacterial infection of the joint.

All types of joints; fibrous, cartilaginous, and synovial joints can get infected. So let’s just use the synovial type as an example. 

A synovial joint consists of a joint capsule which has an outer fibrous layer, and an inner synovial membrane filled with synovial fluid. 

The synovial fluid is a clear viscous fluid that looks like the white of an egg, and it helps lubricate the joint and absorb shock. 

The synovial membrane has blood vessels that supply the joint with nutrients and oxygen. 

The tips of the bones that come together to form the joints are covered by an articular cartilage, which is a slippery smooth layer of cartilage that also absorbs shock and reduces friction during movement.

Now, there are various ways by which a bacterium can get into your joint. 

First, it can be from a preexisting infection in adjacent tissue, usually the bone, from where a bacterial infection can spread to the articulating part of the bone and then makes its way right into the joint. 

It can also develop from hematogenous spread which is where the bacteria is somewhere else in the body like the lungs, and then travels through the bloodstream and gets into the joint.

So, let’s say a child falls on some dirty planks of wood and a nail pierces through their knee, infecting the synovial membrane with bacteria. 

That bacteria could either come from the nail and be living in the environment, like Clostridium tetani which causes tetanus, or it could be bacteria that lives on the skin surface and gets shoved deep into the joint at the moment that the skin is pierced, like Staphylococcus aureus.

Once bacteria get into the synovial cavity, they start destroying the articular cartilage with their toxins. 

One example of a toxin is chondrocyte proteases, which is a powerful enzyme that’s capable of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypothesis_testing:_One-tailed_and_two-tailed_tests</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W998JnN1QiuW9yddB-ub-vQMSUmgLHUD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypothesis testing: One-tailed and two-tailed tests]]></video:title><video:description><![CDATA[Let’s say you want to figure out if a certain medication can lower the systolic blood pressure, so we recruit 100 people, give 50 of them the medication and 50 of them the placebo. 

The placebo looks and tastes like the medication but is completely harmless and ineffective - like a tiny capsule filled with water.

After six months of taking the medication or the placebo, you measure the blood pressure of each person in the study.

Now, the unit of measurement for blood pressure is millimeters of mercury, but we’ll just keep it simple and call it “units”. 

You find that the mean blood pressure in the medication group is 130 units, and the mean blood pressure in the placebo group is 145 units. 

At this point, you might use a statistical test, like unpaired or 2-sample t-test, to see if there’s a significant difference between the two groups’ means. 

Typically, an unpaired t-test starts with two hypotheses. 

The first hypothesis is called the null hypothesis, and it basically says there’s no difference in the means of the two groups. 

For example, our null hypothesis would state that there’s no difference in the mean blood pressure for people that take the placebo compared to people that take the medication.

On the other hand, the alternate hypothesis for a t-test can be either one-sided or two-sided, and this has to be determined at the beginning of the study. 

The alternate hypothesis for a one-sided t-test would either state that medication lowers mean blood pressure compared to the placebo or that medication raises mean blood pressure compared to the placebo. 

The alternate hypothesis for a two-sided t-test would simply state that the mean blood pressure for the medication group is different than the placebo group, but it wouldn’t specify if medication would raise or lower the mean blood pressure. 

Typically, researchers choose to use two-sided t-tests, since they usually don’t know how a treatment will affect the people in the study.

One way t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombophilia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hEag_iveQROj-_P7eDKi0wXvQHa-gZW6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombophilia: Clinical]]></video:title><video:description><![CDATA[In the 1800’s, the German physician Rudolph Virchow identified a triad of risk factors for thrombosis; endothelial injury, stasis, and hypercoagulability. 

The last category, hypercoagulability or thrombophilia, occurs when the normal physiological balance between clot formation and clot lysis is tipped towards clot formation. 

Before going into the individual thrombophilia disorders, let’s go through the normal coagulation system. The coagulation pathway is divided into an extrinsic and intrinsic pathways, which join into a common pathway that ultimately forms a clot made of strong fibrin mesh. 

Let&amp;#39;s start with the extrinsic pathway. It starts when trauma damages a blood vessel, and exposes the cells under the endothelial layer, which have tissue factor in their membrane. 

Activated factor VII binds to tissue factor, forming a complex that then binds to and activates factor X. 

The intrinsic pathway starts when a circulating factor XII, activates factor XI, which then activates factor IX. 

Finally, factor IX forms a complex with factor VIII, and this complex binds to and activates factor X. 

In the common pathway, activated factor X activates factor V, which converts prothrombin to thrombin, or factor II. 

Thrombin then converts fibrinogen into fibrin, which cross-links to form a fibrin clot. 

In order to regulate coagulation, the liver makes protein S, which activates protein C. 

Protein C inactivates factors V and VIII. 

Finally, a protein called antithrombin III inhibits factor X and factor II. 

The prothrombin time, or PT assesses the extrinsic and common coagulation pathways, while the partial thromboplastin time, or PTT assess the intrinsic and common coagulation pathways.

Alright, so you can imagine that increasing or decreasing certain factors in the coagulation pathway can lead to thrombophilia. 

Disorders that cause thrombophilia can be genetically inherited, like factor V Leiden, prothrombin gene mutation, and protein C ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Suicide</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UXNB_fuARMyxzQ5uUiq-SvoPTZOS3jP5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Suicide]]></video:title><video:description><![CDATA[Every 40 seconds someone around the world dies by suicide. The US Centers for Disease Control cite suicide as the second leading cause of death among individuals aged 15 to 34, right after unintentional injuries like car crashes. And it’s a major cause of death among the elderly as well. In fact, for every one that dies by suicide, there are over 20 others that have attempted suicide!  

Now, prior to any suicide or attempted suicide, a person usually has suicidal thoughts, and that’s called suicidal ideation. There’s a range - from passive suicidal ideation, where a person thinks they would be better off dead, to active suicidal ideation, where a person starts to make specific plans to die by suicide. 

Fortunately, most people with suicidal ideation never attempt suicide, but there’s no reliable way to identify those who will. Having said that, there are some predictive risk factors to consider. To identify individuals at higher risk of completing suicide, there’s a risk assessment scale, which can be remembered with the acronym SAD PERSONS. S stands for male sex, A for age younger than 19 or older than 45, D for Depression, P for Previous suicide attempt, E for Excess alcohol or substance use, R for Rational thinking loss - having a distorted sense of reality, S for Separated or Single, O for Organized plan - like overdosing on pills, N for No social support and S for Sickness. More risk factors - means a higher suicide risk. 

There are a few mental health conditions that can increase the risk for suicide- in particular, clinical depression and alcohol or substance addiction.  Clinical depression, which is sometimes called major depressive disorder or unipolar depression, is a relatively common but very serious condition that interferes with someone’s day to day life like working, studying, eating, sleeping— essentially leading to an overall feeling that life isn’t enjoyable. Sometimes, this feeling is so intense that a person loses hope or meaning in ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/erythema-multiforme</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TWT1liRMRSiEauCWs0dlvJIMR4eikCEu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Erythema multiforme]]></video:title><video:description><![CDATA[Erythema multiforme is an acute, immune-mediated condition that affects skin and mucous membranes such as the mouth and genitals. 

The skin is the largest organ in our body, and it’s divided into three layers - the epidermis, dermis, and hypodermis. 

The epidermis forms the thin outermost layer of skin. 

Underneath, is the thicker dermis layer. 

And finally, there’s the hypodermis, the deepest layer. 

The epidermis itself is made of multiple layers of developing keratinocytes - which are flat pancake-shaped cells that are named for the keratin protein that they make. 

Keratinocytes start their life at the lowest layer of the epidermis called the  stratum basale, or basal layer, which is made of a single layer of stem cells called basal cells that continually divide and produce new keratinocytes.

These new keratinocytes then migrate upwards to form the other layers of the epidermis, such as the spinous and granular cell layers. 

Below the epidermis is the basement membrane which is a thin layer of delicate tissue containing collagen, laminins, and other proteins. 

Basal cells are attached to the basement membrane, and help form the dermoepidermal junction.

Similar to how the skin lines the outside of the body, mucosa lines the inside of the body. And it’s named for the surface it covers.

So there’s oral mucosa, nasal mucosa, bronchial mucosa, gastric mucosa, and so forth. 

Mucosa is made up of one or more layers of epithelial cells that sits on top of a layer of connective tissue called lamina propria.

Just like with the skin, there is a basement membrane that sits between and attaches the epithelial layer and the lamina propria.

Now, basal epithelial cells, as well as most cells in the body, have a protein called major histocompatibility complex or MHC class I molecule on the surface of their membrane.  This protein presents peptides from within the cell to immune cells called cytotoxic T cells.

If a cytotoxic T cell recognises the peptides ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iZ-FfXHFRpSNJSkeI7nP4LanRiemoyl-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breast cancer]]></video:title><video:description><![CDATA[Breast cancer, or breast carcinoma, is an uncontrolled growth of epithelial cells within the breast. It’s the second most common cancer in women, but can also, on rare occasion, affect men as well.

Breast cancer is also the second leading cause of cancer deaths in women after lung cancer. This is largely due to the fact that oftentimes breast cancers don’t cause any pain or discomfort until they’ve spread to nearby tissues.

The breasts are milk-producing glands that sit on the chest wall, on either side of the breast-bone. They lie on top of the ribs and the pectoral muscles, and they’re divided into three main parts.

The glandular tissue that makes the milk, is made up of 15 to 20 lobules. Inside each of these lie a bunch of grape-like structures called the alveoli, which are modified sweat glands surrounded by a basement membrane made largely of collagen.

Zooming in on the alveoli, there’s a layer of alveolar cells that secrete breast milk into the lumen which is the space in the center of the gland.

Wrapping around the alveolus are special myoepithelial cells that squeeze down and push the milk out of the lumen of the alveolus, down the lactiferous ducts, and out one of the pores on the nipple.

Now, surrounding the glandular tissue is the stroma, which contains adipose or fat tissue, and this makes up the majority of the breast.

Suspensory ligaments called Cooperʼs ligaments, run through the stroma and help keep it in place. These ligaments attach to the inner surface of the breast skin on one end and the pectoralis muscles on the other.

Just below the skin over the breast, there’s a network of tiny lymphatic vessels that drain the lymph, which is a fluid containing cellular waste products and white blood cells. These lymphatic vessels mainly drain into a group of lymph nodes in the axilla, or the armpit.

Now, the cells of glandular tissue have receptors for certain hormones like, estrogen and progesterone, which are released by the ovaries, an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Varicella_zoster_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hNoNPsM7QASjqzErqG1nfA8nQ6_N79rI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Varicella zoster virus]]></video:title><video:description><![CDATA[Varicella zoster virus is one of the herpesviruses and it causes two diseases - varicella or chickenpox, and herpes zoster also known as shingles. 

Zoster actually refers to a type of belt used by ancient Greek warriors because of the belt like appearance of shingles. 

Now, let’s first talk a bit about the nervous system - it consists of two parts. 

The central nervous system which includes the brain and the spinal cord, and the peripheral nervous system includes the nerves that fan out from the central nervous system to reach the skin, muscles, and organs. 

Peripheral nerves that originate from the brain are called cranial nerves, and they’re in charge of motor and sensory innervation of the head and neck.

A specific cranial nerve, cranial nerve V, is the trigeminal nerve and it’s responsible for the sensation in the face. 

Its sensory neurons create a nerve cell cluster called trigeminal ganglion, located in the bones on the side of the face between the eyes and ears.

The peripheral nerves originating from the spinal cord are called the spinal nerves. 

Each nerve is formed by a dorsal and a ventral root.

Ventral roots contains neurons that carry motor innervation from the spinal cord to the muscles.  

Sensory information, like touch, temperature, pain, and pressure from the skin and other tissues travel through 1st order sensory neurons, in the dorsal root ganglion near the spinal cord, then through the dorsal root, and into the spinal cord, where it synapses with the 2nd order neurons. 

Now, each spinal nerve is in charge of the sensation of a specific area of the skin, called a dermatome. 

For example, if you step on a lego, the pain would be carried by the S1 nerve, but if you hit your big toe on a table leg, the pain would be carried by the L5 nerve.

Varicella zoster virus is a double-stranded DNA virus, protected by a protein coat called capsid, which is enveloped in a lipid membrane. 

The virus initially enters respiratory epithelial ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Patent_ductus_arteriosus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PLD6Kw01S8CPHbLjSHwUi9M8TiG1oUPR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Patent ductus arteriosus]]></video:title><video:description><![CDATA[With patent ductus arteriosus, or PDA, “patent” comes from the Latin word patere, meaning “to lie open”, while ductus arteriosus refers to a blood vessel that normally connects the pulmonary artery to the aorta. During fetal development, the ductus arteriosus allows blood to bypass the lungs, but normally it closes soon after birth. So, in patent ductus arteriosus, this blood vessel fails to close and remains open. 

But before we proceed, first, let’s look at how fetal circulation works. During fetal development, the baby’s lungs are filled with fluid and not yet involved in breathing, so the fetus relies entirely on oxygen-rich blood from the mother. This oxygen-rich blood travels from the placenta through the umbilical vein and eventually reaches the right atrium of the heart. From here, most of it takes a shortcut through the opening between the right and left atria, called the foramen ovale. This allows oxygen-rich blood to completely bypass the lungs and enter the left atrium directly. From the left atrium, blood enters the left ventricle, and from there it’s pumped into the aorta and systemic circulation.  

However, not all blood follows this path. A small amount still reaches the right ventricle and gets pumped into the pulmonary artery. However, since the fetal lungs are not yet functioning, the pulmonary vessels are squeezed, creating high resistance that makes it difficult for blood to flow into the lungs. As a result, most of the blood follows the path of least resistance and slips from the pulmonary artery through another fetal shunt called the ductus arteriosus into the aorta.  

Anatomically, the ductus arteriosus sits right on the aortic arch, just after the arteries that branch off to supply the brain and upper extremities. This setup allows oxygen-rich blood from the left ventricle to reach the brain and upper extremities first, while blood from the right ventricle via the ductus arteriosus supplies the lower body. This arrangement helps]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DNA_cloning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nC6C2UDPTn6DU0c-v52NiY6fQyW0qdzH/_.jpg</video:thumbnail_loc><video:title><![CDATA[DNA cloning]]></video:title><video:description><![CDATA[When you hear the term cloning - you might conjure up images of two versions of yourself, one that’s working all day, while the other parties like a rockstar. 

While that might be possible in the future, for the moment cloning really works at the level of copying a piece of DNA - like a gene - many times over. 

But this is just as cool and has huge implications. 

It basically involves taking a gene from our DNA, inserting it into a plasmid - which is a small, circular bit of bacterial DNA, and then making bacteria multiply that gene - gene replication, and use it to make proteins for us - gene expression!

Ok, so our DNA and plasmid DNA have some things in common - first off, they are both double stranded molecules, with each strand made up of sequences of 4 nucleotides -  adenine, or A, guanine, or G, cytosine, or C and thymine, or T -  arranged in a specific order, like words in a sentence. 

Secondly, to form the double helix, the nucleotides use their bases - A, T, C, G to form hydrogen bonds with bases on the opposing strand. 

Bases form bonds according to the rule of “complementary base pairing” - which states that in DNA, A always pairs with T by means of two hydrogen bonds, while C always pairs with G, with three hydrogen bonds. 

However, the difference between our DNA and plasmids is that our DNA is organized as 46 linear chromosomes, whereas plasmids are circular in shape - like a molecular DNA necklace. 

Now, the first step in DNA cloning is digesting our DNA, which contains the target gene we want to clone, by using restriction enzymes which bind to specific nucleotide sequences, called restriction sites. 

There’s a huge number of these restriction enzymes that recognize hundreds of different DNA sequences - so say we used the restriction enzyme ecoRI - which binds to every G A A T T C sequence of DNA, and breaks the DNA between the G and the first A. 

We can use this enzyme to cleave both our double stranded DNA, containing the target ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Guillain-Barre_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UoKM9ICfQnSkAtpbOUpUNYOBR9GnmeE0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Guillain-Barre syndrome]]></video:title><video:description><![CDATA[Guillain-Barré syndrome is named after two neurologists- Georges Guillain and Jean Barré, and it’s a demyelinating disease of the peripheral nervous system, which includes all of the neurons that extend beyond the brain and the spinal cord. 

Guillain-Barré, or GBS for short, is also called acute inflammatory demyelinating polyneuropathy.

Neurons are made up of three main parts. 

The dendrites, which are little branches that receive signals from other neurons, the soma or cell body, which has all of the neuron’s main organelles, and the axon, which transmits the signal to the next neuron in the series. 

For peripheral nerves, the cell body can either be located in the spinal cord, where it’s called a spinal nerve, or the brain, where it’s called a cranial nerve. 

Myelin is the protective sheath that surrounds the axons of the peripheral neurons, allowing them to quickly send electrical impulses. 

This myelin is produced by Schwann cells, which are a group of cells that support neurons.

In Guillain-Barré syndrome, demyelination happens when the immune system inappropriately attacks and destroys the myelin, which makes communication between neurons break down, ultimately leading to all sorts of sensory, motor, and cognitive problems. 

The cause of Guillain- Barré syndrome is unknown, but it’s known to develop after a bacterial infection, like Campylobacter jejuni and Mycoplasma pneumoniae, or a viral infection, like cytomegalovirus and Epstein-Barr virus. 

Specifically, some strains of Campylobacter jejuni have a particular kind of oligosaccharides on their membrane, that are identical to gangliosides found on the surface of motor neurons. 

So  as a result, immune cells mistakenly attack and destroy the gangliosides, damaging the neurons. 

This is called molecular mimicry, because from the perspective of the immune cells, a host substance is mimicking a foreign protein. 

When a normal component of the cells triggers an immune response that compone]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Two-sample_t-test</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2-WwXGgbSlazYZYB1CmRe5x8Q7mMy7Ja/_.jpg</video:thumbnail_loc><video:title><![CDATA[Two-sample t-test]]></video:title><video:description><![CDATA[The Student’s t-test or simply, the t-test, is a type of parametric statistical test used to determine if there’s a significant difference between the means or averages of two groups. 

And significance is normally defined by a p-value of less than 0.05 or 5%. 

Now when doing any parametric test, there are three key assumptions that we have to make about the population.

First, the sample population must have been recruited randomly. 

Choosing names randomly ensures that the people included in the study will have similar characteristics to the target population. 

This is important because that ensures that the results of the t-test can be applied to the target population - meaning it has good external validity! 

The second assumption is that each individual in the sample was recruited independently from other individuals in the sample.

In other words, no individuals influenced whether or not any other individual was included in the study. 

For example, if two friends decided to get their blood pressures measured on the same day, and they were both included in the study, these two individuals would not be independent of each other and the second assumption would not be met. 

Like random sampling, independent recruitment of individuals is important because it ensures that the sample population approximates the target population. 

The third assumption is that the sample size is large enough to approximate the target population, which usually means having more than 20 people. 

If it’s impossible to get a large sample size, then the sample population must follow a normal bell-shaped distribution for the characteristic being studied because that’s what we would expect to see in the target population.

Okay, now let’s say you want to figure out if a certain medication lowers systolic blood pressure.

So you find 25 people who have been on the medication for 6 weeks, and figure out that the mean systolic blood pressure for the whole group is 130 mmHg. The]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Food_allergy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FCJcyTv9RCGhKSQJGZ19cUBBT3i4ECdV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Food allergy]]></video:title><video:description><![CDATA[A food allergy is a medical condition where there’s an abnormal immune reaction to some food. Now, a variety of food proteins can cause food allergies, but the most common are known as the big eight, these include proteins within milk, eggs, peanuts, tree nuts, seafood, shellfish, soy, and wheat. 

Food is essential to life, and normally food doesn’t cause an allergic reaction - in fact, the process that allows for that is called oral tolerance. Let’s see how that works. Normally, when food travels through the stomach and intestines, the proteins within them are broken down by gastric acid and proteases into tiny fragments, called oligopeptides - small strings of amino acids. These oligopeptides reach the Peyer’s patches which are bits of tissue along the intestinal wall where M-cells live. M-cells are intestinal epithelial cells in the gut that grab protein fragments from the intestines and then transfer them to antigen-presenting cells like dendritic cells. Dendritic cells present them on their cell surface to a nearby helper T cell. The protein fragments are presented by the dendritic cell using an MHC class II molecule, which is basically a serving platter for the helper T cells. The helper T cell is key because it largely controls the immune response. Now here’s the catch, even if a helper T cell binds to that oligopeptide, another type of T cell called a regulatory T cell can release cytokines so that the helper T cell undergoes anergy. Anergy is a bit like turning off that helper T cell so that it doesn’t induce an immune response. In other words, regulatory T cells release cytokines in the lining of the intestines to help prevent the helper T cells from ever getting stimulated by food.  

Now, in food allergy, this process doesn’t work properly. An allergic reaction towards food happens in two steps, a first exposure, or sensitization, and then a subsequent exposure, which usually gets a lot more serious. So, let’s say a person eats shrimp for the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_hormone_synthesis_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NjjcBCt3SUGhMXK6PXA5NVmmR7yR1zhy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenal hormone synthesis inhibitors]]></video:title><video:description><![CDATA[Adrenal hormone synthesis inhibitors or AHSIs are a group of medications which basically inhibit the synthesis of adrenocortical hormones, more specifically cortisol, which is a glucocorticoid hormone produced by the adrenal cortex. 

Normally, the hypothalamus, which is located at the base of the brain, secretes corticotropin-releasing hormone, known as CRH, which stimulates the pituitary gland to secrete adrenocorticotropic hormone, known as ACTH. 

ACTH, then, travels to the pair of adrenal glands, on top of each kidney, where it specifically targets cells in the adrenal cortex.  

This causes the adrenocortical cells to take up cholesterol from the blood, and it also stimulates an enzyme called cholesterol desmolase inside these cells, which converts cholesterol to pregnenolone. 

Then, another enzyme called 3 beta- hydroxysteroid dehydrogenase, (or 3 beta- HSD) turns some of this pregnenolone into progesterone. 

Now, the synthesis of cortisol starts when pregnenolone and progesterone move into the zona fasciculata. 

The enzyme 17 alpha-hydroxylase turns pregnenolone into 17 alpha- hydroxypregnenolone and turns progesterone into 17 alpha hydroxyprogesterone. 

17 alpha hydroxypregnenolone is then turned into 17 alpha hydroxyprogesterone by the enzyme 3 beta- hydroxysteroid dehydrogenase. 

Then, all of the 17 alpha hydroxyprogesterone is turned into 11 deoxycortisol by the enzyme 21 hydroxylase. 

11 deoxycortisol is finally turned into cortisol by the enzyme 11 beta-hydroxylase. 

Cortisol is also known as the stress hormone. 

In times of stress, the body needs to have plenty of energy substrates around, so cortisol increases gluconeogenesis, which is the synthesis of new glucose molecules, proteolysis, which is the breakdown of protein and lipolysis, which is the breakdown of fat. 

Cortisol also helps to maintain the blood pressure by increasing the sensitivity of peripheral blood vessels to catecholamines- epinephrine and norepinephrine, and thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Writing_great_answer_explanations</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iQegtc0OTSSZQb3gK4zAhTm7TA_qWFSI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Writing great answer explanations]]></video:title><video:description><![CDATA[When you’re answering a question on an exam, you typically want to know one thing - What’s the answer? 

Even if you get the answer right, you might want to find out if you got it right for the right reason.

That’s why writing a good answer explanation is so critical - it’s a great opportunity to teach the learner something new in a way that’s likely to really stick. 

Now it all starts off with writing a great question that makes the learner apply what they know to a clinical situation. 

Here’s an example. Once the learner picks an answer, they might get an explanation like this one.

The first key, is to put yourself in the shoes of a learner and offer a very carefully reasoned main explanation that moves smoothly from the question to the answer using a logical set of steps. 

A question written in the style of a patient vignette has specific features, and a good explanation dives into those features, rather than simply restating generalities that can be found in any textbook. 

The reason for this is two-fold. First, it makes the information more memorable and easier to remember.

Second, this reflects the reality of how patients and clinical reasoning work in the real-world. 

For example, in our question - the answer clearly addresses an important change in clinical guidelines where it says: “Previous guidelines have included a step that includes endotracheal intubation and suctioning for infants born through meconium-stained fluid“.

The trick is to pull out the key learning points and explain them clearly, using a tone that is professional yet approachable. 

If, instead, the answer explanation was just a single line that read, “This patient needs positive pressure ventilation”, then that doesn’t really tell the reader anything except the answer - a good explanation explains why that’s the right answer. 

That’s why it’s important to really flesh out the answer with a typical length for the main explanation being about one to two paragraphs.

Now ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adaptive_teaching</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CfvHMd9hSuSSdo90p0Fk3GKwTzqefzF7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adaptive teaching]]></video:title><video:description><![CDATA[Adaptive teaching is a way of teaching that addresses the needs of learners that have different levels of knowledge and backgrounds, rather than a “one size fits all” approach. 

In medicine, it’s used to teach adaptive learners who learn through real-world problems - usually a clinical issue affecting a patient. 

To show how this works, let’s say there’s clinical instructor named Dr. Michael who loves teaching endocrinology. 

He might have learning objectives listed in his course syllabus; things like “Recognize the most common symptoms of endocrine disorders” or “Differentiate between primary and secondary endocrine disorders”.

The syllabus might list out specific “flipped classroom” segments in his course, like one in which he provides his students with his notes and PowerPoint slides so that they can review beforehand, and come prepared to discuss a case about precocious puberty. 

Altogether, this makes up the declared curriculum which is basically everything that a teacher expects to teach in a course, and also what they plan to draw from in a final exam or assessment. 

Often times, though, there ends up being a difference between what a teacher expects to teach and what is actually taught.

In our example, it’s totally possible that Dr. Michael’s students don’t remember normal endocrine physiology and are therefore struggling to understand the diseases. 

To adapt to this situation, Dr. Michael might spontaneously include a ‘team learning’ exercise, where he breaks the students into groups to answer multiple choice questions about various hormones using audience response ‘clickers.’ 

The time spent on this topic might mean that the class won’t ever get a chance to discuss some of the more rare endocrine diseases, and this is where the declared and taught curriculum diverge.

Now, let’s say that Dr. Michael also likes to work with his students outside the classroom through a web-based learning platform. 

He might review questions and flash]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multimedia_learning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9DOXWKTNQZuijJ22YjKKNudfTaa2uSij/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multimedia learning]]></video:title><video:description><![CDATA[We’ve all been there. You’re sitting in a lecture with a professor who’s reading PowerPoint slides densely packed with text, and you’re scrambling to take everything in. You leave wondering if you’ll remember anything. Maybe you even thought about how the information could have been presented better. Well, it turns out that there’s a whole body of research on multimedia learning, and it applies not only to slideshow presentations but to any media format, including books, audio, and video presentations.

Most people process information based on what they hear and see. 

So, if you’re attending a lecture where a professor’s talking directly about what’s on screen, that information goes into your sensory memory, where it remains for half a second or less. 

It stays for such a short period of time because there’s such a massive amount of sensory information around you that it’s only possible to focus your attention on a fraction of it. 

For example, you probably know that the fan in your fridge or freezer is on, but you usually don’t notice it when you’re cooking. 

Now, if you focus on specific sensory information, it enters your working memory, where it sticks around for a little longer—about thirty seconds. 

Working memory ignores useless background noise, like filler words, or things you already know, taking in only the most relevant details. 

Comparing these details with things you’ve already learned solidifies that newfound knowledge, organizing and storing it so it’s easier to recall. 

So, the next time someone asks you what you’re thinking about, they’re asking you what’s in your working memory at that moment.

Your long-term memory is where information is stored after you’ve processed it, and it remains there until it deteriorates slowly over time. 

With this model of learning in mind, you can use a variety of strategies to optimize how you learn using instructional media. 

We’re going to focus on a typical lecture pres]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preparing_to_apply_to_medical_school</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j4ud6PpHSBOLvGdgCe6SGIPvQ5eWiWvG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preparing to apply to medical school]]></video:title><video:description><![CDATA[Becoming a physician is a long and noble journey, and the very first step is applying to medical school. 

The specifics of that process differ around the world, so we’ll go over the specifics of applying in the US medical system, but some features of a strong candidate are universal—a person that is scientifically curious, hard-working, and compassionate. 

One way to think about any career is to think about the intersection of four goals: what do you love? What are you good at? What can you be paid for? And what does the world need?  

Most would agree that becoming a physician offers a reasonable salary and is also what the world needs, but it may not be what a person loves or is good at. 

Figuring that out is what a potential medical school applicant should do before they apply to medical school. 

It’s also what medical schools are trying to do when they evaluate their applicants.  

To figure out if medicine is right for you, you have to get to know yourself, and you have to get to know medicine. 

Medicine offers a bunch of career options that are growing every day, so that by the time a current applicant is ready to start working, there will be new opportunities that don’t even currently exist.

In order to get to know yourself, the first key is to find great advisors and mentors, starting with a pre-health advisor, which you can find at a lot of schools. 

In addition, find a great teacher, family friend, or clinician who can help serve as a mentor; someone who has the time to get to know you and is able and willing to help you grow your mind as well as your character. 

It’s best to have a few of these folks in your life because they can help you develop in different and often complementary ways. 

Next, it’s good to get involved in a variety of projects to explore your interests and expose yourself to the wide range of opportunities that are available. 

Students often get involved in lab-based and clinical research studies, as well a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Road_to_residency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gyYH1OEdSbKAkdRdxmdyF9kjSgyp8Xz4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Road to residency]]></video:title><video:description><![CDATA[For every medical or osteopathic student aspiring to be a clinician, a key stop along the way is residency. 

In total, there are 23 major types of residency programs, and to ultimately find one that is a good fit you need to figure out what sort of training you’re looking for, complete the application process, and participate in the match. 

We’ll go over the specifics of applying to a US residency program, but some aspects of the process are universal.

One way to think about any career is to think about the intersection of four goals—What can you be paid for? What does the world need? What do you love? and What are you good at?  

Most would agree that becoming a physician offers a reasonable salary, but some professions pay much more than others especially when it’s broken down by an hourly rate. 

The pay rate, as well as the number of hours and type of hours, meaning night shifts versus day shifts and taking call, are all important factors to consider. 

The world also needs physicians, but some types of physicians are more important to certain communities. 

For example, really great primary care physicians are in high demand especially in lower income communities.

That leaves what you love and what you’re good at.

Figuring that out is often the biggest challenge for medical students, but hopefully you’ve had a variety of clinical experiences to help you figure out whether you like to work with adults or children, in an operating room or in a clinic, in front of a microscope or a light box. 

We can also flip this around and ask—what do residency program directors think is important in selecting an applicant? 

Well the National Resident Matching Program conducts surveys where they ask that exact question, and out of 33 items, the top five across all specialties were 1. USMLE Step 1/ COMLEX 1 score, 2. Letters of recommendation in the specialty, 3. The Dean’s letter, 4. USMLE Step 2 (CK) score, and 5. Grades in clerkships. 

At the very bottom of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Editing_Wikipedia_articles_during_medical_school</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5nDK4n6yTdihqXc8lCrjnbHWRVm4lcVC/_.png</video:thumbnail_loc><video:title><![CDATA[Editing Wikipedia articles during medical school]]></video:title><video:description><![CDATA[Editing Wikipedia as a health professional student is a great way to not only “learn by teaching” but also to ensure patients and your fellow healthcare professionals get accurate information. 

Wikipedia is one of the most well-known websites around the world and individual articles can get thousands of views a day, so improving them is both rewarding and incredibly impactful. 

To get started, the first thing you need to do is select an article, which may be easier than you think. 

If you look at the WikiProject Medicine page, you’ll see that there’s already a community dedicated to this work. 

There’s a handy chart which organizes over 37,000 English Wikipedia health-related articles by importance and quality, and this is a great way to find a good article to get started with. 

If you’re interested in other domains, there are more WikiProjects like anatomy, pharmacology, and women’s health, and of course you can always just search around for an article that catches your eye.

Once you’ve found an article you’re excited to improve, the next step is to start editing. 

You can start by going to the top right corner of the page and select the button labeled “edit.” 

Ideally, though, you should be logged in to your account first, at which point it’ll say “edit source”. 

The visual editor is easy to use, and works almost the same way as any word processing software. 

As you’re editing, be sure to cite your sources by clicking the cite icon in the upper bar. 

If you’re using the visual editor, adding the PubMed ID to your citations incorporates all the metadata of the citation. 

Also on the article is the talk page. 

The talk pages are where people interested in a topic can collaborate with one another.

In addition to directly editing pages, another area that might be useful to you is your sandbox, which you’ll be able to see once you make an account and log in. 

The sandbox serves as your own personal area to experiment with writing for Wikipedia ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myeloproliferative_neoplasms:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i6fjBY0LR0_Fk02Tba5DOp2zQGSdPlNx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myeloproliferative neoplasms: Clinical]]></video:title><video:description><![CDATA[Myeloproliferative neoplasms are a group of neoplastic disorders characterized by proliferation of the bone marrow cells from the myeloid lineage. That includes red blood cells, platelets, megakaryocytes, as well as granulocytes, which include neutrophils, basophils, mast cells, and eosinophils. 

Each disorder may potentially cause proliferation of all the myeloid cells, however, myeloproliferative neoplasms can cause proliferation of all of the myeloid cells, but they’re classified based on the dominant cell line involved. 

So there’s polycythemia vera, for red blood cells, essential thrombocythemia for megakaryocytes and platelets, chronic myeloid leukemia, or CML for granulocytes, and the odd one out, primary myelofibrosis, which doesn’t really have a dominant cell line, but instead is characterized by bone marrow fibrosis. 

Now, these are diagnoses of exclusion. So for example, when you see an increase in platelets, or thrombocytosis, you have to think through all of the other causes before considering essential thrombocythemia. 

Alright, first up is polycythemia; which is when the hemoglobin level more than 16.5 grams per deciliter in men or more than 16.0 grams per deciliter in women, or a hematocrit more than 49% in men, or more than 48% in women. 

Women have a lower cutoff because they normally lose some blood through the menses. 

Now, polycythemia is classified into primary polycythemia, called polycythemia vera, and secondary polycythemia, which is further subclassified into relative polycythemia, appropriate absolute polycythemia, and inappropriate absolute polycythemia.

To differentiate the causes of polycythemia, we’ll be looking at four laboratory parameters: plasma volume, RBC mass, oxygen saturation, and erythropoietin levels. 

So, starting with secondary polycythemia - relative polycythemia happens when something like dehydration, diuretic use or a burn injury causes a decrease in plasma volume, resulting in an apparent increase of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_papillomavirus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5en8EORqQJujL4_6ktLxvjZ5Q9GFnsl9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human papillomavirus]]></video:title><video:description><![CDATA[Human papillomaviruses, or HPV for short, are a group of non-enveloped DNA viruses that specifically infect human epithelial cells.

There are over 100 different types of HPVs which can be categorized by the epithelial cells they prefer to infect; like cutaneous epithelial cells of the skin, especially the face, hands and feet; and epithelial cells of mucous membranes, especially the respiratory tract including the pharynx, and nasal and oral cavities; and anal and genital regions. 

Some types can cause benign tumors, called papillomas or warts; and some can lead to carcinomas, or cancer of the epithelial cells.

HPV may have contributed to both actor Michael Douglas’s throat cancer diagnosis, and former first lady of Argentina, Eva Perón’s fatal cervical cancer.

Epithelial cells line the outer surfaces of organs and blood vessels and separate the interior of the body from the external world.

They primarily serve as a protective barrier to invasion by pathogenic bacteria, fungi, parasites and viruses; and to water loss. 

In locations like the skin, anus, genitals, and respiratory tract, they can be stratified, having more than one layer of epithelial cells. 

At the base, the layer closest to the interior of the body, these cells are less mature, rounded stem cells, also called basal cells. 

Basal cells divide and replenish all the cells found in the epithelium. 

As the basal cells divide and mature, they move toward the outermost layer, flattening out and becoming more squamous shaped in appearance. 

Once they reach the top layer, these mature, flat cells are exfoliated, or shed, from the epithelium.  

Now, typically basal cells are well protected under all those layers. 

But if there are abrasions or cuts in the epithelium, HPV can gain access to and infect the basal cells. 

Once that happens, HPV can replicate with or without being incorporated into the basal cell’s DNA through the activities of two particular viral genes called E6 and E7. 

T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Probability</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IhVj0VxDQiiQl3NZE_b8U2mZTwapWkMh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Probability]]></video:title><video:description><![CDATA[Probability is the chance that an event or outcome will occur, and it’s calculated by dividing the number of times an event happened by the number of times the event could have happened.

For example, let’s say you have one six-sided die and you want to know the probability of rolling a certain number, like a three. 

Typically, probability is written with a capital P, and P of A represents the probability of “event A” happening. 

In this situation, event A is rolling a 6. Since a die has six sides, there are six possible numbers you could roll, so the probability of rolling a three is 1 divided by 6, or 0.167. 

Probability can be written as a decimal or as a percent, so the chance of rolling a three is 0.167 times 100 or 16.7%.

Now, there are eight basic rules in probability. 

The first rule states that the probability of event A can range anywhere from 0 - or 0% - to 1 - or 100%. 

The larger the probability is, the higher the chance that the event will occur. 

The second rule states that the sum of the probabilities of all possible outcomes has to equal 1. 

For example, the probability of rolling each side of the die is 0.167, and when we add up 0.167 six times, it equals 1. 

Sometimes we might want to find the probability that an event won’t occur - like if we wanted to figure out the probability of not rolling a three. 

The probability of an event not occurring is called the complement, and it’s written as the probability of the event, except it has a prime symbol - which is just an apostrophe. 

The third rule of probability states that the probability that an event doesn’t occur is 1 minus the probability that it does occur.

So, the probability of not rolling a three is 1 minus 0.167, or 0.833. 

Turning that around, it also means that the probability of the event occurring equals 1 minus the complement. This is helpful in situations where we want to figure out the probability that an event occurs, but only know the probability that the eve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/One-way_ANOVA</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sCKkHYAARIOWJMFAEmIVoVNKSAGKRmYp/_.jpg</video:thumbnail_loc><video:title><![CDATA[One-way ANOVA]]></video:title><video:description><![CDATA[Analysis of variance, or simply, ANOVA, is a type of parametric statistical test used to determine if there’s a significant difference between the means or averages of three or more groups. 

And significance is normally defined by a p-value of less than 0.05 or 5%. 

Now when doing any parametric test, there are three key assumptions that we have to make about the population.

First, the sample population must have been recruited randomly. Choosing names randomly ensures that the people included in the study will have similar characteristics to the target population.

This is important because that ensures that the results of the t-test can be applied to the target population - meaning it has good external validity! 

The second assumption is that each individual in the sample was recruited independently from other individuals in the sample. In other words, no individuals influenced whether or not any other individual was included in the study. 

For example, if two friends decided to get their blood pressures measured on the same day, and they were both included in the study, these two individuals would not be independent of each other and the second assumption would not be met.

Like random sampling, independent recruitment of individuals is important because it ensures that the sample population approximates the target population. 

The third assumption is that the sample size is large enough to approximate the target population, which usually means having more than 20 people.

If it’s impossible to get a large sample size, then the sample population must follow a normal bell-shaped distribution for the characteristic being studied because that’s what we would expect to see in the target population.

Okay, now let’s say there are three medications available for lowering systolic blood pressure, and you want to figure out if any of the medications work differently than the others. 

Let’s say that you find 10 people who take Medication A for 6 weeks, an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I5wzLhRWQsWTlqkVkKWFTum7Q2WYnxHu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to pharmacology]]></video:title><video:description><![CDATA[Pharmacology is the study of medications, or chemical compounds, which interact with various living systems, from tiny molecules to cells, to tissues and whole organisms in order to produce a certain effect.

Every day, more and more new medications are designed to fight diseases, from infections to cancer, heart failure, and depression. But the process of developing a new medication can take a lot of time and money, and it typically consists of three steps. Step 1 is discovery, and that’s when a candidate compound is picked out as a possible therapeutic agent for a specific disease. Step 2 is preclinical research, during which this compound is tested on cell cultures and animals, like mice and rats, mainly to see if it causes any serious harm on living organisms. And, finally, step 3 is clinical development, during which clinical trials are performed. That’s where the compound is tested on humans to see if it’s safe and effective in treating diseases.

For a new medication, clinical trials are done in 4 phases, which can be remembered with the mnemonic “All medications need the SEAL of approval,” which stands for Safety, Efficacy, Approval, and Long term. Phase I trials test the medication in a small group of healthy individuals to see if it’s Safe for humans. 

Phase II trials aim to find out more about how Effective the medication is or how well it works at a certain dose. This is done by testing it on a moderately sized group of individuals affected by the condition in question. 

In phase III trials, the new medication is compared to the standard treatment to find out if it’s actually just as good as or even better than the existing one. Phase III trials generally involve a much larger number of individuals, and aim to replicate the exact setting in which the medication will be administered in real life, which will then be used as the basis for Approval by regulatory organizations for the market. 

This whole process can take up to 10 years or more, d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_obstructive_pulmonary_disease_(COPD):_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HROKAcwZSlmV2skSoX5GpB8FTrGdNb7M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic obstructive pulmonary disease (COPD): Clinical]]></video:title><video:description><![CDATA[Chronic obstructive pulmonary disease, or COPD is characterized by obstruction of airflow due to either inflammation of the airways, or chronic bronchitis, and destruction of the alveolar wall with dilation of the airspaces, or emphysema. 

These events are due to inflammation that’s often triggered by inhalation of toxic substances, like tobacco smoke, as well as occupational pollutants like dust and silica. 

Most people have elements of both chronic bronchitis and emphysema, so they’re often clumped together under the term COPD. 

Alright, now chronic bronchitis is characterized by an inflammatory process that leads to increased mucus production, which obstructs the airways and leads to air trapping behind those mucus plugs. 

Chronic bronchitis is clinically defined as having a productive cough for more than 3 months each year for 2 or more consecutive years. 

Now, zooming in for a moment, the body maintains a balance between elastases, which destroy elastin in the alveolar wall and respiratory bronchioles, and anti-elastases, which stop elastase from doing just that. 

In emphysema an inflammatory response to tobacco smoke tips the balance towards elastases, causing excessive destruction of the alveolar wall. 

Without elastin, the elastic recoil that normally maintains the patency of the alveoli and respiratory bronchioles during exhalation is lost, and so these small airways collapse when the person tries to breathe out. 

If air can’t get out, it becomes trapped in the alveoli, causing the airspaces to “puff up”. 

Also, by destroying the alveolar-pulmonary capillary interface, gas exchange is impaired, resulting in hypoxemia and retention of carbon dioxide or CO2. 

But not all cases of COPD are directly related to smoking. 

In people under 45 years of age with COPD, it’s important to consider alpha-1 antitrypsin deficiency which is an autosomal dominant disorder. 

Alpha-1 antitrypsin is a protein synthesized in the liver and it inhibits neutro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Homocystinuria</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pMKV5BoJRH6kus47BJAkF3UUSTGzWbFJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Homocystinuria]]></video:title><video:description><![CDATA[In homocystinuria, “homocysteine” is a metabolite of the amino acid methionine, and “uria” means, a substance present in urine. 

So people with homocystinuria have large amounts of homocysteine in their urine, as well as other problems in the connective tissue, muscles, brain, heart, and blood vessels. 

Now, amino acids are the basic building blocks that make up proteins. 

There are 20 amino acids used in the human body and they all contain a carboxyl (-COOH) group and an amine (-NH2) group.  

Methionine is one of the essential amino acids, meaning our bodies can&amp;#39;t create it, but they must be acquired through food that’s rich in protein like meat, eggs, dairy, avocados, beans, etc. 

So the proteins you eat are broken down into amino acids in the gastrointestinal tract by gastric acid and digestive enzymes.

The amino acids are then absorbed by the small intestine into the bloodstream, and then travel to the cells of the body, where they are used for protein synthesis. 

Since the body can’t store these amino acids, any excess amino acids are converted into glucose or ketones and used for energy. 

Now methionine is also used to synthesize another amino acid, cysteine. 

First, methionine is converted into the amino acid homocysteine through multiple steps. 

Next, the enzyme cystathionine beta- synthase, which requires vitamin B6 as a substrate, combines homocysteine and serine to create cystathionine. 

Finally, the enzyme cystathionase converts cystathionine into cysteine.  

Any homocysteine that does not undergo this process can be converted back into methionine by methionine synthase, which requires vitamin B12, or cobalamin, and folate as substrates.

There are two types of homocystinuria: familial and acquired. 

Familial homocystinuria is an autosomal recessive genetic disorder that first manifests early in life. 

It’s usually caused by cystathionine beta-synthase deficiency, but it can also be caused by decreased B12 affinity in cys]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acid_reducing_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JVZ7f9FLTKadf3DczhwuEQjIRamO70MG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acid reducing medications]]></video:title><video:description><![CDATA[Acid reducing medications include antacids that directly lower the acidity of stomach contents, and antisecretory medications that act on parietal cells in the stomach to decrease acid secretion. They are used to treat conditions like gastroesophageal reflux disorder and peptic ulcer disease by decreasing the acidity of the stomach and allowing the epithelial linings to heal. 

Now, the stomach is composed of four regions: the cardia, the fundus, the body, and the pyloric antrum. There’s also a pyloric sphincter, or valve, at the end of the stomach, which closes while eating, keeping food inside for the stomach to digest. The epithelial layer of the stomach contains different gastric glands which secrete a variety of substances. 

Starting with the cardia, it contains mostly foveolar cells that secrete a protective mucus, which is mostly made up of water and glycoproteins. The fundus and the body contain both the parietal cells and enterochromaffin-like cells, and the antrum and pyloric areas contain G-cells. Now gastric acid is mainly composed of HCl, or hydrochloric acid, which is mainly secreted by the parietal cells. Parietal cells have M3, CCK2, and H2 membrane receptors, which modulate their secretory behavior. When food enters the stomach, it causes the stomach walls to expand, which leads to the activation of these receptors. 

First, stomach expansion causes the branches of the vagus nerve that innervates the stomach to release acetylcholine, which activates M3 receptors. Next, the G cells in the antrum of the stomach release gastrin, which activate the CCK2 receptors. Gastrin and acetylcholine activate the enterochromaffin-like cells, which release histamine, that then activates H2 receptors. 

Activation of M3, CCK2, and H2 receptors increases the conversion of H20 and CO2 to H+ and HCO3- by carbonic anhydrase. The H+ is then pumped out of the cell and into the stomach via the H+/K+-ATPase pump. These H+ ions combine with Cl- ions to form hydroc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sciatica</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gKZodmxgTEKpCfBHJQd9kUKCTZW4dWOl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sciatica]]></video:title><video:description><![CDATA[Sciatica is a condition where there’s pain that starts in the lower back which then travels down the leg. Since the pain is associated with injury or compression of the sciatic nerve and follows the path of the sciatic nerve, it makes sense to name it sciatica.

The sciatic nerve is the longest and widest nerve in the body. It’s formed by the spinal nerves L4, L5, and S1-3, which leave the spinal canal through intervertebral foramen, an opening located between the vertebrae and behind the intervertebral discs. These nerves travel to the area in front of the sacrum, and join to make the sacral plexus.

All the nerves in the plexus, except S3 are split into two divisions: anterior and posterior. Anterior divisions of the L4, L5, S1, S2 and the entire S3 nerve create the tibial nerve, while posterior divisions of the L4, L5, S1 and S2 form the common fibular nerve. These two nerves are bound together by connective tissue and make up the sciatic nerve.

The sciatic nerve then passes beneath the piriformis muscle and through the greater sciatic foramen which is an opening formed by the pelvic bone, sacrospinous, and sacrotuberous ligaments.

It then travels down the back of the thigh to the back of the knee where it splits into the tibial and common fibular nerves. The sciatic nerve innervates the muscles in the back of the thigh. The Tibial nerve innervates the muscles of the posterior compartment of the leg and intrinsic flexors of the foot.

The Common fibular nerve is in charge of the muscles in the anterior and lateral compartments of the leg and intrinsic extensors of the foot. Now, each spinal nerve is in charge of the sensation of a specific area of the skin, called a dermatome.

Dermatomes of the spinal nerves of the sacral plexus cover almost the entire surface of the thigh, leg and foot. L4 covers the medial side of the leg, L5 covers the lateral side. S1 covers part of the dorsum and the entire sole of the foot, S2 the back of the leg, while S3 cove]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteomyelitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KxQNfC8QRduPupKhK98o-7zkRhiF8Npx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteomyelitis]]></video:title><video:description><![CDATA[Osteomyelitis can be broken down. Osteo- refers to bones, –myel stands for myelo and relates to the bone marrow, and lastly, –itis refers to inflammation. 

So, osteomyelitis is an inflammation of the bone or bone marrow, and it typically results from an infection.

Normally, if we look at a cross-section of a bone, we can see that it has a hard-external layer known as the cortical bone and a softer internal layer of spongy bone that looks like honeycombs.

There’s also another layer called the periosteum that covers the cortical bone - like the lamination of a basketball card - and it&amp;#39;s where the muscles, tendons, and ligaments are attached. 

If we zoom into a cross-section of cortical bone, we can see that it has many pipe-like structures called osteons running through the length of the bone. 

Each pipe has an empty center called a Haversian canal which contains the nerves and blood vessels that supply the osteon. 

At the outer-border of the osteon is a ring of cells called osteoblasts which synthesize bone. 

Along with these cells are osteoclasts that break down bone.

In bones, like the long femur bones, the tips of the bone are called the epiphysis, while the shaft is called the diaphysis of the bone. 

Between the epiphysis and diaphysis, we have the metaphysis. It contains the growth plate, the part of the bone that grows during childhood. 

In osteomyelitis, microorganisms, such as bacteria, reach the bone to cause an infection in a few different ways. 

Bacteria particularly affect certain high-risk individuals like those with a weak immune system, and those with poor blood circulation due to uncontrolled diabetes. 

In fact, a major way that bacteria reach the bone is through the bloodstream, and it&amp;#39;s called hematogenous spread. For example, this might happen in a person who uses contaminated needles to inject drugs or in individuals undergoing hemodialysis that may be contaminated by a bacteria or even through the dental ex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Erectile_dysfunction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/elVN1T1FSUSobwwnNb3SAAavSPKauHor/_.jpg</video:thumbnail_loc><video:title><![CDATA[Erectile dysfunction]]></video:title><video:description><![CDATA[In erectile dysfunction, an individual is unable to develop or maintain an erection during sex. 

This disorder is also called impotence and like other sexual dysfunction, this condition becomes more common with age. 

Sex can be important within relationships, so erectile dysfunction often carries with it emotional and psychological stigma.

In both males and females,, sexual activity involves a sequence of events called the sexual response cycle. 

This cycle has four phases, excitement, plateau, orgasm, and resolution. 

During the excitement phase, muscle tension, heart rate, and blood flow to the genitals increases. 

In males, this is called an erection. 

When these reach the maximum level, it’s called the plateau phase. 

Next, the accumulated sexual tension gets released during orgasm, causing ejaculation in males. 

Immediately after orgasm comes the resolution phase, where the body slowly returns to its original, un-excited state.

Alright, let’s take a closer look at the penis which is made of  three long cylindrical bodies: the corpus spongiosum that surrounds the penile urethra, and the two corpora cavernosa made of erectile tissue. 

The corpora cavernosa are wrapped in a fibrous coat called the tunica albuginea, and each corpus cavernosum is made up of blood-filled spaces called the cavernosal spaces. 

These areas are lined with endothelial cells surrounded by smooth muscle.  

Running down the centre of each corpus cavernosum is a large artery called the deep artery which gives off smaller arteries that supply the cavernosal spaces.  

Next, blood get drained from these spaces by small emissary veins, which drain into the deep dorsal vein. 

This vein then carries the blood back into the systemic circulation. 

Now, the penis receives both somatic and autonomic innervation through the cavernous nerves, which innervate both the corpus spongiosum, and the corpora cavernosa.  

You can remember the functions of these fibers with the mnemonic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dentinogenesis_and_the_dentin-pulp_complex</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E6WHtXiDRC6I9PXXk6eJ9IATRTyvVkch/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dentinogenesis and the dentin-pulp complex]]></video:title><video:description><![CDATA[In total, an adult has 32 teeth, and they do everything from chew on gum, to rip apart a delicious burger. 

Each tooth contains both enamel and dentin.

So, the physical properties of enamel and dentin are complementary, there’s the extremely hard and unyielding enamel on the outside and the dentin foundation below which is somewhat flexible and absorbs stress from chewing. 

By volume, the majority of a tooth is made of dentin, which is a hard, whitish-yellow mineralized tissue. 

In fact, a good example of how dentin looks is ivory in elephant tusks, which are solid dentin all the way through.

So, if we cut a human tooth in half, we see a number of layers. 

From the outside to the inside, the tooth crown is covered with translucent-ish enamel. 

Next, there’s the dentinoenamel junction, which is where enamel and dentin meet. 

Right under that is a thin layer of mantle dentin. 

Next follows a layer of primary dentin. 

As we move towards the middle, primary dentin becomes somewhat softer, and is called secondary dentin. 

Mantle dentin and primary dentin are made before we’re born, whereas secondary dentin grows continuously to support the primary dentin. 

The secondary dentin grows from the soft, unmineralized dentin, called predentin, which is just above the pulp. 

Additionally, in some places, there’s tertiary dentin which is a sort of band-aid that helps fix up injured teeth. 

It is also important to know that the tooth is covered by enamel only on its crown, the root is covered by a slightly softer substance called cementum.

The process of creating dentin is called dentinogenesis. 

For primary teeth, it mostly happens around the 14th week of fetal development, and for permanent teeth, it mostly happens when an infant is about 3 months old. 

After that, the process continues to happen, but at a very slow pace. 

Dentinogenesis is performed by odontoblasts, and it’s done from the outside inwards. 

So the process begins with creation of the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Periapical_lesions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/teXDSOb_SC6SblsYfrWhzsuJTpCq0iMN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Periapical lesions]]></video:title><video:description><![CDATA[Bacterial infections of the tooth and the surrounding tissues progress rather slowly, but every step is so much more severe than the previous one. 

Cariogenic bacteria will first tear enamel down. 

Then they’ll bore through dentin. When they or their toxic waste get into the pulp, pulpitis occurs.

Without immediate treatment, pulpitis can cause irreversible damage and require a root canal. 

If no treatment is performed, the pulp will eventually die off through necrosis. 

At that point, the tooth is considered dead, and in essence, it becomes a staging area for bacteria to spread further. 

Our immune system will, at that point, try to stage a defense around the apices of the dental root. 

We call that “battlefield” apical periodontitis, which is one of the periapical lesions.

The primary form of defense our body has against infection is the polymorphonuclear leukocyte, also known as the neutrophil. 

It is the finest soldier serving our body, and its task is to locate and destroy microbes that intrude into the body, wherever that might be. This is usually a very effective force, and most of the times sufficient. 

When an infection occurs, neutrophils will mobilize in huge numbers, head to the site of infection, and leave the circulatory system, searching for bacteria to destroy. 

They achieve this through three methods. 

First is degranulation, where neutrophils release a bunch of granules containing various enzymes, that hurt bacteria. 

Then, they will use neutrophil extracellular traps, or NETs, to immobilize the wounded bacteria. 

These are actually nets, made out of neutrophil DNA! 

Finally, neutrophils will then gobble up the bacteria through phagocytosis as a final means of its destruction. 

All of this works really well, most of the time. 

But, fighting infection is a bloody affair and many of the neutrophils perish during the fight. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/bullous-pemphigoid</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2cqKdJVlQeyJdaCFa44NW87hRqOH9ECi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bullous pemphigoid]]></video:title><video:description><![CDATA[Bullous pemphigoid is an autoimmune skin disease that causes the skin to form bullae or blisters.

Now, the skin is divided into three layers--the epidermis, dermis, and hypodermis. 

The epidermis forms the thin outermost layer of skin.  

Underneath, is the thicker dermis layer, and finally, there’s the hypodermis that anchors the skin to the underlying muscle. 

The epidermis itself is made of multiple layers of developing keratinocytes - which are flat pancake-shaped cells that are named for the keratin protein that they’re filled with. 

Keratinocytes start their life at the lowest layer of the epidermis called the  stratum basale, or basal layer which is made of a single layer of stem cells, called basal cells that continually divide and produce new keratinocytes. 

The stratum basale also contains another group of cells called melanocytes, which secrete melanin.

Melanin is a pigment protein, or coloring substance.

Below the epidermis is the basement membrane which is a thin layer of delicate tissue containing collagen, laminins, and other proteins. 

Basal cells are attached to the basement membrane by hemidesmosomes, a protein complex that stems from the bottom of the basal cells. 

Just like an anchor digs into the seafloor and holds a boat in place, hemidesmosomes dig into the basement membrane and hold basal cells in place.  

The exact cause of bullous pemphigoid is unclear, but it’s thought that in a person with a genetic precondition, it can be triggered by medications like furosemide, captopril, penicillamine, non steroid anti-inflammatory drugs (or NSAIDs), and antibiotics. 

Bullous pemphigoid is a type II hypersensitivity reaction, which is when the immune system produces antibodies that bind to the body’s own cells. 

Immune cells called B cells produce IgG antibodies, which are Y shaped molecules with 2 regions, an antigen binding fragment region - or Fab region, and fragment crystallizable region or Fc region. 

The Fab region of the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dental_occlusion_(Angle_classifications)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H1mgYfeYShSI-G9jIPO9bN9pSlqpthXA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dental occlusion (Angle classifications)]]></video:title><video:description><![CDATA[The mouth is made up of two key bones: the mandible, which is the bone beneath the bottom row of teeth; and the maxilla, which is the bone above the top row of teeth. 

The bones are lined by the gums and have an alveolus, or socket, for each tooth. 

Since the mouth is symmetrically divided down the middle, let’s look at one side of a mouth containing the permanent, or adult, teeth. The teeth that pair up vertically have the same names. 

Starting in the center, first, there are the central incisors and then the lateral incisors. 

And incisors are used for cutting into something like a juicy peach. 

Next, are the canines, which get their name from being the same teeth that are extra long and sharp in dogs. 

They’re also called the cuspids, which comes from the word cusp, meaning point. 

These are used for gripping and tearing into food like a piece of meat.

Then, there are the first and second premolars or bicuspids which have two cusps each. 

Next comes the first permanent molars and the second permanent molars.

Molars usually have four to five cusps, and are great for crushing and grinding food. 

Lastly, there are the third permanent molars, or wisdom teeth, which, in some people, never erupt at all.

All together, that makes 32 permanent teeth.The front teeth from canine to canine are called anterior teeth. 

The rest are called the posterior teeth.

Each tooth has five surfaces that are named based on their location and function. 

Each tooth has one chewing surface.

The chewing surface of posterior teeth are called occlusal surfaces, and the cutting edges of anterior teeth are called incisal edges.

Each tooth has two proximal surfaces which are surfaces that face adjacent teeth. 

Proximal surfaces are mesial when they are closer to the midline of the mouth and distal when they are away from the midline. 

Tooth surfaces next to the face, the ones resting next to cheek or lips, on the upper and lower teeth are called facial surfaces. 

Faci]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/pemphigus-vulgaris</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ii4M0u9oQmy5_eAYFv5CDnKPRGSnkYSd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pemphigus vulgaris]]></video:title><video:description><![CDATA[Pemphigus vulgaris is a rare autoimmune skin disorder that causes blisters or bullae because there’s separation of skin cells. 

Now, the skin is divided into three layers--the epidermis, dermis, and hypodermis. 

The epidermis forms the thin outermost layer of skin.  

Underneath, is the thicker dermis layer, and finally, there’s the hypodermis that anchors the skin to the underlying muscle.  

The epidermis itself is made of multiple layers of developing keratinocytes - which are flat pancake-shaped cells that are named for the keratin protein that they’re filled with. 

Keratinocytes start their life at the lowest layer of the epidermis called the stratum basale, or basal layer which is made of a single layer of stem cells, called basal cells that continually divide and produce new keratinocytes. 

Below the epidermis is the basement membrane which is a thin layer of delicate tissue containing collagen, laminins, and other proteins. 

Hemidesmosomes are a protein complex that attach basal cells to the basement membrane.

As keratinocytes in the stratum basale mature and lose the ability to divide, they migrate into the next layer, called the stratum spinosum.

The next layer up is the stratum granulosum, then stratum lucidum, and finally stratum corneum. 

The cells of the epidermis are bound together by protein complexes called desmosomes, most of which are in stratum spinosum. 

Similar to how the skin lines the outside of the body, mucosa lines the inside of the body, and it’s named for the surface it covers. 

So there’s oral mucosa, nasal mucosa, bronchial mucosa, gastric mucosa, intestinal mucosa, and so forth. 

Mucosa is made up of one or more layers of epithelial cells that sits on top of a layer of connective tissue called lamina propria. 

Just like with the skin, the mucosal cells are attached to each other by protein complexes called desmosomes, and the basal cells are attached to the basal membrane by protein complexes called hemidesm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_dysplasia_of_the_hip</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zNDQjciLSniOwvyFSxIBihgGQU__ityr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developmental dysplasia of the hip]]></video:title><video:description><![CDATA[Congenital hip dysplasia, or developmental dysplasia of the hip, is a problem where the socket or acetabulum - and the femoral head are misaligned, resulting in an unstable hip joint. 

Typically, the problem is present at birth, but sometimes it appears later as the bones develop over time.

The hip joint is a ball and socket type because the ball-shaped head of the femur sits and rotates within the acetabulum which is a cup-shaped socket. 

The hip joint is supported by a tough fibrous joint capsule, which is made up of three main ligaments, the iliofemoral, the pubofemoral, and the ischiofemoral. 

The main job of the joint capsule is to hold articulating bones together and make sure the joint stays stable when the hip is moving. 

Now, the acetabulum itself is a combination of parts of three pelvic bones that join together - the ischium, the ileum, and the pubis.

At the bottom of the acetabulum known as  the acetabular fossa, arises a ligament, called the ligamentum teres that attaches to the fovea capitis, which is a depression found on the tip of the femoral head. 

This ligament helps with joint stability especially during hip flexion and abduction.

Now, the edge of the acetabulum has a thick bony circular rim covered by a ring of cartilage known as the acetabular labrum. 

At its lower end, there’s a depression called the acetabular notch, which is covered by the transverse ligament which fills the gap within the circumference of the acetabulum. 

Now, the normal development of a hip joint requires that the femoral head stays fitted within the acetabulum so that they both grow together keeping their sizes and shapes proportional. 

In congenital hip dysplasia, the femoral head dislocates out of its acetabulum during development, and as a result, the ball and the socket grow out of proportion to one another, so that they’re unable to form a normal stable joint.

The cause of the dislocation isn’t always known. But one situation that can give rise ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/lichen-planus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VPuG-nYtQWO51pQrDuPE6s2LQPanp2N8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lichen planus]]></video:title><video:description><![CDATA[With lichen planus, lichen means tree moss and planus refers to flat, and the reason it’s called that, is that lichen planus is a flat-topped skin rash that looks a bit like tree moss. 

Lichen planus is an immune-mediated disorder, meaning that the immune system has started attacking its own skin, resulting in a skin rash. 

Lichen planus can also affect mucous membrane. 

Now, the skin is divided into three layers--the epidermis, dermis, and hypodermis. 

The epidermis forms the thin outermost layer of skin. 

Underneath, is the thicker dermis layer that contains the nerves and blood vessels. 

And finally, there’s the hypodermis which is made of fat and connective tissue that anchors the skin to the underlying muscle.

The epidermis itself is made of multiple layers of developing keratinocytes - which are flat pancake-shaped cells that are named for the keratin protein that they’re filled with.

Keratinocytes start their life at the lowest layer of the epidermis called the stratum basale, or basal layer, which is made of a single layer of stem cells that continually divide and produce new keratinocytes. 

These new keratinocytes then migrate upwards to form the other layers of the epidermis. 

The stratum basale also contains another group of cells - melanocytes, which secrete a protein pigment, or coloring substance, called melanin. 

As keratinocytes in the stratum basale mature and lose the ability to divide, they migrate into the next layer, called the stratum spinosum which is about 8 to 10 cell layers thick. 

The next layer up is the stratum granulosum which is 3 to 5 cell layers thick. Keratinocytes in this layer begin the process of keratinization, which is the process where the keratinocytes flatten out and die.

Keratinization leads to development of the stratum lucidum layer which is 2 to 3 cell layers thick of translucent, dead keratinocytes. 

Finally, there’s the stratum corneum, or the uppermost and thickest layer of the epidermis, which]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_and_physiology_of_the_teeth</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Lr4SFs-qSBGp5H0oCc1zPRVcTiGqq24b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy and physiology of the teeth]]></video:title><video:description><![CDATA[In the mouth, the bone holding the bottom row of teeth is the mandible, and the bone holding the top row of teeth is the maxilla. 

The mandible and maxilla - like most bones in the human body - have a core of less dense cancellous bone, wrapped in an outer layer of more dense alveolar bone. 

The part of the mandible and maxilla that are in the mouth are covered by the gums. And the teeth rest in bony sockets within the mandible and maxilla and are surrounded by the gums. 

Usually, at around six months of age, infants will have their first pair of deciduous teeth, also called milk teeth or baby teeth, erupt through the gums and into the mouth. 

New deciduous teeth continue to erupt every one to two months until the baby is around two years old and has a full set of deciduous teeth. 

Since the mouth is symmetrically divided down the middle, let’s look at just one side of it. 

The teeth that pair up vertically have the same names. 

Starting at the front of the mouth, in the center, there are the central incisors and then the lateral incisors. These teeth are shaped like chisels and are good at biting off small bits of food.

Next, are the canines, which got their name from being the same teeth that are extra long and sharp in dogs. They’re also called the cuspids, which comes from the word cusp, meaning point. They’re good for puncturing holes, tearing things, and are an essential part of any vampire costume. 

Both incisors and canines typically have one root each. 

Then, there are the first molars and the second molars. Molars usually have four to five cusps, and are great for crushing and grinding food. That makes 20 deciduous teeth in total. 

As the permanent teeth grow in the bone below the deciduous teeth throughout childhood, the roots of the deciduous teeth begin to get absorbed into the gums. This loosens them and allows them to fall out, making room for the permanent teeth to take their places. 

These permanent teeth are also called t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adult_brain_tumors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tgvCaXwVTcC3fiU7f7-39ejsS4WATipx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adult brain tumors]]></video:title><video:description><![CDATA[Adult brain tumors are masses of abnormal cells that generally occur in adults, and result from the uncontrolled growth of those cells within the brain. 

OK - let’s start with some basic brain anatomy. First off, there’s the cerebral cortex which is the part of the brain that’s supratentorial or above the tentorium, and the cerebellum, which is infratentorial or below the tentorium. 

And the brain has four interconnected cavities called ventricles, which are filled with cerebrospinal fluid - a fluid that helps provide buoyancy and protection, as well as metabolic fuel for the brain. 

Highest up, are two C-shaped lateral ventricles that lie deep in each cerebral hemisphere. 

The two lateral ventricles drain their cerebrospinal fluid into the third ventricle, which is a narrow, funnel-shaped, cavity at the center of the brain. 

The third ventricle makes a bit more cerebrospinal fluid and then sends all of the cerebrospinal fluid to the fourth ventricle via the cerebral aqueduct.

The fourth ventricle is a tent-shaped cavity located between the brainstem and the cerebellum. 

After the fourth ventricle, the cerebrospinal fluid enters the subarachnoid space, which is the space between the arachnoid and pia mater, two of the inner linings of the meninges which cover and protect both the brain and spine. 

So this makes it possible for cerebrospinal fluid to also flow through the central canal of the spine.

Now, focusing in on cells within the brain - there are many different types with specialized functions. 

For example, neurons communicate neurologic information through neurotransmitter regulated electrical impulses. 

Then there are cells that secrete hormones into circulation and regulate the functions of other cells throughout the body. 

These cells are found in glands, like the supratentorial pineal gland which is located just behind the third ventricle. 

Or the infratentorial pituitary gland located near the front of the third ventricle. 

There]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_brain_tumors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ILT3xNywTja8YQbNQ4v5wN0iRKWrTyuw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric brain tumors]]></video:title><video:description><![CDATA[Pediatric brain tumors are masses of abnormal cells that generally occur in children, and result from the uncontrolled growth of those cells within the brain. 

OK - let’s start with some basic brain anatomy. First off, there’s the cerebral cortex which is the part of the brain that’s supratentorial or above the tentorium, and the cerebellum, which is infratentorial or below the tentorium. 

And the brain has four interconnected cavities called ventricles, which are filled with cerebrospinal fluid - a fluid that helps provide buoyancy and protection, as well as metabolic fuel for the brain. 

Highest up, are two C-shaped lateral ventricles that lie deep in each cerebral hemisphere.

The two lateral ventricles drain their cerebrospinal fluid into the third ventricle, which is a narrow, funnel-shaped, cavity at the center of the brain. 

The third ventricle makes a bit more cerebrospinal fluid and then sends all of it to the fourth ventricle via the cerebral aqueduct.

The fourth ventricle is a tent-shaped cavity located between the brainstem and the cerebellum.

After the fourth ventricle, the cerebrospinal fluid enters the subarachnoid space, which is the space between the arachnoid and pia mater, two of the inner linings of the meninges which cover and protect both the brain and the spine. 

So this makes it possible for cerebrospinal fluid to also flow through the central canal of the spine.

Now, focusing in on cells within the brain - there are many different types with specialized functions. 

For example, neurons communicate neurologic information through neurotransmitter regulated electrical impulses.

Then there are cells that secrete hormones into circulation and regulate the functions of other cells throughout the body. 

These cells are found in glands, like the supratentorial pineal gland which is located just behind the third ventricle. Or the infratentorial pituitary gland located near the front of the third ventricle. 

There is also a categ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bleeding_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HsRtoAqNRUC_LR_ilm9W5CcQRXykYKT8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bleeding disorders: Clinical]]></video:title><video:description><![CDATA[Bleeding disorders are classified into problems with primary hemostasis - which is formation of the weak platelet plug, and problems with secondary hemostasis - which is making a strong fibrin clot through activation of the intrinsic, extrinsic and common coagulation pathways. 

The first clue in distinguishing between primary and secondary hemostasis is the clinical presentation.

Primary hemostatic problems usually cause petechiae - which are pinpoint superficial skin bleeds, anterior epistaxis - which are usually mild nosebleeds, immediate bleeding after surgical procedures, like tooth extraction, or bleeding from mucosal surfaces, like gingival, gastrointestinal, or vaginal bleeding. 

Primary hemostatic problems can be further subdivided into two groups. 

The first is a decrease in platelet number, thrombocytopenia - which may be caused by decreased production, increased destruction, or sequestration. 

The second is a decrease in platelet function, like in von Willebrand disease, Bernard-Soulier disease, Glanzmann thrombasthenia, uremic platelet dysfunction, and as a result of medications like aspirin, non-steroidal anti-inflammatory drugs or NSAIDs, and clopidogrel. 

Patients with primary hemostatic problems often have a prolonged bleeding time, which involves mildly pricking the patient, and then timing how long it takes for them to stop bleeding - normally, this occurs within two to five minutes. 

Bleeding time is rarely measured nowadays, because they’ve been replaced by another screening tool called platelet function analyzers.

In contrast, patients with secondary hemostatic problems can develop large bruises called ecchymoses, deep tissue hematomas or hemarthrosis - which is bleeding inside the joint space, posterior epistaxis - which causes a severe nosebleed, persistent bleeding after surgical procedures, as well as intracerebral hemorrhage. 

Secondary hemostatic problems are usually due to a decrease in the number of clotting factors, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Asthma:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Gvoo3MQNS_SA7PvuqKLcKzcNRluRDvPz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Asthma: Clinical]]></video:title><video:description><![CDATA[Asthma is an episodic, chronic respiratory disorder characterized by airway obstruction caused by inflammation and hyperresponsiveness of the bronchial smooth muscle. The two golden words in asthma are “reversible”, which means the obstruction can virtually disappear with medications like bronchodilators, and “inducible”, which means the obstruction can occur in response to a variety of stimuli; including allergens like house dust mites, pet animal dander, like cat dander, and pollen, or irritants like tobacco smoke, respiratory tract infections, like a common cold or pneumonia, cold or dry air, and even emotional stress. Now, atopy is the genetic predisposition of an individual towards developing IgE antibodies to otherwise harmless environmental antigens, making that individual strongly predisposed to developing three allergic disorders, eczema or atopic dermatitis, allergic rhinitis, and asthma, collectively coined the atopic triad. Because of this genetic component, asthma is usually diagnosed in early childhood, and may or may not carry on into adulthood.

So, let’s say a genetically predisposed child is exposed to a potential allergen for the first time. First off, dendritic cells take up the allergen and present it to a type 2 helper T-cell, or Th2 cell. In asthma, Th2 cells make the mistake of thinking this harmless antigen is an allergen, so they release cytokines that stimulate B cells to make IgE antibodies. IgE antibodies then prime mast cells, which cautiously anticipate the next event. When the child is re-exposed to the allergen, the mast cells spill out vasoactive mediators like histamine and leukotrienes, which cause bronchoconstriction and inflammation. Once the child is no longer exposed to the allergen, the immune system relaxes, and everything goes back to normal, until the next event. Now, not all asthma episodes are triggered this way by an allergen. A unique form of asthma is aspirin sensitive asthma, which is characterized by ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacodynamics:_Desensitization_and_tolerance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zKpC2ZBlQX2THmFFXyx8irXTQ0_Z1bCV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacodynamics: Desensitization and tolerance]]></video:title><video:description><![CDATA[Pharmacodynamics refers to the mechanisms and effects of medications within the body. Or more simply, it’s what medications do to the body and how they do it.

Alright, so in order to have an effect, most medications have to reach their target cells and bind to a receptor.

Receptors are specialized proteins both on the cell membrane and inside the cell, that can bind to a ligand. 

Now, that ligand could be an agonist, which is a molecule that binds and activates a receptor. 

This means the receptor changes its shape or activity, and that gives rise to a signal cascade of intracellular molecules - the second messengers, which ultimately results in some change in the cell’s function.

Okay, now if we massively expose the receptors to their agonists, we will get a huge downstream signal cascade and cellular response. 

But if we continuously or persistently flood that receptor with the same agonist at the same dose, what will happen, is that the ability of the agonist to produce that response will drop. 

This is actually a defense mechanism, whereby cells prevent their overstimulation by agonists. 

If this happens very rapidly, like within a few minutes, it’s called desensitization or tachyphylaxis. 

If this happens more gradually, like over the course of days to weeks, it’s called tolerance. 

Desensitization can occur with the initial dose of a medication, while tolerance typically happens with repeated doses.  

Alright, so, there are several mechanisms responsible for these phenomena. First, chronic exposure to agonists cause a decrease in the number of receptors. 

The decrease in the number of the receptors could result from the reduced synthesis of new receptors, also known as downregulation.

Also, chronic exposure increases the degradation of preexisting receptors through endocytosis, also known as sequestration or internalization. 

This is when the cell swallows up the receptor in vesicles pinching off from the cell membrane and sends them to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchodilators:_Leukotriene_antagonists_and_methylxanthines</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7KiIPTCYQ4_k92neNOa3HE8cRPaPaq0G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchodilators: Leukotriene antagonists and methylxanthines]]></video:title><video:description><![CDATA[In obstructive lung diseases like asthma, individuals suffer from reversible narrowing of the airways, medications like bronchodilators are helpful in keeping the airways open.

Now, based on their mechanism of action, bronchodilators can be broadly divided into four main groups;  β2-agonists, muscarinic antagonists, leukotrienes antagonist and methylxanthines. 

In this video, we’ll focus on the leukotriene modifying agents and methylxanthines.

So, if we take a look at the lungs, you’ve got the trachea, which branches off into right and left bronchi, and then continues to branch into thousands of bronchioles. 

In the bronchioles you’ve got the lumen, the mucosa, which includes the inner lining of epithelial cells, as well as the lamina propria which contains many cells like the type 2 helper T cells, B cells, and mast cells. 

Surrounding the lamina propria, there is a layer of smooth muscles and submucosa. 

The submucosal layer contains mucus-secreting glands and blood vessels.

Now, the molecular pathway that leads to asthma is actually pretty complex but it is often initiated by an environmental trigger. 

Allergens from environmental triggers, like air pollutants or cigarette smoke, are picked up by dendritic cells which present them to a type 2 helper T cell or Th2 cell in the lamina propria. These cells then produce cytokines like IL-4 and IL-5 which causes the inflammatory response. 

IL-4 is especially important because it leads to the production of IgE antibodies by B cells, and these antibodies bind to FcεR1 receptors on mast cells to activate them. 

These mast cells use an enzyme called phospholipase A2 to take membrane phospholipids and make a 20 carbon polyunsaturated fatty acid called arachidonic acid. 

Arachidonic acid is then metabolized by two important enzymes: one is cyclooxygenase-2 or COX-2, which makes prostaglandins, another one is 5-lipoxygenase or  5-LOX, which makes leukotrienes. 

Now, IL-5 on the other hand, activates eosi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cauda_equina_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xXFNAOWxR3uatWFfG29LKg8USk2XPklo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cauda equina syndrome]]></video:title><video:description><![CDATA[Cauda equina syndrome is a condition caused by damage to the bundle of peripheral nerves protruding from the bottom of the spinal cord, called the cauda equina. 

The latin words cauda equina mean horse’s tail, which is what early anatomists thought this nerve bundle looked like.

The spinal column is made of individual bones, called vertebrae. 

Each vertebra is made of a large anterior portion called the body, and the posterior part called the vertebral arch. 

The central cavity between the body and the arch is called the vertebral foramen. 

Now the spinal column is made of 33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal. 

Other than C1 and C2, each two adjacent vertebrae are, separated by an intervertebral disc, which allows for a slight movement of the vertebrae, and acts as a shock absorber. 

The sacral and coccygeal vertebrae are fused together to form the sacral bone and coccyx, or tailbone respectively. 

Now if you cut the spinal column in half lengthwise you can see that all the vertebral foramina together form the vertebral, or the spinal canal, which is occupied by the spinal cord.  

The spinal cord is connected to the brain and travels through the spinal canal to the second lumbar vertebra, where it ends in a cone, called conus medullaris. 

There are 31 pairs of nerves originating from the spinal cord called spinal nerves; there are 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal. 

Each nerve leaves the spinal canal through the corresponding intervertebral foramen, which are openings between two adjacent vertebrae. 

Since the spinal cord is shorter than the spinal canal, the nerves of the lumbar, sacral and coccygeal regions have to travel down the spinal canal to reach their corresponding openings, forming a nerve bundle below the spinal cord called the cauda equina. 

These nerves carry motor innervation for the genitals, both internal and external anal sphincter,  detrusor vesicae, which is a m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Benign_prostatic_hyperplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z2R4XK7RTZeyTqBqS9lD8tnzSMSBYsLD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Benign prostatic hyperplasia]]></video:title><video:description><![CDATA[In benign prostatic hyperplasia, or BPH, prostatic refers to the prostate gland, hyperplasia means an increase in the number of cells, and benign means that these cells aren’t malignant, so they don’t invade neighboring tissues. 

So, benign prostatic hyperplasia is the non-cancerous growth of the prostate gland. 

This condition is common in men over 50, and is often considered a normal part of aging.

The prostate is a small gland, about the size and shape of a walnut, that sits under the bladder and in front of the rectum. 

The urethra which is the tube through which urine leaves the bladder, goes through the prostate before reaching the penis. 

And that part of the urethra is called the prostatic urethra. 

The prostate is covered by a capsule of tough connective tissue and smooth muscle. 

Beneath this layer, the prostate can be divided into a few zones.  

The peripheral zone, which is the outermost posterior section, is the largest of the zone and contain about 70% of the prostate’s glandular tissue. 

Moving inward, the next section is the central zone which contains about 25% of the glandular tissue as well as the ejaculatory ducts that join with the prostatic urethra.

Last, is the transitional zone, which contains around 5% of the glandular tissue as well as a portion of the prostatic urethra. 

The transitional zone gets its name because it contains transitional cells which are also found in the bladder. 

At the microscopic level, each of the tiny glands that make up the prostate is surrounded by a basement membrane made largely of collagen. 

Sitting within that basement membrane, is a ring of cube-shaped basal cells as well as a few neuroendocrine cells interspersed throughout. 

Finally, there’s an inner ring of luminal columnar cells, which are within the lumen or center of the gland. Luminal cells secrete substances into the prostatic fluid, that make it slightly alkaline that give it nutrients which nourish the sperm and help it surviv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antidiarrheals</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0AdJqbmaT9O10UC1-lBWqr97S5G33c5P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antidiarrheals]]></video:title><video:description><![CDATA[Antidiarrheal medications are used to treat diarrhea, a word which actually means “flow through.” 

Diarrhea can be defined as stool that contains fluid weight over 200g of fluid per day. 

Increased frequency of bowel movement is also common, but not always present. 

It’s important to note that these medications are typically used to treat mild to moderate diarrhea; therefore, they should not be used in individuals with severe illness, bloody diarrhea, or high fever because they can mask or exacerbate the underlying condition.

Now, the small and large intestine are where most of the absorption happens in the GI tract. 

Both regions contain smooth muscles which perform what’s called peristalsis, which is a series of coordinated wave-like muscle contractions that help squeeze the chyme or the food bolus after it leaves the stomach, in one direction.  

Lining the luminal surface of the intestine is a layer called the mucosa, which secretes and absorbs different molecules to change the contents of the intestinal lumen. 

The mucosa of the small intestine has a lot of tiny ridges and grooves, each of which projects little finger-like fibers called villi. 

And in turn, each villus is covered in teeny tiny little microvilli. 

All of this gives the small intestine plenty of surface area to absorb nutrients and ions. 

The large intestine mainly absorbs excess water from the chyme, and that helps condense it into dry fecal matter, which eventually ends up in the rectum.

There are four main causes for diarrhea: osmotic, secretory, inflammatory, and diarrhea associated with deranged, or unstable, intestinal motility. 

Osmotic diarrhea is caused by poor absorption of certain molecules, which leads to an excessive amount of solutes in the intestinal lumen. 

The extra solutes cause fluid retention due to osmosis, which is when water moves from intestinal cells across semipermeable membranes into the lumen so that solute concentrations are equal on both si]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Advanced_cardiac_life_support_(ACLS):_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/umMtiKW9SlqeQV6KLudPJfOoTDeyVkx-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Advanced cardiac life support (ACLS): Clinical]]></video:title><video:description><![CDATA[Advanced cardiac life support, or ACLS, is a structured way to respond to an unresponsive person with cardiac arrhythmias and cardiac arrest. 

ACLS can be done by an individual or by a team that’s led by a team leader.

When we suspect a person may be in need of assistance, the first thing we need to do is determine their level of consciousness. 

Talk loudly at them, rub their sternum, or apply pressure to their nail beds or ear lobes, while simultaneously checking for absent or abnormal breathing. 

If they&amp;#39;re not responsive, check their carotid pulse for about 10 seconds. If there&amp;#39;s no pulse, first immediately activate the emergency response system to get more help and an AED or defibrillator. Then, move on to the ACLS algorithm.

The first thing to do is cardiopulmonary resuscitation or CPR, which combines chest compressions and artificial ventilation.

The big picture goal of CPR is to maintain blood flow to the brain while a patient is pulseless. Because the patient’s heart is not functioning, the team is mechanically squeezing the heart to ensure blood flows to the brain. 

In a person over 8 years of age, chest compressions are done by placing the heel of one hand in the center of the chest, then placing the other hand on top, interlocking the fingers, and without flexing the elbows, pushing down on the chest to a depth of at least 5 centimeters or 2 inches - which is about the same size as a closed fist lengthwise. 

Compressions are done at a rate of about 100 compressions per minute, which you can remember if you do them to the beat of “Staying alive” by the Bee Gees. 

Additionally, the team attempts to artificially ventilate the patient so oxygen can enter the lungs and carbon dioxide can leave the lungs. 

Artificial ventilation includes a variety of ways to assist respiration for a person who isn’t breathing or making sufficient respiratory effort on their own. 

The options for ventilation usually involve a bag valve mask]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Drug_administration_and_dosing_regimens</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ohz-7avUS1ahc1NSfvg_cl1sTkOHDTsS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Drug administration and dosing regimens]]></video:title><video:description><![CDATA[Every medication can be administered through various means, known as routes of administration; and various schedules, meaning at a particular frequency and amount, or dose, which is known as the dosing regimen.

Alright, so routes of administration are broken down into three main categories: enteral, parenteral, and topical. In enteral administration, which is the most common form, the medication is administered through the gastrointestinal tract. This could mean that it’s swallowed by the mouth, also known as peroral administration; placed under the tongue, also known as sublingual administration; between the gums and the inner lining of the cheek, also known as buccal administration; or finally, into the rectum, also known as rectal administration. 

On the other hand, parenteral administration includes any route that bypasses the gastrointestinal tract, to pump the medication directly into the circulation, such as through an injection into a vein, intravenously, or IV for short; under the skin, subcutaneously, or SC for short; or into muscle, intramuscularly, or IM for short. Finally, there’s topical administration, where the medication is applied directly upon a particular area of the skin or mucous membrane to achieve a local or systemic effect. An example of this is an antifungal cream used to treat athlete&amp;#39;s foot locally or a clonidine patch to treat hypertension systemically.

Now, choosing the route of administration depends on many factors. First of all, these include the chemical properties of the medication itself, such as its stability, and its ability to cross certain barriers of absorption. 

For example, a perorally administered medication needs to be able to resist tough, acidic conditions within the stomach, and then readily pass through the walls of the intestines into the blood. In addition to this, blood coming from the gastrointestinal tract is first directed to the liver. And that’s where many medications get broken down or ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pneumothorax:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g2udY-d1Ri6Nm8h-UY5hMW5OTqa72Boh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pneumothorax: Clinical]]></video:title><video:description><![CDATA[The pleura is the blanket that covers our lungs, and it’s made of two layers, the inner visceral pleura and the outer parietal pleura. In between those two layers is a space. 

If air gets in that space, it’s called a pneumothorax. Pneumothoraces can be classified into two broad categories: spontaneous or traumatic. 

Spontaneous pneumothorax is further subclassified into primary and secondary. A primary spontaneous pneumothorax occurs without a triggering event in an otherwise normal lung. 

Most commonly, an individual at risk of primary spontaneous pneumothorax is a tall, thin, young male presenting with symptoms that started at rest. 

This is because there are more mechanical shear forces at the apex of the lung, that can make the pleura rupture, especially after for some reason holding their breath like diving or inhaling and holding a recreational drug or medication in their lungs. 

Another risk factor for a primary pneumothorax is smoking cigarettes and systemic syndromes like Marfan disease. 

Then there’s a secondary pneumothorax; that is a spontaneous pneumothorax that occurs in a lung with pre-existing lung disease, like chronic obstructive pulmonary disease or COPD, asthma, interstitial lung disease, tuberculosis, cystic fibrosis, or lung cancer. 

In COPD, destruction of the alveolar sacs leads to formation of large alveolar blebs, which are small balloons that can eventually rupture, leaking air into the pleural space. 

Traumatic pneumothorax occurs secondary to injury of the pleura after blunt or penetrating trauma to the chest like a stab wound, or as a complication of a procedure, such as a lung biopsy, thoracentesis, central line insertion, or mechanical ventilation. 

Now, any pneumothorax, regardless of how it forms, can potentially become a tension pneumothorax, but it most often happens in a traumatic pneumothorax, which most often occurs due to a punctured lung. 

Causes can include a broken rib puncturing through the pleural spac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Correlation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NORGdGDsR0_P9sW5HKMB5-zpRpO7LuTL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Correlation]]></video:title><video:description><![CDATA[Correlation is a statistical technique that shows whether two quantitative variables are related, and also how strongly they’re related. 

For example, let’s say you want to figure out if drinking more soda is correlated with having a higher body mass index or BMI. 

So, you ask 100 people how many sugary beverages they drink in a week and then check each person’s height and weight to calculate their BMI.  

You could plot these measurements or data points on a scatterplot, with the number of beverages on the x-axis and BMI on the y-axis, and where each data point represents one individual. 

Typically, a trendline is drawn to best represent the pattern of data points on the plot, with roughly half the points above the line and half the points below the line. 

Now, a positive correlation means that BMI increases as the number of beverages increases, and, if the two variables have a perfect positive correlation, then the trendline will pass through every single data point. 

Now imagine that there’s a negative correlation. That means that the BMI decreases as the number of beverages increases, and, with a perfect negative correlation, the trendline also passes through every data point. 

Finally, if there’s no correlation, then the data points will be randomly spread out all over the scatterplot, and the trendline will be flat with no positive or negative direction.

To figure out how strongly two variables are correlated, we can use the Pearson’s correlation test, which is a parametric test that measures how close or spread out the data points are from the trendline. 

The Pearson’s correlation test calculates a correlation coefficient, which is a number that represents how well the two variables are correlated, and usually it’s written with a lowercase r. 

The correlation coefficient can range from negative 1 - which represents perfect negative correlation - to positive 1 - which represents perfect positive correlation. 

A correlation coefficient of 0 ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Information_bias</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r7lIezUHSR6dmpFaTSzkcx8zQTSrsmGQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Information bias]]></video:title><video:description><![CDATA[Information bias or measurement bias is a type of bias or error that can occur when researchers are unable to collect accurate data. 

Typically, information can be misclassified in two ways - differential, when information collected from one group is accurate but information collected from the other group is inaccurate, and non- differential, when information collected from both groups is inaccurate. 

For example, let’s say you want to figure out if flossing teeth prevents cavities. 

So you follow 100 people who floss, and 100 people who don’t floss, over the course of ten years, and find out that 30% of the flossers and 60% of the non- flossers ended up getting cavities.

Now, we can divide these proportions, 60% divided by 30%, and conclude that people who don’t floss have 2 times the risk of getting cavities compared to people that do floss. 

Now, in this study we assume that every person in the flossing group is going to floss their teeth every single day for ten years, and every person in the non- flossing group is not going to floss their teeth for ten years. 

But sometimes people in one of the study groups don’t stick with their exposure for the entire study period. 

For example, maybe some people in the flossing group stopped flossing halfway through the study, because they ran out of floss and just never bought more. 

In this case, they would still be counted by the researchers as part of the flossing group even though they technically switched over to the non- flossing group. 

On the other hand, everyone in the non- flossing group stayed in the non-flossing group, meaning that they all really didn’t floss for the entire ten years. 

This would cause differential misclassification, because information collected from the non- flossing group would be accurate, but information collected from the flossing group would be inaccurate. 

So how does differential misclassification affect the results of a study?

Let’s assume that flossing actually ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gene_regulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pq5oRWnxTsW570MHXDR6CcBkRjiUN_w-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gene regulation]]></video:title><video:description><![CDATA[Our DNA is like a library - found in the nucleus of our cells - with thousands of books. 

Some of these books - called genes - are extremely important, because they carry the recipes for every single protein found in the cell. 

Some of these proteins are necessary in all the cells - like the cytoskeletal proteins. 

But other proteins, like neurotransmitters, are necessary only in certain cell types - like neurons. 

Gene regulation is what allows the right cells to make the right proteins at the right time. 

Now, on the molecular level, DNA is made up of two strands of nucleotides, so each gene is just a segment of this nucleotide sequence. 

And there are four types of nucleotides: adenine, guanine, thymine, and cytosine - or A, G, T, C. 

Now, the entire DNA molecule is wrapped around structural proteins called histones that package the DNA into nucleosomes - like when we roll yarn into a ball to keep it compact and organized. 

Altogether, the entire yarn with the DNA plus the histones - is called chromatin.

The process of decoding the information stored in the DNA is called gene expression - and it includes transcription and translation. 

Transcription is where the enzyme RNA polymerase uses the gene as a template to create a molecule that can leave the nucleus. 

This molecule is called messenger RNA or mRNA and it has the same nucleotide sequence as the gene, with one tweak: it has uracil nucleotides - or U - instead of thymine. 

This message is encoded so that any 3 nucleotide equate a specific codon which codes for an amino acid or is a stop codon which means that the protein is complete. 

In translation, specialized proteins in the cytoplasm - called ribosomes - use the mRNA template to create a string of amino acids that make up the protein. 

Gene regulation can occur at the level of transcription, post-transcriptional which is between transcription and translation, or translation. 

Let’s start with transcriptional regulation - and to u]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Uterine_fibroid</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UyA3SWsTQJSSc6AI2ZM3IM-sR6iWtCyw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Uterine fibroid]]></video:title><video:description><![CDATA[Uterine fibroids, are also called leiomyomas. Leio- means smooth, myo- means muscle, and -oma means tumor, so these are benign smooth muscle tumors of the uterus. 

In fact, fibroids are the most common type of tumor in females.

The uterus is a hollow organ that sits behind the urinary bladder and in front of the rectum. 

The top of the uterus above the openings of the fallopian tubes is called the fundus, and the region below the openings is called the uterine body. 

The uterus tapers down into the uterine isthmus and finally the cervix, which protrudes into the vagina.

Zooming into the cervix, there are two openings, a superior opening up top, and an inferior opening down below, both of which have mucus plugs to keep the uterus closed off except during menstruation and right before ovulation. 

The uterus is anchored to the sacrum by utero- sacral ligaments, to the anterior body wall by round ligaments, and it’s supported laterally by cardinal ligaments as well as the mesometrium, which is part of the broad ligament. 

The wall of the uterus has three layers: the perimetrium, which is a layer continuous with the lining of the peritoneal cavity, the myometrium, which is made of smooth muscle that contracts during childbirth to help push the baby out, and the endometrium, a mucosal layer, that undergoes monthly cyclic changes. 

Now, uterine fibroids are smooth muscle tumors, and they’re monoclonal meaning that they arise from a single cell of the myometrium that starts dividing uncontrollably. 

Overall, fibroids most commonly affect women of African descent. 

They’re sometimes linked to a genetic mutation, with the most common being a somatic mutation with the mediator complex subunit 12 or MED12 gene. 

Mediator complex subunit 12 is part of a group of proteins that control gene activity by regulating how transcription factors bind to RNA polymerase II. 

Another factor in fibroid development is steroid hormones. 

Fibroids have a love affair with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maple_syrup_urine_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jHWzXge1SmieT6NXvYmK-KUhSz6F-CAU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Maple syrup urine disease]]></video:title><video:description><![CDATA[Maple syrup urine disease is a rare genetic metabolic disorder where the body cannot break down branched chain amino acids like valine, leucine, and isoleucine completely, causing buildup of these amino acids and their toxic metabolic byproducts. 

It was named maple syrup urine disease since the urine that contain these metabolites smell like maple syrup. 

Other names for this disease include branched- chain ketoacid dehydrogenase deficiency, or BCKD deficiency, and branched- chain ketoaciduria. 

Now, amino acids are the basic building blocks that make up proteins. 

There are 20 amino acids used in the human body and they all contain a carboxyl group (-COOH) and an amine (-NH2) group. 

The branched chain amino acids have a side chain containing 3 or more carbons, and they include valine, leucine, and isoleucine. 

These 3 are essential amino acids, meaning our bodies can’t create them, so they must be acquired through protein rich foods like meat, eggs, dairy, avocados, beans, etc.

So the proteins you eat are broken down into amino acids in the gastrointestinal tract by gastric acid and digestive enzymes. 

The amino acids are then absorbed by the small intestine into the bloodstream, which then travel to the cells of the body, where they are used for protein synthesis. 

Since the body can’t store these amino acids, any extra amino acids are converted into glucose or ketones and used for energy. 

Branched chain amino acids: valine, leucine and isoleucine, require special steps during their catabolism. 

First, the enzyme branched- chain amino transferase, or BCAT, strip off their alpha amino group and transfers it to an alpha ketoglutarate to form glutamate. 

This also converts the branched- chain amino acids into branched- chain keto acids. 

Valine into alpha-ketoisovalerate, or KIV, leucine is converted into alpha-ketoisocaproate, or KIC, and isoleucine into alpha-keto-beta-methylvalerate, or KMV. 

In the second step, branched-chain alpha-keto]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adenosine_deaminase_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SickPE26RwmFbRs2yCNS-EylRFqkedjH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adenosine deaminase deficiency]]></video:title><video:description><![CDATA[Adenosine deaminase deficiency, or ADA deficiency, is a rare genetic disease, that results in severe combined immunodeficiency, or SCID for short. 

SCID can be caused by a number of causes, so this particular variation is called ADA-SCID.

Let’s take a step back. Our cells have all the instructions on how to live and behave written on their own copy of DNA. 

DNA is made out of four nucleotides, which can also do all kinds of cool stuff in their free time, like provide energy to various processes in the cell. 

Nucleotides are made out of a sugar, in this case deoxyribose, one to three phosphate groups, and a nucleobase, which can be adenine, thymine, cytosine, or guanine. 

So, the name of a deoxyribose-containing, triphosphatic nucleotide, based on adenine, that makes up DNA would be deoxyadenosine triphosphate, or dATP, for short. 

These nucleotides are needed in equal proportions in order to make cellular division run smoothly. 

Now, nucleotides have a functional lifetime of their own, and our body has mechanisms on how to break them up into their building blocks, to be either excreted or recycled. 

Let’s focus on deoxyadenosine triphosphate. 

First the enzyme adenosine deaminase removes an amine group from it, turning it into deoxyinosine monophosphate, or dIMP. 

Then purine nucleoside phosphorylase comes in and removes the phosphate and the deoxyribose from dIMP, making hypoxanthine.

Hypoxanthine is then oxidised twice by xanthine oxidase - first to become xanthine, and then finally, to uric acid. 

Uric acid can then be excreted by the kidneys, in the form of urine.

Now one class of cells that divides quickly and therefore relies heavily on cell division to work smoothly are lymphocytes. 

Lymphocytes protect the body from pathogens, like bacteria and viruses in two ways. 

First, B lymphocytes, or B cells, produce immune proteins called antibodies, which seek out and latch on onto an invader, marking it for destruction by other cells. 

Sec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Patau_syndrome_(Trisomy_13)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7Oncy6WpR52Nt_EJVpFMPP9FS1aM0Lys/_.jpg</video:thumbnail_loc><video:title><![CDATA[Patau syndrome (Trisomy 13)]]></video:title><video:description><![CDATA[Patau syndrome is a chromosomal disorder where a person inherits an extra copy of chromosome 13, or a part of it. 

So instead of having two, they have three copies of chromosome 13, and so Patau syndrome is also known as trisomy 13.

Patau syndrome is named after Dr. Klaus Patau, who first described the chromosomal nature of the syndrome. 

All right, our DNA is like this humongous blueprint of information on how to make a human. 

Usually this massive document is packaged up nicely into storage bins called chromosomes. 

Actually, we usually have 46 chromosomes that we use to neatly organize all our information, depending on how you define organize. 

Each of the 46 chromosomes is actually part of a pair of chromosomes, since you get one from each parent, so 23 pairs. 

If you wanted to make another human, first you’d have to find someone that feels the same way, and then you both contribute half of your chromosomes, so one from each pair, right? Fifty-fifty. 

Now, what if someone contributes one too many? Say Dad contributes 23 and Mom contributes 24, is that possible? 

Yes, and it’s the basis of trisomies, in other words, having three copies of a particular chromosome. 

Trisomy 13, or Patau syndrome, is the least common, but most severe trisomy in live births. 

Alright, so in order to package up half the chromosomes into either a sperm cell or an egg cell, you actually start with a single cell that has 46 chromosomes, let’s just say we’re making an egg cell for the mother. 

I’m just going to show one pair of chromosomes, but remember that all 23 pairs do this. 

So the process of meiosis starts, which is what produces our sex cells, and the chromosomes replicate, and so now they’re sort of shaped like an ‘X’—even though there are two copies of DNA here, we still say it’s one chromosome since they’re hooked together in the middle by this thing called a centromere. 

OK, then the cell then splits in two, and pulls apart the paired chromosomes, so in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clostridium_difficile_(Pseudomembranous_colitis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2O4GxBkdRdi02PsalGXQBcZOTjOu2nAW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clostridium difficile (Pseudomembranous colitis)]]></video:title><video:description><![CDATA[Clostridium difficile is difficult to treat, hence the name. 

Clostridia, as a family, are obligate anaerobes, meaning they don’t require oxygen to thrive, in fact, they’re better off without it. 

In nature, they thrive in deep, compact soil, and when they feel the stress of fresh oxygenated air, they often produce spores, which are extremely resilient to the environment. 

When conditions improve, the spores can sprout into fully fledged Clostridia. 

In the lab, when doing a gram stain, Clostridium difficile is gram positive, or purple and look like big cylinders or rods. 

Now, Clostridium difficile can sometimes establish residence in our colon typically after a person has accidentally ingested the bacteria that originally were living in another person’s colon. 

This is called the fecal-oral route, and it usually results from eating with unwashed hands. 

In fact, around 5% of the population are asymptomatic carriers of Clostridium difficile, but the vast majority of these individuals don’t seem to have an issue with it! 

That’s because there are a number of bacterial species living in the intestines that make up the microbiome. 

These various bacterial species called the normal flora, coexist in an environment where they live together and compete for resources. 

A healthy normal flora, therefore doesn’t allow Clostridium difficile to dominate the intestines. 

However, if the diversity of that normal flora is disturbed - by antibiotics - for instance, then organisms that are resistant to antibiotics like Clostridium difficile can thrive while other bacteria might die out. 

That can allow for overgrowth of Clostridium difficile. 

Another way to disturb the equilibrium of the gut biome is use of chemotherapy or prolonged use of elemental diet, which is gastric tube feeding of elemental liquid nutrients, often seen in intensive care units.

In these situations, once again, the normal flora gets disturbed and it tilts the equilibrium towards Clost]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Edwards_syndrome_(Trisomy_18)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E5kbj-qZT3SJ033LeWODBc3GSWKiiGwp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Edwards syndrome (Trisomy 18)]]></video:title><video:description><![CDATA[Edwards syndrome, named after the British geneticist, John Edwards, who first identified it, is a chromosomal disorder where a person inherits an extra copy of chromosome 18 or a part of it. So instead of having two, they have three chromosomes 18 and so Edwards syndrome is also known as trisomy 18, in other words, “three chromosome 18s”. 

All right, our DNA is like this humongous blueprint of information on how to make a human. Usually this massive document is packaged up nicely into a storage bin called a chromosome. Usually we have 46 chromosomes that we use to neatly organize all our information, depending on how you define organize. Each of the 46 chromosomes is actually part of a pair of chromosomes, since you get one from each parent, so 23 pairs. If you wanted to make another human, first you’d have to find someone that feels the same way, and then you both contribute half of your chromosomes, so one from each pair, right? Fifty-fifty. Now, what if someone contributes one too many? Say Dad contributes 23 and Mom contributes 24, is that possible? Yes, and it’s the basis of trisomies, in other words, having three copies of a particular chromosome. Now the most common trisomy in live births is trisomy 21, or Down syndrome. But the second most common trisomy in live births is trisomy 18, or Edwards syndrome.  

Alright, so in order to package up half the chromosomes into either a sperm cell or an egg cell, you actually start with a single cell that has 46 chromosomes, let’s just say we’re making an egg cell for the mother, I’m just going to show one pair of chromosomes, but remember that all 23 pairs do this. So the process of meiosis starts, which is what produces our sex cells, and the chromosomes replicate, and so now they’re sort of shaped like an ‘X’—even though there are two copies of DNA here, we still say it’s one chromosome since they’re hooked together in the middle by this thing called a centromere. OK then the cell splits in two, and pulls]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Carbonic_anhydrase_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ot0wieCiRcScrXrH0NpkBFvLQWujHmug/_.jpg</video:thumbnail_loc><video:title><![CDATA[Carbonic anhydrase inhibitors]]></video:title><video:description><![CDATA[Diuretics are medications that act on the kidneys to increase production of urine, and to eliminate water, certain metabolic wastes, and electrolytes from the body. 

There are 5 main types of diuretics; carbonic anhydrase inhibitors, osmotic diuretics, thiazide and thiazide-like diuretics, loop diuretics, and last but not least, potassium sparing diuretics - which is the only class of diuretic that retains potassium, rather than wastes it. 

Now, the basic unit of the kidney is called a nephron, and each nephron is made up of a glomerulus, which filters the blood. The filtered content goes through the renal tubule, where excess waste, and molecules such as ions and water, are removed or filtered through an exchange between the tubule and the peritubular capillaries. So the renal tubule plays a huge role in secretion and reabsorption of fluid and ions - such as sodium, potassium, and chloride - in order to maintain homeostasis - or the balance of fluid and ions in our body. 

The renal tubule has a few segments of its own: the proximal convoluted tubule, the U- shaped loop of Henle, with a thin descending, a thin ascending limb, and a thick ascending limb, and finally, the distal convoluted tubule, which empties into the collecting duct, which collects the urine. 

The luminal side of the proximal convoluted tubule is lined by tubule cells, which are also known as brush border cells. The apical surface of these cells, which faces the tubular lumen, is  lined with microvilli. Microvilli are tiny projections that increase the cell’s surface area to help it reabsorb more solutes or water. 

On the other side is the basolateral surface, which faces the interstitium, or the space between the tubule and the peritubular capillaries. When a molecule of bicarbonate approaches the apical surface of the brush border cell it binds to hydrogen to form carbonic acid. At that point, an enzyme called carbonic anhydrase type 4, which lurks in the tubule]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_respiratory_distress_syndrome:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pUQo_WLlSJm-mbTzNEgKlVE1TkKQNy3Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute respiratory distress syndrome: Clinical]]></video:title><video:description><![CDATA[Acute respiratory distress syndrome, or ARDS is a condition where there’s inflammation throughout the lungs leading to pulmonary edema. 

The main site of injury in ARDS is the alveolar-capillary membrane. 

Now, any damage to the alveolar epithelium or the capillary endothelium increases the permeability of the alveolar-capillary membrane, causing fluid to move into the alveoli. 

Oxygen and carbon dioxide have to travel across this fluid, so it acts as a barrier against normal gas exchange. 

The fluid also dilutes out the surfactant molecules coating the alveoli, and as a result the alveoli are less able to remain open and compliant, so they become stiff. 

If the injury continues, the alveoli eventually collapse. 

Now, the pulmonary edema from ARDS causes the same problems as pulmonary edema from congestive heart failure, but because the triggering events are different, the term non-cardiogenic pulmonary edema is often used for ARDS. 

Now, ARDS is not a primary lung disease, rather it arises as a complication of a systemic injury that causes widespread inflammation which results in damage to the alveolar-capillary membranes within the lung. 

The most common underlying systemic cause of ARDS is sepsis, which causes systemic inflammation in response to an infection. 

But other insults include trauma, severe burns, near-drowning, disseminated intravascular coagulation or DIC, acute pancreatitis, massive blood transfusions, aspiration of gastric contents, and toxic smoke inhalation.

The list basically includes any serious injury that directly or indirectly affects the entire body.

So, as you would guess, individuals with ARDS are very sick, and have severe shortness of breath, tachypnea, hypoxemia, and diffuse crackles on auscultation of the chest. At that point, it’s important to look for an underlying cause, like a pneumonia, urinary tract infection, or an infected intravenous line - all of which might result in sepsis. 

Other clues might include ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyponatremia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SLVAcFd9TlKdum60mrco0wGkSSG9jyNT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyponatremia: Clinical]]></video:title><video:description><![CDATA[Hyponatremia means a lower than normal concentration of sodium in the blood, generally below 135 mEq/L.

However, since the concentration of sodium depends on both sodium and water levels in the body, hyponatremia actually translates as too much water in the extracellular compartment. 

Ok, now remember that total body water is distributed either in the intracellular compartment, meaning inside the cells, or the extracellular compartment, meaning outside the cells. 

Both the intracellular and extracellular compartments have the same amount of solutes dissolved in that water - so the same osmolality, normally between 275 and 290 milliosmoles per kilogram. 

Serum osmolality can be calculated using the formula: twice the concentration of sodium measured in milliequivalents per liter, plus the serum concentration of glucose divided by 18, measured in milligrams per deciliter, plus BUN, which stands for blood urea nitrogen, divided by 2.8, also in milligrams per deciliter - so if you remember one thing from this formula, it should be that sodium is the major determinant of serum osmolality.

Ok, now just to make matters more interesting, some of these solutes, like sodium and glucose, can’t freely cross cell membranes, so they generate an osmotic pressure inside the compartment. 

This confers each compartment its tonicity - meaning how likely it is that compartment will draw water out of the other one. 

Normally, the intracellular and extracellular compartment are isotonic to each other - meaning, they have the same concentration of osmotically active solutes. 

However, small variations in solute concentrations, like having more sodium in the extracellular compartment, can alter that equilibrium, so water moves across cell membranes in order to restore the balance.

Water moves according to the rules of osmosis - or from the hypotonic compartment, where there’s more water, to the hypertonic compartment, where there’s less water. And water does that until t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Valvular_heart_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/msyO97ctRlSxlaDnUspv_sIORKu_uS_G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Valvular heart disease: Clinical]]></video:title><video:description><![CDATA[Valvular heart disease involves damage or a defect in one or more of the four valves of the heart, so the aortic and bicuspid or mitral valves on the left side of the heart, and the pulmonary and tricuspid valves on the right side of the heart. 				

Normally, the valvular leaflets are very thin and when the cusps close they&amp;#39;re perfectly apposed. 

Valvular heart diseases are divided into stenosis - in which there’s narrowing of the valvular orifice that prevents adequate outflow of blood - and insufficiency or regurgitation, in which the valvular leaflets fail to close correctly and are unable to prevent backflow of blood. 

These two are not mutually exclusive, which means they can both be present in the same individual and even in the same valve, for instance if thickening of the leaflets results in inappropriate closure as well as a narrow orifice. 

Individuals with valvular heart disease are generally asymptomatic for a prolonged period, even for decades, and as soon as they become symptomatic, their life expectancy deteriorates very quickly. 

The main symptoms are dyspnea, syncope, and angina. Both stenosis and regurgitation lead to turbulent flow when blood flows across the affected valve, which produces heart sounds called pathologic murmurs that are loud enough to be heard upon auscultation with a stethoscope. 

When presentation suggests valvular heart disease, you should proceed with echocardiography to confirm the diagnosis of valvular disease and determine its severity. 

A transthoracic echocardiogram is typically done, but a transesophageal echocardiogram may be needed in selected individuals, like those with a nondiagnostic transthoracic echocardiogram.

Doppler echocardiography allows determination the speed and direction of blood flow, which makes it the most sensitive noninvasive technique for detecting the regurgitant jet. 

In some cases cardiovascular magnetic resonance imaging may be indicated to quantify the severity]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infective_endocarditis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SmkhgDOkT0iWW6bNYyLtGMzNT1m4REGB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infective endocarditis: Clinical]]></video:title><video:description><![CDATA[Infective endocarditis is an infection of the endocardium, the inner layer of the heart. 

Most cases are due to a bacterial or fungal infection of the endocardial lining the heart valves. 

But in order to reach the heart valves, a microbe has to first get into the bloodstream. 

There are a few ways that might happen - microbes can hop into a blood vessel near an open wound or an abscess, or during a dental or surgical procedure, or they can go directly in when a person gets injected with an infected needle which sometimes happens while using illicit drugs.

Microbes generally like to latch onto heart valves that are already damaged, because it makes it easier for them to adhere and form vegetations.

Risk factors for infective endocarditis include cardiac factors, like prior infective endocarditis, a prosthetic valve or implantable cardiac device like a pacemaker, or valvular or congenital heart disease; and noncardiac factors like intravenous drug use, having an intravenous catheter, immunosuppression, or a recent dental or surgical procedure. 

Clinically, infective endocarditis is categorized as either native valve endocarditis when it affects a previously normal heart valve, or prosthetic valve endocarditis when it affects an artificial heart valve. 

Native valve endocarditis is mainly caused by Staphylococcus aureus, viridans Streptococci, and is often seen in intravenous drug users, since these bacteria are normally present in the skin. 

Prosthetic valve endocarditis is mostly caused by Staphylococcus aureus as well - specifically methicillin resistant Staphylococcus Aureus or MRSA, since it’s frequently nosocomial.

Infective endocarditis causes fever, fatigue, dyspnea, and weight loss. 

Typically there’s an acute infection, which occurs within two weeks, but in some cases it might be subacute or chronic and happen over a few months. 

Upon auscultation, there’s usually a heart murmur from blood flowing past the vegetation and creati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastroesophageal_reflux_disease_(GERD):_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yVbFsyzjTc_DP8xP_4VUInd-RWmIpFDd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastroesophageal reflux disease (GERD): Clinical]]></video:title><video:description><![CDATA[The esophagus is a 25-30 centimeter long tube that food and liquids pass through, from the pharynx to the stomach.

The esophageal wall is made of 4 layers: the inner mucosa, which is made of stratified squamous epithelium, except at the lower esophageal sphincter, where it joins the gastric epithelium to form the gastroesophageal junction; the submucosa, a muscular layer; and an outer layer called adventitia. 

At the top and bottom of the esophagus there are the upper and lower esophageal sphincters, respectively. Both relax during swallowing to allow the passing of food or liquids, propelled by peristaltic contractions. 

Additionally, the lower esophageal sphincter is closed between meals to prevent acid reflux and has a resting pressure of 10 to 45 millimeters of mercury. 

When the lower esophageal sphincter pressure is lower than normal, gastric acid reaches the esophagus and the pH of the esophagus drops from 7 to 4, and this is called acid reflux. 

Some degree of acid reflux is normal, and it happens mostly after a meal, but it doesn’t cause esophageal damage or associated symptoms.

Gastroesophageal reflux disease, or GERD, happens when the resting pressure of the lower esophageal sphincter is below 10 millimeters of mercury, which allows the backflow of gastric acid in the esophagus, causing esophageal lesions and symptoms that mostly happen at night.  

GERD can be caused by a hiatal hernia, where the stomach and lower part of the esophagus slide above the diaphragm and this usually happens in overweight, obese individuals. It can also occur during pregnancy due to increased pressure in the abdomen from the growing fetus. 

Other common causes are products that increase the production of gastric acid or decrease the tone of the lower esophageal sphincter, like alcohol, spicy foods, caffeinated drinks including coffee, tea, and soda, citrus fruits, tomatoes, and even peppermint! 

With GERD, typical symptoms include heartburn and regurgitation.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diffuse_parenchymal_lung_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OuVtSzcTRyiXEKxHv_Uuw4yOTkul_MlM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diffuse parenchymal lung disease: Clinical]]></video:title><video:description><![CDATA[Diffuse parenchymal lung diseases, or DPLDs are a group of rare lung disorders that affect the interstitium of the alveolar wall, the alveoli, as well as the blood vessels and pleura of the lungs. 

Previously, they were called interstitial lung diseases because we thought that they only affected the interstitium. 

Now, there are literally hundreds of DPLDs out there, so it’s more important to know how to classify them based on their key features than to memorize the names of an ever-growing list of diseases. 

DPLDs can be broadly classified into those with a known cause, and those with an unknown cause which are also called idiopathic. 

DPLDs that have a known cause can be subclassified into connective tissue diseases, like systemic lupus erythematosus, rheumatoid arthritis, or systemic sclerosis; occupational exposures, like asbestosis, silicosis and berylliosis; granulomatous diseases, like sarcoidosis and hypersensitivity pneumonitis; and treatment-induced causes, like the antiarrhythmic amiodarone, the antibiotic nitrafurantoin, the chemotherapeutic agents methotrexate, bleomycin and busulfan, as well as exposure to radiation. 

Now, idiopathic DPLDs include many subtypes, but the most important one is idiopathic pulmonary fibrosis. 

In all scenarios, tobacco smoking can potentially worsen an existing DPLD. 

Now, DPLDs are classified this way because the known causes are often more treatable and relatively reversible compared to the idiopathic causes. 

Consequently, when approaching a individual, it’s crucial to first think through the known causes. 

Additionally, it’s important to understand that DPLDs are rare, and that other causes of respiratory symptoms like pneumonia and heart failure should be considered. 

Alright, now regardless of the cause, DPLDs share similar clinical, radiographic and pathological manifestations, which is why all these diseases are clumped under the DPLD umbrella. 

Individuals with DPLD commonly present with short]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pleural_effusion:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EqnHrh48QOWAhccW0nCwxETcT2Wf5njv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pleural effusion: Clinical]]></video:title><video:description><![CDATA[Our lungs are covered by two layers of pleura, the inner visceral pleura, and the outer parietal pleura. 

Sandwiched between these layers is the pleural space, which normally contains about 10 milliliters of fluid and that provides a bit of lubrication, so that the lungs can smoothly expand within the chest cavity without encountering much friction. 

Too much fluid in that space results in a pleural effusion, which can actually hinder lung expansion.  

Now, pleural effusions can be broadly classified into transudative and exudative effusions. 

Transudative effusions are often caused by systemic diseases, and result from either an increase in the intravascular hydrostatic pressure, such as in congestive heart failure, or as a result of a decrease in the intravascular oncotic pressure due to a decrease in serum albumin, like in liver cirrhosis, nephrotic syndrome, or malnutrition. 

Exudative effusions, on the other hand, are usually due to local diseases that may cause inflammation, resulting in increased capillary permeability. 

These include infections like pneumonia or tuberculosis, primary lung or metastatic malignancy, autoimmune diseases like systemic lupus erythematosus or rheumatoid arthritis, or pancreatitis. 

One more specific type of effusion is a chylothorax, and it results from impaired lymphatic drainage of the pleura, which can happen after accidental damage during surgery, trauma, or cancer invasion. 

Interestingly, pulmonary embolism can cause both transudative and exudative effusions. 

The transudative component is thought to occur due to obstruction of the pulmonary circulation, causing an increased hydrostatic pressure in that area. 

The exudative component occurs due to release of vasoactive mediators from the platelet-rich clots which increase capillary permeability. 

Now, regardless of the cause, the symptoms of a pleural effusion include progressively worsening shortness of breath, due to limited expansion of the lungs, and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypercholesterolemia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HJTax70GTP6MSlrZ72x9AdghTRWjSGvL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypercholesterolemia: Clinical]]></video:title><video:description><![CDATA[Cholesterol is a lipid molecule that helps maintain the structure of cell membranes, and is a precursor to steroid hormones, bile acids, and vitamin D. 

Although, every day, some new cholesterol comes in through the diet, most of the cholesterol we need is obtained through recycling existing cholesterol. 

Most of that recycling happens in the intestines and is facilitated by bile acids which help us reabsorb cholesterol and bring it back into the bloodstream.  

There are two main types of cholesterol: HDL or High Density Lipoprotein which is sometimes called “good cholesterol”, and LDL or Low Density Lipoprotein which is sometimes called “bad cholesterol”. But good and bad is overly simplistic, and like all things - the subtleties matter.

LDL is produced by the liver and it carries cholesterol out to the rest of the body. 

If all of the cholesterol from LDL is not completely distributed to the peripheral cells, then HDL brings some of that cholesterol back from the peripheral tissues and sends it to the liver. 

Now, what makes LDL bad and HDL good is that, whenever there’s a high blood concentration of LDL, the LDL can be ingested by macrophages that sit along vessel walls, forming atherosclerotic plaques. 

Over decades, large atherosclerotic plaques can lead to myocardial infarctions, strokes, and peripheral vascular disease. That’s why we want to keep LDL blood levels under control. 

On the other hand, HDL can remove cholesterol from cells and that can help reverse the process of atherosclerosis.

A diagnosis of hypercholesterolemia requires measuring total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. 

Cholesterol is measured either as milligrams per deciliter (mg/dL) or millimoles per liter of blood (mmol/L), and it’s recommended to test cholesterol every five years for people aged 20 years or older. 

Hypercholesterolemia is defined as having cholesterol levels that predict a higher risk of atherosclerosis and cardiovascul]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gallbladder_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/drtdMkJkRzy8kCE8hz1jF5apQfmW4QyM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gallbladder disorders: Clinical]]></video:title><video:description><![CDATA[The gallbladder is a small, pouch-like organ that stores the bile produced by the liver. 

After a fatty meal, the gallbladder contracts and releases bile to help break down fats in the diet. 

Bile is made up mostly of water, bile salts, bilirubin and fats, as well as cholesterol. 

Now, the most common gallbladder diseases have to do with an imbalance in bile fluid composition, which leads to the formation of stones either in the gallbladder or somewhere along the biliary tree. 

The biliary tree is made up of the left and right hepatic duct which come together and form the common hepatic duct, as well the cystic duct, which unites with the common hepatic duct to form the common bile duct, also known as choleducus duct.

Finally, the common bile duct joins with the main pancreatic canal to open in the second part of the duodenum.  

Now, most gallbladder diseases are related to either the presence of stones in the gallbladder or in the common bile duct, and whether those locations are infected as the result of an obstruction caused by the gallstones.

A gallstone in the gallbladder is called cholelithiasis, and a gallstone in the common bile duct is called choledocolithiasis, and both are associated with mild inflammation. But, if the gallstones block the normal bile flow this can cause severe inflammation in the biliary tree. 

When there’s a lot of inflammation, the gallbladder and common bile duct tissue becomes extremely susceptible to infection. An infection of an obstructed gallbladder is called cholecystitis, and an infection of an obstructed common bile duct is called cholangitis, or ascending cholangitis. 

In cholelithiasis, gallstones often develop from an imbalance in bile composition. 

For example, if there’s too much cholesterol, cholesterol gallstones  form, and that happens mostly in female individuals during the reproductive period, especially over the age of forty. Other risk factors include being overweight and native American. 

If, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiomyopathies:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CMGwueJ-TI6Q0fCGLm1uUtegRYaw7GdH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiomyopathies: Clinical]]></video:title><video:description><![CDATA[Cardiomyopathy is a broad term used to describe a variety of issues that result from disease of the myocardium. 

When cardiomyopathy develops as a way to compensate for some other underlying disease, like hypertension or valve diseases, it’s called secondary cardiomyopathy, but when it develops all by itself it’s called primary cardiomyopathy.

Now, there are three main types of cardiomyopathy. The most common type is dilated cardiomyopathy, that’s where all four chambers of the heart dilate, or get bigger, and the heart walls become thin and lose contractility. 

Next up is hypertrophic cardiomyopathy and that’s where the walls get thick, heavy, and hypercontractile. 

Finally, there’s restrictive cardiomyopathy which is where the heart muscle is restricted, meaning it becomes stiff and less compliant, and that prevents the heart from filling properly. 

The muscles and size of the ventricles, though, stay about the same size and only get slightly enlarged. 

Restrictive cardiomyopathy may be idiopathic or secondary to a disorder that either deposits harmful substances, like iron or amyloid, in the heart tissue, or there’s fibrosis caused by immune cells or radiation. 

In all three types of cardiomyopathy, over time the heart may be unable to do its job effectively, leading to heart failure signs and symptoms like: fatigue, dyspnea, and swelling of the feet. 

Individuals may also develop acute symptoms like presyncope or syncope, which is a sudden loss of consciousness usually lasting a few seconds. These individuals are at an increased risk of myocardial infarction. 

And because cardiomyopathies affect the cardiac muscle as well as the pacemaker cells that run through the cardiac muscle - they can lead to arrhythmias like atrial fibrillation, ventricular ectopic beats, ventricular tachycardia or fibrillation, and atrioventricular block. 

On auscultation, hypertrophic cardiomyopathy causes a crescendo-decrescendo murmur between S1 and S2, so during s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypernatremia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bW6q2FgHSCu41YNjM9rFkuaBRWSIWsYA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypernatremia: Clinical]]></video:title><video:description><![CDATA[With hypernatremia, there’s a higher than normal concentration of sodium in the blood - above 145 milliequivalents per liter. 

However, since the concentration of sodium depends on both sodium and water levels in the body, hypernatremia actually translates as too little water in the extracellular compartment. 

Ok, now remember that total body water is distributed either in the intracellular compartment, meaning inside the cells, or the extracellular compartment, meaning outside the cells. 

Now, both the intracellular and extracellular compartments have the same amount of solutes dissolved in that water - so the same osmolality, normally between 275 and 290 milliosmoles per kilogram. 

Serum osmolality can be calculated using the formula: twice the concentration of sodium measured in milliequivalents per liter, plus the serum concentration of glucose divided by 18, measured in milligrams per deciliter, plus BUN, which stands for blood urea nitrogen, divided by 2.8, also in milligrams per deciliter - so if you remember one thing from this formula, it should be that sodium is the major determinant of serum osmolality. 

Ok, now just to make matters more interesting, some of these solutes, like sodium and glucose, can’t freely cross cell membranes, so they generate an osmotic pressure inside the compartment, which is a measurement of how likely it is that this compartment will draw water out of the other one. 

Normally, the intracellular and extracellular compartments are isotonic to each other - meaning, they have the same concentration of osmotically active solutes.

However, small variations in solute concentrations, like having more sodium in the extracellular compartment, can alter that equilibrium, so water moves across cell membranes in order to restore the balance. 

Water moves according to the rules of osmosis - or from the hypotonic compartment, where there’s more water, to the hypertonic compartment, where there’s less water. And water does tha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Class_I_antiarrhythmics:_Sodium_channel_blockers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/63SqPW4SQIugJPIFZYU85dDnQ52RkzSQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Class I antiarrhythmics: Sodium channel blockers]]></video:title><video:description><![CDATA[Antiarrhythmic drugs help control arrhythmias or abnormal heartbeats. 

There are four main groups of antiarrhythmic medications: class I, sodium-channel blockers; class II, beta-blockers; class III, potassium-channel blockers; class IV, calcium-channel blockers; and miscellaneous antiarrhythmics, or unclassified antiarrhythmics. 

We’ll focus on class I antiarrhythmics which are further broken down into 1a, 1b, and 1c. All three groups work on Na+ channels in the cardiac myocytes, so class I medications are also called Na+ channel blockers. 

Normally, an electrical signal starts at the sinoatrial or SA node in the right atrium, then propagates throughout both atria, making them contract. 

The signal gets delayed a bit as it goes through the atrioventricular or AV node, then goes through the Bundle of His to the Purkinje fibers of both ventricles, making them contract as well. 

When a heartbeat doesn’t follow this path, it’s called an arrhythmia, and there are two main causes - abnormal automaticity and abnormal reentry. 

Abnormal automaticity is when an area of the heart, say, a part of the ventricle, begins to fire off action potentials at a rate that’s even faster than the SA node. 

As a result, this area of the heart essentially flips roles with the SA node, firing so fast that the pacemaker cells in the SA node don’t get a chance to fire. At that point, the heartbeat is being driven by the ventricles. 

Alternatively, there can be an abnormal reentry which often results from scar tissue in a ventricle after a heart attack. 

Scar tissue doesn’t conduct electricity, so the signal just goes around and around the scar, and each cycle can cause the ventricles to contract. 

Alternatively, there might be an accessory, or extra pathway between the atria and the ventricles like the bundle of Kent in Wolff-Parkinson-White syndrome. 

Here, the signal might move back up the accessory pathway, since oftentimes it’s bidirectional, meaning the signal can go ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Class_II_antiarrhythmics:_Beta_blockers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z9-5IFX4TPKK-udHXZFbIMfaRGqYQqqu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Class II antiarrhythmics: Beta blockers]]></video:title><video:description><![CDATA[Antiarrhythmic medications help control arrhythmias or abnormal heartbeats. 

There are four main groups of antiarrhythmic medications: class I, sodium-channel blockers; class II, beta-blockers; class III, potassium-channel blockers; class IV, calcium-channel blockers; and miscellaneous antiarrhythmics, or unclassified antiarrhythmics. Now, we’ll focus on class II antiarrhythmics in this video.

First, let’s start with the two main types of cells within the heart; pacemaker cells and non-pacemaker cells. 

Pacemaker cells build the electrical conduction system of the heart, which consists of the sinoatrial node, or SA node; the atrioventricular node, or AV node; the bundle of His; and the Purkinje fibers.

Pacemaker cells have a special property called automaticity, which is the ability to spontaneously depolarize and fire action potentials. 

On the other hand, non-pacemaker cells, also known as cardiomyocytes, make up the atria and ventricles; and they give the heart its ability to contract and pump blood throughout the body.

Now, in contrast to non-pacemaker cells, whose action potential has 5 phases, an action potential in pacemaker cells has only 3 phases. 

Here’s a graph of the membrane potential vs. time. Phase 4, also known as the pacemaker potential, starts with the opening of the pacemaker channels. 

The current through these channels is called pacemaker current or funny current (If), and it mainly consists of sodium ions. 

These sodium ions cause the membrane potential to begin to spontaneously depolarize and as the membrane potential depolarizes, voltage-dependent T-type calcium channels open up, thereby further depolarizing the pacemaker cell. 

As calcium enters the cell, voltage-dependent L-type calcium channels open up, causing more calcium to rush into the cell, ultimately depolarizing the membrane to its threshold potential. 

This marks the start of phase 0, which is also known as the depolarization phase. 

Now phase 0 is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Class_III_antiarrhythmics:_Potassium_channel_blockers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NEgIeeBPTAewf5c27Jbdfk1RS0m-pVQV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Class III antiarrhythmics: Potassium channel blockers]]></video:title><video:description><![CDATA[Antiarrhythmic medications help control arrhythmias, or abnormal heart beats. 

There are five main groups of antiarrhythmic medications: class I, also known as sodium-channel blockers; class II, also called beta-blockers; class III, also known as potassium-channel blockers; class IV, also called calcium-channel blockers; and miscellaneous antiarrhythmics, or unclassified antiarrhythmics. Now, we’ll focus on class III antiarrhythmic medications.

Normally, an electrical signal starts at the sinoatrial or SA node in the right atrium, then propagates out through both atria, making them contract. 

The signal gets delayed a bit as it goes through the atrioventricular or AV node, then goes through the Bundle of His to the Purkinje fibers of both ventricles, making them contract as well.

When the signal doesn’t follow this pathway, we get abnormal heartbeats called an arrhythmia, and there are two main causes - abnormal automaticity and abnormal reentry.

Abnormal automaticity is when an area of the heart, say, a part of the ventricle, begins to fire off action potentials at a rate that’s even faster than the SA node. 

As a result, this area of the heart essentially flips roles with the SA node, firing so fast that the pacemaker cells in the SA node don’t get a chance to fire. At that point, the heartbeat is being driven by the ventricles. 

Alternatively, there can be an abnormal reentry which often results from scar tissue in a ventricle after a heart attack. 

Scar tissue doesn’t conduct electricity, so the signal just goes around and around the scar, and each cycle can cause the ventricles to contract. 

Alternatively, there might be an accessory, or extra pathway between the atria and the ventricles, like the bundle of Kent in Wolff-Parkinson-White syndrome. 

Here, the signal might move back up the accessory pathway, since oftentimes it’s bidirectional, meaning the signal can go from atrium to ventricle as well as from ventricle to atrium. 

This create]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Class_IV_antiarrhythmics:_Calcium_channel_blockers_and_others</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/htJwT642R26LDhRSQfhFYVg9SACZUoC5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Class IV antiarrhythmics: Calcium channel blockers and others]]></video:title><video:description><![CDATA[Antiarrhythmic medications help control arrhythmias, or abnormal heartbeats. There are four main groups of antiarrhythmic medications: class I, sodium-channel blockers; class II, beta-blockers; class III, potassium-channel blockers; class IV, calcium-channel blockers; and miscellaneous antiarrhythmics, or unclassified antiarrhythmics. Now, we’ll focus on class IV and miscellaneous antiarrhythmics in this video. 

First, let’s start with two main types of cells within the heart; pacemaker cells and non-pacemaker cells. Pacemaker cells build the electrical conduction system of the heart, which consists of the sinoatrial node, or SA node; the atrioventricular node, or AV node; the bundle of His; and the Purkinje fibers.  

Pacemaker cells have a special property called automaticity, which is the ability to spontaneously depolarize and fire action potentials.  

On the other hand, non-pacemaker cells, also known as cardiomyocytes, make up the atria and ventricles; and they give the heart its ability to contract and pump blood throughout the body. 

Now, in contrast to non-pacemaker cells, whose action potential has 5 phases (0, 1, 2, 3, and 4 ), an action potential in pacemaker cells has only 3 phases (4, 0, and 3). Here’s a graph of the membrane potential vs. time for a pacemaker cell. Phase 4, also known as the pacemaker potential, starts with the opening of the pacemaker channels. The current through these channels is called pacemaker current or funny current (If), and it mainly consists of sodium ions. These sodium ions cause the membrane potential to begin to spontaneously depolarize and as the membrane potential depolarizes, voltage-dependent T-type calcium channels open up, thereby further depolarizing the pacemaker cell. As calcium enters the cell, voltage-dependent L-type calcium channels open up, causing more calcium to rush into the cell, ultimately depolarizing the membrane to its threshold potential. This marks the start of phase 0, whic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ACE_inhibitors,_ARBs_and_direct_renin_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GY2ON2JLTuiDw6IdpAqVJoenT_ylcGc2/_.jpg</video:thumbnail_loc><video:title><![CDATA[ACE inhibitors, ARBs and direct renin inhibitors]]></video:title><video:description><![CDATA[Antihypertensives are a class of medication used to treat hypertension, or high blood pressure. 

Certain antihypertensives act upon the renin-angiotensin-aldosterone system to decrease blood pressure by inhibiting vasoconstriction and water reabsorption in the kidneys. 

Hypertension affects over a billion people around the world, and it’s a major risk factor for heart disease and stroke. 

Blood pressure is the force that blood exerts on the walls of blood vessels. 

Now, there’s a number of factors that determine blood pressure. For example, imagine a hose connected to a pump where the hose is the blood vessel and the pump is the heart. If more water is pumped out, the pressure in the hose increases. 

Now if we squeeze the hose, narrowing the diameter, the pressure inside would be greater and the water will shoot out more strongly. This is similar to how the diameter of the blood vessels can affect blood pressure, which can change in response to different stimuli. 

One important mechanism that regulates blood pressure is the Renin-Angiotensin-Aldosterone System - or RAAS for short - which is a cascade of events that ends up increasing blood pressure.

When blood pressure is low, blood flow to the kidneys decreases. The kidneys respond by secreting renin into the bloodstream.

Renin is a proteolytic enzyme that breaks down a protein made in the liver called angiotensinogen, and this gives rise to angiotensin I. 

When it reaches the lungs, angiotensin I is converted into angiotensin II by an enzyme called Angiotensin-converting enzyme, or ACE for short. 

Now, angio- refers to the blood vessels; and -tens, well it means “to tense.” 

So angiotensin II binds to receptors in vascular smooth muscle and causes them to constrict, which increases the blood pressure.

Finally, angiotensin II also stimulates the release of aldosterone by the adrenal glands. 

Aldosterone increases reabsorption of sodium in the kidneys which also increases water reabsorption. T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sympatholytics:_Alpha-2_agonists</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VQX1wBj2TlmoppOiyQT-NVSxTqSRVDgb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sympatholytics: Alpha-2 agonists]]></video:title><video:description><![CDATA[Central anti-adrenergics are a class of medications that’s not very commonly used these days. Their mechanism of action is to target the adrenergic neurons in the central nervous system, and prevent them from effectively releasing the catecholamines: norepinephrine and epinephrine.    

So, the nervous system is divided into the central nervous system, so the brain and spinal cord; and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles; and the autonomic nervous system, which controls the involuntary movement of smooth muscles and glands of our organs.

Now, the autonomic nervous system - which includes both the sympathetic and parasympathetic nervous systems - is made up of a relay that includes two neurons. We’ll focus on just the sympathetic nervous system. Signals for the autonomic nervous system start in the hypothalamus, at the base of the brain. Hypothalamic neurons have really long axons that carry signals all the way down to the thoracic and lumbar spinal cord nuclei, where they synapse with preganglionic neuron cell bodies. Here, they release the neurotransmitter norepinephrine, which causes the preganglionic neurons to transmit the signals down their relatively short axon, which exits the central nervous system via the spinal cord. These short nerve fibers reach the nearby sympathetic ganglion, which consists of many postganglionic neuron cell bodies. The postganglionic neurons are also called adrenergic neurons, because they release the neurotransmitter norepinephrine, which is also called noradrenaline; and to a much lesser degree, epinephrine, or adrenaline. These two catecholamines activate the adrenergic receptors on many different organs, which allow the sympathetic nervous system to trigger the fight or flight response that incre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenergic_antagonists:_Alpha_blockers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NXyoRzrJSYSNf3WYB-dR4yX6S5qdV9oc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenergic antagonists: Alpha blockers]]></video:title><video:description><![CDATA[Alpha blocker and beta blockers are two types of postsynaptic anti-adrenergic medications that prevent their respective receptors from being stimulated by catecholamines, like norepinephrine and epinephrine.  

The nervous system is divided into the central nervous system, so the brain and spinal cord; and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs.

The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles; and the autonomic nervous system, which is further divided into the sympathetic and the parasympathetic, and controls the involuntary movement of the smooth muscles and glands of our organs.

Now, the autonomic nervous system - which includes both the sympathetic and parasympathetic nervous system - is made up of a relay that includes two neurons. 

We’ll focus on just the sympathetic nervous system.

Signals for the autonomic nervous system start in the hypothalamus, at the base of the brain.

Hypothalamic neurons have really long axons that carry signals all the way down to the thoracic and lumbar spinal cord nuclei, where they synapse with preganglionic neuron cell bodies. 

From there, the signal goes from the preganglionic neurons down its relatively short axon, exits the spinal cord, and reaches the nearby sympathetic ganglion, which is made up of lots of postganglionic neuron cell bodies. 

The postganglionic neurons are also called adrenergic neurons because they release the neurotransmitter norepinephrine, which is also called noradrenalin; and to a much lesser degree, epinephrine, or adrenaline.

These two catecholamines activate the adrenergic receptors on the many different organs, which allow the sympathetic nervous system to trigger the fight or flight response that increases the heart rate and blood pressure, as well as slowing digestion. 

All of this maximizes blood flow to th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenergic_antagonists:_Presynaptic</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vElNE2HdTqW15v3BCwcLhYONT0_uBPF8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenergic antagonists: Presynaptic]]></video:title><video:description><![CDATA[Peripheral presynaptic anti-adrenergics are a class of medication that’s not very commonly used these days. Their mechanism of action is to target the presynaptic adrenergic neurons in the peripheral nervous system, and prevent them from effectively releasing the catecholamines, norepinephrine, and epinephrine.

The nervous system is divided into the central nervous system, so the brain and spinal cord; and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles; and the autonomic nervous system, which is further divided into the sympathetic and the parasympathetic, and controls the involuntary movement of the smooth muscles and glands of our organs.

Now, the autonomic nervous system - which includes both the sympathetic and parasympathetic nervous system - is made up of a relay that includes two neurons. We’ll focus on just the sympathetic nervous system. Signals for the autonomic nervous system start in the hypothalamus, at the base of the brain. Hypothalamic neurons have really long axons that carry signals all the way down to the thoracic and lumbar spinal cord nuclei, where they synapse with preganglionic neuron cell bodies. From there, the signal goes from the preganglionic neurons down its relatively short axon, exits the spinal cord, and reaches the nearby sympathetic ganglion, which is made up of lots of postganglionic neuron cell bodies. The postganglionic neurons are also called adrenergic neurons because they release the neurotransmitter norepinephrine, which is also called noradrenalin; and to a much lesser degree, epinephrine, or adrenaline. These two catecholamines activate the adrenergic receptors on many different organs, which allow the sympathetic nervous system to trigger the fight or flight response that  increases the heart rate ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/cGMP_mediated_smooth_muscle_vasodilators</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_i5M3UPjQhSmS7WSuKxGcc8GRjir9SKF/_.jpg</video:thumbnail_loc><video:title><![CDATA[cGMP mediated smooth muscle vasodilators]]></video:title><video:description><![CDATA[cGMP-mediated smooth muscle vasodilators, as their name implies, are medications that promote dilation of blood vessels by potentiating the effect of cyclic guanosine monophosphate, or cGMP for short. These medications are mainly used to treat hypertension, heart failure, and angina pectoris, which is a pain caused by reduced blood flow to the heart muscle. All right, first, let’s focus on the structure of blood vessels. Blood vessels have three layers, also called “tunics,” or coverings, that surround the vessel lumen, which is the hollow part of the vessel that contains the blood. The innermost tunic is the tunica intima, which includes the endothelial cells; the next one is the tunica media, or middle tunic, which is mostly made of smooth muscle cells and sheets of elastin protein; and finally, there’s the tunica externa, or outside tunic, which is made up of loosely woven fibers of collagen. Moreover, the tunica media can contract, causing vasoconstriction, where the lumen gets a lot smaller; or it can relax, or vasodilate, causing the lumen’s diameter to increase, allowing for more blood flow. 

Now, within endothelial cells of the tunica intima, there’s an enzyme called nitric oxide synthase, which uses the amino acid L-arginine and molecular oxygen to synthesize nitric oxide or NO for short. Once synthesized, nitric oxide diffuses to adjacent smooth muscle cells in the tunica media, where it binds and activates an enzyme guanylyl cyclase. This enzyme converts guanosine triphosphate, GTP, into cyclic guanosine monophosphate, cGMP, which is a second messenger that induces relaxation of smooth muscle cells in vessel walls. All right, now moving on to pharmacology. cGMP-mediated smooth muscle vasodilators are subdivided into two main groups: antianginal medications, which are used to treat anginal pain, when oxygen delivery to the heart is inadequate for normal heart function; and antihypertensive medications, which are used to treat high blood pre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Miscellaneous_lipid-lowering_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tJukByLtTCG6ZatH_f3ipdhYTamERoRl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Miscellaneous lipid-lowering medications]]></video:title><video:description><![CDATA[Lipid-lowering medications work to decrease levels of cholesterol and triglycerides in the body. 

Several medications fall outside the more commonly used classes like statins and fibrates, so in this video, we&amp;#39;re going to discuss the bile acid resins, niacin or vitamin B3, ezetimibe, and the PCSK9 inhibitors.

Although it’s got a bad reputation, cholesterol is actually a critical component of our cells and is used to build the cell membrane. 

It also has other uses like the synthesis of: steroid hormones, vitamin D, and bile. 

Normally, we get our cholesterol from the food we eat, but it can also be synthesized by the liver. 

So when we eat a box of chili fries, the fats and cholesterol are absorbed in the small intestine. 

However, they’re not water soluble, so they can’t travel freely in the blood. 

To fix this, our body makes shipping boxes called lipoproteins. 

These containers consist of a shell made of phospholipids and protein tags that act as instructions for their destination. 

So after absorption, the small intestinal cells package the fats and cholesterol into the largest but least dense lipoproteins, called chylomicrons. 

These are released into the lymphatic system and then enter the bloodstream via the subclavian vein. Then they travel through the blood to reach adipose tissue and the liver. 

Now, the liver can also synthesize intrinsic cholesterol through the mevalonate pathway, which happens in the smooth endoplasmic reticulum of liver cells. 

It begins with 2 acetyl-CoA molecules getting joined together by the enzyme acetyl-CoA acyl-transferase. The result is a 4-carbon molecule called acetoacetyl-CoA. 

Next, the enzyme HMG-CoA synthase combines acetoacetyl-CoA and acetyl-CoA to form a 6-carbon molecule called 3-hydroxy-3-methylglutaryl CoA, or HMG-CoA. 

Then, an enzyme called HMG-CoA reductase reduces HMG-CoA into mevalonate. This step with HMG-CoA reductase is the rate-limiting step of cholesterol synthesis. 

In ot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lipid-lowering_medications:_Fibrates</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yjyTYgrdQ-WpdTJJs3ysRzviSmuN9hAm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lipid-lowering medications: Fibrates]]></video:title><video:description><![CDATA[Fibrates are a group of lipid-lowering medications, along with statins and niacin. 

These medications are very effective at lowering triglyceride levels in the blood, but are less effective at controlling cholesterol.  

Now, triglycerides make up most of your body fat, and they consist of a glycerol and 3 fatty acids. 

So when we eat a box of chili fries, the fatty acids and cholesterol are absorbed into the cells in the small intestine.

The fatty acids are then converted into triglycerides. 

However, triglycerides and cholesterol are not water soluble, so they can’t travel freely in the blood. To fix this, our body makes “shipping boxes” called lipoproteins.

These containers consist of a shell made of phospholipids and protein tags that act as instructions for their destination. 

So after absorption, the small intestinal cells package the triglycerides and cholesterol into the largest, but least dense lipoproteins, called chylomicrons. 

These are released into the lymphatic system and then enter the bloodstream via the subclavian vein. Then, they travel through the blood to reach the liver and other tissues in the body. 

Now in the blood vessels near these tissues, we have an enzyme called lipoprotein lipase, which can break down triglycerides into fatty acids.  

Cells in the nearby tissue can then use these fatty acids to generate ATP. 

Adipose tissue can synthesize a lot of lipoprotein lipases, which means they have access to a lot of fatty acids.  

Now, instead of using the fatty acids for energy, they pick them up, convert them back into triglycerides, and store them for later use. 

Okay, so we can also synthesize fatty acids from glucose in the liver which are then converted into triglycerides. 

These triglycerides and some cholesterol are packed into the next kind of lipoproteins called very-low-density lipoproteins or VLDL, which are smaller and more dense than chylomicrons. 

This package is sent into the bloodstream to carry the ene]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Positive_inotropic_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3gp3WPEoRJSKXXmgy6VJpJbLQ_uaT7Bn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Positive inotropic medications]]></video:title><video:description><![CDATA[Positive inotropic medications, as their name implies, are a diverse group of medications that increase the strength of heart muscle contraction. 

As a result, they increase the stroke volume and thus, the cardiac output. 

Positive inotropic medications include cardiac glycosides, like digoxin; beta agonists, like dobutamine; and phosphodiesterase inhibitors, like milrinone. 

They are used in conditions where the heart can’t pump enough blood to the body’s tissues, like in systolic heart failure. 

Alright, the heart needs to squeeze out a certain volume of blood each minute, called the cardiac output, which can be rephrased as the heart rate multiplied by the stroke volume, which is the volume of blood squeezed out with each heartbeat. 

Okay, now the stroke volume depends on the preload, or the amount of blood that returns to the heart; the afterload, or peripheral resistance; and the strength of the contraction, or contractility, of the cardiac muscle. 

Now, muscle contraction is initiated with an action potential which modifies receptors allowing calcium ions to flow from the sarcoplasmic reticulum into the sarcoplasm. 

This allows myosin heads to bind to the actin. 

These two proteins are ultimately responsible for cell contraction. 

In order for a muscle to relax, calcium ions must be pumped back into the sarcoplasmic reticulum. 

When the frequency of stimulation is increased, more calcium ions accumulate in the sarcoplasm, and the strength of contraction increases.

Alright, now there are conditions in which the strength of the heart’s contraction is impaired, and the heart can’t pump out enough blood to meet the body’s demands, this is called heart failure. 

For example, in systolic heart failure, the heart’s ventricles can’t pump blood hard enough during systole, so as a result, the cardiac output decreases. 

This is typically due to some kind of damage to the myocardium so the heart can’t contract as forcefully or pump blood as efficien]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mineralocorticoids_and_mineralocorticoid_antagonists</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rS-N_UWUS9aQHez0cC_7Siy1TU2FW2Yn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mineralocorticoids and mineralocorticoid antagonists]]></video:title><video:description><![CDATA[With mineralocorticoids, “corticoids” refers to the steroid hormones produced by the adrenal cortex, and “mineral” refers to how these hormones regulate sodium reabsorption and potassium excretion in the distal convoluted and collecting tubules of the kidney. 

Aldosterone is the major natural mineralocorticoid in humans and there are two major classes of medications targeting the actions of mineralocorticoids: mineralocorticoid-receptor agonists, which mimic the role of aldosterone; and mineralocorticoid-receptor antagonists, that block the action of aldosterone.

Alright, but first things first. 

Aldosterone is part of a hormone family, or axis, that works together and is called the renin-angiotensin-aldosterone system. 

Normally, when the blood pressure is low, the kidney gets less blood, which causes it to release renin into the blood. 

Renin converts a prohormone called angiotensinogen into angiotensin I, and another enzyme called angiotensin converting enzyme, or ACE, converts angiotensin I into angiotensin II.  

Angiotensin II has many effects like causing vasoconstriction and stimulating the release of antidiuretic hormone from the pituitary glands. 

In the adrenal glands, it triggers the secretion of aldosterone. 

In the kidneys, aldosterone affects two types of cells along the distal convoluted and collecting tubule of the nephron. 

First, it binds to mineralocorticoid receptors in the cytoplasm of principal cells, forming an aldosterone-receptor complex. 

This complex is translocated to the nucleus of the cell, where it enhances two types of cells along the distal convoluted and collecting tubule of the nephron. 

First, it binds to mineralocorticoid receptors in the cytoplasm of principal cells, forming an aldosterone-receptor complex. 

This complex is translocated to the nucleus of the cell, where it enhances gene expression of epithelial sodium channels (ENaC) and sodium/potassium ion pumps. 

Eventually, this leads to their increase]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperthyroidism_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zwnFn8lFTo_mDR3v9xfKp7dtQ3KNXZDH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperthyroidism medications]]></video:title><video:description><![CDATA[In hyperthyroidism, ‘hyper’ refers to having too much, and ‘thyroid’ refers to thyroid hormones, so hyperthyroidism refers to a condition where there’s excess thyroid hormones. 

Medications used to treat hyperthyroidism either reduce the level of thyroid hormones or treat the symptoms by targeting the affected tissue. 

There are 2 different thyroid hormones; triiodothyronine or T3, and thyroxine or T4.  

Now, if we zoom into the thyroid gland, we’ll find thousands of follicles, which are small, hollow spheres whose walls are lined with follicular cells, or thyrocytes. 

Zooming further into these follicular cells, we’ll see their apical side that surrounds a central lumen filled with a viscous fluid called the colloid. 

The colloid contains the precursor hormone thyroglobulin. 

The basolateral side of follicular cells is in contact with blood vessels that supply these cells. 

Synthesis of thyroid hormones begins when follicular cells take in inorganic iodide ions from the blood, along with two sodium ions, via a sodium- iodide symporter. 

This step is known as ‘iodide trap’. 

The iodide ion is pumped via the pendrin protein, into the viscous fluid inside the follicle called the colloid, which contains thyroglobulin; the precursor of thyroid hormone. 

In the colloid, inorganic iodide undergoes oxidation via the enzyme thyroid peroxidase or TPO, to become organic iodide, which then binds to the tyrosine in thyroglobulin. 

This step is known as iodination. 

Some tyrosine residues bind to only one iodine and form monoiodotyrosine or MIT, whereas others bind to two iodine atoms to form diiodotyrosine or DIT. 

These molecules are then coupled together by the same enzyme thyroid peroxidase. 

This process is known as coupling. 

Coupling one MIT with one DIT creates T3, while coupling 2 DIT molecules creates T4. 

T4 is generally created in greater amounts than T3, with T3 being the more active form with a half life of 1 to 2 days, while T4 is less ac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypothyroidism_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9BJjOoVuTHewciUHY5sWFnfHTYmrmbyx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypothyroidism medications]]></video:title><video:description><![CDATA[In hypothyroidism, ‘hypo’ refers to having too little, and ‘thyroid’ refers to thyroid hormones, so hypothyroidism refers to a condition where there’s not enough thyroid hormones. 

Now, as treatment for hypothyroidism, we can use thyroid hormone analogues as a replacement to supply the body with normal levels of thyroid hormones. 

There are 2 different thyroid hormones; triiodothyronine or T3, and thyroxine or T4. 

They’re two tyrosine-based, iodine-containing hormones that are secreted by the thyroid gland, which is located anteriorly in the neck and consists of two lobes that look like two thumbs hooked together in the shape of a “V”. 

Now, if we zoom into the thyroid gland, we’ll find thousands of follicles, which are small hollow spheres whose walls are lined with follicular cells or thyrocytes. 

Zooming in, these follicular cells have an apical side that surrounds a central lumen filled with a viscous fluid called the colloid. 

The colloid contains the precursor hormone thyroglobulin. 

The basolateral side of follicular cells is in contact with blood vessels that supply these cells.

Now, synthesis of thyroid hormones inside the follicles involves a few important steps. 

First, the inorganic iodide ions, present in a low concentration in the blood, are actively taken up by the basolateral side of the follicular cells, along with two sodium ions, via a sodium-iodide symporter. 

This step is known as ‘iodide trap’. 

The iodide ion is then pumped into the colloid via the pendrin protein, where it undergoes oxidation with the enzyme “thyroid peroxidase” or TPO, which changes it into an organic iodine atom. 

It’s then attached to tyrosine amino acid residues which are found throughout thyroglobulin. 

This step is known as iodination. 

Some tyrosine residues are bound by only one iodine, whereas others are bound by two iodine atoms, yielding monoiodotyrosine or MIT, and diiodotyrosine or DIT, respectively. 

These molecules are then coupled tog]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Laxatives_and_cathartics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RHMSzPMBSsaN2PoTSA7Ep382SGSSGugx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Laxatives and cathartics]]></video:title><video:description><![CDATA[Laxatives and cathartics are medications that increase the passage of stool. 

Laxatives ease the passage of fully formed fecal matter from the rectum; while cathartics have a stronger effect, and cause the evacuation of the entire colon, usually in the form of watery, unformed stool.  

Some medications can function both as a laxative and a cathartic, depending on the dosage. 

Both types of medications are used to treat constipation, which is partly characterized by a decrease in stool passage frequency; small, hard stools; or difficulty with initiating bowel movements. 

Normal stool frequency is usually at least 3 times per week for someone on a typical Western diet.  

Now, the small and large intestines are where most of the absorption happens in the GI tract.  

The small intestine contains smooth muscles that perform peristalsis, which is a series of coordinated wave-like muscle contractions that help push the food bolus through the GI tract. 

Lining the luminal surface of the intestine is a layer called the mucosa, which absorbs nutrients or secretes different molecules, like ions and water, into the lumen. 

The undigested component of the food bolus eventually reaches the large intestine and becomes feces or stool. 

The large intestine mainly absorbs excess water from the stool and that helps condense it into a more solid form. 

However, stool should still be 70-80% water by weight, so if the feces becomes too dry, it could condense into a large, hard mass that’s difficult to pass. 

So instead of peristalsis, which only pushes the food bolus in one direction, the colon undergoes segmental contraction, which pushes the feces in both directions within the haustra to constantly mix it with water; kind of like how a cement truck keeps churning to keep the cement from drying.  

Now, constipation can occur due to a poor diet or a malfunction within the GI tract itself,  although, up to 60 percent of chronic constipation does not have a clear caus]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiplatelet_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wnOIYFQuRfWBiR8RI6EqbrGPTNqgYVd2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiplatelet medications]]></video:title><video:description><![CDATA[Antiplatelet medications prevent blood clot formation during hemostasis, where hemo means blood, and stasis means to halt or stop. 

Hemostasis is divided into primary hemostasis, where circulating cell fragments called platelets form a plug at the site of an injured blood vessel, and secondary hemostasis, which involves multiple coagulation factors working together to form a fibrin mesh to stabilize the platelet plug. 

Antiplatelet medications inhibit the steps of primary hemostasis to prevent the platelet plug from forming.

Primary hemostasis can be further divided into five steps: endothelial injury, exposure, adhesion, activation, and aggregation. 

Endothelial injury is when the innermost layer of the artery, called the endothelium, gets damaged. 

The second step is exposure, where the damaged endothelium exposes the underlying collagen. 

The underlying collagen and endothelial cells then release a protein called Von Willebrand&amp;#39;s factor, or vWF, that binds to this collagen. 

The third step is adhesion where circulating platelets bind to the vWF via a surface protein called GPIB. The fourth step is activation, where platelets become active after binding to vWF. 

First, the platelet changes shape and its membrane forms tentacle-like arms allowing it to grab onto other platelets. 

Second, platelets release more vWF, as well as serotonin, a tiny molecule that attracts more platelets to the area. 

Third, the platelets also release adenosine diphosphate or ADP, and thromboxane A2, or TXA2. These two molecules can activate other platelets that haven’t bound to vWF. 

ADP and TXA2 also cause platelets to express new surface proteins called GPIIb/IIIa, which is needed for the fifth step, aggregation. 

Now each platelet has multiple GPIIb/IIIa receptors that can bind to circulating proteins called fibrinogen.  When two platelets attach to the same fibrinogen protein, they are linked together. 

This allows platelets to rapidly aggregate at the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticoagulants:_Direct_factor_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WBjoPywOT5qNuw7rH6ix-NzzT5e9K4a0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticoagulants: Direct factor inhibitors]]></video:title><video:description><![CDATA[Anticoagulant medications help to prevent thrombi, or blood clots from forming. These medications work by interfering with the normal function of proteins called clotting factors in a chemical process called the coagulation cascade, or secondary hemostasis where hemo refers to blood, and stasis means to halt or stop.  While the most common anticoagulants like warfarin and heparin act on multiple coagulation factors, in this video we’re gonna focus on anticoagulants  that work on a single coagulation factor; either thrombin or activated factor X. 

Now, before we discuss heparin in detail we need to talk about the coagulation cascade which is where heparin exerts its effect. The coagulation cascade starts via two pathways --the extrinsic and intrinsic pathways. The intrinsic pathway starts when circulating factor XII comes into contact with the surface of activated platelets or collagen. Activated factor XII, then activates factor XI, which activates factor IX which activates factor X. Factor X starts the common pathway where it activates factor II, or thrombin, which activates factor I that builds the fibrin mesh. When factor II gets activated it also activates 4 other factors: V, VIII, IX, and XIII. Factor V gets activated and acts as a cofactor for X, factor VIII acts as a cofactor for factor IX, and factor XIII helps factor I, or fibrin, form crosslinks. In the extrinsic pathway, exposed tissue factor activates factor VII, which activates factor X and starts the common pathway. 

Now, the most common point of clot regulation is when a coagulation factor called thrombin is produced. Thrombin, or activated factor II, is a very important clotting factor, because it has multiple pro-coagulative functions. Think of thrombin as the accelerator on a car--the pedal that takes secondary hemostasis from 20 miles per hour to 100 miles per hour! First, thrombin binds to receptors on platelets causing them to get activated. Activated platelets change their shap]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombolytics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VGYGrgYIQHm3FpGKblmf4SvzSs2pRCdR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombolytics]]></video:title><video:description><![CDATA[Thrombolytics, also called fibrinolytics, are medications that break up blood clots formed during hemostasis, where hemo means blood, and stasis means to halt or stop. 

Hemostasis is divided into primary hemostasis, which involves the formation of a platelet plug at the site of an injured blood vessel, and secondary hemostasis, which involves multiple coagulation factors working together to form a fibrin mesh to stabilize the platelet plug.  

Together, these two processes create a blood clot which stops the bleeding.  

Sometimes blood clots could cause problems, like when they form in a coronary artery to cause a heart attack, or when they break off and travel to the brain and cause a stroke. 

In these instances we can use thrombolytics to break up the clot and restore blood flow.

Thrombolytic medications were actually derived physiologically--from what is known as the fibrinolytic system. 

Approximately two days after an injury occurs to a blood vessel and the blood clot forms, it’s time for the body to dissolve the blood clot through a process called fibrinolysis, which is the gradual degradation of the fibrin mesh. 

To do this, a circulating protein produced by the liver called plasminogen, gets converted by an enzyme called tissue plasminogen activator, or tPA, into its active form called plasmin. 

Normally, healthy endothelial cells release only tiny amounts of tPA, but when they’re exposed to coagulation factors produced during 2ndary hemostasis, Factor Xa and thrombin in particular, they start making lots of tPA. 

But it’s important that plasmin activity doesn’t get out of hand, either. 

So the endothelial cells also release plasminogen activator inhibitor 1 and antiplasmin which are proteins that bind and sequester tPA and plasmin respectively. 

It’s all about always reaching that zen balance of coagulation and anticoagulation. 

Now, during an injury, more coagulation factors get activated, which causes more tPA to get released by the e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DNA_alkylating_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/swe7NlufS123X6iZWCI_h_U8TBmtK-WW/_.jpg</video:thumbnail_loc><video:title><![CDATA[DNA alkylating medications]]></video:title><video:description><![CDATA[DNA alkylating medications are a class of drugs that are mainly used as anticancer agents. They disrupt the structure of DNA by adding an alkyl group to the guanine base and can affect all phases of the cell cycle. 

Alright, the cell cycle refers to the events that somatic cells, which includes all of the cells in our bodies except the reproductive cells, go through from the moment they’re formed until the moment they divide into two identical daughter cells. This cycle varies in length depending on the type of cell. For rapidly dividing cells, like skin cells, it takes less than a day, whereas for other cells, like liver cells, the cell cycle can last years.  

Now, the cell cycle can be divided in two phases: interphase and mitosis. Interphase comprises of the G1 phase, during which the cell grows and performs its cell functions, the S phase, during which DNA is replicated, and the G2 phase, during which the cell grows again before entering mitosis. Mitosis can be broken down into prophase, metaphase, anaphase, and telophase, during which the replicated DNA divides equally for the two daughter cells, and ends with cytokinesis, which is when the cell membrane actually divides to form the two new cells. There’s also a G0 phase which is an extended G1 phase where the cell is resting and not actively preparing to divide.   

Alright, now imagine a cancer cell. This cell is going through the phases of the cell cycle without regulation, and its DNA also replicates more frequently and with less error-correcting than healthy cells. Therefore, it’s more sensitive to DNA damage. 

Here’s a DNA base, guanine. Alkylating agents attach an alkyl group at the number 7 nitrogen atom of guanine. Based on their mechanism of action, alkylating agents are characterized as monofunctional, or bifunctional. When monofunctional alkylating agents attach an alkyl group to guanine, repair enzymes recognize there’s something wrong, so they attempt to replace the alkylated bases an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Monoclonal_antibodies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gacKXYsRSESqqaKOsql2bEFjTE6ea5K4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Monoclonal antibodies]]></video:title><video:description><![CDATA[With monoclonal antibodies, antibodies means that they target a specific antigen on the cell surface with an antibody-antigen binding; and monoclonal means that each antibody is produced from a specific B cell line consisting of identical B cells. 

Okay, now monoclonal antibodies are used for the treatment of cancer and various autoimmune diseases like multiple sclerosis and rheumatoid arthritis. 

In this video, we are focusing on the monoclonal antibodies that are used for cancer. 

Normally, all of our cells grow and divide through a tightly regulated cell cycle once they receive growth factor signals. 

During the cell cycle, if a cell appears abnormal in any way to the immune cells that do constant surveillance, the cell has to fix the problem or undergo apoptosis, or programmed cell death - a bit like cellular suicide, rather than proceed to the next phase of the cell cycle. 

But cells can become mutated due to environmental or genetic factors. 

A mutated cell becomes cancerous when it starts to divide uncontrollably. 

As cancer cells start piling up on each other, they form a small tumor mass and they need to induce blood vessel growth, called angiogenesis, to supply themselves with enough energy. 

Some tumors produce vascular endothelial growth factor, or VEGF, which binds to VEGF receptors found on vascular endothelial cells and stimulates angiogenesis. 

Also, many tumors overexpress growth factor receptors like the epidermal growth factor receptor, or EGFR, and the human epidermal receptor 2, or HER2, that stimulate cell proliferation and tumor growth. 

Malignant tumors are ones that are able to break through the basement membrane. 

Some of these malignant tumors go a step further and detach from their basement membrane at the primary tumor site, enter nearby blood vessels or the lymphatic system, and establish secondary sites of tumor growth throughout the body—a process called metastasis. 

Now, the monoclonal antibodies that are used f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antimetabolites_for_cancer_treatment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4SO-h2IcSIyPV0ov67Iacsg_S0mm1M8J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antimetabolites for cancer treatment]]></video:title><video:description><![CDATA[Antimetabolites are a diverse group of medications that are used for the treatment of various conditions including cancer, infections and autoimmune disorders. 

In this video, we are focusing on the antimetabolites used in cancer treatment.   

Alright, during the S phase of the cell cycle, the cell performs DNA replication. 

DNA is composed of a sequence of deoxyribonucleotides and each deoxyribonucleotide is made out of a phosphate group, a five carbon sugar like deoxyribose, and a nucleobase, which can be either a pyrimidine like cytosine, or thymidine, or a purine like adenine or guanine.

Now, nucleotide synthesis starts with ribose-5-phosphate, which is specific for RNA, and an enzyme called ribose phosphate pyrophosphokinase uses an ATP to remove two phosphate groups from it, attaching them to ribose-5-phosphate, creating a phosphoribosyl pyrophosphate, or PRPP. 

Because it catalyzes the synthesis of PRPP, the enzyme ribose phosphate pyrophosphokinase is also known as PRPP synthetase. 

Next step is to make pyrimidines. The amino acid glutamine, bicarbonate, and water are used to form a molecule called carbamoyl phosphate which is then joined to aspartate and together, they form a ringed molecule called carbamoyl aspartic acid, which gets dehydrated to create a molecule called orotate. 

Next, an enzyme moves the phosphoribose unit from PRPP to orotate and that forms orotidine monophosphate, or OMP. 

Next, the enzyme UMP synthase converts orotidine monophosphate into uridine monophosphate, or UMP. 

That UMP gets phosphorylated twice by nucleoside diphosphate kinase, to become uridine triphosphate, or UTP. 

Finally, the enzyme CTP synthase, converts uridine triphosphate into cytidine triphosphate, or CTP. 

Now, purine synthesis starts with the amino acids glutamine, aspartate, and glycine, together with bicarbonate and formate, which is the anion derived from formic acid. 

These undergo a ten-step pathway and the result is inosine monoph]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anti-tumor_antibiotics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zH1SZuA9SF6s_Ia2sKX6Aw0IQniw0kD6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anti-tumor antibiotics]]></video:title><video:description><![CDATA[All right, we know that antibiotics kill microbes, but a certain class of antibiotics called antitumor antibiotics can kill cancer too. Antitumor antibiotics include products that are produced from Streptomyces bacteria like: bleomycin; anthracyclines like doxorubicin and daunorubicin; and dactinomycin, also called actinomycin D. These medications interfere with DNA replication and often damage the DNA itself, leading to cell death. Most of them are cell cycle non-specific. Now, the cell cycle refers to the events that somatic cells go through in order to divide into two identical daughter cells. 

The cell cycle can be divided in two phases: interphase and mitosis. Interphase starts with the G1 phase during which the cell grows and performs its cell functions. At the end of G1, there’s a control point called the G1 checkpoint - where the cell checks to see if the DNA is damaged and it synthesized the right proteins in the correct amount. If there is any reason for the cell not to divide, the cell can either enter a non-dividing state, called the G0 phase, where the DNA repair mechanisms try to fix the problem, or the cell can self-destruct in a process called apoptosis. 

Now, if the cell does get the go-ahead at the G1 checkpoint, it enters the S phase during which DNA is replicated. All right, so during DNA replication, we unzip the double helix with the enzyme DNA helicase, and this creates a replication fork, with the two prongs of the fork being the two strands that are separated from one another. Now, as DNA helicase does its thing, the segments of DNA ahead of it start to overwind, meaning, the double helix becomes more tightly wound. Overwinding of the DNA can slow down replication, so the enzyme DNA topoisomerase works ahead of DNA helicase to loosen up the tight DNA coils. 

Next, RNA primase creates a matching RNA primer on one pron of the replication fork. This is the area where the next enzyme, DNA polymerase, can bind to the DNA to use it as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Microtubule_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ahBJ3c8zTOG5TC7K1NQJq96bSiyGKKaF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Microtubule inhibitors]]></video:title><video:description><![CDATA[Microtubule inhibitors, as their name implies, disrupt the microtubules and inhibit mitosis, which is a specific phase of the cell cycle. 

Anticancer agents in this class include the vinca alkaloids and the taxanes.

But first things first. 

The cytoskeleton is a network of proteins within the cell that gives each cell its shape, and it anchors organelles in place. 

But it’s also a dynamic network, which can change shape when the cell wants to move, contract, divide, or pull in or push out molecules. 

It’s made up of three proteins: actin filaments, intermediate filaments, and microtubules. 

Microtubules are made of alternating round proteins called α- and β-tubulins, which form long strands called protofilaments. 

Thirteen of these protofilaments come together to form a single microtubule. 

Microtubules play a super important role in cell division. 

During cell division there are two centrosomes inside the cell, and each centrosome is made out of two centrioles.

 Each centriole is in turn made up of nine sets of microtubule triplets. 

Now cell division, or mitosis, can be divided into four subphases: prophase, metaphase, anaphase, and telophase. 

During prophase, the membrane around the nucleus disintegrates, and the chromosomes condense. 

During metaphase, chromosomes move towards the middle of the cell, on a line called the metaphase plate. 

Each chromosome is made up of a pair of sister chromatids which are joined together in the centromere where there’s a specific protein complex called the kinetochore. 

When the chromosomes are in place, each centrosome sends out thread-like projections called spindle fibers, that attach to the centromere of each chromosome. 

Spindle fibers consist of microtubules that originate from the centrioles and polymerize in the direction of the kinetochores. 

Next, during anaphase, the centrosomes start pulling on the spindle fibers to pull the sister chromatids apart, forming the mitotic spindle. 

It looks ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Platinum_containing_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hDXdBjqBSzOZB2R2EUrxVgKPScqkftIF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Platinum containing medications]]></video:title><video:description><![CDATA[Platinum containing agents, informally called platins, are a class of medications that are used to treat cancer. 

They disrupt the structure of DNA by acting on consecutive guanine bases within a strand of DNA and can affect all phases of the cell cycle.

Okay, now the cell cycle refers to the events that somatic cells, which includes all of the cells in our bodies except the reproductive cells, go through from the moment they’re formed until the moment they divide into two identical daughter cells. 

This cycle varies in length depending on the type of cell. 

For rapidly dividing cells, like skin cells, it takes less than a day, whereas for other cells, like liver cells, the cell cycle can last years. 

Now, the cell cycle can be divided in two phases: interphase and mitosis. 

Interphase comprises of the G1 phase, during which the cell grows and performs its cell functions, the S phase, during which DNA is replicated, and the G2 phase, during which the cell grows again before entering mitosis. 

Mitosis can be broken down into prophase, metaphase, anaphase, and telophase, during which the replicated DNA divides equally for the two daughter cells, and ends with cytokinesis, which is when the cell membrane actually divides to form the two new cells. 

There’s also a G0 phase which is an extended G1 phase, where the cell is resting and not actively preparing to divide. 

Alright, now imagine a cancer cell. 

This cell is going through the phases of the cell cycle without regulation, and its DNA also replicates more frequently, with less error-correcting than healthy cells. 

Therefore, it’s more sensitive to DNA damage. 

Here’s a DNA base, guanine. 

Platinum containing agents attach at the number 7 nitrogen atom of two adjacent guanines on the same strand of DNA leading to the formation of cross-bridges, or intra-strand cross-linking of the DNA. 

The resultant cross-linking inhibits DNA repair and prevents DNA from being separated for replication, even]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Topoisomerase_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qdQPmmvyQJ6Z6jMJ1_25XP-uS0OGR5CO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Topoisomerase inhibitors]]></video:title><video:description><![CDATA[Topoisomerase inhibitors, as their name implies, are a class of medications that act by blocking an enzyme called topoisomerase. 

They are mainly used as anticancer agents that target specific phases of the cell cycle. 

An interesting fact about these agents is that they are natural products, meaning they are extracted from roots, plants, or trees.

But first things first. 

The cell cycle refers to the events that somatic cells - which includes all of the cells in our bodies except the reproductive cells - go through from the moment they’re formed until the moment they divide into two identical daughter cells. 

This cycle varies in length depending on the type of cell. 

For rapidly dividing cells, like skin cells, it takes less than a day, whereas for other cells, like liver cells, the cell cycle can last for years. 

Now, the cell cycle can be divided into two phases: interphase and mitosis. 

Interphase comprises of the G1 phase, during which the cell grows and performs its functions, the S phase, during which DNA is replicated, and the G2 phase, during which the cell grows again before entering mitosis, or the M phase. 

Mitosis can be broken down into prophase, metaphase, anaphase, and telophase, during which the replicated DNA divides equally for the two daughter cells, and ends with cytokinesis, which is when the cell membrane actually divides to form the two new cells.  

Okay, so during DNA replication, we unzip the double helix with the enzyme DNA helicase and this creates a replication fork, with the two prongs of the fork represented by the two strands that are separated from one another. 

Now, as DNA helicase unzips the DNA, the segments of DNA ahead of it start to overwind - meaning, the double helix becomes more tightly wound. 

Overwinding of the DNA can slow down replication, so the enzyme DNA topoisomerase works ahead of DNA helicase to loosen up the tight DNA coils. 

It achieves this by gently snapping one strand, loosening the ove]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Protein_synthesis_inhibitors:_Aminoglycosides</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jF6_0fIPQg2GU-jks5ZLOJagSq2H73Ik/_.jpg</video:thumbnail_loc><video:title><![CDATA[Protein synthesis inhibitors: Aminoglycosides]]></video:title><video:description><![CDATA[Aminoglycosides are antimicrobial antibiotics that inhibit bacterial ribosomes, which are the organelles that make proteins. 

Genes are used to synthesize proteins in two steps: transcription and translation. 

During transcription, a specific gene on the DNA is “read,” and a copy is made called a messenger RNA, or mRNA. 

Translation is also known as protein synthesis, and it’s when ribosomes use mRNA to assemble proteins from amino acids within the cytoplasm. 

Now, prokaryotic cells, like bacteria, have smaller ribosomes than eukaryotic cells, like those found in humans.   

Bacterial ribosomes are made up of a 50S subunit and a 30S subunit which combine to form a 70S ribosome.  

Eukaryotic ribosomes are made up of a 60S and a 40S subunit that form a 80S ribosome. 

Since these proteins are different, we can create medications that  selectively interfere with the bacterial ones.

In both eukaryotic and prokaryotic cells, protein synthesis involves initiation, elongation, and termination. 

In bacteria, initiation occurs when the 50S and 30S subunits bind to the mRNA sequence to form a ribosome-mRNA complex, also known as initiation complex. 

The mRNA serves as a blueprint for the protein that will be synthesized. 

It’s made up of three nucleotide long sequences, called codons. 

Transport RNA, or tRNA, carrying different amino acids can bind to these codons with their matching anticodons. 

The complete ribosome-mRNA complex has 3 sites where tRNA can enter and bind. 

These are called the A, or aminoacyl site, the P, or peptidyl site, and the E, or exit site.

Elongation starts when the first tRNA, carrying a formylmethionine amino acid, enters the P site and binds to the start codon. 

This causes a conformational change in the ribosome, which unlocks the A site for the next tRNA.  

A process called proofreading occurs here where only tRNAs with the matching anticodon can bind to corresponding mRNA codon. 

After the next tRNA binds at the A site]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antimetabolites:_Sulfonamides_and_trimethoprim</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6kjlnt9XT9uDRTzg3x_YhEFgTD6HLQ0L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antimetabolites: Sulfonamides and trimethoprim]]></video:title><video:description><![CDATA[Antimetabolites are medications that interfere with the synthesis of DNA. 

Some antimetabolites are used in chemotherapy to kill cancer cells, while others are used as antibiotics since they inhibit bacterial folate synthesis. 

Folate, or folic acid, also known as vitamin B9, is necessary for the synthesis of nucleic acids, which are the building blocks of DNA and RNA. 

Simply put, a lack of folate results in a lack of nucleic acids, which then results in decreased DNA and RNA synthesis, leading to hindered cell division and function. 

Now, a key difference between our cells and bacterial cells is that we get all of our folate through our diet, while bacteria can make their own folate from scratch. 

Because of this, we can target the bacterial folate synthesis pathway to minimize the damage done to our cells. 

So in order to synthesize folate, the bacteria will first use the host’s para-aminobenzoic acid, or  pABA, and convert it to dihydropteroic acid via the enzyme dihydropteroate synthetase, or DHPS. 

In the second step, dihydropteroic acid is converted into dihydrofolic acid by dihydrofolate synthetase. 

The third step is the conversion of dihydrofolic acid into tetrahydrofolic acid via dihydrofolate reductase. 

Tetrahydrofolic acid is a folic acid derivative and can be used to synthesize purines like adenine and guanine, which are used to build DNA and RNA, as well as thymidine, which is only used in DNA. 

Now, the first group of antimetabolite antibiotics are the sulfonamides, which include sulfamethoxazole, or SMX, sulfisoxazole, and sulfadiazine. 

These medications bind to dihydropteroate synthetase, or DHPS, in the first step of folate synthesis and prevents the bacteria from making dihydropteroic acid. 

These medications can be given peroral or injected into a vein, but they need to be metabolized by the liver in order to work. 

Now, they are broad spectrum and can treat a variety of gram positive and gram negative bacteria, as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antituberculosis_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i7LXqx7RRcGWRZ-KWoEADEX_TXK2tf9v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antituberculosis medications]]></video:title><video:description><![CDATA[Antituberculosis medications are agents used to treat tuberculosis, a disease caused by the bacteria Mycobacterium tuberculosis. 

Mycobacteria are an interesting bunch, they’re slender, rod-shaped, and need oxygen to survive, in other words, they’re “strict aerobes.” 

They’ve got an unusually waxy cell wall, which is mainly a result of the production of mycolic acid. 

This waxy cell wall makes them incredibly hardy, and allows them to resist weak disinfectants and survive on dry surfaces for months at a time. 

Antituberculosis medications act mainly by preventing the production of mycolic acid and the synthesis of this cell wall.

Although about two billion people worldwide are infected with tuberculosis, or simply ‘TB, the vast majority, about 90-95%, don’t develop symptoms. And this is because usually the immune system can contain it. 

So Mycobacterium tuberculosis is usually transmitted via inhalation, which is how they gain entry into the lungs. 

TB can avoid the mucus traps and make its way to the deep airways and alveoli where we have macrophages which eat up foreign cells, digest, and destroy them. 

With TB, they recognize foreign proteins on their cell surface, and phagocytize them, or essentially package them into a space called a phagosome. 

With most cases, the macrophage then fuses the phagosome with a lysosome, which has hydrolytic enzymes that can pretty much break down any biochemical molecule. 

TB’s tricky though, and once inside the macrophage, they produce a protein that inhibits this fusion, which allows the mycobacterium to survive. 

It doesn’t just survive, though, it proliferates, and creates a localized infection.

Three weeks after initial infection, cell-mediated immunity kicks in, and immune cells surround the site of TB infection, creating a granuloma. 

The tissue inside the middle dies as a result, a process referred to as caseous necrosis. This area is known as a “Ghon focus”. 

In some cases, the mycobacteria is kil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Miscellaneous_cell_wall_synthesis_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I79InzuJTta7Y7mxJuMMCVpnQlObIk43/_.jpg</video:thumbnail_loc><video:title><![CDATA[Miscellaneous cell wall synthesis inhibitors]]></video:title><video:description><![CDATA[Beta lactam antibiotics, such as penicillins and cephalosporins, have a beta-lactam ring in their structure, which gives them their name. 

These medications inhibit cell wall synthesis in bacteria. Unfortunately for us, bacteria are becoming increasingly resilient to beta lactams, so we’ve come up non-beta lactam medications to inhibit cell wall synthesis.  

So, our body is made out of eukaryotic cells. 

Bacterias belong to a different type of cells, called the prokaryotes. 

From the outside to inside, they have a slimy capsule made out of polysaccharides. 

Then, there’s a cell wall in most prokaryotes. 

A cell wall is a structural layer, which encapsulates bacteria, and offers structural support and protection, like a suit of armor. It also offers some filtering capabilities, as not everything can pass freely through it.

Finally, on the inside, there’s a pretty standard cell membrane. 

Should something happen to this wall, say, if its synthesis mysteriously stopped, its owner’s life expectancy will turn to that of a snowflake in Sahara. And that’s exactly what we’re hoping to do. 

Bacterial cell walls are made of a substance called peptidoglycan, or murein.

Peptidoglycan is a very strong, crystal lattice resembling three-dimensional structure, composed out of long using “strands” of amino polysaccharides, running in parallel. 

These are made of made out segments of N-acetylglucosamine, or NAG, and N-acetylmuramic acid, or NAM, in an alternating pattern - so, NAG, NAM, NAG, NAM, and so on, like a pearl necklace. 

These strands are also cross linked by short, four to five amino acids long, or tetrapeptide chains, protruding from NAM subunits. 

Those pentapeptides reach out and link to pentapeptide chains from the neighboring strands, for structural stability, a sub-process known as transpeptidation. 

All of this is made possible by enzymes called DD-transpeptidases, that are also better known as penicillin binding proteins, or PBPs. 

These en]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cell_wall_synthesis_inhibitors:_Cephalosporins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q8ediG-IQhamdYqiWzAveP8jSfCm1Bfp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cell wall synthesis inhibitors: Cephalosporins]]></video:title><video:description><![CDATA[Cephalosporins are antibiotics which got their name from a mold known as cephalosporium, from which they were originally extracted.

They belong to the pharmacological group of beta-lactam antibiotics. 

What all beta-lactams have in common is a beta-lactam ring in their structure, which gives them their name, and also the mechanism of action - which is the inhibition of cell wall synthesis in bacteria.

So, our body is made out of eukaryotic cells. 

Bacterias belong to a different type of cells, called the prokaryotes. 

From the outside to inside, they have a slimy capsule made out of polysaccharides. 

Then, there’s a cell wall in most prokaryotes. 

A cell wall is a structural layer, which encapsulates bacteria, and offers structural support and protection, like a suit of armor. It also offers some filtering capabilities, as not everything can pass freely through it. 

Finally, on the inside, there’s a pretty standard cell membrane. 

Should something happen to this wall, say, if its synthesis mysteriously stopped, its owner’s life expectancy will turn to that of a snowflake in Sahara. And that’s exactly what we’re hoping to do. 

Bacterial cell walls are made of a substance called peptidoglycan, or murein. 

Peptidoglycan is a very strong, crystal lattice resembling three-dimensional structure, composed out of long using “strands” of amino polysaccharides, running in parallel. 

These are made of made out segments of N-acetylglucosamine, or NAG, and N-acetylmuramic acid, or NAM, in an alternating pattern - so, NAG, NAM, NAG, NAM, and so on, like a pearl necklace. 

These strands are also cross linked by short, four to five amino acids long, or tetrapeptide chains, protruding from NAM subunits. 

Those pentapeptides reach out and link to pentapeptide chains from the neighboring strands, for structural stability, a sub-process known as transpeptidation. 

All of this is made possible by enzymes called DD-transpeptidases, that are also better known as p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DNA_synthesis_inhibitors:_Metronidazole</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DWhLXw9sRcWCnsnYZXpV7j7ARtiTrMXc/_.jpg</video:thumbnail_loc><video:title><![CDATA[DNA synthesis inhibitors: Metronidazole]]></video:title><video:description><![CDATA[DNA synthesis inhibitors are a group of antibiotics that target the synthesis of DNA in bacteria and other organisms. Metronidazole, a 5-nitroimidazole, prevents the synthesis of nucleic acids, which are the building blocks of DNA, and is effective against many bacteria and protozoans.         

Metronidazole and related 5-nitroimidazoles are relatively nontoxic to humans. This is because in order to function, they need to be reduced by a protein called ferredoxin, which contains sulfur and iron. This protein is commonly found in anaerobic bacteria and protozoans, but is not as available in humans and aerobic bacteria. Now, this protein can donate an electron to metronidazole, causing it to form free radicals which will damage the DNA, causing it to fragment. Without the DNA as a template, the organism can’t synthesize any more nucleic acids like DNA or mRNA, which will lead to cell death.  

Metronidazole can be taken orally, but it’s also available in an IV form and as topical creams. It penetrates well into body tissues and fluids, including vaginal secretions, seminal fluid, saliva, breast milk, cerebrospinal fluid, and crosses over the placenta.  

This medication can treat many anaerobic bacterial infections like Clostridioides difficile, which can cause pseudomembranous enterocolitis in people taking other antibiotics. Another common organism treated by this medication is Helicobacter pylori, a common bacteria that causes gastritis and peptic ulcers. However, it should be used in combination with other antimicrobials and proton pump inhibitors as part of a triple therapy for the best outcome when treating this condition. Next, Gardnerella vaginalis and other anaerobes that can cause bacterial vaginosis are all treated by metronidazole.  

For protozoan infections, it’s the medication of choice for amoebiasis, an infection of the gut caused by Entamoeba histolytica. It’s the medication of choice against Trichomonas vaginalis as well, which causes vag]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/DNA_synthesis_inhibitors:_Fluoroquinolones</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mnPWO_RvTTG4yj4EmYLbUlCMT4ChADtc/_.jpg</video:thumbnail_loc><video:title><![CDATA[DNA synthesis inhibitors: Fluoroquinolones]]></video:title><video:description><![CDATA[Our bodies consist of eukaryotic cells, while bacterias consist of prokaryotic cells. 

So, in order to treat bacterial infections we can develop antimicrobials that only target prokaryotic cells while leaving our cells mostly unharmed. 

One of these targets is bacterial DNA, and we call these medications DNA inhibitors or nucleic acid inhibitors. 

There are plenty of processes and enzymes involved that we can target and the quinolones and fluoroquinolones inhibit an enzyme called DNA topoisomerase.

So there are many different types of topoisomerases but we’ll be looking at topoisomerase II, also called DNA gyrase, and topoisomerase IV. 

Both types of topoisomerases cause double strand breaks in DNA, but at different points during mitosis. 

Topoisomerase II plays a role in condensing the chromosomes by making a double strand break in the DNA so that it can be more tightly wound, causing a supercoil. 

When enough supercoils are induced, the DNA condenses. 

Topoisomerase IV plays a role later on, after the chromosome has been replicated, where it causes a double strand break in the DNA so the new DNA strand can be disentangled from the original. 

Now, quinolones are created to target bacterial topoisomerases, but it was soon discovered that by adding a fluorine molecule to the quinolones, they become more effective. 

So these newer medications, called fluoroquinolones, replaced the older quinolones in most clinical settings.  

Common fluoroquinolones include ciprofloxacin, ofloxacin, balofloxacin, levofloxacin, gemifloxacin, and moxifloxacin. 

One way to tell a fluoroquinolone apart from other antimicrobials is that they all have the suffix “-floxacin.”  

These medications can be taken peroral or via IV, but ciprofloxacin and ofloxacin are also available in otic formulations, while moxifloxacin is also available in ophthalmic solutions. 

Now fluoroquinolones are broad spectrum bactericidal  antibiotics and ciprofloxacin in particular is widely u]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Miscellaneous_protein_synthesis_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4jjztvjJTOC6TboPgTkZYedYQ_a2tRo9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Miscellaneous protein synthesis inhibitors]]></video:title><video:description><![CDATA[Protein synthesis inhibitors include many different classes of medications that prevent bacterial ribosomes from synthesizing proteins. The ones that target the 50S subunit of the ribosome include chloramphenicol, macrolides, lincosamides, and oxazolidinones. 

Okay, first, let’s look at how genes become proteins. There’s two steps: transcription and translation. During transcription, a specific gene on the DNA is “read” and a copy is made called a messenger RNA, or mRNA, which is like a blueprint with instructions on what protein to build. Translation is also known as protein synthesis, and it’s when organelles called ribosomes assemble the protein from amino acids within the cytoplasm.  

Now, prokaryotic cells, like bacteria, have smaller ribosomes than eukaryotic cells, like those found in humans. Bacterial ribosomes are made up of a 50S subunit and a 30S subunit which combine to form a 70S ribosome. Eukaryotic ribosomes are made up of a 60S and a 40S subunit that form a 80S ribosome. Since these proteins are different, we can create medications that  selectively interfere with the bacterial ones. 

Protein synthesis involves initiation, elongation, and termination. In bacteria, initiation occurs when the 50S and 30S subunits bind to the mRNA sequence to form a ribosome-mRNA complex, also called the initiation complex. The mRNA serves as a blueprint for the protein that will be synthesized. It’s made up of three nucleotide-long sequences, called codons, on top of which transport RNA, or tRNA, carrying amino acids can bind with their matching anticodon. The complete ribosome has 3 sites where tRNA can enter and bind. These are called the A, or aminoacyl site, the P, or peptidyl site, and the E, or exit site. 

Elongation starts when the first tRNA, carrying a formylmethionine amino acid, enters the P site and binds to the start codon. This causes a conformational change which unlocks the A site for the next tRNA. The next tRNA binds at the A site, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cell_wall_synthesis_inhibitors:_Penicillins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JRJDIqjgSKmN14bqFKvphJNbQ3mu9cz0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cell wall synthesis inhibitors: Penicillins]]></video:title><video:description><![CDATA[Penicillins are antibiotics that got their name from the Penicillium mold, from which they were originally extracted. 

They belong to the pharmacological group of beta-lactam antibiotics. 

What all beta-lactams have in common is a beta-lactam ring in their structure, which gives them their name, and also the mechanism of action - the inhibition of cell wall synthesis in bacteria.

So, our body consists of multiple eukaryotic cells, while bacterias are prokaryotic, meaning they are primitive, single cellular organisms.

Most have a slimy capsule made out of polysaccharides  and a cell wall which encapsulates and protects the bacteria like a suit of armor and offers structural support. 

Bacterial cell walls are made of a substance called peptidoglycan, or murein. 

Peptidoglycan is a molecule composed out of long strands of amino polysaccharides running in parallel. 

These are made of segments of N-acetylglucosamine, or NAG, and N-acetylmuramic acid, or NAM, in an alternating pattern - so, NAG, NAM, NAG, NAM, and so on, like a pearl necklace. 

At the tips of the NAM subunits are tetrapeptide and pentapeptide chains, protruding from NAM subunits. 

These peptide chains can link to other peptide chains from the neighboring strands through a process known as transpeptidation. 

This is carried out by an enzyme called DD-transpeptidases, or penicillin binding proteins, or PBPs.  

Now these enzymes are like locks and there are specific binding area for the pentapeptides keys to fit into. 

Once the key goes in the lock, the PBP enzymes fuse them together, creating a stable link between the two amino polysaccharide strands and strengthen the cell wall. 

In essence, all beta lactam antibiotics, like the penicillins, somewhat resemble the tetrapeptide chains. 

Inside the bacteria, PBP enzymes will mistakenly bind to the beta lactams antibiotic molecule instead of a tetrapeptide and stick inside the PBP forever, like chewing gum in a keyhole, permanently disa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Protein_synthesis_inhibitors:_Tetracyclines</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EuLJhdwkRo2LOFDjuXXsE5a5RzaieYb-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Protein synthesis inhibitors: Tetracyclines]]></video:title><video:description><![CDATA[Tetracyclines are antimicrobial antibiotics that inhibit bacterial ribosomes which are the organelles that make proteins. 

Genes become proteins in two steps: transcription and translation. 

During transcription, a specific gene on the DNA is “read” and a copy is made called a messenger RNA, which is like a blueprint with instructions on what protein to build. 

Translation is also known as protein synthesis, and it’s when organelles called ribosomes assemble the protein from amino acids within the cytoplasm. 

Now, prokaryotic cells, like bacteria, have smaller ribosomes than eukaryotic cells, like those found in humans.   

Bacterial ribosomes are made up of a 50S subunit and a 30S subunit which combine to form a 70S ribosome.  

Eukaryotic ribosomes are made up of a 60S and a 40S subunits that form an 80S ribosome. 

Since these proteins are different, we can created medications that  selectively interfere with the bacterial ones.

In both eukaryotic and prokaryotic cells, protein synthesis involves initiation, elongation, and termination. 

In bacteria, initiation occurs when the 50S and 30S subunits bind to the mRNA sequence to form a ribosome-mRNA complex. 

The mRNA serves as a blueprint for the protein that will be synthesized. It’s made up of three nucleotide long sequences, called codons. 

Transport RNA, or tRNA, carrying different amino acids can bind to these codons with their matching anticodons. 

The complete ribosome-mRNA complex has 3 sites where tRNA can enter and bind. 

These are called the A, or aminoacyl site, the P, or peptidyl site, and the E, or exit site.

Elongation starts when the first tRNA, carrying a formylmethionine amino acid, enters the P site and binds to the start codon. 

This causes a conformational change in the ribosome which unlocks the A site for the next tRNA.  

A process called proofreading occurs here where only tRNAs with the matching anticodon can bind to corresponding mRNA codon. 

After the next tRNA bin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Echinocandins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZWUXj8n9QIeBMbJoVMUYaOQzQvu7flre/_.jpg</video:thumbnail_loc><video:title><![CDATA[Echinocandins]]></video:title><video:description><![CDATA[Echinocandins are a novel class of medications used to treat mycoses, or fungal infections. 

Mycoses can be localized skin infections, or develop into systemic infections in immunodeficient patients. 

Antifungals work either through fungistatic action, meaning that they inhibit fungal growth, or through fungicidal action, meaning they kill the fungi.

Now, most fungi have a protective cell wall made of different carbohydrate molecules. 

Some fungal species have beta glucans which are polysaccharide polymers that are cross linked with other carbohydrate molecules to make a strong fungal cell wall.

Beta glucans are produced by an enzyme on the cell membrane called beta-1,3-D-glucan synthase. 

This enzyme is not found in human cells which makes it a good target for antifungal medications.  

Now, echinocandins are a type of medication that noncompetitively bind to and inhibit beta-1,3-D-glucan synthase. 

This weakens the cell wall and prevents it from being repaired. 

The cell wall gradually deforms more and more until it ruptures, causing the cell to die.  

Echinocandins are only available via IV since they are not well absorbed through the GI tract.  

Medications in this class include anidulafungin, micafungin, and caspofungin. 

They are only effective against fungal species that have beta-1,3-D-glucan synthase, but it’s extremely rare for these organisms to have resistance to these medications. 

Because of this, echinocandins are often used to treat fungal infections that are resistant to the more common antifungal medications like amphotericin-B and the “azole” medications like fluconazole. 

Echinocandins are used to treat mucocutaneous candidiasis, which affect the skin, nails, and oral mucosa, or disseminated candidiasis, where the infection spreads to multiple organ systems through the blood, causing endocarditis, endophthalmitis, and osteomyelitis. 

This is only seen in people with a compromised immune system like those with an HIV infect]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Azoles</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QT0tsVlnS-6UU1d5JBWI_Dj3QfmH_9vN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Azoles]]></video:title><video:description><![CDATA[The “azole” antifungals are a family of medications used to treat mycoses, or fungal infections. 

Mycoses can be superficial, like on the skin or hair, or develop into systemic infections in immunodeficient people. 

Antifungals work either through fungistatic action, meaning that they inhibit fungal growth, or through fungicidal action, meaning they kill the fungi. 

Azoles are divided into two major families of antifungals: imidazoles and triazoles.

Most fungal cells have a tough outer cell wall and an inner cell membrane. 

The cell membrane is mostly made of phospholipids with some sterol or modified steroid molecules mixed in.  

Humans have cholesterol, while fungi have ergosterol. 

Both sterol molecules help keep the cell membrane stable at a wide range of temperatures. 

Now, the precursor to both molecules is lanosterol. 

Fungi have a cytochrome p450 enzyme called fourteen-alpha-demethylase in their mitochondria and endoplasmic reticulums, which converts lanosterol to ergosterol. 

Without ergosterol, the structure of the cell membrane will be disrupted. 

This will cause membrane-bound proteins, like ion channels, to stop working properly. 

The membrane also becomes fragile, which eventually leads to inhibition of fungal growth.

The azole antifungals include imidazoles, like clotrimazole, isoconazole, miconazole, butoconazole, fenticonazole, and ketoconazole; as well as triazoles like fluconazole, itraconazole and voriconazole. 

The only difference between the two groups is the imidazoles contain an imidazole ring, while triazoles contain triazole rings. 

These medications work by inhibiting the fourteen-alpha-demethylase enzyme. 

However, they also inhibit human cytochrome P450 enzymes to a lesser degree. 

Because of this, the vast majority of azoles come in topical form, and they’re commonly used to treat superficial mycoses. 

Azole creams are used for treating dermatophytosis, or ringworm, which is a red, itchy, scaly, circular rash]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Miscellaneous_antifungal_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pVC6NjwcSvGCF9ZFlMDcEntUSe2lcM0X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Miscellaneous antifungal medications]]></video:title><video:description><![CDATA[Antifungal agents are a class of medications used to treat mycoses, or fungal infections. 

Mycoses can be superficial, meaning they are localized on the skin, or develop into systemic infections in immunodeficient patients. 

Antifungals work either through fungistatic action, meaning that they inhibit fungal growth, or through fungicidal action, meaning they kill the fungi. 

Now, antifungals include the azole family and a novel class of medications, echinocandins; but there are also many other antifungals with similar or different mechanisms that we’ll talk about in this video.

Okay, most fungal cells have a tough outer cell wall and an inner cell membrane. 

The cell membrane is mostly made of phospholipids with some sterol or modified steroid molecules mixed in. 

Humans have cholesterol, while fungi have ergosterol. Both sterol molecules help keep the cell membrane stable at a wide range of temperatures. 

Now, the precursor to both molecules is lanosterol. 

The precursor of lanosterol is squalene. 

The conversion of squalene to lanosterol is catalyzed by an enzyme called squalene epoxidase. 

Fungi have a cytochrome p450 enzyme called fourteen-alpha-demethylase in their mitochondria and endoplasmic reticulums, which converts lanosterol to ergosterol. 

Without ergosterol, the structure of the cell membrane will be disrupted. 

This will cause membrane-bound proteins, like ion channels, to stop working properly. 

The membrane also becomes fragile, which eventually leads to inhibition of fungal growth.

Okay, let’s start with polyenes, which are naturally-derived antifungal antibiotics that alter cell membrane permeability. 

They include amphotericin, also called amphotericin B, and nystatin. 

Polyenes have both hydrophilic, meaning they love water, and lipophilic, meaning they love fats, characteristics. 

They bind to ergosterol, and the hydrophilic core causes the formation of artificial pores in the cell membrane, thereby creating a leaky me]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anti-mite_and_louse_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VRXheuS3SWeYsmiBY8wA1_qdR4KnloSN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anti-mite and louse medications]]></video:title><video:description><![CDATA[Mites and lice are arthropod ectoparasites, (or external parasites), that live on the surface of the body, like the skin or hair. 

Ectoparasiticides are topical medications used to treat these infestations. 

Endectocides on the other hand, are multi-purpose antiparasitics that work on both external parasites and some internal parasites, like roundworms.

Now, lice are wingless insects that live off of the blood of their hosts. 

There are 3 types of lice that infest humans: head louse that lives in the hair of the scalp; body louse that lives in the hair of the axilla, back, and pubic region; and pubic louse, also called crab louse, that lives in pubic and axillary hair, but also the eyebrows. 

Lice infestation is called pediculosis and the main symptom is pruritus, (or itchiness), which is caused by an allergic reaction to louse’s saliva.  

Scratching of the bites could also lead to bacterial skin infections. 

Another common ectoparasite is the Sarcoptes scabiei mite which causes scabies. 

These tiny critters are eight-legged arthropods that are related to spiders. 

Unlike spiders, scabies mites burrow into the skin and cause a pimple like rash locally. 

Even worse, they tunnel around under the skin, forming elevated tracks that are visible on the skin surface. 

The burrowing causes intense itching that’s more frequent at night when the mites are more active. 

The most common sites for scabies are between the fingers, on the flexor surface of the wrist, and the extensor surface of the elbow and knees. 

They can also be found around the areola of the breast and the pubic region.       

Permethrin is an ectoparasiticide and an insecticide. It’s the first line medication for both scabies and pediculosis. 

This medication is used topically in the form of creams, lotions, or shampoos.

Once taken in by the parasite, permethrin binds to sodium channels on the membrane of neurons, and prolongs their inactive state. This results in delayed repolariza]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antimalarials</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0wL2OSCQTsunIvhql0GDnKJJTeaOYR_p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antimalarials]]></video:title><video:description><![CDATA[Malaria is an infection that can be caused by a few different types of plasmodium species, which are single-celled parasites that are spread by mosquitoes. There are hundreds of types of Plasmodium species, but the five that cause malarial disease in humans are Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, Plasmodium ovale, and Plasmodium knowlesi. Once the plasmodium gets into the bloodstream, it infects liver cells and red blood cells, which causes a variety of symptoms and sometimes even leads to death. We rely on groups of medications commonly known as antimalarials, in order to prevent and treat malaria. 

Now, malaria is transmitted when a plasmodium-infected female of the Anopheles mosquito hunts for a blood meal in the evening and throughout the night. They’re kind of like tiny flying vampires, with the mosquito being drawn to carbon dioxide that gets breathed out, as well as bodily smells, like foot odor. At this point, the Plasmodium is in a stage of development called a sporozoite, waiting patiently in the mosquito’s salivary gland. 

When the mosquito bites a person with its proboscis, the worm-like sporozoites spill out of the mosquito’s saliva and make it into the bloodstream. The sporozoites then travel to the liver, where they invade hepatocytes.  

There, they begin asexual reproduction, also known as schizogony. Over the next 1-2 weeks, P. falciparum, P. malariae, and P. knowlesi sporozoites multiply asexually and mature into merozoites, while host hepatic parenchymal cells die. In contrast, Plasmodium vivax and Plasmodium ovale sporozoites enter into a dormant hepatic phase, where they are called hypnozoites. They can remain in this dormant phase for months to years until they wake up and begin schizogony.  

In both cases, when the merozoites are released into the blood, they enter the erythrocytic phase, where they invade red blood cells. Once inside the red blood cell, Plasmodium feeds on hemoglobin via a process ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Herpesvirus_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KKRcwE6zQDeT-8ZwGm9btSJSQkK5rarp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Herpesvirus medications]]></video:title><video:description><![CDATA[Anti-herpes medications are a group of antiviral agents that treat herpes infections including herpes simplex virus, or HSV, but they can also treat other viral infections like varicella zoster virus, or VZV, and cytomegalovirus, or CMV. 

They act by inhibiting viral DNA synthesis and thus, inhibiting viral proliferation. 

Alright, now let’s start with HSV, which infects skin and mucosal epithelial cells. 

There are two types of HSV, HSV1 and HSV2. 

Generally speaking, HSV1 tends to cause infections “above the waist” mostly involving the lips, or labia, which is referred to as herpes labialis, and the mouth and the gingiva, which is called gingivostomatitis. 

In rare cases, HSV1 can spread to the esophagus, causing esophagitis, or to the central nervous system, causing meningitis or encephalitis, typically affecting the temporal lobe. 

On the other hand, HSV2 tends to cause infections “below the waist” affecting the genital organs, which is referred to as herpes genitalis. 

HSV can also pass from a mother to a baby usually when the baby passes through the infected maternal vaginal secretions and can cause severe neonatal infections. 

The typical presentation of a herpes infection is clusters of small, painful, fluid-filled blisters, that ooze and ulcerate. They eventually heal after a few weeks. 

However, HSV also infects the nearby sensory neurons, which aren’t destroyed, but instead, they become a permanent home for the herpes virus. This is referred to as the latent phase of the infection and is typically asymptomatic. 

From time to time, the herpes virus from the sensory neurons make a few viral copies of itself which can get released and infect the epithelial cells. 

Alright, now let’s move on to varicella zoster virus. VZV causes a primary infection called varicella or chickenpox, which is characterized by a rash on the scalp, face, and trunk that contains macules, papules, vesicles, and scabs at the same time. 

Now, from the neurons in t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/At-Dk8aQQUiwgLFce51toD_jQ1_ZnU0k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis medications]]></video:title><video:description><![CDATA[Anti-hepatitis medications are a group of antiviral agents used to treat viral hepatitis, which is the inflammation of the liver caused by some sort of virus that targets and damages liver cells. 

Now, viral hepatitis can be acute or chronic. 

Acute hepatitis lasts for six months or less, and usually resolves on its own without any antiviral treatment. 

Chronic hepatitis lasts for more than six months, sometimes even for decades. 

Anti-hepatitis medications are mainly used to treat chronic hepatitis and the two main viruses are hepatitis B virus, or HBV, and hepatitis C virus, or HCV.

Alright, so, HCV is a single stranded RNA virus. 

What this means is that HCV inject its RNA into the host’s cell and it can immediately use its host’s ribosomes and translate the proteins needed to make more viruses, like capsomere proteins and enzymes like RNA-dependent RNA polymerase. 

This RNA-dependent RNA polymerase uses the viral RNA as a template, and uses the hepatocyte’s nucleotides to transcribe a complementary strand of RNA, which is then used to form new baby viruses! 

HBV on the other hand is a double stranded DNA virus.

Once the DNA gets injected into a new cell, it enters the cell’s nucleus and is replicated by the host cell’s machinery.  

It’s also transcribed into several messenger RNAs and a pregenomic RNA, and then the messenger RNAs are used to make capsomere proteins and enzymes like DNA polymerase. 

DNA polymerase uses the pregenomic RNA to synthesize new copies of the viral DNA, which is combined with the capsomere proteins to assemble new viruses. 

With each type of virus, whether it’s RNA or DNA, it’s turning your own cells into virus making factories and pumping out new viruses. 

This process strains, damages and potentially kills the infected hepatocytes. 

When these liver cells die, the liver gets inflamed and that’s called hepatitis.

The anti-hepatitis medications can be divided into two groups based on their mechanism of action; n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Protease_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KzH9IcAqS6aRLOLZQa_wC0yoSpSyN0sl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Protease inhibitors]]></video:title><video:description><![CDATA[Protease inhibitors are an important part of HAART, or highly active antiretroviral therapy, which is the combination of medications used in the treatment of AIDS. 

AIDS is caused by an RNA containing retrovirus called human immunodeficiency virus, or HIV. 

Protease inhibitors, or PIs, work by inhibiting the enzyme HIV-1 protease, which prevents the formation of new viruses and further infection of the host’s cells.

HIV is a single-stranded, positive-sense, enveloped RNA retrovirus that targets cells in the immune system that have molecules called CD4 on their membranes. 

These include macrophages, dendritic cells, and especially CD4+ T-helper cells. 

HIV attaches to the CD4 molecule via a protein called gp120 found on its envelope. 

Now, inside its envelope, HIV contains a nucleocapsid which is a capsule containing a single-stranded RNA and some viral enzymes, like reverse transcriptase, integrase, and aspartate protease, also known as a mature HIV-1 protease. 

As HIV binds to the receptors, the viral envelope fuses with the cell membrane of the immune cell, releasing the contents of the nucleocapsid into the helpless host cell’s cytoplasm. 

Once it’s inside the CD4+ cell, reverse transcriptase gets to work immediately. 

It uses the single-stranded viral RNA as a template and uses the nucleotides present in the cytoplasm of the CD4+ cell to transcribe a complementary double-stranded “proviral” DNA. 

This proviral DNA enters the T-helper cell’s nucleus and pops itself into the cell’s DNA, ready to be transcribed into messenger RNA (mRNA).  

These mRNA travel to the ribosomes which translate this into long Gag-Pol polyproteins, which are a bunch of viral proteins joined together. 

Now, human cells don’t come with the equipment to process these long polyprotein chains, but one of the enzymes that HIV releases into the cell is a protease called aspartate protease, or HIV-1 protease. 

This enzyme cuts the polyprotein into individual, functional vi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-nucleoside_reverse_transcriptase_inhibitors_(NNRTIs)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7UJYU61IS5mqs39OfRCz4ZbZSD_5-_Cg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-nucleoside reverse transcriptase inhibitors (NNRTIs)]]></video:title><video:description><![CDATA[Reverse transcriptase inhibitors are an important part of HAART, or highly active antiretroviral therapy, which is the combination of medications used in the treatment of AIDS. 

AIDS is caused by a RNA containing retrovirus called human immunodeficiency virus, or HIV. The “retro” part of retrovirus isn’t referring to its style, but refers to it needing to use an enzyme called reverse transcriptase to transcribe a piece of “proviral” DNA  from its RNA. 

As the name suggests, reverse transcriptase inhibitors go and inhibit this enzyme, and prevent HIV replication. 

They can either be nucleoside reverse transcriptase inhibitors, or NRTIs, which resemble nucleosides, which are the building blocks of nucleic acids like DNA and RNA; or non-nucleoside reverse transcriptase inhibitors, or NNRTIs, which dont resemble nucleosides.

HIV is a single-stranded, positive-sense, enveloped RNA retrovirus that targets cells in the immune system that have a molecule called CD4 on their membrane. 

These include macrophages, dendritic cells, and especially CD4+ T-helper cells.   Normally, the CD4 molecule helps these cells attach to and communicate with other immune cells, which is particularly important when the cells are launching attacks against foreign pathogens. 

HIV attaches to the CD4 molecule via a protein called gp120 found on its envelope.  Now, inside its envelope, HIV contains a nucleocapsid which is a capsule containing a single-stranded RNA and some viral enzymes, like reverse transcriptase and integrase. 

As HIV bind to the receptors, the viral envelope fuses with the cell membrane of the immune cell, releasing the contents of the nucleocapsid into the helpless host cell’s cytoplasm.  

Once it’s inside the CD4+ cell, reverse transcriptase gets to work immediately. It uses the single stranded viral RNA as a template, and uses the nucleotides present in the cytoplasm of the CD4+ cell to transcribe a complementary double-stranded “proviral” DNA. 

Proviral j]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nucleoside_reverse_transcriptase_inhibitors_(NRTIs)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_w7CdcogQ5CDKjfSINaeteZMQR2ZJ1Ux/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nucleoside reverse transcriptase inhibitors (NRTIs)]]></video:title><video:description><![CDATA[Reverse transcriptase inhibitors are an important part of HAART, or highly active antiretroviral therapy, which is the combination of medications used in the treatment of AIDS. 

AIDS is caused by a RNA containing retrovirus called human immunodeficiency virus, or HIV. 

The “retro” part of retrovirus isn’t referring to its style, but refers to it needing to use an enzyme called reverse transcriptase to transcribe a piece of “proviral” DNA  from its RNA. 

As the name suggests, reverse transcriptase inhibitors go and inhibit this enzyme, and prevent HIV replication. 

Based on their structure, they can be classified into nucleoside reverse transcriptase inhibitors, or NRTIs; and non-nucleoside reverse transcriptase inhibitors, or NNRTIs. 

NRTIs resemble nucleosides, which are tiny molecules which when attached to a phosphate group give rise to nucleotides, which are building blocks of nucleic acids like DNA and RNA. 

HIV is a single-stranded, positive-sense, enveloped RNA retrovirus that targets cells in the immune system that have a molecule called CD4 on their membrane. 

These include macrophages, dendritic cells, and especially CD4+ T-helper cells.  

Normally, the CD4 molecule helps these cells attach to and communicate with other immune cells, which is particularly important when the cells are launching attacks against foreign pathogens. 

HIV attaches to the CD4 molecule via a protein called gp120 found on its envelope.  

Now, inside its envelope, HIV contains a nucleocapsid which is a capsule containing a single-stranded RNA and some viral enzymes, like reverse transcriptase and integrase. 

As HIV bind to the receptors, the viral envelope fuses with the cell membrane of the immune cell, releasing the contents of the nucleocapsid into the helpless host cell’s cytoplasm.  

Once it’s inside the CD4+ cell, reverse transcriptase gets to work immediately. 

It uses the single stranded viral RNA as a template, and uses the nucleotides present in the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuraminidase_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KRqXGG7iQ-il_yCo-rCBZ1MgTkWmn_0a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuraminidase inhibitors]]></video:title><video:description><![CDATA[Neuraminidase inhibitors are antiviral medications mainly used to treat influenza, which is the virus that causes the flu. 

There are three types of influenza viruses that infect humans; type A, type B, and type C, and each one has a slightly different genome and set of proteins. 

Now, neuraminidase inhibitors work by preventing the release of new viruses from infected cells, thereby limiting the duration of the illness. 

Alright, first let’s focus on influenza A and influenza B. 

These viruses have two types of glycoproteins on their protective envelope: H protein, or hemagglutinin; and N protein, or neuraminidase. 

When the flu virus enters the body, it uses hemagglutinin to bind to sialic acid sugars on the surface of epithelial cells in the upper respiratory tract. 

Once bound, the cell swallows up the virus in a process called endocytosis. 

Next, the virus releases its viral RNA which moves into the cell’s nucleus. 

Now, these RNAs are negative-sense, meaning they need to be transcribed by RNA polymerase into positive-sense mRNA strands. 

These strands leave the nucleus and are translated into proteins by ribosomes. 

These proteins are then assembled into new viruses. 

Now that we have a cell that’s pretty much a virus-producing factory, it will continue to produce more and more viruses which bud off the host cell’s plasma membrane and leave the body. 

However, the same hemagglutinin that allowed the virus to attach to the sialic acid sugar on the cell surface, can bind to these sugars again and prevent the viruses from leaving the host cell. 

So, in order to be released, the virus uses the neuraminidase proteins to cleave the sialic acid and free itself. 

So in short, hemagglutinin allows the virus to enter the cell, while neuraminidase lets the virus leave the cell.  

Now, neuraminidase inhibitors, as their name implies, bind and inhibit the enzyme neuraminidase, thereby preventing the release of new viruses. 

Common medications in t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antigout_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P-qaCmAmQ9W-gH89a0-sGCNiQ9GFnyOF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antigout medications]]></video:title><video:description><![CDATA[Antigout medications, as their name implies, are medications used to treat gout, which is a form of inflammatory arthritis. 

The underlying cause of gout is hyperuricemia - which is too much uric acid in the blood, resulting in the formation of monosodium urate crystals. 

These sharp, needle-like crystals deposit in areas of slow blood flow, such as joint spaces, or kidney filtration tubules. 

Antigout medications work by preventing the buildup of uric acid, or by reducing inflammation. 

Now, uric acid is a natural waste product of purines, which are one of the building blocks of DNA and RNA. 

During their metabolism, purines are first degraded to hypoxanthine, which is then oxidized twice by xanthine oxidase; first to become xanthine, and then finally, to uric acid. 

Uric acid circulates in the bloodstream until it reaches the kidneys where it’s secreted into the proximal tubules, and eventually excreted in the urine. 

Now, hyperuricemia occurs when levels of circulating uric acid exceed normal levels, which is around 1.5-6 mg/dL for women and 2.5-8 mg/dL for men. 

Urate crystal deposition occurs when concentration of circulating uric acid exceeds its rate of solubility, which is about 6.8 mg/dL. 

Now, antigout medications are subdivided into two main groups: chronic gout medications, which are used to prevent the buildup of uric acid in the blood; and acute gout medications, which are used to reduce inflammation. 

Chronic gout medications include xanthine oxidase inhibitors, such as allopurinol and febuxostat; uricosuric medications, such as probenecid and sulfinpyrazone; and recombinant urate oxidases, such as rasburicase and pegloticase. 

On the other hand, acute gout medications include non-steroidal anti-inflammatory drugs (or NSAIDs), glucocorticoids, and colchicine.

Alright, let’s start with xanthine oxidase inhibitors. Allopurinol is a purine analog that works by competitive inhibition of xanthine oxidase. 

But, besides being an ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-steroidal_anti-inflammatory_drugs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hESMNv73RDWPAEMuiyLB1wbKRz6C5HOi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-steroidal anti-inflammatory drugs]]></video:title><video:description><![CDATA[Non-steroidal anti-inflammatory drugs or NSAIDs are mainly used to treat inflammation, pain, and fever. These conditions are related to an increased production of pro-inflammatory chemicals called prostaglandins.

NSAIDs work by decreasing the production of prostaglandins, thereby reducing inflammation, relieving pain, and reducing fever.

In order to understand how NSAIDs work, first we need to talk briefly about inflammation, which is the body’s response to a harmful stimulus, such as infection or injury. 

So, during inflammation, your immune cells use an enzyme called phospholipase A2 to take membrane phospholipids and make a 20-carbon polyunsaturated fatty acid, called arachidonic acid. 

Arachidonic acid is a substrate for an enzyme called cyclooxygenase or COX. 

The enzyme cyclooxygenase exists in two different isoforms: COX-1 and COX-2. 

COX-1 is a constitutive enzyme, meaning that it’s always active, while on the other hand, COX-2 is an inducible enzyme, meaning that it must be turned on to function. This is usually triggered by immune cells and vascular endothelial cells during inflammation. 

Both enzymes produce prostaglandin E2 (PGE2) and prostacyclin (PGI2), which cause vasodilation and attract different immune cells to the area. 

They also act on neurons that detect pain, called nociceptors, and make them more sensitive to stimuli by lowering their threshold for activation. 

Finally, they stimulate the hypothalamus to increase the body temperature, causing fever. 

Prostaglandin E2 also has other effects like causing uterine contractions, decreasing the secretion of acid, and increasing the production of protective mucus in the stomach.

So, in conditions such as inflammation, pain, or fever, NSAIDs can be used to inhibit cyclooxygenase and decrease the production of prostaglandins. 

Depending on how they interact with these enzymes, NSAIDs are subdivided into 2 main groups: irreversible COX inhibitors, like aspirin; and reversible COX ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoporosis_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/su37xKT-RzWumz0XbM7SpbEkQ5KWDKZ3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteoporosis medications]]></video:title><video:description><![CDATA[Osteoporosis medications are medications used to treat osteoporosis, which is a condition where decreased bone strength increases the risk of a broken bone. 

Osteoporosis is most commonly associated with the elderly, menopause, hyperparathyroidism, malabsorption, and with the use of some medications, like corticosteroids. 

So, the underlying cause of osteoporosis is an imbalance between bone resorption and bone formation, which are normal processes of bone remodeling. 

Now in bone remodeling, the process begins when osteoblasts sense micro fractures near their location. 

The osteoblasts produce a substance called RANKL, or receptor activator of nuclear factor κβ ligand, which binds to RANK receptors on the surface of nearby monocytes.

RANKL induces those monocytes to fuse together to form a multinucleated osteoclast cell.

RANKL also helps the osteoclast mature and activate so that they can start resorbing bones. 

The osteoclast starts secreting lysosomal enzymes, mostly collagenase, which digests the collagen protein in the organic matrix. This drills pits on the bone surface known as the Howship’s lacunae. 

Osteoclasts also start producing hydrochloric acid, or HCl, which dissolves hydroxyapatite into soluble calcium – Ca2+ and phosphate – PO42- ions, and these ions get released into the bloodstream. 

Moreover, osteoblasts and osteoclasts are controlled by two hormones: parathyroid hormone, which is released by parathyroid glands; and calcitonin, which is released by the thyroid gland. 

At low concentrations, parathyroid hormone works by stimulating the activity of osteoblasts, thereby promoting bone formation; while at high concentrations, parathyroid hormone stimulates bone resorption. 

On the other hand, calcitonin works by inhibiting osteoclast activity, thereby decreasing bone resorption. 

Alright, moving on to pharmacology! Osteoporosis medications are subdivided into two main groups: non-hormonal medications, which include bisphosphonat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticonvulsants_and_anxiolytics:_Barbiturates</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LfwUHoApSXC6MZLRFHQd58oqTa2bc2kY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticonvulsants and anxiolytics: Barbiturates]]></video:title><video:description><![CDATA[Barbiturates are a class of medications that are used as anticonvulsants to manage seizure disorders; to induce anesthesia in surgical procedures; as anxiolytics to relieve anxiety; and to manage insomnia. Barbiturates enhance the effect of gamma-aminobutyric acid, or GABA, which is the major inhibitory neurotransmitter in the brain, by binding to its receptor.

It’s pretty well-established that your brain’s really important. It controls your feelings, your movements, your sleep, your memory… It controls everything, whether you’re aware of it or not. The cells that make up our brain are called neurons. Neurons communicate with each other through neurotransmitters. When one neuron is stimulated, it’ll release excitatory neurotransmitters like glutamate, which bind to receptors on the next neuron. This causes the next neuron to depolarize and release its own excitatory neurotransmitters, propagating the signal throughout the brain.

Now, we also have inhibitory neurons that will shut down this chain of events. These neurons release the main inhibitory neurotransmitter in the nervous system, gamma-aminobutyric acid, or GABA, which binds to GABA receptors on other neurons. These receptors are large multi-unit complexes that form ligand-gated ion channels, which open up to let Cl- ions into the cell. The influx of negatively charged ions causes hyperpolarization, where the cell’s membrane potential becomes more negative, which means it’s much more difficult for it to depolarize and fire off an action potential, and that means it’s less responsive to stimuli.

Now, there are cases where neurons in the brain start sending out more excitatory signals than normal. This can occur due to either too much excitation by the excitatory neurotransmitters, or too little inhibition by the inhibitory neurotransmitters like GABA. Excessive excitatory signals can cause psychiatric disorders like anxiety, and neurological disorders like seizures and epilepsy.

Okay, so one way ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticonvulsants_and_anxiolytics:_Benzodiazepines</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WTSGPrtbRb2Y1zlQPW1yXw1GSQm2YwMy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticonvulsants and anxiolytics: Benzodiazepines]]></video:title><video:description><![CDATA[Benzodiazepines are a class of medications that act as a central nervous system depressant.  They have a wide variety of uses including anxiolytic effects, or to relieve anxiety; as anticonvulsants, or to manage seizure disorders; as a hypnotic for insomnia; as an anesthetic; and to treat withdrawal syndromes. They act by enhancing the main inhibitory neurotransmitter gamma-aminobutyric acid, or GABA, by binding to its receptor.  

It’s pretty well-established that your brain’s really important. It controls your feelings, your movements, your sleep, your memory… It controls everything, whether you’re aware of it or not. The cells that make up our brain are called neurons. Neurons communicate with each other through neurotransmitters. When one neuron is stimulated, it’ll release excitatory neurotransmitters like glutamate which bind to receptors on the next neuron. This causes the next neuron to depolarize and release its own excitatory neurotransmitters, propagating the signal throughout the brain.  

Now, we also have inhibitory neurons that will shut down this chain of events. These neurons release the main inhibitory neurotransmitter gamma-aminobutyric acid, or GABA, which binds to GABA receptors on other neurons. These receptors are large, multi unit complexes that form ligand-gated ion channels that open up to let Cl- ions into the cell. The influx of negatively charged ions causes hyperpolarization, where the cell’s membrane potential becomes more negative, which means it’s much more difficult for it to depolarize and fire off an action potential, meaning it’s less responsive to stimuli.  

Alright, now there are cases where neurons in the brain start sending out more excitatory signals than normal. This can occur due to either too much excitation by the excitatory neurotransmitters, or too little inhibition by the inhibitory neurotransmitters like GABA. Excessive excitatory signals can cause psychiatric disorders like anxiety, and neurological disor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/General_anesthetics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/p3qn9xHKRwSdlLI60Qi-O6f0SWOoHe_O/_.jpg</video:thumbnail_loc><video:title><![CDATA[General anesthetics]]></video:title><video:description><![CDATA[General anesthetics are medications used to induce an anesthetic state in patients who are about to go under surgery. 

The anesthetic state refers to a number of conditions that make surgery tolerable for the patient and more manageable for the surgeon. 

The conditions include: unconsciousness, where the person isn’t aware of themselves or their environment; sedation, so they don’t move in response to painful stimulation; analgesia, so they don’t feel pain; and amnesia, so they don’t remember the procedure.

Local anesthetics are different in the fact that they only block pain sensation in a specific part of the body, and don’t affect consciousness.  

Okay, to achieve the anesthetic state, general anesthetics depress the central nervous system. In other words, they diminish the total amount of action potentials that are constantly firing in the brain. The generation of these action potentials depends on excitatory and inhibitory synapses. 

Excitatory, means that the neurotransmitters released into the synaptic space stimulate the postsynaptic neuron to start an action potential. 

The main neurotransmitter involved is glutamate, which binds to postsynaptic NMDA receptors, so some general anesthetics work by blocking these receptors. 

Inhibitory synapses, on the other side, do the opposite; they release the inhibitory neurotransmitter called GABA, which binds to the postsynaptic neuron and keep it from firing. 

So certain anesthetics work by stimulating these GABA receptors or by increasing their sensitivity to GABA. 

Moving on, there are two main phases in anesthesia: induction, which is when the patient enters the anesthetic state; and maintenance, when the anesthetic state is prolonged for as long as required. 

Some anesthetics are better for induction, while others are better for maintenance. 

Now, depending on how they’re administered, there are two classes of general anesthetics: parenteral and inhalational anesthetics. 

Parenteral anestheti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Local_anesthetics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hvb1SjthSr23qlumusXYttqJSqG-1Fhm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Local anesthetics]]></video:title><video:description><![CDATA[Local anesthetics are medications used to reversibly block pain sensation in a specific part of the body in order to perform small surgical procedures. 

The common suffix for local anesthetics is -caine, like procaine, tetracaine, lidocaine, Michael Caine - no wait, that’s the actor. 

Anyway, so there are two classes of local anesthetics - called esters and amides.

Both classes inhibit conduction of action potentials across nerve fibers by blocking sodium (Na+) channels - and thus the perception of pain by the brain.

Pain is sensed by receptors called free nerve endings which are the 1st order neurons in the pain pathway. These neurons send their axons to synapse with 2nd order neurons in the spinal cord which carries the sensory information to the brain, and you feel pain. 

Free nerve endings can be triggered in several ways; by mechanical stimulation, like getting punched; by thermal stimulation like heat and cold; or by chemical stimulation from molecules like bradykinin and histamine. 

These noxious stimuli trigger the opening of cation channels on the membrane called transient receptor potential channels.  This allows Na+ and other positive ions to flow into the cell. The extra positive charge that flows in makes the cell less negative, - which is called depolarization. 

This depolarization causes nearby voltage-gated sodium channels to open up as well, setting off this chain reaction that continues down the entire length of the axon. 

Now, voltage-gated Na+ channels are unique because they have inactivation gates on the intracellular side. 

At resting membrane potential, the channel is closed. When the membrane depolarizes, the channel opens and sodium ions rush into the cell. A few milliseconds later, the  inactivation gate closes and blocks Na+ from entering the cell even though the channel is still open.  This ends the depolarization process.

Finally, when the cell repolarizes, the inactivation gate opens, the activation gate closes, and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Migraine_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zVIpT2jYS8SR6T-dZjpBOcOMQ2CDg58c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Migraine medications]]></video:title><video:description><![CDATA[Migraine medications include a wide variety of drugs used to treat a specific type of headache called migraine.

Migraines are the second most common primary headache. 

They’re often preceded by symptoms like irritability, depression, and fatigue that can begin hours to days before the headache itself. Sometimes there can be an aura where people experience strange smells, lights, visual disturbances, or even hallucinations before the onset of the migraine. 

The migraine itself usually feels like a pounding or pulsating, typically localized to one side of the head and can last from hours to days. 

As if this was not bad enough, these headaches tend to come with nausea and vomiting, irritability, and pain or discomfort with lights, sounds, and smells called photophobia, phonophobia, and osmophobia, respectively. 

During childhood, individuals can have nausea and vomiting without the headaches; and that’s called an abdominal migraine. 

After a migraine is over, it can leave people feeling sore at the location of the pain and generally fatigued. 

To remember the main features of migraines, you can use the mnemonic POUND, where P stands for pulsatile headache, O stands for one-day duration, U stands for unilateral, N for nausea, and D for disabling. 

Although the underlying mechanism causing migraines isn’t well understood, there are some clues. 

Concentrations of the neurotransmitter, serotonin, increase during the aura, triggering vasoconstriction, and then decrease to lower-than-normal levels during the migraine attack, triggering vasodilation. This change in the blood vessel size may be a trigger for pain receptors, causing the headache. 

The initial vasoconstriction may also trigger cortical spreading depression, which is a phenomenon when the brain becomes hypersensitive to certain stimuli like lights, sounds, and smells. 

Migraines are often associated with specific triggers like the smell of cigarette smoke, foods like chocolate or cheese]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nonbenzodiazepine_anticonvulsants</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c7iOWbprTiiTyd_faO9hymECQcu6Tadj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nonbenzodiazepine anticonvulsants]]></video:title><video:description><![CDATA[Anticonvulsants are a type of medication used to treat the various types of seizure disorders.  

These include benzodiazepines and barbiturates which increase the activity of inhibitory neurons, but there are also many other classes of anticonvulsants with different mechanisms that we’ll talk about in this video.

Okay, so the cells that make up our brain are called neurons. 

Neurons communicate with each other through neurotransmitters. 

When one neuron is stimulated, it releases excitatory neurotransmitters that bind to receptors on the next neuron. This causes the next neuron to depolarize and release its own excitatory neurotransmitters, propagating the signal throughout the brain.

The main excitatory neurotransmitter in our brain is glutamate which can bind to several types of receptors that are basically ligand-gated ion channels, which open up and allow  Na+ and Ca2+ to flow in, and K+ to flow out. 

In the end, when it’s all added up, there’s an influx of positive charge that makes the cell less negative,and the neuron becomes depolarized. This causes nearby voltage-gated Na+ channels to open on the surface of the membrane, causing more Na+ to enter. This in turn triggers other nearby voltage-gated Na+ channels to open.

So this series of depolarization travels down the neuron like a wave and it’s called an action potential.

When it reaches the end of the neuron, called the synaptic terminal, it triggers the opening of voltage-gated Ca2+ channels, causing an influx of calcium ions which stimulates the release of neurotransmitters that are stored in synaptic vesicles. 

Okay, we also have inhibitory neurons that shut down this chain of events. 

These neurons release the main inhibitory neurotransmitter called gamma-aminobutyric acid or GABA, which binds to GABA receptors on other neurons. 

These GABA receptors are also ligand-gated ion channels, but they open up to let the negatively charged Cl-, into the cell. 

The influx of negative ions c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuromuscular_blockers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E149d8EiT268yxpPybcPi38YSTS_tIZj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuromuscular blockers]]></video:title><video:description><![CDATA[Neuromuscular blockers are a class of medications that prevent acetylcholine from acting at the neuromuscular junction, which prevents the triggering of skeletal muscle contractions.

Okay, first things first. In order for a skeletal muscle to contract, your brain sends a signal, in the form of an action potential in an upper motor neuron. 

The upper motor neuron then activates a lower motor neuron in the spinal cord.

From here, the action potential is sent through an axon down to its ending branches, called axon terminals, to muscle fibers which they innervate.

The place where an axon terminal meets the muscle fiber is the neuromuscular junction. 

The neuromuscular junction has three main parts: a presynaptic membrane, which is the membrane of an axon terminal; a postsynaptic membrane, which is the membrane of a skeletal muscle fiber and is also called a motor end-plate; and a synaptic cleft, which is the gap between the presynaptic and postsynaptic membranes.

When an action potential reaches the axon terminal, synaptic vesicles that contain neurotransmitters, called acetylcholine, fuse with the cell membrane of the axon terminal, releasing the acetylcholine into the synaptic cleft. 

The acetylcholine then diffuses over to the motor end plate on the muscle fiber and binds to ligand-gated ion channels, also called nicotinic receptors.

When that happens, these ligand-gated ion channels open up, letting lots of sodium ions rush into the skeletal muscle fiber, and a few potassium ions leak out of the cell as well. But overall there’s an increase in positive charge on the inside of the muscle fiber causing it to depolarize. 

This causes the voltage-gated sodium ion channels on the membrane to open up, and there’s a huge influx of sodium ions into the muscle fiber. 

This leads to a generation of an action potential, which rapidly spreads along the entire membrane, causing the whole muscle fiber to contract. 

When the signal sent from the lower motor n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anti-parkinson_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8SyRlTAUS9i9j5jP6CVcEyZBSiqg2jsK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anti-parkinson medications]]></video:title><video:description><![CDATA[Anti-parkinson medications are used to treat Parkinson’s disease, which is a movement disorder where the dopamine-producing neurons in the substantia nigra of the brain undergo degeneration. It’s a progressive, adult-onset disease, and is more common with age, affecting about 1% of people over 60. The substantia nigra is a part of the basal ganglia, a collection of nuclei in the brain that control movement through their connections with the motor cortex. The substantia nigra actually can be split into two sub-regions. First, there’s the pars reticulata, which receives signals from another part of the basal ganglia called the striatum, and relays messages to the thalamus via neurons rich in the neurotransmitter GABA, also known as gamma-aminobutyric acid. Second, there’s the pars compacta, and this is the part of the substantia nigra affected in Parkinson’s. 

The pars compacta sends messages to the striatum via neurons rich in the neurotransmitter dopamine, forming the nigrostriatal pathway, which helps to stimulate the cerebral cortex and initiate movement. In Parkinson’s disease, the neurons in the substantia die, so the individual may experience hypokinesia, which is difficulty initiating movements, and bradykinesia, or slowed movements. The substantia nigra also helps to calibrate and fine tune a person’s movements, which leads to the other clinical features of Parkinson’s, like “pill-rolling” tremor, which is the repetitive, involuntary rubbing of the thumb and index finger, as well as rigidity, stooped posture, and an expressionless, mask-like face. As the neurodegeneration progresses, non-motor dysfunction can appear, including depression, dementia, sleep disturbances, and difficulty smelling. 

Now, in order to treat Parkinson’s disease we can use medications that directly or indirectly increase the stimulation of the dopamine receptors in the brain. Now within the brain, dopamine is found mainly in one of the four 4 dopamine pathways: the nigrostr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholinomimetics:_Direct_agonists</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IL2o8SbGSUO9WTKLDHA4P3LjQ1G6tWSM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholinomimetics: Direct agonists]]></video:title><video:description><![CDATA[The nervous system is divided into the central nervous system, that is the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. 

The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles, and the autonomic nervous system, which controls the involuntary activity of the smooth muscles and glands of our organs, and is further divided into the sympathetic and the parasympathetic nervous systems.

Parasympathetic neurons in the central nervous system project preganglionic fibers towards parasympathetic ganglia, which are collections of neurons near the organ they are supposed to affect.From there, postganglionic fibers project towards the target cell. 

Both the preganglionic and postganglionic neurons release the neurotransmitter acetylcholine. 

Acetylcholine released from preganglionic fibers acts on nicotinic receptors on the postganglionic neurons. 

And acetylcholine released from postganglionic neurons acts on muscarinic and nicotinic receptors on target organs.

Nicotinic receptors are coupled to ion channels that let sodium in and potassium out, causing depolarization. 

Muscarinic receptors are G-protein coupled receptors, which means they trigger secondary messenger proteins that activate a cascade of enzymes inside the cell. 

The physiologic effects of the muscarinic and nicotinic stimulation can be remembered with the mnemonic: DUMB HAVES, so defecation; urination; muscle excitation; bronchospasm; heart bradycardia; autonomic ganglia stimulation; vasodilation; eye miosis, which is constriction of the pupil, and eye accommodation, which is contraction of the ciliary muscles of the iris to facilitate looking at near objects; and secretions from the lacrimal, salivary and sweat glands as well as glands in the GI tract. 

Now, medications that directly act on muscarinic or ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholinomimetics:_Indirect_agonists_(anticholinesterases)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7PRePrTnRFiAEcUBL9f9BaDVSJm-lgow/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholinomimetics: Indirect agonists (anticholinesterases)]]></video:title><video:description><![CDATA[The nervous system is divided into the central nervous system, that is the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. 

The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles; and the autonomic nervous system, which controls the involuntary activity of the smooth muscles and glands of our organs, and is further divided into the sympathetic and parasympathetic nervous systems.

Parasympathetic neurons in the central nervous system project preganglionic fibers towards parasympathetic ganglia, which are collections of neurons near the organ they are supposed to affect. 

From there, postganglionic fibers project towards the target cell. 

Both the preganglionic and postganglionic neurons release the neurotransmitter acetylcholine.

Acetylcholine released from preganglionic fibers acts on nicotinic receptors on the postganglionic neurons. 

And acetylcholine released from postganglionic neurons acts on muscarinic and nicotinic receptors on target organs. 

Nicotinic receptors are coupled to ion channels that let sodium in and potassium out, causing depolarization. 

Muscarinic receptors are G-protein coupled receptors, which means they trigger secondary messenger proteins that activating a cascade of enzymes inside the cell. 

The physiologic effects of the muscarinic and nicotinic stimulation can be remembered with the mnemonic: DUMB HAVES, so defecation; urination; muscle excitation; bronchospasm; heart bradycardia; autonomic ganglia stimulation; vasodilation; eye miosis, which is constriction of the pupil, and eye accommodation, which is contraction of the ciliary muscles of the iris to facilitate looking at near objects; and secretions from the lacrimal, salivary, and sweat glands, as well as the glands in the GI tract. 

Now, medications that act on muscarinic or ni]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscarinic_antagonists</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2PRs4-aHStKhjBZH90qZspF8Si6QkouQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscarinic antagonists]]></video:title><video:description><![CDATA[Muscarinic antagonists, or antimuscarinic medications, are a class of medications that prevent muscarinic receptors of the parasympathetic nervous system from getting stimulated by acetylcholine.

Okay, first things first, the nervous system is divided into the central nervous system, so the brain and spinal cord; and the peripheral nervous system. 

The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles; and the autonomic nervous system, which is further divided into the sympathetic and parasympathetic nervous systems, and controls the involuntary movement of the smooth muscles, and the glands of our organs.

Now, the autonomic nervous system is made up of a relay that includes two neurons. 

We’ll focus on just the parasympathetic nervous system. 

Signals for the parasympathetic nervous system start in the hypothalamus. 

These hypothalamic neurons synapse with nuclei in the brainstem or spinal cord, which send out signals to preganglionic neurons that travel to the rest of the body. 

Their targets are the parasympathetic ganglion, which consist of many postganglionic neuron cell bodies and are located nearby or directly in the target organs. 

The postganglionic neurons extend the rest of the way to the target cell, where they release the neurotransmitter acetylcholine, which is why they are also called cholinergic neurons. 

Acetylcholine binds to a type of receptor, known as muscarinic receptors, on the cells of target organs, which allow the parasympathetic nervous system to trigger a ‘rest and digest’ response, meaning that it keeps body-energy use as low as possible to stimulate activities like digestion.

It acts in the heart, slowing the heart rate and reducing the cardiac output. 

In the gastrointestinal tract, it increases its motility to stimulate digestion and defecation. 

In the bladder, it causes constriction of the bladder muscle, called the detrusor muscl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Opioid_agonists,_mixed_agonist-antagonists_and_partial_agonists</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G6NEPp82RtKTVymxbyPX_sACTcuQ8L3B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Opioid agonists, mixed agonist-antagonists and partial agonists]]></video:title><video:description><![CDATA[Opioid medications are used mainly to control pain. Some of them are also used to treat diarrhea and cough. When treating pain, the goal should be to use short-acting opioids at the lowest effective dose for the shortest duration possible, and slowly increase the dose only as needed.   

As a class, opioids share one thing in common – they bind to opioid receptors in the brain, spinal cord, and gastrointestinal tract. Some are endogenous, meaning they are produced naturally by the body, like endorphins, named for “endogenous morphine” due to their similar effects in the body. But others are exogenous, meaning they come from outside the body, like heroin and morphine, which come from the opium poppy; a flowering plant that oozes a milky white liquid. 

To understand how opioids work, let’s zoom in on a region of the spinal cord that has opioid receptors. Normally, in the absence of endorphins, nociceptive fibers carry pain signals from the body to the dorsal, or posterior, horn of the spinal cord, where they release neurotransmitters like glutamate, substance P and calcitonin gene-related peptide. These neurotransmitters cause pain signals to be transmitted to the brain via ascending pain pathways. 

Now, let’s say someone goes to play a rigorous game of badminton. Exercise releases endorphins, which activate the three major opioid receptors located on neurons called the mu, kappa, and delta receptors.  

As endorphins or other opioids bind to these receptors on the presynaptic terminals of nociceptive fibers, they inhibit the opening of calcium channels, preventing calcium influx, and thereby blocking the release of pain-causing neurotransmitters like glutamate, substance P and calcitonin gene-related peptide.  

At the same time, endorphins also bind to postsynaptic neurons,  

opening potassium channels here, leading to hyperpolarization and decreased excitability of the neuron. These effects together reduce the transmission of pain signals to the brain.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Opioid_antagonists</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/91gcduREQQ_jxQrCz8gjSONhSDuroj4s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Opioid antagonists]]></video:title><video:description><![CDATA[Opioid antagonists, like the name suggests, are medications that block opioid receptors. They’re used mainly to urgently reverse the side effects of opioid agonists and to help individuals who are recovering from opioid use disorder.  

Now, opioids work by binding to opioid receptors in the brain, spinal cord, and gastrointestinal tract. Some are endogenous, meaning they are produced naturally by the body, like endorphins, named for “endogenous morphine” due to their similar effects in the body. But others are exogenous, meaning they come from outside the body, like heroin and morphine, which come from the opium poppy; a flowering plant that oozes a milky white liquid. 

To understand how opioids work, let’s zoom in on a region of the spinal cord that has opioid receptors. Normally, in the absence of endorphins, nociceptive fibers carry pain signals from the body to the dorsal, or posterior, horn of the spinal cord, where they release neurotransmitters like glutamate, substance P and calcitonin gene-related peptide. These neurotransmitters cause pain signals to be transmitted to the brain via ascending pain pathways.   

Now, let’s say someone goes to play a rigorous game of badminton. Exercise releases endorphins which activate the three major opioid receptors located on neurons, called the mu, kappa, and delta receptors. As endorphins or other opioids bind to these receptors on the presynaptic terminals of nociceptive fibers, they inhibit the opening of calcium channels, preventing calcium influx, and thereby blocking the release of pain-causing neurotransmitters like glutamate, substance P and calcitonin gene-related peptide. At the same time, endorphins also bind to postsynaptic neurons, opening potassium channels here, leading to hyperpolarization and decreased excitability of the neuron. These effects together reduce the transmission of pain signals to the brain.  

Now, opioids also have action on the body’s dopaminergic, noradrenergic, and se]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atypical_antidepressants</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6XcY6gxpSzq2I6UfdATd1o0OR1m82hSQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atypical antidepressants]]></video:title><video:description><![CDATA[Atypical antidepressants are mainly used to treat major depressive disorder. This disorder causes a persistent feeling of sadness and loss of interest in everyday activities. Even though the exact cause of depression is still unknown, there&amp;#39;s some evidence that suggests it’s related to low levels of neurotransmitters like serotonin, norepinephrine, and dopamine. Typical antidepressants like selective serotonin reuptake inhibitors or tricyclic antidepressants work by increasing the levels of serotonin and norepinephrine, while atypical antidepressants often have multiple mechanisms of action.  

All right, now within the brain, there are many different types of neurons, but we’re going to focus only on three: serotonergic neurons, which produce serotonin; noradrenergic neurons, which produce norepinephrine; and dopaminergic neurons, which produce dopamine. Each of these neurons synthesizes and stores their neurotransmitters in small vesicles. So, when an action potential reaches the presynaptic membrane, these vesicles fuse with the membrane, releasing neurotransmitters into the synaptic cleft. Once released, serotonin (or 5-HT) binds to 5-HT2 receptors on the postsynaptic membrane, thereby increasing neural stimulation, and regulating mood, feeding, and reproductive behavior. On the other hand, norepinephrine binds to norepinephrine receptors on the postsynaptic membrane, boosting alertness. And finally, dopamine binds to dopamine receptors, thereby stimulating cognitive functions, motivation, and awakeness.

As long as there’s a high enough concentration of neurotransmitters in the synaptic cleft, the postsynaptic neurons will continue to fire. Now, serotonergic neurons on their presynaptic membrane have serotonin transporters (or SERT); noradrenergic neurons have norepinephrine transporters (or NET); while dopaminergic neurons have dopamine transporters (or DAT). These membrane proteins transport neurotransmitters from the synaptic cleft back in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atypical_antipsychotics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H-eNxg25RmKE3GNc32ehGYheTxCZtg2V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atypical antipsychotics]]></video:title><video:description><![CDATA[Antipsychotics, as their name implies, are mainly used to treat schizophrenia and other psychotic conditions. 

Even though the exact cause of schizophrenia is still unknown, there&amp;#39;s some evidence that suggests it’s related to altered levels of the neurotransmitter dopamine.

Now, antipsychotics are subdivided into two main categories: the first generation or typical antipsychotics, and the second generation or atypical antipsychotics. 

Alright, within the brain, dopamine is found in 4 main dopamine pathways: the mesolimbic pathway, which controls motivation and desire; mesocortical pathway, which helps regulate emotions; nigrostriatal pathway, which contains motor neurons that bypass the medullary pyramids, to control involuntary movements and coordination; and lastly, tuberoinfundibular pathway, which releases dopamine to limit the secretion of prolactin. 

Other regions of the central nervous system that are rich in dopamine receptors, include the chemoreceptor trigger zone, which initiates the vomiting reflex; and the medullary periventricular pathway, which regulates eating behavior. 

However, in schizophrenia, altered levels of dopamine mainly affect the mesolimbic pathway and mesocortical pathway.

There’s usually high levels of dopamine in the mesolimbic pathway, which cause positive symptoms of schizophrenia, such as delusions, hallucinations, and disorganized thought. 

On the other hand, low levels of dopamine in the mesocortical pathway cause negative symptoms of schizophrenia, such as lack of motivation, social withdrawal and “flat affect”, which basically means lack of emotions.

Now, in conditions such as schizophrenia, atypical antipsychotics block dopamine D2 receptors in the mesolimbic pathway, thereby alleviating positive symptoms of schizophrenia. 

But, they also block serotonin 5-HT2A receptors in the mesocortical pathway. 

These receptors are found on inhibitory neurons that regulate dopaminergic neurons and decrease dopa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psychomotor_stimulants</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fkl20WzTTk64tkKck4UKquhGQUC2xu1N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psychomotor stimulants]]></video:title><video:description><![CDATA[Psychomotor stimulants are drugs that stimulate the central nervous system to increase motor activity and to produce euphoria, excitement, and a feeling of having lots of energy. 

Unfortunately, some drugs of abuse, like methamphetamine or cocaine, belong to this class of substances. 

However, there are a few medications in this class that do have clinical applications so let’s go over those.

To understand how psychomotor stimulants work, let’s zoom in on one of the synapses of the brain. 

Normally electrical signals, or action potentials, travel down the axon to the axon terminal, where they trigger the release of chemical messengers, called neurotransmitters, from synaptic vesicles into the synapse. 

The neurotransmitters travel across the synapse and bind to receptors on the postsynaptic neuron, where they give the cell a message. 

After the neurotransmitters have done their job, they unbind from the receptors, and can: diffuse away, get degraded by enzymes, or get picked up by proteins and returned to their original release site in a process called reuptake.

Psychomotor stimulants, in general, increase the release of certain neurotransmitters, but their biggest effect is blocking reuptake receptors on presynaptic axon terminals. 

Both actions keep neurotransmitters - like dopamine, norepinephrine, and serotonin - in the synapse longer, and increases their effects.

For example, increased concentrations of dopamine in the brain’s reward pathway, which includes the nucleus accumbens, ventral tegmentum, and prefrontal cortex, produce intense feelings of euphoria, pleasure, and the emotional “high” associated with psychomotor stimulants.

The physical “high” or feeling of hyper-stimulation is caused by increased norepinephrine concentrations throughout the brain, which produces a variety of effects throughout the body like increased energy, constricted blood vessels, dilated pupils, increased body temperature, increased heart rate, and increased bl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Monoamine_oxidase_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9aSqHVaKSLCfJB0EmjC3mJ4fQXaxv886/_.jpg</video:thumbnail_loc><video:title><![CDATA[Monoamine oxidase inhibitors]]></video:title><video:description><![CDATA[Monoamine oxidase inhibitors, or MAOIs, are a class of medications used in the treatment of depression, which is a mood disorder that causes a persistent feeling of sadness and loss of interest in everyday activities. 

Even though the exact cause of depression is still unknown, there is some evidence that suggests it’s related to low levels of serotonin, norepinephrine, and dopamine, which are also called monoamines because they have only one amine group. 

Now, monoamine oxidase inhibitors work by increasing levels of serotonin, norepinephrine, and dopamine, which helps to alleviate the symptoms of depression. 

Alright, now within the brain, there are many different types of neurons, but we’re going to focus only on three: serotonergic neurons that release serotonin, noradrenergic neurons that release norepinephrine, and dopaminergic neurons that release dopamine. 

Each of these neurons synthesizes and stores neurotransmitters in small vesicles, so when an action potential reaches the presynaptic membrane, these vesicles fuse with the membrane, releasing neurotransmitters in the synaptic cleft.

Serotonergic neurons release serotonin, which then binds to 5-HT2 receptors, thereby increasing neural stimulation and regulating mood, feeding, and reproductive behavior. 

On the other hand, noradrenergic neurons release norepinephrine, which hooks up to norepinephrine receptors (NE receptors), boosting alertness and focus. 

Lastly, dopaminergic neurons release dopamine, which binds to dopamine receptors,  stimulating cognitive functions, motivation, and awakeness. 

As long as there’s a high enough concentration of neurotransmitters in the synaptic cleft, the postsynaptic neurons will continue to fire. 

Now, each of these presynaptic neurons has small reuptake proteins, which pump the neurotransmitters from the synaptic cleft back into presynaptic neurons. 

Once inside the neuron, a class of enzymes called monoamine oxidases will break down some of these ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Serotonin_and_norepinephrine_reuptake_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2ImBkEdpQ4u3Ra8ycyD3Hi1iTY_st6Rb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Serotonin and norepinephrine reuptake inhibitors]]></video:title><video:description><![CDATA[Serotonin norepinephrine reuptake inhibitors, or SNRIs, are mainly used to treat major depressive disorder.  This disorder causes a persistent feeling of sadness and loss of interest in everyday activities. Even though the exact cause of depression is still unknown, there&amp;#39;s some evidence that suggests it’s related to low levels of neurotransmitters like serotonin, norepinephrine, and dopamine. Serotonin norepinephrine reuptake inhibitors work by increasing the levels of serotonin and norepinephrine to alleviate the symptoms of depression.

Alright, now within the brain, there are many different types of neurons, but we’re going to focus only on two: serotonergic neurons which produce serotonin, and noradrenergic neurons which produces norepinephrine. Each of these neurons synthesizes and stores their neurotransmitters in small vesicles. So, when an action potential reaches the presynaptic membrane, these vesicles fuse with the membrane, releasing neurotransmitters in the synaptic cleft. Once released, serotonin or 5-HT binds to 5-HT2 receptors on the postsynaptic membrane, thereby increasing neural stimulation and regulating mood, feeding, and reproductive behavior. On the other hand, norepinephrine binds to norepinephrine receptors on the postsynaptic membrane, boosting alertness. As long as there’s a high enough concentration of neurotransmitters in the synaptic cleft, the postsynaptic neurons will continue to fire. Now, serotonergic neurons on their presynaptic membrane have serotonin transporters or SERT, while noradrenergic neurons have norepinephrine transporters or NET. These membrane proteins transport the serotonin and norepinephrine in the synaptic cleft back into presynaptic neurons. This leads to decreased neurotransmitter concentration within the synaptic cleft, causing the postsynaptic neurons to stop firing. 

So, in conditions such as major depressive disorder, where there are low levels of serotonin and norepinephrine, SNRIs can b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Selective_serotonin_reuptake_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aHBpg6tPQieZmw2xatLrZuD_Qn_f32_P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Selective serotonin reuptake inhibitors]]></video:title><video:description><![CDATA[Selective Serotonin Reuptake inhibitors, or SSRIs, are mainly used to treat major depressive disorder.  This disorder causes a persistent feeling of sadness and loss of interest in everyday activities. Even though the exact cause of depression is still unknown, there&amp;#39;s some evidence that suggests it’s related to low levels of neurotransmitters like serotonin, norepinephrine, and dopamine. Selective serotonin reuptake inhibitors work by increasing the levels of serotonin to alleviate the symptoms of depression.

Now, serotonin is a neurotransmitter that helps regulate mood, emotions and feeding behavior.  Presynaptic serotonergic neurons use the amino acid tryptophan to synthesize serotonin, which is also called 5-hydroxytryptamine, or 5-HT. Once synthesized, serotonin is stored in small vesicles within the presynaptic neuron. When an action potential reaches the presynaptic membrane, the vesicles fuse with the membrane and release the serotonin into the synaptic cleft.  The serotonin drift around until they bind to 5HT2 receptors on the postsynaptic neuron, and cause it to fire off its own action potential.  As long as there’s a high enough concentration of serotonin in the synaptic cleft, the postsynaptic neuron will continue to fire. On the presynaptic neuron, there are serotonin reuptake transporters or SERTs. This protein functions like a little trap door on the cell membrane; when a sodium, a chloride and a serotonin binds to the surface of this protein on the extracellular side, it flips over and sends the serotonin and the ions into the cell.  When a potassium ion binds to the protein on the intracellular side, the trapdoor resets again, so more serotonin can attach. This way, serotonin is taken back into the presynaptic neuron, its concentration in the synaptic cleft decreases, and the postsynaptic neuron stops firing.

Now, in conditions such as major depressive disorder, where there’s a low serotonin level, selective serotonin reupt]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tricyclic_antidepressants</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_qjYYYj_QwGZF_9ODojSAgJoQYGK8s6M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tricyclic antidepressants]]></video:title><video:description><![CDATA[Tricyclic antidepressants, or TCAs, are mainly used to treat major depressive disorder. 

This disorder causes a persistent feeling of sadness and loss of interest in everyday activities. 

Even though the exact cause of depression is still unknown, there&amp;#39;s some evidence that suggests it’s related to low levels of neurotransmitters like serotonin, norepinephrine, and dopamine. 

Tricyclic antidepressants work by increasing the levels of serotonin and norepinephrine to alleviate the symptoms of depression.

Alright, now within the brain, there are many different types of neurons, but we’re just going to focus on two: serotonergic neurons which produce serotonin, and noradrenergic neurons which produces norepinephrine.

Each of these neurons synthesizes and stores their neurotransmitters in small vesicles. 

So, when an action potential reaches the presynaptic membrane, these vesicles fuse with the membrane, releasing neurotransmitters into the synaptic cleft. 

Once released, serotonin or 5-HT binds to 5-HT2 receptors on the postsynaptic membrane, thereby increasing neural stimulation and regulating mood, feeding, and reproductive behavior. 

On the other hand, norepinephrine binds to norepinephrine receptors on the postsynaptic membrane, boosting alertness. 

As long as there’s a high enough concentration of neurotransmitters in the synaptic cleft, the postsynaptic neurons will continue to fire. 

Now, serotonergic neurons, on their presynaptic membrane, have serotonin transporters or SERT, while noradrenergic neurons have norepinephrine transporters or NET. 

These membrane proteins transport the serotonin and norepinephrine in the synaptic cleft back into presynaptic neurons. 

This leads to decreased neurotransmitter concentration within the synaptic cleft, causing the postsynaptic neurons to stop firing. 

So, in conditions such as major depressive disorder, tricyclic antidepressants can be used to increase the levels of serotonin and nor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Typical_antipsychotics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KMOQO4dLQ3ymAAv3Q9hUySj7RpCz9ctl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Typical antipsychotics]]></video:title><video:description><![CDATA[Antipsychotics, as their name implies, are mainly used to treat schizophrenia and other psychotic conditions. Even though the exact cause of schizophrenia is still unknown, there&amp;#39;s some evidence that suggests it’s related to altered levels of the neurotransmitter dopamine. Now, antipsychotics are subdivided into two main categories: the first generation or typical antipsychotics, and the second generation or atypical antipsychotics. 

Alright, within the brain, dopamine is found in 4 main dopamine pathways: the mesolimbic pathway, which controls motivation and desire; the mesocortical pathway, which helps regulate emotions; the nigrostriatal pathway, which contains motor neurons that bypass the medullary pyramids, to control involuntary movements and coordination; and lastly, the tuberoinfundibular pathway, which releases dopamine to limit the secretion of prolactin. Other regions of the central nervous system that are rich in dopamine receptors include the chemoreceptor trigger zone, which initiates the vomiting reflex, and the medullary periventricular pathway, which regulates eating behavior. 

However, in schizophrenia, altered levels of dopamine mainly affect the mesolimbic pathway and mesocortical pathway. There’s usually high levels of dopamine in the mesolimbic pathway which cause positive symptoms of schizophrenia, such as delusions, hallucinations, and disorganized thought. On the other hand, low levels of dopamine in the mesocortical pathway cause negative symptoms of schizophrenia, such as lack of motivation, social withdrawal, and “flat affect,” which basically means a lack of emotions.

When it comes to treating schizophrenia, some typical antipsychotics like haloperidol, trifluoperazine, and fluphenazine have a  higher potency, which means you need less of it to achieve a therapeutic effect. The lower potency antipsychotics include thioridazine and chlorpromazine and they require larger doses to achieve the same therapeutic effect a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Loop_diuretics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0M3pn1NmRhS5ZL6Wx-6I_wvNSAKb2j7u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Loop diuretics]]></video:title><video:description><![CDATA[Diuretics are medications that act on the kidneys to increase production of urine - and therefore, eliminates water from the body. There are 5 main types of diuretics - carbonic anhydrase inhibitors; osmotic diuretics; thiazide and thiazide-like diuretics; potassium sparing diuretics; and last but not least, loop diuretics - which we’ll get intimately acquainted with during this video. 

Now, the basic unit of the kidney is called a nephron, and each nephron is made up of a glomerulus, which filters the blood. Blood enters the glomerulus with the afferent arteriole, and exits the glomerulus from the efferent arteriole. The filtered content then goes through the renal tubule, where excess waste, and molecules (such as ions and water), are removed or filtered through an exchange between the tubule and the peritubular capillaries. So the renal tubule plays a huge role in secretion and reabsorption of fluid and ions - such as sodium, potassium, and chloride - in order to maintain homeostasis, or the balance of fluid and ions in our body. The renal tubule has a few segments of its own: the proximal convoluted tubule; the U-shaped loop of Henle, with a thin descending, a thin ascending limb, and a thick ascending limb; and finally, the distal convoluted tubule, which empties into the collecting duct, which collects the urine. 

Different kinds of diuretics act on different segments of the renal tubule. Now, loop diuretics - as you might have guessed - act on the loop of Henle. To be more specific, they mainly target the thick ascending limb. The thick ascending limb is impermeable to water and it is lined with cuboidal cells that have Na+K+2Cl- cotransporters on the apical surface. These transporters reabsorb sodium, potassium, and chloride from inside the thick ascending limb back into the blood. As such, they shuttle one sodium into the cell, down its concentration gradient, and that powers the movement of one potassium and two chlorides into the cell as well.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmotic_diuretics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jnwca9ryRY2rBgFE9QfGJpvXTJugeZ0t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osmotic diuretics]]></video:title><video:description><![CDATA[Diuretics are medications that act on the kidneys to increase production of urine, and therefore, elimination of water from the body. 

There are 5 main types of diuretics: carbonic anhydrase inhibitors; loop diuretics; thiazide and thiazide-like diuretics; potassium sparing diuretics; and last but not least, osmotic diuretics - which we’ll get intimately acquainted with during this video. 

Now, the basic unit of the kidney is called a nephron, and each nephron is made up of a glomerulus, which filters the blood. The filtered content goes through the renal tubule, where excess waste, and molecules (such as ions and water), are removed or filtered through an exchange between the tubule and the peritubular capillaries. So the renal tubule plays a huge role in secretion and reabsorption of fluid and ions - such as sodium, potassium, and chloride - in order to maintain homeostasis - or the the balance of fluid and ions in our body. 

The renal tubule has a few segments of its own: the proximal convoluted tubule; the U-shaped loop of Henle, with a thin descending, a thin ascending, and a thick ascending limb; and finally, the distal convoluted tubule, which empties into the collecting duct, which collects the urine. 

The prototypal osmotic diuretic is mannitol; other osmotic diuretics like glycerin and isosorbide are rarely used. 

Following IV administration, mannitol travels through the bloodstream and acts like you’d expect an osmotically active molecule to act: it sucks water out of the cells it encounters along the way, and all that extra water reaches the kidneys as increased renal blood flow. 

Once at the kidneys, it gets secreted by the glomerulus into the renal tubule. Some of the segments of the renal tubule, like the proximal convoluted tubule and the thin descending limb, are freely permeable to water. So any osmotic agent that ends up here will tend to make water stay inside the tubule, rather than be reabsorbed. 

Now, this increased volume lea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Potassium_sparing_diuretics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o_xt93dRRQ6Hq__NFtg32QbKTCKby3vM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Potassium sparing diuretics]]></video:title><video:description><![CDATA[Diuretics are medications that act on the kidneys to increase production of urine, and to eliminate water, certain metabolic wastes, and electrolytes from the body. 

There are 5 main types of diuretics; carbonic anhydrase inhibitors, osmotic diuretics, thiazide and thiazide-like diuretics, loop diuretics,, and last but not least, potassium sparing diuretics - which is the only class of diuretic that retains potassium, rather than wasting it. 

Now, the basic unit of the kidney is called a nephron, and each nephron is made up of a glomerulus, which filters the blood. T. 

The filtered content then goes through the renal tubule, where excess waste, and molecules, such as ions and water, are removed or filtered through an exchange between the tubule and the peritubular capillaries. 

So the renal tubule plays a huge role in secretion and reabsorption of fluid and ions - such as sodium, potassium, chloride, and magnesium - in order to maintain homeostasis - or the balance of fluid and ions in our body. 

The renal tubule has a few segments of its own: the proximal convoluted tubule, the U-shaped loop of Henle, with a thin descending, a thin ascending limb, and a thick ascending limb, and finally, the distal convoluted tubule, which empties into the collecting duct, which collects the urine. 

Different kinds of diuretics act on different segments of the renal tubule. Now, potassium sparing diuretics act on the cortical collecting tubules. Here, there are principal cells and α-intercalated cells dispersed amongst the tubule cells. 

The principal cell has two pumps on the apical surface, an ATP-dependent potassium pump that pushes potassium into the tubule, and an epithelial sodium channel pump, called ENaC for short, that pulls sodium into the cell. 

There’s also a Na/K ATPase pump on the basolateral surface that again moves 2 potassium ions into the cell for every 3 sodium ions out. 

Now, the alpha intercalated cells mainly get rid of hydrogen ions from th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thiazide_and_thiazide-like_diuretics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4e7pRGepQ_WeG9JzGoc7_aOpS620ux7w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thiazide and thiazide-like diuretics]]></video:title><video:description><![CDATA[Diuretics are medications that act on the kidneys to increase production of urine, therefore elimination of water from the body. 

There are 5 main types of diuretics - carbonic anhydrase inhibitors, osmotic diuretics, loop diuretics, potassium sparing diuretics, and last but not least, thiazide and thiazide-like diuretics - which we’ll get intimately acquainted with during this video.

Now, the basic unit of the kidney is called a nephron, and each nephron is made up of a glomerulus, which filters the blood. The filtered content goes through the renal tubule, where excess waste and molecules, such as ions and water, are removed or filtered through an exchange between the tubule and the peritubular capillaries.

So the renal tubule plays a huge role in secretion and reabsorption of fluid and ions - such as sodium, potassium, and chloride, in order to maintain homeostasis - or the balance of fluid and ions in our body. 

The renal tubule has a few segments of its own: the proximal convoluted tubule; the U-shaped loop of Henle, with a thin descending, a thin ascending, and a thick ascending limb; and finally, the distal convoluted tubule, which empties into the collecting duct, which collects the urine.

Alright, so thiazide and thiazide-like diuretics are taken perorally, and once in the blood, they travel to the kidneys where they are secreted by the proximal convoluted tubule into the lumen of the renal tubule. 

An important point to make here is that they are secreted by the same secretory system that secretes uric acid into the tubule, so they compete with the secretion of uric acid, therefore increasing uric acid levels in the blood. 

Next, they travel along with the filtrate until they reach the distal convoluted tubule. This part of the nephron is lined by epithelial cells. 

Now, on the luminal side of these cells, there’s a nifty little sodium-chloride transporter. This channel reabsorbs one sodium and one chloride ion together from the tubule, i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Estrogens_and_antiestrogens</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TqkWYzNLT9CZ51o61saej-V4To2JS45T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Estrogens and antiestrogens]]></video:title><video:description><![CDATA[Synthetic estrogens are a class of medications that act like natural estrogens and are mainly used for primary hypogonadism, primary amenorrhea, estrogen deficiency, and as contraceptives. 

Now, antiestrogens, or estrogen antagonists include full antagonists, which antagonize natural estrogens in all tissues, and selective estrogen receptor modulators, or SERMs, which act as estrogen antagonists in some tissues but also act as estrogen agonists in others. 

Full antagonists and SERMs are used for breast cancer, and SERMs are also used for osteoporosis.

But first let’s talk a bit about natural estrogen, which plays a big role in the menstrual cycle. 

The hypothalamus, which is part of the brain, secretes gonadotropin-releasing hormone, or GnRH, which travels to the nearby pituitary gland and stimulates it to secrete two hormones follicle stimulating hormone, or FSH, and luteinizing hormone, or LH.

FSH and LH make the ovarian follicles, which are scattered throughout the ovaries, develop and secrete the female sex hormones, estrogens and progesterone. 

These hormones gradually increase during the first 2 weeks of the cycle, called the follicular phase, but estrogen is the main hormone synthesized during this phase. 

The high estrogen levels stimulate the thickening of the endometrium, the growth of endometrial glands, and the emergence of spiral arteries from the basal layer. 

The high estrogen levels also make the pituitary more sensitive to the actions of hypothalamic GnRH, acting as a positive feedback signal, and at the end of the follicular phase, it leads to a massive surge of FSH and LH that leads to ovulation where one of the follicles releases an ovocyte. 

Okay, now the 2 weeks following ovulation is called the luteal phase, where the follicle that released the oocyte becomes the corpus luteum. 

This structure mainly synthesizes progesterone which helps maintain the uterine lining so a fertilized oocyte can implant.

Other than the menstrua]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Progestins_and_antiprogestins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tzfr81fCQ0ing2SImwLRaijzSDymRK5y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Progestins and antiprogestins]]></video:title><video:description><![CDATA[Progestins are a group of synthetic progestogens that have similar effects to those of natural progesterone.

They can be divided into two categories: the progesterone derivatives and the testosterone derivatives. 

They are mainly used as contraceptives, in hormone replacement therapy, or HRT, and in the treatment of various gynecologic conditions. 

Now, antiprogestins act as progesterone antagonists and include mifepristone and ulipristal. 

Mifepristone is used for medical abortion while ulipristal is used as an emergency contraceptive. 

The hypothalamus secretes gonadotropin-releasing hormone, or GnRH, which travels to the nearby pituitary gland and stimulates it to secrete two hormones, follicle stimulating hormone, or FSH, and luteinizing hormone, or LH. 

During the two weeks following ovulation, which is referred to as the ovarian luteal phase, the remnant of the ovarian follicle becomes the corpus luteum, which is made up of luteinized theca and granulosa cells, meaning that these cells have been exposed to the high luteinizing hormone levels that occur just before ovulation. 

The luteinized cells secrete more progesterone than estrogen and progesterone becomes the dominant hormone.

Under the influence of progesterone, the uterus enters into the secretory phase of the endometrial cycle.

During this time, spiral arteries continue to grow, and the endometrial glands continue to produce more secretions that make the endometrium more receptive to the implantation of a fertilized gamete.

After day 15 of the cycle, the optimal window for fertilization begins to close and the corpus luteum gradually degenerates into the nonfunctional corpus albicans. 

The corpus albicans doesn’t make hormones, so estrogen and progesterone levels slowly decrease.

When progesterone reaches its lowest level, the spiral arteries collapse and the functional layer of the endometrium prepares to shed during menstruation. 

This shedding marks the beginning of a new mens]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Uterine_stimulants_and_relaxants</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4YznTcpxSf6KOqREV5svv83wTp6Mrndf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Uterine stimulants and relaxants]]></video:title><video:description><![CDATA[Uterine stimulants and relaxants, as their names suggest, are medications used to induce or inhibit contractions of the uterus. 

Uterine stimulants are also called uterotonics, because they increase the tone of the muscles of the uterus. 

They’re mainly used to induce or facilitate labor, to reduce postpartum hemorrhage, and to induce abortion. 

Uterine relaxants are also called tocolytics, where ‘toco-’ refers to childbirth, and ‘-lytic’ means to terminate. 

They’re used to stop premature labor inorder to give time for the fetal lungs to mature.

So, the uterus is a super important organ in the female body, because not only does it allow the development of the baby during pregnancy, but it also generates the force necessary to push out that tiny human during labor. 

This force results from the muscle contractions that take place in the middle layer of the uterus, the myometrium.

The regulation of these muscle contractions happens at the cellular level, and it all comes down to the activity of myosin light-chain kinase by calcium ions. 

This enzyme phosphorylates myosin, inducing muscle contraction. 

On the other hand, this enzyme can be turned off via phosphorylation by protein kinase A, which causes the muscles to relax. 

Now, during labor, uterine contractions become stronger and more frequent. 

Normally, this happens at some point when the fetus is considered full term, which means all their organs are functional and it’s able to live outside mommy’s womb.  This typically happens between 37 and 42 weeks’ gestation.

Sometimes labor doesn’t start even though it’s been more than 42 weeks. In these cases, it should be induced by the administration of uterine stimulants which include oxytocin, ergonovine, and prostaglandins. 

In other situations the baby, the mother, or both, are at risk if the pregnancy continued.  

These include fetal growth restriction, isoimmunization, premature rupture of the membranes, pre-eclampsia, or eclampsia.  

Uter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aromatase_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZACaqN2ZQPyi1BPpd_pxzZnjQeWerAQT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aromatase inhibitors]]></video:title><video:description><![CDATA[Aromatase inhibitors, or AIs, are a type of medication used to treat breast cancer in postmenopausal people. However, they should only be used if the breast cancer is positive for estrogen receptors.

Breast cancer, or breast carcinoma, is an uncontrolled growth of epithelial cells within the breast. It’s the most common cancer in female individuals, and the second leading cause of cancer deaths after lung cancer. 

Breasts are made up of 15 to 20 lobules, and inside each of these lie a bunch of grape-like structures called the alveoli. Zooming in on the alveoli, there’s a layer of alveolar cells that secrete breast milk into the lumen, which is the space in the center of the gland. These alveolar cells have receptors for certain hormones like, estrogen and progesterone, which are released by the ovaries, and prolactin which is released by the pituitary gland. These hormones stimulate the alveolar cells to divide and increase in number, which makes the lobule enlarge. 

Just like healthy alveolar cells, some breast cancer cells have hormone receptors that allow them to grow in the presence of the hormones. When breast cancer cells have estrogen receptors, the cancer is called an ER-positive carcinoma. In this case, hormonal therapy is useful for adjuvant treatment, and includes medications which block the formation or effects of estrogen.

Aromatase inhibitors block the formation of estrogen by inhibiting the aromatase enzyme that converts androgen to estrogen. Now, before menopause, estrogen is mainly synthesized by the ovaries, where there’s a lot of androgen waiting to be converted. And the amount of aromatase enzyme in the ovary depends on the stimulation by gonadotropin. So, even if we gave this medication to premenopausal people with breast cancer, gonadotropin would induce synthesis of more aromatase, which would synthesize more estrogen. However, in postmenopausal people, estrogen is synthesized by other tissues, like the adrenal glands and fat tis]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/PDE5_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xFHEdB4_Q32kfhhAww8GaaqEQoexsZN3/_.jpg</video:thumbnail_loc><video:title><![CDATA[PDE5 inhibitors]]></video:title><video:description><![CDATA[Phosphodiesterase type 5, or PDE5, inhibitors are a class of medications used to treat erectile dysfunction and pulmonary hypertension. 

As their name implies, they inhibit the PDE5 enzyme in endothelial cells, which allows for smooth muscle relaxation and thus, promotes blood vessel dilation. 

They include sildenafil, vardenafil, and tadalafil.  

Alright, first, let’s focus on the structure of blood vessels. 

Blood vessels have three layers, also called “tunics,” or coverings, that surround the vessel lumen, the hollow part of the vessel that contains the blood.

The innermost tunic is the tunica intima, which includes the endothelial cells; the next one is the tunica media, or middle tunic, which is mostly made of smooth muscle cells and sheets of elastin protein; and finally, there’s the tunica externa, or outside tunic, which is made up of loosely woven fibers of collagen. 

Moreover, the tunica media can contract, causing vasoconstriction, where the lumen gets a lot smaller; or it can relax, or vasodilate, causing the lumen’s diameter to increase, allowing for more blood flow. 

Now, within endothelial cells of the tunica intima, there’s an enzyme called nitric oxide synthase, which uses the amino acid L-arginine and molecular oxygen to synthesize nitric oxide or NO for short. 

Once synthesized, nitric oxide diffuses to adjacent smooth muscle cells in the tunica media, where it binds and activates an enzyme called guanylyl cyclase. 

This enzyme converts guanosine triphosphate, GTP, into cyclic guanosine monophosphate, cGMP, which is a second messenger that induces relaxation of smooth muscle cells in vessel walls. 

Alright, now the cGMP-specific phosphodiesterase type 5, or PDE5, is an enzyme found in various tissues, mainly in the corpus cavernosum of the penis and the retina. 

It’s also found in lower concentrations in other tissues including platelets, vascular and visceral smooth muscle, and skeletal muscle. 

Recently it’s been discovered]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antihistamines_for_allergies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lyzOKPDZTIW23vPJ_5fbXeTuQRmQw4v1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antihistamines for allergies]]></video:title><video:description><![CDATA[Antihistamines for allergies, also known as H1 blockers, are medications that are primarily used to treat allergic reactions, such as urticaria, angioedema, and allergic rhinitis. 

These conditions are related to an increased release of histamine. 

Now, H1 blockers work by blocking the effects of histamine in tissues that have H1 receptors, thereby alleviating symptoms of allergic reactions. 

In order to understand how antihistamines work, first we need to talk briefly about histamine and allergic reactions. 

Histamine is a small molecule that’s mainly produced by mast cells and basophils. 

Once released, they cause local inflammation and vasodilation. However, they are also present in the brain as neurotransmitters, and they are produced by enterochromaffin cells in the stomach to increase gastric acid secretion. 

Okay, so in order to develop an allergic reaction, an allergen, say pollen, needs to enter the body and cause the activation of B cells. 

Activated B-cells produce IgE antibodies that get released into the bloodstream and bind to mast cells. 

The mast cells are now “primed,” meaning that if pollen enters the body again in the future, the mast cells degranulate and release their histamine into the local tissue. 

Now, there are 4 types of histamine receptors: H1, H2, H3, and H4 receptors. 

Since we’re going to talk about antihistamines for allergies, we’re going to focus only on histamine H1 receptors. 

These receptors are predominantly found on endothelial cells, smooth muscle cells, sensory nerve endings, and in the brain. 

On endothelial cells, stimulation of H1 receptors, causes blood capillaries to dilate and become leaky, eventually leading to redness and edema. 

On the flip side, on smooth muscle cells in the lungs, stimulation of H1 receptors results in bronchoconstriction, while on sensory nerve endings leads to pain and itching. 

Finally, in the brain, H1 receptors promote wakefulness and appetite suppression.

No]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_corticosteroids_and_mast_cell_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yP_0pNzITpS8FV1Ixzp-E2nTQxiFRt4t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary corticosteroids and mast cell inhibitors]]></video:title><video:description><![CDATA[In obstructive lung diseases like asthma, where individuals suffer from reversible narrowing of the airways, medications like bronchodilators are helpful in keeping the airways open. 

But, most of the times, narrowing of the airways actually occurs as a result of inflammation and excessive release of various inflammatory chemical mediators like leukotrienes and prostaglandins. 

So, to effectively manage the disease, it’s important to give medications that will control the inflammation.   

So, if we take a look at the lungs, you’ve got the trachea, which branches off into right and left bronchi, and then continues to branch into thousands of bronchioles. 

In the bronchioles you’ve got the lumen, the mucosa, which includes the inner lining of epithelial cells, as well as the lamina propria which contains many cells like the type 2 helper cells, B cells, and mast cells. 

Surrounding the lamina propria, there is a layer of smooth muscles and submucosa. 

The submucosal layer contains mucus-secreting glands and blood vessels. 

Now, the molecular pathway that leads to asthma is actually pretty complex, but it is often initiated by an environmental trigger.

Allergens from environmental triggers, like  air pollutants or cigarette smoke, are picked up by dendritic cells which, present them to a type 2 helper cell or Th2 cell in the lamina propria. 

These cells then produce cytokines like IL-4 and IL-5 which causes the inflammatory response. 

IL-4 is especially important because it leads to the production of IgE antibodies by B-cells, and these antibodies bind to FcεR1 receptors on mast cells to activate them. 

These mast cells use an enzyme called phospholipase A2 to take membrane phospholipids and make a 20 carbon polyunsaturated fatty acid called arachidonic acid. 

Arachidonic acid is then metabolized by two important enzymes: one is cyclooxygenase-2 or COX-2, which makes prostaglandins, another one is 5-lipoxygenase or  5-LOX, which makes leukotrienes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchodilators:_Beta_2-agonists_and_muscarinic_antagonists</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nTva7YekTQyLuaUtDOOmdvVTRliN9PPQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchodilators: Beta 2-agonists and muscarinic antagonists]]></video:title><video:description><![CDATA[In obstructive lung diseases like asthma, where individuals suffer from reversible narrowing of the airways, medications like bronchodilators are helpful in keeping the airways open.

Now, based on their mechanism of action, bronchodilators can be broadly divided into four main groups;  β2-agonists, muscarinic antagonists, leukotrienes antagonist and methylxanthines. 

In this video, we will focus on the bronchodilators like β2-agonist and muscarinic antagonist which mimics or inhibits the regulatory effects of the autonomic nervous system on bronchial smooth muscle.

So, if we take a look at the lungs, you’ve got the trachea, which branches off into right and left bronchi, and then continues to branch into thousands of bronchioles.

In the bronchioles you’ve got the lumen, the mucosa, which includes the inner lining of epithelial cells, as well as the lamina propria which contains many cells like the type 2 helper cells, B cells, and mast cells.

Surrounding the lamina propria, there is a layer of smooth muscles and submucosa. These muscles are innervated by the nerves of the autonomic nervous system, which means they can’t be controlled consciously. 

The autonomic nervous system is made up the sympathetic system which is involved in the “fight or flight” response, like running from angry raccoons, and parasympathetic system which is involved in the “rest and digest” response, like taking a nap after a big dinner. 

So let’s say that racoons are chasing you, the sympathetic nerves activates and release norepinephrine which bind to  β2 adrenergic receptors on the smooth muscles in the respiratory tract, causing them to relax.  The diameter of the airways increase and more oxygen gets to the lungs. 

When you’re resting, there’s less need for the extra oxygen, so the parasympathetic nerves release acetylcholine, which bind to muscarinic M3 receptors in the respiratory tract, causing smooth muscle contraction and narrowing the airways.  

Now, in conditions]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lithium</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rS5iEJsLTje086goGcG71VeYQ4isOWXl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lithium]]></video:title><video:description><![CDATA[Lithium is mainly used for the treatment of bipolar disorder, which is a mental health condition characterized by periods of lowered mood and depression; as well as periods of heightened mood and mania. Although the mechanism of action is not well understood, lithium acts as a mood stabilizer, that can smooth out the highs and lows they experience.  

Alright, almost everyone has ups and downs throughout their life. They can feel happy on a sunny day or a bit down when it’s raining outside. They might also have some extreme highs, like when they meet the love of their life, and they might even have some pretty serious lows after losing a job or a person they were close to.  

However, in bipolar disorder, which used to be called manic depression, the individual has dramatic shifts in emotions, mood, and energy levels, involving extreme lows and extreme highs. These shifts usually happen over several days or weeks.  

The low moods are identical to those in major depressive disorder, also known as unipolar depression. Individuals with this feel hopeless and discouraged; have a lack of energy and mental focus; and have physical symptoms, like eating and sleeping too much or too little. But along with these lows, they have periods of high moods as well, which are called manic episodes or hypomanic episodes, depending on their level of severity. In a manic state, people feel energetic; overly happy and optimistic; or even euphoric with really high self-esteem.  

And on the surface, these might seem like very positive characteristics, but when an individual is in a full manic episode, these symptoms can reach a dangerous extreme. Patients experiencing mania can behave recklessly, they can have pressured speech, where they talk constantly at a rapid-fire pace, or they might have racing thoughts, and feel as if they don’t need sleep. Manic episodes also include delusions of grandeur, for example they might believe that they are on a personal mission from God, or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/von_Hippel-Lindau_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_ivncDphRgqny9FuTMlLCK7BQIaCfmXh/_.jpg</video:thumbnail_loc><video:title><![CDATA[von Hippel-Lindau disease]]></video:title><video:description><![CDATA[Von-Hippel Lindau or VHL is a genetic disease that affects people of all ethnicities and is characterized by tumor development in the CNS, kidneys, adrenal glands and pancreas. 

Okay, the VHL gene is a tumor suppressor gene on the short arm of chromosome 3. 

It codes for proteins that degrade hypoxia-inducible transcription factor, or HIF. HIF upregulates genes that code for platelet-derived and vascular endothelial growth factors, both of which promote new blood vessel formation and cell growth.

In VHL disease, this tumor suppressor gene is mutated which increases HIF, PDGF, VEGF, and ultimately the risk of tumor  formation. 

VHL disease is about as common as Huntington Disease, occurring in 1 in 36,000 people. 

It is inherited in an autosomal dominant pattern, meaning that a VHL patient has a 50% chance of passing it on to each kid they have. 

20% of VHL patients have a de novo or new mutation, meaning they are the first VHL patient in their family. 

Alright, the most common tumor type in VHL is hemangioblastoma, a benign blood vessel tumor  occurring in about 60% of VHL patients. 

In the central nervous system, these can occur in the retina, brain, and spinal cord.  

In the eyes, it can cause blindness by detaching the retina. 

In the brain and spinal cord, a tumor or the accompanying cyst causes problems when it pushes against surrounding tissue. 

For example, if the tumor is in the cerebellum, it can cause ataxia, or the loss of balance. 

If it blocks the flow of cerebrospinal fluid, intracranial pressure can rise causing headaches, nausea, and vomiting. 

Less common are benign cysts and cyst-like tumors called cystadenomas. 

The most concerning, occurring in ~25% of VHL patients, is the endolymphatic sac tumor of the inner ear which can cause deafness. 

Cystadenomas can develop in the broad ligament in women, and the epididymis in men, and incidental cysts can occur in the liver, lung, kidney and pancreas in both men and women. 

Some tumors associated with VHL can be cancerous.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Erb-Duchenne_palsy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-m91QF1DRIiJoL9DT9jMDhJHSaC1Vk01/_.jpg</video:thumbnail_loc><video:title><![CDATA[Erb-Duchenne palsy]]></video:title><video:description><![CDATA[Erb-Duchenne palsy, is named after the neurologists Wilhelm Erb and Duchenne de Boulogne who first described it.  

In this disorder, there’s paralysis to the muscles of the shoulder and the upper arm, and it happens when the nerves that innervate these muscles are damaged. 

People with this disorder have their arm stuck in a position that looks like a waiter discreetly trying to get a tip, so it’s also called waiter’s tip deformity.

Okay, so the nervous system has two parts: the central nervous system, which consists of the brain, brainstem, and spinal cord, and the peripheral nervous system, which includes all of the nerves that fan out from the central nervous system. 

Broadly speaking, the nervous system is split into an afferent and an efferent division. 

The afferent division brings sensory information from sensory receptors in the peripheral nervous system to the central nervous system, and the efferent division sends motor information from the central nervous system to organs like skeletal muscles, which causes them to contract.   

Now, part of the peripheral nervous system are spinal nerves, which branch off the spinal cord. 

There are 31 pairs of spinal nerves, which are grouped into eight pairs of cervical nerves, twelve pairs of thoracic nerves, five pairs of lumbar nerves, five pairs of sacral nerves, and one pair of coccygeal nerves.

The brachial plexus is a network of spinal nerves that innervate the shoulder, arm, and hand, by supplying afferent or sensory nerve fibers from the skin, as well as efferent or motor nerve fibers to the muscles. 

In terms of anatomy, the brachial plexus is divided into five roots, which come from the last four cervical nerves; C5, C6, C7, and C8,  as well as the first thoracic nerve or T1. 

The five roots will then combine to form three trunks: C5 and C6 merge to form the superior or upper trunk, C7 remains as the middle trunk, and C8 and T1 merge to form the inferior or lower trunk. 

These trunks then]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Klumpke_paralysis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l-QYiGCaQr2imvkmy4pFCcg1S2a8JrWP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Klumpke paralysis]]></video:title><video:description><![CDATA[Klumpke’s palsy, named after the neuroanatomist Augusta Déjerine-Klumpke who first described it, is when there is muscle paralysis in the hand, caused by nerve damage. This causes all the fingers to stay in a flexed position so it’s also called “total claw hand.”

Now, we have 31 pairs of spinal nerves which branch off the spinal cord.  

These are grouped into eight pairs of cervical nerves, twelve pairs of thoracic nerves, five pairs of lumbar nerves, five pairs of sacral nerves, and one pair of coccygeal nerves.

Now, some of the cervical and thoracic nerves form the  brachial plexus, which is a network of nerves that controls the muscles and sensations in the shoulder, arm, and hand. 

In terms of anatomy, the brachial plexus is divided into five roots, which come from the last four cervical nerves -  C5, C6, C7, and C8 - as well as the first thoracic nerve or T1. 

The five roots combine to form three trunks: C5 and C6 merge to form the superior or upper trunk, C7 remains as the middle trunk, and C8 and T1 merge to form the inferior or lower trunk. 

These trunks then form six divisions, which will regroup with each other to form three cords. 

These cords give off five terminal branches. 

The main three are the median nerve - which is made up of contributions from C5, C6, C7, C8, and T1 - the radial nerve, which is made up of contributions from C5, C6, C7, C8, and T1, and finally, the ulnar nerve, which is made up of contributions from C8, T1, and occasionally C7.

Klumpke’s palsy occurs when there’s a stretch or tear at the the C8 or T1 roots, or at the lower trunk. This happens when an abducted arm is pulled further away from the body. 

In infants, this could happen when the baby is pulled out of the birth canal by the arm during delivery. 

In adults a trauma to the shoulder, like when someone tries to grab a tree branch while falling, can cause the nerves to be torn. This leads to dysfunction of the median and ulnar nerves since they contain fi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rheumatoid_arthritis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zaXgtFpOTIqrSR-E0woyt1qSR7Gc7zSj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rheumatoid arthritis: Clinical]]></video:title><video:description><![CDATA[Rheumatoid arthritis is a chronic inflammatory disorder that gradually affects synovial joints, but can also cause extra-articular disease as well. Rheumatoid arthritis has been linked to HLA-DR1 and HLA-DR4. Each time there’s a flare, there’s an increase in synovial and immune cells, and over time, that results in a thick, swollen synovial membrane with granulation tissue - called a pannus. The pannus can damage cartilage and other soft tissues and also erode bone. Typically, rheumatoid arthritis affects at least three joints, generally ones in the hands and feet. The disease tends to be symmetric, progressive, and over time it causes joint deformities like crooked fingers.

So the typical articular manifestations in rheumatoid arthritis are pain, swelling, and loss of mobility in the affected joints, but doesn’t usually cause redness or warmth because the inflammatory process is so gradual. Usually, there’s morning stiffness that improves after 30 minutes of movement. The most frequent sites of involvement are the proximal interphalangeal joints and metacarpo-phalangeal joints of the hand, whereas the distal interphalangeal joints is rarely involved because there’s very little synovium in that joint. When these joints are affected, it typically causes reduced grip strength.  

In the feet, usually the metatarsophalangeal joints are affected, and it causes a person to bear more weight on the heels and hyperextend the toes. Other joints that can be involved are the wrists, elbows, shoulders, knees, and ankles. Hip involvement usually only happens later in the disease, and that can cause pain in the groin, thigh, or low back. One very dangerous spot is the C1-C2 joint, which is only synovial joint in the spine. When it’s affected it can cause neck pain, and if it’s not managed properly it can lead to spinal cord compression and tetraplegia. 

The system inflammation in rheumatoid arthritis results in cytokines that can cause extra-articular symptoms. For ex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Methemoglobinemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lXX8vkuaREWLPCtRJydIR2jCQdy9ZEHB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Methemoglobinemia]]></video:title><video:description><![CDATA[Methemoglobinemia is a disorder characterized by elevated levels of methemoglobin in the blood, which leads to tissue hypoxia. 

Normally, our red blood cells are loaded with millions of copies of a protein called hemoglobin.

Each hemoglobin protein is made of four globin subunits, each with an iron containing heme group.

Oxygen can bind to the iron molecule, so each hemoglobin molecule can bind four molecules of oxygen. 

The iron molecules, called ferrum in latin, are usually in the ferrous state, which means that the iron atom has lost two electrons to form Fe2+. 

When iron is in the ferrous state, it can bind oxygen easily when it reaches the lungs, and release oxygen easily when it reaches the other tissues in the body that need oxygen.  

Now, methemoglobin is an oxidized form of hemoglobin, and is normally spontaneously formed in our blood in small amounts. 

In methemoglobin, one of the iron molecules is in the ferric state, which means that the iron atom has lost three electrons, instead of two, to form Fe3+. 

The heme with the Fe3+ is like the lazy co-worker with a decreased ability to bind oxygen. 

The other three heme groups still have iron in the Fe2+ state, and they try to compensate for the slacker by binding to oxygen more tightly. 

However, this ends up being more harmful than helpful, as it prevents them from releasing oxygen to the tissues. 

Too much methemoglobin can eventually lead to tissue hypoxia, so in order to protect ourselves, we have a few enzyme systems that convert methemoglobin to normal hemoglobin. 

The most important one is cytochrome b5 reductase, also known as methemoglobin reductase, because it uses a NADH as a reducing agent to donate electrons to an iron in the Fe3+ state and reduces it to the Fe2+ state. So it’s like the boss that comes by to make the lazy heme productive again. 

This enzyme is found in red blood cells and other cells like neutrophils, and helps to keep the level of methemoglobin in our bloo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Slipped_capital_femoral_epiphysis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8uaiWf7STqSyegwDKmr5EiJsRguEO9tP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Slipped capital femoral epiphysis]]></video:title><video:description><![CDATA[Slipped capital femoral epiphysis, is a common hip disorder in adolescence, in which the growth plate fractures. 

The result is a slippage between the neck of the femur and the overlying head of femur also called the capital or epiphysis. 

Normally, a growing femur has 4 main parts. 

There’s the diaphysis, which is the long and hard part also called the shaft of the bone, and it extends to the metaphysis, at the level of the femoral neck. 

Above the femoral neck, lies the cartilaginous growth plate also called the physis. 

The cartilaginous growth plate has cells which divide and enable the bone to grow in length. 

These cells are very active in adolescence and they enable a growth spurt.

During this period, the growth plate is relatively weak and vulnerable to shearing forces. 

Eventually, the cartilaginous growth plate ossifies and fuses with the epiphysis. This happens around the age of 16 in females, and 19 in males. 

Now, before the growth plate ossifies, it’s supported by the perichondrial ring, which is dense connective tissue that extends from the metaphysis to the epiphysis. 

The perichondrial ring helps resist shearing forces so that the femoral head and the femoral neck don’t slip away from one another.

You see - the ball-shaped head of the femur comes and sits within the cup-shaped socket called the acetabulum. 

This makes a ball and socket type of joint, which is kept stable by tough fibrous joint capsule, and a rope-like ligament known as the ligamentum teres. 

The ligamentum teres arises from the base of the acetabulum known as the acetabular fossa, and it attaches to the fovea capitis, the depression found on the tip of the femoral head.

Around the femoral neck there are epiphyseal blood vessels that supply the cells of the femoral head with nourishment.

In slipped capital femoral epiphysis, the perichondrial ring becomes too weak to resist the shearing forces between the femoral head and the femoral neck, causing the two to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/albinism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PyJK0NtwQMuX_3G5aAHysk5ISNKqMrW6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Albinism]]></video:title><video:description><![CDATA[Albinism, meaning white, is a non-contagious, congenital condition that is defined by a drastic reduction or complete lack of pigmentation in the hair, skin and eyes. 

Albinism is often portrayed negatively, like Silas the antagonist in the book “The Da Vinci Code”, which contributes to his diminished quality of life with the disease. 

The skin is divided into three layers--the epidermis, dermis, and hypodermis. 

The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. 

Just above is the dermis, which contains hair follicles, nerves and blood vessels. 

And just above, the outermost layer of skin, is the epidermis. 

The epidermis itself has multiple cell layers that are mostly keratinocytes - which are named for the keratin protein that they’re filled with. 

Keratin is a strong, fibrous protein that allows keratinocytes to protect themselves from getting destroyed when you rub your hands through the sand at the beach.

Keratinocytes start their life at the deepest layer of the epidermis called the stratum basale, or basal layer, which is made of a single layer of small, cuboidal to low columnar stem cells that continually divide and produce new keratinocytes that continue to mature as they migrate up through the epidermal layers.

But the stratum basale also contains another group of cells - melanocytes, which secrete a protein pigment, or coloring substance, called melanin. 

Melanin is actually a broad term that constitutes several types of melanin found in people of differing skin color. 

These subtypes of melanin range in color from black to reddish yellow and their relative quantity and rate at which they are metabolized define a person’s skin color.

When keratinocytes are exposed to the sun, they send a chemical signal to the melanocytes, which stimulates the melanocytes to produce melanin through a multistep enzymatic reaction that begins with tyrosine. 

Once it’s made, the melanocytes move the mel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Systemic_lupus_erythematosus_(SLE):_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JsRmPkJUTAaPtuMhr3uTA25YTqWC4s9N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Systemic lupus erythematosus (SLE): Clinical]]></video:title><video:description><![CDATA[Systemic Lupus Erythematosus, or lupus, is an autoimmune disease, where essentially any tissue or organ can be the target of inflammation. 

Often there are periods of illness, called flares, and periods of remission during which there are few symptoms.

The diagnosis of lupus is made when 4 or more out of 11 criteria are met. 

The first three have to do with the skin. 

The first is a malar rash, sometimes just called a “butterfly rash”, which is a rash over the cheeks that spares the nasolabial folds and appears after sun exposure. 

Second is a discoid rash, which is chronic erythematous rash in sun-exposed areas like the arms and legs that are plaque-like or patchy redness and can scar.

Third, is a general photosensitivity of the skin — essentially a catch-all category for other rashes that happen to sun-exposed areas — typically only lasting a couple of days. 

Lupus can also damage the inner membrane or mucosa of various tissues, so the fourth criteria is ulcers in the mouth or nose. 

The fifth criteria is serositis which is inflammation of the serosa, which is like the outer membrane of an organ or tissue.

It can manifest as pleuritis, which is inflammation of the lining around the lungs and chest cavity; as pericarditis, which is inflammation of the lining of the heart; or as peritonitis, which is inflammation of the lining of the abdomen.

Now, in addition to pericarditis, it’s worth noting that lupus can also cause inflammation of the myocardium, leading to myocarditis, or the endocardium, leading to Libman-Sacks endocarditis, where clumps of fibrin and immune cells form vegetations on the mitral valve. 

The sixth criteria is arthritis, and two or more joints have to get inflammed to meet the criteria. 

The seventh criteria is evidence of kidney damage based on protein or cells in the urine. 

It’s generally caused by lupus nephritis, which is a type of glomerulonephritis due to immune complex deposition along the glomerular basement membra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lung_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XsYuDC4sR_yQp80Kni_OKoE3TGyyeM4f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lung cancer: Clinical]]></video:title><video:description><![CDATA[Lung cancer is the leading cause of cancer death worldwide in both males and females. It’s broadly classified into non-small cell lung cancer; accounting for 85% of all lung cancers, and small cell lung cancer, accounting for the remaining 15%. 

Small cell lung cancers are centrally located in the lung. Non-small cell lung cancer is further subclassified into four subtypes, the most common one is adenocarcinoma, which usually develops at the periphery of the lung. There’s also the term bronchoalveolar carcinoma which refers to adenocarcinoma-in-situ, which is where the adenocarcinoma tumor isn’t quite as aggressive and hasn’t yet crossed the basement membrane. The other 3 subtypes of non-small cell cancer include squamous cell carcinoma and carcinoid tumors; which are usually centrally located, as well as the rare large cell carcinoma; which can be located either centrally or peripherally.

Now the most important risk factor for the development of lung cancer is tobacco smoking, which accounts for more than 90% of cases. This usually comes in the form of cigarettes, but also includes cigars, pipes, and hookah, also called shisha. There is a dose-dependent linear relationship between the pack-years - the number of cigarette packs per day times the number of years of smoking - and the risk of lung cancer. Second-hand smoking, which is involuntarily inhaling tobacco smoked by other people, also increases the risk of lung cancer. 

Additionally individuals exposed to asbestos for a long period of time such as those working in shipbuilding or construction industry, are also at increased risk. Although classically associated with mesothelioma, which is a malignancy of the pleura, asbestos more commonly causes adenocarcinoma. Other risk factors include radon exposure, which is found in high concentrations in basements, as well as exposure of chest radiation, such as in treatment of lymphoma.

Individuals with lung cancer typically present with symptoms or are as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pericardial_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c46qJMBGR6yw2mMbtlVlJm0VTNWfmdCW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pericardial disease: Clinical]]></video:title><video:description><![CDATA[The pericardium is a sac that covers the heart and the roots of the great vessels. 

The pericardium has two layers, an inner serous layer and an outer fibrous layer, and the space between the two layers is the pericardial cavity. 

The pericardial cavity is normally filled with about 50 mL of serous fluid that cushions the heart from any kind of external jerk or shock - like a shock absorber. 

The pericardium also fixes the heart to the mediastinum, to prevent it from twisting, so that the big vessels don’t get pinched shut. 

Pericardial disease is inflammation of the pericardium due to a variety of causes - from infections, to autoimmune disorders, cancer, and trauma. 

In pericarditis, the pericardium is inflamed and irritated. 

If the inflammation leads to the accumulation of excess fluid in the pericardial sac then it’s called a pericardial effusion, and in its worst form, that extra fluid can cause tamponade physiology. 

Finally, there’s constrictive pericarditis, which is where the inflammation is chronic and leads to fibrosis. 

In pericarditis, the two inflamed layers of the pericardium rub against one another every time the heart beats. This causes severe, sharp retrosternal chest pain, that radiates to the neck, shoulders, and back, and it typically happens with each breath during inspiration. 

That’s because in inspiration the lungs expand, filling the thoracic cavity and compressing the pericardium. 

The pain typically worsens when a person is supine and improves when a person is sitting upright and leaning forward. 

Upon auscultation, there’s a pericardial friction rub, which is a scratchy, grating, high-pitched rub resembling the sound of leather-on-leather rubbing against each other.

On ECG, there’s widespread ST segment elevation in several leads, which distinguishes it from the ST elevation in myocardial infarction which is only present in the leads that correspond to the infarcted tissue.

Also, a very specific ECG find]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronary_steal_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bwO8tU5zSim9x8r9e9XK37kETfOPJnIS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronary steal syndrome]]></video:title><video:description><![CDATA[Coronary steal syndrome is a condition that occurs due to dilation of coronary arteries in the presence of coronary artery disease, which is when there’s a partial or complete blockage in the lumen of another coronary artery. 

The result is a redirection of blood flow from heart muscle supplied by the blocked artery, to other regions of the heart. 

Coronary steal syndrome is a finding observed during a pharmacological cardiac stress test, which is used to diagnose coronary artery disease. 

Now, the heart pumps out blood for all of our organs and tissues to use - but the heart also needs blood. 

So it also pumps blood to itself, through the coronary arteries on the outside of the heart. 

And coronary arteries are linked to one another through teeny tiny blood vessels called collateral vessels, which are normally in an inactive state, meaning blood doesn’t flow through them. 

Now, with coronary artery disease, there’s ischemia, or reduced blood flow to the region of myocardium supplied by that artery. 

In this context, collateral circulation may become active. For example, let’s say two coronary arteries, 

A and B, are linked by a collateral vessel, and coronary artery B has developed a block. 

As a result of ischemia, in the myocardium supplied by coronary artery B, the myocardial cells don’t receive enough oxygen, which is called hypoxia. 

In response to hypoxia, myocardial cells release signalling molecules called cytokines, which cause dilation of the segment of coronary artery B beyond the blockage. 

This slightly improves the blood flow and ameliorates hypoxia.  

But at the end of the day, blood flow within coronary artery B is still decreased, while blood flow in coronary artery A remains the same. 

This creates a pressure gradient across the collateral vessel, which pulls blood from the region of higher pressure, of coronary artery A, through the collateral vessel, and into the region of lower pressure, or the dilated segment of coronary]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastroesophageal_reflux_disease_(GERD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kJxv6FjxTKatlylgMtsm12qjTvCOTHHW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastroesophageal reflux disease (GERD)]]></video:title><video:description><![CDATA[Gastro- refers to the stomach, esophageal stands for esophagus, and reflux means “to flow back”.

So gastroesophageal reflux disease, or GERD, is when stomach acid flows back into the esophagus. 

The presence of acid in the esophagus can lead to Barrett’s esophagus, a serious complication of GERD where the normal mucosa of the esophagus is replaced by one that’s similar to that of the intestines. 

Barrett’s esophagus poses a higher risk of developing esophageal adenocarcinoma.

Normally, the wall of the entire gastrointestinal tract is made of 4 layers: the inner mucosa, the submucosa, a muscular layer, and an outer layer called the adventitia. 

The mucosa is further divided into three layers - an innermost epithelial layer, a middle layer called the lamina propria, and an outermost layer, in contact with the submucosa, called the muscularis mucosae, which is made up of smooth muscle that contracts and helps with the breakdown of food. 

Now, the stomach mucosa is different from the esophageal mucosa. 

Inside the stomach, the epithelial layer is made up of cylindrical cells, which dive into the lamina propria, forming pits. 

These pits are the gastric glands, and there are many of them scattered throughout the stomach. 

Distributed among the cylindrical gland cells, there’s different types of secretory cells. 

First, there’s G cells, which are a type of neuroendocrine cells that secrete a hormone called gastrin in response to food entering the stomach. 

Gastrin stimulates another type of cells, the parietal cells, to release hydrochloric acid. 

And then, there’s chief cells, which secrete an enzyme called pepsinogen.

Hydrochloric acid and pepsinogen are useful for digestion, but they can be quite aggressive for the delicate mucosa. 

Luckily though, the stomach also has some defense mechanism in place.

First, the gastric glands also have foveolar cells, also called surface mucus cells, because they are closer to the surface of the stomach, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G9gByvt6SG_6JpFrVrQpB-gnRsmZvQLX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal cancer]]></video:title><video:description><![CDATA[Esophageal cancer is when malignant or cancerous cells arise in the esophagus. This cancer can appear in any segment of the esophagus and it’s further classified into squamous cell carcinoma and adenocarcinoma - depending on the type of cells it originates from. Squamous cell carcinoma, as you can tell by its name, arises from squamous epithelium. On the other hand, adeno- means gland. So, adenocarcinoma arises from columnar glandular epithelium. Esophageal cancer is generally considered a poor prognosis cancer, because it doesn&amp;#39;t cause symptoms until later stages.

The esophagus is a long tube going from the pharynx to the stomach, and it’s connected to the pharynx through the upper esophageal sphincter, and to the stomach through the lower esophageal sphincter. Both relax during swallowing to allow the passage of food or liquids. Additionally, the lower esophageal sphincter is tightly closed between meals to prevent acid reflux. Now, the esophageal wall has four layers - from the outside in, these are the adventitia ; the muscular layer; the submucosa and the mucosa. The mucosa comes into direct contact with food, and it protects the esophageal wall from friction. The mucosa also has three layers of its own: a layer made of stratified squamous epithelium; a layer of connective tissue, called the lamina propria; and a layer of muscle cells, called the muscularis mucosae. Finally, at the lower esophageal sphincter, the squamous epithelium joins the columnar gastric epithelium to form the gastroesophageal junction. 

Now, squamous cell carcinoma is the most common type of esophageal cancer worldwide, and it originates in the squamous epithelium of the esophagus, most often in the upper two thirds. When this epithelium is repeatedly exposed to risk factors like alcohol, cigarette smoke, or hot fluids, it gets damaged, so the squamous cells divide to replace the old damaged cells. With each division, there is a risk that a mutation can occur in ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastric_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mYn6ZkyYRGWMbgXQP52RWRaaS5OsQv3W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastric cancer]]></video:title><video:description><![CDATA[Gastric cancer is when malignant or cancerous cells arise in the stomach. 

This cancer can appear in any part of the stomach and it’s classified into adenocarcinoma, lymphoma, carcinoid tumor, and leiomyosarcoma; depending on the type of cells it originates from. 

Adeno- means gland; so, adenocarcinoma arises from columnar glandular epithelium. 

Lymphoma arises from lymphocytes. 

Carcinoid tumor is originated in the G-cells of the stomach. 

And leiomyosarcoma arises from smooth muscle cells from the gastric wall. 

Gastric cancer is generally considered a poor prognosis cancer, because it doesn&amp;#39;t cause specific symptoms until later stages.

The stomach has four regions: the cardia, the fundus, the body, and the pyloric antrum. 

There’s also a pyloric sphincter or valve at the end of the stomach, which closes while eating, keeping food inside for the stomach to digest. 

Now, the gastric wall is made up of four layers: from the outside in, there’s the adventitia, or serosa; the muscular layer; the submucosa; and the mucosa. 

The mucosa comes into direct contact with food, and it also has three layers of its own. 

The innermost layer is the epithelial layer and it absorbs and secretes mucus and digestive enzymes. 

The middle layer is the lamina propria and it has blood, lymph vessels, and mucosa associated lymphoid tissue, or MALT for short, which are nodules of immune cells called lymphocytes, in charge of eliminating pathogens that could pass through the epithelial layer. 

The outermost layer of the mucosa is the muscularis mucosa, and it’s a layer of smooth muscle that contracts and helps with the break down food. 

The epithelial layer dips down below the surface of the stomach lining to form gastric pits. 

And these pits are contiguous with gastric glands below which contain various epithelial cell types, each secreting a variety of substances. 

So for example, foveolar cells, or surface mucus cells, secrete mucus, which is a mix of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Portal_hypertension</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Bd_Alwi0TcG3jHul0cfuoK--R2ixLBqB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Portal hypertension]]></video:title><video:description><![CDATA[Portal hypertension means increased blood pressure in the hepatic portal system - or portal venous system. 

Most commonly, this happens because of hepatic cirrhosis, which is when the liver tissue is replaced by fibrotic, functionless tissue. 

Now, the portal venous system comprises the portal vein and its tributaries - namely, the splenic, and mesenteric veins. 

This blood contains all the nutrients absorbed in the GI tract, but it also carries toxins that the liver metabolizes so that they can be safely excreted by the kidneys. 

Once the liver processes all these substances, it sends the blood to the heart, through the inferior vena cava, to enter the systemic venous system. 

Now, there’s a few points in the boundaries of the hepatic portal system, where it could be connected with the systemic venous system that collects blood from the rest of the body: the inferior portion of the esophagus, the superior portion of the anal canal, and the round ligament of the liver - which used to be the umbilical vein during fetal life. 

At birth, the umbilical cord is cut, and the umbilical vein collapses to form the round ligament. 

Normally, the round ligament stays shut because pressures in the portal venous system and the systemic venous system are the same, between 5 and 10  Millimeters of Mercury 

But in some situations, an obstruction may prevent blood flow from the portal vein towards the inferior vena cava. 

When this happens, venous blood accumulates in the hepatic portal system, causing pressure to rise above 5 to 10 12 mmHg - which defines portal hypertension of mercury. 

Portal hypertension leads to the formation of portosystemic shunts - which is when blood is diverted away from the portal venous system and backs up into systemic veins. 

So first, less blood gets to the liver, causing diminished liver function and decreased blood detoxification, which leads to a buildup of toxic metabolites, like ammonia, in the blood. 

Ammonia and other toxi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myelodysplastic_syndromes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OYGPJ1XnSgioWzXNYJ_7K8DsTEGTykS-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myelodysplastic syndromes]]></video:title><video:description><![CDATA[Myelodysplastic syndromes, or MDS, are a group of rare blood disorders associated with faulty development of blood cells in the bone marrow. 

MDS can affect individuals of all ages, but it’s more common after the age of 60.

Blood cells develop from hematopoietic stem cells, through a process called hematopoiesis. 

This involves a number of divisions, and eventually, results in three types of blood cells: red blood cells, which carry oxygen around our bodies, white blood cells to help fight disease causing pathogens, and platelets that help form clots to stop bleeding. 

Once these cells are fully mature, they leave the bone marrow and enter the bloodstream.

In MDS, hematopoietic stem cells are damaged, so they give rise to faulty blood cells, which don’t mature, but instead persist as immature cells, called blasts. 

These immature blood cells usually die in the bone marrow or soon after they go into the blood, so you can’t really count on them to do the job of mature blood cells. 

As the condition progresses, immature blood cells gradually take over the bone marrow, which displaces and reduces the normal ones.

In most cases, the cause of MDS is not known. 

When this happens, it&amp;#39;s classified as primary MDS. 

In rare cases, they can be caused by chemo or radiation therapy, and this is called secondary MDS. 

MDS comprises a spectrum of diseases with differing potential for remaining stable or progressing to acute myeloid leukemia, or AML. 

The most common feature of MDS is anemia, caused by low red blood cell levels. 

Symptoms of anemia include dizziness, irritability, headaches, and pale skin. 

Low white blood cell levels increase the risk of bacterial and fungal infections. 

Finally, low levels of platelets cause excessive bruising following minimal injury and easy bleeding. 

Now, MDS usually worsens with time, as normal bone marrow function diminishes. 

40-50 percent of the time, MDS deteriorates into a form of cancer known as acut]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polycythemia_vera_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0Qx-XjxyRB2IhMtdIMTDxQIcT4q1WsqW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polycythemia vera (NORD)]]></video:title><video:description><![CDATA[In polycythemia vera, there are increased blood cell levels due to overproduction by the bone marrow, which is a soft tissue found within the bones. 

Normally, about 45% of the total blood volume is made up of erythrocytes, or red blood cells, and their main function is to carry oxygen to tissues and bring carbon dioxide to the lungs so it can be expired. This value is called the hematocrit. 

In polycythemia vera there’s an increase in red blood cell production. 

It typically begins with a mutation in a single hematopoietic stem cell, which gives rise to red blood cells, white blood cells, and platelets.

In 90 percent of the affected individuals there is a mutation of the Janus Kinase 2 or JAK2 gene. 

Normally, the kidneys produce erythropoietin which is a hormone that binds to receptors on the hematopoietic stem cells and activates JAK2 gene. 

When that happens, it causes the cell to divide and thus produce more blood cells. 

However, when there’s a mutation, it keeps JAK2 gene activated, and these cells are able to divide even in the absence of erythropoietin. 

The mutated cells proliferate, and rapidly become the predominant hematopoietic cells in the bone marrow. 

In time these cells start to die out and that’s when scar tissue forms. 

At that point, the bone marrow can no longer produce blood cells, leading to anemia or low red blood cell levels, thrombocytopenia or low platelet levels, and leukopenia or low white blood cell levels. This is known as the spent phase. 

And once the disease is in the spent phase, it’s really a different disease altogether - at that point it’s myelofibrosis.

The most common symptoms of polycythemia vera are fatigue, dizziness, increased sweating, redness in the face, blurred vision, and itchy skin especially after a hot shower. 

Itchiness develops due to the increased number of basophils and mast cells which contain histamine that causes itching when released. 

Splenomegaly or spleen enlargement is also comm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myelofibrosis_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ak4_Vu7VSk_7NqaYimv5liGvRbWtTPwL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myelofibrosis (NORD)]]></video:title><video:description><![CDATA[Myelofibrosis is a disease in which the bone marrow within a bone gets replaced by connective tissue in a process called fibrosis. 

Since the bone marrow’s main role is to produce erythrocytes or red blood cells, leukocytes or white blood cells, and thrombocytes or platelets, the process of fibrosis interferes with production of these cell types. 

Now, normally, the vast majority of bone marrow is made of hematopoietic cells which are the early progenitor cells that can differentiate into other cell types.

In addition to these cells there are fibroblasts, which are connective tissue cells.

Now, myelofibrosis can be primary or secondary. 

Primary myelofibrosis is caused by a gene mutation within hematopoietic cells, which activates a set of enzymes that together are called the JAK-STAT pathway. 

The mutation specifically causes the enzymes in the JAK-STAT pathway to go into overdrive so that the cells begin to mature and divide rapidly, quickly filling up the bone marrow. 

A large majority of these cells turn into megakaryocytes which go on to make platelets. 

These megakaryocytes release cytokines, which are molecules that create inflammation. 

And one of these cytokines is fibroblast growth factor which activates fibroblasts. 

The activated fibroblasts engage in the process of fibrosis - they make lots of connective tissue that ultimately begins to fill up and scar the bone marrow and replaces hematopoietic cells. 

In response, the hematopoietic cells migrate to liver, spleen, and lungs - a process called extramedullary hematopoiesis. 

These tissues enlarge and sometimes become dysfunctional. 

The extramedullary hematopoiesis is often not able to fully compensate for the loss of bone marrow hematopoiesis, and it can lead to a shortage of all blood cell lines - called pancytopenia. 

Secondary myelofibrosis can develop in conditions like essential thrombocythemia, which is where excess platelets are produced, and polycythemia vera, which is where excess red blood cells are produced.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antithrombin_III_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RxTGVNiMSaan2fVLLEzSxP7_SKy2xl00/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antithrombin III deficiency]]></video:title><video:description><![CDATA[Antithrombin III is an anticoagulant protein which is made by the liver. So antithrombin III deficiency is when a genetic mutation makes antithrombin III either deficient or defective. This causes excessive clot formation, and the clots can get lodged in small vessels that nourish different organs and tissues, causing strokes.  

Antithrombin III deficiency presents as a hemostasis disorder. Hemostasis is the process where blood flow is stopped after there’s damage to a blood vessel, and it has two steps. Primary hemostasis involves the formation of a platelet plug at the site of injury, and secondary hemostasis involves the coagulation cascade, where several clotting factors come into play to form a fibrin mesh over the platelet plug to reinforce it - forming a blood clot. 

Hemostasis can be both stimulated, and inhibited by several factors. In the first category, there’s thrombin, or factor II, which accelerates hemostasis by increasing platelet activation, and cleaving several factors involved in secondary hemostasis to their active form. 

On the other hand, the most important factor that inhibits hemostasis is antithrombin III. Antithrombin III binds excess thrombin and factor X from secondary hemostasis, and also inhibits coagulation factors VII, IX, XI and XII - which are also key players in secondary hemostasis.  

So, antithrombin helps regulate clot formation, preventing clots from growing too large and blocking blood flow to tissues supplied by the vessel. It also prevents clots from getting so big that small parts of the growing clot break off in the form of emboli. Finally, the anticoagulant properties of antithrombin III can also be enhanced by an anticoagulant medication called heparin - which binds to antithrombin and increases its affinity for its target proteins. So, the two major consequences of antithrombin III deficiency are increased risk of thrombosis and insensitivity to heparin. 

Antithrombin deficiencies can be acquired, or gene]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Factor_V_Leiden</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PUt_CgWvSTqt4wx7BsV9fVaoQNy4Op-e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Factor V Leiden]]></video:title><video:description><![CDATA[Factor V Leiden is a disorder where blood clots form more easily due to a mutation in a clotting protein called factor V. Factor V Leiden is the most common hypercoagulable disorder in people of caucasian descent, and was named after the town Leiden in Holland, where the disease was first described.

Now, Factor V Leiden is a hemostasis disorder. 

Hemostasis is the process where blood flow is stopped after there’s damage to a blood vessel, and it has two steps. 

Primary hemostasis involves the formation of a platelet plug at the site of injury, and secondary hemostasis involves the coagulation cascade, where several clotting factors come into play to form a fibrin mesh over the platelet plug to reinforce it - forming a blood clot. 

Hemostasis can be both stimulated, and inhibited by several factors. 

One way to stimulate hemostasis is with thrombin, or factor II, which increases platelet activation, and cleaves several factors involved in secondary hemostasis to their active form.

So one way to inhibit hemostasis is actually to inhibit thrombin. 

This happens with the help of anticoagulant proteins like protein C. Protein C is a vitamin K dependent circulating plasma protein produced in the liver along with a cofactor called protein S. 

Both protein C and S interact with a protein called thrombomodulin, which is on the surface of intact endothelial cells that line our blood vessels. 

So, let’s say you cut your finger and now a blood clot has formed. 

When there’s a lot of thrombin around a damaged blood vessel, excess thrombin binds to thrombomodulin and it can no longer participate in the coagulation cascade. 

So in a sense, the undamaged cells help ensure that the coagulation process is limited to the injury site. 

Furthermore, the thrombin-thrombomodulin complex binds to protein C. Protein S then joins the party, forming a complex that includes protein C, protein S, and thrombin-thrombomodulin. Protein S binding to this complex activates]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Protein_C_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_Ob2NNgmRsyPcwnbv2Rr3eBDQlG345v2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Protein C deficiency]]></video:title><video:description><![CDATA[Protein C and S are two anticoagulation proteins that inactivate coagulation factors Va and VIIIa in the coagulation cascade. This means, they act like brakes on coagulation, limiting clot formation and preventing clots from growing too big. So, when either of these proteins is deficient, it leads to a hypercoagulable state, meaning a person is at increased risk of developing a clot that could block blood flow.  The most common places for such clots to develop are in the deep veins of the legs and in the vessels that carry de-oxygenated blood through the lungs. 

Normally, protein C and protein S are 2 of many proteins or enzymes that regulate the complex process called hemostasis. This is where a solid clot forms in the flowing, liquid blood to plug the defect in a damaged blood vessel. It has two steps; Primary hemostasis involves the formation of a platelet plug at the site of injury, and secondary hemostasis involves coagulation, where several clotting factors come into play to form a fibrin mesh over the platelet plug to reinforce it, and form the blood clot. The main role of protein C and protein S is to prevent excess coagulation, or fibrin formation, during secondary hemostasis.

Protein C and S prevent excess coagulation by interacting with several other proteins involved in a complex system of checks and balances. So, it starts with a protein called thrombomodulin, which is on endothelial cells that line our blood vessels, and together with thrombin, they form a complex that also includes protein C and protein S. 

When protein S joins this complex, it activates the proteolytic site of protein C, which cleaves and inactivates active factor V, a cofactor for factor X in the common pathway, and factor VIII, a cofactor for factor IX in the intrinsic pathway. The factor V degradation product also binds to this complex and further enhances its ability to cleave more active factor V and active factor VIII. By inhibiting both the intrinsic and common pa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Protein_S_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GKomxmRuRKilzFOrnkdBF6TQTNSCQsdu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Protein S deficiency]]></video:title><video:description><![CDATA[Protein C and S are two anticoagulation proteins that inactivate coagulation factors Va and VIIIa in the coagulation cascade. This means, they act like brakes on coagulation, limiting clot formation and preventing clots from growing too big. So, when either of these proteins is deficient, it leads to a hypercoagulable state, meaning a person is at increased risk of developing a clot that could block blood flow.  The most common places for such clots to develop are in the deep veins of the legs and in the vessels that carry de-oxygenated blood through the lungs. 

Normally, protein C and protein S are 2 of many proteins or enzymes that regulate the complex process called hemostasis. This is where a solid clot forms in the flowing, liquid blood to plug the defect in a damaged blood vessel. It has two steps; Primary hemostasis involves the formation of a platelet plug at the site of injury, and secondary hemostasis involves coagulation, where several clotting factors come into play to form a fibrin mesh over the platelet plug to reinforce it, and form the blood clot. The main role of protein C and protein S is to prevent excess coagulation, or fibrin formation, during secondary hemostasis.

Protein C and S prevent excess coagulation by interacting with several other proteins involved in a complex system of checks and balances. So, it starts with a protein called thrombomodulin, which is on endothelial cells that line our blood vessels, and together with thrombin, they form a complex that also includes protein C and protein S. 

When protein S joins this complex, it activates the proteolytic site of protein C, which cleaves and inactivates active factor V, a cofactor for factor X in the common pathway, and factor VIII, a cofactor for factor IX in the intrinsic pathway. The factor V degradation product also binds to this complex and further enhances its ability to cleave more active factor V and active factor VIII. By inhibiting both the intrinsic and common pa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sideroblastic_anemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nKhiRqpoTNWzCCKb_4Gd8V2oRO2Uvnzp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sideroblastic anemia]]></video:title><video:description><![CDATA[With sideroblastic anemia, sidero- means iron and -blastic meaning immature and anemia refers to a condition where there’s a decrease in the number of healthy red blood cells, or RBCs in the body. 

So sideroblastic anemia is a type of blood disorder where there’s a buildup of iron in the RBC’s in the body causing them to be immature and dysfunctional. 

This buildup occurs because these RBC’s are unable to incorporate iron into hemoglobin which is necessary for RBC’s to transport oxygen. 

In order to better understand sideroblastic anemia, we need to first take a look at hemoglobin,  the main protein within RBC’s that’s responsible for carrying oxygen. 

Now hemoglobin is made up of hemes and globins. 

There are 4 globin subunits, typically two alpha and two beta, and each one has its own heme group.  

This heme is a large molecule that’s made up of four pyrrole subunits that forms a ring, and this structure is called a porphyrin.  

In the middle, there is an ionically bond iron 2+ and the iron is what binds to and carries the oxygen molecule. 

So each hemoglobin can carry four oxygen molecules when it’s fully saturated. 

The process of heme synthesis occurs both within the mitochondria and the cytosol of a cell and requires multiple enzymes to catalyze the numerous steps.  

It begins in the mitochondria where succinyl CoA binds to glycine via delta-ALA synthase which uses vitamin B6 as a cofactor to produce delta-aminolevulinic acid, or ALA. 

Then, in the cytosol, delta-aminolevulinic acid is converted to porphobilinogen, or PBG, via delta-ALA dehydratase. 

From there, four molecules of porphobilinogen condense together to form hydroxymethylbilane with the help of porphobilinogen deaminase. 

Note that porphobilinogen deaminase is sometimes called uroporphyrinogen I synthase or hydroxymethylbilane synthase, or HMBS for short. 

Afterwards, hydroxymethylbilane is converted to uroporphyrinogen III and catalyzed to coproporphyrinogen III via uropor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Iron_deficiency_anemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3eXcU2QtQgifZNi_lkRi9OzIRkaDa2W_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Iron deficiency anemia]]></video:title><video:description><![CDATA[Anemia is a condition where there’s a decrease in the number of healthy red blood cells, or RBCs, in the body. 

So, iron deficiency anemia means anemia caused by a deficiency in iron. 

Iron deficiency anemia is also the most common type of anemia worldwide. 

If we take a close look at our red blood cells, we’ll notice that they’re loaded with millions of copies of the same exact protein called hemoglobin, which binds to oxygen and turns our blood cells into little oxygen transporters, and basically allow us to move oxygen to all the tissues in our body. 

If we take an even closer look at those hemoglobin proteins, we’ll find that they’re made of four heme molecules, which have, right in the middle, iron. 

This iron molecule is what binds to oxygen, so each hemoglobin molecule can bind four molecules of oxygen. 

In addition, iron is also an important part of proteins like myoglobin, which delivers and stores oxygen in muscles; and mitochondrial enzymes like cytochrome oxidase, which help generate ATP.

Normally, when a red blood cell dies, some iron is recycled from it. 

But, we also lose about 1 milligram of iron every day  - some through the sweat, some in shedded skin cells, and some in shedded cells in the gastrointestinal tract, which get out of the body through feces. 

But most of us take in 10-20 mg of dietary iron every day, and absorb about 10% of it, or about 1 or 2 milligrams - so it all evens out at the end of the day! 

Now, our diet contains two forms of iron. 

The first is heme iron, or iron bound to hemoglobin or myoglobin, which comes from animal products like meat. 

Heme iron is in the ferrous, or Fe2+, state. 

The other form is non-heme iron, which is free iron molecules in the ferric, or Fe3+, state. 

Non-heme iron comes from plant based foods like spinach and beans. 

Now, when food is broken down in the stomach, iron is released. 

Heme iron is absorbed directly into the duodenal cells, where it is broken down to release Fe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Beta-thalassemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J-lpx4ivQJSBUZdKJ-pRxpDKRFCrDpbp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Beta-thalassemia]]></video:title><video:description><![CDATA[Beta thalassemia is a genetic disorder where there’s a deficiency in production of the β-globin chains of hemoglobin, which is the oxygen-carrying protein in red blood cells - or RBCs for short. Beta thalassemia is most commonly seen in Mediterranean, African and South East Asian  populations.

Normally, hemoglobin is made up of four globin chains, each bound to a heme group. There are four major globin chain types -  alpha (α), beta (β), gamma (γ), and delta (δ). These four globin chains combine in different ways to give rise to different kinds of hemoglobin. First, there’s hemoglobin F (or HbF), where F stands for fetal hemoglobin, and it’s made up of two α-globin and two γ-globin chains. Hemoglobin A (or HbA), the major adult hemoglobin form, is made up of two α-globin and two β-globin chains. Finally, hemoglobin A2 (or HbA2)) accounts for a small fraction of adult hemoglobin in the blood, and it’s made up of two α-globin and two δ-globin chains.
With beta thalassemia, there’s either a partial or complete β-globin chain deficiency, due to a point mutation, which is when a single nucleotide in DNA is replaced by another nucleotide, in the beta globin gene present on chromosome 11. And most often, these mutations occur in two regions of the gene called the promoter sequences and splice sites, which affects the way the mRNA is read. The result is either a reduced, or completely absent beta globin chain synthesis.

And since this is an autosomal recessive disease, two mutated copies of this gene, one from each parent, are needed to develop the disease. If the person has just one mutated gene that codes for either a reduced production or absent production of beta globin chains, then they have beta thalassemia minor. If the person has two mutated genes that code for reduced beta globin chain synthesis, then they’re said to have beta thalassemia intermedia. If the person has two β0 mutations then no beta globin chains are produced, and they’re said to have bet]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia_of_chronic_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cNTiy6smQoaQq8Sd2ilJg5CEQYi_D8NR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia of chronic disease]]></video:title><video:description><![CDATA[Anemia of chronic disease refers to a low red blood cell, or RBC, count that may be associated with many chronic disease states like infections, malignancy, diabetes, or autoimmune disorders. The disease used to be called anemia of chronic inflammation because the underlying cause anemia is the continuous inflammation generated by chronic disease, which impairs iron metabolism and, in turn, RBC production. The anemia itself is usually mild and it’s the second most common type of iron deficiency anemia. 

RBCs are produced in the bone marrow, in response to erythropoietin - which is a molecule secreted by the kidneys in response to low levels of oxygen in the blood. Taking a closer look at our RBCs, we can see they’re loaded with millions of copies of the same exact protein called hemoglobin, which binds to oxygen and turns our RBCs into little oxygen transporters that move oxygen to all the tissues in our body. Zooming in even closer, each hemoglobin molecule is made up of four smaller heme molecules, which have iron right in the middle. Oxygen binds to the iron, so each hemoglobin molecule can bind four molecules of oxygen. In addition, iron is also an important part of proteins like myoglobin, which delivers and stores oxygen in muscles; and mitochondrial enzymes like cytochrome oxidase, which help generate ATP.

Now, we get the iron required for RBC production from our diet. Following breakdown of food in the stomach, iron is released as Fe2+ ions, and then it’s absorbed in the small intestine - specifically, the duodenum. Inside the duodenal cells, an enzyme called hephaestin oxidizes Fe2+ to Fe3+ ions. This form of iron binds to a protein called ferritin, which temporarily stores the iron. When iron is needed in the body, some iron molecules are released from ferritin and transported into the blood, where they bind to an iron transport protein called transferrin that carries iron to various target tissues and releases them there.

Now, the mechanisms ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aplastic_anemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w5YkP003SR6mqvNYcWvo_H07Rcq3aFo_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aplastic anemia]]></video:title><video:description><![CDATA[Aplastic anemia is a pancytopenia, meaning all blood cell lines are decreased - so the term aplastic anemia, which just refers to low red blood cell count, is actually a misnomer. 

So with aplastic anemia, there’s actually anemia, as well as leukocytopenia, or low white blood cells, as well as thrombocytopenia, or low platelet levels. 

This condition takes many forms, ranging from mild to severe depending on the cause. 

Now, blood cells are produced in the bones of the body, mainly in the bones of the pelvis, ribs and sternum, through a process called hematopoiesis. 

This process starts in the bone marrow, the innermost portion of bone, where the hematopoietic stem cells reside. 

These serve as progenitor cells for all the different cell types found in the blood. 

First, hematopoietic stem cells, also called hemocytoblasts, can become lymphoid progenitors or myeloid progenitors. 

The lymphoid progenitors can develop into lymphoblasts, which can then differentiate into some white blood cells like T-lymphocytes, B-lymphocytes, or natural killer cells. 

The myeloid progenitors can differentiate into erythrocytes, or red blood cells, megakaryocytes, which eventually give rise to platelets, or myeloblasts, which can then become other white blood cells like monocytes, neutrophils, basophils, and eosinophils. 

The most common cause of aplastic anemia is autoimmune destruction of hematopoietic stem cells. 

The details of this mechanism are not fully understood, but research shows that there are alterations in the immunologic appearance of hematopoietic stem cells because of genetic disorders, or after exposure to environmental agents, like radiation or toxins. 

This means that the hematopoietic stem cells start expressing non-self antigens and the immune system subsequently targets them for destruction.

As the immune system destroys hematopoietic stem cells a whole host of complications arise. 

Due to the low red blood cell count tissues cannot proper]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autoimmune_hemolytic_anemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MJHCn-iJRLaEXTXZP7G7R91fSNCfBGRW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autoimmune hemolytic anemia]]></video:title><video:description><![CDATA[Autoimmune hemolytic anemia refers to increased red blood cell hemolysis, or breakdown, that results when a person’s own antibodies target red blood cells for destruction. 

And this results in a lower than normal amount of red blood cells anemia. 

The disease is most often idiopathic, or without a known cause, but it can be related to a medication side effect, or an underlying disease process. 

Normally, red blood cells, or RBCs, are made in the bone marrow and contain hemoglobin, which is an oxygen binding protein that delivers oxygen to tissues. 

Red blood cells live about 100-120 days after which they are recycled in the bone marrow or consumed by macrophages in the spleen, liver, or lymphatic system.

Now, autoimmune hemolytic anemia is an extrinsic type of hemolytic anemia, because the immune system mistakenly believes our own red blood cells are foreign, or non-self, structures, so it secretes antibodies against proteins found on the RBC membrane. 

If there had been a primary defect in the RBC membrane, then it would have been called an intrinsic hemolytic anemia. 

And usually, hemolysis happens in the spleen or liver, so this is considered an extravascular hemolytic anemia - although in severe cases, RBC hemolysis can also happen intravascularly, or inside blood vessels. 

Now, autoimmune hemolytic anemia gets classified as either warm or cold. 

Warm is the more common type, and it’s when hemolysis occurs at temperatures greater than or equal to core human body temperature of 37º celsius. 

Cold autoimmune hemolytic anemia is much rarer, and it occurs when people’s blood is exposed to cold temperatures, usually in the range of 0º to 10º celsius - like when a person goes out into cold weather during winter.

Warm autoimmune hemolytic anemia is almost always due to IgG antibodies, termed “warm agglutinins” that react with antigens, which are proteins on the surface of the red blood cell. 

The main red blood cell antigen that reacts with these ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glucose-6-phosphate_dehydrogenase_(G6PD)_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b7zCaJmPTlm_kzn_RhV2PWGJQxe2tUHZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glucose-6-phosphate dehydrogenase (G6PD) deficiency]]></video:title><video:description><![CDATA[Glucose-6-phosphate dehydrogenase deficiency, or G6PD deficiency, is a genetic disorder characterized by decreased levels of glucose-6-phosphate dehydrogenase, which leads to the destruction of red blood cells. 

Normally, as a part of the metabolic process, our body produces free radicals like hydrogen peroxide, or H2O2. 

Free radicals can damage the cells in many ways including destroying the DNA, proteins, and the cell membrane.  

Now, we have a molecule in our body called  glutathione which acts as an antioxidant and goes around and neutralizes these free radicals.

In order to function, these molecules need to be in the reduced state where they can donate an electron to the H2O2 and convert them into harmless water and oxygen.  

However this causes the glutathione to become oxidized, so before it can get back to work, an enzyme called glutathione reductase will use an NADPH as an electron donor and and reduce the oxidized glutathione back into its working state.  

After giving up its electron, the NADPH will become NADP+.   

So to replenish the supply of NADPH, we have the glucose-6-phosphate dehydrogenase enzyme, or G6PD, which reduces NADP+ back to NADPH by oxidizing a glucose-6-phosphate.  

Glucose-6-phosphate is a metabolite of glucose so we usually have a ready supply of this molecule as long as we are not starving.  

Now G6PD deficiency is caused by mutations on the G6PD gene which is found on the X chromosome and thus it’s an X-linked recessive genetic condition and it almost exclusively manifests as a disease in men, since they have one X and one Y chromosome, so if the one and only chromosome has the mutation, then they have the disorder. 

Women on the other hand have two X chromosomes, so those with an X chromosome that has the mutation, still have another X chromosome with a normal copy of the gene and thus females are usually carriers and only transmit the disease to their sons. 

The G6PD mutations cause defective G6PD enzymes to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Waldenstrom_macroglobulinemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Er77Upx3S3qAG6d9Hrs1NHuqRSiM16ey/_.jpg</video:thumbnail_loc><video:title><![CDATA[Waldenstrom macroglobulinemia]]></video:title><video:description><![CDATA[Waldenstrom Macroglobulinemia, or Waldenstrom syndrome, is a rare type of malignant lymphoma. 

It is characterized by the overproduction of an antibody called immunoglobulin M, or  IgM, in the blood. 

Like all antibodies, IgM is produced by a subpopulation of white blood cells called B lymphocytes, or B-cells for short. B-cells start off as stem cells within the bone marrow, where they undergo a series of developmental phases. 

When they’re mature enough, they leave the bone bone marrow and enter the blood, and from there, they go into secondary lymph organs such as the spleen and lymph nodes. 

Within the secondary lymph organs,these B-cells can then further differentiate into plasma cells which ultimately give rise to the immunoglobulins. 

Thus, Waldenstrom’s macroglobulinemia is more specifically referred to as a lymphoplasmacytic lymphoma.

Now, IgM is actually composed of 5 separate antibodies bound together, thus creating a pentamer, which is a very large, or MACRO-globulin. 

These macroglobulins increase the thickness of blood and aggregate with one another causing a condition known as hyperviscosity syndrome. 

Hyperviscosity causes blood vessels to become engorged, causes hypercoagulability, and reduces the overall rate of blood flow.

Like with many cancers, the exact cause of this overproduction is not well understood but it is hypothesized to be due to mutations in the MYD88 and CXCR4 genes. 

When mutated, these genes allow lymphoplasmacytic cells to avoid programmed cell death, so they end up proliferating excessively. 

The overproduction of lymphoplasmacytic cells in the bone marrow can also crowd out and interfere with the production of normal red blood cells and platelets.  

Although commonly asymptomatic, the symptoms that do occur are mainly attributed to hyperviscosity syndrome,  which leads to mucosal bleeding from the nose and gums.

In the eyes, distension of retinal veins causes retinopathy or blurring and loss of vision. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_intermittent_porphyria</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Awl8Am9JQTuyL8DtFUScZSA8QPi1f5fA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute intermittent porphyria]]></video:title><video:description><![CDATA[Acute intermittent porphyria is a rare autosomal dominant disorder that belongs to a family of disorders called porphyria. These disorders all affect the production of heme which is a major component of red blood cells.  Now, heme synthesis is also called porphyrin synthesis and when halted, it results in the buildup of one of its precursor molecules. 

In order to better understand acute intermittent porphyria, we need to first take a look at hemoglobin, the main protein within red blood cells that’s responsible for carrying oxygen.  Now hemoglobin is made up of hemes and globins.  There are 4 globin subunits, typically two alpha and two beta, and each one has its own heme group.  This heme is a large molecule that’s made up of four pyrrole subunits that forms a ring, and this structure is called a porphyrin.  In the middle, there is an ionically bonded iron 2+ and the iron is what binds to and carries the oxygen molecule.  So each hemoglobin can carry four oxygen molecules when it’s fully saturated. 

The process of heme synthesis occurs both within the mitochondria and the cytosol of a cell and requires multiple enzymes to catalyze the numerous steps.  It starts in the mitochondria where succinyl CoA binds to glycine via delta-ALA synthase to produce delta-aminolevulinic acid, or ALA. Then, in the cytosol, delta-aminolevulinic acid is converted to porphobilinogen, or PBG, via delta-ALA dehydratase. From there, four molecules of porphobilinogen condense together to form hydroxymethylbilane with the help of porphobilinogen deaminase. Note that porphobilinogen deaminase is sometimes called uroporphyrinogen I synthase or hydroxymethylbilane synthase, or HMBS for short. 

Afterwards, hydroxymethylbilane is converted to uroporphyrinogen III and catalyzed to coproporphyrinogen III via uroporphyrinogen III cosynthase and uroporphyrinogen decarboxylase, respectively. Next, coproporphyrinogen III is brought back into the mitochondria and converted into protoporph]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heparin-induced_thrombocytopenia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DdcnlqO8QryulaREPTlnXemvQT6t5vBF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heparin-induced thrombocytopenia]]></video:title><video:description><![CDATA[The term heparin-induced thrombocytopenia can be divided into two parts. 

Heparin refers to an anticoagulant medication which prevents blood clots from forming, and thrombocytopenia refers to decreased number of thrombocytes, or platelets, in the blood. 

So, heparin-induced thrombocytopenia or, HIT, is a complication caused by heparin that results in decreased platelets in the blood. 

Okay, so imagine you’re making dinner and accidentally cut one of your fingers. 

Now, if your body doesn’t stop the bleeding, you will keep losing blood until there’s not enough to supply the vital organs like the heart and brain. 

Now to prevent this from happening the body has a process called hemostasis.  

This process has two phases: primary and secondary hemostasis.

In primary hemostasis, platelets aggregate to form a plug at the site of an injured blood vessel. 

While these platelets are aggregating, coagulation, or secondary hemostasis starts. 

This is where numerous enzymes that are always floating around in the blood called clotting factors get proteolytically activated, meaning that activation happens when a small piece is chopped off - a bit like pulling the pin out of a grenade. 

These factors activate one another, eventually leading to the activation of fibrin or factor Ia.

That results in a fibrin mesh which forms around the platelet plug to reinforce it and hold it together. 

Without primary and secondary hemostasis, our body would suffer massive blood loss from even the most minor injuries; imagine losing all of your blood from something as simple as a pinprick! 

Okay, so heparin induced thrombocytopenia is caused by heparin. 

This medication works by activating an enzyme called antithrombin III, which inhibits coagulation factors Xa, also known as thrombin.  

This halts secondary hemostasis and prevents existing blood clots from growing larger, so it’s often given to people who suffer from pulmonary embolisms, strokes, and myocardial infarction]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immune_thrombocytopenia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fpnnlTzMSmiEz2yqHahCnM0dSR6-EVDh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immune thrombocytopenia]]></video:title><video:description><![CDATA[Immune thrombocytopenic purpura or ITP is an autoimmune condition in which the body produces antibodies against its own thrombocytes or platelets, which are destroyed. And this result in purpura, or small bleeding spots beneath the skin. 

Normally, when there’s any kind of damage to the blood vessel, hemostasis occurs, which is the process that stops the bleeding and plugs the damaged vessel to limit the blood loss. 

And there are two steps: primary and secondary hemostasis. During primary hemostasis, platelets aggregate to form a plug at the site of an injured blood vessel. 

Platelet aggregation is mediated by surface proteins found on platelets, called GP2B3A receptors. While these platelets are aggregating, secondary hemostasis kicks in. 

Secondary hemostasis is also called coagulation, because that’s when clotting factors come into play one after another, with a view to cleaving fibrinogen into fibrin. 

Then, fibrin forms a protein mesh, kinda like a giant net that covers the platelet plug and stabilizes it. 

Now, in ITP, the spleen produces certain IgG autoantibodies which bind to the platelet receptor Gp2B3A, and target the platelet-antibody complexes for destruction in the spleen. 

This leads to  lowering of platelet counts in the blood, which makes it harder for bleeding to stop. Now, ITP can be acute or chronic. 

Acute ITP usually affects children, a couple of  weeks after a viral infection, and resolves spontaneously within two months. 

Chronic ITP usually affect females of reproductive age, and persist more than six months. Chronic ITP can also be primary, when it occurs without an underlying trigger, or secondary, when it’s triggered by another condition like hepatitis C, HIV, or lupus. 

Most of the time, ITP is asymptomatic. In some cases, it can cause purpura, which are red or purple spots on the skin, measuring 0.3 to 1 cm in diameter. 

In severe cases of ITP, when platelet levels get very low, there may be frequent mucosal bleedi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Burns</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2xFW9MkuQkiyUWZfcV2VpNkYT3_b0-kR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Burns]]></video:title><video:description><![CDATA[A burn is the damage that happens after something really hot like a fire, hot water or steam, or even a hot object comes into contact with skin.

But burn injuries can also be caused by extreme cold; electricity; some chemicals, like strong acids; or radiation, like from the sun or medical treatments. 

Ultimately burns cause damage and inflammation of the skin. 

The skin plays an important role in protecting underlying muscles, bones, ligaments and internal organs; forming a barrier to infectious pathogens; and preventing water loss from the body.

Now, the skin is divided into three layers--the epidermis, dermis, and hypodermis. 

The epidermis forms the thin outermost layer of skin, and it’s made up of several layers of keratinocytes - which make and secrete glycolipids, which help to prevent water from easily seeping into and out of the body.

Underneath the epidermis is the thicker dermis layer that contains the nerves and blood vessels. 

But the dermis is divided into two layers - a thin papillary layer just below the epidermis, and a deeper reticular layer. 

The papillary layer contains fibroblasts which produce a connective tissue protein called collagen. 

The fibroblasts are arranged in finger-like projections called papillae; each of which contains blood vessels and nerve endings. 

Nerve endings found in this layer sense pain and fine touch, which allows you to feel something like a feather touching your arm. 

The reticular layer of the dermis is even thicker than the papillary layer. 

The collagen in the reticular layer is packed very tightly together, making it excellent tissue support. 

In addition, fibroblasts in the reticular layer secrete elastin--which is a stretchy protein that gives skin its flexibility. 

The reticular layer also contains the skin’s accessory structures like oil and sweat glands, hair follicles, lymphatic vessels, and nerves - and all of the blood vessels that serve these tissues. A type of nerve ending found he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/stevens-johnson-syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m3XkWRT0QVy8idvAOWuov8-sSWSZ91l6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stevens-Johnson syndrome]]></video:title><video:description><![CDATA[Stevens-Johnson Syndrome is named for the physicians who first reported an acute, immune-mediated condition that affects the skin and mucous membranes such as the mouth and genitals. 

Stevens-Johnson syndrome and toxic epidermal necrolysis are considered to be  the same condition, but are along a spectrum where toxic epidermal necrolysis is the more severe form.

Both can be fatal if not treated, and the risk of fatality increases with severity.

The skin plays an important role in protecting underlying muscles, bones, ligaments, and internal organs by forming a barrier to infectious pathogens; and preventing water loss from the body. 

The outermost layer of the skin is the epidermis and, itself, is made of several layers of cells. 

The deepest layer is called the stratum basale, or the base layer. 

And cells here are anchored to a basement membrane, a thin layer of delicate tissue containing proteins like collagen and laminins, which attach the epidermis to the underlying skin layer called the dermis. 

Similar to how the skin lines the outside of the body, mucous membranes, or mucosa, line the inner body surfaces like the mouth, tongue, respiratory tract, conjunctiva of the eyes, genitals, and anus. 

Mucosa is made up of one or more layers of epithelial cells, which, again, are attached to a basement membrane that sits on top of a layer called the lamina propria.

Now, most cells in the body have a protein called major histocompatibility complex or MHC class I molecule on the surface of their membrane.

This protein presents peptides from within the cell to immune cells called cytotoxic T cells, also called a CD8+ T cells.

If the cell is healthy, the cytotoxic T cell doesn’t recognize the peptides as foreign, and nothing happens. 

But if a cell is infected, say with a virus, the cytotoxic T cell can recognize the peptides as foreign and trigger an immune response. 

Once all infected cells have been destroyed, the immune response resolves.

Steven]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/psoriasis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lktKhJ1vRWCFcXSEFY31r60fTpGIppG_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psoriasis]]></video:title><video:description><![CDATA[Psoriasis is a non-contagious, chronic autoimmune disease that causes skin inflammation, and is linked to other autoimmune deficiencies such as psoriatic arthritis. 

It can be incredibly itchy and form silver plaques on the skin that can be embarrassing, and have both physical and psychological effects. 

Afflicted reality TV star Kim Kardashian, and singer Cyndi Lauper have each spoken out on how psoriasis can have a significantly negative impact on the quality of life.  

Normally, the skin is divided into three layers--the epidermis, dermis, and hypodermis. 

The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. 

Just above the hypodermis is the dermis, which contains nerves, sweat glands, lymph and blood vessels. 

Just above the dermis is the epidermis.

The epidermis itself has multiple cell layers that are composed of developing keratinocytes - which are named for the keratin protein that they’re filled with. 

Keratin is a strong, fibrous protein that allows keratinocytes to protect themselves from getting destroyed when you rub your hands through the sand at the beach. 

Keratinocytes start their life at the lowest layer of the epidermis called the stratum basale, or basal layer, which is made of a single layer of small, cuboidal to low columnar stem cells that continually divide and produce new keratinocytes. 

These new keratinocytes migrate upwards, forming the other layers of the epidermis. 

As keratinocytes in the stratum basale begin to mature and lose the ability to divide, they migrate into the next layer, called the stratum spinosum which is about 8 to 10 cell layers thick. 

The stratum spinosum also has dendritic cells lurking around, which are star-shaped immune cells constantly patrolling for invading microbes as part of the body’s immune defense system. 

The next layer up is the stratum granulosum which is 3 to 5 cell layers thick. 

Keratinocytes in this layer begin the process of ke]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/vitiligo</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TAMyIVWPSsGPFVdQ6kfO3l9DSXivfdll/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vitiligo]]></video:title><video:description><![CDATA[Vitiligo, likely meaning blemish, is a non-contagious skin condition that is defined by patches of discoloration, or depigmentation.

Though vitiligo can affect any race or ethnicity, it tends to be most noticeable in people with darker skin, like Canadian fashion model Winnie Harlow. 

Given the effect on a person’s appearance, pigment loss can really impact a person’s quality of life.

The skin is divided into three layers--the epidermis, dermis, and hypodermis. 

The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. 

Just above is the dermis, which contains hair follicles, nerves and blood vessels.

And just above, the outermost layer of skin, is the epidermis. 

The epidermis itself has multiple cell layers that are mostly keratinocytes - which are named for the keratin protein that they’re filled with. 

Keratin is a strong, fibrous protein that allows keratinocytes to protect themselves from getting destroyed when you rub your hands through the sand at the beach. 

Keratinocytes start their life at the deepest layer of the epidermis called the stratum basale, or basal layer, which is made of a single layer of small, cuboidal to low columnar stem cells that continually divide and produce new keratinocytes that continue to mature as they migrate up through the epidermal layers. 

But the stratum basale also contains another group of cells - melanocytes, which secrete a protein pigment, or coloring substance, called melanin. 

Melanin is actually a broad term that constitutes several types of melanin found in people of differing skin color. 

These subtypes of melanin range in color from black to reddish yellow and their relative quantity and rate at which they are metabolized define a person’s skin color.

When keratinocytes are exposed to the sun, they send a chemical signal to the melanocytes, which stimulates the melanocytes into making more melanin. 

The melanocytes move the melanin into small sacs ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cri_du_chat_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wKjAPOOnRxCg4uY6IhKJzizsQEmdtA6q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cri du chat syndrome]]></video:title><video:description><![CDATA[Cri du chat syndrome is a rare genetic disorder caused by a genetic mutation where a portion of chromosome 5 is deleted, or missing. The name is a French term that refers to the characteristic high-pitched cry of the affected babies, which sounds like the cry of a cat or “le cri du chat”. 

Alright, let’s break this down. Our DNA is packaged up into 46 chromosomes, which contains the genes that are pretty much instructions for making proteins. These proteins control everything from growth and development to the day-to-day functioning of the cells. Each of the 46 chromosomes is actually made up of a pair of chromosomes and you get one from each parent, so 23 pairs. Now, these chromosomes have two rod-shaped arms, one short and one long, hooked together in the middle by a centromere. These two short arms are referred to as p arms from the French term “petit” that means small. In cri du chat syndrome, a part of one of the short arms of chromosome 5 is missing and so cri du chat syndrome is also known as 5p deletion syndrome, or 5p minus.

Okay, so 80-85% of the cases of cri du chat syndrome are the result of de novo deletion, which means they occur on their own without being inherited. However, in 10% of the cases, the deletion is inherited from a parent who has a balanced translocation. Translocation means that a part from one chromosome switches places with a part from another chromosome. and it’s balanced when there is no genetic material gained or lost, so the person doesn’t experience any adverse affect. As an example, let’s say this woman has 23 pairs of normal chromosomes. And here is her boyfriend, and in his karyotype we can see that a part of chromosome 5 has switched places with a part of chromosome 11. But he remains normal because no genetic material is gained or lost. But if these two have a baby, the baby will randomly inherit 2 copies of each chromosome, one from mom and one from dad. Now since both mom and dad have two copies of each chromoso]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Williams_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SHPj_hCyT0S3dgEBGJrtwYW6T0qCuvmK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Williams syndrome]]></video:title><video:description><![CDATA[Williams syndrome, also known as Williams-Beuren syndrome, is named after Dr. J. C. P. Williams who first described it. This is a chromosome disorder in which a small portion of chromosome 7 is deleted, which results in physical and developmental problems.   

Now, our DNA is this humongous blueprint on how to make a human and it’s usually packaged up nicely into 46  chromosomes. These 46 chromosomes come in 23 pairs - and each pair has one chromosome from each parent.  Now, the individual chromosomes are shaped like an “X” with two short arms and two long arms linked together in the center by a centromere. These two short arms are also referred to as p arms from the French term “petit” meaning small. What&amp;#39;s more, the two long arms are also referred to as q arms, since &amp;#39;q&amp;#39; follows &amp;#39;p&amp;#39; in the alphabet.  

In Williams syndrome, about 26 to 28 genes, including the elastin gene (ELN) on the long arm of chromosome 7 are missing due to a microdeletion. In most cases, this occurs randomly during the formation of sex cells in one of the parents. So a sperm cell or an ovum can potentially carry this microdeletion on the long arm of its chromosome 7 and go on to fuse with another sex cell - forming a new organism which has the microdeletion. Rarely, the cause of Williams syndrome can also be an inherited in an autosomal dominant fashion - so when a person with Williams syndrome has children, there is a 50% chance they’ll pass down their own microdeletion to the offspring.  

Now, the precise location of the microdeletion is at band 7q11.23, just like the directions to an address: 7 stands for chromosome 7, &amp;#39;q&amp;#39; refers to the long arm, 11.23 refers to the specific region on the chromosome-  and then it gets very specific: region 1, band 1, sub-band 2, sub-sub-band 3. This section of DNA spans about 26 to 28 genes and 1.5 to 1.8 million base pairs - so this is considered a microdeletion, because w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ehlers-Danlos_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nc7XUZ_1Tt2Bcz6gZ3nGzPeLR5yzC59i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ehlers-Danlos syndrome]]></video:title><video:description><![CDATA[Ehlers-Danlos syndrome is a group of related genetic conditions that are all caused by defective collagen synthesis. Normally, collagen provides strength and elasticity to our bodies, and it&amp;#39;s found in the skin, ligaments, tendons, and bones. In Ehlers-Danlos syndrome, defective collagen leads to stretchy skin, easy bruising, and joints that are super flexible. 

Now, the cells that produce collagen are fibroblasts, and they make five types of collagen. These five types have specific parts of the body they call home. Type I collagen makes its home in the skin, tendons, organs, and bones. Type II collagen makes its home in the cartilage. Type III collagen, in reticular fibers, form a supporting mesh for soft organs like the liver and blood vessels. Type IV collagen is found in a foundation called the basal lamina, on which the epithelial cells sit. Finally, there’s type V collagen which is in cell surfaces, hair, and placenta, as well as in places where type I collagen is found.

The synthesis of collagen, like any other protein, starts with the genes. The name of the genes that encode for a collagen type usually starts with the prefix COL, followed by the collagen number type, and the pro-alpha-chain it encodes. There are many genes that encode for the different types of collagen, like COL1A1, COL1A2, COL3A1, COL5A1, and COL5A2. Let’s take the genes COL5A1 and COL5A2 that encode for type V collagen as an example. In COL5A1, COL stands for collagen. The five stands for type V collagen and the A1 refers to an alpha-1-chain. So, COL5A1 encodes a collagen type V alpha-1-chain. Now, to synthesize type V collagen, for example. COL5A1 and COL5A2 get transcribed from DNA to mRNA and then get translated from mRNA into a string of amino acids that make up a protein. This process happens many times over. Now, this string of amino acids consists mostly of glycine and two other random amino acids, usually, proline and lysine that repeat over and over as amino ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Turner_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CXI8DX8NS82B2cnssBGrA9lHRsqJ88ec/_.jpg</video:thumbnail_loc><video:title><![CDATA[Turner syndrome]]></video:title><video:description><![CDATA[Turner syndrome, named after Henry Turner who first described it, is a chromosomal disorder affecting females where one X chromosome is either completely or partially absent. 

Now, our DNA is this humongous blueprint of information on how to make a human, which is usually packaged up nicely into 46  chromosomes. These 46 chromosomes come in 23 pairs - and each pair has one chromosome from each parent.  One of these pairs, the sex chromosomes, determines person’s biological sex and it can be composed of either two X chromosomes for females or an X and a Y chromosome for males.

So, if you wanted to make another human, first you’d have to find someone that feels the same way, and then you both contribute half of your chromosomes. In order to package up half the chromosomes into either a sperm cell or an egg cell, you actually start with a single cell that has 46 chromosomes. Let’s just say we’re making a sperm cell - for simplicity, we’re only going to show one pair of chromosomes, but remember that all 23 pairs do this. First step is meiosis, which is what produces our sex cells, and the chromosomes replicate, and so now they’re sort of shaped like an ‘X’—even though there are two copies of DNA here, we still say it’s one chromosome since they’re hooked together in the middle by this thing called a centromere. OK then the cell splits in two, and pulls apart the paired chromosomes, so in each of these cells you’ve now got 23  chromosomes. Now the two copies of the chromosome get pulled apart, and the cells split again, which means four cells, each still with 23 chromosomes. Now these are ready to pair up with an egg cell from mom that has 23 chromosomes as well, totaling to 46 chromosomes, and voila–nine months down the road you’ve got yourself a baby.

Usually, each parent contributes one chromosome to each pair. Fifty-fifty. Sometimes though, one parent might contribute one chromosome too many, which is called trisomy, or one chromosome less, which is cal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulpitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GO-24mttRqWweFPwQTKcXLqvSk29MYMc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulpitis]]></video:title><video:description><![CDATA[Pulpitis is inflammation of dental pulp, and it’s usually caused by bacterial infections.

The dental pulp is the soft inner section of the tooth, that houses the nerves and blood vessels that nourish the tooth.

If the pulp gets inflamed, these nerves get activated, really intensively. 

Pulpitis usually starts with either an injury to the tooth, such as a fracture, or commonly from tooth decay which is when there’s erosion of the overlying enamel and dentin layers, opening up a direct route to the pulp.

Bacteria can then access the dental pulp, and generate an infection.  

The most common bacteria include the mutans group streptococci, such as Streptococcus mutans and Streptococcus sobrinus. 

The bacterial infection typically leads to an inflammatory response from the immune system.The inflammation causes tissue swelling.

But because the dental pulp is encased in a tough layer of dentin, there’s very little room for tissue to expand. 

That means that the tissues get squeezed and there’s a lot of pressure on the nerves. 

Clinically, pulpitis can be divided into two types - reversible and irreversible. 

In reversible pulpitis, healthy pulp reacts to the presence of an irritant, for example, a deep carious lesion that isn’t actually within the dental pulp. 

Now, irreversible pulpitis is more serious because the pulp is actually damaged. For example, there may be a bacterial infection within the dental pulp. 

Usually, when there’s an active infection within such an enclosed space it is virtually impossible for the dental pulp to heal. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacokinetics:_Drug_absorption_and_distribution</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yybfYx7aQgqmdyrMrxpzsZkCS5yxgcP0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacokinetics: Drug absorption and distribution]]></video:title><video:description><![CDATA[Pharmacokinetics refers to the movement and modification of a medication inside the body. In other words, it’s what the body does to a medication and how it does it. 

Okay, first things first. A medication needs a way to be administered, or a route of administration. Depending on the form of the chemical preparation, like a pill, solution, spray, or ointment; and the part of the body being treated, the medication can be administered through various means or routes: such as swallowed by the mouth or orally, injected into a vein or intravenously, injected into a muscle or intramuscularly, inhaled into the lungs, sprayed into the nose or nasally, and applied onto the skin or cutaneously.

Once a medication is administered, it first has to be absorbed into the circulation; then distributed throughout the body; metabolized or broken down; and finally, excreted in the urine or feces. This process can be broken down into four components with the acronym ADME; which stands for Absorption, Distribution, Metabolism, and Excretion. Now, the loss of drug through chemical metabolism, which makes it inactive, and through physical excretion out of the body, can together be referred to as elimination.

Okay, so let’s start with absorption. Absorption is the process of moving the medication from the site of administration into the circulation. With the exception of intravenous administration, a medication will need to cross one or more cell membranes before it reaches the circulation. Movement across the cell membrane can occur via passive transport, which requires no energy, and active transport, which requires energy in the form of adenosine triphosphate, or ATP.

Two types of passive transport are used; facilitated diffusion and passive diffusion. Facilitated diffusion helps larger, water-soluble, and polar medications move across the membrane through transport proteins like channels and carrier proteins. Passive diffusion helps small, lipid-soluble, and nonpolar medic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peptic_ulcers_and_stomach_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DD5KDmXmQxGdlsPnnyXFwavaTAaHNq0c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peptic ulcers and stomach cancer: Clinical]]></video:title><video:description><![CDATA[Peptic ulcers are deep erosions in the lining of the stomach or duodenum that lead to inflammation in the gastric or duodenal wall. 

Sometimes, peptic ulcers develop acutely like after a toxic ingestion or ischemia, but more often the erosions are chronic, developing slowly over time. 

Chronic ulcers are mostly benign, but they can sometimes develop into a malignant ulcer, termed stomach cancer, which is why an upper endoscopy with biopsy is essential to the diagnosis. 

Chronic ulcers sometimes don’t cause any symptoms. When they do, the most common symptom is dyspepsia. 

Dyspepsia includes epigastric pain related to eating food, early satiety, postprandial belching, and nausea. 

With gastric ulcers, epigastric pain worsens when eating a meal because of the hydrochloric acid that’s produced in response to food. 

With duodenal ulcers, epigastric pain is relieved while eating a meal, but it typically recurs 2 to 5 hours later or it can appear at night. That’s because with duodenal ulcers, Helicobacter pylori is involved in most cases and it increases the hydrochloric acid production by indirectly increasing gastrin production and when there’s no food to act as a buffer, the pain worsens. 

Sometimes peptic ulcers can erode deep into the gastric and duodenal wall resulting in complications. 

If an ulcer erodes into a blood vessel, then it can cause hematemesis or melena. 

If there’s an ulcer in the pyloric antrum or in the duodenum, then it can cause gastric outlet obstruction. That can worsen the symptoms and even cause the individual to lose weight. 

Peptic ulcers can also perforate into the peritoneal cavity causing peritonitis, and that causes severe abdominal pain and fevers.

With stomach cancer, things get a little more complicated. Risk factors include chronic mucosal inflammation, like in Helicobacter pylori infection, atrophic gastritis, and surgery on the stomach; as well as environmental triggers like tobacco, and occupational exposures t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_mellitus:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q5BCDOEUTgS_n8lJntEoWp3OTiGt8P_L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes mellitus: Clinical]]></video:title><video:description><![CDATA[In diabetes mellitus, the body has trouble moving glucose from your blood into the cells – so blood sugar levels are constantly high. Insulin stimulates the movement of glucose into the cells, and glucagon stimulates the movement of glucose into the blood. In type I diabetes the blood glucose stays high because of an autoimmune destruction of the pancreas, which leads to low insulin levels. In type II diabetes, the body makes insulin, but the cells are insulin resistant - meaning they don’t “respond” to insulin by taking glucose in.

Cells’ inability to use insulin translates in classical symptoms of diabetes like polyuria – individuals pee a lot -, polydipsia – they drink a lot of water -, sometimes polyphagia – they eat a lot – and unexplained weight loss. Both type I and type II diabetes get these symptoms – however, with type I, the onset is usually abrupt and usually affects people under 30. With type II, the symptoms gradually worsen over a few months, and individuals usually have risk factors like being over 45 years old, having a first degree relative with type II diabetes mellitus, a body mass index (BMI) over 25, a sedentary lifestyle, or cardiovascular disease, like hypertension. 

Now, type II diabetes accounts for about 90% of the diabetes cases, so let’s start there. Diagnosing type II diabetes relies on determining blood sugar levels using one of four tests.  The first, and most common test, is a fasting glucose test and it’s where the person doesn’t eat or drink anything except water for 8 hours. Levels of 100 milligrams per deciliter to 125 milligrams per deciliter indicates prediabetes and a level of 126 milligrams per deciliter or higher indicates diabetes. Usually this test is done twice, and two results over 126 milligrams per deciliter are sufficient to diagnose a person with diabetes. Second, we have the oral glucose tolerance test, and it’s where a person is given 75 grams of glucose, and then blood samples are taken at time interva]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cystinuria_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L1yL3hU0RO2yrBpESD582387RnWtap8p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cystinuria (NORD)]]></video:title><video:description><![CDATA[Cystinuria is an inherited metabolic disorder named because of high levels of the amino acid cystine found in urine. The chemically similar amino acids arginine, lysine, and ornithine are also found in high levels. 

The kidneys are two bean-shaped organs in the body that filter out waste products and excess water from blood to produce urine. Typically, amino acids are recovered from urine and reabsorbed into the blood by the kidneys. But in cystinuria, impaired reabsorption of cystine, arginine, lysine, and ornithine leads to excessive amounts in urine. At high concentration, cystine clumps together to form crystals and stones, also called calculi. These can be found along the urinary tract, including the kidneys, ureters, and urinary bladder. 

While high levels of cystine, arginine, lysine, and ornithine in the urine are characteristics of the disorder, the main signs and symptoms are caused only by the cystine crystals and stones. As they stick together and grow larger, they form lemon-yellow stones. Stones are jagged and can cause sharp pains in the sides and lower back that can radiate to the lower abdomen and groin when they cause obstruction of the ureters. The pain can come in waves and may be present when urinating. Stones can also cause injury to tissues in the urinary tract, which can lead to blood in the urine. Frequent recurrences may ultimately lead to lasting kidney damage. Depending on their size, stones may obstruct the urinary tract and slow or stop the flow of urine. This can lead to additional complications, like urinary tract infections. Some individuals won’t form stones, but others typically begin having these symptoms between 10 and 30 years old.

With a normal pH of urine, high levels of arginine, lysine, and ornithine can be excreted in massive amounts without additional complications. But high levels of cystine are not as soluble and need urine with a higher pH to completely dissolve. Undissolved cystine clumps together to form ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Phenylketonuria_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5LakIS_VSNumMjRacAJmgJmSRgWiYw2b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Phenylketonuria (NORD)]]></video:title><video:description><![CDATA[Phenylketonuria or PKU is a rare metabolic disease that can lead to severe brain disorders caused by the accumulation of the amino acid phenylalanine to toxic levels in the blood and brain.

Amino acids are the basic building blocks that make up proteins. Phenylalanine, or Phe, is one of the essential amino acids.  It is necessary for life, but our bodies can&amp;#39;t make it; therefore, Phe must be acquired through foods that contain protein. Normally, once Phe enters the body, most of it is converted to tyrosine by the enzyme phenylalanine hydroxylase. Tyrosine is then turned into neurotransmitters important for normal brain development and function.

PKU is an autosomal recessive genetic disorder that affects function of the phenylalanine hydroxylase enzyme. The phenylalanine hydroxylase gene is located on chromosome 12 and over 600 mutations have been described. The degree of enzyme function can vary. When untreated, people with PKU develop symptoms such as severe intellectual disability, psychiatric disorders, and seizures. A pregnant woman with PKU must pay special attention to her Phe levels to reduce the risk of Maternal PKU Syndrome that can result in heart defects, microcephaly, and developmental disability in her baby.

In PKU, elevated Phe levels and reduced tyrosine levels can change the way the brain functions. This is because Phe uses the same transporters to get across the blood-brain barrier as other amino acids including- tyrosine and tryptophan. Tyrosine is needed to synthesize dopamine and norepinephrine, and tryptophan is needed to synthesize the neurotransmitter serotonin. As Phe levels rise, it occupies all the transporters, making it hard for tyrosine and tryptophan to get across the blood-brain barrier. As a result, dopamine, norepinephrine, and serotonin levels in the brain begin to fall, leading to abnormal brain development and intellectual disability.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fetal_alcohol_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EOAZwJ-1Q5mWrxjlD9GcaN09RliMuovT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fetal alcohol syndrome]]></video:title><video:description><![CDATA[Fetal alcohol syndrome, or FAS, occurs because of maternal use of alcohol during pregnancy. 

It’s currently the leading cause of intellectual disability in the US and can cause characteristic physical abnormalities.

Normally, the fetus is connected to the placenta by the umbilical cord, so the fetus gets oxygen and nutrients from the mother. 

Unfortunately, ethanol and toxic alcohol metabolites like acetaldehyde also pass freely through the placenta, but the fetal liver doesn’t have the necessary enzymes to metabolize them, so they build up inside the fetus really fast.

In FAS, ethanol interferes with cell division and proliferation, cell growth and differentiation, and with the migration of mature cells to their final location in the developing embryo, which affects the development of various fetal tissues, including the brain. 

Alcohol-induced brain damage includes partial or complete agenesis of the corpus callosum, which links the two hemispheres together, so it either forms incompletely, or not at all. 

This causes intellectual disability and seizures. 

When the frontal cortex and the hippocampus are affected, this causes poor memory and communication skills, as well as intellectual disability. 

The cerebellum can also be smaller in size, called   hypoplasia, leading to trouble with movement and balance.

The most common symptom of FAS is growth retardation, resulting in low height and weight. 

Microcephaly can also occur, which results from an overall decrease in brain growth. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glycogen_storage_disease_type_I</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ECrBhPe4S-q-rnfjPQXnJR26SwmLUJqk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glycogen storage disease type I]]></video:title><video:description><![CDATA[Glycogen storage disease type I, also called Von-Gierke’s disease, is a genetic disorder caused by a mutation in the glucose 6 phosphatase gene on chromosome 17. 

The end result is that glycogen can’t be broken down into glucose in liver cells, so glucose metabolism goes awry, resulting in symptoms like low blood sugar, weakness and poor growth. 

Glucose is such an important energy source, that our body stores excess glucose in liver cells and skeletal muscle cells in the form of glycogen. 

Glycogen is basically an enormous molecule or polymer, that’s made up of glucose molecules linked together by glycosidic bonds. 

And glycogen has a main chain, as well as multiple branches sprouting off of it. 

These branches allow glycogen to be compact and also allow it to rapidly add and remove glucose to and from the big glycogen molecule. 

Talk about a molecular sugar rush!

Now, glucose molecules are usually added to glycogen in response to insulin, which is secreted by the pancreas after meals. 

That’s when there’s high blood sugar, or plenty of glucose floating around in the bloodstream. 

So, it makes sense for some of this glucose to be stored as glycogen, right? 

Now when it’s been a while after a meal, so when you’re fasting, blood sugar levels take a dip. In response, the pancreas secretes glucagon and the adrenal glands secrete epinephrine. 

It turns out that glucagon tells the liver cells to break glycogen down into individual glucose molecules, and epinephrine tells skeletal muscle cells to do the same. 

In both the liver and skeletal muscle cells, glycogen breakdown begins with the branches, and it results in the release of glucose-6-phosphate - which is just like glucose, but with a phosphate clinging to it. 

In liver cells, an enzyme called glucose-6-phosphatase removes the phosphate off of the 6th carbon, releasing free glucose into the bloodstream, for all the organs and tissues to enjoy - very generous! 

Skeletal muscle cells, on the ot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glycogen_storage_disease_type_II_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jh71KXQ4S7_Ore6PS8SyF9z_QX6wKFKA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glycogen storage disease type II (NORD)]]></video:title><video:description><![CDATA[Pompe disease, also called glycogen storage disease type II, is a genetically inherited condition caused by insufficient functioning of an enzyme called lysosomal acid alpha-1,4-glucosidase, or just acid alpha-glucosidase, and it’s caused by a mutation of the GAA gene. It’s named after the Dutch pathologist, Dr. J.C. Pompe, who first described it in 1932.

Glucose is used for energy by most cells of the body, and it’s stored inside the cells as a compact, branch-shaped molecule called glycogen. When a cell needs energy, it uses enzymes to remove glucose molecules from the branches. One of the organelles within the cell is the lysosome, which functions a bit like a tiny recycling plant. The lysosome contains enzymes that break down cellular substances so that they can be recycled. Now for some reason, and it’s not really understood why, but small amounts of glycogen end up in the lysosomes, where it’s broken down by an enzyme called acid alpha-glucosidase, to release glucose from the glycogen chain. 

In Pompe disease, a mutation of the GAA gene prevents the production of enough functional acid alpha-glucosidase, and as a result, lysosomes can’t break down glycogen. This leads to a buildup of glycogen within the cytoplasm and lysosomes, and that leads to cellular damage and destruction.

Now, normally, glycogen is found in the largest amounts in the cytoplasm of liver cells and all three types of muscle cell. In individuals with Pompe, glycogen mostly accumulates in the lysosomes of those cells. Skeletal muscles include various muscles of the body as well as the diaphragm which is the primary breathing muscle. Cardiac muscle makes up the majority of the heart, and smooth muscle is found in the walls of blood vessels and many other organs.

Pompe disease is an autosomal recessive condition - so in other words, both parents must be carriers. The severity of the condition depends on how much functional acid alpha-glucosidase is produced. If little to no enzyme]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mitochondrial_myopathy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0pYV6U-iTlSwPZNXEfz1xJH9T4OV_yQf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mitochondrial myopathy]]></video:title><video:description><![CDATA[Primary mitochondrial myopathy is a rare genetic disorder that occurs when there are mutated mitochondria in muscle cells, especially skeletal muscle cells.

These mitochondria are unable to generate adenosine triphosphate, or ATP, which is a form of energy used by our cells.

As a result, muscle cells, which require a lot of energy to function, stop functioning properly.

The mitochondria are the main energy producing factories of a cell, and they do so with the help of the electron transport chain, and the enzyme ATP synthase.

The electron transport chain is made up of complexes of proteins or lipids, called electron carriers, embedded within the inner mitochondrial membrane which pass electrons along like the baton in a relay race.

This movement of electrons helps establish a proton gradient that drives ATP synthase to phosphorylate adenosine diphosphate or ADP into ATP.

Primary mitochondrial myopathy is caused by a mutation either in the mitochondrial DNA or nuclear DNA, which results in the abnormal production of mitochondrial proteins, impairing the function of the electron transport chain.

Mutations in the nuclear DNA are commonly inherited in an autosomal dominant fashion, which means one mutated gene is enough to cause the disease; or autosomal recessive fashion, which means two mutated genes, one from each parent, are needed to cause the disease.

Mutations in the mitochondrial DNA follow maternal inheritance , meaning that only an affected woman can pass on the disease to her children.

This is because, typically during fertilization, the father&amp;#39;s mitochondria are left behind while the sperm’s nucleus alone enters the egg.

The exception is the mitochondrial DNA single deletion, a common cause of primary mitochondrial myopathy, which is always sporadic and cannot be transmitted to the offspring.

In primary mitochondrial myopathy, muscle cells are unable to generate ATP, which results in muscle weakness and fatigue.

Sometimes there]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mucopolysaccharide_storage_disease_type_2_(Hunter_syndrome)_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rtEVZLAqTIKOZne6mCTMvYQTSKqO4-cJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mucopolysaccharide storage disease type 2 (Hunter syndrome) (NORD)]]></video:title><video:description><![CDATA[Hunter syndrome is a rare genetic metabolic disorder that occurs when lysosomal enzymes are absent. 

Hunter syndrome is also known as mucopolysaccharidosis type 2.

Mucopolysaccharides or glycosaminoglycans are types of complex sugars, which are produced by the cells and exported to the extracellular space. 

Examples include heparan sulfate and dermatan sulfate.

Both heparan sulfate and dermatan sulfate can be found on almost all cell surfaces as well as in the basement membrane, which separates epithelial cells from the connective tissue that lies beneath. 

When mucopolysaccharides like heparin sulfate and dermatan sulfate need to get degraded, they are taken over to a lysosome, which contains enzymes needed to break down the mucopolysaccharides. 

Each mucopolysaccharide requires multiple enzymes to fully degrade, and some mucopolysaccharides share certain enzymes in common. 

For example, both heparan sulfate and dermatan sulfate need the iduronate sulfatase and alpha-L-iduronidase enzymes to get broken down. 

Hunter syndrome is caused by a deficiency in iduronate sulfatase, and the result is that heparan sulfate and dermatan sulfate can’t be degraded, so they build up in various tissues. 

Hunter Syndrome is an X-linked recessive disorder so it’s more common in males. 

Early symptoms appear in infants, and they include an enlarged liver and spleen leading to abdominal hernias and recurrent ear infections.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mucopolysaccharide_storage_disease_type_1_(Hurler_syndrome)_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zhH-JyJ4QkaAOSwoJetjNzYJQXe0xnAn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mucopolysaccharide storage disease type 1 (Hurler syndrome) (NORD)]]></video:title><video:description><![CDATA[Mucopolysaccharidosis type I, or MPS I, is a rare genetic metabolic disorder caused by  deficiency of a lysosomal enzyme required to break down mucopolysaccharides. 

The disorder presents as a spectrum ranging from severe forms, classically known as Hurler syndrome, which are associated with life-threatening complications, to attenuated forms, classically known as Scheie syndrome or Hurler-Scheie syndrome. 

This disease can cause significant disability but it can also have a near-normal life expectancy. 

However, since presentation varies greatly between individuals, these designations are imprecise, so Hurler syndrome is generally used for severely affected individuals and attenuated mucopolysaccharidosis type I is used for all others. 

Mucopolysaccharides, also known as glycosaminoglycans, are complex sugars produced by cells and exported to the extracellular space. 

They include various molecules including heparan sulfate and dermatan sulfate, and they can be found on almost all cell surfaces as well as in the basement membrane, which separates epithelial cells from the connective tissue underneath. 

Mucopolysaccharides are degraded inside the cell, where they’re engulfed by a lysosome, that releases enzymes, which breakdown mucopolysaccharides. 

Each mucopolysaccharide requires multiple enzymes to fully degrade, and some mucopolysaccharides are degraded by the same enzymes. 

For example, both heparan sulfate and dermatan sulfate need the lysosomal enzymes iduronate sulfatase and alpha-L-iduronidase to be broken down.

MPS I is an autosomal recessive disorder, caused by a variation in the IDUA gene, which results in alpha-L-iduronidase deficiency. 

This deficiency prevents heparan sulfate and dermatan sulfate from being degraded, and as a result they build up in various tissues, leading to many complications as well as distinctive facial features, like a prominent forehead, a flat nose bridge, and enlarged lips, tongue, and gums. 

MPS I is als]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fabry_disease_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E1YnbMEAStOxX4nQSw0YKuArTyOgSvkW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fabry disease (NORD)]]></video:title><video:description><![CDATA[Fabry disease is a rare X-linked condition caused by mutations or pathogenic variants in the GLA gene that codes for a lysosomal enzyme called alpha galactosidase A or alpha-gal A. 

The alpha-gal enzyme normally breaks down large molecules called globotriaosylceramide or GL3 and other glycosphingolipids, so that small parts of the big molecules can be recycled for the body to use again.  

Without alpha-gal, these GL3 molecules build up inside the lysosomes, the recycling centers of the cells, causing a variety of symptoms and health issues. 

Fabry disease affects males and females, and it has two forms: classic and nonclassic/later onset. In classic 

Fabry disease, symptoms start in childhood and include burning, tingling, prickling, and painful neuropathic pain in the hands and feet, frequently triggered by exercise, fatigue, stress, or illness. 

There may also be a gradual decrease of sweating in childhood until many teens and adults stop sweating entirely. 

In some people living with Fabry disease, small reddish-purple rashes called angiokeratomas appear around the lower abdomen and “bathing trunk” region of the body.  

There may also be gastrointestinal symptoms like cramps, frequent bowel movements, constipation, and diarrhea. 

Many patients have a whorl or verticillata in their cornea, that can be found during a split lamp eye exam - but it doesn’t typically affect vision. 

Without treatment, Fabry disease complications can include kidney disease, abnormal heart rhythms, heart enlargement, and an increased stroke risk.

Nonclassic or later-onset Fabry disease doesn’t cause the earlier symptoms of pain and gastrointestinal issues in childhood, but some adults develop multiple symptoms as young adults. 

Others may only show signs of Fabry disease in a specific organ - like the heart or the kidneys. However, these individuals also have a higher risk of Fabry-associated complications. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Metachromatic_leukodystrophy_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2F0VzzvQQ0_sCKRhmL9tFYUCSDWxA2am/_.jpg</video:thumbnail_loc><video:title><![CDATA[Metachromatic leukodystrophy (NORD)]]></video:title><video:description><![CDATA[Metachromatic leukodystrophy, or MLD, is a rare lysosomal storage disorder that results from mutations in the ARSA gene, which codes for arylsulfatase A - an enzyme that normally breaks down a fat called sulfatide. 

Without this enzyme, sulfatide accumulates in neurons and myelin-producing cells like Schwann cells and oligodendrocytes, resulting in their degeneration. 

MLD is an autosomal recessive disorder, which means that two mutated copies of the gene, one from each parent, are needed to develop the disease. 

In rare cases, MLD can also be caused by mutations in the PSAP gene, which codes for saposin B, which is a protein that activates arylsulfatase A. 

Without arylsulfatase A, cells cannot recycle sulfatides. 

The sulfatide accumulates within cells of the nervous system like Schwann cells and oligodendrocytes, and aggregates to forms intracellular granules. 

These sulfatide aggregates are called metachromatic since they appear differently colored than the cellular material when stained and seen under the microscope. 

Sulfatide granules interferes with the cells’ ability to produce myelin, resulting in demyelination, or loss of myelin sheath, of the neurons. 

The end result is impaired nerve impulse transmission. 

Demyelination in MLD occurs both in the central as well as peripheral nervous system, resulting in a variety of symptoms. 

Common symptoms include peripheral neuropathy, which is the loss of sensation in the extremities, diminished deep tendon reflexes, visual disturbances, difficulty in speaking, difficulty in walking, ataxia, behavior and personality changes, and seizures. 

Now, there are three forms of MLD based on the age at onset of symptoms - late-infantile form, juvenile form, and adult form. In the late-infantile form, symptoms develop within the first three years of life, and include irritability and developmental delay. 

In the juvenile form, symptoms usually develop between the age of 4 and adolescence, which is around]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Niemann-Pick_disease_types_A_and_B_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zK5mxCiXQcqUcR5pPYUdybyNQCmAGbYB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Niemann-Pick disease types A and B (NORD)]]></video:title><video:description><![CDATA[Niemann-Pick disease type A and type B, or NPD-A and NPD-B, which are subtypes of acid sphingomyelinase or ASM deficiency, are rare, genetically inherited conditions characterized by the inability to break down a fat called sphingomyelin due to a deficiency of the enzyme, acid sphingomyelinase. 

There’s also Niemann-Pick disease type C, which is known to be caused by mutations in the genes NPC1 and NPC2, and is therefore considered to be distinct from types A and B. 

Sphingomyelin is a fat that&amp;#39;s included in the membrane of many different cells. 

When cells become old or damaged, they are often phagocytized, or eaten, by macrophages, which are cells of the immune system. 

They contain organelles called lysosomes that are said to function as recycling centers because they break down large, potentially harmful substances to be reused by the body. 

They break down sphingomyelin by using an enzyme called acid sphingomyelinase, which is a product of the sphingomyelin phosphodiesterase 1, or SMPD1 gene. 

In Niemann-Pick disease types A and B, there’s a mutation in the SMPD1 gene that causes a defect in the production of sphingomyelinase, leading to an inability to break down sphingomyelin. 

In NPD-A there’s almost a complete absence of sphingomyelinase activity, while NPD-B has some residual sphingomyelinase activity remaining. 

While the mechanism isn’t completely understood, sphingomyelin primarily accumulates in the lysosomes of macrophages, which travel throughout the body and cause damage in multiple organs and tissues. 

The macrophages develop a characteristic lipid-laden appearance under microscopes and are called “foam cells.” 

Sphingomyelin can also build up in other cell types in the body, reflecting impaired intracellular recycling of membranes and damaged organelles in lysosomes due to sphingomyelinase deficiency.

Signs and symptoms of NPD-A present early in life, and are usually life-threatening. 

These include enlargement of th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tay-Sachs_disease_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oDID0CSyT7Gmyc0Aq9IftWnVQrK4MXiG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tay-Sachs disease (NORD)]]></video:title><video:description><![CDATA[Tay-Sachs disease, or TSD for short, is a lysosomal storage disorder caused by a mutation in a gene on chromosome 15, which codes for a lysosomal enzyme called beta-hexosaminidase A, or HEX-A for short. 

This enzyme normally breaks down a lipid called GM2 ganglioside. 

GM2 is found mainly in neurons, so without HEX-A, it accumulates inside lysosomes. 

TSD is also known as GM2 gangliosidosis, type I. 

This results in progressive symptoms of central nervous system or CNS degeneration, like decreased muscle tone, visual difficulties and seizures, which usually begin by 3 to 6 months of age, proceeding to death by age 4. 

TSD is an  autosomal recessive genetic condition, so males and females are affected equally, inheriting one mutated HEX-A gene from each asymptomatic or heterozygous parent in order to develop the homozygous condition. 

This also means that TSD tends to occur in isolated, inbred populations or communities, which accounts for the predominant occurrence of the disease in infants of Ashkenazi Jewish heritage, and in certain French Canadian, Amish, and Cajun populations. 

These mutations can result in either no synthesis, or defective synthesis of HEX-A, resulting in either a total deficiency of HEX A or varying degrees of enzyme activity depending on the specific mutation. 

So with some mutations, GM2 accumulates over a longer period of time, accounting for a more gradual onset of CNS symptoms in some people. 

Depending on age of onset, TSD can be infantile, with onset at 3 to 6 months; juvenile, with onset at 2-5 years; chronic, with onset in the first or second decade of life; and late-onset, with the first indication of symptoms in the 2nd-3rd decade of life. 

Common signs for the first 3 forms are signs of CNS degeneration, like decreased muscle tone, abnormally increased reflexes, seizures and visual disturbances. 

For adult-onset, there may be motor difficulties and some adults may manifest bipolar type psychological symptoms. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Folate_(Vitamin_B9)_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ReyxiRxPTzu-nbH8Ej7gBjkHT4mcj8nU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Folate (Vitamin B9) deficiency]]></video:title><video:description><![CDATA[Folate deficiency is a clinical condition that occurs because of low level of folate or folic acid in the body. This can lead to a variety of problems ranging from anemia in individuals from all age groups to neural tube malformation in fetuses. 

Folate, also known as vitamin B9, mainly comes from eating leafy greens and citrus fruits like oranges and lemons and, nowadays, many countries fortify foods like grains and cereals with folate. 

Now, folic acid present in these food items is generally in polyglutamate form, which are basically chains of an amino acid called glutamic acid. 

Because of the carboxyl group present in its structure, the chain is negatively charged making it polar and soluble in water, which is a polar molecule but not soluble in lipids which are nonpolar molecules. 

So the polyglutamate residues of folic acid are almost non-absorbable from the GI tract, where all the cells are surfaced with lipid cell membranes. 

So, to make them absorbable, when polyglutamate residues reach a portion of the small intestine called the jejunum, special enzymes present at the jejunal mucosa cut down the polyglutamate residues into monoglutamate. 

Monoglutamate is smaller, and is less negatively charged, so these monoglutamate residues of folic acids can pass through the cell membrane and enter the jejunal cells, where they are converted into tetrahydrofolic acid or in short THF by the enzyme tetrahydrofolate reductase. 

These THFs then get methylated into a more stable form called methyl-THF. Once formed, the methyl-THF then leaves the jejunal cell and enters the bloodstream.

Some of it goes to the liver and get stored for a short period of 2-3 months, while most of it is used up for metabolic activity inside various cells around the body. 

Folic acid is used to synthesize DNA precursors, which is essential for DNA replication and cell division.

On target cells, there’s a specialized membrane protein called Folic Acid Transporter or FAT, which]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vitamin_B12_deficiency</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EAiQCz5xR_aZuP-jGf_dis65Q1_a_iVk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vitamin B12 deficiency]]></video:title><video:description><![CDATA[Vitamin B12 deficiency refers to low levels of Vitamin B12 in the body. 

This can lead to a variety of problems ranging from anemia to soreness of the tongue and neurological dysfunction.

Vitamin B12, also known as cobalamin, is a complex organometallic compound found in animal and dairy products like meat, eggs or milk. 

Dairy and animal products are broken down in the stomach by pepsin, which is the active form of a gastric enzyme called pepsinogen, to release B12. 

Then, a protein made by parietal cells in the stomach, called intrinsic factor, can bind to B12, and the B12-intrinsic factor complex passes into the intestines. 

When the complex reaches the terminal ileum, the enterocytes, which are the special cells lining the intestines, recognize intrinsic factor and absorb the whole complex. 

Inside the enterocytes, intrinsic factor gets removed and a special protein called transcobalamin-II binds the free B12 and transports it into the blood and from there, to various target tissues. 

Some of the transcobalamin-B12 complex gets to the liver, where B12 can be stored for several years.

B12 is used to synthesize DNA precursors, which is essential for cell division. 

First, vitamin B12 accepts a methyl group from methyl tetrahydrofolate or methyl-THF, making methylcobalamin and free tetrahydrofolate, or THF in the process. 

THF then gets an extra “methylene” group from serine, an amino acid found within the cells. 

THF quickly transfers the methylene to a nucleotide called deoxyuridine monophosphate, or d-UMP for short. 

As a result, d-UMP becomes d-TMP or deoxythymidine monophosphate, which can then be converted to thymidine, one of the nucleotides used to build DNA.

Going back, the methylcobalamin that was formed along with THF transfers its methyl group to homocysteine and converts it into an essential amino acid called methionine, thus lowering the levels of homocysteine in the body, too much of which can be harmful. 

Alternatively, B12 c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adenovirus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CV1G3q4dQe2ZZ2R5tdqkWjepRJyFRM6m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adenovirus]]></video:title><video:description><![CDATA[Adenoviruses are a group of viruses that cause respiratory, gastrointestinal, and genitourinary infections. 

There are about 60 serotypes of the virus, divided into 7 subgroups, from A to G. 

Common respiratory infections caused by adenoviruses include a sore throat, the common cold and pneumonia, whereas diarrhea is the most common gastrointestinal ailment. 

Adenoviruses can also cause cystitis, which is the inflammation of the bladder, as well as eye conditions like conjunctivitis. 

Adenoviruses are double-stranded linear DNA viruses surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. 

And they’re “naked” because the capsid isn’t covered by a lipid membrane. 

Their capsid is unique among viruses because it has fiber-like projections from each of the 12 vertices of the shell. 

Adenovirus is primarily transmitted by respiratory droplets when someone coughs or sneezes and by the fecal-oral route. 

In other words, you catch it by ingesting the stool or vomit particles of someone who is sick. Yuck. 

This can happen if infected stool ends up in the water supply or on agricultural fields, if flies land on it, and transfers stool particles to other places, or by touching contaminated surfaces. 

You can summarize it as the four Fs: fluids, fields, flies, and fingers. As a result, adenovirus can end up in food and drinking water. 

Two less common modes of transmission are from mother to newborn via the cervical fluid in the birth canal, and following an organ transplant from a donor who has an adenovirus infection. 

After entering the body, the virus heads for epithelial cells, like those that make up the respiratory, GI, or urinary mucosa, where it uses its fiber projections to bind to the coxsackie-adenovirus receptor on cell membranes. This allows it to get inside the cells. 

Once inside, adenovirus has multiple cytopathic, or cell-damaging, effects, like blocking synthesis of cellular]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bacillus_anthracis_(Anthrax)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wq3J9ukQSxmx2yIsHpT_QJgSSO6Pf31a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bacillus anthracis (Anthrax)]]></video:title><video:description><![CDATA[With Bacillus anthracis, bacillus means little rod and anthracis means coal. 

So Bacillus anthracis is a rod-shaped bacteria that causes a disease called anthrax, that’s associated with characteristic black skin lesions. 

Throughout history, Bacillus anthracis, or B. anthracis for short, has caused a number of plagues in Europe, and it’s also been used as biological warfare. 

Not a good reputation! 

Ok, now B. Anthracis has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria. 

Also, it is a non-motile bacteria and a facultative anaerobe, meaning it can survive with or without oxygen. 

B. Anthracis is also a non beta-hemolytic bacteria, because when cultivated on a medium called blood agar, B. Anthracis colonies don’t cause beta-hemolysis, where hemolysis, or breakdown of the red blood cells that surround the colonies makes the blood agar change color from red to transparent yellow.

Finally, Bacillus Anthracis is a spore-forming bacteria, so it can undergo endosporulation when it feels threatened by the environment, like when the temperature becomes too high or too low, in case of extreme dryness, or when there’s harmful radiation around. 

Endosporulation means that the bacteria starts by replicating its DNA, and then it forms a wall inside the cell, isolating the big portion of the cell, let’s call it the mother cell, from the small portion of the cell.  

Next, the plasma membrane of the cell surrounds the newly formed small portion and then pinches it off, forming a separate body known as a forespore. 

Next, the forespore gets completely engulfed by the mother cell, something like a cell within a cell. 

Finally, inside the dying mother cell, the forespore loses water and accumulates calcium, and at the same time gets wrapped in a super tough cortex from the dying mother cell. 

At this point, the endospore is able to resist heat, due to the presence of dipicolinic acid found in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bacillus_cereus_(Food_poisoning)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QcYeVP5GRpujSIM_94q_-4n-QpGuEG1s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bacillus cereus (Food poisoning)]]></video:title><video:description><![CDATA[With Bacillus Cereus or just B. Cereus, “bacillus” means little rod, and “cereus” means wax. 

So Bacillus Cereus refers to a rod-shaped bacteria that looks like a wax-candle. 

Most often, this bacteria causes food poisoning, but it can also cause more serious infections, mainly in immunocompromised individuals. 

B. cereus has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.

Also, it is a motile bacteria, as it has thread-like flagella that can help it swim in a liquid media, or swarm on a solid surface such as culture media.

It’s also aerobic, meaning it requires oxygen for growth.

B. cereus is catalase positive, meaning it produces catalase enzyme. 

This can be tested by adding a few drops of hydrogen peroxide to a colony of bacteria, and catalase makes hydrogen peroxide dissociate into water and oxygen, making the mixture foam. 

It is also a beta-hemolytic bacteria, because when cultivated on a medium called blood agar, B. cereus colonies cause beta-hemolysis, also called complete hemolysis. 

That’s because B. cereus makes a toxin called beta-hemolysin, that causes complete lysis of the hemoglobin in the red blood cells, making the blood agar change color from red to transparent yellow around the colonies

Finally, Bacillus Cereus is a spore-forming bacteria, so it can undergo endosporulation when it feels threatened by the environment, like when the temperature becomes too high or too low, in case of extreme dryness, or when there’s harmful radiation around. 

Endosporulation means that the bacteria starts by replicating its DNA, and then it forms a wall inside the cell, isolating a portion from the rest of the cell - let’s call it the mother cell. 

Next, the plasma membrane of the cell surrounds the mother cell and then pinches it off, forming a separate body known as a forespore. 

The forespore then invaginates into the mother cell and gets completely engulfed by it. 

Insid]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Corynebacterium_diphtheriae_(Diphtheria)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wm7rcWptS8_C6pbF2783lawgREqJzMSY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Corynebacterium diphtheriae (Diphtheria)]]></video:title><video:description><![CDATA[Corynebacterium diphtheriae or just C. diphtheriae takes its name from the Greek;. “Coryne” that means club, and “diphtheriae,” which means leather. 

So to sum this up, C. diphtheriae is a club-looking bacteria that causes diphtheria, an infection with a characteristic tough leathery membrane that forms in the pharynx. 

C diphtheria has four main subspecies; C. diphtheriae mitis, C. diphtheriae Intermedius, C. diphtheriae Gravis, and C. diphtheriae Belfanti. 

OK, now, C. diphtheriae has a thick peptidoglycan cell wall that takes in purple dye when Gram-stained - so it’s a gram-positive bacteria. 

It is aerobic, which means it requires oxygen to grow, and it doesn’t form spores. 

Now, when stained with Albert’s stain, these bacteria demonstrate some unique features. 

They look like green, club-shaped bacteria with metachromatic granules, which are these dark blue dots made of phosphate, located at the bacterial poles. 

When many, and clustered together, these bacteria seem to be arranged in a characteristic pattern that resembles Chinese letters. 

Finally, C. diphtheriae is a fastidious bacteria. 

This means it can only grow on special nutrients-enriched media. 

The medium commonly used to grow this bug is cysteine-tellurite blood agar on which C. diphtheriae grow into black colonies.

Alright, any of the C. diphtheriae subspecies can be either toxigenic or not, depending on whether or not they produce the diphtheria toxin, or DT for short. 

DT is a cytotoxic protein, where cytotoxic means it causes damage to host cells. 

In fact, all the C. diphtheriae subspecies start out as non-toxigenic, but they become toxigenic after they’re infected by a beta-bacteriophage. 

This is a kind of virus that attaches to bacteria and merges its own genome with the bacteria’s. 

The beta-bacteriophage genome contains tox-genes, which code for diphtheria toxin production. 

Following this, C. diphtheriae can make DT, and, in turn, cause diphtheria. 

Now, D]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Listeria_monocytogenes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/anFGh8W8Tg2ZK63WLzeRAFtiQcWRjtox/_.jpg</video:thumbnail_loc><video:title><![CDATA[Listeria monocytogenes]]></video:title><video:description><![CDATA[Listeria monocytogenes or just L. monocytogenes, is a gram-positive bacteria that causes listeriosis. Listeria was discovered by a Scottish doctor, J.H.H. Pirie, who named it in honor of British surgeon Joseph Lister,.  It’s also called “monocytogenes” because when it was inoculated in rabbits, their monocyte levels increased. 

Ok now, L. monocytogenes is a rod-shaped bacteria with a thick peptidoglycan cell wall. So when gram-stained, it takes in purple dye, making it a gram-positive bacteria. It is catalase positive and oxidase negative - which means it produces the enzyme catalase, but not oxidase. L. monocytogenes is a facultative intracellular pathogen, meaning it can live both outside or inside of its host’s cells. It doesn’t form spores and it is facultatively anaerobic, meaning that it can survive in both aerobic and anaerobic environments.

Now, when L. monocytogenes is cultivated on blood agar medium, its colonies cause beta-hemolysis, also called complete hemolysis. That’s because it produces toxins called beta hemolysins, which hydrolyze the hemoglobin within red blood cells to transparent yellow color byproducts.

L. monocytogenes is a motile bacteria, with a very interesting way to move, that depends on both its location, and the temperature. In an extracellular environment, this bacteria moves by beating its flagella creating a characteristic tumbling motility. But this is only possible at 37 degrees Celsius and below. That’s because FlaA, the gene that codes for flagellin, which is the structural protein that makes up the flagella becomes downregulated as the temperature rises up to 37 degree Celsius. So above 37 degrees, there’s reduced production of flagellin proteins, meaning no flagella being made, rendering L. monocytogenes non-motile.

In an intracellular environment, L. monocytogenes moves by an actin-based motility. It start with this bacteria producing a protein called Actin assembly-inducing protein or just ACTA, which recruits s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clostridium_botulinum_(Botulism)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SNFggd5FQ4Kps36mkUvgVZu7QX_xdesK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clostridium botulinum (Botulism)]]></video:title><video:description><![CDATA[Clostridia, as a family, are obligate anaerobes, meaning that oxygen is toxic to them.

In nature, they thrive in deep, compact soil, and when they feel the stress of fresh oxygenated air, they often produce spores, which are metabolically inert and extremely resilient to the environment. 

Then, when environmental conditions improve, the spores are able to sprout into fully fledged Clostridia. 

When doing a Gram stain, Clostridium botulinum stains purple, or Gram positive, and it’s a bacillus, meaning that it looks like a big cylinder or rod under the microscope. 

Clostridium botulinum is notorious for producing a toxin, called botulinum toxin, which causes botulism.

Historically, to preserve foods, processes like sausage making and canning became popular. 

Unfortunately, since these environments block out air, if a Clostridium botulinum spore gets in during the food preparation process, it can grow and produce botulinum toxin, contaminating the food. 

In fact, this is how Clostridium botulinum gets its name, since botulus means sausage in Latin. 

When it infects a can, the can begins to bulge with air because the bacteria metabolized sugars into short chain fatty acids that form a gas. 

And although the short chain fatty acids are mostly made up of carbon dioxide and hydrogen, the gas is particularly foul smelling. 

Now, nerves that use the neurotransmitter acetylcholine are those we use for muscle control. 

Upon ingesting a contaminated food product, botulinum toxin works by binding specifically to these nerves, inhibiting muscle contraction. 

The toxin comes in eight distinct types, named type A, B, C, D, E, F, G, and H, and they vary in their toxicity. 

The neuron takes in the botulinum toxin by endocytosis, creating a small vesicle that floats within the neuron’s cytoplasm. 

The toxin then activates and slips out of the vesicle, and starts to cleave SNARE proteins. 

SNARE proteins tug vesicles containing acetylcholine to the plasma membr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clostridium_perfringens</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ihxKw1NrTJaeyE_i1G3nsD1ySLC99KAW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clostridium perfringens]]></video:title><video:description><![CDATA[Clostridium perfringens is from the family of Clostridia, and as a family, they’re obligate anaerobes, meaning they don’t require oxygen to thrive, in fact, they’re better off without it. 

Anaerobes, clostridia included, tend to lack the enzymes catalase or superoxide dismutase, so oxygen is actually toxic to them. 

In nature, they thrive in deep, compact soil, and when they feel the stress of fresh oxygenated air, they often produce spores, which are extremely resilient to the environment, and can even survive cooking. 

When conditions improve, for example, when food is slowly cooled or stored, the spores can sprout into full-fledged Clostridia. 

In fact, at an optimum temperature, Clostridium perfringens has one of the fastest growing rates of any bacterium! In the lab, when doing a gram stain, Clostridium perfringens is Gram-positive, or purple when Gram stained, and look like big cylinders or rods, also called bacilli.

Clostridium perfringens is a common cause of food poisoning, in fact, it’s sometimes called “the cafeteria germ”. 

That’s because it typically infects food that’s prepared in large quantities, and then kept warm for prolonged periods, such as in cafeterias or buffets. 

Clostridium perfringens are found in the environment and they can accidentally contaminate food when it’s been left out for a while. 

If a person eats food contaminated with C. perfringens, the bacteria will soon colonize the gut. 

Within 24 hours, the bacteria starts to make clostridium perfringens enterotoxin, or CPE. 

The CPE specifically targets the tight junctions that connect epithelial cells lining the intestines to one another. 

When the tight junctions get destroyed, it causes inflammation and compromises the structural integrity of the intestinal wall. 

Fortunately, CPE is heat labile, so prolonged cooking at 72°C or above will inactivate it. 

And that’s one reason why freshly cooked food is best to eat - the other reason is that it’s simply tastier ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clostridium_tetani_(Tetanus)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U06xYHEkT1yAnc2U5lFiX5edQiK5LXXi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clostridium tetani (Tetanus)]]></video:title><video:description><![CDATA[Tetanus means “being taut”, which is a good description of the disease caused by bacteria called Clostridium tetani.  

Clostridia, as a family, are obligate anaerobes, meaning that oxygen is toxic to them. In nature, they thrive in deep, compact soil, and when they feel the stress of fresh oxygenated air, they often produce spores, which are metabolically inert and extremely resilient to the environment. 

Then, when environmental conditions improve, the spores are able to sprout into fully fledged Clostridia. 

When doing a Gram stain, Clostridium tetani stains purple, or Gram positive, and it’s a bacillus, meaning that it looks like a big cylinder or rod under the microscope. 

Clostridium tetani is notorious for one of its toxins, called tetanospasmin, which can severely disrupt the neuromuscular system of mammals. 

Tetanospasmin works by entering special inhibitory neurons called Renshaw cells. 

Once they get inside, tetanospasmin cleaves SNARE proteins, which are proteins that pull vesicles that are loaded with neurotransmitters to the neuron membrane. 

When the SNARE proteins are cleaved, it prevents the release of inhibitory neurotransmitters, like glycine and GABA. 

You can think of SNARE proteins as the rails and the vesicles as trains that are loaded with neurotransmitters. 

And tetanospasmin destroys the “rails”, so that the “trains” can’t move. 

The role of Renshaw cells and inhibitory neurotransmitters is to fine tune the action of the alpha motor neuron, which is in charge of sending the actual signal for contraction to the muscle. 

In tetanus, Renshaw cells fail to work, and the alpha motor neuron keeps firing without any inhibitory control, causing muscle rigidity and spasm. 

Spores of Clostridium tetani are most often introduced into the body through penetrating trauma, like a puncture wound. Puncture wounds are usually anaerobic and warm, and are therefore optimal for growth of Clostridium tetani. 

And an important point is that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Norovirus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bQEZY6h3RUKOMCslupKN07hxQlm8zrHE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Norovirus]]></video:title><video:description><![CDATA[You’ve probably had the stomach flu, at least once, right? Chances are, it was due to norovirus, which is one of the most common causes of viral gastroenteritis. 

Sometimes it’s also called the Norwalk virus, after the town in Ohio where a big outbreak in 1968 allowed scientists to isolate the virus. 

There are several genogroups of norovirus, but only groups I, II, and IV can cause disease in humans.

Norovirus is part of the caliciviridae family of viruses. 

They are naked viruses surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. 

And they’re “naked” because the capsid isn’t covered by a lipid membrane. 

They’re also single strand RNA viruses. 

This means that their RNA is actually mRNA - and the host cell ribosomes use this mRNA to make only long polyprotein chain, which is then broken into smaller pieces by viral proteases. 

This all happens in the cytoplasm of the host cell, since that’s where ribosomes are found, and results in several viral proteins.

The exact role of each specific viral protein is still a bit of a mystery, but we do know that they mainly affect the small intestine. 

The small intestine has lots of tiny ridges and grooves, each of which projects little finger-like fibers called villi. 

And in turn, each villus is covered in teeny tiny little microvilli. This is called the brush border. 

All of this gives the small intestines plenty of surface area to absorb nutrients. 

Norovirus blunts the villi and shortens microvilli, and this disrupts the ability of the brush border to absorb certain nutrients, specifically fat and a simple sugar called D-xylose. 

It also lowers the activity of alkaline phosphatase and trehalase, which are digestive enzymes produced by brush border cells.

Under a microscope, intestinal cells infected by Norovirus have an intact mucosa and epithelium, but there are a lot of lymphocytes in the lamina propria layer of the mucosa. 

Inter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chlamydia_trachomatis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hAI4x-4cTLCuLr0e2sn1ganXT8e6PTKA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chlamydia trachomatis]]></video:title><video:description><![CDATA[Chlamydia trachomatis or just C. trachomatis, is a gram-negative bacteria that strictly infects humans, and it’s divided into 15 serotypes, also known as serovars. 

A serovar groups together bacteria with similar surface antigens, and so are likely to cause the same type of infection. 

Serotypes A through C cause chlamydia conjunctivitis in adults, which also called trachoma. 

Serotypes D through K cause a genital infection called chlamydia. 

Lastly, serotypes L1, L2 and L3 - and there’s no particular reason that these are numbered - infect the lymph nodes, causing a disease called lymphogranuloma venereum, or LVG. 

No matter the serotype, C. trachomatis is a gram-negative bacteria, meaning it cannot retain the crystal violet stain used during gram staining. 

However, unlike other common gram-negative bacteria which have a thin layer of murein, also known as peptidoglycan in their cell wall, the cell wall of C. trachomatis has no any murein at all - so it can’t retain pink safranin dye used during Gram staining, either.

So, C. trachomatis is best stained with Giemsa stain, which colors them pinkish-blue. 

What is more, unlike most bacteria, chlamydia requires vial cells or embryonated hen&amp;#39;s egg for culture, which is technically difficult and expensive, so cultures are only done for research purposes. 

Chlamydia trachomatis is also non-motile, and an obligate aerobe, meaning it absolutely depends on oxygen to survive. 

It’s also an obligate intracellular pathogen, because it’s unable to make its own ATP for energy, so it needs to use another cell’s resources.

Ok now, when C. trachomatis enters a host cell, it undergoes a life cycle that alternates between two distinct forms. 

The first is the small spore-looking form called the elementary body, and it’s the infective form of this bacteria. 

After the elementary body enters the host cell, it gets enclosed in a vacuole called an inclusion, where it transforms into a metabolically ac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Francisella_tularensis_(Tularemia)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ljp6_0CiTVqchoOiEczNqjeAR-2CXGMe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Francisella tularensis (Tularemia)]]></video:title><video:description><![CDATA[Francisella tularensis is a Gram-negative coccobacillus, which means that shape-wise, it’s somewhere between a spherical coccus and a rod-like bacillus.

In humans, it causes a zoonotic infection called tularemia, also called rabbit fever. 

This bacteria is also considered a category A bioterrorism agent which means it is of highest concern for bioterrorism use, because of its low infectious dose and high associated mortality.

Now, Francisella tularensis has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. 

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye.

Alright, now Francisella tularensis is non-motile, non-spore forming, facultative intracellular which means it can survive both outside and inside the cell and aerobic which means it can survive only in the presence of oxygen. 

Also, it’s oxidase and urease negative which means it doesn’t produce these enzymes.

Finally, Francisella tularensis is a fastidious bacteria which requires enriched medium for growth. 

And Francisella tularensis really loves cysteine, so it only grows in about 47 to 72 hours on cysteine-enriched mediums like cysteine enriched chocolate agar, BCYE and CHAB. 

Cysteine enriched chocolate agar, named so for its color, actually contains cysteine and lysed red blood cells - so no chocolate products were harmed in the making of this medium. 

BCYE stands for buffered charcoal yeast extract, so it contains activated charcoal, yeast extract, and L-cysteine. 

On these two mediums, Francisella tularensis forms round, grey-white colonies. 

Finally, CHAB is a glucose cysteine agar that contains thiamine and blood, and on CHAB, Francisella tularensis forms greenish-white, round, smooth, mucoid colonies.

Now, Francisella tularensis has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.

So first, Francisella tularensis is]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brucella</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KpgmJ9D9TGe7AIPJLPg79QF3S0SV_YRj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brucella]]></video:title><video:description><![CDATA[Brucella is a genus of Gram-negative coccobacilli, and it groups together several species including Brucella abortus, Brucella melitensis, Brucella canis and Brucella suis. 

All cause a systemic disease called brucellosis, but each of them has a different host, and causes a different form of the disease.

Now, Brucella it’s a non-motile bacteria that doesn’t form spores. 

It’s a strict aerobe, meaning that it needs oxygen to survive, and also, it’s facultative intracellular which means it can survive both inside and outside the cell.

Finally, it’s urease and catalase positive which means it produces both these enzymes.

Brucella is usually isolated on blood cultures, with biphasic methods like the Ruiz-Castaneda methods.

Biphasic means that the blood culture bottle has both a solid phase, and a liquid phase. 

Now, Brucella is a very slow growing bacteria, so colonies usually grow in the solid medium after 6 to 8 weeks of incubation. 

The colonies are raised, convex with smooth, shiny corners. 

On the bright side, there are now some modern automated blood culture systems called the Bactec systems, which are more effective and can isolate Brucella after only 1 week. Neat!

Now, Brucella can enter the body one of two ways. 

First, there may be direct contact with infected animals - and the host is different for each Brucella species. 

So, B. abortus is transmitted by cattle, B. melitensis is transmitted by small ruminants such as goats and sheep, B. canis is transmitted by dogs and B. suis is transmitted by swine and rodents. 

In this case the bacteria enters through skin lesions, mucous membranes and inhalation. 

The second way is ingestion of contaminated animal products such as unpasteurized milk, cheese and undercooked meat.

So, once the bacteria is inside the bloodstream, it’s ingested by phagocytes like macrophages and neutrophils.

Normally, phagocytes destroy invading bacteria by wrapping them up in vesicles called phagosomes, which will m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Haemophilus_ducreyi_(Chancroid)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5kEo2R4kTCKvScLVpvX2h4xFQJyukIc7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Haemophilus ducreyi (Chancroid)]]></video:title><video:description><![CDATA[Haemophilus ducreyi is a Gram-negative coccobacillus, which means that shape-wise, it’s somewhere between a spherical coccus and a rod-like bacillus. 

Haemophilus ducreyi is an obligate human pathogen and causes a sexually transmitted disease, called chancroid.

Now, Haemophilus ducreyi has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye used during Gram staining. 

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. 

So, under the microscope, the bacteria look like short or relatively long pink rods with rounded ends, that usually grow in chains, so they’re sometimes compared to a “school of fish”.

Now, Haemophilus ducreyi is: non-motile, so it doesn’t move / facultatively anaerobic, which means it can survive in both aerobic and anaerobic environments / oxidase positive which means it produces an enzyme called oxidase / and catalase negative, which means it doesn’t produce an enzyme called catalase.

Finally, Haemophilus ducreyi can be cultivated on chocolate agar, because this medium contains essential nutrients that Haemophilus ducreyi need to grow, like factor X, also called hemin. 

They’re fastidious bacteria that only grow in a CO2 environment, at a temperature between 33 and 35 degrees Celsius, and it forms small, grey or translucent colonies.

Now, Haemophilus ducreyi enters the body through mucosal and skin breaks and has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.

Now, Haemophilus ducreyi is encapsulated, so it has a polysaccharide layer called a capsule, that acts like a shield, protecting the bacteria against phagocytic cells like macrophages and neutrophils. 

On the capsule there are  fimbria-like proteins, such as Flp1, Flp2 and Flp3 and uses them to attach to subcutaneous epithelial cells and fibroblasts. 

Underneath the capsule there’s an outer membrane which consist of lipo-oligo-sacch]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pasteurella_multocida</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r6_ZYop0S2mBk7LoeH4ThtmITHuRtmo2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pasteurella multocida]]></video:title><video:description><![CDATA[Pasteurella multocida is a gram-negative coccobacillus which is involved in a zoonotic infection. 

Most often, it causes soft tissue and respiratory infections. 

There are 3 subspecies that cause disease in humans: Pasteurella multocida subspecia multocida, Pasteurella multocida subspecia septica and Pasteurella multocida subspecia gallicida. 

All of these subspecies are encapsulated, meaning they have a polysaccharide layer called a capsule. 

And depending on the capsular antigens found on the capsule, they can be grouped in 5 different serogroups: A, B, D, E and F. 

Each of them is involved in a different type of disease and only serogroups A and D cause disease in humans. 

So, serotype A causes respiratory infections and serotype D causes soft tissue infections like cellulitis.

Now, Pasteurella multocida has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during gram staining. 

Instead, like any other gram-negative bacteria, it stains pink with safranin dye. 

But, sometimes, it can have a bipolar staining which means that only the poles of the bacteria stain pink, and the rest of it remains unstained, so the bacteria look like safety pins under the microscope.

Alright, now Pasteurella multocida is non-motile, non-spore forming, and facultative anaerobic which means it can survive in both aerobic and anaerobic environments. 

It’s oxidase and catalase positive, which means it can produce both these enzymes, and it’s also nitrate reduction positive which means it can produce an enzyme that hydrolyzes nitrate into nitrite.

Finally, Pasteurella multocida grows well at 37ºc on sheep blood agar, which is the preferred culture medium, but it can also grow on chocolate agar, Mueller-Hinton agar or brain heart infusion agar. 

The colonies are opaque or grey, and small - they’re only about 1-2 millimeters in diameter each.

Now, Pasteurella multocida has a number of virulence factors, that are like assault weaponry that help it]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Campylobacter_jejuni</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jyepw4TERaK1g5uuX5YY9iPiRI6JFwHc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Campylobacter jejuni]]></video:title><video:description><![CDATA[With Campylobacter jejuni, “campylo” means curved, “bacter” means rod, while “jejuni” refers to the jejunum, which is a segment of the small intestines found between the duodenum and the ileum. 

So, Campylobacter jejuni is a comma-shaped bacteria, and it’s one of the most common causes of bacterial gastroenteritis worldwide. 

It&amp;#39;s commonly found in foods like poultry, and unpasteurized milk.

Now, let’s talk microbe anatomy and physiology. Campylobacter jejuni is a comma-shaped bacteria that has a thin peptidoglycan cell wall, which doesn’t take in the purple dye when Gram stained, and instead appears pink or red – which makes it a gram-negative bacteria. 

It also  has a flagellum at one end which it uses to get around, so it’s a motile bacteria. 

In addition to this, it’s oxidase-positive, meaning that it can use oxygen to create stored energy or ATP. 

Lastly, Campylobacter jejuni is a microaerophile that loves warmth, so it grows best in low-oxygen environments, at 42 degrees Celsius, on blood agar varieties like Skirrow, Butzler, and Campy-BAP.

Alright, Campylobacter jejuni is usually transmitted from animals to humans, via the fecal-oral route. 

In other words, you catch it by ingesting stool particles containing the bacteria. 

Campylobacter jejuni usually resides in the gastrointestinal tract of birds. 

So, when people eat raw and undercooked poultry, there&amp;#39;s a possibility of infection. 

Similarly, cows are common carriers, so people that drink unpasteurized milk can also risk infection. 

There’s also direct contact with infected pets, notably puppies which excrete the bacteria in their stool. 

Kids are the most susceptible to getting infected after playing with an infected pet. 

Lastly, infected stool can end up in sources of freshwater, like rivers, and cause infection. 

Once inside our body, Campylobacter jejuni has a number of virulence factors that it can use to attach to host cells and cause disease. 

First,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Helicobacter_pylori</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j189duquRxCiJYaiTS0k3uAgRvifJdiD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Helicobacter pylori]]></video:title><video:description><![CDATA[Helicobacter pylori, or H. pylori for short, is a bacterium found in the stomach of over half of the world’s population. 

In some individuals it can cause inflammation of the stomach lining; and can result in peptic ulcers.

In fact, complications from H. pylori ulcers is thought to have been the cause of death for the famous writer, James Joyce. 

H. pylori is a gram-negative bacteria that’s shaped like a curved rod and it has 2 to 6 flagella, kind of like multiple tails, all at one end which it uses for movement. 

It’s positive for urease, oxidase and catalase; and is a microaerophile, so that means it needs oxygen to survive, but requires less than the levels typically found in the atmosphere. 

Now in the stomach, there are four regions - the cardia, the fundus, the body, and the pylorus.

And the pylorus itself is made up of two main parts: the antrum; and the pyloric canal, which connects to the first section of the small intestines called the duodenum. 

Ok, now normally, the inner wall of the entire gastrointestinal tract is lined with mucosa, which consists of three cell layers.

The innermost layer is the epithelial layer and it absorbs and secretes mucus and digestive enzymes. 

The middle layer is the lamina propria and it has blood and lymph vessels. 

The outermost layer of the mucosa is the muscularis mucosa, and it’s a layer of smooth muscle that contracts and helps with the break down food. 

The epithelial layer dips down below the surface of the stomach lining to form gastric pits. 

And these pits are contiguous with gastric glands below which contain various epithelial cell types - each secreting a variety of substances. 

So for example, foveolar cells, or surface mucus cells, secrete mucus, which is a mix of water and glycoproteins that coats the stomach epithelial cells. 

With all of these digestive enzymes and hydrochloric acid floating around, the stomach and duodenal mucosa would get digested if not for this mucus which coats ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vibrio_cholerae_(Cholera)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jTbs5YYVR5a2HV4UgM7VEss7Tf6fh8eW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vibrio cholerae (Cholera)]]></video:title><video:description><![CDATA[Cholera is a contagious infection caused by the bacteria Vibrio cholerae, which can in turn cause severe gastroenteritis and excessive watery diarrhea for several days.

Rapid dehydration and electrolyte imbalances can be fatal as suspected in the deaths of James K. Polk, the 11th President of the United States; and Charles the Tenth, King of France.    

V. cholerae is a gram-negative, curved bacteria which looks like little red or pink comma-shapes on a gram stain. 

It’s positive for oxidase and grows in alkaline media. 

It has pili and a single polar flagellum, kind of like a tail, at one end which it uses for movement through the gastrointestinal tract. 

It’s a facultative anaerobe so that means it can undergo respiratory and fermentative metabolism.  

Transmission of V. cholerae typically occurs through a fecal to oral route.

This includes consuming untreated sewage water, and anything that comes in contact with it, like raw or undercooked fish including shellfish; and improper hygiene, like a lack of hand washing after a bowel movement. 

Cholera tends to be more common in developing countries and places lacking advanced sanitation and sewage treatment facilities, with high rates in some locations in Africa and South America. 

People who have low gastric acidity or have an O-blood type are particularly at risk for a severe infection.  

Now, when V. cholerae enters the stomach it shuts down protein production to conserve energy and nutrients, and to survive the acidic environment.

But once V. cholerae is in the intestines, it uses its flagella to move toward the intestinal walls; propel through the mucous layer on top of the epithelial cells lining the intestines; and attach to the finger-like cellular projections, called villi, on the surface of the epithelial cells. 

There, V. cholerae can begin to multiply and produce toxins. 

And though V. cholerae does not enter the epithelial cells itself, the toxins do and they can cause a lot of trou]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Moraxella_catarrhalis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Gq-JoslVQkKGlcD6haaHZGHzRACMq0bJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Moraxella catarrhalis]]></video:title><video:description><![CDATA[Moraxella catarrhalis is a Gram-negative diplococcus, which means it’s a spherical-shaped bacteria that usually hangs out in pairs of two.  

Moraxella has had a bunch of names over the last century. 

When it was first discovered it was named Micrococcus catarrhalis, then its name was changed into Neisseria catarrhalis. 

Later it was moved to another genus, called Branhamella, and finally it was moved again to genus Moraxella, species Moraxella catarrhalis. 

It normally colonizes the upper respiratory tract, and usually causes otitis media in children. 

Now, Moraxella catarrhalis has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. 

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye.

Moraxella catarrhalis is also non-motile, non-spore forming, aerobic, which means it needs oxygen to survive, and oxidase positive, which means it produces an enzyme called oxidase. 

However, it’s maltose fermentation negative which means it cannot ferment maltose. 

To check for this, a pure sample from the culture is transferred to a sterile tube containing a mix of phenol red and maltose, which is then incubated at 36 degree Celsius for 24 hours. 

If acidic fermentation of maltose occurs, the resulting byproducts make the solution go yellow. 

With Moraxella catarrhalis, the solution stays red. 

Finally, it grows well on blood and chocolate agar and it doesn’t grow on modified Thayer-Martin agar, like other Gram-negative diplococci, such as Neisseria species. 

So, on blood and chocolate agar it grows into round, gray-white colonies. 

Finally, Moraxella catarrhalis colonies are positive for the hockey puck test, which means a loop is used to push the colonies across the plate. 

Moraxella colonies are sturdy, and can be slid across the plate without breaking, which means a positive hockey puck test. 

Now, Moraxella catarrhalis is an opportunistic pathogen, which means that it doesn’t usual]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neisseria_gonorrhoeae</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Lb-s-QFBSpa3Uo1JjMNyXbyySFe-JNFy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neisseria gonorrhoeae]]></video:title><video:description><![CDATA[Neisseria gonorrhoeae, also known as N. gonorrhoeae to its friends, is a gram-negative oval bacterium that infects humans, causing a number of infections including gonorrhea. 

The word Neisseria came from Neisser Albert, a German physician who discovered it, while gonorrhea is from the Greek words “gonos” which means &amp;quot;seed&amp;quot;, and “rhoe” which means &amp;quot;flow&amp;quot;, meaning &amp;quot;flow of seed&amp;quot;, an illustration referring to the penile purulent discharge, which was mistakenly thought to be semen in infected males.

Now, a little bit of microbe anatomy and physiology. N. gonorrhoeae is a gram-negative bacterium, because its cell wall has a thin peptidoglycan layer and so it doesn’t retain purple dye used during Gram staining. 

Instead, like any other Gram-negative bacteria, N. gonorrhoeae  stains pink with safranin dye. 

N. gonorrhoeae typically live in  pairs called diplococci, stacked side to side, so the pair looks like a coffee bean. 

They are also non-motile, non-spore forming, and obligate aerobes, which means that they absolutely need oxygen to grow. 

Finally, they’re catalase and oxidase positive - which means they produce both these enzymes. 

N. gonorrhoeae grows on a special chocolate medium called Thayer-Martin agar, which mainly consists of sheep blood... err, yum? 

Some antimicrobials, like vancomycin and nystatin are usually added to the Thayer-Martin agar, to inhibit the possible growth of undesired bacteria or fungi, and maximize the growth of Neisseria species.

However, other Neisseria species, like N. meningitidis, have the same properties.

So the maltose fermentation test is done to differentiate the two. 

The gist of it is that N. gonorrhoeae can’t ferment maltose, whereas N. meningitidis can. 

To check for this, a pure sample from the culture of the suspected bacteria, is transferred to a sterile tube containing phenol red-maltose broth, which is then incubated at 36 degrees Celsius f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neisseria_meningitidis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N2bv3cLMRamY1ZBx-6dfdml8TfeuuWrz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neisseria meningitidis]]></video:title><video:description><![CDATA[Neisseria meningitidis, also called N. meningitidis or just meningococcus, is a gram-negative round bacterium that causes meningitis in humans, as well as life-threatening conditions like sepsis and disseminated intravascular coagulation. 

Now, N. meningitidis has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. 

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. 

N. meningitidis typically live in pairs called diplococci, stacked side to side, so the pair looks like a coffee bean. 

They are also non-motile, non-spore forming, and obligate aerobes, which means that they absolutely need oxygen to grow. 

Finally, they’re catalase and oxidase positive - which means they produce both these enzymes. 

N. meningitidis grows on a special chocolate medium called Thayer-Martin agar, which mainly consists of sheep’s blood... err, yum? 

Some antimicrobials, like vancomycin and nystatin are usually added to the Thayer-Martin agar, to inhibit the possible growth of undesired bacteria or fungi, and maximize the growth of Neisseria species.

However, other Neisseria species, like N gonorrhoeae, also share these properties. 

So the maltose fermentation test is done to differentiate the two. 

The gist of it is that N. meningitidis can ferment maltose, whereas N. gonorrhoeae cannot. 

To check for this, a pure sample from the culture is transferred to a sterile tube containing a mix of phenol red and maltose, which is then incubated at 36 degrees Celsius for 24 hours. 

N. meningitidis causes acidic fermentation of maltose, and the resulting byproducts make the solution go yellow. 

With N. gonorrhoeae, the solution stays red. 

Now, N. meningitidis has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system. 

First, N. meningitidis is encapsulated - meaning it’s covered by a polysaccharide layer called a capsu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Enterococcus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jcT1kf5iTlaFVeiKl93E0DB3QTuWNZlP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Enterococcus]]></video:title><video:description><![CDATA[With Enterococcus, entero- refers to the intestines, while -coccus means round shape. 

So Enterococcus is a genus of round bacteria that commonly colonizes the gut of humans and animals. 

Enterococcus is also called Group D streptococcus in Lancefield classification developed by an American microbiologist Rebecca Lancefield. 

There are two species that can cause infections in humans and these are Enterococcus faecalis, amounting for the majority of infections, and Enterococcus faecium, which causes disease more rarely. 

Now, looking at an individual bacterium, Enterococcus has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria. 

When there’s more of them, Enterococci grow in short chains, usually in pairs. 

They’re non-spore forming, facultative anaerobes, meaning that they can survive in both aerobic and anaerobic environments and catalase negative, which means they don’t produce an enzyme called catalase. 

Enterococci also can tolerate extreme environmental conditions including high sodium chloride concentrations, high pH and even high temperatures. 

They can survive at 60 degrees Celsius for up to 30 minutes!

Ok, now, enterococcus is pyrrolidonyl arylamidase positive, because it makes an enzyme called L-pyrrolidonyl arylamidase. 

To test for this, a small sample is taken from a suspected bacterial colony, and then inoculated to a disk pad that’s embedded with pyrrolidonyl beta naphthylamide - another joy of a word. 

With Enterococcus, pyrrolidonyl arylamidase hydrolyzes pyrrolidonyl beta-naphthylamide to produce beta-naphthylamide. 

Try saying that 3 times fast! Finally, another reagent called N-methylamino-cinnamaldehyde is added to the disk, and it reacts with beta-naphthylamide, resulting in a bright red color that confirms Enterococcus is pyrrolidonyl arylamidase positive.

Now, most commonly, Enterococci are gamma hemolytic which means that when cultivated on blood agar the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Actinomyces_israelii</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q5baWRr_Qb_Emk8eRA9FwQ6xTSu2xcOv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Actinomyces israelii]]></video:title><video:description><![CDATA[Actinomyces israelii, or just A. israelii, is a gram-positive rod-shaped bacteria that causes a human infection called actinomycosis. 

Calling this bug actinomyces implies that it’s morphologically similar to fungus, because both form microscopic branching filaments (or mycelium), while the word Israelii comes from James Adolf Israel, the German surgeon who first described it.

OK, A. israelii is a rod-shaped gram-positive bacteria, we’ve got that part down, but what this means is that it goes purple when gram-stained. 

When there’s many of them, they arrange themselves in the shape of purple branching filaments.

They are anaerobes, meaning they grow better without oxygen, they are also non-motile, and don’t form spores.

But wait… that sounds exactly like Nocardia, another group of rod shaped, gram-positive, filamentous bacteria with a lot of other similar features. 

To distinguish them, an acid-fast stain, also called Ziehl-Neelsen stain is done. 

With this test, a red dye called carbon fuchsin, binds to lipids in the cell wall, coloring them red. 

Then alcohol is applied to wash out any dye that hasn’t colored bacteria, and a second dye, methylene blue, is applied. 

In bacteria who don’t have a lot of lipids in their cell wall, like A. Israelii, all the red dye is washed off by alcohol, so it looks blue under the microscope, making it a non-acid-fast bacteria. 

On the other hand, Nocardia has plenty of lipids in its cell wall, so it retains the carbon fuchsin, and it looks red under the microscope, making it an acid-fast bacteria. 

Another difference is that A. Israelii is catalase negative, so it doesn’t make an enzyme called catalase, whereas Nocardia is catalase positive. 

Finally, A. israelii is cultivated on blood agar, and then incubated in anaerobic conditions. 

It’s a slow-glowing microbe, so it takes up to 21 days to form colonies, which look like white round plaques, with some little grooves in the middle, forming a characteristic m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Yellow_fever_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pU_j44tAQTuOdKbM8n4Q4VrHQjuE6yNq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Yellow fever virus]]></video:title><video:description><![CDATA[Yellow fever virus causes a disease called yellow fever, named so because severe forms of the disease result in  jaundice, which is a yellowish pigmentation of the skin and mucous membranes. Yellow fever virus belongs to the flaviviridae family of viruses, which also includes dengue fever virus and Zika virus. Interestingly, the flaviviridae family is actually named after the yellow fever virus, flavus being Latin for yellow. The virus is endemic to regions of Africa and South America. 

Yellow fever virus is an enveloped virus with an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. Inside the capsid there’s a single-stranded, positive-sense ribonucleic acid, or RNA. This means that their RNA is actually mRNA, which can directly be translated by the host cell ribosomes into new copies of the viral proteins, which get assembled into new viruses. 

Yellow fever virus doesn’t just affect humans, but also other primates like monkeys and apes. And it’s also considered an arbovirus because it’s transmitted via certain arthropod vectors, or carriers, specifically mosquitoes in the Haemagogus and Aedes genera. Haemogogus mosquitoes transmit the virus among monkeys in the jungle, and that’s called the Sylvatic cycle. If an unsuspecting person on a trek chances upon one of these mosquitoes in the jungle, then they get infected too, and end up spreading the virus to other people. Aedes mosquitoes, most commonly Aedes aegypti, transmit the virus in urban areas, and that’s called the urban cycle.

Alright, so when a mosquito bites you, it releases the yellow fever virus in between your skin cells. The virus especially targets dendritic cells, which are specialized immune cells that normally eat up, or phagocytose, antigens in the skin and transfer them to immune cells in the lymph nodes. The virus then latches onto specific receptors on the dendritic cell membrane, which allows the virus to be endocytosed, or engulfed,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gardnerella_vaginalis_(Bacterial_vaginosis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8_nHp-ufRReEVCFKRVqX-H-URfOY4IK-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gardnerella vaginalis (Bacterial vaginosis)]]></video:title><video:description><![CDATA[Gardnerella vaginalis, or G. Vaginalis for short, is a gram-variable coccobacillus present in low numbers in normal vaginal flora. 

Normally, the vaginal flora is made up mostly of Lactobacilli, which keep vaginal pH below 4.5. 

When the number of Lactobacilli decreases, that results in an imbalance of vaginal flora which increases the vaginal pH. 

This allows G. vaginalis to proliferate, causing Bacterial Vaginosis, or BV which is the most common vaginal infection in females of reproductive age.

Now, G. vaginalis is gram-variable, which means it can stain either positive or negative with Gram-staining. 

Ok, so normally, whether a bacteria is Gram-positive or Gram-negative is determined by the amount of peptidoglycan in their cell wall. 

Bacteria with a thick peptidoglycan wall take in the purple dye used during Gram staining, so they’re Gram-positive. 

Bacteria with a thin peptidoglycan wall can’t retain the purple dye, and instead stain pink with the Safranin dye used during Gram-staining. 

So, Gram-variable bacteria, like G. vaginalis, first appear Gram-positive and then, as the culture ages, they gradually lose the peptidoglycan in their wall, and once their wall is too thin to retain purple color, they become Gram-negative.  

Finally, G. vaginalis is non-spore forming, non-motile and facultative anaerobic which means it can survive in both aerobic and anaerobic environments.

Now, when vaginal pH increases, G. vaginalis can use a number of virulence factors to cause disease. 

What is more, along with G. vaginalis, a number of other anaerobic bacteria species can proliferate, like Mobiluncus, Bacteroides or Prevotella which are also present in low numbers in normal vaginal flora - resulting in a mixed infection.

Ok, now, G. vaginalis produces a cytotoxin called vaginolysin and an enzyme called sialidase, and both of these help it adhere to the vaginal epithelial cells and colonize the vaginal epithelium. 

Also, sialidases can cleave the sia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mycoplasma_pneumoniae</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sgs-qetoSYavcXRfnmVQrvYCRMuc-ibg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mycoplasma pneumoniae]]></video:title><video:description><![CDATA[Mycoplasma pneumoniae is a small bacterium which causes atypical pneumonia in young adults.  

Mycoplasma, as a genus, have a cell membrane that is packed with sterols, but they lack a proper, rigid cell wall. 

Therefore, they don’t take up dye under Gram staining, so they can’t be visualized with light microscopy. 

Additionally, they are highly pleomorphic bacteria, meaning they have no fixed shape and size, and they’re also osmotically unstable in the external environment. 

So, to survive, Mycoplasmas invade host cells and live intracellularly. 

Now, Mycoplasma pneumoniae is a facultative anaerobe, meaning it can live without oxygen if it has to, but it grows better in an aerobic environment. 

So it prefers places like lungs or respiratory airways, where there is an unlimited flow of oxygen. 

As a result, some people may carry this bacteria in their nose or throat, and when they sneeze or cough, these organisms get out in the form of small respiratory droplets. 

And when other people inhale these droplets, they may get infected, especially when they spend a lot of time together in close quarters. 

So Mycoplasma pneumoniae infections occur mostly in children who go to school, young adults in college, or military recruits.

Following inhalation of the pathogen droplets, Mycoplasma pneumoniae attaches to an epithelial cell in the respiratory tract, using a specialized attachment organelle which has an adhesive protein complex, called ‘adhesion protein P1’ at its tip. 

Adhesion protein P1 attaches to the host cell surface, like the respiratory epithelial cell, and holds on for dear life.

This makes it much harder for the mucociliary clearance mechanisms, which normally remove any foreign pathogen out of the respiratory tract, to clear the bacteria. 

So Mycoplasma pneumoniae multiplies and damages the respiratory epithelial cells in the process.

When they reach the lungs, this starts a local inflammatory response, and lung tissue fills with white ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mycobacterium_leprae</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1m2MOkhyTs_4n2NgIU3a-5B6TxuuxlrY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mycobacterium leprae]]></video:title><video:description><![CDATA[Mycobacterium leprae is a rod-shaped bacteria which was first discovered in 1873 by Hansen. 

Mycobacterium leprae is a non tuberculous mycobacteria and it causes a disease called leprosy, or Hansen disease. In US, the animal reservoir for Mycobacterium leprae are armadillos.

Now, Mycobacterium leprae it’s an acid-fast bacillus which means it’s resistant to decolorization by acids and it has a high content of mycolic acid in its cell wall, which makes it waxy, hydrophobic and impermeable to routine stain such as Gram stain. 

So, it needs special staining methods to be visualized such as Ziehl-Neelsen staining which uses carbol fuchsin combined with phenol which is able to penetrate the waxy mycobacterial cell wall. 

So, the stain binds to the mycolic acid in the mycobacterial cell wall and after staining, an acid decolorizing solution is applied which removes the red dye from the background cells, tissue fibres, and any organisms in the smear except Mycobacteria, which retain the dye. 

So Mycobacterium leprae appears bright red on a blue background. Other staining methods can be used such as Kinyoun staining, in which the bacteria appear bright red on a green background and fluorescence microscopy using specific fluorescent dyes such as auramine-rhodamine stain.

Now, Mycobacterium leprae is an obligate intracellular microorganism, which means it can survive only inside cells, and it’s an obligate aerobe which means it can survive only in the presence of oxygen.

Finally, Mycobacterium leprae grows best at cool temperatures, between 27 to 33 degrees Celsius, and it proliferates slowly and it cannot be cultivated in vitro. 

Instead, it can be inoculated in nine-banded armadillos, which have a much lower body temperature than most mammals and, like humans, are susceptible to leprosy.

Now, Mycobacterium leprae can enter the body through the lungs or broken skin. 

Once inside the body, it goes for regions in which the temperature is lower than the rest ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_parainfluenza_viruses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vkkc-BJlS0_RIIHVDS2rSR6qTkqkVboj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human parainfluenza viruses]]></video:title><video:description><![CDATA[Human parainfluenza viruses, or HPIV, are a group of viruses that commonly cause respiratory tract infections, especially in children.

In fact, they are the second most common cause of acute respiratory infections in children under 5 years of age. 

Parainfluenza viruses are part of the paramyxoviridae family of viruses, and there are four types that infect humans - types I, II, III, and IV. 

Now, parainfluenza viruses are enveloped viruses which means that they are covered by a lipid membrane. 

Inside the lipid membrane is a nucleocapsid which contains a single stranded, negative sense RNA genome and an RNA polymerase enzyme. 

And, on the lipid membrane are two glycoproteins - HN, or hemagglutinin-neuraminidase, protein; and F, or fusion, protein. 

Parainfluenza viruses are transmitted when an infected person sneezes or coughs, which spreads thousands of droplets containing the virus into the surrounding area up to about two meters, or six feet, away. 

These droplets can then land in the mouths or noses of people nearby, or be inhaled into their lungs.

The virus can also survive on surfaces for a few hours, so it’s possible to get the virus by touching an infected surface, like a contaminated doorknob, and then touch your own eyes, nose, or mouth.

When the parainfluenza virus enters the body, it uses hemagglutinin to bind to sialic acid sugars on the surface of epithelial cells in the respiratory tract. 

Once bound, the fusion, or F protein helps the virus fuse with the epithelial cell membrane and release the nucleocapsid into the cytoplasm. 

In the cytoplasm, an enzyme called RNA polymerase transcribes the negative sense viral RNA into positive-sense mRNA strands, which is then translated by host cell ribosomes into viral proteins and assembled into new viruses. 

These viruses leave the cell by using neuraminidase, which cleaves the sialic acid sugars of the cell membrane, allow the newly created viruses to simply bud out of the cell. 

The n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rhinovirus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4eJSE_ArQD_m805rQixrW_R4RcOVasYt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rhinovirus]]></video:title><video:description><![CDATA[Human Rhinovirus (HRV) is a communicable, infectious virus that causes inflammation of the nasal mucosa, or rhinitis.

It mainly causes upper respiratory tract infections, and gets its rhino- name, meaning nose, because it commonly causes a runny nose, nasal congestion, and sneezing, as well as a sore throat and cough. 

There are over 100 serologic known types and all of them can cause a &amp;quot;common cold” in humans!

Now, rhinovirus belongs to the picornaviridae family of viruses. 

They are naked viruses, about 30 nanometers in diameter, and they’re surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. 

And they’re “naked” because the capsid isn’t covered by a lipid membrane. 

They’re also single-stranded, positive-sense ribonucleic acid, or RNA, viruses. 

This means that their RNA is actually mRNA, which the host cell ribosomes use to make viral proteins. 

Unlike other picornaviruses, rhinoviruses are acid labile. 

That means they can be destroyed by stomach acid, so they don’t typically infect the GI tract and don’t spread through a fecal-to-oral route. 

On the other hand, rhinoviruses commonly infect the epithelium of the respiratory mucosa, which lines the nasal cavity.  

So rhinovirus transmission occurs through contact with infected respiratory secretions, like snot and aerosols, particularly from nose blowing or sneezing. 

Touching an infected surface, like a door handle or shaking hands, and then touching an uninfected respiratory mucosa is a main way to transfer an infection - that’s because rhinoviruses can survive up to 2 hours on the skin, and 4 days on surfaces. 

Once rhinovirus has been introduced to the respiratory mucosa, it targets cell surface receptors expressed at the surface of nasal epithelial cells. 

Rhinoviruses can target a few specific receptors for entry, but one in particular is intercellular adhesion molecule-1, or ICAM-1. 

This attachment allows f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/BK_virus_(Hemorrhagic_cystitis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WXbNSkxFSp_7WsrdSF_G9ZmBRK6yRKcY/_.jpg</video:thumbnail_loc><video:title><![CDATA[BK virus (Hemorrhagic cystitis)]]></video:title><video:description><![CDATA[BK virus, or BKV, is named after the initials of the patient in whom the virus was first identified. BK virus typically infects the urinary system of immunocompromised individuals, or those with a weakened immune system, especially those receiving immunosuppressive medications following organ transplants.  

Major clinical manifestations of BKV infection include hemorrhagic cystitis, which is inflammation of the urinary bladder associated with bloody urine, in bone marrow transplant recipients; ureteral stenosis, or narrowing, and nephropathy in kidney transplant recipients. 

BK virus belongs to the polyomavirus family along with the JC virus. These contain a circular double-stranded DNA genome which is surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. They are also called non-enveloped viruses since the capsid isn’t covered by a lipid membrane. 

It turns out that the vast majority of the population is infected with BK virus during their childhood. The virus is thought to be transmitted from person to person through respiratory droplets when someone coughs or sneezes and by ingesting contaminated food and water.  

Once inside, the virus moves through the bloodstream and eventually reaches the kidneys, specifically the renal tubular epithelial cells, where it starts to replicate. But, the cytotoxic CD8+ T cells of our immune system keep the virus in check by killing any cell that has replicating BK virus inside it. However, the sneaky little viruses are not eliminated, but instead they hit the snooze button, and go into a latent phase within the kidney epithelial cells. In other words, they’re not dividing or causing disease.  

Most people with a healthy immune system are able to keep BK virus in the latent phase in the kidney epithelial cells for their entire life. But things can change if the immune system gets weaker. This can happen for various reasons, like an HIV-infected individual]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/JC_virus_(Progressive_multifocal_leukoencephalopathy)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nJWCiCmgRVmukdpvnaMd6Tl2QTiEkgjE/_.jpg</video:thumbnail_loc><video:title><![CDATA[JC virus (Progressive multifocal leukoencephalopathy)]]></video:title><video:description><![CDATA[In progressive multifocal leukoencephalopathy, progressive means that the disease worsens over time, multifocal means the disease affects multiple locations, leuko refers to white, and encephalopathy refers to a disease of the brain.

So progressive multifocal leukoencephalopathy or simply PML, is a disease of the white matter of the brain that affects multiple locations and worsens over time. 

If we look at a cross section of the brain, it can be divided into two areas: the outermost area is the grey matter, which is made up of neuron cell bodies, and the innermost area is the white matter, which is made up of the axons that come off of the neuron cell bodies. 

The axons transmit electrical impulses to the next neuron in the series. 

The axons are surrounded by a fatty protective sheath called myelin that helps increase the speed at which electrical impulses are sent. 

Myelin is produced by a special type of cells called oligodendrocytes. 

The cause of progressive multifocal leukoencephalopathy is the John Cunningham virus, or simply JC virus, named after the first patient in whom the virus was identified. 

JC virus is a non-enveloped virus with closed circular double-stranded DNA genome. 

It’s thought that the virus is transmitted from person to person through the respiratory and gastrointestinal tract, and that it then moves through the bloodstream and eventually reaches kidney epithelial cells. 

JC virus enters these kidney cells and starts replicating, but the cytotoxic CD8+ T cells of our immune system keep the virus in check by killing any cell that has replicating JV virus. 

So to be clear, the virus is not eliminated, but instead it remains latent in the kidneys, meaning that it isn’t dividing and causing disease. 

And It turns out that the vast majority of the population is infected by JC virus - that might include you! 

Most people with a healthy immune system are able to keep JC virus in the latent phase in the kidney epithelial cell]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rotavirus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Sifz_AuEReq7xbPkRMP7TCIwSQG9Xvk9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rotavirus]]></video:title><video:description><![CDATA[Rotavirus is a common cause of viral gastroenteritis, commonly called the stomach flu, in children. 

In fact, it’s believed that almost every child has had the vaccine or been infected by this virus at least once before the age of five. 

There are at least eight strains of rotaviruses, named A to H, but most rotavirus gastroenteritis infections in humans are due to group A strains.

Rotavirus is part of the reovirus family, where reo- stands for respiratory, enteric, and orphan. 

This tells us that this family of viruses affect either the respiratory system, the intestines, or they’re “orphans” who don’t cause any disease, as far as we can tell. 

They are surrounded by a double icosahedral capsid, which is a two-layered spherical protein shell made up of 20 equilateral triangular faces. 

And they’re “naked” because the capsid isn’t covered by a lipid membrane. 

They’re RNA viruses with double stranded linear RNA with 10 to 12 segments. 

This means that they must first transcribe their genetic material into single stranded mRNA before host cell ribosomes can use it to make viral proteins. 

Transcription happens inside the capsid, using a viral enzyme called RNA-dependent RNA polymerase.

Then the mRNA enters the host cell’s cytoplasm where ribosomes are found. 

Rotavirus is transmitted from person to person via the fecal-oral route.

In other words, you catch it by ingesting the stool or vomit particles of someone who is sick. Yuck. 

This can happen if infected stool ends up in the water supply or on agricultural fields, if flies land on it, and transfers stool particles to other places, or by touching contaminated surfaces. 

You can summarize it as the four Fs: fluids, fields, flies, and fingers. 

As a result, rotavirus can end up in food and drinking water - and from there, it makes its way to the small intestine. 

Now, the small intestine has lots of tiny ridges and grooves, each of which projects little finger-like fibers called villi. 

An]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rabies_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AhR5w9wnRSKwLiSnztBdRKlVQruvJCXH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rabies virus]]></video:title><video:description><![CDATA[Rabies virus, formally called Rabies lyssavirus, affects the central nervous system and causes encephalitis, or acute inflammation of the brain. 

It’s a viral infection transmitted by infected animals, like dogs and bats, and once symptoms develop, it’s usually fatal.

The rabies virus is part of the rhabdoviridae family of viruses. 

All rhabdoviruses are single-strand RNA viruses surrounded by a helical capsid, or a helix-shaped protein layer, all within a distinct bullet-shaped outer envelope, which is covered in glycoprotein spikes. 

They’re also negative sense RNA viruses, which means that before it can be used to make proteins their genetic material has to be transcribed into mRNA. 

And these viruses carry their own RNA polymerase to do just that.  

To understand how rabies works, first let’s look at the human nervous system. 

The nervous system is divided into the central nervous system, so the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs.

Neurons, the main cells of the nervous system, have nerve fibers that extend out from the neuron cell body- these are either dendrites that receive signals from other neurons, or axons that send signals along to other neurons. 

Where two neurons come together is called a synapse, and that’s where one end of an axon releases neurotransmitters, further relaying the signal to the dendrites or directly to the cell body of the next neuron in the series. 

Some synapses allow neurons to relay signals to other types of cells, like the neuromuscular junction where motor neurons innervate muscle cells by releasing the neurotransmitter acetylcholine. 

Acetylcholine binds to nicotinic receptors on the muscle cell membrane, which are ion channels that open when acetylcholine binds to them; and they allow positive ions like sodium and calcium to cross the cell membrane, triggering a muscle contraction.

Rabies m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rickettsia_rickettsii_(Rocky_Mountain_spotted_fever)_and_other_Rickettsia_species</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/etdUmN9CQgKuX2z561FBCwp4QcGiWeb-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species]]></video:title><video:description><![CDATA[The Rickettsiae are a genus of Gram-negative coccobacilli, which includes two major groups of bacteria. 

First, there’s the spotted-fever group, the main species in this group is Rickettsia rickettsii, which causes a disease called Rocky Mountain spotted fever. 

Second, there’s the typhus group of Rickettsia species - which cause different forms of typhus. 

This group includes Rickettsia prowazekii, which causes a disease called epidemic typhus, and Rickettsia typhi, which causes murine typhus, also called endemic typhus.

Now, Rickettsiae are small bacteria, measuring only 0.7 to 2 micrometers in diameter. 

They have a plasma membrane that’s surrounded by a microcapsule. 

And inside the bacteria, there’s cytosol, which contains ribosomes and a single circular chromosome. 

Also, these bacteria have a thin wall, that doesn’t retain the crystal violet dye during gram staining, so they’re classically considered Gram-negative bacteria. 

However, they are very weak Gram-negative bacteria, so special staining methods are needed to visualize them, such as Giemsa, Gimenez or Machiavello. 

So, on Giemsa staining, the bacteria appear bluish-purple, on Gimenez staining they look red, on a bluish-green background and on Machiavello staining they look bright red, on a blue background.

Finally, they’re non-motile and obligate intracellular which means they can survive only inside cells and this is because it can’t make two important energetic compounds, NAD+ and coenzyme A, by itself, and instead it gets them from eukaryotic cells. 

So, they can be grown in vitro in the yolk sac of developing chicken embryos, but they are more conveniently cultured on cell culture monolayers, such as chicken embryo fibroblasts, mouse L cells, and golden hamster cells. 

Now, each of these species has different vectors. 

Rickettsia rickettsii is spread through tick bites, Rickettsia prowakezii is spread via lice feces, and Rickettsia typhi is transmitted through rat fleas. 

B]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bacteroides_fragilis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OaWUF_m2TxqmcbwitoY-kPLdQBmYwo-i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bacteroides fragilis]]></video:title><video:description><![CDATA[With Bacteroides fragilis, ‘bacter-’ means rod, ‘-oides’ means shape and ‘fragilis’ means fragile. 

So, Bacteroides fragilis is a Gram-negative, rod-shaped bacterium. 

Although it&amp;#39;s generally considered a rod-shaped, its can range from a sphere to a rod shape, so it’s considered a pleomorphic bacterium. 

Bacteroides fragilis inhabits the human colon, and from all the Bacteroides species, it’s  responsible for most human infections.

Now, a little bit more about this microbe. For starters, Bacteroides fragilis is Gram-negative, which means that it has a thin peptidoglycan cell wall that can&amp;#39;t readily retain purple dye when Gram stained. 

Additionally, it&amp;#39;s a non-spore-forming and non-motile bacteria. 

It’s also an obligate anaerobe, meaning that it can only live without oxygen. 

Another fact is that it’s bile resistant and seems to like bile, which makes sense since it lives in the colon. 

So, not only can it grow anaerobically in blood agar, but it can also readily grow in bile esculin agar, also known as Bacteroides Bile Esculin. 

After 48 hours of incubation at 35°C  Bacteroides fragilis forms dark colonies with brown-black halos due to the hydrolysis of esculin. 

Finally, a disk test can be done, which identifies Bacteroides fragilis by its resistance to antibiotics like kanamycin, vancomycin, and colistin. 

Ok, so normally, Bacteroides fragilis colonizes the human colon peacefully, without causing any trouble. 

However, trauma or surgery may damage the intestinal wall, which allows Bacteroides fragilis to slip into the bloodstream. 

From there, it can travel to virtually any organ in the body. 

Alternatively, it can slip into the sterile peritoneal cavity accompanied by aerobic bacteria like E. coli, which are also part of the normal gut flora - so peritoneal infections are usually considered “polymicrobial” infection, to reflect that there’s more than one culprit. 

Now, in the peritoneal cavity, Bacteroides fra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bartonella_henselae_(Cat-scratch_disease_and_Bacillary_angiomatosis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2MauhE7xSaS8UvvmB3qTn42IRFqLhQq5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bartonella henselae (Cat-scratch disease and Bacillary angiomatosis)]]></video:title><video:description><![CDATA[Bartonella henselae is a zoonotic bacteria which may cause Cat-scratch disease, or CSD, in humans. 

Zoonotic bacteria refers to any bacteria which can be transmitted between animals and people. 

Now, Bartonella henselae spreads between cats with the help of a cat flea, called Ctenocephalides felis, which feeds on the blood of an infected cat. Then, it drops its feces, which contain Bartonella henselae, on the cat’s body. 

Finally, when the cat grooms or scratches, Bartonella henselae gets on its teeth and claws, and the cat may infect a human by scratching or biting - hence the name, “cat scratch disease”, or “cat scratch fever”. 

There’s also bacillary angiomatosis, which is a severe form of cat scratch disease, that develops primarily in immunocompromised individuals. 

Now, Bartonella henselae is  a gram-negative bacillus, in other words, it&amp;#39;s a rod-shaped bacteria that stains red or pink with Gram staining. 

This is largely due to the fact that Bartonella henselae has a thin peptidoglycan wall that doesn’t retain crystal violet dye during Gram staining. 

Sometimes, though, it doesn’t readily gram stain, so the silver nitrate-based Warthin-Starry stain is used for direct visualization.

Bartonella henselae is a facultative intracellular bacteria, which means that it&amp;#39;s adapted to live inside cells to avoid the immune system. 

Specifically, it hides inside endothelial cells lining up the interior surface of the blood vessels and lymph vessels.

Once inside the endothelial cell, Bartonella henselae can trigger an increased production of interleukin-10, which suppresses the action of immune cells; and interleukin-8, which promotes endothelial cell proliferation. 

In humans, the response to infection depends on the immune system. 

Immunocompetent individuals develop a simple form of the cat-scratch disease. 

The most characteristic symptom is the swelling of a single lymph node or a cluster of lymph nodes, usually in the armpits, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Enterobacter</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wnn6zHNvQMyT8W5NARwfmUgDQDWOrz71/_.jpg</video:thumbnail_loc><video:title><![CDATA[Enterobacter]]></video:title><video:description><![CDATA[Enterobacter is a genus of Gram-negative rod-shaped bacteria which belongs to a family of bacteria called the Enterobacteriaceae. 

There are several species which cause infection in humans and the most important are Enterobacter cloacae and Enterobacter aerogenes. 

It’s an opportunistic pathogen, which can be normally found in the intestinal flora and causes a wide variety of hospital-acquired infections, mainly respiratory and urinary infections.

Now, a little bit of microbe anatomy and physiology. First, Enterobacter has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. 

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. 

And since it’s a Gram-negative bacillus, it looks like a little pink rod under the microscope.

Enterobacter is motile, non-spore forming, facultative anaerobic which means it can survive in both aerobic and anaerobic environments and oxidase negative which means it doesn’t produce an enzyme called oxidase.

Alright, now Enterobacter is urease positive which means it can produce an enzyme called urease that dissociates urea into carbon dioxide and ammonia.

This can be tested by transferring a pure sample of bacteria from the culture to a sterile tube containing a mixture of “urea agar” broth and phenol red. Then, the mixture is incubated. 

So, with Enterobacter, urease makes urea dissociate into carbon dioxide and ammonia. 

Ammonia then makes the mixture change color from orange-yellow to bright pink. 

Finally, Enterobacter grows well on MacConkey agar which is a medium that contains a pH sensitive dye and lactose. 

This medium helps identify whether Gram-negative bacteria are lactose fermenters or not. 

Some Enterobacteriaceae, like Enterobacter, Klebsiella and Escherichia coli, can ferment lactose, which results in the production of acid, that makes the pH sensitive dye turn pink - so their colonies will be pink, while others, like Salmonella and Shi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cyanotic_congenital_heart_defects:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UnELKmq7Ti6-D0XJHdcGImbVRdG3DzrW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cyanotic congenital heart defects: Pathology review]]></video:title><video:description><![CDATA[At the pediatric cardiology clinic, two mothers were chatting about their kids. One mom spoke about a 5 year old boy named Blake, who was a bluish color at birth and had a continuous machine-like heart murmur between the scapulas. 

Another mom spoke about her 12 year old son, Paul, who was healthy at birth, but when he was breastfeeding or crying, his skin turned pale, and then blue. As a child, Paul got out of breath easily and needed to squat down to recover. And during his school physical, he was found to have a heart murmur. 

Both Blake and Paul have cyanotic congenital heart defects, or CHDs, which usually start causing problems within the first 3-8 weeks of life. They can be broadly grouped into life-threatening cyanotic heart defects, or the less dangerous acyanotic heart defects. 

Let’s go over 5 of the life-threatening cyanotic congenital heart defects: persistent truncus arteriosus, transposition of the great vessels, tetralogy of fallot, total anomalous pulmonary venous return, and tricuspid atresia.

Now the first 3 are caused by outflow tract defects that develop during the formation of the aorta and pulmonary artery. In fetal development the heart looks like a long tube; the top part is the truncus arteriosus and the part inferior to that is the bulbus cordis. Neural crest cells migrate into the bulbus cordis and trigger the formation of the aorticopulmonary septum. This structure is formed when two endocardial cushions appear on the right-superior and left-inferior walls. These grow like a spiral - imagine a corkscrew - and they wrap around each other forming a single septum that divides the truncus into the roots of the aorta. One root connects to the primitive left ventricle, and the other connects to the pulmonary artery and primitive right ventricle. That’s how blood gets routed to the right place!

Okay, so if the aorticopulmonary septum doesn’t form, or forms incompletely, the result is a persistent truncus arteriosus. For your exam]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Escherichia_coli</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4x3y1HQtRfKlNy6aIckS2RYISH_ThQRs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Escherichia coli]]></video:title><video:description><![CDATA[Escherichia coli or just E. Coli, is a gram-negative rod-shaped bacteria named after Dr. Escherich Theodor, who discovered it in feces, thus concluding that it colonizes the colon.

Alright, now E. Coli is gram-negative because its cell wall has a thin peptidoglycan layer so it cannot retain the crystal violet stain, but instead, it stains pink with Safranin dye used during Gram staining. 

So it looks like a little pink rod under the microscope. 

Also, E. Coli is a catalase positive bacteria, and that means it produces an enzyme called catalase. 

This can be tested by adding a few drops of hydrogen peroxide to a colony of bacteria, and catalase makes hydrogen peroxide dissociate into water and oxygen, making the mixture foam. 

E. Coli is also a lactose fermenter, because it can produce an enzyme called beta B-galactosidase that cleaves lactose into glucose and galactose monomers. 

To test this, E. Coli can be cultivated on lactose-containing media such as Phenol lactose, and as it ferments it, the fermentation results in the production of acids that turn the red of phenol to yellow. 

It is also a facultative anaerobe, meaning it lives in environments with or without oxygen. 

Now, taking a closer look to this bacteria, E. Coli is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule. 

E. Coli is a motile bacteria, because it has helical whip-like threads called flagella that it can use to move around. 

When E coli is cultivated on eosin methylene blue agar, it grows into black colonies with a greenish-black metallic sheen.

Alright, most of E. Coli are harmless, and they can peacefully colonize the human gut without causing any trouble. 

However, some strains of E. Coli are pathogenic, meaning they can cause illness. It starts with this bacteria using little thread-like extensions called fimbriae to attach to the host cell surface. 

E coli has many different strains that can do that, and they cause different diseases. Thes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Legionella_pneumophila_(Legionnaires_disease_and_Pontiac_fever)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/URM5UC59RcWTZIyIWgHV7AwmRrCu2w4-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Legionella pneumophila (Legionnaires disease and Pontiac fever)]]></video:title><video:description><![CDATA[Legionella pneumophila is a Gram-negative bacillus, which means is shaped like a rod, and can be found in many water systems, such as hot water tanks, cooling towers, large air conditioning systems or hot tubs. 

It is typically transmitted by inhaling infected aerosols, like contaminated water sprays, jets, or mists and causes a disease called legionellosis with two distinct entities. 

The first one, Legionnaires’ disease got its name from a deadly outbreak of pneumonia in 1976 among people attending a convention of the American Legion, and the second one, Pontiac fever, got its name from Pontiac, Michigan, where the first case was recognized. 

Now, Legionella pneumophila has a very thin peptidoglycan layer, so it stains like a Gram-negative bacteria. 

But it stains pretty weakly as a Gram-negative bacteria, so it’s best visualized with silver stain. 

Legionella pneumophila is non-spore forming, aerobic, which means it needs oxygen to survive, facultative intracellular, which means it can survive both inside and outside the cell, and oxidase and catalase positive, which means it produces both of these enzymes. 

Finally, it needs special nutrients to grow, such as cysteine and iron, so it grows on a special medium called buffered charcoal yeast extract, or BCYE, which contains cysteine and iron that are essentially for growth of Legionella. 

So, on this medium, it forms grey-white colonies with a cut-glass appearance.

Now, Legionella pneumophila can enter the body through inhalation of contaminated water droplets. 

Once it reaches the lungs, it gets ingested by alveolar macrophages and inside macrophages, it gets wrapped up in a vesicle called phagosome, which normally merges with lysosomes to kill invading bacteria. 

However, Legionella has a type IVB secretion system, which uses effector proteins to prevent phagolysosomal fusion. 

As a result, Legionella is able to survive and replicate inside macrophages. 

When the cells become too small for ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Salmonella_(non-typhoidal)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7xpMvwK3Sua3R6XSeuQfKSr4QSyLkQb8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Salmonella (non-typhoidal)]]></video:title><video:description><![CDATA[Salmonella is a bacterium belonging to the family Enterobacteriaceae. 

There are two main species: Salmonella bongori and Salmonella enterica, and the latter has six subspecies. 

One of the subspecies is enterica, which has over 2500 serotypes that can be divided into two main groups based on the clinical symptoms they cause- so typhoidal or non-typhoidal Salmonella. 

The non-typhoidal group, can infect humans and animals and cause a variety of disease states. 

But, the most common serotype, Salmonella enteritidis, causes intestinal inflammation, called gastroenteritis, or commonly called “food poisoning”.  

OK, but generally, Salmonella are encapsulated gram-negative, rod bacteria – meaning, they have a polysaccharide layer outside the cell envelope and look like little red or pink sticks on a gram stain. 

They’re facultative intracellular pathogens, meaning they can live both outside or inside of its host’s cells. 

And have flagella, making them motile, but don’t form spores. 

They’re also facultative anaerobes, so they can undergo respiratory and fermentative metabolism; and they can ferment glucose but not lactose; are oxidase negative, and produce hydrogen sulfide gas. 

And while a variety of media can be used to selectively identify Salmonella, among them is Triple Sugar Iron agar which produces a black precipitate when hydrogen sulfide is produced. 

Now, once Salmonella is ingested and reaches the distal ileum of the small intestine, it tends to target the epithelial layer of the mucosal lining where it uses surface appendages to adhere to microfold cells, or M-cells. 

And these M-cells eat, or phagocytose, the bacteria from the intestinal lumen and spit it out into the underlying Peyer’s patches - a type of mucosal immune tissue that extends into the submucosa. 

When encountering non-typhoidal Salmonella, the immune system responds strongly by releasing proinflammatory cytokines that recruit additional immune cells, particularly neutrop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Proteus_mirabilis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GS2y4WCYR-eOr-9LOM16cbE6RzS_3kMz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Proteus mirabilis]]></video:title><video:description><![CDATA[Proteus mirabilis is a Gram-negative bacillus which belongs to a family of bacteria called the Enterobacteriaceae. 

It is widely distributed in soil and water and can also be found in the normal human intestinal flora. 

In humans, it causes urinary tract infections, or UTIs for short.

Now, Proteus mirabilis has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. Instead, like any other Gram-negative bacteria, it stains pink with safranin dye.

And since it’s a Gram-negative bacillus, it looks like a little pink rod under the microscope.

Alright, now Proteus mirabilis is non-spore forming and highly motile. 

It’s also facultative anaerobic which means it can survive in both aerobic and anaerobic environments,  non-lactose fermenter, oxidase negative which means it doesn’t produce this enzyme, and urease positive which means it can produce an enzyme called urease.

Now, it grows well on blood agar and MacConkey agar. 

On blood agar, it has a swarming growth, so it moves and forms a thin filmy layer of concentric circles, which look like the ripples after you throw a rock into a lake. 

On MacConkey agar, however, it doesn’t swarm so it forms smooth, pale or colourless colonies.

Finally, the triple sugar iron test, or TSI for short can be done to assess hydrogen sulfide production. 

This medium contains three sugars - lactose, glucose and sucrose, as well as iron and a pH sensitive dye. 

Proteus mirabilis produces hydrogen sulfide, that reacts with the iron, and a black precipitate forms in the test tube.

Ok, now Proteus mirabilis has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.

First, Proteus mirabilis has flagella, which are lash-like appendages that comes out from the cell body, and confer the bacteria its motility. 

Now, when Proteus mirabilis comes in contact with solid surfaces, especially urinary catheters,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pseudomonas_aeruginosa</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L6LeSdmxTN69eNcbr5ITuOyGSFOwNl55/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pseudomonas aeruginosa]]></video:title><video:description><![CDATA[Pseudomonas aeruginosa, or P. aeruginosa, is a gram-negative bacterium that is abundant in the environment. 

It tends to opportunistically infect high-risk individuals, and is well known for its multi-drug resistance, making it hard to treat.

P. aeruginosa is an encapsulated, gram-negative, rod bacterium, that’s an obligate aerobe, so it uses oxygen for metabolism through cellular respiration.

It does not ferment lactose and does not make spores; but it’s catalase, citrate, and oxidase positive. 

It has a flagellum, kind of like a tail, at one end for motility; and has multiple hair-like appendages, called pili, all over that help with adhesion to other cells.

It also has a number of multidrug efflux pumps that efficiently pump medications out of the bacteria making it resistant to a variety of antibiotics.

In addition it’s able to make beta-lactamases that degrade beta-lactam antibiotics as well as aminoglycoside-modifying enzymes that alter aminoglycoside antibiotics - rendering them ineffective. In short, it’s defenses are strong.

P. aeruginosa is everywhere in the environment - in soil; in the home, and in hospitals - where it’s found on improperly cleaned medical equipment and devices, various surfaces, and on the hands of health care workers. 

It can survive for months on dry surfaces and inanimate objects – but particularly loves humid or wet conditions; like hot tubs, contact lens cases, catheters, and medical ventilators.

Transmission can occur when broken skin or mucous membranes come in contact with contaminated surfaces; or when aerosols containing P. aeruginosa are inhaled after an infected person coughs or sneezes.    

Now, a P. aeruginosa infection is actually not too common in the general population. 

It’s an opportunistic bacterium, meaning that it frequently causes infections in high-risk individuals like those with cystic fibrosis, chronic granulomatous disease, and type 2 diabetes mellitus. 

It’s also common among individual]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Serratia_marcescens</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IGUK-vzoRECr9kua4piZA62YSAO2R9HP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Serratia marcescens]]></video:title><video:description><![CDATA[Serratia marcescens is a Gram-negative bacteria which belongs to a family of bacteria called the Enterobacteriaceae. 

Now, the genus consists of at least 20 species, of which eight are known to have caused infections in humans, with Serratia marcescens being the main human pathogen. 

Serratia marcescens is widely distributed in water, soil and plants and it causes a variety of hospital-acquired infections.

Now, Serratia marcescens has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. 

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. 

And since it’s a Gram-negative bacillus, it looks like a little pink rod under the microscope.

Ok, now Serratia marcescens is motile and also facultative anaerobic which means it can survive in both aerobic and anaerobic environments. 

It’s urease positive which means it can produce an enzyme called urease that dissociates urea into carbon dioxide and ammonia. 

This can be tested by transferring a pure sample of bacteria from the culture to a sterile tube containing a mixture of “urea agar” broth and phenol red. 

Then, the mixture is incubated. So, with Serratia marcescens, urease makes urea dissociate into carbon dioxide and ammonia. 

Ammonia then makes the mixture change color from orange-yellow to bright pink. 

Also, it’s catalase positive which means it can produce an enzyme called catalase. 

To test for this, a few drops of hydrogen peroxide are added to the colony of the suspected bacteria. 

So, if catalase is present, it makes the hydrogen peroxide dissociate into water and oxygen, causing the mixture to foam. 

Furthermore, it produces another three enzymes, DNase, lipase, and gelatinase, which are unique to Serratia and this can help easily differentiate it from other Enterobacteriaceae. 

Finally, Serratia marcescens grows well on MacConkey agar which is a medium that contains a pH sensitive dye and lactose. 

This medium helps ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Yersinia_enterocolitica</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fr9tHNrlReyKliWRzrrQoZXlSJ2laa9U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Yersinia enterocolitica]]></video:title><video:description><![CDATA[Yersinia enterocolitica is a Gram-negative bacillus that belongs to a family of bacteria called the Enterobacteriaceae. 

The Yersinia genus got its name from Alexandre Yersin, who discovered it, and enterocolitica refers to intestine and colon, so Yersinia enterocolitica causes a diarrheal illness, called yersiniosis. 

Now, a little bit of microbe anatomy and physiology. 

First, Yersinia enterocolitica has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. 

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. 

And since it’s a Gram-negative bacillus, it looks like a little pink rod under the microscope.

Interestingly, Yersinia enterocolitica can be both motile and non-motile depending on the temperature. 

So, at 25 degrees Celsius it’s motile and at 37 degrees Celsius it’s non-motile. 

It’s facultative anaerobe, so it can survive in both aerobic and anaerobic environments, and also facultative intracellular which means it can survive both outside and inside the cells. 

Finally, it’s non-spore forming, so it doesn’t make spores, and oxidase negative, so it doesn’t produce this enzyme.

Yersinia enterocolitica grows well on MacConkey agar, which is a medium that contains a pH sensitive dye and lactose. 

This medium helps identify whether Gram-negative bacteria are lactose fermenters or not. 

Some Enterobacteriaceae, like Klebsiella, Escherichia coli and Enterobacter, can ferment lactose, which results in the production of acid, and this makes the pH sensitive dye turn pink - so their colonies will be pink. 

Yersinia enterocolitica, however, is a non-lactose fermenter, so it forms colorless colonies on MacConkey agar.

Yersinia enterocolitica also grows on Cefsulodin-Irgasan-Novobiocin agar, or CIN agar for short. 

After 24 hours of incubation, it forms white, sharp-bordered colonies with a deep-red center, that looks like bull’s eyes colonies. 

Finally, the triple sugar iro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leptospira</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UXSheVDeQlCj5YPbUoOuBzADTOSPmHXr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leptospira]]></video:title><video:description><![CDATA[With Leptospira, “lepto” means thin, and “spira” means coil. 

So Leptospira is a genus of spiral bacteria known to cause leptospirosis, a zoonotic infection, meaning it can be transmitted from animals such as rodents, to humans; especially people who work in sewers and waters contaminated by these animals’ urine. 

The Leptospira genus has over 20 species, and the most common species that causes leptospirosis in humans is Leptospira interrogans.

Now, Leptospira is a tiny spiral bacteria, that stains poorly with Gram staining, because it doesn’t retain the Gram dyes well, so it’s classically considered gram-negative. 

It’s also too tiny to be seen with a light microscope, so to visualize it, a darkfield microscope with use of immunofluorescence is required. 

Leptospira is also a motile bacteria because it has flagella that help it move around. 

Finally, it doesn’t form spores and it’s aerobic, meaning it needs oxygen to grow.  

Currently, little is known about the pathogenesis of this bacteria, but we do know that it possesses a number of virulence factors, which are like assault weaponry that help it attack and destroy the host cells.

These include toxins and some immunogenic molecules such as lipopolysaccharide, or LPS, that triggers an immune response, causing inflammation. 

For example, Leptospira interrogans, the most common cause of leptospirosis, has adhesins, which are proteins that help this bacteria attach to the host’s cells - usually epithelium, monocytes, and macrophages. 

It also releases Sphingomyelinase C toxin, which destroys red blood cells as well as the endothelium of the capillaries, causing hemorrhage. 

Most commonly, Leptospira gets into the host system via abrasions or cuts on the skin. 

Alternatively, it can get in through the conjunctive of the eyes, especially in people who go swimming in contaminated waters. 

Rarely, infection can follow eating contaminated food. 

Serious problems start when this bacteria gets into t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Staphylococcus_epidermidis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OAYmcMslQZyYnKbc7QG9C1fpQX6PF3iB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Staphylococcus epidermidis]]></video:title><video:description><![CDATA[Staphylococcus epidermidis or simply Staph epidermidis can be broken down into staph which means grapes, coccus which means round shape, and epidermidis referring to the superficial layer of the skin.  So, Staphylococcus epidermidis are round bacteria that tend to live clustered together as if they were grapes, and they are part of the normal skin flora even though they may also be found living on the mucosa of the gut.

Now, a little bit of microbe anatomy and physiology. Staph epidermidis has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.  It’s non-motile and doesn’t form spores, and also, it’s a facultative anaerobe, meaning that it can survive in both aerobic and anaerobic environments. 

Staph epidermidis is catalase positive, so it makes an enzyme called catalase. We can use this to differentiate Staph epidermidis from other gram positive cocci, like streptococci and enterococci, which are catalase negative. To test for this, a few drops of hydrogen peroxide are added to the colony of the suspected bacteria. So, if catalase is present, like in staph epidermidis, it makes the hydrogen peroxide dissociate into water and oxygen, causing the mixture to foam. 

Staph epidermidis is also urease positive, meaning it produces an enzyme called urease that dissociates urea into carbon dioxide and ammonia. This can be tested by transferring a pure sample of bacteria from the culture to a sterile tube containing a mixture of “urea agar” broth and phenol red. Then, the mixture is incubated. So, with Staph epidermidis, urease does it’s thing, making urea dissociate into carbon dioxide and ammonia. Ammonia then makes the mixture change color from orange-yellow to bright pink. This doesn’t happen with urease negative Gram-positive cocci, like Streptococcus pneumoniae or Enterococcus faecalis. 

Furthermore, unlike many other Staphylococcus species, Staph epidermidis and its close relative, Sta]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Staphylococcus_saprophyticus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XFuaei4oQXuUyjaiRV7QCXlOQR67xU5R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Staphylococcus saprophyticus]]></video:title><video:description><![CDATA[With Staphylococcus saprophyticus, sometimes called Staph saprophyticus, “staph” means grapes, “coccus” means round-shape, while “saprophyticus” refers to organisms that grow on decaying organic material.  

So, Staphylococcus saprophyticus are round bacteria that tend to live in grape-like clusters, and are commonly found on contaminated meat products. 

Now, a little bit of microbe anatomy and physiology. 

Staph saprophyticus has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.  

It’s non-motile and doesn’t form spores, and also, it’s a facultative anaerobe, meaning that it can live with or without oxygen.

Staph saprophyticus is catalase positive, so it makes an enzyme called catalase. 

We can use this to differentiate Staph saprophyticus from other gram positive cocci, like streptococci and enterococci, which are catalase negative. 

To test for this, a few drops of hydrogen peroxide are added to the colony of the suspected bacteria. 

So, if catalase is present, like in staph saprophyticus, it makes hydrogen peroxide dissociate into water and oxygen, making the mixture foam. 

Staph saprophyticus is also urease positive, meaning it produces an enzyme called urease that dissociates urea into carbon dioxide and ammonia. 

This can be tested by transferring a pure sample of bacteria from the culture to a sterile tube containing a mixture of “urea agar” broth and phenol red. Then, the mixture is incubated. 

So, with Staph saprophyticus, urease makes urea dissociate into carbon dioxide and ammonia. 

Ammonia then makes the mixture change color from orange-yellow to bright pink. 

This doesn’t happen with urease negative Gram-positive cocci, like Streptococcus pneumoniae or Enterococcus faecalis. 

Furthermore, unlike many Staphylococcus species, Staph saprophyticus and its close relative, Staph epidermidis, are both coagulase negative, meaning they don’t produce an enzyme called coagula]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Streptococcus_agalactiae_(Group_B_Strep)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X0o3lGWdRReK1NjrqwBn91EXTx6CarzS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Streptococcus agalactiae (Group B Strep)]]></video:title><video:description><![CDATA[With Streptococcus agalactiae sometimes called Strep agalactiae, strepto means a chain, coccus means round shape, and agalactiae literally means “no milk”. 

So, Strep agalactiae refers to the round bacteria that grow in chains and that was previously known to infect cattle, resulting in reduced milk production. 

Later on, Strep agalactiae was found to also be a human potential pathogen responsible for a number of infections that most commonly affect pregnant women and newborns. 

Strep agalactiae are also called Group B Strep – GBS - in Lancefield classification developed by an American microbiologist Rebecca Lancefield. 

Ok now, a little bit of microbe anatomy and physiology. 

Strep agalactiae has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria. 

It’s non-motile and doesn’t form spores, and also, it’s a facultative anaerobe, meaning that it can survive in both aerobic and anaerobic environments. 

Now, a particular trait of Streptococcus species is that they are catalase negative, meaning they do not produce an enzyme called catalase. 

This is unlike other common gram positive cocci, like Staphylococcus, which are catalase positive. 

When cultivated on a medium called blood agar, Strep agalactiae colonies cause beta hemolysis, also called complete hemolysis. 

That’s because Strep agalactiae makes a toxin called beta-hemolysin, that causes complete lysis of the hemoglobin in the red blood cells, making them blood agar change color from red to transparent yellow around the colonies. 

However, other Streptococcus species, like Strep pyogenes, are also beta hemolytic. 

So to identify Strep agalactiae specifically, the bacitracin test, the hippurate test, or the CAMP test can be done. 

With the bacitracin test, a disk of bacitracin is added to the blood agar. 

Strep agalactiae is bacitracin resistant, so the colonies remain intact, whereas Strep pyogenes is bacitracin sensitive, so ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Streptococcus_pneumoniae</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HBZJw4FmQr6RO228TClnAn89RQmrqsMd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Streptococcus pneumoniae]]></video:title><video:description><![CDATA[Streptococcus pneumoniae or Strep. pneumoniae can be broken down into strepto- which means chain, -coccus, which means round shape, and pneumoniae, which refers to the fact that it causes pneumonia - no surprises there.

So, Strep pneumoniae are round bacteria that tend to grow in chains, usually in lancet-looking pairs called diplococci. 

They’re the most common cause of community-acquired pneumonia - meaning pneumonia acquired somewhere other than the hospital.

Ok now, a little bit of microbe anatomy and physiology. 

Strep pneumoniae has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria. 

They’re non-motile and don’t form spores, and also, they’re facultative anaerobes, meaning that they can survive in both aerobic and anaerobic environments. 

Finally, they’re catalase negative - which means they don’t produce an enzyme called catalase.

Ok, now, when cultivated on a medium called blood agar, Strep pneumoniae colonies cause alpha hemolysis, also called green hemolysis, because they produce hydrogen peroxide, which partially oxidizes initially red hemoglobin in the blood agar to green methemoglobin. 

Other Streptococcus species, like Strep viridans, are also alpha hemolytic. 

So, an optochin test is done to distinguish Strep pneumoniae. That’s where a few drops of optochin are added to the culture. 

Strep pneumoniae are optochin sensitive, meaning the bacteria dies after adding optochin, whereas Strep viridans are optochin resistant - meaning they survive. 

Now, Strep pneumoniae has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system. 

So first, Strep pneumoniae is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule. 

The capsule has pili and fimbriae, which are hair-like extensions that help it attach to a host cell. 

Once attached to a mucosal surface like in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Streptococcus_viridans</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NI7AsDmuQJmXeCrFt8O5ZC54TVGx9j7d/_.jpg</video:thumbnail_loc><video:title><![CDATA[Streptococcus viridans]]></video:title><video:description><![CDATA[The term “streptococcus viridans”, refers to five groups of Streptococci that include Streptococcus anginosus group, mitis group, sanguinis group, salivarius group, and finally the mutans group. 

And each of these groups has approximately 30 species  that can cause disease in humans. 

So the more correct term would be “viridans streptococci”, to reflect that there’s more than one of them. 

Generally speaking, viridans streptococci can’t be assigned to a Lancefield group based on their cell wall antigens. 

However, in the Streptococcus anginosus group, some species can be assigned to Lancefield groups A, C, F or G. 

Now, viridans streptococci have a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so they’re gram-positive bacteria. 

They’re also catalase negative - which means they don’t produce an enzyme called catalase. 	 	 	
Ok, now, when cultivated on a medium called blood agar, viridans streptococci colonies cause alpha hemolysis, also called green hemolysis, because they produce hydrogen peroxide, which partially oxidizes initially red hemoglobin in the blood agar to green methemoglobin. 

One way to remember this is to think that &amp;#39;viridans’ means ‘green’ in Latin. 

Some species in the Streptococcus anginosus group, however, can also be beta-hemolytic or nonhemolytic. 

These guys are special little snowflakes. 

Now, other Streptococcus species, like Streptococcus pneumoniae, are also alpha hemolytic. 

So, an optochin test is done to distinguish them. 

That’s where an optochin-containing paper disc is placed on a plate of blood agar that has been inoculated with the bacteria. 

With Strep pneumoniae, the growth of the bacteria is inhibited in the zone that surrounds the optochin disc, meaning that Strep pneumoniae is optochin sensitive.  

On the flip side, viridans streptococci are optochin resistant - meaning there’s no inhibition of the growth around the optochin disc.

Another test that can be used to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rubella_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cVrTHBtMS6WhvZ9H2C7xe5E0SlS9idnc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rubella virus]]></video:title><video:description><![CDATA[Rubella, the infection formerly known as “German Measles,&amp;#39;&amp;#39; is caused by the Rubella virus. 

Thanks to vaccination, it’s a disease we see less and less, although because some groups are under-immunized, it’s still possible to see outbreaks.

The Rubella virus is part of the Togaviridae family. 

Togaviruses are single-strand RNA viruses surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces, all within a spherical outer lipid envelope. 

They’re also positive sense RNA viruses, which means that their genetic material is actually mRNA, so it can be used right away by the host cell to make viral proteins. 

Now, the Rubella virus is transmitted through respiratory droplets, which are released into the environment when you sneeze or cough on another person. 

Within the nasopharynx mucous membrane, the virus binds to a specific receptor on the membrane of epithelial cells. 

It’s then surrounded by a little section of cell membrane that pinches off to form an endosome, that’s brought into the cell.  

The low pH in the endosome uncoats the viral RNA and the virus causes changes to the endosome. 

Now, when the Rubella virus enters the cell it also rearranges some of the organelles, gathering the endoplasmic reticulum, golgi apparatus, and mitochondria around the endosome. 

The result is a membrane-bound Viral Replication Complex where - like the name says - the virus replicates. 

So, after the virus replicates, its structural proteins are synthesized using the rough endoplasmic reticulum and these proteins are then transported to the golgi apparatus to be assembled and surrounded by membrane, a process called viral budding. 

The new virus copy eventually exits the cell by exocytosis and enters nearby lymphatic and blood vessels, travelling to lymph nodes where it will replicate once again. 

From the lymph nodes, it enters blood vessels again, and spreads to various parts of the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoporosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IinO6oLGQv6RaMEqmepHNKz_TtCdCHc8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteoporosis]]></video:title><video:description><![CDATA[Osteo- refers to bones and -porosis means pores. So, osteoporosis is when there’s a higher breakdown of bone in comparison to the formation of new bone which results in porous bones, meaning a decrease in bone density to the point of potential fracture.  

Looking at a cross-section of a bone, there’s a hard-external layer known as the cortical bone and a softer internal layer of spongy bone or trabecular bone that is composed of trabeculae. The trabeculae are like a framework of beams that give structural support to the spongy bone.  The cortical bone, in turn, is made up of many functional, pipe-like units called osteons, which run through the length of the bone. In the center of these osteons, there are hollow spaces called Haversian canals, which contain the blood supply and innervation for the bone cells. Around the Haversian canals, there are concentric lamellae, which look a bit like tree rings. The lamellae have an organic part, which is mostly collagen, and an inorganic part called hydroxyapatite, which is mostly calcium phosphate. In between neighboring lamellae, there are spaces called lacunae, which contain bone cells called osteocytes. 

At first glance, bone may appear inert and unchanging, but it’s actually a very dynamic tissue. In fact, spongy bone is replaced every 3 to 4 years and compact bone is replaced every 10 years, in a process called bone remodeling, which has two steps: bone resorption, when specialized cells called osteoclasts break down bone, and bone formation, which is when another type of cells called osteoblasts form new bone.  

Bone remodeling as a whole is highly dependent on serum calcium levels, which, in turn, are kept in the normal range by a balance between parathyroid hormone, or PTH, calcitonin and vitamin D.  

Parathyroid hormone is produced by the parathyroid glands in response to low serum calcium, and it increases bone resorption to release calcium into the bloodstream. On the other hand, calcitonin is p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteomalacia_and_rickets</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W75fqUr5RZq0Q0yMjjJtoaRhTAm43qEJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteomalacia and rickets]]></video:title><video:description><![CDATA[Bone softening caused by a faulty process of bone mineralization manifests as either rickets in children or osteomalacia in adults. 

Inadequate bone mineralization could be due to a deficient or impaired metabolism of vitamin D, phosphate or calcium. 

But first, a bit about bones. Now, long bones, like the femur, are made up of two epiphyses, which are its ends, and the diaphysis, which is the shaft. 

Between each epiphysis and the diaphysis, there’s a region called the metaphysis.

And the metaphysis contains the epiphyseal plate, or the growth plate, which is the part of the bone that grows during childhood. 

Once growth stops, the growth plate is replaced by an epiphyseal line, and this is known as epiphyseal closure.

Now, for bones to grow and develop properly, special bone cells, called osteoblasts, are hard at work. 

To build bone, osteoblasts secrete osteoid, which is an organic matrix made of type 1 collagen.

These collagen fibers are the framework for the osteoblasts&amp;#39; work. 

Osteoblasts then deposit calcium and phosphate crystals into the framework. 

This process is called bone mineralization, and it confers strength to the growing bones.

Bone mineralization is dependent on an enzyme called alkaline phosphatase - which increases in response to osteoblast activity. 

So, at the end of the day, bones are like a storage warehouse for calcium and phosphate. 

Now, the levels of calcium and phosphate in the bone, but also in the blood, are regulated by vitamin D and parathyroid hormone, or PTH. 

Vitamin D-wise, two steps are necessary for optimal metabolism: first, there must be enough vitamin D in the body, either from food, or created in the skin in response to sunlight exposure.

Secondly, vitamin D must become metabolically active, and this process also has two steps. 

First one happens in the liver, where inactive vitamin D is converted into 25-hydroxy-vitamin D by the enzyme 25-Hydroxylase.  

25-hydroxy-vitami]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lordosis,_kyphosis,_and_scoliosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LA6TC6ZQQWGGSjRk2Y8rH2VPQt6k5VDw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lordosis, kyphosis, and scoliosis]]></video:title><video:description><![CDATA[Lordosis, kyphosis, and scoliosis refer to curvatures of the spine.

Lordosis refers to the normal inward curvatures of the spine at the cervical and lumbar regions, while kyphosis refers to the normal outward curvature of the spine specifically at the thoracic region. 

These terms get used interchangeably with hyperlordosis and hyperkyphosis, which means that the curves look abnormally pronounced. 

Finally there’s scoliosis which always refers to the abnormal sideways curves of the spine.

Now, the bony spine is made of vertebral bones, and there are intervertebral discs that sit between adjacent vertebrae. 

The spine is made of 33 vertebrae, which can be divided into 5 regions. 

The cervical region has 7 vertebrae, the thoracic region has 12 vertebrae, the lumbar region has 5 vertebrae, the sacral region has 5 vertebrae, and the small tail-like coccygeal region is made up of 4 fused vertebrae. 

Normally, the cervical and the lumbar spines slightly curve inward. 

This results from the fact that the intervertebral discs in these two regions are thicker anteriorly than posteriorly, which causes this part of the spine to lean forward. 

On the other hand, the thoracic and the sacral spines are normally curved backward, which is normal kyphosis.

Lordosis and kyphosis are typically associated with underlying conditions. 

For example, in osteoporosis the bones become porous and weak, and can develop compression fractures causing the bones to collapse a bit. 

This can cause a spinal deformity and can also impinge on nearby nerves. 

Misaligned vertebrae can also exert too much pressure on the intervertebral discs, causing them to degenerate. 

Other conditions include spondylolisthesis, in which a vertebrae slips out of its normal position, or conditions like Ehlers-Danlos syndrome and Marfan syndrome, where bones and connective tissues overgrow, causing spinal instability. 

Obesity can also put excess unbalanced weight on the spine causing it to defor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Compartment_syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J5LgO0IiRryPAZfTvpioNdGPR7WpGXcm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Compartment syndrome]]></video:title><video:description><![CDATA[With compartment syndrome, compartment refers to separate sections of the body that contain muscles, nerves, and blood vessels surrounded by a layer of fibrous connective tissue, called fascia.  

When the pressure within these compartments rises, normal blood flow can be cut off, leading to tissue damage due to hypoxia, or the lack of oxygen.

Compartment syndrome typically happens in the limbs, usually in the lower leg or the forearm. 

Now, if we remove the skin and then we remove the fat tissue from the lower leg, we would uncover the fascia.  

Fascia surrounds the muscles,  keeping them tightly together while they contract to move the limb, and it also help attach these muscles to the bones.

Now if we look at a cross section of the lower leg, we can see that the fascia sends intermuscular septa that together with the interosseous membrane between the tibia and fibula divide the lower leg into four compartments. 

The anterior, lateral, deep posterior and superficial posterior compartments all contain their own muscles, and blood vessels. 

For example, the anterior compartment holds the muscles that perform dorsiflexion of the foot and also aid in it’s inversion and eversion; the deep peroneal nerve that innervates them; and its blood supply comes from the anterior tibial artery and veins.

Since the fascia is not elastic it can’t stretch much. Therefore any increase of the cellular and extracellular volume or a decrease of the volume capacity, like with some external compression, will lead to the increase of the pressure inside the compartment. 

This will compress the structures within, and the first ones to feel the effect of compression are the veins, because the pressure inside their lumen is normally low. 

As the pressure increases, the arteries will become compressed next and this obstructs the normal blood flow. 

This cuts off the oxygen supply and hypoxia develops, which causes cells to start releasing substances like histamine and nitric]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rotator_cuff_tear</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8iWVXLmcQ_6AH2XbOqwuiDHqTjquaKMu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rotator cuff tear]]></video:title><video:description><![CDATA[The rotator cuff refers to a group of four muscles and their tendons, which help to stabilize the shoulder when it’s moving particularly during rotational motion. So, a rotator cuff tear is when one or more of the tendons of the muscles of the rotator cuff are torn.

The shoulder is a complex of bones, ligaments, muscles and their tendons that all work together to connect the upper limb to the chest, allowing necessary movement and providing stability.

The round head of the humerus fits and rotates inside the shallow glenoid cavity of the scapula. Just above the glenoid cavity, the scapula extends two bony processes; the acromion and the coracoid processes which serve as attachment for ligaments and muscle tendons.

The ligaments of the capsule of the glenohumeral joint hold the head of the humerus inside the glenoid cavity. The coracoacromial ligament forms an arch between the coracoid process and the acromion and it prevents the head of the humerus from upward dislocation.

In addition to these ligaments, the shoulder is supported by the four rotator cuff muscles, also called the SITS muscles, for Supraspinatus, Infraspinatus, Teres minor, and Subscapularis.

The SITS muscles form a cuff that surrounds the head of the humerus to make it stable and help it move, specifically in abduction, as well as internal and external rotation. Below the acromion lies the acromial bursa, which is a small sac filled with rubbery synovial fluid, that provides lubrication and prevents the rotator cuff tendons, especially the supraspinatus tendon, from rubbing against the acromion as the joint moves.

A rotator cuff tear may occur when the tendons are violently stretched like when you jerkily lift up something which is too heavy, or accidentally fall on an outstretched arm. This most commonly affects the supraspinatus tendon at its insertion on the greater tubercle of the head of the humerus, because it’s under a lot of tension when the shoulder is abducted.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cervical_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PYxY_imISsqaHMs-AC7nd4hETGSqKcQM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cervical cancer]]></video:title><video:description><![CDATA[Cervical cancer is a cancer of the female reproductive system that originates in the cervix. 

It’s one of the most common cancers in women and it’s usually the result of an infection by the human papillomavirus, or HPV. 

It has also played a huge role in scientific research thanks to cervical cancer cells from a woman called Henrietta Lacks, which were the first human cells to be grown in a laboratory and which continue to be used to this day in labs around the world.

The cervix is also called the neck of the uterus, and it protrudes into the vagina.

The interior cavity of the cervix is called the cervical canal and it can be divided into two sections. 

The endocervix is closer to the uterus, not visible to the naked eye, and it’s lined by columnar epithelial cells that produce mucus.

The ectocervix is the continuous with the vagina and it’s lined by mature squamous epithelial cells.  

Where the squamous epithelium of the ectocervix and the columnar epithelium of the endocervix meet, there’s a line called the squamocolumnar junction. 

And right where the two types of cells meet, there’s the transformation zone - which is where sub-columnar reserve cells multiply and transform into immature squamous epithelium through a process called metaplasia. 

Normally, mature cells are stuck in the G1, or Growth 1, phase of the cell cycle, which is when cells grow take care of regular cellular business, like synthesizing proteins and producing energy. 

Eventually, whenever new cells are needed, they’ll exit G1 and keep going through the rest of the cell cycle to eventually divide in two new identical daughter cells.

Sometimes though, cells can be pushed out of G1 and go through the cell reproduction cycle faster than the body needs new cells. 

This uncontrolled growth and multiplication is called dysplasia and it’s exactly how cervical cancer develops from precancerous cells. 

Dysplasia in the epithelial layer of the cervix, also called cervical intraepith]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endometrial_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wxd2uUCXT8y7pDgUzoOST_QeSXuKeCR7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endometrial cancer]]></video:title><video:description><![CDATA[Endometrial carcinoma, or endometrial cancer, is when malignant or cancer cells arise in the glands of the endometrium, the lining of the uterus. 

The uterus is a hollow organ that sits behind the urinary bladder and in front of the rectum. 

The top of the uterus above the openings of the fallopian tubes is called the fundus, and the region below the openings is called the uterine body. 

The uterus tapers down into the uterine isthmus and finally the cervix, which protrudes into the vagina.

Zooming into the cervix, there are two openings, a superior opening up top, and an inferior opening down below, both of which have mucus plugs to keep the uterus closed off except during menstruation and right before ovulation. 

The uterus is anchored to the sacrum by utero-sacral ligaments, to the anterior body wall by round ligaments, and it’s supported laterally by cardinal ligaments as well as the mesometrium, which is part of the broad ligament. 

The wall of the uterus has three layers: the perimetrium, which is a layer continuous with the lining of the peritoneal cavity, the myometrium, which is made of smooth muscle that contracts during childbirth to help push the baby out, and the endometrium, a mucosal layer, that undergoes monthly cyclic changes. 

The endometrium is itself made up of a single layer of simple columnar epithelium, which has ciliated and secretory cells, that sit on top of connective tissue, or stroma. 

There any many grooves in the stroma which is lined by the epithelium and these are the uterine glands which secrete a glycogen rich fluid that’s essential for the developing embryo during early pregnancy.

Endometrial carcinoma involves the abnormal growth of the epithelial cells that make up endometrial glands, and there are two main types. 

The most common is Type 1 endometrial carcinoma, which is also called endometrioid carcinoma because the tumours grow in a way that looks like normal endometrial glands. 

It usually involves sever]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pelvic_inflammatory_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sITsuxdmTF67wqHy8R-95l41QnCOxo1f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pelvic inflammatory disease]]></video:title><video:description><![CDATA[Pelvic inflammatory disease, or PID, is an infection of the upper female reproductive system, including the uterus, fallopian tubes, and ovaries. 

It can cause a number of serious complications, including infertility. 

The female reproductive system includes all of internal and external organs that help with reproduction. 

The internal sex organs are the ovaries, which are the female gonads, the fallopian tubes, two muscular tubes that connect the ovaries to the uterus, and the uterus, which is the strong muscular sack that a fetus can develop in. 

The neck of the uterus is called the cervix, and it protrudes into the vagina. 

At the opening of the vagina are the external sex organs, and these are usually just called the genitals and they’re in the vulva region.

They include the labia, the clitoris, and the mons pubis. 

The vagina, uterus, and fallopian tubes all have a mucosa, which is a layer of epithelial cells that lines the inside of these organs. 

PID usually develops from a bacterial infection in the vagina or cervix which causes inflammation of this mucosal layer. 

About 60 percent of the time, this changes the composition of the bacterial flora in the vagina, also called bacterial vaginosis. 

Because the reproductive tract is essentially one long tunnel that starts at the ovaries and ends at the external sex organs, the infection can travel up the tract pretty easily. 

Some mechanisms can make it even easier! For example, the cervical mucus, which normally acts as a barrier preventing bacteria from entering the uterus, may become less effective. 

The mucus can become thinner as a result of normal variations throughout the menstrual cycle, or alternatively, it can become less effective in the context of bacterial vaginosis, which is when the normal balance of the vaginal flora is altered, and anaerobic bacteria proliferate and degrade the cervical mucus. 

Other factors contributing to an infection may be retrograde menstruation, which ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amenorrhea</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3FqMMdS3Q7G3rxpEOvNa6alARhG8t6mr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amenorrhea]]></video:title><video:description><![CDATA[Amenorrhea means no menstruation.

It’s normal before puberty, during pregnancy and lactation, and after menopause.

Sometimes though, menstruation either never starts, which is called primary amenorrhea, or suddenly stops in a person who’s previously menstruating, which is called secondary amenorrhea. 

Now, menstruation, and the menstrual cycle as a whole are controlled by the hypothalamus and the pituitary gland, all the way up in the brain. 

The hypothalamus secretes gonadotropin-releasing hormone, or GnRH, which makes the nearby anterior pituitary gland release follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH. 

In the first two weeks of a normal 28-day cycle, the ovaries go through the follicular phase, meaning that out of the many follicles scattered throughout the ovaries, a couple of them enter a race to become the dominant follicle, that will be released at ovulation. 

All the developing follicles secrete loads of estrogen, which negatively inhibits pituitary FSH.

In the meantime, the uterus goes through two phases: the menstrual and proliferative phase. 

During the menstrual phase, the functional layer of the endometrium is shed and eliminated through the vagina, leading to menstruation, which lasts an average of five days. 

It’s followed by the proliferative phase, during which the rising levels of ovarian estrogen make the functional layer of the endometrium thicken and sprout endometrial glands. 

Additionally, spiral arteries emerge to nourish the growing functional endometrium. 

After ovulation, the ovaries enter the luteal phase, which lasts for the two weeks following ovulation. 

During the luteal phase, the remnant of the ovarian follicle, called the corpus luteum, makes progesterone, which negatively inhibits pituitary LH. 

Progesterone makes the endometrium go through the secretory phase, during which it thickens some more, and spiral arteries continue to grow. 

If the egg is not fertilized by a sperm, estr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endometriosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7VigLAJDRSyW5Fph8G044QMaRvm_-5ba/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endometriosis]]></video:title><video:description><![CDATA[Endo- means internal and -metrium means womb, so endometrium is the innermost layer of the womb, and endometriosis is where these endometrial cells grow outside of the womb.                                      

The female internal sex organs are the ovaries, which are the female gonads; the fallopian tubes, two muscular tubes that connect the ovaries to the uterus; and the uterus, which is the strong muscular sack that a fetus can develop in. 

It’s a hollow organ that sits behind the urinary bladder and in front of the rectum. 

The top of the uterus above the openings of the fallopian tubes is called the fundus, and the region below the openings is called the uterine body. 

The uterus tapers down into the uterine isthmus and finally the cervix, which protrudes into the vagina. 

It’s is anchored to the sacrum by utero-sacral ligaments, to the anterior body wall by round ligaments, and it’s supported laterally by cardinal ligaments as well as the mesometrium, which is part of the broad ligament. 

The wall of the uterus has three layers: the perimetrium, which is a layer continuous with the lining of the peritoneal cavity, the myometrium, which is made of smooth muscle that contracts during childbirth to help push the baby out, and the endometrium, a mucosal layer, that undergoes monthly cyclic changes.

In endometriosis, the cells that make up the endometrium migrate and implant themselves in other parts of the body. 

Once there, they will set up camp and start growing to form a mass of endometrial tissue.  

Most often, this affects the ovaries, fallopian tubes, and uterine ligaments. 

But it can also affect other structures in the pelvis and abdomen like the perimetrium, the rectovaginal septum, the recto-uterine pouch, also called the pouch of Douglas, and even the intestines or bladder!

Although we are unsure of the exact cause of the endometrial cell migration, there are at least five main theories that try to explain this phenomenon. 

First,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ovarian_cyst</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7qJtY_iJTwWxx5lbhwv8-XLET3msme_-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovarian cyst]]></video:title><video:description><![CDATA[“Cyst” comes from kustis, which means “pouch”, so ovarian cysts are fluid-filled sacs on or in the ovaries. They are very common in females of reproductive age, but can affect females of any age.

The ovaries are a pair of white-ish organs about the size of walnuts. They’re held in place, slightly above and on either side of the uterus and fallopian tubes by ligaments. 

Specifically, there’s the broad ligament, the ovarian ligament, and the suspensory ligament. And the suspensory ligament is particularly important because the ovarian artery, ovarian vein, and ovarian nerve plexus pass through it to reach the ovary. 

If you slice the ovary open and look at it (don’t try this at home) there’s an inner layer called the medulla, which contains most of the blood vessels and nerves and an outer layer called the cortex, which has ovarian follicles scattered throughout it. 

Each follicle is initially made up of an immature sex cell, or primary oocyte, which is the female sex cell, and layers of theca and granulosa cells surrounding the oocyte. 

Now, there’s actually loads going on with the ovaries throughout the menstrual cycle, which is controlled by the hypothalamus and the pituitary up in the brain. 

The hypothalamus secretes gonadotropin-releasing hormone, or GnRH, which makes the nearby anterior pituitary gland release follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH. 

In the first two weeks of an average 28-day cycle, the ovaries go through the follicular phase, meaning that out of the many follicles scattered throughout the ovaries, a couple of them enter a race to become the dominant follicle, that will be released at ovulation, while the rest regress and die off. 

All the developing follicles secrete loads of estrogen, which negatively inhibits pituitary FSH, and they also make a few androgens like testosterone.

At ovulation, the oocyte is released into the fallopian tube, and the luteal phase begins - which lasts for the last ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_cytomegalovirus_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sNjltt_wSRGcnpod--NKBUuFTq6cjf5h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital cytomegalovirus (NORD)]]></video:title><video:description><![CDATA[Congenital cytomegalovirus infection is the infection of a fetus with cytomegalovirus, or CMV, during intrauterine life.

CMV is among the most common infections that cause defects during fetal development.

It is often grouped with other bacteria, parasites, and viruses that cause similar illnesses in the newborn, known under the acronym TORCH, which includes Toxoplasma.

Other pathogens - usually syphilis; Rubella; Cytomegalovirus, and Herpes simplex virus.

CMV belongs to the herpesviridae family of viruses.

Herpesviruses are double-stranded DNA viruses which are surrounded by a lipid envelope.

CMV is usually transmitted through contact with blood and other body fluids like breast milk, saliva, genital secretions, and urine of an infected person; or from transplanted organs.

Congenital CMV infection occurs when a pregnant woman is infected by CMV for the first time during the pregnancy, or there&amp;#39;s reactivation of an old infection, or reinfection with a new strain of CMV.

The virus in the mother travels through the placenta to the growing fetus.

The exact mechanism by which CMV causes infection and defects in the developing fetus is still unknown, but it’s thought to be because of two things.

First, CMV can be cytopathic, or cell-damaging, as it replicates within the cells.

It breaks down the cytoskeletons which maintain the cell structure which results in enlarged cells with intranuclear viral inclusion bodies, giving it the classic “owl&amp;#39;s eye” appearance.

It is also possible CMV slows down the process of mitosis, or cell division.

Since mitosis helps drive the development of the fetus, tissue with infected cells might not grow properly.

Second, CMV invades the endothelium of blood vessels, resulting in vasculitis, or inflammation of blood vessels.

Vasculitis can affect placental as well as fetal blood vessels, causing narrowing of the vessel wall. And, as a result, not enough blood flows to developing organs, causing abnorm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obsessive-compulsive_disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vj23KhIuQTWIfD7XTH33JIOQQ3iVRQsN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obsessive-compulsive disorder]]></video:title><video:description><![CDATA[Double-checking things is a pretty common human behavior, like—did I shut the garage-door? Better double-check. How about locking the front door? Double-check. Gas-stove and oven off? Double-check. We all do it. 

But what if you feel compelled to triple-check it, or even quadruple check it, or quintuple check it even, then it might be considered an obsession. 

Now, what if you have to do a certain ritual with the gas-stove and oven before leaving the home each time, like: make sure the gas-stove is off, wipe down the gas stove to clean it, double-check that the burners are off, make sure the oven is off, wipe down the oven to clean it, and then open the oven door to make sure no heat is coming out, and then leave the house. 

Then that might be a compulsion.

Obsessive-compulsive disorder, or OCD, is a specific type of anxiety disorder characterized by these obsessions or compulsions. 

Obsessions are recurrent and intrusive thoughts that are typically unwanted and tough to get out of your brain. 

These unwanted thoughts like, “My house is unsafe!” cause anxiety, and usually they lead to compulsions, which are actions that might be performed to try and reduce the anxiety associated with obsessions. 

As you might imagine, these thoughts and rituals can have a serious impact on someone’s daily life. 

OCD affects around 3% of the population, and usually starts in childhood or in the teen years. 

Celebrities like David Beckham and Howie Mandel are known to be affected by OCD. 

A more severe example is that of Howard Hughes, business tycoon, entrepreneur, and inspiration for the movie Citizen Kane, who was affected by relatively incapacitating OCD later in his life.

A very common compulsion is cleaning, which often stems from an obsession with germs or contamination. 

Another common compulsion is checking: people who have this compulsion usually have an associated obsession that something’s unsafe, so they’ll check to make sure that something’s definit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Calcium_channel_blockers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yFXRAtIDSbeOt-8wroW-sXNfTSOHxw3r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Calcium channel blockers]]></video:title><video:description><![CDATA[Calcium entry blockers, or calcium channel blockers - CCBs for short - are vasodilators, or medications that promote dilation of blood vessels. These medications are mainly used to treat hypertension, or high blood pressure, and angina pectoris, which is a pain caused by reduced blood flow to the heart muscle. Now, by definition, blood pressure is the force that blood exerts on the walls of blood vessels and it’s basically what keeps blood flowing and perfusing tissues to deliver oxygen and nutrients. Hypertension happens when this pressure is higher than it should be. In most cases, the cause is unknown. 

But basically, we can do a number of things to help lower the blood pressure. First, we can decrease the heart rate or the myocardial contractility, so the heart pumps less blood into the blood vessels. In other words, diminish the amount of blood that exerts force upon the same area. Or, we can vasodilate the peripheral blood vessels, which increases the area for the same amount of liquid that exerts force. Angina, on the other hand, is a type of chest pain caused by insufficient oxygen supply to the myocardium to meet its demand. Generally, the underlying cause is the presence of atheromatous plaques in the coronary arteries which decreases the blood flow to the heart. So, to help diminish the symptoms, it’s important to decrease the oxygen demand of the heart, again by decreasing heart rate or myocardial contractility; and increasing the oxygen supply by vasodilating the coronary arteries.

Now, let’s look at how calcium channels affect heart function. First off, the heart rate depends on the rate that the pacemaker cells in the sinus and atrioventricular node generate action potentials. These action potentials start automatically when sodium channels slowly let in a stream of sodium ions, which causes the membrane potential of the pacemaker cells to become more positive. When this reaches the threshold membrane potential, it’s the cue for voltage-ga]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acetaminophen_(Paracetamol)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UbwPyEazRl_6Lcm4hYDQWxJqRDqHyj-b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acetaminophen (Paracetamol)]]></video:title><video:description><![CDATA[Acetaminophen, also known as paracetamol, is mainly used to treat pain and fever. These conditions are related to an increased production of pro-inflammatory chemicals called prostaglandins.

Now, acetaminophen works by decreasing the production of prostaglandins, thereby relieving pain, and reducing fever.

In order to understand how acetaminophen works, first we need to talk briefly about inflammation, which is the body’s response to a harmful stimulus, such as infection or injury. 

So, during inflammation, your immune cells use an enzyme called phospholipase A2 to take membrane phospholipids and make a 20 carbon polyunsaturated fatty acid, called arachidonic acid.

Arachidonic acid is a substrate for an enzyme called cyclooxygenase or COX. 

The enzyme cyclooxygenase exists in two different isoforms: COX-1 and COX-2. 

COX-1 is a constitutive enzyme, meaning that it’s always active, while on the other hand, COX-2 is an inducible enzyme, meaning that it must be turned on to function. This is usually triggered by immune cells and vascular endothelial cells during inflammation. 

Both enzymes produce prostaglandin E2 (PGE2) and prostacyclin (PGI2), which cause vasodilation and attract different immune cells to the area. 

They also act on neurons that detect pain, called nociceptors, and make them more sensitive to stimuli by lowering their threshold for activation. 

Finally, they stimulate the hypothalamus to increase the body temperature, causing fever. 

Prostaglandin E2 also has other effects like causing uterine contractions, decreasing the secretion of acid, and increasing the production of protective mucus in the stomach.

Alright, now let’s focus on acetaminophen. Acetaminophen is administered orally, rectally, or intravenously; and it works by reversibly inhibiting COX in the central nervous system, thereby decreasing production of the prostaglandins that cause fever and pain. 

It’s important to note that acetaminophen is not consider]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glucocorticoids</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cDmjL0HwTYKradX6UUWFvw3CS-S1Hk4I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glucocorticoids]]></video:title><video:description><![CDATA[Glucocorticoids are a group of steroid hormones, which are secreted by the two adrenal glands that sit like hats, one on top of each kidney. Each one has an inner layer called the medulla and an outer layer called the cortex. The adrenal cortex secretes different corticosteroid hormones: like glucocorticoids under the control of adrenocorticotropic hormone, or ACTH. 

Normally the hypothalamus, located at the base of the brain, secretes corticotropin releasing hormone, known as CRH, which stimulates the anterior pituitary gland to secrete adrenocorticotropic hormone, known as ACTH. ACTH then travels to the pair of adrenal glands and binds to the ACTH receptors on adrenocortical cells. This causes the adrenocortical cells to release the glucocorticoids from the zona fasciculata, which have powerful anti-inflammatory and metabolic effects. These glucocorticoids have a negative feedback effect on the hypothalamic-pituitary-adrenal axis, meaning excess corticosteroids suppress the release of both CRH and ACTH into the circulation.

Now, once made, glucocorticoids enter the circulation and travel via the blood to reach the target cells. Steroids are lipophilic molecules, so they cross the cell membrane, enter inside the cell, and bind with a cytoplasmic receptor protein, called a ‘glucocorticoid receptor’. Now, this ‘glucocorticoid-receptor complex’ undergoes some structural changes, which allow them to enter inside the nucleus and bind with the ‘glucocorticoid response elements’ or GRE on the chromatin. Now, this induces transcription of specific mRNA that’s used to synthesize different proteins, which in turn modifies various cell functions and metabolic effects in the body.

The most important glucocorticoid in humans is cortisol, and it’s generally released during times of stress, like during an illness or starvation. Cortisol helps to regulate both the immune response as well as cellular metabolism like gluconeogenesis. With regard to the immune response, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ribonucleotide_reductase_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kLpDVxJkQWWcHAinQKTsMFfmTAq8Iw-Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ribonucleotide reductase inhibitors]]></video:title><video:description><![CDATA[Ribonucleotide reductase inhibitors, as their name implies, are a class of medications that act by blocking an enzyme called ribonucleotide reductase. They are mainly used as anticancer agents that target a specific phase of the cell cycle. 

At a quick glance, the life of a cell - its cell cycle - has an interphase, made up of subphases G1, S, and G2, during which the cell is preparing for division; and mitosis, during which the cell actively divides.

During the S phase, the cell performs DNA replication - which is when its 46 chromosomes are duplicated so that each daughter cell can get its own copy of the genetic material.  

Now, a single chromosome is made up of a single DNA molecule that has two strands, which wrap around one another to form a double helix. 

Each single strand of DNA is composed of a sequence of DNA nucleotides. 

Now, nucleotides are the building blocks of nucleic acids such as deoxyribonucleic acid, or DNA; and ribonucleic acid, or RNA. 

The most basic structure of the nucleotide can be broken down into three subunits; a five carbon sugar, a phosphate group, and a nitrogenous base, also known as a nucleobase. 

The five carbon sugar is either deoxyribose in DNA or ribose in RNA. 

Now, the nucleobases can be either pyrimidines or purines. 

The 3 pyrimidine bases are cytosine, or C; thymine, or T, which is DNA specific; and uracil, or U, which is RNA specific. 

There are also two purine bases, adenine, or A; and guanine, or G. 

Now, if we link up just the sugar and the nucleobase, we’ve got ourselves a nucleoside. 

To make a nucleotide, all we’ve got to do is add a phosphate group to the 5th carbon of the sugar on a nucleoside. 

Okay, so in order to make DNA nucleotides we use RNA nucleotides. 

RNA nucleotides are usually in the monophosphate form and we need to change them into the diphosphate form for DNA. 

So a cytoplasmic enzyme called ribonucleotide reductase, also known as ribonucleoside diphosphate reductase, will r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_for_neurodegenerative_diseases</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gV8TvfIoSLG-7syyx-20m8K0SxmIAbCl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for neurodegenerative diseases]]></video:title><video:description><![CDATA[Huntington disease, or HD, is a rare neurodegenerative disease that involves a repeated sequence of DNA that causes an abnormal protein to form, leading to abnormal movements and cognitive problems. 

In most people, a gene called huntingtin or HTT on chromosome 4, contains a triplet repeat, where the nucleotides C, A, and G are repeated 10-35 times in a row. In people with Huntington disease, this repeat goes on for 36 or more times in a row. 

CAG codes for the amino acid glutamine, so people with Huntington disease will have 36 or more glutamines in a row in the huntingtin protein. 

So, in addition to being a triplet repeat disorder, HD is, more specifically, a “polyglutamine” disease. 

The specific way in which extra glutamines causes HD symptoms isn’t fully worked out, but some clues are that the mutated protein aggregates within the neuronal cells of the caudate and putamen of the basal ganglia causing neuronal cell death. 

Cell death might be related to excitotoxicity, which is excessive signaling of these neurons, which leads to high intracellular calcium.

Now the symptoms of HD involve progressive CNS disturbances including movement, cognitive, and mood symptoms and they start appearing around the age of 40.  

Remember, the age of onset depends on the number of CAG repeats, so more repeats means earlier onset. 

Over time, if enough of the neurons die in the caudate and putamen, which together form the dorsal striatum, then it can cause actual loss of brain tissue volume in that area and expansion of the lateral ventricles. 

The death of neurons also cause neurotransmitter imbalance in these regions and there’s a decrease in inhibitory neurotransmitters like GABA, and an increase in stimulatory neurons like dopamine. 

This also decreases acetylcholine, which is released by interneurons that help other neurons communicate. 

Now, the affected areas play an important role in movement, particularly inhibiting it, so cell death in the basal gan]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sympathomimetics:_Direct_agonists</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kgSE1pqCT46-mtiRLKoHknGiRgG-jlxC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sympathomimetics: Direct agonists]]></video:title><video:description><![CDATA[Alpha agonists and beta agonists are two types of adrenergic medications that stimulate their respective receptors and mimic the effect of endogenous catecholamines, like norepinephrine and epinephrine.

The nervous system is divided into the central nervous system and the peripheral nervous system.

The peripheral nervous system can be further divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles; and the autonomic nervous system, which controls the involuntary movement of the smooth muscles and glands of our organs; this system is then further divided into the sympathetic and parasympathetic nervous systems.

Now, the autonomic nervous system is made up of a relay that includes two neurons.

We’ll focus on just the sympathetic nervous system.

Signals for the autonomic nervous system start in the hypothalamus, at the base of the brain. 

Hypothalamic neurons have really long axons that carry signals all the way down to the thoracic and lumbar spinal cord nuclei, where they synapse with preganglionic neuron cell bodies. 

From there, the signal goes from the preganglionic neurons down its relatively short axon, exits the spinal cord, and reaches the nearby sympathetic ganglion, which is made up of lots of postganglionic neuron cell bodies. 

The postganglionic neurons are also called adrenergic neurons, because they release the neurotransmitter norepinephrine, which is also called noradrenalin; and to a much lesser degree, epinephrine also known as adrenaline. 

These two catecholamines activate the adrenergic receptors on many different organs, which allows the sympathetic nervous system to trigger the fight or flight response that increases the heart rate and blood pressure, as well as slowing down digestion.

This response maximizes blood flow to the muscles and brain, and can help you either run away from a threat, or fight it, which is why it’s also called the fight or flight response.

Now, there are two ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacodynamics:_Agonist,_partial_agonist_and_antagonist</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RHUmZF7fSgC8H0hSWrHTCXfZQveSuAIZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacodynamics: Agonist, partial agonist and antagonist]]></video:title><video:description><![CDATA[Pharmacodynamics refers to the mechanisms and effects of medications within the body. Or more simply, it’s what medications do to the body and how they do it.

Alright, so, in order to have an effect, many medications have to reach their target cells and bind to a receptor. Receptors are specialized proteins found inside the cell or on its membrane.  When they bind to a signal molecule called a “ligand”, they can alter their shape or activity, which ultimately results in some change in the cell’s activity or behavior. You can imagine the ligand as the key that fits into the lock, which is the receptor, causing it to open or activate.  Now, depending on the effect a medication has on its receptor, they are often divided into two major categories: agonists and antagonists. An agonist is a medication that mimics the action of the signal ligand by binding to and activating a receptor. On the other hand, an antagonist is a medication that typically binds to a receptor without activating them, but instead, decreases the receptor&amp;#39;s ability to be activated by another agonist. 

Okay, now the maximal effect or response an agonist can produce, abbreviated as Emax, is determined both by the number of receptors bound to the agonist, which depends mainly on the amount of the agonist given, also known as dose, as well as its intrinsic activity, which is the ability of the agonist to fully or partially activate its receptors.  Let’s plot all this into a nice graph to show the relationship between the dose given, on the x axis, usually on a logarithmic scale, and the response produced, on the y axis. So full agonists, upon binding to the receptor at high doses, are capable of producing a maximal response of 100% Emax on the y axis. This represents the point where all available receptors are bound to an agonist. In contrast, partial agonists, even at very high doses, when they occupy all of the receptors, result in a smaller response, so their Emax will be lower. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/MEN_syndromes:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sHQ-8j73T-mBlWE5lC1cI5PyQSOSUQGw/_.jpg</video:thumbnail_loc><video:title><![CDATA[MEN syndromes: Clinical]]></video:title><video:description><![CDATA[The multiple endocrine neoplasias, or MEN for short, are a group of inherited diseases which cause tumors to grow in endocrine glands, like the pancreas, pituitary, thyroid, adrenals, and parathyroid glands.

So in multiple endocrine neoplasias there’s overproduction of various hormones. 

Multiple endocrine neoplasias are caused by a dominant mutation in either the MEN 1 gene which is a tumor suppressor gene or the RET gene which is a proto oncogene.

A MEN1 mutation causes MEN type 1, and a RET mutation causes MEN type 2A and 2B.

In multiple endocrine neoplasia type 1, there are three types of tumors: pituitary, parathyroid, pancreatic - 3 “p’s”. 

But the gastrinomas that occur in the pancreas, are actually more often found in the duodenum, so to keep things accurate 2 “p’s” and a “g” for gastrointestinal gastrinoma is better.

Now in MEN1, the most common tumors are parathyroid tumors which create excess parathyroid hormone. That leads to bone breakdown, which causes serum calcium levels to rise, and that allows calcium kidney stones to form. This is similar to what happens in an isolated parathyroid adenoma. 

The key differences are that MEN1-associated hyperparathyroidism has an earlier age of onset, around 25 years, and tends to affect 3 or 4 of the parathyroid glands, rather than just one. 

A silver lining is that MEN1 associated hyperparathyroidism almost never progresses to a malignant parathyroid cancer. 

Management of hyperparathyroidism can be surgical or nonsurgical. 

Surgery is indicated in individuals who meet at least one criteria in the biochemical, skeletal, renal, or age categories. 

The biochemical criteria are a moderately elevated serum parathyroid hormone, and a serum calcium level that’s adjusted for albumin, of over 12 milligrams per deciliter. 

Skeletal criteria include diminished bone density, and previous asymptomatic vertebral fractures demonstrated on imaging studies.

Renal criteria are the presence of kidney stones, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastroparesis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dp26ts8WQxa7QqKU0k78arwrRLynrwW9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastroparesis: Clinical]]></video:title><video:description><![CDATA[The gastrointestinal system depends on the coordination of the sympathetic and parasympathetic nervous systems, pacemaker cells and neurons within the walls of the stomach and intestine, and the smooth muscle in the gastrointestinal walls. If any part  is disturbed, then it can lead to gastroparesis, which is delayed gastric emptying in the absence of a mechanical obstruction.  

Gastroparesis is usually idiopathic, but it’s associated with a number of diseases like diabetes mellitus, hypothyroidism, neurological conditions like Parkinson’s disease, viral infections, or even an autoimmune attack. 

There are also iatrogenic causes like inadvertent vagal nerve damage during surgery, or can be due to medications like opioids, alpha-2-adrenergic agonists like clonidine, tricyclic antidepressants like amitriptyline, and anticholinergics like atropine.

Individuals with gastroparesis can have symptoms like nausea, vomiting, upper abdominal pain, early satiety, bloating, and in severe cases, unintentional weight loss. On physical examination, there’s usually epigastric distention or tenderness in the upper abdomen, but without guarding or rigidity. 

When gastroparesis is suspected, individuals should undergo an upper endoscopy to make sure that there’s no mechanical obstruction. 

Because an upper endoscopy may not always reveal a mechanical obstruction, after the upper endoscopy, an abdominal CT or magnetic resonance enterography can be done to confirm that there is no mechanical obstruction. 

Now, to establish the diagnosis of gastroparesis, a scintigraphic gastric emptying test should be done. 

For this test, medications that affect the gastric motility should be stopped at least 48 hours before the test is done. In addition, individuals with diabetes mellitus should have their glucose blood levels measured before the test and if they are hyperglycemic, then this should be treated before the test is done as well.

For the test to be accurate, glucose level]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Taking_a_good_patient_history</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9Sr2MWBTSvuxpy5Gz1kT91nJSpi0XMy_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Taking a good patient history]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Taking a good patient history through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_avoid_burnout</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eIRuC3evQySJRotkeYGu9-mvS9WWtzmC/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to avoid burnout]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to avoid burnout through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Writing_a_good_progress_note</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rko12ImSRuuYFq4KuVl3hGncQoeYbT9s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Writing a good progress note]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Writing a good progress note through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Repeated_measures_ANOVA</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hj6vYS6TTr6iG9rLS9c_x6T-RWuj9BG-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Repeated measures ANOVA]]></video:title><video:description><![CDATA[Analysis of variance, or simply, ANOVA, is a type of parametric statistical test used to determine if there’s a significant difference between the means or averages of three or more groups. And significance is normally defined by a p-value of less than 0.05 or 5%. 

Now when doing any parametric test, there are three key assumptions that we have to make about the population. First, the sample population must have been recruited randomly. Choosing names randomly ensures that the people included in the study will have similar characteristics to the target population. This is important because that ensures that the results of the test can be applied to the target population - meaning it has good external validity! The second assumption is that each individual in the sample was recruited independently from other individuals in the sample. In other words, no individuals influenced whether or not any other individual was included in the study. For example, if two friends decided to get their blood pressures measured on the same day, and they were both included in the study, these two individuals would not be independent of each other and the second assumption would not be met. Like random sampling, independent recruitment of individuals is important because it ensures that the sample population approximates the target population. The third assumption is that the sample size is large enough to approximate the target population, which usually means having more than 20 people. If it’s impossible to get a large sample size, then the sample population must follow a normal bell-shaped distribution for the characteristic being studied because that’s what we would expect to see in the target population.

Okay, now let’s say there’s a certain blood pressure medication, called Medication A, and you want to figure out if it helps lower systolic blood pressure after taking it for three months and after taking it for six months. So, you find 10 people and give each of them M]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Two-way_ANOVA</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cc4YQ3GBQweq8ds5gp1zLEWWRhmr4TbB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Two-way ANOVA]]></video:title><video:description><![CDATA[Analysis of variance, or simply, ANOVA, is a type of parametric statistical test used to determine if there’s a significant difference between the means or averages of three or more groups. 

And significance is normally defined by a p-value of less than 0.05 or 5%. 

Now when doing any parametric test, there are three key assumptions that we have to make about the population. 

First, the sample population must have been recruited randomly. Choosing names randomly ensures that the people included in the study will have similar characteristics to the target population. This is important because that ensures that the results of the t-test can be applied to the target population - meaning it has good external validity! 

The second assumption is that each individual in the sample was recruited independently from other individuals in the sample. In other words, no individuals influenced whether or not any other individual was included in the study. 

For example, if two friends decided to get their blood pressures measured on the same day, and they were both included in the study, these two individuals would not be independent of each other and the second assumption would not be met. 

Like random sampling, independent recruitment of individuals is important because it ensures that the sample population approximates the target population. 

The third assumption is that the sample size is large enough to approximate the target population, which usually means having more than 20 people.

If it’s impossible to get a large sample size, then the sample population must follow a normal bell-shaped distribution for the characteristic being studied because that’s what we would expect to see in the target population.

Okay, now let’s say there are three medications available for lowering systolic blood pressure, and you want to figure out if any of the medications work differently than the others. Additionally, you want to figure out if the medications work differently]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacokinetics:_Drug_metabolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RO81Ayl3RZi83r3DKYaV6Zn1T4usLho1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacokinetics: Drug metabolism]]></video:title><video:description><![CDATA[Pharmacokinetics refers to the movement and modification of medication inside the body. Or more simply, it’s what the body does to the medication and how it does it.

Alright, so once the medication get administered, it first has to be absorbed into the circulation, then distributed to various tissues throughout the body; metabolized or broken down; and finally, eliminated or excreted in the urine or feces. 

You can remember this as ADME - Absorption, Distribution, Metabolism, and  Excretion.

Okay, let’s focus on the metabolism. This is the process of converting a medication into a less, or more active form. These forms are also known as metabolites.

So in most cases, metabolic reactions turn an active medication into a less active, or inactive metabolite, which is then ready to get excreted. 

Some medications though, are administered in an inactive form, also known as a prodrug, which needs to be metabolized into an active form within the body before they can produce the desired effect. But even those medications will eventually need to go through further metabolism in order to get inactivated and excreted.

Now, all these reactions are broken down into two main phases: phase I and phase II. 

This classification is somewhat misleading though. For some medications Phase II may occur before Phase I, while others may undergo only Phase I or only Phase II. 

In any case, both phases take place primarily in the liver, and to a much lesser degree, in the lungs, kidneys, and the walls of the small intestine.

So, let’s zoom into a liver cell, also known as a hepatocyte.

Phase I reactions are typically carried out by a class of enzymes called cytochrome P450, or CYP450 for short. 

These enzymes hang out mainly in cell compartments, like the endoplasmic reticulum and the mitochondria. 

They are often abbreviated as CYP followed by a number, which indicates the family; followed by a letter for the subfamily, and then a number again for the form, like CYP3A4]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malabsorption:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dGKvFQOkQx20ZOil4ckrgzTsS2W2pHjQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malabsorption: Clinical]]></video:title><video:description><![CDATA[With malabsorption, nutrients are no longer effectively absorbed in the small intestines. Nutrients can either be macronutrients, such as fats, proteins and carbs or micronutrients like vitamins and minerals. Malabsorption can either be global meaning that the absorption of all nutrients is affected or it can be partial meaning that only specific nutrients cannot be absorbed. Malabsorption presents differently based on which nutrients are being malabsorbed, the severity of the disease, and the underlying cause. Global malabsorption can present with chronic or recurrent diarrhea with pale, greasy, voluminous and terrible smelling stools and unintentional weight loss. In contrast, partial malabsorption causes symptoms specific to the nutrient involved. 

With fat malabsorption, symptoms include steatorrhea - meaning fatty stools. To confirm that it’s really steatorrhea, a fecal fat test can be done to check for fat. If it’s negative and fat malabsorption is still suspected, then a 72 hours stool collection should be done because that’s the gold standard for diagnosing fat malabsorption. To do that, an individual has to have a diet that includes 70 to 120 grams of dietary fat per day, which is the equivalent of eating about 300 grams of cheese per day. Stool is collected for 72 hours, and if there’s more than 6 grams of fat per day, then it’s considered fat malabsorption. Typically if there’s steatorrhea, the stool fat exceeds 20 grams per day. 

If fat malabsorption is present, then the fat soluble vitamins - A, D, E, and K, might also not be getting absorbed. Vitamin A deficiency causes symptoms like night blindness and thickened skin due to hyperkeratosis. Vitamin D deficiency causes symptoms like paresthesias, and fractures due to osteomalacia. Vitamin E deficiency can cause symptoms like muscle weakness. And finally, vitamin K deficiency causes symptoms like easy bruising, excessive bleeding from wounds, gastrointestinal bleeds, or hematuria.

With prote]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_nodules_and_thyroid_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W8xb8To3R3K-UiSf3V3ApdZVT8imKsXm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid nodules and thyroid cancer: Clinical]]></video:title><video:description><![CDATA[Thyroid nodules are lumps on the thyroid gland that represent clusters of abnormally growing thyroid cells. They’re actually fairly common, and they’re often felt on palpation, or they’re discovered incidentally, like during an ultrasound of the thyroid gland. 

There may be a single nodule or multiple nodules, and sometimes they form on a pre-existing goiter - which is when the thyroid is enlarged, usually due to an autoimmune attack on the thyroid gland, like with Hashimoto’s thyroiditis, or Graves’ disease. 

The key thing to identify is whether or not the nodule is benign or is a thyroid cancer.

The thyroid is sensitive to radiation, so an important risk factor for thyroid cancer is prior radiation in the head or neck region, which might have been given for another malignancy in the area, like lymphoma. 

Other risk factors for thyroid cancer include a family history of thyroid cancer or being over age 65, since nodules are more likely to be malignant in older individuals. 

Because thyroid nodules are fairly uncommon in young individuals, if they appear in a person below 20 years of age, they’re usually cancerous.

Finally, having symptoms related to the nodule like voice changes or a hoarse voice, and difficulty breathing or swallowing suggest that the nodule is an invading adjacent tissues and structures, a sign of thyroid cancer. 

On a physical examination, a nodule is more likely to be thyroid cancer if it’s firm and hard on palpation, or if it’s fixed - meaning, it doesn’t move when the individual swallows. 

Another warning sign is the presence of a swollen lymph node in the neck region, especially when the lymph node doesn’t hurt on palpation, and is only on one side. 

The next step in evaluating the risk that a thyroid nodule is cancerous, is getting a TSH level and a thyroid ultrasound. Depending on the results of these tests,  a fine needle aspiration may or may not be needed. 

Now, TSH is normally secreted by the pituitary gland which r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZOgefCZqSmeqD__ySBPCwLzxQgORMoaL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal disorders: Clinical]]></video:title><video:description><![CDATA[The esophagus is a 25- 30 centimeter long tube through which food and liquids pass from the pharynx to the stomach. The esophageal wall is composed of 4 layers: inner mucosa which is made of stratified squamous epithelium except at the lower esophageal sphincter where it joins the gastric epithelium to form the gastroesophageal junction, submucosa, a muscular layer made of skeletal muscle in the upper third, smooth muscle in the lower third and a combination of the two in the middle and finally an outer layer of connective tissue called adventitia. At the top and bottom of the esophagus there are the upper and lower esophageal sphincter, respectively. Both relax during swallowing to allow the passing of food or liquids propelled by peristaltic contractions. Additionally, the lower esophageal sphincter also prevents acid reflux from leaving the stomach between meals. 

Some esophageal disorders are functional meaning that they affect the muscles and nerves which control the motility of the esophagus, whereas other esophageal disorders are mechanical meaning that there’s something within or just outside the esophagus that blocks the passageway. With esophageal dysphagia, it’s important to know what type of food produces the symptoms: if dysphagia is related to the ingestion of both liquids and solids, the most probable cause is a functional disorder. On the other hand, dysphagia for solids only means that the lumen of the esophagus is really narrow, often less than 13 millimeters due to a mechanical cause like a malignancy or esophageal stricture. Dysphagia can also be intermittent or progressive. Usually, intermittent dysphagia is related to both solids and liquids and appears in functional disorders, whereas progressive dysphagia means that something is growing inside the esophagus and dysphagia gradually worsens. Esophageal dysphagia also needs to be distinguished from oropharyngeal dysphagia. With esophageal dysphagia, the individual can easily initiate ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypothyroidism_and_thyroiditis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Svu2juauSj_Bmd8nOhNiXgeTSYSTcmZ1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypothyroidism and thyroiditis: Clinical]]></video:title><video:description><![CDATA[Hypothyroidism is a condition that’s caused by having insufficient thyroid hormones. 

Thyroid hormone production is under the control of the hypothalamus and the pituitary. 

The hypothalamus secretes thyrotropin releasing hormone, or TRH, and TRH stimulates the anterior pituitary to secrete thyroid-stimulating hormone, or TSH. 

TSH then binds to TSH receptors, which makes the thyroid secrete thyroxine, or T4 and triiodothyronine, or T3, in the blood. But this is not a one-way street - there’s also negative feedback happening, meaning when thyroid hormone levels rise, that inhibits the production of TSH and TRH, halting further production of T3 and T4 - to keep everything in balance. 

Normally, some thyroid hormones travel through the bloodstream bound to thyroid binding globulin, and some are in their free form. And the thyroid actually makes more T4 than T3, and that T4 is converted to the more potent T3 in the periphery. 

Thyroid hormones then increase the rate of metabolism in all cells, so they make us think, move, and talk faster, and they also increase heat generation. They also activate the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response, increasing cardiac output.

So with hypothyroidism, it’s like the entire body is functioning in slow motion - but this happens gradually, so it can take years before symptoms are even recognized. These include weight gain despite a loss in appetite because of the lower basal metabolic rate; cold sensitivity because the body is producing less heat; and slower heart rate, mental slowness, lethargy, and constipation because of the decreased effect of thyroid hormones on the sympathetic nervous system. 

With hypothyroidism, glycosaminoglycans also accumulate in the skin and soft tissues, causing myxedema, or swelling, and an enlarged swollen tongue. Individuals may also have a puffy face - like a person who’s just woken up, coarse hair, periorbital edema, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophagitis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sxvnK4phQTijY7gbtyBUS5nwRZOuaRDF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophagitis: Clinical]]></video:title><video:description><![CDATA[The esophagus is a 25-30 centimeter long muscular tube through which food and liquids pass from the pharynx to the stomach. At the top and bottom of the esophagus there are the upper and lower esophageal sphincter, respectively. 

Esophagitis is inflammation of the esophagus, and it usually causes dysphagia or difficulty in swallowing, odynophagia or painful swallowing, and retrosternal chest pain. 

If the cause is unclear, the usual workup includes an upper endoscopy with a biopsy. And in case of retrosternal chest pain, an electrocardiogram should always be done in order to rule out cardiac ischemia.

Now, the most common cause is gastroesophageal reflux disease or GERD, and in that situation it’s called reflux esophagitis. 

In reflux esophagitis, the tone of the lower esophageal sphincter is lower than normal so it doesn’t have a tight grip and allows gastric acid to easily pass into the esophagus. Over time, that leads to inflammatory lesions in the esophagus. 

In addition to the classic symptoms, reflux esophagitis can also cause heartburn and regurgitation. 

In some cases, gastric acid can irritate the respiratory tract, cause symptoms like coughing, voice changes, and a feeling of a lump in the throat. 

An upper endoscopy usually shows signs of erosion and these lesions can be classified using the Savary-Miller system or the  Los Angeles system, both of which use a 4-point grading scale, where grade 1 or A is mild esophagitis and grade 4 or D is severe esophagitis. 

Treatment of reflux esophagitis starts with proton pump inhibitors or PPIs such as omeprazole for 8 weeks. If symptoms disappear, then the dose of PPI is gradually decreased. If PPIs are needed for more than 6 months, then it’s replaced by histamine 2 receptor agonists or H2RAs. Now, if the symptoms recur, then the lowest dose of the medication that last controlled the symptoms is restarted. 

For individuals with severe erosive esophagitis, a repeat upper endoscopy should be done ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shared_decision-making</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O6Pt8-7PSku8Zxp1Vx6a1CCOSiOzFlqq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shared decision-making]]></video:title><video:description><![CDATA[Everyone has preferences - everything from coffee versus tea to more serious ones like buying versus renting.

These preferences are particularly important when it comes to your health - for example, do you prefer to take medications which may have side effects or do you prefer to hold off on medications to see if things improve on their own? 

Probably depends on the situation, right? 

Well shared decision making between an individual, their family and the entire healthcare team - helps ensure that an individual’s preferences are respected and prioritized. 

And some conditions like breast cancer, prostate cancer, heart conditions, and back pain are especially sensitive to individual preferences.

In fact, informed choices typically lead to better outcomes.

Now, to make a well-informed choice, individuals need reliable information about the pro’s and con’s of a treatment option. 

That can come from a decision aid like a pamphlet, video, or a website.  

Let’s take the example of back pain. Imagine that there’s an elderly woman named Ramona who has been struggling with chronic back pain. 

She goes online and finds a variety of options - wearing a back brace, trying yoga, surgery, and losing weight - just to name a few - but it’s hard to know what information to trust.

Shared decision making is a process that can help her navigate these choices with a healthcare professional. 

One approach is called the three-talk model. 

The first part is called team talk and it’s where a clinician describes choices, offers support, and asks about an individual&amp;#39;s goals. 

Ramona shares that she lives alone, but can no longer take long walks or pick up her grandson because of her pain. 

In fact, that’s the main reason that she’s taking her pain more seriously now. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinician's_Corner:_Diagnostic_errors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S-JEwttqQ6m2FqqivOUNHhJzS7e2kM_z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinician&apos;s Corner: Diagnostic errors]]></video:title><video:description><![CDATA[Every year, there are millions of medical diagnostic errors that result in a certain number of deaths. 

Thinking an individual has disease X, when they have disease Y. 

One way to minimize these errors was popularized in the book Thinking Fast and Slow, by Daniel Kahneman, which discusses System 1 and System 2 thinking. 

System 1 thinking is fast.

It’s what people call a “snap decision.” 

For example, if asked what 1 + 1 is, most people automatically blurt out “2” without consciously thinking about it. 

System 2 thinking, on the other hand, is slow. 

It’s analytical and takes more conscious effort. 

If asked what 17 x 24 was, most people need a bit of time to get to the answer which is 408. 

We fluidly switch back-and-forth from System 1 to System 2, and while they’re not two physically separate systems in the brain, they do represent a model that can help us to better understand the different ways that the brain operates.  

When it comes to making a diagnosis, System 1 instantly kicks in when we recognize a pattern in a clinical presentation. 

For example, let’s say a 35-year-old man with major depressive disorder, hypertension, and diabetes comes to a busy primary care clinic with worsening feelings of anxiety, rapid breathing, and occasional right-sided chest pain over the past 30 minutes. 

He says, “It feels like the world is closing in on me.” 

Some clinicians would make a fast, System 1 diagnosis that the patient is having a panic attack. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_give_a_good_oral_presentation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ymxxElwCQyey1jjugOUQeDz4QcafdZei/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to give a good oral presentation]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to give a good oral presentation through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal_bleeding:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FyO1NaGYQZqhbMcNLYM_3O94SNmxVi4M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal bleeding: Clinical]]></video:title><video:description><![CDATA[Gastrointestinal bleeding can be divided into upper and lower GI bleeding. 

Upper GI bleeding arises above the ligament of Treitz- also called the suspensory ligament of the duodenum- and it includes bleeding from the esophagus, stomach, or duodenum. 

Common causes of upper GI bleeding include peptic ulcer disease, erosive esophagitis, esophageal varices, an arteriovenous malformation or an AVM, Mallory-Weiss syndrome and cancers of the upper GI tract.

Lower GI bleeding arises below the ligament of Treitz and includes bleeding from the small intestines past the ligament of Treitz, large intestines, rectum, and anus. 

Common causes of lower GI bleeding include diverticulosis, hemorrhoids, colorectal cancer, AVMs, and intestinal ischemia.

Now, both upper and lower GI bleedings can be either visible or occult- meaning that there’s no visible evidence of bleeding. This is usually detected by a fecal occult blood test or if there are signs of iron deficiency anemia. 

Okay, first things first. A visible upper GI bleed causes hematemesis- which is vomiting of blood, and suggests moderate to severe ongoing bleeding.

If the blood looks like coffee-grounds - it suggests that the blood has been oxidized by acid in the stomach so that the iron in the blood has turned black. It’s a sign that bleeding was a small quantity or has stopped. 

Melena refers to black and tarry stools, and that most often result from upper GI bleeding. In fact, it takes about 50 milliliters of blood in the stomach to turn the stools black. 

A lower GI bleeding can cause hematochezia- which is fresh blood passing through the anus which may or may not be mixed with stool. 

In rare cases, if there’s a large upper GI bleed, that can cause hematochezia as well.

In an individual with a GI bleed, the first step is evaluating their hemodynamic stability. 

In mild hypovolemia, less than 15% of the blood volume was lost, and it causes a resting tachycardia. 

In moderate hypovolemia, 15% to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_masses_and_tumors:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mq2qPYsoS0Ks_-_NhnxWGGNeRvK2eV1T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenal masses and tumors: Clinical]]></video:title><video:description><![CDATA[Adrenal masses emerge from either the adrenal cortex or the adrenal medulla. Usually, they are asymptomatic, and they are discovered incidentally on an abdominal CT or MRI scan performed for another reason - which is why they’re sometimes also called incidentalomas. They can be benign, in which case, they’re  most commonly adenomas, or malignant, in which case they’re called carcinomas. With regard to hormone secretion, these masses can be non-functional, meaning they don’t secrete hormones, or functional, meaning they secrete hormones like normal adrenal tissue would, and they can cause specific symptoms depending on which hormone they secrete. So the two main questions that any adrenal mass rises are whether or not it is malignant, and whether or not it is functional.

As far as benign versus malignant goes, the first clues are based on the CT or MRI imaging: the size of the mass, its shape and borders, and CT attenuation, which is expressed in Hounsfield units, noted HU. 

Adenomas are usually smaller than 4 centimeters, have a regular shape and borders, and have an unenhanced CT attenuation lower than 10 Hounsfield units, which means they have about the same density as fat. Additionally, on a contrast CT scan, adenomas typically washout the contrast pretty quickly - usually more than 50% is washed out 10 minutes after the contrast injection. 

Carcinomas, on the other hand, are usually larger than 4 centimeters, irregular, have a CT attenuation higher than 20 Hounsfield units, and can present with calcifications, local invasion and necrosis. They also have more blood vessels nourishing the tumor, so contrast stays around longer, with less than 50% being washed out 10 minutes after the contrast medium is injected. 

Finally, another difference can be spotted on an MRI. Here, adenomas have isointensity with the liver, meaning, they’re about the same shade of grey, on both T1 and T2 weighted MRI sequences, whereas carcinomas are hypointense compared with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diarrhea:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KV__iLlORr2A1ko6U1xdwUEPTuOPLTDK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diarrhea: Clinical]]></video:title><video:description><![CDATA[Diarrhea is defined as having more than 3 liquidy stools in 24 hours or having a stool weight of over 200 grams per day, but nobody measures stool weight since that can get messy - especially if you’re having diarrhea! 

Diarrhea is also classified as acute if it lasts for less than 2 weeks, persistent if it lasts for 2 to 4 weeks, and chronic if it lasts for more than a month. 

Diarrhea can also be classified as either inflammatory or non-inflammatory. 

Inflammatory diarrhea causes inflammation of the gastrointestinal epithelium and this usually happens with invasive pathogens or as a result of a chronic inflammatory bowel disease, and usually there are systemic symptoms like fever. 

In contrast, non-inflammatory diarrhea can be either secretory or osmotic, and neither one usually causes systemic symptoms like fever. 

With secretory diarrhea, there’s increased water and electrolyte secretion and decreased absorption. 

With osmotic diarrhea, some of the ingested nutrients aren’t fully absorbed, and they remain in the intestinal lumen and pull in water through the process of osmosis! 

Now, most cases of acute diarrhea are caused by pathogens, mostly viruses, but also bacteria, protozoa, and parasites that mostly spread through fecal-oral transmission. 

The minority of cases of acute diarrhea are due to non-infectious causes like stress, medications, or a toxic ingestion. 

Most people with acute diarrhea don’t need to come to the hospital, because symptoms aren’t severe and resolve within 2 weeks. But in terms of figuring out the cause, it’s helpful to ask the right questions - like playing Sherlock Holmes. 

With infectious organisms, diarrhea is non-inflammatory and secretory, stools are watery and usually associated with vomiting and this is mostly caused by viruses, such as norovirus and rotavirus. 

Watery diarrhea can also be related to the ingestion of contaminated food - food poisoning - and in this case timing offers a clue. If diarrhea occu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_bowel_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iFqFW4CcSZaekY3cA96jkAz4RL2oryfO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory bowel disease: Clinical]]></video:title><video:description><![CDATA[Inflammatory bowel diseases are mainly broken down into two autoimmune conditions - ulcerative colitis and Crohn&amp;#39;s disease - both of which cause chronic inflammation in the gastrointestinal tract. 

Ulcerative colitis mostly appears in individuals aged from 20 to 30 years old. 

The chronic inflammation only involves the mucosal layer of the colon or the rectum and inflammation usually starts in the rectum and goes retrograde through the colon. 

Ulcerative colitis can involve only the rectum, in which case it’s called ulcerative proctitis, can involve the rectum and the sigmoid colon - called ulcerative proctosigmoiditis, or can involve the rectum, sigmoid colon and the colon up to the splenic flexure - called distal ulcerative colitis. In some cases, it can also pass the splenic flexure, but spare the cecum - called extensive colitis and finally it can involve the entire colon including the cecum - called pancolitis. 

The onset of the disease is gradual and symptoms are progressive over a few weeks. There may be systemic symptoms, such as fatigue, fever, unintentional weight loss, as well as dyspnea and palpitations due to iron deficiency anemia caused by blood loss. 

Gastrointestinal symptoms include bloody diarrhea, colicky abdominal pain, and tenesmus. 

Extraintestinal manifestations can sometimes occur, and they include arthritis, uveitis and episcleritis, and skin lesions like pyoderma gangrenosum and erythema nodosum, as well as primary sclerosing cholangitis and venous or arterial thromboembolism.

Acute complications of ulcerative colitis include severe gastrointestinal bleeding and fulminant colitis- which is continuous bleeding and over 10 stools per day. 

Another complication is toxic megacolon, which is where the nerves and muscles are damaged and the colon becomes atonic and dilated. In severe cases, it can lead to perforation with peritonitis which causes fevers and severe abdominal pain. 

Finally, long-term complica]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_infectious_rashes:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Oh4Xh1ezQD6GrV20V1qvEDP4SlKHXE4O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric infectious rashes: Clinical]]></video:title><video:description><![CDATA[When approaching a child with a rash, the first step is to put it into one of four categories - maculopapular, vesicular, petechial or purpuric, and desquamating rashes. 

A maculopapular rash has macules, which are up to 5 mm in diameter, and completely flat, meaning that you can’t feel them if you run your finger over them. It also has papules, which are raised bumps that are up to 1 cm in diameter. 

A vesicular rash has vesicles, which are up to 5 mm in diameter, and look like clear blisters filled with fluid. 

A petechial rash and a purpuric rashes, both have flat, red-brown spots that represent bleeding into the skin. These spots do not blanch or turn white when they get pressed. If the spots are smaller than 2 mm in diameter it’s a petechial rash, and if the spots are larger than 2 mm it’s a purpuric rash. 

Finally, there are desquamating rashes, which cause peeling of the skin, like after a sunburn.

Let’s start with maculopapular rashes. First up is erythema infectiosum, or fifth disease, which is caused by parvovirus B19. The virus causes flu-like symptoms along with a fever, that lasts a few days. 

Typically, just as the symptoms start to improve, a rash breaks out on both cheeks, often called &amp;quot;slapped‑cheeks” rash. There can also be a maculopapular, lacy rash on the body, that becomes more prominent after sun or heat exposure. 

Most of the time, everything resolves in a week, but sometimes there can be complications like anemia due to reduced production of reticulocytes that lasts for a few weeks. 

This can be dangerous in children with chronic hemolytic diseases, like sickle cell disease who rely on a high reticulocyte count and can have an aplastic crisis. So in these situations, packed red blood cell transfusions may be needed. 

In addition, if a pregnant female gets parvovirus B19, she can transmitted the infection to her fetus. The virus can get into the fetal bone marrow, and can cause anemia, which is called &amp;quot;hy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colorectal_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sRnyGMjEQJGQXEZD1yJFP7V3RMy1SkT7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colorectal cancer: Clinical]]></video:title><video:description><![CDATA[Colorectal cancer or CRC is a malignancy that arises in the large intestines, which includes both the colon and rectum. It is the most common cancer of the gastrointestinal tract, and a major cause of death and disease around the world. Most colorectal tumors develop due to sporadic mutations, but some are caused by inherited conditions like familial adenomatous polyposis and Lynch syndrome.

Individuals at high-risk for CRC include those with inflammatory bowel disease, especially ulcerative colitis, hereditary colorectal cancer syndromes, such as familial adenomatous polyposis, and those with a family history of colorectal cancer or adenomatous polyps. Individuals at medium-risk for CRC include the elderly, and those that smoke, drink alcohol, eat red meat, and are obese. Finally, well established protective factors include a high-fiber diet full of fruits and vegetables.

Sometimes, especially early on, colorectal cancer is asymptomatic and it’s discovered by screening using either stool based tests or direct visualization. One stool based test is the guaiac-based fecal occult blood test or gFOBT which detects blood in the stool. Another test is fecal immunochemical test or FIT. This time instead of guaiac, there’s an antibody that attaches to any hemoglobin that’s present in the stool. Finally there’s the FIT-DNA test-which combines FIT with a test that detects genes associated with colorectal cancer in the stool, such as             mutations in the adenomatous polyposis coli gene or APC gene. One direct visualization test is a colonoscopy, which is when a camera is inserted retrograde into the colon and rectum using a flexible tube and biopsies are taken. Another one is a flexible sigmoidoscopy, which uses a flexible tube to visualize the rectum and sigmoid colon. Finally, there’s CT colonography or a virtual colonoscopy- which is where CT scans are digitally assembled to produce 3-dimensional views of the colon.

If a suspicious lesion is seen ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Seronegative_arthritis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cjBsV9VkQSyX_ezioOji5nwPSzmyXDue/_.jpg</video:thumbnail_loc><video:title><![CDATA[Seronegative arthritis: Clinical]]></video:title><video:description><![CDATA[Seronegative arthritis refers to a group of four chronic diseases - ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and enteropathic arthritis. 

All of them are negative for rheumatoid factor, they’re all positive for HLA-B27, and they typically all run in families. 

Another feature they share is that they usually affect the bones in the spine and nearby joints. That’s why they’re sometimes called seronegative spondyloarthritides, where spondylo means vertebra. 

Other features include inflammatory back pain that causes morning stiffness which improves after 30 minutes of movement. 

These diseases also cause peripheral arthritis that’s generally asymmetric, and axial arthritis like sacroiliitis and spondylitis, affecting the sacroiliac and vertebral joints, respectively. 

Individuals also present enthesitis – meaning inflammation at the sites where tendons or ligaments insert into the bone and dactylitis, also known as sausage fingers. 

They also cause extra-articular symptoms like involvement of the eyes with anterior uveitis, skin with psoriasis, the heart with aortic regurgitation or pericarditis, genitourinary involvement due to nerve compression at the spinal cord, and gastrointestinal involvement with inflammatory bowel disease - both Crohn&amp;#39;s disease or ulcerative colitis. 

Seronegative spondyloarthritides typically have a good response to NSAIDs and an elevated CRP in blood tests. 

To meet the diagnostic criteria for seronegative spondyloarthritis, an individual has to have evidence of sacroiliitis on imaging plus one of these spondyloarthritis features, or HLA-B27 positivity plus two additional spondyloarthritis features. 

Once the criteria for a seronegative spondyloarthritis have been met, it’s time to figure out which one it is.

First up is ankylosing spondylitis. It typically affects young males, causing fever and pain and stiffness in the low back, hips, buttocks, and thighs, especially in the mornings or aft]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Logistic_regression</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qQSy1xeBTWiMPLz3vDhbEGoLQ8ua6fe_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Logistic regression]]></video:title><video:description><![CDATA[Logistic regression is a type of statistical method that’s used to describe the relationship between an outcome variable and one or more exposure variables. 

In logistic regression, the outcome variable is always categorical, and the exposure variables can be either categorical or quantitative. 

For example, let’s say you want to figure out if smoking more cigarettes increases the chance of having a heart attack. In this case, the number of cigarettes is a quantitative exposure and whether or not a person has a heart attack is a categorical outcome.

Now, to figure this out, you might ask 200 people how many cigarettes they smoke in a day, and then follow that group of people for five years and see who has a heart attack and who doesn’t. 

You could organize your data in a table like this—where the first column, or variable, is the number of cigarettes a person smokes, the second column is if they had a heart attack or not, and the rest of the columns are other characteristics, or variables, that you collected about each person, like their age, sex, and body mass index, or BMI. 

Usually, for binary variables, like yes or no, we use the numbers zero and 1 to represent the two possible answers.

So, for the heart attack variable, we might say that zero represents “no” and 1 represents “yes”. We could do the same thing for sex, where zero represents females and 1 represents males.

Now, let’s just look at the first two variables, so how many cigarettes they smoke and if they had a heart attack or not. You could plot these measurements, or data points, on a scatterplot, with the number of cigarettes on the x-axis, and heart attack on the y-axis, and where each data point represents one individual. 

This scatterplot might seem a little funny looking, and that’s because all of the data points are clustered on two points on the y-axis—they’re either on the zero, which represents no, or the 1, which represents yes. 

This scatterplot can help us figure out how]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diverticular_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qbghp_HgQSicqgfBxLrLQSnbQ7OUM78y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diverticular disease: Clinical]]></video:title><video:description><![CDATA[Diverticula are small outpouchings that form along the walls of a hollow structure. 

In the context of the large intestine, they’re called colonic diverticula, but they can form in the small intestine, as well as other spots like along the esophagus. 

Diverticula usually form at weak spots along the wall, like where a blood vessel penetrates the muscle layer of the intestine. 

Now there are two types of diverticula. The first is a true diverticula which is a herniation that involves all layers of the intestinal wall - like a Meckel’s diverticulum. 

The second is a false or pseudodiverticula which is where only the mucosa and submucosa slide through the intestinal wall, and these end up being more common. 

Risk factors for diverticula, including eating a high-fat, red meat diet that’s low in fiber.  

Diverticulosis is the presence of diverticula and when there’s colonic diverticula, typically these happen in the left and sigmoid colon- the rectum is usually spared. 

Sometimes it’s asymptomatic, and diverticulosis is diagnosed incidentally during an abdominal scan or a colonoscopy that was needed for another reason. 

When diverticulosis is symptomatic, it’s called diverticular disease. 

Typically diverticular disease causes some abdominal pain and a CT-scan usually shows some bowel thickening. But at this stage, treatment is mainly encouraging a high-fiber diet with grains and vegetables. 

But at any point diverticulosis can cause complications. 

One complication is bleeding due to weakening and breaking of blood vessels near a diverticula.

Mild bleeding can cause painless hematochezia, but severe bleeding can lead to hypovolemic shock. 

When there’s bleeding, depending on the severity, lab work and resuscitation are usually done. 

Labs include a CBC to look for signs of anemia and assess the platelet count.

If there are signs of hypovolemia, intravenous fluids are given. 

To see if the bleeding is coming from the upper GI tract, gastric lava]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stroke:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LIgTahLCTpKw7qL7stxlvE1ERxiSuKNU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stroke: Clinical]]></video:title><video:description><![CDATA[A stroke is a when there’s a sudden focal neurological deficit due to a part of the brain losing its blood supply. 

There are two types of strokes - ischemic strokes and hemorrhagic strokes. 

The majority are ischemic strokes and there are three types: thrombotic, embolic, and hypoxic strokes.

Thrombotic strokes are caused by local arterial obstruction due to inflammatory diseases like atherosclerosis, and non-inflammatory diseases like fibromuscular dysplasia. 

Thrombotic strokes affect large vessels like the internal carotid artery, as well as small vessels like the penetrating arteries that branch off of the basilar artery. 

When they affect these small arteries they’re called lacunar strokes, and they typically cause symptoms like hemiparesis, ataxia, dysarthria, and numbness in the contralateral face, arm, and leg.

An embolic stroke is when the blood vessel is blocked by an embolus. 

If it arises from the heart, it’s called cardioembolic, and that usually occurs in the setting of atrial fibrillation. 

That’s because in atrial fibrillation, blood stagnates in the atria and can become clotted. 

That clot can then travel up to the blood vessels supplying the brain. 

Alternatively, an embolus might dislodge from a thrombus or atherosclerotic plaque in the carotid artery, and that results in a thromboembolic or atheroembolic stroke. 

More rarely, there might be a paradoxical embolus which dislodges from a thrombus in the veins - like a deep vein thrombosis, and then slips through an atrial septal defect or patent foramen ovale. 

It enters the left atrium, and from there it can head off to the blood vessels supplying the brain. 

Finally, there’s a hypoxic stroke which is sometimes called a hypoxic ischemic injury, which develops when there’s systemic hypoperfusion or hypoxemia. 

This commonly occurs in infants due to ischemia during birth, but can also be due to things like septic shock or drowning. 

Now, the minority of strokes are hemo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pneumonia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hl6lHbw4R623TbbAuNc35pDMR66uIDGK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pneumonia: Clinical]]></video:title><video:description><![CDATA[Pneumonia is due to inflammation of the lung alveoli from an infection. Typically, fluid that’s filled with white blood cells starts to fill up the alveoli, and that inflammatory fluid essentially replaces the air that’s normally in the alveoli, and that fluid interferes with gas exchange. 

Pneumonia typically causes a fever, cough, and shortness of breath, along with tachypnea and tachycardia, and occasionally hypoxemia. If the infection is near the pleural surface, it can cause pleuritic chest pain, which is pain that worsens with inspiration. On chest exam, there’s dullness on percussion; increased tactile fremitus, which is an increased sensation of vibration when palpating over the affected area and asking the individual to speak; and egophony, which is increased resonance of transmitted sounds and makes the letter “E” sound like the letter “A”. On auscultation, bronchial breath sounds or inspiratory crackles may be heard. 

The diagnosis of pneumonia is based on having clinical signs and symptoms along with abnormal chest imaging, most commonly a chest x-ray. In pneumonia, a chest x-ray typically shows either a lobar consolidation or a diffuse, interstitial infiltrate. Pneumonia has to be distinguished from atelectasis which is when there’s collapse of a region of the lung, a complication that often occurs in individuals after surgery. On a chest x-ray, atelectasis shows up as a wedge-shaped region with it’s apex at the hilum with an ipsilateral shift of structures due to volume loss. In contrast, in a pneumonia there’s usually normal or increased volume with a consolidation that doesn’t have an apex at the hilum and no shift in structures. Now, in addition to imaging, some lab tests suggestive of pneumonia include an elevated white blood cell count, and elevated markers of inflammation like procalcitonin and C-reactive protein. It’s thought that these generally increase much more in bacterial pneumonia versus viral pneumonia.  

For individuals wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Joint_pain:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0rS4JAFRTLaCWXgMFCKjaDKoQuueY77o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Joint pain: Clinical]]></video:title><video:description><![CDATA[Joint pain is associated with a variety of disorders, so identifying the underlying cause can be hard.

First off, there’s the pain itself and there’s the underlying condition.

The underlying condition causing the joint pain which can either be acute or chronic. 

In acute conditions, like a trauma, the joint pain develops right away, whereas in an infection or a bone or soft tissue malignancy the joint pain develop over days to weeks. 

Alternatively, in chronic conditions like osteoarthritis, the joint pain happens over weeks to months, and in inflammatory conditions, that typically cause intermittent flares of joint pain, which are acute attacks, but the cause is still chronic.

The first step is to see how many joints are involved. 

Generally speaking, joint pain can be monoarticular, meaning only one joint is involved, or polyarticular, meaning two or more joints are involved.

The major causes of monoarticular joint pain are trauma, infection, malignancy, and osteoarthritis. 

The major causes of polyarticular joint pain are inflammatory autoimmune diseases, like lupus, as well as other systemic diseases like sarcoidosis. 

Now, in the early stages and during flares, some inflammatory diseases can cause monoarticular pain. 

So the next step is to figure out if the joint pain is inflammatory or non-inflammatory. 

In non-inflammatory disease, the joint pain tends to be acute, worsen with movement and is relieved by rest. 

On the other hand, in inflammatory diseases, symptoms tend to be more chronic, and worsen with immobility, leading to morning stiffness. 

In addition, with inflammatory conditions, there’s usually swelling, loss of function, redness, and warmth. 

Additionally, inflammatory conditions may cause an effusion or synovitis. 

In contrast, in non-inflammatory conditions, there might be swelling and loss of function, but there’s usually no redness or warmth. 

Finally, inflammatory diseases can cause a wide variety of extra-articular ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatitis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2RJCRPp7R4OFxfAg0PxfxmpaRMCIQs61/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatitis: Clinical]]></video:title><video:description><![CDATA[Pancreatitis is inflammation of the pancreas. 

In acute pancreatitis, the pancreas’ own digestive enzymes get suddenly get activated within the pancreas and cause autodigestion which results in inflammation and hemorrhaging. 

In chronic pancreatitis, there are indolent causes of inflammation that damage the pancreas, leading to impairment of both endocrine and exocrine functions of the pancreas.

Now, first thing’s first. Acute pancreatitis is usually caused by gallstones and ethanol abuse, but there are other causes as well, and the full list can be remembered using the mnemonic “I GET SMASHED”: where ‘I’ refers to unknown, or Idiopathic, causes; ‘G’ is obstruction by Gallstones, ‘E’ is Ethanol abuse; ‘T’ is a pancreatic Trauma, which is more likely if the trauma is the result of a puncture injury, like a knife wound rather than a punch; ‘S’ is the use of Steroids; ‘M’ is infection with Mumps virus, ‘A’ is the result of Autoimmune diseases; the second ‘S’ is the result of a Scorpion sting—which is probably the most exciting item on this list and one of the more rare causes - so check your shoes!; ‘H’ is a cheat and stands for both Hypertriglyceridemia and for Hypercalcemia; ‘E’ is trauma from an Endoscopic retrograde cholangiopancreatography or ERCP which is a technique used to diagnose and treat various biliary and pancreatic diseases; and finally ‘D’ stands for Drugs, like sulfa drugs, reverse-transcriptase inhibitors, and protease inhibitors. 

Individuals with acute pancreatitis usually have severe epigastric abdominal pain that radiates to the back, along with nausea and vomiting over several hours. 

In mild cases, there may be tenderness in the epigastrium, and in severe cases, there might be hypovolemic shock which can cause tachypnea, hypoxemia, and hypotension or systemic inflammatory response syndrome or SIRS, which can cause those same symptoms as well as fever. 

So for SIRS - three of the hallmarks - tachypnea, hypotension, and fever - are]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Linear_regression</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WiMoXSocQ-qyWryxRLFQIe48QI25QMsR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Linear regression]]></video:title><video:description><![CDATA[Let’s say you want to figure out if smoking more cigarettes leads to a lower forced expiratory volume, or FEV, which is the total amount of air, in liters per second, that a person can exhale in a single forced breath. 

And let’s say that healthy men generally have an FEV of around 4 liters per second. 

Now, to figure out if men who smoke have a lower FEV, you might ask 100 men how many cigarettes they smoke in a day, and then measure each man’s FEV. 

You could plot these measurements, or data points, on a scatterplot, with the number of cigarettes, which is the exposure, on the x-axis, and FEV, which is the outcome, on the y-axis, and where each data point represents one individual. 

Typically, a linear trend line, or model, is drawn to represent the pattern of data points on the plot.

Theoretically, there are lots of lines that can be drawn to represent the data points, but the best trend line is the one with the smallest amount of error, which is a measurement of how far away an individual data point is from the trend line.

Usually, we look at the squared error, which is the distance between the data point and the line, squared. 

For example, if a data point is very close to the trend line, then the squared error is small. 

On the other hand, if a data point is very far from the trend line, then the squared error is large.

If you add up all the squared error for a line, you get the total squared error, and a line with a smaller total squared error is considered a better fit for the data than a line with a larger total squared error.

Now, when two variables are linearly related, we might want to know specifically what happens to the outcome variable when the exposure variable changes. 

For example, we might want to know how a person’s FEV changes if they smoke five cigarettes per day compared to if they smoke ten cigarettes per day. 

To figure this out, we have to use linear regression, which is a statistical method that calculates an equatio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mood_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dkvMhnsSRDaAM70yir-SWf12TMCE1YQS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mood disorders: Clinical]]></video:title><video:description><![CDATA[Mood disorders are a group of illnesses that describe serious changes in the emotional status that can interfere with day-to- day activities like working, studying, eating, and sleeping. Mood disorders can precipitate a substance addiction, and in some cases can lead to suicide.

Risk factors for mood disorders include a family history and personal trauma. However, the underlying cause is poorly understood. There’s usually an imbalance of serotonin, norepinephrine, and dopamine, which are neurotransmitters that help regulate mood, reward-motivated behavior, appetite, and sleep

Each of these neurotransmitters is thought to have an impact on specific symptoms, like norepinephrine on anxiety or attention, serotonin on obsessions and compulsions, and dopamine on attention, motivation, and pleasure. 

Now, depression has also been associated with hyperactivity of the hypothalamic–pituitary–adrenal or HPA axis, leading to increased cortisol levels, as well as decreased hippocampal and frontal lobe volumes, decreased sleep latency and slow-wave sleep. 

Mood disorders can be seen as a spectrum. At one end of the spectrum we have depressive disorders which include major depressive disorder; substance or medication-induced depressive disorder, depressive disorder due to another medical condition, adjustment disorder with depressed mood, premenstrual dysphoric disorder and persistent depressive disorder (previously known as dysthymia).  

All of these are characterized by depressive episodes, which consist of nine major symptoms - the exception being persistent depressive disorder which accounts for only six of the milder symptoms. 

First, a person feels depressed, hopeless, or lacks a sense of purpose most of the day, every day. Second, there’s anhedonia - which means a diminished interest in an activity that used to be really pleasurable - like no longer enjoying cooking or gardening, if that was once a hobby. Third, either weight gain or weight loss, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_lower_airway_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IJczyVDjTjWj5lqZnuQy9qnjSSuA3mtl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric lower airway conditions: Clinical]]></video:title><video:description><![CDATA[The lower airways include the trachea, bronchi, bronchioles and lungs and can be affected by a number of distinct pathologies in children.

Let’s start with foreign body aspiration, which is where young toddlers might get something like a small coin or a peanut, lodged in their respiratory tract. 

Most of the time, the foreign body goes into the right mainstem bronchus because it’s wider and more vertical than the left. 

In general, if the blockage affects a larger airway or causes a more complete blockage of an airway, then it causes more severe symptoms. 

Typically, children have a sudden onset of shortness of breath, along with coughing, gagging, choking, or drooling.

On auscultation, breath sounds are diminished in blocked area. 

If there’s partial obstruction of the extrathoracic portion of the trachea, that can cause inspiratory stridor.

If there’s expiratory wheezing, that means that there’s partial obstruction of either the intrathoracic trachea, bronchi, or bronchioles. And that wheezing will be localized to the blocked area. 

If there are no sounds like this on auscultation, it may be because there’s a complete obstruction of an airway. 

If a foreign body aspiration is suspected, it’s important to do a neck or chest radiograph. 

Objects like coins and batteries are radiopaque, and will be visible. Whereas objects like a piece of food are radiolucent, so they don’t show up. 

Fortunately, there are still indirect signs of the obstruction that can be seen on a chest Xray. In a complete obstruction, there’s atelectasis distal to the obstruction. 

In a partial obstruction, there’s focal hyperlucency and reduced pulmonary markings distal to the obstruction, due to air trapping. In other words, the foreign body acts like a one way valve that allows air to enter, but not escape. 

If there’s a lot of air trapping, it can cause a mediastinal shift away from the affected side. 

If the radiographs look suspicious for a foreign body aspiration, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cystic_fibrosis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/B9ItiVmdTy_fohK9HKniJNvoQDeFwHaj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cystic fibrosis: Clinical]]></video:title><video:description><![CDATA[Cystic fibrosis, or CF, is an autosomal recessive disorder in which there’s a mutated “cystic fibrosis transmembrane conductance regulator” or CFTR protein. 

The mutated CFTR protein causes secretions to be abnormally thick and sticky - and they build up in the lungs, pancreas, and other organ systems. 

The CFTR protein is a channel protein that pumps chloride ions into various secretions. Those chloride ions help draw water into the secretions, which helps to thin out the secretion. 

The most common mutation that leads to cystic fibrosis is the “∆F508” mutation. This mutation causes the CFTR protein to not make it to the cell membrane. 

Without CFTR protein on the epithelial surface, chloride ions aren’t pumped into the secretions, and that leaves the secretions thick and sticky.

In some countries, diagnosis of cystic fibrosis is done with newborn screening. Usually it’s done by detection of a pancreatic enzyme called immunoreactive trypsinogen or IRT, which is released into the fetal blood when there’s pancreatic damage from CF. 

A confirmatory test is the quantitative pilocarpine iontophoresis, better known as the sweat test, which detects high levels of chloride in the sweat.

The reason for this is that in the lungs and pancreas a mutated CFTR means that chloride can’t go out, but in the sweat glands a mutated CFTR means that chloride can’t come in, or be reabsorbed. 

So if chloride levels in the sweat are high, meaning over 60 mmol/L, CF diagnosis is very likely, while  intermediate levels, from 30 to 59 mmol/L in infants below 6 months or 40 to 59 mmol/L in older infants, children, and adults, mean CF diagnosis is possible.

In both cases, DNA testing is done to detect the most common cystic fibrosis-related mutations. 

If two or more of these mutations are detected, one in each chromosome then the diagnosis of CF is confirmed. 

Having said that, even if only one DNA mutation or no mutation at all is detected, an individual may still have c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sickle_cell_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AYoygK6mSwq7VtOiYuko2wp6ROK0PuZB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sickle cell disease: Clinical]]></video:title><video:description><![CDATA[In sickle cell disease, also called sickle cell anemia, red blood cells take the shape of a crescent, or sickle, and that makes it easier for them to be destroyed, causing anemia. 

Sickle cell disease is an autosomal recessive disorder caused by a mutated hemoglobin gene that encodes for an abnormal adult hemoglobin called hemoglobin S for sickle, or HbS for short. 

A mutation in both copies of the gene is needed to get the disease. If the person has just one copy of the mutation and one normal hemoglobin A gene, or HbA for short, then they have sickle trait and they’re said to be a sickle cell carrier. 

Having sickle trait typically doesn’t cause health problems unless a person is exposed to extreme conditions like high altitude or dehydration, where some sickle cell disease-like symptoms begin to crop up.

Now in individuals with sickle cell disease, when there’s acidosis, hypoxia, or dehydration, HbS changes its shape, and aggregates with other HbS proteins to form long chains that distort the red blood cell into a crescent shape, that looks like a sickle - which is the name of a blade used to cut grain. 

Sickling leads to two important things - vaso-occlusion and hemolysis. 

Hemolysis can be intravascular- meaning red blood cells are prematurely destroyed within the vasculature, or extravascular, meaning that they get engulfed by macrophages in the spleen and liver. These two processes are independent from each other, but usually, both are happening to some degree. 

So, in intravascular hemolysis, hemoglobin and the enzyme lactate dehydrogenase, or LDH, spill out directly into the plasma. The hemoglobin gets bound by a protein called haptoglobin and gets recycled into unconjugated bilirubin. 

In extravascular hemolysis, red blood cells are destroyed by macrophages, so the hemoglobin and LDH are kept within the cytoplasm of the macrophage. Over time, the excess unconjugated bilirubin leads to scleral icterus, jaundice, and bilirubin gallstones. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cushing_syndrome:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_ICGW-GcQMWUYrDOOpw8FQaoSiemBI22/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cushing syndrome: Clinical]]></video:title><video:description><![CDATA[Cushing syndrome or Cushing’s disease is an endocrine disorder with elevated cortisol levels in the blood.

Cortisol production is normally under the control of the hypothalamus and pituitary.

The hypothalamus, secretes corticotropin-releasing hormone, or CRH, which makes the pituitary gland secrete adrenocorticotropic hormone, or ACTH. 

ACTH then stimulates the release of cortisol from the adrenal glands. 

For cortisol levels to stay within the normal range, there’s also a negative feedback mechanism in place. This means that high levels of cortisol tell the hypothalamus and the pituitary to decrease their production of CRH and ACTH, respectively. 

Now, with Cushing syndrome, the high cortisol levels are usually due to a benign tumor of the pituitary, called an adenoma, that secretes excess ACTH.

Excess cortisol can also appear in the context of some other tissue that secretes ACTH or an adrenal mass that secretes too much cortisol. 

In fact, even exogenous glucocorticoids, given for an autoimmune condition, can also cause Cushing syndrome. 

No matter the cause, the symptoms are the result of the effects of excess cortisol on various target tissues. 

There’s increased breakdown of most types of tissue, which leads to muscle wasting and thin extremities; skin thinning; easy bruising; abdominal striae, or lines; and bone thinning, or osteoporosis, which can lead to fractures. At the same time, there’s fat redistribution, so classic findings include a round, full moon shaped face, a buffalo hump - which is a fatty hump on the upper back, and truncal obesity - where fat gathers around the abdomen and trunk rather than in the limbs. 

Finally, excess cortisol causes hypertension and hyperglycemia which can progress to diabetes mellitus, as well as increased vulnerability to infections - particularly fungal infections of the skin. 

Individuals might also experience poor wound healing, menstrual irregularities, and psychiatric disturbances.

When Cushin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/skin-cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A8YeemL2S-iV0OhKxcS2DPAVRouyoYnc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skin cancer]]></video:title><video:description><![CDATA[Skin cancer is an uncontrolled growth of cells within the skin. 

There are three main types: basal cell carcinoma, squamous cell carcinoma, and melanoma. 

Some skin cancers can spread to other locations in the body and can be fatal, as seen with singer-songwriter Bob Marley, who died shortly after being diagnosed with melanoma.

The skin is divided into three layers--the epidermis, dermis, and hypodermis. 

The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. 

Just above is the dermis, which contains hair follicles, nerves and blood vessels. 

And just above that, the outermost layer of skin, is the epidermis. 

The epidermis itself has multiple cell layers that are mostly keratinocytes - which are named for the keratin protein that they’re filled with. 

Keratin is a strong, fibrous protein that allows keratinocytes to protect themselves from getting destroyed, when you rub your hands through the sand at the beach. 

Keratinocytes start their life at the deepest layer of the epidermis called the stratum basale, or basal layer, which is made of a single layer of small, cuboidal to low columnar stem cells that continually divide and produce new keratinocytes that continue to mature as they migrate up through the epidermal layers, flattening out to a pancake-like squamous shape as they ascend.

But the stratum basale also contains another group of cells - melanocytes, which secrete a protein pigment, or coloring substance, called melanin. 

Melanin is actually a broad term that constitutes several types of melanin found in people of differing skin color. 

These subtypes of melanin range in color from black to reddish yellow and their relative quantity and rate at which they are metabolized define a person’s skin color. 

When keratinocytes are exposed to the sun, they send a chemical signal to the melanocytes, which stimulates them into making more melanin. 

The melanocytes move the melanin into small sacs ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kawasaki_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YquRCx9nSKadCI65vkgoZGTiRGaQQrtt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kawasaki disease: Clinical]]></video:title><video:description><![CDATA[Kawasaki disease is a vasculitic disease in which medium-sized arteries throughout the body become inflamed. 

It typically affects young children from 1 to 5 years old, but can sometimes affect teenagers and even adults. 

It is usually a self-limited condition, with fever and manifestations of acute inflammation for at least five days, lasting for an average of 12 days without therapy, and it’s not very responsive to treatment with paracetamol or ibuprofen. 

The most frequent and characteristic signs and symptoms, included in the diagnostic criteria, can be remembered with the mnemonic CRASH. 

First off, they may typically present with bilateral bulbar Conjunctival injection, which typically begins within days of the onset of fever, and leads to photophobia or discomfort or pain to the eyes due to light exposure. 

Then there’s polymorphous Rash that usually begins during the first few days of illness due to sensitivity to sunlight. 

A stands for lymphadenopathy, which tends to primarily involve the anterior cervical nodes overlying the sternocleidomastoid muscles. 

Next up, there are oral mucous membrane changes, including injected or fissured lips, injected pharynx, or Strawberry tongue. 

And finally, there are peripheral extremity changes, including erythema of palms or soles, edema of Hands or feet, and periungual desquamation. 

To make a diagnosis of Kawasaki, individuals must meet at least four of these features. Other common features include irritability, rhinorrhea, cough, vomiting, diarrhea, abdominal pain, and joint pain. 

A severe complication of Kawasaki disease is cardiovascular disease, which most commonly presents as coronary artery aneurysms, and can lead to arrhythmias, myocardial infarction, and ultimately, heart failure.

Typically, an ECG and echocardiography are done in individuals with Kawasaki to look for cardiovascular involvement.

On rare occasion, if echocardiography isn’t able to image the coronary arteries, comput]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_myopathies:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m5EIff-xRTCB3K-xZnoHYpNhQXqfWZlL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory myopathies: Clinical]]></video:title><video:description><![CDATA[Inflammatory myopathies refers to a group of three disorders - polymyositis, dermatomyositis, and inclusion body myositis. 

They’re all autoimmune disorders that cause muscle inflammation, leading to progressive muscle weakness and wasting. 

Sometimes, the muscles can be tender or painful. In severe cases, it can involve the respiratory muscles, which can be life threatening. 

Usually, there’s also systemic symptoms like fever, fatigue, and weight loss; as well as other organ-specific symptoms. 

There can be subcutaneous calcification in the skin; joint pain and arthritis; cardiovascular conditions like arrhythmias, myocarditis, and pericarditis; gastrointestinal conditions like gastroesophageal reflux disease and dysphagia; respiratory problems like aspiration pneumonia; and vascular problems like Raynaud’s phenomenon, where arterial spasm causes reduced blood flow to the fingers. 

Let’s start off with polymyositis, which typically affects adults, and it’s characterized by bilateral muscle weakness that mostly affects proximal, large muscle groups, like the shoulder or hips and spares the distal muscles like muscles in the hands. 

Individuals might have difficulty rising from a chair, lifting their arms, or climbing stairs. 

The muscle weakness usually worsens gradually over several months, and over time there can be muscle atrophy.

Dermatomyositis has the same muscular presentation as polymyositis, but it mainly affects children, and in addition to muscle weakness, children can have a skin rash. 

One type of rash is the heliotrope or lilac rash, which is a pruritic purplish rash that can appear on or around the eyelids. 

A similar rash may appear on sun-exposed areas, like the chest, shoulders, or thighs. 

This rash is similar to the malar rash of individuals with lupus, but it typically extends beyond the nasolabial folds, which is a region that’s usually spared in lupus. 

Another rash is one that causes Gottron’s papules, which are flat, re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypopituitarism:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sYDbwcXyS6OwWCtHnRn1v57WRt6d7XgK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypopituitarism: Clinical]]></video:title><video:description><![CDATA[Hypopituitarism refers to the decreased secretion of one, some, or all of the anterior pituitary hormones, and it usually happens when there’s a pituitary or hypothalamic disease. 

The hypothalamus and the pituitary work together to make 5 different hormones.

First, the hypothalamus secretes corticotropin releasing hormone, which stimulates pituitary production of adrenocorticotropin hormone, or ACTH.

ACTH makes the adrenal glands release cortisol, a hormone in charge of the stress response and keeping blood pressure and blood sugar in the normal range.

Second, the hypothalamus secretes Thyroid Releasing Hormone (TRH), which stimulates pituitary production of thyroid stimulating hormone, or TSH, which then makes the thyroid gland release thyroid hormones, T3 and T4. 

Thyroid hormones speed up the basal metabolic rate in all cells, so it keeps cellular processes going at an optimal rate.

Third, there’s hypothalamic growth-hormone releasing hormone, which stimulates pituitary production of growth hormone, or GH. 

GH acts directly on target tissues to stimulate growth and development. 

Fourth, the hypothalamus has a word to say about reproduction - it makes gonadotropin releasing hormone, or GnRH, which stimulates pituitary production of gonadotropins, Follicle-Stimulating Hormone, or FSH; and Luteinizing Hormone (LH), that stimulate ovarian or testicular production of sex cells and sex hormones.

Fifth, the anterior pituitary makes one hormone without the help of the hypothalamus - that’s prolactin. 

Prolactin secretion is important in females, where is plays a role in breast milk production. 

Ok, so that being said, the clinical presentation of hypopituitarism varies, depending on which pituitary hormones are deficient. 

ACTH deficiency may present with mild symptoms, like orthostatic hypotension and reflex tachycardia, weakness and lethargy. 

Sometimes mild symptoms of ACTH deficiency can worsen during periods of stress, like illness or during ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypokinetic_movement_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ly-D6Zv3QYO6YSHTtutisOhcT1mfcSEj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypokinetic movement disorders: Clinical]]></video:title><video:description><![CDATA[The cerebrum, cerebellum, and basal ganglia all help coordinate movements, so movement disorders can be traced back to these structures. 

Broadly - there are hypokinetic disorders which cause slowness of movement, and hyperkinetic disorders, which cause excessive involuntary movement. We’ll be talking about the hypokinetic disorders.

Alright, when it comes to hypokinetic disorders, the term “parkinsonism” refers to several conditions including Parkinson’s disease itself, and other syndromes called “parkinson-plus” syndromes, which cause parkinsonism plus other clinical features.

These “parkinson-plus” syndromes include Lewy body dementia, multiple system atrophy, and progressive supranuclear palsy. 

Parkinsonism can also be caused by medications, including antipsychotics like haloperidol and anti-emetics like metoclopramide. 

The four cardinal symptoms of parkinsonism can be remembered with the mnemonic “TRAP”. 

“T” for tremor, which is classically described as a resting, pill-rolling tremor, because it looks like someone is rolling a pill between their thumb and index finger. 

“R” stands for rigidity, which is often described as a cogwheel-like rigidity. This means that when attempting to passively move a limb, there are a series of stops or stalls, kind of like a cog on a wheel. There’s also lead-pipe rigidity, which is when a limb is rigid throughout the entire passive movement, kind of like trying to move a lead-pipe. 

Cogwheel and lead-pipe rigidities are distinct from clasp-knife rigidity that results from upper motor neuron lesions. 

In clasp-knife rigidity, the limb is initially rigid like a lead-pipe, but then it gives away, kind of like opening a clasp-knife. 

“A” stands for akinesia, which is the absence of movement, and is a severe form of the more common finding of bradykinesia, which is slowness of movement. This can manifest as a narrow-based shuffling gait or a decreased facial expression, almost to the point where the individual’]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Headaches:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6cE604NrQh_NeX8ms6qQ5OY-QU2SwLP4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Headaches: Clinical]]></video:title><video:description><![CDATA[We’ve all had them. Headaches can be debilitating, and they occur when any of the pain-sensitive structures in the head and neck are stimulated. These include the meninges, blood vessels, nerves, and muscles. 

Headaches can be classified into primary and secondary headaches. Primary headaches include tension, migraine, and cluster headaches, whereas secondary headaches are those that are due to another underlying disorder. 

When an individual has a headache, especially if it feels different from their usual headaches, it’s important to think through causes of secondary headaches to avoid missing something important or life-threatening. 

The mnemonic “SNOOP”, without the “D-O-double G”, summarizes some of the red flags. 

“S” is for systemic symptoms like fever or weight loss. 

“N” is for neurological symptoms, like weakness, sensory deficits, or vision loss. 

The first “O” is for a new or sudden onset headache. 

The second “O” is for other associated conditions, like trauma. 

The “P” stands for progression or pattern, such as a headache that is worsening in severity or frequency. 

Any of these findings warrant further investigation like brain imaging with a CT scan, or MRI, and in some cases a lumbar puncture.

Some clinical features may point towards a specific diagnosis, some of which may be life-threatening! 

For example, if the headache develops suddenly, and feels like a 10 out of 10 in terms of pain right at its onset, or if it’s called “the worst headache of my life”, then it might be a subarachnoid hemorrhage. And it’s typically caused by rupture of an intracranial aneurysm. 

Now, if someone has a sudden headache after a trauma, and it radiates down one side of the neck and is associated with Horner syndrome then it could be due to a carotid or vertebral artery dissection. This is also associated with pulsatile tinnitus which is a pulsating ringing sensation in the ears. If left untreated, the dissection could extend into the intracranial]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_insufficiency:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V2lg8TuDQumpgx7ejldscmMmSriF6Gun/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenal insufficiency: Clinical]]></video:title><video:description><![CDATA[Adrenal insufficiency is a condition in which the adrenal glands don’t produce enough adrenal hormones - particularly cortisol, but sometimes aldosterone can be deficient as well. 

Cortisol production is normally under the control of the hypothalamus and pituitary. The hypothalamus secretes corticotropin-releasing hormone, or CRH, which makes the pituitary gland secrete adrenocorticotropic hormone, or ACTH. 

ACTH then stimulates the release of cortisol from the adrenal glands. Aldosterone, on the other hand, is the final product of a physiological chain called the renin-angiotensin-aldosterone system, or RAAS for short. 

Renin is produced by the kidneys, so aldosterone production is actually independent of hypothalamic and pituitary stimulation. This is important, because adrenal insufficiency actually comes in three distinct flavors. 

First, there’s primary adrenal insufficiency, or Addison’s disease, when there’s a problem with the adrenal glands themselves. In this case, both cortisol and aldosterone production are deficient. 

The most common cause for primary adrenal insufficiency in high income countries is autoimmune destruction of the adrenal gland. Another common cause can be due to tuberculosis, HIV, or disseminated fungal infections. 

Finally, bilateral adrenal metastases from cancer somewhere else in the body, like the lungs, breast, or colon, can also cause adrenal insufficiency. 

Then, there’s secondary adrenal insufficiency, which occurs due to insufficient pituitary ACTH secretion. 

Since ACTH only stimulates cortisol production, in this case there’s a cortisol deficiency, but aldosterone levels are normal. 

This can happen with panhypopituitarism, when the entire pituitary gland is affected, and all stimulatory hormones secreted by it are deficient. 

Panhypopituitarism can be a result of any condition that affects the entire pituitary - like when the pituitary is affected by trauma or compressed by a large central nervous system t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperthyroidism:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jYcJnIYqTyyJHBGWdRq2yQP6Qb67XfRK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperthyroidism: Clinical]]></video:title><video:description><![CDATA[Hyperthyroidism, which is sometimes referred to as thyrotoxicosis, is a condition that’s caused by having excess thyroid hormones. 

Thyroid hormone production is under the control of the hypothalamus and the pituitary.

The hypothalamus secretes thyrotropin releasing hormone, or TRH, which makes the anterior pituitary secrete thyroid-stimulating hormone, or TSH.

TSH then binds to TSH receptors, which makes the thyroid secrete thyroxine, or T4, and triiodothyronine, or T3, in the blood. But this is not a one-way street - there’s also negative feedback happening, meaning when thyroid hormone levels rise, that inhibits the production of TSH and TRH, halting further production of T3 and T4 - to keep everything in balance. 

Normally, some thyroid hormones travel through the bloodstream bound to thyroxine-binding globulin, and some are in their free form. 

And the thyroid actually makes more T4 than T3, and that T4 is converted to the more potent T3 in the periphery. 

Thyroid hormones then increase the rate of metabolism in all cells, so they make us think, move, and talk faster, and they also increase heat generation. They also activate the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response, increasing cardiac output.

Thyroid hormones are important - and the occasional increase is like getting a boost to fight off a zombie or to stay warm during a snowstorm! 

But with hyperthyroidism, it’s like the entire body is buzzing at twice the normal rate. So individuals with hyperthyroidism tend to be hyperactive and talk really fast, and present with tremor in the extremities - as if they’ve had too much coffee. Also, making so much internal heat makes them sweat a lot and uncomfortable in warm temperatures.

It can also cause anxiety, irritability, and mood swings, as well as difficulty sleeping - again, think too much coffee. 

Hyperthyroidism can also cause an increased appetite, unexplained weight loss, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Venous_thromboembolism:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rmjAWc-vQTGxk_1ON4VAQJr3TT61zfsP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Venous thromboembolism: Clinical]]></video:title><video:description><![CDATA[Our bodies are constantly maintaining a fine balance between making and breaking blood clots. In the late 1800s, doctor Rudolf Virchow identified three factors that contribute towards the formation of clots: hypercoagulability, stasis of the blood, and endothelial injury. If there’s any factor that tips the balance towards forming clots then a venous thromboembolism, or VTE can develop. VTE can cause two clinical presentations: deep vein thrombosis, or DVT, and pulmonary embolism, or PE. They are clumped together because they share the same pathophysiology, and often a DVT leads to a PE. 

Risk factors for VTE revolve around Virchow’s triad, and can be remembered with the mnemonic “THROMBOSIS”: “T” is for trauma or history of travel. “H” is for hospitalization and hormones, meaning any form of exogenous estrogen such as hormone replacement therapy, tamoxifen or combined oral contraceptives, which promote the formation of clots in the venous circulation. “R” is for relatives, that is family history of inherited hypercoagulable disorders, like Factor V Leiden. “O” is for old age. “M” is for having any malignancy. “B” is for long bone fractures. “O” is for obesity and obstetrics; that is pregnancy and the early post-partum period. “S” is for any form of major surgery, especially orthopedic surgery as well as smoking. “I” is for immobilization, such as a paralyzed limb. And the final “S” is for other sickness, like antiphospholipid syndrome, nephrotic syndrome, and paroxysmal nocturnal hemoglobinuria. 

Alright, now DVTs usually involve the deep veins of the lower extremity, such as the proximal iliac and femoral veins, or the distal popliteal veins. Upper extremity DVTs are very rare, and if they do happen, it’s usually because of an indwelling intravascular catheter. Now, individuals with DVT usually develop a swollen, red and painful unilateral limb. That sounds nonspecific, so it’s important to differentiate DVT from superficial thrombophlebitis, celluliti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meningitis,_encephalitis_and_brain_abscesses:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WV2W1FJ9TfWD50MhN748AeUrSfGKXJcC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meningitis, encephalitis and brain abscesses: Clinical]]></video:title><video:description><![CDATA[In order to properly “osmose” new information, your brain is protected from the rest of the body by three meningeal layers.

From outside to inside they’re the dura mater, arachnoid mater, and pia mater, with cerebrospinal fluid in the space between the arachnoid and pia.

If pathogens make their way into these layers, the inflammatory response results in meningitis.

If they find a way to penetrate into the brain parenchyma itself, the inflammatory response results in encephalitis. 

And if a pathogen walls itself off - it’s called a brain abscess.  

Meningitis can be caused by viruses, bacteria - including mycobacteria like TB, fungi, and parasites.

When it’s caused by viruses, tuberculosis, fungi  or parasites, it’s called aseptic meningitis, because routine bacterial cultures of the cerebrospinal fluid are negative. 

Sometimes, the infection may spill over from the meninges into the brain parenchyma, and that’s called meningoencephalitis. 

Now, the most common causes of acute bacterial meningitis depend on the individual’s age.

For example, in infants less than 3 months, the most common causes in a descending order are group B streptococci, Escherichia coli, and Listeria monocytogenes. 

In adolescents 13 to 17 years old, the most common causes are Neisseria meningitidis, followed by Streptococcus pneumoniae, and Haemophilus influenzae. 

In non-adolescent children 3 months to 12 years and in adults, Streptococcus pneumoniae is the most common cause, followed by Neisseria meningitidis and Haemophilus influenzae.

It’s also important to consider Listeria monocytogenes in adults over the age of 50 or those who are immunocompromised. 

Also, Staphylococcus aureus is more common in individuals with a history of neurosurgical procedures or trauma to the head. 

Other less common, but extremely important bacterial causes include Mycobacterium tuberculosis, lyme meningitis, rocky mountain spotted fever, and neurosyphilis. These are separated from the oth]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperkinetic_movement_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/traE1gicTvq45G_PDTWZY9RHRayS93KG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperkinetic movement disorders: Clinical]]></video:title><video:description><![CDATA[The cerebrum, cerebellum, and basal ganglia all help coordinate movements, so movement disorders can be traced back to these structures. 

Broadly - there are hypokinetic disorders which cause slowness of movement, and hyperkinetic disorders, which cause excessive involuntary movement. We’ll be talking about the hyperkinetic disorders. 

First up is tremor, which is an involuntary, rhythmic movement of a body part, and is the most common of all of the movement disorders. 

Tremors can be classified into resting, postural, and action tremors.

Resting tremors develop when the affected body part is resting, and is gravity-dependent, and they usually disappear when the person begins a voluntary movement. 

Action tremors are further grouped into kinetic tremors and postural tremors.

Kinetic tremors are simple - if they occur uniformly throughout a voluntary movement - intentional - if it worsens as the affected body part approaches the target - and task-specific - if it occurs during a specific task, like writing. 

Intention tremors are often associated with a problem with the cerebellum, and can accompany other cerebellar signs like ataxia and dysmetria. 

Postural tremors occur when the individual is in a specific position, such as extending their arms out.

One very specific type of tremor is called a flapping tremor, or asterixis, and it’s induced when a person fully extends their wrists. In a flapping tremor a person will flap their wrists, like a bird flapping it’s wings. It’s a classic sign of a metabolic disorder, like hepatic encephalopathy in liver disease, uremic encephalopathy in kidney disease, and carbon dioxide retention in lung disease.

A specific and extremely common tremor disorder is essential tremor. It’s thought to be inherited in an autosomal dominant way, although there can be incomplete penetrance, meaning that some affected individuals may not develop all of the features.

Individuals with essential tremor usually develop a unilate]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anthelmintic_medications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VAFWhGEwRgi0yk8VKJfmpXRyTNKsskmu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anthelmintic medications]]></video:title><video:description><![CDATA[Anthelmintics are a group of antiparasitic antibiotics that treat infections by parasitic worms or helminths. 

They are roughly divided into two groups: vermifuges, which stun helminths; and vermicides, which kill them. 

Now “helminth” is not a term based on taxonomy; instead, it’s a practical term used for many multicellular, worm-like parasites that can infect humans. These include cestodes, trematodes, and nematodes.

Cestodes are tapeworms that can grow to prodigious size, some even reaching over 20 feet, or 7 meters! 

Species like Taenia solium, or pork tapeworm, and Taenia saginata, or beef tapeworm, are transmitted via undercooked pork and beef. 

Once eaten, they hang out in the small intestine, living off of the nutrient-rich fluid around them. 

They are also hermaphrodites and can lay over 50,000 eggs in their lifetime, so you’re never lonely when you have tapeworms! 

The disease itself, taeniasis, can be asymptomatic or it can cause GI symptoms, like abdominal pain, nausea, diarrhea, and weight loss. 

However, if the eggs of the Taenia solium found in human feces is ingested, it could cause cysticercosis. This is where newly hatched larvae burrow into different parts of the body like the eyes, which can cause blindness; and also the brain, which can lead to seizures and death.

Next are trematodes, which  are more commonly known as flukes. 

Common species that infect humans include Schistosoma species, or blood flukes, that cause schistosomiasis, also called snail fever. 

These parasites live inside freshwater snails and pop out as free swimming larva that search for unsuspecting swimmers, and penetrate the skin through hair follicles to make their way into capillary beds, where they feed on blood. 

Liver flukes like Clonorchis and Opisthorchis species also use snails as a host, but their larvae invade fish, that are then eaten by humans.  

Once ingested, the fluke burrows through the intestinal wall and head straight for the liver and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperkalemia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VJVpUk9fTO6fNQgTGOtZG5OoRCm4ERqI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperkalemia: Clinical]]></video:title><video:description><![CDATA[With hyperkalemia, there’s too much potassium in the extracellular fluid, generally over 5 mEq/L. 

Common causes include metabolic acidosis; a hyperglycemic hyperosmolar state; the use of medication, like potassium sparing diuretics; and tissue breakdown, like with a crush injury. 

In addition, individuals with acute or chronic kidney disease, can develop hyperkalemia when there’s a high potassium intake. 

Hyperkalemia is often asymptomatic, but it can cause symptoms like palpitations, paresthesias, and muscle weakness. 

Ultimately if hyperkalemia is severe enough, it can lead to a flaccid paralysis that starts in the lower extremities and ascends upward. 

In addition, severe hyperkalemia can affect renal function - causing a person to become oliguric- meaning their daily urine output can fall below 400 milliliters.

Whenever potassium levels are above 5 mEq/L, the first to do is an EKG. 

If the EKG is normal and the individual doesn’t have symptoms of hyperkalemia, and if there’s no apparent cause of hyperkalemia, then it may be due to pseudohyperkalemia. This happens when potassium moves out of the cells during or after a blood draw. 

For example, potassium gets released from muscle cells during muscle contraction, so if a person repeatedly clenches their fist during the blood draw, then potassium levels can rise - in fact, they can go up by up to 2 mEq/L in that forearm! 

Also during blood drawing, some of the red cells can be harmed and release potassium. 

Pseudohyperkalemia can also happen when there’s thrombocytosis or leukocytosis. 

For example in chronic lymphocytic leukemia, the lymphocytes are frail, so they break easily and release potassium. The key is to simply repeat the serum potassium level and to obtain a CBC. 

If pseudohyperkalemia is ruled out, then there’s a true hyperkalemia. 

There may be EKG changes, but they don’t always correlate with the severity and progression of hyperkalemia.

Oftentimes, a potassium level between 6]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bone_tumors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jqf7KoEEROeMHvqbUPDylOQWS1mDjoUR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bone tumors]]></video:title><video:description><![CDATA[Bone tumors form when a bone cell divides uncontrollably and forms a mass or tumor. 

If the tumor remains confined and doesn’t spread into surrounding tissues, then it’s considered benign. 

But if the tumor invades into surrounding tissues and metastasizes or spreads through blood or lymph, then it’s considered malignant.

Malignant tumors can either be primary which is when they arise from the bone cells, or secondary, which is when a tumor developed somewhere else in the body, metastasized, and spread to the bones. 

The most common sources of tumor cells that affect the bones but start somewhere else in the body, are the breast, prostate, the lungs, the thyroid, and the kidneys.

Now, even though the bones vary in size and shape, they are all made of the same types of cells, and chief among them are osteoblasts which build up new bone, and osteoclasts which help with bone breakdown or resorption.

Now in addition to these, there are some more primitive cells in the bone marrow called human mesenchymal stem cells and neuroectodermal cells, which have the ability to differentiate into many cell types including nerve, fat, bone, and cartilage cells. 

Now, in terms of anatomy, looking at a long- bone like the femur - it has two epiphyses, which are the ends that contribute to joints with other bones. 

Between the two epiphyses, is the diaphysis, also called the bone shaft.

In children and adolescents, there is an additional narrow portion between the epiphysis and the diaphysis called the metaphysis. 

The metaphysis contains the growth plate, the part of the bone that grows during childhood. 

In adults the growth plate has ossified and fused with the diaphysis and the epiphysis.

Now, there are genes that promote normal cell growth called proto-oncogenes. 

With mutations, proto-oncogenes become oncogenes, and these overstimulate the cell growth. 

To balance out cell growth, there are other genes called tumor suppressor genes which promote apoptosis]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenergic_antagonists:_Beta_blockers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F0T96DkETUW-EhFu4Z3yNEMcTReWUg8_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenergic antagonists: Beta blockers]]></video:title><video:description><![CDATA[Alpha blockers and beta blockers are two types of postsynaptic anti-adrenergic medications that prevent their respective receptors from being stimulated by catecholamines, like norepinephrine and epinephrine.   

The nervous system is divided into the central nervous system, so the brain and spinal cord; and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. The peripheral nervous system can be divided into the somatic nervous system, which controls voluntary movement of our skeletal muscles; and the autonomic nervous system, which controls the involuntary movement of the smooth muscles and glands of our organs; this system is then further divided into the sympathetic and parasympathetic nervous systems. 

Now, the autonomic nervous system is made up of a relay that includes two neurons. We’ll focus on just the sympathetic nervous system. Signals for the autonomic nervous system start in the hypothalamus, at the base of the brain. Hypothalamic neurons have really long axons that carry signals all the way down to the thoracic and lumbar spinal cord nuclei, where they synapse with preganglionic neuron cell bodies. From there, the signal goes from the preganglionic neurons down its relatively short axon, exits the spinal cord, and reaches the nearby sympathetic ganglion, which is made up of lots of postganglionic neuron cell bodies. The postganglionic neurons are also called adrenergic neurons, because they release the neurotransmitter norepinephrine, which is also called noradrenalin; and to a much lesser degree, epinephrine also known as adrenaline. These two catecholamines activate the adrenergic receptors on many different organs, which allows the sympathetic nervous system to trigger the fight or flight response that increases the heart rate and blood pressure, as well as slowing down digestion. This response maximizes blood flow to the muscles and brain, and can help you either]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pituitary_adenomas_and_pituitary_hyperfunction:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/II4Sq9RcTLy87MMaIDV1DZeLSmWEX_cY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pituitary adenomas and pituitary hyperfunction: Clinical]]></video:title><video:description><![CDATA[Pituitary adenomas are benign tumors of the anterior pituitary that derive from one of the five types of pituitary hormone producing cells. 

One group of cells are the somatotrophs which secrete growth hormone, or GH. 

Then, there are the corticotrophs, and they secrete adrenocorticotropic hormone, or ACTH for short. 

ACTH makes the adrenal glands secrete cortisol.

Another cell group are the lactotrophs which secrete prolactin, which stimulates breast milk production, and inhibits ovulation and spermatogenesis. 

There are also thyrotrophs which secrete thyroid stimulating hormone, or TSH. 

Last but not least, there are gonadotroph cells, which secrete luteinizing hormone, or LH, and follicle-stimulating hormone, or FSH, both of which stimulate the ovaries or testes.

Sometimes, pituitary adenomas can be entirely asymptomatic, and they’re discovered incidentally on a head MRI performed for another reason, like a head trauma. 

On an unenhanced MRI, meaning, without contrast, normal pituitary tissue has a greater signal intensity than brain tissue - so it looks whiter.  

A pituitary adenoma, on the other hand, has a signal that is similar to surrounding brain tissue - so it’s “just as grey” instead. 

Following administration of Gadolinium as contrast, normal pituitary tissue lights up like a christmas tree. 

An adenoma typically takes in more contrast than the central nervous system, but less than the healthy part of the pituitary - so grey-wise, it’s somewhere in between the two.  

The MRI helps ascertain the size of the tumor - pituitary adenomas smaller than 1 centimeter are called microadenomas, whereas those larger than 1 centimeter are called macroadenomas. 

Both micro and macroadenomas can be functional, meaning that they secrete hormones, or non-functional, meaning they don’t - so any individual with a confirmed pituitary adenoma should be screened for hormone hypersecretion. 

Functional adenomas typically secrete prolactin, growth hormon]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lipid-lowering_medications:_Statins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0bMk6GBWQfKZzb8PxBHvorfhTTS7uyQd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lipid-lowering medications: Statins]]></video:title><video:description><![CDATA[Statins lower overall lipid levels in the body, and work by inhibiting the enzyme HMG-CoA reductase, which is the rate-limiting step of cholesterol metabolism. 

They are an incredibly important class of medications because they’ve been shown to decrease complications associated with cardiovascular disease like strokes, heart attacks, and peripheral vascular disease.

Although it’s got a bad reputation, cholesterol is actually a critical component of our cells and is used to build the cell membrane. 

It also has other uses like the synthesis of steroid hormones, vitamin D, and bile. Normally, we get our cholesterol from the food we eat, but it can also be synthesized by the liver. 

So when we eat a box of chili fries, the fats and cholesterol are absorbed in the small intestine. However, they’re not water soluble, so they can’t travel freely in the blood. 

To fix this, our body makes shipping boxes called lipoproteins.

These containers consist of a shell made of phospholipids and protein tags that act as instructions for their destination. 

So after absorption, the small intestinal cells package the fats and cholesterol into the largest but least dense lipoproteins, called chylomicrons. 

These are released into the lymphatic system and then enter the bloodstream via the subclavian vein. Then they travel through the blood to reach adipose tissue and the liver. 

Now, the liver can also synthesize intrinsic cholesterol through the mevalonate pathway, which happens in the smooth endoplasmic reticulum of liver cells. 

It begins with 2 acetyl-CoA molecules getting joined together by the enzyme acetyl-CoA acyl-transferase. 

The result is a 4-carbon molecule called acetoacetyl-CoA.

Next, the enzyme HMG-CoA synthase combines acetoacetyl-CoA and acetyl-CoA to form a 6-carbon molecule called 3-hydroxy-3-methylglutaryl CoA, or HMG-CoA. 

Then, an enzyme called HMG-CoA reductase reduces HMG-CoA into mevalonate. 

This step with HMG-CoA reductase is the rate-l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Jaundice:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FLUq0EgFT4ymA9AEwnjraTNARNSf-whO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Jaundice: Clinical]]></video:title><video:description><![CDATA[Jaundice -also called icterus- is the yellowish pigmentation of the skin and sclera- and appears when total bilirubin levels exceed 2 mg/dL in adults. 

Total hyperbilirubinemia can be predominantly due to unconjugated- or indirect bilirubin or it can be due to conjugated-or direct bilirubin and it largely depends on where bilirubin metabolism is disrupted. 

So jaundice can be thought of as prehepatic, hepatocellular, or posthepatic. 

A workup for jaundice includes total and conjugated bilirubin, AST, ALT, and alkaline phosphatase, which are markers of liver injury. 

In addition, albumin, PT, PTT, and INR which are markers of hepatocellular function are done. 

If total bilirubin levels are elevated and conjugated bilirubin levels are normal and there’s no other evidence of liver injury or liver dysfunction, then that means that there’s a high amount of unconjugated bilirubin - and the jaundice is most likely due to a prehepatic cause. At that point, additional labs can be sent, like a CBC, LDH, haptoglobin, and a blood smear. 

Common prehepatic causes of excess unconjugated bilirubin include hemolytic anemia and dyserythropoiesis- which is macrophages inappropriately destroy too many red blood cells. These show anemia, an elevated LDH, a decreased haptoglobin, and can show schistocytes on a blood smear.

Now, if the additional lab work comes back normal, then the cause of this jaundice may be hepatocellular. 

One example of this is Gilbert syndrome, which is a genetic condition that causes a decrease in the enzyme uridine glucuronyl transferase. As a result, hepatocytes are less effective at conjugating bilirubin. Individuals are usually asymptomatic, but when there’s a trigger like fasting - adipocytes release a lot of unconjugated bilirubin and that can overwhelm the hepatocytes. 

Usually during an episode of jaundice, the unconjugated bilirubin doesn’t rise above 3 milligrams per deciliter and it resolves within 24 hours after resuming a normal d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypokalemia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TYYXd_GbQu_lhR_rnuKCoYRuTP6W3r6-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypokalemia: Clinical]]></video:title><video:description><![CDATA[Hypokalemia happens when there’s too little potassium in the extracellular fluid, generally under 3.5 mEq/L and it’s usually due to a low potassium intake, abuse of laxatives, vomiting, metabolic alkalosis and the use of diuretics- both loop and thiazides.  

Hypokalemia can be asymptomatic or can cause symptoms like palpitations or smooth muscle weakness leading to an ileus which can cause nausea and vomiting. 

In severe cases, there can be muscle weakness in the skeletal muscles, which can lead to diaphragmatic paralysis and difficulty breathing. 

Whenever potassium levels are below 3.5 mEq/L, the first thing to do is an EKG. 

There may be EKG changes, but they don’t always correlate with the severity and progression of hypokalemia. 

The EKG typically shows ST segment depression, a depressed T wave, and an increase in the amplitude of the U wave, best seen in leads V4 to V6. 

Sometimes, the T and U waves merge to form a T-U wave which can be mistaken for a prolonged QT interval. 

In severe cases, the QRS duration is prolonged, the ST becomes markedly depressed, and the T waves are inverted. 

Common causes of hypokalemia are diarrhea, vomiting, or diuretic use. But if these aren’t the cause, then urinary potassium is assessed in order to see if hypokalemia is caused by renal losses. 

The best way to do that is to measure the 24-hour urine potassium, but because that takes a full day, in an urgent setting, a spot urine potassium to creatinine ratio can be obtained instead. 

Next, an ABG is done to assess acid-base status. 

In metabolic acidosis it would show a pH below 7.35 and a bicarbonate-or HCO3 level below 22 mEq/L. 

If metabolic acidosis is associated with a low urine potassium to creatinine ratio, then the cause may be gastrointestinal, like laxative abuse. 

If metabolic acidosis is associated with a high urine potassium to creatinine ratio, then the cause may be diabetic ketoacidosis or type 1 or 2 renal tubular acidosis. 

Now, if the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dementia_and_delirium:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wmTbvg9dTB_pqIT36ZeoZLC_SBmY3yCS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dementia and delirium: Clinical]]></video:title><video:description><![CDATA[The brain is responsible for various mental functions, including memory, language, visuospatial function,  concentration, executive function, praxis, which is the ability to carry out complex motor activities, and personality. A subtle decline in cognitive function like a slowed reaction time, is a common part of normal aging, and usually doesn’t impair daily functioning and independence - this is called mild cognitive impairment. On the other hand, if there’s a decline in cognitive skill that does impair daily functioning and independence, then it’s called dementia. The major risk factor for most forms of dementia is advancing age, but dementia is not considered an inevitable consequence of normal aging. 

Most of the time, in dementia, a close family member or friend notices the individual’s change in cognition. This includes impaired memory, which leads to repeating conversations or misplacing belongings. Language impairment can make it hard to think of common words. Additionally, concentration and executive function are impaired, so individuals have a hard time with complex tasks, like managing their finances. Impairment in praxis leads to an inability to perform complex motor tasks, such as buttoning one’s shirt. Visuospatial impairment can lead to an inability with recognizing familiar faces or using simple instruments like utensils. Sometimes, family members will notice a change in the individual’s personality. To do a neurological examination, the Montreal cognitive assessment or MOCA or the mini-mental status examination, or MMSE, can be done to assess orientation, registration, recall, attention, and language. For example, orientation is assessed by asking individual what time it is, where they are, or who the president is. Registration is assessed telling the individual three words - like dog, table, and cake, and then asking them to repeat it immediately. Then, they’re asked to repeat those]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Traumatic_brain_injury:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rcp43hzvQ5GEGWF5_FZ26HB3QtWKRt8p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Traumatic brain injury: Clinical]]></video:title><video:description><![CDATA[When an external force damages the head - the result is head trauma, and if there’s temporary or permanent brain dysfunction, we call it a traumatic brain injury, or TBI. This external force could be a blunt impact, like a baseball bat, a penetrating injury, like a gunshot wound, a blast wave, like an explosion, or an accelerating-decelerating force, like in a motor vehicle crash. The most common causes of TBIs are falls and motor vehicle crashes, and high-risk groups include the elderly and individuals using alcohol and illicit drugs. When TBIs occur in children, non-accidental trauma, or child abuse, should always be considered. 

TBIs can cause primary injuries which are a direct result of the external force. These include skull injuries like fractures; blood vessel injuries like an epidural or subdural hematoma, or a subarachnoid or intracerebral hemorrhage; and brain parenchymal injuries like brain contusions and diffuse axonal injury. Sometimes, primary injuries can lead to secondary injuries - like cerebral herniation, seizures, and increased intracranial pressure. 

When an individual has a suspected head trauma, the initial evaluation starts with the primary survey, during which the “ABCDEs” are assessed. “A” is for airway, and individuals with a traumatic brain injury may not be able to protect their airway, leading to aspiration and hypoxia, which can worsens the brain injury. These individuals may require endotracheal intubation and mechanical ventilation. “B” is for breathing, and if there’s increased intracranial pressure, it can lead to an irregular breathing pattern - which is part of the Cushing triad. “C” is for circulation, and hypertension and bradycardia are the two remaining features in the Cushing’s triad. There may also be hypotension, which can reduce brain perfusion. 

“D” is for disability, which can be assessed using a 15-point Glasgow Coma Scale, or GCS, where the minimum possible score is 3. The GCS score has 3 parts: eye move]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Seizures:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YpXWyH9PR8yEdI3e-zRSwckNShKqZWML/_.jpg</video:thumbnail_loc><video:title><![CDATA[Seizures: Clinical]]></video:title><video:description><![CDATA[A seizure is a paroxysmal motor, sensory or autonomic event that occurs due to abnormal, excessive and synchronous electrical discharges from neurons in the brain, and  usually lasts less than 5 minutes.

If a seizure lasts more than 5 minutes, it’s called status epilepticus. 

And the term “convulsion”, refers specifically to motor seizures. 

Now, a seizure is different from epilepsy.

Epilepsy is a chronic disease of the brain that predisposes an individual to having recurrent unprovoked seizures; that is seizures without a clear triggering cause. 

Epilepsy is typically diagnosed when an individual has two or more unprovoked seizures separated by at least twenty-four hours. 

Epilepsy can also be diagnosed when an individual has one seizure and a high likelihood of having another one. 

There are many different forms and causes of epilepsy. 

Seizures are classified into generalized and focal seizures. 

Generalized seizures arise from both cerebral hemispheres at the same time, while focal seizures arise from specific areas in one cerebral hemisphere. 

Now, generalized seizures are subclassified into motor and non-motor seizures. 

Regardless of the subtype, generalized seizures almost always cause a sudden impairment of consciousness. 

Generalized motor seizures include tonic, clonic, tonic-clonic, atonic, and myoclonic seizures. 

Tonic seizures involve sudden stiffening of the muscles, while clonic seizures involve rhythmic twitching of the muscles. However, these clinical features are usually combined, so individuals commonly have a tonic-clonic seizure. 

In a generalized tonic-clonic seizure, a person may have a sudden contraction of their vocal cord muscles, causing them to involuntarily scream or cry during a seizure. 

Contraction of the ocular muscles can cause uprolling of the eyes. 

Contraction of the oropharyngeal muscles can impair swallowing, causing respiratory secretions to pool in the oropharynx. 

Contraction of the jaw muscles m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acing_the_USMLE®_Step_1</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d977r6vfR2qs4Xzd0_CIjFlQTR2AxJ9T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acing the USMLE® Step 1]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Acing the USMLE® Step 1 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Viral_hepatitis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-pCRsnggQU2-nzAyrSvXVTcuRZCD0LM1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Viral hepatitis: Clinical]]></video:title><video:description><![CDATA[Viral hepatitis is liver inflammation caused by a viral infection and it can either be acute or chronic, and five important causes are hepatitis A, B, C, D and E. 

Acute viral hepatitis lasts for less than six months and the individual has nausea, vomiting, and right upper quadrant pain. Sometimes if there’s a high total bilirubin, it can lead to jaundice, pruritus, dark urine, and clay- colored stools. 

Chronic viral hepatitis lasts for more than six months and the individual can sometimes be asymptomatic. Other times, chronic viral hepatitis can cause fever, fatigue, and loss of appetite, as well as extrahepatic symptoms like arthralgias and skin rashes. 

On the physical examination, with acute hepatitis, there’s typically hepatomegaly, but with chronic hepatitis, the liver may feel normal on palpation, and if  there’s cirrhosis, the lower margin of the liver can feel irregular. 

A diagnostic workup for viral hepatitis includes a CBC, AST, ALT, total bilirubin and unconjugated bilirubin, alkaline phosphatase, and PT, PTT, INR. 

Thrombocytopenia, prolonged PT and prolonged PTT as well as an elevated INR can be present in both acute and chronic hepatitis. 

In acute hepatitis, levels of AST, ALT are over 100 international units per liter and sometimes the alkaline phosphatase and total bilirubin are elevated as well. If the total bilirubin is above 2 milligrams per deciliter, then an individual can appear jaundiced. 

With chronic hepatitis, elevation of AST and ALT persists for more than six months but levels don’t usually rise above  400 international units per liter. In addition, total bilirubin and alkaline phosphatase levels can also be elevated. 

During viral hepatitis, medications that are metabolized by the liver, like aspirin, or medications that can damage the liver, like acetaminophen, should be used with caution, because they can further damage the liver.  

Okay, now let’s start with hepatitis A which only causes acute hepatitis. It’s ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cirrhosis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zkX3LrGFRYmrdBl2UMsZ9A8bS6yhDfbP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cirrhosis: Clinical]]></video:title><video:description><![CDATA[Cirrhosis is when chronic inflammation and liver damage causes the liver to become fibrotic and develop scar tissue. 

At a cellular level, the hepatocytes become impaired and this leads to hepatic dysfunction and portal hypertension. 

Cirrhosis is usually irreversible, so it’s usually called “end-stage” or “late-stage” liver damage, and often requires a liver transplant. However, in some cases, early treatment can slow down and even reverse the cirrhosis. 

Compensated cirrhosis is when there are enough healthy cells to make up for the damaged ones, but minor complications like hemorrhoids can still occur. 

Decompensated cirrhosis is when healthy cells can no longer keep up with the workload, causing major complications like hepatic encephalopathy, ascites, and esophageal and gastric variceal hemorrhage. 

In compensated cirrhosis, although there aren’t any major complications, there may still be some symptoms such as loss of appetite, fatigue, and muscle cramps. There may also be easy bruising and excessive bleeding because there aren’t enough clotting factors produced by the liver. 

Cirrhosis can also impair estrogen metabolism, causing amenorrhea and irregular menstrual bleeding in females, and low libido and gynecomastia in males.

On physical exam, there may be hepatomegaly - where the liver can feel firm and nodular, but when there’s a lot of scarring, the liver may be small so that it can’t be felt at all. 

Another sign is spider angiomas- or spider nevi- which are swollen blood vessels just beneath the skin surface- on the truck, face and upper limbs. 

Palmar erythema- which is redness of the hands- can sometimes be seen. 

There can also be hypertrophic osteoarthropathy- which is when there’s nail clubbing and periostitis- which is inflammation around the small hand joints.  

Sometimes, there are Dupuytren contracture, which is when one or more fingers are permanently flexed. 

Portal hypertension can lead to splenomegaly, along with caput ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_deliver_bad_news</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SLGNBLbiS3mlPeDJa6rS-Hr7RTGOBhOg/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to deliver bad news]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to deliver bad news through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Child_abuse:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4ibHlvK4R9awAjG-pLKxygCXT_iqiCv0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Child abuse: Clinical]]></video:title><video:description><![CDATA[Every year, approximately 40 million children around the world suffer from child abuse - also called non-accidental trauma. 

Child abuse is defined as anything that the parent or caregiver does or doesn’t do that causes harm to a child. 

There are four main types of abuse - physical abuse, emotional abuse, sexual abuse, and neglect. 

Physical abuse includes any intentional physical injury, which results in a physical mark or bruise - and in an extreme form leads to fractures, internal bleeding, and death. 

Emotional abuse includes saying and doing things that undermine a child’s emotional development or self-esteem, such as threats, criticisms, or rejection. 

Sexual abuse is any form of sexual exploitation of a child. 

And neglect is failure of the caregiver to cater for the basic needs of a child, ranging from food, clothing, and shelter, to medical attention, an education, and also love and support. 

Neglect also includes abandonment, which is leaving a child alone or unsupervised for a long period of time.

Now, although it’s not considered abuse - corporal punishment - like spanking is no longer considered an appropriate way to discipline a child. 

Spanking young children can cause serious injury, and the child is often unlikely to understand the connection between the behavior and the punishment. 

Repeated spanking may cause agitated, aggressive behavior in the child, and models aggression as a way to resolve conflict. 

Spanking and even threats of spanking, alters the parent–child relationship, making other forms of discipline less effective when physical punishment is no longer an option, such as with adolescents. 

Finally, because spanking can help the parent relieve their anger, it can increase the chance that a parent will spank a child in the future. 

In some situations, repeated spanking can lead to more aggression which can lead to leaving a physical mark - a sign of physical abuse. 

Child abuse is particularly common among childr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Appendicitis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-s54fjBQR4u3iTZmo2lhi3pnRi6r_B2U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Appendicitis: Clinical]]></video:title><video:description><![CDATA[Appendicitis is when the appendix gets inflamed, and it’s the most common surgical emergency of the abdomen. 

Normally, the appendix can be found in a retrocecal location, as well as preileal, postileal, pelvic and subcecal. 

Since the appendix is a hollow tube, the most common cause of inflammation is something getting stuck in or obstructing that tube. 

That something could be a fecalith, a hardened lump of fecal matter, an undigested seed, or even intestinal parasites like pinworms. 

Another cause of obstruction, especially in children and adolescents, is lymphoid follicle growth, also called lymphoid hyperplasia. 

Lymphoid follicles in the appendix grow in size during adolescence, and they can sometimes obstruct the tube. 

Exposure to viral infections like adenovirus and measles can also cause these follicles to grow as well.

Early on acute appendicitis causes periumbilical abdominal pain, nausea, and vomiting. 

Sometimes there can be other atypical symptoms like indigestion, flatulence, diarrhea, and malaise. 

Within 24 to 48 hours, the appendix becomes more swollen and inflamed, and it begins to irritate the abdominal wall, causing the pain to get more severe and localized to the right lower quadrant, as well as causing a fever. 

This classic migration of pain may not be seen in children under three years old. 

McBurney’s sign is tenderness at McBurney&amp;#39;s point - which is located one-third of the distance from the anterior superior iliac spine to the belly button, and it’s a classic sign of appendicitis. 

Another sign of appendicitis is Rovsing’s sign, which is when palpation of the left lower quadrant causes pain in the right lower quadrant.

The obturator sign when the inflamed appendix lies in the pelvis and causes irritation of the obturator internus muscle. 

The iliopsoas sign is when there’s pain on extension of the right hip, which is found in retrocecal appendicitis. 

Now if obstruction persists, the pressure in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Metabolic_and_respiratory_alkalosis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c4mpB_VKSt_CfM5jfpNgI39BT26eKm57/_.jpg</video:thumbnail_loc><video:title><![CDATA[Metabolic and respiratory alkalosis: Clinical]]></video:title><video:description><![CDATA[In metabolic alkalosis, the blood pH is above 7.45, and it’s due to a bicarbonate or HCO3 concentration in the blood over 27 mEq/L. 

Individuals with metabolic alkalosis can be asymptomatic or can cause hypoventilation, due to respiratory compensation. 

Associated symptoms are related to the underlying cause. 

For example, if there’s a history of vomiting, nasogastric suction, laxative abuse or use of loop or thiazide diuretics, then there may be symptoms of dehydration. 

The diagnosis is usually based on an ABG, and in addition to a pH above 7.45, and HCO3 levels above 27 mEq/L, if there’s respiratory compensation, the pCO2 is usually above 45 mm Hg. 

Generally, for every 1 mEq/L elevation in HCO3 above the normal level of 27 mEq/L, pCO2 increases by about 0.7 mm Hg above the normal level of 45 mm Hg, but pCO2 doesn’t usually rise above 55 mm Hg, regardless of HCO3 levels. 

Let’s take an example and say that HCO3 level is 30 mEq/L - so it’s 3 mEq/L above the baseline. 

This means that our pCO2 should be 45- which is the baseline for pCO2- plus 3 times 0.7, which equals 47.1 mm Hg. 

In addition, electrolytes are also done to see if there’s any imbalances, like hypokalemia. 

Now, if the cause of metabolic alkalosis isn’t obvious from the history, then a spot urine chloride is measured. 

If the urine chloride is below 20 mEq/L, that suggests volume depletion from a variety of causes like vomiting which leads to loss of hydrochloric acid, so the treatment is really aimed at addressing the underlying cause of vomiting. 

A related cause is aggressive nasogastric suction, so the treatment is stopping or slowing the removal of gastric secretions. 

Another cause is  loop or thiazide diuretics which block hydrogen ion and chloride ion reabsorption in the kidney.

Chloride is a negatively charged ion, so loss of chloride leads to increased reabsorption of bicarbonate to compensate for the loss. 

The loss of chloride causes the urine chloride to go above]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/BRUE,_ALTE,_and_SIDS:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/faSiKJClRFKELbLmEMdo4zQDS4at1mG6/_.jpg</video:thumbnail_loc><video:title><![CDATA[BRUE, ALTE, and SIDS: Clinical]]></video:title><video:description><![CDATA[In 1986, the term ALTE which stands for Apparent Life-threatening Event was used to represent an episode that can happen in any child, but mostly in infants, less than 1 year of age causing at least one of the following 5 symptoms: a sudden change in color, like cyanosis, pallor, or erythema; a change in muscle tone, like hypotonia; or apnea lasting over 20 seconds; choking; or gagging. Names are important and the term ALTE caused some problems. 

It was vague, causing caregivers to worry, and most of the time it referred to events that were normal variations of an infant’s normal behavior.

So, in 2016, ALTE was replaced by BRUE - a Brief, Resolved, Unexplained Event. 

Brief means that the episode lasts less than 1 minute, typically 20-30 seconds. 

Resolved means that the event is over and the infant has returned to their baseline. 

And unexplained - is self-explanatory. 

The event has to happen specifically in an infant under 1 year old and involve one or more of the following 4 symptoms: a sudden change in color, like cyanosis, pallor, but not erythema; muscle tone, either hypotonia or hypertonia; breathing, which includes any irregular or diminished breathing like apnea; or an altered level of responsiveness or consciousness. 

The key distinction with ALTE is that BRUE has age and time limits, doesn’t accept erythema as a color change and doesn’t include choking or gagging. 

Instead, it includes hypertonia in muscle tone changes, irregular or diminished breathing in breathing changes, and an extra category of symptoms: the change in the level of responsiveness or  consciousness.

When an infant who has had a BRUE is brought for evaluation, the first thing to do is to assess the vital signs - to make sure that they’ve normalized. 

After that a careful history is taken that reviews potential causes of sudden events that can spontaneously resolve. 

One is GERD, which usually causes spitting up after feeding and Sandifer’s sign, or arching of the b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endometrial_hyperplasia_and_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ml_Oi9RaTemk-6Se8tRefu0STpCaXDRj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endometrial hyperplasia and cancer: Clinical]]></video:title><video:description><![CDATA[Endometrial cancer or endometrial carcinoma is when cancer cells arise in the glands within the lining of the uterus. 

Initially the abnormal growth is called endometrial hyperplasia, a precancerous lesion that can eventually progress to endometrial cancer. 

Now, the main cause of endometrial hyperplasia and cancer is excess estrogen - either endogenous or exogenous. 

In fact, estrogen has a cumulative effect throughout a female’s lifetime - so risk factors include early menarche or late menopause, both of which increase the number of ovulatory cycles, each of which contributes to a spike in estrogen. 

Females who have never been pregnant are also at risk - because they don’t have a pause in their menstrual cycles.

Additionally, obese females are also at risk, because excess adipose tissue converts adrenal androgens to estrogen.

Another risk factor is chronic anovulation, like with polycystic ovarian syndrome. That’s because the ovarian follicles keep secreting estrogen, and there’s no luteal phase progesterone to counteract its effects on the endometrium.

Iatrogenic causes include hormone replacement therapy with estrogen, as well as tamoxifen, a breast cancer medication that blocks the estrogen receptor in the breast, but stimulates the estrogen receptor in the uterus.

Finally, there’s Lynch syndrome, an autosomal dominant disorder which causes non-polypoid tumors to sprout in the colon, and also increases the risk of endometrial cancer. 

Endometrial cancer can cause different symptoms based on age and reproductive status. 

In premenopausal females below 45 years old, there might be abnormal vaginal bleeding or anovulation. 

In females between the age of 45 and the onset of menopause, there might be intermenstrual bleeding, menstrual cycles shorter than 21 days, and heavy periods that last over 7 days. 

Finally, in postmenopausal females, any vaginal bleeding should prompt an endometrial evaluation.

Alternatively, an endometrial evaluation m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vasculitis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YU1_CHDjSE6ZkbbYS0RYBcnNRNqsTdRe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vasculitis: Clinical]]></video:title><video:description><![CDATA[Vasculitides are a group of disorders that cause vasculitis, which is inflammation in the walls of the blood vessels. 

Since blood vessels pass through organs - vasculitis damages those organs, and mimics a variety of diseases. 

There are usually systemic symptoms like fever, fatigue, joint pain, and weight loss; as well as organ-specific symptoms that may literally involve any organ.  

Whenever vasculitis is suspected, there’s inflammation, which is often reflected by an increased ESR, CRP, and increased white blood cell count, and sometimes requires a biopsy of whichever organ or tissue is involved. 

The vasculitides are divided into groups based on the size of the arteries that are mainly involved. 

There’s large vessel, medium vessel, and small vessel vasculitis which affects small arteries and capillaries.

Starting with large vessel vasculitis, the first condition is Giant cell arteritis, also called temporal arteritis. 

This is the most common vasculitis in individuals over the age of 50. 

The most frequently affected arteries are the external carotid, ophthalmic, and temporal arteries. 

Symptoms include a headache and vision loss, and a worrisome complication is that there’s a high risk for a stroke. 

Often, the temporal artery can become tender and rigid. 

In addition, individuals can get jaw claudication, which is when there’s temporal artery insufficiency causing ischemia of the masticatory muscles, leading to pain while chewing. 

Diagnosis of giant cell arteritis is done with temporal artery biopsy, looking for giant cells in the tissue.

The next large vessel vasculitis is Takayasu arteritis. 

This is an extremely rare condition affecting mostly young women, generally younger than 40 years old, with increased incidence in the Asian populations. 

Takayasu arteritis primarily affects the aorta and its major branches. 

And the inflammation can cause turbulent blood flow which results in vascular bruits on auscultation of any involve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sjogren_syndrome:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rRoJuCI2TdOrpK_9fTErm92aToWMUW2T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sjogren syndrome: Clinical]]></video:title><video:description><![CDATA[Sjogren&amp;#39;s syndrome is a common autoimmune disorder, that mostly occurs in females, where the immune system attacks various exocrine glands, which are glands that pour their secretions into a duct. 

Most commonly the salivary glands and the lacrimal or tear glands are affected. 

If Sjogren syndrome is primary or occurs alone - it’s called sicca syndrome, and that’s associated with anti-SSA/RO and anti-SSB/LA antibodies. 

Alternatively it can be secondary, which means that it is accompanied by other autoimmune diseases like lupus, rheumatoid arthritis, and scleroderma. 

Sjögren&amp;#39;s syndrome causes dryness of various body surfaces. 

Lacrimal gland involvement leads to dryness of the eyes, blurry vision, itching, redness and burning and ultimately to keratoconjunctivitis, which is the inflammation and ulceration of the cornea and conjunctiva. 

Salivary gland involvement leads to xerostomia, or dry mouth, difficulty in tasting and swallowing, cracks and fissures in the mouth, and eventually tooth decay. 

In the nose and airways, it causes ulceration and bleeding, and if this affects the larynx, it can lead to difficulty speaking.

In some people there may be dryness of the skin and vagina. 

Finally the salivary and lacrimal glands can swell up and compress nearby structures like nerves, causing pain. 

In addition, Sjögren&amp;#39;s syndrome can also affect organs beyond the exocrine glands as well, and sometimes it can overlap into another autoimmune disorder. 

Systemic symptoms include fever, fatigue, myalgia, unintentional weight loss, and lymphadenopathy. 

There can be vascular conditions like palpable purpura, due to bleeding within the skin. 

These purpura can develop into large ulcers that can get infected. 

Another vascular condition is Raynaud’s phenomenon, which is where arterial spasm reduce the blood flow to the fingers for a few minutes at a time. 

The fingers turn white and then blue, often with numbness or pain, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_allergies:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pBIb2Sw5TAC7D5w8xlYelG8FRGu8j3H3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric allergies: Clinical]]></video:title><video:description><![CDATA[Allergies are an IgE-mediated Type I hypersensitivity reaction against a specific allergen. These include environmental triggers, like viral infections, animal dander, latex, pollen, and insect stings; foods, like nuts, shellfish, and eggs; and medications, like penicillins and sulfonamides. And these usually present first during childhood.

Now, allergic reactions happen in two steps. 

Step one - exposure to the allergen causes allergen-specific IgE antibodies to bind to the surface of mast cells and basophils.

Step two - a repeat exposure to the allergen causes those mast cells and basophils to release proinflammatory molecules like histamine.

Generally, there are acute allergic reactions which resolve within 6 weeks, and chronic allergies which persist for more than 6 weeks. 

Among the acute allergic reactions, the most common trigger is a viral upper respiratory tract infection. 

One outcome is urticaria, also called hives, which are slightly raised, well-defined wheals that are 1 mm to 10 cm in diameter. They’re usually red, blanch with pressure, are extremely itchy, and can pop up anywhere in the body. 

The key feature is that these lesions come and go very rapidly - meaning one might appear on the leg as another disappears from the arm. The reaction involves the epidermis and dermis layers of the skin, and the whole thing typically resolves within 24 hours.

Typically no treatment is needed, but if the itching is really bad, topical cooling moisturizers or oral second-generation histamine H1 blockers can be used like loratadine, desloratadine, fexofenadine, cetirizine, or levocetirizine. If these don’t work, immunomodulatory agents, like cyclosporine or methotrexate can also be used. 

Now, if there’s recurrent urticaria, it’s good to try to identify a trigger, so that it can be avoided. 

One way is with in vivo skin prick tests, which is where small drops of up to 40 allergens, like pollens, fungi, animal dander, house dust mites, and variou]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amenorrhea:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uwtMb9lSQ0OZm0zrOoIFyRMxR3GVqC8t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amenorrhea: Clinical]]></video:title><video:description><![CDATA[Amenorrhea means no menstruation, and that’s normal in females before puberty, during pregnancy and lactation, and after menopause. 

Now, for menstruation to happen, a female must normal anatomy and a functioning hypothalamo-pituitary-ovarian axis. 

In other words, the hypothalamus must secrete gonadotropin releasing hormone, or GnRH, to stimulate pituitary production of FSH and LH. 

And, finally, the ovarian follicles must secrete estrogen and progesterone in response to FSH and LH stimulation. 

In childhood and early adolescence, estrogen leads to the development of secondary sex characteristics - like the development of breasts, and the appearance of axillary and pubic hair. 

And eventually, usually 2 to 3 years after the breasts have started developing, the first menstruation, or the menarche, occurs. 

Menstruation marks the beginning of the menstrual cycle, and that cycle repeats every 28 days on average from puberty until menopause. Ovulation happens on day 14 of this average 28 day cycle. 

If the oocyte is fertilized by a sperm, then the remains of the follicle keep secreting estrogen and progesterone to help with pregnancy until the placenta develops, and no menstrual bleeding occurs. 

In the absence of pregnancy, estrogen and progesterone levels gradually decrease, and when they get really low, on day 28, this leads to menstruation, and the beginning of a new cycle.  

So physiology aside, primary amenorrhea is when a female has not begun breast development by age 13 or hasn’t had menarche by age 15. 

Secondary amenorrhea is when a female started have menstrual periods, but then stopped having them. 

A pregnancy test is the first step for both primary and secondary amenorrhea, because some females can be pregnant even before they’ve had their first period. 

If the individual is not pregnant, then the next step for primary amenorrhea is staging a female’s development using the Tanner scale.

The Tanner scale centers on two criteria, the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_pyelonephritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KxJseecFRG6dWG98yVG2de4QQs6nhwYr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute pyelonephritis]]></video:title><video:description><![CDATA[With acute pyelonephritis, pyelo- means pelvis, and -neph- refers to the kidney, so in this case it’s the renal pelvis, which is the funnel-like structure of the kidney that drains urine into the ureter, and -itis means inflammation. So acute pyelonephritis describes an inflamed kidney that develops relatively quickly, usually as a result of a bacterial infection.

Now a urinary tract infection, or UTI, is any infection of the urinary tract, which includes the upper portion of the tract—the kidneys and the ureters, and the lower portion of the tract—the bladder and urethra. So acute pyelonephritis is a type of upper urinary tract infection.

Acute pyelonephritis is most often caused by ascending infection, meaning bacteria start by colonizing the urethra and bladder, which would be a lower urinary tract infections, and make their way up the ureters and kidney, therefore upper UTI shares a lot of the same risk factors as lower UTI, things like female sex, sexual intercourse, indwelling catheters, diabetes mellitus, and urinary tract obstruction. 

One major factor that increases the risk of an upper UTI from a lower UTI spreading upward is vesicoureteral reflux, or VUR, which is where urine is allowed to move backward up the urinary tract, which can happen if the vesicoureteral orifice fails.
The vesicoureteral orifice is the one-way valve that allows urine to flow from each ureter into the bladder, but not in the reverse direction. 

VUR can be the result of a primary congenital defect or it can be caused by bladder outlet obstruction, which increases pressure in the bladder and distorts the valve. 

As kind of a double-whammy, obstruction also leads to urinary stasis, where urine stands still, which makes it easier for bacteria to adhere and colonize the urinary tract. 

So, for ascending infections that cause acute pyelonephritis, the most common organisms are E coli, Proteus species, and Enterobacter species, all of which are commonly found in the bowel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_do's_and_don'ts_of_patient_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cNZMnc7ySZC2qVbDUNDG0lsvSSaJ3PJe/_.jpg</video:thumbnail_loc><video:title><![CDATA[The do&apos;s and don&apos;ts of patient care]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of The do&apos;s and don&apos;ts of patient care through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_strike_a_balance_in_medical_school</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BHpGobdWSvOajgxH7Tvm1KoaQimGVw0U/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to strike a balance in medical school]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to strike a balance in medical school through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_navigate_your_way_in_the_hospital</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_R3-3HH0SZ_fjQITC-8NhlsjSbu_IwpI/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to navigate your way in the hospital]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to navigate your way in the hospital through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Study_tips_for_SHELF_exams_and_the_USMLE®_Step_2</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fsaBt5u7QxGoxMvvVOYj5HQiSlyuihry/_.jpg</video:thumbnail_loc><video:title><![CDATA[Study tips for SHELF exams and the USMLE® Step 2]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Study tips for SHELF exams and the USMLE® Step 2 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bike_helmet_safety:_Information_for_patients_and_families</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ePdhWYrtRaKSqngNW_94KqdoRpqu6OUM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bike helmet safety: Information for patients and families]]></video:title><video:description><![CDATA[Bicycle riding is about as safe as walking. 

But when you’re riding in traffic or down a mountain trail, it can be dangerous.

Wearing a safe bicycle helmet correctly is the best way to protect your head in a crash. 

Helmets have changed over the years and there are helmets made for lots of different activities. 

Some are multi-purpose, but they may not be made for riding. 

Start by picking one that’s certified for biking.

To choose a helmet, first find the circumference of your head where a hatband or sweatband might sit. 

Use a fabric tape measure or piece of string and measure it with a ruler. 

Next, make sure the helmet’s not on backwards. Hey, it happens! 

Turn the dial to adjust the tension until it&amp;#39;s snug --  nod and shake your head. 

The helmet should stay in place. 

Adjust the helmet so that the front edge is level across your forehead, and 1 or 2 fingerbreadths above your eyebrows. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_What_is_acute_flaccid_myelitis,_the_polio-like_paralyzing_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rqM1cMxQT9Gu_NVzK0yYvYPbTk_p5_Xp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: What is acute flaccid myelitis, the polio-like paralyzing disease]]></video:title><video:description><![CDATA[Acute flaccid myelitis—or AFM—is inflammation of the spinal cord that causes sudden muscle weakness. 

It’s a rare condition, fewer than one in a million people will get it a year, and it mainly affects children. 

This disease has been in the news recently it looks like there are going to be more cases of AFM in 2018 than we saw last year. 

This disease causes polio-like symptoms and while it can be caused by poliovirus, it can also be caused by environmental toxins, West Nile Virus, autoimmune diseases, and enteroviruses—especially enterovirus 68. 

Unfortunately, the cause for many cases has not been determined. 

Let’s break down what happens. The spinal cord, of course, is part of your nervous system and roughly speaking it allows for communication between your brain and all of the nerves that snake through the rest of your body. 

When you step on a lego with your bare foot, your brain receives an inbound message about pain, and then sends an outbound message that tells your leg muscles to lift your foot, and your throat muscles to howl in pain. 

Both the inbound and outbound messages are sent through the spinal cord. 

The cells that transmit these messages are called neurons, and they can be incredibly long—even up to a few feet long! 

These neurons have different parts to them.

They receive information through structures called dendrites, which  then enter the cell body, which is like the cell’s headquarters. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_flu_vaccine:_Information_for_patients_and_families</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s9lBp7qUQtq7X4DAlOGiTXzCSQ2tOtlB/_.jpg</video:thumbnail_loc><video:title><![CDATA[The flu vaccine: Information for patients and families]]></video:title><video:description><![CDATA[Influenza, or simply the flu, is caused by influenza virus. Almost everyone has had the flu at some point—high fever, runny nose, sore throat, muscle pains, headaches, coughing, sneezing, and feeling tired—it’s terrible.  

Good news is that it usually improves in a week, but occasionally someone can go from being completely healthy to being seriously ill—requiring hospitalization or even care in the ICU.  

The flu spreads when a sick person sneezes or coughs, and sends thousands of virus-containing droplets into the local area. If they’re lucky, these viruses might land directly on another person’s nose or mouth,  but more often they end up landing on nearby objects like a table. But the flu virus is hardy—and it can survive for hours in the environment.  

To make matters worse, a person may be contagious a day before their symptoms even begin, and up to two weeks afterwards—even after they feel much better! So, while it’s great that Debbie is back to work this week after recovering from the flu. It’s not so great that Debbie brought contaminated doughnuts to share. Thanks Debbie! 

OK, so if you don’t want to feel like garbage with the flu for a week, or get your friends, family and coworkers sick, the most effective way to prevent influenza is through vaccination, which can be done as an injection or nasal spray. These vaccines usually contain a mix of three weakened or inactivated influenza virus strains that are predicted to be the ones that will dominate for a specific season. And because flu viruses mutate rapidly these vaccines are updated every year.  

So how well do they work? Well it depends. First, high-risk individuals like pregnant people, those with a chronic health condition, or those under 6 months or over 65 years of age—are more susceptible to the flu despite being vaccinated.  

Second, since the vaccine is based on predictions, some years are better than others. On average, though, the flu vaccine reduces the risk of illness by roug]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Are_you_eating_plastic</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EC7Ft7aOTZ_fdwiyy3LlgtBvRa_Eauv0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Are you eating plastic]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Knowledge Shot: Are you eating plastic through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Are_you_at_risk_of_an_adenovirus_infection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dn8KI7s0R9iWTK3ydlUwz-RrQUy9Gyhn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Are you at risk of an adenovirus infection]]></video:title><video:description><![CDATA[Adenoviruses have been in the news recently as there was a recent outbreak of adenovirus infections in New Jersey that has been responsible for the deaths of at least 10 children. 

So what are adenoviruses and how dangerous are they? 

Adenoviruses are, actually, a common group of viruses that are mostly known for causing mild upper respiratory illnesses like a mild cold, but they can also cause severe problems like pneumonia. 

They can also cause diarrhea, pink eye, bladder infections, and even neurological diseases if the infection hits the brain or spinal cord.

These viruses circulate year round and are spread when a person sneezes or coughs which releases the viruses into the air.  

If the virus lands on another person’s nose, mouth, or eyes - bullseye! 

Alternatively, the virus might land on nearby objects like a light switch—where they can be difficult to remove with cleaning products, and remain infectious for weeks. 

They can also be passed by close personal contact, like when that aggressive aunt pinches your cheek at family dinners.

The good news is that hand washing with soap and water, and avoiding close personal contact with infected people—usually removes the threat. 

On the flip side, if you are sick, it’s good to stay home to avoid spreading the illness, to cover your nose and mouth when you sneeze, cough into your elbow when you cough, and to wash your hands frequently. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Managing_diabetes_during_the_holidays:_Information_for_patients_and_families</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AWcOB3qMTw_dS4SJuwYe95TpSZWSiuGm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Managing diabetes during the holidays: Information for patients and families]]></video:title><video:description><![CDATA[Turkey, giblet gravy, wine, mashed potatoes, stuffing, green bean casserole, wine, sweet potato casserole, wine, dinner rolls, cranberry sauce, wine, pumpkin pie, pecan pie, and my mother’s favorite (even though I don’t know what it is) green fluff. 

These are staples that I’m planning to have on my Thanksgiving table which don’t even account for snacks that will be served throughout the day before the feast. 

American Thanksgiving is famous for its gut-busting portions and rich dishes, but there are a number of holidays this time of year that can be just as challenging for someone with diabetes. 

So, how do you keep to a diabetes management plan when temptations, travel, and parties throw you off your routine? 

Here are a few tips to help keep blood sugar under control. 

1) Plan ahead. 

Are you in charge of hosting a holiday party? Make healthy menu decisions. 

Are you invited to a party? Offer to bring a healthy dish to share. 

2) Mimic your regular routine as much as possible. 

For example, don’t skip meals to prepare for a feast. 

Have your normal breakfast and try to eat as close to your usual meal times as possible. 

If the party happens later than your usual dinner time, try having a small snack at the regular mealtime and cut back when the holiday feast is served. 

3) Be smart about alcohol.

Alcohol can interfere with blood sugar levels and diabetes medications. 

It also lowers your inhibitions, making you more likely to overeat.

So, if you do choose to imbibe, limit your intake, sip your drink slowly, and don’t drink on an empty stomach. 

4) Beat the buffet. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_What_do_you_need_to_know_about_wildfire_smoke_and_your_health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z04971s1RL_QpkiJO_thd3QITfeqRCNz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: What do you need to know about wildfire smoke and your health]]></video:title><video:description><![CDATA[Wildfires, like the ones currently ravenging California can choke the air of the surrounding communities with smoke. 

People living in those communities can end up breathing this smoky air for days or even months until the fire is brought under control.

To describe how bad the air is government agencies commonly use a scale called the Air Quality Index, or AQI, to describe the air quality in a given area--the higher the number the more polluted the air is. 

Recently, in San Francisco the AQI reached 271 which is roughly ten times the air pollution the city has on an average day. 

It’s been estimated that breathing this air for a day has the equivalent health risks of smoking 10 cigarettes. 

So, what are the health risks to inhaling wildfire smoke and how can you decrease your risks?  

Wildfire smoke is full of gases and tiny particles from burning vegetation and building materials that can irritate your eyes, nasal passages, throat, and lungs. 

They can also trigger an immune response leading to inflammation. 

All of this can lead to coughing, difficulty breathing, a fast heartbeat, chest pain, and it can even trigger an asthma attack.

Young children are one of the groups with the highest risk for difficulties with exposure to smoky air —because their respiratory tracts are still developing and they breathe more air per pound of body weight than adults. 

Other high-risk groups include the elderly, and people with heart and lung diseases—like asthma. 

So how can you decrease your risks for breathing in smoky air? 

First: Pay attention to the news and listen for public warnings and recommendations about smoke. 

Second: limit your exposure. 

If it is smoky outdoors it’s better to stay indoors with the windows and doors closed.

In addition, if you’re using an air conditioner, make sure that it’s recirculating air and not drawing air in from the outside. 

Third: Avoid strenuous outdoor activity.

This is one of the few times where it’s advised t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Firearm_Injury_is_a_public_health_issue:_here's_what_you_can_do.</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oMO_5smHRiqgJy6zqLluWmRWT7CtEfgj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Firearm Injury is a public health issue: here&apos;s what you can do.]]></video:title><video:description><![CDATA[As a result of suicides, homicides, accidents, and mass shootings, firearms-related injuries and deaths have been at epidemic levels in the United States for at least three decades. 

However, health-promoting organizations and health professionals alike have been forbidden from framing this problem as a public health issue. This has to change. 

The Centers for Disease Control and Prevention—the CDC—has played an integral role in public health research, such as clarifying the link between tobacco and lung cancer. 

However, since the passage of the 1996 Dickey Amendment the CDC has been blocked from doing research that might yield results that could be used to improve firearm safety. 

At times, individual providers have been stifled by so-called “gag laws,” like the one Florida enacted in 2011 that punished physicians, and especially pediatricians, for asking their patients about firearm safety with a fine of up to $10,000 and even loss of their medical license. 

This law was finally struck down as unconstitutional in 2017, and currently no such law exists in the US. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Vaping_versus_smoking:_what_are_the_risks</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y_UcZMQyQP2zNcXiwpSytyXmRVewpsLv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Vaping versus smoking: what are the risks]]></video:title><video:description><![CDATA[Electronic cigarettes, or e-cigarettes, are handheld devices that recreate the feeling of smoking regular cigarettes but are widely believed to be a much safer form of tobacco. 

That’s partly why  there’s been a spike in e-cigarette use, or vaping, over the past few years, especially in pre-teens and teenagers.

So what are the differences between vaping and smoking, and how safe is vaping? 

Let’s start with cigarette smoking, which remains the leading cause of preventable deaths - killing nearly half a million people a year in the United States alone, with nearly a tenth of those deaths among non-smokers who are exposed to secondhand smoke.

Cigarettes are usually composed of tobacco, paper, a filter, and additives. 

These additives can be any number of hundreds of things like sugars which improve the taste of the cigarette, ammonia which enhances the effects felt by nicotine, and menthol which can ease the throat irritation caused by smoking. 

When the cigarette burns, it produces smoke, which is then inhaled to deliver the nicotine to the lungs. 

Burning produces thousands of toxic chemicals like formaldehyde and carbon monoxide which damage the inner lining of arteries which increases the risk of cancers, heart attacks, and stroke. 

In general, it’s thought that nicotine is responsible for the addictive qualities of cigarette smoke, while the toxins are responsible for the negative health consequences of smoking. 

This is where e-cigarettes come in. 

These devices have a mouthpiece, a heating element, a power source, and a reservoir filled with a liquid called e-liquid which contains nicotine and other chemicals. 

Some of them, like the popular JUUL device, are designed to look like a USB thumb drive to be more discrete. 

These devices work by heating the e-liquid to create an aerosol, called vapor, that can be inhaled and delivers a similar dose of nicotine as cigarette smoke. 

Because there’s no combustion, there are 10 to 100 times lower ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Glioblastoma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jkrIxCCsSCi2o1cCueKVFxa1SIOpVEZ0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Glioblastoma]]></video:title><video:description><![CDATA[In glioblastoma, ”-blastoma” refers to a malignant, or invasive tumor, formed by immature, precursor cells, often called blasts, and “glio-“ to glial cells, particularly astrocytes, which make up the “glue” or supportive tissue of the central nervous system, so glioblastoma is basically an aggressive cancer of the central nervous system that arises from precursor glial cells specifically bound to differentiate into astrocytes. 

Actually, this is the most common primary malignant tumor of the central nervous system in adults, with “primary” meaning that it originates inside the central nervous system.

Okay, normally, the human central nervous system, aka the brain and spinal cord, apart from neurons, contains trillions of another type of cells, known as glia. 

Glial cells are sort of the “glue” of the nervous tissue, but they are also involved in every single aspect of neuronal function. 

There is a wide variety of glial cells, but all of them originate from some common precursor cell that, through various steps, chooses to differentiate into a specific type of glial cell. 

The most abundant one is the astrocyte. In greek, “astro” means star, so astrocytes are star-shaped cells, each of which has thousands of projections waving around and taking up neurotransmitters, cleaning up after neuronal activity, while also surrounding the endothelial cells that line the brain capillaries, in order to help create the blood- brain barrier.

What sets them apart histologically is that they express high amounts of an intermediate filament protein, called glial fibrillary acidic protein, or GFAP for short.

Now, sometimes, astrocytes or their precursors develop mutations in genes controlling their replication. 

More specifically, there are typically mutations that lead to overexpression of genes promoting cell proliferation, such as growth factor receptors, and others that cause loss of function of tumor suppressor genes, such as p53. 

The net result is that cells]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Oxytocin:_the_Love_Hormone.</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gWuDa332SLGqVaciogZjfqX3Rkab9_G2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Oxytocin: the Love Hormone.]]></video:title><video:description><![CDATA[Alright, real quick…

Valentine’s Day is here, and love is in the air. Well, actually, a more accurate thing to say is, our brains are hopped up on oxytocin.

So what is oxytocin, and why is it considered the love hormone?

Well, oxytocin is a neuropeptide, which means that it’s a short-chain polypeptide that’s used as a neurotransmitter, relaying a signal from one neuron to another. 

Oxytocin is released by the pituitary gland and binds to oxytocin receptors, which can be found on cells in the brain, as well as the rest of the body. 

Oxytocin is crucial during the delivery of a baby; it helps with cervical dilation and contractions. Then, during breastfeeding, oxytocin gets released in response to a baby’s suckling, or even a baby’s cry, as part of the reflex that allows milk to be let down from the nipples.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_CRISPR-Cas9_and_the_age_of_gene-edited_humans</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e0RLu_e-R0ylgoYkha8wd6mHRUezOYx8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: CRISPR-Cas9 and the age of gene-edited humans]]></video:title><video:description><![CDATA[Genome or gene editing is when targeted changes are made like insertions and deletions, right in an organism’s genome. 

Over the past decade, the CRISPR-Cas9 system has become a very popular method of genome editing because it’s fast, cheap, precise, and relatively easy to use. 

The way it works is that researchers create a piece of RNA with a ‘guide’ sequence which is complementary to a targeted bit of DNA in the host’s genome. 

In other words, if the DNA has a sequence that reads 5′  -GGCTAT- 3′, then the RNA guide sequence is exactly the opposite and reads 3′ - CCGAUA -5′.

And remember it’s a U for Uracil instead of a T for Thymidine because the guide sequence is made of RNA and not DNA.

The Cas9 protein then attaches to the RNA and the whole thing binds to the target DNA sequence in the host genome. 

The Cas9-RNA complex then makes a double-strand cut in the genomic DNA, and an alternative piece of DNA can be spliced in right at that spot. 

CRISPR-Cas9 technology works in a variety of cell types and organisms, and it’s been used to study diseases, and generate tissues from stem cells, like heart muscle tissue and neuronal tissue.

Now, it’s also possible to treat a whole, multicellular organism with genome editing. 

For example, a mouse with liver disease due to a genetic defect was treated with a CRISPR-Cas9-mediated genetic change, and it improved the mouse’s symptoms.

One important point to note about this mouse example, however, is that the change was made to somatic cells, rather than germline cells, meaning these genomic modifications aren’t passed to the next generation.

That said, CRISPR-Cas9 technology is able to alter the DNA in germline cells, and if that’s done, then the engineered changes can be transmitted across generations. 

And this has been done in several organisms including mice, monkeys, and most recently in humans. 

Last month, Chinese scientist He Jiankui, claimed at a conference that he has edited the genes of twin g]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Could_you_get_an_MD_online</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i6jtvv7zRta3WP1vlz_XMaqYQvu7fTQY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Could you get an MD online]]></video:title><video:description><![CDATA[Today, you can get an online degree in a variety of fields in the healthcare system—everything from paramedic training, to medical billing, to dental hygiene, to phlebotomy. 

Within the field of nursing, there are over 300 programs that offer bachelors, masters, and even doctorate degrees. 

Of course, if the training involves patient care these programs also require hands-on training in a clinical setting. 

There is one healthcare degree that is not offered online, however, and that is the Doctor of Medicine or MD.

For more than a century, MD training in the United States has included 2-years of preclinical training that’s largely done in the classroom, followed by 2-years of clinical apprenticeship. 

The classroom-based teaching is usually done with passive lectures that are more often than not inefficient and unpopular. 

In many schools fewer than one-third of the class even attend these lectures after the first semester. 

Further, a recent study has shown that in-class attendance doesn’t predict how well a medical student will perform academically.

So, if the majority of future physicians aren’t attending class, what are they doing? 

The answer is that these students are learning online. 

Many students stream their professor’s lectures at 1.5x – 2x speeds while at home or at a coffee shop. 

They also invest in external resources such as osmosis.org to enhance their comprehension and retention of their class materials—not to mention increasing their test scores.

While there are examples of innovative models of medical education, there is no “online medical school” that enables completion of parts or all of the preclinical training virtually. 

This is in part due to the stringent requirements by the Liaison Committee for Medical Education (LCME) which accredits medical education programs.

But there are a few trends that suggest there’s growing appetite for innovation in physician training.

First, the vast majority of medical students are di]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Is_Santa_Claus_at_risk_of_a_heart_attack</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BYBexYzrTmqygalg2cc0ViiRQYyk_pnG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Is Santa Claus at risk of a heart attack]]></video:title><video:description><![CDATA[Alright, real quick - ooh!

Osmosis videos often include famous people who have had a disease, and it’s for two reasons. One, it helps destigmatize having the disease; and two, it helps to serve as a memory anchor for remembering the specifics of the disease. 

Today, we’re discussing one of the biggest celebrities of all: Santa Claus (ho, ho, ho!). Indeed, because of his age, his relationship with iconic brands such as Coca Cola, and his ability to pander to children with promises of presents - and to parents with threats of withholding those presents from their children for misbehavior - Santa Claus has become one of the most beloved and recognizable figures around the world. 

While Santa Claus has never been known to have any serious illnesses or conditions, we’re concerned he might be a ticking time bomb for having a heart attack.

Much of what we know about this enigmatic cultural icon, including one of his many pseudonyms, comes from a single chance encounter with a scholar named Clement Clarke Moore in 1822, who chronicled the meeting in, “A Visit from St. Nicholas,” more popularly known as, “’Twas the Night Before Christmas.” As Moore recounts: 

“His droll little mouth was drawn up like a bow, 
And the beard on his chin was as white as the snow; 
The stump of a pipe he held tight in his teeth,
And the smoke, it encircled his head like a wreath;
He had a broad face and a little round belly,
That shook when he laughed, like a bowl full of jelly.
He was chubby and plump, a right jolly old elf.”

From this description, it’s clear Santa Claus has several of the key cardiovascular risk factors, which increases potential of having a heart attack.

Remember, heart attacks typically occur when an artery has plaque buildup, and that plaque suddenly breaks, blocking the blood from getting through and reaching the heart muscle. It&amp;#39;s a bit like a plump individual getting stuck in a chimney and blocking the smoke from getting through to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growing_your_seed_habit</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1H2kvQSfRVO7UPN9S5D51Fs6RWWKzCGV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growing your seed habit]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Growing your seed habit through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Direct_to_consumer_advertising</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/czREIID5SXqRQRYBmosPRaBNSY26V9qW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Direct to consumer advertising]]></video:title><video:description><![CDATA[At some point, you’ve probably seen a commercial with green meadows, sunshine, and smiling attractive people, celebrating a prescription drug! 

The ad usually suggests that you “ask your doctor today about” that drug, before rattling off a long list of side effects. 

These kinds of advertisements are a form of direct-to-consumer advertising, or DTCA, which means that the ad comes directly from pharmaceutical companies and is directed at consumers like you and me. 

Although it may feel normal,  DTCA is currently only legal in two countries; the United States and New Zealand. 

In the United States, DTCA of prescription medications took off in 1997, when the FDA eased restrictions. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_What_over-the-counter_painkiller_is_the_best_at_killing_pain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Mwjh2uUUQM_JQ2qwo826aFqWR_6qFVdM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: What over-the-counter painkiller is the best at killing pain]]></video:title><video:description><![CDATA[We’ve all had days with nagging headaches, muscle and joint soreness, or general aches and pains, that don’t require medical attention, but require something to take the edge off the pain. 

That something is often an over-the-counter, or OTC, painkiller. 

There are a variety of brands, which each have different active ingredients, so which OTC painkillers are the best at decreasing pain? 

In general, OTC painkillers can be classified in two categories: non-steroidal anti-inflammatory drugs or NSAIDs and acetaminophen. 

Inflammation and fever result from pro-inflammatory chemicals called prostaglandins, and NSAIDs work by decreasing levels of these prostaglandins. 

The most common OTC variations of NSAIDs include Aspirin which is found in brands like Bufferin and Bayer; Ibuprofen, found in brands like Advil and Motrin; and Naproxen, found in Aleve. 

NSAIDs are generally safe, but chronic use can irritate the stomach lining and cause ulcers. 

NSAIDs, are also believed to decrease blood flow through the kidneys which can lead to kidney problems in people with other risk factors for kidney disease.

Similarly, while the mechanism isn’t completely clear, NSAIDs, with the exception of Aspirin, can cause cardiovascular damage with extended use. 

Finally, NSAIDs have been linked to developmental defects in fetuses so it’s generally recommended for pregnant women to avoid NSAIDs, especially late in the pregnancy. 

Unlike NSAIDs, it’s unclear how Acetaminophen exactly works, but it’s thought to block enzymes in the brain and spinal cord that produce chemicals that promote pain and fever. 

One key difference though, is that acetaminophen doesn’t decrease inflammation. 

It’s found in hundreds of brands like Tylenol, and it’s commonly mixed with other active ingredients as well. 

Examples include Excedrin which works for migraines and is a mix of acetaminophen, aspirin, and caffeine; and Vicodin, which is a prescription strength painkiller that contains ace]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_How_well_do_fluoride_treatments_work_at_preventing_tooth_decay</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NwL3gsdyTNqyXrW0J4E3O3xFRf2du8x5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: How well do fluoride treatments work at preventing tooth decay]]></video:title><video:description><![CDATA[Alright, real quick - ooh!

Currently, about two-thirds of US households have fluoridated water, and the CDC has made nationwide fluoridation of drinking water a top priority for the prevention of cavities. 

The use of fluoride, however, is something of a hot button issue. For example, a recent study showed that consumer-generated videos versus industry-generated videos on YouTube were much more likely to have an anti-fluoride sentiment. 

This is not new. In 1945, Grand Rapids, Michigan, became the first city to implement community fluoridation of the water supply, and in the decades that followed, several conspiracy theories developed around the practice, including speculation of a plot to impose a communist regime in the United States. 

Of course, fluoride is not just found in tap water. It&amp;#39;s also found naturally and fortified in certain foods, can be found in varnish or gels at the dentist&amp;#39;s office, and is a common ingredient in mouth rinses and toothpastes.

So how does fluoride prevent cavities, and what does the research say about the benefits of its use?

Now, in general, there&amp;#39;s bacteria on your teeth, which can form micro-colonies. And when these micro-colonies coalesce, it creates a layer of dental plaque. Bacteria have a hard time getting into the tooth due to the outer layer of enamel, which is composed of a hard substance called hydroxyapatite, a type of calcium phosphate crystal with the chemical formula Ca10(PO4)6(OH)2. 

Now, if the bacteria on the tooth&amp;#39;s surface start to overgrow, they can metabolize sugary foods and drinks and generate acid, which can cause the hydroxyapatite to break down. Without hydroxyapatite, the enamel surface of the tooth can weaken and allow bacteria to enter, causing permanent damage. This is called a cavity. If it goes on long enough, the bacteria can infect the root of the tooth, and this can be extremely painful. 

So this is where fluoride comes in. Fluoride can re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_What_over-the-counter_medicine_works_best_at_kicking_the_cough_of_the_common_cold_and_bronchitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KD8TTImXRwimOxD-I2H9C-AVTU_uMkuU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: What over-the-counter medicine works best at kicking the cough of the common cold and bronchitis]]></video:title><video:description><![CDATA[The common cold causes a sore throat, headache, sneezing, a runny nose or nasal congestion, and coughing which usually starts a few days after the other symptoms, but often develops into the worst symptom and can linger for a few weeks.

Bronchitis causes chest congestion, shortness of breath, wheezing, and once again, a lingering cough. 

Both are viral infections so antibiotics don’t work, but the symptoms can be rough, so, what’s the best medication for treating a cough due to the cold or bronchitis? 

Unfortunately, many over-the-counter cough remedies haven’t been recently tested and when they have been, many are found to be ineffective. 

Also, simply taking something for a cough can make a person feel better, so there’s also a placebo effect at work. 

In general, there are three ways to study how well a cough medication works. 

The first way is a survey that simply asks people if a medication helped them recover from their cough.

The second way is called the challenge method because healthy people are challenged with citric acid or capsaicin—the molecules that make hot peppers hot—both of which can induce coughing. 

Then the medication is given to see if it reduces the coughing. 

The third way, cough counting, involves a person with a cough wearing a recording device that counts the number of coughs they have before and after they take a medication. 

This last way is considered the best (yes, really) by regulatory agencies like the Food and Drug Administration, but the results don’t always correlate with results from surveys and challenge studies. 

So, with this in mind, a recent review in the British Medical Journal took a look at the effect of various over-the-counter cough medications by looking at all three types of measurements. 

Now, the availability for each medication varies by country. 

For example, codeine is only available with a prescription and Levodropropizine is not readily available in the United States. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medical_school_and_disability</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lFGo86muTzSzmJBDY8ziSgWVQMWSAzE2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medical school and disability]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Medical school and disability through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Does_exercise_help_decrease_insomnia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/la_VPz20Toawa7dF0B7iwYEoSRSG4c1G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Does exercise help decrease insomnia]]></video:title><video:description><![CDATA[Insomnia affects about a third of all people at some point in their life and it makes it difficult to either fall asleep or stay asleep. 

Sometimes it’s a mild, short-term symptom but if it’s severe and lasts a long time it’s considered a disorder. 

Either way, it leaves the person feeling exhausted. Unfortunately, treating insomnia is challenging.

For example, sleep medications often have dangerous side-effects and can be habit forming, so they’re generally recommended for temporary use only after other options have been tried. 

Another treatment is cognitive behavioral therapy, which is effective, but requires clinical supervision which costs time and money. 

This is where exercise comes in.

Exercise is safe, can be done quickly and cheaply, and doesn’t require the help of a highly trained clinician. 

Also, exercise has been shown to improve sleep quality in a number of studies, and that’s why exercise is a core recommendation from the National Sleep Foundation to improve sleep. 

That said, while there are a number of clear benefits to exercise, only a few studies have looked at the relationship between physical exercise and insomnia, so whether or not exercise improves sleep for people with insomnia remains unclear.  

To answer this question researchers looked at a number of studies that explored the link between exercise and symptoms of insomnia or insomnia disorder. 

They specifically looked at randomised clinical trials, where at least 30 minutes of either aerobic exercise, like cycling, or mind-body exercise, like yoga or Tai chi, were done per session, for at least 120 total minutes a week for several weeks, to see if that improved overall sleep in adults with insomnia. 

To measure sleep quality, the studies either used subjective data, like questionnaires and diaries or objective data, like actigraphy, which measures body movement through the night, or polysomnography, which measures brain waves, heart rate, and breathing through the ni]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_study_smarter</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YS0miCbmQGeYIrw63ube1dMpTFK5a3ls/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to study smarter]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to study smarter through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disruptive,_impulse-control_and_conduct_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8dQt-pB3RFuMhbTTvCyNRXkuQDWol4R1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disruptive, impulse-control and conduct disorders: Clinical]]></video:title><video:description><![CDATA[From time to time, everyone has moments when they behave poorly, but those with disruptive, impulse-control, and conduct disorders repeatedly have trouble controlling their behavior, and often end up destroying things or hurting those around them. 

For example, they might get irritated and then end up punching their fist through a door.

There are various biological, psychological, and environmental factors that contribute to disruptive, impulse-control, and conduct disorders. 

Biological factors, include having a family history. 

In addition, having abnormalities in the prefrontal cortex and amygdala are specifically linked to intermittent explosive disorder.

Psychological factors include having a difficult temperament like being withdrawn and unable to adapt to new situations, and having difficulty with delayed gratification. 

Environmental factors include physical or sexual abuse, harsh discipline, parental neglect or rejection, frequent change of caregivers, parental criminality, and a family history of substance-related disorders.

All of the disorders are marked by difficulty controlling emotions and behaviors, leading to destruction of property or hurting others as well as troubles with authority.

Individuals are usually unable to restrain their impulses and their responses are typically out of proportion to the provocation, and cause high levels of psychosocial impairment. 

A person may feel increasing tension like feeling a tightening in their muscles, and a compulsion to act on their destructive or explosive impulses, as well as a sense of pleasure and release after they’ve done so.

According to DSM-5, this group of conditions includes seven disorders: intermittent explosive disorder, oppositional defiant disorder, conduct disorder, pyromania, kleptomania, and the last two are other specified and unspecified disruptive, impulse-control, and conduct disorders. 

The most studied condition is intermittent explosive disorder. 

First, diagno]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eating_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QdQuk4UuSxaPaPAteSSlj3jZT-KH-SIz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eating disorders: Clinical]]></video:title><video:description><![CDATA[An eating disorder is a mental disorder characterized by abnormal eating habits that negatively affect a person&amp;#39;s physical or mental health. Eating disorders are quite common, and while in many cultures there is a misconception that they only affect women, they can, in fact, affect anybody regardless of gender or sex, but most often occur in teenagers who struggle with low self-esteem and the social pressure to look a certain way. They’re tied to both biological factors - like genetics and hormones, as well as environmental factors - like psychosocial pressure to have the socially-defined “ideal body” perpetuated by social and traditional media, or having careers that promote weight loss like modeling and sports; also bullying, loneliness, and childhood trauma are all linked to eating disorders. 
The most common eating disorders include anorexia nervosa, bulimia nervosa, and binge-eating disorder. Besides that, there are other conditions, which include umination, avoidant or restrictive food intake disorder, and finally pica. There are also two other diagnoses, other specified eating disorder, and unspecified eating disorder, reserved for symptoms that don&amp;#39;t fit any of the primary disorders.
If an individual is suspected to have an eating disorder, a number of screening instruments have been developed to identify those who need further evaluation. A very simple instrument is the SCOFF questionnaire, which consists of five questions. The acronym SCOFF relates to one of the words in each question  - Sick, Control, One, Fat, and Food. The questions are: Do you make yourself Sick because you feel uncomfortably full? Do you worry you have lost Control over how much you eat? Have you recently lost more than One stone - so 14 pounds or 6.35 kilograms - in a three-month period? Do you believe yourself to be Fat when others say you are too thin? And finally, would you say that Food dominates your life? One point is assigned for every &amp;qu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preoperative_evaluation:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lfBm3aumTgSkMC4UPtuR3FrBRMWbM2U4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preoperative evaluation: Clinical]]></video:title><video:description><![CDATA[A preoperative evaluation is done before an individual can undergo surgery, to assess their health. This is important because surgery and anesthesia are stressful events that can exacerbate underlying diseases. 

The goal of a preoperative evaluation is to identify diseases and risk factors that can increase the risk of surgery and anesthesia, and to come up with strategies to reduce that risk.

The American Society of Anesthesiologists created the ASA physical status classification system for preoperative evaluations. 

This classifies individuals into six groups: 1 is a healthy person; 2 is someone with mild systemic disease; 3 is someone with severe systemic disease; 4 is someone with severe systemic disease that is a constant threat to life; 5 is a moribund person who is not expected to survive for long without the operation; and finally, 6 is a declared brain-dead person whose organs are being removed as a donor. 

If the surgery is an emergency, the physical status classification is followed by “E” for emergency. 

In addition to the ASA physical status, other operative risk factors include age, comorbid conditions in addition to systemic diseases, the operative procedure, the type of anesthesia, and finally the surgical team and resources. 

That includes the surgical and anesthesia team, duration of surgery and anesthesia, equipment, medications, blood, and postoperative care. 

The first key risk factor is age, and much of the risk associated with age is due to comorbidities like cognitive and functional impairment, malnutrition, and frailty. 

Next is exercise capacity, because those with good exercise tolerance generally have low risk. Next is a complete medication history, specifically including over-the-counter, complementary, and alternative medications, which could cause an increased risk of bleeding. 

Most medications should be continued up to and including the morning of the operation, but some should be discontinued preoperatively. 

For]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vaccinations:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MGu0wtgFSp_feXyO1x0cj6V8RDGXEVMg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vaccinations: Clinical]]></video:title><video:description><![CDATA[Vaccination is the process of generating a protective adaptive immune response against microbes by exposing the body to non-pathogenic forms of microbes or components of microbes. 

There are four main types of vaccines: Live attenuated, inactivated, subunit, and toxoid vaccines. 

Live attenuated vaccines contain pathogens that have been weakened in the laboratory and they’re used to protect against Measles, Mumps, Rubella, and Varicella - the MMR-V vaccine, Rotavirus, polio- the Oral Polio Vaccine or OPV, influenza- the nasal flu vaccine and Yellow fever. 

Inactivated vaccines use a pathogen that has been killed in the laboratory and include vaccines against Hepatitis A, polio- the Inactivated Polio Vaccine or IPV, and Influenza- the inactivated influenza vaccine. 

Subunit vaccines contain just a portion of the pathogens- like polysaccharides or proteins and this is done in vaccines against Haemophilus influenzae type B, Hepatitis B, human papillomavirus or HPV, Bordetella pertussis, Streptococcus pneumoniae, Neisseria meningitidis, and varicella zoster virus. 

Finally, toxoid vaccines contain inactivated toxins produced by pathogens, and this is used in vaccines against Clostridium tetani which makes tetanus toxin and Corynebacterium diphtheriae which makes diphtheria toxin.

Toxoid vaccines are often combined with subunit vaccines to make a more immunogenic or strong vaccine. For example the TDaP and DTaP vaccine provides coverage against the toxins for tetanus and diphtheria, as well as the toxin and non-toxin antigens that are part of pertussis. 

All of these vaccines can be administered one of four ways: intramuscularly, intradermally, subcutaneously, or orally. 

Every year, each country publishes a routine vaccination schedule that includes which vaccines a child should be given depending on their age, as well as vaccine contraindications.

One contraindication for all vaccines is having a severe allergic reactions like anaphylaxis when given ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_impress_your_attendings</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2kOHoRaVSBSm1oaxgw1Iqs9xQyOWDE68/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to impress your attendings]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to impress your attendings through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Essential_thrombocythemia_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ScCABUxkR5KJuUg9h7KDg2zdTpyXHmRw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Essential thrombocythemia (NORD)]]></video:title><video:description><![CDATA[Essential thrombocythemia is a slowly progressive disease where the bone marrow produces too many platelets.

In rare cases, essential thrombocythemia can develop into myelofibrosis and acute leukemia.

Now, the vast majority of bone marrow is made of hematopoietic cells which are the early progenitor cells that can differentiate into other cell types.

In the case of platelets, progenitor cells differentiate into megakaryocytes, which are responsible for creating platelets.

In essential thrombocythemia there’s a genetic mutation that occurs in the Janus Kinase 2 gene, also called JAK2, or somewhere along this pathway of cell signalling. 

Normally, the liver and kidneys produce a a tiny hormone called thrombopoietin which binds to hematopoietic cell receptors. 

When it binds, those cells activate the JAK2 gene which makes them divide and mature into megakaryocytes and platelets. 

Cells can also develop mutations in the thrombopoietin receptor, MPL, or in the chaperone protein, Calreticulin or CalR.

Now, when there’s a genetic mutation in CalR, the signalling pathway remains active all the time, and that means that platelets keep getting produced even in the absence of thrombopoietin. 

Although there are lots of platelets that are made, many of them end up being misshapen - they’re large and irregularly shaped. 

Now, all of these excess platelets end up causing an increased risk of blood clots in the deep veins of the legs, lungs, and even sites where clots don’t usually form, like the abdomen. 

As a result, there’s an increased risk of stroke, heart attack, and miscarriage. 

Now, if the number of platelets is extremely high, over 1.5 million, then there’s an increased risk of bleeding. 

That’s counterintuitive, but it’s because platelets use up free Von Willebrand factor, and low concentrations of circulating Von Willebrand factor means that it may not be enough available at the site of an injury, and that can lead to bleeding. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Proteins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zUihZ3bMTbC1iMqORfOFdWAsSuOpH1C4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Proteins]]></video:title><video:description><![CDATA[Protein is an essential part of the human diet. It’s found in a variety of foods like eggs, dairy, seafood, legumes, meats, nuts, and seeds. 

Regardless of the source, the protein that we eat gets broken down and reformed into new proteins in our bodies. 

These proteins do everything from fighting infections to helping cells divide. You name it, they’re doing it.

At its simplest, a protein is a chain of amino acids, bound to one another by peptide bonds. Like a string of beads. 

These strings get twisted and folded into a final protein shape.

When we eat protein, it gets broken down into its individual amino acids.

Most amino acids have a central carbon atom bonded to one amino or nitrogen-containing group and one carboxylic acid group - that’s why it’s called an amino acid. 

The carbon also has one hydrogen atom and a side chain which is unique to each amino acid. The exception to this is proline which has a tiny little ring structure instead.

Although there are hundreds of amino acids in nature, humans use only about 20 of them to make basically every type of protein. 

They include: alanine, arginine, asparagine, aspartic acid, cysteine, glutamic acid, glutamine, glycine, histidine, isoleucine, leucine, lysine, methionine, phenylalanine, proline, serine, threonine, tryptophan, tyrosine, and valine. Phew, that’s 20. 

One way to divide them is by defining which ones our bodies can make ourselves, and which ones we cannot. 

There are 5 amino acids - alanine, asparagine, aspartic acid, glutamic acid, and serine - that we can get from foods, but we can also make ourselves. These are called nonessential amino acids. 

Then, there are 6 of them that we call conditionally essential because healthy bodies can make them under normal circumstances - arginine, cysteine, glutamine, glycine, proline, and tyrosine. But we can’t make them in cases like starvation or certain inborn errors of metabolism. 

Finally, there are 9 of them that we can only get from ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_tract_infections:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wMfDJ-y9SRyvGmdK8PRZPRw8QReQflJk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary tract infections: Clinical]]></video:title><video:description><![CDATA[Urinary tract infections or UTIs are infections that affect part of the urinary tract. 

They’re usually caused by bacteria found in fecal flora, which normally colonizes the urethral meatus. 

However, when those bacteria make their way up the urethra and into the bladder, they can cause lower UTIs, like cystitis, which is the inflammation of the bladder, or upper UTIs, like acute pyelonephritis, which is the inflammation of the renal pelvis and kidneys. 

Both cystitis and acute pyelonephritis can be uncomplicated or complicated. 

By complicated, we mean that the individual has an associated structural or functional condition of the genitourinary tract or an underlying disease which increases the risk of a severe infection. 

So a complicated UTI is one that happens in a male, a pregnant female, and individuals with indwelling urinary catheters. 

Additionally, it’s considered a complicated UTI when it happens in individuals with poorly controlled diabetes mellitus, immunocompromised individuals, those with urologic conditions- like urethral strictures, and those that have had urologic procedures.

So let’s start with uncomplicated cystitis. 

The most common pathogens are Enterobacteriaceae which include Escherichia coli, Klebsiella pneumoniae, and Proteus mirabilis. 

Another pathogen is Staphylococcus saprophyticus. 

Uncomplicated cystitis usually appears in women, because they have a shorter urethra than men, making the urethral meatus closer to the anal orifice.

Risk factors for cystitis are recent sexual intercourse, as well as the use of spermicide-coated condoms, or general spermicides- because spermicides facilitate the growth of E.coli. 

Shortly after a sexual intercourse, symptoms include dysuria, urinary frequency, urinary urgency, and suprapubic pain. In females over 65 years, symptoms can include chronic dysuria or urinary incontinence. 

Now, in young women with typical symptoms, no further testing is necessary to make the diagnosis. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integrase_and_entry_inhibitors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L_vvd4K2QB_pLoFxc9N7SfCrR72gPzoC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integrase and entry inhibitors]]></video:title><video:description><![CDATA[Entry inhibitors and integrase inhibitors are groups of medications that are used in HAART, or highly active antiretroviral therapy, which is the combination of medications used in the treatment of AIDS. 

AIDS is caused by a retrovirus called human immunodeficiency virus, or HIV. 

Entry inhibitors act by preventing the binding of HIV to the CD4+ cell receptors, thereby preventing its entry into the cell. 

Integrase inhibitors inhibit the viral integrase enzyme, which is needed to incorporate the HIV proviral DNA into the host cell DNA. 

HIV is a single-stranded, positive-sense, enveloped RNA retrovirus that targets cells in the immune system that have a molecule called CD4 on their membrane. 

These include macrophages, dendritic cells, and especially CD4+ T-helper cells.

Normally, the CD4 molecule helps these cells attach to and activate other immune cells when there’s an infection. 

HIV has 2 proteins, gp120 and gp41 that form a complex on its envelope, which it uses to attach to the CD4 molecules. 

Next, it uses this complex to attach to a co-receptor on the immune cell before it can gain entry. 

The most common co-receptor that HIV binds to the CXCR4 co-receptor on T-cells; or the CCR5 co-receptor found on T-cells, macrophages, monocytes, and dendritic cells. 

When HIV binds to the CD4 and the co-receptors, the viral envelope fuses with the cell membrane of the immune cell, releasing its single-stranded RNA and some viral enzymes, like reverse transcriptase and integrase into the helpless host cell’s cytoplasm.

Once it’s inside the CD4+ cell, reverse transcriptase gets to work immediately. 

It uses the single stranded viral RNA as a template, and uses the nucleotides present in the cytoplasm of the CD4+ cell to transcribe a complementary double-stranded “proviral” DNA. 

Integrase then helps to integrate this proviral DNA into the normal DNA of the cell. 

Now it’s ready to be transcribed into new viruses, pretty sneaky, huh?

Well here’s th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anxiety_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vDQYBnVRReOTzgsRpp4QBXrgRPOEG9b8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anxiety disorders: Clinical]]></video:title><video:description><![CDATA[Normally, anxiety works to set the body on high-alert during stressful times. In anxiety disorders, these normal feelings of anxiety go into overdrive, worsening performance on the job, at school, and in relationships. Anxiety disorders are extremely common affecting up to 30 percent of adults at some point in their lives. 

Anxiety disorders are caused by a combination of genetics, stress, environmental and social factors. For example, it may be due to having a low level of the neurotransmitter GABA - which is linked to anxiety, a tough job like police work, increased caffeine intake, and going through a divorce. 

There’s also a strong correlation with trauma like humiliation, bullying, and sexual abuse, especially if it occurred during childhood. 

There’s also evidence that individuals tend to mirror the anxiety of those around them. That’s why threats to the community - like violence and global warming - are able to directly and indirectly raise anxiety. 

According to DSM-5, there are nine anxiety disorders: the archetype - generalized anxiety disorder, and the other eight illness that feature similar symptoms - separation anxiety disorder, selective mutism, specific phobia, social anxiety disorder, agoraphobia, panic disorder, substance or medication-induced anxiety disorder, and anxiety disorder due to another medical condition. 

The two key symptoms in anxiety disorders are fear and uncontrollable anxiety. Fear is the emotional response to a real or perceived imminent threat, whereas anxiety is the anticipation of a future threat. 

Fear causes a fight or flight response when your life is threatened, while anxiety is often associated with feelings of imminent danger and causes avoidant behaviors. For example, fear is what you might feel during an exam, while anxiety is the dread you may feel the night before the exam.

Fear and anxiety can easily get out of hand and turn into panic attacks. Panic attacks are short uninterrupted periods of up to t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Can_a_smartphone_app_help_you_quit_smoking</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hbjohtSOQUSlRJHSVmATTs1vRrKTGgcu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Can a smartphone app help you quit smoking]]></video:title><video:description><![CDATA[We all know that smoking cigarettes is dangerous, and quitting smoking is one of the best things you can do for your health. 

The problem is quitting nicotine is extremely difficult. 

But now, there’s a new tool to help people quit—smartphones. 

The appeal of smartphones is that they are on a person’s body almost all the time and they can serve up apps to people around the world. 

But can a digital app actually help you quit smoking irl? 

To address this question researchers ran a full-scale, long-term, global trial to see how effective a smartphone app is at helping someone quit smoking.

The trial worked like this: over a 5-month period, an app designed to help you stop smoking was available for a free download in the Apple App Store in the USA, UK, Australia, and Singapore. 

The study focused on people over age 18 who smoked daily—some of these people were randomized into an intervention group that received a version of the app that had features designed to help them quit, while other people were randomized into a control group that received a version of the app that only gave them unstructured information about quitting smoking. 

Both versions of the app recorded the date that a person quit smoking and then followed-up with their progress after 24 hours, 10 days, 1 month, 3 months, and 6 months. 

The 1 month follow-up was considered the primary outcome of the study. 

The study was double-blinded—meaning that neither the participants or the researchers knew which group they were in. 

Now the app designed to help smokers quit had four main features. 

First, it gave them a decision-aid feature that guided the user through the risks and benefits of different quitting strategies—like nicotine replacement therapy, or hypnosis—to help the user decide which strategy interested them the most so that they could use it along with the app. 

Second, the app sent out push notifications like daily motivational messages. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Helping_a_patient_with_a_rare_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZtauVUlmRvWZMoe7bNVTDv8sR6OOL_Cl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Helping a patient with a rare disease]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Helping a patient with a rare disease through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bowel_obstruction:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K37Fig3-RXiUztTscTXlwVldTAqBba8Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bowel obstruction: Clinical]]></video:title><video:description><![CDATA[Bowel obstruction is when the normal flow of contents moving through the intestines is interrupted. 

Bowel obstruction can be defined as partial or complete. 

Partial obstruction is when gas or liquid stool can pass through the point of narrowing, while complete obstruction is when no substance can pass - and this is defined as obstipation. 

The causes of bowel obstruction can be either functional or mechanical causes. 

Functional, or adynamic causes disrupt peristalsis, which are the waves that move through the smooth muscles of the bowel walls. 

Mechanical causes are actual blockages in the large or small intestines of the bowel, and these mechanical causes are the ones that are usually treated surgically.  

Among mechanical causes, one cause of small bowel obstruction in individuals who have previously undergone surgery, are postoperative adhesions. 

Adhesions are fibrous bands of scar tissue that causes organs to attach to the surgical site or to other organs, causing the lumen of the bowel to get kinked or pinched tight in certain spots. 

Another cause of small intestinal obstructions is hernias - which is when a portion of the bowel protrudes out of the abdominal cavity and can get trapped or tightly pinched at the point where it pokes out. 

Large bowel obstructions, on the other hand, are most often due to a volvulus - which is when a loop of intestine twists upon itself, kinking off the lumen. 

Sometimes the volvulus can occur around a mass like in colorectal cancer. 

Other mechanical causes of both small and large bowel obstruction include inflammatory bowel disease which can cause strictures and adhesions, ingestion of a foreign body which can get lodged along the gastrointestinal tract, and intussusception - which is where a part of the intestine folds into the lumen of an adjacent section of bowel.

One unique situation is called a closed-loop obstruction, and it’s where the intestine is obstructed at two location]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Trauma-_and_stressor-related_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7nYZYHDEQHintAuVeIX5Itf9RYGB9myo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Trauma- and stressor-related disorders: Clinical]]></video:title><video:description><![CDATA[Everyone experiences trauma at some point in their lives, and most of the time, with support from loved ones - people are able to recover. 

But in individuals with trauma and stressor-related disorders like post-traumatic stress disorder, these experiences lead to symptoms like flashbacks and nightmares, hypervigilance, and aggressiveness - all of which can profoundly impact their life in a negative way. 

Trauma and stressor-related disorders are thought to be caused by a combination of genetics, biological factors, and environmental factors. 

The genetic link is based on the fact that those with a family history of mental issues tend to develop the disorders more frequently. 

Biological factors include high levels of stress hormones like adrenaline and cortisol, even in the absence of stressful situations. 

Environmental factors include things like family neglect in early childhood or jobs with high trauma exposure like being a fire-fighter or soldier. That’s because repeated trauma increases the risk of trauma and stressor-related conditions.

Trauma can be thought of as an overwhelming amount of stress that exceeds one’s ability to cope or process the emotions involved with that experience. 

A traumatic event can involve one or repeated experiences over time. 

For example, the experiences include things like serious road accidents, poverty, neglect in early childhood, military combat, and sexual abuse. 

Psychological distress following a traumatic event most commonly causes anhedonia or lost interest in activities that were once enjoyable and a decreased ability to feel pleasure, dysphoria or a profound state of unease or dissatisfaction, externalized anger or aggression, and dissociative symptoms such as detachment from reality or self. 

Most individuals develop depression, anxiety, and have problems with substance abuse which is often a way to self-medicate symptoms. 

For diagnosis, the symptoms should cause distress and prevent in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Schizophrenia_spectrum_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WVyNRgAjSOaJNmzGamE8CpdwSwWb5BU5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Schizophrenia spectrum disorders: Clinical]]></video:title><video:description><![CDATA[Psychotic disorders are a group of conditions - including schizophrenia - that are characterized by individuals having difficulty thinking clearly, making good decisions, distinguishing reality from imagination, and behaving appropriately. 

This makes it very hard to handle daily life and social interactions, and if symptoms go untreated, individuals are at risk of harming themselves.

The underlying pathophysiology is still mostly a mystery, but there are some clues. Some psychotic disorders such as schizophrenia run in families, which suggests a genetic basis, and it’s also thought to be related to trauma, drug abuse, stress, infections, and autoimmune disorders.

Another clue is that some individuals benefit from antipsychotic medications which block the dopamine receptor D2, which suggests that for those people, excess dopamine levels may contribute to the disease. 

In fact, interestingly, one of the most effective antipsychotic drugs, clozapine, is a weak D2 antagonist. 

Now, according to DSM-V, psychotic disorders include seven main disorders distinguished by the duration and severity of symptoms, and the presence of mood episodes - either depressive, manic or hypomanic ones. 

Depressive episodes persist for a two-week period and consist of diminished interest or pleasure in activities, significant weight loss or gain, inability to sleep or oversleeping, psychomotor agitation, feelings of worthlessness, decreased ability to think, and finally recurrent thoughts of death, or suicidality. 

Manic and hypomanic episodes feature symptoms like grandiosity, racing thoughts, short attention, and rapid speech. 

Schizophrenia is the most common psychotic disorders. 

By comparison, conditions with less severe symptoms include schizotypal personality disorder, delusional disorder, and brief psychotic disorder. 

On the flip side, there are the conditions with more severe symptoms like schizophreniform disorder, schizoaffective disorder]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obsessive_compulsive_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w0U2grsbRvuaz1-kA20pNrrNS6_pcrT7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obsessive compulsive disorders: Clinical]]></video:title><video:description><![CDATA[We all have unwanted thoughts at times that we can’t just shake off. And we also have things we want to do only in a particular way - no matter if we’re talking about washing dishes or superstitions. 

But individuals with obsessive-compulsive disorder or OCD and related disorders, like hoarding disorder, experience these obsessive ways of thinking and acting in such an extreme way that it causes distress and begins to negatively impact their lives.

The causes of obsessive-compulsive disorders are not fully understood, but there are a number of risk factors. 

Biological factors include hormonal imbalances, neurologic conditions,  and having a family history of OCD, confirming a genetic component. 

Psychological factors include trauma like sexual abuse or bullying early in life, and environmental factors include streptococcal infections, stress, and an unhealthy lifestyle. 

Now, according to DSM-5, the most common disorder is obsessive-compulsive disorder. 

The other 8 include hoarding disorder, body dysmorphic disorder, trichotillomania or hair-pulling disorder, excoriation or skin-picking disorder, substance or medication-induced obsessive-compulsive and related disorder, and obsessive-compulsive and related disorder due to another medical condition. 

The last two are: other specified obsessive-compulsive and related disorder and unspecified obsessive-compulsive and related disorder, which are reserved for symptoms that don&amp;#39;t fit any of the main disorders.

In terms of symptoms, the group is mainly characterized by obsessions and compulsions.

Obsessions are repeated, persistent, and unwanted thoughts, urges, or mental images that are intrusive and cause distress or anxiety. 

They are hard to get rid of and usually disappear only after performing a certain action or series of actions called compulsions. 

Compulsions are repetitive actions like hand washing or mental acts such as praying, counting, or repeating words silently that the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_surgical_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/57pt88I9TP6jdpkPc1Ob_frYTLqhW5DS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal surgical conditions: Clinical]]></video:title><video:description><![CDATA[You can think of the esophagus as a 25 to 30 centimeter long tube, that has a wall composed of 4 layers. 

The esophageal mucosa is made of different layers, there’s an inner stratified squamous epithelium layer, the submucosa, a muscular layer that’s made of skeletal muscle in the upper third, smooth muscle in the lower third, and a combination of the two in the middle; and finally an outer layer of connective tissue called adventitia.

At the top and bottom of the esophagus there are the upper and lower esophageal sphincter, respectively. 

Both relax during swallowing to allow the passing of food or liquids propelled by peristaltic contractions. 

Additionally, the lower esophageal sphincter prevents acid from refluxing back into the esophagus between meals.  

There are three main ways to evaluate the esophagus. 

First, there’s an upper gastrointestinal tract radiography or a Barium swallow which uses orally ingested barium as contrast for an X-ray of the esophagus, stomach, and duodenum. 

Second, there’s an upper endoscopy which is when a flexible tube with a camera is sent through the mouth to visualize the esophagus, stomach, and duodenum - and take a biopsy if needed. 

Third, is esophageal manometry which is where a pressure-sensitive catheter is inserted through the nose and sent into the esophagus to measure the strength of peristaltic contractions, esophageal sphincters contractions during swallows. 

There are two types of esophageal manometry. 

In Classical manometry there are 4 to 8 pressure sensors placed at different levels of the esophagus and a normal reading looks something like this. 

In high resolution manometry there are more pressure sensors and the reading is color coded and looks like a surface map, where red indicates the strongest contractions, and blue indicates the weakest contractions, so that it looks something like this.

There are a number of esophageal conditions that can be treated surgically. 

First, there’s Z]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UbrNQmS6T2WtvIpjsYmGpcfTQ22JIlIl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breast cancer: Clinical]]></video:title><video:description><![CDATA[Breast cancer, or breast carcinoma, is an uncontrolled growth of epithelial cells within the breast. 

It’s the most common cancer in women, but can rarely affect men as well. 

Now, estrogen and progesterone stimulate breast cells to grow and divide, and exposure to them over long periods of time increases the risk of breast cancer. 

More menstrual cycles over a lifetime means a higher cumulative exposure to these hormones. That’s why factors that increase the number of menstrual cycles increases the risk of breast cancer. 

That includes things like early menarche, or a first menstrual bleeding before 11 years of age, and late menopause, after 54 years of age. 

On the flip side, some factors that are associated with fewer lifetime menstrual cycles - like pregnancy and a longer time breastfeeding - decrease the risk of breast cancer. 

Similarly, hormone replacement therapy used to treat menopause symptoms, also increases that risk. 

Another risk factor is exposure to ionizing radiation, like from chest X-rays and CT scans or previous radiation therapy for other cancers located in the chest. 

Breast cancer has been linked to mutations in tumor suppressor genes, like BRCA1, BRCA2, and TP53, which normally prevent uncontrolled cell division. 

Some breast cancers have mutations in the ERBB2 gene which causes an increase in human epidermal growth factor receptor 2, or HER2, which promotes cell division. 

Finally, some breast cancer cells have estrogen or ER receptors and progesterone or PR receptors, which allow them to divide faster in the presence of these hormones. 

Breast cancer is the second leading cause of cancer deaths in women after lung cancer, and this is largely due to the fact that breast cancers often don’t cause pain or discomfort until they’ve metastasized.

Now, breast self-examination isn’t recommended for screening purposes, because it hasn’t shown an overall benefit. 

In fact, it’s led to a higher rate of breast biop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kidney_stones:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BndMzxyzR9CJ2zgo3_7Q0du7R-2RYvhK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kidney stones: Clinical]]></video:title><video:description><![CDATA[Kidney stones, also called nephrolithiasis, urolithiasis, or renal calculi, can form in the kidneys, but also in the ureters, bladder, or the urethra. 

They appear when solutes in the urine precipitate and crystalize. Depending on which solute precipitates to form the stone, there can be calcium oxalate, calcium phosphate, uric acid, cystine, and struvite stones. 

Risk factors for developing kidney stones depend on their composition. 

Risk factors for calcium oxalate stones include high urine calcium, high urine oxalate, low urine citrate, and dietary factors include low calcium, low potassium, and low fluid intake, as well as a high oxalate, and a high animal protein intake. 

Calcium phosphate stones usually develop in individuals with renal tubular acidosis type I and II. 

Uric acid stones can form when urine pH is persistently below 5.5, which can happen with chronic diarrhea or conditions like gout, diabetes, and obesity. 

Cystine stones occur in the setting of cystinuria - a genetic condition where too much cystine is excreted. 

Finally, struvite stones, also called staghorn calculi, are made up of magnesium ammonium phosphate, and the main risk factor is a urinary tract infection with a bacterium that produces urease - like Proteus and Klebsiella. These bacteria increase urine pH, making it a favorable environment for magnesium ammonium phosphate to precipitate.  

Sometimes, kidney stones can be asymptomatic and discovered incidentally during an ultrasound or a CT-scan. 

Other times a kidney stone can cause symptoms due to urinary obstruction and renal distention.

It can cause renal colic, which is when there’s acute pain that’s so intense that it requires IV pain medication. 

Passing a large stone through a narrow ureter has been compared to passing a baby’s head through the vaginal canal! The difference is that you don’t have to raise and nurture the stone once it passes. 

In renal colic, the location of the pain depends on where the st]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinician's_Corner:_Endocarditis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0gdLUaSSQ06pREwySbMsPj3GRfufMvUC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinician&apos;s Corner: Endocarditis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinician&apos;s Corner: Endocarditis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Can_using_a_range_hood_decrease_your_chance_of_having_an_asthma_attack</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pHxdJ_yAQBydanGUnJCTyH8USb2IypAQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Can using a range hood decrease your chance of having an asthma attack]]></video:title><video:description><![CDATA[In the United States alone roughly 24 million people, including 6 million children, have asthma, and air pollution is a known trigger for asthma attacks. 

That’s because microscopic particles, called particulate matter, float around in the air, get breathed in and irritate the airways. 

The most obvious air pollution, like city smog or wildfire smoke, is outdoors, and being exposed to higher levels of outdoor particulate matter is known to cause higher levels of asthma. 

That said, on average, Americans are spending over 80% of their day indoors. 

So indoor air pollution is important to consider as well. 

The most obvious cause of indoor air pollution is second-hand smoke from cigarettes—which is a major risk factor for asthma—but it can also come from dust, mold, pet dander, air conditioners, and cooking. 

Now, cooking habits differ from one region to another.

For example, cooking over open fires indoors is common in some parts of the world, and improving ventilation in those situations can improve asthma. 

But what about cooking over modern stovetops? Well, it turns out that cooking over a stovetop definitely produces airborne particles—just consider what it’s like to clean grease off the stovetop after cooking bacon. 

But is it enough particulate matter to trigger asthma? 

Well, a study was done that looked at household behaviors, particulate matter levels, and asthma severity. 

The study included 35 low-income households in the San Francisco Bay Area that had children, between the ages of 6 and 10 years old, with asthma, but no other major illness.

To measure particulate matter levels, particle sensors were placed in the main living area of each home and they measured the air every five minutes over the course of a month. 

A temperature sensor was placed next to the stove, to know when the stove was on, so that air quality in the living area could be compared to stove use. 

Asthma severity was measured using standardized interviews and by]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Increasing_daily_physical_activity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iJ0EFSlCTxadZwEYe5WH9WVhRkeDgOQw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Increasing daily physical activity]]></video:title><video:description><![CDATA[Our lives are becoming more and more sedentary.

Most of us have jobs that are sedentary, and we spend more time in the car or in front of screens than ever before. 

To combat this, some people have started to try to increase their daily step count. 

But it can be hard to stay motivated over time. 

So researchers set out to figure out how to best motivate people that are trying to increase their daily step count. 

They first compared setting a static goal, which is where there’s one step count goal that doesn’t change, to setting an adaptive goal, which is where the goal changes based on how active a person has recently been. 

They also compared giving cash rewards immediately after a person reaches a goal, to giving cash rewards months later for just participating in the study.  

The researchers recruited 96 overweight and inactive adults and had them wear pedometers while they were awake and recorded their daily step counts at baseline for about 10 days. 

So from day 1 to day 10, individuals in all four groups instructed to not change their daily behaviors so the researchers could get a feel their usual routine. 

Now, on day 11 of the study, which was the beginning of the intervention phase all participants were sent an email that encouraged them to strive for an ultimate target of 10,000 steps per day on at least 5 days a week. 

They were then randomized into four groups: an adaptive goal and immediate reward group, an adaptive goal and delayed reward group, a static goal and immediate reward group, and a static goal and delayed reward group. 

Individuals in each of these four groups were then monitored for an additional 110 days—a little under 4 months.

For the two static groups, 10,000 steps a day remained the goal for the rest of the study. 

The adaptive goal groups, however, were given daily goals based on a person’s step counts for the last 9 days. 

More specifically, they took the step counts over the prior 9 days, ordered them lowest]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacokinetics:_Drug_elimination_and_clearance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-jgJrjiTRvqngqQjN2gfELclTqmBL_5o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacokinetics: Drug elimination and clearance]]></video:title><video:description><![CDATA[Pharmacokinetics refers to the movement and modification of medication inside the body. 

Or more simply, it’s what the body does to this medication and how it does it.

Alright, so once the medication is administered, it first has to be absorbed into the circulation, then distributed to various tissues throughout the body, metabolized or broken down, and finally, eliminated or excreted in the urine or feces. 

You can remember this as ADME- Absorption, Distribution, Metabolism, and Excretion.

Okay, now let’s focus on a process called elimination, which is often confused with the process of excretion. 

Elimination is the removal of a medication from the body.  

Now this can be accomplished through metabolism, where the medication is broken down into inactive metabolites, or through excretion which is when the intact medication is transported out of the body.  

This can happen through a number of ways, but the most common route is through urination. 

So, the major function of the kidneys is to clear metabolic waste material and foreign substances, like medications, from the body by filtering the blood.  

Now, zooming in on a nephron’s tubule, each one is lined by cells that have two surfaces. 

One is the apical surface, which faces the tubular lumen, and the other is the basolateral surface, which faces the peritubular capillaries, which run alongside the nephron.

Alright, so first, certain medications in the circulation can be filtered out with the other metabolic wastes when the blood goes through the glomerulus. 

Second, as the filtrate makes its way through the proximal convoluted tubule, certain medications from the peritubular capillaries get secreted into the tubular lumen. 

For polar, water-soluble medications, this is mainly done actively through active secretion, meaning that it requires specific carrier proteins on the basolateral membrane of the tubular cells, which uses ATP for energy. 

Non- polar, lipid- soluble drugs, on the other ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abdominal_pain:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/B2TduLjNQUKg5gfpSh50ugdEQ4e6zp_e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abdominal pain: Clinical]]></video:title><video:description><![CDATA[Abdominal pain is a very common complaint, and the differential diagnosis is wide, ranging from benign to life-threatening conditions. Life-threatening conditions include a ruptured abdominal aortic aneurysm, mesenteric ischemia, perforation anywhere along the gastrointestinal tract, acute bowel obstruction, acute pancreatitis, peritonitis, ectopic pregnancy, ovarian torsion, and myocardial infarction.

There are three main types of abdominal pain: visceral, parietal, and referred pain. Visceral pain happens when the nerves that run through the walls of an organ get stretched. The pain isn&amp;#39;t usually well localized and feels like a dull ache or cramp. Hollow organs cause an intermittent colicky type of pain, whereas solid organs cause a more constant pain. 

Sometimes, as a disease evolves, visceral pain can become parietal pain, which is also called somatic pain. That’s the pain that results from irritation to the parietal peritoneal wall. Parietal pain is sharp and can be localized by pointing to a specific spot. Finally, there’s referred pain which is when the brain mistakenly identifies pain as coming from one region like the shoulder when it’s actually coming from a different region like the diaphragm.

Abdominal pain can often be separated into the abdominal area that’s involved. Foregut organs - so the stomach, duodenum, pancreas, and biliary tract - cause epigastric pain. Epigastric pain that’s associated with bloating, abdominal fullness, heartburn, or nausea is called dyspepsia, and it’s generally due to gastroesophageal reflux disease, gastritis, pancreatitis, or peptic ulcer disease - meaning an ulcer of the stomach or duodenum.

Left upper quadrant pain can overlap with the causes of epigastric pain, like pancreatitis which causes pain that radiates to the back, but may also be due to the spleen. Right upper quadrant pain generally involves the liver or biliary tree, like acute hepatitis, gallstones, or acute cholecystitis, but it may ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hernias:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zIBtBrbnRJWVBJcXHAvsoOT5RHuC1X5M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hernias: Clinical]]></video:title><video:description><![CDATA[A hernia is when an organ protrudes or bulges out through the body wall that normally contains it.

So an abdominal wall hernia is when an organ protrudes through the abdominal wall, which is made up of a few layers. 

The deepest layer is the visceral peritoneum, which covers many of the abdominal organs, and lines the peritoneal space. 

That layer wraps around to form the parietal peritoneum.

Then moving outwards, there’s the extraperitoneal fat, the transversalis fascia, the muscle layer with the internal and external oblique and transversus abdominis aponeurosis, and a layer of fascia, which has different names in different regions. 

Anything that increases the pressure of the abdominal cavity may result in a sac that forms in the abdominal wall through which organs may protrude. 

The organ that’s usually involved in a hernia is the gastrointestinal tract, but it can also involve other organs like the omentum, the bladder, and even the ovary. 

Abdominal hernias vary in size and location. 

Small hernias can be asymptomatic or they can cause pain and create a small bulge that can worsen with increased abdominal pressure from coughing or straining. 

Over time, hernias can grow and lead to bowel obstruction, causing severe pain, nausea, vomiting, or constipation.

Larger hernias can put pressure on the overlying skin, causing erythema and ulceration.

Generally speaking, there are four types of abdominal wall hernias - groin, ventral, pelvic, and flank hernias. 

The most common type are groin hernias, and they occur at the lower margin of the abdomen where the thigh meets the hip. 

Groin hernias are classified into inguinal and femoral hernias, and inguinal hernias are further classified into direct inguinal and indirect inguinal hernias. 

Direct inguinal protrude medial to the inferior epigastric vessels within Hesselbach&amp;#39;s triangle, which is formed by the inguinal ligament inferiorly, the inferior epigastric vessels laterally]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dizziness_and_vertigo:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h6aYofkGTmmY5t8PrWysekdGT6OISwvI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dizziness and vertigo: Clinical]]></video:title><video:description><![CDATA[The term “dizziness” can be used to refer to a number of related symptoms like presyncope, disequilibrium, what’s called “non-specific dizziness”, and vertigo. 

Asking individuals specific questions about how they experience dizziness can help clarify the symptom. Let’s go through each of these. 

Pre-syncope is the prodromal phase that occurs before syncope. 

Individuals often complain of seconds to minutes of “nearly blacking out” or “nearly fainting”, and “feeling lightheaded when standing,” along with palpitations, sweating, a feeling of warmth, nausea or even blurry vision. Sometimes there’s a history of cardiac disease, such as congestive heart failure or coronary artery disease may be present. 

Presyncope could be due to vasovagal syncope, orthostatic hypotension, or cardiac arrhythmias, so the workup usually includes an electrocardiogram, or ECG. 

Disequilibrium refers to a sense of imbalance specifically while walking, and usually is due to neurologic disorders like Parkinson’s disease, cerebellar disorders, peripheral neuropathy, or cervical spine disease. 

This is often described as “feeling the ground moving” or “feeling like you’re on a boat”. 

Non-specific dizziness is a more vague term that has a variety of causes ranging from anxiety or panic attacks, to hypoglycemia, or side effects of medications like anticholinergics. 

Finally, there’s vertigo which can be thought of as having an illusion of self-motion, or movement of the surrounding environment. 

We’ve all experienced vertigo. It’s that spinny sensation you get after swinging a small child around or the woozy feeling of seasickness. Yeah, that’s vertigo. 

Vertigo arises when there’s a mismatch between other sensory systems and the vestibular system. 

The vestibular system is made of the vestibular apparatus; including the three semicircular canals, the utricle and saccule, the vestibular nerve, and the vestibular structures in the brainstem and cerebellum. 

Vertigo can be br]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_tackle_your_first_semester_of_medical_school</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7TDtvApNQ3GoKvIp1-JUiODYRAeX1wwJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to tackle your first semester of medical school]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to tackle your first semester of medical school through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_succeed_in_the_NRMP®_match</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1xnHURovS7OmwLOk4Zk_FqD6TUCjZcyJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to succeed in the NRMP® match]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to succeed in the NRMP® match through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Can_a_positive_mindset_help_treat_peanut_allergies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9Fs6qh0jTl_BLkxoAQ8Eyx7RTFG6yeTl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Can a positive mindset help treat peanut allergies]]></video:title><video:description><![CDATA[Peanut allergies are a common and severe type of food allergy. 

In people who are allergic, peanuts can cause skin reactions, itching in the mouth and throat, digestive problems, shortness of breath, and even anaphylaxis, which requires a shot of adrenaline with an EpiPen and a trip to the emergency room. 

A promising treatment for peanut allergies is oral immunotherapy—and the way it works is by giving someone with the allergy tiny traces of peanuts and increasing the dose gradually over time so that they can slowly get desensitized to them.

Doing this can trigger mild symptoms, and sometimes those symptoms make a person quit the treatment, but the symptoms may actually be a sign that the treatment is working. So how these mild symptoms are perceived really matters. 

To better understand how patients’ perception of these mild symptoms can affect the outcome of the treatment researchers recruited 50 families with children aged 7 to 17 years old with peanut allergies, who were about to undergo oral immunotherapy. 

The families were randomized into two groups. 

In the first group, the families were told that the mild symptoms should be interpreted as evidence that the treatment is working.

In the second group, the families were told that the symptoms were an unfortunate side effect of the treatment. 

Families came for a total of 8 visits over the course of seven months, to participate in small-group activities that are related to the treatment. 

At each of these visits the messaging about the mild symptoms was reinforced. 

Importantly, both groups were given identical instructions for oral immunotherapy and training in recognizing dangerous side-effects and how to use an EpiPen. 

They also had equal access to helpful resources like over-the-phone staff support. 

The only difference between the groups was the messaging about the symptoms. 

At the end of the study, the researchers asked the families about their views on the symptoms, and looked at]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Empathetic_listening_for_clinicians</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UDjC0OBiShKlTbKlN0NcCn7nQ1_NcON8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Empathetic listening for clinicians]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Empathetic listening for clinicians through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Third-year_medical_student_explains_how_to_set_up_an_Osmosis_Study_Schedule</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jYMbjvkiRA6aFsvx4DcHHEaaR5m_11tl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Third-year medical student explains how to set up an Osmosis Study Schedule]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Third-year medical student explains how to set up an Osmosis Study Schedule through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Knowledge_Shot:_Why_we_should_care_for_our_caregivers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5cHNUh6CS8iA5M6minYRPPZiQkekSQDA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Knowledge Shot: Why we should care for our caregivers]]></video:title><video:description><![CDATA[In January 2019, Medscape released their annual National Physician Burnout, Depression, and Suicide report and found that 44% of the 15,000 physicians surveyed felt burned out, that’s a 5% increase from the 39% they saw in their 2013 survey. 

Another study by Mayo Clinic researchers found a 9% increase in burnout among physicians from 2011 to 2014. 

Currently, there are 300 to 400 physicians who die by suicide each year, a rate that’s nearly double that of the general population. 

To be honest, even the term ‘burnout’ itself is problematic, because it inaccurately represents these feelings of demoralization, physical and emotional exhaustion often felt by caregivers. 

The term ‘burnout’ suggests that individual caregivers are ‘breaking’ as a result of individual character flaws like not being resilient or hard-working enough, rather than as a result of a health care system that is broken and overstretched. 

Often the realities of the healthcare system - limited access for the poor, layers of paperwork and bureaucracy, and inadequate time for meaningful conversations contradict the morals and values of the caregivers within that system. 

So instead of “burnout” the term “moral injury”, recently suggested by Dr. Zubin Damania, more accurately and honorably describes the demoralization and exhaustion felt by these caregivers.  

Based on these reports, the medical community has taken a closer look at exactly how early in a clinician’s training moral injury begins to appear. 

The results are not encouraging.

A recent review found that around 44% of medical students around the world feel moral injury. 

Another review found that 29% of residents had a major depressive episode during training as compared to 8% of similarly aged individuals in the general population. 

Similarly, a study of nearly 1,200 inpatient nurses found that the depression rate was 18%, roughly twice that of the general population. 

Yet another study found that 20% of employed fema]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_hemorrhage:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/imxSRrbdSiS6z8CA9tQ2nRQfTpKZE-fI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postpartum hemorrhage: Clinical]]></video:title><video:description><![CDATA[Postpartum hemorrhage is worrisome when more than 500 milliliters of blood are lost after a vaginal delivery, or more than 1000 milliliters of blood are lost after a C-section.

Postpartum hemorrhage usually occurs in the 24 hours following delivery, in which case it’s called early, or primary postpartum hemorrhage.

But in rare situations, it happens later than 24 hours after delivery, and that’s where it’s called late, or secondary postpartum hemorrhage.

Postpartum hemorrhage, like any ongoing bleeding, can be classified according to the degree of hypovolemia and vital signs status.

Stage 1 is when 500 to 1000 milliliters of blood have been lost. Blood pressure is usually normal, but there may be palpitations, tachycardia and slight dizziness.

Stage 2 is when 1000 to 1500 milliliters have been lost. Systolic blood pressure drops to 80 to 100 mmHg, tachycardia is obvious, and there may be weakness and sweating.

Stage 3 is when 1500 to 2000 milliliters have been lost. Systolic blood pressure drops between 70 and 80 mmHg, and there may be restlessness, pallor and low urine output.

Finally, stage 4 is when more than 2000 milliliters have been lost, systolic blood pressure is less than 70 mmHg, and symptoms may include cardiovascular and respiratory collapse, loss of consciousness and and anuria.

Now, before elucidating the cause, some immediate measures should be taken in order to compensate the blood loss. These follow an A-B-C pattern.

A stands for airway, so you’ll want to protect the airway, especially when there’s loss of consciousness.

B stands for breathing, so you’ll want to administer Oxygen through a non-rebreather mask.

C stands for circulation - meaning measuring vital signs and establishing the degree of hypovolemia, inserting two large caliber peripheral IV catheters - of at least 14 gauge or even larger-gauge -, and starting fluid resuscitation immediately, with 500 milliliters of normal saline or lactated Ringer’s solution given over]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertensive_disorders_of_pregnancy:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R8kruoDoQuCAtjRNgyIC0SZSTCOXCFii/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertensive disorders of pregnancy: Clinical]]></video:title><video:description><![CDATA[Hypertensive disorders of pregnancy are diseases that cause high blood pressure during pregnancy - either a systolic blood pressure higher than 140 mmHg, or a diastolic blood pressure higher than 90 mmHg, or both. To make the diagnosis, two separate blood pressure measurements taken at least 4 hours apart have to be elevated. 

Hypertensive disorders of pregnancy are organized by their time of onset and the presence of proteinuria. 

Before 20 weeks gestation, chronic hypertension is usually the cause of hypertension, and there isn’t usually proteinuria. 

Chronic hypertension in pregnancy requires antihypertensive medication when systolic blood pressure is over 160 mmHg, or when diastolic blood pressure is over 110 mmHg, and options include labetalol, nifedipine or methyldopa, with a goal to get blood pressure below 150 over 100 mmHg. 

Delivery is recommended between 38 and 40 weeks of gestation in females not requiring medication; between 37 and 40 weeks for females with hypertension controlled with medication, and between 36 and 38 weeks for females with severe and difficult to control hypertension. 

After 20 weeks gestation, the possible causes are gestational hypertension, which doesn’t cause proteinuria, and preeclampsia and eclampsia, both of which do cause proteinuria.

Gestational hypertension is relatively benign, but many females with gestational hypertension progress to developing preeclampsia. 

Females with non-severe gestational hypertension, meaning less than 160 over 110 mmHg, can be managed as outpatients, with weekly or twice weekly follow-up visits to measure blood pressure and protein excretion. 

Females are instructed to monitor their blood pressure and fetal kick count daily, and at each visit starting at 32 weeks of gestation, a fetal ultrasound, a non-stress test or NST should be done, and  sometimes a biophysical profile is indicated. 

On an ultrasound, fetal growth and the amount of amniotic fluid can be estimated.

An NST is]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Personality_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ngu6ixPpR2_mvIxHKtPS6OmlQYWtwUD0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Personality disorders: Clinical]]></video:title><video:description><![CDATA[If you were to describe a friend’s personality, you might say they are creative, or easy-going but nervous in groups. Basically, you’re summarizing the personal traits that make them who they are—either how they think or how they act. 

Sometimes these thought patterns or behaviors which make up a person’s personality can actually be harmful in the sense that they interfere with their day-to-day functioning in their personal life, at work, or in social settings. If this were the case, we would say that the individual has a personality disorder.

Now to diagnose a personality disorder, there are general criteria as well as features specific to the individual personality disorders. 

The first general criteria for personality disorder is the presence of a constant pattern of inner experience and behavior that deviates substantially from the cultural norm, manifested in two or more of the following four areas: cognition - like, for example, deviations in the ways individuals perceive themselves, other people or events; affectivity such as changes in the range, intensity, and appropriateness of emotional responses; interpersonal functioning; and impulse control. 

Second, this pattern is inflexible and present in most personal and social situations, including relationships, work and school. 

And lastly, the pattern is stable, of long duration, and its onset is in adolescence or early adulthood. 

The patterns should not be attributable to a substance like alcohol or another medical condition.

The DSM-5 lists ten personality disorders that are split into clusters A, B, and C. 

Alright so cluster A personality disorders include paranoid personality disorder, schizoid personality disorder, and schizotypal personality disorder.

In paranoid personality disorder, there’s distrust and suspiciousness of others, which make individuals think that everything people do in relation to them is malevolent. This is shown by at least four of the following seven patterns. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ovarian_cysts,_cancer,_and_other_adnexal_masses:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HJKPCwSVR5OvuHijwjSgRw-uQD_tgFZD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovarian cysts, cancer, and other adnexal masses: Clinical]]></video:title><video:description><![CDATA[Adnexal masses can affect the ovary or the fallopian tube. They can develop in females of all ages, and can be discovered incidentally during a pelvic ultrasound, or when they cause symptoms like pain or pressure on the affected side.

When encountering an adnexal mass the  first step is to assess whether or not it’s a medical emergency, and, if it’s not, whether the mass is benign or malignant. 

Medical emergencies are adnexal masses that cause severe and abrupt pain, along with other symptoms like nausea, vomiting, fever, or vaginal bleeding. 

In addition, any kind of pelvic pain or bleeding in a pregnant female during her first trimester is considered a medical emergency - so the first step is to get a pregnancy test. 

If the pregnancy test is negative, the likely causes are ovarian torsion, a ruptured ovarian cyst, and a tubo-ovarian abscess.

In ovarian torsion, the ovary twists around the suspensory ligament, which suspends the ovary and contains the ovarian blood vessels within it. 

Risk factors include an ovarian mass - like a cyst or cancer, and an ovary greater than 5 centimeters in diameter. 

In both cases, twisting the vessel cuts of the blood supply to the ovary - causing ovarian ischemia. 

An ultrasound may show that one ovary is larger than the other one, because of edema and blood pooling up in the ovarian veins, and the affected ovary might look like a twisted mass. 

A Doppler ultrasound shows decreased or absent blood flow within the ovary, and the “whirlpool sign” may be present, which is when blood flow inside the ovarian vessels seems to flow in a spiral around a central axis.

Urgent surgical detorsion of the ovary is required to avoid ischemic injury and loss of the ovary and fallopian tube. 

Ovaries that are hemorrhagic or edematous are more likely to be viable, than necrotic appearing ovaries. 

If the ovary can’t be saved, a unilateral salpingo-oophorectomy is often done. That’s where the affected ovary and fallopian tube ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anal_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fkVXU3BuQ7qKFpPYUvXRXBQgSp2Z2Qmr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anal conditions: Clinical]]></video:title><video:description><![CDATA[The anus is the final 3 to 4 centimeters of the gastrointestinal tract, and it extends from the rectum to the anal margin. 

The top and bottom of the anal canal are surrounded by the internal and the external anal sphincters, which are two muscular rings that control defecation. 

The internal sphincter is under involuntary control, while the external sphincter is under voluntary control. 

Within the anal canal, there are mucosal membrane infoldings that form the anal columns. 

And at the base of these columns, there is the dentate or pectinate line, which divides the upper two thirds and lower third of the anal canal. 

Above the dentate line, there’s the mucosa is lined by simple columnar epithelium, and below the dentate line, there’s the anoderm, which has no hair and sebaceous and sweat glands, and is lined by squamous epithelium.

Now, hemorrhoids are normal vascular structures in the anal canal that act as cushions for the stool as it passes through. 

Hemorrhoidal disease is when hemorrhoids get swollen or inflamed; but the term &amp;quot;hemorrhoid&amp;quot; is often used to refer to the disease. 

Hemorrhoids are often caused by chronically or recurrently increased abdominal pressure, from a variety of causes. 

For example, straining during bowel movements, chronic diarrhea or constipation, obesity, pregnancy, and old age. 

Complications of hemorrhoids can include anemia due to chronic blood loss; strangulation if the blood supply to an internal hemorrhoid is cut off, leading to ischemia; and thrombosed hemorrhoids, which is when blood pools inside a hemorrhoid and forms clots. 

Internal hemorrhoids are ones above the dentate line, and external hemorrhoids are ones below the dentate line. 

Internal hemorrhoids are subclassified into four grades based on the degree of prolapse from the anal canal. 

Grade I hemorrhoids don’t protrude outside the anal canal. 

Grade II hemorrhoids protrude outside the anus during bowel movement, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_upper_airway_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/phsdXke0R2GstbVV3B-eYha-TwCpZJ4O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric upper airway conditions: Clinical]]></video:title><video:description><![CDATA[The upper airways include the nasal cavity, paranasal sinuses, pharynx and larynx. 

In children, the upper airways can be affected by mechanical obstruction - like in a foreign body aspiration or by a structural defect like in laryngomalacia. There can also be inflammation in these anatomic regions due to an infection. 

Let’s start with foreign body aspiration, which most commonly occurs in young toddlers who get something like a small coin or a peanut, lodged in their respiratory tree. 

Most of the time, the foreign body goes into the lower respiratory tract, because of gravity and because that main bronchus is a bit larger. But if it’s large and unlucky enough to get stuck in an upper, larger airway, then symptoms are more severe. 

Typically, if there’s a partial upper airway obstruction, children begin coughing, gagging, choking, or drooling, and on auscultation, there’s inspiratory stridor. 

But, if there’s a complete obstruction, children may be unable to cough or speak and can even pass out. And in this case, we should immediately start Basic Life Saving, or BLS maneuvers to relieve obstruction.

For infants less than one year of age, five back blows are delivered, followed by five chest thrusts. And for children one year of age or older, five abdominal thrusts or Heimlich maneuver should be performed. 

Okay, now, if the child is stable, then usually a chest Xray is done - and objects like coins and batteries are radiopaque, and are visible, whereas pieces of food are usually radiolucent, so don’t show up. 

If an upper airway foreign body aspiration is suspected, then it’s important to do a neck radiograph.

Sometimes, there are indirect signs of obstruction, like a subglottic density or swelling. 

A CT scan can also be done to confirm the suspicion. 

Alternatively, the child can be taken for laryngoscopy to visualize and remove the object. 

If the object gets lodged in the nose, there may be unilateral, foul- smelling rhinorrhea or ep]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postoperative_evaluation:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r3ovFjlEQEGw9gqrC6ZKMA9BSZquBkrf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postoperative evaluation: Clinical]]></video:title><video:description><![CDATA[The goal of a postoperative evaluation is to recognize and manage issues that arise in the immediate postoperative period.

Generally, right after any procedure requiring anesthesia, individuals are monitored in a post-anesthesia care unit or PACU for things like respiratory distress or cardiac complications.

Signs of respiratory distress include tachypnea - with a respiratory rate over 30 breaths per minute, or bradypnea - with a respiratory rate below 8 breaths per minute; SpO2 lower than 93 percent; or in severe cases cyanosis and use of accessory respiratory muscles. If there’s a concern, an arterial blood gas and a chest X-ray can be obtained.

Also cardiac monitoring is done to assess their heart rate and blood pressure, because postoperatively, individuals are at increased risk of cardiovascular complications like hypo- or hypertension, cardiac arrhythmias, myocardial ischemia, and even heart failure.

Individuals are also assessed for their mental status, temperature, pain level, neuromuscular function, ability to pass gas and stool, and presence of nausea or vomiting.

Last but not least, a person’s hydration status along with intake and output - like fluid administration, urine output, bleeding, and wound drainage - are all carefully tracked. Now, the most common postoperative complication is nausea and vomiting.

Risk factors include preoperative nausea and vomiting, female gender, having a history of postoperative nausea and vomiting or motion sickness, use of volatile anesthetics, longer duration of anesthesia, and the type of surgery, with cholecystectomy, gynecologic, and laparoscopic procedures showing slightly higher risk compared with other general surgical procedures.

To help minimize this, inhalation agents which more commonly cause those symptoms, can be avoided.

Instead, total intravenous anesthesia or TIVA can be used along with propofol, which helps with induction and maintenance of anesthesia.

In addition, preventive measures i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_adrenal_hyperplasia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bR6IfVYcTWiZE_UY_UArC4bHTNe1sDc_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital adrenal hyperplasia: Clinical]]></video:title><video:description><![CDATA[Congenital adrenal hyperplasia is a disease where there are enlarged adrenal glands that are present at birth, and it can be caused by a number of enzyme deficiencies in the adrenocortical steroid pathway. 

These enzyme deficiencies result in low levels of multiple adrenocortical steroids, with cortisol always being one of them. 

Low level of cortisol make the pituitary release more ACTH, which stimulates proliferation of adrenal cells, resulting in the enlargement, or hyperplasia, of the adrenal gland. 

Adrenal steroid hormone production takes place in the three layers of the adrenal cortex - the zona glomerulosa, where aldosterone synthesis takes place, the zona fasciculata, that’s in charge of cortisol production and finally, the zona reticularis is where androgens are made. 

Ok, now the first step for the synthesis of all three adrenal hormones is when cholesterol desmolase converts cholesterol to pregnenolone. 

In the zona glomerulosa, pregnenolone is first converted to progesterone, with the help of 3-beta-hydroxysteroid dehydrogenase, or 3-beta-HSD. 

Progesterone becomes 11-deoxycorticosterone under the influence of 21-hydroxylase.

11-deoxycorticosterone becomes corticosterone with the help of 11-beta hydroxylase, and finally, aldosterone synthase turns corticosterone into...well, aldosterone, what’d you expect.

Some of the pregnenolone and progesterone can be used to make cortisol, by making their way in the zona glomerulosa. 

Here, 17 alpha -hydroxylase turns pregnenolone into 17 hydroxypregnenolone and turns progesterone into 17 hydroxyprogesterone. 

17 hydroxypregnenolone is then also turned into 17 hydroxyprogesterone by the enzyme 3 beta-hydroxysteroid dehydrogenase. 

Then, all of the 17 hydroxyprogesterone is turned into 11 deoxycortisol by the same 21 hydroxylase enzyme, and 11 beta-hydroxylase makes 11 deoxycortisol become cortisol. 

Finally, some of the 17 hydroxypregnenolone and 17 hydroxyprogesterone are also used to make and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sleep_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5L4QNNWVQGCeVp-Qko_KfYF1Rym9Zqh2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sleep disorders: Clinical]]></video:title><video:description><![CDATA[Many of us have trouble falling asleep from time to time - usually because of stress or illness. 

But when sleep problems become a regular occurrence and interfere with daily life, that’s a sign of a sleep disorder like insomnia and sleep apnea. 

If left untreated, sleep disorders can increase the risk of accidents and debilitating conditions such as depression.

Sleep disorders are usually caused by factors that interrupt the sleep cycle - which is a period of sleep that lasts about 90 minutes, during which we move through five stages. 

Over the course of the night, there are four or five sleep cycles. 

The first four stages make up non-rapid eye movement or NREM sleep which is roughly 80% of the sleep cycle, while the fifth part is rapid eye movement or REM sleep, which accounts for the last 20% of the sleep cycle. 

Across the four stages of NREM, we move from very light sleep during Stage 1, to very deep sleep in Stage 4.

During NREM there’s minimal muscle activity and our eyes don’t move much. 

During REM sleep, the eyes dart around, and this is where dreaming occurs, memories are consolidated, and where we get the most rest.

The stages can be interrupted by various things. Heavy smoking, stress, and jet lag can make it hard to fall asleep, and substances like alcohol, caffeine, cocaine, and other stimulants can reduce NREM sleep. 

The ability to fall asleep quickly also decreases with age, especially in those with medical conditions that cause dyspnea, pain, nocturia, or nausea.

Individuals end up feeling really tired during the day and are often unable to perform at work, at school, and can struggle to have a healthy sex life. 

Often the fatigue can lead to irritability and difficulty focusing, and can worsen feelings of depression and anxiety. 

Some individuals get into a vicious cycle where they drink a lot of coffee to stay awake, and that can worsen the underlying problem. 

There are nine sleep-wake disorders according to DSM-5.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Metabolic_and_respiratory_acidosis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7ZZLg11qRr6XJKxbsaVqpab5REK4Vxqt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Metabolic and respiratory acidosis: Clinical]]></video:title><video:description><![CDATA[In metabolic acidosis, the blood pH is below 7.35, and it’s due to a bicarbonate or HCO3 concentration in the blood of less than 22 mEq/L. 

With metabolic acidosis, the respiratory center is stimulated in order to compensate for the acidosis and the individual hyperventilates, leading to dyspnea. 

In addition, associated symptoms are related to the underlying cause, for example, in diabetic ketoacidosis there’s nausea and vomiting. 

First thing’s first. Serum chemistries are obtained including serum bicarbonate or HCO3, potassium, sodium and chloride in order to see if there’s any electrolyte imbalance, and BUN and Creatinine are checked to assess renal function.

The diagnosis is usually based on an ABG, and in addition to a pH below 7.35, and HCO3 levels below 22  mEq/L, if there’s respiratory compensation, the pCO2 levels will be under 35 mm Hg. 

Generally, for every 1  mEq/L reduction in HCO3 levels, there’s a 1.2 mm Hg fall in pCO2. 

Additionally, we can verify if the respiratory compensation is appropriate by using Winter’s formula and comparing the calculated value with the measured pCO2 from the ABG. 

It goes like this. Arterial pCO2 equals 1.5 times serum HCO3 plus 8 plus or minus 2. So if our HCO3 is 15, then the calculated arterial pCO2 is: 1.5 times 15 plus 8 plus or minus 2. So 1.5 times 15 is 22.5, and 22.5 plus 8 is 30.5, so it’s 30.5 plus or minus 2, so the range is 28.5 to 32.5. 

So if the measured pCO2 is between 28.5 and 32.5, then there’s an appropriate respiratory compensation for the metabolic acidosis. 

If the measured pCO2 comes back greater than 32.5, then there’s a metabolic acidosis and an associated respiratory acidosis. 

And if the measured pCO2 is lower than 28.5, then there’s a metabolic acidosis and an associated respiratory alkalosis. 

Generally, when pH levels are below 7.1, treatment is urgent and IV sodium bicarbonate or Tromethamine or THAM is given.

Next, we have to calculate the serum anion gap- which ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dissociative_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K5iHBBMMSDiL4g_-DWrhlb4HSTKhu2Nt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dissociative disorders: Clinical]]></video:title><video:description><![CDATA[Dissociative disorders cause a disconnection or a lack of continuity between the individuals and their own thoughts, memories, actions, and identity. 

For example, people might have out of body experiences or they might not remember important aspects of a traumatic event that they’ve been through - and that can cause distress and impairment. 

Switching off from reality is a normal defense mechanism that helps the person cope during a traumatic time. In other words, it&amp;#39;s a form of denial. 

This behaviour becomes pathological when the traumatic event has ended but the person still hasn’t dealt with it properly. 

People who dissociate may feel disconnected from themselves and the world around them, and these experiences can last for a relatively short time - hours or days, or for much longer - weeks or months. 

When diagnosing a dissociative disorder, all other mental disorders should be ruled out. 

Also, the symptoms should not be attributable to the physiological effects of a substance and should cause significant distress or impairment in all areas of functioning.

Environmental factors that contribute to dissociative disorders include a history of psychological trauma, especially traumatic experiences like physical, sexual or emotional abuse during childhood, or experiences such as war, kidnapping, or even serious medical procedures. 

According to DSM-5, there are five related conditions: dissociative identity disorder, dissociative amnesia, depersonalization/derealization disorder, other specified dissociative disorder, and unspecified dissociative disorder.

First, there’s dissociative identity disorder which is where individuals have two or more distinct personality states. 

When a person is experiencing another identity they typically lose their normal sense of self and control, and can have differences in emotion, behavior, consciousness, memory, perception, cognition, sensations, and movement. 

For example, individuals might sudden]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disorders_of_consciousness:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CrBnmzWBQ5C8WC1P1dhPxbt5RPGaWnSX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disorders of consciousness: Clinical]]></video:title><video:description><![CDATA[One of the many higher-order functions of our brains is maintaining consciousness. 

Consciousness includes both arousal or wakefulness, as well as awareness. 

Now, arousal is maintained by a network of neurons in the pons and midbrain that form the ascending reticular activating system, or ARAS. 

The ARAS sends out neuronal connections to both cerebral cortices, which are responsible for producing awareness.

So damage to the ARAS in the brainstem, both cerebral hemispheres, or damage to the tracts connecting them can affect a person’s consciousness. 

Now, a coma is a state of profoundly decreased arousal resembling sleep, however, a comatose individual cannot be aroused by external stimuli. 

“Stupor”, “obtundation”, and “lethargy” are terms that reflect states that fall between normal arousal and a coma, but individuals in these states can be aroused by external stimuli. 

Arousability is assessed by noise stimulation, such as shouting in the individual’s ear, or somatosensory stimulation, like pressing on the supraorbital ridge or squeezing the trapezius muscle. 

Now, the differential diagnosis for coma is large, but they fall into 4 broad categories: toxic, such as opioid toxicity, infectious, such as sepsis or meningitis and encephalitis, metabolic, which includes electrolyte imbalances or organ dysfunction, and structural, such as a stroke or subdural hemorrhage. 

When a person is found to already be in a comatose state, it’s helpful to get information from witnesses, family members, friends, and paramedics, as well as from medical alert bracelets. 

If the comatose state had an abrupt onset it may be due to stroke, seizure, subarachnoid hemorrhage, or cardiac arrest. Whereas a gradual onset may be due to a brain tumor, subdural hematoma, infection, or metabolic disorder. 

Prior to the coma, transient neurological symptoms like hemiparesis, hemisensory loss, or diplopia suggest a stroke.

A history of a fall may suggest traumatic brain injury,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_be_a_lifelong_learner</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FaGM22tgSHCzSy4SllRPCfPCTUOo9rQY/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to be a lifelong learner]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to be a lifelong learner through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Patients_Perspective:_Congenital_Hip_Dysplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_j2-brPtQsycN2kYDYODCXafT9_wPbCo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Patients Perspective: Congenital Hip Dysplasia]]></video:title><video:description><![CDATA[C: I’m Caitlin Walker.

D: And I’m David Walker. And, uh, we have two kids, Mikey and Ellie, and Ellie was diagnosed with hip dysplasia.

The diagnosis happened pretty early on. It was one of those situations where, uh, Caitlin noticed something, uh, going on with like a ‘click,’ - 

C: Literally about thirty minutes after she was born. And they gave her to me, uh, I could hear the ‘click.’ When we heard the click, it was right away that she saw a doctor, uh, because as soon as I had notified the nurse, while she was - while I was holding her and I could hear the click, I had told the nurse in the delivery room. So she got the in-house pediatrician to come over to our room. 

The first pediatrician did not notice anything. Another pediatrician came up to the room, and then she checked out Ellie and confirmed that there was a click. 

D: The only reason that we, uh, were really concerned about the click to begin with was because our son, he had a hip dysplasia, but not as severely. 

C: After the in-house pediatrician looked at her, it had been about a day before she saw her primary pediatrician. Um, and then from there, it was about four days until she saw the specialist, um, at the children’s hospital. Then they ultimately confirmed with the ultrasound.

Um, I wasn’t really sure of the extent of what it was going to be; since our son had a very mild case of that, he didn’t need a harness or anything. 

Once I found out she needed to get a harness, my perspective on the thing sort of changed a little bit. So she had to wear the harness for about six weeks. She had to wear that harness full time, twenty-four-seven. 

Initially, we didn’t put a shirt underneath her harness, because they put some padding underneath the harness and told us that was going to be enough, that she would be fine. But it was really about two days after she had the harness when we started to notice the chafing and the redness. So we ended up putting a shirt underneath her harness, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_kidney_injury:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ronp-bz4TpSglkLxqPRrVjt0Su_nF0wA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute kidney injury: Clinical]]></video:title><video:description><![CDATA[With acute kidney injury, or AKI, there’s a decrease in kidney function that typically happens over a few days. This leads to the retention of urea and other nitrogenous waste products- such as ammonia and uric acid and dysregulation of extracellular volume and electrolytes. 

The most commonly used diagnostic criteria for AKI are the Kidney Disease: Improving Global Outcomes or KDIGO guidelines. The KDIGO guidelines define AKI as an increase in serum creatinine of at least 0.3 milligrams per deciliter within 48 hours or as an increase in serum creatinine by 1.5 times the baseline serum creatinine within the last 7 days or when the urine volume has been less than 0.5 milliliters per kilogram per hour for six hours. Based on these criteria, there are three stages of AKI, where stage 1 is mild and stage 3 is severe AKI. In stage 1 AKI, there’s an increase in serum creatinine to 1.5 to 1.9 times the baseline serum creatinine or an increase in serum creatinine by 0.3 milligrams per deciliter or a decrease in urine output to below 0.5 milliliters per kilogram per hour for 6 to 12 hours. In stage 2 AKI, there’s an increase in serum creatinine to 2 to 2.9 times the baseline serum creatinine or a decrease in urine output to less than 0.5 milliliters per kilogram per hour for more than 12 hours. In stage 3 AKI, there’s an increase in serum creatinine to 3 times the baseline serum creatinine or an increase in serum creatinine to more than 4 milligrams per deciliter or a decrease in urine output to less than 0.3 milliliters per kilogram per hour for more than 24 hours or anuria- meaning less than 100 milliliters per day of urine- for more than 12 hours or where renal replacement therapy has been initiated. All individuals are classified according to whichever criteria places them in the most severe stage of injury. 

Once diagnosed, the causes of AKI can be split into prerenal, intrarenal, and post-renal causes. In prerenal AKI, there’s decreased blood flow into the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prebiotics_and_probiotics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3xUo8ykFTDOJavKj-VhjMtSeQ6GuSKRY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prebiotics and probiotics]]></video:title><video:description><![CDATA[The gastrointestinal tract is home to trillions of microbes, collectively called the gut microbiome.

It was previously thought that there were about ten times as many microbial cells in our bodies as there are human cells, but more recent estimates have it at closer to a one-to-one ratio, with the balance tipped just slightly toward the microbes. 

In other words, it looks like we’re slightly more microbe than human!

The gut microbiome is dominated by two main groups of bacteria: Bacteroidetes and Firmicutes, with much smaller numbers of Proteobacteria, Verrucomicrobia, Actinobacteria, and Fusobacteria. 

The amount and types of bacteria can vary drastically from person to person, and there’s no clear consensus on what makes up a “healthy” microbiome.

Microbes are found throughout the gastrointestinal tract, but most are in the large intestine, or colon. And since what we eat and drink passes through the gastrointestinal tract every day - it’s no surprise that our diet affects our gut microbiome. 

For example, people who eat a high-fiber diet tend to have higher levels of Prevotella, and those with a diet higher in protein and fat have more Bacteroides, both of which are members of the Bacteroidetes group. 

In fact, studies have shown that even a single day of a strict animal-based diet or plant-based diet can alter the microbiome composition, but we often revert back to our regular microbiome once our diets go back to normal.

Two parts of our diet that are uniquely able to affect the microbiome are probiotics and prebiotics.

Probiotics are live microorganisms that offer a health benefit - for example, by helping to enhance or restore health to our gut microbiome. 

Many of the microorganisms that naturally live in our bodies are similar to microorganisms found in probiotic foods, drinks, and dietary supplements.

Probiotic bacteria are found in fermented dairy products like yogurt and kefir as well as foods like kimchi and sauerkraut, though not al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Paying_for_medical_school</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Dkcc58lZS9C4JUaQiINwwyNnQIW2GIcg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Paying for medical school]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Paying for medical school through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brain_tumors:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5H0IlEbxSeSxvfMECF7B9JDZTBCvGQJb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brain tumors: Clinical]]></video:title><video:description><![CDATA[Brain tumors are broadly classified into primary tumors originating from cells within the central nervous system, and metastatic tumors originating from cells outside the central nervous system. 

Primary brain tumors are the most common solid tumors in children, while metastatic tumors are more common in adults. 

The most common primary brain tumors in both adults and children are gliomas, a subset of these are called astrocytomas. 

In adults, gliomas are followed by meningiomas, and in children, medulloblastomas and ependymomas are next on the list. These are followed by the less common schwannomas, oligodendrogliomas, craniopharyngioma, choroid plexus tumors, germinomas, hemangioblastomas, and primary central nervous system lymphoma. 

Also, in children, most brain tumors are located below the cerebellar tentorium, or are infratentorial. Whereas in adults, most brain tumors are above it, or are supratentorial. Just remember that adults are taller than children. 

Now, in order of decreasing frequency, metastatic brain tumors most commonly come from cancers of the lung, breast, and melanoma. 

The main environmental risk factor for brain tumors is exposure to ionizing radiation, which can come from therapeutic radiotherapy for cancer, or diagnostic imaging like CT scans. 

Electromagnetic radiation from cell phones and microwaves is currently being researched as potential risk factors in humans. 

Immunocompromised people, like organ transplant recipients or individuals with AIDS are at high risk of primary central nervous system lymphoma caused by the Epstein-Barr virus, or EBV. 

Meningiomas are particularly more common in women, possibly because the tumor cells possess estrogen and progesterone receptors. 

A small proportion of brain tumors occur secondary to genetic syndromes. 

For example neurofibromatosis type 1 is associated with optic nerve gliomas and schwannomas, whereas neurofibromatosis type 2 is associated with bilateral schwannomas. 

T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alveolar_surface_tension_and_surfactant</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oMKx66cDSg6l_lXpb9ghVwNUQhmOR7T2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alveolar surface tension and surfactant]]></video:title><video:description><![CDATA[The alveoli are the tiny air sacs in the lungs where gas exchange happens. And their walls are lined by a thin film of water, which creates a force at their surface called surface tension. 

Surface tension tends to collapse the pulmonary alveoli, and, as you can imagine, this could turn into a big problem - not being able to breathe in. 

Luckily, alveolar cells have found a way to counteract surface tension by producing surfactant, which is a phospholipoprotein that reduces the surface tension, keeping the alveoli open so that we can breathe properly. 

That being said, take a deep breath, because we’re about to delve into the physics of surface tension. 

The water molecules, known as H2O to their friends, stay close together because of hydrogen bonds that form between the negatively charged oxygen ion of one molecule and the positively charged hydrogen ion of another molecule. 

Within the bulk of water, the molecules are equally pulled in every direction by neighboring molecules, so the resulting net force is zero. 

However, when you add air into the mix, the whole system becomes unbalanced, because at the water-air interface, water molecules are not surrounded by other water molecules. 

This creates too many cohesive forces between water molecules at the surface, that pull the water molecules at the surface closer together, making the surface of the water shrink to the minimum surface area possible. 

Now, the interior of the alveoli is also spherical, so the net force of surface tension is directed to the center of the alveoli, which tends to collapse the alveolar walls towards the center. 

The magnitude of this force is predicted by Laplace law, which states that the pressure collapsing the alveolus is directly proportional to the surface tension generated by molecules of fluid lining the alveolus, and inversely proportional to the radius of the alveoli. So the smaller the alveoli, the larger the collapsing pressure.

Now, when we breathe o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Measuring_cardiac_output_(Fick_principle)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n3eO7-LITtuTGlg3_0rBLxW0Rmqp8Yzq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Measuring cardiac output (Fick principle)]]></video:title><video:description><![CDATA[Cardiac output is defined as the volume of blood ejected by the left ventricle per unit time. 

The volume of blood is called the stroke volume, and the unit used to measure cardiac output is one minute. 

So cardiac output can be calculated as stroke volume which is the volume of blood pumped out of the left ventricle per beat, times the number of heartbeats per minute, which is around 70. 

Another way to calculate cardiac output is by using the Fick Principle, which simply states that at rest, the oxygen going into an organ minus the oxygen left out of an organ must equal how much oxygen that organ has used. 

Using the Fick Principle’s equation of (cardiac output = oxygen consumption/arterio-venous oxygen difference), cardiac output can be calculated. 

Both methods render normal cardiac output to around 5 litres per minute on average. 

To measure cardiac output, we first have to take a look at the left ventricle. 

There’s a moment when the left ventricle is fully relaxed. 

It occurs at the end of filling or diastole, also called the end-diastolic point, and the volume of blood within the left ventricle is called the end-diastolic volume, and it’s about 120 milliliters. 

Then the left ventricle contracts, forcing blood through the aorta and into the whole arterial system. 

After that is another moment when the left ventricle is fully contracted. 

It occurs at the end of contraction or systole, also called the end-systolic point, and the volume of blood within the left ventricle is called end-systolic volume, and it’s about 50 milliliters. 

So, end-diastolic volume minus end-systolic volume, gives us the stroke volume, which is the volume of blood that the left ventricle ejects with every heartbeat, or stroke. 

In this case, the stroke volume is 120 minus 50, which equals 70 milliliters.

Every minute, though, our heart beats about 70 times, on average. 

So if we multiply the stroke volume times the heart rate, or times our heart beats per minu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_preload</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rl7TpybhTXCNGA9oSPI6qi02QMuDw7XN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac preload]]></video:title><video:description><![CDATA[Cardiac preload is one of the main factors that influence how much blood the heart pumps out with each heartbeat, or stroke. 

Now, remember that the heart has two upper chambers: the left atrium, which receives oxygenated blood from the lungs via the pulmonary veins; and the right atrium, which receives deoxygenated blood from all of our organs and tissues via the superior and inferior vena cava. 

From the atria, the blood flows into the lower chambers of the heart: the left ventricle, which pumps oxygenated blood to all our organs and tissues via the aorta; and the right ventricle, which pumps the deoxygenated blood back to the lungs via the pulmonary arteries. 

Alright, now, each heartbeat consists of two phases: systole, which is when the heart contracts and pumps the blood out of the ventricles; and diastole, which is when the heart relaxes and ventricles fill with blood. 

And as the left ventricle fills with blood during diastole, the pressure within it rises. 

The pressure at the end of diastole is called the left ventricular end-diastolic pressure, which is a key determinant of cardiac preload.  

So, cardiac preload can be defined as the ventricular wall stress at the end of diastole. 

And it can be calculated using the law of Laplace, which states that wall stress   =   pressure (P)   x   radius (R)    /    2 x wall thickness (W). 

Another way to say this is that cardiac preload is directly proportional to the end-diastolic pressure and radius of the left ventricle, and indirectly proportional to two times the ventricular wall thickness. 

To visualize this, let’s look at a cross-section of the left ventricle, which looks a bit like a doughnut, with little dough. A diet doughnut, if you will. 

Now, the little dough circle represents the wall of the left ventricle, and its thickness is the ventricular wall thickness, or W. Pressure, or P, on the other hand, is determined by the volume of blood inside the ventricle at the end of diastol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_afterload</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BQn_d5mPSB2yZgIOyHHykkuuROqTkflx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac afterload]]></video:title><video:description><![CDATA[Cardiac afterload is one of the main factors that influence how much blood the heart pumps out with each heartbeat, or stroke. 

Now, remember that the heart has two upper chambers: the left atrium, which receives oxygenated blood from the lungs via the pulmonary veins; and the right atrium, which receives deoxygenated blood from all of our organs and tissues via the superior and inferior vena cava. 

From the atria, the blood flows into the lower chambers of the heart: the left ventricle, which pumps oxygenated blood to all our organs and tissues via the aorta; and the right ventricle, which pumps the deoxygenated blood back to the lungs via the pulmonary arteries. 

Alright, now, each heartbeat consists of two phases: systole, which is when the heart contracts and pumps the blood out of the ventricles; and diastole, which is when the heart relaxes and ventricles fill with blood. 

And as the left ventricle fills with blood during diastole, the pressure within it rises. 

Then the left ventricle contracts, increasing the pressure within the left ventricle even more and forcing blood through the aortic valve into the aorta and whole arterial system. 

So, cardiac afterload can be defined as the ventricular wall stress during systole or ejection. 

And it can be calculated using the law of Laplace, which states that wall stress   =   pressure (P)   x   radius (R)    /    2 x wall thickness (W). 

Another way to say this is that cardiac afterload is directly proportional to the pressure inside the left ventricle during ejection as well as the radius of the left ventricle, and indirectly proportional to two times the ventricular wall thickness. 

To visualize this, let’s look at a cross-section of the left ventricle, which looks a bit like a doughnut, with little dough. 

A diet doughnut, if you will. Now, the little dough circle represents the wall of the left ventricle, and its thickness is the ventricular wall thickness, or W. Pressure, or P, on the other ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Law_of_Laplace</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yw-1TaFPT4a6bccXmlE7b2niTDis_d2s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Law of Laplace]]></video:title><video:description><![CDATA[The law of Laplace, named in honor of French scholar Pierre Simon Laplace, is a law in physics that states that the tension in the walls of a hollow sphere or cylinder is dependent on the pressure of its contents and its radius. 

The concept was then later applied to medicine since there are many hollow spherical and cylindrical shaped organs in our bodies that deal with pressures. 

Important examples include the blood vessels and the chambers of the heart.

Okay, so according to the law of Laplace, wall tension is proportional to pressure (P) times radius (r). 

Now, let&amp;#39;s break it down. 

The wall tension is the force in the container’s walls that resists the force trying to expand it.  

So if we’re blowing up a balloon, we can think of the wall tension as the force created by the elastic rubber wall that resists the outward force applied by the pressure inside the balloon. 

Now if we break the wall tension into components, we have a vertical vector of force that’s counteracting the expansion of the balloon and a horizontal vector of force that’s stretching and tearing the balloon’s wall.

So, for pressure, if we were to blow more air into a balloon, we would expect the pressure inside to build up and the wall tension of the balloon would increase as the walls push back against the expansion. 

If the pressure trying to expand the balloon is greater than the wall tension, the balloon will expand... or pop! 

Now another factor is the radius.  

A smaller radius means more pressure is needed to overcome the wall tension in order for the container to expand.  

This is why it’s harder to blow up a small, deflated balloon than it is to blow up a half inflated balloon.   

An example of this can be seen in the alveoli in the lungs of a newborn.  

Let’s plug in some easy, imaginary numbers and forego units to make this concept easier to understand!  

Normally, an unused alveolus in a newborn is collapsed, so let’s say it has a radius of 2, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breaking_down_USMLE®-style_questions:_1</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s65HTU3LQjydZ5_pu2eY6T-vQE2kloaA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breaking down USMLE®-style questions: 1]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Breaking down USMLE®-style questions: 1 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breaking_down_USMLE®-style_questions:_2</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JjV8HvP4TY6kieYLwDazIZgCRselxwof/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breaking down USMLE®-style questions: 2]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Breaking down USMLE®-style questions: 2 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breaking_down_USMLE®-style_questions:_3</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JNtwa4cVQ7yia2dmfMR6IxasRgO0oh63/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breaking down USMLE®-style questions: 3]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Breaking down USMLE®-style questions: 3 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breaking_down_USMLE®-style_questions:_4</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tm8VRWpoTiWg1lxMyg-FCwg8Ro2Sjr_p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breaking down USMLE®-style questions: 4]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Breaking down USMLE®-style questions: 4 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breaking_down_USMLE®-style_questions:_5</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CMr0MQsTSm25VBEJY4twPcnVQHqgGNxk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breaking down USMLE®-style questions: 5]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Breaking down USMLE®-style questions: 5 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breaking_down_USMLE®-style_questions:_6</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xIc6MSF9Tqy69k1jF3M5Uk1YTm2Sr0sD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breaking down USMLE®-style questions: 6]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Breaking down USMLE®-style questions: 6 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breaking_down_USMLE®-style_questions:_7</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SlEvG9vaTxKJSeqGz6mb6HQNRUS5Ridb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breaking down USMLE®-style questions: 7]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Breaking down USMLE®-style questions: 7 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breaking_down_USMLE®-style_questions:_8</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X6O5EktrSHqS3QZw47Y5lV0kQAGhJVzt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breaking down USMLE®-style questions: 8]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Breaking down USMLE®-style questions: 8 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Phosphate,_calcium_and_magnesium_homeostasis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/owOgHDT5RTKi4UgwjhNdDVJgQ8Oui_Ko/_.jpg</video:thumbnail_loc><video:title><![CDATA[Phosphate, calcium and magnesium homeostasis]]></video:title><video:description><![CDATA[Phosphate is a negative ion noted as PO4, while calcium, noted as Ca and magnesium, noted as Mg, are positive ions. 

Now, about 85 percent of the phosphate, along with 99 percent of calcium and about 60 percent of magnesium are located in the bone matrix. 

Phosphate and calcium combine to form calcium phosphate, which makes up the hard bone matrix of bones and teeth, and magnesium helps strengthen it.  

Okay, now, let’s start talking specifics about phosphate. The remaining 15 percent of phosphate is found almost entirely in the intracellular fluid, or ICF, while only less than 0.5 percent is found in the extracellular fluid, or ECF.

Now, most of the ECF is made up of plasma and in the plasma, 90% of phosphate circulates free, while 10 percent is bound to plasma proteins. 

Phosphate plasma levels range between 2.5 and 4.5 milligrams per deciliter. 

Phosphate is a component of nucleotides that make up the DNA and RNA, high-energy molecules, like adenosine tri-phosphate and metabolic intermediates. 

Phosphate also acts as a buffer for hydrogen. 

Okay, now, phosphate comes from our diet and the daily recommended phosphate intake is about 1 gram per day and we can get it from chicken, turkey or pork. 

Once ingested, phosphate is absorbed in the GI tract into the bloodstream and then goes where it’s needed- such as the bone- and the rest is excreted. 

Okay, let’s see how phosphate is handled by the kidneys. See, the kidneys are made up of lots and lots of nephrons, and each nephron is made up of a renal corpuscle and a renal tubule. 

The renal corpuscle, in turn, is made up of the glomerulus, which is a tiny clump of capillaries, and Bowman’s capsule surrounding it. 

So, blood gets to the glomerulus through the afferent arteriole, which is a branch of the renal artery,  and leaves the glomerulus through the efferent arterioles. 

These vessels act like a coffee filter, allowing everything but red blood cells and proteins to pass from the bloodstream]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Potassium_homeostasis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2iW0cpjzQ0SbLLiWV66MDjQGTXygmO9X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Potassium homeostasis]]></video:title><video:description><![CDATA[Potassium or Kalium is a positive ion, or a cation, noted with a K. About 98% of total body potassium is found in the intracellular fluid, or the ICF for short, which makes for an intracellular potassium concentration of about 150 milliequivalents per liter.

The remaining 2 percent is in the extracellular fluid, or the ECF, which consists of plasma and interstitial fluid.

However, since we can only measure the plasma level of potassium, which is about 4.5 milliequivalents per liter, that level is often used to define the normal extracellular concentration of potassium. 

Maintaining the normal potassium concentration in the ECF and ICF is essential for the normal functioning of excitable cells like nerve cells and muscle cells, including cardiomyocytes.

Now, across all cell membranes, when there’s no stimulus, there are negative electrical charges on the inside and positive electrical charges on the outside.

This creates a potential difference  called the resting membrane potential.

Once there’s a stimulus- like when a muscle contracts-, an electrochemical impulse is generated and transmitted along the cell membrane and that generates an action potential.        

Okay, now, we get potassium from our diet.

The daily recommended potassium intake is about 40 to 50 milliequivalents per liter which is about 1.6 to 2 grams of potassium - which is the equivalent of 5 bananas per day.

Once ingested, potassium is reabsorbed in the blood by the GI tract and travels unbound to plasma proteins.

Most of potassium gets inside the cells, a little amount can be lost through sweat and the GI tract and the rest is filtered by the kidneys and excreted.

Knowing this, potassium needs to be carefully regulated in order for its concentration to remain constant.

Potassium balance depends on the total amount of potassium in the body which in turn is determined by potassium intake and excretion and it’s called the external potassium balance.

Potassium balance also depen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cerebral_circulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/282BpRdoRKi4DCmnmeZfZIjHSmuGo6XN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cerebral circulation]]></video:title><video:description><![CDATA[With cerebral circulation, cerebral stands for &amp;quot;brain,&amp;quot; and circulation, refers to “blood flow.” 

So, cerebral circulation is the movement of blood through the vessels that supply the brain and surrounding structures. 

Our brain is responsible for complex functions such as thinking, feeling, memory, movement, vision, and speech. 

Therefore, some of the devastating effects of oxygen deprivation to the brain include strokes, seizures, coma, and even death. 

As a result, the brain requires a very efficient cerebral circulation to provide oxygen and nutrients, and remove carbon dioxide and  wastes. 

Now, like any other organ in the body, the blood supply to the brain, originates from the aorta. 

Arising from the heart’s left ventricle, it goes on to form the aortic arch. Here, the brachiocephalic artery, originates first. 

This branch gives off the right subclavian artery and the right common carotid artery. 

Then a bit further along the aortic arch, the left common carotid artery arises, followed by the left subclavian artery. 

The subclavian arteries give off right and left vertebral arteries, which ascend through the intervertebral feramina up to the brain. 

Because the consequences of hypoxia to the brain are so devastating, the brain is safeguarded by having a dual circulation, an anterior circulation, originating from the carotids, and a posterior circulation, originating from the vertebral arteries. 

The two circulations eventually meet up, creating what’s known as the circle of Willis. 

Alright, the anterior circulation starts in the neck, where the common carotid splits into the external and internal branches, the internal carotid arteries, passes through the carotid canal of the temporal bone of the skull and into the cranial cavity to supply the brain. 

Once, it enters the cranial cavity, the internal carotid artery gives off branches. First are the middle cerebral arteries that supply blood to the temporal and parie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronary_circulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IxzMQW7MRDqofGwU5gWi7KwJQW_42Ffw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronary circulation]]></video:title><video:description><![CDATA[Introduction

With coronary circulation, coronary comes from the Latin word “coronarius,” meaning &amp;quot;crown.&amp;quot; This is because the coronary blood vessels surrounding the heart resembles a little crown! And circulation refers to “the flow of blood.” So, coronary circulation is the movement of blood throughout the vessels that supply the myocardium also known as  the heart muscle. 

Now, the heart is a pump, primarily made up of cardiac muscle cells known as cardiomyocytes. And like any other cell, they require a steady supply of oxygen, nutrients, and a way to eliminate wastes. And although the heart is continually pumping blood throughout its chambers, the myocardium is too thick for the diffusion of blood to happen effectively. So, instead, the coronary circulation provides an efficient way for the exchange of substances to occur.  

Coronary Circulation

Okay, the coronary circulation system is mainly made up of arteries and veins. To begin, the arterial supply of the heart starts with the branching out of the left and right coronary arteries from the base of the aorta. It’s like a superhighway that carries oxygenated blood from the heart to the rest of the body.

Left Coronary Artery

Now, the left coronary artery heads along the left coronary sulcus, a groove on the outer surface of the heart that marks the point of division between the ventricles and the atria.  Not too far along the sulcus, the left coronary artery divides into two major branches. The first is the left anterior descending artery or LAD.  It travels down the anterior interventricular sulcus, and it supplies the anterior 2/3 of the interventricular septum, the anterolateral papillary muscle, and the anterior surface of the left ventricle.  The second branch is the left circumflex artery or LCX. It goes along the coronary sulcus, around the left side of the heart and supplies the left atrium and the posterior walls of the left ventricle.   

Right Coronary Artery

Altern]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Microcirculation_and_Starling_forces</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F6q8cUcnQomZhIm_vURNNt60SLCKQu-h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Microcirculation and Starling forces]]></video:title><video:description><![CDATA[With microcirculation and Starling forces, microcirculation refers to the blood that flows through the smallest vessels in the circulatory system called capillaries. 

And Starling forces, named after British physiologist Ernest Starling, sometimes called Starling pressures, are the forces that drive the exchange of fluid through the walls of the capillaries.

The capillaries have a single layer of endothelial cells lining their walls with clefts between these cells. 

Normally, blood flows into smaller and smaller arteries, eventually reaching the arterioles, the metarterioles, and then the capillaries. In the capillary bed, due to the capillary’s thin walls and clefts, substances like nutrients or waste products can move from the blood into surrounding tissues and vice-versa. 

After the capillaries, blood moves into venules, and then finally into veins. Intertwined with these capillaries are the lymphatic capillaries, which return interstitial fluid and proteins to the vascular system. 

Lymphatic capillaries can also empty into larger lymphatic vessels and eventually into the thoracic duct, which empties lymphatic fluid directly into the large veins. 

So, arterioles, metarterioles, capillaries, venules, and lymphatic vessels together make up the microcirculation. 

Now, the arterioles that come before the capillaries act as floodgates, regulating blood flow into the capillaries. 

So if the arterioles constrict, the resistance increases, and if they dilate, the resistance decreases. 

Therefore, the arterioles generally determine total peripheral resistance, or the amount of resistance opposing blood flow. 

This means arterioles play a key role in regulating the blood flow to an organ. 

Now, there are 2 mechanisms that help them do their job, intrinsic and extrinsic control. 

Intrinsic control of blood flow is based on the level of metabolites in the surrounding tissue. 

For example, adenosine and carbon dioxide will cause]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_changes_at_high_altitude_and_altitude_sickness</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OZyUtMFQQeyFMRxpPWx6yif9TQmw6H5M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary changes at high altitude and altitude sickness]]></video:title><video:description><![CDATA[The air we breathe in has the same amount of oxygen (about 21 percent or just 0.21) at all altitudes. This is referred to as the Fraction of Inspired Oxygen or FiO2. However, the atmospheric air pressure, or Patm, decreases with altitude from about 760 mmHg at sea level to about 500 mmHg at the top of a 3000 meter mountain. So the problem is not that there’s proportionally less oxygen at high altitudes, but rather the problem is that the lower air pressure means that the same oxygen proportion will result in a lower partial pressure of oxygen in the alveoli, or PAO2 for short. So when there’s an increase in altitude, the amount of oxygen getting to the alveoli reduces. But luckily, the body makes physiological changes to keep the tissues well oxygenated even at low atmospheric pressures. Now if that fails, it can lead to altitude sickness.  

OK, so normally, the respiratory mucosa is a bit moist, and at 37 degree Celsius (a normal body temperature), some water molecules exist as water vapor. These molecules create a pressure of their own known as the vapor pressure or pH2O, which is about 47 mm Hg. So the air we breathe in mixes up with these vapors and becomes humidified.

Now, at the end of inspiration, the air pressure within the alveoli becomes equal to the Patm, or the air pressure outside the body, but the composition is a bit different due to the humidification that takes place in the respiratory tract and alveoli. So if we want to know how much of the dry air remains within the alveoli, we have to subtract this vapor pressure from the mixture and then,  multiply the dry air pressure with FiO2, to get the amount of oxygen that gets into the alveoli.

OK, now, across the alveolo-capillary membrane, gas exchange is happening all the time. Some oxygen molecules are diffusing across the membrane and binding to the hemoglobin within red blood cells. At the same time, red blood cells are dropping off carbon dioxide which diffuses from the blood]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chest_trauma:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G1s2VpHaQ5e2ruOqWc6CedPsSZ2IdXho/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chest trauma: Clinical]]></video:title><video:description><![CDATA[The chest wall houses a number of vital structures in the body - the heart and the pericardium, the lungs and the pleura, the aorta, and the esophagus - all protected within the rib cage and sternum. 

And trauma to the chest wall is responsible for over one-fourth of trauma deaths. 

Chest trauma can be blunt, such as from motor vehicle accidents, or penetrating, such as from a stab or gunshot wound. 

Chest trauma evaluation starts with the primary survey, which includes the ABCDEs: airway, breathing, circulation, disability, and exposure, and the goal is to quickly assess and treat life-threatening injuries. 

It starts with checking the patency of the airway and whether the individual requires endotracheal intubation. 

As for breathing, you can look, listen, and feel. 

So look at the respiratory rate, oxygen saturation, and breathing pattern. 

If the person is hypoxemic, a 100% oxygen non-rebreather mask should be given. 

Also if there’s asymmetric breathing it could indicate a weak chest segment due to rib fractures. 

Next, listen for breath sounds for signs like decreased air entry in tension pneumothorax or hemothorax, or muffled heart sounds in cardiac tamponade. 

After that feel for tenderness along the chest wall, which can occur with rib fractures.

In circulation, check the blood pressure and heart rate.

If there are signs of shock it could be due to a number of causes like bleeding into the pleura or pericardium, obstruction of cardiac output in the setting of a tension pneumothorax, or inadequate cardiac output in the setting of myocardial injury. 

Also, as part of circulation, it’s important to look for other sources of bleeding, to insert two large-bore intravenous lines, and to prepare for the need for blood products. 

It’s specifically important to assess for signs of inadequate end-organ perfusion, such as altered mental status, decrease urine output, cool or pale skin, and a delayed capillary refill. 

Bedsides ultrasound can a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_gastrointestinal_bleeding:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jukOy-WVTzqMamQzJTvDuIe2SV_DQYB-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric gastrointestinal bleeding: Clinical]]></video:title><video:description><![CDATA[Pediatric gastrointestinal bleeding can be divided into upper and lower GI bleeding.

Upper GI bleeding arises above the ligament of Treitz- also called the suspensory ligament of the duodenum- and it includes bleeding from the esophagus, stomach, or duodenum. 

Common causes of pediatric upper GI bleeding include peptic ulcer disease, and esophageal bleeding.

Lower GI bleeding arises below the ligament of Treitz and includes bleeding from the small intestines past the ligament of Treitz, large intestines, rectum, and anus. 

Common causes of lower GI bleeding include anal fissures, allergic, necrotizing or infectious enterocolitis, malrotation with volvulus, intussusception, Meckel’s diverticulum, juvenile polyps and inflammatory bowel disease. 

Now, both upper and lower GI bleedings can be either visible or occult- meaning that there’s no visible evidence of bleeding. This is usually detected by a fecal occult blood test or if there are signs of iron deficiency anemia. 

Okay, first things first. Visible upper GI bleeds may cause blood in the vomit, which might be fresh and bright red, known as hematemesis- and suggests moderate to severe ongoing bleeding, or it might look like coffee- grounds, which suggests that the blood has been oxidized by acid in the stomach so that the iron in the blood has turned black. This is a sign that bleeding was a small quantity or has stopped. 

Blood in the stool or diaper may present as black and tarry stools, known as melena, which suggest small quantity bleeding, about 50 milliliters of blood, and that most often results from upper GI bleeding.

If there is fresh, bright red blood passing through the anus which may or may not be mixed with stool, it’s usually lower GI bleeding, known as hematochezia. 

In rare cases, if there’s a large upper GI bleed, that can cause hematochezia as well.

In any child with active GI bleed, the first thing to do is evaluate the general appearance, meanin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neck_trauma:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FGf3xuBgSqGLOJW6KbxLBOa6THiILRWG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neck trauma: Clinical]]></video:title><video:description><![CDATA[The neck is a compact tube packed with many vital structures including blood vessels like the carotid artery and internal jugular vein, nerves like the brachial plexus, parts of the airway like the larynx and trachea, and parts of the digestive tract, such as the pharynx and esophagus. As a result, even seemingly innocuous traumatic injury can be lethal. The cervical spine is the most flexible and mobile part of the vertebral column. 

But, that flexibility comes with a price, making the cervical spine the most vulnerable part of the vertebral column to trauma. Now, neck trauma can be classified into penetrating neck injury, like that from a knife stab, and blunt neck injury, like that from a car crash. 

Before delving into penetrating neck injuries, it’s crucial to review the anatomy. The neck is anatomically divided into three zones. From bottom to top, zone I, or the lower zone, is from the clavicles to the cricoid cartilage, zone II, or the middle zone, is from the cricoid cartilage to the angle of the mandible, and zone III, or the upper zone, is from the angle of the mandible to the base of the skull. To help you remember the order of the zones, think of going up an elevator, so zones I, II, III from bottom to top. The neck is enveloped by the superficial and deep cervical fascia, and sandwiched between them is the platysma muscle. 

Anatomically, the neck can also be described in triangles. The sternocleidomastoid muscle separates the neck into two triangles. The anterior triangle contains most of the major anatomic structures, including the larynx, trachea, pharynx, esophagus and major vascular structures; while the posterior triangle contains muscles, the spinal accessory nerve, and the spinal column.

Penetrating neck injury is most often caused by gunshot wounds and stab wounds. The platysma muscle defines penetrating neck injury. So, if the platysma muscle is violated, then the likelihood of injury to the deep aerodigestive and neurovascular s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bites_and_stings:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T2Xj7NX3SoKZwfjYsVeWhAHARDeXi7C4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bites and stings: Clinical]]></video:title><video:description><![CDATA[Bites and stings can be caused by a variety of animals, insects, snakes or yes, even humans! 

The most common mammalian bites are from dogs, cats, and humans. And each bite transmits the polymicrobial flora that can be found in the mouth - including Staphylococcus aureus, group A Streptococcus species, Klebsiella, Enterococci, Prevotella and many more. 

Dog bites can transmit a gram negative rod called Capnocytophaga canimorsus, which can cause gangrene at the bite site and can disseminate and cause sepsis, especially in asplenic individuals and those with liver disease.

Cat bites or scratches - particularly from kittens - can transmit Bartonella henselae, which causes cat scratch disease. 

Both dog and cat bites can also transmit Pasteurella multocida which can cause cellulitis at the bite injury. 

Finally, human bites can transmit Eikenella corrodens which is a gram negative anaerobe which can cause local and disseminated infection - including being a cause of culture-negative endocarditis - one of the HACEK organisms.

In general, bite wound infections cause local cellulitis and in some cases can lead to a local abscess and fevers. 

Dog bites are the most common ones of all, and because dogs have strong jaws they often cause serious tissue injury, but infections aren’t that common. 

In contrast, cats have long, thin teeth, that create deep puncture wounds, which very often get infected. Cat bites can even reach the underlying joint space or periosteum, leading to septic arthritis or osteomyelitis. 

Like cat bites, human bites also have a high risk of infection. 

Most human bites happen due to aggressive play between children, but can also happen among adults. 

In a child, if the bite mark is over 2.5 centimeters in diameter, then it’s likely an adult bite, and should raise the suspicion of child abuse. 

The most common human bite occurs when a clenched fist hits a person’s tooth, and that results in a laceration over the 3rd and 4th metacarpa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Substance_misuse_and_addiction:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4QXQwl1RSSKWajiEVkmI-eyRRdamwjhy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Substance misuse and addiction: Clinical]]></video:title><video:description><![CDATA[People use substances or recreational drugs for various reasons. Initially it’s usually for fun or curiosity or to treat pain, but over time people can become reliant on them and it can lead to a substance-related and addictive disorders. 

Addictive disorders are uniquely challenging to treat because they’re medical conditions that cause social support networks to fall apart.

In addition, an individual craves and seeks out substances, despite facing harmful consequences. 

The addictive potential from substances come from their effect on the brain&amp;#39;s reward system and their ability to affect emotion, mood, and perception. 

They typically cause a dramatic increase in dopamine levels, which results in euphoria or a so-called “high.” 

Individuals typically make repeated attempts to quit and often relapse. 

Substance-related and addictive disorders are linked to biological factors - which is why individuals with a family history of substance use are at higher risk. 

There are also psychological factors, like using substances to self-medicate for mental health problems like PTSD and depression. 

Finally, there are environmental factors like neglect and abuse that put individuals at higher risk.

So substance-related and addictive disorders includes substance use disorders and substance-induced disorders which comprise three conditions: intoxication, withdrawal, and other substance or medication-induced mental disorders. 

There are 10 classes of drugs that can lead to substance-related disorders, each with its own particular presentation: alcohol; opioids; stimulants which includes amphetamine-type substances and cocaine; cannabis; caffeine; hallucinogens - which includes phencyclidine (PCP) as well as other hallucinogens; inhalants; one category for sedatives, hypnotics, and anxiolytics; tobacco; and a category for other substances. 

Caffeine can only lead to intoxication and withdrawal, but not substance use disorder. 

The]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_cysts_and_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qRdFBmYvT__516DDx3n7AumBQkec2--U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal cysts and cancer: Clinical]]></video:title><video:description><![CDATA[Renal masses can develop in both adults and children, and  sometimes, they’re due to genetic mutations. 

These masses may be either cysts or tumors, and they can be discovered incidentally during an abdominal ultrasound or a CT-scan or when an individual has symptoms like abdominal or flank pain. 

Renal cysts can be simple or complex, and they can also be solitary - meaning there’s just one cyst, or there can be multiple cysts - sometimes affecting both kidneys.

Simple cysts are the most common type of renal mass, and they typically occur in adults with otherwise healthy kidneys. 

On an abdominal ultrasound, they’re usually smaller than 1 centimeter, but can be up to 4 centimeters. They’re round and have a thin regular wall and are filled with liquid which makes them anechoic - so it basically looks like a small balloon filled with black fluid. 

Additionally, there can also be some fine septa and calcifications within the simple cyst. 

Usually they’re asymptomatic, and don’t need treatment. 

On the other hand, complex cysts are larger than 1 centimeter. On an ultrasound, they have thick, irregular walls and are multilocular- meaning they have septations within, that separate the cyst cavity into compartiments.

Complex cysts can cause symptoms like flank pain, and they can cause complications like infections, hemorrhage, and hypertension.

An infected cyst can cause symptoms like fever and fatigue. 

Sometimes, the infection can spread to the renal parenchyma, causing an acute pyelonephritis with symptoms like fever, acute flank pain or diffuse abdominal tenderness.

A CBC shows leukocytosis and neutrophilia, and the ESR and CRP are elevated. 

If the infection is limited to the cyst, then the urinalysis may be normal, whereas if the cyst causes acute pyelonephritis then pyuria, bacteriuria and proteinuria are present. 

Blood cultures may be positive with both a simple cyst infection and acute pyelonephritis, whereas urine cultures are typically po]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypoglycemics:_Insulin_secretagogues</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MjNk0pU7S8CWScjyx9hqyq-1SYGuzjGx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypoglycemics: Insulin secretagogues]]></video:title><video:description><![CDATA[Hypoglycemics are used to treat high blood sugar, a condition commonly known as diabetes mellitus. 

As a quick review, Type 1 diabetes mellitus, which most commonly affects children and adolescents, arises when certain cells of the pancreas known as beta cells are unable to produce enough insulin to maintain normal blood glucose levels. 

This is in contrast to Type 2 diabetes mellitus where the body is able to produce insulin, but the tissues don’t respond as well to it, or in other words, these individuals are insulin resistant.

In this video, we’ll be focusing specifically on the use of insulin secretagogues like sulfonylurea for the treatment of Type 2 diabetes. 

In general, diabetes mellitus occurs when your body has trouble moving glucose from your blood into your cells. 

This leads to high levels of glucose in your blood and not enough in your cells, and remember that your cells need glucose as a source of energy. 

So not letting glucose enter, means that the cells starve for energy despite having glucose right on their doorstep. 

Insulin reduces the amount of glucose in the blood by binding to insulin receptors embedded in the cell membrane of various insulin-responsive tissues like muscle cells and adipose tissue.  

When activated, the insulin receptors cause vesicles containing glucose transporter that are inside the cell to fuse with the cell membrane, allowing glucose to be transported into the cell. 

Now in Type 2 diabetes, the body usually makes insulin, but the tissues don’t respond as well to it. 

The exact reason why cells don’t “respond” isn’t fully understood, but the cells don’t move their glucose transporters to their membrane in response, which if you remember, is needed for glucose to get into the cell, these cells are therefore insulin resistant. 

Since tissues don’t respond as well to normal levels of insulin, the body ends up producing more insulin in order to get the same effect and move glucose out of the blood. 

They]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Burns:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FZZfLf2eRMezCoePeaEPmxHYRxarTdtt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Burns: Clinical]]></video:title><video:description><![CDATA[The skin is the largest organ of the body, and is made of the epidermis, the dermis, and the hypodermis. 

Burns result from exposure of skin cells to an overwhelming amount of energy in the form of heat, causing cellular necrosis. 

The degree of injury depends on the temperature, the duration of exposure, and the baseline structural integrity of the skin; which means younger children and elderly individuals are at higher risk of injury, because their skin is relatively weaker. 

Okay, burns can be classified based on the cause, or by the depth of injury which corresponds to the severity of the burn. 

Burns are most commonly thermal, which can result from scalds, such as hot water, or flames, such as from house-fires. 

Less commonly, burns can be electrical, like from exposure to lightning strike or high-voltage electrical current, or from exposure to chemical substances, which can be acidic or alkaline. 

Based on depth, burns can be first, second, or third degree. 

First degree burns are also called superficial burns, and involve the epidermis only. 

A prime example would be a simple sunburn from a day on the beach, which appears red, with no blisters.  

Second degree burns are further subclassified into superficial partial thickness burns, which involve the epidermis and the superficial dermis, and deep partial-thickness burns, which involve the epidermis and the deep dermis. 

Superficial partial thickness burns appear red and are often blistered, whereas deep partial thickness burns appear red or white, with no blisters. 

Third degree burns are full-thickness burns, extending through and destroying the entire dermis. 

These appear leather-like with a charred appearance and tense feel. 

Usually, third degree burns are surrounded by a rim of second degree burns. 

Fourth degree burns extend beyond the dermis, destroying fascia, muscle or bone. 

Because third and fourth degree burns destroy the entire skin, they destroy the skin nerve endings, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Insulin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0hfd4MuaSliAtFYs2pjOrX-USue5aq3n/_.jpg</video:thumbnail_loc><video:title><![CDATA[Insulin]]></video:title><video:description><![CDATA[Insulin is a hormone that’s involved in lowering the blood sugar levels or glycemia after a meal. Insulin comes from the latin insula, which means island, because this hormone is produced by some small islands of cells scattered throughout the pancreas that are called pancreatic islets or islets of Langerhans.

The pancreas lies in the upper left part of the abdomen, right behind the stomach. The vast majority of the pancreas is made up by exocrine glands in charge of secreting digestive enzymes into the small intestine to help digestion. But about 1 to 2% of the mass of the pancreas is made up by the islets of Langerhans, which are endocrine glands made up by five different cell types, and each cell type secretes a specific hormone. The most abundant are the beta cells, which produce insulin. But you can also find alpha cells that secrete glucagon, delta cells that secrete somatostatin, gamma cells that secrete pancreatic polypeptide, and finally epsilon cells that secrete ghrelin.

Let’s focus on beta cells. Beta cells are in charge of producing insulin, which is a peptide hormone encoded by the INS gene on chromosome 11. Insulin is first synthesized as a single polypeptide called preproinsulin. A short tail called leader or signal peptide is cleaved from preproinsulin to form proinsulin. Proinsulin consists of three peptide chains in the order B, C for connecting peptide, and A. Proinsulin is then further cleaved at two positions, releasing a fragment called the C-peptide, and leaving the B- and A- chains, and two disulfide bonds which link the B- and A- chains together to form insulin. This mature insulin is stored inside granules within the beta cells where it waits until it’s released into the blood.

The most important trigger for insulin secretion is glucose. Beta cells are sensitive to glucose concentrations in blood, and when blood glucose levels rise, beta cells secrete insulin into the blood to help lower those levels and store glucose. Other s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Toxidromes:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xj4G9-jhS4aZcEuvnm8JY80zTRCBGmqv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Toxidromes: Clinical]]></video:title><video:description><![CDATA[Accidental and intentional intoxications or drug overdoses produce toxidromes, which are a combination of symptoms and characteristic findings for a particular substance or class of substances. 

Sometimes there’s more than one substance that’s used, so there are a combination of findings. 

The general goals of management include stabilizing the clinical condition and controlling the symptoms, as well as finding the causing substance and give specific treatment. 

Individuals who present only mild toxicity can be observed in the emergency department until they are asymptomatic, while those with significant toxicity should be admitted to an intensive care unit or ICU.

The initial step in evaluating a person who may have a toxidrome is to assess the A, B, C’s - airway, breathing and circulation. 

The respiratory rate and oxygen saturation should be assessed and if the oxygen saturation is lower than 92%, high-flow oxygen can be given by face mask. 

In individuals with severe respiratory distress, intubation and mechanical ventilation may be needed right away. 

Next, an electrocardiogram is done along with continuous cardiac monitoring to assess for cardiac arrhythmias. 

If the individual is hypotensive, then 2 liters of IV isotonic crystalloid solution is given, followed by a norepinephrine drip. 

Next, if the individual has neurological symptoms- like confusion or delirium, then IV thiamine is given to prevent Wernicke’s encephalopathy. That’s usually caused by vitamin B1 deficiency, which is often due to ethanol abuse and can cause the triad of nystagmus, ataxia, and confusion. 

Additionally, if the individual presents with respiratory depression, then an opioid overdose is the most likely cause. In this case, 0.05 milligrams of iv naloxone or 0.1 milligrams of intramuscular naloxone is administered. The dosage is then doubled every 2 minutes until reversal of respiratory depression. 

Now, if the individual presents within two hours from the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neonatal_jaundice:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dJ_Ylj5uR3C2oMRtSW2ubzn7R5CEieaG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neonatal jaundice: Clinical]]></video:title><video:description><![CDATA[Neonatal jaundice -also called icterus- is the yellowish pigmentation of the skin and sclera that appears when total bilirubin levels rise above the 95th percentile for age, which is usually around 2 mg/dL. 

Total hyperbilirubinemia can be predominantly due to unconjugated- or indirect bilirubin or it can be due to conjugated-or direct bilirubin and it largely depends on where bilirubin metabolism is disrupted.

So jaundice can be thought of as prehepatic, hepatocellular, or posthepatic. 

If total bilirubin levels are elevated and conjugated bilirubin levels are normal, then that means that there’s a high amount of unconjugated bilirubin. 

Normal conjugated bilirubin levels are defined as less than 1 milligrams per deciliter if the total bilirubin is lower than 5 milligrams per deciliter or less than 20 percent of the total bilirubin if the total serum bilirubin is higher than 5 milligrams per deciliter. 

Unconjugated hyperbilirubinemia is almost always a completely normal phenomenon, called physiologic jaundice of the newborn. It’s extremely common and develops in the majority of infants, especially preterm infants, within the first two days to 1 week of life. 

At birth, newborns have a high hematocrit, but their red blood cells have a shorter life. As a result, when that large number of red blood cells turn over, a lot of hemoglobin gets released. That hemoglobin gets broken down into unconjugated bilirubin.

Now, newborn livers are relatively inefficient at conjugating bilirubin and they’re also inefficient at excreting this conjugated bilirubin into the intestinal tract, and that inefficiency leads to unconjugated hyperbilirubinemia.

Usually, this is totally benign, because the total bilirubin rises slower than 0.2 milligrams per deciliter per hour or 5 milligrams per deciliter per day, and the overall level doesn’t exceed 18 milligrams per deciliter, and resolves spontaneously within 1 week in full-term infants or 2 weeks in preterm infants. 

A]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Miscellaneous_hypoglycemics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v_c8qPLeS1yqcrJ8WZrJbsiuSICsqZB6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Miscellaneous hypoglycemics]]></video:title><video:description><![CDATA[Hypoglycemics are used to treat high blood sugar, a condition commonly known as diabetes mellitus. 

As a quick review, Type 1 diabetes mellitus, which most commonly affects children and adolescents, arises when certain cells of the pancreas known as beta cells are unable to produce enough insulin to maintain normal blood glucose levels. 

This is in contrast to Type 2 diabetes mellitus where the body is able to produce insulin, but the tissues don’t respond as well to it, or in other words, these individuals are insulin resistant.

Many hypoglycemics, like sulfonylureas, promote the release of insulin from the beta cells of the pancreas and therefore are known as insulin secretagogues. 

In this video, however, we’ll be focusing specifically on the use of non-secretagogues in the treatment of Type 2 diabetes. 

These medications include multiple classes of medications such as biguanides, thiazolidinediones, alpha glucosidase inhibitors, amylin analogues, and sodium glucose transporter 2 inhibitors.  

It’s important to note, however, that diet and exercise should always be the first step in managing diabetes before initiating medications, and should generally be continued while on medication as well.

There are two classes of medications that increase insulin sensitivity and decrease the production of new glucose and they include biguanides and thiazolidinediones. Let&amp;#39;s start with the biguanides. 

Biguanides are the first line of therapy for the treatment of type 2 diabetes. There is one main medication in the biguanide class and that is metFORMIN. 

It&amp;#39;s main mechanism of action is to decrease the production of new glucose from the liver, or to inhibit hepatic gluconeogenesis. 

Although the exact mechanism remains unknown, it’s believed that metFORMIN does this by increasing the activity of a liver enzyme known as AMP-dependent protein kinase (or AMPK). 

AMPK has many complex functions, namely it plays a role in insulin sig]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chlamydia_pneumoniae</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XWOMI2l_QJGsk4TDuX0pdpBIR8GF4zwz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chlamydia pneumoniae]]></video:title><video:description><![CDATA[With Chlamydia pneumoniae, which also used to be called Chlamydophila pneumoniae in the past, Chlamydia comes from “cloak” and pneumoniae means, well, pneumonia. 

So, Chlamydia pneumoniae are bacteria that hide inside host cells, particularly cells of the respiratory tract, and they cause pneumonia in humans. 

Now, Chlamydia pneumoniae is classically considered Gram-negative, because it can&amp;#39;t retain the crystal violet dye used during gram staining. 

Additionally, it has an outer lipopolysaccharide membrane which all Gram-negative bacteria also have. However, other Gram-negative bacteria also have a thin peptidoglycan layer under the lipopolysaccharide membrane, whereas Chlamydia pneumoniae doesn’t. 

Without it, Chlamydia can’t retain the pink safranin dye used during Gram staining, so they’re not technically Gram-negative either, which is why they’re more correctly called atypical bacteria. 

To visualize them, a Giemsa stain is required, which makes them look blue or reddish blue. 

Now, Chlamydia pneumoniae is non-motile and round-shaped, and is also an obligate aerobe, meaning that they depend on oxygen for survival. 

Additionally, Chlamydia pneumoniae are obligate intracellular pathogens which means they are unable to generate ATP so they rely on other cells for energy. 

When outside of a host cell, Chlamydia pneumoniae are metabolically inactive. 

So, this means that they can’t grow on artificial mediums but rather, require a host cell for culture. 

Ok now, when C. pneumoniae enters a host cell, it undergoes a life cycle that alternates between two distinct forms. 

The first is the small spore-looking form called the elementary body, and it’s the infective form of this bacteria. 

After the elementary body enters the host cell, it gets enclosed in a vacuole called an inclusion, where it transforms into a metabolically active, star-looking form, called the reticulate body. 

The reticulate body can use the host cell resources to divid]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abdominal_trauma:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d61nDg25T6yhdowEHzzXQQriQl2EXxK2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abdominal trauma: Clinical]]></video:title><video:description><![CDATA[Abdominal trauma is defined as injury anywhere between the nipple line and inguinal creases, and can be blunt, like from motor vehicle accidents, or penetrating, like from stab wounds or gunshot wounds. 

As with any trauma, evaluation begins with the primary survey, which includes the ABCDEs; airway, breathing, circulation, disability and exposure. 

The main goal of the primary survey is to assess and treat for immediately life-threatening injuries. 

Okay, so if the individual is talking to you with a clear voice, their airway is intact. If not, assess their ability to maintain the airway, or if they needed assisted ventilation with a bag-valve mask or even endotracheal intubation. 

As for “breathing”, look for tracheal deviation and listen to the breath sounds. 

Also, if the individual is hypoxic, provide 100% oxygen using a non-rebreather mask. 

Next, look at the heart rate and blood pressure, as tachycardia or hypotension may indicate hemorrhagic shock. 

Assess for signs of inadequate end-organ perfusion, such as altered mental status, decrease urine output, cool or pale skin, and delayed capillary refill. 

Also, insert two large-bore intravenous lines, and prepare for the need for blood products. 

Bedside ultrasound can also be used in the primary survey - and it’s called focused assessment with sonography for trauma, or the FAST exam. 

The ultrasound probe explores the pericardial cavity, then the right flank, also called the hepatorenal recess or Morison’s pouch, and then the left flank which looks for perisplenic fluid, and finally the suprapubic region to look for fluid around the bladder. 

When views are added to look for a pneumothorax, hemothorax, or cardiac tamponade, it’s called an extended FAST or E-FAST. 

The FAST exam is non-invasive, portable, and great at detecting intra abdominal bleeding, but it does require skill to use it properly and doesn’t identify which organ is injured. 

For example, fluid in the hepatorena]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infertility:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SqKGiHEzQzW4Z-BoR7nqX3rcRnGXbgxL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infertility: Clinical]]></video:title><video:description><![CDATA[Infertility is classically defined as the inability of a couple to conceive after 12 months of sexual intercourse without using contraception. Sometimes, the evaluation for infertility begins at 6 months, depending on female and male factors. Female factors include age over 35, other gynecologic conditions like endometriosis, prior pelvic inflammatory disease or suspected uterine pathology, like in women who have undergone uterine surgery in the past. Evaluation should also start at 6 months in females with risk factors for premature ovarian failure, like previous ovarian surgery, chemotherapy or pelvic radiation therapy, autoimmune disease, smoking, or a family history. Male factors include history of testicular surgery or radiation, chemotherapy, adult mumps, impotence or other sexual dysfunction, or history of fertility issues with a prior partner. 

The infertility work-up is done for both partners at the same time. In males, the semen analysis can identify most causes of infertility. This is when semen is collected in a sterile cup after 2 to 7 days of ejaculatory abstinence - meaning no semen release through sexual intercourse or masturbation - and then analyzed under a microscope. Because sperm concentrations tend to vary a lot between semen samples, at least two samples should be collected at least one week apart. The standard semen analysis can give information about semen volume, as well as sperm count, motility and morphology. 

Semen volume is normally greater than 2 milliliters, sperm concentration should be above 15 million spermatozoa per milliliter of ejaculate, and total sperm count should be over 40 million spermatozoa per ejaculate. Total sperm motility should be over 40%, meaning over 40% of sperm should be moving, with at least 32% showing forward motility. The last parameter is morphology - at least 4% of sperm should have a head, a neck, and a single tail. That may sound like a low bar, but that’s all it takes.

Sperm number abnormal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gestational_trophoblastic_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q7vDue4LSt22t7ZprjSAHhOcT4qb3EcB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gestational trophoblastic disease: Clinical]]></video:title><video:description><![CDATA[Gestational trophoblastic disease includes both benign and malignant proliferations of placental cells. 

At the benign end of the spectrum, there’s moles - and no, we’re not talking about the cute little brown ones above the upper lip. In this case, moles refer to a molar pregnancy, and they are also called hydatidiform moles. 

At the malignant end, there’s invasive moles, which derive from the benign moles, and choriocarcinoma - which is placental cancer that most frequently occurs in the absence of a molar pregnancy. 

Risk factors for molar pregnancies include maternal age extremes - like younger than 20, or older than 35, and a previous molar pregnancy. 

Moles result from errors in normal fertilization. 

Normally, at fertilization, a single egg with 23 chromosomes fuses with a single sperm with 23 chromosomes, resulting in a new organism with 46 chromosomes. This can go wrong in two ways, so we have two kinds of moles - complete, or classic, and incomplete, or partial mole. Both lead to an abnormal proliferation of placental cells, and an abnormal placenta. 

The difference is that a complete mole appears when a chromosomally empty egg fuses with a normal sperm, and the sperm genetic material duplicates to form a 46 chromosome organism. However, this organism doesn’t have both maternal and paternal chromosomes, so the mole develops into a mass rather than developing into a fetus. 

An incomplete mole, on the other hand, appears when a normal egg is fertilized by two sperm - which forms an organism with 69 chromosomes, that usually develops into non-viable fetal parts.

With a complete mole, the placenta secretes a huge amount of HCG. So affected females present with signs of pregnancy, like missed periods, and a positive urine pregnancy test. 

Vaginal bleeding is another sign, which may range from light spotting to heavy bleeding, and parts of the mole may even be eliminated, and they look like grapes, or cherry-like clusters. 

Additionally, this]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Somatic_symptom_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7SfdVpL5Q5GNWqT2mLODqaByTfGxqX2A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Somatic symptom disorders: Clinical]]></video:title><video:description><![CDATA[Somatic symptom disorders, formerly known as somatoform disorders, are unexplained physical symptoms that are recurrent and cause significant distress and impairment to someone’s daily life.

The exact cause of somatic symptom disorders isn&amp;#39;t clear, but there may be biological causes like having an increased sensitivity to pain. 

Many symptoms are also affected by a person’s emotional response to symptoms - so they’re affected by attitude and personality. 

Some conditions may also be learned behaviors like learning that being sick attracts attention. And this can especially happen when a person develops the condition in early childhood. 

Somatic symptom disorders are more commonly seen in people with a history of substance abuse, anxiety, and depression.

Somatic symptoms can be wide-ranging like pain, tingling, shortness of breath, to general fatigue and weakness. 

In somatic symptom disorder, the history, physical exam, test results, and imaging are either normal or don’t explain a person&amp;#39;s symptoms. 

Often, in addition to the symptoms themselves, individuals have a lot of anxiety about the symptoms. 

The complaints are recurrent and should occur for at least six months. 

Finally, the symptoms should not be better explained by another mental disorder, and it should cause significant distress or impairment in all areas of functioning.

The seven conditions in the category in DSM-5 called somatic symptom and related disorders include somatic symptom disorder, illness anxiety disorder, conversion disorder, psychological factors affecting other medical conditions, factitious disorder, other specified somatic symptom and related disorder, and finally, unspecified somatic symptom and related disorder.

The most studied condition in this category is somatic symptom disorder. 

First, individuals must have at least one somatic symptom which causes significant interference with daily life. 

Second, they must have persistent and excessive]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lower_back_pain:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b7gxnRB9QJeBmtE4d38W8ifVQ3i4R5vK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lower back pain: Clinical]]></video:title><video:description><![CDATA[Back pain can originate from the spinal cord, the nerve roots, the vertebral column, the surrounding muscles and ligaments, or even extra-spinal structures such as abdominal organs. 

Most lower back pain is considered non-specific musculoskeletal back pain, and is due to strained muscles and ligaments in the back. But sometimes it’s due to a specific disorder, and these can be categorized into 6 groups: degenerative disorders, mechanical disorders such as disk herniation and lumbar spinal stenosis, infections such as osteomyelitis and spinal epidural abscess, spinal epidural hematoma, inflammatory disorders such as ankylosing spondylitis, and cancers, such as multiple myeloma. 

Specific disorders are often identified with a thorough history, and to help remember some common clues there’s the mnemonic: “TUNA FISH”.

“T” is for trauma. “U” is for unexplained weight loss, which may suggest a cancer. “N” is for neurological symptoms, like sensory loss, pain, or weakness in the legs, loss of sensation in the perineal area - which is called saddle anesthesia - as well as bowel, bladder, or sexual dysfunction. 

“A” is for age over 50, which increases the risk of cancer. 

“F” is for fever, which may indicate an infection. 

“I” is for intravenous drug use or an immunocompromised state, both of which also increase the risk of infection. 

“S” is for steroid use, which can cause secondary osteoporosis and vertebral fractures. 

And finally, “H” is for a history of cancer. 

On physical examination there might be some clues that suggest a specific disorder as well. 

For example, erythema might be due to an underlying infection or and inflammatory process like psoriatic arthritis.

On palpation, if there’s a midline, point of focal tenderness then that could be due to an infection, cancer, or fracture.

Also, if there’s a problem with the straight leg test then that could be due to a radiculopathy. 

If there’s no specific finding in the history or physical that ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Elimination_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u3zjjfyYS3uC9_bMf6BIuwcaSN2Rxxv2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Elimination disorders: Clinical]]></video:title><video:description><![CDATA[Elimination disorders involve the elimination of feces - encopresis - or urine -enuresis, and they usually occur in children who struggle with going to the bathroom. 

Although it is not uncommon for them to have occasional &amp;quot;accidents&amp;quot;, when these behaviors occur for longer than three months particularly in children older than 5 years, they might have an elimination disorder.

There are many predisposing factors, including genetics, psychological factors, delayed or lax toilet training, and psychosocial stress. 

Enuresis has been associated with delays in the development of normal circadian rhythms of urine production, resulting in nocturnal polyuria, and with reduced functional bladder capacities and bladder hyperreactivity. 

In encopresis, painful defecation can lead to constipation and a cycle of withholding behaviors that make encopresis more likely. 

Constipation may develop for psychological reasons like anxiety about defecating, a more general pattern of anxiety, dehydration associated with a febrile illness, hypothyroidism, or medication side effect like anticonvulsants. 

Once constipation has developed, it may be complicated by an anal fissure, painful defecation, and further fecal retention. 

Although there are minimum age requirements for diagnosis, these are based on developmental age or ‘mental age’ and not solely on chronological age or ‘real age.’ 

Both encopresis and enuresis may be voluntary or involuntary, and although they typically occur separately, they might also co-occur.

Associated symptoms include low self-esteem, loss of appetite, abdominal pain, decreased interest in physical activity and withdrawal from friends and family as children often feel ashamed and end up avoiding situations that can lead to embarrassing accidents like at school or camps. 

According to DSM-5, there are four elimination disorders including enuresis, encopresis, other specified elimination disorder, and unspecified eliminat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skin_and_soft_tissue_infections:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZF5uHLl2QteMuG_nygiXjO31Q9SQ8-eO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skin and soft tissue infections: Clinical]]></video:title><video:description><![CDATA[Focal skin and soft tissue infections are often due to bacteria infections, and include conditions like impetigo, folliculitis, cellulitis, erysipelas, furuncles and carbuncles, and necrotizing fasciitis. 

The first step is getting a full history. 

In impetigo, there’s usually no pain, whereas in necrotizing fasciitis the pain is severe. 

Most skin infections tend to be localized and around a particular anatomic structure. 

For example, folliculitis, furuncles, and carbuncles involve the hair follicle. 

Also, a superficial infection like impetigo or folliculitis causes itchiness.

In erysipelas, the fever is high and abrupt in onset, and in necrotizing fasciitis the fever usually persists. 

Some individuals have had contact with other individuals with skin infections, and this is commonly the case with community-acquired methicillin-resistant S. aureus, which causes cellulitis and furuncles. 

On physical exam, there may be signs of systemic illness like fever and chills, and signs of toxicity like lethargy, tachycardia, and hypotension. 

Additionally, there may be adenopathy, which can occur in non-bullous impetigo and cellulitis, bullae which can be seen in bullous impetigo, and crepitus with edema that exceeds the rash border, which can be seen in necrotizing fasciitis. 

The rash may be papular as in folliculitis, vesicular or pustular like in impetigo, or there may be macular erythema like in cellulitis.

Additional labwork should be done when there are signs and symptoms of systemic toxicity. 

A Gram’s stain, skin and swab cultures can help identify a specific pathogen like community-acquired methicillin-resistant S. aureus. 

Blood cultures are unlikely to be positive in simple localized infections like impetigo and folliculitis, but should be taken when there’s deep tissue involvement like necrotizing fasciitis or erysipelas.

Other tests include a CBC, C-reactive protein level, and liver and kidney function tests. 

An x-ray can be done wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-corticosteroid_immunosuppressants_and_immunotherapies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VY7c1iRLT7CnoxyoAVoMQ-yaQauC_zpK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-corticosteroid immunosuppressants and immunotherapies]]></video:title><video:description><![CDATA[Non-corticosteroid immunosuppressants are a class of medications that suppress the immune system and they’re used primarily to reduce the immune response after organ transplantation and inorder to prevent transplant rejection. 

Imagine the immune system as an army ready to fight against anything foreign that might cause harm like microorganisms and toxins but without harming the body’s own cells. To make that work, the immune system is trained to distinguish non-self or foreign, from self. 

The soldiers of the army are our immune cells which are basically white blood cells. 

A specific type of the immune cells are the T cells and there are two main types: cytotoxic T cells and helper T cells. 

Cytotoxic T cells kill infected or cancerous cells, whereas T helper cells primarily support other immune cells. 

These cells like the generals on the battlefield: they secrete cytokines that coordinate the efforts of all the immune cells and that explains why immunosuppressants primarily act by inhibiting their action. 

Okay but first things first. When a T cell is initially formed it’s considered naive but later when that T cell encounters an antigen, it gets activated and turns into an effector T cell. This process requires two signals.

The first signal is the antigen itself, which is usually presented to the helper T cell by an antigen presenting cell like a macrophage. 

The second signal is called costimulation, and it’s when a ligand called CD28 on the surface of a T cell binds to a ligand called B7 on the antigen presenting cell. 

Once activated, the T helper cell begins making lots of a cytokine called interleukin 2, or IL-2. 

At the same time, the T helper cell also upregulates its IL-2 alpha receptor which is found on its surface. 

When IL-2 binds to these receptors it activates a signal pathway called the mammalian target of rapamycin, or mTOR, pathway. 

The mTOR pathway regulates cell proliferation and so the T cell starts to rapidly undergo D]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/What_are_mind_maps_and_how_do_you_use_them_effectively</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UWYyRQNAQ4ayGGLQSfCr5tLKQN2NEgod/_.jpg</video:thumbnail_loc><video:title><![CDATA[What are mind maps and how do you use them effectively]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of What are mind maps and how do you use them effectively through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peripheral_vascular_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vn5HTA6HTDia3pIl19htr7IGQzmB-PmW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peripheral vascular disease: Clinical]]></video:title><video:description><![CDATA[Peripheral vascular disease is an abnormal narrowing of arteries other than the ones that supply the heart or brain, and it most often affects the ones in the legs. 

Risk factors include being older than 60 years, smoking, hypertension, hyperlipidemia, diabetes, and metabolic syndrome. 

The most common underlying mechanism of peripheral artery disease is atherosclerosis, which results in the accumulation of lipid and fibrous material between the layers of the arterial wall.

Eventually, the affected artery becomes progressively narrower, and this may lead to pain, ulceration, and even gangrene.

Now, most people with peripheral vascular disease actually don’t have symptoms until occlusion becomes significant, which is when 70% of the vessel lumen is obstructed. 

Symptoms include intermittent claudication, which includes pain, numbness, or tiredness in the legs during walking or standing, and is relieved by rest.

This is because the blood supply may be enough to meet the muscle needs at rest, but not the increased needs during activity, leading to ischemia – so basically, occurs when oxygen demand is greater than oxygen supply. 

The perceived level of symptoms from intermittent claudication can be mild to extremely severe depending on the degree of blood supply. 

Intermittent claudication can present unilaterally or bilaterally, as buttock and hip, thigh, calf, or foot pain, singly or in combination. 

In addition, pulses in one or both groins are diminished, and bilateral aortoiliac disease that is severe enough almost always causes erectile dysfunction.

The triad of intermittent claudication, absent or diminished femoral pulses, and erectile dysfunction is known as Leriche syndrome.

Location of pain depends upon the artery involved. Lower aorta or iliac artery involvement causes pain in the hips and buttocks. 

Iliac or common femoral artery involvement causes pain in the thigh. 

Superficial femoral artery involvement causes pain in upper two thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexual_dysfunctions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6AtJh_4GTXiALhpdv3nklp_eSGKpsmT3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sexual dysfunctions: Clinical]]></video:title><video:description><![CDATA[Sexual dysfunctions are a group of dysfunctions that prevent individuals from wanting or enjoying sexual activity. They can have a profound impact on a person’s life, and can lead to high levels of distress and anxiety.

There are many factors which may lead to sexual dysfunctions.

Emotional factors include depression, sexual fears or guilt, past sexual trauma, and anxiety. 

Physical factors include pain and discomfort during sex. 

Additionally, drugs, such as alcohol, nicotine, or narcotics, premenstrual syndrome, pregnancy, the postpartum period, and menopause can all affect a person’s libido and the ability to experience sexual pleasure.

Sexual dysfunctions can be divided into four subtypes: lifelong or acquired and generalized or situational.

Lifelong is when the sexual problem has been present from first sexual experiences; acquired applies to problems that develop after a period of relatively normal sexual function; generalized is when the problem occurs across many types of stimulation, situations, or partners; and situational refers to sexual difficulties that only occur in certain contexts. 

In all the disorders, the sexual dysfunction should not be better explained by a nonsexual mental disorder or as a consequence of severe relationship distress or other stressors, and it shouldn’t be attributable to another medical condition. 

Additionally, the symptoms must persist for at least 6 months and should cause significant distress. 

Sexual dysfunctions can be further divided into three categories: male sexual disorders which include delayed ejaculation, erectile disorder, male hypoactive sexual desire disorder, and premature ejaculation; female sexual disorders which include female orgasmic disorder, female sexual interest or arousal disorder, and genito-pelvic pain or penetration disorder; and three common disorders, namely substance or medication-induced sexual dysfunction, other specified sexual dysfunction, and unspecified sexua]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parathyroid_conditions_and_calcium_imbalance:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/B2oxHC52Sl2DoY6S5yDWR5wFQPCDH65J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parathyroid conditions and calcium imbalance: Clinical]]></video:title><video:description><![CDATA[There are a number of ways you can measure calcium in the blood. 

First, there’s total calcium levels and this is made up of three fractions. 

About 40 percent of the calcium is bound to albumin and about 15 percent is bound to minerals and the remaining 45 percent freely circulates the body and it’s called ionized calcium. 

Total calcium levels range between 8.5 to 10.5 milligrams per deciliter, while ionized calcium ranges between 4.8 and 5.7 milligrams per deciliter. 

When total calcium levels fall below 8.5 milligrams per deciliter, it’s considered hypocalcemia and when total calcium levels rise above 10.5 milligrams per deciliter, it’s considered hypercalcemia. 

Okay, let’s start with hypocalcemia. 

Individuals with hypocalcemia can be asymptomatic or have symptoms like tetany - which are intermittent muscular spasms - and perioral tingling. 

On clinical examination, there may be a positive Chvostek’s sign. That’s when the facial muscles contract in response to tapping the skin over the facial nerve, just 2 centimeters anterior to the ear. 

Another sign is the Trousseau sign. That’s where a blood pressure cuff is placed over the individual’s arm and is inflated to a pressure above the systolic blood pressure and is held like that for 3 minutes. 

A positive Trousseau sign is when there’s a muscle spasm in the arm and forearm. 

Now, the first thing to do in hypocalcemia is redo the lab work to make sure that the reading is accurate. 

If hypocalcemia is confirmed, then the next thing is to check albumin levels. 

Since most of the total calcium is bound to albumin, any rise or fall in the albumin will affect total calcium levels, leading to pseudohypocalcemia. 

Normal albumin levels are 4 milligrams per deciliter and normal total calcium levels are 10 milligrams per deciliter. 

For every 1 milligram per deciliter drop in albumin, calcium levels lower by 0.8 milligrams per deciliter. So, based on this, the corrected calcium levels can be calc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nephritic_and_nephrotic_syndromes:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3GK16sQdSNOOUNiZwarhUA35SS6MT_Lx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nephritic and nephrotic syndromes: Clinical]]></video:title><video:description><![CDATA[Glomerular diseases damage the glomeruli which disrupts the filtration process, and allows  blood or proteins to get into the urine. Usually a kidney biopsy is needed to determine the cause. 

Specifically, microscopy and immunofluorescence along with electron microscopy can be done on the kidney biopsy to classify the disease. 

Some glomerular diseases cause a clinical syndrome like nephrotic syndrome or nephritic syndrome. 

But other times, a glomerular disease, may only cause an isolated symptom like hematuria. 

For example, IgA nephropathy can cause isolated hematuria, or it can cause nephritic syndrome. 

Now when an individual is suspected of having renal disease, BUN and creatinine levels are checked and based on creatinine levels, the eGFR is calculated to assess renal function. 

Additionally, urinalysis is done both by microscopy and dipstick, and a 24-hour protein collection is done as well. 

Microscopy gives information about what the cells in the urine look like. 

Now, the dipstick test is more of a qualitative and semiquantitative test- try saying that three times fast. It can give information about what’s in the urine- such as blood or proteins, but can’t exactly say how much of it there is. 

That’s why a 24-hour protein collection is done in order to determine how much protein is lost through urine. 

The 24 hour protein collection can show moderate proteinuria which is between 1 and 3.5 grams per day and this usually indicates nephritic syndrome or isolated proteinuria, or it can show severe proteinuria, which is greater than 3.5 grams per day and this is nephrotic syndrome range proteinuria.  

An alternative to a 24-hour protein collection, is calculating the urine protein/creatinine ratio using spot urine samples. This is calculated by dividing the urine protein by the urine creatinine. 

Glomerular disease can manifest in a number of ways. First, there’s isolated hematuria which can be macroscopic if it’s seen by the naked eye, o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Food_allergies_and_EpiPens:_Information_for_patients_and_families_(The_Primary_School)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FgH6uNzhT1WFblrxblhGoEoXQ3O1_J20/_.jpg</video:thumbnail_loc><video:title><![CDATA[Food allergies and EpiPens: Information for patients and families (The Primary School)]]></video:title><video:description><![CDATA[A food allergy is a medical condition where there’s an abnormal immune reaction to some food. 

It’s different from food intolerances because it involves the immune system. 

Now, any food can cause allergies. But, the most common are the big eight: milk; eggs; peanuts; tree nuts, like almonds, walnuts, and pecans; seafood, like bass, flounder, and cod; shellfish, like crabs, lobster, and shrimp; soy; and wheat. 

Now, normally food doesn’t cause an allergic reaction. 

But a food allergy can develop in two steps; a first exposure; and then a second exposure later, which usually is a lot more serious. 

So, let’s say a person eats shrimp for the first time, and for some reason has an immune response where antibodies are produced in his body that specifically recognize shrimp as a bad actor, called an allergen. 

These shrimp-specific antibodies then stay in the body and lay around, looking out for shrimp. 

If that same person has a second exposure to shrimp, maybe even months later, the shrimp-specific antibodies spot the shrimp and cause the immune system to leap into action, releasing a bunch of molecules in the body which cause many of the symptoms of an allergic reaction. 

A life-threatening reaction, called anaphylaxis, can develop minutes to hours after even a very small second exposure to the food allergen, even if it is just breathing in allergen dust or contacting a contaminated surface. 

And while symptoms can vary between people and reactions, they can include minor skin rash or hives, to more serious symptoms like itching, swelling or tingling of the eyes, lips, tongue, mouth or throat; vomiting; diarrhea; stomach cramps; dizziness and fainting; plus wheezing, coughing, and difficulty breathing. 

Sometimes symptoms can improve for a bit, but then get worse again over a few hours. 

With every re-exposure to the food allergen, the reaction can get even more severe and in some cases be life threatening.

Early recognition and management of al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Childhood_oral_health:_Information_for_patients_and_families_(The_Primary_School)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/obcW_0kJSG2FRouF8eqS_cDiRjKu9Cak/_.jpg</video:thumbnail_loc><video:title><![CDATA[Childhood oral health: Information for patients and families (The Primary School)]]></video:title><video:description><![CDATA[Oral health is much more than just a pretty smile. 

In fact, poor oral health can impact a child’s growth and development, behavior, social interactions, and even their ability to learn in the classroom. 

This is because the pain from cavities can make it hard for a child to concentrate and complete a task in school, can cause a poor night’s sleep, and eventually can cause poor school attendance.

Cavities can also develop into other serious infections in their mouth and can lead to hospitalization. 

Children with tooth decay can also become self conscious about the way their teeth look, and it can make them shy or even withdraw from their peers. 

Now, although cavities are the most common chronic childhood disease, the good news is that they’re completely preventable with some healthy habits.

First, let’s go over how and why cavities might form. 

Each tooth is covered by a thin layer of sticky plaque. 

The plaque can stick to a sugar called sucrose which is found in various foods and drinks. 

The plaque also houses bacteria which use sucrose for energy, and generate an acid that can slowly destroy the surface of the teeth.

Over time, if more and more acid is released by the bacteria, the tooth can break down and a hole can appear on the surface of the tooth. 

This is called a cavity. 

There are several ways to prevent cavities.

First off, it’s important to minimize foods and drinks with lots of sugar like fruit juice, soft drinks, or sports drinks, as well as products that stick to the teeth like hard candy, honey, gummy vitamins, fruit leather, or dried fruits like raisins.

In fact, it’s best to replace all juice or soda in the home or classroom with water. 

Next, each time a child consumes food or drink with sugar the bacteria in the dental plaque make acid for 20 to 40 minutes.

So, it’s best to give children food at regular intervals during the day, rather than having them eat throughout the day without any breaks. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ADHD:_Information_for_patients_and_families_(The_Primary_School)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BhNL9g-eRoSvxdabGKD6zZe3Sh_V_txf/_.jpg</video:thumbnail_loc><video:title><![CDATA[ADHD: Information for patients and families (The Primary School)]]></video:title><video:description><![CDATA[ADHD, which is the abbreviation for attention-deficit hyperactivity disorder, is the most common mental health diagnosis affecting children in America, and there are concerns about both underdiagnosis and overdiagnosis. 

ADHD refers to a spectrum of behaviors. 

There are genetic and environmental exposures that play a role in the development of ADHD, however, at this point in time we cannot know what specifically caused an individual child’s ADHD. 

ADHD is different for everyone.  

For some children ADHD causes hyperactivity, for others ADHD causes only difficulty focusing or keeping attention, and in some kids ADHD causes challenges with both. 

As a result, some children with ADHD may only have challenges with inattention. They may not have disruptive behaviors but rather only struggle to keep focused on a task at hand. 

Other children with ADHD are hyperactive; they often struggle to sit still, have trouble waiting, interrupt others during conversations, and have difficulty following classroom rules. In addition, they can be impulsive, make rash decisions and make careless mistakes. 

Again, there are many children with ADHD who have both inattentive and hyperactive symptoms. 

Regardless of the symptoms, many students with  ADHD can begin to fall behind in their academic work and can sometimes miss days from school because of significant behavior problems in the classroom. 

To make matters worse, ADHD can take a toll on children’s friendships; their disruptive and impulsive behavior can result in being shunned or bullied by peers. 

Needless to say, ADHD can be hard on children as well as their teachers and families.

The first and probably the most important step is noticing that the child can’t keep attention, something that both teachers and parents are uniquely able to do. 

Teachers are very helpful in identifying children since the classroom setting is often the place where children exhibit symptoms. The expectations to pay attention and co]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Childhood_nutrition_and_obesity:_Information_for_patients_and_families_(The_Primary_School)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4r5xpur4QR_666ixc7wM6-g3QtK5gzrv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Childhood nutrition and obesity: Information for patients and families (The Primary School)]]></video:title><video:description><![CDATA[With obesity rates rising for children worldwide, it’s important for everyone, including parents, teachers, and all caregivers, to know what they can do to help children avoid gaining unhealthy amounts of weight. 

With the exception of a very few children, obesity is most often the result of unhealthy eating habits. 

Some important other related factors include a person’s genetics, environment, behavior, and socioeconomic status.

Childhood obesity leads to long-term health consequences that last into adulthood. 

These include high blood pressure, elevated blood fats, type two diabetes mellitus, liver disease, arthritis, asthma, anxiety, depression, and many other diseases.

Obesity also comes with social stigma that can lead to low self-esteem, bullying, or other forms of mistreatment. 

If children are already overweight or obese, there are various ways to help them return to a healthy weight - including working with their pediatrician, dietitians, physical therapists, and behavioral counselors. 

Now, preventing obesity starts with a conversation about healthy eating behaviors including what, when, and how much to eat as well as how much physical activity to get. 

Here are three practices for home and school to help children build healthy eating habits for life:  limit sugar intake, control portion size, and pay attention to the types of food children eat. 

One of the first things that can be done is limiting sugar intake, particularly sweet beverages. 

Children between ages 2 to 18 years old should consume less than 25g, or roughly 6 teaspoons, of added sugar each day.  

This is less sugar than many may realize. 

One can of soda contains about 39 grams, or 9 teaspoons of sugar. 

Juice also contains concentrated sugar even though it’s a natural product. 

One apple juice carton contains about 28 grams, or 7 teaspoons of sugar. 

Having either one of these beverages is more sugar than a child should be consuming in an entire day, so it’s best to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Toxic_stress:_Information_for_patients_and_families_(The_Primary_School)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mTgKaJgwStmYJBpniXBpNMwzTDq4ZhKu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Toxic stress: Information for patients and families (The Primary School)]]></video:title><video:description><![CDATA[Everyday we encounter stressful situations, like our first day of school, meeting new people, or going through a job interview. 

In these situations, the body responds by activating our sympathetic nervous system. 

That’s the system that diverts blood away from organs like the intestines or the bladder, so that we can increase blood flow and energy to organs like the brain, heart, and muscles, which help us respond or cope. 

This is sometimes called the fight-or-flight response because it’s the same system that kept our ancestors safe in dangerous situations. 

Short bursts of stress are helpful, especially if the stress is addressed in a positive way, which often means with the help of a supportive social environment with parents, friends, or teachers that care. 

In fact, even a hug from a loved one can release hormones that can ease the stress and make it more tolerable - in that situation it’s called tolerable stress. 

But if there’s a stressful situation like the loss of a parent, and there isn’t a strong support structure to help cope with the stress, then the stress can persist and it can have negative effects like insecurity, anger, and fatigue. 

And when the stress system gets activated repeatedly, like when a child experiences physical abuse or chronic neglect, and if there’s no supportive social environment, then the stress can be overwhelming and have a lasting, biological impact. 

Basically, the brain and body adapt to chronic exposure to threat, by developing a heightened alarm state, and the body feels threatened all the time, even after the threat is removed. 

This type of stress isn’t tolerable and when it becomes chronic, it’s called toxic stress. 

And events that trigger toxic stress in children are called adverse childhood experiences.

Symptoms of toxic stress include difficulty sleeping, anxiety, fearfulness, and irritability. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Androgens_and_antiandrogens</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r1X9bcDgQXiWyw66xy4vKklhTguqpJ0z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Androgens and antiandrogens]]></video:title><video:description><![CDATA[Androgens are a class of steroid hormones that act as agonists to androgen receptors. 

Testosterone is the principal endogenous androgen, while synthetic androgens include testosterone derivatives and anabolic steroids. 

They bind to and activate androgen receptors and are used in the treatment of conditions where testosterone levels in the body drop lower than normal, such as primary or secondary hypogonadism. 

Now, antiandrogens or androgen antagonists include androgen receptor inhibitors, 5α-reductase inhibitors, and inhibitors of testosterone synthesis. 

They prevent the biological effects of androgens like testosterone in the body and are used in the treatment of prostate cancer, benign prostatic hyperplasia, hair loss in males, and hirsutism in females. 

Testosterone, the primary male hormone, is an androgen, andro meaning male and gen meaning “to produce,” which means testosterone helps generate the characteristics associated with male sexuality. 

The effects of testosterone are first seen in the fetus, where it guides development of the male urogenital tract and external genitalia, as well as testicular descent through the inguinal canal. 

Testosterone is primarily secreted by the fetal testicles. 

The fetal ovaries also secrete testosterone but at much lower levels, and this largely explains the differences in fetal development between boys and girls.

In puberty, the hypothalamic-pituitary axis regulates testosterone levels and gonadal function. 

The hypothalamus secretes gonadotropin-releasing hormone which causes the pituitary gland to secrete luteinizing hormone or LH and follicle-stimulating hormone or FSH. 

These hormones travel to the testes and cause leydig cells to convert cholesterol into testosterone through a number of steps. 

Two important intermediate molecules in that process are dehydroepiandrosterone, also called DHEA, and the molecule that it gets converted into - androstenedione. 

The last step is to have the testicu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_bone_tumors:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-kAv1SEDTay7L-y2GOAPHQLdSxGAgJbA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric bone tumors: Clinical]]></video:title><video:description><![CDATA[Osteosarcoma and Ewing&amp;#39;s sarcoma are primary skeletal malignancies that can occur in children. 

The tumors cause similar signs and symptoms, so the diagnosis is based on radiography findings and biopsy results. 

Both bone tumors cause a dull, aching pain that is mostly non-responsive to NSAIDs or acetaminophen. 

One particular aspect of the pain in bone tumors is that the initial mild pain becomes increasingly severe over a few months and sometimes gets worse at night. 

Additionally, the site might be swollen and occasionally there can be pathologic fractures after seemingly minor trauma. 

Palpation might also reveal a soft tissue mass. 

In osteosarcoma, the tumors are mostly on the metaphysis of a long bone like the femur or tibia, while Ewing’s sarcoma most frequently involves the diaphyseal or meta-diaphyseal regions of long bones like the femur, or the pelvis. 

Other locations for these tumors include the hip, spine, chest wall, and for Ewing’s sarcoma, even soft tissues. 

Usually there’s an isolated localized tumor, but some individuals also have pulmonary metastases, and that can happen for both Osteosarcoma and Ewing&amp;#39;s sarcoma. In those situations, individuals can also have dyspnea or cough.

Finally, systemic symptoms such as fever, weight loss, and decreased appetite are quite rare.

If there’s suspicion of a bone tumor, the first step is local plain radiographs.

Let’s start with osteosarcoma which is a tumor derived from neuroectodermal tissue. 

Plain films of the tumor site often reveal medullary and cortical bone destruction and a wide zone of transition with a moth-eaten appearance. 

The associated soft tissue mass is variably ossified in a radial or &amp;quot;sunburst&amp;quot; pattern, which is characteristic for osteosarcomas, alongside Codman triangle which is a triangular area of new subperiosteal bone that is created when a tumor raises the periosteum away from the bone. 

Laboratory evaluation is usually n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_constipation:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OealGSUaShGRmV4QRW_hSIG3TBqG5EYA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric constipation: Clinical]]></video:title><video:description><![CDATA[Constipation in children is a decreased stooling frequency or increased difficulty of passing stool, as compared to a child’s baseline. 

Normally, full-term neonates pass meconium, which is the very first stool which is usually thick and green-black, within the first 48 hours of life. Premature neonates, meaning those born before the start of the 37th week of gestation, can take a bit longer. After that, during the first three months of life, infants have about two to four stools a day. By the age of two years, toddlers generally have one or two stools per day. And by age four, children typically have one bowel movement per day.

If a neonate doesn’t pass meconium within the first 48 hours of life, has abdominal distention, refuses to feed, or has bilious vomiting, it should raise suspicion for imperforate anus, meconium ileus, and Hirschsprung disease. In an imperforate anus there’s a non-patent or tiny anal opening, which is anteriorly displaced relative to the base of the scrotum or vagina. In some cases, there can also be a fistula between the rectum and the urethra, bladder, or vagina, through which some meconium may drain.

About half of the neonates with an imperforate anus also have other congenital anomalies associated with VACTERL syndrome. VACTERL stands for Vertebral defects, Anal atresia, Cardiac anomalies, Tracheoesophageal fistula, Esophageal atresia, Renal anomalies, and Limb anomalies. So, the next step is to perform a posteroanterior and lateral-view x-ray of the sacrum, called a cross-table x-ray. This can help distinguish between a high-type or low-type defect, meaning that the intestine ends high or low in the pelvis and whether it’s associated with other sacral abnormalities. In addition, an ultrasound of the spine, heart, abdomen and limbs are needed to look for vertebral, cardiac, renal and limb abnormalities. Also, an NG tube can be placed and a chest X-ray can be obtained to look for signs of tracheoesophageal fistula and esophag]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Virilization:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/16GuQdOOSUOZI8t-EOCwLB2NQGeSYAVB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Virilization: Clinical]]></video:title><video:description><![CDATA[Hirsutism and virilization reflect excess androgen production in a genetically female individual, and are characterized by excess male-pattern hair growth.

Both hirsutism and virilization may or may not be associated with weight gain, acne, and even male pattern balding.

With virilization, however, females may also have a deepened voice and clitoromegaly, which are not seen with hirsutism. 

The excess androgens can come either from the ovary - and the main androgen here is testosterone - or the adrenal glands - which mainly secrete an androgen called dehydroepiandrosterone sulphate. 

Ok, now excess hair growth can be quantified using the Ferriman-Gallwey score. This score requires assessing the amount of hair present in nine body areas: the upper lip, chin, chest, upper and lower back, upper and lower abdomen, upper arms, and thighs. 

Hair growth in each of the nine areas are graded from 0, meaning no terminal hair growth, to 4, meaning extensive terminal hair growth.

Ethnicity must be taken into account when interpreting the score, as the normal amount of body hair can vary between ethnic groups.

So, for females of caucasian and african descent, scores between 8 and 15 indicate mild hirsutism, 16 to 25 indicate moderate hirsutism, and scores greater than 25 indicate severe hirsutism. 

For females of Asian descent, who have naturally sparse body hair, a score greater than 2 is sufficient to establish the presence of hirsutism, whereas for females of Mediterranean, Hispanic, and Middle Eastern descent, who naturally have more body hair, only a score higher than 10 is considered abnormal. 

Given this variation, the most important consideration is not necessarily the amount of body hair a female has, but rather if the pattern of hair growth has changed, or the rate of growth has increased. 

In order to elucidate the cause of excess body hair growth, the first step is to rule out any medications which may cause it - like minoxidil, or exogenous andro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Contraception:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4fwGwKOST1ONvY-5u4xx2b8SRNyyATyc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Contraception: Clinical]]></video:title><video:description><![CDATA[Contraception refers to various methods that can be used to prevent pregnancy, and they can be categorized by their efficacy. 

Think of efficacy as the number of pregnancies that occur in 100 females using that method over the course of a year. Ideally that number to be as low as possible.

Tier 1 methods are the most effective, with less than 1 pregnancy in 100 females in a year. These include types of long active reversible contraception, or LARC, which includes intrauterine devices and contraceptive implants, and irreversible methods, like a vasectomy and bilateral tubal ligation. Of course, these can sometimes be reversed, but the reversal success rates vary.  

Tier 2 methods are a little less effective, with 4 to 7 pregnancies in 100 females in a year. These include hormonal contraception, like contraceptive pills, patches, vaginal rings, and hormonal injections. 

Finally, tier 3 methods are the least effective, with over 13 pregnancies in 100 females in a year. These include the male and female condoms, diaphragms and cervical caps, spermicides and sponges, and “natural” contraceptive methods like withdrawal of periodic abstinence during the fertile period. 

Now, keep in mind that condoms are the only contraceptive method that also protect against sexually transmitted infections - so they should always be used when that’s a concern. 

So, let’s start with tier 1 methods - specifically, LARC. 

First, there’s intrauterine devices, which can be hormonal, meaning they contain a progestin called levonorgestrel, or non-hormonal, meaning they’re made out of copper. 

Both hormonal and copper IUDs are good choices in adolescent and adult females who want a long term, highly effective contraceptive method, and in females who want to avoid estrogen exposure because they may have other risk factors for deep vein thrombosis and pulmonary embolism, like smoking and being over age 35. 

Contraindications for both hormonal and copper IUDs include known or susp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neurodevelopmental_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zSYJPOpRRo_AE7nyVEaOkAVcSAqAy54Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neurodevelopmental disorders: Clinical]]></video:title><video:description><![CDATA[Pediatric neurodevelopmental disorders cause developmental deficits in areas like movement, language, and cognition, which can interfere with how a person functions independently in society. 

In some cases there are specific genes that are thought to play a role. But there are also a number of environmental risk factors like maternal use of alcohol, tobacco, or illicit drugs during pregnancy; preterm birth; and prenatal or childhood exposure to environmental contaminants like lead.

Now the range of deficits can vary from a tic disorder that affects facial movements to global impairments in language and cognition.

Sometimes, there are deficits and delays in achieving development milestones like having fluent speech by age 6. 

The neurodevelopmental disorders frequently co-occur; for example, individuals with autism spectrum disorder often have cognitive disability, and many children with attention-deficit/hyperactivity disorder or ADHD also have a learning disorder. Usually the symptoms occur in the early developmental period, but sometimes they’re not fully seen until a person is older like in some learning disorders.

For diagnosis, the areas where the deficits are must be substantially below those expected for the individual’s chronological age, and they significantly interfere with most of the daily activities that are appropriate to their chronological age, and impact academic productivity, prevocational and vocational activities, leisure, and play.

According to DSM-5, there are twelve conditions that can be divided into six categories: autism spectrum disorder; ADHD; specific learning disorder; intellectual disabilities which consists of intellectual disability and global developmental delay; communication disorders which include language disorder, speech sound disorder, childhood-onset fluency disorder, and social communication disorder; and motor disorders which is made up of developmental coordination disorder, stereotypic movement d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cervical_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GZFpJUZ1SLeabczhRzXOA1C5T_2uBtyZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cervical cancer: Clinical]]></video:title><video:description><![CDATA[Cervical cancer arises in the cervix, most frequently at the transformation zone - which is where the glandular epithelium of the endocervix meets the squamous epithelium of the exocervix. 

The most frequent type of cervical cancer is squamous carcinoma, and it’s almost always due to human papillomavirus, or HPV.

HPV strains 16 and 18 account for most cases, and strains 31, 33, 45, 52, and 58 account for the rest. 

However, it can take up to two decades for HPV infection to progress through precancerous lesions of increasing severity, and finally to cancer. 

So there are two key elements that make cervical cancer unique among cancers. 

First, vaccinating against high risk HPV strains can help prevent cervical cancer. 

Second, a pap smear can be done to screen for precancerous lesions. 

And if they’re found, it’s possible to remove the precancerous lesions before they progress to cancer.

As a result, cervical cancer is one of the most preventable gynecologic malignancies. 

Cervical cancer screening is the cornerstone of prevention, and should be done in both vaccinated and unvaccinated females between the ages of 21 to 65, with regular pap tests. 

With the pap test, a thin, long brush is used to scrape cervical cells off the cervix. 

The test takes about 2 minutes, but it can cause slight discomfort as well as light spotting may occur afterwards. 

A normal pap test is when microscopy shows no cervical cell abnormalities. And when that’s the result, screening can be repeated in 3 years. 

Cervical cell abnormalities can show up as either atypical squamous cells, or ASC or cervical squamous intraepithelial lesions, or CSIL. 

Atypical squamous cells look mildly atypical, and don’t necessarily develop into cervical cancer, whereas cervical squamous intraepithelial lesions are full-blown dysplastic, and have a greater chance of becoming cervical cancer.

ASC results can further be classified as either ASC-US, where US stands for unknown significance]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ij9ZlG3xRu6OSfjqjzsjuQfaR0W6Ilgq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock: Clinical]]></video:title><video:description><![CDATA[Shock is most commonly due to hypotension, which is a systolic blood pressure less than 90 mm Hg, or a mean arterial pressure less than 65 mm Hg, that leads to inadequate tissue perfusion and injury to various organ systems, like the brain, heart, kidneys, and liver. 

If left untreated, shock can cause irreversible multi-organ failure and death. 

Shock can be thought of with the following equation.  The mean arterial pressure is equal to the cardiac output times the systemic vascular resistance.

The cardiac output is equal to the heart rate times the stroke volume, and the stroke volume is dependent on the preload and the contractility.

So, the causes of shock can be either due to a decline in the cardiac output or the systemic vascular resistance. When one parameter declines, normally the other increases to try to compensate. 

A decrease in the cardiac output can be due to a decreased preload, decreased contractility or a heart rate that’s too fast or too slow. 

Decreased preload can be due to extracellular fluid volume depletion, such as from diarrhea, excessive diuresis, dehydration, or hemorrhage. These are all causes of hypovolemic shock. 

Preload can also decrease if there is something obstructing the entry of blood into or out of a cardiac chamber, and this is called obstructive shock. 

For example, tension pneumothorax and pericardial tamponade can compress the inferior vena cava, obstructing blood flow to the right ventricle, decreasing the cardiac output.

A massive pulmonary embolism can obstruct blood from circulating through the pulmonary vessels and getting to the left ventricle. 

Cardiogenic shock is when the decline in cardiac output is secondary to a decrease in contractility, such as in congestive heart failure, myocardial infarction, myocardial contusion, or due to dysrhythmias. 

Okay, on the other hand of the equation, we have things that decrease the systemic vascular resistance, or in other words result in peripheral vasodil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscle_weakness:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_iTDUgOJRNubjwMSBPMMHL2hTpmKegsq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscle weakness: Clinical]]></video:title><video:description><![CDATA[Muscle weakness is a decrease in muscle power. It’s sometimes confused for fatigue which is the inability to sustain an activity, or with bradykinesia, which is a slowness of muscle movement. 

So to measure weakness, there should be a decrease in power compared to what you would expect. 

Muscle power can be graded on a scale from 0 to 5. 5 is normal power. 4 is a slight decrease in power. 3 is active movement against gravity, but not to resistance. 2 is active movement, but not against gravity or resistance. 1 is a small trace contraction, like a flicker of a finger. And 0 is complete paralysis. 

Now, muscle weakness can generally arise from a problem in a few locations: the upper motor neuron; lower motor neuron; and the neuromuscular junction, or the NMJ, which includes the synapse and the muscle itself. 

The next part of the exam is assessing muscle tone; which is the resistance to passive stretch. 

In upper motor neuron lesions, the tone is increased and it’s called spastic paralysis. 

In lower motor neuron and NMJ lesions, the tone is decreased and it’s called flaccid paralysis. 

Next is muscle bulk, which is usually normal in upper motor neuron and NMJ lesions, whereas severe atrophy occurs in lower motor neuron lesions. 

Next, reflexes are usually hyperactive in upper motor neuron lesions, preserved in NMJ lesions, and hypoactive or absent in lower motor neuron lesions. 

Next are fasciculations, which are small muscle twitches under the skin that only occur in lower motor neuron lesions. 

Finally, the Babinski reflex and pronator drift are both unique clinical features of upper motor neuron lesions. 

A Babinski reflex is induced by lightly stroking the lateral aspect of the sole of the foot. 

Plantarflexion of the toes is the normal response, while dorsiflexion of the big toe and fanning of the other toes is a Babinski reflex. 

A Babinski reflex is normal in the first 18 months of life because the corticospinal tracts aren’t f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexually_transmitted_infections:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pwuDHwfvQV24MDvjPDYe80yGSFyrROcX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sexually transmitted infections: Clinical]]></video:title><video:description><![CDATA[Sexually transmitted infections or STIs are infections that get transmitted through sexual fluids or skin-to-skin contact during sexual intercourse. Some STIs primarily affect the genital organs- like gonorrhea and chlamydia, while others affect the whole body- like syphilis, HIV, and hepatitis B. Generally, with STIs, all partners with whom there has been sexual contact in the 60 days prior to the diagnosis should be evaluated and treated. On a side note, in this video we’ll be using the term “female” to refer to individuals who have female reproductive sex organs, and the term “male” to refer to those who have male reproductive sex organs. 

Okay, let’s start with infections that mainly affect the genital organs like Neisseria gonorrhoeae- which causes gonorrhea, Chlamydia trachomatis which causes chlamydia, and Mycoplasma genitalium - an increasingly recognized pathogen. These infections are usually asymptomatic, but in females, they can cause cervicitis and urethritis. Cervicitis causes changes in vaginal discharge, pruritus in the genital area, intermenstrual vaginal bleeding, or post-coital bleeding. With urethritis, there can be symptoms that suggest a urinary tract infection, like dysuria and frequency. If left untreated, these bacteria can ascend in the reproductive tract and cause pelvic inflammatory disease or PID- which is the inflammation of the uterus, fallopian tubes, the ovaries and of course, the cervix. Acute PID causes lower abdominal pain that worsens during sexual intercourse or sudden movement, post-coital bleeding, and intermenstrual bleeding. Chronic PID causes a low grade fever, weight loss, and abdominal pain. Sometimes, PID can be complicated by a tubo-ovarian abscess which can involve the fallopian tubes, ovaries, or other nearby pelvic organs. Now, in males, these infections can cause urethritis or epididymitis. With urethritis, there’s dysuria and penile discharge, and with epididymitis, there’s unilateral testicular pain and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Asthma:_Information_for_patients_and_families_(The_Primary_School)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v7h5zEr2QAWb5BQE88TK0nV4QQas8x7w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Asthma: Information for patients and families (The Primary School)]]></video:title><video:description><![CDATA[Asthma is a health problem that can make it hard to breathe. 

This can be very frustrating and scary. For kids, it can make them miss a lot of school. 

But - if you know what to do, asthma can be controlled.

With the help of parents, teachers, nurses, and doctors, the good news is that children with asthma can live healthy, active lives.  

They can go to school, play sports, play the trumpet--or whatever they love to do!

When you breathe, air moves from your nose or mouth into your lungs by passing through small tubes, called airways.  

People with asthma have trouble breathing because these airways get narrower, making it hard for air to move in and out. 

Let’s take a closer look at the airways inside the lungs. 

One reason that asthma makes it hard to breathe is that it causes a lot of irritation and swelling, making the walls of the airways get thick. 

The muscles around the airways also get irritated and squeeze, making them even more narrow. 

With-- asthma, the irritation also leads to more mucus, which can clog the airways. 

Breathing with asthma can feel like breathing through a thin straw - it is hard to move air in and out, and can be very tiring.

Asthma is different for everyone. 

The most common symptoms are coughing, chest tightness, getting tired easily, and wheezing.

Wheezing is a high-pitched whistling sound that comes from the air trying to get in and out of the lungs through narrow airways. 

In some children, cough may be the only symptom, and may increase at night or while napping, making it hard to sleep. 

Some people with asthma have symptoms almost every day. 

Others have symptoms once every few months. 

But asthma is a chronic disease, which means it never really goes away, so people with asthma should always have their medications ready.

Sometimes, asthma symptoms can suddenly get worse.  

This is called an asthma attack. 

During an asthma attack, it can be so hard to breathe that it is hard to talk. 

If a child]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Yersinia_pestis_(Plague)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M9zON2TuSaqeNWN0ZjHzbWQeRrOZqoIw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Yersinia pestis (Plague)]]></video:title><video:description><![CDATA[Yersinia pestis is a Gram-negative coccobacillus which belongs to a family of bacteria called the Enterobacteriaceae. 

It causes a disease called plague, which is transmitted by rodents, mainly rats, as well as prairie dogs, and their fleas. 

Plague is highly contagious, and there have been three major pandemics in human history - one of them, known as the Black Death, killed up to one-third of the European population. Yikes!

Now, Yersinia pestis has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. 

Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. 

On Wright-Giemsa and Wayson staining it has a bipolar staining which means that only the poles of the bacteria stain, and the rest of it remains unstained, so the bacteria look like safety pins under the microscope.

Alright, now Yersinia pestis is non-motile, non-spore forming, facultative anaerobic which means it can survive in both aerobic and anaerobic environments and facultative intracellular which means it can survive both inside and outside the cells. 

It’s oxidase and urease negative which means it doesn’t produce these enzymes and catalase positive which means it produces an enzyme called catalase. 

Also, it’s indole negative which means it doesn’t convert tryptophan into indole.

Yersinia pestis grows well on MacConkey agar, sheep blood agar, and chocolate agar. 

MacConkey agar is used to identify if a bacteria ferments lactose or not, and it contains a pH sensitive dye and lactose. 

So, if a bacteria ferments lactose, it means that it’s able to ferment lactose and produce acid which causes the pH sensitive dye to turn pink leading to formation of pink colonies. 

Non-lactose fermenters, like Yersinia pestis, aren’t able to modify the PH sensitive dye, grow into colorless colonies. 

Next, on sheep blood agar and chocolate agar, Yersinia pestis forms opaque, yellow colonies that look like fried eggs. 

Finally, the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vulvovaginitis:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b9o1fJMvT0OYKRQxwitwVrMpS8mxEHiz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vulvovaginitis: Clinical]]></video:title><video:description><![CDATA[In females of reproductive age, the vagina is normally colonized by a bacterial species, called Döderlein lactobacilli, which convert glucose into lactic acid. This biochemical process keeps the vaginal PH at an acidic 4.5 - which is not suitable for the growth of pathogenic organisms. 

Vulvovaginitis refers to the inflammation of the vagina and the vulva, which usually go hand in hand - given their close proximity. When there’s inflammation there are typically symptoms like a change in the color, volume or smell of vaginal discharge, itching, a burning sensation, irritation, dyspareunia, or pain during sex, and dysuria, or pain during urination. Inflammation can be due to an infection, or non-infectious causes that lead to an imbalance in the normal vaginal flora. Non-infectious etiologies include atrophic vaginitis in postmenopausal females, and retained foreign bodies, like tampons or condoms. These can usually be ruled out by doing a thorough speculum exam, that will show a pale, smooth and shiny vaginal epithelium with atrophic vaginitis, or identify the retained foreign body, which can then be removed. For atrophic vaginitis, treatment is with local estrogen creams. 

Infectious vulvovaginitis is almost always due to bacterial vaginosis, candida vulvovaginitis, or trichomoniasis. Bacterial vaginosis and candida vulvovaginitis are due to an imbalance in the normal vaginal flora, and trichomoniasis is a sexually transmitted infection. Other sexually transmitted infections, like gonorrhea, chlamydia or mycoplasma, typically cause cervicitis, but rarely can also cause vaginitis.

Ok, now, bacterial vaginosis develops when the number of lactobacilli decreases, and that leads to an increase in pH, allowing other bacterial species like Gardnerella vaginalis to proliferate. A risk factor for developing bacterial vaginosis is having a new sex partner or having multiple sexual partners. However, bacterial vaginosis is not considered a sexually transmitted inf]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_kidney_disease:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OiJFzkXCQsi2uSOyCEcaqDq1Sbm9qr89/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic kidney disease: Clinical]]></video:title><video:description><![CDATA[Chronic kidney disease, or CKD, describes a decrease in kidney function with an estimated glomerular filtration rate—or eGFR—below 60 milliliters per minute per 1.73 square meters, that happens over a minimum of three months, regardless of the cause. 

Now, if there’s already kidney damage- like with glomerular disease, tubulointerstitial disease, vascular disease or congenital renal disease- but the eGFR is above 60 milliliters per minute per 1.73 square meters, then this is still CKD, because all these conditions progressively affect the renal function and over time, without treatment, eGFR decreases. 

Now, the causes of CKD can be split into three categories: prerenal, intrarenal, and postrenal causes.

Prerenal CKD causes are due to a decrease in renal perfusion like in heart failure and cirrhosis.

Intrarenal CKD causes can be further classified into renal vascular disease, glomerular disease and tubulointerstitial disease. 

Renal vascular disease includes hypertension and renal artery stenosis. 

Glomerular diseases include nephritic and nephrotic diseases. 

And tubulointerstitial disease includes polycystic kidney disease. 

Other causes of intrarenal CKD are nephrotoxic substances like lead and certain medications like cisplatin. 

Finally, there’s postrenal CKD, which is most commonly caused by prostate disease. 

Also, repeated episodes of pyelonephritis can lead to CKD. 

Diagnosing CKD usually requires having past measurements of the eGFR, albuminuria or proteinuria and past urine dipstick and sediment examinations. 

If that isn’t possible, the individual needs to have multiple assessments over a period of three months to confirm that the problem is chronic. 

That means getting a serum creatinine to calculate the eGFR, along with urinalysis- both by dipstick and microscopy-  to identify any abnormalities in the urine- such as hematuria and checking the urine albumin levels. 

Additionally, an abdominal ultrasound is done because CKD can ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abnormal_uterine_bleeding:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jf2zWQ7JQf_pL20KUqflCnx3QNGZz0xB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abnormal uterine bleeding: Clinical]]></video:title><video:description><![CDATA[Vaginal bleeding occurs in females of reproductive age, meaning between the age of menarche, which happens around 11, and menopause, which happens around 50. 

Normal vaginal bleeding is called menstruation, and it usually lasts less than 8 days, and no more than 80 milliliters—or slightly less than 6 tablespoons—of blood are lost. 

The first day of menstrual bleeding marks the beginning of the menstrual cycle, which normally repeats itself every 24 to 38 days. 

Additionally, normal menstrual cycles are regular, meaning that the shortest and longest cycles in a 12 month period don’t usually vary by more than 9 days. 

Pathological vaginal bleeding, or “abnormal uterine bleeding”, on the other hand, describes any variation in normal bleeding patterns - in terms of age, frequency, regularity, duration, or volume.  

Age-wise, any kind of bleeding is considered abnormal before menarche and after menopause. 

Abnormalities in frequency and regularity can mean that cycles either occur irregularly, or that they are very short or very long. This also includes unscheduled intermenstrual bleeding - bleeding between cycles. 

Finally, volume-wise, vaginal bleeding that is profuse enough to cause changes in hemodynamic status, even in the context of an otherwise normal menstrual cycle is considered pathological. 

So, the first step in assessing vaginal bleeding is checking the hemodynamic status, by looking for signs of hypovolemia.

Mild hypovolemia can cause mild tachycardia and orthostatic hypotension, whereas severe hypovolemia can cause severe tachycardia, hypotension, oliguria and delayed capillary refill. 

If there’s hypovolemia, lab work includes a CBC, which usually shows a normal hemoglobin level, because the individual is losing whole blood. 

Over the next 24 hours, there’s a physiologic compensation of holding onto more water, and IV fluids are usually given - and that decreases the hemoglobin level. 

Importantly, cross-matching for blood transfusio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aortic_aneurysms_and_dissections:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yai-ojGjQ9is7SBfLnhxz2gQRYqHyjLB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aortic aneurysms and dissections: Clinical]]></video:title><video:description><![CDATA[An aneurysm is a full-thickness dilation of a segment of a blood vessel so that it’s 50 percent greater than its normal diameter, and it’s usually caused by a weakness in the blood vessel wall.

True aneurysms involve all three layers of the arterial wall - the tunica intima, which has endothelial cells; the tunica media, which has smooth muscle; and the tunica adventitia, which has connective tissue as well as vasa vasorum which are the vessels nourishing the aortic wall itself.

There are two major types of aneurysms: fusiform aneurysms, which are uniform in shape with symmetrical dilatation and involves the entire circumference of the aortic wall; and saccular aneurysms, which are localized outpouchings of only a portion of the aortic wall.

Aortic aneurysms are classified by their location along the aorta. Abdominal aortic aneurysms involve the segment of the aorta within the abdominal cavity. Thoracic aortic aneurysms are found within the chest; and these are further classified as ascending or descending aneurysms. Finally, there’s thoracoabdominal aortic aneurysms, which involve both the thoracic and abdominal aorta.

AAAs are the most common form of aneurysm, usually involving the infrarenal segment of the aorta, inferior to the renal arteries and superior to the iliac bifurcation. An AAA is defined as dilation with a transverse diameter exceeding 3 centimeters.

Most individuals with abdominal aortic aneurysm, or AAA, have no symptoms and are only detected as an incidental finding on imaging studies performed to evaluate an unrelated condition. Some cases, especially in thinner individuals, may be discovered on a routine physical examination as a pulsating abdominal mass that can be felt on palpation and heard as a bruit on auscultation.

For earlier detection of asymptomatic AAAs, it’s generally recommended to perform one-time screening with ultrasound in males that are 65 to 75 years old who have ever smoked, as well as in males 60 year]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Newborn_management:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wTLdVa-CQU6klqrlD3N54xCjRk60mzXY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Newborn management: Clinical]]></video:title><video:description><![CDATA[Newborn management, especially in the first &amp;#39;golden minute’ after birth, is vital to ensure a successful transition from intrauterine to extrauterine life. 

It consists of a series of steps, like the Apgar score, performed at specific times to detect any problems the newborn might have, and to deliver effective resuscitation. We can divide the delivery room timeline into 5 parts.

Ok, part one includes what happens before delivery. This includes making sure the right equipment for resuscitation is nearby; knowing how the baby will be delivered and its gestational age; and if the mother had regular prenatal care. 

The next step is assessing any risk factors that might anticipate resuscitation, to allow a team skilled in neonatal resuscitation to be present during delivery. 

Maternal risk factors include age under 20 or over 35 years; diabetes mellitus or hypertension; substance use disorder; and previous history of stillbirth, fetal loss or early neonatal death. 

Fetal risk factors include prematurity or gestational age under 37 weeks; postmaturity or gestational age over 42 weeks; congenital anomalies like gastroschisis and omphalocele; intrauterine growth restriction; or pregnancy complications like in utero infections. 

Part two consist of the first 30 seconds of life. Once the baby is delivered, the time of birth is noted. Next, a few initial steps are performed to ensure a smooth transition and perhaps to stimulate the newborn to start breathing if it didn’t come out doing so. 

First, the newborn is dried with towels. 

Second, the newborn should be kept warm by setting the temperature in the delivery room at 26°C and by using blankets or a radiant warmer bed. Pre-term babies with less than 28 weeks of gestation should be wrapped in plastic without being dried first. This step is important because hypothermia contributes to hypoglycemia, acidosis and even mortality.

Third, the nose and mouth are cleared of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bowel_obstruction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/94aZWZQ3QXCGsCY4UpHKl_x7R-etzgdS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bowel obstruction]]></video:title><video:description><![CDATA[Bowel obstruction is when the normal flow of contents moving through the intestines is interrupted. 

The causes of bowel obstruction can be either mechanical or functional, also called ileus. 

Mechanical obstruction is caused by actual blockages in the large or small intestine, and it can be defined as partial or complete. 

Partial obstruction is when gas or liquid stool can pass through the point of narrowing, while complete obstruction is when nothing can pass. 

Functional causes disrupt peristalsis, which are the waves of contraction that move through the smooth muscles of the bowel wall that pushes food through the intestines.  

The small and large intestines are tube-shaped structures through which chyme, or food that has been partly digested by the stomach, and stools pass until they’re excreted. 

Now if we zoom into a cross-section of the intestinal wall, it’s lined by four layers of tissue: First, there’s the adventitia, or serosa; which is the outermost layer that faces the abdominal or peritoneal cavity. This is the space between the abdominal wall and the abdominal organs, and it’s lined by peritoneal membranes that contains a thin film of serous fluid. 

Moving on, there’s the muscularis externa, which is smooth muscle that contract to move food through the bowel. 

Deep beneath this layer is the submucosa, which has connective tissue as well as glands, blood and lymph vessels that supply the intestinal wall. 

And finally, the innermost layer is the mucosa and it’s composed of a few of its own layers: the muscularis mucosae, which has smooth muscle, the lamina propria, which is rich with blood and lymph vessels, and the innermost layer which is the epithelial lining that faces the lumen. 

Okay, so let’s go over some mechanical causes for bowel obstruction. 

The most common cause in the small intestine is postoperative adhesions. 

After a surgery, the scar tissue that forms during the healing process can form fibrous bands that ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alopecia:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qoY7kTOhQkatTYT6uJy4SgpMSo_M376B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alopecia: Clinical]]></video:title><video:description><![CDATA[Alopecia refers to a loss of hair from part of the head or body and it can occur in a wide variety of disorders. 

Assessment begins with obtaining a description of hair loss and the areas involved, as well as a medical history and family history. 

Physical examination involves inspection of the scalp and other body sites. 

Assessment of activity on the scalp may be done with a hair pull test, done by gripping about 20 hairs and gently pulling upward and away from the skin. Normally, about three hairs may fall out with each pull, while if more than 10 hairs are removed, the test is considered positive.

A noninvasive method of examining hair and scalp is trichoscopy, which is performed with the use of a dermatoscope. This traditionally consists of a magnifier, a non-polarised light source, a transparent plate and a liquid medium between the instrument and the skin.

In some cases, diagnostic techniques such as microscopic examination of cut or plucked hair fibers and scalp biopsies may provide additional information. 

The pluck test is conducted by pulling hair out by the roots. 

The root of the plucked hair is then examined under a microscope to determine the phase of growth, and is used to diagnose if there’s a defect of anagen or telogen. 

Anagen hairs have sheaths attached to their roots, while telogen hairs have tiny bulbs without sheaths at their roots. 

Finally, getting a scalp biopsy from the centre of the lesion gives confirmation of permanent hair loss, whereas a biopsy from the edge or an area of active inflammation may shed light on the underlying disease, and depending on the suspected diagnosis, additional laboratory studies may be performed.

Broadly, hair loss disorders can be divided into cicatricial or scarring alopecias, non scarring alopecias, and structural hair disorders. 

Cicatricial alopecias are characterized by irreversible damage to the hair follicle that results in interruption of hair cycling and permanent hair loss if n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tooth_decay_and_cavities</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZWpe49UjQQen9jM7R8LO3UBjQv_jjkt0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tooth decay and cavities]]></video:title><video:description><![CDATA[Dental caries disease, also called tooth decay, refers to demineralization or weakening of the teeth, and the end result of caries disease is a caries lesion. 

An advanced caries lesion can progress to a point where the tooth surface forms a cavitation or a hole, which is the physical evidence of tooth breakdown. 

Let&amp;#39;s start by building a model of a tooth and its surrounding structures. 

In the mouth, the bone beneath the bottom row of teeth is the mandible, and the bone above the top row of teeth is the maxilla. Both bones have an alveolus, or socket, for each tooth. 

The socket is lined on the inside by a periodontal ligament. 

Protecting the alveolus on the outside, is a layer of soft, supportive tissue called the gingiva, or gums, that sits on top of the bone and covers the root surface from the bone to the cementoenamel junction - where the cementum and enamel come together.

The tooth itself can be roughly divided into a few parts. The first part is the root, and it sits within the alveolus. 

The root is covered by cementum, which is a bonelike substance that the periodontal ligament’s fibers attach to. 

Next, there’s the neck, which is the transition between the root portion covered by bone and the crown. 

The crown is the visible part of the tooth that protrudes from the gingiva, and it’s covered in enamel, which has such a high mineral content that it’s the hardest substance in the human body.

When the teeth are developing, enamel is made before the tooth erupts into the mouth by a group of cells called the ameloblasts that die once the tooth erupts - meaning that the teeth lose the ability to make more enamel forever. 

Now, let’s fill the tooth in from the inside out. Blood vessels and nerves come from the jaw bones, and enter the center of the root through a narrow passage, called the apical foramen. 

From there, they enter the soft center of the tooth, called the pulp, where they provide nutrition and sensation. 

The ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_orthopedic_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8ZHt93RWR6eZidgKvPVVvZVXRKGwUfgx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric orthopedic conditions: Clinical]]></video:title><video:description><![CDATA[Pediatric bone pathologies typically cause pain, and it can vary in terms of intensity and radiation.

Pain usually involves the hip, knee, and back, and it usually worsens over time. If it involves one leg, the pain can lead to limping, and in some cases, individuals might not be able to bear weight.

The symptoms might be unilateral or bilateral, and they might worsen after physical effort and improve with rest. Arm pain is usually related to fractures or arm injuries secondary to trauma and an x-ray or CT of the arm is enough for diagnosis.

The conditions can be divided into those lead to hip pain which include developmental dysplasia of the hip, Legg-Calve-Perthes, slipped capital femoral epiphysis, and transient synovitis; those that cause knee pain, mostly represented by Osgood-Schlatter disease; and conditions that lead to back pain, usually congenital scoliosis. 

First, developmental dysplasia of the hip or DDH is mostly associated with newborns, and it’s a spectrum of conditions that includes abnormal development of the acetabulum and proximal femur, and mechanical instability of the hip joint. 

DDH results from laxity of the ligaments around the joint or from in utero positioning. 

First, history might reveal associated risk factors like a positive family history of DDH, female gender, breech presentation at more than at 34 weeks of gestation, and tight lower extremity swaddling. 

Physical examination might detect limited range of motion of the hips and legs, asymmetry of the limbs if only one side is affected, or asymmetric skin creases in the thigh and groin. 

In those up to 6 months of age, DDH can be detected by the Barlow and Ortolani tests, which are also widely used as screening tests. The tests begin with the individual laying on their back on a stable surface with the hip flexed to 90° and in neutral rotation, which is when the limb is turned neither toward nor away from the body&amp;#39;s midline.

During the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_vomiting:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FtV4IO2YQn_zMcU6JKeAnoLgS6emLchc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric vomiting: Clinical]]></video:title><video:description><![CDATA[Causes of vomiting vary a lot depending on the age group of the child, and usually it’s split into newborns or infants that are less than 3 months of age, infants that are over 3 months of age—or children—and adolescents. 

First looking at newborns or young infants, less than 3 months of age, it may be very common to spit up a little bit of milk or formula, usually within the first hour after being fed. This is considered normal gastroesophageal reflux, or GER, and generally the vomiting is small-volume, non-projectile or not forceful, formula- or breast milk-colored, and the infant is looking healthy. It usually goes away on its own, but what can also help is feeding the baby in an upright position, burping it frequently during feeding breaks—meaning before switching breasts for breastfeeding moms and every 2 to 3 ounces for bottle-feeding moms—as well as after the baby is done eating, and avoiding active play right after feeds.

On the flip side, vomiting is considered pathologic when it occurs in large volumes, is projectile or has a green or bright yellow color given by bile, or when there are signs of illness, like fever, weight loss, or feeding refusal. 

Pathologic vomiting can be caused by obstruction of the gastrointestinal tract. Now, if the obstruction is after the junction of the duodenum with the bile ducts at the ampulla of Vater, then the vomiting is bilious. This may be caused by intestinal malrotation with volvulus, atresia or stenosis of the lower duodenum or intestines, or by Hirschprung’s disease. 

In intestinal malrotation with volvulus, there’s twisting of the mesentery around the superior mesenteric artery leading to intestinal obstruction, infarction, and necrosis. 

This causes symptoms like acute, bilious vomiting, accompanied with abdominal distention and bloody diarrhea. In fact, bowel infarction can also damage the intestinal wall and allow the bacteria in the gut to move into the body, which can cause sepsis. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eczematous_rashes:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QY_WHLo8QEqvpVr4ZOEXJYRIS5mwBPW5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eczematous rashes: Clinical]]></video:title><video:description><![CDATA[An eczematous rash, or simply eczema, is a group of inflammatory skin conditions characterized by redness, itching, and sometimes oozing vesicular lesions, which may become scaly, crusted, or hardened. 

This group includes atopic dermatitis, contact dermatitis, seborrheic dermatitis, dyshidrosis, nummular or discoid dermatitis, and stasis dermatitis. 

Now, every type of eczema has a different set of additional symptoms, and also the area of the skin on which the symptoms appear tends to be different. 

That’s why diagnosis is based mostly on the history and physical examination, and a patch test may be done to determine whether there is an allergic component. Finally, in uncertain cases, a skin biopsy may be useful.

Atopic dermatitis, also called atopic eczema, is a chronic inflammatory skin disease that’s particularly common among young children, but can last into adulthood. 

Atopic dermatitis results from an allergy, more specifically, it happens when the immune system attacks the skin causing a dry, itchy rash on flexor surfaces of the body, areas like the creases of the wrists, the insides of the elbows, and the backs of the knees, as well as exposed skin surfaces like on the face, the hands, and the feet. 

Atopic dermatitis can worsen in the presence of allergens like cigarette smoke, mold, and dust mites, as well as changes in the weather, and even emotional stress. 

Although it usually causes patches of red itchy skin that come and go, the skin can occasionally even blister and peel. Over time, the skin can become lichenified, which literally means turned to leather. 

Atopic dermatitis is generally a clinical diagnosis, based on evidence of itchy skin, plus three or more criteria, which include having a history of dermatitis involving the skin creases, visible dermatitis involving flexural surfaces, personal or family history of asthma or hay fever, presence of generally dry skin within the past year, and either symptoms beginning in a child ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Routine_prenatal_care:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BKsBxfy0Rei3Xu3fsOyGzEOQSzexoaZ1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Routine prenatal care: Clinical]]></video:title><video:description><![CDATA[Prenatal care refers to evaluations that can be done during pregnancy, to assess maternal and fetal health, and intervene when possible to ensure the birth of a healthy baby with minimal risk for the mother. Prenatal care also includes preconception counseling, which seeks to identify a spectrum of social, behavioral, environmental, and biomedical risks to a woman&amp;#39;s fertility and pregnancy outcome with the goal of reducing these risks through education, counseling, and appropriate intervention. Now, pregnancy consists of three trimesters, the first lasting for the first 12 weeks of pregnancy, the second between weeks 13 and 27, and the third from weeks 28 to 40, and during each of these trimesters, the obstetrical consult focuses on different aspects of maternal and fetal health. Prenatal visits are usually done every 4 weeks until week 28, every two weeks from week 28 to 36, and then weekly until delivery.  

So, the initial prenatal visit may occur either when the individual suspects they are pregnant, or because they wish to conceive in the near future. No matter the case, at the initial prenatal visit, the history should be focused on obstetrical history, family history, and identifying any potential risks during pregnancy.

The obstetrical history comprises of gravidity, parity and abortions. Gravidity, or G, means the number of times the individual has been pregnant so far, including the current pregnancy. Parity, or P, refers to the number of times the individual has carried the pregnancy to a viable gestational age - meaning more than 24 weeks. Finally, abortions, or A, refers to the number of pregnancies that were lost for any reason. So, for example, if the individual is currently pregnant, has been pregnant once before, and that pregnancy resulted in a live birth at 38 weeks, you’d say that as Gravida 2, Para1, Abortions0, or G2P1A0. Alternatively, if that previous pregnancy had resulted in a miscarriage at 12 weeks, you’d say that as G]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_heart_defects:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tpneyh-fR9SxHFIQzEOBI4q1S4GP2uZj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital heart defects: Clinical]]></video:title><video:description><![CDATA[Congenital heart defects are usually divided into two categories based on the presence or absence of cyanosis, as well as by how it sounds on cardiac auscultation. 

Acyanotic defects cause left to right shunting, and include four conditions: ventricular septal defect or VSD, atrial septal defect or ASD, patent ductus arteriosus or PDA, and coarctation.

Cyanotic defects present right to left shunting, and include five conditions: tetralogy, transposition, truncus arteriosus, total anomalous pulmonary venous return, and hypoplastic left heart syndrome. 

Usually the diagnosis is then confirmed by echocardiography. 

An ECG should be performed as part of the initial work-up. 

Chest x-ray is important when there’s suspicion of heart failure, and, sometimes a CT or MRI are done if the diagnosis is inconclusive. 

Rarely, cardiac catheterisation with angiography is used if the diagnosis remains uncertain after non-invasive studies.

Regarding infective endocarditis prophylaxis, it is recommended for high risk individuals: those with a cyanotic congenital heart disease that has not been fully repaired; a congenital heart defect that&amp;#39;s been completely repaired with prosthetic material or a device for the first six months after the repair procedure; repaired anomalies with residual defects, such as persisting leaks or abnormal flow.

Most heart defects can also be detected prenatally by standard obstetric ultrasound examination. However, small ventricular septal defects or atrial septal defects, minor valve lesions, partial anomalous pulmonary venous connection, and coronary artery anomalies are often not detected prenatally.

The optimal gestational age for screening for structural fetal cardiac anomalies is 18 to 22 weeks of gestation, although in some cases it can be done as early as 10 weeks of gestation. 

In the first two days of life, a pulse oximetry saturation less than 90% in the right hand or either foot requires urgent ec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Methods_of_regression_analysis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-tLqSQwzRkKIu6g3teLO-b-0ThW4uYs8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Methods of regression analysis]]></video:title><video:description><![CDATA[There are four basic types of statistical analyses commonly used in epidemiological research, and the analysis you pick depends on two main criteria. 

The first criterion is the type of data you have, which can be either individual data or binned data, which is also called group data. 

So, for example, let’s say we want to know how many people out of 100 people developed lung cancer the past 5 years. 

With individual data, we have information about each person, so we can tell whether or not each of the 100 people developed lung cancer. 

So let’s say that 6 people developed lung cancer. If we have individual data, we can look at the individual characteristics for each of those 6 people, like their sex, age, race, or past history of migraines, and we can compare them to the people that didn’t developed lung cancer. 

On the other hand, if we have group data, we don’t actually know which specific individuals out of the 100 people developed lung cancer. 

So even though we know that 6 people had them, we don’t know which 6 people they were or any of their individual characteristics.

The second criterion is the type of outcome or y-variable you’re measuring, which can be either quantitative, categorical, or time to event. 

Quantitative variables have a numeric value, like a person’s forced expiratory volume, which is the total amount of air, in liters, that a person can exhale in a single forced breath. 

A very fit person might have an FEV of 5, while a less fit person might have an FEV of 3.

On the other hand, categorical variables have distinct levels. 

For example, we could use a categorical variable to characterize if a person was diagnosed with lung cancer in the past five years or if they were not. 

And finally, time to event variables describe how long a person was followed before the event or outcome occurred. 

For example, if we started following a person at age 50 and they developed lung cancer at age 53, then their time to event would be 3]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prostate_gland_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UOZ0UmurRimIMwPl3Wm0t58MQtiD3QsC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prostate gland histology]]></video:title><video:description><![CDATA[The prostate gland is a large and dense exocrine gland that’s responsible for secreting a white alkaline fluid that makes up about 30 to 50 percent of the seminal fluid volume. 

It’s the largest accessory sex gland in the male reproductive system, measuring approximately 3 cm in length and width, and a height of 5 cm. 

The average weight of a normal prostate gland is about 11 grams. 

Due to its similar size and shape, it’s sometimes compared to a walnut. 

The gland surrounds the most proximal portion of the urethra or prostatic urethra, just below the bladder and consists of 30 to 50 branched tubuloalveolar glands, such as the ones seen in this low power image of the prostate. 

The glands all drain into converging ducts that eventually empty into the prostatic urethra.

The alkaline fluid that’s secreted by the prostate gland also includes various small molecules, fibrinolysin, citric acid, and the clinically important prostatic acid phosphatase or PAP, and prostate-specific antigen or PSA. 

Normally, only a small amount of PSA will leak into the prostate’s vasculature and circulate in an individual’s blood. 

But a high level of circulating or serum PSA is a sign of abnormal prostatic tissue, which could be caused by prostate cancer, inflammation, or benign prostatic hyperplasia. 

Because of this association, a PSA serum level is often used as a tumor marker for prostate cancer. 

And even after a patient has had their prostate cancer removed, PSA is used to monitor for a possible recurrence of the prostate cancer. 

PSA and PAP immunostains can also be used on tissue samples to assist with the diagnosis of prostate cancer, such as this section from a lymph node, where a PSA stain is highlighting a metastatic prostate adenocarcinoma in brown. 

Similar to this image at 40x magnification, the prostate will have glandular structures called acini that are surrounded by supporting fibromuscular stroma. 

Each acinus has two layers of cells: an epi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Study_designs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ff1211LcQwiUeKul6ODyktfwTBi8Tw-P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Study designs]]></video:title><video:description><![CDATA[There are six basic types of epidemiological study designs, and they can each be distinguished using certain criteria.

The first criterion for deciding which study design to use is whether you have individual or group data. 

For example, let’s say we want to know how many people out of 100 people had migraines in the past year. 

Now, with individual data, we have information about each person, so we can tell whether or not each of the 100 people had a migraine. 

So, let’s say that 9 people had migraines. If we have individual data, we can look at the individual characteristics for each of the 9 people that had migraines, like their sex, age, race, or past history of migraines, and we can compare them to the people that didn’t have migraines.

On the other hand, if we have group data, we don’t actually know which specific individuals out of the 100 people had migraines. 

So even though we know that 9 people had them, we don’t know which 9 people they were or any of their individual characteristics. 

Now, ecological studies are a type of study design that uses group data to figure out if there is a potential association between two variables. 

For example, let’s say you want to figure out if people who sleep less are more likely to get migraines. 

And perhaps you have information about average sleep duration for populations in ten different cities. 

You could plot this information on a graph with average sleep duration on the x-axis and the prevalence of migraines—which is the number of people that suffer from migraines, per 100,000 people—on the y-axis.

Generally, we can see that the less sleep a city gets, the higher the prevalence of migraines is for that city. 

The thing is, we can’t actually say that getting less sleep causes migraines, since we don’t have information about each individual in each city. 

All we can say is that there’s an association between sleep duration and prevalence of migraines. 

Ecological studies are helpful for maki]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prevention</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Cld2dG2HT72a9bLorAlUf0bFQMeuleif/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prevention]]></video:title><video:description><![CDATA[In epidemiology, there are three different types of prevention—primary, secondary, and tertiary. 

To get a clearer picture of what each type of prevention is and when it occurs, let’s first take a look at a timeline of the natural history of a disease, and we’ll use cervical cancer as an example. 

Cervical cancer is cancer of the cervix, and around 13 thousand women are diagnosed each year. 

Most cases of cervical cancer are diagnosed in women ages 35 to 44, though older women are also at risk.   

In the natural history of a disease, the first step is the biologic onset of the disease. 

So, in the case of cervical cancer, this is when a group of cells in the cervix become cancerous and begin to rapidly divide, forming a tumor. 

At this stage, the person probably doesn’t even realize that they have the disease, since they’re still asymptomatic. 

At some point later, symptoms will start to show, like vaginal bleeding after sexual intercourse, or having unusual vaginal discharge. 

And at this point, the person might go to a health clinic to talk with someone about their symptoms, and they’ll be diagnosed with cervical cancer. 

Finally, the person will receive some type of treatment, like radiation therapy or chemotherapy, and this will eventually lead to an outcome, like remission, or in severe cases, death. 

Now, this progression can be split into two phases. 

The preclinical phase is the time between the biological onset of the disease and when symptoms start to show, and the clinical phase is the time between when symptoms start to show and time when therapy is complete.

Now, let’s talk about how prevention fits into this timeline. 

The first type of prevention is primary prevention, and it’s all about stopping the onset of disease. 

And this is what you probably think of when you hear the word ‘prevention’, and one way to remember this is because primary and prevent both start with the letter P. 

In primary prevention, you’re trying to ensu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fever_of_unknown_origin:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5LLx7V_0Qjm99nb8NQQFL4N6T76YxmQl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fever of unknown origin: Clinical]]></video:title><video:description><![CDATA[Fever is one of the most common complaints in children. 

Now, fever of unknown origin, or FUO, is defined as a temperature higher than 101ºF or 38.3ºC that lasts for at least eight days and has no underlying cause in spite of a formal evaluation. 

Okay, so, causes of FUO can be divided into two large categories: infectious and non- infectious. 

Infectious causes include generalized infections, especially bacterial ones, like Brucellosis, Cat scratch disease caused by Bartonella henselae infection, Lyme disease caused by Borrelia infection, Mycobacterial infections such as tuberculosis, Salmonellosis causing typhoid fever, Typhus caused by Rickettsial infections, Tularemia caused by Francissela tularensis, Psittacosis caused by Chlamydophila psittaci, Pasteurella along with various others infections from Campylobacter, Yersinia Legionella infections, Vibrio parahaemolyticus or vulnificus. 

Likewise, there are viral infections, including Adenovirus, Influenza, CMV, EBV, arboviruses, and HIV; there are parasitic infections, like Malaria, Toxoplasmosis, and Babesiosis; and there are fungal infections like Blastomycosis, Cryptosporidiosis, Histoplasmosis, and Coccidioidomycosis. 

But there are also localized infections, like pneumonia, bone and joint infections, such as osteomyelitis and septic arthritis, infective endocarditis, meningitis or encephalitis, intra abdominal abscesses, hepatitis, upper respiratory tract infections such as mastoiditis and sinusitis, dental infections, and urinary tract infections such as pyelonephritis.

Non-infectious causes include inflammatory conditions like Kawasaki disease, autoimmune conditions like Juvenile idiopathic arthritis, rheumatoid arthritis, polyarteritis nodosa, and systemic lupus erythematosus; neoplasms like leukemia and lymphoma; inflammatory bowel disease; immunodeficiencies; familial dysautonomia, and periodic fever syndromes like familial Mediterranean fever, cyclic neutropenia, and periodic fever with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypersensitivity_skin_reactions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/seg_rP7VQ06NOePmmxcOJaZIQWW3opxT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypersensitivity skin reactions: Clinical]]></video:title><video:description><![CDATA[Hypersensitivity skin reactions are due to an exaggerated immune system reaction towards an antigen, and some reactions can be life-threatening. 

Hypersensitivity skin reactions include urticaria, erythema multiforme, Staphylococcal scalded skin syndrome, drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, and toxic epidermal necrolysis.

Urticaria, also called hives, are slightly raised, well-defined wheals that are 1 millimeter to 10 centimeters in diameter. They’re usually red, blanch with pressure, are extremely itchy, and can pop up anywhere in the body. 

The key feature is that these lesions come and go very rapidly - meaning one might appear on the leg as another disappears from the arm. 

The reaction involves the epidermis and dermis layers of the skin, and the whole thing typically resolves within 24 hours. 

Typically no treatment is needed, but if the itching is really bad, topical cooling moisturizers or oral second-generation histamine H1 blockers can be used like loratadine, desloratadine, fexofenadine, cetirizine, or levocetirizine. If these don’t work, immunomodulatory agents, like cyclosporine or methotrexate can also be used. 

Now, if there’s recurrent urticaria, it’s good to try to identify a trigger, so that it can be avoided. 

One way is with in vivo skin prick tests, which is where small drops of up to 40 allergens, like pollens, fungi, animal dander, house dust mites, and various foods, are pricked into the skin on the forearm or upper back. 

After that, if there are signs of urticaria within about 20 minutes, that implies that the substance is a trigger. 

Unfortunately, it’s a bit uncomfortable and requires that the individual doesn’t take any antihistamines and doesn’t have any other skin diseases. 

Another way is with in vitro blood tests that look for IgE antibodies against specific allergens, such as foods, insect venoms, pollen, mold, latex, or antibiotics. This takes longer, is more expensi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_milestones:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8NoN7E6uSOSrA_ocB9Ezk8gDSpm9DDgc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developmental milestones: Clinical]]></video:title><video:description><![CDATA[When we talk about healthy child development, we often speak of milestones that children hit at certain ages. 

By looking at these milestones, we can see how the child is developing and keep an eye out for any potential problems. 

There are ten age stages when milestones should be checked: two months, four months, six months, nine months, twelve months (or one year), eighteen months, two years, three years, four years, and five years. 

And there are four types of milestones that should be assessed: gross and fine motor, communication, cognitive, and social.

It’s worth noting that development is different from growth. 

Growth is when children are getting bigger in size - specifically gaining weight, getting taller, and increasing their head circumference, while development refers to complex things like walking, speaking, turning a page in a book, and smiling at familiar faces. 

Developmental milestones are like a checklist of abilities that kids learn in time, but not all children learn them at the same pace. 

For instance, some kids may begin walking as early as ten months, while others don&amp;#39;t do it until they’re fourteen months. 

It’s considered pathologic when the milestone isn’t hit at all or when it takes kids too long to develop that milestone compared with other children.

Now, at two months, for gross motor milestones, a baby can keep their head steady when held and also bring their head and chest up and look forward while on their stomach, and for fine motor milestones, their eyes track objects past the midline. 

Second, for communication milestones, a baby can turn the head when someone is speaking, and can coo - which is a noise that resembles speech.

Third, for cognitive milestones, a baby can start showing a preference for their usual caregiver over a stranger, paying attention to new things or sounds, and looking at objects until they reach their midline. 

And fourth, for social milestones, a baby can smile in response ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Premature_rupture_of_membranes:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z8fSXxEIR2ieH9DNiSl_7Qk2SPmD_6KE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Premature rupture of membranes: Clinical]]></video:title><video:description><![CDATA[The fetal membranes are also called the chorioamniotic membranes, and they make up the amniotic sac. 

Inside the amniotic sac, there’s amniotic fluid, so throughout pregnancy, the fetus develops in a bubble of fluid that protects it from shock and infections.

When the amniotic sac ruptures, it releases the amniotic fluid, which is why a lot of individuals describe it as “their water breaking”. 

Normally, this occurs right before labor, or sometimes even during labor, and it’s associated with uterine contractions.  

If the membranes rupture in the absence of uterine contractions, that has different names depending on when it happens during the pregnancy. 

If they rupture after 37 weeks, that’s simply called premature rupture of membranes, or PROM for short.

So premature doesn’t have anything to do with a premature delivery, but rather with it occuring before labor, in the absence of uterine contractions - which is why, sometimes, the term prelabor rupture of membranes is also used. 

If the membranes rupture before 37 weeks gestation, that’s called preterm premature rupture of membranes, or pPROM for short. 

And no matter when it happens during pregnancy, if more than 18 hours pass between rupture of membranes and delivery of the fetus and placenta, that’s called prolonged rupture of membranes.

Risk factors for PROM and pPROM include PROM or pPROM in a previous pregnancy, genital or urinary tract infections, smoking, as well as polyhydramnios, which means there’s too much amniotic fluid, and abdominal trauma.

Diagnosing premature rupture of membranes requires a speculum exam and specific tests. 

Bear in mind that a digital examination of the cervix should be avoided, as it can increase the risk of infection, and may precipitate labor in females with pPROM. 

Ok, now the speculum exam shows fluid pooling in the posterior vaginal fornix. 

The fluid may be clear, or there may be blood or meconium in it, which is actually not a cause for concern.

To]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vaginal_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_6FHqaZ-TL6ydMAvVy1MZ0u9RHikLXsM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vaginal cancer: Clinical]]></video:title><video:description><![CDATA[Vaginal cancer is a rare gynecologic malignancy. 

The most frequent histologic subtype is squamous carcinoma, which develops from the squamous epithelium of the vagina, in which case, it’s in relation to an HPV infection, particularly high risk strains, like HPV 16 and 18. 

Sometimes, however, clear cell adenocarcinoma can occur, which develops from the glandular cells of the vagina, in which case it’s almost always because of exposure to a medication called diethylstilbestrol, or DES for short. 

So, risk factors for vaginal cancer depend on the histologic subtype. 

For vaginal squamous cell carcinoma, they’re the same as for cervical cancer: multiple lifetime sexual partners, early age at first sexual intercourse, as well as smoking, and immunocompromising conditions, like an HIV infection.

For vaginal adenocarcinoma, the only known risk factors are in utero exposure to DES. 

This medication was prescribed to females between 1940 and 1970 to prevent pregnancy complications, like miscarriage - so their daughters would be at risk for developing vaginal adenocarcinoma.

Most of the time, vaginal cancer is asymptomatic. 

If there are symptoms, abnormal postcoital or postmenopausal vaginal bleeding are the most common ones, and a watery, blood-tinged or foul-smelling vaginal discharge may be present as well. 

In later stages, when the cancer has spread further than the vagina, pelvic pain may be present. 

When the bladder is involved, there may also be symptoms like urinary frequency, and if the cancer has spread to the rectum, there may be constipation. 

The speculum examination can usually identify any suspicious or abnormal looking masses inside the vagina, most commonly located on the upper third of the posterior vaginal wall. 

Most commonly, vaginal cancer looks like a mass, but it can also look like a plaque or an ulcer. 

In addition, if there are enlarged inguinal lymph nodes, that may be a sign of metastatic disease. 

If a mass is visible ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_creation_process</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0meX3-dsRFKjA3TLA5J5E6QZTfe3AIRs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video creation process]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Video creation process through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alpha-thalassemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UG2ZDgEbQl_uOHSZjL2GxVIVSWmZskLE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alpha-thalassemia]]></video:title><video:description><![CDATA[Alpha-thalassemia is a genetic disorder where there’s a deficiency in production of the alpha globin chains of hemoglobin, which is the oxygen-carrying protein in red blood cells. 

Normally, hemoglobin is made up of four globin chains, each bound to a heme group. There are four major types of globin chains- alpha (α), beta (β), gamma (γ), and delta (δ). These four globin chains combine in different ways to give rise different kinds of hemoglobin. First, there’s hemoglobin F (or HbF), where F stands for fetal hemoglobin, and it’s made up of two α-globin and two γ-globin chains. Hemoglobin A (or HbA) is the major form of adult hemoglobin, made up of two α-globin and two β-globin chains. Finally, hemoglobin A2 (or HbA2) amounts for a small fraction of adult hemoglobin in the blood, and it’s made up of two α-globin and two δ-globin chains.
Alpha chain synthesis is controlled by four alpha genes, two on each copy of chromosome 16. And alpha thalassemia is caused by mutations in the alpha genes, most commonly a gene deletion. The mutations are inherited in an autosomal recessive pattern, which means that you need mutated genes from both parents to get the disease.
If a person has one defective alpha gene, they’re called a silent carrier, because they don’t have symptoms, but can still pass the gene to their children. If a person has two defective alpha genes, the person has alpha thalassemia minor, which causes mild symptoms. This can either be caused by a ‘cis’ deletion, where mutated genes are on the same chromosome; or a ‘trans’ deletion when the mutated genes are on two different chromosomes. Cis-deletion variants are more prevalent in Asian populations, whereas, trans-deletion variants are more prevalent in African populations. 

If there are three defective alpha genes, there’s moderate disease, called hemoglobin H, or HbH, disease. This is caused by excess beta chains, which clump together within developing red blood cells to form tetramers (β4), and giv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endometritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WwhQttuxRey7pF-MV7-n2c7MTOWNkGXR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endometritis]]></video:title><video:description><![CDATA[Endometritis is an inflammation of the endometrium, which is the inner lining of the uterus. 

It is usually caused by an infection of the endometrium from bacteria that normally live in the female lower genital tract, but it could also be caused by bacteria from outside the body.

The female reproductive system is divided into upper and lower genital tracts. 

The upper genital tract consists of the uterus, ovaries, and fallopian tubes. 

The lower genital tract in turn consists of the cervix, vagina and the external genitals, which includes the labia and the clitoris. 

Now, The uterus consists of 3 layers, an outer thin layer called the perimetrium or the serosa, a middle smooth muscle layer called the myometrium, and the innermost layer, the endometrium. 

The endometrium has two layers, an inner functional layer made up mainly of glands and supporting connective tissue, called stroma, and an outer thin basal layer  which regenerates the overlying functional layer after each menstrual cycle. 

Alright, normally, there are many species of bacteria living in the female’s lower genital tract, and this is called the normal flora. 

These include Ureaplasma urealyticum, Peptostreptococcus and group B Streptococcus. 

Under normal conditions, these bacteria live there happily without causing any harm, however, if they reach the upper genital tract, they can cause an infection like endometritis if they make it to the uterus. 

Endometritis is a common problem during pregnancy because bacteria can easily reach the uterus during childbirth. 

Okay, so normally the fetus is surrounded by membranes and amniotic fluid, and the uterus’s opening is sealed by a mucous plug. 

This mucus plug has antimicrobial properties, preventing bacteria from reaching the uterus. Typically, during vaginal delivery, the mucus plug is shed, the cervix widens, and the membranes around the fetus rupture, so the baby can be delivered. 

However, bacteria in the lower genital tract can ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abnormal_labor:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bM51JJvMRe2ap-ZbDGjSkG6kRj2SKsvj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abnormal labor: Clinical]]></video:title><video:description><![CDATA[Abnormal labor is defined as the abnormal onset of labor - either too early or too late in the pregnancy - or abnormal duration of the stages of labor. 

Normally, labor onset occurs between weeks 37 and 42 of pregnancies, and labor itself has three stages.

Stage I is when the cervix dilates to 10 centimeters, and it’s divided into a latent phase, covering dilation from 0 to 6 centimeters, and an active phase, when the cervix dilates completely. 

Stage II is when the fetus passes through the birthing canal. 

If everything goes well, the baby is delivered and labor progresses to stage III, which is the delivery of the placenta. 

Ok then! Preterm labor is when regular uterine contractions and cervical changes, which include cervical effacement, or thinning and dilation, start before 37 weeks gestation, but later than 20 or 24 weeks. 

Earlier than that, the delivery is called an abortion, because the fetus hasn’t developed enough to survive in the outer world, even with all the neonatal care measured that we have at our disposal. 

And the reason we say 20 or 24, is because the OB world is not in full agreement on this matter, either. 

Alright - now, risk factors for preterm labor include lifestyle factors, like smoking, alcohol consumption, or illicit drug use, like cocaine or heroin.

Other risk factors include a prior preterm labor, multiple gestation, aka twins or triplets, short cervical length, meaning the cervix is less than 25 millimeters long on ultrasound before 24 weeks gestation, as well as prior cervical surgery, like a cone biopsy that’s done to diagnose or treat cervical cancer. 

And then a myriad of other conditions can increase the risk of preterm birth, such as urinary or genital infections, and also obstetric complications like preeclampsia, eclampsia and HELLP syndrome, all of which are associated with hypertension during pregnancy and more, placenta praevia, when the placenta is inserted in close proximity of the cervix, or covers ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Papulosquamous_skin_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hpG0FUicQeKIrn7OYEzvvprSSEm-5qjB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Papulosquamous skin disorders: Clinical]]></video:title><video:description><![CDATA[Papulosquamous disorders are a heterogeneous group of disorders whose etiology primarily is unknown, that present with both red papules and scaling. 

The major entities in this group include psoriasis, parapsoriasis, lichen planus, pityriasis rosea, and seborrheic dermatitis. 

Diagnosis is most often clinical, taking into account the location and distribution of the papulosquamous skin lesions. Only a few cases may require further investigation with skin biopsy to confirm diagnosis and choose the appropriate treatment.

Psoriasis is a chronic and complex immune-mediated disease that causes skin inflammation, presenting as well-demarcated, erythematous plaques with silver scales that can be incredibly pruritic or itchy. 

For some individuals, having psoriasis may have psychosocial effects with a significant negative impact on the quality of life. 

The causes of psoriasis aren’t clear but there’s definitely a genetic component and environmental triggers like trauma, stress, or smoking. 

Symptoms of psoriasis can vary, and there are a few subtypes. 

Plaque psoriasis is the most common. It appears as flattened areas of epidermal elevation that are inflamed and red or salmon-colored, from the underlying dilated blood vessels, and are topped with white-silvery scales.

Plaques are typically itchy and found on the scalp and in tensor regions, like the elbows, groin, lower back, and knees. 

Guttate psoriasis appears as small, red, individual spots on the trunk and limbs. 

This subset usually starts in childhood, and is sometimes triggered by an infection, like strep throat. 

Inverse psoriasis appears as smooth and shiny red lesions that lack scales and typically form within skin folds like in the genital region, under arms or under the breasts.

Pustular psoriasis appears as areas of red skin with small, white elevations of cloudy pus, formed from dead immune cells. They are usually tender and form on the hands and feet. 

Erythrodermic psoriasis is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endometrial_hyperplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UFMrOiPvRPCUXesch1bSPqKAQRiOBLO8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endometrial hyperplasia]]></video:title><video:description><![CDATA[With endometrial hyperplasia, endometrial refers to the endometrium, which is the inner lining of the uterus, and hyperplasia means increased growth, so endometrial hyperplasia means excessive growth of the inner lining of the uterus.

The uterus consists of 3 layers, an outer thin layer called the perimetrium or the serosa, a middle smooth muscle layer called the myometrium, and the innermost layer, the endometrium. 

The endometrium has two layers, an inner functional layer made up mainly of glands and supporting connective tissue, called stroma, and an outer thin basal layer  which regenerates the overlying functional layer after each menstrual cycle. 

Now, the growth of the functional layer is regulated by the hormones secreted by the ovaries. Each ovary is made up of a number of ovarian follicles. 

Each follicle consists of an oocyte, which is the female germ cell, surrounded by an outer layer made up of theca cells, which secrete androgens, also known as the male hormones, and an inner layer made up of granulosa cells, which secrete estrogen. 

Now estrogen stimulates the growth of endometrial glands and stroma. 

This effect of estrogen predominates during the first phase of the menstrual cycle. 

This is also called the proliferative phase because it’s when the lining of the endometrium grows.  

At the end of this phase, ovulation occurs, where one ovarian follicle expels the oocyte into the fallopian tube and it travels to the uterus.  

During the second phase of the menstrual cycle, also called the secretory phase, the remaining structure of the follicle, now called the luteal body, begins to secrete progesterone.

Progesterone counteracts the effect of estrogen on the endometrium by stopping its growth. 

At the same time, it causes the glands to produce secretions that acts as nutrients for any developing embryo.

Endometrial hyperplasia most often results when the endometrium is exposed to high levels of estrogen for a prolonged time. 

Th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_ophthalmological_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fRvs2YmVQg6GuEiHiguV5N2GRJeXEdOD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric ophthalmological conditions: Clinical]]></video:title><video:description><![CDATA[In children, some causes of vision changes don’t typically cause pain and these include amblyopia, strabismus, and congenital cataracts. 

Causes of vision changes that do cause pain include retinoblastoma, conjunctivitis, corneal abrasion, and retinal detachment.

Routine vision checks are done at well-child visits, and they should be done at least once when a child is between three and five years of age. And it can be done with red reflex testing, which is where an ophthalmoscope is used to compare the reflex in both eyes for asymmetry. It’s done in a dark room, where the light is directed into both eyes at the same time from a distance of 1 to 2 feet. If screening detects an abnormal red reflex further testing is required. 

Sometimes, a concern is raised when parents notice that their child doesn’t seem to track their face or follow objects, or they might notice nystagmus, which are involuntary eye movement. 

Parents might also notice that the normal &amp;quot;red eye&amp;quot; glow of the pupil is missing in photos. 

Older children may complain of blurred vision, but most are unaware of their visual deficit. 

Diplopia or double vision; visual inattentiveness, which is when people ignore things on a portion of their visual field; gray cloudiness of the pupil which is normally black; and photophobia may also be present. 

Risk factors include a history of prematurity, a family history of childhood cataract, retinoblastoma, retinal dysplasia, childhood glaucoma, or recent eye trauma.

The first eye pathology that’s not painful is amblyopia, where the diminished vision is usually in one eye, and is secondary to abnormal visual stimulation of the visual cortex.

Because the retina is not stimulated with a clear, focused image, or because the visual axes may be misaligned, there’s abnormal visual stimulation of the visual cortex and suppression of the retinal image formed by 1 o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunodeficiencies:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zoOrYQgBRfGQ4BY6VsNTpT4XRoajmb7D/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunodeficiencies: Clinical]]></video:title><video:description><![CDATA[Immunodeficiencies can be classified into primary and secondary immunodeficiencies. 

Primary immunodeficiencies are relatively rare, genetic and typically inherited defects in one or more of the elements of the immune system. 

Secondary immunodeficiencies are much more common, acquired disorders that occur as a result of some extrinsic factor affecting the immune system.

Both primary and secondary immunodeficiencies can cause frequent or recurrent infections- specifically six or more new infections anywhere in the body within one year or four or more new ear infections within one year. Sometimes these infections turn out to be unusually severe. 

Specifically, it’s unusual for two or more serious sinus infections or pneumonias to occur within one year or two or more episodes of sepsis or meningitis to occur in a lifetime. 

Serious means that they cause persistent fever or confinement to bed for a week or more, are difficult to treat requiring two or more months of antibiotics with little effect or a need for IV antibiotics or hospitalization or cause unusual complications. 

These include organ abscesses, non healing wounds, chronic diarrhea or failure to thrive meaning failure to gain weight or grow normally, persistent laboratory abnormalities such as leukocytosis or elevated ESR and CRP or persistent imaging abnormalities, such as bronchiectasis. 

And then, it’s also concerning if the pathogens are opportunistic organisms, such as Candida albicans, nontuberculous Mycobacteria or Pneumocystis jiroveci, which usually don’t cause serious infections in individuals with a normal immune system. 

Okay, now secondary immunodeficiencies usually occur well after infancy while most primary immunodeficiencies are inherited and present during the first few years. 

Secondary immunodeficiencies can be caused by underlying diseases like HIV infection, malnutrition, diabetes mellitus, malignancy, splenectomy, for example due to sickle cell disease, trauma or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vulvar_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JR5x2gIcSe6NFY8YqHsB9rlES0yUBAUv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vulvar cancer: Clinical]]></video:title><video:description><![CDATA[Over 90% of vulvar cancers are squamous cell carcinomas, which develop from the squamous epithelium of the vulva. 

The other 10% of vulvar cancers are melanomas, which develop from melanocytes, and vulvar adenocarcinomas, which develop from glandular cells, like those that make up Bartholin’s glands on either side of the vaginal opening. 

A particular type of adenocarcinoma is Paget’s disease of the vulva - which is a type of cancer that usually develops in the ducts of the breast, but can rarely develop in other locations, such as the vulva. 

Ok, now, more than 50% of vulvar squamous cell carcinomas are in relation to an HPV infection, particularly high risk strains, like HPV 16 and 18 - just like with cervical cancer. 

And just like cervical cancer, vulvar cancer starts out as vulvar intraepithelial neoplasia, and it may take many years for it to even progress to cancer. 

Other risk factors for squamous cell carcinomas include smoking, immunosuppressive conditions like an HIV infection, and lichen sclerosus, which is a skin disorder than frequently affects the genitals, making the skin become very thin and white, like cigarette paper. 

For the melanoma type of vulvar cancers, risk factors include a family history of melanoma, or a personal history of melanoma or dysplastic nevi, which are atypical moles, in other locations on the body.  

Additionally, individuals with cervical or vaginal cancer have a higher risk of vulvar cancer, probably because they can all be caused by high risk HPV strains. 

Symptoms vary depending on histologic subtype, but at the end of the day, there’s always a vulvar lesion, and pruritus - the fancy word for itching. 

Sometimes there may also be associated pain, bleeding or discharge. Squamous cell carcinomas usually look like a red, pink or white bump, or it may look like a wart, or an open sore that doesn’t heal. 

Vulvar melanomas, on the other hand, are usually black or dark brown - and sometimes they may start in a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leg_ulcers:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g6J96t56TxaTKRaOK6R_Fk5XRkWLP-kE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leg ulcers: Clinical]]></video:title><video:description><![CDATA[An ulcer is an unhealed sore or open wound that may appear on the skin or mucosal surfaces due to destruction of the epidermis that extends into the dermis and may reach subcutaneous fat or deeper tissues. 

Skin ulcers may take a very long time to heal. For optimal wound healing, the wound bed needs to be well vascularized, free of devitalized tissue, clear of infection, and moist. 

The general approach to treating any ulcer starts from wound debridement to remove the accumulation of devitalized tissue, as well as decreasing the bacterial load to prevent infections. 

This is usually done through irrigation, typically warm isotonic saline solution; while surgical debridement with a scalpel or other sharp instruments is done for removing large areas of necrotic tissue, for chronic non healing ulcers, or when there are signs of infection. 

In addition, individuals with infected ulcers should have wound cultures sent and should get started on antibiotic therapy. 

Then, a dressing is applied to the ulcer to help the wound heal more quickly by providing a sterile, breathable and moist environment, as well as reducing the risk of infection. Dressings are typically changed daily or every other day. 

Nonhealing ulcers may progress to gangrene, which is a hard, dry texture, usually in the distal toes and fingers, often with a clear demarcation between viable and black, necrotic tissue. 

When gangrene has set in, aggressive debridement or amputation of the affected area may be required.

Skin ulcers most often appear on the legs, and can result from multiple causes. 

Biopsies are not usually necessary for most ulcers, but can be helpful when the diagnosis is uncertain. 

The most common causes are venous insufficiency, arterial insufficiency, and neuropathy. So they’re often classified as venous, arterial, or neuropathic. 

Venous ulcers are associated with venous insufficiency due to valve dysfunction, which causes stasis of blood in the legs, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fpVLmS_CTFaj4NH8tLJ4XIxdQVSjRGKi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital disorders: Clinical]]></video:title><video:description><![CDATA[Congenital anomalies appear as the baby develops in utero and vary in severity and presentation, ultimately impacting the infant&amp;#39;s health, development, and survival. 

We can talk about some of the more common and severe defects, beginning with the head and then making our way down the body: cleft lip, esophageal atresia, congenital diaphragmatic hernia, gastroschisis, omphalocele, biliary atresia, bladder exstrophy, and open neural tube defects.

So first, a cleft lip is when the individual’s upper lip doesn’t form completely and has an opening in it. It is usually associated with a cleft palate, which is when the palate doesn’t form completely and has an opening in it. 

Now, these defects can occur as isolated malformations or as part of a syndrome involving multiple other organs, including the heart. 

Regarding prenatal diagnosis, cleft lip can be diagnosed with accuracy via ultrasound after 13 or 14 weeks of gestation. Ultrasound images in the coronal view and axial planes can help see the fetal lip and palate and assess if there are any associated abnormalities like lower limbs or the vertebral column defects. 

After birth, diagnosis is clinical. 

Early management is mostly supportive, and it aims to help the baby eat. It can be done with devices like specially designed bottle nipples, dental appliances, a feeder that can be squeezed to deliver formula, and an artificial palate molded to the individual’s own palate. 

However, surgical closure is the definitive treatment. For a cleft palate, a 2-stage procedure is often done. First, the cleft lip, nose, and soft palate are repaired at age 3 to 6 months. Then, the residual hard palate cleft is repaired at age 15 to 18 months. 

Esophageal atresia is a birth defect resulting in an interrupted esophagus. This way, the esophagus has two separate sections—the upper and lower esophagus—that do not connect. One or more fistulas between the esophagus and trachea may also occur. 

Prenatal diagnos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neonatal_ICU_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/14yjM11tRlu56p7ajA72d5DTR3K9_hAJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neonatal ICU conditions: Clinical]]></video:title><video:description><![CDATA[Preterm infants sometimes develop life-threatening complications that require immediate Neonatal ICU admission and management.

Some common issues that occur in a preterm infant include intraventricular hemorrhage, retinopathy of prematurity, apnea of prematurity, bronchopulmonary dysplasia, persistent pulmonary hypertension of the newborn, respiratory distress syndrome, feeding difficulties, gastroesophageal reflux disease, necrotizing enterocolitis, neonatal jaundice, and fetal growth restriction.

Now, prematurity is defined as a birth that occurs before 37 completed weeks of gestation.

The different degrees of prematurity can be defined by gestational age and birth weight.

The classification based upon gestational age is as follows: late preterm birth is when the gestational age is between 34 and less than 37 weeks; moderate preterm birth is between 32 and less than 34 weeks; very preterm birth is under 32 weeks; and extremely preterm birth - when the gestational age is below 28 weeks.

The birth weight classification is as follows: low birth weight is when the baby weighs less than 2500 grams, very low birth weight is under 1500 grams; and extremely low birth weight is when the baby weighs less than 1000 grams.

First, in intraventricular hemorrhage, bleeding in the germinal matrix occurs within the first day after birth.

The germinal matrix is located between the caudate nucleus and the thalamus, at the level of the foramen of Monro.

The etiology is multifactorial but it’s primarily attributed to vascular fragility and to disturbances in cerebral blood flow.

On examination, there are three possible presentations in the preterm infant. First, the silent presentation is detected by routine ultrasound screening.

Second, the saltatory or stuttering course evolves over hours to several days and it’s characterized by nonspecific findings, like altered consciousness, hypotonia, and abnormal eye movements and position. The respiratory function is can a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_ear,_nose,_and_throat_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PFNAvmJIQ7aKbKwSQVPSS3A5TGq3xNJB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric ear, nose, and throat conditions: Clinical]]></video:title><video:description><![CDATA[The most common ear, nose, and throat issues that occur in children can be divided into four categories. 

First, ear pathologies associated with ear pain and hearing loss include otitis externa, otitis media, mastoiditis, aural atresia, and ear foreign bodies. 

Second, nose-related conditions associated with rhinorrhea include viral and bacterial sinusitis, foreign bodies, and nose bleeding - mostly anterior posterior epistaxis. 

Third, breathing difficulties usually include nasal polyps, adenoids, and choanal atresia. 

And fourth, throat pathologies that cause a sore throat include viral and bacterial pharyngitis.

Let’s begin with ear pathologies. First, otitis externa or external otitis refers to inflammation of the external auditory canal usually caused by Pseudomonas aeruginosa or Staphylococcus aureus. Diagnosis is clinical.

On presentation, individuals show signs of external ear canal inflammation like ear pain, pruritus, discharge, and hearing loss due to ear canal edema. The auricle and tragus might also show signs of erythema and might be painful when touched. Individuals might have a history of tympanic membrane perforation, ear infection, recent ear instrumentation, or hearing devices use. 

Pneumatic otoscopy is needed to see if the tympanic membrane is affected. 

In otitis externa, otoscopy detects a swollen and erythematous ear canal and an erythematous tympanic membrane, which might be only partially visible due to canal edema. 

The tympanic membrane is typically mobile with pneumatic insufflation, moving inwards and outwards, respectively. 

Now, there should be no evidence of middle ear fluid or a perforated tympanic membrane as this is rare in otitis externa but common in otitis media. 

If there are signs of external ear inflammation that appear over 48 hours within three weeks and the tympanic membrane has preserved its mobility and integrity, a diagnosis can be established. 

Treatment begins with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vaginal_versus_cesarean_delivery:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jyy2OlGhTGO4KGxMJjDwjuI0TO_xYj55/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vaginal versus cesarean delivery: Clinical]]></video:title><video:description><![CDATA[Vaginal and cesarean delivery are the two ways that a baby can be born. With vaginal delivery, the baby comes into the world through the mother’s vagina, or birth canal, and the process is called labor, whereas with cesarean delivery, also called a c-section, surgery is done to get the baby out. 

Now, generally speaking, vaginal delivery is the preferred option. 

But in some cases, complications may arise during labor, or a vaginal delivery may be contraindicated in the first place, and a c-section may be done. 

And finally, a c-section may be performed on maternal request. 

Ok, now, vaginal delivery, or labor, has three stages. 

Stage I is when the cervix dilates to 10 centimeters, and it’s divided into a latent phase, covering dilation from 0 to 6 centimeters, and an active phase, when the cervix dilates completely.

Stage II is when the fetus passes through the birthing canal. 

If everything goes well, the baby is delivered and labor progresses to stage III, which is the delivery of the placenta. 

Complications that may arise during labor come in two flavors. 

First, labor may fail to progress as expected, and second, there may be non-reassuring fetal status, sometimes called fetal distress, during delivery; and both are indications for a C-section. 

So, in the first category, the indications are active phase arrest and prolonged second stage. 

Active phase arrest means there’s there’s no cervical change during the active phase after 4 hours of adequate uterine contractions, or 6 hours without adequate uterine contractions. 

Remember that adequate uterine contractions are higher than 200 Montevideo units, or MVU.

A prolonged second stage, on the other hand, is when it takes longer than 3 hours in primiparas and 2 hours in multiparas for the baby to descend through the birth canal.

In this case, an emergency C-section is indicated if the fetal head is not engaged, meaning it hasn’t reached the inlet of the pelvic brim during that time. 

Now]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tips_on_how_to_be_a_learner_and_an_educator</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/p953Mhj4RY26VCdCD8JHlH2bTK_AixJU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tips on how to be a learner and an educator]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Tips on how to be a learner and an educator through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypopigmentation_skin_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i1qOoNu-Tl6iIl5w7P4qn8JkT2SxbVMB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypopigmentation skin disorders: Clinical]]></video:title><video:description><![CDATA[Hypopigmentation refers to an area of skin becoming lighter than the baseline skin color due to a decreased amount of melanin pigment in the skin, which is produced by melanocytes.

Its most severe presentation is depigmentation, in which there’s absence of all pigment. 

Most causes of hypopigmentation are not serious, and diagnosis can be made based upon a detailed history and physical examination, taking into account the course of the disorder, and lesion morphology, distribution, pattern, and extent of hypopigmentation, as well as additional cutaneous and extracutaneous signs and symptoms. 

Individuals may be examined under a Wood&amp;#39;s lamp, which emits low wave ultraviolet A light that allows a better visualization of variations in skin pigmentation. This is done in a darkened room with the Wood&amp;#39;s lamp held at 4 to 5 inches from the skin, to observe any subsequent fluorescence. 

Hypopigmented lesions emit a bright blue-white fluorescence and appear sharply delineated - the brighter they appear, the lower the amount of melanin pigment. 

Examination under a Wood&amp;#39;s lamp is especially helpful in fair skinned individuals to identify hypopigmented or depigmented lesions that may not be visible to the naked eye. 

Finally, cases where the diagnosis is uncertain may get a skin biopsy to evaluate the number and location of melanocytes and melanin in the affected skin areas.

One of the most common and well known hypopigmentation disorders is vitiligo. 

The exact cause isn’t known, but there’s an autoimmune destruction of melanocytes, leading to complete depigmentation of well defined patches that can range in size from millimeters to centimeters and can sometimes expand and merge with other patches over time. 

These patches are classified into two broad categories. There’s non-segmental vitiligo, which is the more common type that affects any age group, and it occurs at various locations that are mirrored on both sid]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ascending_and_descending_spinal_tracts</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BRsTVdZ0Qyyop596eBQgnoqbQhWrIjOE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ascending and descending spinal tracts]]></video:title><video:description><![CDATA[Ascending and descending spinal tracts are pathways that carry information up and down the spinal cord between brain and body.

The ascending tracts carry sensory information from the body, like pain, for example, up the spinal cord to the brain.

Descending tracts carry motor information, like instructions to move the arm, from the brain down the spinal cord to the body.

Both types of tracts are made up of neuronal axons that gather into long columns called funiculi, meaning long ropes, which are found inside the ventral, lateral and dorsal parts of the spinal cord.

Ascending tracts are sensory pathways that begin at the spinal cord and stretch all the way up to the cerebral cortex.

There are three types of ascending tracts, dorsal column-medial lemniscus system, spinothalamic (or anterolateral) system, and spinocerebellar system. They are made up of four successively connected neurons.

First order neurons are found inside dorsal root ganglions from where they gather sensory input and send it to the second order neurons, usually found inside the spinal cord or brainstem.

They further transmit it to the third order neurons found inside the thalamus, and then the fourth order neurons in the cerebral cortex.

While ascending through the spinal cord these tracts cross over to the opposite side of the central nervous system, or CNS, meaning that the left side of the brain receives sensory input from the right side of the body and vice versa.

These crossings are called decussations and they happen at different levels of the CNS for each of these tracts.

Let’s start with the dorsal column-medial lemniscus system which is a sensory pathway that transmits delicate sensations like vibration, proprioception or sensation of the position of bodyparts, two-point discrimination, and touch.

Throughout the body there are receptors like mechanoreceptors found in the skin that sense touch, or proprioceptors, like the muscle spindles and Golgi tendon organs in the mu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Salmonella_typhi_(typhoid_fever)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qBLb6FQKR4a99zFIEkJ00cLjRtKv7tCe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Salmonella typhi (typhoid fever)]]></video:title><video:description><![CDATA[Salmonella is a bacterium belonging to the family Enterobacteriaceae. 

There are two main species: Salmonella bongori and Salmonella enterica, which itself has six subspecies. 

One of the subspecies is enterica, which has over 2500 serotypes that can be divided into two main groups based on the clinical symptoms they cause typhoidal or non-typhoidal Salmonella. 

The typhoidal group, which includes serotype Salmonella typhi (S. typhi), specifically infects humans and causes enteric fever, which is more commonly called  typhoid fever. 

If left untreated, it can be fatal and throughout history, has been the cause of death of aviator and engineer Wilbur Wright, one of the Wright brothers; Dr. Hashimoto, the first to describe Hashimoto&amp;#39;s thyroiditis; and several people in New York City infected by “Typhoid Mary” in the first documented asymptomatic carrier of the disease in the United States.   

OK, but generally, Salmonella are encapsulated gram-negative, rod bacteria – meaning, they have a polysaccharide layer outside the cell envelope and look like little red or pink sticks on a gram stain. 

They’re facultative intracellular pathogens, meaning they can live both outside or inside of its host’s cells. 

And have flagella, making them motile, but don’t form spores. 

They’re also facultative anaerobes, so they can undergo respiratory and fermentative metabolism; and they can ferment glucose but not lactose; are oxidase negative; and produce hydrogen sulfide gas. 

And while a variety of media can be used to selectively identify Salmonella, among them is Triple Sugar Iron agar which produces a black precipitate when hydrogen sulfide is produced. 

Now, once Salmonella is ingested and reaches the distal ileum of the small intestine, it targets the epithelial layer of the mucosal lining. 

Here, it uses surface appendages to adhere to microfold cells, or M-cells. And these M-cells eat, or phagocytose, the bacteria from the intestinal lumen and spit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Theoretical_Foundations_of_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HAeIjGyOT669_DlQx7QXUcgsQcSv0WRh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Theoretical Foundations of Nursing]]></video:title><video:description><![CDATA[The field of nursing has a unique professional culture, with particular ways of doing things and thinking about things. 

Broadly speaking, these ideas can be described as a Nursing knowledge, and it guides  the day to day responsibilities of nurses and distinguishes nurses from other health care providers like physicians, pharmacists, and therapists. 

Now this body of knowledge can be organized into categories. 

Going from abstract to concrete, the four categories are: a metaparadigm, philosophies, conceptual models or frameworks, and the last category is theories. 

Nursing metaparadigm

Let’s start by looking at the most abstract category which is the nursing metaparadigm. 

The metaparadigm consists of four fundamental concepts that define the nursing discipline and together they form the foundation for the field.  

The four concepts are: person, nursing, health, and environment. 

Let’s go through them one by one. 

Person refers to the recipient of nursing care. 

It could be an individual, a family, or a community. 

It could also refer to a group of people that require a specific type of health care, for example, premature infants or people on dialysis. 

Nursing refers to the care the person receives from the nurse. 

For example, administering a medication, taking a person’s blood pressure, or even health education. 

Health refers to a person’s overall level of wellness, and not simply the absence of disease. 

It incorporates the physical, psychosocial, and spiritual aspects of a person’s life. 

It also includes the person’s view of their own health and their health-related behaviors such as diet, level of activity, and habits like smoking. 

Finally, environment refers to the context in which nursing care is provided. 

It could mean the physical location that the care is given, like an operating room or the patient’s home, but it also includes factors like a person’s socioeconomic situation.

Now, it’s important for nurses to consider all]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Opsoclonus_myoclonus_syndrome_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KXJO2ZvWRxW6HEwnt4luQ7SRSxq1243W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Opsoclonus myoclonus syndrome (NORD)]]></video:title><video:description><![CDATA[Opsoclonus-myoclonus syndrome is also called OMS or dancing eyes-dancing feet syndrome. 

Opsoclonus describes seemingly random, involuntary, and rapid eye movements in the horizontal, vertical, and diagonal directions. 

Myoclonus describes lightening-like limb movements or limb jerks, that can also be more tremulous. 

The syndrome also causes ataxia, which often results in the inability to walk, sit or crawl, and the loss of previously attained abilities, like speech. 

Generally speaking, OMS is thought to be an autoimmune condition in which the body attacks the nervous system, resulting in the characteristic signs and symptoms. 

The precise cause of OMS is unknown, but in children, it’s often due to a paraneoplastic syndrome. 

The idea is that a hidden or occult tumor - like a neuroblastoma or ganglioneuroblastoma - triggers the body’s immune system, and the resulting antibodies unintentionally target healthy cells of the nervous system. 

CD20+ B-cells that get into the CSF fluid seem to play an important role. 

One brain area that gets affected is the cerebellum, which plays an important role in coordinating body movements. 

In older children and adolescents OMS is thought to be triggered by an infection, and in adults, it’s often due to a paraneoplastic process due to lung or breast cancer, for example.

In children with OMS, there’s almost always ataxia, so it’s sometimes referred to as OMAS - with the A representing ataxia. 

In fact, most toddlers with OMS are initially misdiagnosed with acute cerebellar ataxia of childhood. 

The diagnosis of OMS is also often based on symptoms like opsoclonus and myoclonus which can appear abruptly, progressing over days to weeks.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Precocious_and_delayed_puberty:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OdPIGmsFRHybC-SD5suyhBJBQ2_QPxdX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Precocious and delayed puberty: Clinical]]></video:title><video:description><![CDATA[Puberty is the natural process of sexual maturation, occurring around the age of 11 for females and 11.5 for males. When it begins too early, it’s called precocious puberty, and when it starts too late, it’s called delayed puberty. 

Now puberty is normally under the control of the hypothalamic-pituitary-gonadal axis. It begins when the hypothalamus starts releasing the gonadotropin-releasing hormone or GnRH, which eventually makes its way through the hypophyseal portal system to the hypophysis. 

Here, GnRH stimulates the pituitary gland to release the two gonadotropin hormones: luteinizing hormone, or LH, and follicle-stimulating hormone, or FSH, into the blood. These two hormones then signal the ovaries and testes to release sex hormones, mostly estrogen in females and testosterone in males. 

Sex hormones then trigger the maturation of the sex organs and the development of secondary sexual characteristics.

These sex-specific physical characteristics can be evaluated with the Tanner scale, which represents a predictable set of steps that males and females go through at puberty. 

There are five stages: In stage 1, the pre-pubertal stage, no pubic hair is present in either sex. Males have a small penis and testes. Females have a flat-chest. 

In stage 2, around a mean age of 10, soft pubic hair appears; there is a measurable enlargement of the testes; and breast buds appear. 

In stage 3, around a mean age of 12, pubic hair becomes coarser; the penis begins to enlarge in both size and length; and breast mounds form. 

In stage 4, around a mean age of 13, pubic hair begins to cover the pubic area; the penis begins to widen; and breast enlargement continues to form a “mound-on-mound” contour of the breast. 

In stage 5, usually after the age of 14, pubic hair extends to the inner thigh; the penis and testes have enlarged to adult size; and the breast takes on an adult contour. 

Puberty lasts for about 4 years, depending on factors such as race, genetic b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_bone_and_joint_infections:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HgpGSsw9RCuAYiax0o_1s-txQGyPehHQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric bone and joint infections: Clinical]]></video:title><video:description><![CDATA[Bone and joint infections comprise mostly of osteomyelitis and septic arthritis, or a combination of the two.

In osteomyelitis, infections most often occur at the ends of long bones where they meet to form joints like the hip and knee, and in septic arthritis, they occur in the joints. 

The source of infection may be hematogenous, secondary to close-by infection or secondary to direct inoculation from trauma and surgery.

Diagnosis is mostly clinical, and it’s based on the rapid onset and localization of symptoms. 

Individuals mostly present constitutional symptoms like irritability, decreased appetite or activity, tachycardia, malaise, and fever. 

Local signs consist of warmth, swelling, point tenderness around a bone or joint, and cellulitis. Joint stiffness is also common, with single joint involvement being more characteristic for bacterial infections. 

If the clinical signs raise suspicion of infection, the next step is asking for additional tests to confirm or infirm diagnosis.

Let’s start with osteomyelitis, which is an infection of the bone. It is usually caused by Staphylococcus aureus, with community-acquired methicillin-resistant S. aureus or MRSA accounting for many of the cases, especially in posttraumatic, post-surgical, and vertebral osteomyelitis. 

Vertebral osteomyelitis is also caused by Mycobacterium tuberculosis in about a quarter of the cases. 

Additionally, Salmonella species and Streptococcus pneumoniae are commonly found in those with sickle cell disease; Gram-negative bacteria, such as Pseudomonas species or Escherichia coli, are common in infections after puncture wounds of the feet or open injuries to bone, and Staphylococcus epidermidis in some of those with prosthetic devices.

The earliest signs generally depend on the age of the individual. In neonates, the affected limb may be limp and moving it might be painful but fever and other symptoms might be absent.

Older infants and children present pain, fever, and local s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_urological_conditions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m1Qg5mxVRA6cfqbppU6JbhPnSJC_HBb1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric urological conditions: Clinical]]></video:title><video:description><![CDATA[Some of the most common urologic issues in children include congenital defects of the urethra - so hypospadias and epispadias; hematuria; pathologies associated with hydronephrosis - so congenital ureteropelvic junction obstruction, ectopic ureter, vesicoureteral reflux, and posterior urethral valves; and lastly, urinary tract infections.

Let’s begin with congenital defects of the urethra. First, hypospadias is a congenital disorder that’s common in males but extremely rare in females.

In hypospadias, the urethral opening or meatus is not at the tip of the penis but on the bottom of the urethra, which is located on the ventral side of the penis. This occurs because the urethral folds along the penile urethra don’t meet up and close properly, leaving an opening along the bottom of the penile shaft. Diagnosis is mostly clinical. 

On examination, there are three possible types of hypospadias in males: glanular, which is near the head of the penis, midshaft, which is the middle of the penis, and penoscrotal—where the penis and scrotum come together. Additional findings include foreskin that fails to become circumferential and appears as a dorsal hood; chordee, which is when the penis has a hook shape and curves inwardly; inguinal hernia, which is a protrusion of bowel through the inguinal canal, and cryptorchidism, which is the absence of testes from the scrotum. The clinical picture might also present with painful urination, recurrent urinary tract infections, sexual dysfunction, infertility, and psychosocial problems, especially as the individual grows and matures sexually. 

Next, an excretory urogram, which uses a series of x-rays to visualize substances passing through the kidneys, bladder, and the urethra is recommended if the clinical picture is severe or if the individual presents symptoms suggestive of urinary tract infection or of an associated defect. 

Common findings on urogram include rotation anomalies of the kidneys, meatal st]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Platelet_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OaAwDMZgQK_r-8KTDUFEmgZqQDy5YRKq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Platelet disorders: Pathology review]]></video:title><video:description><![CDATA[At the family medicine center, a mother came in with her 5 year old child, Alana.  

Several days ago, Alana developed bloody diarrhea after eating undercooked ground beef and her mother noticed her face was pale and she only urinated once in the past 12 hours. 

Next to her, there’s a 30 year old person named Danika, who came in complaining of increased bruising for the past several months. 

She has no other symptoms and physical examination shows multiple ecchymoses on the extremities. 

Both Alana and Danika are suffering from a hemostasis disorder. 

Hemostasis disorders, also known as bleeding disorders, can be broadly divided into three groups. 

The first includes problems with primary hemostasis, which is when there’s a problem forming the initial platelet plug, and so, they’re referred to as platelet disorders. 

Now, the second group includes problems with secondary hemostasis, which is making a strong fibrin clot through activation of the intrinsic, extrinsic and common coagulation pathways, and are also known as coagulation disorders. 

And the last group includes disorders that affect both primary and secondary hemostasis and are known as mixed platelet and coagulation disorders. 

For this video, let’s focus on the platelet disorders.  

These can be further subdivided into two categories. In the first category, there’s thrombocytopenia, which is defined as a platelet count below 150,000 per microliter, with the normal range being between 150,000 and 450,000. 

Thrombocytopenia can be caused by increased platelet destruction, which can be immune-mediated, like in heparin induced thrombocytopenia, or HIT, and immune thrombocytopenic purpura, or ITP. 

Other cases can be non-immune mediated, like thrombotic thrombocytopenic purpura, or TTP, and hemolytic-uremic syndrome, or HUS. 

Thrombocytopenia from these cases is often due to an increased consumption of platelets during the formation of abnormal clots. 

And as a result, there are fewer pl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gallbladder_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D6w2JinTSoip4HZfRdkXU8BsTCqL4hzp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gallbladder histology]]></video:title><video:description><![CDATA[The gallbladder is a muscular pear-shaped storage sac attached to the lower surface of the liver.

In addition to being able to store about 50 mL of bile, it also concentrates the bile before secreting it into the duodenum after meals.

Bile is produced by the liver and secreted into a network of intrahepatic bile ducts before reaching the common hepatic duct.

The common hepatic duct then connects with the cystic duct, which allows the bile to flow into the gallbladder.

When the gallbladder contracts, bile is pushed back out of the gallbladder through the cystic duct and flows into the common bile duct, which joins with the main pancreatic duct before emptying into the duodenum.

Focusing on the gallbladder, at low magnification the gallbladder wall has three main layers: the inner mucosa, tunica muscularis, and its outer layer of connective tissue called the external adventitia or serosa.

If we first take a closer look at the mucosa, we can see that the mucosa has many mucosal folds or rugae, but they’re not long enough to be considered villi.

Some of the folds of the mucosa are deep enough to form the appearance of cross-bridges when seen under a microscope, such as the two in this image.

If we increase the magnification to 40x, we can see that the mucosal epithelium is lined with simple columnar cells that are overlying the lamina propria, which contains dense irregular connective tissue, many immune cells, and small capillaries.

The gallbladder’s mucosal folds may look similar to portions of the intestine but can be distinguished by the gallbladder’s lack of intestinal crypts at the base of the mucosal folds.

In the bottom left of this image, we can see a portion of the next layer underneath the mucosa, called the tunica muscularis.

Here we can see more of the tunica muscularis or the muscular layer of the gallbladder.

The muscles in this layer are grouped in bundles of smooth muscle, but they are actually randomly oriented.

The contraction o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pituitary_gland_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s0l4kfi6TSujJZtvPw8zRFAqRi27QZel/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pituitary gland histology]]></video:title><video:description><![CDATA[The pituitary gland, is a small gland with a diameter of approximately 1 cm.

It sits within a saddle-shaped bony cavity called the sella turcica, at the base of the brain.

The gland is divided into two main parts, the anterior pituitary or adenohypophysis; and the posterior pituitary or neurohypophysis.

Each part originates from different embryological sources, which is reflected in their different structure and function.

“Adeno” means “related to glands” and the adenohypophysis consists primarily of glandular epithelial tissue.

In comparison, the neurohypophysis consists mainly of neural secretory tissue, since the neurohypophysis arises from a bud of nervous tissue that grows down from the hypothalamus.

In this low power, para-sagittal section of the pituitary gland, the anterior and posterior parts of the pituitary can be identified pretty easily when stained with Masson’s trichrome.

Generally, this stain will stain nuclei and basophilic structures blue, collagen will be blue or green, and non-basophilic cytoplasm and red blood cells will be red.

The posterior pituitary is composed of mostly unmyelinated axons, which don’t have nuclei or a large amount of collagen.

So as a result, the posterior pituitary doesn’t stain well and will look significantly lighter when compared to the anterior pituitary.

Whether it’s stained with Masson’s trichrome or Hematoxylin and eosin.

In between the anterior pituitary and posterior pituitary, is a thin strip of cystic tissue, called the pars intermedia, which is part of the anterior pituitary because the cysts are actually remnants of Rathke’s pouch, which is the embryological structure that eventually develops into the anterior pituitary.

Zooming in closer to the pars intermedia, the colloid-filled cysts can be seen more clearly, along with irregular clusters of basophilic cells, that often invade the neighboring neurohypophysis as well.

Looking even closer, we can see a portion of the pars intermedia that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Paraphilic_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CZjVSlgWTyWBjzVKHGvifEbNTdeKFP12/_.jpg</video:thumbnail_loc><video:title><![CDATA[Paraphilic disorders: Clinical]]></video:title><video:description><![CDATA[Paraphilic disorders are conditions where there’s a recurrent, intense urge or sexually arousing fantasy that’s distressing or disabling because it involves inanimate objects, children or nonconsenting adults, or suffering or humiliation of oneself or another person.

Psychological factors are thought to play a major role, especially events in childhood that led the individual to associate sexual pleasure with a specific event or object. 

Often, a child who is the victim or observer of inappropriate sexual behaviors - including online, learns to later imitate the behavior. 

Other causes include childhood sexual abuse, substance abuse, hypersexuality, exhibitionism, and a history of antisocial behavior and sexual anxiety.

Paraphilia refers to a persistent sexual interest in things other than sex or foreplay with physically mature, consenting human partners. 

However, for a paraphilia to turn into a paraphilic disorder, there are some additional criteria. 

First, in paraphilic disorders the symptoms last for at least 6 months. 

Second, the sexual urges must manifest as either fantasies, urges that cannot be controlled, or sexual behaviors like masturbation. 

Third, the individual must have acted on these unusual sexual urges with a nonconsenting person, or they must cause anxiety, obsessions, guilt, or shame; or impairment in important areas of functioning - including sex.

According to DSM-V, there are ten disorders included in this category: voyeuristic disorder, exhibitionistic disorder, frotteuristic disorder, sexual masochism disorder, sexual sadism disorder, pedophilic disorder, fetishistic disorder, transvestic disorder, and other specified and unspecified paraphilic disorder. 

The other specified and unspecified paraphilic disorder diagnoses can be applied to the various other paraphilias that cause distress or impairment. 

In voyeuristic disorder the individual is at least 18 years old and experiences sexual arousal from observing an unsusp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blistering_skin_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uIx2GP8aSkCTsRVnR4fCE-GVTnGh7MdP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blistering skin disorders: Clinical]]></video:title><video:description><![CDATA[Blistering skin disorders are characterized by the presence of blisters, which are bubbles that pop up when serum collects in pockets under the top layer of the skin. 

Blisters occur as a result of a loss of adhesion between cells within the epidermis - called acantholysis; edema between epidermal cells - called spongiosis; and dissociation between the epidermis and dermis. 

Blisters that form within the epidermis tend to be more fragile than subepidermal blisters. 

Blisters that are smaller than 1 centimeter in diameter are called vesicles, while blisters that are larger than 1 centimeter in size are called bullae.

There are various causes for blistering disorders, including autoimmune disorders, drug reactions, infections, genetic disorders, and traumatic injury. These conditions range from benign to life-threatening conditions. 

Life-threatening cutaneous blistering disorders include toxic epidermal necrolysis, staphylococcal scalded skin syndrome, disseminated herpes simplex virus infection, and disseminated herpes zoster. 

Broadly speaking, blistering skin disorders may be divided into generalized or localized disorders. 

Among generalized blisters, some cause systemic illness, whereas others don’t. Generalized blistering disorders that are not usually associated with systemic illness include miliaria crystallina, bullous impetigo, linear IgA bullous dermatosis, epidermolysis bullosa, pemphigus, pemphigoid, and dermatitis herpetiformis.

Miliaria crystallina typically results in multiple tiny vesicles on the face and trunk, due to obstruction of eccrine sweat gland ducts in the setting of excessive warmth. 

Usually, the rash of miliaria resolves on its own, the key is to avoid overheating the body by wearing lighter clothing, staying hydrated, and keeping a cool environment, for instance by using air conditioner. A soothing ointment like calamine lotion can also help.

Bullous impetigo is caused by Staphylococcus aureus, which produces exfolia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_incontinence:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jQqUyIgcSPCOUI-z7w8zbeQkTaicDwGF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary incontinence: Pathology review]]></video:title><video:description><![CDATA[In the Urology ward, two people are coming in. The first is Oleg, a 70 year old man who says that he frequently has to use the bathroom and also complains of a weak urinary stream. The second is Samantha, a 55 year old woman who says that she “pees” a little when she laughs. Samantha also has 2 children and both were born by vaginal delivery. Now, both these individuals seem to have urinary incontinence. 

Urinary incontinence is a problem where the process of urination happens involuntarily, meaning that a person might urinate without intending to. This is particularly problematic because it affects a person’s personal hygiene as well as their social life in a way that can be very limiting.

Let’s talk about physiology real quick. Okay, so as urine flows from the kidneys into the bladder, the bladder starts to fill. Lining the bladder is a layer of transitional epithelium containing “umbrella cells”. These cells physically stretch out as the bladder fills, just like an umbrella opening up in slow-motion. This expansion is further aided by the relaxation of the muscular layer within the bladder’s walls, called the detrusor muscle. At some point, the bladder fills up with urine that will eventually exit the body through the urethra. 

Now, the urethra is wrapped up in some muscles that can prevent urine from leaking out. The first one is the internal sphincter muscle, which is made of smooth muscle and is under involuntary control and typically opens up when the bladder is about half full. The second one is the external sphincter muscle, and it’s made of skeletal muscle and is under voluntary control. This is the reason that it’s possible to stop urine mid-stream by tightening up that muscle. Once urine has passed through the external sphincter muscle, it can no longer be stopped.

Now, when specialized nerves in the bladder wall sense that the bladder is about half full, they send impulses to the spinal cord at levels S2 and S3, also known as the micturiti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_and_urinary_tract_masses:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XI36OqQjSi6iznlUyPsbouo-Q-_sVaD4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal and urinary tract masses: Pathology review]]></video:title><video:description><![CDATA[In the Emergency Department, two people came in. One of them is 68 years old Randy who has left flank pain and gross hematuria. On the physical examination, there’s also a palpable mass in the left abdomen. Randy also has a history of heavy smoking for the past 40 years. The other person is 54 year old Uriah who came in because of painless hematuria. A while ago, Uriah took cyclophosphamide for a condition he had called Hodgkin’s disease. Both individuals had an ultrasound done, which showed a mass in Randy’s left kidney and a mass in Uriah’s bladder. 

Okay, Randy has a mass in his left kidney, while Uriah has a mass in his bladder. Let’s first talk about renal masses, which can develop in both adults and children. These masses may be either cysts or tumor. In turn, renal cysts can be either simple or complex, while tumors can be benign, like renal oncocytoma, or malignant, like renal cell carcinoma.  Regarding masses of the urinary tract, the main concerns are transitional cell carcinoma and squamous carcinoma of the bladder.  

Let’s look at them one by one.  Simple cysts are very common and account for most of renal masses. They are typically small and occur in adults with otherwise healthy kidneys. On an abdominal ultrasound, they’re perfectly round and have a thin wall and are filled with fluid. This liquid is basically the produced by the kidney. The ultrafiltrate is the plasma without proteins that results after the filtration process, that happens in the glomeruli, specifically in Bowman’s capsule.  This makes simple cysts anechoic on ultrasound, since the fluid does not produce an echo and thus appear black. Usually they’re asymptomatic and are discovered incidentally during an ultrasound or a CT-scan done for other reasons. On the other hand, complex cysts are larger than simple cysts. Additionally, on an ultrasound, they have thick, irregular walls and are multilocular- meaning they have septations within, that separate the cyst cavity into com]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nephrotic_syndromes:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-YTx7T7MS8ullZJlNua61PwaSyWBkjtE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nephrotic syndromes: Pathology review]]></video:title><video:description><![CDATA[On the Nephrology ward, two people came in with the same symptoms: peripheral and periorbital edema. 

One of them is a 10 year old caucasian boy named Brian who had recently been stung by a bee, and the other one is a 55 year old Hispanic individual named Gregory. 

Lab tests show that both of them have hypoalbuminemia, hyperlipidemia and urinalysis showed frothy urine with fatty casts. 

A 24-hour protein collection was done which showed massive proteinuria with more than 3.5 grams of protein lost through urine per day. 

Both Brian and Gregory have nephrotic syndrome, but Brian has minimal change disease, while Gregory has focal segmental glo-merulo-sclerosis. 

Nephrotic syndrome happens when the glomeruli are damaged and they become more permeable, so they start letting plasma proteins pass from the blood to the nephron and then into the urine.  

This leads to proteinuria, which is when more than 3.5 grams of protein is excreted through the urine per day. 

One of the proteins lost through urine is albumin and this leads to hypoalbuminemia.  

This causes peripheral and periorbital edema since there’s less oncotic pressure in the blood vessels and the fluid leaks out.  

On your tests, a nephrotic patient could also present with a hypercoagulable state and you will need to understand the pathology. 

The reason for this is that the person is also losing antithrombin III proteins which is the body’s anticoagulant. 

This means that individuals with nephrotic syndrome are prone to thrombotic and thromboembolic complications. 

Immunoglobulins are another type of proteins lost through urine, which means that there’s a higher risk for infection. 

Now, apart from proteins, lipids are also lost through urine, which gives the urine a frothy or foamy appearance. 

On microscopy, there could be fatty casts, which are hyaline from dead epithelial cells that contained a lot of fat globules.  

If these casts contain a lot of cholesterol then, under polari]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatitis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/muLy77mzRuizrUy-vSk1NrTkQr2e_qGp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatitis: Pathology review]]></video:title><video:description><![CDATA[While in the Emergency Department, two individuals came in with severe epigastric pain. Michael who is 45, complains of pain that radiates to his back, vomiting, and nausea.  

All of these symptoms appeared after he came home from partying at the bar a few hours ago. 

On the clinical examination, there’s epigastric tenderness without guarding or rebound, decreased bowel sounds, and purple discoloration around the periumbilical region. He also tends to bend over to relieve the pain. 

Anna, who is 29 years old, on the other hand, says the pain started abruptly and that it doesn’t radiate anywhere. She also noticed it gets worse after her meals. On examination, she presents with epigastric pain, scleral icterus, and fever. 

Both were admitted and started on IV fluids. 

Blood tests were ordered, which revealed lipase and amylase levels that were 3 times more than normal.

Ok, so from what we can gather, both people have acute pancreatitis. 

Let’s begin with a bit of physiology. The pancreas is located in the epigastric region, behind the stomach, and it is mostly a retroperitoneal organ. 

It has both endocrine functions, by releasing hormones like insulin and glucagon, and exocrine functions by secreting enzymes needed for food digestion. 

The exocrine pancreas releases digestive enzymes through smaller ducts which drain in the main pancreatic duct. 

The main pancreatic duct, which travels through the length of the pancreas, joins the common bile duct at the ampulla of Vater and drains into the duodenum. 

Now, the main pancreatic enzymes include pancreatic amylase which breaks down carbohydrates; trypsin and chymotrypsin, which break down proteins; and lipase which breaks down lipids.  

To protect the pancreas from destroying itself, the acinar cells of the pancreas manufacture zymogen, or the inactive form, of trypsin, called trypsinogen. 

When this zymogen is released into the small intestine, it is cleaved by enteropeptidase enzymes found in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Karyotyping</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CQ1TeVJkTw_-xHc2kGz2SnV_QXu8SUfi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Karyotyping]]></video:title><video:description><![CDATA[Karyotyping is the simple process of seeing what a person’s chromosomes look like. 

But don’t think of it as a chromosome beauty contest - karyotyping is actually used to detect chromosome number or structure abnormalities, in order to diagnose genetic disorders, like Down syndrome; or even some types of cancer, like leukemia.

Ok, now, chromosomes are found in the nucleus of our cells and they contain our DNA. 

You can think of DNA like a library, with thousands of books called genes that carry recipes for how to make every single protein found in the cell. 

In human somatic cells, so all cells besides the gametes; there are 23 pairs of homologous chromosomes, and in each pair, one chromosome came from each parent. 

This adds up to 46 chromosomes in total. 

Of these 23 pairs, 22 are somatic pairs, which contain genes that code for traits like hair color; and one sexual pair, which determines the biological sex of an individual. 

In genetically female individuals, there are two X chromosomes, while in genetically male individuals, there’s an X and a Y chromosome. 

However, chromosomes actually look different depending on the phases of the cell cycle - which is the series of events that somatic cells go through from the moment they’re formed until they divide into two identical daughter cells. 

The cell cycle has two phases: interphase, when the cell prepares to divide, and mitosis, when the cell is dividing. 

In early interphase, each chromosome has a single copy of the genetic information, called a chromatid, so there’s 46 chromosomes and 46 chromatids. 

But in later interphase, as the cell prepares for mitosis, each chromosome is copied and pasted, so the amount of DNA, aka the number of chromatids, doubles up. 

But two identical chromatids remain joined in a region called the centromere - so they still count as one chromosome. 

So right before mitosis, there are 46 chromosomes and 92 chromatids. 

This way, the two resulting daughter cells h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Short_bowel_syndrome_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VtaN2qJcTMeRdcv3awfc2rYvSRqigVUu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Short bowel syndrome (NORD)]]></video:title><video:description><![CDATA[In short bowel syndrome, bowel is another word for the intestines. 

It’s a condition that occurs when either the small intestine and/or the large intestine become physically shorter when a portion is removed by surgery, or functionally shorter, when a portion is damaged in a way that makes it nonfunctional. 

This can lead to poor absorption of water and vital nutrients from food.

Normally, digestion begins when food is chewed and travels into the stomach where it’s dissolved by stomach acid, enzymes, and physical churning. 

Then, it’s sent to the first portion of the small intestine, which is called the duodenum. 

This is where more enzymes are added from the pancreas to digest macronutrients, including proteins, carbohydrates, and fats, while bile is added from the liver and gallbladder to help absorb fats. 

It’s also where the absorption of some minerals like calcium, iron, and magnesium begins. 

The next section is called the jejunum, and it has long projections on its surface, giving it a large surface area for absorption. 

It plays the biggest role in the digestion and absorption of most nutrients, including the breakdown-products of macronutrients, zinc, water-soluble vitamins, and fat soluble vitamins, namely A, D, E, and K. 

The third section is called the ileum, and it has tight intercellular junctions, allowing it to efficiently absorb fluid and begin concentrating the intestinal contents. 

Unlike the jejunum, the ileum is also capable of undergoing structural and functional adaptations to compensate for the jejunum if needed. 

The final portion is called the terminal ileum, and it absorbs vitamin B12 and bile salts which are recycled. 

It ends with the ileocecal valve, which prevents intestinal contents from going into the large intestine too quickly and the backward flow of material. 

The large intestine functions to absorb water, electrolytes like sodium and potassium, short-chain fatty acids, and bacteria within it produce vitami]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Monosodium_glutamate</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wKT8lgLNTCiRW9uh956fd84_Te23eE0w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Monosodium glutamate]]></video:title><video:description><![CDATA[Savory foods are inherently delicious—but have you ever wondered why? 

In 1908, a Japanese professor pondered this question when exploring what made kelp broth taste so good. 

He recognized a unique taste in it, that was different from the four well-known tastes of sweet, sour, bitter, and salty. 

It turns out that glutamate, an amino acid made by many plants and animals, was the source of this distinctive taste, which became known as “umami” in reference to “umai”, the Japanese word for delicious. 

The professor isolated glutamate from seaweed to produce a crystallized salt form of glutamate which combined one molecule of glutamate with the ion sodium - to make it more tasty. 

This umami seasoning is still widely used today, and is known as monosodium glutamate, or MSG.

Glutamate is the most abundant amino acid found in nature, and it’s one of the 20 amino acids that make up proteins in the human body. 

Because glutamate is synthesized as part of normal metabolism, it is considered a non-essential amino acid. 

In other words, we don’t technically need to get it from food. 

Our bodies synthesize about 50 grams of glutamate each day and store about 4.5 pounds of glutamate in major organs like the brain, muscles, kidneys, and liver. 

On average we eat about 10 to 20 grams of glutamate each day, mostly from protein-containing foods like meat, cheese, nuts, and legumes.

Whether consumed from food or MSG, glutamate is metabolized in the same way. 

In the saliva in the mouth, MSG separates into its original two parts…glutamate and sodium…and then glutamate binds to its receptors to elicit an umami, or savory, flavor sensation. 

In the stomach, there are more glutamate receptors, and these activate the vagus nerve. 

The vagus nerve notifies the brain that protein-rich foods have entered the stomach, and then the brain tells the stomach and intestines to prepare for protein digestion.

After leaving the stomach, glutamate enters the small intestine w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heart_failure:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ls764QvVSOqL8-77xs-0kLpxQKy7Ksmo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heart failure: Pathology review]]></video:title><video:description><![CDATA[On the cardiology ward, there were two people who had been admitted to the hospital repeatedly.  

The first one is 70 year old Lidia, who had a myocardial infarction about 3 years ago. 

She presents with fatigue, and dyspnea. 

She says that she usually wakes up at night because of shortness of breath, but using more pillows when sleeping helps relieve it somewhat. 

On examination, she has pitting edema in her legs and on auscultation, an S3 sound is heard. 

The other person is 81 year old Richard who has been a smoker for the past 50 years. 

He is also experiencing fatigue, and has pitting edema, but on further examination, there’s also jugular venous distention and hepatomegaly.

Okay, so, both these individuals suffer from heart failure. 

Heart failure is a clinical syndrome used to describe the inability of the heart to pump enough blood or a point at which the heart can’t supply enough blood to meet the body’s demands. 

This can happen in two ways, either the heart’s ventricles can’t pump blood hard enough during systole, called systolic heart failure, or not enough blood fills into the ventricles during diastole, called diastolic heart failure. 

In both cases, blood backs up into the lungs, causing congestion or fluid buildup, which is why it’s also often known as congestive heart failure, or just CHF. 

Alright, first up is systolic heart failure. 

One way to think about this is that the heart needs to squeeze out a certain volume of blood each minute, called cardiac output, which can be calculated as the heart rate multiplied by the stroke volume. 

The heart rate is pretty intuitive, but the stroke volume is a little tricky. 

For example, an adult heart might beat 70 times per minute and the left ventricle might squeeze out 70ml per beat, so 70 x 70 equals a cardiac output of 4900 ml per minute, which is almost 5 liters per minute. 

Now, the stroke volume is only a fraction of the total volume. 

The total volume might be closer to 110 ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mixed_platelet_and_coagulation_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lVz11-S3TiKRKysu2ivklauKSrGRVonf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mixed platelet and coagulation disorders: Pathology review]]></video:title><video:description><![CDATA[At the emergency department, a 70 year old male named Max is admitted because of high fever with chills, and hypotension. He complains of having urinary urgency, frequency and dysuria, or painful urination, for the last few days. A few hours after admission, he rapidly deteriorates and starts to bleed from venipuncture sites. Urine and blood cultures are ordered and are both positive for gram negative rods. Lab tests show low platelet count, and bleeding time, PT and PTT are prolonged, fibrinogen is decreased and d-dimers are elevated. Peripheral blood smear shows schistocytes. Now, there’s also an 18 year old female, named Sylvia, that came in with recurrent severe nose bleeds. She also complains of heavy menstrual periods. Family history reveals her father also suffered from bleeding diathesis. Lab tests show normal platelet count, prolonged bleeding time and PTT, and normal PT. 

Both Max and Sylvia are suffering from a hemostasis disorder. Hemostasis disorders, also known as bleeding disorders, can be broadly divided into three groups. The first includes problems with primary hemostasis, which is the formation of the weak platelet plug, and so, they’re referred to as platelet disorders. Now, the second group includes problems with secondary hemostasis, which is making a strong fibrin clot through activation of the intrinsic, extrinsic and common coagulation pathways, and are also known as coagulation disorders. And the last group includes disorders that affect both primary and secondary hemostasis and are known as mixed platelet and coagulation disorders. Okay, in this video, we will focus on mixed platelet and coagulation disorders, that include disseminated intravascular coagulation, or DIC, and von Willebrand disease. 

Alright, so let’s take a closer look at these disorders, starting with DIC, which is a massive overactivation of the coagulation system including both platelets and clotting factors. For your exams, it’s important to know that DIC ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-hemolytic_normocytic_anemia:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HT0brWVASxWEo-u1e27paUWYSbuDUrJr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-hemolytic normocytic anemia: Pathology review]]></video:title><video:description><![CDATA[At the family medicine center, Sofia, a 32-year-old black person of African descent, came to visit the doctor because she has been feeling fatigue as well as exertional dyspnea. 

Her medical history includes systemic lupus erythematosus. 

Next to Sofia, a father from Ireland brings his 14-year-old son, John, who’s been less active and has bruised easily for the past month. 

John’s medical history includes recurrent upper respiratory tract infections before the onset of the current symptoms. 

During the clinical examination, his spleen cannot be palpated. 

CBC is ordered for both people and they show low hemoglobin with normal MCV and reticulocyte count index lower than 2%. 

John also has leukopenia and thrombocytopenia. 

Both John and Sofia are suffering from anemia, which is defined as lower than average levels of hemoglobin, typically below 13.5 grams per deciliterg/dL in adult men and below 12.0 g/dL in adult women. 

For children, this level varies based on the age. 

Now, anemias can be broadly grouped into 3 categories based on mean corpuscular volume, or MCV, which reflects the volume of an RBC. 

So, microcytic anemia is where the MCV is lower than 80 femtolitersfL, normocytic is when, with an the MCV is between 80 and 100 femtolitersfL, and macrocytic is when the, with an MCV is larger than 100 femtolitersfL. 

Alright, the normocytic anemias can be further classified as hemolytic where there’s increased destruction of red blood cells and non-hemolytic where there’s decreased production of red blood cells in the bone marrow. 

When there’s hemolysis, the bone marrow revs up and starts pumping out reticulocytes which are immature red blood cells, but when there’s a bone marrow problem the reticulocyte count is low. 

So for your exams, if you run into a normocytic anemia and the reticulocyte production index, or RPI, is higher than 2%, think hemolytic anemia, since the red blood cells are being destroyed and the body compensates by producing]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_failure:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZZULLaYTRU61DoO5EDuoTzeaRtC3os2A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal failure: Pathology review]]></video:title><video:description><![CDATA[On the Nephrology ward, two people came in. The first one is 55 year old Matilda, who came in with oliguria, fever and a rash on her arm. Matilda also has a history of taking NSAIDs for her knee-pain. The second one is 34 year old George, which came in with oliguria, hypotension, tachycardia and cold extremities. George says that he’s also been having diarrhea for a few days now. BUN and creatinine levels were high for both of them. 

Both Matilda and George have renal failure. Now, renal failure is when the kidneys aren’t functioning properly. Before talking specifics, let’s remember some basic renal physiology. Now the kidney’s job is to regulate what’s in the blood, so they might remove waste, or make sure electrolyte levels are steady, or regulate the overall amount of water, and even make hormones, such as erythropoietin, which stimulates red blood cell production. Okay, so blood gets into the kidney through the renal artery, into tiny clumps of arterioles called glomeruli where filtration happens. After filtration, the stuff that’s filtered out, called the filtrate, moves into the renal tubules, where reabsorption and secretion of fluid and electrolytes happens. Along with fluid and electrolytes, though, waste-containing compounds are also filtered, like urea and creatinine, although some urea is actually reabsorbed back into the blood, whereas only a little bit of creatinine is reabsorbed. In fact, in the blood, the normal ratio of blood urea nitrogen, or BUN, to creatinine is between 5 and 20 to 1—meaning the blood carries 5 to 20 molecules of urea for every one molecule of creatinine, and this is a pretty good way to assess kidney function! So, when we want to check renal function, we look at BUN and creatinine levels and if there’s something wrong, then levels of both BUN and creatinine will be high.

Now, back to renal failure. There are two types of renal failure: acute and chronic. Now, acute renal failure is now called acute kidney injury. Th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_tubular_acidosis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ci81eXckTWu_DZW3B2lj5T-3SWiaoQbD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal tubular acidosis: Pathology review]]></video:title><video:description><![CDATA[In the Emergency Department, two people came in with rapid, shallow breathing and tachycardia. The first one is 45 year old Olga who also has systemic lupus erythematosus and the second one is 39 year old Fred. An arterial blood gas was taken, along with electrolytes. Results showed that Olga had low pH, low bicarbonate and pCO2 levels and her potassium level was also low. Fred also had low pH, low bicarbonate and pCO2 levels, but his potassium level was high.   Based on the ABG results, the diagnosis of normal anion gap metabolic acidosis was made. In order to identify the cause of their normal gap metabolic acidosis, more investigations were done and the urine anion gap showed that both individuals had a low urinary anion gap, which suggests that the cause was renal.

Okay, now, a normal anion gap metabolic acidosis can have renal causes. Like when a lot of bicarbonate is lost through the urinary tract-  which happens in type II renal tubular acidosis. A normal anion gap metabolic acidosis can also happen when too many hydrogen ions are retained, like in type I and type IV renal tubular acidosis. Now, there’s also a type III renal tubular acidosis, where both the proximal and distal tubules are affected. This is a pretty rare situation and the causes are not well understood, so it’s unlikely to be tested.

Okay, now, let’s review the physiology of the tubules. The proximal tubule is affected in RTA type II. It’s lined by brush border cells which have two surfaces:  One is the apical surface that faces the tubular lumen and is lined with microvilli, and the other is the basolateral surface, which faces the peritubular capillaries. Now, a lot of bicarbonate is reabsorbed here.  When bicarbonate approaches the apical surface it binds to hydrogen to form carbonic acid, which will be split into water and carbon dioxide by carbonic anhydrase. The water and carbon dioxide diffuse into the cells where carbonic anhydrase facilitates the reverse reaction and combi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Appendicitis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eDWfWtgfRyK4rbWFiLNWZfNcRu2oK7sI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Appendicitis: Pathology review]]></video:title><video:description><![CDATA[While in the Emergency Department, Bella, a 22-year-old woman, presents with abdominal pain that started 6 hours ago. The pain was initially located around the umbilical area but it has migrated to the right lower quadrant in the past few hours. The pain is sharp, like being stabbed with a knife and it gets worse with movement. A physical examination showed tenderness of the right lower quadrant with moderate guarding and a low-grade fever of 100.4°F. Shortly after, Edward, who’s 11, presents with generalized abdominal pain with vomiting and diarrhea. On examination, he appears ill and has a temperature of 104°F. His abdomen is tense with generalized tenderness and guarding. No bowel sounds are present. Blood tests were ordered in both cases, detecting an increased white blood cell count of 12,000 cells per microliter with 85 percent neutrophils.

Now, both people have appendicitis. Now the appendix is the little close-ended hollow tube that’s attached to the cecum of the large intestine, and sometimes it’s called the vermiform appendix, where vermiform means “worm-shaped.” Normally, the appendix can be found in a retrocecal location, as well as pre-ileal, post-ileal, pelvic subcecal, and paracecal. Its function is actually unknown, though some theories suggest it might be a “safe-house” for the gut flora and that it plays a part in the lymphatic and immune system. 

Ok, so appendicitis usually occurs because something gets stuck and obstructs the appendix. That something could be a fecalith, which is a hardened lump of fecal matter, a piece of undigested material like gum or seeds, or even a clump of intestinal parasites like pinworms. Another cause of obstruction could be lymphoid follicle growth, also called lymphoid hyperplasia, and a high yield fact is that unlike a fecalith, this is more common in children. Now, because the intestinal lumen is always secreting mucus and fluids from its mucosa, fluid and mucus build up in the obstructed appe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diverticular_disease:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5QXr_lKhRxqkuaCXqgMyzjRSQ6SQOcrr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diverticular disease: Pathology review]]></video:title><video:description><![CDATA[At the gastroenterology clinic, there is a 62- year- old male from Germany, named Karl, who came in for his regular colonoscopy. 

He is totally asymptomatic, except for occasional vague abdominal discomfort after meals. 

Next, a 65- year- old Native American named James came to the emergency department after two episodes of painlessly passing fresh, red blood in his stool.  

Finally, Zendaya, a 78- year- old African- American female, was brought to the hospital from a nursing home by paramedics, due to a severe pain in the left lower abdomen which started this morning. 

Her temperature was measured at 101.8°F or 38.8°C at the nursing home. 

On further history, they all had diets low in fiber and high in fat and red meat and suffered from chronic  constipation. 

Zendaya’s nursing home attendant reports that lately her constipation has been even worse than usual; in fact, her last bowel movement was more than three days ago.

Karl, James and Zendaya all have diverticula in the colon. 

Diverticula are small outpouchings that form along the walls of a hollow structure, most commonly, the large intestine. 

According to their pathogenesis, diverticula can be broadly grouped into traction and pulsion diverticula. 

Traction diverticula occur due to the pulling forces of an adjacent inflammatory site, resulting in scarring and outpouching of all layers of the intestinal wall. 

These are also known as true diverticula. 

Next, there’s pulsion diverticula, which are a result of high pressures created during a strained bowel movement. 

The pressure pushes on the mucosa and submucosa until they bubble out through weak spots along the wall, like where a blood vessel penetrates the muscle layer of the intestine. 

These are also known as false or pseudodiverticula since they don’t involve all layers of the intestinal wall. 

For your exams, it’s important to know that, most of the time, diverticula in the large intestine, and particularly, the left and sigmoid]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autoimmune_bullous_skin_disorders:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bzXGtfEKRYy3PhLTmbkWOzziT3Spyj9H/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autoimmune bullous skin disorders: Clinical]]></video:title><video:description><![CDATA[Autoimmune bullous disorders are a group of disorders in which the immune system mistakenly attacks the skin and mucosal membranes.

The lesions start as blisters, and then evolve into erosions, ulcers, and finally crusts. Often times this pattern occurs recurrently.  

There are four main autoimmune bullous disorders - pemphigus, pemphigoid, dermatitis herpetiformis, and linear IgA bullous dermatosis. 

Now for diagnosis, a history and physical can be followed up with a skin biopsy, serologic studies, and microbiologic tests.

A skin biopsy with light microscopy can reveal the skin layer involved in blister formation and the type of inflammatory cell infiltrate. 

If it’s a small vesicle, then the entire lesion should be removed. For larger lesions, a specimen should be obtained from the edge of a blister, and it should contain both portions of the blister and intact skin.

Direct immunofluorescence studies are typically done when an autoimmune blistering disorder is suspected, because they can detect the antibody or complement deposition pattern and skin level of involvement. 

For example, in pemphigus vulgaris and pemphigus foliaceus there’s intercellular antibody deposition in the epidermis, whereas in bullous pemphigoid there’s linear antibody deposition along the basement membrane. 

Finally, it’s important to take a biopsy from normal-appearing skin adjacent to the blister, also called a perilesional biopsy, to get reliable results.

Also serologic testing may be useful for the evaluation of autoimmune blistering disorders, using indirect immunofluorescence to detect antibodies within the circulation. 

If the target of circulating antibodies associated with specific autoimmune blistering diseases is known, antigen-specific testing can be used, such as ELISA, immunoblotting, and immunohistochemistry.

Let’s start off with pemphigus. Pemphigus includes a group of rare, but potentially life-threatening blistering disorders caused by autoantibodies th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atoms_and_the_periodic_table</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uWY4pdJ8Sn2NC_7xVZhQelCmQ5ewkn5t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atoms and the periodic table]]></video:title><video:description><![CDATA[One of the first models of the atom was the “plum pudding” model, which was proposed by the physicist J. J. Thomson in the nineteenth century. 

In the “plum pudding” model, atoms were thought to have a cloud of positive charge, and within that cloud there were tiny electrons with negative charge. 

Sort of like the mid-nineteenth century british dessert — plum pudding --- where the plums were the electrons sitting within a delicious positive charge of pudding. 

However, in the 20th century the physicist Ernest Rutherford realized that the plum pudding model wasn’t quite right. 

He did a famous experiment where he took positively-charged alpha particles, and shot them at a piece of gold foil. 

Most of these alpha particles passed straight through the gold foil and hit the detector, but some of them actually bounced off of the gold foil and hit the sides of the detector. 

His explanation for this was that the atoms are mostly empty space, and that the majority of the alpha particles travel straight through the foil and strike the back wall of the detector, but that on very rare occasions, the alpha particles bounce off of something. 

He visualized a very small but very dense object in the middle of the atom, that he called the nucleus, which the alpha particles were bouncing off of on those rare occasions. 

Since the alpha particles are positively charged, Rutherford figured that the nucleus must also be positively charged since like charges repel.

So Rutherford gave us the idea that the modern atom consists of mostly empty space containing electrons, which are miniscule in size compared to the atom overall. 

But in the middle of that empty space there is a very small but very dense nucleus. 

Later, scientists showed that the nucleus actually consists of two types of particles: protons and neutrons. 

Protons have a positive charge but neutrons have no charge.

Now, when looking at the periodic table you can find the simplest atom, which is hydroge]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_and_parathyroid_gland_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cDIjtauxTn_dWGeOGKb8m7kIR4u1HE_8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid and parathyroid gland histology]]></video:title><video:description><![CDATA[The thyroid gland is a butterfly-shaped endocrine gland with average weight of 25-30 grams, and located anterior and inferior to the larynx. 

It produces two types of hormones; the iodine-containing hormones tri-iodothyronine or T3, thyroxine or T4, and calcitonin. 

The parathyroid glands consist of four small ovoid glands weigh 30 milligrams each and are located on the posterior surface of the thyroid gland. 

They are responsible for secreting parathyroid hormone, or PTH for short.

Let’s first look at the thyroid gland, which has a thin capsule of connective tissue surrounding it that can be seen in this low power image, mostly on the right side. 

The connective tissue extends inward along with blood vessels, lymphatics, and nerves. 

Although there aren’t any nerves clearly visible in this image. 

The thyroid gland is unique because it’s the only endocrine gland that stores its inactive hormones extracellularly in follicles. 

The follicles can vary in size quite a lot, from 50 to 500 um. 

Each follicle is filled with a gel-like mass called colloid, which stains dark pink with H&amp;amp;E. 

The colloid consists mostly of thyroglobulin and thyroid hormones that are bound to the colloid. 

We can see that some follicles have colloid with a “scalloped” pale edge. 

This is where the follicle has extracted some of the stored colloid in preparation for hormone activation and secretion. 

On the other hand, the clear space around the colloid is just an artifact that was caused by the colloid shrinking in comparison to the follicular wall. 

The follicular epithelium is made of a single layer of simple cuboidal cells with round central nuclei and dark chromatin. 

These cells are responsible for secreting thyroid hormones when needed. 

The nuclear features of these cells are particularly important because they are the main feature looked at when diagnosing papillary thyroid carcinoma. 

In papillary thyroid carcinoma, the nuclei will be large and irre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cartilage_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/61OgLuPgT0GqIT3uSrUvDP5rSJ_i9WYm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cartilage histology]]></video:title><video:description><![CDATA[Cartilage is an avascular, smooth, and elastic tissue with various forms that allow it to function in a variety of ways.

It can act as a smooth surface for bone articulation within joints, play a role in bone formation, and also provide structural support, such as the cartilage rings in the trachea.

The majority of the tissue consists of extracellular matrix or ECM, and only a relatively small number of chondrocyte cells.

Mature chondrocytes are responsible for secreting and maintaining the extracellular matrix of the cartilage.

Based on the appearance and specific function, cartilage is separated into three main types: hyaline cartilage, elastic cartilage, and fibrocartilage.

Hyaline cartilage has a “glassy” appearance and can be found on many articular surfaces as well as cartilage that provides structural support.

Elastic cartilage contains a dense network of branching elastic fibers that allow it to be more flexible, which is why it’s often found in structures that need to be firm, yet still flexible.

Some examples include the epiglottis, larynx, and the pinna of the external ear.

And finally, fibrocartilage contains dense connective tissue with collagen fibers, as well as bands of extracellular matrix.

This type of cartilage is found in structures such as the meniscus and intervertebral discs.

Let’s first focus on hyaline cartilage, which is the most common type of cartilage.

This image is an example of hyaline cartilage on the articulating surface of a long bone, with the articulating surface located at the top of the image.

The image on the right is a longitudinal section of the trachea, which is an example of hyaline cartilage providing structural support.

Both images were stained with hematoxylin and eosin or H&amp;amp;E for short. With this stain, the cartilage stains a dark purple due to its strong affinity for hematoxylin.

If we take a closer look at the tracheal hyaline cartilage, it has an outer layer of dense irregular connect]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aortic_dissections_and_aneurysms:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oFG4VVk1S7_mbLKwki-6V0FBSVeRZbRx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aortic dissections and aneurysms: Pathology review]]></video:title><video:description><![CDATA[Ronda is a 55 year old with a history of hypertension, diabetes and coronary artery disease who came to the emergency department with a 1 hour history of sudden chest pain that’s described as “something’s tearing inside my chest!” She says this pain is different from the occasional chest pain she gets when she exercises.  She was given nitroglycerin in the ER but the pain did not improve. Her blood pressure is 175/95 in the right arm, but 130/80 in the left arm. An ECG shows left axis deviation, but no ST segment changes. Her troponin levels are normal. This is what her chest x-ray looked like. After seeing this x-ray, a CT of the chest was performed, and this is what it looked like. 

Okay, so the aorta is subject to a lot of stress, so a lot can go wrong. First let’s look at aortic aneurysms which is an outpouching that occurs due to weakening of the aortic wall. A true aneurysm involves all three vessel layers; the tunica intima, media and adventitia. A dissection occurs when there is a tear in the tunica intima, allowing blood to literally “dissect” into the vessel wall. This may create the appearance of an aneurysm, but because it doesn’t involve all three layers, it’s a false, or pseudoaneurysm. 

Now, that we got the basic terminology down, let’s take a closer look at aortic aneurysms. These usually occur in the abdominal aorta, but can also occur in the thoracic aorta. The most high yield and most important risk factor for abdominal aortic aneurysms is atherosclerosis. In atherosclerosis, chronic inflammation results in the release of enzymes called matrix metalloproteinases, or MMPs, which degrade the extracellular matrix in the tunica media, weakening the aortic wall.  

Abdominal aortic aneurysms, or AAAs, are most common below the origin of the renal arteries, which corresponds to the L2 vertebral level. This is because below this level, the abdominal aorta lacks “vasa vasorum”, which sounds like a graduation title, but are in fact small blood ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Significant_figures</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SsStfJrAQZqZX9E4svrkp9AfSQavdBqM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Significant figures]]></video:title><video:description><![CDATA[Significant figures are important for calculations involving measurements. 

For example, we can look at a thermometer that has markings of 5 degrees Celsius. 

So if we zoom in, and see a measurement that is between 25 and 30, you have to guess on the second digit. 

It might look like it’s 26 or 27, it’s hard to say. 

So if it is 27 degrees, then that measurement has two digits, the first digit we know for certain, and the second digit is estimated and therefore uncertain. 

But both are considered significant figures. 

Now let’s look at a different thermometer, which has markings of 1 degrees Celsius. 

So this time, the measurement is between the markings for 26° C and 27° C. 

So you don’t have to guess on the second digit, you know that it’s 27. 

But you have to guess on the third digit, which looks like it might be 27.2 degrees Celsius. 

In this case, the uncertain digit is the last two. 

But all three digits are considered significant figures for this measurement.

In general, when reporting measurements, the precision of your measuring device determines the number of significant digits. 

If any estimation is involved in reading a number from your device --- like a thermometer or a graduated cylinder --- then you record a measurement rounded to one decimal place beyond the decimal place of the markings. 

If you use a digital measurement, like a digital scale or pH probe, then there’s no estimation involved. 

You can just record however many significant figures are reported by the measurement device. 

So the number of significant figures is affected by the instrument used to perform a measurement. 

As another example, for finding the volume of a liquid, the most common way would be to use a graduated cylinder. In order to maximize the precision of our measurement, we would pour liquid into our graduated cylinder and then locate the bottom of the meniscus. 

We can draw a line there, and then read it off our measurement device. 

So in this]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cirrhosis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gdbrHc_gTQix3souMVa1XSmxQaudMYjl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cirrhosis: Pathology review]]></video:title><video:description><![CDATA[At the family medicine clinic, a 52- year- old male immigrant from Africa, named Jamar, came in for a checkup for the first time in a decade. On questioning, he admits to an extensive history of alcohol abuse. Physical examination reveals gynecomastia, palmar erythema and spider angiomata, as well as a palpable spleen.

Next, a 70- year- old Caucasian female, named Eleanor, with a history of chronic hepatitis C infection, is brought to the emergency department by paramedics due to altered mental status. She is completely disoriented and unable to provide an adequate history. Neurologic examination also reveals asterixis.

Lab tests of both show increased aspartate aminotransferase, or AST, and alanine aminotransferase or ALT. There’s also decreased albumin and increased prothrombin time. The difference is that Jamar has an AST level twice as high as ALT, in contrast with Eleanor, who has an ALT higher than AST. Eleanor, in particular, also has high serum levels of ammonia.

Both Jamar and Eleanor have cirrhosis. This is when chronic inflammation damages the liver causing it to become fibrotic. Normally, the liver is highly regenerative but scar tissue can replace liver cells which prevents regeneration and when this goes on for too long, it reaches the point where the damage is no longer reversible. If enough of the liver is replaced by scar tissue in advanced cirrhosis, a liver transplant might be needed. . Now, if we zoom into a hepatic lobule, we can see that it’s made of sheets of hepatocytes with sinusoids between them. The sinusoids are made of branches of the portal vein and hepatic artery, and together with the bile duct, form the portal triad which runs towards the central vein.

Now, there’s a space around each sinusoid, called the perisinusoidal space which contains stellate cells. When the hepatocytes are injured, they cluster together and form regenerative nodules. Here, they secrete paracrine factors that activate the stellate cells, which th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_renal_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pyQgFTnISC_8Gkrit2XJdvJ5RnmX_3m5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital renal disorders: Pathology review]]></video:title><video:description><![CDATA[Two people came to the Nephrology ward one day. 

The first is 29 year old Dan, who presents with hypertension, gross hematuria, and flank pain. 

Dan’s family history showed that his grandmother died of a berry aneurysm. 

Next is 35 year old Heather. 

She doesn’t present have any symptoms, but she has been referred to the nephrology clinic because her primary care doctor discovered that she her kidneys have a “weird shape” on an abdominal x-ray. 

Both individuals underwent abdominal ultrasound.  

Dan had many cysts of different sizes on both kidneys, while Heather’s kidneys are located lower than normal and appear fused together.  

Both Dan and Heather have congenital renal disorders. 

The renal system starts developing during week 4 of intrauterine life.  

It comes from the mesoderm, which is one of the three primitive germinal layers.  

More specifically, it develops from a portion of the mesoderm called the intermediate mesoderm. 

The intermediate mesoderm on either side of the embryo condenses to form a cylindrical structure called the urogenital ridge, and a portion of the urogenital ridge called the nephrogenic cord gives rise to urinary structures. 

During renal development, the nephrogenic cord gives rise to three sets of structures: the nonfunctional pronephros in the embryo’s head region which regresses by the end of week 4. 

Then, the mesonephros forms,  appears in the thoracic and upper lumbar region and acts as temporary kidneys until they regress in week 12. 

Finally the metanephros develops in the pelvic region, and it forms the permanent kidneys. 

Ok, the metanephros sprout small buds called the ureteric buds. 

At the same time, the intermediate mesoderm gives rise to another tissue called the metanephric blastema. 

The blastema release growth factors that stimulates the ureteric bud to become the ureter, the renal pelvis, the renal calyces, and the collecting ducts. 

Meanwhile, the ureteric bud release growth factors that ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parathyroid_disorders_and_calcium_imbalance:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SCFrbgIORIudO0niYyX-4YlFRuehhQtr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parathyroid disorders and calcium imbalance: Pathology review]]></video:title><video:description><![CDATA[On the Endocrinology ward, two individuals came in. The first person is 47 year old Melania who recently went through a surgical procedure called thyroidectomy due to thyroid cancer. Melania came in with tetany and on the clinical examination, there was a positive Chvostek’s sign. The other person is 55 year old Emma, who came in with constipation, muscle weakness and bone pain. She has a history of kidney stones, specifically calcium stones and she also said that she’s been feeling down lately. Calcium, phosphate and PTH levels were taken in both individuals. Melania had low levels of calcium, high levels of phosphate and low levels of PTH, whereas Emma had high levels of calcium, low levels of phosphate and high levels of PTH. 

Both individuals seem to have a problem in their parathyroids. First, a bit of physiology. The 4 parathyroid glands are on the posterior of the thyroid gland, and their main job is to keep blood calcium levels stable. Changes in the body’s levels of extracellular calcium and phosphate levels are detected by surface receptors in the parathyroid’s chief cells. Both decreased calcium levels and increased phosphate levels can signal the chief cells to release more parathyroid hormone or PTH.  PTH affects many organs.  In the bones it binds to osteoblasts, the bone building cells, and causes them to release RANK ligands, or RANK-L, and monocyte colony-stimulating factor, or M-CSF. These will cause osteoclast precursors to mature into osteoclasts that break down bones and release calcium and phosphate into the blood.  PTH also gets the kidneys to reabsorb more calcium and excrete more phosphate. It also activates calcitriol, also known as 1,25-dihydroxycholecalciferol, or active vitamin D. Active vitamin D then goes on to cause the gastrointestinal tract to increase calcium absorption. Altogether, these effects help to increase extracellular levels of calcium with they’re low.

Now, let’s talk about hypoparathyroidism, where ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocarditis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u6r1UWyIQfK-gQsvsPYr0pT1SmWQJP9H/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocarditis: Pathology review]]></video:title><video:description><![CDATA[Two people came into the cardiology ward. 

One of them was 25 year old Darren, who came in with a fever, chills and fatigue. 

On the clinical examination, his fingernails had splinter hemorrhages and the palm of his hands had some erythematous flat lesions. 

There were also some track marks on his forearm. 

The other one is 75 year old Anna, who also had a fever and the same splinter hemorrhages and erythematous flat lesions that we previously saw. 

On auscultation, a heart murmur was heard. 

On her history, she said she was at the dentist  2 weeks ago. 

Okay, so both people likely have endocarditis, or inflammation of the inner layer of the heart. 

Remember that the heart’s wall is made up of three layers, the epicardium being the outermost layer, then the myocardium, and the endocardium, which is the layer that gets inflamed. 

The inflammation can affect the heart valves, the mural endocardium or even prosthetic valves!  

The most common cases of endocarditis are due to a microbial infection, and this is called infective endocarditis  but in some cases, endocarditis can also be non-infective. 

For non-infective endocarditis, the first step is usually damage to the endocardium. 

Damage exposes the underlying collagen and tissue factor, which causes platelets and fibrin to adhere, which forms tiny blood clots. 

This is called Nonbacterial Thrombotic Endocarditis or NBTE.  

Tiny clots and fibrin can develop into vegetation, especially on the heart valves which damages them and makes it harder for them to open or close.  

Although the exact cause of NBTE is unknown, it’s thought that a proinflammatory state where cytokines levels are elevated can increase clot formation. 

This can happen with hypercoagulable states, like when there’s a malignancy, especially pancreatic adenocarcinoma. 

Another situation where NBTE can happen is with systemic lupus erythematosus, 

This is an autoimmune disease involving antigen-antibody complexes, and in thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_tract_infections:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KGoMm99QSc_8-9DBG7VBlwJsSpG4wAzI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary tract infections: Pathology review]]></video:title><video:description><![CDATA[Two people came to the Nephrology ward. 

The first one is 25 year old Carmen who recently returned from her honeymoon and now complains of suprapubic pain, dysuria and urinary frequency. 

The other one is 35 year old Pamela who has had dysuria, fever, nausea and flank pain for the past 2 days. 

On physical exam, she has costovertebral angle tenderness. 

CBC and urinalysis were done for both people. 

They showed that Carmen had a normal white blood cell count, but on the dipstick test, leukocyte esterase and nitrites were both positive. 

For Pamela, the white blood count was high, the dipstick test showed positive leukocyte esterase and nitrites, and on microscopy, there’s white blood cell casts in the urine. 

Both Pamela and Carmen have urinary tract infections, or UTIs. 

This includes the lower portion of the tract like the bladder and urethra, and the upper portion of the tract like the kidneys and ureters. 

UTIs are almost always caused by an ascending infection, where bacteria moves from the rectal area to the urethra and then migrate up the urethra and into the bladder. 

Normally, bacteria would be washed away with urination, but in some cases, like with E. Coli, that doesn’t happen. 

Instead, E. Coli uses little thread-like extensions called fimbriae to bind the uroepithelial cells and  colonize the bladder mucosa, causing cystitis. 

From the bladder, the infection can go up the ureter and into the kidney, where they attract neutrophils into the renal interstitium, causing pyelonephritis. 

As neutrophils die off, they make their way through the urinary tract and appear in the urine. 

The neutrophils and the surrounding inflammatory protein debris is even “casted” into the shape of the tubule, creating white blood cell casts and hyaline casts.  

For your exams remember that other factors like sexual intercourse or an indwelling catheter can also let bacteria into the urinary tract. 

So remember, in ascending infections bacteria moves f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antepartum_hemorrhage:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BMkQO2pRT3_VWvr3sQwTKw8LTtaC8eZh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antepartum hemorrhage: Clinical]]></video:title><video:description><![CDATA[Vaginal bleeding may affect as many as 40% of pregnant individuals. Most frequently, it occurs during the first trimester of pregnancy, meaning until week 12, but sometimes it can happen during the second or third trimesters, or between weeks 13 and 27, and weeks 28 to 40, respectively. 

The first step when confronted with vaginal bleeding during pregnancy is to assess the hemodynamic stability of the individual, based on the degree of hypovolemia and vital sign status. 

Stage 1 hypovolemia is when 500 to 1000 milliliters of blood have been lost. Blood pressure is usually normal, but there may be palpitations, tachycardia and slight dizziness. 

Stage 2 is when 1000 to 1500 milliliters have been lost. Systolic blood pressure drops to 80 to 100 mmHg, tachycardia is obvious, and there may be weakness and sweating. 

Stage 3 is when 1500 to 2000 milliliters have been lost. Systolic blood pressure drops between 70 and 80 mmHg, and there may be restlessness, pallor and low urine output. 

Finally, stage 4 is when more than 2000 milliliters have been lost, systolic blood pressure is less than 70 mmHg, and symptoms may include cardiovascular and respiratory collapse, loss of consciousness and anuria. 

Now, before elucidating the cause, some immediate measures should be taken in order to compensate the blood loss. These follow an A-B-C pattern.

A stands for airway, so you’ll want to protect the airway, especially when there’s loss of consciousness. 

B stands for breathing, so you’ll want to administer Oxygen through a non-rebreather mask. 

C stands for circulation - meaning measuring vital signs and establishing the degree of hypovolemia, inserting two large caliber peripheral IV catheters - of at least 14 gauge or even larger gauge -, and starting fluid resuscitation immediately, with 500 milliliters of normal saline or lactated Ringer’s solution given over 30 minutes. 

Afterwards, the rate of fluid is adjusted depending on their hemodynamic status. In ind]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coagulation_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vk7M1Tw_QzyFTDK3MsWoneXTRp6ZLJrI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coagulation disorders: Pathology review]]></video:title><video:description><![CDATA[At the hematology ward, there’s Braden, a 5 year old male, who developed prolonged bleeding after circumcision. 

His mother is worried because he has a history of recurrent hemarthrosis after minor falls. 

Family history reveals a relative of his mother who suffered from bleeding diathesis. 

Now, there’s also a 3 day old preterm baby, called Harlow, who is bleeding severely from the umbilicus. 

Her mother states that she did not get the standard care after delivery. CBC, PT and PTT are ordered for both patients. 

They both have normal platelet count. 

Now, Braden has normal PT but elevated PTT, while Harlow has both PT and PTT elevated. 

Both Braden and Harlow are suffering from a hemostasis disorder. 

Hemostasis disorders, also known as bleeding disorders, can be broadly divided into three groups. 

The first includes problems with primary hemostasis, which is the formation of the platelet plug, so they are also called platelet disorders. 

The second group includes problems with secondary hemostasis, which is making a strong fibrin clot through activation of the intrinsic, extrinsic and common coagulation pathways, and so they’re known as coagulation disorders. 

And the last group includes disorders that affect both primary and secondary hemostasis and are known as mixed platelet and coagulation disorders. 

Let’s focus on coagulation disorders that are usually due to a decrease in the number of clotting factors and causes include hemophilia and vitamin K deficiency. 

So, let’s look at hemophilia first. 

They are a group of inherited bleeding disorders caused by deficiencies in various coagulation factors. 

Hemophilia A and B are X-linked recessive disorders  so a high yield fact is that they almost exclusively affect males while females are carriers.  

A big hint for hemophilia is a family history of a maternal relative with a bleeding disorder. 

Hemophilia A causes a deficiency in factor VIII, while hemophilia B leads to a deficiency in f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_and_vascular_tumors:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wfFwUhaMQR60cQfikOGsMNuoRmi0vy3I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac and vascular tumors: Pathology review]]></video:title><video:description><![CDATA[Two people came to the clinic one day. Kara is a 66 year old woman who came to the clinic after noticing gradually developing left arm swelling and redness over the past 3 months. Physical examination reveals a tender purplish lesion along the left armpit. She has a history of hypertension, diabetes, and breast cancer that was treated 10 years ago with a modified radical mastectomy and radiation therapy.

Klay is a healthy 1 year old infant brought by his parents due to a rapidly growing “red bump” on his face. He has no history of trauma, and the lesion didn’t appear elsewhere. Physical examination reveals a raised, bright red nodule on the left side of his face and no other abnormal findings.

Now, both Kara and Klay have vascular tumors. There are many types so it’s best to classify them into benign and malignant tumors. Starting with the most common benign vascular tumor in children; the strawberry hemangioma, where Hemangioma means a benign tumor of the blood vessels. A strawberry hemangioma appears as a superficial, bright red skin lesion that looks kind of like a strawberry, and it commonly affects the face. Histologically, these lesions are confined to the epidermis. Now a typical strawberry hemangioma develops in infancy and grows pretty fast, but fortunately, it goes away on its own by 5 to 10 years of age. So in terms of management, exams like to bring up a very concerned parent, but the correct answer will almost always be to reassure the parent that the lesion will regress without treatment.

Now, a related disorder is cherry hemangioma, which is the most common benign vascular tumor in adults. This tumor appears dark red, like a cherry. Histologically, this lesion extends to the superficial papillary dermis, so they reach much deeper than strawberry hemangiomas. These tumors increase in frequency with age, and unlike strawberry hemangiomas, they do not regress spontaneously.

Cavernous hemangiomas are soft, bluish lesions, and unlike strawber]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kidney_stones:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Cd0Qc3ZmSuCq91yq-GOzaJcDSpu_ycs1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kidney stones: Pathology review]]></video:title><video:description><![CDATA[In the Emergency Department, two people with similar symptoms came in. 

One of them is 35 year old Conrad who has a terrible left flank pain, along with nausea and vomiting and the other one is 40 year old Sam who has left flank pain, but also has dysuria. 

An electrolyte panel and urinalysis was done in both individuals. 

Results showed that Conrad had normal levels of calcium in the blood, but urinalysis showed hypercalciuria and hematuria. 

Sam’s urinalysis showed positive leukocyte esterase, as well as positive nitrites and hematuria. Abdominal CT showed radiopaque masses in their ureters.  

Now, the suspicion is that both individuals have kidney stones, but there are actually several types of kidney stones and we need to know what we’re dealing with in order to give the right treatment. 

Okay, let’s first talk about how kidney stones form. 

Urine’s a combination of water, which acts as a solvent, and all sorts of particles, or solutes. 

In general, when certain solutes become too concentrated in the solvent, they become supersaturated. 

Urinary supersaturation of certain solutes results in precipitation out of the solution and formation of crystals. 

Those crystals then act as a nidus, or place where more solutes can deposit and over time it builds up a crystalline structure. 

This can happen if there’s an increase in the solute, or a decrease in the solvent, as would be the case with dehydration. 

This means that  dehydration leads to a low urine volume which can further put a person at risk for kidney stones.

Okay, let’s now talk about the different types of stones. 

There are four main types of stones. 

Calcium stones are present in about 80 percent of the cases, while struvite stones are present in about 15 percent of the cases and uric acid stones are present in about 5 percent of the cases. 

Finally, a super rare type of stone is a cysteine stone. 

Let’s start with calcium stones.  

With calcium stones, in most cases, the inorg]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombotic_thrombocytopenic_purpura</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZZFWELcgTlGkpFmuBd6Rsyv3QP_s4m2l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombotic thrombocytopenic purpura]]></video:title><video:description><![CDATA[Thrombotic Thrombocytopenic Purpura, often referred to as TTP, is a rare, serious blood disease that results in many small blood clots forming throughout the body. 

Typically, blood clot formation starts the tissue injury. Right away, some cells begin to release a protein called von Willebrand factor. This von Willebrand factor sticks to exposed fibers in the torn tissue and becomes like glue, allowing platelets to stick to the site. 

As the platelets pile on top of one another, they link together into a mesh, which we call a clot. In TTP, there is often a severe deficiency of the enzyme ADAMTS13 which breaks down von Willebrand factor when it’s no longer needed. 

Without this von Willebrand factor regulation by ADAMTS13, small blood clots can form more frequently throughout the body.

The small blood clots formed in a person with TTP can block normal blood flow through arteries and veins, leading to clinical findings that include decreased platelets, increased red blood cell destruction, and neurological issues such as headaches, mental changes, confusion, speech abnormalities, partial paralysis, seizures, or coma.

TTP can cause a wide range of other symptoms. Due to the low number of platelets, small areas of abnormal bleeding in the skin may occur which can be seen as a rash-like appearance or a purplish discoloration. 

Other symptoms may affect the entire body including fever, weakness, fatigue, and extreme paleness. There can also be episodes of unusually heavy bleeding or abdominal pain accompanied by nausea and vomiting. 

Acute kidney failure occurs in less than 10% of people with TTP and requires dialysis. Due to the lack of blood and urine filtration when the kidneys stop working properly, increased water, salt, and protein retention can occur causing an onset of symptoms within days including foot swelling, shortness of breath, headaches, fever, and an irregular heartbeat.

Although the exact cause of TTP is unknown, it’s associated with a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Reading_a_chest_X-ray</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qsC0Z-ybTm2iUmnSCMBR3KEKQ4WmfQaf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Reading a chest X-ray]]></video:title><video:description><![CDATA[You can think of X-rays as photos made from high-energy photons that penetrate the body tissues so that we can see what’s going on inside.  Just like visible light, X-rays are less likely to penetrate denser materials.  Conventional x-rays that show white bones on a black background are like photographic negatives.  The darkest parts of the film like the lungs are areas where more photons can penetrate the body.  In contrast, the sharp, bright white areas are where the dense bone material blocks photons from getting through.   

Let’s go through this chest X-ray using an easy-to-remember checklist - associated with the first 7 letters of the alphabet: ABCDEFG. 

A stands for Assessment.  To avoid errors and wasted time, you should always begin by assessing the patient and exam data.  You want to verify the patient’s data with the exam data (medical record number, date of the exam, etc.) to ensure that you are looking at the right study and patient. 

You also need to assess image quality, because this will impact the accuracy of the test in detecting pathology.  For example, to ensure there isn’t excess rotation of the patient, you should make sure that the medial ends of the spinous processes are equally distant from the border of the vertebral bodies. Rotation throws off the usual X-ray anatomy and introduces unwanted variation. Next, a good inspiration film should show at least the 10th or 11th posterior ribs. If the lungs are not fully expanded, we might miss important diseases.  Finally, we need to make sure that the exposure isn’t too bright or too dark.  To check for this, you can look for fine markings in the lung fields to make sure they are visible. If the fine lung markings aren’t visible, then the X-ray may fail to detect some diseases.

A also reminds us to make sure there isn’t “Air where it shouldn’t be.”  Finding air where it should not be - or more commonly “ruling it out” - remains one of the most important uses of medical X-rays.  Diagno]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Benign_hyperpigmented_skin_lesions:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vhkGzFucQSqrHrbb3kBWt3__Q7Sb6Dec/_.jpg</video:thumbnail_loc><video:title><![CDATA[Benign hyperpigmented skin lesions: Clinical]]></video:title><video:description><![CDATA[Hyperpigmentation is the darkening or increase in the natural color of the skin, most often due to hypermelanosis, which is an increased deposition of melanin in the epidermis or dermis. 

This can be associated with a multitude of clinical conditions, ranging from normal variations of skin color to acquired and inherited syndromes. 

Diagnosis of hyperpigmentation includes physical examination and a detailed history. 

A complete skin examination should be performed under visible light to observe important clinical parameters, including the extent of the pigmentary abnormality, distribution, pattern, color hue and morphology of individual lesions. 

Under natural light, epidermal hypermelanosis appears light brown to dark brown in color, while dermal hypermelanosis has a bluish or ashen gray hue with margins less defined than epidermal hypermelanosis. 

Complete skin examination should include observing these general features with the naked eye, and then further examine them through dermoscopy. 

Next, hyperpigmented skin lesions may be examined under a Wood&amp;#39;s lamp, which emits low wave ultraviolet. 

A light that allows a better visualization of variations in skin pigmentation. 

This is done in a darkened room with the Wood&amp;#39;s lamp held at 4 to 5 inches from the skin, to observe any subsequent fluorescence. 

Under a Wood&amp;#39;s lamp, epidermal hypermelanosis shows enhanced pigmentation, while dermal hypermelanosis doesn’t. 

Finally, a skin biopsy for histopathologic evaluation is not routinely performed for the diagnosis of all hyperpigmented lesions, but it may be necessary when the clinical diagnosis is uncertain or suggests malignancy.

The most frequent benign hyperpigmented skin lesions are melanocytic nevi, most commonly known as moles. 

These are benign proliferations of a type of melanocyte called nevus cells, which cluster as nests within the lower epi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leukemias:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4gvH8SD2QCSZZ4bVh08P88WwTXWTCo8Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leukemias: Pathology review]]></video:title><video:description><![CDATA[A 65-year-old man, named Mike is admitted to the hospital for a lower respiratory tract infection. He reports easy bruising for the past months, and a few hours after admission, he rapidly deteriorates and starts to bleed from venipuncture sites. Lab tests show low platelet count, and bleeding time, PT and PTT are prolonged. Fibrinogen is decreased and d-dimer is elevated. Peripheral blood smear shows schistocytes. Bone marrow biopsy shows more than 30% blast cells with Auer rods in the cytoplasm.  

Next, there’s a mother with her 5-year-old son, Luke. Luke’s mother has noticed that he’s been less active and had recurrent upper respiratory tract infections in the past few months. Clinical examination reveals diffuse lymphadenopathy. CBC shows anemia and leukopenia, while bone marrow biopsy shows more than 30% blast cells.   

The last person is a 40-year-old woman, named Mia, who reports recurrent upper respiratory tract infection, progressive fatigue, and abdominal fullness. Clinical examination reveals severe splenomegaly. CBC shows anemia, increased WBCs, while blood smear shows increased granulocytes and immature forms of myeloid cells. The lap score is low. Bone marrow biopsy shows blast count of 8%.  

Okay, so all three people have leukemia. Leukemias can occur when there’s uncontrolled proliferation of immature white blood cells.  The most immature type of cells are called blast cells, but sometimes cells near maturity that resemble normal white blood cells can also be affected.   Whatever the stage, these abnormal cells accumulate in the bone marrow or blood.  This differentiates them from lymphomas which can also arise from white blood cells, but they typically form solid tumors in lymphatic tissue such as lymph nodes, thymus, or spleen. 

Leukemias are most commonly caused by genetic mutations. These mutations can be chromosomal deletions, where part of a chromosome is missing; trisomies, where there’s one extra chromosome; and translocati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Happy_Birthday_from_Osmosis!</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gSZx5lr4SKKpw32bmlPJGAbjQI6vYlYa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Happy Birthday from Osmosis!]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Happy Birthday from Osmosis! through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autoimmune_polyglandular_syndrome_type_1_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Dgqk0eaNREOMDVmMik1gDJzCQGuiKr9v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autoimmune polyglandular syndrome type 1 (NORD)]]></video:title><video:description><![CDATA[Autoimmune polyglandular syndrome type 1, also called APS type 1, or autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, also called APECED, is a rare, genetically inherited condition. 

Autoimmune means that the body’s immune system begins to attack its own tissues, and polyglandular means that multiple hormone-producing organs are affected.

Normally, your body should only react to things that are foreign or not-self. 

This is maintained by a process called immune tolerance where only non-self-reactive B-cells and T-cells, are allowed to mature, whereas self-reactive ones aren’t. 

For T-cells, this process takes place in the thymus, where a gene called AIRE, or autoimmune regulator, is expressed by thymic medullary epithelial cells. 

When T-cells are developing, this gene leads to the production of thousands of the body’s proteins, and this serves as a test to see whether the T-cells react to self proteins. 

If one does, that T-cell either undergoes apoptosis and dies, or it becomes a regulatory T-cell, or T-reg, that helps to eliminate other immune cells that react to self antigens.

In APS type 1, there’s a genetic mutation in AIRE that’s usually inherited in an autosomal recessive fashion. 

This means that the thymic medullary epithelial cells lose the ability to display the body’s different self-proteins. 

Since they can no longer test whether T-cells are self-reactive or not, the process of immune tolerance does not occur normally, and self-reactive T-cells are allowed to live. 

Regulatory T-cells are no longer produced normally either, so the body loses a second mechanism for destroying autoimmune cells. 

This allows for the production of antibodies and lymphocytes that target normal tissues of the body. It is still unclear why, but certain glandular tissues, including the adrenal glands and parathyroid glands, are particularly targeted. 

There are multiple characteristic signs and symptoms of APS type 1. 

One of them is polye]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bone_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/db-sBVPdT12tdgzzA3OLcpixQAuTJ6BK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bone histology]]></video:title><video:description><![CDATA[Bones are composed primarily of an extracellular calcified material called the bone matrix or collagen matrix.

It also has three main types of cells: osteocytes, osteoblasts, and osteoclasts. 

Osteocytes are found in cavities or lacunae between the layers of the bone matrix and assist with the nutrition of the bone. 

Osteoblasts are found mostly along the surface of bones, but also within the bone matrix itself. 

They’re responsible for both synthesizing and mediating the mineralization of the bone matrix. 

Osteoclasts are large multinucleated cells that are responsible for removing calcified bone matrix and allow for the constant turnover and remodelling of bones. 

Morphologically, there are two main types of bone. 

The compact or cortical bone is the dense portion that’s found closer to the surface of bones. 

The deeper portion of bones have interconnecting cavities and is called the cancellous or trabecular bone. 

In this electron microscopy or EM image of the tibia, the compact bone is also blue, and the more central trabecular bone is yellow. Microscopically, both compact and trabecular bones will be organized or arranged in two forms. 

Layered or lamellar bone has a bone matrix that’s arranged in sheets. 

80% of lamellar bone is found within the compact bone and only 20% is found within the trabecular bone. The more immature woven bone, has collagen fibers that are arranged randomly. 

This form of bone is found mostly within developing and growing bones, as well as bones that have healed after being fractured.

Alright, let’s compare sections of a long bone and a flat bone. 

This long bone is a partial cross-section of the head of a long bone, and the flat bone is a cross-section from the skull. 

Both sections have been decalcified in order to make it easier to cut the bone into thin sections, but the collagen is still present in the slides. 

Since the denser compact bone is typically found closer to the surface, it’s seen in the long ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_distress_syndrome:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4QlvoxUfTbuVZZfG6NVirJ7yR8mzLGHP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory distress syndrome: Pathology review]]></video:title><video:description><![CDATA[Two people are admitted to the emergency department. 

Mike, a 55-year-old man, presents with shortness of breath, high fever, and cough. 

A chest x-ray was ordered and it showed a right lower lobe infiltrate, which is suggestive of pneumonia. 

He was then started on IV antibiotics but the following day Mike became hypoxic and hypotensive. 

Because his hypotension didn’t improve despite intubation, IV fluids, and vasopressors, he is diagnosed with septic shock. 

Next, a repeat x-ray detected newly-developed bilateral alveolar opacities, heart echography ruled out heart failure, and arterial blood gas analysis revealed a PF ratio of 109 milligrams Mercury. 

Then there was Dona, an infant delivered by cesarean section at 36 weeks’ gestational age, with an Apgar score of 9 at birth. 

A few hours after delivery, she develops tachypnea, chest wall retractions with nasal flaring, and tachycardia. 

Aside from increased work of breathing, her physical examination findings are normal. 

A chest x-ray was ordered and it showed diffuse reticulogranular ground glass appearance with air bronchograms.

Now, both people are in respiratory distress. 

But first, a bit of physiology. 

Normally, when you breathe in, the air reaches the alveoli, which are made up of two types of pneumocytes. 

First, type I pneumocytes are thin, and have a large surface area that that facilitate gas exchange. 

More important for the exams are the type II pneumocytes, which are smaller, thicker and have the ability to proliferate in response to lung injury. 

They are in charge of making a fluid called surfactant which contains various phospholipids.  

This lets it act like droplets of oil that coats the inside of the alveoli, decreasing surface tension, so if it’s missing, the alveoli will collapse. 

These cells also act like stem cells, meaning they can give rise to type I cells and type II pneumocytes.

Ok so acute respiratory distress syndrome, or ARDS, is characterized by rapi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Perinatal_infections:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-kLpTos8Rv2RGBvfDWHXdewZRAeLHepH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Perinatal infections: Clinical]]></video:title><video:description><![CDATA[Perinatal infections are a significant cause of impaired growth, developmental anomalies, and mortality. They can be divided into two categories. 

The first category is in-utero infections acquired transplacentally or through ruptured membranes, which lead to congenital defects. They are mostly represented by TORCH infections, an acronym that includes infections caused by Toxoplasma, Other agents - usually syphilis; Rubella; Cytomegalovirus, and Herpes simplex virus. 

The second category belongs to intrapartum infections, which are acquired as the newborn passes through the birth canal, mostly caused by group B streptococcus, Hepatitis B virus, and HIV.

Let’s begin with TORCH infections. In some cases, intrauterine infection may be suspected on the basis of laboratory results obtained during pregnancy, like positive syphilis serology with increasing titers, and on ultrasonography findings. 

After birth, although most infections are asymptomatic, common early signs include fever, microcephaly, cataract, hearing loss, congenital heart disease, hepatosplenomegaly, thrombocytopenia, and jaundice. Late signs include vision loss, intellectual disability, deafness, and seizures.

First, congenital toxoplasmosis is caused by the protozoan parasite Toxoplasma gondii. Prenatal diagnosis is based on ultrasonography signs of congenital infection, like ventriculomegaly, intracranial calcifications, and fetal growth restriction. It is then confirmed by polymerase chain reaction or PCR testing of the amniotic fluid. 

If PCR doesn’t confirm the presence of Toxoplasma DNA, those suspected of congenital toxoplasmosis will still need a complete diagnosis evaluation after birth. Postnatal diagnosis evaluation begins with a complete clinical examination. 

The most common early and late symptoms are cataract, microcephaly, hepatomegaly, jaundice, and purpura. Evaluation continues with serologic tests performed as soon as possib]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Macrocytic_anemia:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2XhBydV2Q5mvX7P9gP0IdM9oQXSxAj3b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Macrocytic anemia: Pathology review]]></video:title><video:description><![CDATA[In the hematology ward, two people came in with the same symptoms: easy fatigability, exertional dyspnea, and weight loss. One of them is a 65 year old caucasian individual named Bobby, and the other one is a 50 year old Hispanic individual named Sara. Bobby complains of frequent falls, while Sara admits she is a chronic user of alcohol. Their lab tests show decreased hemoglobin levels. 

Both Bobby and Sara are suffering from anemia, which is defined as lower than average levels of hemoglobin, typically below 13.5 g/dL in adult men and below 12.0 g/dL in adult women. Now, anemias can be broadly grouped into 3 categories based on mean corpuscular volume, or MCV, which reflects the volume of a Red Blood Cell or RBC. So microcytic anemia is where the MCV is lower than 80 fL, normocytic, with an MCV between 80 and 100 fL, and macrocytic, with an MCV larger than 100 fL. Now, let’s focus on the macrocytic anemias. The two most common causes are vitamin B12 deficiency and folate deficiency.  Orotic aciduria, Fanconi anemia, Diamond-Blackfan anemia are also macrocytic.  Finally, liver diseases and hypothyroidism can also cause this type of anemia, but their mechanisms are not well understood. 

Okay! Macrocytic anemias can be classified based on the presence of megaloblasts. These are large, immature red blood cells produced when the cytoplasm develops normally, but the DNA synthesis is impaired and cell division is delayed. So when there’s defective DNA synthesis or defective DNA repair like in folate deficiency, vitamin B12 deficiency, orotic aciduria, and Fanconi anemia there’s megaloblastic macrocytic anemia. Megaloblastic anemia can also affect white blood cell production, so the bone marrow starts releasing large, immature neutrophils, with hypersegmented nuclei, meaning their nucleus has more than 5 lobes. These are called hypersegmented neutrophils and are a key finding on the peripheral blood smear of individuals suffering from megaloblastic anemia. 

So]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Extrinsic_hemolytic_normocytic_anemia:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TtbYV733SFmD_9338tEYTsr9R1SWgfjt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Extrinsic hemolytic normocytic anemia: Pathology review]]></video:title><video:description><![CDATA[At the family medicine center, two people came in with progressive fatigue. 

One of them is a 60 years old named Will whose past medical history included an aortic valve replacement with a mechanical valve due to severe aortic stenosis. 

There’s Hanna, a 28 years old female of African descent. 

She was diagnosed a year ago with systemic lupus erythematosus, or SLE. CBC is ordered for both people and it shows low hemoglobin with normal mean corpuscular volume, or MCV and reticulocyte count index over 2%. 

They also have increased LDH. Now, Will has schistocytes on peripheral blood smear, while Hanna has spherocytes. 

Both Will and Hannah are suffering from anemia, which is defined as lower than average levels of hemoglobin, typically below 13.5 g/dL in adult men and below 12.0 g/dL in adult women. 

For children, this level varies based on the age. Now, anemias can be broadly grouped into 3 categories based on =MCV, which reflects the volume of an RBC. 

So microcytic anemia is where the MCV is lower than 80 fL, normocytic, with an MCV between 80 and 100 fL, and macrocytic, with an MCV larger than 100 fL. 

Normocytic anemias can be further classified as hemolytic when there’s increased destruction of RBCs, or hemolysis, and non-hemolytic when there’s decreased production of RBCs from the bone marrow. 

When there’s hemolysis, the bone marrow revs up and starts pumping out immature RBCs called reticulocytes, but when there’s a bone marrow problem reticulocyte count is low. 

So for your exams, it’s important to know that in hemolytic anemias there’s an increased reticulocyte production index of over 2%, while in non-hemolytic anemias it’s lower than 2%. 

Alright, now hemolytic anemias can be classified as intrinsic or extrinsic hemolytic anemias. 

In intrinsic hemolytic anemias, RBCs are destroyed because they’re defective, while in extrinsic hemolytic anemias, RBCs are normal but are later destroyed outside the bone marrow. 

In this video, let’s fo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myeloproliferative_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LsAa59RLT0_q3iAXfnPAEgVNQGSdd5bE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myeloproliferative disorders: Pathology review]]></video:title><video:description><![CDATA[A 70 year old female named Jenny is brought by her husband to the emergency department complaining of blurred vision and headache. Her face appears plethoric and her husband says that Jenny has been complaining of extreme itchiness after showers for the last few days. She has no significant past medical history. CBC shows increased hematocrit and slightly increased platelets. Uric acid is also increased. Next to Jenny, there’s a 65 year old male named Seth that came in with fatigue and progressive weight loss due to early satiety. Past medical history is unremarkable. Clinical examination reveals a very enlarged spleen. CBC shows pancytopenia and peripheral blood smear shows teardrop cells.

Both Jenny and Seth suffer from myeloproliferative neoplasms. These are a group of malignant neoplasms characterized by proliferation of the bone marrow cells from the myeloid lineage. That includes RBCs, platelets, as well as granulocytes, which include neutrophils, basophils, mast cells, and eosinophils. Each disorder can potentially cause proliferation of all of the myeloid cells, but they’re classified based on the dominant cell line involved. So there’s polycythemia vera, for RBCs, essential thrombocythemia for platelets, chronic myeloid leukemia, or CML, for granulocytes, and the odd one out, primary myelofibrosis, which doesn’t really have a dominant cell line, but instead is characterized by bone marrow fibrosis.

Okay, now CML is associated with the 9:22 translocation, which is when there’s fusion of the BCR gene on chromosome 22 and the ABL tyrosine kinase gene on chromosome 9. This is called the Philadelphia chromosome. Now, in this video, let’s focus on the myeloproliferative disorders that are not associated with Philadelphia chromosome, or the “Philadelphia chromosome negative myeloproliferative disorders,” like polycythemia vera, essential thrombocythemia, and primary myelofibrosis. All right, so let’s take a closer look at these myeloproliferative ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heart_blocks:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S_u-aj5RT6uiYVqVpG-WNVByRC69LVuI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heart blocks: Pathology review]]></video:title><video:description><![CDATA[Mikey is a 22 year old male college student from Vermont who was sent to the emergency department after passing out. 

His vital signs show a heart rate of 40 beats per minute and a blood pressure of 90/50. On examination, there is an erythematous circular rash with central clearing. 

His friends mention they recently went on a hiking trip. His ECG is as follows. 

Natasha is a 60 year old female with chronic hypertension, diabetes, and peripheral vascular disease who comes to the emergency room complaining of sudden-onset, squeezing retrosternal chest pain accompanied by shortness of breath and sweating. 

Her ECG is as follows. On laboratory evaluation, her troponin levels are significantly elevated. 

Alright, so the normal electrical activity of the heart starts in the sinoatrial or SA node located near the opening of the superior vena cava into the right atrium. 

Electrical activity is then conducted through the atrium to the atrioventricular, or AV node, after which it goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers which deliver the current to the right and left ventricles. 

Now, normally there is delay in conduction at the AV node and the Bundle of His, which gives some time for ventricular filling before the ventricle contracts. 

A “heart block”, or AV block, occurs when conduction is delayed for too long at the AV node or the bundle of His. Also, electrical activity may be blocked at the level of the bundle branches, which are called bundle branch blocks. 

Okay, on the ECG, the normal delay in the AV node is represented by the PR interval, which is normally less than 5 small boxes, or 200 milliseconds. 

There are three main types of AV block. 

1st degree AV block is technically not really a block, it’s more of a delay. 

Every single atrial impulse eventually makes it to the ventricles. 

The high yield concept here is that  the only abnormality is a prolonged PR inter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malabsorption_syndromes:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/itXNibfnTuuooZwL0Mpu8g04Tw2u-zbH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malabsorption syndromes: Pathology review]]></video:title><video:description><![CDATA[At the gastroenterology clinic, there is a 53 year- old man from the United Kingdom, named George, who came in complaining of periodic foul-smelling, bulky and frothy stools, as well as recurrent abdominal pain after meals and weight loss, despite not dieting. 

On further history, he admits that he has been consuming alcohol with almost every meal for the last 10 years. 

An upright abdominal x-ray shows calcifications in the epigastric area. 

Next to him is a 9 year- old girl from Iran, named Yasmin, whose parents are concerned about her short stature and inadequate weight gain despite following a balanced diet. 

On examination, her height and weight are below the 3rd percentile for her age and sex. 

She also has an itchy rash consisting of small vesicles on both of her knees. 

At first glance, you’d think George’s and Yasmin symptoms have nothing in common. 

But the fact is, they both have different forms of malabsorption syndromes. 

With malabsorption, nutrients are no longer effectively absorbed in the small intestine. 

Nutrients can either be macronutrients, such as fats, proteins and carbs or micronutrients like vitamins and minerals. 

Malabsorption can either be global, meaning that the absorption of all nutrients is affected, or it can be partial, meaning that only specific nutrients cannot be absorbed. 

In general, unabsorbed nutrients are allowed to linger in the gastrointestinal lumen for longer than usual, disrupting the proper formation of stool, which results in diarrhea, bloating and flatulence. 

And since these nutrients are lost in the stool, malabsorption will also lead to unintentional weight loss and various nutritional deficiencies. 

For macronutrients, let’s start big, with fat malabsorption which causes steatorrhea, meaning fatty, greasy, floating, voluminous and terribly smelling stools. 

And it’s important to know that screening for fat malabsorption is done with a fecal fat test, known as Sudan III stain. 

A hig]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_nodules_and_thyroid_cancer:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OWDXDF5iQ7mFj4OyPBAimm9sQDipNKWy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid nodules and thyroid cancer: Pathology review]]></video:title><video:description><![CDATA[On the endocrinology ward, two individuals came in. 

Both individuals complained about feeling a lump on their necks, but reports no other symptoms. 

The first one is 49 year old Dasha who as a child, lived close to Chernobyl. 

The other one is 27 year old Mike, who’s family history involves multiple endocrine neoplasia type 2A. 

On exam, they each had a painless mass on their thyroid. 

Both people had normal T3, T4, and TSH levels. 

They underwent thyroid echography, which showed cold nodules. 

Afterwards, fine-needle biopsies were done. 

Both individuals had tumors on their thyroids. 

First, let’s refresh some info on the thyroid. 

The thyroid gland is an endocrine gland located in the neck. 

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. 

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, tri-iodo-thyronine or T3, and thyroxine or T4. 

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Once inside the cell T­4 is mostly converted into T3, at which point it can exert its effect. 

T3, among other effects, speeds up the basal metabolic rate, increases cardiac output, stimulates bone resorption and activates the sympathetic nervous system. 

The thyroid is also made up of parafollicular or C cells, which are near the follicles. 

These cells produce calcitonin, a hormone that lowers blood calcium levels by inhibiting osteoclasts.  

Calcitonin also inhibits renal tubular cell reabsorption of calcium, allowing the calcium to be excreted in the urine. 

Now, DNA mutations can cause thyroid cells to become cancerous. 

For example, a mutation might change a proto-oncogenes like RET and BRAF, which are genes that code for proteins that promote cell growth and proliferation, into oncogenes. 

That would mean that the proteins force the cell to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis's_vision,_mission,_and_values</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ShMegpRERkecpOTPxjxDHt71RzOSZEkg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osmosis&apos;s vision, mission, and values]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis&apos;s vision, mission, and values through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dyslipidemias:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x0CRrq_XSgu5Vdr69LPgP0XsT9On2U37/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dyslipidemias: Pathology review]]></video:title><video:description><![CDATA[Jamie is a 24-year-old male presenting to the emergency department complaining of sudden onset chest pain and shortness of breath when playing soccer. 

On further evaluation, his ECG showed ST-segment elevation and laboratory evaluation showed elevated troponin I levels. 

After instituting treatment, Jamie and his family inquire about the odd early onset of his disease. 

The physical examination of the skin showed numerous xanthomas.  

A lipid panel is ordered and shows marked elevation of LDL.

Jamie had a myocardial infarction which was caused by an underlying lipid disorder.  

Lipid disorders include both hyper and hypolipidemia.  

Hyperlipidemia  can manifest as a high level of cholesterol, a high level of triglycerides, or a combination of both. 

Hypolipidemia is the opposite where there’s a low level of these lipids. 

So let’s do a quick overview of the physiology of lipid metabolism. 

After eating a fatty meal, cholesterol and fatty acids enter the intestinal cells.  

The fatty acids are assembled into triglycerides, and then they, along with a small amount of cholesterol, are packaged together with lipoproteins to form chylomicrons.  

Chylomicrons move into the lymphatic vessels and eventually end up getting emptied into the left and right subclavian veins where they enter into the blood.  

Now an enzyme in capillaries called lipoprotein lipase breaks down the chylomicrons to free the triglycerides, and then it also breaks the triglycerides down into fatty acids. 

These can be taken up by nearby tissues to generate energy, like in the muscle cells, or for storage, like in adipocytes. 

The remains of the chylomicrons will contain lipoproteins and a small amount of triglyceride and cholesterol, so these chylomicron remnants head to the liver to deposit the leftover lipid molecules.  

The Liver is also synthesizing fatty acids and cholesterol and it will combine these with the ones from the chylomicron remnants and package them together]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiomyopathies:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n5ebWNbUTfeiMipuPsq63jQSRai6BRrE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiomyopathies: Pathology review]]></video:title><video:description><![CDATA[Aman is a 60 year old male who came into the clinic with shortness of breath and lower limb edema for the past 3 months. He has a history of hypertension, hyperlipidemia and chronic alcohol use. On auscultation, an additional S3 sound is heard. An echocardiogram is performed, which shows dilated ventricular chambers and a reduced ejection fraction. Alexandra is a 23 year old professional volleyball player who came to the clinic after multiple episodes of “passing out” during her games. At first, she presumed it was due to dehydration, but she is now concerned. She has a family history of sudden cardiac death in multiple relatives. An echocardiogram shows asymmetric hypertrophy of the interventricular septum, and a normal ejection fraction.

Both Aman and Alexandra have cardiomyopathies. From outside to inside, the heart is made of the epicardium, myocardium, and endocardium. Diseases that affect the myocardium are called cardiomyopathies. The three main subtypes are dilated, hypertrophic and restrictive cardiomyopathy.

Let’s start with dilated cardiomyopathy, which is the most common one, accounting for almost 90% of all cases. Now, In dilated cardiomyopathy the ventricular walls become thin and weak. As a consequence, the ventricular chambers dilate. Because the ventricular wall is thinner, muscle contraction is weaker and the heart can’t pump blood efficiently throughout the body. So we have a systolic dysfunction with normal diastole.

Okay, when it comes to the etiology of dilated cardiomyopathy, the large majority of cases are idiopathic, meaning the cause can’t be identified. However, there are many secondary causes that must be excluded first. Examples include toxins like chronic alcohol or cocaine abuse, nutritional deficiencies like thiamine deficiency, also called beri-beri, or selenium deficiency. Another cause is myocarditis, which is inflammation of the heart muscle, usually caused by viruses like Coxsackie B, but can also be related to autoi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pneumonia:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r3u4Mg2lTFq4tlIcNJrzZoCVTuOXThBm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pneumonia: Pathology review]]></video:title><video:description><![CDATA[Two people came to your clinic one day. 

Mariah is a 54-year-old smoker, who came in with  with productive cough with yellow sputum and left-sided chest pain. 

Physical examination reveals fever, tachycardia, and tachypnea. Her lung sounds are barely audible, but it had crackles at the left base. 

Next is Jeremy, a 64-year-old man who was hospitalized for a stroke 2 weeks ago.  

He recently developed a cough and right-sided chest pain. 

He is tachycardic and has a fever of 38.4°C. 

Examination reveals fremitus, decreased breath sounds, and dullness to percussion in the right lower lung field. 

Chest x-rays were performed which showed a left lower lobe infiltrate in Mariah’s case, and a right lower lobe infiltrate in Jeremy’s.

Now, both people have pneumonia. 

So pneumonia is an infection of the lung tissue.  

Some microbes can overcome the innate defenses of the lungs and immune system to colonize the bronchioles or alveoli. 

These pathogens then triggers an inflammatory response.   

Inflammatory cells, such as white blood cells, dead bacteria, proteins and fluid from the damaged tissue, form a fluid called exudate which can be coughed up and expelled from the body.  

However they can also accumulate in the lungs, filling up the alveoli. 

We can divide pneumonia into “classic” pneumonia or “atypical pneumonia based on symptoms. 

So with classical pneumonia, high yield symptoms might include dyspnea, or shortness of breath, fatigue, and fever. 

Individuals might also develop pleuritic chest pain, which is characterized by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling; and productive cough with yellow sputum. 

Besides these, High yield signs that might come up on your exam include dullness to percussion, which suggests that there’s a lung consolidation. 

This occurs because the air in the alveoli is replaced by pus and fluid so the sound will lose its normal tympanic or drum-like quality. 

Ther]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lymphomas:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DfyoGTI1TdSZJKEImd_P4hQIRn6ii6vi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lymphomas: Pathology review]]></video:title><video:description><![CDATA[At the family medicine center, there is a 25 year old male, named Hogan, who came in because of a painless non-erythematous mass on his neck. Next to Hogan, there is a 30 year old male immigrant from Africa, named Burak, who has noticed a painless mass on his jaw. He also complains of drenching night sweats, and unexplained weight loss over the last few months. Biopsy is ordered for both people.  In Hogan’s there’s binucleated B cells surrounded by mainly lymphocytes. Burak’s biopsy showed numerous lymphocytes with some tingible-body macrophages. CBC is normal for both. 

Both Hogan and Burak have lymphoma.  Lymphomas are tumors derived from lymphocytes, which are B and T cells. They can be broadly grouped into two categories; Hodgkin and non-Hodgkin lymphomas. 

In contrast, non-Hodgkin lymphomas don’t have Reed-Sternberg cells can sometimes spread non-contiguously, and can involve extranodal sites like the skin, gastrointestinal tract, and brain. Non-Hodgkin’s lymphomas can occur in both children and adults. Finally, overall prognosis is better with Hodgkin lymphomas.

Let’s start by looking at  Hodgkin lymphoma.  This type of lymphoma typically arise from B-cells and spread in a contiguous manner, meaning it spreads to nearby lymph nodes, and rarely involve extranodal sites. It has a bimodal age distribution, affecting young adults in their 20s and adults older than 60 years of age. Histologically, it’s characterized by the presence of Reed-Sternberg cells and for your exams, remember that these are binucleated, neoplastic B cells that look kind of like owl eyes. The large mononuclear version of Reed-Sternberg cells are called Hodgkin cells. These abnormal, neoplastic cells are usually surrounded by non-neoplastic inflammatory cells, mostly T cells, and sometimes eosinophils.  They can also activate fibroblasts, which secrete collagen. 

Okay, now Hodgkin lymphoma includes two major subgroups, the first and more common is classical Hodgkin lymphoma]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nephritic_syndromes:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9BXJDObkRW2cVF_rOmXxBpr3QPa1dd-6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nephritic syndromes: Pathology review]]></video:title><video:description><![CDATA[On the nephrology ward, two people came in with the same symptoms: peripheral and periorbital edema, along with cola-colored urine, arterial hypertension and decreased urine output. 

The first person is 10 year old Timmy who had a throat infection two weeks ago. 

The second one is 45 year old Dorothy, who also presents with hemoptysis. 

Lab tests show that both of them have increased creatinine and BUN. 

On urinalysis, there’s hematuria and red blood cell casts in the urine.  

A 24-hour protein collection was done and showed that both Timmy and Dorothy had proteinuria, but in both cases it was less than 3.5 grams per day.

Now, both Timmy and Dorothy have nephritic syndrome. 

Nephritic syndrome is typically caused by inflammation that damages the glomerular basement membrane, leading to hematuria and red blood cell casts in the urine.  

Eventually, this damage can lead to renal failure, where the individual can present with oliguria, arterial hypertension, due to sodium retention, and peripheral and periorbital edema. 

Lab tests show high levels of BUN and creatinine and on urinalysis, there’s hematuria, proteinuria and RBC casts in the urine. 

A 24-hour protein collection is necessary to quantify how many proteins are lost through urine. 

Now, nephritic syndrome can be differentiated from nephrotic syndrome because the proteinuria is generally under 3.5 grams per day, or within the “subnephrotic range”. 

In severe cases though, proteinuria can reach over 3.5 grams per day. 

In order to determine the cause, a careful history and a kidney biopsy can help diagnose the particular disease. 

Okay, let’s start talking about the different disorders that could cause nephritic syndrome. 

To make things simpler, we can categorize these into three groups; those caused by type III hypersensitivity, like poststreptococcal glomerulonephritis, IgA nephropathy, and  Diffuse proliferative glomerulonephritis; those with multiple potential causes, like  membran]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Penis_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wz7fdJdySnKv5RbdYv4572ovTg2lnSh4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Penis histology]]></video:title><video:description><![CDATA[The penis is composed of three cylindrical columns of erectile tissue, which are bound together by a dense fibroelastic layer called the tunica albuginea. 

In this very low power, transverse cross-section of the penis, the upper two columns are the dorsal corpora cavernosa of the penis, and the lower column is the ventral corpus spongiosum, which also contains the penile urethra. 

At the distal end of the penis, the corpus spongiosum expands to become the glans penis. 

The tunica albuginea is surrounded by a layer of superficial fascia that contains connective tissue, prominent blood vessels, and nerves. 

The dorsal side of the penis, which is the top side of this image, typically has the major blood vessels present, whereas the blood vessels within the columns of erectile tissue are significantly smaller. 

Surrounding the superficial fascia is the outermost sheath of penile skin, which can only be partially seen in the upper left of this image. 

The penile skin moves freely over the underlying tissues due to the loose hypodermis. 

Unless circumcised, it extends over the glans as the prepuce or foreskin, which acts as a retractable protective fold of skin.

If we take a closer look at the corpora cavernosa at 10x magnification, we can see that the tissue is highly vascular, with a lot of red blood cells visible within the wide and irregularly-shaped vascular sinuses. 

These sinuses are surrounded by walls or trabeculae that contain mostly elastic connective tissue and smooth muscle. 

If we zoom in a little closer, we can see a few cross-sections of smooth muscle that stain darker than the surrounding tissue. 

The sinuses are supplied by constricted thick-walled arteries and arterioles called helicine arteries. 

As their name suggests, the helicine arteries are normally coiled when the penis is flaccid. 

But during an erection, following the parasympathetic stimulation, the smooth muscle surrounding the sinuses and arteries relax, causing the arteries to dilate and straighten out. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperthyroidism:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6PVf2vh6Q3y7K_0peKZw3GeMSombFkaY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperthyroidism: Pathology review]]></video:title><video:description><![CDATA[On the Endocrinology ward, two individuals came in. 

The first one is 55 year old Gregor, who came in complaining about weight loss, heat intolerance, chest pain, palpitations and insomnia.

On the clinical examination, he’s anxious and restless. 

He had warm and moist skin, his eyelids were retracted and there was exophthalmos of both eyes and tachycardia. 

The other person is 37 year old Josie who migrated to the US from Panama. 

She came in with similar symptoms as Gregor but on clinical examination, she also had a goiter.  

According to her, she recently had a contrast imaging procedure for a different problem. 

TSH and levels of T3 and T4 were taken for both individuals. 

Levels of TSH were low, while levels of T3 and T4 were high. 

Okay, so both individuals had hyperthyroidism. 

First, a bit of physiology. 

Normally, the hypothalamus detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone, or TRH, into the hypophyseal portal system. 

The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin, or simply TSH. 

TSH stimulates the thyroid gland which is a gland located in the neck. 

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. 

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4. 

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. 

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body. 

Once inside the cell T­4 is mostly converted into T3, and it can exert its effect. T3 speeds up the cell’s basal metabolic rate. 

T3 increases cardiac output, stimulates bone resorption, thinning out the bones, and activates the sympathetic nervous system. 

Thyroid hormones are also involved ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Deep_vein_thrombosis_and_pulmonary_embolism:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4Z9vtk5pRbO25CU-cTCj9scySDW-gcmV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Deep vein thrombosis and pulmonary embolism: Pathology review]]></video:title><video:description><![CDATA[Hannah is a 42 year old woman who came to the emergency department due to pain in her right calf. 

She reports flying from Japan back to the United States 2 days ago. 

She denies fever, chills, or history of trauma to the leg. 

She reports a 25 pack year smoking history for 20 years, and she takes oral contraceptive pills. 

On physical examination, she is stable, and her BMI is 32. 

Her right leg is shown in this image. 

On laboratory investigation, her D-dimer levels are elevated. 

Deep vein thrombosis, or DVT and pulmonary embolism, or PE are a spectrum of clinical manifestations that result from venous thromboembolism. 

The pathogenesis and risk factors of both DVT and PE centers around Virchow’s triad, that is; stasis of blood flow, hypercoagulability, and endothelial injury. 

Board exams like to test your ability to identify a PE by using scenarios that promote venous stasis such as paralysis after a stroke, the postoperative period, as well as long drives or flights. 

People with varicose veins are also at risk of DVT, because incompetent venous valves prevent proper venous outflow, causing stasis. 

An interesting risk factor is pregnancy, where the enlarged uterus may compress the iliac veins, causing stasis of venous outflow. 

Another similar cause is May-Thurner syndrome where the left iliac vein gets sandwiched between the right iliac artery anteriorly and the lumbar vertebrae posteriorly, which also leads to venous stasis. 

Now, the coagulation system is normally balancing clot formation and clot lysis. 

Hypercoagulability occurs is when the scale is tipped towards clot formation. 

This may be genetic, such as factor V Leiden, or antithrombin III deficiency. 

Or it may be acquired, like when there’s high estrogen during pregnancy or when using estrogen-containing oral contraceptive pills. 

Also, nephrotic syndrome causes loss of antithrombin III in the urine, resulting in hypercoagulability. 

This is especially prominent in mem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Microcytic_anemia:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yA167WSCQaGPIEiIOIjh15IgSB24PwN4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Microcytic anemia: Pathology review]]></video:title><video:description><![CDATA[At the family medicine center, there is a 60-year-old Indigenous American named Istu who came to visit the doctor because of his progressive fatigue and difficulty in swallowing. Next to him, there is a mother from Greece with her child, Thalia, who is 10 months old. Little Thalia appeared healthy at birth but in the past 2 months, her mother noticed that her face was often pale, she’s been less active, and there was a mass in her belly.   

Both Istu and Thalia are suffering from anemia, which is defined as lower than average levels of hemoglobin, typically below 13.5 g/dL in adult men and below 12.0 g/dL in adult women. For children, this level varies based on the age.  Now, anemias can be broadly grouped into 3 categories based on mean corpuscular volume, or MCV, which reflects the volume of a Red blood cell or RBC. So microcytic anemia is where the MCV is lower than 80 fL, normocytic, with an MCV between 80 and 100 fL, and macrocytic, with an MCV larger than 100 fL. Now, let’s  focus on the microcytic anemias, and the most common causes are iron deficiency anemia, lead poisoning, sideroblastic anemia, and thalassemias. Although microcytic anemia can also present in anemia of chronic disease, which is caused by Inflammatory conditions like rheumatoid arthritis, and systemic lupus erythematosus or SLE, it’s usually classified as normocytic anemia.  

Now iron deficiency anemia, lead poisoning, and sideroblastic anemia are caused by defective heme synthesis, while thalassemias are caused by defective globin chains. Normally, RBCs are loaded with millions of copies of a protein called hemoglobin. Hemoglobin is actually made up of four peptide, or globin, chains, each bound to a heme group. Those 4 heme molecules have, right in the middle, iron, which binds to oxygen and allows it to move in our body.

Okay, so let’s look at iron deficiency anemia which could be caused by decreased intake, decreased absorption, increased demand, or increased loss of iron. F]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vasculitis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pLXsHQuKRk_Je6TJXHCFaRtaRsCD-vXu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vasculitis: Pathology review]]></video:title><video:description><![CDATA[At the clinic, two very different people with very different symptoms showed up. Novakova is a 60 year old woman from Czech Republic who’s been having a headache by the right temple, progressive jaw pain during chewing, and shoulder and hip stiffness, particularly in the morning. Her ESR levels are elevated, and she is beginning to develop vision loss in the right eye. The other person is Hikaru, a cute 3-year-old Japanese boy brought by his mother. He has a red, swollen tongue, unilateral neck swelling, a desquamating rash, and a fever for the past 6 days. An ECG reveals elevation of the ST segment, and an echocardiogram shows evidence of a coronary artery aneurysm.

At first glance, you’d think Novakova and Hikaru symptoms have nothing in common. But the fact is, they both have different forms of vasculitis. The majority of vasculitides are caused by some form of immune-mediated damage. Some are type III hypersensitivities caused by immune complexes that deposit in vessels and cause damage. They could also be triggered by autoantibodies, like anti-neutrophil cytoplasmic antibodies, or ANCA. Lastly, they might be caused by cell-mediated immunity due to monocytes, macrophages or lymphocytes.

Whatever the cause, immune cells cause inflammation, which damages the endothelial wall, exposing the underlying collagen. This results in thrombosis and could lead to ischemia of the organs supplied by the affected vessels. Also, inflammation weakens the structural integrity of the blood vessel wall, leading to aneurysms. In addition, inflammation can spread to the supplied organ itself, causing tissue damage. 

Since vasculitides are systemic inflammatory disorders, non-specific symptoms like fever, arthritis, myalgia, weight loss, and night sweats might be present. The symptoms specific to each disease depends on which blood vessels are affected, and we can classify vasculitides into large, medium, and small-vessel vasculitis.

For large vessel vasculitis, let]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cytomegalovirus_infection_after_transplant_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3-_7xL49SgKyOeWP07YE4hp1SG2aaQTN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cytomegalovirus infection after transplant (NORD)]]></video:title><video:description><![CDATA[Cytomegalovirus, or CMV, is an enveloped double-stranded DNA virus that belongs to the herpesviridae family. It&amp;#39;s one of the most common viruses to cause severe infection in individuals undergoing transplantation of bone marrow or solid organs like the liver or kidney. It can affect almost every organ in the body resulting in encephalitis, retinitis, pneumonia, hepatitis, gastroenteritis, and of course, transplant rejection.

In the post-transplantation period, the recipient is usually given immunosuppressive medication in order to prevent their immune system from recognizing the transplanted tissue as foreign and causing rejection. However, one major disadvantage of this approach is that the weakened immune system is unable to protect the body against pathogens like CMV.

CMV can be transmitted through blood and other body fluids like saliva, genital secretions, and urine of an infected person; or from the transplanted organ itself!

During the primary infection, the virus usually invades the epithelial cells, like those that make up the oral, GI, or urinary mucosa; and starts to multiply. CMV damages the infected cells by breaking down the cytoskeletons which maintain the cell structure. That results in enlarged cells with intranuclear viral inclusion bodies, giving it the typical owl&amp;#39;s eye appearance.

CMV also infects monocytes in the blood and sets up a latent infection, which means that the virus remains dormant for long periods of time. The dormant virus can reactivate at times when the immune system weakens, causing disease.

Most of the time primary infection occurs years before the transplant with resultant  reactivation of the virus during immunosuppressive therapy. In about 25% of transplants primary infection occurs which is usually much more severe compared to reactivation.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cystinosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vP4N8kijTiOONITBi9FiAvkIQBm__8ic/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cystinosis]]></video:title><video:description><![CDATA[With cystinosis, “cystin-” refers to cystine, an amino acid, and “-osis” implies disease. 

So, cystinosis is a rare condition caused by mutations of the CTNS gene that leads to a cystine buildup in the body. 

This can cause tissue damage, especially in the kidneys and eyes.

Cystine is an amino acid that comes from our diet. 

When food travels through the stomach and intestines, the proteins within, are broken down into tiny fragments, called oligopeptides, or small strings of amino acids. 

Turnover of muscle, bone and other parts of the body provide another source of protein that can be broken down into oligopeptides. 

Many of these oligopeptides end up in specialized vesicles, called lysosomes, found inside all of our cells. 

Here, they are further broken up into amino acids like cystine. 

Now, cystine, like any other amino acid has to leave the lysosome, and it does this with the help of a specific protein. 

Generally, genes tell our bodies how to make proteins. 

So, the CTNS gene encodes for the protein cystinosin, a transporter that is found embedded in the lysosomal membrane. 

It’s function is to export cystine out of the lysosome.

Now, in cystinosis, any one of over 100 mutations can affect the CTNS gene, leading to a defective cystine transporter. 

Without a working transporter, cystine has no way of leaving the lysosome, so it accumulates, turning into cystine crystals in the process. 

Crystals that slowly damage organs like the kidneys and eyes.

In general, humans have two copies of their genes, so both must be damaged for there to be so little cystine transport that cystinosis occurs. 

That means that a person with cystinosis must receive a mutated CTNS gene from both the mother and father. 

For each such mating, there is a 25% chance that both parents will pass down their own CTNS mutation to the offspring.

Now, depending on the CTNS gene mutation, three types of cystinosis can develop that differ in the age of onset and severi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypopituitarism:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/87YKByZSR0CzVG13BTcWu60MRUCd1vqr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypopituitarism: Pathology review]]></video:title><video:description><![CDATA[On your rounds, you admit 28-year-old Regina who presents with an 8-month history of depression, cold intolerance, fatigue, and reduced libido. 

History revealed she delivered a healthy baby eight months ago, and that the delivery was complicated by a severe postpartum hemorrhage. 

She has also been unable to breastfeed and hasn’t had her menstruation since giving birth. Physical examination is remarkable for bradycardia, weight loss, and delayed relaxation of her reflexes. 

Then you see Alexander, a 58-year-old male with difficulty seeing things in his peripheral vision. He also describes a loss of sex drive, erectile dysfunction, and significant weight gain, all starting approximately two years ago. 

The examination revealed moderate obesity, bilateral gynecomastia, and bitemporal hemianopsia. 

Basal serum hormone measurements were performed, showing decreased T4 levels in Regina and decreased FSH, LH, and testosterone levels in Alexander.

Both people have hypopituitarism. So hypopituitarism refers to the decreased secretion of one, some, or all of the anterior pituitary hormones. 

These hormones are ACTH, or adrenocorticotropic hormone; TSH, or thyroid stimulating hormone; GH, or growth hormone;  FSH, or follicle-stimulating hormone; LH, or luteinizing hormone, and prolactin.

Posterior pituitary hormone deficiency can also occur, but it’s extremely rare. This part of the pituitary gland releases oxytocin and antidiuretic hormone, or ADH.

Hypopituitarism typically occurs because of an acquired or congenital issue where the  hypothalamus or pituitary is injured. Now, the clinical picture of hypopituitarism depends on which hormone is missing. 

First, ACTH deficiency can present with symptoms such as orthostatic hypotension and tachycardia, weakness and lethargy, especially during periods of stress, like illness or during surgery.

Stress can also precipitate an adrenal crisis where the individuals have vascular collapse and shock, nausea, vomiti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gaucher_disease_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OdW8NPrwTDWRPKhs3e_09nr6Rb2BXYLv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gaucher disease (NORD)]]></video:title><video:description><![CDATA[Gaucher disease is an inherited condition characterized by insufficient levels of the enzyme glucocerebrosidase, also called beta-glucosidase. 

It’s named for the French physician, Philippe Gaucher, who first described the condition. 

Glucocerebroside is a glycolipid, which is a molecule containing both sugar and fat, that&amp;#39;s included in the membrane of many different cells. 

Glucocerebroside is formed through a set of reactions in the cell that require enzymes. 

Once the glucocerebroside is made it becomes a part of various cells and when these cells become old or damaged, they are often engulfed, or eaten, by immune cells called macrophages. 

Macrophages contain lysosomes, which are organelles that act as  the cells’ digestive center. Inside lysosomes, large, potentially harmful substances are broken down, to be either discharged or reused by the body. 

One example is glucocerebroside which is broken down by the enzyme glucocerebrosidase, or GBA, which is a product of the GBA gene. 

In Gaucher disease, the GBA gene is faulty, meaning it has a mutation that leads to a reduction in the level or activity of glucocerebrosidase. 

Hence, glucocerebroside can’t be broken down and it accumulates inside the lysosomes of macrophages. 

So under a microscope, macrophages have a characteristic lipid-laden, or “fatty” appearance, similar to “crumpled tissue-paper.” 

These transformed macrophages are called Gaucher cells, and they accumulate in multiple organs and tissues, including the bone marrow, liver, and spleen. 

While the reason is unclear, Gaucher cells and other nearby macrophages secrete damaging lysosomal enzymes and inflammatory signals into the surrounding area. 

This causes an immune response and production of scar tissue, resulting in many characteristic signs and symptoms. 

GBA gene mutations are inherited in an autosomal recessive manner.

There are a few subtypes of Gaucher disease. In type 1, some individuals are asymptomatic, bu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cushing_syndrome_and_Cushing_disease:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xYV7iEXoSzGp0b0K5GHLQTAXQHyIZ_j-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cushing syndrome and Cushing disease: Pathology review]]></video:title><video:description><![CDATA[On the Endocrinology ward, two people came in with similar symptoms. One of them is 45 year old Samantha, who complains of gaining a lot of weight lately. Samantha also suffers from severe asthma for which she’s taking oral glucocorticoids. She also had many viral and bacterial infections lately. On clinical examination, there’s truncal obesity, a large hump behind her neck, and striae on her abdomen. Her arterial pressure was elevated and she also had hyperglycemia. The other person is 38 year old Dan who is also obese, and has an abnormally round face. He has arterial hypertension and hyperglycemia. Unlike Samantha, Dan is not taking any medications. A 24 hour urine free cortisol was done in both individuals and levels were high. Further investigations were done, including ACTH levels.   

Now, both individuals suffer from an endocrine disorder that involves high levels of cortisol. This is generally called Cushing syndrome. Now, if Cushing syndrome results from a pituitary adenoma making excess ACTH, it’s called Cushing disease.  

Normally, the hypothalamus secretes corticotropin-releasing hormone, known as CRH,  

which stimulates the pituitary gland to secrete adrenocorticotropic hormone, known as ACTH. ACTH travels to the adrenal glands where it targets cells in the adrenal cortex.  

The adrenal cortex is the outer part of the adrenal gland and is subdivided into three layers-  

the zona glomerulosa, the zona fasciculata, and the zona reticularis.  

Zona fasciculata is the middle zone and also the widest zone, and ACTH specifically stimulates cells in this zone to secrete cortisol. This is a class of steroids, or lipid-soluble hormones, called glucocorticoids. Glucocorticoids are not soluble in water, so most cortisol in the blood is bound to a special carrier protein and only about 5% is unbound or free. In fact, only this small fraction of free cortisol is biologically active, and its levels are carefully controlled. Excess free cortisol is fil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pituitary_tumors:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g-PI03XJQIm1YWuuCgjFiKUzSoCIajKH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pituitary tumors: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you see a 6 year-old named Alex who presents with severe headaches and vision impairment which began six months ago. More specifically, he has some difficulty seeing things on the periphery, what he describes as tunnel vision. Examination reveals bitemporal hemianopia and a much taller stature than expected for his age, with disproportionately long arms and legs. Soon after, you see Maria, who says she has been unsuccessfully trying to have a baby for the last two years. She also mentions that she hasn’t had her menstruation in 3 months, but had milky nipple discharge. Hormone serum measurements were performed in both, showing an increase in insulin-like growth factor-1 levels in Alex and an increase in prolactin levels in Maria.

Now, both seem to have a disease affecting the pituitary. But first, a bit of physiology. The pituitary is a small gland situated in a tiny bony space called the sella turcica. It is linked to the hypothalamus by the pituitary stalk, and it is divided into the anterior pituitary and the posterior pituitary. The posterior pituitary is not glandular; thus it doesn’t make its own hormones.  Instead, it stores and secretes oxytocin and antidiuretic hormone which are produced in the hypothalamus. By contrast, the anterior pituitary has five types of hormone producing cells. First, lactotrophs secrete prolactin, which stimulates breast milk production and inhibits ovulation and spermatogenesis. Second, somatotrophs secrete growth hormone, or GH. GH acts directly on target tissues to stimulate growth and development. Then, corticotrophs secrete adrenocorticotropic hormone, or ACTH for short. ACTH makes the adrenal glands secrete cortisol. Cortisol is in charge of the stress response and keeping blood pressure and blood sugar in the normal range. Fourth, thyrotrophs secrete thyroid stimulating hormone, or TSH. TSH makes the thyroid gland release thyroid hormones, T3 and T4. Thyroid hormones speed up the basa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cystic_fibrosis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5BKiE5DXQ_GS04FMVB-64Zw9QM6ozJMJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cystic fibrosis: Pathology review]]></video:title><video:description><![CDATA[A newborn was delivered two days ago at home without any complications. Today, he was brought in for examination. The baby has a fever and a distended abdomen that&amp;#39;s rigid on palpation. The mother mentions her son started vomiting a green fluid and that he has yet to pass his first stool. She also says she didn’t have access to prenatal care throughout the pregnancy. An x-ray was performed, and it showed air-fluid levels and dilated bowel loops, along with a “soap bubble” appearance. A pilocarpine-induced sweat test was done which showed a Cl- level over 60.

Now, the newborn seems to have cystic fibrosis. But first, a little physiology. Normally, elements like ions and water come in and out of the cell through specific channels located on the cell’s membrane. A very high yield fact you need to know is that there’s this particular channel called “cystic fibrosis transmembrane conductance regulator” or the CFTR protein, which is an ATP-gated channel, meaning it works by using ATP for energy. It transports negatively charged  Cl-.  In cells that produce mucus, it secretes the ion out of the cell, and in cells of the sweat glands, it reabsorbs Cl- back into the cell. Now, normally, cells in mucus membranes pump out chloride ions into the thick mucus, which helps attract water and make it less viscous. This mucus will protect the lining of organs and tissues like the airways, digestive system, and reproductive system. For example, the mucus produced by the glands in the airways allows the tiny cilia to sweep back and forth. This sweeping motion helps move the mucus and the bacteria or foreign particles trapped in it, out of the airways. Additionally, the CFTR protein also regulates the function of other channels, such as those that transport positively charged sodium ions.
Now, cystic fibrosis, or CF, is an autosomal recessive disorder where there’s a mutation in the CFTR gene, and it is considered to be the most common lethal genetic disease in the C]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_brain_tumors:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v38rWiRpRcGB56aDUOpCScIqQKGtxmEL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric brain tumors: Pathology review]]></video:title><video:description><![CDATA[In the neurology ward, two children came in with the same symptoms: morning headaches, nausea, vomiting, and frequent falls. One of them is a 12 year old named Greg, and the other is a 14 year old individual named Suzan. Greg’s symptoms started a few months ago and retained the same level of severity, while Suzan’s symptoms started a few weeks ago and are rapidly worsening. A brain MRI with contrast is ordered for both of them, which showed a well circumscribed cystic lesion in the cerebellum for Greg, and a solid, heterogeneous mass in the cerebellum that compresses the fourth ventricle in Suzan. 

Okay, so both Greg and Suzan have pediatric brain tumors. Brain tumors occur when there’s uncontrolled growth of abnormal cells within the brain. They are broadly classified into primary tumors originating from cells within the nervous system, and metastatic tumors originating from cells outside the nervous system. Primary brain tumors are the most common solid tumors in children and can be either benign or malignant. Now, for the exams, it’s important to remember that the most common primary brain tumor in both adults and children are gliomas, and more specifically, a subset of these called astrocytomas. In children, medulloblastomas and ependymomas are next on the list, while in adults gliomas are followed by meningiomas. Less common brain tumors include craniopharyngioma, pinealomas, pituitary adenomas, oligodendrogliomas, hemangioblastomas, and schwannomas. Now, metastatic tumors are much more common in adults and are always malignant. In order of decreasing frequency, they most commonly come from cancers of the lung, breast, skin melanomas, kidneys and colon. 

Okay, brain tumors can also be categorized based upon their location as either supratentorial, or above the cerebellar tentorium, and infratentorial tumors, or below the tentorium, though some tumors can form in either. In children, a very high yield concept is that most brain tumors are infratentor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pericardial_disease:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SaqFcY18SwqksO7KnDpzPGj1RcicByh7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pericardial disease: Pathology review]]></video:title><video:description><![CDATA[Two people came to the emergency department. One of them is 55 year old Pamela who has  sharp retrosternal chest pain that gets worse when she breathes in. On chest auscultation, a friction rub can be heard. The other person is 43 year old Thomas, who had been in a car accident and now presents severe hypotension and on physical examination, his neck veins are distended, his heart rate is really high. On chest auscultation there’s barely audible heart sounds. An ECG was ordered for both individuals. Pamela had ST-segment elevation in several leads and also PR depression, while Thomas has low-voltage QRS complexes. 

Okay, based on what we know about the individuals, we can assume that both suffer from pericardial disease. But first, a bit of physiology. The pericardium is a sac that covers the heart and the roots of the great vessels. The pericardium has two layers, an inner serous layer and an outer fibrous layer. The space between the two layers is the pericardial cavity that cushions the heart from any kind of external jerk or shock - like a shock absorber. The pericardium also fixes the heart to the mediastinum, to prevent it from twisting, so that the large vessels don’t get pinched shut. 

Now for pericardial disease, we should start by talking about inflammation in the pericardium, which is called pericarditis. People who develop pericarditis are also at risk of developing a pericardial effusion where the inflammation causes fluid to accumulate around the heart. 

Pericarditis is in most cases idiopathic. It can also be due to a viral infection, like Coxsackie B virus. Pericarditis can also be seen in autoimmune diseases, like rheumatoid arthritis or systemic lupus erythematosus, because the immune system attacks our own tissues, including the pericardium. For your exams, other high yield causes include myocardial infarction and Dressler syndrome which occurs several weeks after a myocardial infarction. Basically, when heart cells die in a myocardia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tuberculosis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ABEAG79dTL_HMMR4zCNPEcZHRjWChRdK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tuberculosis: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you meet Josh, an HIV-positive 25-year-old man who presents with a 2-month history of non-productive cough. He also describes poor appetite and significant weight loss, fever, night sweats, and excessive tiredness. He denies dyspnea or hemoptysis. Physical examination is unremarkable. A PPD intradermal test was performed and it was negative. His chest X-ray showed a peri-hilar lesion with central necrosis and calcification as well as lymphadenopathy of nearby nodes. 

Now, this person seems to suffer from tuberculosis, or TB for short. But first, a bit of microbiology. Mycobacteria tuberculosis are slender, rod-shaped, Gram positive bacteria that need oxygen to survive, in other words, they’re “strict aerobes”. One piece of high-yield information is that although they are classified as Gram positive - meaning they have an outer cell wall, it is the same wall that makes the bacteria special. This is  because Mycobacterium have an unusually waxy cell wall made of mycolic acid, which is composed of long chains of branched lipids, which won&amp;#39;t stain with Gram. This makes them “acid-fast” so the Ziehl-Neelsen stain has to be applied, a dye that will not be washed away by acids, giving the bacteria a bright red color. The wall also makes the bacteria incredibly hardy, and allows them to resist weak disinfectants, antibiotics, and allow them to survive on dry surfaces for months at a time. 

Okay, so Tuberculosis is a type of pulmonary infection caused by Mycobacterium tuberculosis, sometimes just called TB bacteria. Before we start, you need to know that there are a few high-yield risk factors for TB. These include immunosuppression, like in people with HIV; iatrogenic immunosuppression, like in people who undergo treatment with corticosteroids; systemic diseases such as COPD, diabetes, and end-stage renal disease; extremes of age; substance abuse; and populations with an increased risk of exposure, like the prison populations, h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Trachea_and_bronchi_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v0Ws23XvTqWkJpuEW0v5epitQxawcbvc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Trachea and bronchi histology]]></video:title><video:description><![CDATA[The trachea is the large airway that extends from the larynx and divides into the two primary bronchi. 

Because the trachea and bronchi share similar functions, their walls are composed of similar tissue types as well, but with a few key differences.

Let’s first look at a low power image of the trachea, stained with Hematoxylin and eosin, or H&amp;amp;E for short. 

At this magnification, we can easily see the C-shaped cartilage ring, which is unique to the trachea. 

Also, you can use the cartilage ring to determine the orientation of the image, since the closed side of the ring points anteriorly and the open side of the ring will always face posteriorly towards the esophagus. 

The free ends of the ring are connected to one another by smooth muscle, called the trachealis muscle. 

The smooth muscle can be differentiated from the  surrounding tissue by the long appearance of their cell bodies when cut longitudinally. 

Their lack of striations also indicates that the muscle is smooth muscle, not skeletal muscle.  

In older individuals, portions of the tracheal cartilage can transform into bone. 

For example, this cross-section of a hen’s trachea shows areas of calcification, with some hyaline cartilage still present on the right.

Looking at the epithelium at 10x magnification, it’s easier to see the different layers of the trachea. 

The lumen of the airway is seen at the bottom left of this image. 

So, the very thin layer lining the trachea’s respiratory epithelium. 

Zooming in much further to approx 100x, the cells that make up the epithelium can be distinguished more easily. 

Similar to the nasal and bronchial epithelium, the tracheal epithelium contains three main types of cells: ciliated pseudostratified columnar cells, the pale-staining mucus-secreting goblet cells, and basal cells which are found closer to the basement membrane. 

The basement membrane can be seen as the pink or eosinophilic band that separates the epithelium from the unde]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Borrelia_species_(Relapsing_fever)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WpWSYszyQ6iXzmnIlGSlYE-xR9OJXRxw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Borrelia species (Relapsing fever)]]></video:title><video:description><![CDATA[Borrelia is a genus of spirochetes, which are long, thin, spiral shaped bacteria, that spin or twist to move around. 

The genus has two major groups. The first one is associated with Lyme disease and the most common species is Borrelia burgdorferi. 

The second group is associated with relapsing fever and the most common species are Borrelia hermsii, Borrelia turicatae, Borrelia parkeri and Borrelia recurrentis. 

Of the second group, the first three species cause tick-borne relapsing fever, while Borrelia recurrentis causes louse-borne relapsing fever. 

By the way, you may know this already, but “louse” is actually singular for “lice” - so body lice are the vector that transmits Borrelia recurrentis. 

Now, all Borrelia species have an outer membrane that contains a substance similar to lipopolysaccharides, an inner membrane, and a layer of peptidoglycan in a periplasmic space, which is the space between the inner and the outer membrane. 

Since the peptidoglycan layer is thin, it doesn’t retain the purple dye used during Gram staining, so they’re classified as Gram-negative. 

However, they can’t be easily visualized with Gram staining. Instead, they’re best seen with the Wright or Giemsa stain, which make the bacteria appear purple, and with dark-field microscopy, which make the bacteria appear white against a dark background. 

Now, Borrelia species are motile, which means they can move around using long, thin filaments called endoflagella, which are located in their periplasmic space. 

The filaments rotate in this space, between the outer membrane and the peptidoglycan layer, propelling the bacterium forward in a corkscrew-like motion.

Finally, the bacteria can be cultivated on Barbour-Stoenner-Kelly medium or by intraperitoneal inoculation of immature laboratory mice, but these tests are not widely available. 

Now, Borrelia can enter the body one of two ways, depending on the type of relapsing fever. 

So, in tick-borne relapsing fever, or TBRF,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sjogren_syndrome:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jQ1SCKURSWi8lfhxv3uDX2d7S-Otfv9a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sjogren syndrome: Pathology review]]></video:title><video:description><![CDATA[On your rounds, you see a 55-year-old female named Patricia who presents with fatigue, dry skin, and red eyes. She mentions that she&amp;#39;s had a recurrent sensation of sand in her eyes and dry mouth every day for the past three months. She also mentioned that when it’s cold outside, the tips of her fingers turn white and hurt.  On examination, there are signs of tooth decay and purpura on both lower extremities. Sialometry was performed, which detected salivary hypofunction.

Ok, so Patricia’s clinical picture is suggestive of Sjogren syndrome. Now, Sjogren syndrome is an autoimmune disorder that mostly affects middle-aged females. The high yield concept here is that the immune system attacks various exocrine glands, especially salivary and lacrimal glands. If Sjogren syndrome is primary or occurs alone, it’s called sicca syndrome. Alternatively, it can be secondary when it is accompanied by other autoimmune diseases like lupus, rheumatoid arthritis, and scleroderma. Now, the exact cause of Sjogren syndrome is unknown, but both genetic and environmental factors are involved. 

In Sjogren syndrome, some helper T-cells perceive nuclear components that leak out of dead or damaged cells in the body as antigens.  These T-cells become active and proliferate and then activate B-cells which start producing anti-nuclear antibodies, or ANAs, against the nuclear antigens. A high yield fact to remember is that the two types of ANA formed in Sjogren syndrome are anti-SSA/RO and anti-SSB/LA antibodies, which are formed against ribonucleoproteins SS-A and SS-B. Next, both T-cells and antibodies enter the circulation and reach the exocrine glands, where activated T-cells secrete cytokines to recruit even more immune cells. This results in a lymphocytic infiltration of the exocrine glands, which ends up damaging the exocrine gland tissue. Eventually, the secreted cytokines also activate fibroblasts, which produce fibrous tissue that replaces the damaged tissue. The en]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Movement_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fS9nqRk3QdiBO931XhnSFB3QTOqtoHcq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Movement disorders: Pathology review]]></video:title><video:description><![CDATA[In the neurology ward, there’s a mother with her child, named Justin, who is 2 years old. Justin’s mother is worried because she palpated a mass in his abdomen while bathing him. Justin also has been having episodes of rapid, dancing eye movements as well as shocklike, jerky movements of his extremities. Next, there’s a 42 year old male, named Oliver. For the past few months, Oliver has been acting strangely according to his sister. He forgets important information and is very aggressive with his family. He also has bursts of wild, dance-like movements of his arms. His sister is very anxious because their father died at age 50 after having similar symptoms. Okay, now next to Oliver, there’s a 58 year old male, named Ashton. His wife has noticed that her husband’s face has become inexpressive and he has been having hand tremor at rest for the past few months. Also, his movements have become slower, and he had frequent falls. His medical history is otherwise insignificant. 

Okay, so all of them have movement disorders. The cerebrum, cerebellum, and basal ganglia all help coordinate movements, so movement disorders can be traced back to these structures. Movement disorders can be broadly grouped into 2 categories, hypokinetic disorders, which cause slowness of movement, and hyperkinetic disorders, which cause excessive involuntary movement. 

Alright, when it comes to hypokinetic disorders, a lot of their symptoms are grouped together under the term “parkinsonism.” This can appear in many conditions including Parkinson’s disease itself, and other syndromes called “parkinson-plus” syndromes. These cause parkinsonism, plus other clinical features. Some Parkinson-plus syndromes include Lewy body dementia, multiple system atrophy, and progressive supranuclear palsy. 

Okay, the four cardinal symptoms of parkinsonism can be remembered with the mnemonic “TRAP”. “T” for tremor, which is classically described as a resting, pill-rolling tremor, because it looks like ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Scleroderma:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iM68msXvQLKqciP8nGDiYfDfQR2dwYhU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Scleroderma: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you see Rosa, a 35-year-old woman who has complained of puffy hands and feet for the past 4 months. 

On examination, the skin on the limbs and trunk is stiff and shiny, with decreased markings. 

Other important findings are sclerodactyly, Raynaud&amp;#39;s phenomenon, and digital ulceration. 

Pulmonary function tests were performed as well, and they showed a pattern suggestive of restrictive lung disease. 

Then you see Haruki, a 65-year old who says that he noticed skin changes recently, stating that the wrinkles on his face have disappeared. 

He also said that his acid reflux got worse in the past 6 months. 

On examination, his hands show Raynaud&amp;#39;s phenomenon and sclerodactyly. 

The skin on his face and the arms below the elbow were tight, shiny, smooth, with no wrinkles. 

Pulmonary function tests are normal. 

Blood tests were performed in both cases, showing increased serum levels of anti-Scl 70 and and-RNA polymerase III antibodies in Rosa, and increased anti-centromere antibodies in Haruki.

Now, both seem to have scleroderma. 

Scleroderma refers to systemic sclerosis, a rare autoimmune disorder in which normal tissue is replaced by thick, dense collagen. 

It affects the skin, blood vessels and internal organs. 

Now, there are two main types of scleroderma, diffuse cutaneous systemic scleroderma; and limited cutaneous systemic scleroderma, which was formerly called CREST syndrome. 

The condition’s pathology is not completely understood, but it’s believed that some individuals have a genetic predisposition to scleroderma which is triggered by external factors. 

These triggers include: viral infection by cyto-megalo-virus and parvovirus B19; exposure to silica dust, organic solvents, vinyl chloride; and medication like cocaine, bleomycin, and pentazocine. 

Okay, for pathology, scleroderma usually starts with an injury to the endothelial cells that line the interior surface of small blood vessels]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal_bleeding:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WFgcBKShRgGZGmfUYaugbj3QQ_qHMpQ0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal bleeding: Pathology review]]></video:title><video:description><![CDATA[A 30-year-old male named Joseph came to the emergency department because of sharp chest pain radiating to his back. He recently graduated from medical school and has been celebrating for the past week at local bars. He says that he was drinking to the point of vomiting and blacking out. He thinks his pain began after a particularly intense night of vomiting and retching. His vital signs show no abnormalities. On the other hand, a 54-year-old lawyer called Lance has been noticing blood in his stool for the past 2 weeks. As he describes the problem, he mentions that there are “streaks of bright red blood” on top of the stool and didn’t notice any pain during bowel movements. Also, he reports a marble-sized, soft mass at the anus that can be pushed back into the anal canal. He denies abdominal pain,  weight loss, or a history of colon cancer. 

Now both people have gastrointestinal bleeding, but with different presentations. Gastrointestinal bleeding can be divided into upper and lower GI bleeding. Upper GI bleeding arises above the ligament of Treitz, also called the suspensory ligament of the duodenum, and it includes bleeding from the esophagus, stomach, or duodenum. Typical presentation includes hematemesis, or vomiting of blood; ‘coffee ground’ vomitus, which suggests that the blood has been oxidized by the acid in the stomach so that the iron in the blood has turned dark; and melena, which refers to black, tarry stools. On the other hand, lower GI bleeding arises below the ligament of Treitz and includes bleeding from the small intestine past the ligament of Treitz, large intestines, rectum, and anus. Typical presentation includes hematochezia, which is fresh blood passing through the anus which may or may not be mixed with stool. 

Now, since these individuals are losing blood, they can develop anemia, or they can even become hemodynamically unstable. In mild hypovolemia, when they lose less than 15% of the blood volume, these individuals can]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Plasma_cell_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dEIgJS2nTAGdn3CemQl00mi_TRqjL17R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Plasma cell disorders: Pathology review]]></video:title><video:description><![CDATA[At the family medicine department, a 70 year old male named Ian came in with progressive fatigue and chronic back pain. His lab tests show anemia with an MCV of 90. as well as increased calcium, blood urea nitrogen and creatinine levels. Peripheral blood smear showed the following. Next to Ian, there’s a 65 year old female named Amanda that complains of progressive fatigue, recurrent nosebleeds and blurred vision. Clinical examination reveals palpable liver and spleen. Her lab tests show anemia with normal MCV, reticulocyte count index over 2%, increased LDH, and a positive Coombs test. 

Although their symptoms are very different, both Ian and Amanda have a plasma cell disorder. Plasma cell disorders are a group of hematological malignancies that are characterized by unregulated proliferation of plasma cells in the bone marrow. They include multiple myeloma, monoclonal gammopathy of unknown significance or MGUS(em-gus), and Waldenström’s macroglobulinemia. Each of them produce a monoclonal or M-protein, which is a unique protein of a single type, like a protein “clone”. Because plasma cells normally make immunoglobulins, it’s not surprising that the M-proteins produced are also immunoglobulins 

Alright, now let’s take a closer look at these different plasma cell disorders, starting with multiple myeloma, which is the most common primary bone tumor in people older than 40 to 50 years of age. In multiple myeloma, the most common M-protein produced is IgG, followed by IgA,  and these immunoglobulins have both a heavy and light chain. More rarely, the myeloma cells can only make the kappa or lambda light chain of the immunoglobulin, and in that situation, the resulting protein is called the Bence-Jones protein. 

A high yield concept is the clinical presentation of multiple myeloma, which can be summarized with the mnemonic CRAB (like the animal), “C” is for hypercalcemia, which results from increased osteoclast activity due to the release of osteoclast acti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Headaches:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z603-Ww7RiSGvYAuD19gCOzRT7m0yRb3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Headaches: Pathology review]]></video:title><video:description><![CDATA[At the neurology department, there’s a 34-year old male, named Andrew, who came in due to  headache. This is the first time he’s had a headache like this and described the pain as “the worst headache of his life”. Neurological examination reveals neck stiffness. His medical history is otherwise insignificant. Next to Andrew, there’s a 30-year old female, named Anna, who complains of recurrent episodes of unilateral, pulsating headaches that usually occur when she’s tired, and last approximately 6 hours each time. Her mother also suffers from similar episodes of headache. Finally, there’s a 40-year old male, named Evan, who has had recurrent attacks of excruciating headaches for the past two months. The pain is located behind his eye, typically occurs in the morning, and lasts for about one hour. He also has nasal congestion and lacrimation of the affected eye. He has no family history of similar episodes. 

All three people suffer from headaches. A headache occurs when any of the pain-sensitive structures in the head and neck are stimulated. These include the meninges, blood vessels, nerves, and muscles. Headaches can be classified into two types. The first are called primary headaches, and they’re more common. These are chronic or recurrent headaches and include tension headaches, migraines, and cluster headaches. Now, the second type are called secondary headaches, and these are acute headaches from a specific underlying cause like a serious head injury, infection, or a brain tumor. 

Alright, now let’s take a closer look at the different types of primary headaches. Tension headaches are the most common type and they’re more common in females. On the exams, the classic description is a headache that is slowly-progressive, bilateral, tight, “band-like” headache with no other associated symptoms. Typically, they lasts from 30 minutes to up to a week, and is usually triggered by stress and dehydration. It is thought that these headaches are due to an increa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertension:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KELHJCPFQhO8qrxYN71QpWnuRmme6CC-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertension: Pathology review]]></video:title><video:description><![CDATA[Anthony is a 40 year old male with a history of type 2 diabetes mellitus presenting to a family medicine clinic for his annual health check-up. His blood pressure measurement is 145 over 95 millimeters of mercury, and his BMI is 32.  On further history, he explains that his job as a truck driver has prevented him from exercising regularly. His father had a history of hypertension and passed away from a stroke. A follow-up appointment showed a blood pressure of 150 over 90. Alicia is a 30 year old female who came in because she’s concerned that she might be pregnant. Her pregnancy test is negative, however, her blood pressure is 170 over 90. On her second appointment, her blood pressure remains elevated. She is placed on lisinopril. A couple of days later, she presents with decreased urine output, and an elevated blood urea nitrogen and creatinine. Finally, Vikander is a 62 year old-male with a history of hypertension.  He complains of headache, altered mental status, and visual changes. On further history, he mentions he is “sick of all the medications he has to take”. Fundoscopic examination reveals a swollen optic disk, and his blood pressure is 200 over 120. 

Okay so all three people present with hypertension.  Now normal blood pressure is less than 120 systolic over 80 diastolic. According to the recent 2017 American Heart Association and American College of Cardiology guidelines, hypertension is currently defined as a blood pressure over 130 systolic and 80 diastolic.  Now, typically, both systolic and diastolic pressures tend to rise or fall together, but that’s not always the case. Sometimes, you can have systolic or diastolic hypertension. This is referred to as isolated systolic hypertension or isolated diastolic hypertension. 

Okay, just because you see an elevated blood pressure on the exam, it does not mean that individual has hypertension. The blood pressure must be persistently elevated in order to define it as hypertension. So on your exam]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skin_cancer:_Clinical_practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ewls3WbHRECEXTvIm6HNr3rXRkiWE4ma/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skin cancer: Clinical]]></video:title><video:description><![CDATA[Skin cancer is differentiated based upon the type of skin cell that’s involved. 

There are three main types of skin cancer: basal cell carcinoma, squamous cell carcinoma - collectively known as non-melanoma skin cancer, and melanoma. 

Diagnosis of skin cancer starts with naked-eye skin examination of the characteristics of the lesion, as well as detailed history of the current skin complaint, asking for the time of onset, duration, location, evolution, and symptoms. 

This is then followed by dermoscopy. Dermoscopy is a noninvasive, in vivo technique used for the evaluation of skin lesions. 

It allows for the visualization of subsurface skin structures in the epidermis, dermoepidermal junction, and upper dermis, which are otherwise not visible to the naked eye. 

There are three dermoscopic criteria to predict malignancy of a pigmented lesion - asymmetric distribution of colors and structures within a lesion, blue-white structures, and atypical network. 

On the other hand, for nonpigmented lesions, the three criteria are ulceration, white zones, and vascular structures and patterns. 

Now, the main purpose of dermoscopy in the evaluation of pigmented and nonpigmented skin lesions to help decide whether or not to monitor the lesion over time with sequential digital dermoscopy imaging to determine its biologic nature, or to perform a skin biopsy, which is needed to confirm diagnosis of skin cancer, showing the type of cells involved. 

Biopsy can also serve as the definitive treatment for lesions that haven’t spread elsewhere. 

The three main types of skin biopsy are shave biopsies, punch biopsies, and excisional biopsies. 

In shave biopsies, a superficial thin piece of skin is removed from the surface using a small sharp blade, so they are typically used for lesions for which sampling of the full thickness of the dermis is not necessary. 

On the other hand, punch biopsies involve the removal of a core-shape piece of tissue using a sharp cutting ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/West_Nile_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bh9J1RGmTQCD3402UmcIJjG6RT6BRkB5/_.jpg</video:thumbnail_loc><video:title><![CDATA[West Nile virus]]></video:title><video:description><![CDATA[West Nile virus is an arthropod-borne virus, or arbovirus, which are viruses that get transmitted through insects called vectors. 

The vector for west nile virus is the mosquito, and gets transmitted in highest frequency through the female Culex species, which feeds on birds. 

The virus was first discovered in Uganda - west of the Nile - but has since been reported throughout the world. 

The virus causes a disease called West Nile fever, which normally causes mild symptoms, but can progress to full blown encephalitis or meningitis. 

Normally, west nile virus is found in birds and mosquitoes. 

Birds act as a reservoir for the virus, meaning the virus can replicate at high enough levels to cause significant viremia, or elevated viral blood counts, which allows for transmission to other uninfected mosquitoes. 

The virus will then replicate inside the mosquito and ultimately move into its salivary glands. 

So when the mosquito bites another animal, it injects its infected saliva into the host, since mosquitoes normally use their saliva as an anticoagulant. 

When the vector mosquito bites a larger animal, like a horse or a human, the virus can&amp;#39;t spread from these larger animals because their blood doesn’t reach high enough levels of the virus to be passed on to any mosquitoes that happen to bite them. 

And this is called a dead end host.

West Nile virus is composed of positive single-stranded RNA. 

This means that their RNA is actually mRNA, and the host cell ribosomes use this mRNA to make a long polyprotein chain, which is then broken into smaller pieces by viral proteases. 

This all happens in the cytoplasm of the host cell, since that’s where ribosomes are found, and results in the production of several viral proteins. 

West Nile virus is surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. 

West Nile virus is also an “enveloped virus” because the capsid is covered by a li]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_cycle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6TxelB_tTh_kM1jCaSLc06WsQvWbDLuI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac cycle]]></video:title><video:description><![CDATA[A cardiac cycle is the sequence of mechanical and electrical events that occurs with every heartbeat. Now, the heart is shaped like a cone and it contains two upper chambers, called atria; and two lower chambers, called ventricles. 

Now, the left atrium receives oxygenated blood from the lungs via the pulmonary veins; while the right atrium receives deoxygenated blood from all of our organs and tissues via the superior and inferior vena cava. 

From the atria, the blood flows into the lower chambers of the heart: the left ventricle, which pumps oxygenated blood to all our organs and tissues via the aorta; and the right ventricle, which pumps the deoxygenated blood back to the lungs via the pulmonary arteries.

Alright, so each heartbeat consists of two phases: systole, which is when the heart contracts and pumps blood out of the ventricles; and diastole, which is when the heart relaxes and ventricles fill with blood. Now, the cardiac cycle graph is used to express events during one cardiac cycle. 

Along the y-axis are aortic pressure, left atrial pressure, and left ventricular pressure, heart sounds, ventricular volume, right atrial pressure curve, and ECG; while along the x-axis is time. 

But, before we continue, here’s something to keep in mind: since there are no valves separating the right atrium from the superior vena cava and the jugular veins, the jugular venous pulse will follow the same pressure changes as the ones that arise in the right atrium. 

In other words, an increase in the atrial pressure will result in an increased jugular venous pulse, and vice versa. Therefore, below the right atrial pressure curve let’s write JVP for jugular venous pulse. 

And right above the graph, we’ll write the seven phases of the cardiac cycle. The first phase is the atrial contraction, which lasts about 0.1 seconds. 

Next, isovolumetric ventricular contraction, rapid ventricular ejection, reduced ventricular ejection, are phases of ventricular systole and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_insipidus_and_SIADH:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vVJG30CGS6mogEOr9RmsVFJ-T7S0Aul_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes insipidus and SIADH: Pathology review]]></video:title><video:description><![CDATA[Okay, so two people were admitted to the Endocrinology ward. One of them is 35 year old Imre, who came in with intense polyuria and polydipsia. Imre was dehydrated and presented with dry mouth, headache, dry skin and dizziness. Several tests were done and results showed increased serum osmolality and further on, a desmopressin test was done. During the test, an ADH analogue was administered and urine osmolality increased. The other person is 45 year old Sienna who came in to do some routine tests because she started taking cyclophosphamide and wanted to make sure that there are no complications. Her lab results showed hyponatremia, decreased blood osmolality, and her urine osmolality was higher than serum osmolality. 

Now, both individuals are unable to maintain normal osmolality. But to understand this we need to  go over a bit of physiology first. In the brain, specifically in the hypothalamus, there are osmoreceptors which can sense the osmolality of the blood, or how concentrated it is. Osmolality is the concentration of dissolved particles in the blood plasma, or the liquid portion of blood. There are a number of dissolved particles in the blood plasma, but the major ones are glucose, sodium, and blood urea nitrogen, and a normal osmolality is between 285 and 295 milliOsmoles per kilogram. 

Now, during periods of dehydration there is an increase in concentration of these particles in the blood and osmolality increases. The osmoreceptors in the hypothalamus sense the change in osmolality and this triggers the sensation of thirst. The water that we drink gets absorbed and dilutes the blood, bringing the osmolality back to normal. 

In addition to osmoreceptors, the hypothalamus also contains the supraoptic and  paraventricular nuclei  that produce antidiuretic hormone, or ADH, which is then sent to the posterior pituitary for storage. ADH is also called vasopressin because it causes smooth muscle around the blood vessels to contract, which increases r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Niemann-Pick_disease_type_C</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6g_fM6xwS1OLQClMh0M-5ehZTbi5Zxyq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Niemann-Pick disease type C]]></video:title><video:description><![CDATA[Niemann-Pick disease type C, or NPC, is a rare genetically inherited condition caused by mutations in either the NPC1 or NPC2 genes. 

These mutations impair intracellular transport of cholesterol and other molecules, which causes progressive neurologic and developmental problems. 

Now, cholesterol reaches the cells packed in lipoproteins, which bind to low density lipoprotein, or LDL, receptors on the cell membrane, to get inside the cell. 

Then, cholesterol reaches the early-endosome, which is an intracellular organelle that eventually matures into a late-endosome, and finally into a lysosome. 

Inside the lysosome, cholesterol is processed and recycled, so that it can be incorporated into the cell membrane. 

To get out of the lysosome, first, cholesterol gets a little help from the NPC2 gene product, a protein that carries cholesterol up to the lysosomal membrane. 

And on this membrane, cholesterol is greeted by the NPC1 gene product, which is a glycoprotein that moves cholesterol out of the lysosome and into the cell. 

So with NPC1 or NPC2 mutations, intracellular cholesterol transport is impaired, so cholesterol accumulates inside lysosomes instead. Mutations can affect people of all ethnic backgrounds, and they’re inherited in an autosomal recessive pattern, which means that an affected individual must have two copies of the mutated gene, one from each parent.

Cholesterol buildup affects almost all cells, so it causes a variety of symptoms. 

The brain and bone marrow are often affected. 

The liver and spleen can be affected too, in which case, they enlarge. 

Liver enlargement disrupts bile flow, causing bilirubin to accumulate in the blood. 

This leads to jaundice, or yellow pigmentation of the skin and whites of the eye. 

An enlarged spleen, on the other hand, may trap platelets, which causes easy bruising and bleeding issues. 

Finally, when this buildup occurs in macrophages, they develop a characteristic lipid-laden appearance under mi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypothyroidism:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oFG92_QGQ-Wc1wGqD5v5LGhHRN6ix0tz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypothyroidism: Pathology review]]></video:title><video:description><![CDATA[In this scenario, there are two individuals at the emergency department. The first one is 23-year-old Hannah who reports lethargy, fatigue, reduced appetite, muscle weakness and constipation. She also says that lately she gained a bit of weight and has a low libido. On clinical examination, she has periorbital edema, dry, cool skin, her nails are brittle, and her reflexes are slow. She also has a moderately enlarged, painless goiter.  

The other one is 33-year-old Quentin, who also presents with lethargy, fatigue, reduced appetite, muscle weakness, constipation and he’s also complaining about feeling cold all the time.  He said that he recently had the flu, but no other illnesses. On clinical examination, there’s periorbital edema, dry, cool skin, brittle nails and hair, and a very painful goiter.  

TSH, free T3, and free T4 are taken, along with antithyroid-peroxidase and antithyroglobulin antibodies. Both Hannah and Quentin have high levels of TSH and low T3 and T4 levels, but Hannah has positive antithyroid-peroxidase and antithyroglobulin antibodies. Both individuals seem to have hypothyroidism.  

First, a bit of physiology. Normally, the hypothalamus detects low serum levels of thyroid hormones and releases thyrotropin-releasing hormone or TRH into the hypophyseal portal system. The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH. TSH stimulates the thyroid gland. 

The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4. Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. Only a small amount of T3 and T4 will travel unbound, or free, in the blood, and this is the form that acts upon nearly every type of cell in the body.  

Once inside the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bone_tumors:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sEZx69wWQSONEDheSRTk4JakSWaQFmZw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bone tumors: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you see two individuals. First is James, a 14-year-old boy who came in for chronic right knee pain, night sweats, and weight loss. He didn’t report falling or any other trauma to the region or any additional symptoms. On examination, his right knee is slightly larger than the left and, on palpation, a hard mass can be felt on the metaphysis of his right femur, close to the knee region. Then you see William, who’s 22 years old and complains of a 1-month history of bone pain along his left tibia, a problem which is worse at night. One interesting observation he made was that the pain responds well to Ibuprofen, a nonsteroidal anti-inflammatory drug. On examination, palpation reveals a bony mass on the anterior surface of the left tibial diaphysis. As expected, X-ray scans were obtained. They showed a distal sunburst appearance and Codman&amp;#39;s triangle in James’ right femur, whereas William’s x-ray scans detected a small lesion under 2 centimeters with a radiolucent core on the anterior surface of his left tibia.

Now, both seem to have some type of bone tumor. But first, a bit of physiology. Even though the bones vary in size and shape, all bones are made of the same types of cells, and chief among them are osteoblasts which build up new bone, and osteoclasts which help with bone breakdown or resorption. Now in addition to these, there are some more primitive cells in the bone marrow called human mesenchymal stem cells and neuroectodermal cells, which can differentiate into many cell types including nerve, fat, bone, and cartilage cells. In terms of anatomy, looking at a long, bone like the femur, it has two epiphysis, which are the ends that contribute to joints with other bones. Between the two epiphyses, is the diaphysis, also called the bone shaft. In children and adolescents, there is an additional narrow portion between the epiphysis and the diaphysis called the metaphysis. The metaphysis contains the growth pla]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mammary_gland_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bKWbcC-WSdWvpHBTw79AhAE4QsSd3RVy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mammary gland histology]]></video:title><video:description><![CDATA[Now, let&amp;#39;s get a closer look. The mammary glands of each breast consist of about 15 to 25 sections called lobes with each lobe containing many smaller structures called lobules.

Each lobule consists of a large number of alveolar glands, which are the small sac-like structures that produce milk.

The milk produced by the alveolar glands drain into the terminal ducts that join together to form the intralobular ducts.

These ducts converge further and form the lactiferous ducts, which drain the lobes and eventually lead to the nipple.

All of the lobules and ducts are also surrounded by fibro-fatty tissue that provide a supportive and protective function.

Before pregnancy, the mammary glands are considered to be in an inactive state, and they’re structurally different from mammary glands that are in the active state.

The active state occurs during pregnancy and during lactation after childbirth.

During pregnancy, the alveolar glands and the duct system will grow in preparation to produce milk for a newborn baby.

This low power image is an example of lactating mammary glands in the active state.

A portion of a lobe can be seen surrounded by a thick layer of connective tissue that contains a small number of fat cells or adipocytes within the connective tissue as well.

Within the lobe, thinner layers of connective tissue separate the lobe into lobules.

In a neighboring lobe, we can also see a couple of large lactiferous ducts.

These ducts are lined with a double layer of columnar or cuboidal cells with a surrounding layer of connective tissue.

If we take a closer look at one of the lobules, we can see some of the smaller intralobular ducts that are typically lined with 1 to 2 layers of cuboidal cells that also have a thin layer of connective tissue that surround the ducts. In this image of a different lobule, we can see a good example of a few alveoli and a longitudinal cross-section of the terminal duct that’s responsible for draining the mil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_mellitus:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Dxkc-4bxQh6IYSSRE0BmwX-YQjClE-pA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes mellitus: Pathology review]]></video:title><video:description><![CDATA[In the Emergency Department, two individuals came in. One of them is 12-year-old Timmy, who is severely dehydrated, presents with rapid and deep breaths, abdominal pain, nausea and vomiting. On the clinical examination, his breath actually smells fruity and sweet. Timmy’s parents said that he had been eating a lot lately, but he actually lost weight. Also, they said that Timmy is also drinking water all the time and going to the bathroom a lot. The other person is 55-year-old Oliver, who also came in with severe dehydration, lethargy; and his family said he had a seizure about 2 hours ago, and in the past month, he had lost some weight, although he had been eating. Both individuals underwent several investigations, including glucose levels, ketones, BMP, and an ABG. Okay, based on both individuals’ symptoms, we can assume that both suffer from diabetes mellitus. 

Diabetes mellitus is a condition where glucose can’t be properly moved from the blood into the cells. This leads to high levels of glucose in the blood and not enough of it inside cells. Since cells need glucose as a source of energy, not letting glucose enter means that the cells starve for energy despite having glucose right on their doorstep.  

In general, the body controls how much glucose is in the blood with two hormones: insulin and glucagon. Both of these hormones are produced in the islets of Langerhans of the pancreas. Insulin is secreted by the beta cells, while glucagon is secreted by the alpha cells.  

Insulin reduces blood glucose levels. It does that by binding to insulin receptors embedded in the cell membrane of insulin-responsive tissues, like muscle cells and adipose tissue. When activated, the insulin receptors cause vesicles containing glucose transporter that are inside the cell to fuse with the cell membrane, allowing glucose to be transported into the cell. 

Okay, now, there are two types of diabetes mellitus, Type 1 and Type 2, and the main difference between them is t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adult_brain_tumors:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PZxu9uFgTCCKssx9FFeAkeMXRdaJdBAg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adult brain tumors: Pathology review]]></video:title><video:description><![CDATA[In the neurology ward, a 64-year old female, named Angela, came in complaining of morning headaches along with nausea and vomiting for the past few weeks. Her husband says that her personality has changed over the last few weeks and she seems more aggressive. Brain MRI revealed a mass in the frontal lobe.Tissue biopsy shows a pseudo-palisading pattern with necrosis in the middle and viable cells lining up in the periphery.

Now, next to Angela, there’s Jerry, a 59-year old male who’s also having morning headaches for the past few months. A brain MRI is ordered and reveals a mass on the brain surface, just under the dura mater. Tissue biopsy shows psammoma bodies. 

Finally, there’s a 40-year old male, named Dan, who complains of ringing in the ears and hearing loss on one side. A brain MRI is done, and showed a mass on the cerebellopontine angle. Tissue biopsy shows a mass with biphasic appearance with alternating hypercellular and hypocellular regions. Tumor cells stain positively for S100.

Okay, Angela, Jerry, and Dan all had brain tumor. Brain tumors occur when there’s uncontrolled growth of abnormal cells within the brain. They are broadly classified into primary tumors originating from cells within the nervous system and metastatic tumors originating from cells outside the nervous system.

Now, brain tumors can occur in both children and adults. In this video, let’s focus on adult brain tumors. In adults, metastatic tumors are much more common than primary tumors, in fact, they account for more than half of the cases. In order of decreasing frequency, they metastasize from the lung, breast, melanoma from the skin, kidneys, and colon. Now, the most common primary brain tumor in adults is glioblastoma multiforme, which is a type of astrocytomas. Meningiomas and pituitary adenomas are next on the list. Less common brain tumors include oligodendrogliomas, hemangioblastomas, and Schwannomas. immunocompromised people, like organ transplant recipients or in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Post-transplant_lymphoproliferative_disorders_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P5DR8CRUSRaqzNqq4ia3d_ybTBqgQVLa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Post-transplant lymphoproliferative disorders (NORD)]]></video:title><video:description><![CDATA[Posttransplant lymphoproliferative disorders, or PTLDs, are uncontrolled growths of cells called lymphocytes that may occur in transplant recipients after receiving a solid organ, such as a kidney or a lung, or stem cells. 

Transplant recipients require medications to suppress their immune systems which may contribute to the development of a PTLD.

Normally, immune cells can differentiate between healthy “self” and “other” cells by inspecting for the presence or absence of the normal “self” major histocompatibility complexes, also called human leukocyte antigens, present on the surface of every cell that contains a nucleus.

Healthy “self” cells are left alone.

“Others” include cells from other people or donors and “self” cells that are infected, damaged, or stressed.

Lymphocytes, are a class of rapidly dividing cells and, therefore, tends to develop mutations more often.

B-lymphocytes, or B-cells, work to develop antibodies toward invading microbes.

There’s also two types of T-lymphocytes, or T-cells.

Cytotoxic T-cells can directly destroy “other” cells and helper T-cells assist other immune cells.

Normally, if B-cells start to replicate out of control, it&amp;#39;s the T-cells that keep them in check, and keep the immune response organized. 

When people receive a transplanted organ or stem cells, they also must take immunosuppressive medications to prevent the immune system from rejecting, or attacking, the transplant.

In PTLDs, immunosuppression also prevents the destruction of abnormal lymphocytes that exhibit uncontrolled replication.

Resulting uncontrolled growth of lymphocytes can either be a benign hyperplasia, meaning there’s a large collection of noncancerous cells, or the cells can become malignant, resulting in a cancer called lymphoma. 

While PTLD may result from the overproduction of T-cells, it is more typically associated with the overproduction of B-cells.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenoleukodystrophy_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mn6nx1ZpR6aN6pCh_ioZbzZ7RAme2MLS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenoleukodystrophy (NORD)]]></video:title><video:description><![CDATA[With adrenoleukodystrophy, sometimes called ALD, adreno- refers to the adrenal glands, while -leuko-, means white, and -dystrophy refers to tissue degradation. So, adrenoleukodystrophy is a rare genetic condition, caused by a mutation in the ABCD1 gene, located in the X-chromosome, that leads to the progressive loss of white matter in the nervous system, and the degradation of adrenal glands. Generally, genes tell our bodies how to make proteins. In this case, the ABCD1 gene directs the body to produce adrenoleukodystrophy protein or ALD protein. ALD protein is a transporter that is found embedded in the membranes of vesicles found in cells that break down specific forms of fatty acids, called peroxisomes. Its function is to import into peroxisomes, a group of fats, naturally present in the human body and in our diets, called very long-chain fatty acids or VLCFAs.

Once inside the peroxisomes, these molecules are broken down into shorter forms of fatty acids. Now, in adrenoleukodystrophy, there’s a mutation in the ABCD1 gene which leads to a defective ALD protein. Without a working ALD protein, VLCFAs have no way of entering the peroxisomes to be broken down, so they accumulate inside cells. This build up of VLCFAs is thought to be damaging to our nerve cells and the glial cells that support them, the cells in our adrenal glands that produce steroid hormones, the cells in the testicles, and some of our immune cells. Adrenoleukodystrophy is inherited in an X-linked fashion. This means that the ABCD1 gene is found on the X-chromosome. Males who carry a ABCD1 gene mutation on their X chromosome will have the condition. 85% of females who carry a ABCD1 gene mutation on one of their X chromosomes present higher levels of VLCFAs and half experience symptoms.

Now, adrenoleukodystrophy has variable expressivity, which means that the symptoms between each person with the condition can differ greatly, even within the same family. For this reason, an affected person]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lung_cancer_and_mesothelioma:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j2D9RCbrSZSAcRV1k60_gA9TS6u6AI7Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lung cancer and mesothelioma: Pathology review]]></video:title><video:description><![CDATA[Two people came to the clinic one day. First is a 65-year-old named Alex, who presents with a two-month history of dry, persistent cough and weight loss of around 7 pounds without dieting. He also says he coughs up blood sometimes but denies fever, dyspnea, sore throat, rhinorrhea or any chest pain. Alex has a history of asthma and hypertension, and smoked 1 pack of cigarettes daily for 45 years. On examination, his breath sounds are diminished at the right lung base. 

The other individual is Clara, who’s an 80-year-old retiree. Before her retirement, Clara was a construction site supervisor. She complains of increasing shortness of breath, which started ten months ago, and new onset of myalgia located on the right side of her chest. Physical examination reveals decreased breath sounds in the right lung base along with dullness to percussion. Chest X-rays were ordered for both people. In Alex’s case, it showed a single, coin-like lesion on the right lung base. Clara’s scan showed pleural effusion, irregular pleural thickening, and two ivory white, calcified pleural plaques at the base of her right lung.

Both people have cancer involving the lung. But first, a bit of physiology. Lining the airways are several types of epithelial cells that serve multiple functions. These include ciliated cells that have hair-like project called cilia that work to sweep foreign particles and pathogens back to the throat to be swallowed. Another type, called goblet cells secrete mucin to moisten the airways and trap foreign pathogens. There are also basal cells that are thought to be able to differentiate into other cells in the epithelium, club cells that act to protect the bronchiolar epithelium, and neuroendocrine cells that secrete hormones into the blood. On the outside, the lungs are covered by the mesothelium which consists of the parietal pleura and the visceral pleura. Between them, there’s the pleural space, where the fluid produced by the epithelial cells is rele]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prostate_disorders_and_cancer:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_ShIwMkLQy2uaorF-_nVwZAdQD_ab9Ir/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prostate disorders and cancer: Pathology review]]></video:title><video:description><![CDATA[On the urology ward, two people came in.  The first is 63-year-old Joseph who complains of difficulty with urination. More specifically, he says he has trouble initiating his stream of urine, and after urination, his bladder still feels full. He also wakes up several times each night feeling the need to urinate. These symptoms have been present for the past few years, but have gradually become worse. Digital rectal examination revealed symmetrically enlarged, smooth, firm, nontender prostate with rubbery or elastic texture. The second is Sam, a 72-year-old African-American individual who comes in with lower back pain that is not relieved by rest or position changes and has been increasing over the past couple of months. He has also noticed recent feelings of fatigue and weight loss, which he attributes to decreased appetite. On further history, he consumes a diet low in fiber and high in saturated fat and red meat. On digital rectal examination, an irregular, hard lump is palpated in the posterior of his prostate. Labs show increased alkaline phosphatase and total PSA levels with decreased free to total PSA ratio.

Both Joseph and Sam have different forms of prostate disorders! Let’s first remind ourselves about physiology real quick. The prostate is a small gland whose job is to secrete an alkaline milky liquid that joins the sperm and the semen. To do that, it sits under the bladder and in front of the rectum. That’s important because when we do digital rectal exam, we’re able to palpate the posterior of the prostate. The urethra goes through the prostate before reaching the penis. And that part of the urethra is called the prostatic urethra. 

Now, the prostate can be divided into a few zones and this is high yield!  The peripheral zone, which is the outermost posterior section, is the largest of the zones and contain about 70% of the prostate’s glandular tissue. Moving inward, the central zone contains about 25% of the glandular tissue. Last, is the tr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Systemic_lupus_erythematosus_(SLE):_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Cu7fonVgSz2obaJGHpMEHqdZRliHYrZi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Systemic lupus erythematosus (SLE): Pathology review]]></video:title><video:description><![CDATA[At the internal medicine department, a 42 year old female named Mary shows up. She complains of multiple skin lesions on the arms, chest and back. She reports having these lesions for about 3 months. In the past, she had similar lesions. She reports morning stiffness involving her fingers and knees, as well as a history of multiple miscarriages. Blood tests revealed pancytopenia as well as a very high ESR and CRP. She was positive for ANA and antiphospholipid antibodies.

Meanwhile, at the emergency department, a 25 year old man named Kyle shows up with flank pain and hematuria. He has a history of migratory arthralgias and photosensitivity. He was positive for ANA and double-stranded DNA antibodies, and also had low complement levels. Blood tests revealed very high ESR and CRP, as well as high creatinine, so a urinalysis was performed, showing proteinuria and red blood cell casts. 

Both individuals actually have very different presentations of the same disease, called Systemic Lupus Erythematosus. This is a systemic, relapsing, and remitting autoimmune disease, where systemic means that essentially any tissue or organ can undergo inflammation; while relapsing and remitting, stands for periods of illness, called relapses or flares; and periods of remission during which there are few or no symptoms. 

Now, lupus develops when the person’s immune system starts recognizing nuclear antigens of the body’s own cells as foreign and tries to attack them. Essentially, B cells start producing antibodies which bind to nuclear antigens in our own cells. Normally, these B cells are destroyed before they fully mature in a process called self tolerance, but in people with lupus this process is impaired. The antibodies released by these B cells form antigen-antibody complexes and these complexes drift around in the blood until they deposit or stick to the vessel wall in all sorts of different organs and tissues like the kidneys, skin, joints, heart.

Deposited ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acid-base_disturbances:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y_AEi07GQquXrB1JTTjXKPvEQrO5RBs0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acid-base disturbances: Pathology review]]></video:title><video:description><![CDATA[Two people came into the Emergency Department one day.  The first one is 33 year old Muriel who came in with abdominal pain, a severe headache and hyperventilation. One of Muriel’s friends said that she caught her drinking antifreeze. The other one is 35 year old Eustace who came in with confusion and hypoventilation. Eustace also has duodenal ulcers, for which he has been taking antacids. Among other tests, an ABG was done for  both individuals. The results showed that Muriel had low pH, along with low levels of bicarbonate and low levels of pCO2, while Eustace had high pH, along with high levels of bicarbonate and high levels of pCO2. 

Okay, based on lab results, both individuals seem to have acid-base disturbances. Now, let’s go back to the basics for a bit. So, in plasma you can find carbon dioxide or CO2 and water or H2O. They are constantly mixing together in order to make bicarbonate ion or HCO3− and hydrogen ion or H+. Similarly, HCO3− and H+ can form CO2 and H2O. 

Now, HCO3 − is mostly regulated by the kidneys and metabolism, while CO2 is regulated by the lungs. The blood pH which corresponds to the hydrogen ion concentration needs to stay in a very narrow range, between 7.37 and 7.42. Basically, the more hydrogen ions, the more acidic the blood is and the lower the pH. Less hydrogen ions means the blood is more alkaline, and the higher the pH. So, let’s say that HCO3− levels decrease for some reason. In this case, the equation shifts to the right and more HCO3− and  H+ will be produced and as a result the blood becomes more acidic, so pH levels decrease. On the other hand, if HCO3− levels rise, less H+ will be produced and the pH rises. Now, if CO2 increases, then the equation shifts to the right and the pH drops. If CO2 decreases, then the equation shifts to the left and the pH rises. Stay with us here. In practice, the Henderson-Hasselbalch equation is used to calculate the pH based on HCO3 and pCO2 values, where pCO2 represents the partial p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atherosclerosis_and_arteriosclerosis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NfwXcAfnQwCRTEPMPMa37AQkScCE_gbp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atherosclerosis and arteriosclerosis: Pathology review]]></video:title><video:description><![CDATA[Mikhail is a 60 year old man with a history of hypertension, diabetes and dyslipidemia who presents to your clinic complaining of sudden-onset retrosternal chest pain associated with shortness of breath. He has a 35-pack-a-year smoking history, and he mentions that he also develops lower limb pain when walking for more than 15 minutes. His father underwent a below the knee amputation of his right lower extremity and died from a stroke. On physical examination, his BMI is 32. On further workup, his ECG and high troponin levels suggest a myocardial infarction. Mikhail goes to the cath lab to undergo per-cutaneous coronary intervention, which showed a clot occluding the left anterior descending coronary artery. After the procedure, his chest pain resolved. However, he started developing a web-like skin rash. 

Mikhail suffers from arteriosclerosis, which is a hardening and thickening of the arterial wall, causing it to lose its elasticity. A specific type of arteriosclerosis is atherosclerosis, which is a chronic inflammatory disorder that affects the endothelium of medium and large arteries, and is characterized by the buildup of cholesterol plaques within the arterial lumen. In a descending order, the most common arteries affected by atherosclerosis are the abdominal aorta, coronary artery, popliteal artery and then the carotid artery. 

Risk factors for atherosclerosis can be divided into modifiable and nonmodifiable risk factors. Modifiable risk factors include hypertension, diabetes mellitus, smoking and dyslipidemia, particularly an increase in LDL levels or a decrease in HDL levels. Non-modifiable risk factors include age, family history, and being of African-American descent. 

The pathogenesis of atherosclerosis is essentially an inflammatory response to endothelial cell injury. The endothelium is  injured by stress against the arterial wall, like in hypertension. This is especially more prominent at arterial bifurcations, such as the carotid artery ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vertigo:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DsF-tWqLTWCYt3B4uBuE2pKfQ5eezE3n/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vertigo: Pathology review]]></video:title><video:description><![CDATA[At the family medicine center, there’s a 55 year old female, named Juliette, who came to visit the doctor because she has had some episodes where she felt like “everything around her was moving”. 

These episodes start abruptly and usually last a few hours. 

She also complains of ringing in her left ear and feels that she can’t hear very well from that ear. 

Her medical history is otherwise insignificant. 

Clinical examination reveals horizontal nystagmus. 

Next to Juliette, there’s a 70 year old male, named Alasdair, who is brought in by his son because an hour ago he felt that “the room around him was moving” and had difficulty in speaking. 

He also complains of “seeing double”. 

Alasdair has hyperlipidemia and hypertension. 

Clinical examination reveals vertical nystagmus. 

Alright, so both Juliette and Alasdair have vertigo. 

People with vertigo will often say they get “dizzy,” which is an imprecise term. 

What they are experiencing is either vertigo, syncope or presyncope, also known as lightheadedness, or disequilibrium. 

The difference is vertigo can be thought of as having an illusion of self-motion, or movement of the surrounding environment; syncope is the feeling of blacking out or fainting; and disequilibrium causes a sensation of being off balance without the sensation of the environment moving. 

Vertigo arises when there’s a mismatch between other sensory systems, like sight and proprioception, and the vestibular system. 

The vestibular system is made of the vestibular apparatus; including the three semicircular canals, the utricle and saccule, the vestibular nerve, and the vestibular structures in the brainstem and cerebellum. 

Vertigo can be broken down into peripheral vertigo, which is due to damage to the vestibular apparatus, or damage to the vestibular nerve, and central vertigo, which is due to damage to the vestibular structures in the brainstem or cerebellum.

Okay, let’s take a closer look at the causes of peripheral v]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_tubular_defects:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d6ZImYG8ToSnEvBBFB99qsjSTTOZu36u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal tubular defects: Pathology review]]></video:title><video:description><![CDATA[In the Emergency Department, two people came in. One of them is 40-year-old Sarah, who came in with rapid, shallow breathing and tachycardia. The other one is 35-year-old Alfred, who came in with slow and shallow breathing. Arterial blood gas was taken, along with electrolytes. Results showed that Sarah had low blood pH, bicarbonate and pCO2 levels and her potassium level was also low. Alfred had a high pH, bicarbonate and pCO2 levels, but his potassium level was low.  

Based on these results, Sarah was diagnosed with metabolic acidosis, while Alfred had metabolic alkalosis. Further investigations were done, like electrolytes and urinalysis. This showed that Sarah had hypophosphatemia and urinalysis showed phosphaturia, aminoaciduria and glucosuria, while Fred had hypokalemia and urinalysis showed hypercalciuria. Now, the results from the labs of both individuals point towards some kind of renal tubular defect that’s causing acid-base disorders.  

Before talking specifics, let&amp;#39;s remember the physiology of the renal tubules. The proximal convoluted tubule or PCT reabsorbs bicarbonate, all glucose, uric acid and amino acids. Apart from this, it also reabsorbs water, potassium, chloride, phosphate and most of the sodium, as well as most of the calcium. PCT also secretes hydrogen and phosphate into the urine.  

The thin descending loop of Henle reabsorbs water and that’s pretty much it. The thick ascending loop of Henle or TAL, on the other hand, reabsorbs potassium, chloride and sodium. Now, in order to reabsorb sodium, potassium and chloride, there’s a Na/K/Cl cotransporter or NKCC2, that’s only found in the kidney and its role is to snatch these ions from the urine and reabsorb them. Apart from this, TAL can also reabsorb calcium and most of the magnesium but doesn’t reabsorb water.  

Now, the distal convoluted tubule or DCT reabsorbs sodium and chloride, through a sodium-chloride cotransporter, as well as calcium and some magnesium.  Again, it]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_cancer:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YFmS2ihrSxa4bnqS7k1CY6TMT3SEyq4T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breast cancer: Pathology review]]></video:title><video:description><![CDATA[64-year-old Cassie comes to the office because of a new breast mass that she found on her monthly self-examination. 

A mammogram shows microcalcification clusters so an excisional biopsy is performed. 

Pathology shows high-grade cells with central necrosis in the lumen and dystrophic calcification in the center of the ducts without invasion of the basement membrane. 

Later that day, a 58-year-old named Linda comes to the physician&amp;#39;s office with eczematous dermatitis of the left nipple and areolar area for the past 24 months. 

Her history reveals that the lesion has been treated unsuccessfully with topical steroids and has progressively distorted the nipple, resulting in nipple inversion. 

Physical examination reveals scaly, crusted, and deformed left nipple with multiple plaques overlying the surrounding areola. 

At first glance, you’d think Cassie and Linda have nothing in common, but the fact is, they have different forms of breast cancer! 

Breast cancer is the most common malignancy in women and it’s typically seen in postmenopausal women, over 50 years of age. 

Most breast cancers are adenocarcinomas and they typically arise from the terminal duct lobular units. 

Breast cancer can present as a palpable hard mass, most commonly located in the upper outer quadrant of the breast. 

Now, some breast cancers can be associated with amplification and overexpression of genes for estrogen receptors, progesterone receptors, and HER2/neu receptors. 

For your exam, you have to remember that these receptors are important therapeutic and prognostic factors of breast cancer. 

In other words, breast cancers that are associated with overexpression of estrogen and progesterone receptors are more susceptible to anti-estrogen medications, such as tamoxifen. 

On the other hand, HER2/neu receptors, also known as erbB2 receptors, are coded by the ERB-B2 gene. 

These receptors are transmembrane glycoproteins with tyrosine kinase activity that plays an im]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuromuscular_junction_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_pYIftt7SxO7VTgdIqYZ3nItQROvfYV0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuromuscular junction disorders: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you see Kira, a 23-year-old female who presents with a series of recurrent symptoms that get worse as the day progresses. These include slurring of speech, difficulty swallowing, and double vision. She also mentions that her head feels heavy and is hard to hold up. She also complained that her arms are so weak she can’t even brush her hair. Additionally, she reports severe fatigue and shortness of breath. On examination, sensation and reflexes are normal. Next, you see a 62-year-old man named Jonathan, who presents with a history of leg muscle weakness that prevents him from doing simple things like climbing stairs or standing up, which gets better the more he uses his legs. He also reports shortness of breath, fatigue, dry mouth, impotence, and unintentional weight loss. Examination reveals a severely underweight man with dilated pupils. Reflexes are initially absent, although these are obtainable after a brief period of exercise. Blood tests were obtained, detecting anti-acetylcholine receptor antibodies in Kira and anti-voltage-gated calcium channels antibodies in Jonathan. 

Now, both seem to have some type of neuromuscular junction disease. But first, a bit of physiology. In normal neuromuscular function, a nerve impulse is carried down the axon from the spinal cord, to the nerve endings, in the neuromuscular junction, where the impulse is transferred to the muscle cell. Here, the nerve impulse leads to the opening of voltage-gated calcium channels, causing an influx of calcium ions into the nerve terminal, which triggers synaptic vesicle fusion with plasma membrane. These synaptic vesicles contain a neurotransmitter called acetylcholine, which is released into the synaptic cleft. The neurotransmitter then binds to nicotinic acetylcholine receptors on muscle cell membranes and activates a chain reaction in the muscles that ultimately results in their contraction.

Ok, so there are two commonly tested diseases affecting the neu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrinsic_hemolytic_normocytic_anemia:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iA--m0KoTCKJqrxZGFW0ChiVSFKO5nuu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intrinsic hemolytic normocytic anemia: Pathology review]]></video:title><video:description><![CDATA[On the hematology ward, there’s a mother with her daughter, Kyra, a five -year old that has developed jaundice and complains of easy fatigability. She is an adopted child with an unknown family history. Clinical examination reveals a palpable spleen. Next to her, there’s a 35-year-old person of African descent, called Darnell, who started trimethoprim-sulfamethoxazole for treatment of acute prostatitis a few weeks ago. Recently, he developed jaundice, dark urine, back pain and fatigue. There’s also a father who brought Billy, his 13-year-old son, to the emergency department because of a painful and prolonged erection. CBC is ordered for all of them and it shows low hemoglobin with normal MCV and reticulocyte count index over 2%. They also have increased LDH. Now, Kyra also has an increased MCHC and spherocytes on peripheral blood smear, while Billy has sickled cells. 

Although their symptoms are very different, they all suffer from anemia, which is defined as lower than average levels of hemoglobin, typically below 13.5 g/dL in adult men and below 12.0 g/dL in adult women.This level varies based on the age for children. Now, anemias can be broadly grouped into 3 categories based on mean corpuscular volume, or MCV, which reflects the volume of a red blood cell. So microcytic anemia is where the MCV is lower than 80 fL, normocytic, with an MCV between 80 and 100 fL, and macrocytic, with an MCV larger than 100 fL. Normocytic anemias can be further classified as hemolytic when there’s increased destruction of RBCs, or hemolysis, and non-hemolytic when there’s decreased production of RBCs from the bone marrow. When there’s hemolysis, the bone marrow revs up and starts pumping out immature RBCs called reticulocytes, but when there’s a bone marrow problem reticulocyte count is low. So for your exams, it’s important to know that in hemolytic anemias there’s an increased reticulocyte production index of over 2%, while in non-hemolytic anemias it’s lower than 2%. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombosis_syndromes_(hypercoagulability):_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x9bTmgtkRkm9xnNchLB33aQ6T8mftZhA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombosis syndromes (hypercoagulability): Pathology review]]></video:title><video:description><![CDATA[At the emergency department, a 30 year old Caucasian female named Celia came in with pain and swelling in her right calf. She has a history of pregnancy loss and her mother has a history of recurrent episodes of venous thromboembolism. Her medical history is otherwise unremarkable. Coagulation studies show normal PTT. Next to Celia, there’s a 60 year old male called Nicholas who developed a painful lesion on his arm after starting anticoagulation therapy with warfarin. Now, there’s also a 26 year old African American female named Mary who has recurrent pregnancy losses. She was diagnosed with systemic lupus erythematosus about a year ago. She has no family history of thrombophilic disorder. 

All of them suffer from thrombophilic disorders, or thrombosis syndromes, which are inherited or acquired diseases that predispose an individual to clot formation. Inherited disorders include factor V Leiden, prothrombin gene mutation, protein C and S deficiency, and antithrombin III deficiency, while the most important acquired disorder is antiphospholipid antibody syndrome. But before going into the individual thrombophilic disorders, let’s go through the normal coagulation system. The coagulation pathway is divided into an extrinsic and an intrinsic pathway, which join into a common pathway that ultimately result in the formation of fibrin clots. The extrinsic pathway starts when trauma damages a blood vessel, and exposes the cells under the endothelial layer, which have tissue factor in their membrane. Activated factor VII binds to tissue factor, forming a complex that then binds to and activates factor X. The intrinsic pathway starts when a circulating factor XII, activates factor XI, which then activates factor IX. Finally, factor IX forms a complex with factor VIII, and this complex binds to and activates factor X. In the common pathway. Activated factor X activates factor V, which converts prothrombin, or factor II, into thrombin. Thrombin then converts f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testicular_tumors:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6uJw_SqASxqqX68p7smazP4KQBWtD1Wt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Testicular tumors: Pathology review]]></video:title><video:description><![CDATA[25-year-old Kyle comes to the office after palpating a lump on his left testicle while showering this morning. On physical examination, there is a nontender, round, firm, rubbery mass in the left testicle that does not transilluminate with light. Scrotal ultrasound shows a 1.4-cm solid mass with no cystic components. Laboratory tests reveal normal serum human chorionic gonadotropin or hCG level, and normal α-fetoprotein or AFP level. Later that day, 32-year-old William comes to the physician&amp;#39;s office complaining of heat intolerance, excessive sweating, palpitations, frequent bowel movements and recent weight loss despite increased appetite. His past medical history is insignificant. On examination, the thyroid gland is normal with no signs of goiter or nodules. However, a hard nodule is palpated in the right testicle which does not transilluminate with light and appears solid on scrotal ultrasound. Laboratory studies show increased serum T4 and T3 levels as well as extremely elevated hCG levels.

Based on the initial presentation, Kyle and William both have some form of testicular mass. In fact, testicular tumors are the most common solid malignancy in males between 20 and 35 years old. 

Okay, now, for your exams, it’s important to know that the main risk factors for developing testicular cancer, especially the germ cell variety, include cryptorchidism, which is when the testicles fail to descend to the scrotum or get stuck in the inguinal canal, as well as Klinefelter syndrome, where biological male individuals inherit more than one X chromosome leading to small, undeveloped testicles. 

For symptoms, a testicular tumor most often comes up as a small, firm lump that is typically painless, but can sometimes cause a sharp or dull pain in the testicles and lower abdomen. In more severe cases, symptoms may arise from a malignant tumor metastasizing to other organs. This is most commonly hematogenous to the lungs, leading to dyspnea or hemoptysis, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bone_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vM4zUp1nQee0Vur68JRpA16CRrekHFM7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bone disorders: Pathology review]]></video:title><video:description><![CDATA[While on your rounds, you see two individuals. First up is Jenna, a 70-year-old female who presents with left hip pain after falling while getting out of bed. She sustained a fracture of the right hip, and preoperative chest x-ray reveals that she had pre-existing asymptomatic vertebral fractures before her fall. She denies any other symptoms and physical examination was otherwise normal. Then you see Gerald,  a 46-year-old male who presents with a mild but noticeable limp and hip pain on the right side after falling from a chair. Examination is unremarkable. In Jenna’s case, a DEXA scan was performed, revealing a T -2.8 score. In Gerald’s case, radiographs of the hip showed a right hip fracture and abnormally dense hip bones.

Both seem to have some type of bone disorder. But first, a bit of physiology. Bones have a hard-external layer of cortical bone and a softer internal layer of spongy bone composed of trabeculae. The trabeculae are like a framework of beams that give structural support to the spongy bone. Now, these are replaced every few years in a process called bone remodeling. The process has two steps: bone resorption, which is when osteoclasts break down bone by releasing hydrogen and collagenases, and bone formation, which is when osteoblasts form new bone by secreting osteoid seam. Osteoid seam is mainly made up of collagen and it acts like a scaffold upon which hydroxyapatite, a combination of calcium and phosphate, deposits. Bone formation requires an alkaline environment, which is why bone cells also produce alkaline phosphatase, an important marker of bone cell activity. 
At a cellular level, remodeling begins when osteoblasts release receptor activator of nuclear factor κβ ligand, or RANKL for short, which binds to RANK receptors on the surface of osteoclast, activating them to begin bone matrix demineralization. Once there’s been sufficient bone demineralization, osteoblasts secrete osteoprotegerin, which inactivates RANKL. This ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gallbladder_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q3jluZW1SQqA223zbdMAuYszRHG9KGoy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gallbladder disorders: Pathology review]]></video:title><video:description><![CDATA[In the emergency department, there is a 45 year old obese female from Spain, named Valencia, who came in with right upper quadrant and epigastric pain that began suddenly a couple of hours ago, right after her lunch. The pain is steady in nature, and radiates to the right shoulder. Her temperature is 38 °C or 100.4 °F and on physical examination, there is pain with deep palpation of the right upper quadrant. At the same time, at the gastroenterology clinic, a 64- year old Caucasian female, named Ashley, is incidentally found to have diffuse gallbladder calcification on an abdominal x- ray. She is totally asymptomatic except for some episodes of vague abdominal pain after meals. Both Valencia and Ashley have gallbladder diseases. 

The gallbladder’s job is to basically store and concentrate bile. When you eat high fat foods, they make their way to the small intestine, and stimulate the enteroendocrine cells to secrete cholecystokinin into the bloodstream. Cholecystokinin, in turn, makes its way to the gallbladder and tells it to squeeze bile out into the small intestine. Now, bile’s a fat emulsifier, essentially helping to break fats or lipids into small “micelles”, making them easier to absorb. Remember that bile is mostly made up of bile salts and acids, cholesterol, phospholipids, proteins, bilirubin and small amounts of various other compounds, like water, electrolytes, and bicarbonate. 

Now, there are multiple types of gallstones, and the process of gallstones formation is called cholelithiasis. So, let’s start with cholesterol gallstones. Remember for your exams that these are the most common type, accounting for around 75–90% of cases of all gallstones. Generally speaking, cholesterol stones have a characteristic yellow color and are radiolucent, meaning that they can’t be seen on X-ray. This is very high yield and is often used as a clue on your exams!  However remember that these stones can be seen on X-ray in rare cases when they bind with e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meniscus_tear</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/evI-aoTyTpSBkd_2OoStm9dXTBatrSZW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meniscus tear]]></video:title><video:description><![CDATA[The menisci are crescent-shaped fibrocartilage cushions found in the knee joint. 

Normally, there’s the medial and lateral menisci between the femur and the tibia. 

So, a meniscus tear, more commonly known as torn knee cartilage, is when one of the menisci of the knee is torn. 

This usually occurs due to trauma during contact sports.

The knee is a complex joint, actually it’s a combination of three joints. 

These are the femoropatellar joint, between the femur and patella, and the two tibiofemoral joints which are formed by the bony prominences, also called the condyles of the tibia and the femur. 

Between the femoral and tibial condyles, there’re the medial and lateral menisci. 

The menisci act to absorb compressive force, which can reach up to three times the body weight while walking! 

In addition, the menisci have a cup-shaped surface which provides a deeper place for the condyles to fit in improving joint’s stability.

Next, the knee joint is supported by a number of ligaments. 

So, within the joint space, there&amp;#39;s the anterior cruciate ligament, or ACL, which runs from the anterior middle edge of the tibia to the lateral condyle of the femur, and the posterior cruciate ligament, or PCL, that runs from the middle posterior edge of the tibia to the medial condyle of the femur. 

Now, outside the joint space, we’ve got one collateral ligament between the femur and the tibia on each side of the joint, which are the lateral collateral ligament, or LCL, and the medial collateral ligament, or MCL. 

The MCL is firmly attached to the medial meniscus, which makes it less mobile compared to the lateral meniscus.

A meniscus tear can occur when the meniscus is violently compressed, called an acute tear, which usually occurs in young athletes. 

Acute tears typically occur when the knee is bent and at the same time excessively twisted, like when you’re playing basketball and then you suddenly change direction, trying to crossover another player.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cervical_cancer:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0yUrlf5JQMm3XDPlV5VleILSRGWtD2Nq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cervical cancer: Pathology review]]></video:title><video:description><![CDATA[At the gynecology clinic, 28-year-old Luciana comes in because she was told that her Pap smear showed abnormal cervical cells. She is totally asymptomatic and her previous pap smear from 3 years ago was normal. 

Next, there is 36-year-old Cassie who presents to the office after noticing vaginal bleeding after sexual intercourse. There’s no associated pain with urinating, bloody urine, constipation or pelvic pain. She admits she has never done a pap test in her life. Pelvic exam shows a friable mass growing on the cervix.

In further history, both have been sexually active with multiple sexual partners and use oral contraceptive pills as their method of contraception. Both Luciana and Cassie have different types of cervical pathologies.

So, first let’s talk physiology real quick!. The cervical canal can be divided into two sections. The endocervix is closer to the uterus, and is lined by columnar epithelial cells. The ectocervix is continuous with the vagina and it’s lined by mature squamous epithelial cells. Where the squamous epithelium of the ectocervix and the columnar epithelium of the endocervix meet, there’s a line called the squamocolumnar junction. For your exams, it’s necessary to remember that, right where the two types of cells meet, there’s the transformation zone, which is where cells multiply and transform into immature squamous epithelium through a process called metaplasia.

Now, metaplasia is when a stimulus, usually a stressor, causes the stem cells in a region to differentiate into another type of cell that replaces the typical cell type in that region. For example with Barrett’s esophagus, chronic stomach acid irritation causes the normal stratified squamous cells that line the esophagus to get replaced by simple columnar cells. This is different from dysplasia where fully differentiated cells turn into immature cells that have varying shape and nuclear morphology. Metaplasia is usually reversible if the stressor is removed while only]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colorectal_polyps_and_cancer:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k77MyEH9QCCkAOPFNiI897B5SdCITFpW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colorectal polyps and cancer: Pathology review]]></video:title><video:description><![CDATA[At the gastroenterology clinic, there is a 63-year-old Caucasian male, named Neil, who&amp;#39;s complaining about progressive fatigue and weight loss in the last 6 months. Laboratory findings reveal positive fecal occult blood test and iron-deficiency anemia. At the same time, an 18-year-old Caucasian male, named Brendon came in for a colonoscopy screening. He was concerned after learning that both his grandfather and uncle were diagnosed with colon cancer in their early thirties. His doctor detected more than one hundred polyps on colonoscopy.

Now, both people have some form of colorectal polyps or cancer. But first let’s start with colorectal polyps, which are overgrowths of epithelial cells in the colon or rectum. They are subdivided into non-neoplastic polyps, such as hamartomatous polyps, hyperplastic polyps, inflammatory pseudopolyps, mucosal, and submucosal polyps; and neoplastic polyps, which include adenomatous and serrated polyps. 

Hamartomatous polyps are solitary, disorganized masses that contain normal tissue found at the site of the polyp. These polyps can occur sporadically, or in genetically inherited conditions, such as juvenile polyposis syndrome or Peutz-Jeghers syndrome; and they have mild malignant potential. 

Next, hyperplastic polyps, are the most common polyps and they are small and typically located in the rectosigmoid region. Usually, these polyps are benign lesions, but in rare cases, they can evolve into serrated polyps, which have malignant potential. 

Inflammatory pseudopolyps are multiple benign pseudopolyps that occur during regenerative and healing phases in chronic inflammation, and they are most commonly seen in inflammatory bowel disease. 

Mucosal polyps, which are clinically insignificant, are usually small, less than 5mm, and they look similar to surrounding normal mucosa. On the flip side, submucosal polyps can include lipomas, leiomyomas, fibromas, or other lesions. 

Now let’s switch focus to neoplastic ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_work</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bClWtnaYTUG1zoUJB5iZX5G2RWmA8tix/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac work]]></video:title><video:description><![CDATA[Cardiac work, also known as stroke work, is similar to the concept of work in physics. In physics, work is defined as force times distance. 

Stroke work can be thought of as the work performed by the left ventricle to eject a volume of blood, defined as stroke volume multiplied by mean aortic pressure.

And here, stroke volume corresponds to distance, whereas mean aortic pressure corresponds to force. Stroke work is best represented by a pressure-volume loop. 

Pressure- volume loops are graphs, where the pressure inside the left ventricle is on the y axis and the volume of the left ventricle is on the x axis. 

Each loop represents changes in ventricular pressure and volume over the course of one cardiac cycle, or one heartbeat, which includes both ventricular systole, or contraction, and diastole, or relaxation. 

The lower right hand corner is the end-diastolic point, and it’s the point in the cardiac cycle when diastole is over. Αt this point, the mitral valve between the left atrium and the left ventricle, closes, leaving the left ventricle filled with the maximum volume of blood, called the end-diastolic volume. 

And then, systole begins, which is when the left ventricle contracts to push that blood into the aorta. Ventricular contraction makes the pressure shoot up, but for a brief period of time, both the mitral and aortic valves are closed, so left ventricular volume doesn’t change. 

This phase is isovolumetric contraction, but it doesn’t last long, because eventually the pressure inside the left ventricle exceeds aortic pressure, making the aortic valve pop open, and that starts the ejection phase. 

During the ejection phase, blood from the left ventricle goes into the aorta, decreasing left ventricular volume. The left ventricle continues to contract, so ventricular pressure rises further, but then falls slightly. 

Finally, when aortic pressure exceeds left ventricular pressure, the aortic valve closes, marking the end of systole, or the en]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Uterine_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s_NXOxcxRcaWKDBKwbBgeXSvSLKnCLBW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Uterine disorders: Pathology review]]></video:title><video:description><![CDATA[29-year-old Carmen presents to the physician’s office complaining of severe lower abdominal pain during her menstrual periods as well as pain during intercourse. 

She has been trying unsuccessfully to get pregnant for the first time for the past 2 years. 

Pelvic examination shows a normal sized uterus. 

Later that day, 44-year-old Susanna comes to her physician reporting heavy menstrual periods that last about 10 days. 

This has been occurring for the past 6 months and is accompanied with a feeling of “fullness” in the lower abdomen as well as fatigue. 

On further history, she has never been pregnant. 

Physical examination shows an enlarged uterus with multiple round masses. 

Laboratory studies reveal iron deficiency anemia.

Based on the initial presentation, Carmen and Susanna both have some form of uterine disorder.  

Let’s first review physiology real quick. 

The uterus consists of 3 layers, an outer layer called the perimetrium or the serosa, a middle smooth muscle layer called the myometrium, and the innermost layer, the endometrium. 

The endometrium has two layers, an inner functional layer made up mainly of glands and supporting connective tissue, called stroma, and an outer thin basal layer  which regenerates the overlying functional layer after each menstrual cycle. 

Okay, now, the first uterine disorder is endometritis or inflammation of the endometrium. 

This is usually caused by normal bacterial flora of the lower genital tract, meaning the cervix, vagina or external genital organs, that travel upwards into the endometrium.  

A high yield risk factor to remember is the retention of products of conception,  like parts of the placental or fetal tissues, following delivery or abortion. 

Another risk factor is the presence of a foreign body, like an intrauterine contraceptive device.  

Both can provide a good environment for bacteria to grow and cause an infection in the uterus. 

Less commonly, endometritis can be caused by outside]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fluorescence_in_situ_hybridization</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XfCh7QriQyq7FjTbB3xT5mtsR7qofuoa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fluorescence in situ hybridization]]></video:title><video:description><![CDATA[Fluorescence in situ hybridization is a cytogenetic technique that uses fluorescent DNA segments, called “probes”, to bind to a known DNA sequence. 

It’s used to localize particular DNA sequences, or lack thereof, on a chromosome in order to detect chromosomal abnormalities, or mutations; like deletion, duplication, or translocation of a DNA segment; which may be the underlying cause of a genetic disease.

Ok, now, our DNA is like a library, found in the nucleus of our cells, that carries our genetic information. 

On the molecular level, DNA is made up of two strands of nucleotides that are coiled around one another to form a double helix.  

There are four different nucleotides: adenine, or A, thymine, or T, cytosine, or C and guanine, or G. A binds with T, and C binds with G; nucleotides on opposite strands form hydrogen bonds to keep the two strands together. 

To fit inside the nucleus, DNA wraps around proteins which further condense to form chromatin fibers. 

These chromatin fibers are loosely or tightly packed depending on the phase of the cell’s cycle. 

The cell cycle represents a series of events that somatic cells, that is, all cells besides the gametes, go through from the moment they’re formed until the moment they divide into two identical daughter cells. 

And it has two phases: interphase, or cell growth in preparation for division, and mitosis, or cellular division. 

During early interphase, chromatin fibers float in a loose state inside the nucleus, like DNA-rich noodles. 

Each of the chromatin noodles represents a single DNA molecule. 

Now, during later interphase, when the cell prepares for mitosis, or cellular division, the DNA noodles replicate and chromatin condenses to form chromosomes. 

Remember that human somatic cells have 23 pairs of chromosomes, so 46 chromosomes in total. 

And right before mitosis, each chromosome carries two identical DNA molecules, called chromatids. 

Chromatids join together in the center in a regi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_gland_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9sSgCUQySWWk5qu5Pn_GT4S4S5WOEYK6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenal gland histology]]></video:title><video:description><![CDATA[The adrenal glands are a pair of endocrine glands that are located just above or superior to the kidneys and are also in the retroperitoneal space of the abdominal cavity. 

The left gland has a semilunar shape and the right gland is flattened and more triangular in appearance. 

The adrenal glands are covered by a capsule made of thick connective tissue. 

The parenchymal tissue has two main regions, the adrenal cortex and the adrenal medulla. 

The cortex is the large outer region of the adrenal gland. 

The cortex can be further divided into three zones that each secrete a different class of steroid hormones. 

Starting with the most superficial zone: the zona glomerulosa secretes mineralocorticoids, the zona fasciculata secretes primarily glucocorticoids, and the zona reticularis secretes primarily gonadocorticoids, or sex hormones. 

The adrenal medulla is the region that’s most centrally located and visibly distinct from the cortex. 

The medulla is responsible for secreting the catecholamines: epinephrine and norepinephrine. 

If we zoom in further, we can see some of the blood vessels of the adrenal gland. 

Just outside of the capsule, there are small afferent blood vessels that are branches of the suprarenal arteries that supply blood to the adrenal gland. 

And within the medulla, there are the large medullary veins that drain blood into the suprarenal veins. 

Now, let’s take a closer look at the outermost layer of the adrenal cortex, the zona glomerulosa. 

This layer is just beneath the capsule and comprises about 15 percent of the cortex. 

The secretory cells are arranged in ovoid or glomerulus-like clusters that are separated by fibrous trabeculae that extends from the capsule. 

The individual cells are either columnar or pyramidal with round nuclei, and a lipid-filled cytoplasm that gives the cytoplasm its pale “foamy” appearance. 

These are the cells that are responsible for secreting aldosterone into nearby capillaries that can be fou]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gout_and_pseudogout:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UILrKgzoQ9WBoQXmlOpNObeeSYqG88ps/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gout and pseudogout: Pathology review]]></video:title><video:description><![CDATA[On your rounds, you see Ashvir, a 50-year-old man who complains of severe pain and swelling in his first toe on the right foot. 

This is the first time he has experienced this and the symptoms  developed in the last 5 hours. 

He described the pain as very severe and that it’s causing him to limp. 

On examination, he is obese and the toe is swollen, red, warm, and painful to the touch. 

Then you see Bianca, a 22-year old who also came in with a pain and swelling of the left big toe and left knee, which developed yesterday. 

However, unlike Ashvir, she is not overweight and has a history of hemochromatosis. 

Synovial fluid analysis was performed in both, detecting negatively bi-refringent crystals in Ashvir, and weakly positively birefringent crystals in Bianca.

Now, both seem to have some type of crystalline arthropathy. 

But let’s talk about physiology first. 

Purines, together with pyrimidines, are key components of nucleic acids like DNA and RNA. 

Purines are first broken down into adenosine monophosphate or AMP and guanosine monophosphate or GMP. 

AMP is converted to inosine via two different mechanisms; either by removing an amino group to form inosine monophosphate or IMP, which is quickly converted to inosine, or by removing a phosphate group to form adenosine, which is also converted to inosine. 

Inosine is then converted to hypoxanthine, and hypoxanthine to xanthine, which is finally metabolized to uric acid. 

These last two steps are catalyzed by the enzyme xanthine oxidase. 

GMP is converted to guanosine, which is then converted to guanine. 

Guanine is deaminated to form xanthine, which is oxidized by xanthine oxidase to form the final product, uric acid. 

Now, under normal physiologic conditions, uric acid circulates in plasma and synovial fluid as urate an-ions. 

However, human tissues have a limited ability to metabolize urate; thus, it is quickly eliminated by the kidney and the gut to maintain urate homeostasis. 

Another wa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neurocutaneous_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xdfJ9iE5SVm3tuAdrS3ala4OTRymxRXJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neurocutaneous disorders: Pathology review]]></video:title><video:description><![CDATA[At the family medicine clinic, a 17 year old male named Heath came in because of lower back pain. Clinical examination reveals lots of small growths on the face, light flat patches throughout his body, and a darker raised patch on his forehead. Heath was adopted early in his life and his family history is unknown. Abdominal ultrasound reveals an angiomyolipoma of the left kidney. Next to Heath, there’s an 8 year old child named Sylvia. Sylvia complains of difficulty seeing what the teacher is writing in school. She also has a purple mark that covers the forehead and her right upper eyelid. Eye examination reveals increased intraocular pressure in the right eye. Her medical history includes an episode of seizure when she was 5 years old. A brain MRI is ordered and reveals brain atrophy. Finally, there’s a 45 year old male named Austin who came in because of a ringing sound in his ears and a gradual loss of hearing. Brain MRI reveals bilateral masses on the cerebellopontine angle. 

Okay, so all of them have a neurocutaneous syndrome. Neurocutaneous syndromes primarily affect the nervous system and the skin. They include Sturge-Weber syndrome, tuberous sclerosis, neurofibromatosis type I and II, and Von Hippel-Lindau disease. For the exams remember that Sturge-Weber occurs due to sporadic mutations, while tuberous sclerosis, neurofibromatosis type I and II, and Von Hippel-Lindau disease are autosomal dominant conditions. 

Alright, now let’s take a closer look at these different disorders, starting with Sturge-Weber syndrome, which is also known as encephalotrigeminal angiomatosis. During week 6 of development, as the cephalic portion of the neural tube grows, a network of tiny blood vessels called a vascular plexus develops. There’s a gene called the GNAQ gene which codes for a guanine nucleotide-binding protein that is involved in the development of that plexus. Normally, around week 9, the GNAQ gene stops getting expressed, leading to the regression of th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Central_nervous_system_infections:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ij3WPfImTqW5iaLunGqUCY85QxyJ8aNZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Central nervous system infections: Pathology review]]></video:title><video:description><![CDATA[At the emergency department, 17-year old Mike is brought in by his parents. He has a fever, headache, and photophobia. On clinical examination, Mike has neck stiffness and Kernig and Brudzinski signs are positive. Lumbar puncture reveals a predominantly neutrophilic pleocytosis, elevated protein, and low glucose. Next to Mike is 27-year old Helen, who came in with a fever, headache, and confusion for the past 72 hours. Kernig and Brudzinski signs are negative. Head CT reveals patchy temporal lobe enhancements. Finally, there’s 60-year Lucia, who is brought by her family because of a seizure. She also complains of headache and has a mild fever. There’s no neck stiffness and Kernig and Brudzinski signs are negative. Two weeks ago Lucia had an episode of otitis media for which she was treated with antipyretics and analgesics. She has no history of epilepsy. Head CT reveals a single ring-enhanced lesion in the right temporal lobe. 

Okay, so all 3 people suffer from a central nervous system infection. CNS infections include meningitis, which is when pathogens infect the meningeal layers; encephalitis, when the pathogens infect the brain parenchyma; meningoencephalitis, where the infection starts in the meninges and then spreads into the brain parenchyma; and abscess which is when pathogens wall themselves off in the brain. 

Okay, so let’s take a closer look at the various forms of CNS infections, starting with meningitis. Meningitis can be caused by any pathogen that infects the meninges. When it’s caused by viruses, mycobacteria, fungi, or parasites, it’s called aseptic meningitis, because routine bacterial cultures of the cerebrospinal fluid are negative. The most common cause of aseptic meningitis is a group of viruses called enteroviruses, like echovirus and coxsackie virus. Despite viral meningitis being much more common, acute bacterial meningitis is more life-threatening.  The bacteria that is most likely to be responsible will depend on the individual]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronary_artery_disease:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Yy_LVQ0DTQuclJjP1mD_BThvSJyqUILq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronary artery disease: Pathology review]]></video:title><video:description><![CDATA[In an urban emergency department, 3 people came in for chest pain. The first is Anish, a 54 year old man with a known history of hypertension, hyperlipidemia, and 25-pack year smoking. He’s complaining of shortness of breath, and squeezing, retrosternal chest pain that radiates to his neck, jaw and left arm.  He’s been having these episodes but they only come after riding his bicycle for at least 20 minutes, and is relieved once he rests. Investigations reveal a normal ECG and normal troponin levels. Next, is Erica, a 66-year old woman with a history of diabetes mellitus who complains of sudden-onset shortness of breath, fatigue and dizziness, but no chest pain. An ECG reveals ST-segment depression, and troponin levels are elevated. Finally, There’s Tyrion, a 45-year old man, with a known history of hypertension, diabetes, and hyperlipidemia. He complains of epigastric abdominal pain at rest, shortness of breath, sweating and lightheadedness for the past 30 minutes. His blood pressure is 80/60, and his heart is 45 beats per minute. An ECG reveals ST-segment elevation in leads II, III and aVF. 

All three have coronary artery disease which is defined as an imbalance between myocardial oxygen demand and supply from the coronary arteries. Reduced oxygen supply to the heart is defined myocardial ischemia, which results in a severely reduced ability of the heart muscle ability to contract. If this is prolonged, it can go on to cause myocardial infarction, otherwise known as heart attack, which refers to death of heart muscle. Now, coronary artery disease is usually caused by atherosclerosis of the coronary arteries. Risk factors for atherosclerosis can be divided into non-modifiable ones, which include age, with men greater than 45 years and women greater than 55 years being at risk, and family history of coronary artery disease, and modifiable ones, like lipid abnormalities including elevated LDL or  low HDL levels, as well as hypertension, diabetes melli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Seizures:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-JszFihcSZeOIb_iGkapie1mS5WS6KZb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Seizures: Pathology review]]></video:title><video:description><![CDATA[On the neurology ward, a 7-year old male, called Stefan, is brought by his mother. His mother is worried because he has several episodes every day where he loses consciousness for a few seconds. His teacher also complains that she often catches him daydreaming during the lesson. Next to Stefan, there’s a 17-year old male, called Jacob, who seems sluggish and tired. His friends brought him because he suddenly started “shaking and jerking” and he lost consciousness for about two minutes. His medical history is otherwise insignificant. Now, there’s also an 11-year old female, called Megan, who also seems lethargic. Her father is very upset because he witnessed an episode of twitching of her left foot that lasted a few minutes. Megan was unconscious and has no memory of the event. Finally, there’s a 19-year old female, called Joanna, that has had repetitive episodes of sudden and rapid jerking movements with loss of consciousness for the past few months. They usually occur when she wakes up in the morning and especially during periods of sleep deprivation. 

Okay, so all of them had a seizure episode. A seizure is a paroxysmal motor, sensory or autonomic event that occurs due to abnormal, excessive and synchronous electrical discharges from neurons in the brain. Seizures usually last less than 5 minutes. If it lasts more than 5 minutes, it’s called status epilepticus. Epilepsy is a chronic disease of the brain that predisposes an individual to having recurrent unprovoked seizures; that is seizures without a clear triggering cause. Epilepsy is typically diagnosed when an individual has two or more unprovoked seizures separated by at least twenty-four hours. 

Okay, now seizures are broadly classified into two types, generalized and focal seizures. Generalized seizures arise from both cerebral hemispheres at the same time, while focal seizures arise from specific areas in one cerebral hemisphere. However, focal seizures can spread to both cerebral hemispheres, c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Demyelinating_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/By-pHOz0TGeIFz8AEnk5lHnqQXO9BUKC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Demyelinating disorders: Pathology review]]></video:title><video:description><![CDATA[At the neurology department, a 23 year old male, named Charles, is brought by his parents because of weakness in his feet that started 2 days ago and worsened over time. During clinical examination, the deep tendon reflexes in his lower extremities are decreased but sensation is intact. Past medical history reveals a case of gastroenteritis about three weeks ago. Next to Charles, there’s a 26 year old female, named Maria, that came in because of an episode of blurring in her left eye and pain during eye movement. She had a similar episode a few months ago that lasted about a week and resolved without any treatment. She also describes an episode where she felt an electric shock-like sensation through her body after having a hot shower.  

Alright, so both of them have a demyelinating disorder. This occurs when myelin, the protective sheath that surrounds the axons of neurons, is destroyed. Now, myelin is produced by oligodendrocytes in the central nervous system, or CNS, which includes the brain and the spinal cord, while in the peripheral nervous system, or PNS, which includes all of the neurons that extend beyond the brain and the spinal cord, it is produced by Schwann cells. Myelin helps the neurons to quickly send electrical impulses. As a result, the destruction of myelin, or demyelination, makes communication between neurons difficult, ultimately leading to all sorts of sensory, motor, and cognitive problems. Okay, now demyelinating disorders can be classified into two groups. The first one includes disorders that affect the myelin in the CNS, such as multiple sclerosis, acute disseminated encephalomyelitis, progressive multifocal encephalopathy and central pontine myelinolysis. The second group includes diseases that affect the myelin in the PNS, like Guillain-Barre syndrome and Charcot-Marie-Tooth. Now, other less high yield demyelinating disorders include Krabbe disease, metachromatic leukodystrophy and adrenoleukodystrophy. 

Alrigh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nasal,_oral_and_pharyngeal_diseases:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pzR0qN2VSIuOtWt1f5ti-T59QSCZK9zW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nasal, oral and pharyngeal diseases: Pathology review]]></video:title><video:description><![CDATA[While in the ENT Clinic, two people present with trouble breathing through the nose and  have frequent nose bleeds. One of them is a 25 year old individual named Andrew, and the other one is an 18 year old individual named Sarah. Andrew says the problems appeared gradually and feels like something is stuck in the nose. Andrew also has a history of aspirin allergy. On examination, everything seems normal, except for a decrease in the sense of smell. Sarah, on the other hand, has noted these problems ever since childhood. Sarah also mentioned that the symptoms get worse during the spring or proximity to flowers. On examination, presentation is nasal congestion and red, itchy, swollen eyes with frequent bouts of sneezing. Blood tests were normal in both individuals.

Now, from what we can gather, both have some type of nasal, oral, or pharyngeal disease. But first, a bit of anatomy. The nasopharynx is an open chamber located below the base of the skull and behind the nasal cavity. The nasopharynx contains structures like the adenoids, also known as the pharyngeal tonsils; the Waldeyer&amp;#39;s tonsillar ring, which is a ring-like arrangement of lymphoid tissue in both the nasopharynx and oropharynx; the Rosenmüller fossa, which is part of the lateral recess of the nasopharynx and a common site of nasopharyngeal cancers; and the eustachian tube orifices. Now, the nasopharynx connects the nasal cavity and oropharynx, which is posterior to the oral cavity that contains structures like the salivary glands, soft and hard palate, tongue, and tonsils. 

Ok, so we can begin with nasal polyps. Now, remember that a nasal polyp is a clump of epithelial cells that undergo hyperplasia and form a growth of tissue along the lining of the nasal cavity. This is most often caused by seasonal allergies, recurrent infections, frequent asthma exacerbations, chronic sinusitis, or acetyl-salicylic acid and nonsteroidal anti-inflammatory drug sensitivity. There are some genetic ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complications_during_pregnancy:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Et8kR8vMTCuz2O3x0RUOwTwJScuv2SUq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complications during pregnancy: Pathology review]]></video:title><video:description><![CDATA[26 year-old Effie is brought to the emergency department with severe lower abdominal pain and bloody vaginal discharge that began a few hours ago. Her last menstrual period was 7 weeks ago. She has been sexually active with multiple partners and uses condoms on occasion. Her past medical history is significant for pelvic inflammatory disease. On examination, her blood pressure is 80/40 mmHg and her pulse is 130 beats per minute. She is pale and her extremities are cold and clammy. Next to her, there’s also 37-year-old Kate who came in noting an abrupt onset of abdominal pain and continuous vaginal bleeding. She is going through week 28 of her fourth pregnancy and was involved in a car crash a couple of hours ago, but did not immediately seek medical care. On presentation, fetal heart rate and movement are significantly diminished. Laboratory studies reveal low platelets, prolonged PT and PTT and elevated d-dimers. Peripheral blood smear shows schistocytes.

Based on their initial presentation, both Effie and Kate have  a form of pregnancy complication.

Now, the most common medical complication of pregnancy is hypertensive disorders of pregnancy. These are diseases that cause high blood pressure during pregnancy, either a systolic blood pressure higher than 140 mmHg, or a diastolic blood pressure higher than 90 mmHg, or both.  So, when hypertension is diagnosed before 20 weeks gestation, it’s usually chronic hypertension, meaning that it’s not due to pregnancy. 

After 20 weeks gestation, new onset hypertension without proteinuria or damage to other organs is gestational hypertension. Now if hypertension gets severe, meaning systolic blood pressure of 160 mmHg or greater and/or diastolic blood pressure of 110 mmHg or greater, it can often lead to organ damage.  One key thing to look out for is the presence of proteinuria, or excessive amounts of protein in the urine, which is a marker of kidney damage. Other affected organs include the brain and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dxSQcfGOQ2SIaMxp5F2H_lckTEiAmKHs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal disorders: Pathology review]]></video:title><video:description><![CDATA[A 33-year-old named Ravi came to the clinic because he has difficulty swallowing food and water over the last 3 months. Physical examination shows significant weight loss, of 7-kg or 15-lb, since his last visit 4 months ago. Esophageal manometry shows incomplete lower esophageal sphincter relaxation in response to swallowing, while barium swallow reveals a dilated esophagus with an area of distal stenosis. At the same time, a 62-year-old man named Frank comes to the clinic because of bad breath, regurgitation of food overnight, and trouble swallowing food. He has had these symptoms for several months. He denies fever, chills, nausea, vomiting, or weight loss. Physical examination shows a mass on the side of the neck. v

Now, both Ravi and Frank have some form of the esophageal disorder. Esophageal disorders can be subdivided into: inflammatory esophageal disorders, or esophagitis, which are characterized by an inflammation of the esophageal lining along with dysphagia, and odynophagia; functional esophageal disorders, which affect the muscles and nerves that control the motility of the esophagus and cause intermittent dysphagia for solids and liquids; and mechanical esophageal disorders, which are characterized by the blockage of the passageway and they typically cause progressive dysphagia for solids. 

Inflammatory esophageal disorders, also known as esophagitis, are characterized by an inflammation of the esophageal lining and based on the cause, they are also subdivided into several types. 

First, there’s reflux esophagitis, which is associated with the reflux of gastric acid from the stomach back into the esophagus. Alternatively, pill-induced esophagitis, where a medication injures the esophagus thereby causing inflammation and possible upper GI bleeding. It is associated with medications such as nonsteroidal anti-inflammatory drugs or NSAIDs, bisphosphonates, tetracyclines, iron, and potassium chloride. In caustic esophagitis, caustic agents, such ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acyanotic_congenital_heart_defects:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0LxT5X_TRP2nsz7ycM2YxhPLSAGQOAqw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acyanotic congenital heart defects: Pathology review]]></video:title><video:description><![CDATA[In a pediatric cardiology clinic, 4-year-old Tara is brought in by her parents because she has not been acting herself over the past month. The mother also mentioned that she can’t keep up with the other children when playing and often gets fatigued or short of breath. Vital signs include a temperature of 37.0 degrees Celsius or 98.6 degrees Fahrenheit, a heart rate of 100 beats per minute, a blood pressure of 110 over 70 mmHg, and a respiratory rate of 18 breaths per minute. On examination, her skin is pink, and auscultation of the heart reveals a holosystolic murmur over the left sternal border. 

Ok, so Tara has some sort of congenital heart defect. Congenital heart diseases are defects in the embryological development of the heart or its major blood vessels. When the defect causes blood to move from the right to the left side, it’s called a right-to-left shunt. This is because deoxygenated blood from the right side goes to the left side, and then enters the systemic circulation. A large amount of deoxygenated blood in the systemic circulation gives the physical appearance of cyanosis, which is a bluish discoloration of the skin. Therefore, right-to-left defects are called cyanotic heart diseases. Conversely, left-to-right shunts are called acyanotic heart defects, because there is no cyanosis. In general, individuals with acyanotic congenital heart diseases could be asymptomatic or present with signs of heart failure, such as exercise intolerance, shortness of breath, and in the case of infants and young children; poor feeding and failure to thrive. 

Okay, of the acyanotic congenital heart diseases, ventricular septal defect, or VSD, is the most common. The ventricular septum normally separates the left and right ventricles, and is made of a membranous component, which is the upper one-third, and a muscular component, which is the lower two-thirds. The defect most commonly occurs in the membranous portion of the septum. Ventricular septal defects are ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_gastrointestinal_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uyj6ZBjYS9WGyNsLj2llqmQYQLK3-EzL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital gastrointestinal disorders: Pathology review]]></video:title><video:description><![CDATA[A newborn infant boy from Syria, named Ahmad, gets transferred to the neonatal intensive care unit due to an opening in the abdominal wall. On examination, there’s a sac protruding from the center of the abdomen, with visible bowel loops. He was born to a 28 year old mother, who received no prenatal care. 

Next, a 5 week old Caucasian boy named Nathaniel is brought to the clinic with bouts of projectile vomiting after every meal. On examination, an olive- shaped mass is palpated in the right upper abdominal quadrant. The baby also has sunken eyes and frontal fontanelle, and poor skin turgor. 

Both children have congenital gastrointestinal disorders. Normally, during the fourth week of fetal development, the embryo starts to change from a flat, three-layer disc to something more shaped like a cylinder, a process called embryonic folding. In the horizontal plane, the two lateral folds eventually come together and close off at the midline, except for at the umbilicus, where the umbilical cord connects the fetus to the placenta. This folding allows for the formation of the gut within the abdominal cavity. If those lateral folds don’t close all the way, an opening is left in the abdominal wall, and that’s called gastroschisis, where gastro- refers to the gastrointestinal tract, and -schisis refers to separation.  

For your exams, a good hint is that this opening is almost always to the right of the umbilicus, although it’s not really known why. This defect allows the bowel, and sometimes other abdominal organs, like the liver and the gallbladder, to protrude out where they are freely exposed to the outside environment. The result is that these organs become irritated and inflamed. 

There is a related condition called an omphalocele, where omphalo- refers to the umbilicus, and -cele refers to hernia or swelling. Normally, during around the sixth week of development, the liver and the intestines grow really quickly, and because the abdominal cavity is still p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Klebsiella_pneumoniae</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S4lN_q6HTt6hjfoud-8m5GYrSSa9TUdN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Klebsiella pneumoniae]]></video:title><video:description><![CDATA[Klebsiella pneumoniae is a Gram-negative rod-shaped bacteria, which belongs to a family of bacteria called the Enterobacteriaceae. 

Klebsiella pneumoniae can normally colonize the oropharynx and the gastrointestinal tract.  

It causes various hospital-acquired infections, such as pneumonia (hence the name)  and is the third most common cause of urinary tract infections. 

Characteristics

Now, Klebsiella pneumoniae has a thin peptidoglycan layer, so like other Gram-negative bacteria, it stains pink. 

And since it’s a bacillus, it looks like a little pink rod under the microscope.

Klebsiella pneumoniae is non-motile, non-spore forming, and facultative anaerobe.  

This means it can live even without oxygen, although it grows better in an aerobic environment. 

So, it prefers places like lungs,throat, or respiratory airways,  as well as ventilators in the ICU where there is an unlimited flow of oxygen. 

Alright, now Klebsiella pneumoniae is  urease positive, which means it can produce an enzyme called urease that dissociates urea into carbon dioxide and ammonia. 

This can be tested by transferring a pure sample of bacteria from the culture to a sterile tube containing a mixture of “urea agar” broth and phenol red. 

Then, the mixture is incubated. 

So, with Klebsiella, urease makes urea dissociate into carbon dioxide and ammonia. 

Ammonia then makes the mixture change color from orange-yellow to bright pink.

Finally, Klebsiella pneumoniae grows well on MacConkey agar, which is a medium that contains a pH sensitive dye and lactose. 

This medium helps identify whether Gram-negative bacteria are lactose fermenters or not. 

Some Enterobacteriaceae like Klebsiella, Enterobacter, and Escherichia coli, can ferment lactose.  

This results in the production of the acid that makes the pH sensitive dye turn pink - so their colonies will be pink. 

Klebsiella has an abundant polysaccharide capsule which leads to the formation of very mucoid and viscous pink ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epstein-Barr_virus_(Infectious_mononucleosis)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k5pOMcloQy__NjGyRypEmVMwRsOimupD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epstein-Barr virus (Infectious mononucleosis)]]></video:title><video:description><![CDATA[The Epstein-Barr virus, or EBV, also known as human herpesvirus-4, or HHV-4, is an enveloped virus of the Herpesviridae family, which contains linear, double-stranded DNA.

It is the most common cause of infectious mononucleosis, more commonly known as “mono.”

EBV infection begins when saliva or respiratory secretions that contain the virus from one person make their way into someone else’s mouth. 

Often, this happens by sharing food or drinks, or by kissing, which is why mono is sometimes called the “kissing disease” and why it is most common in adolescents and young adults, aged 15-24, because young people are often doing the smooching. 

When EBV reaches the new person’s mouth, it infects two types of cells in the oropharynx: epithelial cells, which line the surfaces of the oropharynx, and B cells, which are lymphocytes, or lymphoid cells, that create antibodies to fight off infections. 

In the epithelial cells, the virus undergoes the lytic cycle, whereby its DNA gets transcribed and translated by cellular enzymes, which help to form viral proteins, which are packaged into new viruses, which can leave the host cell destroyed, or lysed, and subsequently infect neighboring epithelial cells. 

The viruses that reach the lymphoid tissue of the oropharynx, the tonsils, infect their main target, B cells, by attaching to their CD21 receptor, also known as the CR2 receptor. 

The infected B cells then enter the latent phase, in which the virus just sort of hangs out in the host cell instead of killing it. 

They then carry and spread the infection along their normal trajectory to the other lymphoid tissues of the body, including the liver, spleen, and lymph nodes.

The body’s immune system reacts to the infection by mounting a humoral response, whereby the B cells create antibodies to fight off the virus, and a cellular response, in which cytotoxic (or CD8+) T cells, which are lymphocytes that mature in the thymus, work to kill the infected B cells. 

This ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreas_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7XQRGNzzTpW7jooCkNLvKNP0QSS2Xqly/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreas histology]]></video:title><video:description><![CDATA[The pancreas is a large gland that has both exocrine and endocrine functions.

The majority of the pancreas consists of exocrine glands that produce about 1.5 liters of alkaline digestive enzymes daily, which is secreted directly into the duodenum.

The pancreas, also contains small endocrine cells found in clusters called islets of Langerhans, which typically stain lighter than the pancreatic tissue around it.

The pancreas has a thin collagenous capsule that surrounds the entire pancreas, although only portions of it can be seen in this image.

The capsule also extends into the pancreas as septa, forming lobules.

This section of the pancreas was prepared with Azan stain, which stains collagen blue-ish purple color in order to highlight structures such as the capsule, septa, as well as the connective tissue that surrounds large blood vessels.

Azan stain will also stain the connective tissue surrounding interlobular ducts a similar color as well.

But these ducts can be differentiated from the blood vessels by the presence of digestive enzymes instead of red blood cells within their lumen as well as their distinct epithelium that lines the lumen.

The epithelium consists of simple columnar cells in this image, but some ducts may also consist of stratified columnar or stratified cuboidal epithelium instead.

To the right of the interlobular ducts is an adipocyte.

The adipocytes actually increase in number within the pancreas as individuals age, which is a normal finding that’s caused by pancreatic atrophy over time.

The main functional tissue of the pancreas is called the parenchyma.

If we take a closer look at this slide stained with hematoxylin and eosin, or H&amp;amp;E for short, we can see that the majority of the parenchyma consists of the exocrine portion of the pancreas. The exocrine secretory cells are arranged in groups that resemble a berry surrounding a central lumen.

In latin acini means “berries,” which is why the groups of exocrine]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_herpesvirus_8_(Kaposi_sarcoma)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/evVJi81STWGp35ExCheeTNgOQ2uS35bn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human herpesvirus 8 (Kaposi sarcoma)]]></video:title><video:description><![CDATA[Human herpesvirus 8, or HHV-8, also called Kaposi’s sarcoma-associated herpesvirus, or KSHV, belongs to the family of human gamma herpesviruses. 

HHV-8 is one of the seven known oncoviruses, meaning viruses that cause cancer in people. 

Specifically, HHV-8 causes Kaposi’s sarcoma, a type of cancer usually seen in individuals with AIDS. 

Human herpesvirus 8 is a large double stranded linear DNA virus surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. 

The capsid is covered by a protein layer called the tegument, and finally enclosed in an envelope, which is a lipid membrane that contains viral glycoproteins and is acquired from the nuclear membrane of host cells. 

HHV-8 is transmitted through sexual contact and once in the body it uses the viral glycoproteins on its envelope to enter a wide variety of cells such as B cells, endothelial cells, macrophages and epithelial cells. 

Now, the virus life cycle has two phases - a latent phase and a lytic phase. 

In the latent phase, the virus just hangs out in the cell without destroying it, and expresses the viral latency-associated nuclear antigen, or LANA-1. 

This may sound harmless, but LANA-1 inhibits p53, a tumor suppressor protein that prevents cancer formation. 

So when LANA-1 inhibits p53, that prevents apoptosis and leads to uncontrolled cellular proliferation. 

In the lytic phase, the virus starts to replicate, so its DNA gets transcribed and translated by cellular enzymes, in order to form viral proteins, which are packaged into new viruses. 

When the virus enters into the lytic phase, thousands of virus particles can be made from a single cell which can destroy the cell and subsequently infect neighboring cells. 

Now, the body’s immune system reacts to the infection by mounting a humoral response, where the B cells create antibodies to fight off the virus, and a cellular response, in which cytotoxic T cells work to kill the inf]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GERD,_peptic_ulcers,_gastritis,_and_stomach_cancer:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2QhKLmRGQKikn7pX6GPrKh2YTaeT7GcY/_.jpg</video:thumbnail_loc><video:title><![CDATA[GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review]]></video:title><video:description><![CDATA[A 61-year-old man, named Shawn, comes to the emergency department because of substernal chest pain and heartburn. 

He mentions that his symptoms worsen typically after coffee, heavy meals or during times of stress. 

He also feels the pain at night when he is lying in bed and has previously been woken from sleep by discomfort. 

He has not noticed any dyspnea, diaphoresis, or palpitations but is currently experiencing some nausea and a sour taste in his mouth. Shawn also denies a history of previous cardiovascular conditions. His ECG is normal. 

Shawn has gastroesophageal reflux disease, or GERD. GERD is a condition caused by a transient lower esophageal sphincter relaxation, which enables stomach contents and acid to re-enter esophagus and damage esophageal mucosa. 

As a result, people with GERD present with symptoms such as retrosternal chest pain, heartburn, regurgitation, and dysphagia. 

It’s important to note that GERD symptoms tend to worsen after eating, when lying down, or bending over. 

Now, if stomach acid gets to the throat, it can cause laryngopharyngeal reflux, which has a different set of symptoms such as acidic taste in the mouth, sore throat, chronic cough, and hoarseness. 

In the mouth, gastric acid can even damage tooth enamel. Finally, if inhaled, stomach acid can cause pneumonia and asthma. 

GERD is commonly associated with conditions such as decreased esophageal motility, gastric outlet obstruction, and hiatal hernia. 

Risk factors for GERD include lifestyle habits such as caffeine, alcohol, and smoking; use of some medications, such as antihistamines and calcium channel blockers; but also, obesity; pregnancy; and Zollinger-Ellison syndrome. 

For your exam, it’s important to know that long-term complications of GERD include esophagitis, esophageal strictures, Barrett&amp;#39;s esophagus, esophageal adenocarcinoma, and pulmonary fibrosis. 

Now, a classic GERD presentation can be diagnosed based on clinical symptoms ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_insufficiency:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7JGkeK4vSmGQ_yLGVzdf85eZRh6tFiv0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenal insufficiency: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you see two individuals. First is Mike, a 50-year-old immigrant from Canada who comes in with a 5-month history of progressive fatigue, weight loss, and muscle pain. Personal history is unremarkable but there’s a family history of autoimmune disease. Examination reveals hypotension, and diffuse skin hyperpigmentation most pronounced around the oral mucosa, palmar creases, and knuckles.

Then you see Teresa, a 25-year-old who presents acute vomiting, abdominal pain, and fever. She was accompanied by her mother, who mentions Teresa recently underwent transsphenoidal resection of a pituitary tumor. Examination reveals severe hypotension and altered mental status. 

Morning cortisol serum measurements showed decreased levels of serum cortisol in both individuals. Both people have adrenal insufficiency although their symptoms are very different.

Now, adrenal insufficiency is a condition where the adrenal glands don’t produce enough adrenal hormones, particularly cortisol and, sometimes, aldosterone. There are actually three types of adrenal insufficiency. First, primary adrenal insufficiency is when there’s a problem with the adrenal glands themselves. As a result, both cortisol and aldosterone production is deficient. It can be acute, usually due to a massive adrenal hemorrhage, or chronic, in which case it is called Addison disease. Now, a high yield concept to remember is that the most common cause for Addison in high income countries is autoimmune mediated damage to the adrenal glands. In the rest of the world, the most common cause is infection, especially from tuberculosis, but it can also be due to HIV or disseminated fungal infections. Finally, bilateral adrenal metastases of cancer from somewhere else in the body,can also cause chronic adrenal insufficiency.

Then, there’s central adrenal insufficiency which can be secondary or tertiary. In secondary adrenal insufficiency, the problem is not with the adrenal glands but with th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Familial_hypercholesterolemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1H8xXxEFRsqzXW5a9PrPvnQiSVWRWede/_.jpg</video:thumbnail_loc><video:title><![CDATA[Familial hypercholesterolemia]]></video:title><video:description><![CDATA[With familial hypercholesterolemia, familial means the disease runs in families, so it has a genetic predisposition, hyper means excess and lastly cholesterolemia refers to the level of cholesterol in the blood. 

So, familial hypercholesterolemia is a genetic disorder associated with high levels of cholesterol in the blood.

Now, cholesterol is a lipid molecule, so a type of fat, that normally helps maintain the structure of cell membranes, and is a precursor to steroid hormones, bile acids, and vitamin D. 

There are two main types of cholesterol: LDL or Low Density Lipoprotein which is sometimes called “bad cholesterol,” nad HDL or High Density Lipoprotein which is sometimes called “good cholesterol.” 

But good and bad is overly simplistic, and like all things - the subtleties matter. 

LDL is produced by the liver and it carries cholesterol out to the rest of the body. 

If all of the cholesterol from LDL is not completely distributed to the peripheral cells, then HDL brings some of that cholesterol back from the peripheral tissues and sends it to the liver. 

Now, what makes LDL bad and HDL good is that, whenever there’s a high blood concentration of LDL, the LDL can be ingested by macrophages that sit along vessel walls, forming atherosclerotic plaques. 

Over decades, large atherosclerotic plaques can lead to myocardial infarctions, strokes, and peripheral vascular disease. 

That’s why we want to keep LDL blood levels under control. 

On the other hand, HDL can remove cholesterol from cells and that can help reverse the process of atherosclerosis.

Now, our body usually keeps LDL cholesterol levels in check by clearing our excess LDL from the plasma. 

This is mainly done by the LDL receptors present on the surface of the liver cells. 

First, the LDL molecules bind to the LDL receptors, which are clustered in specialized regions of the cell membrane called coated pits. 

After binding, the coated pits along with the receptor-bound LDL are interna]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parvovirus_B19</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kQww_-WSSBWeZod2XVGHPRRbTvWTzueV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parvovirus B19]]></video:title><video:description><![CDATA[Parvovirus B19 is the smallest known DNA animal virus, coming in at an itty bitty 18 to 28 nanometers in diameter. 

In comparison, the average size of a single human red blood cell is a whopping 7200 nanometers!

While it’s mostly known for causing fifth disease, or “slapped cheek syndrome,” in children, parvovirus B19 can also affect adults and it can cause serious illness in individuals with pre-existing conditions like sickle-cell anemia and HIV.

Parvovirus B19 is part of the parvoviridae family.

It’s a single-stranded DNA virus surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. 

And it’s “naked” because the capsid isn’t covered by a lipid membrane.

Parvovirus B19 is primarily transmitted by respiratory droplets when someone coughs or sneezes. 

You can also catch it via an infected blood transfusion and a pregnant female can also transmit it through the placenta to her unborn child. 

Now, although the virus first enters cells of the respiratory tract by binding to receptors on host cells, it doesn’t replicate in them. 

Instead it keeps travelling through cells and into the circulatory system until it reaches bone marrow, where red blood cells are made, a process called erythropoiesis. 

Once there, parvovirus B19 uses receptor-mediated endocytosis to enter erythroid progenitor cells, also called proerythroblasts, the early cells that eventually become red blood cells. 

It then uses these cells’ DNA replication machinery in the nucleus to replicate its DNA and assemble new copies of the virus. 

Why not simply replicate in cells of the respiratory system? 

Well it turns out that Parvovirus B19 needs two things: it prefers to bind to a specific receptor, the P antigen, which is found in large numbers on proerythroblasts’ cell membrane and it needs cells that pass through the S phase of the cell cycle, which is the phase where cell DNA is replicated. 

Since the body is constantly p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physiological_changes_during_exercise</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yrFZSrtZQHarfcEEGYUTU2LrTQWrAmtK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physiological changes during exercise]]></video:title><video:description><![CDATA[During physical exercise, our organs and tissues are working hard to keep us moving; or, technically speaking, for our musculoskeletal system to do its job. 

Now it’s fairly obvious that during exercise, skeletal muscles work, or contract, harder and faster than when we’re at rest, so they use a lot of energy in a short time, so they need a lot more blood and oxygen to keep going. 

So organ systems like the cardiovascular and respiratory system have to make some quick physiological adjustments, to meet the skeletal muscles demand. 

Moreover, the endocrine system also kicks things into high gear, by secreting hormones like cortisol and adrenaline, that speed up intracellular processes to keep us going.

But before we delve into the specifics of that, let’s remember how muscle contraction works on a microscopic level. 

So, skeletal muscles are made up of muscle fibers which are actually the skeletal muscle cells.  

We just call them “fibers” because they are long, multinucleated cells, meaning they have more than one nucleus. 

Their structure also differs from other cells because their cytoplasm, sometimes also called sarcoplasm, is filled with stacks of long filaments called myofibrils, which are made up of contractile units called sarcomeres. 

And finally, sarcomeres are made up of the thick myosin filaments, and thin actin filaments, which can slide over one another, shortening the sarcomeres. 

So when all the sarcomeres in a muscle fiber do that in sync, that results in shortening of the muscle as a whole, or muscle contraction. 

And this process is powered by energy in the shape of ATP molecules, where adenosine-triphosphate. 

The three phosphates in the molecule are linked in a chain, and between two adjacent phosphate molecules, there are high-energy phosphate bonds. 

ATP molecules attach to a part of the myosin filament called the myosin head. 

The myosin head is actually an ATPase, or  an enzyme that can cleave an ATP molecule into ADP a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Streptococcus_pyogenes_(Group_A_Strep)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tWH1I7eYTIyKTomRNps-m3QzSeyTgVc9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Streptococcus pyogenes (Group A Strep)]]></video:title><video:description><![CDATA[Streptococcus pyogenes, sometimes called Strep pyogenes, can be broken down into “strepto” which means chain, “coccus”, which refers to round shape, “pyo” which means pus, and “genes” which refers to forming. 

So, Strep pyogenes are round bacteria that grow in chains, responsible for a number of infections that often present with pus. Strep pyogenes are also called Group A Strep – GAS - in Lancefield classification developed by American microbiologist Rebecca Lancefield. 

Ok now, Strep pyogenes has a thick peptidoglycan cell wall, which takes in purple dye when Gram-stained - so this is a gram-positive bacteria. 

It’s non-motile and doesn’t form spores, and it’s also a facultative anaerobe, meaning it can survive in both aerobic and anaerobic environments. 

Finally, Strep pyogenes is catalase negative, meaning it doesn’t make an enzyme called catalase. 

However, unlike other common cocci like Enterococci, Strep pyogenes is pyrrolidonyl arylamidase positive, because it makes an enzyme called L-pyrrolidonyl arylamidase. 

To test for this, a small sample is taken from a suspected bacterial colony, and then inoculated to a disk pad that’s embedded with pyrrolidonyl beta naphthylamide - another joy of a word. 

With Strep pyogenes, pyrrolidonyl arylamidase hydrolyzes pyrrolidonyl beta—naphthylamide to produce beta-naphthylamide. 

Try saying that 3 times fast! Finally, another reagent called N-methylamino-cinnamaldehyde is added to the disk, and it reacts with beta—naphthylamide, resulting in a bright red color that confirms Strep pyogenes is pyrrolidonyl arylamidase positive.

When cultivated on a medium called blood agar, Strep pyogenes colonies cause  beta-hemolysis, also called complete hemolysis. That’s because Strep pyogenes makes toxins known as streptolysins, which hydrolyze the hemoglobin in red blood cells to transparent yellow color byproducts. 

But some other Streptococcus species, like Strep agalactiae, are also beta-hemolytic. So a bacitrac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obstructive_lung_diseases:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F1OT8GWpQUukNkNyLdjYMr3fTqWHivyq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obstructive lung diseases: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you see two individuals. First is Elsa, a 66-year-old with a history of smoking 2 packs a day for the past 35 years. She came in with progressive shortness of breath and chronic, productive cough, which appeared two and a half years ago but recently got worse. On examination, she presents with pursed-lip breathing, barrel chest, and diminished breath sounds with wheezing. Spirometry was requested, and it showed signs of moderate respiratory obstruction, including an important reduction in forced expiratory volume in one second. The other individual is James, a 7-year-old with a history of wheezing and coughing episodes that began 2 years ago. The episodes used to be only during the winter, but in the past 6 months, they increased in frequency and severity. His father has a history of asthma, and the child himself has eczema. Physical examination and spirometry was normal.

Now, both seem to have some type of obstructive lung disease. But first a bit of physiology. The respiratory tree can be divided into the conducting zone, which consists of large airways like nose, pharynx, larynx, trachea, and bronchi; and the respiratory zone, consisting of respiratory bronchioles, alveolar ducts, and alveoli. Lining the lumen of the airways you’ve got the epithelium, mostly composed of one layer of ciliated pseudostratified columnar epithelial cells up until the beginning of terminal bronchioles, where it is replaced by cuboidal cells. 

The ciliated pseudostratified columnar epithelial cells have hair-like projections called cilia. The cilia are responsible for eliminating larger particles like dust that reach the terminal bronchioles by moving them towards the pharynx, where they are coughed out. The epithelium also contains the goblet cell which makes the mucus within the airway. Going deeper past that layer you’ve got the basement membrane and loose connective tissue, called the lamina propria, which together with the epithelium makes up t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_endocrine_neoplasia:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oX1zpWYtQ8S1uumC9d39nTTtRnKNjOYu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple endocrine neoplasia: Pathology review]]></video:title><video:description><![CDATA[Two individuals came in for genetic testing based on recommendations from their primary care physicians. The first one is 24 year old Kurt, who was previously diagnosed with Zollinger-Ellison syndrome and also has an adenoma in one of his parathyroid glands. On the clinical examination, doctors observed that he has gynecomastia. His mother also has parathyroid adenomas. The other one is 19 year old Courtney, who was previously diagnosed with parathyroid hyperplasia and pheochromocytoma. Her father has recently been diagnosed with thyroid medullary cancer.

Although their presentation and family history differ, both people have multiple endocrine neoplasias, or MEN for short. These are a group of inherited diseases which cause tumors to grow in the endocrine glands of the body. The endocrine glands affected in multiple endocrine neoplasia are the pituitary gland, thyroid gland, parathyroid glands, adrenal glands, and the pancreas. So in multiple endocrine neoplasias, there are tumors that form in these glands that lead to overproduction of hormones. 

Multiple endocrine neoplasias are caused by genetic mutations in one of two genes: either MEN1 or RET, which codes for receptor tyrosine kinase.  For your exams, remember that both of these genes have a dominant inheritance pattern, so only one copy of the mutated gene is needed to get the disease. 

Okay, let’s start with the MEN1 gene that is found on chromosome 11 and codes for a tumor suppressor protein called menin, which - under normal circumstances - stops a cell from dividing uncontrollably. MEN1 mutations cause MEN type 1. For your tests, you absolutely have to know that there are three types of tumors associated with MEN type 1: parathyroid, pancreatic, and pituitary. 

The most common tumor is a parathyroid adenoma. Increased parathyroid hormone production causes increased bone breakdown, which leads to hypercalcemia. The clinical manifestations of hypercalcemia can be recalled by the mnemonic: “Sto]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myalgias_and_myositis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WT4PnI3nT2yZaRVmmvB3ASMIRJ6k8gP1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myalgias and myositis: Pathology review]]></video:title><video:description><![CDATA[On your rounds, you see two individuals. First is Yu Yan, a 58-year-old female who presents with a 2-week history of fatigue, weight loss, fevers, and bilateral pain with stiffness in the shoulder and hip girdles. These symptoms are worse at night and last for more than an hour. She also mentions that she finds it hard to get out of bed in the morning due to stiffness. On examination, her wrists and finger joints are painful and swollen, but there’s no muscle weakness. Then you see Elizabeth, a 38-year-old female who has a 4-year history of body pain. The pain was initially limited to her neck, but it has gradually spread and she now complains of constant pain all over. She does not sleep well and is chronically fatigued. Examination revealed many tender points throughout her body but no sign of joint swelling or muscle weakness. Blood tests were performed in both. In Yu Yan’s case, there was an increase in inflammatory markers, but creatine kinase levels were normal. In Elizabeth’s, blood tests were completely normal.

Both people have myalgias, or muscle pain.  There are many causes but let’s start with myopathies, which are neuromuscular disorders in which the primary symptom is muscle weakness due to muscle cell dysfunction. There are two main inflammatory myopathies, polymyositis and dermatomyositis. 

First, polymyositis is an autoimmune disease where there’s inflammatory infiltration in striated muscles that cause muscle damage. Now, the cause is still unknown, but polymyositis is often associated with other autoimmune diseases, including Sjogren syndrome, rheumatoid arthritis, scleroderma, and mixed connective tissue disease. It is thought that there’s an overexpression MHC class I molecules and muscular autoantigens, which end up triggering a primarily cell-mediated immune response that inappropriately activates CD4+ and CD8+ T-cells. This is probably due to molecular mimicry, which is when an immune cell mistakes a protein in the body as bei]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchioles_and_alveoli_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QC5WdLwaSwWmYplNGwGJJjYoSzq_Z6dY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchioles and alveoli histology]]></video:title><video:description><![CDATA[Bronchioles are air-conducting passageways that are typically less than 1 mm in diameter. The smallest bronchioles, called terminal bronchioles, are the most distal airways that are still a part of the conducting portion of the respiratory system. The terminal bronchioles then lead to the first portion of the airways that have a respiratory function, called respiratory bronchioles. These bronchioles then lead to the alveolar ducts, which are transitional airways that gradually become increasingly involved in gas exchange and lead to the alveolar sacs and their individual alveoli.

If we compare images from a bronchus and bronchiole at low magnification, we can see that the larger bronchus has large supporting cartilage plates that aren’t seen in the smaller bronchiole. The bronchi also contain sero-mucous glands that are not present in bronchioles, but the bronchioles will still have a surrounding layer of smooth muscle present. The larger proximal bronchioles, similar to the one in this image, are called the primary bronchioles. If we zoom in to 40x, we can see that the primary bronchioles have ciliated, pseudostratified columnar epithelium with goblet cells. When using a Hematoxylin and Eosin stain, the goblet cells will appear lighter than the surrounding epithelial cells and as their name suggests, these cells are often shaped similarly to the top portion of a goblet. Moving distally through the airways, the bronchioles&amp;#39; diameter gradually decreases and the terminal bronchioles will have a diameter less than 0.5 mm. The epithelium also transitions from ciliated pseudostratified columnar epithelium to an epithelium that consists mostly of ciliated simple columnar and cuboidal cells with exocrine club or Clara cells instead of goblet cells. The Clara cells can be identified by their tall columnar and non-ciliated appearance, as well as their dome-shaped apical ends that contain secretory granules.

If a patient has bronchial asthma, there will b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Live_AMA_with_Rishi_Desai,_MD,_MPH:_COVID-19</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RUxkEPD7TRSZPjShzZv7DpNfTKeKLtzX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Live Ask-Me-Anything with Rishi Desai, MD, MPH: COVID-19]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Live Ask-Me-Anything with Rishi Desai, MD, MPH: COVID-19 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/N95_mask_fitting</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AGBynfmGS7m3Nc6mS3tJUJRASHGQsw2-/_.jpg</video:thumbnail_loc><video:title><![CDATA[N95 mask fitting]]></video:title><video:description><![CDATA[This video covers how to apply an N95 mask. 

Normally, you’d do everything on this list, but to keep things concise this video will focus on the steps in blue and will also include a summary.

Hold the N95 mask in the palm of your hand. 

Check the mask to ensure it is in good condition. 

To apply it, point its nose up and let its elastics dangle towards the floor. 

Place the mask on your face, pull the bottom strap around your head, rest it below your ears. Top strap goes on the crown of your head. 

Remember, this order is important. Bottom strap always first. 

Mold the nose piece to fit your nose. Remember, comfort is important too. Less so, however.

Check for a good seal. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nocardia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/edHLWuIiR4KB0-BDXr-a6xW3RLeZsLnP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nocardia]]></video:title><video:description><![CDATA[Nocardia is a genus of Gram-positive branching filamentous rods that are often found in soil. 

There are over 80 species of Nocardia and around 30 of them causes disease in humans, and the most notable ones are Nocardia asteroides, Nocardia brasiliensis, Nocardia cyriacigeorgica, Nocardia farcinica and Nocardia nova. 

Nocardia causes a disease called nocardiosis which has three major forms - pulmonary, cutaneous and disseminated.

OK, Nocardia is a rod-shaped Gram-positive bacteria, we’ve got that part down, and this means it goes purple when Gram-stained. 

When there’s many of them, they arrange themselves in the shape of purple branching filaments. 

They are obligate aerobes, meaning they need oxygen to grow, they are also non-motile, and don’t form spores. 

But wait… that sounds exactly like Actinomyces israelii, another group of rod shaped, gram-positive, filamentous bacteria with a lot of other similar features. 

To distinguish them, an acid-fast stain, also called Ziehl-Neelsen stain is done. 

With this test, a red dye called carbon fuchsin, binds to lipids in the cell wall, coloring them red. 

Then alcohol is applied to wash out any dye that hasn’t colored bacteria, and a second dye, methylene blue, is applied. 

Now, Nocardia is a weak acid-fast bacteria which means that a less concentrated solution of alcohol is needed during staining and that’s because the mycolic acids in its cell wall have intermediate-length. 

So, because it has plenty of lipids in its cell wall, it retains the carbon fuchsin, and it looks red under the microscope, making it an acid-fast bacteria. 

On the other hand, in bacteria who don’t have a lot of lipids in their cell wall, like A. Israelii, all the red dye is washed off by alcohol, so it looks blue under the microscope, making it a non-acid-fast bacteria. 

Also, Nocardia can be visualized with auramine-rhodamine stain using fluorescence microscopy, which can show a reddish-yellow fluorescence. 

This stain is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vaginal_and_vulvar_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7AceICW_SGmjaxD9UG6XIW0OQ-2WDBse/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vaginal and vulvar disorders: Pathology review]]></video:title><video:description><![CDATA[62-year-old Tess comes to the emergency department with vaginal bleeding for the past couple of hours. She also mentions that she has occasionally noticed some watery, foul-smelling vaginal discharge. After ensuring that she is hemodynamically stable, history reveals that her last menstrual period was about 10 years ago and she has had multiple sexual partners. On speculum examination, a suspicious-looking mass is identified in the upper third of the posterior vaginal wall. 

Later that day, 69-year-old Oshun comes to the physician&amp;#39;s office complaining of an intense burning sensation, itching and pain in her genital region. Her last menstrual period was at the age of 48. On further history, she has been smoking 1.5 packs daily for 40 years. On examination, a white, asymmetrical lump with irregular borders and 1.2 cm in size is seen in the right labia majora.

All right, both Tess and Oshun have some type of vaginal or vulvar condition. Let’s take a look at the Anatomy real quick. The external sex organs, together referred to as the vulva, contain the labia majora, which cover the labia minora, and between the two labia minora there is a space called the vulvar vestibule that includes the opening of the vagina and the the urethral opening. Now, vaginal and vulvar conditions are classified into non- neoplastic ones including bartholin cyst, lichen sclerosus, lichen simplex chronicus, and imperforate hymen and neoplastic ones, which are relatively rare cancers of the female genital tract. 

Okay, let’s start with the first non-neoplastic condition, which is the Bartholin cyst. The Bartholin glands are two small glands that lie underneath the vestibule and on each side of the vaginal opening. Normally, they secrete a mucus- like fluid that drains through ducts into the vestibule in order to lubricate the vagina. But when their ducts get blocked, the fluid builds up, causing cystic dilation of the gland. For your exams, remember that blockage typically]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ovarian_cysts_and_tumors:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X7AXUKInRnOUoGd8xRSqcV-NRrOkxxnj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovarian cysts and tumors: Pathology review]]></video:title><video:description><![CDATA[65-year-old Rebecca presents to the clinic with several months of abdominal discomfort, bloating, and a change in bowel habits. Her past medical history is significant for endometriosis. Menarche was at age 10 and menopause at age 57. She has never been pregnant. On physical examination, a slightly painful nodule is palpated around the umbilicus. Transvaginal ultrasound showed a large, irregular cyst with heterogeneous fluid in her right ovary. Later that day, 6-year-old Gloriana is brought to the office by her mother, who is worried that her daughter is more “womanly” and taller than the other girls her age. Over the last few months, she has also occasionally complained of vague abdominal pain. Physical examination reveals coarse pubic hair and significant breast enlargement. The child’s height is also in the 96th percentile. Laboratory studies also showed increased inhibin b levels.

Based on the initial presentation, Rebecca and Gloriana’s symptoms are caused by some form of ovarian mass. Broadly speaking, ovarian masses include ovarian cysts and tumors. Starting with ovarian cysts, these are fluid-filled sacs on or in the ovaries and can be classified into simple and complex cysts. 

Simple cysts are generally small, they contain a clear serous liquid, and have a smooth internal lining. The classic example is a follicular cyst which is a dominant follicle that fails to rupture before ovulation and keeps growing. This can happen, if say, the normal surge of LH that causes ovulation just doesn’t happen during a given menstrual cycle. In fact, follicular cysts are the most common type of ovarian mass in young individuals. 

For your test, remember that if you encounter multiple follicular cysts, they are usually associated with polycystic ovary syndrome, or PCOS. This is caused by a dysfunction in the hypothalamic-pituitary-ovarian axis that causes chronic anovulation, which may lead to amenorrhea, or absent menstruation, and excess androgen production, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Scleroderma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dZ-W3I5NRz_wLX5V8j1iUFfNQ-ad-KqA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Scleroderma]]></video:title><video:description><![CDATA[Learning medicine is hard work. Osmosis makes it easy! It takes your lectures and notes to create a personalized study plan with exclusive videos, practice questions, and flashcards, and so much more. Try it free today!  

Scleroderma refers to systemic sclerosis, a rare autoimmune disorder in which normal tissue is replaced with thick, dense connective tissue. It affects the skin, blood vessels and internal organs. Now, there are two main types of scleroderma: limited cutaneous systemic scleroderma, better known as CREST syndrome; and diffuse cutaneous systemic scleroderma. The word scleroderma comes from the Greek words ‘sclero,’ meaning hard, and ‘derma,’ meaning skin, which points to the hard skin as its most visible feature.

So, normally, when there’s an infection in the body, macrophages will eat some of the invading organisms and break them down. In addition to destroying the pathogen, they also present a fragment of the pathogen, called an antigen, to naive T cells. When the naive T-cells bind to this presented antigen, they mature into T-helper cells, also called CD4+ T-cells, and they go on to help and recruit more immune cells. The T-helper cells release cytokines, which increase the activity of macrophages and attract nearby neutrophils. Macrophages also release cytokines, like TGF-β, that tell fibroblasts to repair damaged tissue after the infection by laying down collagen.

Scleroderma affects women three times more often than men. The exact pathology of scleroderma is not completely understood, but generally, it’s thought that some individuals have a genetic predisposition to scleroderma which is triggered by external triggers. Some known triggers include viral infection by cytomegalovirus and parvovirus B19; exposure to silica dust, organic solvents, and vinyl chloride; and drugs and medications like cocaine, bleomycin, and pentazocine.

It’s thought that there’s initially an injury to endothelial cells lining the small arteries. These cel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_herpesvirus_6_(Roseola)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GIAThxMPRjuRTP5MWWpxNEGdRsKf4x0v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human herpesvirus 6 (Roseola)]]></video:title><video:description><![CDATA[Human herpesvirus 6, or HHV-6, is a double stranded DNA virus which belongs to the Herpesviridae family, subfamily Betaherpesvirinae, genus Roseolovirus. HHV-6 primary infection is the cause of the common childhood disease called roseola infantum, also known as exanthema subitum or sixth disease.

Human herpesvirus 6 is a double stranded linear DNA virus surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. 

The capsid is covered by a protein layer called the tegument, and finally enclosed in an envelope, which is a lipid membrane that contains viral glycoproteins and is acquired from the nuclear membrane of host cells. 

Now, HHV-6 infection begins when a person comes in contact with respiratory secretions from another person who contains the virus. 

Once in the body, the virus attaches to dendritic cells, which are antigen-presenting cells that can be found in the skin, nose, lungs, stomach and intestines. 

These cells are able to process antigens like viral proteins and present them on the cell surface to the T cells. 

So, when the virus attaches to dendritic cells, it activates them, and they migrate to the lymph nodes where they interact with CD4+ T lymphocytes. 

When dendritic cells and T cells interact, the virus gets ingested by T cells and they get infected. 

Inside T cells, the virus can replicate most efficiently, so it undergoes the lytic cycle, where its DNA gets transcribed and translated by cellular enzymes, to form viral proteins, which are packaged into new viruses that can leave the cell destroyed and subsequently infect neighboring cells. 

The virus can also replicate into a wide variety of other cells such as monocytes, macrophages, natural killer cells, astrocytes, megakaryocytes and glial cells - but not as efficiently as inside T cells. 

Finally, HHV-6 can go into a latent state in monocytes, where the virus just hangs out inside the cell instead of killing it. 

T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Haemophilus_influenzae</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IH-K0nEfTbOY4n9wSpNyPCe_TGe7o6-8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Haemophilus influenzae]]></video:title><video:description><![CDATA[Haemophilus influenzae is a small Gram-negative coccobacillus which can normally colonize the human respiratory tract. There are two major categories of H. influenzae  - encapsulated strains and unencapsulated strains. 

Encapsulated strains are classified into six serotypes based on their capsular antigens - a, b, c, d, e and f, and unencapsulated strains are called nontypable, because they lack the polysaccharide capsule, and, consequently, capsular antigens. 

The strains that cause disease in humans are most often Haemophilus influenzae type b, or Hib for short and Haemophilus influenzae nontypable.

Now, Haemophilus influenzae has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining. Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. 

And since it’s a coccobacillus, it’s shaped somewhere between round, like a coccus, and linear, like a bacillus. Haemophilus influenzae is non-motile, so it doesn’t move, and facultative anaerobic which means it can survive both in aerobic and anaerobic environments. It’s also catalase and oxidase positive which means it produces both these enzymes.

Finally, Haemophilus influenzae can be cultivated on chocolate agar, because this medium contains essential nutrients that Haemophilus influenzae needs to grow, like factor X, also called hemin, and factor V, also called nicotinamide adenine nucleotide. 

Another way to grow it is to grow it with Staphylococcus aureus colonies, on blood agar, which provides factor V via red blood cells hemolysis. 

On both blood agar and chocolate agar, Haemophilus influenzae grows into convex, smooth, gray or transparent colonies. Now, Haemophilus influenzae has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.

So first, encapsulated strains of Haemophilus influenzae are covered by a polysaccharide layer called a capsule. Now,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nasal_cavity_and_larynx_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x7F2IvMWTN_qPnnt2icokKcLTv6aG7uK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nasal cavity and larynx histology]]></video:title><video:description><![CDATA[The nasal cavity is separated into two spaces, or fossae, by the nasal septum.

The nasal septum can be seen along the midline.

The nasal turbinates project into the nasal cavity in order to help increase the total available surface area.

Both the paranasal sinuses, as well as the majority of the nasal cavity, are lined with respiratory mucosa.

Only the roof of the nasal cavity is lined with olfactory mucosa instead.

This image of a human’s nasal mucosa, at 10x magnification, was prepared with Alcian blue and Van Gieson stains.

If we zoom in, to 40x magnification, we can see that the epithelium consists of pseudostratified ciliated columnar cells, along with many goblet cells that can be easily identified in light blue, because of the Alcian Blue stain.

This epithelium is also referred to as respiratory epithelium and generally can be found in the conducting portions of the respiratory tract.

The supporting connective tissue called the lamina propria is deep to the epithelium and contains many blood vessels and seromucous glands.
If we compare the respiratory epithelium to the olfactory epithelium, we can see that the olfactory epithelium also has pseudostratified columnar cells, but it’s significantly thicker and is composed of a combination of olfactory, sustentacular, and basal cells.

The surface of the olfactory epithelium is also lined with modified cilia that function as olfactory receptors, which allows the olfactory cells to sense smells.

Moving on to the larynx, this image is a low power, coronal section of the larynx.

There are two pairs of folds within the larynx, the upper folds are the vestibular folds (or false vocal cords), and the lower folds are the actual vocal folds, (or true vocal cords).

Between the folds on each side are narrow spaces simply called ventricles.

Each true vocal cord will need relatively large muscles in order to move the vocal cords for speech.

These muscles, called the vocalis muscles are stained dark]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Imaging_features_of_COVID-19_(LifeBridge_Health)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oP_d0cSfTyiE4QQnsZQG27_NT5OO63do/_.jpg</video:thumbnail_loc><video:title><![CDATA[Imaging features of COVID-19 (LifeBridge Health)]]></video:title><video:description><![CDATA[As of March 16th, so in just the first three months of the outbreak, there have been 167,511 cases of COVID-19 and 6,606 deaths, working out to a mortality rate of 3.9%. 

On top of that, every case of COVID-19, leads to roughly 2.3 new cases, meaning that the outbreak is still spreading. 

Many countries have been affected, and there are numerous cases of community spread, meaning that individuals are getting sick without being around any sick contacts or having traveled to outbreak areas. 

In that context, healthcare workers need diagnostic tools to investigate cases of potential COVID-19 that are both sensitive and specific.

The gold standard for diagnosis of COVID-19 is RT-PCR, or reverse transcription polymerase chain reaction. 

In the early days of the epidemic in China RT-PCR was only 30 to 70% sensitive whereas Chest CT was reportedly much more sensitive in that context.  

However, more recent data from the US labs at the University of Washington suggests that second generation COVID RT-PCR tests are faring much better, with 95%+ sensitivity.  

Despite its usefulness in the early days of the epidemic in China, Chest CT findings are no longer part of the diagnostic criteria for COVID.   

There are still clearly issues with access to RT-PCR and related wait times in the US and elsewhere.  

Nevertheless, over the past several weeks, several major US radiology societies have come out with statements making it clear that CT should be used sparingly in COVID and only when it will impact management.  

However, because there will be certain cases when imaging is indicated, as well as patients imaged for other reasons whose scans reveal findings potentially suggestive of COVID, it is essential that healthcare providers be familiar with the imaging features of the infection.

Typically, when a patient has symptoms of COVID-19, like fever, cough, or shortness of breath, they may get a chest X-ray. 

The most common abnormal finding is “ground glass” o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/What_is_Osteopathic_Medicine_(DO)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2erpPtBbTVmq2XpQ5PQiEd3aThS1rEEc/_.jpg</video:thumbnail_loc><video:title><![CDATA[What is Osteopathic Medicine (DO)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of What is Osteopathic Medicine (DO) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peripheral_artery_disease:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uGIDVkBtTdS1oZfWLBS_7BxHQs6T58JE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peripheral artery disease: Pathology review]]></video:title><video:description><![CDATA[Tariq is a 52-year-old individual who presents to the clinic complaining of left leg pain. He describes the pain as “cramping” and mostly located in his calf. He also mentions that the pain comes every time he walks from his home to the supermarket, and is relieved when he rests. Tariq also has a known history of hypertension, diabetes mellitus, and a myocardial infarction 2 years ago. On physical examination, there is a noticeable decrease in hair growth on the left side compared to the right, and the skin appears dry and shiny. There is no leg swelling, and there’s no back pain.

Peripheral artery disease is insufficient tissue perfusion due to narrowing or occlusion of the aorta or one of its peripheral branches supplying the limbs. Similar to coronary artery and cerebrovascular disease, the development of an atherosclerotic plaque that narrows or completely occludes an artery is the number one cause of peripheral artery disease, and so these diseases often coexist together. 

So on the exam, an important clue may be an individual with a past medical history of a myocardial infarction or a stroke. In addition, look for risk factors of atherosclerosis, such as hypertension, diabetes mellitus, smoking and hyperlipidemia.

The symptoms of peripheral artery disease depend on how bad the occlusion is. In the early stages of the disease individuals may be completely asymptomatic. One of the first symptoms is intermittent claudication. This is characterized by cramping pain in the affected area that comes about during exercise, and is relieved with rest. 

Individuals often describe a specific and often consistent distance that brings about the pain, such as walking 2 blocks. The location of the pain can also help give a clue about which artery is occluded. For example, hip claudication indicates aortic or iliac artery occlusion, whereas calf claudication points towards femoral or popliteal artery occlusion. 

In addition to claudication, chronic limb ischemia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Body_temperature_regulation_(thermoregulation)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PvqtPMUsT_aWxi54T0QQ3zx6SJ_EVUfz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Body temperature regulation (thermoregulation)]]></video:title><video:description><![CDATA[Body temperature regulation, also known as thermoregulation, is how an organism keeps its body temperature within certain limits. 

For humans, the normal body temperature ranges between 36.1°C, or 97 °F, and 37°C, or 98.6°F. 

When body temperature increases above 38.5° C, or 101.3°F,  that’s called hyperthermia. 

The opposite condition, when body temperature decreases below 35 °C, or 95 °F, is known as hypothermia.

Thermoregulation is needed in response to internal and external temperature variations. 

Internal temperature variations are sensed by specialized nerve cells, called thermoreceptors, located in the anterior hypothalamus. 

Now, the hypothalamus works as a thermostat. 

The front part or the anterior hypothalamus responds to increased environmental temperatures and it also controls the core temperature of the body. 

The back part or the posterior hypothalamus, on the other hand, responds to decreased environmental temperatures.

Changes in the external temperature are sensed by the skin thermoreceptors, which are specialized nerve cells located in the skin. 

For example, during winter, when the environmental temperature is less than the body temperature, the skin receptors sense these variations and send the information to the anterior hypothalamus which will then inform the posterior hypothalamus that the body has to generate heat. 

Now, besides the behavioral habits, such as putting more clothes on or drinking hot tea, there are several other physiologic mechanisms through which heat production is increased.

First, thyroid hormone action is stimulated. 

Thyroid hormones are thyroxine or T4 and triiodothyronine or T3, which is the active form. 

One of their roles is to increase heat production and they do that by stimulating conversion of T4 to T3. 

T3 then increases the production of the energy molecule adenosine triphosphate or ATP in the body. 

ATP is basically the energy currency in the cell and the more we have, the more of it]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skeletal_muscle_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Htae7HWtSIyb40dsaKYU5ofnTfOExVuY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skeletal muscle histology]]></video:title><video:description><![CDATA[Now, let’s get a closer look! There are three types of muscles: skeletal, cardiac, and smooth muscle. Each of them has distinct functions as well as structural characteristics that can be identified histologically.

Let’s focus on skeletal muscles, which are composed of large, elongated, branching, and cylindrical cells with multiple nuclei that are located along the periphery. These cells are often also called muscle fibers. In this longitudinal section of skeletal muscle, the muscle fibers are the narrow strands that are all arranged in the same direction. The muscle fibers are also arranged in parallel bundles called fascicles.

With longitudinal sections of skeletal muscle, the nuclei may not always look like they’re in the periphery, but with a transverse section, it’s much easier to visualize. It’s also easier to identify the endomysium, which is the connective tissue that surrounds the polygonal muscle fibers. The perimysium is also easier to identify, since it’s an even thicker layer of connective tissue that surrounds the fascicles.

Skeletal muscle has a rich network of capillaries, and if we zoom in further, we can see that the capillaries are typically seen at the corners of the polygonal muscle fibers. Although it’s not always easy to see with H&amp;amp;E staining, the subtypes of skeletal muscle can sometimes be differentiated. In this example, the Type I or slow twitch muscle fiber is distinguished by its smaller size and darker stain when compared to the neighboring Type II or fast twitch muscle fibers.

The muscle fibers contain many myofibrils that are made up of contractile proteins called myofilaments. The myofilaments consist of thin actin filaments and thick myosin filaments that are arranged in parallel and also form the basic unit of the striated muscles called a sarcomere. The myofilaments mainly consist of thin actin filaments and thick myosin filaments. The alignment and structure of the sarcomeres result in perpendicular bands ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ovary_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H_JzLc3ERIiXZ7wjUI56pGElTN25egO6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovary histology]]></video:title><video:description><![CDATA[The internal female reproductive organs consist of the ovaries, uterine or fallopian tubes, uterus, and vagina.

The ovaries are almond-shaped structures that produce steroid hormones like estrogen and progesterone, as well as the female gametes or oocytes.

Each ovary is typically about 3 centimeters long, 1.5 centimeters wide, and 1 centimeter thick, with a thin outer capsule.

The capsule is made up of a thin layer of simple cuboidal epithelium that’s only one cell thick, and an underlying dense layer of connective tissue called the tunica albuginea.

The majority of the ovary consists of the cortex, which is the outer region where oocytes and ovarian follicles develop.

Ovarian follicles are the fluid-filled structures that each contain an oocyte.

This cortex of the ovary has highly cellular connective tissue in comparison to the inner region of ovaries called the medulla, which consists mostly of loose fibroelastic connective tissue with many large, tortuous blood vessels, lymphatic vessels, and nerve fibers.

Alright, let’s take a closer look at the cortex.

The primordial follicles are the follicles found in the outer cortex that develop during fetal life.

At this stage, they actually stop developing, which is called arrested development, and they stay this way until they’re needed for ovulation.

The primary oocyte is the large round cell that makes up the majority of each primordial follicle.

The primary oocytes have a prominent nucleus and a diameter that’s about 25 to 30 um.

The outermost layer of the primordial follicles is a single layer of flattened follicular cells, which are pregranulosa cells.

The zona pellucida is a very thin, pink or eosinophilic layer of glycoproteins that sits between the primary oocyte and the outer follicular cells.

When a primordial follicle continues developing, the next stage of follicular development is called the primary follicle.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arteriole,_venule_and_capillary_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C44BuaJEQwGAAuWkvBCwSX26Q2CB-O3_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arteriole, venule and capillary histology]]></video:title><video:description><![CDATA[The circulatory system consists of two functional parts, the lymphatic system and the blood circulatory system. 

The microvasculature is part of the blood circulatory system and consists of the arterioles, capillaries, and venules. 

This is the portion of the circulatory system that’s responsible for the exchange of gases, nutrients, fluids, and metabolic waste. 

The majority of this exchange occurs in the capillaries. 

The arterioles are continuations of the small muscular arteries that can constrict in order to control the amount of blood that flows into the capillary beds. 

There are also muscular precapillary sphincters between the arterioles and capillaries called precapillary sphincters, that also help control how much blood flows to the capillary beds. 

The capillaries drain the blood into the postcapillary venules, then the collecting venules, and finally the small muscular venules. 

The small muscular venules gradually increases in diameter and eventually drain into small veins.

Alright, this image is an example of an arteriole from the abdominal mesentery. 

Similar to most blood vessels, the arteriolar wall has three main layers, the tunica intima, tunica media, and tunica externa. 

The tunica intima consists of an internal elastic membrane or lamina and an inner lining of flat endothelial cells with round nuclei. 

The tunica media consists of 1 to 2 layers of circularly arranged smooth muscle. 

The tunica externa surrounding the smooth muscle is a very thin layer of fibrous tissue that can be difficult to identify in images like this. 

Here’s an example of a smaller arteriole. 

We can see 3 nuclei from endothelial cells and two smooth muscle nuclei. 

In smaller arterioles like this one, the internal elastic lamina is not present. 

After the arterioles, blood flows into the capillaries, which are the blood vessels with the smallest diameter in the body. 

The walls of the capillaries are composed of only a single layer of endothel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thymus_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fe5b2solRxCJvxFqbYb4FI3xRQG4lWia/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thymus histology]]></video:title><video:description><![CDATA[The lymphatic system is an essential part of the immune system and it consists of a network of lymphatic vessels, tissues, and organs.

The lymphatic vessels drain interstitial fluid or lymph from peripheral tissues back into the blood.

Lymphoid tissue and organs contain a lot of lymphocytes and other white blood cells.

The primary lymphoid organs include the thymus and bone marrow.

And the secondary lymphoid organs include the tonsils, lymph nodes, spleen, and mucosa-associated lymphoid tissue or MALT for short.

The thymus is a flat encapsulated lymphoid organ located in the anterior superior mediastinum, right behind the sternum.

During embryonic development, the thymus originates from the embryo’s third pair of pharyngeal pouches.

This organ is most active during childhood, reaching its largest size around puberty, with a weight of approximately 30 to 40 grams.

After puberty, the thymus will begin to slowly involute or decrease in size, with less lymphatic tissue and an increase in adipocytes.

The thymus plays an important role in the maturation of T cells, which includes negative selection or central tolerance.

This process, along with regulatory T cells help prevent autoimmunity.

This is a low power image of a neonatal thymus.

At this magnification, the thin collagenous capsule is a little hard to see, but if we zoom in a little further, we can see the capsule more clearly, as well as the connective tissue that extends inward from the capsule into the thymus, forming incomplete lobules.

When compared to an adult’s thymus, we can see that the adult thymus has noticeably more fatty infiltrate, which is seen by the white spaces scattered throughout the organ.

The lobules of both adult and neonatal thymi have inner regions that stain light purple and pink, which is called the thymic medulla; and the outer regions of the lobules are more basophilic or dark purple, which represents the cortex of the thymus.

The clear distinction between the in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Traumatic_brain_injury:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y5GI4GeCSGW4rZBIdylujVy8TfKWATbX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Traumatic brain injury: Pathology review]]></video:title><video:description><![CDATA[At the emergency department, 65-year-old Christian came in complaining of headaches, vision problems, and memory loss. These symptoms have gradually progressed over the past couple of weeks. On examination, there’s slurred speech, and his gait is unsteady. He has a history of chronic alcohol abuse. Head CT shows a “crescent-shaped” hyperdense mass that crosses the suture lines. Later that day, 33-year-old Max is brought in after a fight. They reported being knocked unconscious, but regained consciousness after an unknown period of time. Head CT is ordered and shows a “lens-shaped” hyperdense mass that doesn’t cross the suture lines.  Max was very agitated and said they felt fine.  They then left the hospital against medical advice.  Later that day, Max lost consciousness again and died at home. 

Okay, so Christian and Max had some form of traumatic brain injury. When an external force damages the head resulting in temporary or permanent brain dysfunction, we call it a traumatic brain injury, or TBI.  Now, as a direct result of the external force, TBIs can cause extra-axial and intra-axial injuries. Extra-axial injuries are within the skull but don’t involve the brain parenchyma. The most high yield ones are epidural and subdural hematomas, as well as a subarachnoid hemorrhage. Intra-axial injuries - on the other hand - do involve the brain parenchyma, and the most high yield one for your exams is diffuse axonal injury. Now, the initial brain injury can impair the normal functioning of the cerebral metabolism and result in complications, such as tissue hypoxia, cognitive impairment, and seizures. Additionally, if the brain injury is associated with intracranial bleeding or severe inflammation followed by edema, the pressure within the skull may rise and result in severe complications. For your exams, it’s important to note that the most important complication of increased intracranial pressure is brain herniation. Trauma initiates a series of mol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Airflow,_pressure,_and_resistance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PNccr0wpTmilJrL-0uiLi0gxRgu5O9z5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Airflow, pressure, and resistance]]></video:title><video:description><![CDATA[When we breathe, air moves between the atmosphere and the alveoli inside the lungs. 

This movement of air is driven by the pressure difference between the two sites; where air flows from an area of higher pressure to an area of lower pressure. 

The journey of air within airways is not easy though, due to the presence of airway resistance. 

Alright, pressure difference and airway resistance determine how much air flows through an airway in a period of time, which is known as airflow. 

Airflow can be measured in liters per minute. 

The relationship between airflow and pressure difference is directly proportional, which can be represented as airflow, or Q, and that is directly proportional, (which looks like a stretched out Greek letter alpha) , to ∆P, which is the pressure difference. Q ∝ ∆P

This means that the higher the pressure difference between two sites, the more air flowing between them. 

On the other hand, the relationship between airflow and airway resistance is inversely proportional, represented as Q ∝ 1R  , where R is airway resistance,  meaning if airway resistance increases, airflow decreases. 

Alright, by setting up these two relationships in one equation, we will get Ohm’s law, which states that airflow Q, equals the pressure difference ∆P, divided by airway resistance R. Q = ΔPR

Now, the pressure difference, or ∆P, between the atmosphere and the alveoli can be created by changing the volume of the lungs during inspiration and expiration. 

So, during inspiration, contraction of  the diaphragm and chest muscles causes the lungs to expand, increasing their volume and the volume of the alveoli. 

Now, if we look at a single alveolus, as its volume has increased, there’s now more room inside for gas particles, so the pressure inside goes down and becomes lower than the atmospheric pressure. 

As a result, air flows from the atmosphere into the alveolus

At the end of inspiration, the alveolus becomes filled with oxygen-rich air from the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/clinical-skills:disinfecting-frequently-touched-surfaces</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0305B83ASg6H4y-e8oRG_0IsRlCGUujv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Disinfecting frequently touched surfaces]]></video:title><video:description><![CDATA[Recently the CDC updated their guidelines on how to disinfect frequently touched surfaces at home in response to the COVID-19 pandemic.

Most common EPA-registered disinfectants that you can get at the grocery store will work just fine, but if you need to, you can make your own using household bleach!

First, make sure you wear gloves and are in a well ventilated area whenever you work with bleach! Also don’t mix bleach with ammonia or any other cleaner. 

Fill up a container with a quart of water or 950mL. 

Then add 4 teaspoons of bleach, and mix. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Beating_Coronavirus:_Flatten_the_Curve_Raise_the_Line</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sy-vFzGPRL_ljH31uL6dLCCCRz68O0wk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Beating coronavirus: Flatten the curve, raise the line!]]></video:title><video:description><![CDATA[COVID-19, caused by a coronavirus, has led to a pandemic that threatens everyone. 

The overriding strategy to limit the damage and to beat this pandemic is to “flatten the curve and raise the line.”  

During a pandemic, health care resources like hospitals and ICU beds can be overwhelmed by the sheer number of patients - above and beyond the baseline number of patients who are already being cared for by the healthcare system, like those with heart attacks, strokes, or other infections.

To visualize the progress of a disease outbreak over time, we can plot an epidemic curve. 

This is a graphic depiction of the number of new outbreak cases by date of onset of the disease. 

The overall shape of the curve can reveal the type of outbreak we’re dealing with and the horizontal line represents the capacity of the community health care system. 

Hospital capacity is defined as the number of beds, staffing, and other measures available for patient care. 

Now, most hospitals in the US and many other countries are already operating close to the capacity line, so when a pandemic occurs, the infectious agent spreads very rapidly, and the curve can rise and cross the line.  

When this happens, the healthcare system can no longer meet the needs COVID 19 patients as well as all of the other types of patients! 

At that point, people are not getting the best care and outcomes like the mortality rate start to rise quickly. 

For these reasons, a large number of lives can be saved by simply ensuring people get sick at a slower rate, and this is called “flattening” of the epidemic curve.  

A flatter curve assumes the same number of people ultimately get infected, but over a longer period of time, which leads to a less overwhelmed health care system. 

Now, a key factor to flatten the curve is social distancing, which refers to measures aimed at reducing close contact between people. 

This is why governments are closing schools, non-critical businesses, and other place]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Using_Osmosis_to_support_distance_learning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RvtLxOgoQEKhzehbi1lo_2YJSY6cR-rS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Using Osmosis to support distance learning]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Using Osmosis to support distance learning through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_transform_live_courses_into_online_courses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wSmltSQjTsCgV2PB2H1DAkAHSHin1dMf/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to transform live courses into online courses]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to transform live courses into online courses through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Managing_your_students_mental_health_during_public_health_emergencies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7GfFf8XVRNqqs1hzMqQD5E_CTe2Cnn27/_.jpg</video:thumbnail_loc><video:title><![CDATA[Supporting your students mental health during public health emergencies]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Supporting your students mental health during public health emergencies through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Supporting_educators_mental_health_during_high-stress_periods</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8ktHVTsVQzCOG-Pkcm00Cuz2SVatMZoW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Supporting educators mental health during high-stress periods]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Supporting educators mental health during high-stress periods through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19:_Tips_for_maximizing_psychological_health_during_stressful_times</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x2bYCbZHSrOZu8iqB8x0qbY2T_S3Vb9B/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19: Tips for maximizing psychological health during stressful times]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of COVID-19: Tips for maximizing psychological health during stressful times through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19:_Guided_Meditation:_30_Minutes_to_De-Stress</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f-iTWo1qS0aIqwbAxFQie8jsTAC2ukj9/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19: Guided Meditation: 30 Minutes to De-Stress]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of COVID-19: Guided Meditation: 30 Minutes to De-Stress through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19:_Ask_Me_Anything_Open_Forum_with_Rishi_Desai,_Md_MPH</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6ozlXjq3S9aGABwFYeHj9Rv_T_GPD6Eb/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19: Ask Me Anything Open Forum with Rishi Desai, Md MPH]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of COVID-19: Ask Me Anything Open Forum with Rishi Desai, Md MPH through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colon_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EHB9M6idQk6nhs79UNYwBUpsTCa85PiP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colon histology]]></video:title><video:description><![CDATA[Now, let&amp;#39;s get a closer look. The large intestine consists of the appendix, cecum, colon, rectum, and anal canal. The colon is mainly responsible for reabsorbing water and electrolytes from the feces within its lumen. The colon is continuous with the rectum, where the feces is stored before defecation. Similar to the rest of the large intestine, the colon has 4 main layers: the mucosa, submucosa, muscularis propria, and a surrounding serosal layer of connective tissue that isn’t seen in this image.

Even at low magnification, we can see that the colon’s mucosa at the top of this image doesn’t have the distinct long villi or finger-like projections that would normally be seen in the small intestine. Taking a closer look at the colon’s mucosa, the lumen of the colon is seen at the top of the image and the first layer of cells lining the mucosa is the epithelium of the mucosa. The epithelium consists of two types of cells, enterocytes and goblet cells. The enterocytes or absorptive cells are the simple columnar cells with microvilli. They’re also called the absorptive cells because of their main function of absorbing water from the colon lumen. And the goblet cells are responsible for secreting mucus. Although the cells aren’t clearly seen in this image, the mucus they produce is easily seen as the globular structures that are stained dark purple from the hematoxylin and eosin stain. The surface epithelium is continuous with straight, unbranched, tubular glands called the crypts of lieberkühn. Unlike the crypts in the small intestine, these crypts extend through the majority of the mucosa, from their openings at the intestinal surface all the way to the muscularis mucosa along the deepest portion of the overall mucosa. It may not always appear to be continuous on histological slides because the path of the crypts may not always travel along the same plane as the section of tissue taken from the colon. The superficial portions of the crypts will typic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Covalent_bonding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ikDFt31XTZisjWvdN8UgOtVQQFi7Z2cO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Covalent bonding]]></video:title><video:description><![CDATA[A covalent bond is where electrons are shared between two nonmetal atoms.  

Let’s start with hydrogen, which is a nonmetal on the left side of the periodic table. 

Hydrogen has an atomic number equal to one which means that it has one proton and one electron. 

If we take two hydrogen atoms, each with its own electron, we can combine them to form a molecule, where each atom contributes one valence electron to the final molecule. 

In other words, these two valence electrons are shared by both atoms in the final molecule. 

We can represent this process by putting two dots between the two hydrogen atoms.  

These two dots represent one covalent bond.  

We can also represent a covalent bond by drawing a straight line between the hydrogen atoms. 

One straight line means one covalent bond and represents two valence electrons. 

Now, in our hydrogen molecule, opposite charges attract. 

So the one electron from the hydrogen atom on the left is attracted to the positively charged nucleus of the hydrogen atom on the right. 

At the same time, the negatively charged electron from the hydrogen on the right is attracted to the positively charged nucleus of the hydrogen on the left. 

So a mutual attractive force holds together the two atoms in a covalent bond.

At the same time, like charges repel, which keeps the two positively-charged nuclei from getting any closer together.

Another way to represent the hydrogen molecule is by writing H with the subscript two. 

This implies that we have two hydrogen atoms in our molecule. 

So hydrogen is an example of a diatomic molecule, which is a molecule composed of two atoms. 

There’s an easy way to remember a list of the elements that form diatomic molecules. 

Imagine a mad scientist who is named Dr. Brinclhof, whose name spells out each of the diatomic molecules: “Br” is bromine, “I” is iodine, “N” is nitrogen, “Cl” is chlorine, “H” is hydrogen, “O” is oxygen, and “F” is fluorine.

Let&amp;#39;s try drawing some o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Quantum_numbers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9RrcfLfNQ3aLgkUtZreUiPEgSS23yhBr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Quantum numbers]]></video:title><video:description><![CDATA[Quantum numbers can be used to understand the electronic structure of atoms. 

Quantum numbers come from Quantum Mechanics which was the successor to the Bohr Model.  

The Bohr model traces to the early 20th century physicist Niels Bohr, who realized that he could use ideas from classical mechanics to formulate a simple picture of an atom. 

His main idea was that an electron orbits around the nucleus at a specific radius in the same way that planets orbit around the Sun. 

Unfortunately, the Bohr model does not remain accurate when dealing with atoms with more electrons than hydrogen.  

For many electron atoms, more sophisticated theories based on quantum mechanics have been developed. 

A main point of these theories is that, rather than imagining an atom as a collection of electrons orbiting the nucleus, it is better to think of the electrons as a diffuse cloud around the nucleus -- corresponding to a probability of electrons existing in various locations. 

Therefore, rather than stating that an electron lies at a given, fixed distance from the nucleus like the Bohr model, these more sophisticated models provide the probability of finding electrons in various locations.

These clouds of likely electron locations have a name -- they are called orbitals. 

Looking at a picture of an electron density model, we can see that all these dots indicate the probability of finding an electron. 

We don&amp;#39;t know exactly where the electron is, but it is somewhere in this cloud around the nucleus. 

If we think about this orbital as being a three-dimensional sphere, we would say there is a 90% probability that the electron is somewhere in that sphere around the nucleus.

Electrons in orbitals are described by four quantum numbers. 

The first quantum number is called the principal quantum number, and it is symbolized by N.  

N is a whole number, like 1, 2, 3, or higher. In a diagram of an atom, electrons with higher values of N -- and thus higher principal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Back_pain:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f8KbnHp5R2CPVcC_J5IvhqZ0SYOPBjE2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Back pain: Pathology review]]></video:title><video:description><![CDATA[At the urgent care clinic, three people came in with lower back pain. The first is Jeff, a 26-year-old, who says his pain began 5 hours ago after trying to lift a 300-pound weight off of the floor at his local gym. He describes the pain as sharp and severe and says the pain goes down the back of his right leg and into his foot. Physical examination reveals a positive straight leg raise test on the right, and a diminished right Achilles tendon reflex. Second is Beth, a 68-year-old, who says she slipped and fell while walking in her kitchen yesterday. Her history includes a wrist fracture from a little over a year ago. Physical examination shows midline spinal tenderness to palpation. Finally, we have Harry, a 71-year-old male, who says his back pain has progressively worsened over the past month, keeping him up at night. He also reports increased urinary frequency.

Back pain is a very common complaint and one for which there are many potential causes. It can originate from the spinal cord, nerve roots, the vertebral column, the surrounding muscles, and ligaments, or even extra-spinal structures, such as abdominal organs. Therefore, the causes of back pain can be subdivided into mechanical causes, such as muscle strain, spinal osteoarthritis, disc herniation, spinal stenosis, vertebral fractures and osteoporosis; and non-mechanical causes, such as bone metastasis, seronegative spondyloarthritis, and vertebral osteomyelitis.

First, let’s start with musculoskeletal causes. The vast majority of cases of back pain are considered non-specific musculoskeletal pain due to strained muscles or ligaments. These individuals have no sensory or motor deficits, and they typically complain about tenderness over the affected muscle or ligament. The treatment for these individuals is prescribing activity as tolerated and NSAIDs for pain management. The next one is spinal osteoarthritis, which can be due to the natural aging process where the cartilage at the tips of bones ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_masses:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OjvpnmJnRq_mdf4SIYDjC3C5ThapHq8g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenal masses: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you see two individuals. First is Jessica, who comes in with lumbar pain, anuria, and constipation. Examination is unremarkable and she doesn’t have any history of kidney disease. The other person is 38-year-old Dan, who is obese and has an abnormally round face. He is also hypertensive and hyperglycemic. Dan is not taking any medications but he’s complaining of severe lumbar pain on the left side. Abdominal CT scans were obtained for both. In Jessica’s case, imaging detected a mass in the right adrenal cortex. In Dan’s case, CT detected a mass in the left adrenal cortex.

Ok, so both seem to have some type of adrenal masses. But first, a little bit of physiology. Each adrenal gland has two main components: the cortex and the medulla. For your exam, something high-yield to keep in mind is that the cortex is composed of 3 zones. The zona glomerulosa, the outer zone, contains clustered cells that produce mineralocorticoids, mainly aldosterone, which regulates blood pressure and electrolyte balance. The zona fasciculata, the middle zone, contains foamy-looking cells in columns that are responsible for the production of glucocorticoids, predominantly cortisol, which increases blood sugar levels via gluconeogenesis, suppresses the immune system, and aids in metabolism. And the innermost zone is the zona reticularis, which has basophilic cells arranged in anastomosing cords that produce gonadocorticoids, especially androgens like dehydroepiandrosterone or DHEA. 

The medulla is composed of special cells called chromaffin cells. These are modified postganglionic sympathetic neurons that originate from the neural crest. Normally, when a fetus is in its 5th week of development, special cells called neural crest cells start migrating along the midline of the embryo. In the thoracic region, neural crest cells differentiate into the neurons of the sympathetic chain on either side of the developing spinal cord. In the lumbar region, neural cres]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis_C_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fzW-78EiQ26RGhwFw6aFb8CWRsisgPbk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis C virus]]></video:title><video:description><![CDATA[Hepatitis C virus is a part of the flaviviridae family, and it can be broken down in hepat- which refers to the liver, and -itis, which means inflammation. 

So this virus affects the liver, causing hepatitis. 

Hepatitis C virus is enveloped, meaning that it is surrounded by a membrane. 

It also has a lipoprotein envelope that’s very similar in structure to two lipoproteins that normally transport cholesterol through the blood: low density lipoprotein, or LDL and very-low-density lipoprotein, or VLDL. 

Underneath the membrane, there’s an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. 

The capsid holds a single strand positive-sense RNA, meaning that it has positive polarity, which is why it can be used directly by the host ribosomes to synthesize viral proteins.

Now, hepatitis C virus can be transmitted through contaminated blood or through sexual contact. 

Once inside the body, hepatitis C virus circulates the blood and reaches the liver, where it infects the main liver cells called hepatocytes; and B lymphocytes, which are a type of immune cells that create antibodies.

First, the virus binds to the cells using its envelope, which is very similar to LDL and VLDL, so it can attach to specific LDL receptors. 

Then, the virus enters the cell by endocytosis, which is when it’s wrapped by the cell membrane and brought inside the cell in a bubble called an endosome. 

Next, the viral membrane fuses with the endosome and releases the capsid which dissolves in the cytoplasm, leaving only viral RNA. 

Then, viral RNA binds to the host ribosomes and is used to create structural and non-structural proteins. 

Structural proteins will be used to make the viral particle, while the non-structural proteins make the replication complex that contains an enzyme called RNA dependent RNA polymerase. 

This enzyme uses the positive-sense viral RNA to create a negative-sense template. 

And the replication complex can]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/ELISA_(Enzyme-linked_immunosorbent_assay)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/asAAA-rWRSubu3omCNvaPMuOQ_K_wYhM/_.jpg</video:thumbnail_loc><video:title><![CDATA[ELISA (Enzyme-linked immunosorbent assay)]]></video:title><video:description><![CDATA[Enzyme-linked immunosorbent assay - or ELISA for short - is a laboratory technique or assay where antibodies or antigens in people’s samples are immobilized in a surface, and then detected by an antibody with an enzyme attached that causes a change of color. 

So it’s useful to diagnose infections, such as HIV, hepatitis B, or malaria; and autoimmune diseases, like Graves’ disease, systemic lupus erythematosus, or rheumatoid arthritis, where the body reacts to its own proteins as if they were foreign antigens. 

Immune response

We are constantly surrounded by harmful microorganisms called pathogens, that could cause a lot of damage if it wasn’t for the immune system. 

These pathogens have unique parts called antigens. 

Now, B lymphocytes are cells of the immune system that can detect those antigens and trigger an immune response by secreting lots and lots of antibodies. 

These antibodies, also called immunoglobulins or Ig, are Y-shaped proteins that have two regions: the constant fragment region, also called Fc, that determines the antibody class - IgD, IgM, IgG, IgA, or IgE; and two fragment-antigen binding, or Fab regions, that recognize and bind to the antigen in order to inactivate it, preventing the pathogen from reaching its target cell and causing damage. 

Principle of ELISA

Now, the basic idea with ELISA is to use that specific link between the antigen and antibody to help diagnose infections or autoimmune diseases. 

More specifically, ELISA can be used to look for either the pathogen’s antigens or the antibodies our body secretes against them. 

More than that, it also makes them visible or measurable by using an antibody against the suspected antigen or antibody. 

But this antibody comes with a +1: it has an enzyme attached, which can modify a substrate called a chromogen. 

Chromogen literally means that it generates color, so the change in color determines whether the test is positive or negative.

So, think of an ELISA test like a cook]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis_A_and_Hepatitis_E_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SnV6TJp7Tr6xdsXQQ4Stn4yVSeqBpkiF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis A and Hepatitis E virus]]></video:title><video:description><![CDATA[Hepatitis A and E are two viruses that cause acute hepatitis.The name comes from the word hepat - meaning liver, and suffix -itis to label inflammatory disease, meaning that hepatitis is an inflammation of the liver. They tend to cause hepatitis epidemics, especially in children and young adults.

Now, even though they cause the same disease, Hepatitis A and E viruses come from different families. Hepatitis A is a picornavirus, while hepatitis E is a hepevirus. They are naked viruses, made of a single strand RNA surrounded by a capsid, which is a spherical protein shell. And they’re “naked” because the capsid isn’t covered by a lipid membrane. 

These viruses are transmitted by the fecal-oral route, in other words, you catch it by ingesting stool particles of someone who is sick - yuck! This usually happens if infected stool ends up in the food, water and shellfish, or on surfaces. So usually, outbreaks can often be traced to the same source of food or water, and they also tend to be common in day-care centers. 

Ok, now, when you eat, food travels through your pharynx, esophagus, stomach, duodenum and intestines. In the intestines all of the nutrients are absorbed and go through hepatic portal venous system, which is a system of veins that carry blood from the spleen, pancreas and intestines to the liver. And just like nutrients, the hepatitis A or E reach the liver through the hepatic portal venous system.

Now, the liver is made of functional units called hepatic lobules. The main cells are called hepatocytes, and their main job is to use a huuuge array of enzymes to detoxify harmful substances from our blood - like drugs or alcohol; synthesize a variety of important proteins, like coagulation factors; and convert cholesterol into bile salts which along with water and bilirubin make up the bile. Bile flows into the bile ducts and eventually reaches the gallbladder, which is a small pear-shaped hollow organ located beneath the liver. This is where bile i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ehrlichia_and_Anaplasma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/17AU_DahSf6Wx9b84MgvYfk8TPu7HdOq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ehrlichia and Anaplasma]]></video:title><video:description><![CDATA[Ehrlichia and Anaplasma are two genera of Gram-negative pleomorphic bacteria, which means they can take different shapes - round like a coccus, or coccobacillary, which means somewhere between a spherical coccus and a rod-like bacillus. 

The most common species that cause disease in humans are Ehrlichia chaffeensis, which causes a disease called human monocytic ehrlichiosis, or HME, and Anaplasma phagocytophilum, which causes a disease called human granulocytic anaplasmosis, or HGA. 

Now, Ehrlichia and Anaplasma have a thin peptidoglycan layer, so they don’t retain the crystal violet dye during Gram staining. 

Instead, like any other Gram-negative bacteria, they stain pink with safranin dye. 

Both are non-motile, non-spore forming, and obligate intracellular which means they can survive only inside cells.

Finally, Ehrlichia and Anaplasma don’t grow on routine culture media and they need to be cultivated in vitro in different cell lines. 

So, Ehrlichia chaffeensis can be isolated in DH82 canine histiocytic cell line and Anaplasma phagocytophilum can be isolated in promyelocytic leukemia HL-60 cell line.

Now, Ehrlichia and Anaplasma enter circulation following a tick bite and once inside the body, they infect circulating leukocytes. 

Ehrlichia primarily targets monocytes and macrophages, and it infects them using tandem repeat proteins, or TRP. 

These bacterial proteins bind to proteins found on the surface of the cell, and they induce phagocytosis - so basically, they make the cell gobble up the bacteria. 

Anaplasma, on the other hand, primarily targets neutrophils, and infects them with the help of a P-selectin glycoprotein which binds on the P-selectin glycoprotein ligand-1, or PSGL-1 found on the surface of neutrophils. 

This activates an intracellular pathway that leads to reorganization of cellular actin which leads to phagocytosis, allowing Anaplasma to enter the cell.

Once inside the cell, both Ehrlichia and Anaplasma live in an early end]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coxiella_burnetii_(Q_fever)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LGaqPUeITNKq1yRCymelSo1JRNm0N4xj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coxiella burnetii (Q fever)]]></video:title><video:description><![CDATA[Coxiella burnetii is a gram-negative rod that causes a condition called Q fever. This bacterium is highly resistant to environmental stressors including high temperatures and ultraviolet light, and spreads to humans from animals like cows, sheep, and goats, so Q fever is considered a zoonotic infection. 

Now, Coxiella burnetii is considered a Gram-negative, obligate intracellular organism. So, it can only replicate inside other cells, like our macrophages. C. burnetii is also non-motile and has a biphasic life cycle that consists of an environmentally stable, non-replicating form called small cell variant, or SCV for short, and a metabolically active, replicating large cell variant, or LCV. When it feels threatened by the environment, like when the temperature becomes too high or too low, in case of extreme dryness, or when there’s harmful radiation around, C. burnetii transforms into the SCV by shrinking and condensing its DNA and periplasmic space. In this form, it is able to resist heat, harsh chemicals, digestive enzymes, and even antibiotics. Remarkably, the SCV can survive for years, waiting for favorable conditions to come, and then convert into the LCV that can then grow and divide inside host cells. 

Now, the primary disease that Coxiella burnetii causes is called Q fever. This disease is most commonly acquired by inhalation of aerosolized C. burnetii from an infected animal.  

Infection can happen during parturition, when large amounts of bacteria are released in birth fluids, or from dust contaminated by animal excrement, such as when cleaning a barn. It can also be picked up through ingestion of raw milk or other unpasteurized dairy products, or by contact with contaminated animal materials.  

So, people at highest risk for infection include those in close contact with farm animals such as farmers and veterinarians, and also slaughterhouse workers.  

In terms of pathogenesis, the exact mechanism of disease is poorly understood. What is kno]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spinocerebellar_ataxia_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QcpPSquUROqz0QX6LxZPkDkESAyzheb4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spinocerebellar ataxia (NORD)]]></video:title><video:description><![CDATA[Spinocerebellar ataxia or SCA refers to a group of rare genetically inherited conditions, caused by mutations in several types of SCA genes. 

These mutations result in degenerative changes in the cerebellum and often, the spinal cord, which causes progressive problems with coordination and balance, known as ataxia.

The cerebellum sits at the back of the skull, posterior to the brainstem. 

Neurons send their axons carrying input from the spinal cord, the brain and the internal ear through the brainstem into the cerebellum.  

Once there, the cerebellum uses this information to coordinate and plan movement as well as maintain balance.

So, with mutations in the SCA genes, the cerebellum, along with the spinal cord, slowly degenerate. 

In fact, many different gene mutations have been identified, each of which is known to cause different types of spinocerebellar ataxia. 

The types are described using &amp;quot;SCA&amp;quot; followed by a number, according to their order of identification, so there’s SCA1 through SCA48, with SCA3 being the most common type. 

However, in about 40% to 25% of the cases, the causative genes are still unknown.

Now, most of these gene mutations are inherited in an autosomal dominant pattern, meaning that one copy of an altered SCA gene is enough to cause the disease. 

Affected individuals have a 50% chance of passing on the altered gene to their child, causing that child to have the disease. 

In some cases, the involved gene contains a triplet repeat, where the nucleotides C, A, and G are repeated multiple times in a row. 

And since CAG codes for the amino acid glutamine, the encoded protein will have multiple extra glutamines in a row. 

The specific way in which extra glutamines causes the disease’s symptoms isn’t fully understood, but the abnormal protein seems to aggregate within the neurons of the cerebellum and spinal cord, causing them to die.

The expanded CAG repeats also affect DNA replication itself. 

When cop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Early_infantile_epileptic_encephalopathy_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qAH3qNP0SJ2ahoGC4IImBq-XQxSrxKfV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Early infantile epileptic encephalopathy (NORD)]]></video:title><video:description><![CDATA[With early infantile epileptic encephalopathy, epilepsy means seizure disorder, encephalopathy means brain dysfunction, often due to damage, and ‘early infantile’ refers to the age of onset of the disease, which is usually within the first three months of life. 

So, early infantile epileptic encephalopathy, or EIEE, is a disorder characterized by recurrent and unprovoked seizures during early infancy, which can result in severe brain damage. 

The nervous system is made up of specialized cells called neurons which receive and send signals from other neurons. 

The two neurons communicate at the synapse, where one neuron sends neurotransmitters to the next neuron. 

Excitatory neurotransmitters, like glutamate, bind to the receptors on neurons and tell them to open up ion channels and relay an electrical signal. 

Inhibitory neurotransmitters like GABA can close the ion channels and dampen down electrical signals.

The most common causes of EIEE are structural brain abnormalities like hemi-megalencephaly where one half of the brain is larger than the other; absence of the corpus callosum, which is a large fiber bundle connecting the left and right hemispheres; and dysplasia, or abnormal development of the cerebral cortex. 

Other causes include metabolic disorders like nonketotic hyperglycemia; and mutations in the genes coding for normal development of the neurons. 

These include the ARX, or Aristaless-related homeobox, gene, and STXBP1, or syntaxin-binding protein 1, gene. 

Regardless of the cause, defective neurons fire synchronously (at the same time) and excessively, resulting in a seizure. 

Infants with EIEE typically present with seizures within the first 3 months of life, often in the first 10 days. 

The seizures can occur during wakefulness and sleep. 

They’re usually generalized tonic-clonic seizures, which means that the muscles in the trunk and extremities suddenly become stiff, the tonic phase, and then jerk, the clonic phase. 

Some indi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mycobacterium_avium_complex_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EhvdrvQBTtibS1nn88FSR8VJRXW__YLf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mycobacterium avium complex (NORD)]]></video:title><video:description><![CDATA[Mycobacterium avium complex, or MAC, includes three species; Mycobacterium avium, Mycobacterium Chimaera, and Mycobacterium intracellulare. 

MAC is the most common nontuberculous mycobacteria, or NTM.

The three different species of MAC are difficult to differentiate and cause the same spectrum of diseases, so they are often grouped together. 

MAC is very different from Mycobacterium tuberculosis. 

MAC lung infection is a chronic disease, often present for several years prior to diagnosis. 

It typically has a more indolent course, and can be difficult to eradicate, with frequent recurrences after completing long courses of treatment. 

In addition, in immunocompromised individuals, MAC can become disseminated, affecting organs other than the lungs, and can cause lymphadenitis.

MAC are non-motile, facultative intracellular bacteria which means they can survive both inside and outside the cell. 

They’re also aerobic which means they need oxygen to survive. 

They have a high content of mycolic acid in their cell wall, which makes them waxy, hydrophobic and impermeable to routine stain such as Gram stain. 

So, they need special staining methods to be visualized such as Ziehl-Neelsen staining which is able to penetrate the waxy mycobacterial cell wall. 

So, the stain binds to the mycolic acid in the mycobacterial cell wall and after staining, an acidic decolorizing solution is applied which removes the red dye from the background cells, tissue fibres, and any organisms in the smear except Mycobacteria, which retain the dye; and this is why they are called “acid-fast,” and they appear bright red on a blue background. 

Finally, MAC are slow growing bacteria, and it typically takes them 10 to 21 days to grow on a medium called Lowenstein Jensen. 

MAC are ubiquitous in soil and water and they are thought to enter the body through inhalation. 

Once inside the body, they adhere to mucosal epithelial cells in the respiratory tract, and infect the macrophag]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Tom_Frieden:_Former_Director_of_the_CDC_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/paMktXcUTGij-YmKcs_TdSRYRYOaSd3k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Tom Frieden: Former Director of the CDC (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Tom Frieden: Former Director of the CDC (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diffusion-limited_and_perfusion-limited_gas_exchange</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pDXEaHHmRsaIfMfnxNZSSjk7SUGNxf9c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diffusion-limited and perfusion-limited gas exchange]]></video:title><video:description><![CDATA[The primary role of the lungs is to ensure gas exchange between the external environment, and the blood within the circulatory system. 

This happens thanks to a series of branching tubes called airways, which conduct the air down into small thin-walled sacs called alveoli, which are wrapped in an intricate network of tiny blood vessels called pulmonary capillaries. 

And the alveolo-capillary membrane, where the layer of alveolar cells lining the alveoli meets the endothelial cells that make up the pulmonary capillary, is where gas exchange occurs. 

Now, before we delve into diffusion, perfusion and their limits, remember that gas exchange across the alveolo-capillary membrane happens according to Fick’s law. 

Fick’s law states that the net rate of diffusion - V of any particular gas across the alveolar-capillary membrane, is proportional to the pressure gradient across the wall; which is the difference between the partial pressure of the gas in the alveolar sacs, or PA, and the partial pressure of the gas in the blood, or Pa, and also proportional to the surface area of the wall, or A, but inversely proportional to the wall’s thickness - T. And this is all times the diffusion constant - D, which varies from gas to gas.
 V=(PA-Pa)ADT
So, diffusion-limited gas exchange means that a gas like oxygen or carbon dioxide can diffuse across the alveolo-capillary membrane as long as the partial pressure gradient is maintained. 

On the other hand, perfusion-limited gas exchange means that if the pressure gradient is not maintained, and the concentration of gases on the two sides of the alveolo-capillary membrane becomes the same, further gas exchange is only possible by increasing blood flow, or perfusion, in the pulmonary capillary.

To understand these concepts, let’s look at a section of an alveolar sac, with a pulmonary capillary running along its surface. 

The capillary carries mixed venous blood, which is low in oxygen and high in carbon dioxide]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Jaundice:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yDMiRCySTy_59tJ5yFkBQgnRS2W8yZPg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Jaundice: Pathology review]]></video:title><video:description><![CDATA[Christine, a 20-hour-old female infant presented with neonatal jaundice. She was born at term following an uncomplicated pregnancy. Physical examination shows she is alert, well-perfused, feeding normally, and afebrile. The skin is yellow in the face, trunk, and limbs, but there’s no organomegaly. Laboratory studies reveal high total bilirubin of 25mg/dL, normal liver function tests, and no evidence of hemolysis. On the other hand, a 17-year-old boy named Steven comes to his primary care physician because his sister has been telling him that periodically, he look a little yellow. Medical history is noncontributory, physical examination shows no abnormalities, but Steven mentions that he has recently started working out and dieting to prepare for prom. Laboratory studies show elevated total bilirubin concentration. A week later, his bilirubin concentration is normal. 

Now, both Christine and Steven have jaundice, but the underlying cause of their problem is different. Jaundice, also called icterus, is the abnormal yellowish pigmentation of the skin, mucous membranes, and sclera due to the deposition of the bilirubin. The reference range for total bilirubin is 0.2 - 1.2 mg/dl; while jaundice typically occurs when total bilirubin levels exceed 2mg/dl. Now for your exam, it’s crucial to know the metabolism of bilirubin! When old red blood cells pass through the spleen, macrophages eat them up and break down the hemoglobin to heme and globin. Heme is then converted into biliverdin by an enzyme heme oxygenase. Biliverdin is further converted into unconjugated or indirect bilirubin by an enzyme biliverdin reductase. 

Unconjugated bilirubin is the form of bilirubin that’s lipid-soluble.Since it’s not water soluble, this form of bilirubin binds tightly to albumin in the blood, therefore, it can’t be filtered by the kidneys and excreted in the urine. Instead, the unconjugated bilirubin undergoes hepatic metabolism of bilirubin, which consists of 3 main phases. The]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Body_Temperature_Assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rjH_54HXQ7SpIQJYtHX_aNIkR0W5-J5b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Body Temperature Assessment]]></video:title><video:description><![CDATA[Hello! This video covers how to assess body temperature. Normally you’d do everything on this list, but to keep things concise, this video will focus on the steps in blue and will also cover special populations like infants and the elderly, and include a summary.

Meet Fred. Fred’s deep core temperature is stable, averaging 37.2 degrees Celsius, or 99 degrees Fahrenheit. Fred’s oral temperature is also normal: 37° Celsius, or 98.6° Fahrenheit. 

Fred’s body temperature is where it should be. But what if it weren’t?

Fred might be hyperthermic or feel feverish, depending on the cause of his excess heat. Fever is when the body’s hypothalamic temperature setpoint increases, often caused by infection, inflammation, or malignancy. Hyperthermia is when the body retains too much heat.

A temperature between 37.5 and 38.3°C (or 99.5 and 100.9°F) is classified as hyperthermic. A temperature above 40°C, or 104°F, can be life-threatening.

Or, Fred could be hypothermic. He might have been exposed to cold for a prolonged period of time, accidentally or in preparation for a medical procedure. A temperature below 34.0°C, or 93.2°F, is classified as hypothermic.

Let’s check. We can measure Fred’s temperature in several ways.

Attach the blue, oral probe stem to the thermometer. Slide a disposable cover over the temperature probe.

Ask Fred to open his mouth and insert the thermometer into one of Fred’s posterior sublingual pockets. At the base of his tongue, not in front of it. Ask Fred to keep his lips closed. Wait 20-30 seconds or until the thermometer chimes.

Is Fred comatose, confused, critically ill, or in shock? Is he unable to close his mouth? Use a rectal probe for the most accurate measurement. Roll Fred over and into the Sims position, with the upper leg bent. Wear gloves.

Attach the red, rectal probe stem to the thermometer. Slide over a disposable probe stem cover, and apply plenty of lubricant. With one hand, separate Fred’s buttocks. Ask Fred to breathe ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic:_Daily_Report_with_Rishi_Desai,_MD,_MPH_4/1/2020</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H_ARa1NQSVqQ9hPuHkVCFIGgSRWGDGmv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic: Daily Report with Rishi Desai, MD, MPH 4/1/2020]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic: Daily Report with Rishi Desai, MD, MPH 4/1/2020 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Pulse_oximetry</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4KC9RSvJR_S5WoT6lom0eP60SFqV1hYG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Pulse oximetry]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical Skills: Pulse oximetry through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_neurological_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kl1S0CAZT2ODwZq8H1kXzHE5TNW42Sjo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital neurological disorders: Pathology review]]></video:title><video:description><![CDATA[At the physician’s office, a 30 year old male named Alex came in because of headaches and dizziness for the past few months. He also often stumbles while walking and recently fell down the stairs. His past medical history is insignificant. MRI of the brain and spinal cord shows herniation of the cerebellar tonsils. 

Next to Alex, there’s a mother with her 4 years old child named Evi who had recurrent urinary tract infections. Evi was born with leg paralysis and leg deformities. Clinical examination reveals a mass on her lower back. 

All right, both of them have a congenital neurological malformation, which occurs when there’s a primary defect in the developmental process of the nervous system. These conditions appear as the baby develops in utero and can vary in severity and presentation, ultimately impacting the infant&amp;#39;s health, development, and survival. The most high yield neurological malformations are neural tube defects, posterior fossa malformations, syringomyelia, and holoprosencephaly. 

Okay, let’s take a closer look at these disorders, starting with neural tube defects, or NTDs, which include spina bifida and anencephaly. They’re relatively common anomalies that develop when a portion of the neural tube - the precursor of the central nervous system-  fails to close as it should during the fourth week of gestation. When the posterior neuropore doesn’t close well, the baby is born with spina bifida, which is Latin for “split spine”. But when the anterior neuropore doesn’t close properly, the forebrain fails to develop, and the baby is born with anencephaly or absence of a major portion of the brain and the skull. In spina bifida, there’s incomplete closure of the vertebrae and membranes of the spinal cord. 

A very high yield risk factor for NTD is folate or vitamin B9 deficiency in the mother. For this reason, folic acid, which is the manufactured form of folate, should be given at least one month prior to conception and during early p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic:_Daily_Report_with_Rishi_Desai,_MD,_MPH_4/3/2020</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/64yq68VhQfudPt0TtKC8klS_SFKsc6jP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic: Daily Report with Rishi Desai, MD, MPH 4/3/2020]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic: Daily Report with Rishi Desai, MD, MPH 4/3/2020 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic:_Daily_Report_with_Rishi_Desai,_MD,_MPH_4/4/2020</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X3-76URNR56kHSFIlF2kMm3GR1iOzsq0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic: Daily Report with Rishi Desai, MD, MPH 4/4/2020]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic: Daily Report with Rishi Desai, MD, MPH 4/4/2020 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Face_coverings_for_the_general_public</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U8-6d8oyS4aFfAaRjce41kyeSDupsx-h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Face coverings for the general public]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Face coverings for the general public through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_BiPAP_and_CPAP</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T4mW05BJTx2knoSWj_ShZ7yrQHarxlqy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: BiPAP and CPAP]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical Skills: BiPAP and CPAP through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Mechanical_ventilation_-_conventional_ventilators</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Xrz-EU7mQFqVnbaXysduBP16Qqi8sh54/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Mechanical ventilation - conventional ventilators]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical Skills: Mechanical ventilation - conventional ventilators through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_High-frequency_oscillatory_ventilation_(HFOV)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5ZSd_WTcSt6h3UAAc6x1iXa6TjKp_fJp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: High-frequency oscillatory ventilation (HFOV)]]></video:title><video:description><![CDATA[Hello! This video covers how to set up a patient on high frequency oscillatory ventilation. Normally you’d do everything on this list, but to keep things concise, this video will focus on the steps in blue and will also cover frequently asked questions, troubleshooting, tips, and a summary.

As a word of caution, we’re not covering every possible type of equipment on the market. Make sure you understand how your own equipment works and how it may affect your procedure.

Here is all the equipment you will need: a high frequency oscillatory ventilator, humidified oxygen source, an oxygen saturation monitor, a cardiac and end tidal or transcutaneous CO2 monitor, neuromuscular blocker medications, personal protective equipment, suction equipment, and a self-inflating bag. 

High frequency oscillatory ventilation, or HFOV, differs from conventional ventilation in that instead of delivering a set number of breaths at a certain pressure or volume, HFOV provides volumes equal to or less than the anatomical dead space using respiratory rates with a range of 3 to 15 Hertz which is also 3 to 15 cycles per second. For clarity, 3 to 15 cycles per second is equivalent to 180 to 900 breaths per minute! Whoah.

The lungs are partially inflated to maximize surface area for gas exchange, and the fast breaths allow for a large volume of gas exchange to occur. The fast, small breaths also help reverse and prevent atelectasis, improve CO2 elimination, and reduce the risk of barotrauma and volutrauma which may occur in conventional ventilation. 

HFOV also can be employed in patients with acute lung injury, which is also called ALI, and acute respiratory distress syndrome, which is also called ARDS, but is not the first choice in these circumstances.

Calibration of the ventilator absolutely MUST be done before attaching the ventilator to a patient. Use a rubber stopper to block the circuit for calibration and performance procedures. The water trap stopcock ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_RT-PCR_Block_testing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AidfVsRHR7yswKEeldq3Q0aPSD6AAtcE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: RT-PCR Block testing]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: RT-PCR Block testing through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_RT-PCR_Ace_Inhibitors_and_ARBs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iYtC7w3-QIGv2pn1loSSYuKcR6aDDkkD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: RT-PCR Ace Inhibitors and ARBs]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: RT-PCR Ace Inhibitors and ARBs through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Recycling_N95_masks</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8vzIEyVWSkiq94g4-aD_Nv4_Ryqkg9vr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Recycling N95 masks]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Recycling N95 masks through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Using_a_metered-dose_inhaler</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Dn3DY1XeTlS4zLEiA4JDRs7FSeOmcmdb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Using a metered-dose inhaler]]></video:title><video:description><![CDATA[Hello. This video will talk about how to administer medication with a metered-dose inhaler. Normally you do everything on this list, but to keep things concise, we’ll focus on the steps in blue, and we’ll also include information on how to clean your inhaler and how to use a spacer device. Plus, we’ll include a summary.

Start by preparing the inhaler. Insert the medication canister into the top of the inhaler and remove the mouthpiece cover from the bottom. Shake the inhaler for at least a few seconds to ensure the contents of the canister are properly mixed. 

Now, grasp the inhaler between your thumb and index and middle fingers, like this. 

Raise the inhaler to the patient’s mouth, holding it about 1 - 2 inches, or about 2 - 4 centimetres away, and aiming towards the back of the throat.

Have the patient open their mouth wide and breathe in nice and deep before exhaling completely. 

Have the patient tilt their head back a little and slowly breathe in over about 2 - 5 seconds as you fully depress the canister. Have them hold their breath for about 10 seconds before allowing them to exhale.

That’s the preferred way to do it, but you can also place the mouthpiece directly into the patient’s mouth. Have the patient exhale fully, and place the mouthpiece between the teeth and over the tongue, aiming towards the back of the throat. Make sure they close their lips around the mouthpiece. 

Have the patient tilt their head back a little and slowly breathe in over about 2 - 5 seconds as you fully depress the canister. Have them hold their breath for 10 seconds before removing the inhaler and allowing them to exhale.

Now, if another dose is needed, wait 20 - 30 seconds before repeating these steps. If you need to administer a different medication, wait 2 - 5 minutes before repeating these steps.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Obtaining_blood_pressure_assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4Wh5TruGRLWyndt0bOiWqyRtT7iH5_pZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Obtaining blood pressure assessment]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical Skills: Obtaining blood pressure assessment through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Respiratory_rate_assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hp3Kz_dtT5WCcNnuSk_EjiIeTden9veb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Respiratory rate assessment]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical Skills: Respiratory rate assessment through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Pulses_assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LGd8G676TGuvSmLEe8q3WbwGQ4KnO5BZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Pulses assessment]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical Skills: Pulses assessment through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_COVID-19_survival_on_surfaces</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g8_YjpmMSBeyV9pcfZxeP2SaQOuIYurS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: COVID-19 survival on surfaces]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: COVID-19 survival on surfaces through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Hydroxychloroquine_+_Azithromycin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YNIKD0DwQACPCi0sZUQ611r5STmhnbah/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Hydroxychloroquine + Azithromycin]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Hydroxychloroquine + Azithromycin through 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video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_How_long_will_the_pandemic_last</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hknxNSwzQT2zvXVFAaehxdRCTnGiz-Lz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: How long will the pandemic last]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: How long will the pandemic last through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Passive_immunity_with_plasma_therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FeUPLcaVQoOFRwj3cY6556dRSp2FCo1A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Passive immunity with plasma therapy]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Passive immunity with plasma therapy through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_COVID-19_vaccines</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R2sxOtFeSf6X1rj1DfNKJ3EbRW_ZaPyP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: COVID-19 vaccines]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: COVID-19 vaccines through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Managing_L_type_COVID-19_patients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PpKmJ2xcQgyz1GUanMcU37KZT42-HGoj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Managing L type COVID-19 patients]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Managing L type COVID-19 patients through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Poonam_Desai:_ER_Physician_in_NYC_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LtlOkJyMQ0q3y27pDBAw7y_IQNSNHJl2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Poonam Desai: ER Physician in NYC (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Poonam Desai: ER Physician in NYC (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Vitamin_D_for_respiratory_infections</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cE5Op5fsRiOq6DEkcUbhyC7nTRSqbZ37/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Vitamin D for respiratory infections]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Vitamin D for respiratory infections through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Caring_for_vulnerable_populations</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/El3_mNUaSAWl6-2hPrmSDPAdRd2xRa6-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Caring for vulnerable populations]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Caring for vulnerable populations through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Remdesivir</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4rjzpmrQST2xPO-C5aHmi1oIT_yibS_l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Remdesivir]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Remdesivir through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_BCG_vaccine</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zIA_k8TzQ02kFNfeRcm0mZZ9QgmWJ0Er/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: BCG vaccine]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: BCG vaccine through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Splitting_ventilators</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ivM7uPcQQ0ebzGYx8OlIdZPhSfy_ev_V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Splitting ventilators]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Splitting ventilators through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Prone_positioning_on_ventilators</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jog6nZ70R7SpE8XLbI_T7vN7RhGSdD4J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Prone positioning on ventilators]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Prone positioning on ventilators through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_learning_from_a_distance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YtKIi9wBRLWa5qV6I_VfGcuJSHWuSJb_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical learning from a distance]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical learning from a distance through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Academic_productivity_and_personal_well-being_during_COVID-19</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y6AQw419Q9eH63MfMhMUQ07TSTm6K4lO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Academic productivity and personal well-being during COVID-19]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Academic productivity and personal well-being during COVID-19 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Curricular_integration_of_online_learning_resources</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UDfwT2UoSCSH8gWDmz5tXhStSQuwsre5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Curricular integration of online learning resources]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Curricular integration of online learning resources through 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video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Human_challenge_studies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XPyXOfeaQEu-oaR825__fMvXQXqkeGyL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Human challenge studies]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Human challenge studies through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Cultural_changes_during_COVID-19</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DGGCHVfBSLCgaCUXRzJAAdSuTpKMyevu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Cultural changes during COVID-19]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Cultural changes during COVID-19 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Trusting_antibody_testing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zn_i_CLVRG_mWS-0CBLthHy0Sp6dm35l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Trusting antibody testing]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Trusting antibody testing through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Children_and_COVID-19</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DDajifeDTlG3_t6poTCJjZQLRH2fCCmS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Children and COVID-19]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Children and COVID-19 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_Digital_surveillance_technology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x5-wNLmFTKCRRILzfWthXWQgQzK88--V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Digital surveillance technology]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: Digital surveillance technology through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_Pandemic,_Daily_Report_with_Rishi_Desai,_MD,_MPH:_COVID-19_and_climate_change</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XHfRAPgNRKK6J1vK4FfaeDsCSUKiewIq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: COVID-19 and climate change]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Coronavirus Pandemic, Daily Report with Rishi Desai, MD, MPH: COVID-19 and climate change through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._David_Shulkin:_9th_U.S._Secretary_of_Veterans_Affairs_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fA5IbImaSRaihCN4bD5L79_9SFCWuuzk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. David Shulkin: 9th U.S. Secretary of Veterans Affairs (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. David Shulkin: 9th U.S. Secretary of Veterans Affairs (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Large_group_video_conferencing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tMzdJVwoQ-W_5Jt4tx8KFrSsTGu4G6I8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Large group video conferencing]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Large group video conferencing through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_wellbeing_during_social_distancing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j0AQ42iESJG8vBsu3mYXlBzTSie7Fhue/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mental wellbeing during social distancing]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Mental wellbeing during social distancing through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Small_group_video_conferencing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oYPcyemdSoe7rHiOBevlVHrCTHOC5LJ0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Small group video conferencing]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Small group video conferencing through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Anne_Schuchat:_Principal_Deputy_Director_of_the_CDC_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fKdOWYqsQQGzNFtytma4rq5rQjig1vxk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Anne Schuchat: Principal Deputy Director of the CDC (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Anne Schuchat: Principal Deputy Director of the CDC (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Giving_oral_medication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tURJjQkbRw_Dzf8Y73ukHD5_RoaEIxjO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Giving oral medication]]></video:title><video:description><![CDATA[Hello. Today I will talk about the different ways to administer oral medication.

Normally you do everything on this list, but to keep things concise, we’ll focus on the steps in blue, and we’ll also include a summary.

Regardless of how you’re administering the medication, sit the patient upright. If they’re not able to sit upright, then they can lie on their side. 

Place tablets into a medicine cup, and have the patient swallow them one at a time. Have a glass of water ready to help the tablets go down.

Now, in some situations, you might want to check if the patient has successfully swallowed the tablets. To do so, have the patient open their mouth before you visually inspect the cheeks and under the tongue.

If the patient is unable to swallow tablets, break them up one at a time in a pill-crusher device, then mix the crushed medication into a teaspoon of soft food, and have the patient eat that.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Removing_indwelling_catheters_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pZrB1sUzSgGnMJN6ujIvkVU6Trqgn81-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Removing indwelling catheters (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Genitourinary: Removing indwelling catheters (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Personal_hygiene:_Introduction_to_bathing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JEYpuSqpQMGyGJbAtXY3EENZTB64WmQV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Personal hygiene: Introduction to bathing]]></video:title><video:description><![CDATA[As a nursing assistant, personal care, including assisting with bathing, is one of the tasks you will need to perform during your daily shifts. The main purpose of bathing is to clean the skin of germs, dirt, dead skin cells, and excess oil; get rid of unpleasant body odors; and It’s also essential for the client’s physical and emotional well-being. 

Bathing provides an opportunity to enhance blood circulation to the skin, soothe muscle aches, as well as boost self-esteem, and generate a feeling of calm and relaxation. For the nursing assistant, it’s also a chance to closely observe the condition of their skin, and talk to the client, understand their needs, and gain their trust.

Now, many factors can affect the frequency of bathing. Generally, this is going to depend on the  facility’s policies and the nurses who come up with the client’s plan of care. Bathing frequency can range from daily to 1-2 times a week. 

Factors to consider include the client’s personal preferences; health condition; physical activity level; mental capacity to get involved in their care; social, cultural, or religious traits; or even the weather.

There are a number of different supplies you need to be familiar with when assisting with bathing. Starting with skin care products: soap can be a bar or liquid, and what it does is it pulls germs, dirt, dead skin cells, and excess oil off the skin. 

These are then washed away as the skin gets rinsed with water. However, keep in mind that soap tends to have a drying effect on the skin, but there are special moisturizing soaps or soapless cleaners to prevent this. 

Lotions and creams can be applied after bathing while the skin is still fairly damp to keep it smooth and moisturized. After the skin has been dried out, body powder can be used to suck in excess moisture or sweat and prevent friction between touching skin areas. 

Body powder should not be used on people with respiratory problems. Talcum powder and other products containi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Bladder_and_bowel_training_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v1SF1TeMQ0y6Q1KuP9rPIqmwQQWTDXvC/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Bladder and bowel training (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of GI/GU: Bladder and bowel training (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Grooming:_Shaving</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qvGzlnoEQyS9YndNcEa7vHqnQ42Pzdm8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Grooming: Shaving]]></video:title><video:description><![CDATA[Shaving promotes comfort, hygiene, and well-being. Most people prefer to shave on their own, but as a nursing assistant, you will come across clients that will require your assistance. Keep in mind that religious, ethnic, and personal preferences are a factor, so always ask the client about what they want before assisting them in shaving. 

Now, to shave a client, you need clean gloves, bath towels, washcloth, tissues, wash basin, shaving cream, electric razor, disposable or safety razor, and aftershave lotion. A mirror can also be provided so the client can check their appearance after shaving. 

Before you proceed with shaving, ask if the client has their own shaving supplies. Also check if the person has fragile skin. Always ask the nurse to see if they’re taking any medications that could cause their blood to be thin and check with them for the type of razor to use. 

Individuals at risk for skin infections or who are more prone to bleeding should use an electric razor instead of disposable or safety razor. Don’t get the electric razor overly wet and make sure to practice electrical device safety. 

If there’s an increased risk of electrical sparks, for example, if the client is on oxygen or if a client has electrical implants, such as a pacemaker, you should avoid using electrical razors.  

Before you continue shaving, make sure that there’s no rust, nicks, or cracks on the razor. Next, prepare your working area by covering the overbed table with paper towels and placing your equipment. Make sure you’ve washed your hands and put on gloves. 

Raise the bed to a height comfortable for you and the client and lower the side rail on the side of the bed that you are standing. Place a towel under the client’s chin to protect the clothing. Fill the wash basin with warm water and check that it’s not too warm or cold. 

The client should also check to make sure the temperature is suitable for them. Soak the washcloth in the wash basin and apply it over th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Basic_needs_of_care_and_activities_of_daily_living</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DRFP5L84T0WgHBHSBTDvGz3NQHWzUkBk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Basic needs of care and activities of daily living]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Basic needs of care and activities of daily living through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assistive_devices_for_ambulation_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CUwCCYROSYmJsYeNAt5Mmun8TQKPbFFj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assistive devices for ambulation (for nursing assistant training)]]></video:title><video:description><![CDATA[Assistive devices for ambulation, or just ambulation devices, are tools used to aid in walking.  The most common types include walkers, canes, and crutches. You need to know when each of these are appropriate and assess if the patient is using them correctly. Remember that a patient’s ambulation device is ordered to fit them specifically, kind of like glasses, so they should not be shared with other patients.  

Let’s start by looking at walkers. These are movable, lightweight devices that consist of a metal frame, 2 hand grips, and 4 legs. Walkers provide great stability due to their wide base, so they are great for people who can bear weight on their feet but have trouble walking due to weakness of the legs or balance issues. When assessing the proper fit of a patient’s walker, make sure that the hand grips are at the patient’s waist level. Check the legs because they should have non-slip tips like a rubber cover. To use a walker, the patient should stand straight while holding the hand grips. When moving forward, they lift it up and move it another 6-10 inches in front of them and set it down. Because many patients have difficulty lifting a walker, many models now have wheels on the front legs. However, these are prone to rolling forward, so brakes are usually built in. So, when the patient is going to stand for a while, make sure the brakes are locked. Using the walker as support, they should move one leg forward and then the other. Once balance is reestablished, repeat the process. 

Next up, we have canes. These are also movable, lightweight devices made of a strong material like wood or metal. Canes consist of a handle, a shaft, and legs. There are single leg, triple leg or quad leg canes, and the ones with multiple legs provide more stability but are also more cumbersome. Canes are used by patients who could bear weight but have weakness in one of their legs, like a stroke patient or those with paralysis in one leg. Crutches and walkers are better ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Grooming:_Foot_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XMS5EjD9R0G78GSQmwsHW-q0RfSmwFFq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Grooming: Foot care]]></video:title><video:description><![CDATA[Foot care is an important part of personal care. Some clients, like those in an advanced age, need help with this task. As a nursing assistant, make sure you assist these clients. 

Foot care includes caring for the skin of the feet as well as the toenails which helps prevent infections and injuries and reduces unpleasant odors. Look for calluses or corns, which are areas with a thickened layer of skin that’s often painful. 

Cracks on the skin or ingrown nails — which is when the edge of the toenail grows into the surrounding skin — can be portals of entry for microbes, leading to infections. 

Long or rough toenails can also harm the client and damage their clothing or bed sheets. In addition, poorly cared for feet and dirty stockings or socks can cause bad odors as well as encourage microbes to grow. 

At the same time, foot care, as part of grooming, also contributes to the overall physical and emotional well-being of the client; it can boost the client’s self-esteem and generate a feeling of comfort. 

In addition, it is a chance to closely observe the condition of the feet and toenails but also spend some time with the client and gain their trust. 

Now, for people with poor blood flow, or compromised circulation, to the feet, foot care is especially important. This can be due to various conditions including diabetes, circulatory disorders, heart problems, or simply advanced age. 

Reduced blood flow results in increased risk for infection, poor wound healing, and reduced sensation, which means they might be unaware of an injury that can lead to complications like infection or gangrene. 

Often, nurses with specialized training will be the ones providing foot care for these clients. Now, before we talk about assisting with foot care, an important term you should be familiar with is tinea pedis, also known as athlete’s foot. 

This is a fungal infection that usually starts in the skin between the toes and appears as a red, itchy rash. It’s more common]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Assisting_with_bowel_elimination</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AFnYcXn-SOuHHOOU3y824cw6SPaqdo18/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Assisting with bowel elimination]]></video:title><video:description><![CDATA[Defecation refers to the excretion of feces, commonly referred to as “poop” or “stool,” which are semi-solid waste products that result from the intestinal digestion of nutrients. Feces form in the colon, and they are stored in the rectum until they can be released through the anus during defecation. The process is also often called a “bowel movement.” 

And usually, bowel movements are also accompanied by “flatus” which is the fancy way of saying gas, or air, passing through the anus. This is not to be confused with flatulence, or excessive gas formation in the stomach and intestines. 

Bowel movements are a physiological way for the body to eliminate waste and prevent us from getting sick, so normal bowel habits and stools are super important to our overall health.

Normal bowel habits vary from person to person. Some people pass a bowel movement once a day, some only every 2 or 3 days, while some people can have 2 or 3 bowel movements per day; and that’s normal if there’s no change in stool quality. Normal stool is usually brown, but color varies depending on diet and fluid intake. 

Stool can be red after eating tomato juice, tomato soup, or foods with red food coloring, like ketchup. Pathologically, red stool can also mean there’s intestinal bleeding. Green foods, on the other hand, can make stool greener. Pathologically, green stools as well as clay-colored, white, yellow, or orange stools can signal a disease or infection. 

Regarding shape and consistency, there’s a useful tool called the Bristol stool chart that can help orient us. According to this chart, there are 7 types of stool, numbered from 1 to 7, which go from hard to soft. 

So, type 1 stools are represented by hard, separate lumps. Type 2 is when the stool is formed, with lumps, and has a “sausage like&amp;#39;&amp;#39; aspect. Types 1 and 2 usually indicate severe and mild constipation, respectively, which means the passage of a hard, dry stool. 

Prolonged constipation can also caus]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Professionalism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y3_ZTdtCSNSAjyv3YjlTLbllQB6ar_pu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Professionalism]]></video:title><video:description><![CDATA[As a nursing assistant, you’re expected to have the skills needed for your job, to know how to make decisions that are best for your clients, and to look and behave in a certain manner. 

The way you present yourself to others is the way others will see your whole team and agency, so you should begin developing professional qualities now.

Let’s see what that means. A professional is a person who has successfully completed education and training that allows them to practice a certain profession. As a nursing assistant, you will be expected to adhere to professional standards and ethical principles.

Professionalism is the way professionals approach their job and how they communicate with others. It refers to both nonverbal communication, like appearance and behavior, and verbal communication, like the kind of language they use and what they say. 

A positive, enthusiastic attitude while on the job, a willingness to learn new skills, and volunteering to help co-workers when they need help are also examples of professionalism.

Strong work ethic, or the type of mindset that professionals have and the principles they use as guidelines for performing their work, is another example of professionalism. 

Having a strong work ethic will make you stand out from your coworkers and make you thrive because your employer and the people you take care of will recognize your dedication to work.

Let’s go over a few important qualities you should develop in order to have a strong work ethic. Punctuality means you should come to work a few minutes early, so you will have time to prepare and start your shift ready to go. 

Reliability means others can depend on you to always arrive at your workplace, stay until your shift is over, and be committed to your work. 

Accountability means you should accept responsibility for your actions and its consequences. Always admit if you have made a mistake, learn from your mistakes, and take the appropriate actions to prevent it fr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexual_orientation_and_gender_identity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5JEWirajTo_FjtIVwCU011R4RaC0NGrc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sexual orientation and gender identity]]></video:title><video:description><![CDATA[In recent years, healthcare centers have started understanding the importance of incorporating Sexual Orientation and Gender Identity, or SOGI, in their medical records.

Traditionally, one’s assigned sex at birth is their biological sex which depends on their sex chromosomes. If they have a Y chromosome, their biological sex is male. If they have 2 X chromosomes, their biological sex is female. However, things aren’t that simple.

For example, a person could have a Y chromosome but they’re missing specific genes that encode for specific male characteristics, so even though they’re chromosomally male, they appear as what is stereotypically described as female.

So you’re thinking biological sex can be linked back to genes, right? Well, things get even more complicated than that. Some genes get expressed at high levels, and others at low levels. So a person may have genes that express a high level of testosterone and little or no estrogen and progesterone, or vice versa.

Finally, hormones like testosterone, estrogen, and progesterone bind to receptors, and some people may have lots of receptors that can easily bind to hormones, whereas others may have very few receptors. In many cases, these people are intersex individuals whose bodies do not fit into the standard definition of male or female.

The bottom line is that biology is messy, and like most things, biological sex exists on a spectrum. Now, separate from the biological construct of sex, is gender identity and gender expression. Gender identity is a person’s own sense of their gender and gender expression is how they present themselves to the world.

Many people identify as either man or woman. But there are also various types of non-binary gender, or gender identities that lie outside of the man-woman dichotomy. For example, someone could identify with multiple genders, such as Native or indigenous Two-Spirits do.

Furthermore, some will identify with a gender that’s neither man nor woman, while ot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Patrice_Harris:_President_of_the_American_Medical_Association_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z3xS3yjzQqOwD06AWXt5HuWISjKSKWrl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Patrice Harris: President of the American Medical Association (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Patrice Harris: President of the American Medical Association (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Conrad_Fischer:_Infectious_Disease_Specialist_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kVQmb_OZSkKBY0yNUOaoIwz7QwCQeMTh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Conrad Fischer: Infectious Disease Specialist (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Conrad Fischer: Infectious Disease Specialist (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/NCLEX_Q&amp;A_with_Jannah_Amiel</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fQF2i3x2RVWfbp95AkeVEgojQM6naWJp/_.jpg</video:thumbnail_loc><video:title><![CDATA[NCLEX Q&amp;A with Jannah Amiel]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of NCLEX Q&amp;A with Jannah Amiel through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Abdi_Mahamud:_Incident_Manager_for_WHO_Western_Pacific_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iAieh2mqS_eF7AJzgDpg_DuxTpe4BiUe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Abdi Mahamud: Incident Manager for WHO Western Pacific (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Abdi Mahamud: Incident Manager for WHO Western Pacific (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Donna_Meyer:_CEO_of_the_Organization_for_Associate_Degree_Nursing_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZnOzNlkKSQecjc9xoBhGHwblTr6nO5P8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Donna Meyer: CEO of the Organization for Associate Degree Nursing (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Donna Meyer: CEO of the Organization for Associate Degree Nursing (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Nutrition</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HDVPOx7_TJWBGPPwxF9iW2MWT6Kvx0RQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Nutrition]]></video:title><video:description><![CDATA[Nutrition is defined as the process of obtaining food and using it for maintenance, growth, and repair. It can be broken down into ingestion, or taking in food; digestion, or breaking it down into nutrients; absorption, or pulling those nutrients into the bloodstream; and, finally, metabolism, or turning these nutrients into energy. 

This energy is calculated in units known as kilocalories, or simply calories. Nutrients found in food can be divided into two groups. 

The first includes carbohydrates, proteins, and fat which provide energy; while the second group, including minerals, vitamins, and water, offers no energy but is still essential for normal body function. 

Starting with carbohydrates which are found almost everywhere from fruits and vegetables to dairy and grains. They are one of the main sources of energy in the body, providing 4 calories per gram. 

There are simple carbohydrates or sugars that the body can readily absorb and the most important of these is glucose. 

Complex carbohydrates, or starches, take longer to break down and absorb. There are also dietary fibers which are found mostly in fruits, vegetables, legumes, bran and oats. 

Fibers are carbohydrates that intestinal enzymes can’t break down at all, so they pass through the intestine undigested and ultimately end up as bulk matter in the stool. 

In this way, they help increase stool weight and prevent constipation. Next, proteins can be found in many animal products, like dairy, meat, poultry, and eggs as well as plant-based products, like beans and peas, soy, nuts, and seeds. 

Just like carbohydrates, each gram of protein provides 4 calories. At the same time, though, proteins can be broken down into amino acids which we largely use to make our own proteins as well as hormones and other molecules needed for the immune response or tissue repair. 

Fats or lipids are found in oils, butter, avocados, and meats. They are a major source of energy, providing 9 calories per gram b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Comfort_promotion:_Handling_linens_and_other_bedmaking_supplies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9W40OGK_ScyMh_IrW3PRe7LvTCKGODYC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Comfort promotion: Handling linens and other bedmaking supplies]]></video:title><video:description><![CDATA[Linens need to be clean, dry, and wrinkle-free in order to prevent pressure ulcers, skin breakdown, and make the client comfortable. 

When making the bed, you’ll work from the bottom to the top, so in that order, basic bedmaking supplies include a bottom sheet, draw sheet, bed protector, top sheet, blanket, bedspread, and pillowcase.

Let’s go over the basic supplies in the order they are applied. The bottom sheet can be fitted to wrap around and under the mattress, or it can be non-fitted, also known as flat. 

The draw sheet is a flat sheet placed over the middle of the bottom sheet, so it covers the area from above the client’s shoulders to below their buttocks. 

If a rubberized mattress is used, the draw sheet is an important moisture absorbing barrier between the client’s body and the mattress. 

Sometimes, a rubberized draw sheet can also be used to protect the mattress from soiling. In that case, it should always be covered with a cotton draw sheet, so there is no direct contact between the client’s skin and the rubber. 

A special type of draw sheet called a lift sheet is made by folding a flat sheet in half, and it’s used to lift or reposition a client. 

Sometimes, you’ll need to use a bed protector, also known as an incontinence pad or soaker pad, which is a square of absorbent fabric backed with waterproof material and usually measures 3x3 feet. 

It’s used for incontinent clients and clients with draining wounds so that urine, feces, and fluids from wounds don’t soil the rest of the linens. 

The top sheet is a flat sheet placed over the draw sheet or the bed protector. Blankets are usually made of woven cotton, and they’re placed over the top sheet. 

A bath blanket is a lightweight cotton blanket that can be used to provide privacy and warmth to the client during a linen change or a bed bath. 

Bedspreads are used to cover all the previous layers. Along with the blanket, they can be used to mark the bed as open or occupied. 

Pillows can b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Urinary_catheters_and_routine_indwelling_catheter_care_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ll0vx53TQAeAp3xaAqjcym11RmCRAh29/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Urinary catheters and routine indwelling catheter care (for nursing assistant training)]]></video:title><video:description><![CDATA[A urinary catheter is a tube that goes into the bladder that drains urine. This is commonly used in a variety of situations, such as before, during, or after an operation, in order to keep the bladder empty. It’s also used to monitor the amount of urine produced by people with urinary incontinence, in those with wounds or pressure ulcers that need to be protected from contact with urine, or to collect sterile urine samples. Catheter care is essential for preventing urinary tract infections because an indwelling catheter is a pathway for bacteria to move up from the perineum into the bladder. This is important because, during normal urination, the urine flow acts as a natural way to “flush” bacteria out of the urinary tract.

Now, the most common types of urine catheters are straight, indwelling, and suprapubic catheters. Both straight and indwelling catheters are inserted into the bladder through the urethra, but the difference is that a straight catheter is removed once the urine is drained, while an indwelling urinary catheter, also called Foley catheter or retention catheter, remains in the bladder and lets the urine drain continuously into a drainage bag. With the suprapubic catheter, “supra-” means above and “pubic” refers to the pubic bone, so it is inserted into the bladder through a surgical incision made above the pubic bone. 

Let’s focus on the indwelling catheter. This consists of a soft balloon that is inflated inside the bladder to keep the catheter from slipping out and a length of tubing, which connects the catheter with a drainage bag for collecting urine. Indwelling catheters may have two or three lumens. In double-lumen indwelling catheters, one is for urine drainage and the other one is used to inflate the balloon. In triple-lumen indwelling catheters, the additional lumen is used to regularly deliver irrigation fluid into the bladder. This can help prevent blood clots from forming, which is important in certain cases, like after a pros]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Incentive_spirometry_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wn8XE23RR3WyMLBuoyr4rkHgRHWd6ecr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Incentive spirometry (for nursing assistant training)]]></video:title><video:description><![CDATA[Incentive spirometry is a respiratory exercise to help clients improve their lung expansion, prevent fluid and mucus from collecting in the lungs, and reduce the risk of developing respiratory complications, like pneumonia and atelectasis.

It is especially important for people with underlying lung diseases, those who are overweight or have other chronic diseases, as well as those recovering from surgery.

Incentive spirometry is performed with a special device called an incentive spirometer, which is made up of a mouthpiece attached to a breathing tube that connects to an air chamber with an adjustable volume indicator.

Flow oriented incentive spirometer uses balls to indicate volume, while the volume oriented spirometer uses pistons. Now, before you start, here are some general considerations.

Clients that are experiencing pain, motor function impairments, and people with dementia or other cognitive impairments might be unable to perform incentive spirometry exercises.

Those who can, should do incentive spirometry 5-10 times every hour while awake. After performing the test, people sometimes feel dizzy and out of breath for a short period of time.

When performing incentive spirometry, first make sure the client is in the sitting or the most erect position possible, ideally in the high-Fowler’s position.

Set the volume indicator at the target volume level. Ask them to exhale completely through the mouth.

Then, tell them to place their lips tightly around the mouthpiece and inhale through the mouth by taking a slow, deep breath. As they inhale, you’ll see the piston or balls rise inside the air chamber.

This shows how deeply the client can inhale. Maximal inspiration is the volume reached when they cannot inhale any more.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain:_Recognizing_and_reporting_pain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/URBb2y7nRd_4uWDaHywEF3-EQjqe9tcg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pain: Recognizing and reporting pain]]></video:title><video:description><![CDATA[Pain is a feeling of discomfort that ranges from mild to severe, usually caused by an underlying condition and is never normal. Acute pain is a sudden, usually severe pain that typically decreases over time once the underlying cause resolves. It can last from days to weeks and is often caused by some sort of tissue damage. This includes trauma (like burns, sprained ankle, broken bones); surgery; or diseases and conditions (like appendicitis). Chronic pain lasts longer than a few months and is usually associated with headaches, back pain, arthritis, nerve pain, and many others. Pain can interfere with the client’s ability to function and their quality of life. So it’s important that nursing assistants know how to recognize and report it. 

Many of your clients will feel pain, but it won’t be the same for everyone. Pain is an individualized sensation that depends on many factors. Each person has a different pain threshold, which is the point when they start noticing pain, and pain tolerance, which is the highest amount of pain they can handle. For example, if you pinch someone with a low pain threshold, they might immediately say it hurts, while someone with a high pain threshold will probably not report any pain at all. Now, the way someone handles pain is not just limited to pain threshold and tolerance. There are other factors to consider like anxiety, rest, energy level, hunger, culture, past experience with pain, and so on. 

Now, as a nursing assistant, you might be the first to notice when a client is in pain. It is easy to notice when the client tells you they feel pain, but sometimes they won’t be able to tell you, or they might not want to. However, a client in pain will usually show some physical signs of pain that you should learn to recognize. These include irritability, restlessness, mood change, insomnia, clenching the jaw, frowning, grimacing, moaning, not wanting to move or change position, redness of the affected part, avoiding the use or r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Comfort_promotion:_Bedmaking</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uZx55UP6QEqyXzPiehAHs-uBTl6UVUYP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Comfort promotion: Bedmaking]]></video:title><video:description><![CDATA[Bed-making is important for maintaining proper hygiene and the comfort for the clients. It is usually done in the morning before visiting hours or while the client is dressing or bathing. 

In hospitals, bed linens are changed daily, while in a long-term care setting, it might be less frequent. However, there are also situations when linens should be changed straight away. 

These include excessive wrinkling and soiling by spilled food and drinks, sweating, urine, feces, vomit, wound drainage, and feeding tube leakage.

Before we talk about bed-making, it’s important to know the different status of beds. Closed beds are not currently being used. 

They are either waiting for a new client to arrive or there’s already a client assigned to it, but they&amp;#39;ll be out of the bed for a while.  

An open bed is a bed currently in use or one that’s prepared for a client who’ll be occupying it soon. 

So it might be for a new client who&amp;#39;s on their way or a current client who’s expected to return shortly, like from a diagnostic test or a bath.

Next, a surgical bed is an open bed that’s prepared for a client who will require a stretcher to be moved to the bed. This could be someone who just had surgery or had an injury that requires them to be carried. 

Finally, occupied beds are beds with individuals who are unable to leave the bed. Now, before we get into the procedures, there are some general considerations for you to follow when making a bed. 

Wash your hands before collecting clean linens. Always take exactly what you need. Never bring extra linens into the clients’ room because, once in the clients’ room, linens are considered contaminated and cannot be used for another client.

When placing clean linens, they should be centered and placed so that the stitching is facing the mattress and make sure there are no wrinkles. Practice infection control when handling linens. 

Hold them away from your body, so they don’t touch your uniform and don’t l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Personal_hygiene:_Perineal_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YicCJZx9R0SHJ3GBmFFjqzgMRhCMAt70/_.jpg</video:thumbnail_loc><video:title><![CDATA[Personal hygiene: Perineal care]]></video:title><video:description><![CDATA[The perineum is defined as the area between the anus and, either the vaginal opening in biological females, or the root of the penis in biological males. The perineal area is close to the sites of fecal and urine excretion. 

Furthermore, it’s the ideal dim, damp, and warm sanctuary for germs to flourish, so keeping this region clean is essential for preventing infections, skin irritation, and getting rid of unpleasant body odors. 

As a nursing assistant, perineal care is one of the most important and sometimes challenging tasks you will need to perform. It’s also a chance to closely observe the condition of their skin in the area.

Now, before we talk about how to assist with perineal care, here are some general considerations. Perineal care is typically done at least once every day during a bath. However, for specific clients, like those with diarrhea, fecal or urinary incontinence, vaginal bleeding or discharge, perineal care might be needed more regularly. 

If they are able, let them perform perineal care on their own but stay close by in case they need help. Otherwise, encourage the client to participate as much as possible and don’t rush the procedure. 

Some clients may also find it comforting to have someone of their own sex present in the room. At all times, respect the client’s privacy and modesty by remembering to close the room’s door and bed curtains. Make sure the client is properly covered. 

Since bathing tends to trigger urination, remember to ask them if they need to use the bathroom, a bedpan, or urinal beforehand. At the same time, make sure to take the proper safety measures to protect yourself from possible exposures to the client’s body fluids or blood.

Okay, so, when assisting with perineal care, first gather the supplies you’ll need including gloves, a bath blanket, paper towels, pre-moistened bath wipes or washcloths, a bed protector, towels, soap, a washbasin, clean clothing, and clean linens. 

Start by filing the wash b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Repositioning_clients_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7drENkosQAa0Ko-3JEAxGgd6SgmxT2-b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Repositioning clients (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Repositioning clients (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Personal_hygiene:_Oral_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q717WIf8RbOovQZl96avpnpoROazlXmF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Personal hygiene: Oral care]]></video:title><video:description><![CDATA[Now, oral hygiene is essential to prevent mouth infections and bad breath. To maintain proper oral hygiene, you have to remember three basic steps: brushing, flossing, and rinsing. 

The frequency of oral hygiene depends on the individual&amp;#39;s condition and comfort level, but it’s typically performed in the morning, after meals, and before bed. 

Clients who are unable to take food and fluids by mouth, like those who are unconscious, will require oral hygiene every 1 or 2 hours to keep their mouths fresh.

Before we continue, there are several important definitions that you should know. Halitosis refers to a chronic bad breath which can be the result of poor oral hygiene or an underlying health problem. 

Dental plaques are films of saliva and microbes that stick to the teeth and can lead to tartar which are crusty deposits. 

Dental caries, also known as tooth decay or cavities, is damage caused by acid-producing bacteria in the mouth. Stomatitis refers to any inflammation that affects mucous membranes of the mouth and lips. 

Next up is gingivitis which is non-destructive inflammation of the gingiva, or gums. If left untreated, gingivitis can lead to periodontitis which is a severe inflammation of the supporting structures of teeth, including soft tissue and bones. 

Moreover, in people over the age of 35, periodontitis is the main cause of tooth loss. If a person has lost a tooth, they can replace it with a prosthetic tooth which is also known as a dental implant. 

On the other hand, dentures are removable replacements of the missing teeth and surrounding tissue which allow people to chew food normally. When a person has no natural teeth left, it’s called edentulous.

Before you start with the procedure, review the client&amp;#39;s medical record and evaluate possible oral hygiene issues. 

These include: restriction of food and water which can cause mucosal dryness; presence of tubes, such as endotracheal, nasogastric, or oxygen tubes which can]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain:_Comfort_measures</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j1_vReHuQmyZNCaNw0NC460yRVyqJJtq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pain: Comfort measures]]></video:title><video:description><![CDATA[Pain is a common complaint found in the hospital, and pain is a subjective experience that may differ from client to client. This means that everyone’s pain is not the same. There are different comfort measures available to assist clients with their individual pain needs. 

These include non-prescription or over the counter pain-relieving medications, such as ibuprofen, which is usually used for mild or moderate pain, or prescription medications, such as narcotics usually used for severe pain, which are prescribed by the healthcare team. 

You can also use heat and cold applications as well as physical therapy treatments like massage, movement therapy, and exercise.

As a nursing assistant, there are several comfort measures you can use to help alleviate your client’s pain. While doing this, make sure you are as gentle as possible in providing comfort measures as even minor movements can cause extreme pain.  

It is also important to remember that before any comfort measures are performed, you need to carry out proper hand hygiene. 

One easy measure is client positioning, which can be used to make sure the client is in a comfortable position and aligned properly, relieving strain on muscles and joints.  

A back massage is also an effective measure to help relieve discomfort as it can be used to comfort and relax clients with the added benefit of stimulating circulation and preventing skin breakdown. 

A good time to give a back massage is after repositioning or after a bath. Always check with a nurse before performing a back massage to make sure it’s appropriate and safe for the client. You can also take the opportunity to check the skin for redness, bruises, and injuries.

Next, helping the client relax can reduce anxiety, which can cause the body to be tense and increase pain. Adjust the room temperature and lighting to create a relaxing environment while also limiting noise in the room. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Promoting_self_care_and_independence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wd3EBH6eTVeq7E6ZPCGuS6mVRcyjzQYC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Promoting self care and independence]]></video:title><video:description><![CDATA[Self-care refers to performing the activities of daily living that help maintain and enhance health; this can include activities like eating, getting dressed, bathing, and toileting. Self-care is important for maintaining physical, emotional, and psychological health and to help prevent existing conditions from getting worse. 

A client&amp;#39;s ability to practice self-care can be impaired by an illness or age-related changes that affect mobility, endurance, mental state, or senses like loss of vision. This can create a sense of powerlessness and hopelessness. Your clients will feel more independent when they are able to perform self-care activities and this will build their self-esteem and maintain their personal dignity.

As a nursing assistant, you will care for many clients who will need your assistance with self-care. First, check the client&amp;#39;s plan of care. It will include interventions aimed at promoting self-care. 

For example, during bathing, some interventions that you could perform include providing partial assistance during bathing, washing and drying hard-to-reach areas, and observing for signs of activity intolerance. You should check with the nurse to find out which activities you can do in order to best assist the client. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Roger_Seheult:_Co-Founder_of_MedCram_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xRtCPJljT82mvkkv0SXoK6qmSGK-Z34P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Roger Seheult: Co-Founder of MedCram (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Roger Seheult: Co-Founder of MedCram (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Jesse_VanWestrienen:_Co-Founder_&amp;_Biology_Lead_at_Biomeme_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rpLz0Fb-SRWKISJUTf3YgvTDTWWOUR3O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Jesse VanWestrienen: Co-Founder &amp; Biology Lead at Biomeme (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Jesse VanWestrienen: Co-Founder &amp; Biology Lead at Biomeme (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arianna_Huffington:_CEO_of_Thrive_Global_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Svwl2L7sSJys3U_5ht96h34aSwu5UoK0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arianna Huffington: CEO of Thrive Global (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Arianna Huffington: CEO of Thrive Global (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Other_ways_of_providing_fluids_and_nutrition</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZtKACyKmSAyRL5Q-SUE_4pn5Q3Kp9o45/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Other ways of providing fluids and nutrition]]></video:title><video:description><![CDATA[There are many reasons why a client might encounter problems with eating or drinking. It could be due to difficulties with chewing, swallowing, or digestion as a result of trauma, surgery, or various medical conditions. 

Several alternative methods of providing them the nutrients and fluids they need are available, and a nursing assistant should be familiar with them.

Okay, let’s start with intravenous, or IV, therapy. This consists of a pre-filled IV bag that delivers fluids, one drop at a time, through a drip chamber and a tube into a catheter that goes directly into a vein, most commonly on the back of the hand or the arm. 

The tube also possesses a clamp that can adjust or pause the flow. Some IV sets are also connected to an electronic pump that regulates the flow rate. 

Now, IV therapy cannot replace normal nutrition, but it’s typically used to provide water as well as glucose, vitamins, and minerals. It’s also a good way to administer IV medications, like antibiotics or pain relievers or even blood!  

What’s most important for you to remember about clients on IVs is to notify the nurse immediately if the catheter is out of place. In this case, the fluid may leak into the surrounding tissue, which is known as infiltration. 

The client will likely report a burning or tight sensation around the IV catheter insertion site, and there’ll be swelling, blanching, and cooling of the skin in the area.  

Also, make sure to let the nurse know if the dressing over the IV site is loose or soiled, the IV bag is empty, the fluid is not flowing into the drip chamber, or blood has flowed back into the IV catheter.

Some IV pumps may also make an alarm sound if there’s something wrong, like air in the catheter, low battery in the pump, blocked flow due to kinks in the tubing, or the client laying on top of or pulling on the IV line.

Next, some clients might receive enteral nutrition, otherwise known as “tube feeding.” This means nutrition is delivered through ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Personal_hygiene:_Bathing_the_client</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MzfQo0LkQEy3cmZh0kqrohBkTkazqq88/_.jpg</video:thumbnail_loc><video:title><![CDATA[Personal hygiene: Bathing the client]]></video:title><video:description><![CDATA[As a nursing assistant, personal care, including assisting with bathing, is one of the most important, and sometimes challenging, tasks you will need to perform during your daily shifts.

Now, before we talk about how to assist with bathing, here are some general considerations. Before beginning the procedure, explain how you will assist them and why bathing is important.

This can be especially helpful for confused clients or those with memory impairment. Ask the client if they have special preferences for certain skin care products. 

Because bathing tends to trigger urination, remember to ask them if they need to use the bathroom, a bedpan, or urinal beforehand. Prepare the shower, tub room, or the bed if they’re doing a bed bath and make sure it’s clean. 

Watch out for a slippery bathtub or bathroom floor, place a non-slip mat and secure it to prevent a fall. Check the water to make sure the temperature is safe and comfortable for the client. 

This should be confirmed by the client by having them dip their finger in the water. Also, make sure that the ambient temperature is comfortable for them when they’re undressed. 

When bathing the client, encourage them to participate as much as possible. When providing a back massage, make sure to avoid reddened skin regions, sores, or bony parts because massaging these areas can damage the skin even more. 

At all times, respect the client’s privacy and modesty by remembering to close the room’s door, all window covers, and ensuring the client is properly covered.

Okay, so, when assisting a person with a shower, tub, or whirlpool bath, first gather the supplies you’ll need including gloves, soap, powder, lotion or cream, deodorant or antiperspirant, a bath blanket, washcloths, towels, and clean clothing. 

In the case of a bath or a whirlpool tub, start by filling the tub halfway. If the client is taking a shower, check if they need a shower chair and place it in the shower. 

In both cases, make sure that t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Oral_feeding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XyILS6nwTkqi-8FWkw0o8bB1SKq0Gx92/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Oral feeding]]></video:title><video:description><![CDATA[As a nursing assistant, you will need to prepare clients for their meals, serve them food, and depending on their needs, assist them in eating. Now, before we talk about how to do these things, here are some general considerations. 

Always check that the name on the tray matches the identification card or bracelet of the client and that the meal served follows the nutritional guidelines for that particular client. 

Make sure to serve food as soon as it’s ready so that serving temperature is optimal. Ask the nurse how much help the client will need and then confirm with the client.

Whenever possible, let them eat in the dining room together with others. However, in some cases, it’s best to provide a private place. 

Finally, try to create a friendly atmosphere, keep them company, and help them as much as they need, while encouraging them to participate as much as possible.

Okay, so, when preparing a client for their meal, first gather the supplies you’ll need, including gloves, soap, washcloths, paper towels, towels, and washbasin as well as equipment for oral hygiene and a bedpan or  urinal. 

Make sure to notify them as early as possible to get ready for the meal. Remember to ask them if they need to be accompanied to the bathroom beforehand or offer them a bedpan or urinal.

Wear your gloves and assist the client with cleaning their hands, face, and teeth. If they can’t get up from the bed, fill the washbasin with water and check that it’s warm enough. 

Then, spread paper towels on the over-bed table, place the basin on top, and help them with hygiene. If the client is incontinent, make sure they are dry and clean. 

If they use eyeglasses, hearing aids, or dentures, check that those devices are properly positioned. Next, check where they’ll be eating and make sure the room is free from disturbing sights, odors, or sounds. 

If they&amp;#39;re eating in the dining room, position them in a chair or wheelchair, so they’re upright; if they’re in bed, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immobility,_basic_positions_and_alignment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lk2aT_CfRwG9PPjznNQZVFEwSomQ21da/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immobility, basic positions and alignment]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Immobility, basic positions and alignment through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Standard_and_transmission-based_precautions_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K79wjvl0S5m-XZ-i6afCRh9cRL_QNJR2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Standard and transmission-based precautions (for nursing assistant training)]]></video:title><video:description><![CDATA[When assisting with client care, a set of protective practices should be applied to prevent the transmission of infection to and from the client.

These include standard precautions which are used for any client, at any time, in any situation and transmission-based precautions for clients with a diagnosed or suspected infectious condition.

Okay, let’s start with standard precautions. So, every time there’s a risk for exposure to blood, all types of body fluids, secretions, and excretions other than sweat, as well as open skin lesions or rashes, mucosal surfaces, and possibly contaminated items or surfaces, make sure to utilize personal protective equipment, or PPE for short.

This includes wearing gloves, a waterproof gown if there’s a possibility that your clothes get contaminated, and protective mask, goggles, or a face shield for procedures where splashes of body fluids are likely.

When moving from a contaminated area to a clean body area, remember to change your gloves and wash your hands thoroughly.

If there’s no access to water or soap and your hands aren’t visibly dirty, you can also use an alcohol-based sanitizer. Remember to still wash your hands afterwards as soon as you can.

Do the same after touching any surfaces in or out of the care setting. Now, in the case of unexpected contact with blood or any body fluids, wipe up any spills, disinfect the area with a facility-approved cleaning product, and practice hand hygiene right away.

In any case, before leaving the client’s room or moving on to another client, remove all your personal protective equipment and practice hand hygiene.

Next, to limit the potential transmission of respiratory infections, standard precautions include wearing a mask when caring for clients with suspicious signs or symptoms, like cough.

It’s also important to instruct these clients to keep at least a 1 meter, or 3 feet, distance between themselves and others or to otherwise wear a mask.

Clients should also remember]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_nursing_process</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-FkgA6rqQCWmXt_p1pC6NUAYTke_I_LS/_.jpg</video:thumbnail_loc><video:title><![CDATA[The nursing process]]></video:title><video:description><![CDATA[As a nursing assistant, you will be heavily involved in client care and the nursing process. The best practice is to focus on the client’s needs which is why it is called client-centered care. 

Clients are considered active participants in their care. They are informed, involved in all decisions, and are encouraged to ask questions. Their preferences and values should always be respected.

The nursing process is a systematic guide nurses use to provide the best care for their clients. It consists of five steps: Assessment, Diagnosis, Planning, Implementation, and Evaluation. 

In the first step, Assessment, the nurse collects and analyzes information about the client. The nursing assistants contribute to this step with the observations they made during client care. 

There are two types of information: subjective and objective. Subjective information is usually collected from the client. So, Subjective information is what clients Say, like, “I’ve been feeling more tired lately,” or, “The pain in my leg is really bad. 

Like an 8 out of 10.” Objective information is measurable, like the client’s height, weight, vital signs, and so on. Keep in mind that the pain scale is a subjective measure because it’s something the client reports and not something you can objectively measure or observe. 

In the next step, Diagnosis, a nursing diagnosis is made based on the collected information and the client’s problem. The third step, Planning, is about setting goals for the client and planning nursing interventions to reach these goals. 

A client care conference is organized so you and other members of the healthcare team can share information about the client. The fourth step, Implementation, involves performing planned interventions. 

As a nursing assistant, the nurse will assign you to perform tasks related to these interventions, like turning a client over in bed to prevent pressure ulcers or helping them with bathing. In the final step, 

Evaluation, the effect]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Becoming_a_nursing_assistant</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BbY2wdDqQJyTeA1RYNIUopIATo6Pn7Tv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Becoming a nursing assistant]]></video:title><video:description><![CDATA[Nursing assistant, or NA, is someone who is trained to help clients with their healthcare needs and activities of daily living under the supervision of a licensed nurse. Nursing assistants have been around for a long time and are well-trained and valuable members of the healthcare team.

Alright, there are many different healthcare facilities where nursing assistants can work. In fact, wherever there’s a need for healthcare, nursing assistants can lend a hand. 

Such places include hospitals, nursing homes, home care, assisted living facilities, hospice organizations, long-term care facilities, correctional institutions, and skilled-nursing facilities. 

In these various settings, nursing assistants provide physical and emotional care for people who are sick, disabled, or injured. 

They help people who require assistance with activities of daily living. This ranges from personal hygiene, turning and repositioning bed-ridden clients, to helping clients eat. 

As part of the healthcare staff, nursing assistants also help to observe the wellness of the clients by measuring their vital signs, weight, and pain level, which they document and report to the rest of the staff.

Now, the minimum training and competency requirements to become a nursing assistant are established by a federal law known as the Omnibus Budget Reconciliation Act of 1987, or simply OBRA. 

The OBRA-required minimum training period for a nursing assistant program is 75 hours, among which 16 must be clinical training supervised by a registered nurse who has a minimum of 2 years of experience. 

75 hours of training is just the minimum set by OBRA, but indeed, the period of training varies among states, and it may go up to 180 hours. So it’s important to get familiar with your state’s program requirements.    

Upon completion of the training program, candidates must take and pass the competency exam in the state they were trained. The exam includes a written or oral component, plus a practi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronavirus_disease_19_(COVID-19)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KG8D2ZdORbGdlhvbWdVncRLiSUaV8hbG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronavirus disease 19 (COVID-19)]]></video:title><video:description><![CDATA[Coronavirus disease 19, or COVID-19 for short, is caused by a pathogen called SARS CoV-2, or severe acute respiratory syndrome coronavirus 2. 

So from its name alone, “severe acute respiratory syndrome coronavirus,” you get that this pathogen is a type of virus that causes a respiratory infection. 

The number two is in the name because this virus is genetically very similar to the SARS coronavirus, which was responsible for the SARS outbreak of 2002.

For someone to become infected with COVID-19, all 6 steps in the chain of infection model must be met. 

In order, these include: the pathogen, the reservoir, the portal of exit, the method of transmission, the portal of entry, and, finally, the susceptible host. 

So for COVID-19, the pathogen is COVID-19, and the reservoir is a place where the virus can survive. Right now, the natural reservoir for COVID-19 is still being investigated. 

Both symptomatic and asymptomatic humans who are infected with COVID-19 can act as reservoirs. 

The virus is then released from the reservoir through a portal of exit, like the respiratory tract. Transmission can happen through respiratory droplets. 

When people cough or sneeze, they can spread the virus directly to other people, or those droplets could end up on surfaces like phones, tables, doorknobs, and faucets. 

The droplets then enter the respiratory tract as well as the mouth or eyes as the portal of entry. Finally, the virus then infects a susceptible host, which is, well, another person.  

Once a person is infected with COVID-19, there’s an incubation period, which is the time between infection and symptom development. 

For COVID-19, the incubation period can last for up to 14 days but is usually around 4 or 5 days. 

Some people don’t develop symptoms at all, but they can still transmit the virus to other people. Others develop symptoms, which can range from mild to severe. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Grooming:_Hair_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NwEMl2a7QdeOX4PSYbmQx9uARp_ZrxoV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Grooming: Hair care]]></video:title><video:description><![CDATA[Hair care is one of several grooming activities that are important for a person’s physical and emotional well-being. Clean and well-maintained hair improves a client’s self-esteem and speeds up their recovery. 

Clients are usually motivated to take care of their hygiene on their own, but as a nursing assistant, you’ll come across individuals who have weak motor skills or other conditions that prevent them from managing their own hair and therefore require your assistance. 

Before we continue, there are several important definitions you’ll need to be familiar with. Dandruff is a skin condition that mainly affects the scalp. This condition is not contagious and it’s typically associated with itching and flaking. 

Dandruff can be caused by seborrheic dermatitis, which is a skin condition that also affects the scalp. It’s characterized by yellow or white patchy scales, crusts, and itching. In infants, seborrheic dermatitis is also known as cradle cap. 

Next up is tinea capitis, a scalp condition caused by a fungal infection, which is also associated with itching and flaking. Next, we have pediculosis capitis, which is a condition caused by small parasitic insects called head lice. Head lice lay their eggs, called nits, onto the shaft of the hair. Nits are easy to confuse with dandruff, but the nits cannot be brushed off while dandruff can. 

The last one is alopecia, more commonly known as hair loss, which can be inherited or acquired. Acquired alopecia can be age-related or it can be caused by chemotherapy and radiation therapy or other problems like poor nutrition.

First, prepare your working area by covering the overbed table with paper towels and placing your equipment. Make sure that your client is in a supine position. When combing their hair, raise the bed and head of the bed to a comfortable height as tolerated by the client; when shampooing and washing their hair, lower the head of the bed until it’s flat. Also, lower the side rail on the si]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain:_Heat_and_cold_applications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8hIHeTxzR7Kh0ekkBP9CWTh6QwCIDpb-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pain: Heat and cold applications]]></video:title><video:description><![CDATA[The application of heat and cold techniques are a great way to help a client alleviate pain and discomfort. In addition to reducing pain, they can reduce muscle spasms, promote healing, improve mobility, and make the client more comfortable. 

They may also be used on their own or in conjunction with other pain relieving techniques, depending on the client and their severity of pain. 

These include non prescription medications like ibuprofen, prescription medications like narcotics, and physical therapy treatments. 

As a nursing assistant, when a client is in pain or discomfort, the first thing you should always do is make sure your clients are in a comfortable position with proper alignment. 

Make sure the wheels on the bed are locked and raise the bed in a good working position that’s comfortable for the client, and cover them so that only the treatment area is exposed. 

Afterwards, even though there are many methods we can use to help with a client’s pain, oftentimes it will be decided on by the health care team to apply heat and cold to different areas of the body to make the client more comfortable. 

In order to apply heat and cold safely, we need to understand the different ways to apply heat and cold and how to do so properly to avoid harm to the client. 

However, as a nursing assistant, make sure you follow your facility’s protocol, the instructions provided when the nurse delegated the task to you and ensure the task is on your list of authorized duties before applying heat and cold application. 

Furthermore, if you are ever unsure on how to use any of the heat and cold applications, consult a nurse on your team or refer to the manufacturers instructions.

Heat application is typically used for musculoskeletal injuries, such as neck and back pain, to reduce pain and relax muscles. 

It also promotes healing by dilating the blood vessels in the area and increasing circulation. Heat can also loosen up stiff joints and may help to reduce swell]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Condom_catheters_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7XfRtW24SmG3RIr8L5IW74dWTKmegqUH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Condom catheters (for nursing assistant training)]]></video:title><video:description><![CDATA[A condom catheter, also known as external urinary catheter or urinary sheath, consists of a flexible sheath that fits over the penis, much like a condom, and is connected to tubing that lets urine flow to a drainage bag. This provides a safe and non-invasive way to commonly manage urinary incontinence or involuntary loss of urine in biological males. 

Condom catheters should be changed on a daily basis. Now, before we talk about how to apply or remove a condom catheter, here are some general considerations. First, ask the nurse to tell you what catheter size to use. That’s important because if it’s too small, it may compress or traumatize the urethra, restricting the flow of urine or blood. And if it’s too large, it could leak or slip off. Clip the hair at the base of the penis or put on a hair guard before applying the catheter to prevent hairs from getting in the catheter. You also need to check the type of the condom catheter used. Some of them are held in place by a self-adhesive coating on their inside, while  others need an external strap of elastic tape. Remember to close the room’s door and bedside curtain and respect the client’s privacy. Before beginning the procedure, unclip the tubing from the bedsheet from the bed linens or the client’s leg, if there is any. Once you are finished replacing the condom catheter, secure the tubing again and make sure that it doesn’t have any kinks and that the condom is not twisted because that will obstruct urine flow. You also need to ensure that the drainage bag is placed below the level of the bladder to prevent the urine from flowing back into the bladder. 

Okay, so, you’re removing a condom catheter, and reapplying a new one. First, cover the over-bed table with paper towels. Then fill the wash basin with water and check that the temperature is comfortably warm. Place the basin together with soap, towels, and washcloths on the over-bed table. Ensure that the wheels on the bed are locked and raise the bed ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Assisting_with_urinary_elimination</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f04xMjNRTj6XXI66WIRSzUxBT5aBgT_1/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Assisting with urinary elimination]]></video:title><video:description><![CDATA[Urination is the process of expelling urine outside the body via the urethra. In the medical field, it’s also called voiding or micturition. Your client might have problems with urinating, so it’s important that you recognize them and be able to assist them. 

Typically, this process starts when you decide to urinate, the brain sends a signal down to the bladder causing it to contract. The sphincter relaxes, and the urine passes through the urethra and outside the body.  

The amount of urine a person passes depends on their age and size, but generally, an adult should pass around 2,200 ml to 2,700 ml per day. If they pass under 300 ml per day, it’s called oliguria. If it’s less than 100ml per day, it’s called anuria. Both often indicate a serious medical condition!  

Frequency of urination can also be an issue. Needing to urinate more than once every 2-3 hours is called urinary frequency, and having to urinate often at night is called nocturia. If there’s pain when urinating, it’s called dysuria. If they leak urine involuntarily, it’s called incontinence. If they feel the urge to urinate but can’t, it’s urinary retention; if they feel sudden, strong urges, it&amp;#39;s called urinary urgency.  

Now typical urine can range from  clear to a light yellow or an amber color, and it should be free of particles . A darker “tea” color could be due to dehydration but also other medical problems. Red urine could be due to hematuria or blood in the urine, but some food, like beets, can also cause this. 

Now, some people might have trouble with urination simply because they are too weak or have other medical conditions that prevent them from getting to the bathroom or using the toilet, so whatever the cause, you’ll need to know how to assist people with voiding. 

Now, before we go into each procedure, some common care tips include: Making sure the path to the toilet is lit before the client goes to the bathroom. Answer call lights promptly, especially if they ar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Grooming:_Hand_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oa7x3ll2S2CbXwN8zXNrmxpwSOKlP9gO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Grooming: Hand care]]></video:title><video:description><![CDATA[Hand care involves cleaning and caring for the hands and fingernails. It is an essential part of personal care and hygiene. Some clients, like those in advanced age, need help with this task. As a nursing assistant, you may be asked to assist these clients. 

Regular hand care contributes to the client’s overall health, generates a feeling of comfort, and promotes their ability to participate more fully in their daily activities. At the same time, hand care can prevent problems from occurring. 

Cracked, dry skin can be a portal of entry for microbes, which can lead to infections. A client with long or rough fingernails may harm themselves, especially if their level of alertness is decreased due to problems such as dementia. As you care for the client’s hands, you can closely observe the condition of the skin and fingernails

Okay, now, let’s go over some important terms. The nails grow from the nail root, which is under the skin. The area where it comes out is covered by a semicircular waxy layer called the cuticle.  There are also nail folds along each side of the nail, and together with the cuticle, they  prevent entry to bacteria and other pathogens. 

Torn and partially disconnected pieces of the cuticle or the nail folds are known as hangnails, and they can result from various causes such as dry skin, cold temperatures, nail biting, or even a bad manicure. 

Hangnails can be irritating and painful, especially when they rub on clothing. They can also bleed and get infected or inflamed, so it’s important to provide proper hand care to prevent hangnails from occurring. In some healthcare facilities, hand care is performed solely by the nurses.

Okay, so, when assisting with hand care, first gather the supplies you’ll need, including gloves, a wash basin, soap, paper towels, towels, washcloths, an orangewood stick, nail clippers (if you’re allowed to clip the client’s nails), an emery board, and hand lotion. If the client has brought their own suppl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Comfort_promotion:_Caring_for_the_client's_environment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2BQApKSkRlWuSDEgHVAvQIB0TtGploYR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Comfort promotion: Caring for the client&apos;s environment]]></video:title><video:description><![CDATA[In a healthcare setting, a client’s, or resident’s, “unit” is referring to their room. The various types of units differ according to the person’s needs. 

For a client that is receiving medical care in their own home, the resident’s unit is the person’s bedroom or living room. 

However, most people that need medical care stay in healthcare facilities, such as hospitals and long-term facilities. 

In hospitals, clients typically stay in commune units with a shared bathroom that can accommodate more than one person. 

There can also be more private units that are designed for one or two people, but these are used for individuals that need more privacy such as those recovering after a surgery. 

A special type of unit is in the intensive care unit, or ICU, or a critical care unit, or CCU, and it’s reserved for individuals that are critically ill, need special equipment and more intense monitoring. 

Also, a hospital usually has birthing suites for people that are about to or just gave birth to a baby. 

Sometimes, a hospital can also have another type of unit called a subacute care unit, or skilled nursing unit, for clients who are not ill enough to be in a regular hospital unit, but have not yet recovered fully to return to their home. 

Now, in a long-term care facility, also known as a nursing home or an assisted living facility, the units are different than in hospitals. 

People stay for a longer period of time and so the facility has to be more home-like. Residents have their own private room or share a room with one or more people. 

Bathrooms can be private or shared and there are also some other common rooms designed for dining and other activities. 

In some long-term facilities, people live in whole apartments that have one or more bedrooms and bathrooms, but share commune dining or activity rooms with other people. 

Now, the condition of a client’s unit affects the person’s well-being and so the resident’s environment must have certain acc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Monitoring_fluid_intake_and_output</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1aaLwQIBQsm06Kd_VTdpK00oQK_80u_K/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Monitoring fluid intake and output]]></video:title><video:description><![CDATA[Normally, the amount of total body water should be balanced through the ingestion and elimination of water: ins and out. To ensure this balance, as a nursing assistant, you may need to track and record all fluid intake and output on an intake and output sheet, commonly known as I&amp;amp;O sheet. 

This is particularly important for certain groups of clients, like those on special fluid orders, including “encourage fluids” and “restrict fluids;” those who are at risk of developing dehydration, or losing too much body fluid, which impairs normal body functions; or those who might develop edema where swelling occurs in tissues due to excess fluid build up. 

High risk of dehydration exists for those who may not be drinking an adequate amount of fluids throughout the day or those who might be losing too much due to receiving certain medications, like diuretics, or through vomiting, diarrhea, bleeding, burns, excessive sweating, fever, or vigorous exercise. Common signs include dry mouth, excessive thirst, and dark urine. 

Likewise, clients at risk of developing edema include those receiving intravenous fluids or those with heart or kidney disease, where the body has trouble eliminating excess fluid. The fluid builds up and causes swelling, especially in the lower extremities. 

Nursing assistants should check with nurses in charge of the client and the nursing plan of care to find out if the client&amp;#39;s intake and output should be monitored. So, every time one of these clients receives or loses fluids in any way, the exact volume can be recorded. These volumes are then totaled at the end of every shift and then at the end of a 24-hour period. 

Okay, so for fluid intake, you’ll need to count anything the client drinks, including water and beverages as well as all foods that are liquid at room temperature, like ice cream, gelatin, sherbert, pudding, custard, ice chips, and popsicles. The nurse will also measure the fluids provided through intravenous t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sensory:_Caring_for_optical_aids</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I_TeZdjRSMqK2vZxl17vKvBmT1ODqx-i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sensory: Caring for optical aids]]></video:title><video:description><![CDATA[Many of your clients will wear glasses or contact lenses, which are commonly used to correct vision. Contact lenses are made to adhere to the cornea, which is a transparent part of the eye in front of the iris. They can be rigid gas permeable or soft lenses. Rigid gas permeable lenses are made of firm plastic that allows oxygen to pass through it and are smaller than the cornea. Soft contact lenses are made of flexible plastic that covers the entire cornea plus a small area around it. 

Now, there are a few common reasons why an individual would need glasses or contact lenses: nearsightedness or myopia, which is a disorder when the eyes can’t focus on faraway objects; farsightedness, or hyperopia, which is a disorder usually present at birth when the eyes can’t focus on close objects; astigmatism, which occurs when the cornea or the lens inside the eye is irregularly shaped, so the vision is distorted or blurry; and presbyopia, which is a natural part of the aging process that occurs when the eyes can no longer focus on objects close-by.

Some of your clients might have an artificial or prosthetic eye because their natural eye was surgically removed, usually, due to an injury, infection, eye tumor or a disorder called glaucoma, which happens when the pressure inside the eye gets too high, causing damage to the nerves and blood vessels. 

Now, some of your clients will be able to take care of their own eyeglasses, contact lenses, or artificial eye, but others might need your help. There are a few things to remember before the procedure. Inform your clients about the procedure, and explain it to them. Your clients aren’t able to see well without their visual aids, so make sure they are not standing or walking during the procedure as they could injure themselves. Eyeglasses, contact lenses, and artificial eyes are expensive, so make sure that they are not damaged or lost. Eyeglasses, contact lenses, and artificial eyes should have their containers labeled wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Oral_fluids</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n6jQwhguSi_Mji0en5kSOgOVRw6bshqj/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Oral fluids]]></video:title><video:description><![CDATA[Water is essential for human life. It’s the main substance in our bodies, making up more than 50% of a person’s body weight, and it’s directly involved in every biochemical reaction in each cell in our body. 

Normally, the amount of total body water should be balanced through the ingestion and elimination of water, ins, and outs. 

About 80% of our water intake comes from drinking fluids, the other 20% comes from the food we eat. 

Water content in food varies, but some fruits and vegetables, like watermelon or strawberries, are 90% water by weight. 

Now, the recommended daily amount of fluid intake for an adult is around 10 to 20 glasses, which is about 1.5 liters to 3 liters. 

As far as water output goes, we eliminate water through breathing, as humidified air leaves the body, as well as through sweating, urinating, and bowel movements. Now, when water losses are greater than the intake, it results in dehydration. 

There are many causes of dehydration, ranging from not drinking an adequate amount of fluids throughout the day, to losing too much through vomiting, diarrhea, bleeding, burns, excessive sweating, or vigorous exercise. 

So, it’s important to encourage clients to maintain proper hydration and recognize the various reasons why a client might not have adequate fluid intake. 

Some groups like children and the elderly are more prone to dehydration. Children have a higher surface area to body mass ratio, so they end up losing more water through their skin. 

The elderly have decreased thirst sensation and might be taking medications that alter their hydration status. 

Oftentimes, they also have chronic diseases that affect their kidneys’ ability to maintain a healthy water balance. 

Individuals in comas or with dementia are also more susceptible to dehydration because they might not be able to express their thirst.

Now, when the opposite happens, meaning that the intake is greater than the water losses, this can result in an excessive amoun]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Comfort_promotion:_Promoting_rest_and_sleep</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mLYMdiXMTmWi0BukRLa0U-MqQ9On8PFv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Comfort promotion: Promoting rest and sleep]]></video:title><video:description><![CDATA[As a nursing assistant, one of your most important tasks is to ensure your clients are resting properly and having high-quality sleep. 

That’s because insufficient rest and sleep can take a huge toll on your clients’ physical and emotional health. 

For example, poor sleep reduces their pain tolerance and makes them more susceptible to infections, heart problems, and diabetes. 

These clients can end up feeling really tired during the day which can make physical activities like walking down the hall more challenging and dangerous, with clients being more likely to sustain a fall injury. 

Often, the fatigue can also lead to irritability and difficulty focusing, present challenges remembering and processing information, and can worsen feelings of depression and anxiety.

Now, the approximate amount of sleep needed in a 24-hour period varies greatly according to the client’s age group. 

The older they are, the less sleep they need. So, newborns might get up to 17 hours of sleep per day, whereas, for adults, the recommended sleep range is typically 7 to 9 hours. 

For older adults, it might be a bit more difficult to achieve this many hours of sleep without interruption through the night which is why naps during the day may help.

Poor sleep duration or quality is usually caused by factors that interrupt the sleep cycle, which is a period of sleep that lasts about 90 minutes, during which we move through five stages. 

Over the course of the night, there are four or five sleep cycles. The first four stages make up non-rapid eye movement, or NREM sleep, which is roughly 80% of the sleep cycle, while the fifth part is rapid eye movement, or REM sleep, which accounts for the last 20% of the sleep cycle. 

Across the four stages of NREM, we move from very light sleep during Stage 1 to very deep sleep in Stage 4. During NREM there’s minimal muscle activity, and our eyes don’t move much. 

During REM sleep, the eyes dart around, and this is where dreaming occurs,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sensory:_Caring_for_hearing_aids</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QxFY9eEIQBqMFqQ7Kk8hs-d9S8uFLb_F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sensory: Caring for hearing aids]]></video:title><video:description><![CDATA[Some of your clients might have a hearing impairment, usually related to long term exposure to noise; infections and disorders; some drugs; genetics; or simply their age. Some of these clients will use hearing aids to improve their hearing. 

Now, hearing aids don’t reverse hearing loss or address the cause, but they can improve an individual’s hearing comprehension by amplifying the sound or by making it louder. 

Traditional hearing aids amplify all sound: speech and background noise (like traffic, background music, and other people talking). This can be really distracting. 

Modern programmable hearing aids have a microchip that analyzes the sound and removes background noise. 

The hearing aids can also have different programs for different environments like a restaurant, library, park, and so on.

There are many different types of hearing aids such as behind the ear, in the outer ear, in-canal, bone-anchored, or attached to glasses. 

All hearing aids have the same basic parts: a microphone that receives sounds and converts them into electrical signals; an amplifier that increases the power of these electrical signals; a receiver that converts the electrical signals back into sound; and batteries.

When caring for clients with hearing aids, there are a few things to remember: Clean the hearing aids daily following manufacturers’ instructions and avoid alcohol wipes; don’t use any hair products or wet the hair of a client while they are wearing their hearing aids; when they are not being used, store hearing aids in a container labeled with the client’s name and room number; keep the hearing aids at room temperature away from heat and moisture; and make sure that there are spare batteries available and replace dead batteries right away. 

Remember that without their hearing aids, your client might be unable to hear and understand what’s going on in their environment.

When caring for clients’ hearing aids, you will need gloves, a towel, a washcloth, fac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mary_Jo_Bondy:_CEO_of_the_Physician_Assistant_Education_Association_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5snDi0mKTlapoXRljAuVHmt7QmKZ4HG_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mary Jo Bondy: CEO of the Physician Assistant Education Association (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Mary Jo Bondy: CEO of the Physician Assistant Education Association (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adele_Webb:_Executive_Dean_of_Healthcare_Initiatives_at_Strategic_Education,_Inc._(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lp6sYmr8SNecqMIyanyjeDyIS-qrH1f6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adele Webb: Executive Dean of Healthcare Initiatives at Strategic Education, Inc. (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Adele Webb: Executive Dean of Healthcare Initiatives at Strategic Education, Inc. (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medical_and_surgical_asepsis_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qZzXrcPQRLGgcWHyFjlgkUPnRi6pNhgl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medical and surgical asepsis (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Medical and surgical asepsis (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Collecting_a_sputum_specimen_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iXMKms7MSxCkff9zmyGfrqCIS5_Wqe1_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Collecting a sputum specimen (for nursing assistant training)]]></video:title><video:description><![CDATA[Sometimes, the clients you care for may have respiratory complaints. A healthcare provider may order a sputum specimen for a client they suspect may have a respiratory infection, such as pneumonia or other respiratory illnesses, like lung cancer.

A nurse may delegate collection of the sputum specimen to a nursing assistant. A sputum specimen is simply a sample of sputum from a particular client.

Sputum, sometimes referred to as “phlegm,” is made up of mucus as well as some other respiratory secretions that can be coughed up, or expectorated, from the lungs, bronchi, and trachea.

If a client is coughing or spitting up blood, or sputum that contains blood, that’s called hemoptysis, where “hemo-” refers to blood, and “-ptysis” refers to spitting up.

Now, before collecting a sputum specimen, there are a few things you should keep in mind and a few supplies you’ll need to gather and prepare.

Coughing up or spitting up mucus into a cup can be both uncomfortable and embarrassing for a client.

So, it’s important you ensure client privacy and comfort as much as possible throughout the duration of the procedure.

Be sure you’re collecting sputum, which is produced in the respiratory tract, and not saliva or spit, which is produced in the mouth.

The supplies you’ll need are clean gloves, a small cup of water, an emesis basin, a sterile specimen container with its lid, facial tissues, disinfectant wipes, client identification labels, the laboratory requisition form, and a small biohazard plastic bag.

All right, first, wash your hands, put on some clean gloves, and greet the client. Identify them using two identifiers: usually their full name and birth date, being sure to check that information against the client’s identification bracelet, labels, and laboratory requisition form.

Next, provide the client with a small cup of water to rinse their mouth in order to clear away any microbes that may be present in their mouth; ask them to spit into an emesis basin a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocrine:_Blood_glucose_testing_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zuz32nT-Slur_Lu6d8YKfLIgQbuyI2G8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocrine: Blood glucose testing (for nursing assistant training)]]></video:title><video:description><![CDATA[Blood glucose testing is a procedure used to measure a client&amp;#39;s blood glucose level using a small portable device called a glucometer. It requires a drop of capillary blood most commonly obtained from a finger and takes a few seconds to show results. This is especially important for people with diabetes mellitus type 1 and type 2 as well as gestational diabetes. Regular blood glucose testing evaluates effects of medications, diet, and exercise to keep blood glucose levels under control. This will prevent future complications like vision impairment, kidney and nerve damage, and cardiovascular disease.

As a nursing assistant, you might be asked to help test a client’s blood glucose, so here are some general considerations. First, check to see if the procedure is within your authorized duties and follow facility policies and/or protocols. Also, make sure to familiarize yourself with the type of glucose meter used at your facility. Next, the clients might have thickened, damaged, edematous, or inflamed areas of skin, so you should ask the nurse to determine the most appropriate site for a puncture. Some need testing only once a day, while others might need it more than once and at specific times, like before meals or drug administration. Clients who have coagulation disorders or take drugs that can alter bleeding time might take longer to stop the bleeding after the procedure. Be sure to check with the nurse and the plan of care to determine how often a client needs their blood glucose checked and what’s the normal range for the client.

Now, before you perform blood glucose testing, gather the necessary supplies including gloves, lancet device, antiseptic swab, washcloth, cotton or gauze, and glucometer and strips; make sure you read the instructions on how to use a glucometer because some steps might differ depending on a manufacturer. For the procedure, make sure your client is comfortably sitting or lying in bed in the semi-Fowler position. If th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Oxygen_therapy_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d9zOQZxXThKGWvsw_d6cja8PRzGNf5So/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Oxygen therapy (for nursing assistant training)]]></video:title><video:description><![CDATA[Oxygen therapy is the delivery of extra oxygen to those with conditions that cause hypoxia, which is when there is not enough oxygen to meet the needs of the body.

This includes clients with various diseases that interfere with the lungs’ ability to properly absorb oxygen from the inhaled air like pneumonia, chronic bronchitis, emphysema, and sleep apnea as well as blood problems like anemia where the blood doesn&amp;#39;t carry enough oxygen and heart problems like heart failure where the heart has trouble pumping blood around the body.

Now, oxygen is considered a medication so, as a nursing assistant, you will provide care for clients receiving oxygen therapy.

However, it’s a nurse’s or respiratory therapist’s task to start and maintain the oxygen therapy, and a healthcare provider will be the one to order when and how to administer supplemental oxygen.

Okay, now, an oxygen setup consists of an oxygen source and a delivery device. There are several sources for oxygen therapy, including a wall outlet, an oxygen tank, a liquid oxygen system, and an oxygen concentrator.

With a wall outlet, oxygen is delivered into each client’s room from a central supply. Next, an oxygen tank is filled with oxygen under pressure and is typically portable, so it can be carried along as the client moves.

However, this should be moved very carefully; if the tank tips over and the valve breaks open, pressurized oxygen can burst out forcefully and result in severe trauma.

Oxygen tanks also have a gauge that shows how much oxygen is left. There are also liquid oxygen systems that consist of a portable component which can be worn over the shoulder.

The portable component needs to be filled by a large reservoir that is kept at home. Finally, oxygen concentrators pull in air from the atmosphere and selectively remove nitrogen to deliver 100% oxygen.

These devices need a power supply and are very easy to use because they have an on-off switch.

They are usually preferred at]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Routine_ostomy_care_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RvuDulfjRj2LSenmmOReOMPJS_GMurrU/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Routine ostomy care (for nursing assistant training)]]></video:title><video:description><![CDATA[An ostomy is a surgically created opening used to connect an internal organ to the abdominal wall, through which waste products, like intestinal contents, are eliminated. The opening that can be seen on the body surface is called a stoma, and it’s usually connected to an ostomy pouch, also called a bag or appliance, where stool and flatus collect. An ostomy can be permanent or temporary, and it can be necessary because of fecal incontinence, an intestinal tumor, bowel trauma, and a bowel inflammatory disease. In these circumstances, part or all of the intestine is removed, and the remaining part of the intestine is brought up through the abdominal wall to allow for elimination of waste products. 

Now, depending on how much bowel is removed, an ostomy can be either an ileostomy or a colostomy. With an ileostomy, a part of the small intestine is connected to the abdominal wall. An ileostomy can be permanent when the entire large intestine is removed or temporary when it’s done to allow the large intestine to heal after trauma or surgery.  With a colostomy, only part of the large intestine is removed, and the remaining part is connected to the abdominal wall. Remember that, normally, in the small intestine, the nutrients are pretty liquid because most of the water is reabsorbed in the large intestine. So, with an ileostomy, the feces are liquid, and they flow at a fairly constant rate. With a colostomy, on the other hand, feces have a different consistency depending on the location of the colostomy. So, if nearly all the large intestine was removed and the colostomy is near the beginning, feces are more liquid. If the colostomy is near the end of the digestive tract, feces are more solid. 

Like ostomies, ostomy appliances also come in different shapes and sizes. There are drainable appliances, also called “open-end” appliances which are sealed with a clip or a Velcro-type system at the bottom, so they can be drained and reused. Then there are closed-end, or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Jeff_Maggioncalda:_CEO_of_Coursera_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zrdu-vmXScScvepTveJjTUaXRfi0eyl4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Jeff Maggioncalda: CEO of Coursera (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Jeff Maggioncalda: CEO of Coursera (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Grooming:_Dressing_and_undressing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pkOSPN4BT4O-kG79HXocEUheSAisBCq_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Grooming: Dressing and undressing]]></video:title><video:description><![CDATA[Changing clothes promotes comfort, hygiene, and well-being. Clients usually change clothes when they wake up in the morning and before they go to sleep at night. Τhey also change clothes for bathing as well as when the clothes get wet or dirty. 

Now, most people are able to dress and undress on their own, but as a nursing assistant, you will come across clients that will require your assistance, such as those that are recovering from a surgery, are weak due to an illness or advanced age, or have a disability on an arm or leg due to a neurological disease, such as a stroke. 

Some clients will only need minimal assistance, like securing a zipper or selecting clothes, while others will require your assistance for the entire procedure of dressing and undressing. Allow the client to dress themselves to the fullest possible extent. 

Now, a client’s clothes can vary depending on the type of the facility. In hospitals, people usually wear gowns, while in long-term facilities they often wear their own clothes during the day and sleepwear, such as nightgowns or pajamas, during the night. 

Keep in mind that it’s very important to allow the client to choose their own clothes whenever  possible. If they’re not able to decide their own clothes, make sure to choose clothes that are comfortable and appropriate for the client’s activities and the environment. 

Also, for clients who have a weakness or disability, be sure to choose clothes that are easy to put on and take off. 

In addition, there are assistive devices, such as hook and loop straps or fasteners instead of buttons, that can make changing clothes much easier. 

Now, before we talk about assisting a client with dressing and undressing, here are some general considerations. 

Before beginning the procedure, find out from the nurse the plan of care, how much help the client usually needs, and if the client has any issues that require extra care, such as a cast, splint, wound, or weakness. 

At all times, res]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Measuring_peak_expiratory_flow_rate_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v8RuRaZ7S1_1QkUYuVOKkWynQGyF_uI_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Measuring peak expiratory flow rate (for nursing assistant training)]]></video:title><video:description><![CDATA[Peak expiratory flow rate, or PEFR for short, is the fastest and the hardest someone can exhale after a full inspiration.

This can be used to measure the client’s ability to push air out of their lungs and, thus, measure the amount of obstruction in the airways of clients with certain respiratory conditions, like asthma.

This is essential to determine how open their lungs are, if their treatment is working properly, and if they need a dose adjustment or even a new medication.

Measurement of PEFR is performed with a special portable handheld device called a peak flow meter.

This is made up of a mouthpiece attached to a numbered scale with a small arrow that moves as the client blows air out, indicating the speed of airflow measured in liters per minute.

Now, before you start assisting a client with measuring PEFR, here are some general considerations.

Clients that are experiencing pain, motor function impairments, and people with dementia or other cognitive impairments might be unable to measure PEFR independently. Those who can, should perform PEFR measurements at home or in a healthcare facility.

Measurements are done regularly at certain times, such as first thing in the morning and last thing at night, before or after using asthma medications, or when experiencing symptoms of an asthma exacerbation, like shortness of breath, cough, or wheezing.

When assisting a client with their PEFR test, first make sure the client is standing erect if they’re able.

The arrow should be set on the zero mark and a clean, disposable mouthpiece should be attached to the device.

Instruct the client to inhale through the mouth by taking a deep breath and placing their lips tightly around the mouthpiece, keeping their tongue away from the opening.

Then, the client should exhale as fast and forcibly as possible. This process should be repeated twice more.

Each time, make sure their head remains in the same position and that arrow is reset to zero. Dispose of the mo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal:_Collecting_a_stool_specimen_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MD5FC6s2ToyjeQ3S-PJdr4fUSYq-IY9U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal: Collecting a stool specimen (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Gastrointestinal: Collecting a stool specimen (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Admissions,_transfers_and_discharges</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/leFMC9MXTmqPQravMP8RspcmQVSNQWZn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Admissions, transfers and discharges]]></video:title><video:description><![CDATA[Admission refers to the official entry of a client into a healthcare facility, and a transfer is moving a person from one room to another, from one department to another, or from one healthcare facility to another. Discharge refers to the official departure of a person from a healthcare facility. These processes can be impactful and disruptive to a client&amp;#39;s normal routine. The good news is that, as a nursing assistant, you can help the clients feel less overwhelmed as they check in and out of the healthcare facility.

Alright, after the new client arrives in the healthcare facility, the admitting nurse fills out the client information on the admission sheet, including the client’s full name, the current address, and date of birth. The client is then given an identification number. As a nursing assistant, you will be asked to escort the client; this is a great opportunity to make a good first impression and help the client feel as comfortable as possible. Some clients may need to be transported in a wheelchair or on a stretcher depending on their health status. Remember, you’re the one who will take care of most of the clients’ basic needs. So, be sure to make them feel welcome and comfortable. First, greet every client by name and title, like Mr. or Mrs. You can find the client&amp;#39;s name in their admission sheet or by asking the nurse. Then, introduce yourself and your title to the client and their family members or guardian if they are present. After the client gets into their assigned room, offer to help them with unpacking and getting changed into a gown or pajamas if needed.  It’s also important to make a list of the client’s belongings to make sure that nothing gets lost. Make sure that the client feels respected and is treated with dignity.

When the client is settled and relaxed, take their vital signs and measure height and weight.  Usually, the nurse comes to make the admission assessment, which involves gathering the client’s ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sxz8ippfTSyv8GKH4oQ_Ut9VRn_MojBs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to disease]]></video:title><video:description><![CDATA[A disease or a disorder is the result of an abnormal change or disturbance in the structure or function of an organ or organ systems. An illness is a more subjective state a person identifies themselves based on physical or mental symptoms. 

Now, diseases can either be acute or chronic. Acute diseases are temporary, and the affected person is expected to recover from them. Chronic diseases continue for a long period of time and can sometimes last for the person’s entire lifetime.

Now, diseases can be divided into several categories. However, a disease can be a part of more than one category. The first category includes infectious diseases, which are caused by tiny organisms, such as viruses, bacteria, fungi, or parasites. Some examples of infectious diseases include pneumonia, urinary tract infections, and the common cold. 

Next up are degenerative diseases, which are the result of a gradual breakdown of the tissues of the body. Some of these diseases are genetic, such as Huntington disease. 

Others are caused by infections, injuries, or aging. However, sometimes there isn’t a known cause. Some examples of degenerative diseases include osteoporosis, arthritis, and Alzheimer disease. 

Next up are nutritional diseases that are caused by an imbalance in certain nutrients. Keep in mind that consuming either too much or too little of a nutrient can lead to a nutritional disease. 

For example, consuming too many calories can lead to obesity, while not getting enough iron in your diet can lead to iron deficiency anemia.

Next on the list are metabolic or endocrine diseases, which are a result of the body not being able to use certain nutrients. They often occur when the body makes too much or not enough of a certain hormone. 

As a result, the organ for which a certain hormone is responsible doesn’t function properly. One example is diabetes, where the body can’t produce or respond  to insulin, which leads to abnormal nutrient metabolism and high blood gluc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integumentary_system:_Wounds</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ftsegr_cTQqVDHBfH9WYzV6yTtOhWQOM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integumentary system: Wounds]]></video:title><video:description><![CDATA[A wound is an injury to the skin and its underlying tissue. An intentional wound is made by a healthcare professional for therapeutic purposes and interventions, like surgery. 

An unintentional wound is a result of an accidental injury like skin tears and trauma from a car crash or a fall. It is possible to prevent unintentional wounds in healthcare settings by using proper techniques to reposition and transfer clients.  

If there is a break in the skin, the wound is open. If the skin is intact, the wound is closed. A bruise is a good example of a closed wound. Immediately after an injury, blood vessels constrict and blood clots are formed to stop the bleeding. 

Once the bleeding is stopped, the first stage of wound healing called the inflammatory stage begins. In this stage, the body is starting to heal itself and clear out any microbes that may have entered the wound. 

The blood flow increases, and there are signs of inflammation, like redness, warmth, swelling, and pain. The second stage is called the proliferative stage. 

In this stage, cells divide to increase their numbers and repair the damage. A structural protein called collagen is laid to make the tissue stronger. 

The last stage is called the maturation stage. This is when the collagen becomes more organized and stronger, the wound matures, and the scar is formed. 

There are a few factors that contribute to wound healing. First, there must be a good blood flow to the area to supply the cells in the area with oxygen and nutrients. 

Next, there’s proper hydration and nutrition. Protein is essential for building collagen, so adequate protein intake is required for wounds to heal properly. 

Lastly, protection from infection is needed because infected wounds take longer to heal. Some other factors can prolong wound healing, like advanced age, low blood flow, diabetes, and malnourishment. 

Sometimes, there can be some complications during wound healing. A wound can be contaminated with micro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Mechanical_ventilation_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rbkwvdfZQqqOdCpYl4WVT47hQi_ekMcf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Mechanical ventilation (for nursing assistant training)]]></video:title><video:description><![CDATA[As a nursing assistant, you will help provide safe care to clients with mechanical ventilation. This is when a machine reduces or even takes over the work of breathing from clients who find it difficult or impossible to do so without help.

The use of mechanical ventilation can range from short to long term and from care in a healthcare facility to home care.

Okay, now, mechanical ventilation can be “invasive” or “noninvasive.” Invasive mechanical ventilation involves the insertion of an artificial airway. An artificial airway is basically a tube that gets placed in the trachea.

One example of this is an endotracheal tube, which is a tube that gets inserted through the mouth and down past the pharynx and larynx into the trachea.

Another is a tracheostomy tube, which is inserted directly through an opening made in the skin of the neck, called a tracheotomy.

Typically, both types of tubes have an inflatable balloon that forms a seal against the tracheal wall. Tracheostomy tubes are also kept in place with a collar or ties wrapped around the client’s neck.

Now, the thing with endotracheal tubes is that because they go through the pharynx and larynx, the client won’t be able to speak, drink, or eat anything via the mouth, which can be extremely uncomfortable for the client.

If mechanical ventilation is required for a long period of time, a tracheostomy tube might be preferred over an endotracheal tube.

Endotracheal tubes can be used only temporarily, for a few weeks, but tracheostomy tubes can be used permanently, such as for clients whose larynx has been surgically removed due to cancer or those with paralyzing conditions that require them to stay on a ventilator permanently.

Now, tracheostomy tubes allow the client to take food or fluids normally through the mouth. Speaking with a tracheostomy tube in place has also been made possible through one-way speaking valves, such as the Passy-Muir valve.

This valve opens as the client breathes in and closes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bloodborne_diseases</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ajfzRLdoTfyqxraE6I2lIgwYTWOX7YMP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bloodborne diseases]]></video:title><video:description><![CDATA[As a nursing assistant, you will come in contact with clients that have serious bloodborne diseases. You have to learn about these diseases, how they can be transmitted, and what you can do to protect yourself at work. 

A bloodborne disease is an infection that is transmitted from an infected person to a non-infected person via the blood or other body fluids such as urine, feces, vomitus, saliva, sweat, semen, vaginal fluids, breast milk, and amniotic fluid. 

In the healthcare environment, transmission can occur via accidental needlesticks and cuts from broken glass items such as blood tubes. 

They can also be transmitted due to direct contact of infected fluids with open skin lesions (like cuts and sores) or with the mouth, the nose, and the eyes. 

Outside of the workplace, they can also be contracted via intravenous drug abuse, unprotected sex, via the placenta from a pregnant person to the fetus, or through blood transfusions. 

Alright, now the most common bloodborne pathogens are human immunodeficiency virus (or HIV), viral hepatitis, malaria, syphilis, and Ebola. 

Of the common bloodborne diseases, the most important ones to know are HIV and viral hepatitis because they pose the biggest threat for U.S. healthcare workers. 

HIV is a virus that targets the cells of the immune system. Over time, the immune system begins to fail and this increases the risk of infections and tumors that a healthy immune system would otherwise be able to fend off. These complications are referred to as AIDS (or acquired immunodeficiency syndrome). 

Now, the acute HIV infection typically presents with flu-like symptoms such as fever, chills, muscle aches, and fatigue. In response, the immune system mounts a counterattack. 

It starts to control the infection, and the person enters the chronic phase, or latent phase, which can last between 2 and 10 years. 

At this point, the individual could still transmit the virus, but they are usually asymptomatic and can still fi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Mark_Rosenberg:_President_Emeritus_for_the_Task_Force_for_Global_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MEwOHsmeRpeyrUFYyyNMqC_vR8uSRUEg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Mark Rosenberg: President Emeritus for the Task Force for Global Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Mark Rosenberg: President Emeritus for the Task Force for Global Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meet_the_Osmosis_Team:_Amin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m71kljmCS8OEkvrIc88FfXUCR7eXjT6c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meet the Osmosis Team: Amin]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Meet the Osmosis Team: Amin through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meet_the_Osmosis_Team:_Samantha</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8SIOXKBuRJWS0Pck_ZJIGVubQ96mOLkI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meet the Osmosis Team: Samantha]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Meet the Osmosis Team: Samantha through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meet_the_Osmosis_Team:_Will</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hGpW67f5QyeZOb6j1VQ2PHuJRQaeo31j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meet the Osmosis Team: Will]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Meet the Osmosis Team: Will through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meet_the_Osmosis_Team:_Zachary</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dBtqufT1R9uRCZiD9Ts0Yf7BRbye_zz8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meet the Osmosis Team: Zachary]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Meet the Osmosis Team: Zachary through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meet_the_Osmosis_Team:_Jake</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:thumbnail_loc><video:title><![CDATA[Meet the Osmosis Team: Jake]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Meet the Osmosis Team: Jake through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meet_the_Osmosis_Team:_Jessica</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ycNU_fMGSZyRJxoYewaaZRuKRXufsvGk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meet the Osmosis Team: Jessica]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Meet the Osmosis Team: Jessica through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meet_the_Osmosis_Team:_Marisa</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bzDE675IRXODcBtc6unFKPGkQE_Yqy0s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meet the Osmosis Team: Marisa]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Meet the Osmosis Team: Marisa through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meet_the_Osmosis_Team:_Pauline</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qnFwWHbPSuKvxELs9-WvwKaGRmWQOx4t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meet the Osmosis Team: Pauline]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Meet the Osmosis Team: Pauline through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integumentary_system:_Pressure_ulcers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Yg_VeKTzSwyKQsWQNXh8PGSWRliR7k6Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integumentary system: Pressure ulcers]]></video:title><video:description><![CDATA[Pressure injuries, also known as bedsores or decubitus ulcers, are painful traumas to the skin and the underlying tissue. Pressure  injuries are usually caused by constant pressure on the skin. 

They could also be caused by pressure combined with friction and shearing. Friction is when skin rubs against a surface. Shearing is when two skin surfaces rub against each other. 

Pressure injuries usually appear over bony prominences, which are parts of the body with the thinnest subcutaneous tissue between the bone and the skin. 

Bony prominences include the back of the head, spine, shoulder blades, elbows, sacrum, hips, knees, ankles, heels, and toes.

When an individual is lying in bed or sitting for a long period of time, the skin and the subcutaneous tissue are squeezed between the bone and the surface they are lying or sitting on. 

The blood vessels can become compressed, which reduces blood flow to the area. Now, if an individual is sliding down in bed, the friction and shearing damage blood vessels, which also reduces blood flow to the area. Without the blood coming in, cells are without oxygen. This leads to cell death and tissue damage.

Factors that increase clients’ risk for developing pressure  injuries, include: immobility; dementia; conditions associated with poor blood flow like advanced age, heart and lung disease, and diabetes; skin conditions like thin skin related to aging, dry skin due to low water intake, or thin subcutaneous tissue due to poor nutrition; and external factors like moisture and irritants from sweat, urine, and feces.

There are four stages of injury, development. In Stage 1 the blood flow is reduced. The skin is warmer than the surrounding areas and appears red but remains intact. 

When pressed on, the area doesn’t blanch or turn white. In Stage 2 only the epidermis and the dermis are affected. It looks like a shallow open wound or a blister. 

In Stage 3 the damage reaches the subcutaneous tissue. There can be drainage ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Range_of_motion_exercises</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sAK2pFhxSvu12I3lIW6KsT_1TUq-fpBw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Range of motion exercises]]></video:title><video:description><![CDATA[Range of motion, or ROM for short, is defined as the normal movement potential of a joint to the extent that is not causing any pain! 

The range of motion is measured in degrees and it’s determined by the type of joint, its articular surfaces, regional muscles, ligaments, and tendons. 

Now, during everyday activities, people typically use all of their joints through their complete range of motion. But this is not the case with  some individuals. 

Some of them have restricted movement due to pain, while others might have conditions that cause muscle weakness or paralysis that prevent them from completing the full motion. 

Either way, if not treated, decreased range of motion can lead to muscle atrophy, which is the wasting away of muscles due to disuse and contractures, a condition where muscles and tendons are permanently shortened. 

To prevent this, range-of-motion exercises, or ROM exercises, are prescribed for these  individuals.

Now, range of motion exercises are typically done to preserve a person’s joint and muscle function, but they can also be used to either increase or prevent further loss in the range of motion. 

They are usually done at least two times a day, and based on the client’s involvement, they can be subdivided into three groups. 

The first group includes active range-of-motion exercises. These exercises are done by your client independently but with your verbal guidance and encouragement. 

The second group covers active-assistive range-of-motion exercises. Here, clients require your help to complete the full motion. These exercises are commonly prescribed to individuals that have some form of muscle weakness. 

The last group includes passive range-of-motion exercises, which are done by a nursing assistant without the active participation of the client. These exercises are commonly done for comatose and paralyzed individuals. 

Now, let’s switch our focus to joint movements. But, before we start, think of a joint as the connec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_system:_Infections</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VL9arLMiSP_ojJImEu7VzkyCTlOQBNEp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory system: Infections]]></video:title><video:description><![CDATA[There are a variety of respiratory infections that can affect a client you’re caring for. Some of the more common infections are pneumonia; influenza, often referred to as “the flu;” and the common cold.

Pneumonia is an inflammation and infection of the lung tissue caused by microbes, such as bacteria or viruses. These microbes can enter the lungs either through normal breathing or through aspiration, where foreign material, like food or vomit, enters into your airway. 

Either way, these microbes will cause infections that cause inflammation, where fluid and pus builds up in the alveoli: the tiny air sacs in the lungs. 

Consequently, gas exchange can’t happen, which makes breathing difficult. Some of the common signs and symptoms of pneumonia include fever, cough, shortness of breath, fatigue, and chest pain that worsens with breathing. 

Cyanosis can occur, where the skin turns bluish due to decreased oxygen in the blood. Pneumonia is usually diagnosed with a chest X-ray and can be treated with antibiotics. 

Supportive treatment includes oxygen and IV fluids. Be mindful to take transmission-based precautions.  

Influenza, or “the flu,” is a respiratory infection caused by the highly contagious influenza virus. It most commonly causes fever as well as generalized body aches, fatigue, and headache. 

It can sometimes cause a cough, sore throat, stuffy nose, and sneezing. Treatment for individuals with the flu generally involves plenty of fluids and rest. 

Sometimes, drugs are given to alleviate symptoms or shorten the duration of the illness, but most people recover in approximately one week. 

Some people, especially elderly individuals, very young children, and those with chronic conditions, have a high risk of developing complications, such as viral pneumonia. 

Because of this, it is important to prevent the spread of the influenza virus with annual flu vaccines and transmission-based precautions.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nervous_system:_Neurodegenerative_diseases</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0n8CeokWSnCcuzvBUggjB264QfekNTFl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nervous system: Neurodegenerative diseases]]></video:title><video:description><![CDATA[Neurodegenerative diseases are a group of disorders characterized by the degeneration, or loss, of neurons, which are the main cells of the nervous system. 

Some of the most famous neurodegenerative diseases include Parkinson disease; Huntington disease; multiple sclerosis; and amyotrophic lateral sclerosis, formerly called Lou Gehrig’s disease.

Okay, let’s start with Parkinson disease. This is a slowly progressive disorder that primarily affects individuals over 50 years old. It is caused by the degeneration of certain neurons in the brain that produce dopamine. 

Dopamine is a neurotransmitter, or a chemical used to relay messages between neurons within the brain, and normally, one of its main roles is to promote movement. 

In Parkinson disease, a decrease in dopamine results in difficulty initiating or controlling movement. This is typically manifested with four main symptoms, which can be remembered with the mnemonic “TRAP.” 

“T” stands for tremor, which is classically described as a resting, pill-rolling tremor because it looks like someone is rolling a pill between their thumb and index finger. 

“R” stands for rigidity, which is caused by tensed up muscles that resist movement. When someone tries to flex the client’s limbs, they could move in a series of stops and jerks, which is called “cogwheel rigidity.” 

If it remains rigid throughout the movement, it’s called “lead pipe rigidity.” “A” stands for akinesia, which is the absence of movement and is a severe form of the more common finding: bradykinesia, which is the slowness of movement. 

This can manifest as a slow, shuffling gait or a decrease in facial expressions almost to the point where the individual’s face looks like they’re wearing a mask. 

“P” stands for postural instability, which causes a stooped posture, problems with balance, and an increased frequency of falls. 

If the muscles involved in speech are also affected, the client might either slur words or talk too quickly to the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Male_reproductive_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TFKQuyvsRYKRMs1HtlB7WpUGRAGM2Tpz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Male reproductive system: Structure and function]]></video:title><video:description><![CDATA[The male reproductive system consists of external sex organs, which include the penis and the scrotum, and internal sex organs, which include the testicles, the epididymis, and the vas deferens. Internal sex organs also include the male accessory sex glands: the seminal vesicles and the prostate gland.

First, let’s focus on the external sex organs. The penis has three main parts: the root, the body, and the glans, which is covered with a fold of skin called foreskin, or prepuce. 

At the top of the glans is the opening of the urethra, which is a tube that carries urine and sperm outside of the body. 

If we do a cross-section of the penile body, you can see two columns of erectile tissue called corpora cavernosa. Corpora cavernosa fills with blood and enables an erection. 

On the other hand, there’s also a spongy tissue around the urethra, called corpus spongiosum. During an erection, corpus spongiosum fills with a small amount of blood to prevent the compression of the urethra. 

Below the penis is a pouch that contains testicles, called the scrotum. The scrotum hangs outside of the body keeping the temperature of the testicles about three degrees lower than body temperature. This is the perfect environment for testicles to produce sperm. 

Besides sperm, testicles also produce testosterone, which is a hormone that is responsible for the normal development of male secondary sex characteristics, such as the growth of body and facial hair, changes in body form, and lowered voice pitch.

Now, sperm production, also known as spermatogenesis, begins in puberty in biological males and continues throughout the lifetime. But, sperm cells that are produced in testicles are actually immature. 

From the testicles, immature sperm cells travel to the epididymis, which is a coiled tube structure, where they mature and gain the ability to move on their own. 

From this moment on, sperm cells are able to “swim” to the egg in the female reproductive tract and fertilize]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HiWd3WcRT1WsPlWDviCAJIfNQ0_a2RPx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary system: Structure and function]]></video:title><video:description><![CDATA[The main function of the urinary system is to control the volume and composition of blood by removing excess fluid and waste products from the body. 

The structures of the urinary system consist of two kidneys, two ureters, the urinary bladder, and the urethra. The kidneys filter the blood to produce urine. 

Once produced, urine will flow through the ureters into the bladder for storage until it’s ready to be excreted through the urethra. Let’s explore each part of the urinary system in more detail, starting with the kidneys. 

They are bean-shaped organs located toward the back of the upper abdominal cavity, one on each side of the spinal column. They’re protected by the bottom of the rib cage and a layer of fat. 

Inside each kidney there are about 1 million nephrons. The nephron is the basic functioning unit of the kidney. 

Each nephron consists of a glomerulus and a series of complicated twisted tubules. The glomerulus is a network of capillaries located within a structure called Bowman’s capsule.

Now, in order to filter blood, the kidneys need a good blood supply, so they are supplied by two large arteries: the left and right renal arteries that branch directly off of the aorta, the largest artery in the body. 

Once inside the kidney, the left and right renal arteries branch into smaller and smaller arteries and eventually give rise to the capillary within the glomerulus. 

These capillaries have tiny openings in them that let small molecules filter out of the blood. Through this process, waste products are removed from the blood, while nutrients remain within the blood.  

At the end of filtration, we’ll basically have two distinct liquids: one is the filtered blood, which remains within the capillaries, and the other one is the filtrate in the Bowman’s capsule, which forms the basis of urine. 

The filtrate leaves the Bowman’s capsule and flows through the tubules that make up the rest of the nephron. These tubules will reabsorb some of the sub]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular:_Applying_antiembolic_stockings_and_sequential_compression_devices_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PW55lO2TTZOjn571Ijf3lVxCRemea25X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular: Applying antiembolic stockings and sequential compression devices (for nursing assistant training)]]></video:title><video:description><![CDATA[Αs a nursing assistant, you will be asked to apply antiembolic stockings and sequential compression devices, or SCDs, in clients that are at risk for deep vein thrombosis, or DVT, such as those who are recovering from a major surgery or have heart and circulatory problems. Make sure you know how they work and how to apply them. 

But first thing’s first: In deep vein thrombosis, deep vein refers to veins that run between the muscles as opposed to superficial veins that you can see on the surface and thrombosis refers to blood clot formation. So a DVT is a blood clot in one of those deep veins, and it typically involves the deep veins of the lower legs or thighs. An individual with DVT will often complain of rapid swelling, redness, and pain on the lower leg. The bad news is that it can lead to life threatening conditions, such as pulmonary embolism where a broken off piece of the clot called an embolus travels to the lungs and causes respiratory problems. 

Alright, antiembolic stockings and SCDs can be used to prevent DVTs. They both work by exerting pressure on the veins of the lower legs, promoting blood return to the heart instead of pooling in the legs. Thus, they decrease the risk for blood clots. Now, antiembolic stockings look similar to conventional stockings, but they are much more elastic. They can extend from the foot to the calf or thigh level. They can provide different levels of pressure, so it&amp;#39;s important to make sure the ones prescribed for the client aren&amp;#39;t so tight that they cut off blood circulation but also not too loose because they won’t promote blood return to the heart. They also leave an opening over or under the toes which can be used by the health care team to check blood circulation in the lower leg as well as the color and the temperature of the skin. Now, sequential compression devices are plastic sleeves that wrap around the client’s legs and consist of multiple compartments that are connected to an air pum]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Performing_urine_testing_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xCoKJALWQ2i36annc60uWnpDRripB554/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Performing urine testing (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Genitourinary: Performing urine testing (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Male_reproductive_system:_Reproductive_system_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_BPcaKiFRvW6HragZYQ4J_h6RLG8wT9T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Male reproductive system: Reproductive system disorders]]></video:title><video:description><![CDATA[The male reproductive system consists of external sex organs, which include the penis and the scrotum, and internal sex organs, which include the testicles, the epididymis, and the vas deferens. Internal sex organs also include the male accessory sex glands: the seminal vesicles and the prostate gland. 

Now, the most common disorders of the male reproductive system include infertility, erectile dysfunction, and cancers.

Let’s start with infertility, which in biological males, is defined as the inability to cause a pregnancy in a biological female after 12 months of trying. 

Some common causes of male infertility include abnormal sperm production and sexually transmitted infections, such as gonorrhea, chlamydia, or HIV.

Now, let’s switch our focus to erectile dysfunction, also known as impotence. In erectile dysfunction, an individual is unable to develop or maintain an erection during sex. This condition becomes more common with age and it could be temporary or permanent. 

The most common causes of erectile dysfunction include: cardiovascular disorders that decrease blood flow to the penis; hormonal disorders associated with low levels of testosterone; emotional disturbances, like excessive stress; and certain medications that can cause erectile dysfunction as a side effect.

Switching gears and moving on to cancers of the male reproductive system, such as testicular, prostate, and penile cancer. Testicular cancers are malignant growths in one or both testicles.

Typically, testicular cancer affects young and middle-aged individuals. They often present as small lumps in the testicle that can be easily felt during testicular self-examination or a physical. 

If detected early, they have a good outcome, but in advanced stages, testicular cancers easily spread to other organs in the body.

Next up is prostate cancer, which is a cancer that originates in the prostate gland. Prostate cancer usually affects individuals older than 50 years of age. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_vital_signs_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n9WDmYtfS86wzbj8v7nd10JqSbO5cJGs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to vital signs (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Introduction to vital signs (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Lois_Nora:_President_Emeritus_of_Northeast_Ohio_Medical_University_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TZATEM56QZ6cJTauIaJKzO0_SlWs9OdT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Lois Nora: President Emeritus of Northeast Ohio Medical University (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Lois Nora: President Emeritus of Northeast Ohio Medical University (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anant_Agarwal:_Senior_VP_University_Planning_&amp;_Strategic_Initiatives_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BHN29GKVSmOPIOWRH3h5GPmoQ0OhJa5l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anant Agarwal: Senior VP University Planning &amp; Strategic Initiatives (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Anant Agarwal: Senior VP University Planning &amp; Strategic Initiatives (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Flatten_the_curve,_raise_the_line_music_video</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LCAwV4m5TxWV1rkv7lGFYIVTQLqvT_t9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Flatten the curve, raise the line music video]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Flatten the curve, raise the line music video through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_a_client_with_COVID-19</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7AAVhvWNS_W2feyC8hBwQSejSH2yF5IN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for a client with COVID-19]]></video:title><video:description><![CDATA[Coronavirus disease 19, or COVID-19 for short, is caused by a pathogen called SARS CoV-2, or severe acute respiratory syndrome coronavirus 2. 

The disease can range from mild to severe, and nursing assistants play a key role in caring for clients with COVID-19 as well as preventing transmission of the disease. 

In the hospital, COVID-19 management revolves around a series of precautions that all medical personnel employ to minimize transmission of the disease and interventions that aim to shorten the course of the disease, maximize the client’s well-being over the course of their illness, and prevent complications of the disease.

The first measure you should employ when caring for a client with COVID-19 is wearing personal protective equipment, which includes  non-sterile gloves, a gown, a mask, goggles, or a face shield as needed. 

Regarding gloves, always wash your hands before putting on gloves and after removing them and use a different pair of gloves for every client and for every procedure you perform. 

Remember that gloves only ensure protection if they are intact and without any holes, fit properly, and cover your wrists. Remove contaminated gloves when you finish the procedure or when you need to touch a commonly used item or surface, such as a light switch, door handle, or faucet. When removing the gloves, turn them inside out and dispose of them safely. 

Next up, there are waterproof gowns, which usually open at the back and cover you from the neck to the knees. Gowns should be used when caring for clients with COVID-19 because there is a chance that they could cough or sneeze, and the droplets could end up contaminating your clothing. Each gown should be used only once, so remember to change the gown between clients. 

PPE also includes wearing a mask that covers the nose and the mouth. Usually, it’s recommended to wear masks when you are closer than 2 meters, or 6 feet, to the client. 

For most cases, a simple surgical mask can be used,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Tracheostomy_suctioning_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/40m7aRxdTEqweIZnaWC04ghaS6eQ_rWL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Tracheostomy suctioning (for nursing assistant training)]]></video:title><video:description><![CDATA[Tracheostomy suctioning is a procedure used to remove secretions from the trachea in individuals with tracheostomy tubes. A tracheostomy tube is an alternative airway for breathing that is inserted through a hole made on the neck and trachea into the tracheal lumen. Tracheostomy tubes are used to bypass an upper airway obstruction; to prevent aspiration; and enable easier suction of tracheal secretions, which can block the normal airflow and lead to an insufficient oxygen supply. 

Generally, nursing assistants should alert the nurse if they think a client requires suctioning. They can assist with tracheostomy suctioning by gathering the required supplies. Now, common signs and symptoms that suggest that a client may require suctioning include a non-productive cough, increased heart and respiratory rate, noisy breathing, shortness of breath, visible secretions, and the presence of coarse breathing sounds or rattling lung sounds. 

Now, there are two types of suction catheters used for tracheostomy suctioning. The first one is a one-time use catheter with a control port, which comes in a sterile kit along with sterile gloves and connecting tubing. This catheter is sterile, which minimizes the risk of infection; it’s transparent, which lets the nurse see the secretions and fluids being suctioned out; and it has the thumb control port, which enables  suction control. One-time use suction catheters typically have a tip with a single opening and come in various sizes. 

For clients who require mechanical ventilation, a closed, or in-line, suction catheter can be used without disconnecting the mechanical ventilator; they are typically used in intensive care units. These catheters are wrapped by a sterile plastic sleeve, so sterile gloves are not necessary. Instead, the nurse can use the regular, or clean, gloves.

Switching gears and moving on to the supplies. If this procedure is within your authorized duties and facility policy and you’re assigned to gather su]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocrine_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/69z3KPmoQDu0R0W_bLwJIalGS42cASgK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocrine system: Structure and function]]></video:title><video:description><![CDATA[The endocrine system is made up of endocrine glands that secrete chemicals called hormones into the bloodstream. When hormones reach their target cell, they bind to a receptor on the cell’s membrane or within that cell, and, in response, the target cell changes what it’s doing. 

So, at the end of the day, the endocrine system helps regulate all sorts of things, like cellular metabolism, which is how cells work; growth and development of the body; reproductive function; and even blood sugar levels after a meal! 

Now, endocrine glands are scattered throughout the body, kind of like a remote work environment. Underneath the brain, there’s the hypothalamus and the pituitary gland. 

The hypothalamus and the pituitary are partners, working together to release hormones that regulate all sorts of things, such as body temperature; blood osmolarity, or how concentrated or dilute the blood is; how the body responds to stress; or even if there’s some sort of danger.

Now, sometimes the pituitary will release a hormone that acts as a messenger that tells another organ what to do. For example, the pituitary sends hormone messengers to the thyroid gland, telling it to secrete thyroid hormones; to the adrenal glands telling them to secrete cortisol; and it tells the gonads, which are the ovaries in females and testes in males, to secrete sex hormones, like estrogen, progesterone, and testosterone. 

Other times, the pituitary releases hormones that go straight to its target tissue. So, antidiuretic hormone’s main role is to tell the kidneys to retain water, depending on the body’s needs. 

Oxytocin dilates the cervix and stimulates uterine contractions during childbirth; it also makes the muscle cells in the breasts contract to eject the milk during breastfeeding. 

So, aside from motherhood, its levels are generally pretty low, but they do increase a little bit during pleasant social interactions, hugs, and physical contact. 

Another hormone, growth hormone, makes ou]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_clients_with_HIV/AIDS</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BpLrmhXdRgOxoDfh_vedwCtISdyoVYTO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for clients with HIV/AIDS]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Caring for clients with HIV/AIDS through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Musculoskeletal_system:_Musculoskeletal_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/94vzpFG5TUqILvm1e5tF2fr9Qo_F5lGL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Musculoskeletal system: Musculoskeletal disorders]]></video:title><video:description><![CDATA[Musculoskeletal disorders are disorders of the bones, joints, and the skeletal muscles, affecting movement. Therefore, any daily activity and quality of life is also affected. 

They make individuals prone to falls and injuries, and dependant on others’ assistance in everyday life activities. Some of these disorders are osteoporosis, arthritis, and muscular dystrophy.

Osteoporosis is a disorder of the bones that causes them to lose their strength and mass, giving them a porous, or sponge-like, appearance. 

This makes them very frail and susceptible to breaking. The most commonly affected bones are of the vertebrae, which can get compressed, leading to a height reduction, back pain, and forward bending of the upper spine, causing a deformity called a dowager’s hump. 

Other commonly affected bones are the hip bones, long bones of the extremities, and the wrist bones. Sometimes, the bones might be so fragile that even normal daily activities, like walking down the stairs, can result in a fracture.

Factors that increase clients’ risk for developing osteoporosis include: advanced age; family history of osteoporosis; small stature; diet that lacks calcium and proteins; vitamin D deficiency that decreases calcium absorption from food; eating disorders, like anorexia nervosa; smoking and consuming alcohol. 

Other risk factors include immobility; sedentary lifestyle; medications, like corticosteroids; and other conditions, like thyroid dysfunction. 

Menopause in biological females is also an important risk factor because there’s decreased production of estrogen: a hormone that has protective effects on the bones.

As a nursing assistant, you should encourage your clients that are at higher risk for osteoporosis to take precautionary measures in order to delay or even prevent its development. 

These include regular exercise, like walking and lifting weights; proper diet rich in calcium and proteins, like dairy products; vitamin D supplements; and avoidin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal_system:_GI_system_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/18j1YgavQY_8XmGK-xI8f0FKTSmS9nzG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal system: GI system disorders]]></video:title><video:description><![CDATA[The gastrointestinal, or GI system, consists of different organs that work together to extract nutrients from the food we eat and then excrete what the body didn’t use in the form of waste. 

Sometimes, these organs can malfunction due to disorders like hernias; gastroesophageal reflux disease, or GERD; ulcers; appendicitis; gallstones; and cancer.

Alright, let’s have a look at these disorders in detail, starting with hernias, which is when an organ pushes through an opening in the tissue that holds it in place. 

Normally, abdominal organs are contained and protected within the abdominal cavity, which is lined by different layers of muscles and connective tissue that make up the abdominal wall. 

Most hernias occur when there is a defect in the abdominal wall through which abdominal organs can bulge out. 

There are several types of hernias, which are classified based on their location. There can be inguinal hernias, femoral hernias, umbilical hernias, and hiatal hernias. 

Both inguinal and femoral hernias occur when a loop of intestines protrudes through the abdominal wall near the groin. An umbilical hernia occurs when a loop of intestines protrudes around the umbilicus. 

A hiatal hernia occurs when an abdominal organ, usually the stomach, protrudes through the hiatus, which is an opening in the diaphragm through which the esophagus passes. 

Hiatal hernias allow stomach acids to move back into the esophagus, resulting in heartburn. Inguinal, femoral, and large umbilical hernias are treated surgically. 

Hiatal hernias are treated with medications and therapeutic measures aimed at controlling heartburn, such as eating smaller meals several times a day; waiting a few hours after a meal before lying down; and refraining from smoking and consuming alcohol and coffee. If these measures are unsuccessful, surgery may be indicated.

In some more serious cases, the muscles of the abdominal wall may squeeze around a herniated organ, cutting off its blood supp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_safety:_Body_mechanics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zzof6NCXROGQIYCz9u-szChuQJSpBXYY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace safety: Body mechanics]]></video:title><video:description><![CDATA[As a nursing assistant, your job involves a great deal of physical activity, like carrying and transferring clients and objects, which might cause an injury to your muscles, bones, and joints. 

This is called work-related musculoskeletal disorder, and the injuries may occur gradually over time or may happen all at once without warning.  

Alright, the most commonly injured parts of the body are the back, neck, shoulders, and arms. In fact, back injuries are the most common and most concerning! 

Symptoms include decreased range of motion, limited mobility, and pain when standing up or changing positions. Also, you may feel numbness or tingling in your thighs or legs, which indicates a nerve injury.

Alright, there are several factors that increase your risk of having a musculoskeletal injury, such as sitting or standing in one position for a long time and assuming a poor posture, like bending or squatting frequently. 

Also, your risk of injury increases if you stretch your body to reach far objects above your shoulders, carry objects when you are feeling tired and fatigued or objects that are too heavy, and twist or bend your body when carrying an object. 

Walking on a slippery floor and working in narrow spaces, like hallways and bathrooms, can be risky as well. Now, there are certain client caring activities that can put you at a higher risk for musculoskeletal  injury. 

These include, transferring clients who are totally dependent on others for movement, transferring combative clients, or transferring clients from bed to the chair or vice versa. 

Also, you may get an injury when changing a client’s position on a bed or chair, if you bend while making their bed or when you are bathing or weighing them, or when trying to stop a client from falling down. 

Now, to understand the reason why work-related injuries occur, we can look at the principles of ergonomics. “Ergo” means work and “nomics” means “study of,” so ergonomics means the study of work. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_clients_with_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_gmkj0mARMGX2kmShUNuBXVwQhqnXDWB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for clients with cancer]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Caring for clients with cancer through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Collecting_a_urine_specimen_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_5E6XaMiTyGY9OLrULumjd47RcmTpIUm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Collecting a urine specimen (for nursing assistant training)]]></video:title><video:description><![CDATA[Urinalysis includes physical examination of the urine, testing of urine, and examination of the urine under a microscope. It can be used to diagnose and monitor various conditions, including kidney disorders; urinary tract infections; and systemic diseases, such as diabetes. 

Now, for the routine urinalysis, a random urine specimen is required, which means that urine can be collected any time during the day without any special measures. When the client is suspected to have a UTI, or urinary tract infection, it’s important to do a clean catch specimen. “Clean catch” refers to cleaning the perineum and the skin on the genitalia to clear away any microbes on the skin that could contaminate the urine sample. The sample should be taken  midstream, meaning it should be collected from the middle of the urine flow. This way, the first and last portion of the urine that’s more likely to contain bacteria from skin are not collected. A properly collected clean catch specimen will help make sure any bacteria found in the urine specimen came from inside the urinary tract. 

Now, before we review the details of collecting a urine specimen, here are some common care tips. Based on facility policies, a nursing assistant can collect a urine specimen under the supervision of and at the direction of a licensed nurse who will provide you with instructions. Always confirm the client’s identity to make sure the procedure is performed on the right person. Make sure that the specimen container is labeled with the client’s name and room number, as well as the date and time the specimen was collected. At all times, respect the client’s privacy and modesty by remembering to close the doors and window covers, and ensuring the client is properly covered. 

Okay, now, when collecting a urine specimen, first, gather the supplies you’ll need, including: gloves, paper towels, a specimen container, a collection device, toilet tissue, and a biohazard transport bag. You may also need a beds]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Female_and_male_reproductive_systems:_Sexually_transmitted_infections</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bzohaw-WSCu0MUJoCCr0eXIwSqaPbmub/_.jpg</video:thumbnail_loc><video:title><![CDATA[Female and male reproductive systems: Sexually transmitted infections]]></video:title><video:description><![CDATA[As their name implies, sexually transmitted infections, or STIs, are infections that get transmitted during sexual intercourse or sexual contact. They are also known as sexually transmitted diseases, or STDs. 

Now, common viral pathogens that can cause sexually transmitted infections include herpes simplex virus, or HSV, that causes genital herpes; human papillomavirus, or HPV, that causes genital warts; and human immunodeficiency virus, or HIV, the virus that causes AIDS. 

Common bacterial pathogens include Neisseria Gonorrhoeae, which causes gonorrhea; Chlamydia Trachomatis, which causes chlamydia; and Treponema Pallidum, which causes syphilis. 

These pathogens are typically transmitted from person to person through sexual fluids, such as vaginal secretions or semen. 

But, it’s important to note that besides external genitalia, sexually transmitted infections can also affect other parts of the body, including eyes, mouth, throat, and anus.

First, let’s focus on sexually transmitted viral infections, starting with herpes simplex virus. There are two types of herpes simplex virus: herpes simplex virus type I and herpes simplex virus type II. 

Herpes simplex virus type I is not technically an STI; instead, it typically infects the lips and causes a small painful blister, commonly known as cold sore. 

On the other hand, herpes simplex virus type II usually affects the genital and perianal area and causes small, painful blisters. Because it affects a person’s genital area, this type is also known as genital herpes. 

It’s important to note that there’s no treatment or vaccine for herpes simplex virus; therefore, outbreaks of small, painful blisters may occur again after the initial blisters disappear.

Moving on to human papillomavirus. This sexually transmitted viral infection is associated with numerous genital warts that have a cauliflower-like surface. 

Genital warts are also known as venereal warts, and they tend to be skin-colored. In biological]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sensory_system:_Eye_and_ear_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5AkIZegyRma7_-JxBlu1deYTR2emO6Wn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sensory system: Eye and ear disorders]]></video:title><video:description><![CDATA[Eyes and ears can be affected by many diseases, which can be caused by infections; uncontrolled high blood sugar, like in diabetes; or simply by aging. We’ll be talking about some of the common eye and ear diseases that you may encounter when caring for clients.

Okay, let’s start with eye disorders. First is conjunctivitis, commonly known as the pink eye. It’s an infection of the thin membrane that lines the eyelids and covers the sclera, called the conjunctiva. 

Clients with conjunctivitis will have pink or red eyes, itchiness or a burning sensation in their eyes, and watery or sticky discharge. 

Conjunctivitis is really contagious as microbes can be easily transmitted from someone’s eyes to their hands and then to surfaces, where they’re picked up by another person. The most common treatment is prescribed eye drops or ointments.

Okay, next is glaucoma, which is when the aqueous humor in the anterior chamber of the eye builds up, causing an increase in the pressure inside the eyes. 

This causes compression of blood vessels and nerves, which initially leads to blurred vision and peripheral vision loss as if the client’s looking through a tunnel. 

If not treated, it can lead to complete blindness. Glaucoma is more common in people over the age of 40, and it’s more common in those with a family history of the disease. 

It can be acute, where the client will suddenly have severe eye pain, vision loss, and nausea and vomiting. When it’s chronic, vision loss develops gradually over time. 

There’s no cure for glaucoma, but medicated eye drops can help keep the pressure within the eye normal.

Okay, now the lens and cornea are both transparent, round structures that help to focus light entering the eyes on the retina, which allows us to see a clear image. 

Now, any problem with focusing the light on the retina leads to refractive errors, which include myopia, hyperopia, presbyopia, and astigmatism. 

Myopia occurs when the eyeball is more oval than ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nervous_system:_Dementia_and_delirium</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2h0NmsLhQmCc-V7qd3ZobzgKTryz4QdP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nervous system: Dementia and delirium]]></video:title><video:description><![CDATA[The brain is responsible for various mental functions, including memory, thinking, language, behavior, mood, and personality. A decline in at least one of these functions can be caused by either dementia or delirium.

Okay, first, it’s important to differentiate between these two. Dementia is generally caused by structural changes in the brain, has a gradual onset, lasts months to years, and the symptoms usually progress over time. 

On the other hand, delirium classically occurs as a consequence of another underlying condition, like an infection or medication toxicity; is acute in onset; lasts only a couple of hours to days; and symptoms fluctuate, meaning they come and go. 

Dementia goes through three main stages. In the early stage, the client&amp;#39;s memory starts to become impaired, which may lead to repeating conversations or misplacing belongings. 

At this point, the client typically recognizes their memory lapses, and this can generate feelings of shame, embarrassment, or frustration. 

In the middle stage, the client has trouble identifying common objects or faces and carrying out tasks that involve multiple steps, like grooming or cooking. 

Language can also become affected, and they can have trouble processing verbal or written communication. Sometimes, family members notice a change in the client’s behavior or personality. Many clients may also experience loss of bladder control, which can lead to urinary incontinence. 

In the late stage, clients become dependent for all everyday activities. Mobility decreases, so they are unable to walk or sit up without assistance. 

Ultimately, this can progress to them becoming bed bound. Their ability to swallow food or fluids as well as communicate through language or facial expressions becomes limited or completely lost. 

Total urinary and fecal incontinence can also be expected at this point. These clients are also susceptible to respiratory and urinary tract infections, which may lead to s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Responsibilities_of_the_nursing_assistant</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JleBQ6F0RWCgQb3DRk41lyFNT0OD158Q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Responsibilities of the nursing assistant]]></video:title><video:description><![CDATA[The responsibilities of a nursing assistant can vary depending on the setting and state where they work, but all nursing assistants operate within defined parameters or range of tasks they are legally permitted to perform. 

In Oregon, the nursing assistant has a list of authorized duties that can be found in the Oregon Administrative Rules, Chapter 851, Division 63. 

All the tasks performed by a nursing assistant will focus on helping nurses perform basic nursing skills that help clients  meet their physical and emotional needs. 

Meeting physical needs involves assisting clients with tasks related to hygiene, safety, food and water, comfort, exercise, and elimination.  

Meeting emotional needs will involve connecting to the client, often by simply being willing to listen attentively when they need someone to talk to. 

Finally, one of the most important duties of the nursing assistant is to act as a liaison between a client and the nursing team by observing and reporting to the nurse when they notice any changes in a client’s physical or mental status. 

Now the standards and authorized duties for a nursing assistant is defined by their state and training, so it’s important to become familiar with these and work within your state’s rules. 

For example, nursing assistants are not permitted to supervise other nursing assistants. Only licensed nurses may supervise nursing assistants. Now, you can mentor and coach another nursing assistant.

You can even assist in the orientation of a new nursing assistant to your facility but a licensed nurse will need to validate their competency and sign-off on their overall orientation. 

Additionally, nursing assistants are not permitted to make diagnoses or prescribe medications or treatment, which are responsibilities of the health care provider. 

In order to be a great nursing assistant, you must also possess certain personal characteristics, workplace skills, and physical capabilities.  

You need to be courteou]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_a_client_with_a_cast_or_traction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iQQZ4fSTR8uv8O0krjWM57eJRZK_3McJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for a client with a cast or traction]]></video:title><video:description><![CDATA[As a nursing assistant, you may come across individuals that have musculoskeletal injuries or traumas. To recover, these clients require immobilization and stabilization, which are techniques used to limit the movement of body parts in order to keep them in the proper position to prevent injury and promote healing. This can be achieved with the use of special devices, such as casts and traction. 

Now, the most common musculoskeletal injuries are fractures, which typically occur due to trauma or a fall. 

Now, a fracture is defined as a complete or partial break in the bone, which occurs when the physical force applied to the bone is stronger than the bone itself. 

Additionally, broken bones can damage surrounding structures, including nerves, blood vessels, muscles, and tendons. 

There are many different types of fractures and many different ways of getting them; for example, repetitive activities, such as running or jumping, can lead to small cracks in the bone, also known as stress fractures. 

Pathologic fractures, on the other hand, occur in bones that are weakened by other conditions, such as bone cancers or osteoporosis. 

Closed fractures, sometimes called simple fractures, occur when the bone breaks, but the overlying skin remains intact. 

On the other hand, open fractures, also known as compound fractures, occur when the fractured ends of the broken bone pierces through the overlying skin. 

In greenstick fractures, one side of the bone breaks, while the other side bends; in impacted fractures, a piece of one bone gets wedged into another bone. 

Finally, comminuted fractures  occur when the bone breaks into multiple fragments, while spiral fractures occur when a strong, twisting force is applied to the bone. 

Spiral fractures are commonly seen in non-accidental traumas, such as physical abuse, like when someone forcefully grabs and twists on an arm. 

Now, for a bone to heal properly, fractured ends must be brought back and aligned into thei]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_clients_with_sensory_impairment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UCZPbJX7RUSBiwNtJDSHq6OaQKy-8_hU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for clients with sensory impairment]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Caring for clients with sensory impairment through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Oropharyngeal_suctioning_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w10H7g8zSR6BQfunmQNxl11TQ3_oNFT7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Oropharyngeal suctioning (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Respiratory: Oropharyngeal suctioning (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_healthcare_team</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UOdlGeo8TDmSbWsPAOxc_KwnQnygC2IX/_.jpg</video:thumbnail_loc><video:title><![CDATA[The healthcare team]]></video:title><video:description><![CDATA[As a nursing assistant, you will work as a part of an interdisciplinary healthcare team. A healthcare team is a group of people from various fields who work together to provide holistic client care, meaning caring for their physical and emotional needs. 

Alright, there are several members of the healthcare team and all their roles are important and complementary to one another. Healthcare team members include the physician, or doctor; dietician; pharmacist; physical therapist; laboratory technician; cleric; social worker; occupational therapist; nurse; advanced practice nurse; and nursing assistant.

Let’s start with physicians, who diagnose and treat diseases. The type of diseases physicians treat varies based on their medical speciality. 

For example, cardiologists treat diseases of the heart, such as myocardial infarction, commonly known as a heart attack. Pulmonologists, on the other hand, treat lung diseases, such as lung infections, also known as pneumonia. 

There are also surgical specialties that use surgery to treat people’s conditions, such as cardiac surgery and neurological surgery.

Another member of the healthcare team is the dietician, or the nutritionist, who evaluates the nutritional needs of the clients and teaches them about those needs. 

Next is the pharmacist, who dispenses prescribed drugs for clients and provides consultation on drug selection and possible interactions between drugs. 

Also, there’s the physical therapist whose main job is the rehabilitation of the clients, which means restoring their normal level of function and movement after an illness or an accident. 

A laboratory technician is the one who collects specimens from the clients, such as blood, stool, and urine, and runs various tests and reports their results. 

Now, as a part of holistic care, a cleric supports the spiritual needs of the client. Also, a social worker helps clients in dealing with emotional, social, and any other issues that affect their condit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Female_reproductive_system:_Reproductive_system_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OLaFsAPrSDmOuJFfSN0E1636RaalxfmS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Female reproductive system: Reproductive system disorders]]></video:title><video:description><![CDATA[The female reproductive system consists of internal sex organs, which include the ovaries, the fallopian tubes, the uterus, and the vagina; and external sex organs, such as the mons pubis, the labia, and the clitoris. Now, the most common disorders of the female reproductive system typically affect the internal sex organs, and they include infertility, menstrual disorders, pelvic organ prolapse, and benign and malignant growths. 

Let’s start with infertility, which is defined as the inability to become pregnant after 12 months of trying. Fertility problems can affect both partners. As a biological female gets older, the likelihood of infertility increases until pregnancy is no longer possible after menopause. Some other common causes of female infertility include hormonal imbalance, ovulation problems, structural abnormalities of the reproductive system and scar tissue from prior surgeries, or infections in the female reproductive tract.

Now, let’s switch our focus to menstrual disorders. Amenorrhea is the absence of menstrual bleeding, and it can be classified as primary or secondary amenorrhea. Primary amenorrhea is defined as the absence of the first menstrual bleeding by the age of 16, and it can be caused by abnormal development of reproductive organs, hormone imbalances, and malnutrition. On the other hand, secondary amenorrhea refers to the absence of menstrual bleeding in individuals who previously had regular menstrual cycles. Moreover, secondary amenorrhea is one of the first signs of pregnancy, but it can also be caused by endocrine disorders or tumors. 

Next up is menorrhagia, which is defined as heavy or prolonged menstrual bleeding. Common causes of menorrhagia include infections, uterine disorders, or hormonal disturbances. Excessive and chronic loss of blood can even lead to anemia. The last one is dysmenorrhea, or extremely painful menstrual bleeding. Dysmenorrhea can be caused by strong uterine contractions, often called menstrual cram]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Communication_with_friends_and_family_of_clients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oPUDtGJFTkGh-Iz3BARG7OVlRBqU4bLn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Communication with friends and family of clients]]></video:title><video:description><![CDATA[Your client&amp;#39;s friends and family can provide support and comfort and help maintain your client&amp;#39;s quality of life. As a nursing assistant, you play an important role in ensuring visits from friends and family are as pleasant as possible.

There are a few things to keep in mind when communicating with your client’s friends and families. First, always treat them with courtesy and respect. 

You must always take into account the family and friends of your client and the impact that an illness, injury, or disability can have on them. 

For example, if family members have always been actively involved in the client’s care, it might be difficult for them to give up the role of caregiver, and they can feel that you don’t provide the care as well as they did. 

Other families might feel guilty when admitting a loved one in a long-term care facility. Other times, families can feel helpless and even second-guess the care you’re providing. 

In all cases, it’s important that you also consider the stress they feel and to not take anything personally. Also, try not to interrupt your client’s visit from friends and family. 

Check on them occasionally, and when you need to provide care, ask them to leave the room and let them know as soon as they’re able to return. 

During a visit, be sure to check to see if you observe your client getting tired; when this happens, politely ask the visitors to come back later, so the client can rest. 

Keep in mind that families are diverse in regards to their relationships and cultural or religious customs. Some family members may want to actively participate in care, such as by bringing home-cooked food or staying with the client overnight. 

Do your best to accommodate them according to the client’s plan of care and facility policies. One of your duties as a nursing assistant is communicating with your client’s family and friends and updating them on the client’s status and care. 

This can help reassure them and he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nervous_system:_Brain_and_spinal_cord_injuries</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WCCArWCLTNiMWdk9xIBQT_tMThWCombR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nervous system: Brain and spinal cord injuries]]></video:title><video:description><![CDATA[Damage to the head or spine that causes the brain or spinal cord to stop working properly is called a brain or spinal cord injury, respectively. 

In most cases, these are traumatic, meaning that they result from an external, physical force, like a fall, a car crash, or a gunshot wound. 

They can also be non-traumatic, which is the case when the brain or spinal cord are not receiving enough oxygen, such as when breathing or heart problems prevent enough oxygen from reaching the brain or spinal column or when blood vessels supplying the brain or spinal cord are compressed by something like a tumor. 

Now, the symptoms of a brain or spinal cord injury can show up at the time of the injury or even hours to days later. In general, these vary depending on the region damaged and the severity  of the injury. 

Starting with brain injuries, symptoms may include confusion, headaches, nausea, vomiting, weakness, numbness, and vision or auditory problems. 

More serious cases can even result in death. Clients can also experience life-long effects, and these may involve the motor function, causing muscle weakness or paralysis; various mental functions, causing thinking, memory, language, behavior, or emotional problems; or the level of consciousness, resulting in a coma. 

This is a state like deep sleep but without a sleep-wake cycle. There’s a profoundly decreased alertness or responsiveness to their environment, like sound or touch. 

Duration of a coma may vary from weeks to months, or rarely, go on for several years. After that time, the client might gradually come out of a coma or progress to a persistent vegetative state. 

In this case, there’s a sleep-wake cycle, but the client still remains unaware and unresponsive to their surroundings and is unable to speak or follow commands.

They might show signs of movement, like opening the eyes or grimacing; however, these are only involuntary actions that are not a response to the environment.

Now, in a spinal cor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_safety:_Emergency_codes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sQg4KhVqQi_N1_PDCBV3aLYoTGaK9X1G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace safety: Emergency codes]]></video:title><video:description><![CDATA[Emergency codes in a healthcare setting are messages intended to alert the staff in a quick and precise manner. 

They are announced over the facility&amp;#39;s public communication systems along with the location of the emergency, which helps to get the message across to all intended personnel. 

At the same time, it helps avoid causing panic to clients and visitors. It&amp;#39;s a code, right? Codes may vary from facility to facility, so as a nursing assistant, you need to be familiar with your facility’s codes, what they mean, and how you should respond. 

The first common code in the healthcare settings is code blue. A code blue is announced when there is an adult client with a medical emergency, usually a cardiopulmonary arrest, who needs an immediate cardiopulmonary resuscitation, or CPR. 

If a pediatric client has a medical emergency, some facilities call a code white. During the code blue or code white situation, your role as a nursing assistant will be assisting physicians, nurses, respiratory therapists, and family members as needed. 

Okay, let’s move on to code red. This is announced when there is fire or smoke somewhere in the building. 

If you’re the one at the scene, notify your supervisor and follow the RACE fire response plan, which involves Removing clients in immediate danger to safety, Activating the alarm, Containing the fire by closing the door and windows, using the fire extinguishers to Extinguish the fire if it’s possible, and Evacuating the building if everything else fails.

Next is code yellow, which is called in the event of a bomb threat. Your facility will outline what you and other healthcare workers should do if a threat is received. 

Above all, it’s important to remain calm and follow instructions to keep you, your co-workers, and your clients safe.

Healthcare facilities often use hazardous materials in client care, such as chemotherapy agents. A code orange is called if there is a spill or release of any substance t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular_system:_Heart_diseases</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l3JAZyfITkWpPDqG3iIdHp0aTpqGaYB9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular system: Heart diseases]]></video:title><video:description><![CDATA[Heart diseases can affect both children and adults. In children, they’re usually congenital, or present from birth, and they can result from abnormal development of the heart during pregnancy. 

In adults, heart diseases are acquired, which means that they develop later in life, and they’re often caused by the person’s lifestyle choices. 

Okay, let’s start with congenital heart diseases, which can affect the atria, the ventricles, the heart valves, and vessels. They can cause blood flow to slow down, stop completely, or change direction. 

There’s no clear cause that’s been identified, but there are a number of risk factors that seem to be associated with congenital heart disease. 

The most well-known factors include a family history of a congenital heart disease, certain viral infections of the mother during pregnancy, maternal diabetes, and exposure to medications and illicit drugs. 

Children with congenital heart diseases could be asymptomatic or present with difficulty breathing; cyanosis, which is when the skin turns blue due to decreased oxygen in the blood; poor feeding; and failure to thrive, which means that the child is not growing as fast as they should. 

Diagnosis is usually made during pregnancy or soon after birth. However, some cases are diagnosed when the child is older. 

Treatment usually requires medications or surgery to correct the defect, and afterwards, children can often grow up to live a normal life without complications. 

Okay, now, let’s switch our focus to acquired heart diseases that are more common in adults. The most common are coronary artery disease; heart failure; and arrhythmia, which is abnormal heart rhythm. 

Risk factors for an acquired heart disease can be divided into non-modifiable, meaning they can’t be changed, and modifiable, which means they can be. 

Non-modifiable risk factors include age, with biological males greater than 45 years and biological females greater than 55 years being more at risk; sex, wi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_system:_Lung_conditions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QRSSbSqkSrSuBFQVlmu3iywlTgipC6UF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory system: Lung conditions]]></video:title><video:description><![CDATA[There are a variety of conditions that can disrupt respiratory function. As a nursing assistant, you will be caring for clients with lung conditions, such as cystic fibrosis, asthma, chronic obstructive pulmonary disease, and cancer.

We’ll begin with cystic fibrosis, which is a chronic disease caused by a genetic defect. The disease causes excessive mucus production by the cells in the mucous membranes lining many of the organ systems in the body, including the respiratory system. 

Normally, the mucus in our respiratory system is thin and watery, and it protects our respiratory tract from microbes, like bacteria and viruses and foreign particles, like dust or dirt, while keeping the respiratory tract warm and moist so that we can breathe comfortably. 

In cystic fibrosis, though, the mucus is thick, sticky, and present in excess. So, it can build up and stick to the walls of the airway, restricting airflow and irritating and inflaming the respiratory tract. 

This causes a client to have difficulty breathing; wheezing; and a productive cough, which means they cough up mucus. 

The thick, sticky mucus is also a great home for microbes, which can often remain in the respiratory tract, making clients with cystic fibrosis more susceptible to infections. 

While there is no cure for cystic fibrosis, treatment is centered around maintaining healthy lung function and preventing complications. 

This is generally accomplished through proper hydration to thin mucus secretions, chest physiotherapy to clear the airway, exercise to keep the respiratory muscles strong, medications to open up the airway and fight off infections, and sometimes lung transplants for clients that don’t respond to these therapies.  

Okay. Next up is asthma. Asthma is a chronic lung condition characterized by reversible episodes of inflammation and constriction, or narrowing, of the bronchi and bronchioles in response to certain triggers, like allergies, exertional activity, cold air, smok]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Pulse_oximetry_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XWdZREQpRaii3yVyC3_KO7NsSsKh5oYV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Pulse oximetry (for nursing assistant training)]]></video:title><video:description><![CDATA[As a nursing assistant, you will help provide safe care to clients who have or are at risk for hypoxia, which is when there is not enough oxygen to meet the needs of the body.

These clients require pulse oximetry, which is a non-invasive, easy, and pain-free method of measuring the amount of oxygen carried by the hemoglobin in the red blood cells.

This is known as arterial blood oxygen saturation, or SaO2 for short. Maintaining a normal SaO2 ensures that the amount of oxygen that travels through the bloodstream to tissues around the body is adequate.

Now, a pulse oximeter consists of a probe, which is attached by a cable to a pulse oximeter. That probe has a light source on one side and a photodetector, or sensor, on the other side.

So, when it gets clipped onto a body part, a light shines through the tissues on one side, and on the other side, the sensor detects how much light has been absorbed by the arterial blood in the tissues.

The principle is that, when hemoglobin is bound to oxygen, it absorbs more light than when it’s not. Now, there are several types of probes, depending on the site they can be placed.

The most commonly and easily used ones are digit probes, which can fit onto a finger or a toe. There are also earlobe probes, which attach to the client&amp;#39;s ear.

Less commonly, if the digits or earlobes are inaccessible, a pulse oximetry probe can be applied across the forehead and secured with a headband.

Both earlobe and forehead probes tend to be more accurate than digit probes in cases when blood flow to the extremities is compromised or if the client moves their hands or feet frequently, creating motion artifacts.

There are also sensor pads that can be used on several different sites, including an adult&amp;#39;s earlobe or nose bridge and a newborn&amp;#39;s palms or soles.

Now, all these probes can be either disposable, which are preferred when multiple clients need to be checked using the same oximeter, or reusable when u]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_safety:_OSHA</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Bei-QhHvRtufvBjywH-mOc27TnGsoxgT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace safety: OSHA]]></video:title><video:description><![CDATA[The Occupational Safety and Health Administration, or OSHA, is a government agency that is responsible for protecting the health and safety of workers across all sectors. OSHA enforces standards and provides education and training necessary to ensure safe working conditions.

In healthcare, OSHA establishes detailed standards and directives, which are aimed at protecting all healthcare professionals, including nursing assistants, from various health hazards, such as infectious diseases. 

For example, OSHA established bloodborne and respiratory pathogens standards, which require employers to provide Hepatitis B vaccination to their workers; set standards for procedures, such as use of puncture-resistant containers for disposal of sharps; and require employers to provide personal protective equipment, including gloves, gowns, masks, and face shields. 

OSHA also enforces standards for safe client handling and to protect healthcare providers from work-related injuries, which can occur when lifting, moving, and repositioning clients; assuming awkward postures, like leaning over the bed for a long time; or performing some repetitive tasks. 

The most common injuries related to handling clients include sprains and strains, which commonly affect the lower back and the shoulder. 

To address this problem, OSHA recommends that the healthcare staff receive training on safe strategies to handle clients. It also encourages the use of assistive devices when moving clients, such as  mechanical lifts and wheel chairs. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Musculoskeletal_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ag0p7lwWTmWJpZXHlqtX6sYnSZWdxnpF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Musculoskeletal system: Structure and function]]></video:title><video:description><![CDATA[Musculoskeletal system is involved in almost every aspect of our lives as it shapes our bodies and makes all the movements possible, like getting up, walking, and playing sports. 

It consists of many different bones and other structures that, together, provide a solid framework for the body, called the skeleton. 

Bones get their strength from storing calcium and phosphate, but they can also release them into the body for other organs to use. By working together, bones and muscles form the joints that are responsible for the movement of the body. 

Now, when we look at the skeleton, we can see that there are several types of bones: four to be precise. In the arms and legs, there are long bones that bear the load of the body and enable extremity movement. 

In the wrists, hands, ankles, and feet, there are short bones that enable more delicate and skillful movement. Then, looking at pelvis, shoulder blades, cranium and rib cage, we can see that they contain flat bones that mainly protect vital organs, like the brain, lungs and heart. 

Inside these flat bones, there is a red bone marrow, which produces blood cells, like red and white blood cells and platelets. 

Finally, bones of the face and the spine are irregular bones of various shapes that enable flexibility and a variety of movement.

Okay, so the place where two or more bones come together is called the joint. Joints provide range of motion, from the fixed joints of the skull that do not move at all to the shoulder joint that provides a variety of motion. 

In order for the joints to function properly, the ends of the bones are covered with the connective tissue called the cartilage that prevents the bones from rubbing against each other and acts as a shock absorber. 

A connective tissue wraps around the joint like a capsule and forms a joint cavity. The inner side of this cavity is covered with a synovial membrane that produces synovial fluid: a substance that lubricates the joint surfaces to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_clients_with_rehabilitation_needs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EXTf2CVMQbyvzr9BqJVUlNlYS2mXqGte/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for clients with rehabilitation needs]]></video:title><video:description><![CDATA[As a nursing assistant, you will care for clients that have some form of physical or mental condition that may interfere with their everyday activities. For example, they may have a stroke or other injuries to the brain or spinal cord, heart attack, amputation, or substance abuse. 

These individuals require rehabilitation, which is a process that helps a client return to their highest possible level of physical, psychological, emotional, and economic function. 

Together, physical therapists, occupational therapists, speech therapists, nursing teams, doctors, psychologists, social workers, dieticians, and clients and their families form the rehabilitation team. 

Rehabilitation care is provided by physical, occupational, and speech therapists, and you should not confuse rehabilitation with restorative care, which is provided by the nursing team. 

Restorative care includes actions and procedures that support rehabilitation care, and the goal is to maintain the skills learned in rehabilitation. 

Now, there are three main phases of the rehabilitation process, and they include the acute, subacute, and chronic phase. 

The acute phase refers to the first 24 hours after an injury or surgery and includes techniques and procedures that keep the person alive, such as life-supporting measures, constant monitoring, and prevention of early complications. The next phase is the subacute phase, which typically lasts 7 days. 

The goal of this phase is the stabilization of the client’s condition and prevention of immobility complications, such as blood clots, which are clumps of blood that can stop blood flowing through a blood vessel; pneumonia, which is an inflammation of the lungs; pressure ulcers, which are caused by breakdown of the skin and the underlying tissue when resting in the same position for too long; and contractures: a condition where muscles and tendons become permanently shortened and rigid. 

Other aspects of this phase include proper nutrition, prop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocrine_system:_Hormone_insufficiency_and_excess</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T0fomhTXSsCylLhTbyqRrKp4TKCFO7nD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocrine system: Hormone insufficiency and excess]]></video:title><video:description><![CDATA[The endocrine system works best when a moderate amount of each hormone is secreted in order to maintain homeostasis, or balance in the body. 

But if too little of a particular hormone is secreted, that causes a hormone insufficiency in the body. Conversely, if too much of a particular hormone is secreted, that causes a hormone excess in the body. Both hormone insufficiency and excess can cause disease. 

A few relatively common causes of hormone deficiency and excess are related to growth hormone, or GH; thyroid hormones; parathyroid hormone, or PTH; and glucocorticoid hormones, especially cortisol.

So let’s look at them one by one, starting with GH. GH normally acts on various tissues in the body, making them, well, grow! 

It’s also very important during childhood and adolescence, which are accelerated growth periods, and it plays a less important role in adults. So, growth hormone deficiency and excess present differently depending on the client’s age. 

In children, growth hormone deficiency leads to short stature, but the person is overall well-proportioned; whereas growth hormone excess causes gigantism, which is when the child is taller than average, but still well-proportioned. 

In adults, on the other hand, growth hormone deficiency doesn’t cause a clinical condition, because adults are, well, pretty much done growing. 

Growth hormone excess in adults, though, causes acromegaly. Individuals with acromegaly are not well-proportioned because the bones in the face, hands, and feet grow too much, causing a characteristic appearance.

Next up, thyroid hormone excess and deficiency are quite common, and these are usually because of a disorder of the thyroid gland. 

Iodine is used to synthesize thyroid hormone, and it can be found in fish, dairy, and also in iodized salt. It can also cause thyroid hormone imbalances if too much or too little is consumed. 

Thyroid hormone excess is called hyperthyroidism, and it’s often caused by Graves disease, whi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stages_of_grief</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BSSwiIyrRf6aXpaxQq3c0VzPSmWbBCLT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stages of grief]]></video:title><video:description><![CDATA[Grief is a normal response to physical or emotional loss, and it’s defined as a state of mental anguish. In a medical setting, grief can be encountered as a response to the loss of a loved one; when a terminally ill client comes to know that their own life may end; or when a client receives a diagnosis of a chronic disease, such as heart failure. 

There are five stages of grief, also called the five stages of dying. These are denial, anger, bargaining, depression, and acceptance.

So let’s imagine a scenario and walk through these stages one by one. Suppose you are caring for a client with final stage lung cancer, and they have been through surgery and several rounds of chemotherapy to manage the disease. 

However, their last computed tomography, or CT, scan shows the cancer has spread so much that there are no more medical or surgical options to prolong their life. 

So, the only recommendation is palliative care, which is when measures are taken to make the patient as comfortable as possible until they die. 

Death may occur within the next couple of weeks, months, or a year; however, it suddenly becomes a near-future certainty. 

When told the news, a grieving client can first react with denial. So, they may reject the news altogether or think that the doctors have made a mistake. 

In this stage, the most important thing is to remain neutral but understanding and compassionate. Refrain from trying to convince the person about the reality of their situation or illness. 

So, if the client says, “These can’t be my scans! I was supposed to get better after chemotherapy! This is a mistake!” You can respond along the lines of, “I am sorry. I understand the news must come as a shock. 

I know this is not an easy time for you.” Denial can last anywhere from a couple of minutes, to a few days or hours, and in some cases, the person never moves past this stage. 

If they do progress past denial, they enter the second stage of grief, which is anger. Anger resu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocrine_system:_Diabetes_mellitus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TZ_iVAPKR6a1dsvNC396oB6dSnKYtVBq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocrine system: Diabetes mellitus]]></video:title><video:description><![CDATA[In diabetes mellitus, the body has trouble moving glucose from your blood into the cells, so blood sugar levels are constantly high. This is called hyperglycemia. 

A hormone made by the pancreas, called insulin, stimulates the movement of glucose into the cells after meals. 

So, in type 1 diabetes, the blood glucose stays high because of an autoimmune destruction of the pancreas, which leads to low insulin levels. 

In type 2 diabetes, on the other hand, the body makes insulin, but the cells are insulin resistant, meaning they don’t “respond” to insulin by taking glucose in. 

In time, constantly high blood sugar levels can cause long-term complications, like cardiovascular disease, kidney problems, neurological disease, eye conditions, slower healing, and increased risk of infections. 

Lack of insulin or cells’ inability to use it translates in classical symptoms of diabetes, like polyuria, which means that individuals pee a lot; polydipsia, which means they drink a lot of water; sometimes polyphagia, which is a fancy way to say they eat a lot; and unexplained weight loss. 

Both type 1  and type 2 diabetes get these symptoms. However, with type  1, the onset is usually abrupt and usually affects people under 30. 

With type 2, the symptoms gradually worsen over a few months, and individuals usually have risk factors, like being over 45 years old or having a first degree relative with type 2 diabetes mellitus; a body mass index, or BMI over 25; a sedentary lifestyle; or cardiovascular disease, like hypertension. 

People with risk factors for type 2 diabetes can develop something called “prediabetes.” That’s when their blood sugar levels are higher than normal but not high enough to meet the criteria for diabetes. 

The good news is that lifestyle changes, like exercising, adopting a healthy diet, and losing weight, can delay or even prevent type 2 diabetes altogether! 

There are three key focuses for the management when caring for people with type 2 ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_safety:_Disaster_preparation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EELR4i3pTP_iQX4AwTLPqA7RRACVokWZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace safety: Disaster preparation]]></video:title><video:description><![CDATA[A disaster is a sudden tragic event that could result in huge losses in terms of property damage, injuries, and deaths. Disasters can be categorized as either natural, such as earthquakes, hurricanes, and floods, or man-made, such as hazardous chemical spills, terrorist attacks, wars, and plane or train crashes. In both cases, healthcare facilities should always be prepared to provide care to the victims.

Now, a disaster can occur at any time, creating an overwhelming situation for healthcare facilities. This is why each healthcare facility must have a disaster plan in place, and it should be adapted to its internal organization and resources. 

For example, a disaster plan of a hospital may focus on admission and treatment of a large number of multiple-injured people, while a disaster plan of a nursing home may focus on ensuring safety and providing care to its clients during a hurricane. 

Alright, there are essential elements that should be included in every disaster plan and can be summarised with the acronym D-I-S-A-S-T-E-R. 

First, it should include Detection, which involves determining if there is a disaster in the area and the possible causes. 

Sometimes, an undetected disaster, like contamination of the water supply, will first be noticed by healthcare workers who recognize an increased number of individuals coming in with similar unexplained symptoms. 

After detection, an Incident command system should be established to help coordinate different facilities, personnel, and equipment to respond to the disaster in an orderly fashion. 

The next step is about ensuring the Safety and Security of the staff. Staff members need to protect themselves by wearing adequate personal protective equipment, or PPEs, especially during exposure to hazardous chemicals and infectious biological agents. 

This prevents increasing the number of victims and the loss of staff who need to provide care to injured people. Another important element in a disaster plan is]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Types_of_personal_protective_equipment_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZEUpYyoaRfmgEedtMM4oxf3PSQ6J7nuh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Types of personal protective equipment (for nursing assistant training)]]></video:title><video:description><![CDATA[When assisting with client care, personal protective equipment, or PPE for short, should be used to avoid transmission of infection to and from the client.

This includes wearing non-sterile gloves, a gown, a mask, goggles, or a face shield as needed. The PPE needed depends on the type of the procedure, the client, and the risk for exposure to body fluids. Okay, let’s take a closer look at the components of PPE, starting with non-sterile gloves.

These should be used every time there is a risk for exposure to blood, all types of body fluids, secretions, and excretions, as well as open skin lesions or rashes; mucosal surfaces, such as when providing perineal care; and possibly contaminated items, such as soiled clothing and linens or contaminated surfaces.

Now, when wearing non-sterile gloves, there are some general considerations for you to follow. First of all, the gloves must be intact without any holes, so make sure you don’t tear them when putting them on.

Long and rough fingernails or rings can also tear the gloves. Also, be sure that they fit properly, meaning that they’re not too loose or too tight, and cover your wrists.

In case you or the client is sensitive to latex, use gloves that are from a different material, such as vinyl. It is also important to use a different pair of gloves for every client and for every procedure.

Also, when caring for a client, change gloves when moving from a contaminated site of their body, such as the perineum, to a site that’s cleaner.

Also, remove contaminated gloves when you need to touch a commonly used item or surface, such as a light switch, door handle, or faucet.

Always consider the outside of the gloves as contaminated and the inside as clean. Now, when removing the gloves, turn the inside out and dispose of them safely.

Afterwards, don’t forget to wash your hands before putting on gloves and after removing them. Moving onto waterproof gowns. These usually open at the back and will cover you from the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U3WvJSM-TM2GlvwinfQTd3G2RCa-a_UP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal system: Structure and function]]></video:title><video:description><![CDATA[The primary functions of the gastrointestinal system are digestion, which is breaking down food that we eat into nutrients; absorption, which is getting those nutrients into the bloodstream; and excretion, which is getting rid of digestive waste as feces. 

The gastrointestinal system is made of hollow, connected organs that make up a canal, called the gastrointestinal tract, as well as a couple of accessory organs that are not part of the canal but play an important role in the food digestion process.

Alright, from top to bottom, the gastrointestinal tract starts with the mouth, then the esophagus, the stomach, the small intestine, the large intestine, and ends with the anus.

Digestion starts after food ingestion, which is putting food into the mouth. The first step is mastication, which is chewing on food to physically break it into small chunks. 

This process is also referred to as mechanical digestion. During mastication, the tongue mixes food with saliva secreted from salivary glands. 

Saliva contains some chemical substances, called enzymes, which start breaking down chemical bonds between food molecules. 

This process is called chemical digestion, and it continues at different levels of the gastrointestinal tract as food moves along. 

As mastication goes on, we get a food-saliva mixture, called a bolus, which is ready to be swallowed. Swallowing takes place through a muscular tube, called the esophagus. 

To move this food bolus along, muscles of the esophagus contract and produce a wave-like movement that pushes food downward into the stomach. This movement is called peristalsis, and it also continues throughout the GI tract. 

When the food arrives in the stomach, it mixes with gastric juice consisting of acid and gastric enzymes, which turns the food bolus into a pulpy soup, called chyme, made of much smaller food particles. 

Next, chyme moves to the first part of the small intestines, called the duodenum, where bile secreted by the liver ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular_system:_Blood,_venous,_and_arterial_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nJCd9UaGTvO8EwggifXtlmunR-a4ZvoG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular system: Blood, venous, and arterial disorders]]></video:title><video:description><![CDATA[Cardiovascular disorders are disorders of the blood, the blood vessels, and the heart, affecting the body’s ability to carry oxygen and nutrients from the heart to the tissues and remove waste products, such as carbon dioxide from the tissues. Some of these disorders are anemia, venous disorders, and atherosclerosis. 

Anemia is a disorder of the red blood cells, or RBCs, that decrease their ability to carry oxygen. This usually develops when there’s low iron or deficiency of certain B vitamins, which leads to decreased production of RBCs. 

Anemia also occurs when the person is losing blood due to a disorder, such as ulcers and cancers of the gastrointestinal system. 

A biological female can also develop anemia due to heavy menstruations. Other causes include decreased production of RBCs from the bone marrow, inherited disorders that cause abnormal shapes in some RBCs, and hemolytic disorders that cause excessive destruction of RBCs. 

Clients with anemia will become tired easily and can have difficulty breathing, and their skin and mucous membrane becomes more pale.   

Okay, moving onto venous disorders. Normally, the veins move the blood towards the heart and they have one-way valves to prevent backflow. 

In venous disorders, veins lose their elasticity and the valves are not working properly, allowing blood to leak backward and pool in the lower legs. 

This makes individuals prone to varicose veins, which is when the veins in the lower legs become enlarged from this additional blood, and they start becoming tortuous, or twisted. 

Although there are probably a lot of factors that play into the development of varicose veins in the legs, biological females tend to be more at risk than biological males; people that stand or cross their knees for long periods of time and those who are obese are also at greater risk. Clients with varicose veins often complain of pain in the legs, swelling, and a sensation of heavy legs. 

Now, varicose veins can progres]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Chest_physiotherapy_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U8PAqdDYRFKkppuoZUtw3X7eSaW2JGCl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Chest physiotherapy (for nursing assistant training)]]></video:title><video:description><![CDATA[Chest physiotherapy, or simply CPT, is a technique that can be performed by certain healthcare workers for people suffering from diseases that impair mucus clearance, such as chronic obstructive pulmonary disease, bronchitis, and cystic fibrosis. The goal of CPT is to help the client clear excessive mucus secretions from the lungs in order to prevent complications, like mucus plugs, infections, and atelectasis. 

Before performing this procedure, be sure this is within your scope of practice and is allowed by your facility&amp;#39;s policy. To start, first gather the supplies you’ll need, including gloves, face shield, and gown for you and pillows for the client’s comfort. In addition, keep suction machine equipment available to assist in clearing airway secretions in case the client’s ability to cough and clear their airway is ineffective. Make sure you know if the client is feeling weak, anxious, or in pain. CPT must be scheduled according to the client’s needs and daily routine and activities. Individuals in pain can take analgesics 20 minutes before beginning CPT. Each CPT session usually lasts between 20 and 40 minutes which can be very exhausting, so try to schedule it between rest periods. Avoid performing CPT around 1 to 2 hours before and after meals. The best times to perform CPT are in the morning to clear secretions that may have accumulated over night as well as at night to clear the lungs before bedtime. Frequency of CPT varies for each client from just once daily to as frequent as every 2 hours. This will depend on each client’s needs and capabilities as well as the healthcare professional orders, so make sure to check the nurse charts.

Now, CPT includes postural drainage, percussion, vibration, and shaking. It involves a lot of touching, so before you begin, make sure you always explain to the client where and how you’ll be touching. Postural drainage involves placing the individual in different positions for 10 to 15 minutes, using ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_system:_Urinary_incontinence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mByWQ_Z4TIewd2bNlsdGR0FjTRe7aWMG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary system: Urinary incontinence]]></video:title><video:description><![CDATA[Urinary incontinence happens when an individual involuntarily passes urine. There are two types of urinary incontinence: temporary or persistent. 

Temporary incontinence is reversible once the cause is resolved. It can be caused by a number of things, including a bladder infection or after removing an indwelling catheter that’s been placed for a long time. 

Persistent incontinence is irreversible. It can be caused by a number of things, such as decreased muscle tone in the muscles of the bladder or the muscles supporting the bladder. 

This can occur after childbirth or from obesity. Other causes include injuries or conditions that affect the spinal cord, the brain, or the nerves that control the bladder or even dementia. 

Urinary incontinence can be challenging to live with because it can be very embarrassing. Moreover, having urinary incontinence can put an individual at risk for having skin problems, such as rashes and pressure ulcers. 

It also puts a person at risk for falling because of rushing to the bathroom to avoid involuntarily losing urine. For the caregiver, the incontinent individual might have specific needs, like needing clothing and bedding changed frequently. 

There are many types of urinary incontinence, such as stress incontinence, urge incontinence, functional incontinence, overflow incontinence, and reflex incontinence. In this video, we’ll be covering stress incontinence, urge incontinence, and overflow incontinence. 

Let’s take them one by one. Stress incontinence is the most common type of urinary incontinence. With stress incontinence, urine is lost whenever the abdominal pressure is increased. 

This can happen when coughing, sneezing, laughing, or during physical exercise. Stress incontinence can also happen if an individual delays going to the bathroom, and the bladder becomes too full. 

Factors that contribute to stress incontinence include childbirth, obesity, or loss of muscle tone as a result of aging. It can also hap]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nervous_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mFy_K3n3T4a5PKX5xkJEUcryTh6lFCqw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nervous system: Structure and function]]></video:title><video:description><![CDATA[The nervous system is involved in nearly everything we do from how we see, to how we walk and talk. Now, the main cells of the nervous system are called neurons. 

These make up the brain, the spinal cord, and the peripheral nerves that reach the rest of the body. The nervous system is responsible for detecting and reacting to changes happening both in and outside of the body. 

To do that, it gathers sensory signals from the internal and external environment, which are then analyzed. Then, motor signals are sent, which results in an action in response to the change. 

So, for example, if you sense pain from touching a hot stove, you jerk your hand away; if you sense your stomach is full, your digestive system starts working harder; if you sense your blood pressure is low, your heart pumps faster.  

Okay, let’s start by looking at the neurons that make up the nervous system. These are composed of a cell body, which contains all the cell’s organelles, and nerve fibers that extend out from the cell body. 

These fibers are either dendrites that receive signals from other neurons or axons that send signals along to other neurons. 

The space between where two neurons come together is called a synapse, and that’s where the axon of one neuron releases chemical messengers called neurotransmitters. 

These will travel through the synapse and reach the dendrite of the next neuron, causing it to send a signal down its axon. This is how a signal can pass from neuron to neuron. 

Now, the nervous system is divided into the central nervous system, including the brain and spinal cord, and the peripheral nervous system, which are the nerves that connect the central nervous system to muscles and other organs in the rest of the body. 

The peripheral nervous system is divided into the somatic nervous system, which controls the voluntary movement of our skeletal muscles and the autonomic nervous system, which is further divided into the sympathetic and parasympatheti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_infection_control</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W-Y77aF0T161WoRVcKhc8UVuSLaKiyYa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to infection control]]></video:title><video:description><![CDATA[Infection control refers to practices that are designed to prevent the spread of infectious diseases in healthcare settings. Infections are caused by different types of tiny and simple pathogenic organisms, meaning organisms that cause diseases. 

As a nursing assistant, it’s important to recognize the common pathogens and how to prevent infection in yourself and your clients. Now let’s look at the pathogens that can cause infections. 

First, we have viruses such as human immunodeficiency virus, or HIV, hepatitis B, and C viruses, and coronavirus. These are the most simple infectious pathogens and are usually made of their genetic material, proteins, and sometimes an envelope. 

Next, we have bacteria, which are more complex. Some examples of these pathogens include Streptococcus pyogenes, which can cause strep throat; Escherichia coli, which is a common cause of urinary tract infections; and Mycobacterium tuberculosis, which is a pathogen that causes tuberculosis. 

Next, we have fungi, which are plant-like organisms. A common one is Candida albicans, which is a normal part of the human flora. However, in certain conditions, it can cause yeast infections in the vagina, mouth, or skin. 

Finally, we have parasites, which can be subdivided into helminths, such as pinworm, which causes intestinal pinworm infection; protozoa, like Toxoplasma gondii, which causes toxoplasmosis that can affect the brain; and insects, such as Sarcoptes scabiei, which is a pathogen that causes scabies on the skin.

In order to cause diseases, pathogens first must invade a person’s body, which is a process known as infection. To do this, they also have to evade a person’s immune system, which is subdivided into non-specific and specific immunity. 

Non-specific immunity includes physical barriers, such as intact skin and mucous membranes, and immune cells that can destroy pathogens, such as white blood cells. 

On the other hand, specific immunity refers to the defense mechanisms]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_and_development</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0LRipdrLRbGnvEYJlBPIqDHSQL__mtu-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development]]></video:title><video:description><![CDATA[Growth involves physical changes in height and weight and appearance of the body, while development refers to a change in functional ability, such as cognitive, motor, and psychological aspects of the individual. 

Okay, growth and development start from the time of conception and progress until a person dies. The progress happens in several stages, and each one of them has its characteristics and particular milestones that must be completed before moving to the next one. 

Milestones of earlier stages are simpler compared to those of the later stages. For example, crawling is achieved before walking because it requires less coordination and effort. 

This growth and development happens in a cephalocaudal fashion, meaning it starts at the head and moves downwards. An example would be an infant first learns to hold their head up before learning to sit. 

Another pattern is proximodistal meaning from the center of the body outwards. An example is that control of the arms develops before control of the fingers. 

It’s also important to note that growth and development occur at different rates in different individuals, which is why you will find people reaching the same milestones at different times. For example, one child may walk at 8 months and speak, while a sibling didn’t walk until the age of 14 months.

Now, let’s have a look at the major stages of growth and development that humans go through during their lifespan. The stage that goes from birth to 1 year of age is called infancy. 

Infancy is a very fast stage in which a person grows up quickly and accomplishes new milestones on a monthly basis. Generally, by the first year of age, the newborn has tripled their birth weight, started eating solid foods, and started to walk. 

Social skills also develop remarkably during the first year. An infant learns to smile, recognize parents and siblings, and say simple words. The next stage goes from year 1 to year 3 of age and is called toddlerhood. 

Children i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal:_Administering_an_enema_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bQGEpPmbSh_gmYPMQC48klbpQtuNCjv6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal: Administering an enema (for nursing assistant training)]]></video:title><video:description><![CDATA[An enema is when fluid is inserted into the rectum and lower colon, and that’s usually done to stimulate the elimination of feces from the rectum. So, an enema can be performed to treat constipation (which is when people have trouble voiding their bowels) or a fecal impaction (which is when the feces form a dry, hard mass in the rectum and can’t be eliminated by the person). Another reason for using an enema is to clean the rectum and lower the colon before a diagnostic or surgical procedure.

Enemas can be classified depending on their purpose or their composition. So in the first category, there are cleansing enemas, which are used to clean the colon of feces entirely. Then there are oil-retention enemas, which are lubricating enemas that soften the feces in order to make them easier to eliminate. Third, there are medicated enemas, which contain medication that can be prescribed for a variety of reasons, like lowering serum potassium levels for example. 
Depending on their composition, the different types of enemas include tap water; normal saline; Harris Flush and carminative, which help with gas elimination; soap suds; and oil-retention enemas, which is an oil-based solution.
Now before we go into the procedural details of administering an enema, here are some come common care tips. Always double-check the client’s ID to make sure the procedure is performed on the right person. Based on  the facility’s policies, a nursing assistant can administer an enema under the supervision and at the direction of a licensed nurse, who will direct you on the type of enema, the amount of solution, and any other special instructions. The client should empty their bladder before the procedure to make sure there are no accidents.  It’s important that there’s a vacant bathroom nearby or a bedpan or bedside commode if the client has mobility problems. You should also close the bed curtains and door, and keep the person covered as much as possible for privacy reasons. Othe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Viral_structure_and_functions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q8FGvlE8RPKZzXh4sGIf_s8BRe6xkxHV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Viral structure and functions]]></video:title><video:description><![CDATA[Viruses are a unique group of pathogens with a simple acellular organization and a distinct pattern of multiplication. 

Despite their simple structure they are a major cause of disease. 

They have no cytoplasmic membrane, cytosol, or functional organelles, but they can infect all types of cells, and numerous viruses can also infect bacteria, which are called bacteriophages. 

Viruses and bacteriophages are not capable of metabolic activity on their own, so instead, they invade other cells and use their metabolic machinery to produce more viral molecules, nucleic acid and proteins which then assemble into new viruses. 

Viruses can exist either extracellularly or intracellularly. 

In the extracellular state, the virus is called a virion and isn’t capable of reproducing.  

A virion consists of a protein coat, called a capsid, surrounding a nucleic acid core which contains the genetic material or the viral genome. 

The nucleic acid and the capsid are collectively called a nucleocapsid. 

Some virions have a phospholipid membrane derived from the host cell, called an envelope which surrounds the nucleocapsid. 

The viruses that have an envelope are called enveloped viruses and these include the herpesviruses and HIV, while the ones that lack the envelope, such as poliovirus, are called non enveloped or naked viruses. 

Once inside the cell, the virus enters the intracellular state, where the capsid is removed and the virus becomes active. 

In this state the virus exists solely as nucleic acids that induce the host to synthesize viral components from which virions are assembled and eventually released. 

Now, the viruses are surrounded by an outer protein coating called the capsid, which protects the viral genome and aids in its transfer between host cells. 

Also, according to their capsid symmetry the viruses can come in many shapes and sizes. 

There are three types of shapes: helical, icosahedral, and complex. 

First, the helical viruses have a capsi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bacterial_structure_and_functions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cemhi2DWRa6Au0FEuE2Tpuq_QoyVrwmm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bacterial structure and functions]]></video:title><video:description><![CDATA[Bacteria are prokaryotic cells that play an important role in human disease and health. 

They can cause disease but are also part of the human microbiota and live on our skin, body and on everyday objects in our environment. 

When compared to eukaryotic cells, the structure of bacteria is less complex due to a lack of nucleus and membrane-bound organelles such as mitochondria, endoplasmic reticulum and Golgi complexes. 

Now, bacterial cells are often surrounded by several layers, which are collectively called the cell envelope. 

Let’s start with the cell wall which is found on the outer surface of the cell membrane and its most important role is to protect the bacteria. 

It consists of peptidoglycan which usually helps differentiate whether bacteria are Gram positive or Gram negative. 

Gram positive bacteria have a single thick layer of peptidoglycan above the plasma membrane, which allows them to retain the staining dye, and Gram negative bacteria have a thinner layer of peptidoglycan sandwiched between the surface membrane and the plasma membrane, so they can’t retain the dye. 

Additionally, the cell wall helps maintain their shape. 

The round shaped bacteria are called cocci, the rod shaped ones are called bacilli, spiral shaped ones are spirilla, and sometimes the same bacteria can have multiple forms, in which case they’re called pleomorphic. 

Some bacteria are covered by a capsule, which acts as a shield that protects the bacteria against phagocytosis, and also helps the bacteria adhere to surfaces. 

The capsule is considered an important virulence factor since the strains that lack a capsule are less virulent. 

Underneath the bacterial cell wall, there’s the plasma membrane which is the most important layer because it encloses the cytoplasm which is a gel-like substance composed mainly of water that also contains cell components, enzymes, and various organic molecules. 

If the plasma membrane is  removed, the cell’s contents spill into t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_face_and_palate</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kffLuJzxTb_R27Q2qnbYkZBCROerFQMg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the face and palate]]></video:title><video:description><![CDATA[Early in embryonic development, during the 3rd week post-fertilization, the embryo is a flat, disc-shaped organism made up of three layers of pluripotent cells called germ layers, which give rise to all the organs and tissues in the body: an inner layer, called endoderm, a central layer, called mesoderm, and an outer layer, called ectoderm. 

By week 4 of development, as a result of the folding of the embryo along the rostrocaudal axis and the lateral axis, it takes on a more recognizably “human” form—but to be honest, it still looks more like a shrimp than a baby. 

At the head end of this little shrimp-like creature, the neural tube expands greatly forming the primitive forebrain, which produces a bulge known as the frontal prominence. 

Lateral to the neural tube is the paraxial mesoderm, which partially segments rostrally to form somitomeres and fully segments caudally to form somites, the first in the series being the occipital somites.

At this point, a small pit called the stomodeum forms between the frontal prominence and the developing cardiac bulge, and it will eventually become the oral cavity. 

At the back of the stomodeum, there’s a two-layered membrane, called the buccopharyngeal membrane, made up of ectoderm and endoderm. 

The buccopharyngeal membrane initially separates the stomodeum from the foregut, but soon disintegrates, allowing free access between the stomodeum and the foregut. 

At the same time, six little bulges or thickenings of the mesoderm, sprout from the primitive pharynx to become the branchial, or pharyngeal, arches. 

These arches are paired, symmetrical bumps that form on each side on the lateral aspect of the embryo, in a craniocaudal fashion, going from head to tail. 

At the same time, neural crest cells from the midbrain and the first two rhombomeres migrate bilaterally to the region and infiltrate the mesoderm bumps where they support the development of embryonic connective tissue needed for craniofacial development]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Oral_Microbiota_and_Systemic_Health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TiIf121mRh_2ywTVV3dxHxo2RX2eBB-_/_.jpg</video:thumbnail_loc><video:title><![CDATA[The Oral Microbiota and Systemic Health]]></video:title><video:description><![CDATA[The human oral microbiota is represented by the community of commensal, symbiotic, and pathogenic microorganisms which are normally found in the oral cavity. 

The oral microbiota is found in saliva, the surface of gum tissue and teeth, and in biofilms, which are basically layers of goop-like material made of exopolysaccharides or EPS, within which bacteria survive in a quiescent or slow-growing state. 

These microbes play an important role in maintaining oral homeostasis, protecting the oral cavity and preventing disease development.

Now, the oral microbiota can be classified into a core microbiota and a variable microbiota.

The core microbiota is the same for all individuals, while the variable microbiota is different between individuals in response to unique lifestyles and phenotypic and genotypic determinants. 

The oral cavity contains over 700 microbial species as well as commensal and opportunistic bacteria, archaea, fungi, protozoa and viruses which are organized into different microbial habitats including the hard palate, tongue dorsum, saliva, palatine tonsils, throat, buccal mucosa, keratinised gingiva, supragingival plaque, subgingival plaque, lips and even dentures!

The major genera with the largest representation in oral cavities include Streptococcus, Prevotella, Haemophilus, Rothia, Veillonella, Neisseria, Fusobacterium and Porphyromonas. 

Now, the oral microbiota can be altered by a series of endogenous and exogenous factors such as diet, smoking, alcohol, antibiotics, or pregnancy. 

This alteration can disrupt the bacterial equilibrium in the oral cavity by increasing harmful bacteria and decreasing the beneficial ones, thus leading to a series of oral infectious diseases such as dental caries or periodontal diseases.

So, a sugar rich diet and frequent snacks can lead to dental caries, while a diet with increased fibrous foods and dairy products help maintain a healthy balance in the oral microbiota. 

Smoking can alter the oral mi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_tongue</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6-z60OmhQ56z-Y00VrEv5MCHQLeRKtlX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the tongue]]></video:title><video:description><![CDATA[The tongue is a muscular structure as well as a sensory organ that starts developing alongside the external face around  week 4 of intrauterine life. 

A fully developed tongue consists of two parts, the anterior two-thirds; and posterior one-third, which is called the root of the tongue; they are separated from each other by a shallow v-shaped groove, known as the terminal sulcus. 

The two parts develop separately, which results in them having different nerve supplies.

Around week 4 of embryonic development, as a result of the folding of the embryo along the rostrocaudal axis and the lateral axis, the embryo takes on a more recognizably “human” form—but to be honest, it still looks more like a shrimp than a baby. 

At the head end of this little shrimp-like creature, the neural tube expands greatly forming the primitive forebrain, which produces a bulge known as the frontal prominence. 

Lateral to the neural tube is the paraxial mesoderm, which partially segments rostrally to form somitomeres and fully segments caudally to form somites, the first in the series being the occipital somites. 

At this point, a small pit called the stomodeum forms between the frontal prominence and the developing cardiac bulge, and it will eventually become the oral cavity. 

At the same time, six little bulges or thickenings of the mesoderm, sprout from the primitive pharynx to become the branchial, or pharyngeal, arches. 

These arches are paired, symmetrical bumps that form on each side on the lateral aspect of the embryo, in a craniocaudal fashion, going from head to tail. 

At the same time, neural crest cells from the midbrain and the first two rhombomeres migrate bilaterally to the region and infiltrate the mesoderm bumps where they support the development of embryonic connective tissue needed for craniofacial development, called ectomesenchyme. 

The pharyngeal arches are separated externally by small clefts on the pharyngeal wall called branchial grooves, and inte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_teeth</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sCFLjRW-Tq_GsvWpWzrKsGTmR6yH36ng/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the teeth]]></video:title><video:description><![CDATA[Odontogenesis, or teeth development, is a process that includes the development of deciduous teeth, also called milk teeth or baby teeth; and permanent teeth. 

Deciduous teeth begin to develop during week 6 - 7 of intrauterine life, whereas, development of permanent teeth begins during week 14 of intrauterine life and continues to even up to 5 years after birth!

Now, teeth are one of the most diverse organs in humans both morphologically and functionally. 

The development of teeth begins around  week 6, and from two tissue components: the primitive oral epithelium derived from ectoderm, and the underlying ectomesenchyme or dental mesenchyme. 

The dental mesenchyme derives from craniofacial neural crest cells that migrate from the developing midbrain and the first two rhombomeres into the first branchial arch.  

Now, the oral epithelium and the dental mesenchyme instructs each other in a sequential and reciprocal way to precisely determine the formation and location of highly specialized teeth, such as incisors, canines, premolars and molars.

The tooth development starts with a thickening of the primitive oral epithelium known as the primary epithelial bands- one on each jaw. 

Each primary epithelial band soon splits into two; an inner, or lingual, dental lamina, and an outer, or buccal, vestibular lamina. 

The vestibular lamina subsequently hollows and forms the vestibule of the mouth, which is the space between the alveolar portion of the jaws, lips, and cheeks. 

Now, signal proteins such as FGFs, BMPs and ectodysplasin cause the cells within the dental lamina to start proliferating and to invaginate in the positions that correspond to the locations of the future teeth. 

These localized enlarged projections within the dental lamina are known as the dental placodes. 

Next, as the dental placodes continue to proliferate, the tooth undergoes morphogenesis which results in different teeth shapes. 

This is guided by interactions between epithelial ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Emerging_coronaviruses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eIeKfzyoQ7GqDghk4O47IL7mSqC1YTEg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Emerging coronaviruses]]></video:title><video:description><![CDATA[Emerging diseases are illnesses that have increased in incidence during the past 20 years, or are expected to increase in the near future. 

Some are zoonotic, meaning they are caused by pathogens that have hopped from infected animals to humans. 

A few examples are coronaviruses, a group of RNA viruses that can cause a variety of respiratory illnesses in humans.

Transmission of emerging zoonotic diseases can occur through animal tissues, environmental sources; or animal hosts, either directly or indirectly through another animal, or even an inanimate carrier, like air. 

And they can even reemerge through similar mechanisms if the pathogen has a natural reservoir, which can be an animal where it naturally survives and reproduces. 

And there are a few factors that help increase their transmission. 

Some of the major ones include: increased close contact between an infected animal and humans, which happens during deforestation, climate change, or large-scale farming and food processing; changes in societal norms, like food preferences, or areas to live, and decreases in vaccination rates or sanitation; or increased globalization that spreads local outbreaks rapidly through trade and travel; and even increased populations vulnerable to infections, like older folks and people with underlying conditions which may make them immunosuppressed.   

Now, Coronaviruses are a group of enveloped, positive-sense single-strand RNA viruses. 

And they were first discovered in the 1930s in domestic poultry that had respiratory, gastrointestinal, liver, and neurologic diseases. 

But since then, they have been found in a variety of animals, and seven coronaviruses are currently known to cause disease in humans. 

A main way they are transmitted person-to-person is through respiratory droplets, which contain the pathogen and come in direct contact with the eyes, nose, or mouth of another person who comes in close contact; or indirectly make its way there by first contam]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lyme_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/caNF65XHTsO850X3gtPT8cpZQw_ltSuN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lyme Disease]]></video:title><video:description><![CDATA[Lyme disease, or Lyme borreliosis, is an infectious, blood-borne bacterial disease that is transmitted by ticks. 

It’s caused by Borrelia burgdorferi species.

Now, the genus Borrelia contains several species. 

Lyme disease in people is caused primarily by Borrelia burgdorferi in North America and by B. afzelii, B. garinii, and B. burgdorferi in Europe and Asia. 

In domestic animals, only B burgdorferi is confirmed to cause Lyme disease..

Borrelia are spirochetes, which means spiral-shaped bacteria. 

They have outer surface proteins, abbreviated as Osp, which play a role in virulence; and sets of flagella that run between the cell wall and outer membrane, which they use to spin or twist to move in a wave-like motion. 

Hard-shelled, Ixodes ticks, or deer ticks, are the vector for B. Burgdorferi, meaning they are the intermediate organism that spreads the bacteria. 

In the northeast and Midwest USA, I. scapularis, the black-legged deer tick is the main vector;  while on the Pacific coast, it’s I. pacificus, the western black-legged tick. 

In Europe and Asia I ricinus and I. persulcatus are the primary vectors. 

Ticks like environments with moderate humidity and temperature so they’re often found in  wooded areas, thick brush, marshes, and tall grass. 

The ticks are small, and even adults are only about 3 mm long, so they can be hard to notice.

Now Ixodes ticks feed on the blood from hosts throughout their life stages of larva, nymph, and adult. 

When they hatch as larvae, they are uninfected. 

When they feed on infected hosts as  larvae or nymphs, they can pick up the  B. burgdorferi bacteria.  

In the younger stages of their life, they often feed on smaller animals like  rodents,  birds and even lizards.  

When they grow into adults, they move on to larger mammals like dogs, cats, or horses.

A tick infected with B. Burgdorferi can transmit the bacteria to humans and  animals through their saliva during feeding. 

In the first few hours after]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_eye_disease_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oTCXW7g2So_yteeojZcq-pydTpC6z7wf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid eye disease (NORD)]]></video:title><video:description><![CDATA[Thyroid eye disease is a rare disease in which progressive inflammation damages muscle, fat and connective tissues around the eyes. 

The disease has an active phase, which can last from six months to two years, where inflammation, swelling, and damage occur. 

The inactive phase occurs when disease progression stops, but the tissue damage and symptoms remain.

Signs and symptoms can vary between individuals, but commonly the white parts of the eyes are inflamed. 

A particularly noticeable change is the eyes appear to be bulging out of the eye socket, called exophthalmos or proptosis, which makes a person appear as if they are always ‘staring’.

Additionally, the eyes can feel irritated, uncomfortable, and have a “gritty” feeling. 

They may also be constantly watery or be dry. 

The eyelids can become inflamed and retracted, so they won’t close completely and blinking or trying to close the eyes can be painful.  

Vision changes may also occur, including blurry vision; double vision; or an intolerance to bright lights. 

In severe cases, vision may be threatened from increased pressure on the main nerve of the eye that carries visual information to the brain; or from dryness leading to erosion of the cornea, which is the outer part of the eye. 

Thyroid eye disease usually occurs during middle age. 

While it’s more frequent among females, males tend to have more severe cases. 

Environmental factors such as smoking may contribute but there’s also a variety of genetic factors. 

Individuals may have an elevated risk if they also have immune diseases like type 1 diabetes or rheumatoid arthritis. 

Because thyroid eye disease occurs so often with Graves’ disease, it’s also called Graves’ orbitopathy, Graves’ ophthalmopathy, and thyroid-associated ophthalmopathy.

The exact underlying process by which thyroid eye disease occurs is not fully understood, but like Graves disease, it’s an autoimmune disorder. 

Normally, the immune system protects the body by i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mechanisms_of_antibiotic_resistance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VR5L6ZGvSdukjVQ89eGaj51RS2GPj05t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mechanisms of antibiotic resistance]]></video:title><video:description><![CDATA[The discovery of antibiotics is one of the most important advancements in clinical medicine and public health. It has laid the foundation for a number of other advancements including the ability to perform surgeries more safely and reduction of infant and maternal mortality rates.

Many antibiotics are derived from other bacteria or fungi. For example, penicillin, secreted by the fungus Penicillium, can kill bacteria. 

This is because microbes use antibiotics to fight off other microbes. But the use of antibiotics, and, more broadly, antimicrobials, which includes medications that target not only bacteria, but also viruses and fungi, has exploded in recent years. 

Antimicrobials have been used on an industrial scale, partially because of overprescription in humans, but more so because of routine use in farm animals! 

In fact, a good number of antimicrobials are excreted from humans and animals unchanged, and these get flushed into waste water, which allows pathogens to be perpetually exposed to antimicrobials. In response to this enormous selective pressure, many pathogens have become highly resistant to antimicrobials.

Now when it comes to bacteria, generally speaking, there are four mechanisms for how they become resistant to antimicrobials. 

The first mechanism is antibiotic inactivation or modification, which is where bacteria develop specific enzymes that destroy and inactivate antimicrobials. 

One example is beta lactamase, which is a bacterial enzyme that destroys antimicrobials that contain a beta lactam ring, like penicillins and cephalosporins. As a result, bacteria that produce beta lactamases are immune to the action of many beta lactam antibiotics.

The second mechanism is the alteration of a target, or binding site. An antibiotic that cannot bind anywhere is rendered useless. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ketosis_in_Cattle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n3pPoqtyRH2-YlFPFcVrupXcSrSHzhQh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ketosis in Cattle]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Ketosis in Cattle through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Feline_Panleukopenia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zMkPKnBhTxKd4wIa3Wjkaj5hRQuD8WbE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Feline Panleukopenia]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Feline Panleukopenia through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_stones_in_dogs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wgkgFrSrQku37XX-ctqHnNoNTzaIicVD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary stones in dogs]]></video:title><video:description><![CDATA[Uroliths, also known as urinary calculi or stones, are caused when minerals in urine form crystals, which then clump together and grow large enough to become visible. 

Blockage of urine flow caused by stones may lead to pain, difficulty urinating, and blood in the urine. Physical examination, radiography, and urinalysis are typically used for diagnosis. 

The most common types found in dogs are struvite, calcium oxalate, urate, cystine, and silica stones. Struvite stones are the most common type in dogs and are primarily made of magnesium ammonium phosphate. 

In most cases they form in the presence of urinary tract infections. Treatment by changing the diet to dissolve the stones is often successful.

Any urinary infection must also be treated. Other options are surgery or lithotripsy (breaking up the stones with ultrasound). 

Calcium oxalate stones may develop in any dog breed, but Miniature Schnauzers, Lhasa Apsos, Yorkshire Terriers, Bichon Frises, Shih Tzus, and Miniature Poodles may be predisposed. 

Treatment options are surgery or lithotripsy. Recurrence is often a problem, but a diet low in oxalate, protein, and sodium may help prevent new stones from forming. 

Keeping urine dilute and acidic may also be beneficial. Urate stones are most common in Dalmatians and dogs with congenital portosystemic vascular shunts. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Thanks_Front_Line_Workers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:thumbnail_loc><video:title><![CDATA[Osmosis Thanks Front Line Workers]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis Thanks Front Line Workers through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Structure_and_function_of_the_human_body</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lxq3-j9eSZSkn9b7bLBNsYmiQCqJvcKP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Structure and function of the human body]]></video:title><video:description><![CDATA[The human body has many different parts. The science that studies the structures and arrangement of those parts is called anatomy, while the study of how they function is called physiology. 

To understand how the human body works, let’s start at a microscopic level and look at cells. Cells are the smallest structural and functional unit of the body. 

Now, cells, with similar structures, join together to form tissues, which are specialized to carry out specific functions. There are four types of tissues. 

We have epithelial tissues that cover external body surfaces and line our internal body cavities; muscle tissues that contract and help carry out some functions, like movement; nerve tissue, which transports electric signals between various body parts and the brain; and the connective tissue, which supports and connects all other tissues. 

Now, when different tissues come together, they form an organ. Organs can carry out tasks that are actually too big to be fulfilled by a single type of tissue. 

One example of an organ is the heart, which is made of different tissues, such as the cardiac muscle tissue that helps the heart pump blood and the nervous tissue that helps regulate its rhythm. 

Okay, now, different organs work together in a systematic way to form organ systems. Organ systems carry out the much more extended functions that an isolated organ couldn’t be able to handle. 

A good example of this is the digestive system that consists of the mouth, esophagus, stomach, small and large intestines, the pancreas, liver, and gallbladder; all of which take part in digestion.  

Okay, let’s shift gears a little bit and take a closer look at the cell. All of the body’s functions start at the cellular level. Cells have structures called organelles that act like very simple organs. 

One of these organelles is the cell’s outer layer, called the cell membrane, or plasma membrane. This plays a role in regulating what enters and leaves the cell. 

Inside th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assistive_devices_for_activities_of_daily_living</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jEvRivZ1QGO2SH2l92R58BBYQ0Ww-XaT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assistive devices for activities of daily living]]></video:title><video:description><![CDATA[Assistive devices for activities of daily living are devices that are made or adapted to help a person perform actions and tasks such as walking, grooming, dressing, eating, and drinking. 

Also, they represent an important part of a client’s life because they boost their self-esteem by aiding them in regaining independence.  

Let’s start with assistive devices for walking, which are also called ambulatory assistive devices or mobility aids. There are three major groups of mobility aids, which include canes, crutches, and walkers. 

Canes are made of plastic, wood, or aluminum, and they can have a straight or half circle handle. 

Canes are prescribed to increase stability in individuals that can bear weight but are unstable or too weak on one side of the body. 

Next, we have crutches, which can be axillary or forearm crutches. Axillary crutches are made of wood or aluminum, and they are characterized by axillary bars; while forearm crutches are made of aluminum, and they are characterized by forearm cuffs. 

These devices are prescribed to increase stability but also to partially or fully reduce the weight bearing on a lower limb. 

Finally, we have walkers. These devices have an aluminum framework and four legs, with or without wheels. 

Walkers afford the greatest stability; therefore, they are prescribed to individuals that can bear weight but are weak or unstable! 

Finally, most assistive devices made of aluminum have a push-button mechanism, which enables their adjustment to a client’s height. 

Next, we have assistive devices for personal hygiene such as combs, brushes, and toothbrushes. These devices can be modified to have built-up handles. 

Built-up handles make grasping easier, which is perfect for people with reduced grip strength. Additionally, combs and brushes can also be designed to have long handles, which allows users to reach their hair without having to lift their arms above the head. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obtaining_height_and_weight</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0GL0fP1RQteWLcTgZkH0zdBrTx_J5UHL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obtaining height and weight]]></video:title><video:description><![CDATA[Weight and height are important indicators of the client’s overall health and nutritional status. The weight can reflect whether the disease is getting better or worse. 

For example, a client with kidney or heart disease will retain fluid in their body, which increases their weight. On the other hand, a client who has cancer may lose a lot of weight. 

Also, the weight is used to calculate doses of medications for the client, which helps to adjust the right dose and decrease adverse effects. 

As a nursing assistant, you will measure the client&amp;#39;s height one time, which is at admission, while the weight may be measured more frequently: at admission; periodically during the client’s stay, maybe even daily; and at discharge.

Alright, there’re a few things to keep in mind to obtain accurate weight measurements. First, the weight should be measured at the same time of the day, so the weights can be compared. 

Actually, it’s best to measure it before breakfast to avoid any weight added by food or fluid the client ingests. Before measuring the client&amp;#39;s weight, instruct them to empty their bladder because a full bladder can also add some weight. 

If they have a urinary bag, empty it first; if the client is wearing incontinence briefs, make sure they’re dry. Also, you should ask them to wear the same type of clothes every time you measure their weight; preferably they should wear a gown or pajamas and take off their footwear. 

Alright, there are different scales to measure the client’s weight. These include the upright scale, chair scale, bed scale, and sling scale. 

The type of scale to use depends on the client&amp;#39;s condition and their ability to stand and move from their bed. Whatever scale you use, always remember to ensure your client&amp;#39;s safety by providing support and assistance to prevent any falls or injuries.

Now, the upright scale is used when the client can stand without assistance. These scales can be dig]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gHd-EgZ4RiGQ4NZbr3iBtVaDSV24cQzH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory system: Structure and function]]></video:title><video:description><![CDATA[The respiratory system consists of the structures in our bodies that allow us to breathe. It is made up of the lungs and a collection of tubes and passages called the “airway.” 

It’s often thought of as consisting of two regions: the upper respiratory tract and lower respiratory tract. The upper respiratory tract includes the nose, nasal cavity, the oral cavity, pharynx, larynx, and the upper part of the trachea; the lower respiratory tract includes the lower part of  trachea, bronchi, bronchioles, and the lungs.

The tubes and passages that make up the airway serve to move air into and out of the lungs. Air enters the body either through the nostrils of the nose and into the nasal cavity, which is the air-filled space behind the nose, or through the mouth, also known as the oral cavity. 

Both entryways lead air to the pharynx: the cavity behind the nose and mouth, more commonly known as the throat. 

From there, air travels down into and through the larynx, otherwise known as the “voice box” because it contains the vocal cords necessary for producing speech. 

After passing through the larynx, air begins to move into the trachea, the tube known as the “windpipe” that branches off at its base into two tubes: the left and right bronchi, which lead to the left and right lung. 

Each of the bronchi branches off further and further within the lungs into many smaller and smaller tubes, called bronchioles, at the end of which are bunches of tiny air sacs, called alveoli, which are surrounded by tiny blood vessels, called capillaries.

Now, healthy lungs are pink, spongy, and elastic. The right lung is divided into 3 lobes, while the left lung is divided into only 2 lobes and is a bit smaller than the right lung because of the space taken up by the heart in the left side of the chest cavity. 

Each of the lungs is covered by the pleura: a 2-layered sac with a fluid-filled space between the two layers. One of the layers is attached to the lung, and the other is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Transferring_clients_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/68qxHpfRR_iNOEpVwYy8MijTQWK5YecV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Transferring clients (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Transferring clients (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assisting_with_ambulation_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vo6o1jpfQq2RPZoakphS08QxRG6H3G2C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assisting with ambulation (for nursing assistant training)]]></video:title><video:description><![CDATA[Ambulation means “walking,” and your client might need to ambulate to get to places or may need to do it to prevent atrophy, which is when muscles waste away from prolonged bed rest. Other health problems from long-term immobility include decreased cardiovascular and pulmonary functions, poor digestion, pressure ulcers, contractures, urinary problems, and many others. So, even if they require assistance, clients are encouraged to ambulate frequently.  

Before we talk about ambulation assistance, here are some general considerations. Explain to the client how far you’ll be walking and how you will assist them. Check if they need an ambulation device, like a cane or walker. If a device is needed, check to see if it’s functional. Make sure the route is not slippery and that there are no obstacles. Make sure IV lines and poles are free from tangles and that the IV pump is unplugged from the wall and has enough battery to last during ambulation. Make sure they’re properly dressed and wearing non-skid footwear. During ambulation, encourage them to walk normally without shuffling or sliding. You might need an additional assistant if the person’s unbalanced, weak, or not cooperative. Finally, and most importantly, be sure not to leave the client’s side at any time during the process.  

Now, before getting a resting person to stand and walk, you need to get them into a sitting, or “dangling,” position, where they sit erect with their feet dangling off the side of the bed. The main reason for this is to protect against falling. One common cause of falls is orthostatic hypotension, where blood rushes into the legs as the person shifts into an upright position, causing a drop in blood pressure and decreased blood flow to the brain. It can result in dizziness or even fainting, especially in the elderly. If you have the person stand in this condition, it could lead to falls, so having them sit in the dangling position will help their body adjust without the risk. 

To]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sensory_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ecgz4GR9RgK6tXXmnFcP7LnKQ56NCflZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sensory system: Structure and function]]></video:title><video:description><![CDATA[The sensory system is a part of the nervous system, and it can be split into two divisions: the general senses and the special senses. 

Both divisions gather information about your surroundings and what’s happening inside your body. The sensation you experience, also called a stimulus, is captured by sensory receptors, which receive the stimulus and convert them into nerve impulses that travel all the way through sensory nerves to the brain for interpretation.

Alright, the general senses include touch, pressure, position, and pain. There are receptors for these distributed all over the body. 

Now for touch, tactile receptors pick up sensory information when something comes in contact with your skin, like when you’re petting a dog. 

Some parts of your body, like the tips of the fingers, are more sensitive to touch because they have more tactile receptors than other areas, like your back. 

Now, in addition to touch, some tactile receptors sense pressure on the skin. This is why we feel uncomfortable after sitting in a certain position for a long time and need to change our position to another one. 

Clients like those with spinal cord injuries might have problems with this sensation, so they stay in the same position, which causes prolonged compression of blood vessels in their skin and a decrease in blood flow to that area. This causes their skin to break down and form pressure ulcers. 

The next general sense is the sense of position. When you’re sitting on your couch, you know your legs are straight or crossed without looking at them. 

This is because position receptors found in joints, muscles, and tendons inform your brain about the position of different parts of the body relative to each other. 

Also, these receptors inform your brain about how much your muscles are contracting or stretching and help prevent injury when you’re doing something like lifting heavy weights at the gym. 

Now, the last general sense is pain. Pain receptors can be foun]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_safety:_Fire_safety</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rUkuYj23SYSx8YjtduMNwZ1BSt_TxNC2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace safety: Fire safety]]></video:title><video:description><![CDATA[Fires are known to cause huge losses in terms of property damages, injuries, and deaths. They pose even greater threats in healthcare facilities where there are many physically weak and sick people unable to get out of their beds or chairs. 

Additionally, healthcare facilities have volatile and flammable chemicals in their setting; the presence of oxygen can aggravate fires and make them hard to control. As a nursing assistant, you should know how to prevent fires and what to do when there’s a fire at your facility. 

There are three important elements that must be present to start a fire: fuel, heat, and oxygen. In a healthcare setting, fuel is anything that can burn, such as bed linens, mattresses, clothing, paper, and so forth. 

Just like fuel, sources of heat are everywhere in healthcare settings. It can be from an electrical spark from a frayed electrical cord; overheated devices, such as irons, furnaces, or radiators; or a lighted candle or cigarette. 

Oxygen in the air we breathe is sufficient to start a fire. Also, note that there are clients in healthcare settings who are on oxygen therapy, which increases the amount of oxygen in the environment.

The first step to preventing damages and losses caused by fires is to know how to prevent them in the first place. Preventing fires is everyone&amp;#39;s responsibility, so let’s focus on what you should do as a nursing assistant. 

For healthcare settings where clients are permitted to smoke, make sure they do so only in designated areas and that there’s somewhere they can extinguish cigarettes and matches. 

Keep an eye on clients who smoke who are mentally disabled or disoriented because they might not follow the rules. Never allow clients, especially those on oxygen therapy, to smoke in the bed. 

This is because a client might fall asleep and drop a cigarette on the bed. Also, do not give clients who are on oxygen anything that can create sparks. 

Even something like a wool or mohair blanket ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_system:_Renal_failure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YucZBCxvTnapqewQk227H-yIQ8ee4nMd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary system: Renal failure]]></video:title><video:description><![CDATA[Renal failure happens when the kidneys don’t function at all or function at a low capacity, meaning that they are unable to filter blood properly. 

As a result, a lot of waste products along with fluid build up in the body, affecting other organs in the body including the heart. In kidney failure, the individual can become very sick very quickly, especially if treatment is delayed.

There are two types of renal failure: acute and chronic. Acute renal failure, or acute kidney injury, happens when there’s a sudden loss of kidney function. 

One cause of acute kidney injury is when there’s a decreased blood flow to the kidneys, which can happen in the case of bleeding, severe diarrhea, or burns. 

Other causes of acute kidney injury include severe infections; severe allergic reactions; poisoning with substances, like antifreeze; or ingesting certain medications that can damage the kidneys, such as large quantities of nonsteroidal anti-inflammatories, like Ibuprofen. 

Chronic kidney failure, or chronic kidney disease, happens when there’s a progressive decrease in kidney function, meaning that the number of functioning nephrons are gradually lost. 

Common causes of chronic kidney disease are diabetes mellitus and hypertension. Both these conditions damage the blood vessels in the glomerulus. 

Other causes include chronic infections, such as chronic pyelonephritis; infection of the kidneys; or blockage in the urinary system, like when there’s a large kidney stone or tumor. 

One of the signs of renal failure is dehydration, which happens due to excessive loss of fluid. This usually happens pretty early in acute kidney injuries because the kidneys aren’t able to reabsorb water back into the bloodstream. 

Another sign is swelling, caused by the build-up of fluid in the tissues of the body. This usually happens later in chronic kidney disease, when the kidneys aren’t able to excrete the excess fluid. 

Another sign is hypertension, which happens mostly due to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular:_Pulse_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x-EfYBFmQI63nsYp4KwOdqYYQbSMAkc6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular: Pulse (for nursing assistant training)]]></video:title><video:description><![CDATA[With every heartbeat, the heart creates a wave, or pulse, that’s sent to arteries all over the body in order to deliver oxygenated blood to our organs and tissues. As a nursing assistant, you need to be able to obtain a pulse and determine its characteristics, including the pulse rate, rhythm, and amplitude, or character. 

Okay, you can calculate the pulse rate by counting the number of pulses in one minute. This is actually equal to the heart rate, or the number of times the heart beats per minute. Normal pulse rate varies among different age groups. So, for those 12 years of age or older, it’s typically between 60 and 100. For school-aged children between 5 and 12 years old, it’s 75 to 110. For preschoolers from 3 to 5, it’s 80 to 120, while for toddlers from 1 to 3, have a normal pulse rate of 80 to 130. Finally, infants under 1 year of age normally have the fastest pulse rate, which ranges from 120 to 160 beats per minute. Besides age, the pulse rate can also be influenced by many factors, including physical activity; body temperature; emotions, like anger, fear, or stress; medications; or even the weather! So, tachycardia is when the pulse rate is faster than normal, and this can occur in response to strenuous exercise, fever, pain, anxiety, or specific medications. In contrast, bradycardia means that the pulse rate is too slow and can be due to heart problems or various medications.

Another important characteristic is the pulse rhythm, which is normally regular, meaning that the intervals between the beats are equal. In an irregular rhythm, also known as arrhythmia, the beats do not follow an even tempo and some of them might even be skipped. Arrhythmia can be a result of heart problems or a complication of a heart attack or heart surgery. It can also be caused by problems with the balance of electrolytes, such as potassium, in the blood.

Then, there’s the pulse amplitude, or character, which refers to how strong, forceful, or full the pulse ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_safety:_Violence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KKIzXh43R__Z3gYYtVHsCOCAS-SKNbs9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace safety: Violence]]></video:title><video:description><![CDATA[As a nursing assistant, you may encounter workplace violence. The National Institute for Occupational Safety and Health, or NIOSH, defines workplace violence as “the act or threat of violence, ranging from verbal abuse to physical assaults, directed toward persons at work or on duty.” 

Some examples of workplace violence include written or verbalized threats; harassment, like being followed, yelled at, or sworn at; or physical harm done by hitting, kicking, stabbing, or shooting. 

Healthcare team members, especially nurses and nursing assistants, may be victims of violent acts from internal sources, such as coworkers, clients, or visitors, or external sources, like robbers and muggers in the facility parking area.

Now, violence can occur anywhere in the healthcare setting, but it is particularly common in emergency rooms, waiting areas, mental health units, and parking lots because these areas are often associated with multiple risk factors linked to violence. 

These risk factors include people with weapons, acutely disturbed or violent individuals, criminals brought in by police, abusers of illicit drugs or alcohol, individuals with mental health issues, upset family members or visitors, long wait times due to understaffing, and poorly lit areas. 

Working alone, especially without easily accessible communication devices, is also associated with an increased risk of workplace violence. 

Lack of staff training to recognize and react appropriately to hostile or assaultive situations can also contribute to increased workplace violence.

Now, as a nursing assistant, your role when it comes to workplace violence is threefold: keep yourself safe, keep others safe, and immediately report any incidents to the nurse. 

You can help keep yourself safe by knowing your way around the care facility, communicating your whereabouts at all times, ensuring you aren’t alone in any poorly lit or low traffic areas, and remaining alert to any suspicious persons or activi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Privacy_and_confidentiality</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OJ1BcCLwT6eUQuJsqEYtn1G5TyS11569/_.jpg</video:thumbnail_loc><video:title><![CDATA[Privacy and confidentiality]]></video:title><video:description><![CDATA[Caring for people puts you in a position where you’ll be entrusted with their private and confidential information. As a nursing assistant, you will have access to your client’s private information, such as health status, medical history, ongoing treatments, prognoses, communication with family and friends, and possibly their financial information. That’s why respecting your client’s privacy and confidentiality is an important aspect of your work.

Alright, in a healthcare setting, the client’s right to privacy and confidentiality is determined by the Omnibus Budget Reconciliation Act, or OBRA. 

Privacy is a client’s right to have control over their personal information and be free from being observed by others not involved in their care, while confidentiality refers to a  client’s right to have their information kept secret. 

Failing to respect your client’s right to privacy and confidentiality constitutes an act of invasion of privacy and has legal implications.

During your job as a nursing assistant, you should follow your facility’s policy when it comes to protecting your client’s privacy and confidentiality. 

Inform your clients about their rights and respect these rights as you carry out your tasks. Some situations where a client&amp;#39;s right to privacy must be respected include while bathing or dressing clients, during a medical procedure and when a client is using the bathroom. 

Before entering a client’s room, be sure to knock and then introduce yourself to the client. Before performing any procedure that requires privacy, ask visitors to leave if they are present and show the visitors a place for them to wait until the procedure is complete. 

Then, close the curtains and doors. Some procedures may require the client to be undressed so make sure you drape body parts that are not necessary to be exposed during the procedure. 

Other components of a client&amp;#39;s right to privacy include having the right to make phone calls in private ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ygf-9GSnT7Cy6iKz6iUElaWsQxO-fAxx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular system: Structure and function]]></video:title><video:description><![CDATA[The cardiovascular system includes the blood, the blood vessels, the heart, and the lymphatic system. It is responsible for carrying nutrients, hormones, and other substances to the body tissues. 

It also carries oxygen to the rest of the body and removes waste products, such as carbon dioxide. Also, it produces the cells of the immune system that help fight infections. Finally, it helps maintain a balance of body fluids and a normal body temperature. 

Okay, let’s take a closer look at the components of the cardiovascular system, starting with the blood. The blood is composed of the plasma and the blood cells. 

The plasma is 90% water, and the other 10% contains nutrients, such as glucose; salts; and proteins, like albumin. 

The blood cells include the red blood cells, or RBCs, also known as erythrocytes; the white blood cells, or WBCs, also known as leukocytes; and the platelets, or PLTs, also known as thrombocytes. 

RBCs are produced in the bone marrow and they have a characteristic disc shape. They live for about 120 days. When they get too old or damaged, the spleen and the liver will break them down. 

They contain a protein called hemoglobin, which is responsible for carrying oxygen to the tissues. As blood circulates through the lungs, the blood gets oxygenated as hemoglobin picks up oxygen molecules. 

As the blood travels through the body, the oxygen is given to tissues, carbon dioxide is picked up, and the blood becomes deoxygenated. 

Now, WBCs are produced by the bone marrow and the lymphatic system. Their major role is to destroy any harmful microbes that enter the body, so their number increases when there is an infection. 

Finally, platelets are not actual cells but fragments of large cells, called megakaryocytes, which are produced by the bone marrow. 

Platelets play an important role in the formation of blood clots, which plugs up any damaged areas in blood vessels to stop bleeding. 

Okay, now blood travels to the tissues through t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Emergency_care:_Falls</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2l6utnHtTC6YB8wgBbx6SaKaR3ikV4tN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Emergency care: Falls]]></video:title><video:description><![CDATA[As a nursing assistant, sometimes you will need to handle some emergencies while providing care for clients; one of these is when a client falls. 

Now, clients at risk for falls should always use assistive devices when ambulating, and a nursing assistant should be present with them during ambulation in the event that they begin to fall. 

If a client does begin to fall or appears unsteady or complains of dizziness, hold your arms up and around the client’s waist or under their arms. 

Grab onto the transfer belt if already in use and bring them closer to your body. Be sure to keep your feet shoulder width apart to give you a wide base of support and keep your back straight. 

Don&amp;#39;t pull their arms trying to stop the fall as this may cause further injury to their bones or joints. Then, let the client slowly slide down while leaning against you until their buttocks rests on your legs.

As they slide down, bend your hips and knees to gently lower the client to the floor; make sure to protect the client’s head from injury. Now, stay with the client, calm them down, and call a nurse to assess them. 

If you find a client on the floor, and you didn’t witness the fall, don’t try to move them as this may worsen any injury they might have had. Stay with the client, calm them down, and call a nurse to assess them. 

Alright, after alerting the nurse in charge, they’ll check the client for injuries. For those with minor or no injuries, you can work on transferring them back to their bed. 

If the client can stand on their own, let them do so while observing them or help them to stand using a transfer belt. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_in_the_News</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8Ic8TLfnT0aXiVdHvCk63zPiTN_Z5YD6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osmosis in the News]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis in the News through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rep._Donna_Shalala:_U.S._Representative_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y2Vw4funQAG8V8DyLRGqFu13SPqGCf7q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rep. Donna Shalala: U.S. Representative (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Rep. Donna Shalala: U.S. Representative (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Joshua_Sharfstein:_Vice_Dean_at_Johns_Hopkins_School_of_Public_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1HSB67GITGy7qE_VjQGUcMqKSC6b8gXB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Joshua Sharfstein: Vice Dean at Johns Hopkins School of Public Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Joshua Sharfstein: Vice Dean at Johns Hopkins School of Public Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gabe_Dalporto:_CEO_of_Udacity_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ivVHaY9zQmKoQcPVAD4eqlClTQ_Goay8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gabe Dalporto: CEO of Udacity (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Gabe Dalporto: CEO of Udacity (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dhiren_Patel:_Vice_President_of_Medical_Affairs_at_Pack_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JRQQIvKMSVaeUEeH1elMplxWSVa801pg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dhiren Patel: Vice President of Medical Affairs at Pack Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dhiren Patel: Vice President of Medical Affairs at Pack Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dean_Ho:_Director_of_the_Institute_for_Digital_Medicine_at_NUS_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oQflVy-zTca50FWY6th7byEBQsiwKt8Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dean Ho: Director of the Institute for Digital Medicine at NUS (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dean Ho: Director of the Institute for Digital Medicine at NUS (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Ted_Wendel:_Senior_VP_of_Strategic_Initiative_&amp;_Planning_at_A.T._Still_University_of_Health_Sciences_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ziqdeBWcQX__vvKgCcqEXJcITduWPcJO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Ted Wendel: Senior VP of Strategic Initiative &amp; Planning at A.T. Still University of Health Sciences (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Ted Wendel: Senior VP of Strategic Initiative &amp; Planning at A.T. Still University of Health Sciences (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Julia_Cheek:_CEO_and_Founder_of_Everlywell_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NC4nneM_SWSwEay7ALAYfm9vT-CWj3d8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Julia Cheek: CEO and Founder of Everlywell (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Julia Cheek: CEO and Founder of Everlywell (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Joe_Habboushe:_Co-founder_and_CEO_of_MDCalc_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JyxXxDLcRPOZpbKI5ES3U0LqQ4mBsofK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Joe Habboushe: Co-founder and CEO of MDCalc (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Joe Habboushe: Co-founder and CEO of MDCalc (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Viral_hepatitis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R7XPeoH5R2y0xBEzeHNvrIqrRji0M8MJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Viral hepatitis: Pathology review]]></video:title><video:description><![CDATA[At your clinic, 44-year-old Colin comes to the office because of abdominal pain for 3 months. 

He has not been to a physician in 10 years and has been using IV drugs since he was 17. 

He does not drink alcohol and has no significant family history. 

His temperature is 38.2°C or 100.76°F, pulse is 98/min, respirations are 19/min, and blood pressure is 126/84 mmHg. 

Physical examination shows a large distended abdomen, yellow sclera, palmar erythema, and spider angioma on his abdomen and extremities. 

Lab results reveal the following: Hepatitis A IgM antibody negative, Hepatitis B surface antigen negative, Hepatitis B surface antibody positive, Hepatitis B core antibody negative, and HCV antibody positive.  

At the same time, a 32-year-old pregnant individual named Megan comes to the emergency department because of vomiting and fever. 

The patient worked as a global health nurse and her medical history is relevant for recent traveling to Nepal. 

Physical examination shows yellowing of the skin and sclera, right upper quadrant tenderness, and hepatomegaly. 

Her temperature is 38.5°C or 101.3°F, pulse is 97/min, respirations are 15/min, and blood pressure is 120/75 mmHg. 

Both Colin and Megan have viral hepatitis, which is inflammation of the liver parenchyma caused by hepatitis viruses A, B, C, D, or E. 

Based on the duration of symptoms, hepatitis can be acute, which lasts less than 6 months, or chronic, which lasts more than 6 months. 

Individuals with acute viral hepatitis typically present with fatigue, malaise, nausea, vomiting, anorexia, low-grade fever, jaundice, dark urine, and right upper quadrant tenderness; whereas individuals with chronic viral hepatitis can be asymptomatic or they can present with non-specific symptoms such as malaise and fatigue. 

Regardless of the virus that’s causing it, histopathology of viral hepatitis is characterized by two main findings: first, there’s hepatocyte injury where the damaged hepatocytes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integumentary_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LEW7lq8xQzuFkukgkEteKH5RQ6ioPDl_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integumentary system: Structure and function]]></video:title><video:description><![CDATA[The integumentary system is the largest organ in our body. It is made up of the skin and its accessory structures, which include the nails; hair; sebaceous, or oil, glands; and sweat glands. 

The primary functions of the integumentary system are covering and protecting our internal organs and tissues, preventing the entry of microbes or harmful substances, preventing excess water loss and dehydration, storing fat and water, regulating our body temperature, providing sensory information, and producing vitamin D.

Now, the skin is divided into the epidermis and the dermis. The epidermis is the outermost and thickest layer, and it&amp;#39;s made of multiple layers of developing cells, which are called keratinocytes because they produce keratin: a protein that makes our skin resistant to water. 

Now, keratinocytes start their life at the lowest layer of the epidermis and then migrate upwards to form the other layers of the epidermis in a process that takes approximately a month. 

Now, the lowest layer of the epidermis also contains another group of cells called melanocytes, which secrete a protein pigment, or coloring substance, called melanin. 

The relative quantity and type of melanin defines a person’s skin and hair color. In addition, melanin acts as a natural sunscreen that protects keratinocytes from excessive exposure to ultraviolet light from the sun. 

However, a little exposure is necessary daily because ultraviolet rays stimulate keratinocytes to synthesize vitamin D, which is needed for calcium absorption. 

Okay, so as keratinocytes mature, they migrate up into the next layer, which also contains immune cells, called Langerhans cells, that lurk around, constantly looking for invading microbes. Finally, as new keratinocytes push up, older, dead cells are sloughed off, forming skin flakes or dandruff. 

Now, below the epidermis lies the dermis, which is made up of elastic connective tissue that gives flexibility to the skin. The dermis lies abo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_safety:_Following_workplace_policies_and_procedures</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BHeCMRZjRjmhP-mgQSICiqJrT9ORxq2Q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace safety: Following workplace policies and procedures]]></video:title><video:description><![CDATA[As a nursing assistant, you will follow workplace policies and procedures to guide you as you provide care to your clients. Alright, before any procedure, you need to be prepared. 

Let’s say that a procedure such as dressing a wound needs to be performed. The first pre-procedure step is washing your hands properly and putting on gloves, especially if there is a possibility of contact with body fluids, such as blood. 

This helps prevent the transmission of infections between you and the clients. The next step is gathering all the materials that you are going to need, which will help save time and promote efficiency. 

After you’ve gathered everything you need and are ready for the procedure, knock on the client’s door, greet the client, and introduce yourself as you enter.

Then, follow your facility&amp;#39;s policy to confirm the client’s identity to make sure the procedure is performed on the right client. Use at least 2 identifiers. 

For example, check their wrist band and ask the client to state their name and date of birth. Never use the client’s room number or bed number to identify a client. 

Next, explain the procedure by telling the client what to expect and encourage their cooperation. If visitors are present, ask them to leave the room and show them a place for them to wait until the procedure is complete. 

Then, close the curtain and doors. Depending on the procedure, make sure you take all necessary safety precautions regarding body mechanics, infection control, and equipment use. 

For example, if you’re going to perform a procedure with the client in bed, raise the bed to a comfortable height to work with as a part of good body mechanics. 

If the procedure requires the client to be out of the bed, lower the bed to its lowest position to minimize the potential damage from falling as you assist the client to step to the floor. 

Before performing the procedure, expose the area of the body where the procedure is going to be carried out a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Female_reproductive_system:_Structure_and_function</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H37e7r01SQO5orP_2InNMrh2T4S2QVO6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Female reproductive system: Structure and function]]></video:title><video:description><![CDATA[The female reproductive system consists of internal sex organs, which include the ovaries, the fallopian tubes, the uterus, and the vagina; and external sex organs, such as the mons pubis, the labia, and the clitoris. 

The ovaries are a pair of white-ish organs about the size of walnuts. They’re located slightly above and on either side of the uterus. 

On the ovarian cross-section, we can see an outer layer, with ovarian follicles scattered throughout it, and an inner layer, where most of the blood vessels and nerves are. 

At birth, there are about two million primordial follicles, which are future ovarian eggs, also called ova. 

Once the egg has matured, it is released from ovaries into the first part of the fallopian tube: the fimbriae. Fimbriae are the finger-like projections that guide the egg into the Fallopian tube. 

The egg then travels to the uterus. The uterus, also known as the womb, is a hollow organ that has several parts and looks like an upside down pear. 

The top of the uterus above the openings of the fallopian tubes is called the fundus, and the region below the openings is called the uterine body. 

The uterus tapers down into the uterine isthmus and finally the cervix, which protrudes into the vagina. 

The wall of the uterus is made up of strong muscles that stretch to accommodate a growing baby and contract during labor and childbirth. 

The uterus is lined with a soft inner layer, called endometrium, that undergoes changes during menstrual cycles. 

Next up is the vagina, which is an approximately 3 inch long muscular canal that extends from the cervix to the vulva. 

During sexual intercourse, the vagina receives the penis, but during birth, it also serves as the birth canal. 

Finally, the vagina has a mucous membrane lining that lubricates the cavity during sexual intercourse and protects the body from infection.

Now, switching gears and moving on to the external sex organs, together referred to as the vulva. The vulva consi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_terminally_ill_clients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DNpCZqogSrGZNcvJ_FAGoLlaQnS-o7kn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for terminally ill clients]]></video:title><video:description><![CDATA[As a nursing assistant, you will be caring for clients that have a terminal illness. It’s important to learn about these diseases and how you can provide the best care for these clients. A terminal illness is a disease for which there’s no cure. 

Common examples include various types of cancers; heart diseases; respiratory problems; kidney disorders; and liver diseases; as well as chronic infections, such as acquired immunodeficiency syndrome, or AIDS, which is caused by the HIV virus. 

Although there’s no definitive treatment for terminal diseases, it’s important to ensure that these clients will receive palliative care, which focuses on alleviating the client’s symptoms in order to make them feel as comfortable as possible. 

The goal of palliative care is to improve the client’s quality of life and it can be provided in healthcare centers, such as hospitals and long-term care facilities, but also at home. 

The most common examples of palliative care are medications to relieve pain and oxygen therapy for clients with difficulty breathing. 

Surgical procedures, chemotherapy, and radiation therapy that will not cure the disease but will reduce the client’s symptoms are also forms of palliative care. 

Clients with a terminal illness that have approximately six months left to live can also receive hospice care. Hospice care focuses on the client’s physical, emotional, and spiritual needs. 

Similarly to palliative care, the goal of hospice care is to improve the quality of life and ensure that the client will live and die with dignity. 

Hospice care is provided by a team of doctors, nurses, nursing assistants, and social workers. It is available in hospitals and long-term care facilities, as well as at home. 

The team also provides support for the family, even after the client’s death. When caring for a terminally ill client, it’s important to be familiar with some terms. 

First, a will is a legal document that states the person’s wishes regardi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19:_Ask_Me_Anything_Open_Forum_July_20,_2020</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OwOWeBQyRqGou2F-phKvZUbDTj6NQwt_/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19: Ask Me Anything Open Forum July 20, 2020]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of COVID-19: Ask Me Anything Open Forum July 20, 2020 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Dan_Weberg:_Head_of_Clinical_Innovation_at_Trusted_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Dp65JSnySy_MKiei7BzGTywsRnuDYSyF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Dan Weberg: Head of Clinical Innovation at Trusted Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Dan Weberg: Head of Clinical Innovation at Trusted Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Brad_Spellberg:_Chief_Medical_Officer,_LA_County_and_USC_Medical_Center_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/czvac-41QU62rHtT3bIO4ibbQsWuI3qJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Brad Spellberg: Chief Medical Officer, LA County and USC Medical Center (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Brad Spellberg: Chief Medical Officer, LA County and USC Medical Center (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Khanderia:_Director,_Echocardiography_Lab,_Aurora_St_Luke_Medical_Center_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cdu_t-sSQOuIpUDI9MU_oEiiRB2UO1JJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Khanderia: Director, Echocardiography Lab, Aurora St Luke Medical Center (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Khanderia: Director, Echocardiography Lab, Aurora St Luke Medical Center (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Vu_Tran:_Co-founder_and_Head_of_Growth_at_Go1_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/54OXeB0_SMmBAsJb57YqbCXsTCGPfRqH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Vu Tran: Co-founder and Head of Growth at Go1 (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Vu Tran: Co-founder and Head of Growth at Go1 (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Overcoming_Test_Anxiety</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qPYpFQhgQqSa5MRJ_idEkv8dRAKVd14X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Overcoming Test Anxiety]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Overcoming Test Anxiety through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Empirical_formulas</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N_76IoA7SaWmLGig_F_lmiT_TaKBnFF6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Empirical formulas]]></video:title><video:description><![CDATA[An empirical formula is a chemical formula that gives the smallest whole number ratio of atoms in a compound. 

As an example, let’s take the molecule ethene, which has two carbons and four hydrogens, so the molecular formula is C2H4. 

But notice that both subscripts are divisible by two. 

So to figure out the empirical formula for ethene, we have to find the smallest whole-number ratio that describes the relative number of different atoms. 

So we divide both the two and the four by two, to get the empirical formula CH2. If we want to get the molecular formula from the empirica

l formula, we need to do the opposite of this: we would multiply all of the subscripts by two. 

This is because, for ethene, the empirical formula is different than the molecular formula. 

For an unknown compound, we would need to determine the common factor of the subscripts (two in the case of ethene) using an experimental technique such as mass spectrometry.

Sometimes the empirical formula and the molecular formula are the same. 

A common example is water, which is H2O. 

That means that there are two hydrogens for every one oxygen. 

Now, let’s suppose we have a mystery compound that is 84.1% carbon and 15.9% hydrogen and we want to figure out the empirical formula for our mystery compound.

A useful trick is to assume that we start with exactly 100 grams of the mystery compound. 

That means we have 84.1 grams of carbon and 15.9 grams of hydrogen. 

Our first step is to convert the masses into moles.  

We can look up the molar mass for carbon and hydrogen on the Periodic Table. 

The molar mass of carbon is 12.0 grams per mole and the molar mass of hydrogen is 1.01 grams per mole.

We take 84.1 grams of carbon and divide it by 12.0 grams per mole. 

The grams cancel out of the division, and after we divide the numbers we are left with around 7 moles of carbon. 

We next take 15.9 grams of hydrogen, and divide this number by by 1.01 grams per mole. 

This tells us that ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dara_Warn:_Chief_Customer_Officer_at_Penn_Foster_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qTLS93-rSOeZ6fMIJ4D_I06RRtesN-QX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dara Warn: Chief Customer Officer at Penn Foster (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dara Warn: Chief Customer Officer at Penn Foster (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brandon_Perthuis:_Chief_Commercial_Officer_of_Fulgent_Genetics_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/onCNO9YQR4aoRpn173vwD4wHQle6-ghi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brandon Perthuis: Chief Commercial Officer of Fulgent Genetics (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Brandon Perthuis: Chief Commercial Officer of Fulgent Genetics (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dan_Rosensweig:_President_and_CEO_of_Chegg.com_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OulMkH_GR7WdgsvHh9NtyKdRRoWQ6SzR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dan Rosensweig: President and CEO of Chegg.com (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dan Rosensweig: President and CEO of Chegg.com (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Things_I_wish_I_knew_when_I_started_Med_School</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qn-vD1olQi_oKsXXtOjiwxcdQ-ODMva0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Things I wish I knew when I started Med School]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Things I wish I knew when I started Med School through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coxsackievirus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cGy6sbspSdC6IILF72uqleOrQou7ci66/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coxsackievirus]]></video:title><video:description><![CDATA[Coxsackievirus, sometimes referred to as Coxsackie’s virus is part of the enterovirus genus of the picornavirus family, named after Coxsackie village in New York, the place where it was first isolated. 

Coxsackievirus is surrounded by an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. Nonetheless, it’s a naked virus because the capsid isn’t covered by a lipid membrane. 

It’s also a positive sense single strand virus. This means that its RNA is actually mRNA – and the host cell ribosomes use this mRNA to make one long polyprotein chain, which is then broken into smaller pieces by viral proteases. This all happens in the cytoplasm of the host cell, since that’s where ribosomes are found, and results in several viral proteins. 

Coxsackievirus is primarily transmitted from person to person via the fecal-oral route. In other words, you catch it by ingesting stool particles of someone who is sick… yuck. This can happen if infected stool ends up in the water supply or on agricultural fields, if flies land on it, and transfer stool particles to other places, or by touching contaminated surfaces. You can summarize it as the four Fs: fluid, fields, flies, and fingers. As a result, coxsackievirus can end up in food and drinking water. It can also be spread by respiratory droplets when someone sneezes or coughs. 

After it enters the body, the virus first replicates in cells of the pharynx and the terminal ileum. From there, the virus enters blood vessels and travels to lymphatic tissue throughout the body. This initial viral presence in the blood is called minor viremia because it’s a relatively small amount of virus.   

Alright, Coxsackievirus counts over two dozens serotypes, but they can be grouped in only two groups; A and B based on their pathophysiology. Starting with Group A, it most commonly affects children under five years, and it generally prefers infecting the skin and mucous membranes. The most known]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Light_microscopy_and_staining_methods</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I4M37nQ3R_GGUZhfHHvgSM_-SmeS30Gb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Light microscopy and staining methods]]></video:title><video:description><![CDATA[Histology is the study of tissues and organs using microscopy. 

Similar to the phrase “form follows function”, the structures of human tissues are closely related to their functions. 

By integrating histology with other disciplines, such as biochemistry, cell biology, and physiology, we can gain a much better understanding of how the body functions. 

While there are many types of microscopy, light microscopy or LM is the most common, largely because of how practical it is in both the clinical setting, as well as in research. 

Other types of microscopy include scanning probe, ultraviolet, virtual, and electron microscopy or EM. 

Light microscopy can be further subdivided based on the specific technique that’s used, such as bright field, immunofluorescence, and dark field microscopy. 

We’ll be focusing primarily on bright field microscopy and some of the various staining methods that go along with it.

Bright field microscopy is not only the simplest type of light microscopy but also the type that most people are familiar with, utilizing ordinary light to examine stained tissue at high magnification. 

In order to visualize the tissue, it needs to be properly prepared first. 

The most common method of tissue preparation has three main steps. 

First is to fix, or preserve the tissue using formalin. 

The next step is tissue processing, which is the step that removes water from the tissue. 

This is done by using ethanol, which replaces the water in all the cells, and  xylene, which removes ethanol by dissolving it, making it easier to embed the tissue in paraffin. 

Embedding the tissue in paraffin wax is the third step, which removes xylene from the tissue and also solidifies into a “paraffin block” that makes it easier to section, or cut the tissue into very thin slices. 

This is done using a machine called a microtome, which most labs use to cut the paraffin block into slices 4 μm in thickness. 

Next, the paraffin slice is mounted ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophagus_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qOP4K6NAT6qmO0ohu-6LsRM8QU6_0Yhr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophagus histology]]></video:title><video:description><![CDATA[The gastrointestinal or GI tract extends as a single tube from the esophagus all the way to the distal portion of the anal canal.

Although different parts of the tract may appear to have very different structures and functions, the wall still maintains 4 main layers all throughout the GI tract: the mucosa, submucosa, muscularis propria, and either an outer serosa or adventitia.

Even in this low power cross-section of the esophagus, we can see the inner mucosa, submucosa, and muscularis propria, although the outer adventitia isn’t present in this image.

All 4 layers have variations to their structure and function in different regions of the GI tract, but the mucosa is the layer that typically has the most significant changes.

The mucosa of the esophagus consists of 3 main layers.

At 20x magnification, we can see each of the layers more clearly.

The epithelium, lamina propria, and muscularis mucosa.

The thick epithelial layer lines the lumen of the esophagus and consists of stratified squamous non-keratinized cells, which has their typical appearance of flat, overlapping cells that are more flat as they move away from the base or basal cell layer.

The lamina propria is a much thinner layer of dense irregular connective tissue.

It provides a supporting function to the epithelium, such as the blood vessels within the connective tissue that supply blood to the epithelium.

The muscularis mucosa is the outermost layer of the mucosa and is comprised of smooth muscle.

The muscle fibers in this image have a circular or dot-like appearance because the fibers run longitudinally or in the same direction as the esophagus.

The lower esophageal sphincter or LES for short is actually not an anatomical sphincter, which means histologically, there is no well-defined thickening or muscle that controls the LES.

Instead, the LES is considered a physiological or functional sphincter.

But when this sphincter isn’t functioning properly, it can lead to gastric acid re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Electrolyte_disturbances:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mc_gjtUbQCi80dtQLqe3F3DhR1OCkg5o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Electrolyte disturbances: Pathology review]]></video:title><video:description><![CDATA[Two people came to the Emergency Department during your shift.  One of them is 75-year-old Karen who has palpitations and muscle weakness. Karen also has heart failure and one of the medications she’s currently on is digitalis. The other one is 25-year-old Carmen who has tetany. On the clinical examination, Carmen has a positive Chvostek sign. In both these individuals, an ECG was done and levels of electrolytes were taken. Karen’s ECG showed a wide QRS complex with peaked T waves and high levels of potassium, while Carmen’s ECG showed prolonged QT and low levels of calcium. 

Okay, now let’s start talking about electrolytes and what happens when their levels are either too high or too low. 

Let’s begin with potassium, which is a cation that’s mostly in the intracellular fluid, or ICF for short. It’s essential for the normal functioning of excitable tissues, such as nerves and muscles, including the cardiac muscle, and also maintains the resting membrane potential.

So, with hyperkalemia, there’s too much potassium in the extracellular fluid or ECF. And in order for there to be hyperkalemia, there are two possibilities. The first is an external balance shift, like when there’s decreased potassium excretion by the kidneys, leading to increased serum potassium. There’s also internal balance shift where potassium moves out of cells, and into the interstitium and blood. One potential cause is hyperosmolarity. Osmolarity reflects the number of solute particles per liter of solvent, and normally, the osmolarity of the ICF equals the osmolarity of the ECF, even though the exact composition of solutes differs. So when there’s hyperosmolarity, this means that there’s something in the ECF that creates an osmotic force capable of dragging water from inside the cells, like glucose, for example. As water leaves the cells, the intracellular potassium concentration increases and this creates a driving force for potassium to leave the cell, leading to a rise in extracell]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_titrations</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GcpXIsDES8iByra_Rl-owXMISNWB2o3e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to titrations]]></video:title><video:description><![CDATA[A titration is a procedure used by chemists to determine the concentration of a particular solute in a solution. 

To understand how titrations work, let’s do an example. 

Let&amp;#39;s say we are given an aqueous solution of hydrochloric acid. 

We do not know the concentration of the solution, but we do know its volume, which is 20 milliliters.

To perform a titration, we need a piece of equipment called a burette. Into this burette, we add a 0.100 molar solution of aqueous sodium hydroxide.  

Since we know the concentration of our sodium hydroxide solution, we call it our “known” solution.   

The known solution is also called  the “titrant.”  

Since we don&amp;#39;t know the concentration of our HCl solution, we call it our “unknown” solution. 

To do a titration, we are going to add the known solution to the unknown. 

Before we start doing this, we need to carefully record the initial volume of the solution in our burette. 

The numerical value of the initial volume does not matter, it just matters that we know the exact starting point so that we can compare it to our ending volume later. 

We also need to add into the hydrochloric acid solution a few drops of phenolphthalein, which is an acid base indicator. 

Phenolphthalein is colorless when it is in an acidic environment. 

But in a basic environment, the indicator will turn the solution pink.  

Next, we open up the stopcock on the burette and allow the sodium hydroxide to gradually drip into the hydrochloric acid solution. 

As the sodium hydroxide is added, the aqueous solution of sodium hydroxide reacts with the aqueous solution of hydrochloric acid in an acid-base neutralization reaction to form an aqueous solution of sodium chloride and water.  

The net ionic equation leaves out all of the ions that don&amp;#39;t participate in the reaction. 

Remember that those ions are called are spectator ions. 

Since sodium ions and chloride ions are present in solution both before and aft]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Valvular_heart_disease:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PeyIgmDqT-Wff7B-Yp8LR1KHRC_9vWaF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Valvular heart disease: Pathology review]]></video:title><video:description><![CDATA[On the Cardiology ward, there are two individuals. One of them is 75 year old Antonia, who’s complaining of chest pain and says she hardly catches her breath after walking. On clinical examination, her pulse feels pretty weak and on auscultation, a systolic murmur is heard. The murmur was louder just after S1 and got quieter and quieter by the end of S2.

The other individual is 38 year old Mark who has a history of rheumatic fever and is complaining of not being able to swallow properly. On clinical examination, his voice sounds raspy and on auscultation, a snap is heard after S2 along with a diastolic rumble. Based on auscultation, both individuals were sent for echocardiography.

Okay, so based on auscultation and symptoms, both individuals seem to have valvular heart disease. Valvular heart disease involves damage or a defect in one or more of the four valves of the heart, so the aortic and mitral valves on the left side of the heart, and the pulmonary and tricuspid valves on the right side of the heart. 

Okay, now, before talking specifics about valvular disease, we’ll first talk about rheumatic fever, which can affect multiple valves. Rheumatic fever can develop after streptococcal infection like strep throat, which is caused by Streptococcus pyogenes. This particular group of streptococcus has an antigen that lumps it into a group called “group A”, and they also produce an enzyme called streptolysin, which causes hemolysis. Some of these strep bacteria have a protein on their cell wall called “M protein”, and this particular protein is highly antigenic, meaning that the immune system sees it and recognizes it as a foreign molecule and produces antibodies against it. 

Now, this becomes a problem when these antigens cause a phenomenon called molecular mimicry. M proteins can be structurally similar to human proteins, which means the antibodies that target them will also target our own tissue. In this case, they are similar to proteins found in the m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dementia:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q3PWChS7QSyozW1MZ3O9aauCQomOId8X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dementia: Pathology review]]></video:title><video:description><![CDATA[At the neurology department, a 60 year old male, named Oliver, is brought in by his son because lately Oliver has become more aggressive, impolite and he seems to have lost his interest in his family. Recently, he has also started repeating conversations. Next, there’s a 72 year old female, named Iris, who is also brought by her son. Iris is always staying at home because she is embarrassed that she’s unable to hold her urine. She also has a hard time finding her things at home because she forgets where she has placed them. Her son has noticed that she is walking strangely, as if her feet stick to the ground. Finally, there’s a 35-year old male, named Alasdair, who is brought by his partner because in the past few weeks he has started repeating conversations and misplacing their belongings. Alasdair also has episodes of jerking movements of his left arm and he has fallen twice in the last few days. His medical history reveals corneal transplantation 6 months ago. 

Okay, so all of these people have dementia. Dementia occurs when there’s a decline in at least one cognitive function and it impairs daily functioning.  Remember that they need to have intact consciousness. Dementia can result from reversible and irreversible causes. Reversible causes include alcohol dependence, hypothyroidism, vitamin B12 deficiency, neurosyphilis, normal pressure hydrocephalus, or NPH, and depression. Irreversible causes include Alzheimer disease, which is by far the most common cause of dementia, vascular dementia, which is the second most common cause, frontotemporal dementia, Lewy body dementia, Parkinson disease, Huntington disease, and Creutzfeldt-Jakob disease, or CJD. 

Okay, so let’s take a closer look at the irreversible causes of dementia, starting with Alzheimer disease, which is a very high yield topic for the exams! In the cell membrane of a neuron, there’s a molecule called amyloid precursor protein, or APP. Normally, old APP gets chopped up by two enzy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Precipitation_reactions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V1P5AuRVTcC5cbTgOpG0JS1NSXi81OQD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Precipitation reactions]]></video:title><video:description><![CDATA[Precipitation is when a chemical reaction occurs between two solutions, and the reaction produces a product that is a solid. 

Let’s look at an example of a precipitation reaction. 

Let’s say we have a beaker with a solution of lead nitrate, and we have another beaker containing a solution of potassium iodide. 

If we pour the potassium iodide solution into the beaker containing the lead nitrate, we observe a cloud of yellow solid appearing in the beaker. 

That yellow solid is our product, which is the precipitate of the reaction. 

We would say that the solid “precipitates out” when it falls to the bottom of the beaker.

Let&amp;#39;s write out the equation for this precipitation reaction. 

One beaker contains an aqueous solution of Lead (II) nitrate, which has the chemical formula Pb(NO3)2. 

The other beaker contains an aqueous solution of potassium iodide, which has the chemical formula KI.

To predict the products of this reaction, we need to know what ions were in solution. 

We can find the ions using the technique of “crossing over” charges. 

Taking lead nitrate, we look at the subscripts in its chemical formula, Pb(NO3)2. 

The subscript on lead is implied to be one, while the subscript on nitrate is 2. 

We “cross over” these subscripts, and say that our solution contains lead 2+ cations, and nitrate “minus” anions. 

We can write these out as 

Pb2+

NO3-

We can now do the same thing for potassium iodide. 

Since that has the formula KI, we know that our solution has potassium “one plus” cations and iodide “one minus” anions. 

We can write these out as well

K+
I-

Now that we know the four ions in our solution, we can figure out the products of the reaction. 

To do this, we take the cation from one reactant, and combine it with the anion from the other reactant. 

Let’s start with our potassium cations. 

These have a charge of plus one, and so we can combine them with the anion from the other reactant which is a nitrate ion. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Making_buffer_solutions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vIYaX8pST_2FRQCjV-dEewntRJ_zNGf4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Making buffer solutions]]></video:title><video:description><![CDATA[Buffer solutions contain relatively high concentrations of a weak acid and its conjugate base.  

When small amounts of acid or base are added to the solution, buffers react with the added acid or base and resist large changes in pH.   

Many biochemical reactions require specific buffers to work properly.  

Therefore, making buffer solutions is an important laboratory skill in biochemistry.

For a brief review of how buffers work, let’s look at a generic buffer that consists of a weak acid, HA, and its conjugate base, A minus. 

If an acid, H plus, is added to the buffer solution, the conjugate base A minus will react with it. 

We can write the balanced equation for this acid-base neutralization reaction as A minus plus H plus gives HA.  

If a base, OH minus, is added to the buffer solution, the weak acid HA will react with it.  

We can write the balanced equation for this acid-base neutralization reaction as OH minus plus HA gives H2O plus A minus. 

Therefore, a buffer resists changes in pH because it contains both an acid, HA, to neutralize added OH minus ions and a base, A minus, to neutralize added H plus ions.  

There are two ways to make a buffer solution. 

The first way to make a buffer solution starts with an aqueous solution of a weak acid, HA.  

Since weak acids have a low percent ionization, in aqueous solution, most of the weak acid will stay as HA, and only a small percentage of HA will turn into A minus.  

So, to represent an aqueous solution of a weak acid HA, in our particulate diagram, we start out with four HA molecules, and zero A minus anions.  

Water molecules are left out of the particulate diagram for clarity.  

Next, we add a solid salt, NaA. 

When NaA dissolves in water, NaA turns into the Na plus ion and the A minus anion.  

So if we add four particles of NaA to the aqueous solution of HA, they will dissociate and form four Na plus ions and four A minus anions.   

Buffers work the best when the concentrations of the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Limiting_reactants_and_percent_yield</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rUihUrhUTK6OZHj802QIZuqbQbGzmFvK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Limiting reactants and percent yield]]></video:title><video:description><![CDATA[Limiting reactants limit the amount of products a chemical reaction can produce. 

Let&amp;#39;s use a simple example. 

Let’s say we have 10 people and 5 chairs. 

If only one person can sit in a chair, then only five people can sit down at a time while five others stand. 

We can write this as a chemical equation:

1 Person + 1 Chair —&amp;gt; 1 Sitting Person

So because it takes one person, and one chair, to produce one sitting person, then we know that with 5 chairs and 10 people we are limited to producing at most 5 sitting people. 

So the number of chairs is the limiting reactant, or limiting reagent, in our example. 

But sometimes figuring out the limiting reactant is not very intuitive. 

And so we will use the chair example to learn how to find the limiting reactant more systematically, by using mole ratios. 

If we want to analyze this problem using mole ratios, we start by looking at the coefficients in the balanced chemical equation. 

In the equation, the coefficients of “Person” and “Chair” are both one---so the mole ratio between the reactants is one-to-one:

Person/Chair = 1/1

Now that we have the mole ratio between the reactants, we pick either one of the numbers that we are given in our problem---we can pick either 5 chairs, or we can pick 10 people, it does not matter. 

Here, suppose we pick 10 people. 

We write this number into our mole ratio equation, and then put an “x” in place of the number of chairs

Person/Chair = 1/1 = 10/x

If we solved the equation, we would find that “x” is equal to “10” 

This represents how many chairs would be needed to have a perfectly balanced reaction with 10 people. 

So, since we know from our problem that we only have 5 chairs, we now know that chairs must be our limiting reactant---we have fewer chairs than we need to react with every person.

Let’s say that instead of picking 10 people as our first number, we instead picked 5 chairs. 

In this case, we would write out the mole ratio wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mole_Conversions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/65hs9a7WQvC9PCiSU17mJr3ASreSFOAV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mole Conversions]]></video:title><video:description><![CDATA[Moles are a counting unit that make it easier for chemists to work with large numbers.  

Just as we say that one dozen eggs is equal to twelve eggs, we can say that one mole of atoms is equal to 6.02 times ten to the 23rd atoms.  

6.02 times ten to the 23rd is called Avogadro’s number.  

An essential skill in chemistry is being able to convert between mass, moles, and number of atoms.  

Suppose we start with two moles of helium, and we want to figure out how many grams of helium we have. 

To convert between grams and moles, we need to use the molar mass.  

The molar mass is the mass of one mole of an element and is found on the periodic table.  

If we look this number up for helium, we find that helium has a molar mass of 4.0 grams per mole. 

So one mole of helium has a mass of 4.0 grams. 

We can use the molar mass as a conversion factor.  

Two moles of helium times four grams of helium per mole of helium is equal to eight grams of helium.  

Notice how “moles of helium” cancels out.  

Let’s consider a related problem, in which we are given 8.0 grams of helium and we want to calculate the number of moles of helium. 

For this problem, we want to divide by the molar mass.  

So 8.0 grams of helium divided by 4.0 grams per mole gives us 2.0 moles of helium.  

Notice how the grams cancel out to give us moles as our unit.  

We can also do this problem by multiplying by one over the molar mass which gives us 8.0 grams of helium times one mole of helium per 4.0 grams of helium. 

Once again, grams cancel out to give moles.  

So the answer is 2.0 moles of helium.  

So to recap, to convert moles to grams, we multiplied by the molar mass. 

To convert grams to moles, we divided by the molar mass. 

Here’s a table to help us keep track of  how to do the different conversions.  

We can also use the number of moles to calculate the number of atoms that are present.  

For example, let&amp;#39;s say we have 0.500 moles of silver, and we want to know ho]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis_B_and_Hepatitis_D_virus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9mEvrUeVQ8ShInwXVT8d1wG5T9eQ-Ewg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis B and Hepatitis D virus]]></video:title><video:description><![CDATA[Hepatitis B virus, or Hep B virus for short, is a member of the hepadnavirus family; hepatitis D virus, or Hep D virus, is a deltavirus. They both cause hepatitis, or inflammation of the liver. Even though they both cause hepatitis, hepatitis D virus cannot cause the disease by itself, and needs hepatitis B virus to replicate.  

Both hep B and D viruses are enveloped, so they’re surrounded by a membrane. To make things interesting, the membrane of both viruses contains hepatitis B viral proteins - specifically, they both have a surface antigen called HBs. Beneath the membrane there is a protein shell called a capsid, which has more antigens. HB core, or HBc, is in the capsid of hepatitis B. There is also an HB envelope or HBe antigen for short, which is a variant of HBc but it’s not really part of the virus. It’s secreted, and can be found in infected individuals&amp;#39; serum. Delta antigen or HDAg for short is in the capsid of hepatitis D virus. 

Inside the capsid, there’s the viral genetic material. Now, hep B is a DNA virus, which means that its capsid contains partial double-stranded circular DNA, which is made of a long and short strand, so there is a part where the long strand is single stranded. And it also has DNA polymerase, which is an enzyme with DNA- and RNA-dependent activity, meaning it can convert DNA to RNA and vice versa. On the other hand, hep D is an RNA virus, so its capsid contains single-stranded circular RNA in a rod-like folded structure, which is why host cell enzymes can use it as double-stranded DNA.

The main source of hepatitis B virus is blood, but it can also be found in other bodily fluids like milk, amniotic fluid, vaginal secretions and semen. So, routes of transmission include: sexual contact; contaminated blood, either following transfusions or injections with contaminated needles, the latter being more common in people who use intravenous drugs. The virus can also be passed from an inf]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Donning_and_doffing_personal_protective_equipment_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Io-vEyVPRfOXuXrsRjyip0WvS0K5-HPd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Donning and doffing personal protective equipment (for nursing assistant training)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Donning and doffing personal protective equipment (for nursing assistant training) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Documentation_and_reporting</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OR7sNQWaTQCqvFVF7xLGp7XoSh_FTaKc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Documentation and reporting]]></video:title><video:description><![CDATA[As a nursing assistant, you represent a connection between your clients and other healthcare professionals. So, a major part of your job is to report and document, or record, all the relevant information that’s related to the clients under your care. 

Now, for this, you need to make observations, which are defined as something you notice about your client, especially any changes in the client’s physical or mental condition. There are two types of observations: objective and subjective. 

Objective observations are typically detected with your senses. For example, you can see a skin rash; you can hear a client’s noisy breathing or coughing; you can smell unpleasant odors; and finally, you can touch a client&amp;#39;s skin and feel if it’s cold, warm, wet, or dry. 

In addition, objective observations can also be measured. For example, you can measure the client’s vital signs, such as body temperature, blood pressure, and pulse. Objective observations provide objective data called signs. 

On the other hand, subjective observations cannot be directly detected or measured. Instead, they include any information reported to you by clients, such as discomfort, dizziness, or weakness. 

As an example, a client may complain about nausea or bloating. You can’t see, hear, smell, feel, or measure their discomfort, but the client can describe it to you. Subjective observations provide subjective data, which are called symptoms.

Now, switching gears and moving on to communication among healthcare team members. The most common way of communication is reporting. 

This is a verbal form of communication  about the client’s condition. As a nursing assistant, there are several things that you should always report to the nurse. 

The first thing to keep in mind are observations that suggest changes in the client’s condition as well as observations concerning the client’s response to a new procedure or therapy. 

Next, make sure you report when a client complains]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Client_rights</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iop6NPghQreXQ7mF9xhKiOsdRdG_R4W2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Client rights]]></video:title><video:description><![CDATA[As a nursing assistant, caring for clients requires knowing and respecting client rights. The rights of clients in hospitals are outlined by the American Hospital Association, or AHA, Patient Care Partnerships, while those of clients in long-term care facilities, such as nursing homes, are outlined under the Omnibus Budget Reconciliation Act, or OBRA for short, which is a federal law enforced by the Centers for Medicare and Medicaid.

Alright, both AHA and OBRA outline rights of clients who are being cared for in healthcare facilities, and these facilities must inform clients about their rights in a way that they can understand. 

This means that written translations or interpreters must be available if needed. Large print should be available for clients with vision impairment. 

Clients also have the right to know the identities of those who are caring for them and to receive compassionate, respectful, quality care in a safe and clean environment that supports quality of life. 

The right of clients to participate in activities and form client groups promotes quality of life. The right to keep personal items in their rooms is an important right that promotes comfort and a home-like setting. 

They have the right to choose their own healthcare providers to be involved in the planning of their care, and to have their personal values and spiritual beliefs respected. 

Respect for privacy of their bodies, their personal affairs and private information are also important rights of the clients. Clients have the right to be free from restraints and all forms of abuse, maltreatment, and neglect.  

If a client has a concern about their treatment or care, they have the right to ask questions, voice concerns, and make complaints. And finally, clients must always be free to exercise all basic civil and religious liberties as a United States citizen.

Alright, let’s take a closer look at a client’s right to make personal choices whenever it is safe for them to do so.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integumentary_system:_Skin_lesions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aAE7YJoSRdOwqhlKYAvhZI11Q6SZWrF6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integumentary system: Skin lesions]]></video:title><video:description><![CDATA[Skin lesions can include any abnormal area of the skin, so there are several terms to describe them. Let’s start with macules, which are flat lesions with a clear border up to 1 centimeter in diameter; patches are similar to a macule but are larger than 1 centimeter. 

Papules are raised bumps that are up to 1 centimeter in diameter, while plaques are like papules but larger than 1 centimeter. A smooth papule or plaque that is transient, meaning that it comes and goes, is called a wheal. 

Pustules are blisters filled with pus. Vesicles are clear blisters filled with fluid that are up to 1 centimeter in diameter, while bullae are fluid-filled blisters larger than 1 centimeter. 

Scales are accumulations of thickened skin on the surface, which become dry and flaky and sometimes peel off. Crusts are dry exudates, which is the liquid that leaks out of blood vessels, containing cells, sebum, pus, or blood.	 	

Now, lesions can appear in groups and form a rash, which includes any skin eruption. Rashes that are limited to one area are called localized, while rashes that occur all over the body are called systemic. 

In addition, there are four categories based on how they look: maculopapular, vesicular, petechial or purpuric, and desquamating rashes. As the name suggests, a maculopapular rash has both macules and papules. 

A vesicular rash has vesicles. Petechial and purpuric rashes both have flat red-brown spots that represent bleeding into the skin. If the spots are smaller than 2 mm in diameter, it’s a petechial rash; if the spots are larger than 2 mm, it’s a purpuric rash. 

Finally, there are desquamating rashes, which cause peeling of the skin, like after a sunburn. Now, rashes can have many different causes, and specific care depends on which rash a client has. 

Rashes may be caused by systemic infections in which the skin itself isn’t infected but develops a rash as a sign of an infection occurring somewhere inside the body. 

As an example, clients wi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_system:_Infections_and_stones</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rc8JECHnSOuWIsPNVqa_v8qwQc6idpuE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary system: Infections and stones]]></video:title><video:description><![CDATA[There are many illnesses that can affect the urinary system. Some of the most common ones include urinary tract infections, or UTIs, and kidney stones. Thankfully, both are easily treated but can cause severe complications if they’re not. 

Urinary tract infections can affect any part of the urinary system, like the urethra, the bladder, or the kidneys. They can be broken down into different diseases depending on which part of the urinary tract the infection is. 

Let’s start with urethritis, which is the infection of the urethra. It usually affects biological males because they have a longer and more curved urethra than females. 

The most common causes of urethritis are the same microorganisms that cause sexually transmitted infections, or STIs, such as gonorrhea, herpes, and chlamydia. 

Moving on with cystitis, which is the infection of the bladder. Cystitis usually affects females. That’s because the urethral opening in females is closer to the anus. 

Now, the anus is often contaminated with microorganisms because feces that contain bacteria from the digestive tract exit the body through the anus. 

Moreover, a female’s urethra is short and straight, meaning that once microorganisms have access to the urinary tract, they have a pretty short journey towards the bladder. This is the reason why it’s important to wipe from front to back when giving perineal care for a female. 

Moving on to pyelonephritis, which is the infection of the kidneys. This can happen when a bladder infection isn’t properly treated. 

Over time, the microorganism can multiply in the bladder, move through the ureters, and reach the kidneys. Left untreated, the infection can cause permanent damage to the kidneys. 

Okay, let’s go over some common signs and symptoms of a urinary tract infection. A UTI often causes urinary frequency, painful urination, a sensation of burning when urinating, and cramping. 

Specific symptoms of cystitis include pelvic pain as well as lower abdominal ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Frank_Sculli:_Co-founder_and_CEO_of_BioDigital_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/er3wEN6qS-Ga0Eba8OWt9ahyRgmTQ42D/_.jpg</video:thumbnail_loc><video:title><![CDATA[Frank Sculli: Co-founder and CEO of BioDigital (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Frank Sculli: Co-founder and CEO of BioDigital (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Jason_Bellet:_Co-founder_and_COO_of_Eko_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VOesDO_ZTkqF0VgnXMfMtpyDT1_AqfiE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Jason Bellet: Co-founder and COO of Eko (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Jason Bellet: Co-founder and COO of Eko (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chip_Paucek:_Co-founder_and_CEO_of_2U,_Inc._(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WM4sLIGjQ9CVL-5cDItGLb7ASmCQGBMC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chip Paucek: Co-founder and CEO of 2U, Inc. (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Chip Paucek: Co-founder and CEO of 2U, Inc. (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/CRISPRCas9</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v5rqqcduTO_n0jp2OCDcU3IaQoGodpBL/_.jpg</video:thumbnail_loc><video:title><![CDATA[CRISPRCas9]]></video:title><video:description><![CDATA[Few laboratory techniques have drawn quite as much attention to themselves as CRISPR/Cas9 has. 

And on some level, everybody has heard of what this tool can do: gene editing, or, put simply, tweaking DNA. 

With gene editing, targeted changes are made, like deletions and insertions, right in an organism’s genome. 

Over the past decade, the CRISPR-Cas9 system has become a very popular method of genome editing because it’s fast, cheap, precise, and relatively easy to use. 

Now, on a molecular level, DNA is made up of two strands of nucleotides, so each gene is just a segment of this nucleotide sequence. 

Nucleotides of DNA are made out of a sugar - deoxyribose, a phosphate, and one of the four nucleobases - adenine, cytosine, guanine, and thymine - or, A, C, G, T for short. 

The nucleotides on one strand pair up using hydrogen bonds with nucleotides on the opposing strand, to create the double-stranded DNA: specifically, A bonds with T, and C bonds with G, so they’re called complementary bases and form base pairs. 

Now, a single strand of DNA can also form bonds with a single strand of RNA, made out of a sugar - ribose, a phosphate, and one of the four nucleobases - but RNA has uracil, U for short, instead of T. 

So, when complementary sequences in DNA and RNA bond,  A bonds with U. 

In other words, if the DNA has a sequence that reads 5′  -GGCTAT- 3′, then the RNA sequence is exactly the opposite and reads 3′ - CCGAUA -5′.   

Now, occasionally double-stranded breaks in the genome occur. 

And when they do, the cell has two main repair mechanisms to correct the damage. 

The most common type is non-homologous end joining, where a protein complex called DNA protein kinase begins by binding to each end of the broken DNA. 

Then it recruits another protein, called artemis - named after the Greek goddess! - to cut off the single- stranded ends. 

It’s like using a tiny bit of sandpaper to smooth the broken ends of the pencil, so that the pencil can be m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Study_for_Success:_Habits_Every_Nursing_Student_Should_Adopt</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GuyvKUhyRXq3SwIDsm6O_cxaSwuPyyHt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Study for Success: Habits Every Nursing Student Should Adopt]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Study for Success: Habits Every Nursing Student Should Adopt through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aromatic_L-amino_acid_decarboxylase_deficiency_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m3w1GRLfRCCNqPW1QoJ_0Ty2RhWd8_pJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aromatic L-amino acid decarboxylase deficiency (NORD)]]></video:title><video:description><![CDATA[Aromatic L-Amino Acid Decarboxylase deficiency, or simply AADC deficiency, is a very rare disease in which there’s a decreased activity of an enzyme called aromatic l-amino acid decarboxylase, or AADC for short. 

The disease affects babies, which most often seem healthy at birth, but then start developing signs and symptoms during the first months of life. 

The severity of the disease can vary between individuals. 

AADC deficiency mainly causes movement disorders. 

One of the most frequent symptoms is hypotonia of the trunk, which means these individuals have very little muscle tone, making them floppy. 

Another frequent symptom is oculogyric crises, which is the abnormal rotation of the eyeballs with elevation of the gaze, as well as uncontrolled movements of the head and neck, agitation, and irritability. 

Oculogyric crises can last for hours, and typically occur every 2 to 5 days. 

Other less frequent movement disorders include decreased movement called hypokinesia, increased muscle tone of the limbs or hypertonia, and involuntary movements like tremors, twisting movements called dystonia, writhing movements or athetosis, dance-like movements of hands and feet called chorea.

AADC deficiency can also affect the autonomic nervous system, which is the part of the nervous system that controls our internal organs. 

Symptoms can include excessive salivation and sweating, droopy eyelids called ptosis, nasal congestion, unstable body temperature, low blood pressure, and low blood sugar or hypoglycemia. 

In addition, AADC deficiency can cause gastrointestinal symptoms like reflux, diarrhea, or constipation. 

Other less frequent symptoms include seizures, decreased or increased sleep, and decreased or increased reflexes.

Finally, children affected with AADC deficiency often have learning disabilities, developmental delay, and fail to reach milestones like talking or walking. 

In addition, they may present feeding difficulties, leading to decreased gr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_Impress_your_Attendings_in_2020</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ShNtVdsRT7iKIfAqylWyz-Z2T1y8yo_G/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to Impress your Attendings in 2020]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to Impress your Attendings in 2020 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_contractility</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jrJ9aN3TTbWKw9NP20b5xaDSQl_w6k2x/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac contractility]]></video:title><video:description><![CDATA[The main job of the heart is to pump blood all over the body, to our organs and tissues and keep them oxygenated. 

It does so by contracting around 70 times per minute. 

The physiological basis of cardiac contractility is the synchronous contraction of heart muscle cells, aka cardiomyocytes. 

Cardiac contractility is a measure of the strength of cardiomyocytes, to contract. 

In order for cardiomyocytes to contract, they first need to depolarize. 

Depolarization is when ions move across the membrane of a cell, and the membrane potential becomes less negative or even slightly positive. 

Think of a really pessimistic negative cell throwing his hands up and enjoying a moment of joy. 

When one cell depolarizes enough - it can cause some ions like calcium to flow into neighboring cells and trigger them to depolarize as well. 

If one cell after another depolarizes, then there’s a depolarization wave which you can imagine would look like a wave moving through a crowd at a football stadium. 

Each depolarization wave causes a heart muscle contraction, so the rate at which depolarization waves ripple through the heart actually sets the heart rate. 

This depolarization wave starts with the sinoatrial node, which sometimes gets called the SA node and then moves through the rest of the heart to cause a contraction. 

So if depolarization waves are going through about once per second, that means that your heart beats once per second, or sixty times in a minute. 

Now let’s zoom in on a cardiomyocyte. 

These hard working cells have branches and intercalated disks along their edges which have small holes called gap junctions that allow ions to flow from one cardiomyocyte to the next. 

When ions like calcium move from that cell into a neighboring cell, this triggers depolarization, and cardiomyocytes depolarize one after another.

Another feature of cardiomyocytes are passageways called transverse tubules, or T-tubules. 

T-tubules are invaginations or tunnels o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shigella</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1oMzx6S4QTaeS45zG8_fYAWgSBiSymk3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shigella]]></video:title><video:description><![CDATA[Shigella is a Gram-negative bacterium that belongs to the Enterobacteriaceae family. 

There are 4 species of Shigella: 

S. dysenteriae, S. flexneri; S. boydii; and S. sonnei, and each has its own serotypes. 

In humans these species can all cause Shigellosis, which is a contagious infection of the intestines, particularly the colon. 

And shigellosis can progress to dysentery, which is when the infection causes inflammation of the colon, resulting in severe abdominal pain and diarrhea.

Now, Shigella is a gram-negative, rod shaped bacterium, meaning it looks like a little red or pink stick on a gram stain. 

And it’s a facultative anaerobe, so it can survive with or without oxygen in the environment. 

It has no flagellum, making it nonmotile; and it doesn’t form spores. 

It’s also a non-lactose fermenter, so it doesn’t ferment lactose; and it’s urease and oxidase-negative, meaning it doesn’t produce these enzymes. 

Finally, it doesn’t produce hydrogen sulfide gas either, and this can be used to selectively identify Shigella on special culture mediums like MacConkey agar. 

On this medium, Shigella mostly forms white, non-lactose fermenting, non-hydrogen sulfide-producing colonies

Now, once Shigella is ingested, it multiplies in the small intestine, and then passes into the colon. 

There, it targets the epithelial layer of the mucosal lining where it infects colonic enterocytes and microfold cells, or M-cells. 

And these M-cells phagocytose, which means they eat the bacteria from the intestinal lumen, and then spit it out into the underlying mucosa-associated lymphoid tissues, or MALTs. 

MALTs are a type of mucosal immune tissue that extends into the submucosa, and contains plenty of immune cells like macrophages. 

The macrophages gobble up Shigella to neutralize the pathogen, but the bacterium induces apoptosis, or programmed cell death, in the macrophage. 

Now, when a macrophage dies, it releases a variety of cytokines, including IL-1β, which a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Von_Willebrand_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BfybuzqiR7i04O3N6p2SMEYYR9aF1ani/_.jpg</video:thumbnail_loc><video:title><![CDATA[Von Willebrand disease]]></video:title><video:description><![CDATA[Von Willebrand disease, named after Finnish doctor Erik Adolf Von Willebrand, who first described the condition, is a bleeding condition associated with either a low amount or poor quality of von Willebrand factor.  

Imagine you are repotting a cactus and a spine pricks you, damaging the tiny blood vessels in your fingertip. As a result, the body triggers primary hemostasis, which is a well-coordinated process that stops bleeding. This injury exposes the collagen in the blood vessel wall, which is rich in von Willebrand factor, and triggers local endothelial cells to release more von Willebrand factor into circulation.  

Once released, the von Willebrand factor sticks to the damaged area and acts like glue, providing a foundation for platelet attachment. Circulating platelets use their glycoprotein IIb receptors to bind this glue-like substance, triggering their activation. They change shape and extend tentacle-like arms to grab onto nearby platelets. Once activated, they release more Von Willebrand factor, along with serotonin and calcium.  

Platelets also release adenosine diphosphate and thromboxane A2, which together activate other platelets that haven’t bound the Von Willebrand factor. These two substances also spark platelets to express new surface proteins called GPIIB/IIIA. Acting like hooks, these proteins enable platelets to catch fibrinogen, which acts like a pair of handcuffs, linking two platelets together. Eventually, this results in a snowball effect, with more platelets piling up, creating a plug that seals the injury. 

Once the body creates the platelet plug, it triggers secondary hemostasis to reinforce the clot with a strong fibrin mesh. This process involves the extrinsic and intrinsic coagulation pathways, which ultimately converge into the common coagulation pathway. 

In the extrinsic pathway, blood vessel injury exposes factor III, also known as tissue factor, which activates factor VII. Next, activated tissue factor, activ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lymph_node_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CobDz6FeQP6tl12hUqn2yUC1S_qubWVU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lymph node histology]]></video:title><video:description><![CDATA[The lymphatic system is an essential part of the immune system and it consists of a network of lymphatic vessels, tissues, and organs.

The lymphatic vessels drain interstitial fluid or lymph from peripheral tissues back into the blood.

Lymphoid tissue and organs contain a lot of lymphocytes and other white blood cells.

The primary lymphoid organs include the thymus and bone marrow.

And the secondary lymphoid organs include the tonsils, lymph nodes, spleen and mucosa-associated lymphoid tissue or MALT for short.

Lymph nodes are small secondary lymphoid organs that are found along lymphatic vessels throughout the body.

They’re encapsulated, bean-shaped structures that usually have a diameter of about 1 cm along the short axis and 2.5 cm along the long axis.

And they support the immune system by filtering the lymph, in order to identify and fight infections.

If we zoom closer, we can more easily identify the outer capsule of connective tissue, as well as the three functional regions of the lymph node.

Just beneath the capsule is the outer cortex, which contains spherical nodules or follicles of B cells, each with a germinal center, similar to the follicles of the spleen.

The germinal center is where B cells differentiate into plasma cells.

The next region is the inner cortex or paracortex, which doesn’t have any nodules.

And finally, the innermost region of the lymph node is the medulla.

The distinction between the inner cortex and medulla is hard to see at this magnification, but the medulla will have cords of lymphoid tissue, as well as passageways for lymph called medullary sinuses.

These sinuses eventually join one another and drain into the efferent lymphatic vessels.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertriglyceridemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mfW5Ic33SoSmbYMkkqJXZQPdR-WYhaZz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertriglyceridemia]]></video:title><video:description><![CDATA[With Hypertriglyceridemia, hyper means high, -emia refers to blood levels, and triglycerides are the most abundant fatty molecules in an organism. 

So, hypertriglyceridemia is when there’s excess triglycerides in the blood. 

Specifically, hypertriglyceridemia is when there are more than 150 mg of triglycerides per deciliter of blood.  

Triglycerides can be deposited in subcutaneous tissue and around organs and function as energy storage in the body. 

We can either get triglycerides from our diet, which are called exogenous triglycerides; or our liver can synthesize them from other molecules, in which case they’re called endogenous triglycerides.  

Now, exogenous triglycerides are first absorbed in the small intestine, and then they undergo a series of changes in order to be transported and deposited in the body. 

So, after triglycerides are absorbed, they enter the intestinal mucosal cells, inside of which they’re coupled with various apolipoproteins and phospholipids to create chylomicrons, which are one type of lipoprotein. 

Lipoproteins are made up of lipids (like triglycerides or cholesterol) or phospholipids and proteins (like apolipoproteins CII, CIII, or E). 

The main job of lipoproteins is to carry insoluble molecules, like triglycerides, from the intestines to the circulation. 

That&amp;#39;s because, normally, triglycerides are insoluble in liquid environments like blood. 

Now, the newly created chylomicrons enter the bloodstream and bind to the wall of capillaries in adipose and skeletal muscle tissue. 

At the binding site, they interact with the lipoprotein lipase enzyme leading to the breakdown of the triglyceride core and liberation of free fatty acids directly into the adipocytes or skeletal muscle cell, where they’re either stored or used for energy. 

After triglycerides leave the chylomicron, what’s left is called a remnant chylomicron. 

Remnant chylomicrons are high in cholesterol esters and they’re cleared from circulation ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sodium_homeostasis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yPdDtpGLRMS9Q9ZhsDU66MrnTsyr78bC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sodium homeostasis]]></video:title><video:description><![CDATA[Sodium is a positive ion or a cation noted with Na. 

Most of the sodium in our body is located outside the cells, in the extracellular fluid, or ECF for short. 

In the extracellular fluid, sodium has a concentration of about 135 milliequivalents (mEq) per liter. 

And remember that sodium concentration doesn’t necessarily reflect the total amount of sodium in the body, but rather the amount of sodium relative to the amount of water in the body. 

So sodium homeostasis refers to the mechanisms employed by the body to maintain a normal sodium concentration in the extracellular fluid. 

Sodium is essential in maintaining water balance, as well as for nerve impulse conduction and muscle contraction. 

Additionally, sodium is an important determinant of the volume and osmolality of the extracellular fluid, which is made up of plasma and interstitial fluid. 

Now, osmolality refers to the total solute concentration in a certain amount of solvent or water. 

By affecting plasma osmolality, sodium determines plasma and blood volume. 

So, at the end of the day, it’s important to maintain the sodium concentration in order to keep enough blood inside our arteries. 

This blood is called the effective arterial blood volume or EABV, and it’s what ends up perfusing our various organs and tissues.

Okay, now, sodium comes from our diet. 

The daily recommended sodium intake is about 2.3 grams per day which is the equivalent of a teaspoon of salt per day. 

Once ingested, sodium is absorbed in the blood by the GI tract, and travels through the bloodstream unbound to plasma proteins. 

At the other end, some sodium is eliminated from the body through sweat and through feces, but most of it comes out, along with water, as pee. 

So the kidneys are the cornerstone of sodium homeostasis.

See, the kidneys are made up of lots and lots of nephrons, and each nephron is made up of a renal corpuscle and a renal tubule. 

The renal corpuscle, in turn, is made up of the glomerulu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Definitions_of_acids_and_bases</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/njOO3H2gTIKGLdJpXnd4QwCKSIyjg5Sb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Definitions of acids and bases]]></video:title><video:description><![CDATA[Acids and bases are substances that are commonly found in our everyday lives.  

For example, acids give fruits like oranges and lemons a sour taste.  

There are several definitions of acids and bases that are used in chemistry. 

Our first definition of acids and bases is from a chemist named Arrhenius. 

An Arrhenius acid is a substance that increases the concentration of hydrogen ions in solution when it is dissolved in water.  

An example of an Arrhenius acid is hydrogen chloride gas, which has the chemical formula HCl. 

When gaseous HCl dissolves in water, it forms hydrogen ions, 

H plus, and chloride anions, Cl minus in aqueous solution.  

Since dissolving HCl in water increases the concentration of hydrogen ions in solution, HCl is an Arrhenius acid.  

An aqueous solution of HCl is called hydrochloric acid.

An Arrhenius base is a substance that increases the concentration of hydroxide ions when it is dissolved in water. 

The hydroxide ion has the formula OH minus.  

An example of an Arrhenius base is sodium hydroxide, which is a white solid and has the chemical formula NaOH.  

When NaOH dissolves in water, it dissociates into Na plus and OH minus.  

Since dissolving NaOH in water increases the concentration of hydroxide ions in solution, sodium hydroxide is an Arrhenius base.

Our second definition of acids and bases is from two chemists, Bronsted and Lowry.  

A Bronsted-Lowry acid is a “proton donor,” and a Bronsted-Lowry base is a “proton acceptor.”  

Before we look at examples of Bronsted-Lowry acids and bases, we need to understand what is meant by the word “proton.”  

A neutral hydrogen atom has a proton in the nucleus and an electron outside of the nucleus. 

We represent a neutral hydrogen atom with an “H” and a single dot next to the H to represent the one valence electron.

If we take this electron away from our neutral hydrogen atom, we are left with a proton.  

So, in acid-base chemistry, whenever we are talking about ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Restrictive_lung_diseases:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HyH7KzCMSFy5F2mn8ZO8tRrrTU2NXRWt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Restrictive lung diseases: Pathology review]]></video:title><video:description><![CDATA[While on your rounds, you see two individuals. First is Alicia, a 28-year-old African American individual who comes in with progressive shortness of breath and cough. She also mentions that she lost weight in the past six months and that she had tuberculosis a few years ago. Examination reveals painful red skin lesions on each side of her nose and the anterior surface of both legs, along the tibia. The rest of the examination was normal. Next, you see a 65-year-old male named Richard, who presents with gradually progressive dyspnea on exertion and dry cough. He has no history of underlying lung disease or other relevant symptoms. On examination, there is nail clubbing but no other signs that could suggest a particular etiology, like pneumonia or COPD. Pulmonary function tests were performed in both cases, showing signs of a restricted pattern, including a significant reduction in forced vital capacity.

Both seem to have some type of restrictive lung disease. But first, a bit of physiology. The lung is compliant, meaning that it can expand and contract because its connective tissue is made up of  proteins like elastin and collagen. Compliance is defined as the volume change produced by a change in the distending pressure, and is expressed as the ratio of ΔV, the change in volume, to ΔP, which is the change in pressure. In other words, the higher the compliance, the easier it is for the lungs to expand.  In contrast, the lung’s tendency to collapse and push the air back out is called elastic recoil, which is balanced by the outward pull of the chest wall. 

Now, remember that breathing also involves the structures around the lungs, like the ribs, intercostal muscles, diaphragm, or pleura. During inhalation, the diaphragm and intercostal muscles contract to pull the ribs up and out and expand the chest cavity. This creates a vacuum that pulls the lungs open to allow air in, which eventually reaches the alveoli and specifically, a thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testicular_cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eAJFLwVITkqg-6qk4Q_FRp3ZRdCj3hsf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Testicular cancer]]></video:title><video:description><![CDATA[Testicular cancers are malignant tumors that form in one or both testes. They usually present as a mass that’s often detected in the early stages since they are on an organ that’s easily accessible during physical examination. Thus, they typically  have a good prognosis.

The testes are a pair of male reproductive glands the size of small plums, that are located in the scrotum. The testes themselves are covered on the outside by the tunica albuginea, a white, fibrous layer. 

If we slice a testis open and look inside, sorry for the cringe moment, we can see septa that partition each testis into lobules. Each lobule contains up to four seminiferous tubules, where sperm is synthesized.

Now let’s zoom in on a single seminiferous tubule, which is the “sperm factory”. A seminiferous tubule has a thick wall of epithelial cells that surround a fluid-filled lumen, a bit like a garden hose.  

The wall of the tubule is made up of two kinds of cells: at the periphery, there’s the germ cells known as spermatogonia, which are the primordial sperm cells that begin dividing over and over in puberty, and give rise to male gametes. 

Next to them are Sertoli cells which are large cells that extend from the margin all the way to the lumen of the tubule. Sertoli cells are supportive cells that provide nutrients to developing sperm cells, and contribute to the blood-testis barrier by only allowing certain molecules, like testosterone, into the seminiferous tubules. 

Outside the tubule, there’s connective tissue with capillaries, as well as Leydig cells - another supportive cell which produces testosterone, which is a hormone necessary for the proper development of sperm.

During fetal development the entire body derives from three layers called germ layers; the ectoderm, mesoderm and endoderm. 

These germ layers are made of germ cells that migrate out and differentiate into all of the different types of tissues. 

Some very special germ cells stay as germ cells, meaning t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abdominal_hernias</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c_kwFfvXSBWTE637XJB_dxImSFGE76Kh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abdominal hernias]]></video:title><video:description><![CDATA[Abdominal hernias, also called external hernias, are when an abdominal organ, or part of an abdominal organ protrudes through the abdominal wall, usually at a site of weakness. They can be classified into midline hernias and groin hernias. Most frequent types of midline hernias are the epigastric and umbilical hernias, while groin hernias can further be classified into inguinal and femoral hernias. There’s also incisional hernias, which is when contents herniate through an incisional scar from a previous abdominal surgery

Now, the abdominal wall is made up of a few layers. The deepest layer is the visceral peritoneum, which covers many of the abdominal organs and lines the peritoneal space. That layer wraps around to form the parietal peritoneum. Then, moving externally, there is the extraperitoneal fat, the transversalis fascia, the muscle layer with the internal and external oblique and transversus abdominis aponeurosis and a layer of fascia which has different names in different regions. Ok, so anything that increases the pressure of the abdominal cavity may result in a sac that forms in the abdominal wall through which organs might protrude.  

When organs protrude through the midline, that results in a midline hernia. Midline hernias include the epigastric hernia, which is when abdominal organs herniate through the linea alba, or the part of the midline between the xiphoid process and the umbilicus. With umbilical hernias, on the other hand, the organ protrudes through the umbilicus. 

And then there’s groin hernias, which can be classified into inguinal hernias, the more common type, and femoral hernias. 

With inguinal hernias, the contents of the abdominal cavity, usually fat or part of the small intestine, protrude through the inguinal canal.

The inguinal canal lies between the muscles of the anterior abdominal wall. The canal is bound superiorly by the internal oblique and transversus abdominis muscles, anteriorly by the external and internal o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacy_school:_Dosage_calculations</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_-sNTTqcQle8zpE2WzLz6yG3SSuf1V4G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacy school: Dosage calculations]]></video:title><video:description><![CDATA[Dosage calculations are used to figure out the right amount of medicine to give a patient based on that particular patient’s needs. 

Different things can affect a patient’s dosage requirements of a medicine, including age, weight, laboratory values, or it may even depend on the medicine itself.  

Some calculations can be simple, while others require conversions and use of proportions.  

This concept can be a bit intimidating at first, but with a little practice, calculating doses will become second nature.

Let’s start out with some basic examples of calculations that you might encounter.  

Let’s say that we have a 140 kilogram person who needs a specific medication for an infection.  

The dosage for this medication is 6 milligrams per kilogram per dose.  

What dose would this patient require in grams?  

We would start out by taking the person’s weight which is 140 kilograms and multiply it by 6 milligrams per kilogram to get 840 milligrams per dose (Figure 1).  

However, we aren’t quite done.  

To convert milligrams to grams, we know that for every 1 milligram of a product, this is equal to 0.001 grams of the same product.  

Since we know that this patient would need 840 milligrams of the medicine, we can then take 840 milligrams and multiply this number by 0.001, which is the same as dividing by a thousand, to get an answer of 0.84 grams (Figure 2).

Now, there may be times when you or someone else has already selected a dose for a patient, but you need to figure out what that dose is per kilogram of the patient’s weight. 

Let’s say that you receive a prescription for a man who’s starting a medicine to treat a heart condition.  

This medicine comes in a concentration of 40 milligrams per milliliter, and he’s supposed to take 1 milliliter daily.  

If he weighs 70 kilograms, what dose is he getting in milligrams per kilogram?  

We will first want to set up a proportion to figure out how many milligrams he is getting per dose.  

If we set up ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ionic_bonding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7f0q1qiyTYKqhKtyN1MLH06mTLS6lvUu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ionic bonding]]></video:title><video:description><![CDATA[When a metal like sodium reacts with a non-metal like chlorine, they form an ionic bond.  

Sodium has the atomic number 11, meaning that it has 11 protons and 11 electrons. 

Due to details of its atomic structure, a sodium atom tends to lose one of its electrons, causing it to go down to 10 electrons. 

When this happens, the particle will still have 11 protons in its nucleus. 

So 11 protons minus 10 electrons gives us an overall “one plus” charge. 

We refer to charged particles as ions. 

A positively charged ion is called a cation.  Metals tend to lose electrons to form cations. 

Chlorine, on the other hand, is a non-metal. 

Non-metals tend to gain electrons to form negatively charged ions called anions. 

A chlorine atom has an atomic number of 17, so it has 17 protons and 17 electrons. 

When the neutral chlorine atom gains an electron it ends up with 18 electrons, but it still has 17 protons in its nucleus, so overall there’s a net charge of one minus. 

Now we have a positively charged sodium cation, and a negatively charged chloride anion. 

Opposite charges attract, so that creates an ionic bond. 

Compounds that contain ionic bonds are called ionic compounds. 

Now, in sodium chloride, it extends beyond just two ions. 

A chloride ion sits next to a sodium ion, which sits next to another chloride ion, and another sodium ion, and on it goes. 

And this entire crystal structure is held together by electrostatic attractions. 

These tasty little crystals form what we call table salt. 

On the periodic table, elements like sodium appear in the first column on the far left of the table. 

These “group 1A” elements tend to lose one electron and form a “one plus” charged cation. 

In contrast, elements like chlorine are in “group 7A” on the other side of the periodic table. 

These atoms tend to gain one electron and form a “one minus”  charged anion. 

So both group 1A elements like sodium, and group 7A elements like chlorine, try to have the same]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Strong_acid-strong_base_titration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LGYbmUmOSbqqa79P7N04s9sHQHe3xVMF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Strong acid-strong base titration]]></video:title><video:description><![CDATA[Let&amp;#39;s consider the titration of a strong acid, hydrochloric acid, with a strong base, sodium hydroxide. 

Let&amp;#39;s say we have 20.00 mL of a 0.500 molar solution of hydrochloric acid in a flask.  

Into the burette, we place the titrant, which is a 0.500 molar solution of sodium hydroxide. 

Before we start the titration, we need to calculate the initial pH of the hydrochloric acid solution.

Because hydrochloric acid is a strong acid, we assume it ionizes 100% in water which means that all the HCl turns into H plus ions and Cl minus ions. 

Therefore if the concentration of HCl is 0.500, that&amp;#39;s also the concentration of H plus ions and Cl minus ions in solution.  

Since pH is equal to the negative log of the concentration of H plus ion, we take the negative log of 0.500, which gives us a pH equal to 0.301. 

Titrations can be represented by titration curves.  

For this titration, we put volume of sodium hydroxide added on the x axis and pH on the y axis.  

Since we haven’t added any strong base yet, our first point is at 0 milliliters of base on the x axis and a pH of 0.301 on the y axis.  

Titrations can also be represented by particulate diagrams.  

Since we haven&amp;#39;t added any of our base yet, the only ions present are H plus and Cl minus. 

Since the concentrations of H plus ions and Cl minus are equal, the diagram has two particles of each ion.  

Next, we open the stopcock on the burette and allow some of the sodium hydroxide solution to go into the flask containing the hydrochloric acid. 

Let&amp;#39;s say we add 10.00 mL of the 0.500 molar solution of sodium hydroxide. 

Because sodium hydroxide is a strong base, we assume that it dissociates 100%, which means that all of the NaOH turns into an Na plus and OH minus.  

Therefore, if the concentration of sodium hydroxide is 0.500, that&amp;#39;s also the concentration of sodium ions and hydroxide ions in solution.

Let’s write an equation for the acid-base neu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_pelvic_cavity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bLEmWcTvRBC_qIz427wlLO2SRFmahYFm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the pelvic cavity]]></video:title><video:description><![CDATA[The pelvic cavity is a funnel-shaped space surrounded by pelvic bones and it contains organs, such as the urinary bladder, rectum, and pelvic genitals, to name a few.

The pelvic cavity and the abdominal cavity together form the larger abdominopelvic cavity.

The pelvic cavity is bounded superiorly by the pelvic inlet, which connects it to the abdominal cavity, and inferiorly, it’s bounded by a group of muscles and the fascia surrounding them, called the pelvic floor or pelvic diaphragm which is suspended above the pelvic outlet, with its central portion dipping below it.

The pelvic cavity also has an anteroinferior wall, two lateral walls, and a posterior wall.

So let’s start with the anteroinferior wall, formed by the bodies and rami of pubic bones, and the pubic symphysis.

Each pubic bone has three parts: a body and a superior and inferior ramus. The body of the pubic bone is the thickest, most anterior part of the pubic bone.

Anteriorly, the bodies of the right and left pubic bones are joined together in the median plane to form the pubic symphysis.

Now, in an anatomical position, the pelvis is tilted in the anterior-posterior plane, making the pubic bones and pubic symphysis act more like a weight bearing floor than an anterior wall.

The lateral walls of the pelvic cavity are formed by the right and left hip bones.

Each hip bone has an inferior opening called the obturator foramen, which is formed by the pubis and the ischium.

The foramen is partially covered by a membrane called the obturator membrane.

This membrane and the pelvic surfaces of the ilium and ischium give origin to a muscle called the obturator internus which pads most of the lateral pelvic wall.

Now, the fibers of the obturator internus muscle fibers converge posteriorly to become tendinous, and then travel through a foramen called the lesser sciatic foramen.

Finally, they attach to a large area on the lateral side of the femur called the greater trochanter.

The medial surf]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bones_and_joints_of_the_thoracic_wall</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T7Fyx_o8S4_bpJRUQ8PojUvPQnCCGALg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bones and joints of the thoracic wall]]></video:title><video:description><![CDATA[The thorax is the area between the neck and abdomen and consists of the thoracic cavity, its contents, and the walls that surround it. 

The thoracic skeleton forms the osteocartilaginous thoracic cage that protects the thoracic viscera and some of the abdominal organs. 

This skeleton is made up of the sternum, 12 pairs of ribs and associated costal cartilages, as well as 12 thoracic vertebrae and intervertebral discs interposed between them. 

The ribs and costal cartilages form the largest part of the thoracic cage and both can be identified numerically, going from 1 to 12 for the ribs, and going from 1 to 10 for the costal cartilage, as ribs 11 and 12 do not have an associated costal cartilage.  

Now, the true thoracic wall includes the thoracic cage and the muscles between the ribs and the skin, as well as subcutaneous tissue, muscles and fascia that cover its anterolateral aspect. 

The structures that cover its posterior aspect are considered to belong to the back. 

Additionally, the mammary glands of the breasts lie within the thoracic wall subcutaneous tissue, and the anterolateral axioappendicular muscles are also  considered part of the thoracic wall. 

Okay, let’s start talking about the ribs, which form most of the thoracic cage. 

They’re curved, flat, lightweight, and highly resilient bones. 

Each rib has a spongy interior that contains bone marrow or hematopoietic tissue which forms blood cells. 

There are three types of ribs based on their connection to the sternum: true, false, and floating ribs. 

The true or vertebrosternal ribs are the first 7 pairs of ribs, and they attach directly to the sternum through their own costal cartilages. 

The false or vertebrochondral ribs are the 8th, 9th, and usually the 10th pair of ribs, and their cartilages are connected to the cartilage of the rib above them. 

Consequently, their connection to the sternum is indirect. 

The floating ribs or vertebral or free ribs are the 11th, the 12th pair of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spinal_cord_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yq3IQAhxSjOgrAZ8A5Isk8DfQkabfkDh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spinal cord disorders: Pathology review]]></video:title><video:description><![CDATA[At the physician’s office, 55-year-old Mario presents complaining of weakness in his hands and feet. These symptoms have gradually progressed over the past couple of months. At first, he struggled to manipulate small objects like buttoning his shirt. Now he also often stumbles while walking and recently fell down the stairs. In addition, his family mentions that his speech has become slightly slurred. He denies any sensory symptoms, memory loss or any bowel or bladder complaints. Later that day, 43-year-old Donna comes in with difficulty walking. She has fallen several times over the last few weeks. Her past medical history is significant for HIV infection, which was diagnosed a few years ago. On neurologic examination, her pupils are small and irregularly shaped and do not react to light, but constrict with accommodation. The sensations of pressure, vibration, fine touch and proprioception are also reduced throughout the lower extremities. She has a wide-based gait and cannot maintain balance with her eyes closed.

Based on the initial presentation, both Mario and Donna have some form of spinal cord disorder. Okay, let’s talk about physiology first real quick. If we zoom in at a cross-section of the spinal cord, we’ll see that it is composed of both grey and white matter. Grey matter is found within the medial portion of the spinal cord and has two dorsal or posterior horns that contain cell bodies of sensory neurons and two ventral or anterior horns that contain cell bodies of motor neurons.  In the center of the grey matter there’s a small cavity called the central canal which is filled with cerebrospinal fluid that provides nutrients and mechanical support. Surrounding the grey matter is white matter, which consists of the axons of various neurons and they are organized into tracts that carry information to and from the brain. 

For your exams, there are a few main tracts to remember. First, there’s the spinothalamic tract which is an ascendi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Van_Ton-Quinlivan:_CEO_of_Futuro_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G-pLQst6QmSkv-m0uvXyTkIkQi2IMco3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Van Ton-Quinlivan: CEO of Futuro Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Van Ton-Quinlivan: CEO of Futuro Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Sherling:_Chief_Medical_&amp;_Strategy_Officer_of_Modernizing_Medicine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jl6Lfgz0QXyuJMPOJbm1m9gcSVSLRPkM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Sherling: Chief Medical &amp; Strategy Officer of Modernizing Medicine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Sherling: Chief Medical &amp; Strategy Officer of Modernizing Medicine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Adam_B._Hill:_Pediatric_Oncologist_at_Riley_Hospital_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sADvEZXZQu2E0bkDk5iftCLGTXCGJTbv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Adam B. Hill: Pediatric Oncologist at Riley Hospital (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Adam B. Hill: Pediatric Oncologist at Riley Hospital (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lendri_Purcell_and_Althea_Hicks:_Jonas_Philanthropies_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hhsQ57_WQlWLozIpQ-vgQZ_vSdOYlzL1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lendri Purcell and Althea Hicks: Jonas Philanthropies (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Lendri Purcell and Althea Hicks: Jonas Philanthropies (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Molarity_and_dilutions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cSzEE1yXTqaYWq-SbtSWZwxNQ9KRVNO9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Molarity and dilutions]]></video:title><video:description><![CDATA[Molarity is a way of  quantifying the concentration of a solution.  

Dilution is a way of decreasing the concentration of a solution.  

Both molarity and dilution are essential concepts for correctly performing chemical experiments in a laboratory.

Let’s say that we have two glasses of water. 

In one glass, we put a small amount of sodium chloride which is table salt. 

We can assume that all of this sodium chloride dissolves into the water to form an aqueous solution. 

In our other glass, we put a much larger amount of sodium chloride which we will also assume completely dissolves in the water. 

Because the first glass has less sodium chloride in the solution, we would say that this glass contains a more dilute solution of sodium chloride.  

Because the second glass has more sodium chloride, we would say that this glass has a more concentrated solution of sodium chloride.  

The words dilute and concentrated allow us to compare our two solutions of sodium chloride; however, they don’t quantify exactly how much more concentrated one solution is compared to another.  

When we are quantifying the concentration of a solution, we need to use the concept of molarity.  

The definition of molarity is moles of solute divided by the total volume of the solution in Liters. 

Let’s use the definition of Molarity to make a solution of sodium hydroxide.   

Suppose we want to make 500. milliliters of a 1.00 M solution of sodium hydroxide.  

So, we know that the definition of molarity is moles of solute divided by liters of solution. 

We plug 1.00 molar into our equation for the molarity. 

We also plug in our desired quantity of the final solution, which is 500. mL. 

But because the definition of Molarity is moles per liter, we need to convert 500. mL to 0.500 L.

So the equation for molarity is that x divided by 0.500 L equals 1.00 molar, where “x” is the number of moles of sodium hydroxide we want in our solution. 

Solving for “x”, we can see that w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cervix_and_vagina_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6MZCUue-Ts2MzQljnqeZUJU0TeOz-7Pe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cervix and vagina histology]]></video:title><video:description><![CDATA[The cervix is the lower, cylindrical part of the uterus that opens into the vagina. Histologically the cervix is different from the rest of the uterus and also has a mucosa that doesn’t shed during menstruation. The cervical mucosa can be separated into three distinct regions: the endocervix, transformation zone, and ectocervix, which is also called the exocervix. The endocervical mucosa forms the wall of the cervical canal and will have a mucus-secreting simple columnar epithelium. The ectocervical mucosa is present in the part of the cervix that protrudes into the upper vagina and surrounds the external os, which is the lower opening of the uterus. This mucosa will have a non-keratinized stratified squamous epithelium that’s continuous with the vagina. The transformation zone is the region between the endo- and ectocervix. There’s an abrupt change from columnar cells to squamous cells within the transformation zone called the squamocolumnar junction. The exact location of the squamocolumnar junction will change or shift depending on the age of the individual as well as changes in the size of the uterus during menstruation. The transformation zone is also the ideal site to collect cells from during a Pap smear or Pap test. Underneath all regions of the cervical mucosa is a thick cervical wall that consists of dense connective tissue. Unlike the uterus, it only has a small amount of smooth muscle present.

The vagina connects the cervix to the external opening of the vagina called the vaginal vestibule. The wall of the vagina doesn’t contain glands and is composed of three main layers: the inner mucosa, which is typically about 150-200 µm in adults; a muscular layer called the muscularis; and an adventitia of connective tissue. The adventitia also contains a large amount of elastic fibers, which allow the vaginal wall to be both strong and flexible, which is particularly beneficial during childbirth.

Let’s first take a closer look at the mucosa of the end]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gas_exchange_in_the_lungs,_blood_and_tissues</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4mcXaHsuQkmOb2_Df5BBFzTDRleYogWu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gas exchange in the lungs, blood and tissues]]></video:title><video:description><![CDATA[Gas exchange is the physical process by which gases move passively, meaning that no energy is required to power the transport, by diffusion across a surface. 

External respiration is another term for gas exchange. 

It describes both the bulk flow of air into and out of the lungs and the transfer of oxygen and carbon dioxide into the bloodstream through diffusion. 

Internal respiration, on the other hand, describes the capillary gas exchange in body tissues. 

While the flow of air from the external environment happens due to pressure changes in the lungs, the mechanisms of alveolar gas exchange are more complex. 

The primary three components of gas exchange are the surface area of the alveolo-capillary membrane, the partial pressure gradients of the gasses, and the matching of ventilation and perfusion.

So, if we were to draw a path for the oxygen molecules entering the body, it would start from the nose or mouth and end up in the lungs, where it reaches the alveoli which are wrapped in an intricate network of tiny blood vessels called pulmonary capillaries. 

So, from the alveoli, the gas molecules will go into the blood in the capillaries. 

Carbon dioxide follows the same path, but in the opposite direction, moving from the blood in the capillaries to the air in the alveoli and then getting exhaled. 

Now, the important role in this process belongs to the alveolo–capillary membrane where the layer of alveolar cells lining the alveoli meets the endothelial cells that make up the pulmonary capillary, and is where gas exchange happens. 

With that in mind, let’s just say that when it comes to the surface area of the alveolo-capillary membrane, bigger is better because a respiratory membrane with a large surface area has more gas to diffuse across it in a given period of time leading to a more efficient gas exchange. 

With emphysema, for example, which is a condition where the alveoli are gradually destroyed, the total surface area that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stomach_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dMi-JszPRoGDtVujK3mrCit1TBGMqRJN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stomach histology]]></video:title><video:description><![CDATA[The stomach is an expanded portion of the gastrointestinal tract or GI tract that partially digests food by breaking it down mechanically and chemically in order to form a pulpy acidic fluid called chyme.

The stomach is divided into 4 anatomical regions: the cardia, fundus, body, and pylorus.

But the stomach is only divided into 3 histological regions: the cardia, fundus, and pylorus.

That’s because the fundus and body are histologically identical, so both regions are called the fundus when referring to their histology.

The cardia is a small area surrounding the opening to the esophagus which contains cardiac glands that secrete mucus.

The fundus is the largest region histologically, since it also includes the body of the stomach as well.

This region of the stomach has fundic or gastric glands that secrete digestive enzymes such as pepsin, and a protective layer of mucus.

The pylorus is the most distal region of the stomach before reaching the pyloric sphincter.

This region will have a combination of pyloric glands that secrete mucus and neuroendocrine cells that secrete gastrin.

Similar to the rest of the GI tract, the wall of the stomach has 4 main layers: the inner mucosa, submucosa, muscularis propria, and outer serosa; although some portions of the GI tract have an outer layer of adventitia instead of serosa.

This low power longitudinal section of the stomach was taken from the cardia of the stomach.

Now, if we take a closer look at the mucosa of the cardia, we can see that the surface of the mucosa has a simple columnar epithelium with many invaginations that form millions of gastric pits.

The gastric pits will comprise about a quarter of the mucosa’s thickness.

At the base of these pits, they join with multiple tubular cardiac glands that secrete mucus that protects the esophagus from gastric reflux and is also a part of the stomach’s gastric juice.

The cardiac glands extend all the way to its underlying layer called the muscularis muc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Small_intestine_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5yMYa5RuRs2UCtwojFDcGnH3T1OIV1K6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Small intestine histology]]></video:title><video:description><![CDATA[The small intestine is the longest portion of the gastrointestinal or GI tract.

It’s approximately 6 meters long in adults and it’s the main site for both digestion and absorption of food in the body.

Although the majority of the small intestine shares similar histological structures, it’s still divided into three main segments.

The duodenum, jejunum, and ileum.

The most proximal segment of the small intestine is the duodenum, and it’s also the shortest segment as well.

The duodenum connects with the jejunum at the duodenojejunal junction.

The jejunum is approximately 2.5 meters long and will gradually transition to the Ileum, which is the last segment of the small intestine.

The ileum is usually about 3.5 meters long and leads to the cecum of the large intestine at the ileocecal junction.

Similar to the rest of the GI tract, the wall of the small intestine has 4 main layers: the mucosa, submucosa, muscularis propria, and in the small intestine the outermost layer is a layer of connective tissue called the serosa.

In these images, the serosa is only present in the image of the duodenum.

Although each segment of the small intestine shares similar overall structures, there are still quite a few differences between each segment that can be seen with light microscopy.

Even at low magnification, we can see that the finger-like projections or villi that extend into the lumen in both the duodenum and jejunum are very tall and slender when compared to the villi of the ileum are significantly shorter, broader, and their tips are flat in comparison to the duodenum and the jejunum.

Let’s take a closer look at the mucosa of the duodenum.

The villi of the entire small intestine are lined with enterocytes, which are simple columnar cells with microvilli.

The microvilli increase the surface area available to the enterocytes for absorption.

The pale cells within the villi are the goblet cells, which secrete mucus for lubrication and physical protection of t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Liver_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WQc7FADDRVCJR8Wq9H0rdm4kQ6_JQ18H/_.jpg</video:thumbnail_loc><video:title><![CDATA[Liver histology]]></video:title><video:description><![CDATA[The liver is the largest internal organ in the body and weighs about 1.5 kg.

It’s surrounded by a capsule of fibrous connective tissue called Glisson’s capsule.

If we look at the liver from an inferior view, which is a view from the bottom of the liver, we can see that the liver is divided into a large left lobe and right lobe, as well as two smaller lobes, called the quadrate and caudate lobes.

The liver parenchyma or functional tissue of the liver is organized into thousands of hepatic lobules, which have a dual blood supply that comes from terminal branches of the hepatic portal vein and hepatic artery.

The blood then flows through sinusoids surrounded by hepatocytes before draining into the lobule’s central vein.

Hepatocytes are the main functional cells of the liver that perform a large variety of functions, including the production of bile, a number of plasma proteins, and non-essential amino acids; the metabolism of fat, carbohydrate, and protein; the storage of glucose, vitamins, and iron; and the breakdown or detoxification of metabolic waste products, drugs, and toxins.

At lower magnification, the hexagonal shape of the hepatic lobules can be identified by their slightly darker edges and the prominent central veins in the center of each lobule.

The portal triad consists of a bile ductule, portal venule, and arteriole.

After identifying the lobule, it can be easier to locate portal triads in an image since they’re typically located at the corners of the lobules.

If we take a closer look at just one portal triad, we can more easily identify the portal venule by its large diameter and thin walls compared to the arteriole, which has a much smaller diameter and thicker walls.

Similar to this image, the portal tract can sometimes have more than one bile duct.

The bile ducts can be identified by their prominent simple cuboidal epithelium.

Also in this image are a couple small lymphatic vessels, which have even thinner walls than the venule.
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pigmentation_skin_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q96tJ4AAQ6i09UDsrBFGSCFhQoiOLnW9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pigmentation skin disorders: Pathology review]]></video:title><video:description><![CDATA[21 year old Holly comes to her primary care provider&amp;#39;s office complaining of pigment changes on her skin for the past year. She denies any history of trauma or recent inflammation of the skin. Her past medical history is significant for autoimmune thyroiditis. Physical examination shows several sharply demarcated depigmented patches on the dorsum of both her hands and wrists. On the same day, 30 year old Maria comes due to some tan spots that recently appeared on her cheeks. Maria tells you she is pregnant and of hispanic descent. Physical examination reveals that no other body area is involved. Based on the initial presentation, Holly and Maria seem to have some form of pigmentation skin disorder. 
All right, so the skin is divided into three main layers, the epidermis, dermis, and hypodermis. Melanocytes are located in the stratum basale layer of the epidermis and they produce a pigment called melanin from tyrosine. Melanin is then taken up by surrounding keratinocytes, and it contributes to the color of our skin, hair, and eyes. Now, what’s high yield is that melanin acts as a natural sunscreen that absorbs and dissipates, or scatters, UV radiation from the sun or other sources such as tanning booths, preventing it from damaging the keratinocytes. Now, as keratinocytes in the stratum basale mature, they migrate into the next layers of the epidermis, called the stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer. 

Before we dive into the various disorders, there are several high yield terms to describe skin lesions. So, macules are flat, well circumcised lesions up to 1 centimeter in diameter, while patches are similar to a macule but are larger than 1 centimeter. Papules are raised bumps that are up to 1 centimeter in diameter, while plaques are like papules but larger than 1 centimeter.
Okay, now, let’s start with pigmentation skin disorders. First, there]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VtExknZpSjSeDryaEUiIsxZWShaIEJJD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock: Pathology review]]></video:title><video:description><![CDATA[Amina is a 42-year-old female who was brought to the emergency department after her car crashed into a tree. According to paramedics, part of the car was on fire upon arrival. During resuscitation, her vitals showed a blood pressure of 70 over 50 and a heart rate of 140. Upon examination, her extremities are cold and clammy and there were multiple first and second-degree burns on her neck, abdomen and lower extremities. Additionally, auscultation reveals decreased air entry on the left side of her chest, and this is Amina’s chest x-ray. Palpation of the pelvis produced significant tenderness, prompting the ED physician to order a pelvic x-ray.   After resuscitating Amina, another individual is rolled into the emergency department. Anastasia, 77 years old, comes in with high fever and chills and a 5-day history of dysuria and flank pain. Her blood pressure is 80 over 40 and heart rate is 120 beats per minute. On examination, her extremities are warm and flushed.

Both people have a life threatening condition called Shock.  Shock  is defined as inadequate organ perfusion that results in hypoxia and cellular damage.. Perfusion of organs is normally maintained by the arterial blood pressure. The mean arterial pressure is equal to the cardiac output times the systemic vascular resistance. So, any alteration to the components of this equation can potentially lead to shock. On the exam, look for hypotension as an initial clue for shock. Others include tachycardia, decreased urine output and altered mental status. 

Now we can classify shock into 2 major categories. There’s “cold” or low cardiac output shock, and “warm” or distributive shock where there’s decreased systemic vascular resistance. Okay, let’s start with “cold” shock. This includes cardiogenic, hypovolemic and obstructive shock. In cardiogenic shock, the cardiac output is compromised because of a problem with the heart. This could range from congestive heart failure, acute myocardial infarct]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_Study_for_Boards_Using_Question_Banks</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S_F6f6QCSaOK9RJKlznyvPITSHucDYjK/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to Study for Boards Using Question Banks]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to Study for Boards Using Question Banks through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Robert_Cain:_President_and_CEO_of_the_AACOM_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pcni_a8yS3mNhUB3TxoL-LdgTl6sURQM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Robert Cain: President and CEO of the AACOM (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Robert Cain: President and CEO of the AACOM (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._David_Skorton:_President_&amp;_CEO_of_the_AAMC_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BYEEIbfARpeDe2Wb64lr1nZLQK_X6E23/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. David Skorton: President &amp; CEO of the AAMC (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. David Skorton: President &amp; CEO of the AAMC (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_orthopedic_surgeon_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zfSESl3RTDyUYbm-kuP9Sv9kRs27Gz6w/_.jpg</video:thumbnail_loc><video:title><![CDATA[The orthopedic surgeon and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Sofia Morales was a young woman who lived in Atlanta, Georgia. 

She worked in a factory and studied at a community college. 

She had recently moved to the US and spoke Spanish as her primary language, but tried practicing English with classmates in the evenings - mostly through a group text chat - when she felt motivated. 

One morning, Sofia woke up and noticed that her left wrist was hurting and that there was a lump there. 

She had felt the pain before, but it was the large lump that had her worried. 

“Could this be a tumor?” she wondered aloud, as she picked up the phone to make an appointment to have it checked out. 

A few days later, Sofia went to see her primary care physician, who examined her wrist. 

With the help of a Spanish language interpreter, her doctor reassured her that it was most likely a ganglion cyst and not a tumor. 

Her doctor also suggested that she get the cyst surgically removed and set up an appointment with the orthopedic surgeon. 

Sofia went home feeling relieved that it wasn’t a bone tumor, and was glad that it would get removed. 

Two weeks went by - and Sofia went with her younger sister to visit the orthopedic surgeon. 

Dr. Margo, an orthopedic surgeon, who examined Sofia’s wrist and agreed that she needed to have the cyst removed. 

Dr. Margo didn’t have an interpreter with her, and was in a rush to get back to the operating room so she asked her teammate, Dr. Alex Hammond, to take over. 

The conversation was quick “Spanish-speaking woman, wrist surgery - cyst removal. 

You got it?” 

“Yep, wrist surgery, got it.” Dr. Hammond responded. 

&amp;quot;She&amp;#39;s in room 2. 

Get the consent and schedule the procedure, thanks so much!” she trailed off as she walked away. 

Dr. Hammond was feeling overwhelmed. 

He was hoping to wrap up some clinic notes and wanted to get to the post-operative unit to see another patient, but now he had to take care of one more thing. 

It had been a stressful day. 

He hasn’t h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_cardiologist_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_dq0iToESxmqocnxyHT7s1S4Q1ixh98S/_.jpg</video:thumbnail_loc><video:title><![CDATA[The cardiologist and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Joseph Hoff was a 66-year-old man. 

He was originally from Germany, and his family moved to the United States when he was 3 years old. 

Joseph grew up in Chicago and then settled in Omaha, Nebraska, where he ran a family business - furniture restoration and repair. 

He loved the midwest and never really wanted to leave. 

One afternoon, Joseph was repairing an old cupboard with his son, when his heart started pounding in his chest. 

He felt out of breath and sat down on the cement floor, and before he knew it, he was lying down on the floor. 

His son ran over and didn’t waste any time, as he called for emergency services.  

About 15 minutes later, Joseph and his son were being taken into the Emergency Department. 

The emergency room team was notified that he was arriving, and a team of folks worked in unison to get him treated. 

Among other things, they set up monitors and IV lines placed, obtained lab work, and performed an ECG.. 

A few minutes later, Dr. Daria Baldwin, the cardiologist, came down to see him. 

She was handed the ECG. 

She look at the tracing and shouted “he has ongoing V-tach, let’s give him amiodarone.”

Within a few hours, Joseph was stable. 

He was sent up to the medical floor for observation. 

Dr. Baldwin swung by to pay him a visit him and explained that she had reviewed his medical chart and that she wanted him to continue taking amiodarone. 

She said, “alright Joseph, we’ll place you on the loading dose of 1200mg of amiodarone. 

Is that clear?” Joseph nodded. 

She also told him to make a follow up appointment with her next week in order to check his condition and reduce the amiodarone dose. 

One week later Joseph arrived for his appointment. 

Dr. Baldwin asked Joseph if he experienced any exhaustion, fluttering in his chest, or shortness of breath lately, but Joseph said no. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_emergency_medicine_resident_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lKDfDWYgTYmQ08v6XGhlMAKcSmWnZWFb/_.jpg</video:thumbnail_loc><video:title><![CDATA[The emergency medicine resident and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Dr. Theodore Watkins was a 31-year-old resident physician from Roswell, New Mexico. 

He regularly went to the gym, ate a plant-based diet, and practiced meditation - in many ways he was the picture of healthy living. 

Theo, as his friends and family called him, lived in a 2 bedroom apartment with his girlfriend and their dog Misty. 

One night, while he was playing with his dog, his alarm rang - he had a night shift in the Emergency Room. 

He scratched Misty’s belly &amp;quot;Time to go! 

See you in the morning!”

The night shift was fairly routine - some laceration repairs, a gunshot wound, a woman with severe panic attacks, and a mix of other complaints. 

The clock in the emergency department showed 5:39am when a nurse announced that there was a 43-year old male with a sudden onset of chest pain being carted in. 

Dr. Watkins quickly drank up the rest of the coffee and replied: “Bring him in.” 

A few moments later, a man was wheeled in on a gurney. 

He was breathing heavily, holding his chest, and turning and twisting in pain. 

Dr. Watkins asked the man some questions as the team begin to set up monitors, get IV access, and give pain medication. 

Through gasps - the patient explained the pain started abruptly when he got out of the bed, and that he felt it everywhere including in his back. 

Within moments information was flowing in. 

The blood pressure in one arm was lower compared to the other one, the ECG was normal, and the lab work had been sent off. 

The nursing team had also paged the overnight attending physician, Dr. Chapman, and when he called back - the phone was handed to Dr. Watkins.

“Dr. Chapman on the phone,” said the sleepy voice from the other side. 

During the next few minutes, Dr. Watkins explained that they have a 43-year-old patient with unusual chest and back pain over the last couple hours, and that there was an irregularity in the inter-arm blood pressures. 

He mentioned that the ECG showed no signs of a STEMI. 

Dr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_gynecologist_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VFhUcrGxTMCgQ9htDOQJajhWSwqhQ3cu/_.jpg</video:thumbnail_loc><video:title><![CDATA[The gynecologist and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Grace Sutton was a 42-year old, African-American psychiatrist from Portland, Maine. 

She finished medical school at the top of the class, and she owned a well-known private practice in Manhattan. 

Her clients raved about her. 

Grace was married to a famous patent attorney in New York, and in her free time, she enjoyed going to charity events and museum exhibitions. 

She lived with her husband in a luxurious loft apartment next to Central Park, and they were planning on having a baby.

It had been a few months since Grace’s last appointment with her gynecologist and she had one final visit at a gynecologist clinic before her big procedure -- in vitro fertilization. 

She was meeting with Dr. Lottie Velazquez, an older woman who seemed calm and confident, and Grace found her presence comforting. 

“Nice to meet you, Dr. Velazquez!” - Grace replied with a smile on her face. 

Grace told Dr. Velazquez that she had been having some mild abdominal pain, but wasn’t sure of the cause - thinking perhaps it was stress related.

During the physical examination, the conversation between the two was relaxed. 

“So, you’re a psychiatrist, right?” Dr. Velazquez prompted. 

Grace replied in a steady manner: “Yes, I am. I think of it as mental wellness and I like to say: Your mind is your best friend.” 

Dr. Velazquez nodded and smiled, “I wish you could say that to my daughter. 

She’s a teenager and she’s going through all sorts of things - she broke up with her boyfriend, got into a fight at school, and smokes regularly.” 

As the conversation continued, Dr. Velazquez kept talking about her daughter and got so worked up that she hardly focused on the physical exam. 

After a few minutes, Dr. Velazquez asked Grace to get dressed. 

When she walked over to the computer to enter the physical exam into the electronic medical record system, Dr. Velazquez realized that she hadn’t done a proper physical exam so she copied the findings from a prior appointment. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_internist_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sqhGEjqaQoSVdqZ8Jf6ERpnvQUWMlw_0/_.jpg</video:thumbnail_loc><video:title><![CDATA[The internist and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Zach Hoover was a 57 year-old man, who lived in Montgomery, Alabama. 

He lived in a small 1-bedroom apartment with his cat Milo. 

During the week he worked as a janitor in the local high school and on weekends he volunteered at the local animal shelter. 

Zach’s only real splurge was a weekly bingo night that he had been attending since his divorce finalized. 

One afternoon, Zach was cleaning the high school yard, when he experienced weakness in his legs. 

Over the next few days, the weakness gradually progressed until he was barely able to get around without the help of a cane. 

One Friday evening he had had enough. 

He filled up Milo’s food bowl to the brim, zipped up his jacket, and called a taxi to take him to the emergency room.  

When Zach arrived at the Emergency Department, he was examined by a young attending physician, Dr. Tia Pearson. 

The conversation was slow and meandering. 

Zach complained about how his weakness was affecting all aspects of his life. 

“I live only a few blocks from here but I still had to take a taxi.” 

He complained. Dr. Pearson listened carefully and questioned Zach more about his condition. 

“Have you experienced any chest pain lately? 

Shortness of breath, headache, or vomiting?” Zach said no. 

He was generally quite healthy, didn’t smoke, didn’t drink, and had even stopped eating red meat and processed foods. 

On physical examination, the heart, lung, and abdominal examinations were all normal. 

“Since your problem isn’t specific enough, I want to run some blood tests and an ECG.” 

Dr. Pearson explained to Zach. 

He agreed and after the tests were run, he waited patiently for the results. 

When lab results came in they showed hyperkalemia - high potassium levels, so Dr. Pearson arranged for Zach to get admitted to the hospital and started ordering some medications to help lower his potassium levels. 

The nurses administered IV medication to treat the hyperkalemia, and got him ready for his hospital a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Questions_to_Ask_When_Choosing_a_Nursing_Program</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wp5ecbiIT5qp9AE9XPijLYyCRfKbzb4-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Questions to Ask When Choosing a Nursing Program]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Questions to Ask When Choosing a Nursing Program through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_moonlighter_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OozD06RyTUKQnpHlW7af5trHSP_VKfJt/_.jpg</video:thumbnail_loc><video:title><![CDATA[The moonlighter and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Dr. Clara Hom was a junior clinical faculty member who shared a 2-bedroom apartment with her older brother, in a suburb just outside of Denver, Colorado. 

During the day, Dr. Hom worked in the cardiology unit, but some evenings she would do night shifts in the Intensive Care Unit. 

She really hated moonlighting, but took on the extra shifts to help pay off her 220,000 dollars in student loans. 

“Another Saturday, another shift. 

Two more of these and then I can have a full weekend off - a golden weekend.” 

Dr. Hom thought aloud as she was leaving her home.

An hour later, Dr. Hom arrived at the Intensive Care Unit. 

The woman who did the day shift was eager to head out and whipped through the sign out. 

She said, “On the right side, beds 1-4 we’re just monitoring for postoperative complications, 5 and 6 are patients with cardiac problems. 

On the left side, we have two patients, 22-years old Sarah Arroyo, and 26-year old Isaac Berg.” 

Arroyo has been having recurrent bleeding post-tonsillectomy, and Berg has ARDS from who knows what, and is now he’s on mechanical ventilation - the plan is to keep him steady on his settings overnight.” 

And like that, the sign-out was completed and Dr. Hom was left alone to settle in for the night. 

The night slipped by quietly, no big issues.

Dr. Hom felt relieved - she liked the money, but being in the ICU scared her and the feeling had never really gone away over the years. 

It was about 6:02am Dr. Hom was called by Sarah Arroyo’s nurse because she had been spitting up some blood. 

Dr. Hom checked her tonsil beds, and she saw bright red streaks running down the back of Sarah’s throat. 

She tried to remain composed, but her stomach began to turn. 

“Nurse, bring me a kidney dish.”  

Dr. Hom advised Sarah to spit the blood out in the kidney dish, rather than swallowing it. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_nurse_and_doctor_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rnkI9B33TcO_rCGZewqQWaa9SLSzmwQj/_.jpg</video:thumbnail_loc><video:title><![CDATA[The nurse and doctor and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Nora Walsh was a young nurse who lived in a two-story house with her parents, in Pittsburgh, Pennsylvania. 

She had two jobs - a full-time job in the Emergency Department and a part-time job as a nursing tutor. 

She took pride in her love of science and decided to name her two small Pomeranians - Pen and Vanco, after 2 types of antibiotics - Penicillin and Vancomycin. 

One day, after wrapping up a tutoring session, she went straight to the Emergency Department to do a night shift. 

In the early morning hours of her shift, a patient - Parviz Elagin - was brought in by his husband. 

Parviz’s skin was covered in hives, his face was swollen, and he was having difficulty breathing. 

Dr. Arturo Reyes screamed from the other side of the room: “He’s got severe anaphylaxis! 

Let’s grab the crash cart - we need the Endotracheal tube, epi, and IV fluids! 

Nora, I need your help on this!” 

Nora left her coffee and rushed over to get the crash cart.

A few seconds later, she was at the bedside quickly opening up the drawers to get access to everything and rubbing her hands together with hand sanitizer. 

“Here you go doc,” Nora said as she passed the endotracheal tube to Dr. Reyes. 

“Nora… I need you to…” Dr. Reyes was trying to tell her something while he was struggling with the intubation. 

It was clear - the patient’s larynx was too narrow for this size of the tube. 

After several failed attempts, Dr. Reyes pulled out the tube and said, “Nora, I need you to get me another tube - We need a smaller diameter. ” Nora rushed. 

A few minutes later, the intubation was complete and everyone in the room took a collective deep breath. 

But Parviz was still critically ill and his blood pressure was starting to drift down - a worrisome sign of shock. 

“Give him 2 milliliters of epinephrine,” Dr. Reyes ordered. 

Nora looked at Dr. Reyes in a strange way, like something was clearly wrong, and asked: “Are you sure, Dr. Reyes?” ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_obstetric_resident_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NnDbxrsYSceSh8TSJYeZBXRRQtGrRDDk/_.jpg</video:thumbnail_loc><video:title><![CDATA[The obstetric resident and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Dr. Frank Mills was a 34-year old obstetrics resident who had lived most of his life near his parents in Richmond, California. 

Recently, he had moved to Miami, where he lived in a 3-bedroom house with a pool, and spent weekends hosting small parties and barbeques. 

Dr. Mills was friendly and charming, but could sometimes come across as arrogant and boastful. 

He enjoyed medicine, but his real passions in life were cooking, surfing, and ping pong - in that order.

It was another night in the maternity unit.

In front of the coffee machine, Dr. Mills was talking his with his colleague Dr. Holt about a party he was planning for the 4th of July. 

A few moments later, a nurse approached them and said, “Dr. Mills, we have a 37-years-old woman who’s 39 weeks pregnant and hypertensive.” 

Dr. Mills said he’d be there in a moment, and then resumed his conversation with Dr. Holt: 

“So, what do you say?

You should come by on Saturday night. 

It’s going to be the best 4th of July ever!” 

He smiled and went to see the patient.

“Hello there, my name is Dr. Mills. 

What seems to be the problem?” he asked the frightened woman. 

The woman explained that over the past few days she’s been having blurry vision, a pounding headache, and feeling more anxious. 

She was spending the weekend with family and thought the symptoms were from being sleep deprived. 

She didn’t want to worry her parents, so she waited until today to check her blood pressure back at her home. 

Normally her blood pressure was around 120/80, but today it was 155/100. 

She knew that she was supposed to call if that happened, so she called and was told to come in. 

Dr. Mills calmed her down and explained the plan, “We’ll be admitting you to the hospital and doing some lab tests to make sure that you and the baby are safe”. 

The woman agreed. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_ophthalmologist_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FF-MW0u6RzGm2JXv__gP3zjmTmeMbgoo/_.jpg</video:thumbnail_loc><video:title><![CDATA[The ophthalmologist and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Rebecca Foley was a middle-aged woman, who lived most of her life with her husband in Arlington, Texas. 

Two years ago, her daughter had twins, so Rebecca started spending more time in Austin to help her daughter and son-in-law take care of the babies and to help around the house. 

For years, Rebecca had a problem with her eyes - she wasn’t able to see close objects clearly, and the problem was getting worse. 

One day she tripped on some steps while coming up in dim light, and fell hard. 

The next day, Rebecca’s daughter convinced her to make an appointment for an eye exam. 

Rebecca arrived for her appointment with her ophthalmologist - an older doctor with a grey beard, Dr. Emmanuel Sullivan. 

After a series of tests Dr. Sullivan concluded: “Rebecca, we have some good news and some bad news.” 

“Give me the bad news first,” Rebecca replied with a smile. 

Dr. Sullivan explained that she had significant myopia or nearsightedness. 

“But the good news is that you’re a candidate for laser eye surgery.” 

He explained that laser eye surgery was a pain-free procedure that could be done in 15 minutes and offered long-lasting results. 

Rebecca agreed and Dr. Sullivan scheduled her for the following Thursday. 

On Thursday morning, the morning ophthalmology meeting was more tense than usual. 

There were two procedure rooms with lasers, and one of the machines wasn’t working. 

To accommodate all of the patients, Dr. Sullivan and his colleague Dr. Mason would have to share the same room. 

When Rebecca came in for her procedure, she felt nervous but the procedure was really quick and she took the rest of the day off. 

Dr. Sullivan had explained that she might experience some vision problems that day, but he told her that everything would be normal the following morning. 

But Rebecca still couldn’t see well the next day or the day after that. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_radiology_fellow_and_the_avoidable_lawsuit_(Coverys)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/caKXmru3SlC420FblvajUwWRQm_bRGB7/_.jpg</video:thumbnail_loc><video:title><![CDATA[The radiology fellow and the avoidable lawsuit (Coverys)]]></video:title><video:description><![CDATA[Patricia Buckley was a retired teacher who lived most of her life in the midwest, but had recently moved to Dayton, Ohio. 

She shared a small 1-bedroom apartment with her trusted companion of many years - a parrot named Mr. Gatsby. 

Most nights she would watch movies, but occasionally she enjoyed hosting small dinner parties. 

One morning, as Patricia was cleaning her house, she suddenly felt tired and dizzy, and as the day progressed, she felt more achy and developed a slight cough. 

“I hope I’m not getting sick right before my trip to Europe,” she thought aloud, as she picked up the phone to make an appointment with her primary care physician. 

The next day, Patricia arrived for her appointment with her primary physician, Dr. Larson. 

The conversation was relaxed. 

Patricia said she was mostly worried about the fatigue. 

She explained, “I’m going to visit my daughter and my lovely grandson in Europe for the summer, and I&amp;#39;m pretty sure I won&amp;#39;t be able to keep up with him or help around the house if I’m exhausted like this.” 

Dr. Larson explained that she thought it was most likely a viral infection, but that she needed to get some blood tests and a chest X-ray just in case Patricia had developed a walking pneumonia or something called parrot fever - both of which could be treated with antibiotics. 

Patricia felt reassured and headed out to get the lab work and chest X-ray done.

A few hours later, an overnight radiology fellow, Dr. Samir Patel, was reading the chest X-ray of patient 7322881. 

He didn’t know Patricia - he just knew her medical record number. 

The reason for the chest X-ray? 

Two words “rule-out pneumonia”. 

He squinted at the image and sipped his Chamomile tea. 

No signs of pneumonia, but he noticed a small oval shape on her left upper lobe. 

“Could this be a tumor? Or tuberculosis?”, he wondered as dictated the report. 

“Findings: No evidence of pneumonia. 1-centimeter oval lesion in the left upper lobe. 

No hilar adenopathy...“ he finished up. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glut1_deficiency_syndrome_(Glut1_Deficiency_Foundation)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pHf-sgM4RDCEW931ZUUsGDqVSN2-3dZW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glut1 deficiency syndrome (Glut1 Deficiency Foundation)]]></video:title><video:description><![CDATA[Glucose transporter type 1 deficiency syndrome, or Glut1 Deficiency, is a rare genetic disorder that impairs brain metabolism. 

Glucose is not transported properly into the brain, which leaves it starving for the metabolic fuel it needs to grow, develop and function normally.  

The condition is caused by over a hundred different mutations in the SLC2A1 gene, which regulates GLUT1 protein production. 

And because it’s an autosomal dominant disorder, just one mutation in one of the two copies of the gene is enough to cause the disease. 

Mutations mostly occur spontaneously, but affected patients do have a 50% chance of passing the altered gene to an offspring.  

Now, normally GLUT1 is the primary transport protein that lets glucose cross the blood brain barrier, where the brain uses it as its main source of energy. 

Without enough glucose, the brain will have impaired growth and function. 

This leads to symptoms that vary widely between individuals, and can even evolve over time as patients age. 

Typically, newborns are asymptomatic, but within a few months they sometimes develop irregular involuntary eye-head movements called aberrant gaze saccades or intermittent involuntary gaze, which is often a first sign of Glut1 Deficiency. 

Various types of seizures are  common in many patients but not always present. These seizures are usually resistant to medication treatments. 

Most Glut1 Deficiency patients also have some form of movement disorder: spasticity where muscles are stiff and tense; ataxia, where balance and movement control is poor; and dystonia where muscles are contracted and twisted. 

Tremors and other involuntary movements such as chorea and dyskinesia are also common, as well as floppiness due to decreased muscle tone. 

Episodes of temporary paralysis on one or both sides of the body, can also occur. 

These symptoms can be constant or paroxysmal, meaning intermittent, and can be triggered or worsened by excessive exercise, stress, il]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stoichiometry_for_atoms,_molecules_and_ions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZzIMSjVLRG__KtIlhoT3MXvCRzeA2ttV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stoichiometry for atoms, molecules and ions]]></video:title><video:description><![CDATA[Stoichiometry deals with the relationships between the quantities of reactants and products in a chemical reaction. 

For example, consider when hydrogen and oxygen react to form water. 

In a balanced chemical equation, the coefficients tell us the relative number of molecules involved. 

2 H2 + O2 → 2 H2O

The balanced equation tells us that two molecules of hydrogen will react with one molecule of oxygen to produce two molecules of water.  

We know that one mole is equal to 6.02 times ten to the twenty-third molecules.  

This incredibly large number is called Avogadro’s number.  

So if we have one molecule of oxygen and we multiply by Avogadro’s number, we have one mole of oxygen.  

If we have two molecules of hydrogen and we multiply that by Avogadro’s number, then we have two moles of hydrogen.  

Notice that the one mole of oxygen and two moles of hydrogen correspond to the coefficients in the balanced equation. 

So two moles of hydrogen will react with one mole of oxygen to produce two moles of water.  

Therefore, the coefficients in a balanced equation tell you the relative number of moles of everything involved in the reaction.  

We can use these mole relationships to find out how much product can be made from a given amount of reactant, or to find out how much of a reactant is needed to form a known amount of product. 

Stoichiometry problems give us information about one substance in the reaction, and ask us to find out about one or more other substances in the reaction.

There are four general types of stoichiometry problems:

The first type of stoichiometry problem is a mole-to-mole conversion: you are given moles of something and asked to find moles of something else. 

Suppose we start with 4 moles of hydrogen, and we are asked to figure out how many moles of oxygen are necessary to completely react with the hydrogen. 

To accomplish this, we need to use a mole ratio. 

Looking at the coefficients in our balanced equation, we can see ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testis,_ductus_deferens,_and_seminal_vesicle_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L4RIB9OdSgKozOGBbuVCZgyoQq2hicVV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Testis, ductus deferens, and seminal vesicle histology]]></video:title><video:description><![CDATA[Testes, or testis when singular, is responsible for the production of sperm, which is called spermatogenesis.

The testes also produce sex hormones, mainly testosterone.

The male genital ducts carry spermatozoa and liquid from the seminiferous tubules in the testes all the way to the penis.

The genital ducts can be split into two groups, the excretory genital ducts and intratesticular ducts.

The intratesticular ducts include the straight tubules (or tubuli recti), rete testis, and efferent ductules.

And the excretory gential ducts include the epididymis, ductus (or vas) deferens, and urethra.

This very low power image is a sagittal section of a testis, which also includes the head of the epididymis located posterior and partially superior to the testis.

The epididymis is a single, long convoluted duct where spermatozoa accumulate and continue to mature even further, including the development of motility.

Accessory glands, such as the seminal vesicles and prostate gland, secrete seminal fluid that provides lubrication and nutrients for the spermatozoa.

The seminal fluid is also slightly alkaline, or basic.

This alkalinity helps protect sperm and prolong their life after they’ve been deposited in the acidic environment of the vagina.

Surrounding each testis is a thick capsule of connective tissue, called the tunica albuginea.

The connective tissue extends inward from the posterior side of the testes and separates the seminiferous tubules into about 250 incomplete pyramid-shaped lobes.

Each lobe contains one to four highly-coiled seminiferous tubules.

Now, if we zoom in all the way to 40x magnification, we can see the individual seminiferous tubules, which have a germinal epithelium that’s responsible for spermatogenesis.

In this one image, we can see the various stages of spermatogenesis.

The spermatogonia are the undifferentiated germ cells that are mainly found along the periphery of the germinal epithelium, against the basement membrane.

T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Central_nervous_system_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BjIul_uRRL2kpyiiqipnPl7_TkqRsxxV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Central nervous system histology]]></video:title><video:description><![CDATA[The central nervous system or CNS consists of the cerebellum, cerebrum, brain stem, and spinal cord.

The neuron is the basic working unit of the nervous system.

And the neuroglia or glial cells are the non-neuronal cells that support and protect the nervous system.

The central neuroglia includes astrocytes, oligodendrocytes, ependymal cells, and microglia.

The peripheral neuroglia includes Schwann cells, satellite cells, and a number of cells associated with specific organs.

Macroscopically the CNS is made of white matter and grey matter.

The difference in appearance is from the lipid-rich myelin sheaths that cover the axons present in white matter.

Whereas the grey matter consists mostly of neuron cell bodies, dendrites, astrocytes, and microglial cells.

In this high power image of white matter from the spinal cord, the axons are surrounded by clear white space, which is where the myelin was present before the tissue was processed to create this slide.

The outermost portion of the cerebrum and cerebellum consist of grey matter, with their white matter present mainly in the deeper regions of the brain.

One the other hand, the spinal cord has the opposite arrangement, with white matter mainly in the periphery and grey matter mostly located closer to the center, forming an “H” or butterfly-shaped appearance when looking at a cross-section of the spinal cord.

In this low power image, we can see the spinal cord’s two posterior or dorsal horns closer to the top of the image and two anterior or ventral horns at the bottom.

The dorsal horns contain mostly sensory neurons and the anterior horns contain mostly upper motor neurons.

A simple way of remembering the location of the motor neurons is to remember that most cars also have their motors in the front or anterior part of the car.

The entire CNS is also covered by layers of connective tissue called the meninges.

The portion of the meninges that can be seen in this low power image is the dura]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skin_cancer:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eX3IyihOQgGOoKPfBcuiMQQ3QFmZIt3S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skin cancer: Pathology review]]></video:title><video:description><![CDATA[62 year old William comes to the dermatology clinic for a routine skin examination. He has been working as a farmer since the age of 20 and rarely wears a hat or sunscreen. Physical examination reveals a pink, pearly lesion with surrounding telangiectasias on his right upper lip. Right after him, 47 year old Shelby comes in because of a large mole on her right shoulder that has recently grown in size. She is light skinned and has many freckles. Physical examination shows an asymmetric lesion, 8 millimeters in diameter, with irregular borders and variegated brown to black pigmentation.

Based on the initial presentation, both William and Shelby seem to have some form of skin cancer. Okay, first, let’s talk about physiology real quick. Normally, the skin is divided into three main layers, the epidermis, dermis, and hypodermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Above the hypodermis is the dermis, containing hair follicles, nerve endings, glands, blood vessels and lymphatics. And above the dermis is the epidermis, which contains 5 layers of developing keratinocytes. Keratinocytes start their life at the lowest layer of the epidermis, so the stratum basale or basal layer. As keratinocytes in the stratum basale mature, they migrate into the next layers of the epidermis, called the stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer.

Now, the stratum basale also contains the melanocytes, which produce a pigment called melanin from tyrosine. Melanin is then taken up by surrounding keratinocytes, and it contributes to the color of our skin, hair, and eyes. Now, what’s high yield is that melanin acts as a natural sunscreen that absorbs and dissipates, or scatters, UV radiation from the sun or other sources such as tanning booths, preventing it from penetrating the skin. 

Now, this is important because UV radiati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spleen_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8Z0zDpaFSEOxm1_QuhSDQX4jRNm1OF4H/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spleen histology]]></video:title><video:description><![CDATA[The lymphatic system is an essential part of the immune system and it consists of a network of lymphatic vessels, tissues, and organs.

The lymphatic vessels drain interstitial fluid or lymph from peripheral tissues back into the blood.

Lymphoid tissue and organs contain a lot of lymphocytes and other white blood cells.

The primary lymphoid organs include the thymus and bone marrow.

And the secondary lymphoid organs include the tonsils, lymph nodes, spleen and mucosa-associated lymphoid tissue or MALT for short.

The spleen is the largest lymphoid organ.

It receives blood from the splenic artery and is the only lymphoid organ that primarily filters blood instead of lymph.

It’s an encapsulated organ that’s typically about 12 cm in length, 7 cm wide, and 3 cm deep.

The spleen’s functional tissue or parenchyma consists of red pulp, with small white nodules of lymphatic tissue scattered throughout called the white pulp.

Although, when looking at the spleen histologically after it’s been stained with H&amp;amp;E, the red pulp is actually stained a combination of pink and purple; and the white pulp is stained dark purple because it contains a large number of basophilic nuclei.

If we take a closer look at the outer edge of the spleen, the capsule that surrounds the spleen is seen as a dense layer of pink connective tissue.

The connective tissue also forms short extensions into the spleen called trabeculae.

The trabeculae will also occasionally surround arteries as they enter the parenchyma of the spleen.

These trabecular arteries are branches of the splenic artery.

The remainder of the tissue seen in this image is the highly vascular red pulp.

Now, if we move to a different region of the spleen, we can see there are areas that are more basophilic and stain mainly purple.

These areas of lymphatic tissue make up the white pulp, which consists mostly of T cells or B cells.

The trabecular arteries from the previous image branch even more and become ce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f0FrIlZdTB_3i1YEl1UfKMIaQ56ZCJpw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood histology]]></video:title><video:description><![CDATA[Blood is composed of specialized cells that circulate in an extracellular fluid called plasma.

Plasma typically consists of about 92% water, 7% protein, and 1% is a combination of other solutes.

The three main types of blood cells are the red blood cells or erythrocytes, white blood cells or leukocytes, and platelets, which are also called thrombocytes.

The total blood volume of an average adult is about 6 L. Leukocytes and thrombocytes only comprise about 1 percent of the blood volume; whereas plasma, which is the largest portion of the blood, is about 55%.

Hematocrit or HCT for short, is the percent of packed red blood cells (or RBCs) in blood, by volume.

Normally, the hematocrit is between 39 to 50 percent in males and 35 to 45 percent in females.

The morphology and characteristics of blood cells can be analyzed histologically by using a common technique called a blood smear or blood film.

A drop of blood is placed on a glass slide, then literally smeared or spread across the slide from left to right, creating a thin layer of cells similar to this image of a blood smear stained with Wright’s stain.

This stain is a mixture of eosin, which is an acidic dye, methylene blue, which is a basic dye, and azures, which are also basic dyes.

It’s commonly used as a differentiating stain for blood smears, bone marrow, and blood parasites.

The head of the blood smear is where the drop of blood was applied to the slide.

When the blood was spread from the head to the right side of the slide, the thin layer of blood gradually became even thinner.

The tail of the smear is the last portion of the smear that visibly tapers even more.

The tail of the smear is not used for examination because the morphology of the cells can appear distorted.

The cells are often abnormally grouped together, and red blood cells will have a loss of central pallor, which could be mistaken for spherocytosis.

If we take a closer look at the blood smear on the left side, there ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Supraventricular_arrhythmias:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nxzb1JXaTACWpI0ikezu6c0YScO1UROA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Supraventricular arrhythmias: Pathology review]]></video:title><video:description><![CDATA[Melissa is a 21 year old college student who is having the time of her life at a party. It’s late, and  unfortunately she has class the next morning, so she drinks a ton of coffee to sober up. On her way out, Melissa collapses to the floor, but wakes up after a couple of seconds. On her way to the emergency room, she tells the paramedics that she’s “aware of her heartbeat”. Then comes Taylor, a 32 year old female who is brought to the emergency room by her partner because she suddenly collapsed for a couple of minutes while cooking dinner. Taylor is now awake, and she tells you that right before collapsing she was feeling dizzy and like her heart was racing, but now she’s fine. They are both placed on different monitors. Melissa’s heart rate is 200 beats per minute and regular, and this is Melissa’s ECG. On the other hand, Taylor’s heart rate is 80 beats per minute and regular, so everything seems fine. However, her ECG shows this. 

All right, so both Melissa and Taylor experienced palpitations and syncope, and their ECGs reveal they both have some form of arrhythmia. The best way to approach arrhythmias is to first: know what a normal ECG looks like, and second: have a good classification system to narrow down the diagnosis. 

First, let’s review the normal electrical conduction pathway in the heart, and how it looks like on an ECG. An ECG tracing specifically shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node and  is then conducted through the atrium, creating the P wave on ECG. From the atrium, electrical activity goes to the atrioventricular, or AV node, after which it goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles. On an ECG, this will create the QRS complex, which represents the depolarization of the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fallopian_tube_and_uterus_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YB9Q4jfVTRSPdTu1fLeLEZp0QU_hx5wj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fallopian tube and uterus histology]]></video:title><video:description><![CDATA[The internal female reproductive organs consist of the ovaries, fallopian tubes, uterus, and vagina.

The fallopian tubes are also often called the uterine tubes or oviducts.

These fibromuscular tubes transport a mature female reproductive cell or egg cell called an ovum from the ovary to the uterus.

Each fallopian tube is about 10-12 cm in length and is divided into four regions: closest to the ovaries is the infundibulum, which has finger-like projections called fimbriae; next is the ampulla; then the isthmus; and finally the intramural part, which travels through the wall of the uterus in order to transport the ovum into either the upper left or right of the uterine cavity.

The ampulla is the longest region and fertilization of an ovum is most likely to occur in this region.

The uterus is a hollow pear-shaped muscular organ that nourishes and supports the growth of an embryo during pregnancy.

The curved top or superior part of the uterus is called the fundus; the largest section in the middle is the body; and the bottom, more cylindrical portion is the cervix.

Although the cervix is part of the uterus, it’s histologically different from the rest of the uterus and will be covered in a separate video.

This video will just focus on the fundus and body of the uterus, which consist of three major layers: the inner endometrium, myometrium, and outer perimetrium, although the perimetrium is too thin to easily see in this image.

The endometrium is the inner mucosal layer that’s lined with simple columnar cells.

The myometrium is a thick and highly vascular wall of smooth muscle.

And the perimetrium consists mostly of a serosal layer or visceral peritoneum that’s continuous with the broad ligament, although, there are portions of the uterus that are surrounded by an adventitial layer of connective tissue instead.

Alright, let’s first take a closer look at the fallopian tubes.

The wall of each fallopian tube also consists of three main layers: an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscular_dystrophies_and_mitochondrial_myopathies:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OWCemLBeSyWdODN1cVHtabJRTreAZodH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscular dystrophies and mitochondrial myopathies: Pathology review]]></video:title><video:description><![CDATA[At the clinic, 32 year old mary comes with her 6 year old son thomas, after noticing he’s often clumsy, weak, and has trouble climbing the stairs of their house. Mary is worried because she had a brother who presented the same symptoms as a child, and developed progressive weakness, until he passed away at 23 years old due to respiratory problems. Upon physical examination, the physician notices that thomas has scoliosis and thick calves. Later that day, 29 year old sarah comes to the clinic with her 10 year old son mike because of progressive muscle weakness and fatigue, as well as vomiting and loss of appetite. In addition, she mentions that he has experienced seizures. 

Based on the clinical findings, the physician concludes that both children have some form of inherited muscular disorder, and orders genetic testing to confirm the diagnosis. Now, let’s go over the two main groups: muscular dystrophies and mitochondrial myopathies.

Muscular dystrophies are a group of genetic disorders characterized by muscle degeneration and weakness. Within that group, dystrophinopathies are the most common, and this includes duchenne muscular dystrophy, or dmd for short, and becker muscular dystrophy, or bmd.

Both duchenne and becker result from mutations in the dystrophin gene, which is found on the x chromosome. For your exams, remember that these are x-linked recessive disorders, which means that all carrier males develop the disease, because they only have one x chromosome and thus one dystrophin gene available. On the other hand, females have two x chromosomes, so even if they have a defective dystrophin gene on one x chromosome, they still have another functional one. However, only one x chromosome gets expressed and the other is inactivated through a process called x-inactivation or lyonization. This inactivation is random which means that every cell could have a chance of having the mutated x chromosome be the active copy. If this is the case for m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_muscle_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y7y59IWLTRiuMnahuA18tvG9Tzan6YJW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac muscle histology]]></video:title><video:description><![CDATA[There are three types of muscles: cardiac, skeletal, and smooth muscle.

Each type has distinct functions as well as structural characteristics that can be identified histologically.

Cardiac muscle makes up the majority of tissue found in the wall of the heart.

Each mature cardiac muscle cell or cardiomyocyte is relatively short, with a length approximately 85-120 µm long and a diameter approximately 15-30 µm.

Histologically, cardiac muscles have quite a few unique characteristics that make it easier to differentiate them from skeletal muscles.

Unlike skeletal muscle, cardiac muscle fibers are branched cells with only 1-2 centrally located nuclei.

Also unique to cardiac muscles are the intercalated discs, which are the specialized junctions between neighboring cells that allow the cells to have synchronized contractions and pump blood out of the heart efficiently.

Let’s first take a look at a longitudinal section of cardiac muscle cells that was stained with Hematoxylin and Eosin (or H&amp;amp;E for short).

If we compare cardiac muscle cells to skeletal muscle cells, we can see there are some key differences between the two muscle types.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration:_Giving_oral_medication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bE4wGsf9S2acqma79xZ3dkgTRTGPhX0g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication administration: Giving oral medication]]></video:title><video:description><![CDATA[Hello. Today I will talk about the different ways to administer oral medication.

Normally you do everything on this list, but to keep things concise, we’ll focus on the steps in blue, and we’ll also include a summary.

Regardless of how you’re administering the medication, sit the patient upright. If they’re not able to sit upright, then they can lie on their side. 

Place tablets into a medicine cup, and have the patient swallow them one at a time. Have a glass of water ready to help the tablets go down.

Now, in some situations, you might want to check if the patient has successfully swallowed the tablets. To do so, have the patient open their mouth before you visually inspect the cheeks and under the tongue.

If the patient is unable to swallow tablets, break them up one at a time in a pill-crusher device, then mix the crushed medication into a teaspoon of soft food, and have the patient eat that.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Celiac_disease:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mvIM6JSKTtSDnLVkkSnqSV8BQ86yQTeJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Celiac disease: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Samantha Wilberson is a 29-year-old female client who was admitted to the Medical-Surgical floor during the night. Ms. Wilberson has a history of celiac disease and was directly admitted to the department by her gastroenterologist after a severe bout of watery diarrhea, vomiting, and dehydration. She says the last time she remembers feeling this sick was over a year ago after she had a bad case of the flu. 

Celiac disease, also known as gluten enteropathy or celiac sprue, is currently understood as an immune-mediated disorder where the gluten in food triggers the body’s immune cells to attack the cells in the small intestine. Celiac disease is hereditary, and people with a first-degree relative with celiac disease, like a parent or sibling, have a 1 in 10 risk of developing it. Some people may be genetically predisposed to Celiac disease. In fact, it is estimated to affect 1 in 100 people worldwide. 

Now, gluten’s found in all sorts of wheats and grains, including rye and barley, and is the main culprit in Celiac disease. The intestine’s inability to fully digest the protein fractions of gluten leads to a build-up of the amino acid glutamine. This accumulation is toxic to the intestinal mucosa, damaging the intestinal villi, which are those small finger-like projections that line the small intestine and help promote nutrient absorption. When the villi become damaged, they can atrophy. This leads to complications like diarrhea, vomiting, fatty stools, abdominal distention, and malabsorption of important nutrients like iron and vitamin B12-- which can lead to anemia. 

Symptoms of Celiac disease are commonly first noticed between the ages of 1 and 5. Usually, there’s a period of time anywhere between 3- 6 months from the time gluten is introduced in the diet and the manifestations of Celiac disease are apparent. And of course, because gluten intake leads to complications, lifelong dietary changes are necessary in order to prevent flare-ups. Occasionally a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_oral_cavity_(dentistry)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6QIeiP_QSLC6HfmAa_ekA_2DRvec1oMt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the oral cavity (dentistry)]]></video:title><video:description><![CDATA[The mouth, or the oral cavity, does a variety of jobs that range from playing the trumpet, or kissing, to more vital roles like  chewing and swallowing your favorite food. 

It’s the point of entry into the gastrointestinal system but also acts as an alternative respiratory pathway in case your nose gets blocked and helps produce and modify sound when you speak or sing.

Now, the oral cavity is a space that extends from the inner surface of the lips to the beginning of the oropharynx, which is marked by the junction of the hard and soft palate above; the anterior pillars, or the palatoglossal arches, laterally; and the terminal sulcus of the tongue below. 

The roof of the oral cavity is formed by the palate, which separates the oral cavity from the nasal cavity above. 

At the bottom, the mylohyoid muscle forms a muscular diaphragm that supports the tongue and the structures of the floor of the mouth. 

Finally, the lateral walls of the oral cavity are formed by the cheeks.

The oral cavity is divided by the teeth and the inner oral mucosa into two parts; the smaller, oral vestibule, and the larger, oral cavity proper. 

The oral vestibule is a small slit-like space between the teeth and inner mucosal lining of the lips and cheeks. 

The mucosa of the lips and cheeks continues onto the gingiva to form the superior and inferior boundaries of the vestibule. 

The oral cavity proper is the space contained within the upper and lower dental arches.

It extends from the inner surface of the teeth and communicates with the oropharynx posteriorly. 

Now, when the mouth is open, the oral vestibule becomes continuous with the oral cavity proper. 

However, some amount of communication is maintained even when the jaws are shut. 

This is achieved through a tiny space called the retromolar fossa, which lies behind the third molar teeth and the ramus of the mandible.

The basic bony framework of the oral cavity is formed by three main bones; the mandible or the lower ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_bowel_disease:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_8GNLu4fSv68aPeOce4sxIFqSiGoxYVw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory bowel disease: Pathology review]]></video:title><video:description><![CDATA[Alex is a 21 year old college student who has a 2 month history of frequent episodes of abdominal pain and bloody diarrhea. Chris is also a 21 year old college student with painful ulcers in the mouth, intermittent abdominal pain, and non-bloody diarrhea that’s been going on for years. In addition, Chris has a history of recurrent kidney stones. 

After careful examination, colonoscopy is ordered in both cases. In Alex’s case, there’s circumferential inflammation that’s continuous throughout an entire section of the rectum and colon. On the other hand, in Chris’ case, there are linear patches of damaged colon with normal mucosa in between, and the rectum is not involved.

Alex and Chris both have inflammatory bowel disease or IBD, which is characterized by chronic gastrointestinal tract inflammation due to autoimmune reactions, as well as systemic symptoms like fatigue, fever and unintentional weight loss. IBD typically has its onset before the age of 30. The exact cause is unknown, but there’s definitely a genetic component because it runs in families. Now, there are two types of IBD - Crohn’s disease and ulcerative colitis. 

Okay, now let’s look at each specific disease, starting with Crohn’s disease, which is mostly caused by an abnormal Th1 cellular response, and a known risk factor is smoking. In Crohn’s disease, the inflammation can pop up anywhere in the GI tract, from the mouth to the anus, but the rectum is often spared. It tends to be most severe at the terminal ileum.

Gastrointestinal symptoms include crampy abdominal pain, watery diarrhea that may or may not be bloody, and sometimes malabsorption symptoms like malnutrition, steatorrhea, or B12 deficiency. A very frequent finding to keep in mind are aphthous ulcers in the mouth. Some individuals may also present esophageal involvement, with odynophagia and dysphagia. 

Extraintestinal symptoms include arthritis, uveitis and episcleritis, and skin lesions like pyoderma gangrenosum and eryt]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Benign_breast_conditions:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yrLc24kVQ3_3Gv93MoXx-Pn0T-m8dcwL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Benign breast conditions: Pathology review]]></video:title><video:description><![CDATA[A 40-year-old musician named Anne-Marie comes to the primary care clinic. She mentions that multiple lumps in her breast would come and go at different times during her menstrual cycles. For the past year, she has also experienced premenstrual breast pain in both breasts. On physical exam, multiple lumps were found on the upper, outer quadrant of the right breast.  At the same time, Ashley, who is a 32-year-old Rehabilitation Technician, comes to the clinic because of a breast lump that she noticed 8 weeks ago. She reports that a lump seems to become more tender and increase in size during her period. Physical examination shows a palpable, mobile, firm mass in the right upper outer quadrant of the right breast. 

At first glance, you’d think Anne-Marie and Ashley both have similar problems, but the fact is, they have different forms of benign breast conditions. Now these include fibrocystic breast changes; benign tumors, such as fibroadenoma, intraductal papilloma, and phyllodes tumor; inflammatory processes, such as fat necrosis and lactational mastitis; and gynecomastia. On your exams, it’s important to differentiate these from possible malignancy based on presentation, history, and other findings.

First, let’s start with fibrocystic breast changes, which are the most common benign lesions of the breast that are typically found in premenopausal women between 20 to 50 years of age. These individuals usually complain about premenstrual breast pain, which is a very high yield fact and the hallmark symptom of this condition; and multiple lumps, which are typically located in the upper lateral quadrant of the breast. But often, these lesions can be bilateral and multifocal. Another high yield fact is that the breast pain and lumps are associated with the phases of the menstrual cycle and cyclic ovarian hormonal stimulation. Fibrocystic breast changes can include simple cysts, which are dilated and fluid-filled ducts; papillary apocrine change or metaplasia; ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Miscellaneous_genetic_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z-seC7SlRyaPUJ5h71mgU2RaTl2Rt7xs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Miscellaneous genetic disorders: Pathology review]]></video:title><video:description><![CDATA[At the clinic, 30 year old Linda comes with her 2 year old toddler for a yearly pediatric checkup. Linda tells the pediatrician that, while she was bathing her son, she noticed that his testes are unusually large. Clinical examination confirms enlarged testes, and additionally, the pediatrician noticed dysmorphic facial features including a long, narrow face; prominent forehead and jaw; and large, protruding ears. Later that day, 27 year old Samantha comes to the clinic with her 5 year old son because she noticed that he often has strange episodes of laughter and smiling. In addition, she mentions that he had experienced seizures several months ago. 

Based on the clinical findings, the pediatrician concludes that both children have some form of genetic disorder, and orders genetic testing to confirm the diagnosis. Now, let’s go over genetic disorders such as fragile X syndrome, imprinting disorders, Cri-du-chat syndrome, and Williams syndrome.

First, let’s start with fragile X syndrome. This is an X-linked disorder caused by inactivation of the  FMR1 gene, which is located on the long arm of the X chromosome. These individuals have over 200 CGG trinucleotide repeats on the FMR1 gene, which leads to its hypermethylation and subsequent inactivation. Fragile X syndrome is the most common cause of inherited intellectual disability, and the second most common cause of genetically associated psychiatric disorders, after Down syndrome. Individuals with fragile X syndrome can have delayed speech and motor development. In addition, individuals may have anxiety disorders, autism, and attention deficit-hyperactivity disorder; as well as mitral valve prolapse. For your exam, it’s important to know the key physical findings of fragile X syndrome includes enlarged testes, also known as macroorchidism; and dysmorphic facial features, like a long narrow face, with large protruding ears, and prominent forehead and jaw. The treatment of fragile X syndrome includes speech,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rheumatoid_arthritis_and_osteoarthritis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/46jssnzFSJCChVTF1DdwfghMSzi18u5e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rheumatoid arthritis and osteoarthritis: Pathology review]]></video:title><video:description><![CDATA[Jody is a 55 year old woman who presents with a 6 month history of bilateral hand and wrist stiffness. 

She mentions that the stiffness lasts for more than an hour a day but tends to improve as she uses the affected joints. 

Examination shows swelling, limited range of movement, and subcutaneous nodules over the proximal interphalangeal joints, but no redness. 

Then you see Kerry, a 60 year old woman who comes in with a 1 year history of pain in the right knee that has gotten progressively worse. 

The pain is worse in the evening or with use of the affected limb and is associated with stiffness, which typically occurs at rest and lasts around 10 to 15 minutes. 

Examination reveals Kerry is obese, has bowing of the right knee, and that the affected joint has a limited range of motion. 

Blood tests are ordered in both cases, showing in Jody&amp;#39;s case high levels of rheumatoid factor (RF) and anti-citrullinated peptide antibody (ACPA), whereas in Kerry&amp;#39;s case both antibodies were absent.

Both people have arthritis. 

Now, a healthy joint usually consists of two bones, each with its own layer of articular cartilage. 

Articular cartilage is a type of connective tissue with a lubricated surface that acts like a protective cushion for bones to smoothly glide against. 

Now, there are many types of joints, including fibrous, cartilaginous, and synovial joints, which have additional components depending on their function. 

For example, synovial joints, like those of the wrist, elbow, knees, shoulders, and hips, are mobile joints that connect two bones via a fibrous capsule that is continuous with the periosteum, which is the outer layer of bones. 

The fibrous capsule is lined with a synovial membrane that has cells that remove debris and produce synovial fluid, which is a viscous fluid found inside the joint capsule to lubricate the joint. 

Together, the synovi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ureter,_bladder_and_urethra_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kW3_1MLfQQ6FJ2oFXssCCZRXTFabSEId/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ureter, bladder and urethra histology]]></video:title><video:description><![CDATA[The ureters are fibromuscular tubes that transport urine from the renal pelvis to the urinary bladder, where it’s stored until it’s emptied through the urethra during urination.

The ureters, bladder, and the initial portion of the urethra are all lined with transitional epithelium, which is also called urothelium.

This specialized epithelium is only found in the urinary system and it allows the conducting passageways and bladder to expand a lot while staying impermeable to water and ions.

Let’s first take a look at a cross-section of the ureter at low magnification, which shows the four main concentric layers of the ureter: the transitional epithelium that lines the mucosa, the lamina propria, the muscularis externa, and the adventitia.

The transitional epithelium is also further divided into 3 layers.

At high magnification, we can see that the most superficial layer consists of large ovoid cells that are called dome or umbrella cells because of their curved apical surface and because they often cover other epithelial cells beneath them.

When the ureter is distended, there are fewer folds in the epithelium, but the epithelium is also able to expand further by flattening and decreasing the amount of overlap of the umbrella cells.

The second layer that comprises the transitional epithelium is an intermediate layer of cuboidal and low columnar cells.

When umbrella cells are damaged, cells from the intermediate layer are able to quickly differentiate in order to replace the damaged umbrella cells.

The third layer of the transitional epithelium is the basal layer, which is a single layer of cuboidal basal cells that rest on the basement membrane.

Although the basement membrane is often hard to identify when using light microscopy.

In this cross-section of the ureter, the lumen is on the far left.

So the first layer starting from the left is the transitional epithelium, which is purple when stained with hematoxylin and eosin.

The next main layer ben]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peripheral_nervous_system_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/a5a22s9AQ7CkuYgISnX3JtMhSDmm7N9e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peripheral nervous system histology]]></video:title><video:description><![CDATA[The peripheral nervous system or PNS consists of all the nerves and ganglia outside of the central nervous system.

The central nervous system consists of the cerebellum, cerebrum, brainstem, and spinal cord.

The peripheral nerves consist of at least one bundle of nerve fibers called a fascicle, which has a surrounding layer of connective tissue called the perineurium.

This cross-section of a larger peripheral nerve was stained with Masson’s trichrome.

If we zoom in to look at just one fascicle, we can see that the thin layer of perineurium surrounding the fascicle is stained a darker blue.

At 40x magnification, we can see the individual nerve fibers, but the structures are not as easy to identify compared to a similar image stained with H&amp;amp;E instead.

The very thin and delicate layer of connective tissue surrounding each nerve fiber is called the endoneurium.

The endoneurium stains a slightly darker pink compared to its contents, which include the individual nerve axons at the center, as well as the Schwann cells or neurolemmocytes that form the myelin sheath around larger nerve fibers.

The myelin sheath can be seen as a thick pink outer ring that surrounds many of the nerve fibers.

The basophilic or purple round nuclei found along the outer edge of the nerves are the nuclei of schwann cells.

Alright, if we take a look at the outer edge of the peripheral nerve, we can see the outermost layer of dense irregular connective tissue called the epineurium.

The epineurium surrounds the entire nerve and also fills the space between fascicles in order to hold the fascicles together along with the blood vessels and loose connective tissue within the nerve.

Now, if we take a look at a longitudinal section of a large peripheral nerve, the nerve fibers have a wavy or zigzag pattern.

This arrangement of the nerve fibers helps to protect the nerves from damage when they’re stretched due to normal movement or if the nerve is connected to flexible ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_coronary_circulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/utqphN6uTHCZLLo7qXvEaARKRi2E3o6J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the coronary circulation]]></video:title><video:description><![CDATA[Our hearts are responsible for sending blood throughout our body and bringing it back to our lungs in a constant exchange of oxygenated and deoxygenated blood.

Here at Osmosis, we also think your hearts are responsible for ‘starting with the heart’ and showing us love every time you watch one of our videos!

But remember, the heart itself also needs its own blood supply, called the coronary circulation, which it gets from the right and left coronary arteries.

The coronary arteries are embedded in fat, and course across the surface of the heart just deep to the epicardium.

Let’s begin with the right coronary artery or RCA, which has its origin in the right aortic sinus and passes to the right side of the pulmonary trunk.

Close to its origin, the RCA gives a sinoatrial nodal branch, which supplies the sinoatrial node. The RCA then descends in the coronary sulcus.

Along the way, it gives off the right marginal branch, which gets close to the apex, but doesn’t reach it and supplies the right border of the heart.

After giving this branch, the RCA turns to the left and continues its journey in the coronary sulcus posteriorly.

Here, the RCA gives yet another branch, the atrioventricular nodal branch, which supplies the AV node.

The RCA usually gives the posterior interventricular branch which descends in the posterior interventricular groove.

This branch supplies areas of both ventricles and sends perforating interventricular septal branches into the IV septum.

Finally, the terminal branch of the RCA continues for a short distance in the coronary sulcus.

The left coronary artery or LCA originates from the left aortic sinus and passes between the left auricle and the left side of the pulmonary trunk and gets in the coronary sulcus.

At the superior end of the anterior interventricular or IV groove, the LCA divides into two branches: the anterior interventricular or IV branch, sometimes called the left anterior descending or LAD and the circumflex branch]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Joints_of_the_wrist_and_hand</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S_RJvP-qR1mD4jzsQNauV8TNT2SZo9n0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Joints of the wrist and hand]]></video:title><video:description><![CDATA[The wrist is a complex joint that serves as the bridge connecting the forearm and the hand together. 

It consists of a main radiocarpal joint, between the radius and the proximal row of the carpal bones minus the pisiform, and the smaller intercarpal joints, which are small joints among the carpals. 

Then we have the hand, which consists of the carpo-metacarpal joints, the intermetacarpal joints, the metacarpophalangeal joints, and the interphalangeal joints. 

Try saying those three times fast!!

Ok, let’s start with the wrist joint. 

First, there’s the radiocarpal joint which is a condyloid type of synovial joint consisting of the distal radius and scaphoid, the lunate, and the triquetrum carpal bones. 

Interestingly enough, the ulna doesn’t participate in the radiocarpal joint.  

It is the articulating surface of the distal radius and the articular disc of the distal radio-ulnar joint which articulate with the proximal row of carpal bones to form the radiocarpal joint. 

The articulating surfaces of the radiocarpal joint are surrounded by the tough joint capsule and synovial membrane, extending from the distal ends of the radius and ulna, to the scaphoid, the lunate, and the triquetrum. 

The joint capsule of the radiocarpal joint is reinforced by a couple of ligaments, both on the dorsal and the palmar sides of the joint. 

The palmar ligaments extend from the distal radius to the two rows of the carpal bones. 

These ligaments strengthen the joint and make it possible for the hand and the radius to move as one unit during supination of the forearm, or turning the palm upwards. 

To remember this, think about cupping both your hands and bringing them together to hold a bowl of ‘soup’, which mimics the movement of supination. 

On the posterior side of the radiocarpal joint there are the dorsal radiocarpal ligaments, which also extend from the distal radius to the carpal bones. 

These ligaments stabilize the wrist joint, and ensure that the hand f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Growing_Popularity_of_PAs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EIhy1zfIToCGoE6U1rXtdv-KTp_SbM-s/_.jpg</video:thumbnail_loc><video:title><![CDATA[The Growing Popularity of PAs]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of The Growing Popularity of PAs through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alagille_syndrome_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BhLKhhuYRpyRBZlt2_9oQjffSiuqC42P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alagille syndrome (NORD)]]></video:title><video:description><![CDATA[Alagille syndrome, or ALGS, is a genetic disorder that can affect multiple organs in the body and cause a variety of abnormalities. 

Alagille syndrome typically affects the liver but it can also cause problems in the heart, kidney, eyes, and bones. 

One of the main liver features of Alagille syndrome is the disruption of bile flow from the liver to the gallbladder. 

Affected individuals have a reduced number of bile ducts in the liver. 

As a result, there is a decrease in bile flow, also known as cholestasis. 

The symptoms and signs of cholestasis include  jaundice, or the yellowing of skin and eyes, severe itching, pale colored stools,  and dark urine. 

Some patients may also have an enlarged spleen or liver. 

Because many necessary vitamins and nutrients need bile to be properly absorbed, people with Alagille syndrome may also experience select vitamin deficiencies, or poor weight gain and growth. 

Deficiencies in specific vitamins may result in vision problems from a lack of Vitamin A, bone weakness from a lack of vitamin D, developmental delays from a lack of Vitamin E, and blood clotting problems from a lack of Vitamin K. 

The heart can also be impacted by Alagille syndrome. 

The most common finding in ALGS patients is peripheral pulmonary arterial stenosis. 

This means that the blood vessels carrying blood to the lungs are narrowed. 

The stenosis typically manifests as a heart murmur, or an extra sound in the heartbeat. 

Symptoms are based on the degree of narrowing of the blood vessel and some people may have no symptoms while others may have dizziness, shortness of breath, increased sweating, chest pains, and cyanosis, or bluish colored skin. 

Children with Alagille syndrome may also have congenital heart defects, or heart problems that one is born with. 

The most common congenital  heart defect in ALGS patients is tetralogy of Fallot. 

Other possible defects include atrial septal defects, patent ductus arteriosus, and  coarctation ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Seronegative_and_septic_arthritis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EKpNaqpaTp6LCKXeVMK3rmwuSW2WdCcJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Seronegative and septic arthritis: Pathology review]]></video:title><video:description><![CDATA[Maurice is a 28 year old male who presents with a 2 year history of gradually progressive low back pain and stiffness. He mentions that the pain wakes him up several times at night, and that the stiffness tends to be worse when he wakes up and improves as he moves. Examination shows mild deformity of the spine and hip, as well as tenderness over the buttock. Then you see Clint, a 63 year old male shows up with a red, warm and swollen left knee, which hurts so much he can barely walk. Clint tells you that symptoms started a few days ago, after he tripped and cut his knee. His body temperature is 38 celsius degrees or 100.4 degrees Fahrenheit. X-rays are ordered in both cases, showing, in Maurice&amp;#39;s case, erosion of the sacroiliac joint. On the other hand, in Clint&amp;#39;s case, X-rays look pretty normal, so an arthrocentesis is performed, revealing that synovial fluid is purulent.

Based on the initial presentation, both cases seem to have some form of arthritis. But first, a bit of physiology real quick. There are many types of joints, including fibrous, cartilaginous, and synovial joints. synovial joints, like those of the wrist, elbow, knees, shoulders, and hips, are mobile joints that connect two bones via a fibrous capsule that is continuous with the periosteum, which is the outer layer of bones. The fibrous capsule is lined with a synovial membrane, which has cells that remove debris and produce synovial fluid. This is a viscous fluid found inside the joint capsule which lubricates joint. Together, the synovial membrane and articular cartilage form the inner lining of the joint space. 

Now, arthritis refers to a group of diseases that cause destruction of one or more joints. First, we have seronegative arthritis, which is called seronegative because there&amp;#39;s an absence of both rheumatoid factor or RF, and anti-cyclic citrullinated peptide antibody or anti-CCP, which are commonly found in rheu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acneiform_skin_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hR-upHJsRguZ409Mwu_mUKxhQ522c9xZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acneiform skin disorders: Pathology review]]></video:title><video:description><![CDATA[At the dermatology clinic, 31-year-old Lauren presents complaining of frequent flushing, mainly on the cheeks, nose, and forehead, for the past five months. She mentions that this seems to get worse after eating anything spicy or drinking alcohol. On examination, there are visible small, superficial, dilated blood vessels around the nares, while no comedones are seen. Based on the initial presentation, Lauren seems to have some form of acneiform skin disorder.

Okay, first, let’s talk about physiology real quick. Normally, the skin is divided into three main layers, the epidermis, dermis, and hypodermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Above the hypodermis is the dermis, containing hair follicles, nerve endings, glands, blood and lymph vessels. And above the dermis is the epidermis, which contains 5 layers of developing keratinocytes. 

Keratinocytes start their life at the lowest layer of the epidermis, so the stratum basale or basal layer. As keratinocytes in the stratum basale mature, they migrate into the next layers of the epidermis, called the stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer.

Before we dive into the various acneiform skin disorders, there are several high yield terms to describe skin lesions. So, macules are flat, well circumcised lesions up to 1 centimeter in diameter, while patches are similar to a macule but are larger than 1 centimeter. Papules are raised bumps that are up to 1 centimeter in diameter, while plaques are like papules but larger than 1 centimeter. Finally, pustules are blisters filled with pus.

All right, onto acneiform skin disorders! Let’s begin with acne vulgaris, which is an extremely common and high yield skin disorder. The cause of acne is not completely understood, but there are a few main factors that contribute to its formation. First, when keratin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breathing_cycle_and_regulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0n4t5KXrR_i-IAERG6KD-fhYQc6HHqx6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breathing cycle and regulation]]></video:title><video:description><![CDATA[Breathing, also known as ventilation, is how the air moves into and out of the lungs. It consists of repetitive cycles of inspiration, when air flows into the lungs; expiration, when air leaves the lungs; and a brief pause, called the rest period, between these two. 

Now, the direction of airflow throughout the breathing cycle depends on the difference between the atmospheric pressure, which is the pressure of the air in the environment, and the alveolar pressure, or the pressure inside the alveoli, which are the tiny sacs of air where gas exchange happens in the lungs. 

An additional parameter is the intrapleural pressure, also called the intrathoracic pressure, which is the pressure of the fluid inside the pleural cavity that surrounds the lungs. 

Intrapleural pressure is usually negative compared to the alveolar or atmospheric pressure, and this is important because the alveolar pressure minus the intrapleural pressure gives the transmural pressure. 

As long as the transmural pressure stays positive, the airways remain open throughout all of the phases of the breathing cycle. 

Ok, now, normal, quiet breathing involves inspiration and expiration of a tidal volume, or VT for short, of about 500 mL, which includes the volume of air that fills the alveoli plus the volume of air that fills the airways. 

Now, according to what is known as Boyle’s law, at a constant temperature, pressure and volume are inversely related to each other, so when the alveolar pressure decreases, more air will enter the lungs, increasing the air volume

With that in mind, let’s establish the starting point for these variables by looking at the lungs during the rest phase of the breathing cycle. 

During rest, the diaphragm is at its balanced position. The alveolar pressure equals the atmospheric pressure to a value of zero centimeters H2O, so there is no pressure gradient, and no air is moving into or out of the lungs. 

The intrapleural pressure is negative, approximately -5]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Artery_and_vein_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qgix02_4QeKC_5huVdqYMnixRMyPLM7L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Artery and vein histology]]></video:title><video:description><![CDATA[The circulatory system consists of two functional parts, the blood circulatory system and the lymphatic system.

The blood circulatory system or cardiovascular system consists of a circuit that transports blood to and from tissues throughout the body.

The heart pumps the blood through a series of arteries that branch into smaller and smaller blood vessels that supply the tissues with blood.

The smallest arteries branch further to become arterioles, which drain the blood into capillaries.

The capillaries form a network of tiny blood vessels that perfuse the tissue.

The capillaries then drain into venules, before converging to form small veins.

The veins continue to join or converge with one another, forming larger and larger veins that eventually drain back into the heart.

Arteries and veins have walls that share a common overall structure that consists of three layers: the tunica intima, tunica media, and tunica adventitia.

The inner layer or tunica intima is lined with a single layer of a specialized epithelium called the endothelium, which acts as a semipermeable barrier.

The subendothelial layer is the layer beneath the endothelium and is still part of the tunica intima.

This layer, which consists of loose connective tissue and occasionally smooth muscle as well.

In some arteries, the tunica intima will also have a very thin layer of elastic tissue along the outer edge of the subendothelial layer called the internal elastic lamina.

The internal elastic lamina has holes throughout the layer, which allow substances from the blood to more easily diffuse through this layer, deeper into the wall.

The middle layer or tunica media consists mostly of smooth muscle.

Arteries will also contain a lot more elastic fibers in comparison to veins.

Both the smooth muscle and elastic fibers are arranged in circular or concentric layers surrounding the lumen of the blood vessel.

Similar to the tunica intima, in arteries, the tunica media may also]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atomic_units_and_moles</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WbElPW0eRc_Gn4xbALhVNxJBRUyHiozJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atomic units and moles]]></video:title><video:description><![CDATA[Atomic mass units and moles are units of measurement in chemistry, which allow us to easily work with very small and very large numbers. 

For example, the mass of a hydrogen atom is 1.6735 times 10 raised to the negative 24th grams.

It is inconvenient to work with numbers like this for such small objects, and so chemists use the atomic mass scale instead. 

One atomic mass unit is equal to 1.66054 times 10 raised to the negative 24 grams. 

So in order to find the mass of a hydrogen atom in atomic mass units, we multiply the mass by the conversion factor consisting of one atomic mass unit divided by 1.66054 times 10 raised to the negative 24 grams. 

The grams cancel out, and we end up finding that one hydrogen atom has a mass of 1.0078 atomic mass units, or a.m.u. 

A hydrogen atom consists of a proton and an electron. 

Electrons have a mass that is negligibly small compared to a proton. 

As a result, we generally round the mass of an electron down to zero, and just estimate that the mass of a hydrogen atom is equal to the mass of one proton inside the atom’s nucleus. 

So one proton has a mass of about one a.m.u. 

For atoms containing neutrons, the mass of a neutron is almost identical to the mass of a proton, and so we say that a neutron also has a mass of about one a.m.u. 

So we can estimate the mass of a given atom by counting the total number of  utrons in the atom’s nucleus, which gives us the mass in a.m.u.

For example, let’s take an atom of carbon-12.  

Carbon-12 has a mass number of 12 which tells us that carbon has a total of 12 protons and neutrons combined.  

Since each proton and neutron has a mass of about 1 a.m.u., we would estimate the mass of the carbon-12 atom to be 12 a.m.u.  

Actually, the atomic mass unit is currently defined as assigning a mass of exactly 12 amu to a carbon-12 atom.  

But many elements exist in different isotopes, which have the same number of protons but different numbers of neutrons. 

As a result, these]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Michael_Gustafson:_President_of_U_Mass_Memorial_Medical_Center_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ckvbxNuFSL2IZP6cVwdFyecGScmjCoXn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Michael Gustafson: President of U Mass Memorial Medical Center (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Michael Gustafson: President of U Mass Memorial Medical Center (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kathy_Boden_Holland:_Group_President,_Adtalem_Global_Education_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lE3dDrx3QKyjbcE9vB4WTQo1TDKWoS9v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kathy Boden Holland: Group President, Adtalem Global Education (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Kathy Boden Holland: Group President, Adtalem Global Education (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abby_Levy_&amp;_Alan_Patricof:_Co-founders_of_Primetime_Partners_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-RzVTI8OQ0G_aM5AjPROkEJPQpiHo-z7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abby Levy &amp; Alan Patricof: Co-founders of Primetime Partners (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Abby Levy &amp; Alan Patricof: Co-founders of Primetime Partners (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Joseph_Kvedar:_President_of_the_American_Telemedicine_Association_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ydy2DhPyQ-a9AkqyyB_I95WKQueUUOma/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Joseph Kvedar: President of the American Telemedicine Association (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Joseph Kvedar: President of the American Telemedicine Association (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mel_Hall:_Former_CEO_of_Press_Ganey_Associates_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qt16hbnnR3iw2JYpiPnGzDd7SaCdrEMZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mel Hall: Former CEO of Press Ganey Associates (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Mel Hall: Former CEO of Press Ganey Associates (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Nicole_Keith:_President_of_the_American_College_of_Sports_Medicine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yBQCJeusS6aF1U0-H3mq9irbQQ_FOtIC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Nicole Keith: President of the American College of Sports Medicine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Nicole Keith: President of the American College of Sports Medicine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Lawrence_Chin:_Dean_of_the_College_of_Medicine_at_SUNY_Upstate_Med_U_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QOuYo-eARjyvz67yIM_8eZb-S06w_0H_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Lawrence Chin: Dean of the College of Medicine at SUNY Upstate Med U (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Lawrence Chin: Dean of the College of Medicine at SUNY Upstate Med U (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cyril_Phillip:_Principal_at_Providence_Ventures_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fzo_wNKuRw2NrPKBDeadBmyFQau6bnoC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cyril Phillip: Principal at Providence Ventures (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Cyril Phillip: Principal at Providence Ventures (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pleural_effusion,_pneumothorax,_hemothorax_and_atelectasis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gj8980RAQIWueCm-0XHhSKBzSzykW907/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review]]></video:title><video:description><![CDATA[During a night shift in the Emergency Department, you see George, a 21 year old, who complains of sharp, stabbing left-sided chest pain and shortness of breath, both of which appeared suddenly while he was playing video games. He is a smoker and mentions his younger brother suffered a pneumothorax last year. On examination, the left side of his chest is slightly more expanded than the right side and his breathing is very shallow. The affected side is also hyperresonant on percussion and there’s diminished breath sounds on auscultation. Then there’s Anna, a 58-year-old with progressively worsening dyspnea, pleuritic chest pain, and fever. She has a history of diabetes and cirrhosis. On examination, her blood pressure and heart rate are both increased, and jugular venous pressure is elevated. Also, the base of her left lung field is dull to percussion with decreased breath sounds. Her lower extremities have pitting edema up to the knee. X-rays were performed in both individuals. In George’s case it showed a retracted visceral pleural edge with a decrease in the left lung volume. In Anna, it showed left sided costophrenic angle blurring. 
Now, they both seem to present with conditions affecting the pleura. But to understand the pathophysiology, it’s a good idea to review the anatomy and physiology first.  Ok, so the pleura covers the lungs and consists of the parietal pleura, which is stuck to the chest wall, and the visceral pleura, which is stuck to the lungs. It extends all the way up to the clavicle and first rib, which is something that will help you understand why neck injuries can cause tension pneumothorax. Also know the inferior limit of the pleura is the 7th rib on the midclavicular line, the 10th rib on the mid axillary line, and the 12th rib on the paravertebral line. Between the layers of the pleura is the pleural space, containing 10 to 20 milliliters of a lubricating fluid that helps reduce friction as the lungs expand and contract. There’s als]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autosomal_trisomies:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iHExkkTkTQidhM5xe0XHRky-TpuDzvSb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autosomal trisomies: Pathology review]]></video:title><video:description><![CDATA[A 1 day old newborn boy, named Nikolas, is brought to the emergency department due to frequent vomiting of a &amp;quot;greenish liquid” immediately after meals. Physical examination shows a flat nasal bridge, small mouth with a protruding tongue, and a single palmar crease on each hand. A plain abdominal x-ray reveals a double bubble appearance on the upper abdomen, with no gas seen distally. The infant was born at home to a 41 year old mother who received no prenatal care and is unable to provide any medical history. Some days later, a 39 year old mother gives birth to a female baby, named Taylor, through emergency cesarean section at 36 weeks of gestation. Taylor is found to have a punched out lesion on the left side of her scalp, where skin is missing. On further examination, her head is smaller compared to infants of the same age and gender, and she has an extra finger on her right hand. The mother lives in a remote area and was not able to receive any prenatal care. Finally, 37 year old Annita visits the prenatal clinic at 16 weeks of gestation for the quadruple screen test. Results show a low level of maternal serum alpha-fetoprotein or AFP for short, low human chorionic gonadotropin or hCG, low unconjugated estriol, and normal inhibin A. She has not undergone any first trimester screening.

Based on the initial presentation, all cases seem to have some form of autosomal trisomy. This is where the baby ends up with three copies of an autosomal chromosome instead of two. For your exams, remember that, in most cases, this results from a process called nondisjunction. This typically occurs during meiosis 1, where a chromosome pair in the egg or sperm cell doesn’t split apart. So the child of this individual could receive 2 chromosomes from that parent and 1 more from the other parent. The resulting zygote will have three autosomal chromosomes or an autosomal trisomy.

Another topic examiners love to focus on is Robertsonian translocation, which means t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skin_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uw0l6Gc7SkaJf3mO7D0t18cQQtOMaBI8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skin histology]]></video:title><video:description><![CDATA[The skin covers and helps protect the body from its environment.

It’s also known as the integument, which is part of the integumentary system.

The integumentary system also consists of structures that are derivatives of the skin, such as nails, hair, and glands within the skin, like sweat glands.

The skin can be split into two general types: thick skin and thin skin.

Thick skin has a much thicker outer layer of epidermis that helps to protect the body in places where it’s regularly exposed to slightly harsher physical conditions.

That’s why it’s typically found in places such as the palms of the hands and soles of the feet.

Thick skin can also be differentiated from thin skin because it doesn’t have hair follicles or oil-producing glands called sebaceous glands.

It does still contain sweat glands though.

The overall thickness is often more than 5mm, whereas thin skin is typically only between 1-2mm thick.

Thin skin has all the same structures as thick skin except it has a thinner epidermis and additional structures such as hair follicles and sebaceous glands.

If we compare histologic images of thick skin and thin skin at low magnification, we can see the three main layers that make up the skin.

At the top of the image is the surface epidermal layer or epidermis that’s significantly thicker in thick skin.

Hair follicles are only found in thin skin, and as we can see in this image, they’re located in the middle layer called the dermis or dermal layer.

The third and deepest layer is called the hypodermis, which consists mainly of adipose and loose connective tissue, although this image of thick skin doesn’t include the hypodermis.

Now, if we look at just the epidermis, there are sub-layers that make up the epidermis.

Starting from the base of the skin is the stratum basalis, spinosum, granulosum, lucidum, and corneum at the surface.

The Stratum Lucidum can only be seen histologically in very thick skin.

If we take a closer look at the ep]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_elbow_joint</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/flQoxjVVQCiQ-1qdf1wcOrsYSRWiEexR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the elbow joint]]></video:title><video:description><![CDATA[The elbow joint is a hinge type of synovial joint, and it’s actually made up of two separate joints which work together as one. 

The first joint, called the humero-ulnar joint, is between the trochlea of the humerus and the trochlear notch of the ulna; and second one, called the humero-radial joint situated between the capitulum of the humerus and the superior aspect of the head of the radius. 

A good way to remember this is thinking of the ‘CRAzy TULips’. The CRA in CRAzy represents the Capitulum which articulates with the RAdius, and the TUL in TULips represents the Trochlea which articulates with the ULna.

The elbow joint is covered by a synovial membrane, which is surrounded by a joint capsule. 

The joint capsule extends from the margins of the articular surfaces of the capitulum and trochlea on the humerus, to the coronoid process anteriorly; and to the olecranon fossa posteriorly. 

On both the medial and lateral sides, the elbow joint is strengthened by two strong ligaments called the collateral ligaments which are thickenings of the elbow joint capsule .

On the medial side, also called the ulnar side, there’s the ulnar collateral ligament, which extends from the medial epicondyle of the humerus to the coronoid process and the olecranon of the ulna. 

The ulnar collateral ligament actually consists of three separate bands: anterior, posterior and oblique. 

The anterior band is the strongest, and it runs from the medial epicondyle to the tubercle of the coronoid process. 

This band helps limit elbow extension. Next, there’s the fan-shaped posterior band, the weakest of all, and it runs from the medial epicondyle to the olecranon of the ulna. 

This helps limit elbow flexion. Finally, there is the thin oblique band, which  makes the socket for the trochlea slightly deeper, reducing the chance of dislocation. 

On the lateral side, there’s  the radial collateral ligament, which extends from the lateral epicondyle of the humerus to the annular li]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bones_of_the_lower_limb</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CQIS4zJmTUO0z_bAcrOViYmSRQOAVrR-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bones of the lower limb]]></video:title><video:description><![CDATA[The foot bone’s connected to the...leg bone. And the leg bone’s connected to the... thigh bone! Alright, as a quick recap… just kidding. The lower limbs actually have an incredibly detail-rich skeleton that can be divided into two functional components: the pelvic girdle, which connects the lower limb to the axial skeleton, and the bones of the free lower limb. 

The pelvic girdle is a bony ring, known as the pelvic ring, consisting of the right and left hip bones, and the sacrum which is common to both the pelvic girdle and axial skeleton. Each hip bone consists of the ilium, ischium, and pubic bone and has three articulations. Posteromedially, it articulates with the sacrum at the sacroiliac joint, anteromedially  it articulates with the other hip bone at the pubic symphysis. And finally, it articulates with the head of the femur to form the hip joint. 

Ok so, the ilium is the largest and most superior part of the hip bone and it can be divided into a body and a wing. The wing, or ala of the ilium,has a lateral and a medial surface, a crest, and two borders: anterior and posterior. Superiorly, there&amp;#39;s the iliac crest, which begins at the anterior superior iliac spine and it extends posteriorly to the posterior superior iliac spine. The crest has an internal and external lip, and serves as an important attachment site for muscles and deep fascia. Next, the lateral surface of the ala has three rough arched lines called the posterior, anterior, and inferior gluteal lines, where the gluteal muscles attach, which are the muscles of your bottom. Next, the medial surface can be divided into two by the internal lip of the iliac crest. The anterior portion is concave, and it forms the iliac fossa - which is where the iliacus muscle attaches.  The posteromedial portion is rough and it presents the auricular surface - which is shaped like an ear and articulates with an identical surface on the sacrum to form the sacroiliac joint.. Next, the anterior borde]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vessels_and_nerves_of_the_forearm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I01wGj3bSpuH7yBEe7USRR9vTZeDcoS7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vessels and nerves of the forearm]]></video:title><video:description><![CDATA[The forearm contains a vast network of vessels and nerves. 

Most of these originate in the axilla, and to get to the forearm,  most of them pass through the cubital fossa, which is a small, triangular  fat-filled pit on the anterior part of the elbow. 

The cubital fossa has three borders. 

The superior border consists of an imaginary line joining the medial and lateral epicondyles of the humerus; the lateral border is the medial border of the brachioradialis muscle; and the medial border is made up by the lateral border of the pronator teres muscle. 

Deep within this region, is the floor of the cubital fossa which is formed by two muscles; the brachialis and supinator. 

Superficially, there’s the roof, which is formed by the antebrachial fascia and reinforced by the bicipital aponeurosis coming from the biceps brachii, as well as the overlying subcutaneous tissue and skin. 

The cubital fossa contains some important structures. 

From medial to lateral, there are the median nerve: the brachial artery which bifurcates into the radial artery laterally, and the ulnar artery medially, the accompanying veins to these deep arteries; the tendon of the biceps brachii muscle; and radial nerve on the most lateral part found between the brachioradialis and brachialis muscles. 

Overlying the brachial artery and median nerve is the bicipital aponeurosis, which protects these structures, in situations like when blood is drawn from superficial veins such as the median cubital vein which lies superficial to the bicipital aponeurosis. 

So that&amp;#39;s the cubital fossa, short and sweet. 

Ok, now let’s see some details about the arteries of the forearm. 

The main arteries are the ulnar and radial artery, which are the terminal branches of the brachial artery arising in the cubital fossa. 

Starting with the ulnar artery, it emerges from the brachial artery in the cubital fossa. 

The ulnar artery runs deep to the superficial and intermediate flexor muscle groups]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_anterior_and_medial_thigh</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TdMpTzBHTg_NCzMXpZfodvjKS3eddYfg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the anterior and medial thigh]]></video:title><video:description><![CDATA[The thigh is the part of the lower limb located between the hip and the knee, and it can be divided into anterior, medial and posterior compartments that surround the femur. These compartments are formed by the intermuscular septa that originate on the inner surface of the fascia lata and attach to the linea aspera of the femur.

And, more importantly, each compartment contains its own muscles, as well as blood vessels and nerves. Each muscle in the three compartments has a proximal origin and distal insertion, a neurovascular supply, and a specific action on the joints of the lower limb.

So, the anterior compartment, which is the largest one, includes the anterior thigh muscles, which can function as flexors of the hip and extensors of the knee. First, the flexors of the hip include the pectineus, iliopsoas, and sartorius.

The pectineus is an almost rectangular muscle located in the anterior part of the superomedial portion of the thigh, and it’s often composed of a superficial and deep layer. It originates on the superior ramus of the pubis and inserts on the pectineal line of the femur, just inferior to the lesser trochanter.

Now, this muscle has a lot of nerve, mainly because of its dual nerve supply. One supply is from the femoral nerve, and the second supply is from a branch of the obturator nerve. Finally, the pectineus has 3 main actions - it adducts, flexes, and medially rotates the thigh. This is one muscle, two nerves, and three actions!

Second, the iliopsoas is the most powerful of the hip flexors. It has most of its mass located in the posterior wall of the abdomen and greater pelvis. Actually, it consists of two parts. Its broad lateral part is called the iliacus muscle, which arises from the floor of the iliac fossa, ala of the sacrum, inner lip of the iliac crest, and anterior sacroiliac ligaments.

And its long medial part is called the psoas major. It originates from the sides of the T12 to L5 vertebrae and the discs between them, as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abdominal_quadrants,_regions_and_planes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4ICcKnVAT4SO55or8XI6a-bKRcKNP4oZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abdominal quadrants, regions and planes]]></video:title><video:description><![CDATA[The abdomen is a part of the body sometimes casually referred to as the belly or torso.

The organs within this area are said to be contained within a space known as the abdominal cavity, which is bounded by the musculo-aponeurotic walls anterolaterally.

Superiorly, the abdominal cavity extends into the thoracic cage to the 4th intercostal space and is separated from the thoracic cavity by the diaphragm.

Some organs found within the upper region of the abdominal cavity, such as the spleen, liver, stomach and parts of the kidneys, are actually protected by your rib cage.

Inferiorly, the lower portion of the abdominal cavity doesn&amp;#39;t have a physical boundary because it’s continuous with the pelvic cavity; so sometimes, they’re lumped together under the term “abdominopelvic cavity”.

However, to better understand the anatomy, the inferior boundary, which separates the abdominal cavity from the pelvic cavity is an imaginary plane called the pelvic inlet, which divides the pelvis into a greater, or false pelvis, above, and a lesser, or true pelvis, below.

Similar to how the ribcage protects some of the superior organs of the abdominal cavity, the greater pelvis protects some of the lower organs of the abdomen, including portions of the ileum, cecum, appendix, and sigmoid.

You may have already noticed how many organs there are inside the abdominal cavity. So to make it easier to describe their location, the abdomen is often divided into anatomical quadrants, of which there are four, or regions, of which there are nine.

Let&amp;#39;s start with the quadrants. To get those four quadrants, imagine a line running down from the xiphoid process, or tip of the sternum, all the way down to the pubic symphysis. This line is the median plane and divides the abdomen into a left and a right half.

The second imaginary line goes straight through the belly button or umbilicus, from left to right. This line creates the transverse or transumbilical]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Salmonellosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cH2zZg2nRVu5gnldgemSfxAaTKym_J7W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Salmonellosis]]></video:title><video:description><![CDATA[Salmonellosis is a bacterial infection caused by Salmonella bacteria,  which have 2 species, S. enterica and S. bongori and over 2400 serotypes. 

Some of these serotypes are named. 

In such cases, people often shorten the scientific name to include only the genus and serotype; for example, S. enterica, subspecies enterica, serotype Typhi is shortened to Salmonella Typhi. 

Salmonellosis is usually transmitted through contaminated food or water and is typically caused by serotypes of the Salmonella enterica species.

All Salmonella bacteria are bacilli, which means rod-shaped bacteria. 

Salmonella has flagella all over its surface, allowing it to move. 

In humans, most cases are caused by the S. Enteritidis and S. Typhimurium serotypes.

Other serotypes of Salmonella enterica cause similar infections in other warm-blooded animals. 

These include S. Gallinarum in poultry, S. Abortusovis in sheep, S. Choleraesuis in pigs, S. Dublin in cattle, and S. Arizonae in reptiles, among others. 

All of these strains can also infect humans. 

In humans, Salmonella is typically transmitted through the fecal-oral route, after infected feces come into contact with various foods including raw meat, poultry, eggs, unpasteurized milk, and crops. 

Salmonella can also be present on the skin of reptiles and birds and be transmitted through contact with these animals. 

When the bacteria are ingested, they travel through the digestive tract, invading and multiplying in intestinal cells. 

Infected cells then release proinflammatory cytokines, causing an inflammatory response. 

This results in gastroenteritis, or inflammation of the intestinal tract, causing abdominal pain and severe diarrhea.  

The bacteria can also enter the blood, termed bacteremia, and cause enteric fever.  

From there, they can make their way to other organs like the liver, lungs, heart, and bone to cause focal Salmonella infection.  

These symptoms and signs usually arise in humans between 12 and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Zoonotic_Influenzas</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S9hng8mWSgCfOCWrKh96AwT8SZOHOtYU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Zoonotic Influenzas]]></video:title><video:description><![CDATA[Zoonotic influenzas spread around the world in yearly outbreaks, resulting in about three to five million cases of severe illness and approximately half a million deaths. 

‘Zoonotic’ means they are caused by pathogens, in this case viruses, that have hopped from infected animals to humans. 

They have been found in a variety of animals, like domestic poultry, wild birds, and pigs. 

In humans, they typically cause mild to severe respiratory symptoms and fever, and they also have the potential to cause epidemics or pandemics. 

Influenza viruses belong to the Orthomyxoviridae family. 

They are segmented, negative sense, single-stranded RNA viruses. 

Only types A and B cause disease in humans, with type A influenza viruses being the most common. 

Influenza viruses are classified based on two surface proteins: hemagglutinin, or H protein, and neuraminidase, or N protein, of which there are many different types. 

So for example, the H1N1 virus that causes swine flu has H protein type 1 and N protein type 1. 

Among other things, these surface proteins determine what species the virus can infect. 

However, influenza A viruses can undergo antigenic shifts where two strains of the virus mix their genome to create a new virus with a different set of H and N proteins.  

This allows the new virus to infect different species from the original strains. 

The most common types of zoonotic influenzas are avian, meaning originating from birds, and swine, meaning originating from pigs. 

Avian flu is caused entirely by influenza A virus and transmission is often through direct contact with infected poultry as the birds are slaughtered or plucked. 

Based on pathogenicity, avian influenza is divided into two types: high pathogenicity  or low pathogenicity. 

The type with the greatest risk is highly pathogenic avian influenza, or HPAI. 

The most well-known HPAI strain is H5N1, which first appeared in China in 1996, and was then responsible for the bird flu outbreak in 2004. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_heart</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K0_KqQC1RdGBP1_FcK2Yi1_HQ1awBea_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the heart]]></video:title><video:description><![CDATA[The heart is a muscular organ just slightly bigger than a person’s loosely clenched fist. It is located in the thorax - more specifically, between the two lungs, in a space called the mediastinum. The heart is covered by a tough membrane called the pericardium, that separates the heart from the other structures in the mediastinum. This position allows the heart to do its job, which is to pump oxygen-rich blood to the entire body, and to send poorly oxygenated blood to the lungs, where gas exchange takes place. The heart is made up of four chambers, and as a whole can be functionally divided into the right heart, made up of the right atrium and the right ventricle, and a left heart, made up of the left atrium and left ventricle. And both atria have pouch-like protrusions called auricles, which can increase their capacity when needed.

Ok, now, poorly oxygenated blood from our bodies and tissues enters the right atrium through the superior vena cava and inferior vena cava. From there, blood passes into the right ventricle, which pumps into the pulmonary trunk, on a voyage towards the lungs and is considered part of the pulmonary circulation. On the other hand, after gas exchange takes place in the lungs, oxygenated blood returns from the lungs through the four pulmonary veins, which drain into the left atrium. Then, oxygenated blood goes in the left ventricle and from there, it’s pumped into the aorta so that it reaches the whole body and is considered part of the systemic circulation.

So, looking at it in three dimensions, the heart looks like an upside down, tipped-over pyramid with four sides, a base that’s mostly posterior and an apex, or tip, that points anteriorly and slightly to the left.

On an anterior or posterior view in two dimensions, the heart is shaped like a trapezoid, so it has a superior and inferior as well as a right and left border. It is important to understand what comprises the borders of the heart because the heart is rotated to the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_lungs_and_tracheobronchial_tree</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hxl6S2AMRKKsmuAL921kf4s5R32xtvKe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the lungs and tracheobronchial tree]]></video:title><video:description><![CDATA[The lungs are a pair of air-filled organs located in the thoracic cavity, on the left and right side, separated by a central mediastinum, which contains the heart, thoracic parts of the great vessels, thoracic parts of the trachea, esophagus, thymus, and other structures.

It’s also important to notice that the heart is turned and extends towards the left side of the thoracic cavity, imposing on the left lung markedly more than the right so the anatomy of the two lungs is not completely symmetrical.

Each lung is covered by a membrane called the pleura, which is subdivided into the visceral pleura that intimately adheres to the lung and the parietal pleura that lines the pulmonary cavity.

Between them, there’s the pleural cavity, which is normally filled with a thin film of fluid.

Now, on the medial part of each lung, there’s the pulmonary hilum, where the root of the lung passes through.

The root of the lungs is made of structures like the main bronchus arteries, and veins.

The lungs are light, soft and spongy, and each of them has an apex a base, 3 surfaces: costal, mediastinal and diaphragmatic, and 3 borders: anterior, inferior and posterior.

The apex is the blunt superior end of the lung above the level of the first rib into the root of the neck, while the base is the concave inferior surface of the lung that rests on the diaphragm.

Now for the specifics.

The right lung is larger and heavier than the left, but it’s shorter and wider, because the right dome of the diaphragm is higher and the heart and pericardium are more to the left.

The right lung is divided into three lobes, superior, middle and inferior, by the horizontal fissure and the oblique fissure, which can be seen on all the surfaces of the lung.

On the other hand, the left lung has a single left oblique fissure, which can also be seen on all surfaces and divides the left lung into two lobes: superior and inferior.

Also on the left lung, there’s a deep cardiac notch on the an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eye_conditions:_Refractive_errors,_lens_disorders_and_glaucoma:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JK5ZRtKzQ162L22u5PZq2XfzTFGlJ9l7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eye conditions: Refractive errors, lens disorders and glaucoma: Pathology review]]></video:title><video:description><![CDATA[At the ophthalmology clinic, 61-year-old Pedro presents with vision impairment that has been progressive over the past couple of years. He denies experiencing any pain. His past medical history is significant for type 2 diabetes mellitus.  Physical examination shows bilateral clouding of the lens. 

Next to him, 68-year-old Eileen comes in. She complains that, about an hour ago she started experiencing excruciating pain in her right eye, accompanied by blurry vision and seeing halos around bright lights. Eileen also tells you that she has since vomited twice. On clinical examination, her right eye is red, with a dilated pupil that fails to react to light. Her left eye appears unremarkable.

Based on the initial presentation, both Pedro and Eileen have some form of eye condition. But first, a bit of physiology. If we take a closer look at a cross-section of an eye, we can see that it’s split into three different chambers: anterior, posterior, and vitreous. The anterior chamber includes the area from the cornea to the iris. The posterior chamber is a really narrow space between the iris and the lens. Finally, the much larger vitreous chamber includes the space between the lens and the back of the eye. 

Now, both the anterior and posterior chambers are located in the anterior segment of the eye, while the vitreous chamber is part of the posterior segment of the eye. Both chambers in the anterior segment, that is, the anterior and posterior chambers, are filled with a clear watery fluid called aqueous humor, while the vitreous chamber is filled with a clear but thicker fluid called the vitreous humor. 

Okay, let’s start with what’s probably the most common group of eye conditions, so refractive errors. Normally, when the eye is in a relaxed state, the refractive power of the cornea and lens help focus light onto the retina. The retina is like a movie screen and the distance from the projector is the axial length of the eye. If it’s too close or too far from ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ventricular_arrhythmias:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3vmCOR4MQg2pOkM8LDIfELosSE_rRGkn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ventricular arrhythmias: Pathology review]]></video:title><video:description><![CDATA[Clint is a 19 year old male that’s brought to the emergency department for acute chest pain. Upon examination, you notice that his heart rate is really fast, about 170 beats per minute. He has a history of depression, and is currently being treated with TCAs. He is otherwise healthy. A few minutes after arriving, Clint loses consciousness. His ECG shows this. 

All right, so based on his presentation and ECG, Clint has some form of arrhythmia. The best way to approach arrhythmias is to one: know what a normal ECG looks like, and two: have a good classification system to narrow down the diagnosis. To help identify an irregular rhythm, you can look at the morphology of the waveform and make sure that there is a P wave before every QRS complex, and a QRS complex after every P wave. 

Now let’s take a look at the heart rate. The resting heart beats at a rate between 60 to 100 times per minute, and each of those beats starts off with depolarization of the sinoatrial node, and so we call it a normal sinus rhythm. It&amp;#39;s also important to know that there is typically a delay in the conduction at the AV node and the Bundle of His, which gives some time for ventricular filling before the ventricle contracts. On the ECG, this is represented by the PR interval, which should be less than 5 small boxes, or 200 milliseconds. 

Now, any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical activity is called an arrhythmia. Arrhythmias could be completely asymptomatic, and be picked up incidentally on an ECG. Arrhythmias can also present with palpitations, which is a sensation of your heart beating too hard or fast, fluttering, or skipping a beat. Additionally, they may alter cardiac output, causing individuals to present with signs of hypotension and decreased brain perfusion, like dizziness, altered mental status, or syncope. 

If an arrhythmia is really fast, the heart muscles now demand more oxygen, and if oxygen supply i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vesiculobullous_and_desquamating_skin_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g44CJzkTQM2J7DUg00T4lEVQQ8CYU2y5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vesiculobullous and desquamating skin disorders: Pathology review]]></video:title><video:description><![CDATA[At the dermatology clinic, 58 year old Alan presents complaining of painful lesions on his skin and mouth for the past two months. On examination, there are flaccid bullae with erosions all over his trunk and extremities, as well as erosions on the oral and gingival mucosa. When lateral pressure is applied to a lesion, the outermost layer seems to slough off. 

On the same day, 17 year old Gabriella comes in with an intensely itchy rash that appeared a couple of weeks ago. She has also experienced frequent nausea and diarrhea after meals. Physical examination shows multiple papules, vesicles, and bullae on both of her knees, forearms, and elbows, as well as her back and buttocks. Lab tests reveal elevated levels of anti-gliadin IgA and IgM. Based on the initial presentation, Alan and Gabriella seem to have some form of vesiculobullous or desquamating skin disorder. 

Okay, first, let’s talk about physiology real quick. Normally, the skin is divided into three main layers, the epidermis, dermis, and hypodermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Above the hypodermis is the dermis, containing hair follicles, nerve endings, glands, blood and lymph vessels. And above the dermis is the epidermis, which contains 5 layers of developing keratinocytes. 

Keratinocytes start their life at the lowest layer of the epidermis, so the stratum basale or basal layer. As keratinocytes in the stratum basale mature, they migrate into the next layers of the epidermis, called the stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer. 

Before we dive into the various inflammatory skin disorders, there are several high yield terms to describe skin lesions. The most important here are the vesicles, which are up to 1 centimeter in diameter and look like clear blisters filled with fluid, and bullae, which are fluid-filled blist]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_breast</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/voqP1hJDTYO6eAVDzKkW_gFJQCyP39QK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the breast]]></video:title><video:description><![CDATA[The breasts are the most prominent superficial structures in the anterior thoracic wall consisting of glandular tissue and a supporting fibrous and fatty matrix.

This glandular tissue, or mammary glands, are found in the subcutaneous tissue overlying the pectoralis major and minor muscles.

The amount of fat surrounding this glandular tissue will determine the size of the breasts.

Breasts have a circular body and a nipple in the center, surrounded by a pigmented area of skin called the areola.

Each breast has the following boundaries: transversally from the lateral border of the sternum to the midaxillary line and vertically from the second through the sixth ribs.

Two thirds of the underlying tissue of the breast is formed by the pectoral fascia covering the pectoralis major and the other third is formed by the fascia that covers the serratus anterior muscle.

A small part of the breast might extend along the inferolateral edge of the pectoralis major, going towards the axillary fossa or the armpit.

Here it forms an axillary process or tail, called the tail of Spence.

Now, let’s take a look at this sagittal section of the female breast.

As you can see, there’s a fine space between the breast and the pectoral fascia.

This is called the retromammary space or bursa, which is a loose subcutaneous tissue plane.

This plane contains a small amount of fat which allows the breast to move a bit on the pectoral fascia.

Breasts contain the mammary glands responsible for lactation in females.

Mammary glands are made up of 12 to 20 lobes, each of them containing many smaller lobules.

These smaller lobules have grape-like clusters of alveoli that contain mammary secretory epithelial cells, the milk producing cells of lactation.

These alveoli, lobules and lobes are connected through a network of ducts called the lactiferous ducts, and eventually form a unique lactiferous duct for each lobe which opens independently to the areola to drain the milk produced dur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_pelvic_girdle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5Wgz7SDXScONdUhZlK9rPNLUTo6JN_Va/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the pelvic girdle]]></video:title><video:description><![CDATA[The pelvic girdle or the bony pelvis is a bony ring, formed by the left and right hip bones and the sacrum, and it surrounds the pelvic cavity, and connects the vertebral column to the lower limbs.

The main functions of the pelvic girdle are to transfer the weight of the upper body to the lower limbs when sitting or standing, and provide attachment points for muscles that help with locomotion and posture.

It also provides support and protection for the abdominopelvic structures. So let’s start with the hip bones.

The right and left hip bones are irregular shaped bones located at the sides of the pelvic cavity, which bound and form the lateral walls of the pelvis.

Each one of these hip bones develop from the fusion of three bones, the ilium, ischium, and pubis. Now, let’s start with the upper part of the hip bone, the ilium. You can think of the ilium as a fan.

It has an upper expanded part representing the spread of the fan called the ala, and a lower narrow part representing the handle of the fan called the body.

Now, there are 4 bumps coming off the ilium called spines. Let’s talk about them!

If we look anteriorly to the ilium, we can see two of the spines. One of them is superior and the other one is inferior. The naming is easy because it follows the rule of (Anterior or Posterior) + (Superior or Inferior).

The superior one is called the anterior superior iliac spine, and the inferior one is called, you guessed it,  the anterior inferior iliac spine.

Now, looking at the ilium from a posterior view, we can see the remaining two spines, one superior and again, one inferior. If we follow the rule just mentioned, we can name them easily.

The superior one is called the posterior superior iliac spine, and the inferior one is called, wait for it,  posterior inferior iliac spine.

The main function of the spines is to provide attachment points for various muscles. For example, the longest muscle in the body is called the sartorius, and it attaches to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bones_of_the_upper_limb</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FvUZimN7SgizIBklClVZ4uY0TFOsgDhV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bones of the upper limb]]></video:title><video:description><![CDATA[The upper limb is connected to the axial skeleton, which is the cranium, vertebral column, and associated thoracic cage, by the bony pectoral girdle at the sternoclavicular joint, which is the connection between the clavicle and sternum. 

Each upper limb is made up of 32 bones, and has a number of different regions. 

First, there’s the pectoral girdle, which consists of 2 bones: the scapula, also called the shoulder blade, and the clavicle, also known as the collarbone. 

Then there’s the arm, which only has one bone, called the humerus. 

Then we have the forearm, which has two bones called the radius and the ulna. 

Next, there’s the wrist, which has 8 carpal bones, and finally, the hand, which has 5 metacarpal bones, and the fingers, who have 14 phalanges in total.

OK, now let’s have a look at the shoulder girdle first. 

The shoulder girdle consists of the scapula and clavicle, and articulates anteriorly with the manubrium of the sternum. 

Starting with the scapula, it’s a flat triangular bone located on the posterior aspect of the shoulder, extending over the second to the seventh ribs. 

The scapula helps to connect the rest of the upper limb to the trunk, while stabilizing and assisting the shoulder during movement while serving as an attachment point for numerous muscles and ligaments. 

Now, like any respectable triangle, the scapula has three borders; the shortest and the thinnest of them is the superior border. 

Then there’s the medial border, which runs parallel to the vertebral column, and finally, there’s the lateral border which is the thickest one. 

The lateral border is also known as the axillary border because it points towards the  axilla, or armpit region. 

The point where the medial and lateral borders meet is the inferior angle, and we also have the superior angle which is the junction of the superior and medial borders. 

At the lateral part of the superior border, there’s a small indentation called the scapular notch through ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vessels_and_nerves_of_the_thoracic_wall</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7hz1UYaIQGOzwGaGTtN2hC5FQOehHg3k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vessels and nerves of the thoracic wall]]></video:title><video:description><![CDATA[There are numerous vessels and nerves that course throughout the bony and muscular architecture of the thoracic wall, and they provide innervation and blood supply to the structures within and around the thoracic cage. 

First,  let’s have a look at the contents of the intercostal space, specifically the neurovascular bundle containing the intercostal nerve, artery and vein. 

It is important to remember the order of these structures, with the most superior structure being the intercostal vein and below it comes the artery and below the artery, the nerve. 

To easily remember this, think V-A-N or think about a VAN that’s blue at the top, red in the middle and yellow in the inferior part. 

The inferior portion of the ribs also have a costal groove which only provides partial protection for these structures, so they can be damaged during penetrating intercostal injuries or any intervention that requires intercostal access 

Now, let’s talk about the nerves. 

There are 12 pairs of thoracic spinal nerves which supply the thoracic wall. 

They leave the intervertebral foramina as soon as they are formed, dividing into anterior and posterior rami. 

Now, the anterior rami of nerves T1 through T11 form the intercostal nerves that run along the intercostal spaces along the inferior borders of the ribs, with the third intercostal nerve travelling between the third and fourth ribs. 

The anterior ramus of nerve T12 that courses inferior to the 12th rib is the subcostal nerve. 

The intercostal nerves give anterior and lateral cutaneous branches to innervate the thorax and abdominal wall, muscular branches to supply the muscles of the thoracic wall, and they give rami communicantes or communicating branches that connect the intercostal nerves to a sympathetic trunk on the same side. 

The posterior rami of thoracic spinal nerves pass posteriorly, lateral to the articular processes of the vertebrae in order to supply the joints, deep back muscles and skin of the pos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_radioulnar_joints</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rsRKHQsBTp220sYhc9vCZ-FyQOivxcGJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the radioulnar joints]]></video:title><video:description><![CDATA[The radioulnar joints are two joints between the two bones of the forearm: the ulna, on the medial side, and the radius, on the lateral side.

There’s one superior, or proximal radioulnar joint, and one inferior, or distal radioulnar joint, and together they allow for the movements of pronation and supination.

This is gonna be short and sweet, so let’s dive right in!

The proximal radioulnar joint is a pivot type of synovial joint, which consists of the head of the radius articulating with the radial notch of the ulna.

The radial head is tightly bound into the radial notch of the ulna by the anular ligament that secures it in place.

The two articulating surfaces are covered by a synovial membrane, over which lies the joint capsule.

The joint capsule of the proximal radioulnar joint is an extension of the elbow’s joint capsule.

Next up, in the distal forearm, the radius and the ulna form another pivot type of synovial joint called the distal radioulnar joint, which is also covered by a fibrous joint capsule lined internally with a synovial membrane.

For this joint, the rounded head of the ulna articulates with the ulnar notch of the distal radius.

The articulating surfaces are mainly bound together by a fibrocartilaginous structure called the articular disc, which is triangular in shape, so it’s also known as the triangular ligament.

The articular disc attaches to the edge of the ulnar notch of the radius, and the base of the styloid process of the ulna.

The distal radioulnar joint is reinforced by the two important ligaments: the anterior and the posterior ligaments.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lysosomal_storage_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6fufLcbYT6yezxuA0QXsd8TgSAmzOSBF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lysosomal storage disorders: Pathology review]]></video:title><video:description><![CDATA[At the pediatric clinic, Abigail, a 5-month-old girl of Ashkenazi Jewish descent, is brought in by her parents because of recurring episodes of seizures, which started about a month ago. Her parents have also noticed that Abigail startles easily at loud noises. Physical examination reveals a low muscle tone with exaggerated reflexes. Upon palpation of the abdomen, the liver and spleen are of normal size. On ophthalmologic examination, a cherry red spot is found on the maculae of both eyes. Next in the clinic, there’s 2-year-old Harry. According to his mother, he recently stopped walking and speaking in sentences, and instead started crawling and babbling again. On further questioning, his mother mentions that Harry seems to have a hard time sitting still and often shows aggressive behavior. Physical examination reveals a prominent forehead, a nose with a flattened bridge and flared nostrils, an enlarged tongue, and thickened lips. On ophthalmologic examination, no corneal clouding is observed.

Based on the initial presentation, both Abigail and Harry seem to have some form of lysosomal storage disorder. These are a group of inherited metabolic disorders that result in the inability to break down certain substances in lysosomes, causing them to build up, and ultimately leading to cell damage and death. Lysosomal storage disorders include sphingolipidoses, caused by the accumulation of a certain type of lipids called sphingolipids. Mucopolysaccharidoses are caused by the accumulation of a type of complex sugars called mucopolysaccharides or glycosaminoglycans. Finally, there’s also mucolipidoses, which are caused by the accumulation of both sphingolipids and mucopolysaccharides.

Okay, let’s start with sphingolipidoses! Gaucher disease is the most common lysosomal storage disorder. It is caused by a mutation in the GBA gene, which codes for the enzyme glucocerebrosidase, also known as beta-glucosidase. For your exams, remember that Gaucher disease]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscles_of_the_thoracic_wall</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/95ttYAtKS8_JT_GeDhI459L3S2SAakUw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscles of the thoracic wall]]></video:title><video:description><![CDATA[The thoracic wall surrounds the thoracic cavity, which is the anatomical region where viscera like the heart and lungs can be found.

The thoracic wall contains a variety of muscles, where many of the muscles that cover and attach to the thoracic wall have a primary action elsewhere, such as the arms, neck, and abdomen, and it is their secondary actions that affect the movements of the thoracic wall.

For example, the pectoralis major and pectoralis minor muscles overlay the thoracic wall but they are primarily involved with movements of the upper limb and their secondary action is to act on the thoracic wall as accessory muscles of respiration.

However, the thoracic wall also does have muscles that have their primary action in the thoracic wall, and these are called the true muscles. They are the serratus posterior, levatores costarum, subcostals, transversus thoracis, and the innermost, internal, and external intercostals.

Let’s start with the two serratus posterior muscles. There’s a serratus posterior superior muscle and serratus posterior inferior muscle on each side. The Serratus posterior superior muscles have their proximal attachment at the nuchal ligament and the spinous processes of C7 through T3 vertebrae and their distal attachment at the superior borders of the 2nd through 5th ribs. Its main action is the elevation of the superior 4 ribs during inspiration.

The serratus posterior inferior muscles have their proximal attachment at the spinous processes of T11 through L2 vertebrae and their distal attachment at the inferior borders of 9th through 12th ribs near their angles. Its main action is depressing the inferior ribs in order to prevent them from being pulled upwards by the diaphragm.

Both of these muscles have also been shown to have a role in proprioception, meaning that they might make you aware of the position of the body. For example, when you’re lying in bed with your eyes closed, these muscles, among others, could send signals t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_eye</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fGbDbBQjRxmEbQjJjSM5bTSsQzmmaN7J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the eye]]></video:title><video:description><![CDATA[To be able to see everything that surrounds us, including this video, we can count on two very special sense organs: the eyes. The eyes can be easily injured, so each of them is protected by a hard bony structure called the orbit. The orbits also protect the muscles, vessels and nerves of the eyes. And between each eye and the orbit protecting it, there’s a soft cushion of fat to prevent any friction or damage to the eyes. Additional protection is ensured by the lacrimal apparatus, which secretes tears to lubricate the eyes, and the eyelids, which close and open as needed.

Okay, now, if you look at a sagittal cut of the eyeball, you’ll see it’s shaped like two spheres fused, a bigger posterior one and a smaller anterior one, both with liquid inside. To keep this shape, the eyeball needs a solid structure: the fibrous layer, which is made of dense connective tissue and forms the skeleton of the eyeball. This layer has two parts: the one that makes the outer layer of the smaller sphere, called the cornea; and the one that makes the outer layer of the bigger sphere, called the sclera. The cornea is transparent and located at the anterior end of the eyeball. It allows light to pass through to the interior of the eyeball. Have you ever needed to use eye drops? Were you able to do that without instinctively closing your eyes once the drop touches your eye? The involuntary blinking is actually because of the corneal reflex! See, when something touches or irritates the cornea, it is  sensed by the ophthalmic nerve, a branch of cranial nerve V.  This sensory signal then reaches the brain stem, and signals the facial nerve, cranial nerve VII, to contract the orbicularis oculi to close our eyes. Now, the sclera is opaque and makes the white shell of the eyes. It occupies the majority of the posterior  eyeball and serves for attachment of the extrinsic muscles of the eye. Also, the sclera is pierced by the optic nerve at the posterior end of the eyeball. The place wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Thoracic_wall</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JCGJG8SnTDqClJpanj4UkQbqS6imdhUf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Thoracic wall]]></video:title><video:description><![CDATA[If it wasn&amp;#39;t for our thoracic wall, many of the important organs in our thoracic cavity would be unprotected and vulnerable to injury.

But sometimes the thoracic wall itself can be injured, which has a wide range of clinical consequences depending on the affected structures.

Let’s start by talking about the ribs.

First, like any other bone in our body, ribs can break, causing rib fractures.

These usually result from direct trauma or crushing injuries.

The middle ribs are the ones most commonly fractured.

The weakest part of a rib is the posterolateral bend, anterior to its angle.

However, direct trauma can cause a rib to fracture anywhere.

The broken part of the rib can harm internal organs, such as the liver, kidney or the spleen.

Rib fractures higher up can cause mediastinal injuries, and if the fracture is lower, then it can tear the diaphragm.

Furthermore, rib fractures at any level have the risk of causing an intrathoracic injury such as a pneumothorax, which is when there’s air in the pleural cavity, and that doesn’t allow the lung on that side to expand properly.

Since ribs move during respiration, coughing, laughing and sneezing are very painful after a rib fracture!

A related injury is a flail chest, which is when three or more ribs fracture in two or more places, which can allow a big segment of the thoracic wall to move freely.

During a normal inspiration, the thoracic wall expands outwards and increases its diameter, whereas during expiration, it decreases its diameter to expel air.

However, when there’s a flail chest, the movement is paradoxical, meaning that during inspiration, the free segment actually moves inward and during expiration, it moves outward.

This is an extremely painful injury that impairs ventilation, and, as a consequence, blood isn’t properly oxygenated.

Management wise, for a flail chest, you want to ensure adequate pain control and supplemental oxygen if needed.

If respiratory failure occurs as a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bones_of_the_cranium</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hcn4ipRWRZ_DfVDCjESaANuwR3alkrer/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bones of the cranium]]></video:title><video:description><![CDATA[The cranium, or skull, is the bony structure that protects the structures found inside our head, and it’s divided into two parts: the viscerocranium and the neurocranium. Viscera- refers to the organs within the body cavities, so the viscerocranium is the lower and anterior part of the skull that forms the orbits, the nasal cavities, and the oral cavities; in other words, the facial skeleton. Neuro-, on the other hand, refers to the nervous system, so the neurocranium, also called the cranial cavity, is the superior and posterior part of the skull that houses the brain, and its membranous coverings - the cranial meninges - and also blood vessels and the proximal parts of the cranial nerves. 

Let’s look at the viscerocranium first, which is actually made up of 15 bones! Only three of them are unpaired bones, and they sit on the midline: the mandible, ethmoid, and vomer; then there are six pairs of paired, symmetrical bones: the maxillae, the inferior nasal conchae, as well as the zygomatic, palatine, nasal, and lacrimal bones. Most of these bones articulate with each other by fibrous - or immovable - joints; except for the mandible, which articulates only with the temporal bones by a synovial - or movable - joint. 

Next, the neurocranium is made up of eight bones: the frontal, ethmoid, sphenoid, and occipital bones, which are singular and placed in the midline; then two temporal and two parietal bones, which are bilaterally paired. All these bones articulate by fibrous joints. In addition, the neurocranium can be further divided into the calvaria - or skullcap - and the cranial base, which would be like the roof and the floor of the neurocranium, respectively. The cranial base is where the foramen magnum is found, where the spinal cord is continuous with the brain. 

Alright, so let’s get started with the bones of the viscerocranium. If you get face to face with a skull, you&amp;#39;ll see the most bones of the viscerocraniu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscles_of_the_forearm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nyH6v51TRUa0ii7NAr10pX64Rhuxby2M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscles of the forearm]]></video:title><video:description><![CDATA[Anatomically speaking, the forearm is the part of the upper limb between the elbow and the wrist joints. 

It contains two bones: the ulna and the radius, which provide support to local muscles supplied by an intricate network of nerves and vessels. 

On the anterior part of the elbow, there’s a triangular fat-filled pit, called the cubital fossa, which is where the majority of important nerves and vessels to the forearm and hand can be found. 

Okay, before we start, it is important to know that, even though some of the muscles of the forearm attach proximally to the humerus, they still belong to the forearm. 

The forearm is divided into two compartments, which are separated by the radius and ulna and the interosseous membrane running between them. 

We have the anterior compartment, which contains flexors and pronators. 

Next, is the posterior compartment, housing the extensors and supinators of the forearm. 

Generally, muscles in the same compartment are innervated by the same nerve. 

So, the muscles of the anterior compartment are generally innervated by the median nerve, with a few muscles being innervated by the ulnar nerve. 

Muscles of the posterior compartment, on the other hand, are innervated by the radial nerve. 

Now, the muscles of the anterior compartment are divided into three groups, or layers: superficial, intermediate, and deep. 

In the superficial layer there are four muscles which all arise from a common tendon attached to the medial epicondyle of the humerus, so this attachment site is called the common flexor origin. 

Muscles attaching to the common flexor origin are the flexor carpi ulnaris, the palmaris longus, the flexor carpi radialis, and the pronator teres muscles.

Now, let&amp;#39;s look at these muscles one by one. 

On the most medial side lies the flexor carpi ulnaris. 

This muscle has two heads: the humeral head that proximally attaches to the medial epicondyle of the humerus and the ulnar head proximally att]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_hip_joint</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J7_qNMieSwGNb2Ku1J4EBJM-Rpq_asjd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the hip joint]]></video:title><video:description><![CDATA[If you have ever wanted to know about the new ‘hip joint’ in town, look no further than the hip joint! 

The hip joint is a large, strong joint connecting the pelvis to the lower limb. Let&amp;#39;s take a closer look! 

The hip joint is a synovial ball and socket joint, where the head of the femur forms approximately two thirds of a sphere, and it articulates with the cup-like acetabulum of the hip bone. 

The femoral head is not entirely round, as it has depression on top of it which is called the fovea for the ligament of the head of the femur. 

Except for the fovea, the femoral head is also covered entirely in articular cartilage which facilitates smooth movement and prevents bone erosion as it slides within the acetabulum.

The acetabulum, on the other hand, is a bowl like structure on the lateral aspect of the hip bone, and you might remember it is formed by the fusion of the ilium, ischium, and pubis. 

The acetabulum is surrounded on the outside by a margin that’s incomplete inferiorly, where the acetabular notch is situated; this makes it look like a bowl with a broken rim. 

On the outside of the acetabulum margin, there’s the acetabular labrum, where labrum is a fancy word for lip, which continues over the acetabular notch with the transverse acetabular ligament. 

The labrum increases the surface area of the acetabulum to allow more than half of the femoral head to fit within the acetabulum for stability. 

There’s also a rough depression in the floor of the acetabulum - the acetabular fossa, right above the notch. 

These two structures, the acetabular notch and fossa, are surrounded by the thick and smooth lunate surface, the articular surface on which the head of the femur slides.

Just like most joints, the hip joint is enclosed within a strong joint capsule formed by  an external fibrous layer, called the fibrous capsule, and an internal layer, called the synovial membrane. 

The fibrous layer attaches proximally to the acetabulum p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Breast</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/euNR0Q37RQaGOrgm_ALGF6k1RTSY1VDO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Breast]]></video:title><video:description><![CDATA[The breasts, formally known as the mammary glands, are situated in the subcutaneous tissue overlying our pectoralis muscles. There are many conditions that can affect the breast, the most well known being breast cancer. Breast cancer, as well as other conditions that can affect the breast, can often go unnoticed, which has serious clinical consequences; so It is important to understand and recognize these conditions as early as possible.

So let’s start with breast cancer, which causes changes to the structure and appearance of the breasts. One of the classic changes is the presentation of a palpable breast mass, which is typically a hard, immobile lesion with irregular borders most commonly found in the upper outer quadrants.

Another indication of more advanced disease are skin changes, specifically the orange-peel appearance, also called the peau d’orange sign, which happens when there’s prominent edema and dimpling of the overlying skin. Larger dimpling of the skin can result from cancerous invasion of the glandular tissue and fibrosis, which may also pull on the suspensory ligaments of the breast and can cause retraction of the nipple.

If the cancer interferes with the lymphatic drainage this can lead to lymphedema, which is when there’s excess fluid in the subcutaneous tissue. This in turn results in deviation of the nipple and the skin appears thickened and leather-like. Cancer cells can spread through contiguity, which is when the adjacent tissue is invaded.

When breast cancer cells invade the retromammary space or the pectoral fascia, or when they metastasize to the interpectoral nodes, the breast elevates when the muscle contracts, and this usually signals advanced cancer. Furthermore, the local cancerous invasion to the pectoral fascia and pectoralis major muscle below may result in deep fixation of the breast tissue.

Breast cancer usually spreads through lymphatic vessels, which basically carry cancer cells from the breast to the lymph nodes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Aseem_Desai:_Cardiologist_&amp;_Author_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Av1ImXfoRwa01A7yslz-NXkcTnyxUZAy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Aseem Desai: Cardiologist &amp; Author (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Aseem Desai: Cardiologist &amp; Author (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Deborah_Trautman:_President_and_CEO_of_American_Association_of_Colleges_of_Nursing_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KvRCOjJxS7GR8ICVCsPuiVnyR6iJqONP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Deborah Trautman: President and CEO of American Association of Colleges of Nursing (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Deborah Trautman: President and CEO of American Association of Colleges of Nursing (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Thomas_Mohr:_Dean_and_Chief_Academic_Officer,_Idaho_College_of_Osteopathic_Medicine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JLAgHLIET8KiHqmGIVZ6dY79RB2fotg6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Thomas Mohr: Dean and Chief Academic Officer, Idaho College of Osteopathic Medicine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Thomas Mohr: Dean and Chief Academic Officer, Idaho College of Osteopathic Medicine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Greg_Osmond:_Chief_Medical_Officer_of_PathologyWatch_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DdbFMY91Qx2cLuZZiAqaYUPWSZyc0JLe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Greg Osmond: Chief Medical Officer of PathologyWatch (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Greg Osmond: Chief Medical Officer of PathologyWatch (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rochelle_Rivas_and_Brian_Spicker:_Maricopa_Community_Colleges_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ajosf-YJQKaUBPY2kwMiLFjMReqteRP5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rochelle Rivas and Brian Spicker: Maricopa Community Colleges (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Rochelle Rivas and Brian Spicker: Maricopa Community Colleges (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mainul_Mondal:_Founder_and_CEO_of_Ellipsis_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PDZcJLJTQmajnc1NM3kYf-0STxOhZLqr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mainul Mondal: Founder and CEO of Ellipsis Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Mainul Mondal: Founder and CEO of Ellipsis Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Ken_Johnson:_Executive_Dean_of_Ohio_University_Heritage_College_of_Osteopathic_Medicine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wgUFuEQNRPms7OoK5tN2H4V3Qny9LoM-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Ken Johnson: Executive Dean of Ohio University Heritage College of Osteopathic Medicine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Ken Johnson: Executive Dean of Ohio University Heritage College of Osteopathic Medicine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_oculomotor_(CN_III),_trochlear_(CN_IV)_and_abducens_(CN_VI)_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eTomqQCZSICZEtRnbPpV9VAfTEiNSsLt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves]]></video:title><video:description><![CDATA[Imagine a world where we had no control over the movements of our eyes.

We would have to move our entire head in that direction to look at something new, something that would surely cause neck issues when playing video games.

Luckily, we do have control over our eye movements, and the cranial nerves which innervate the extrinsic ocular muscles that move the eyeball are the oculomotor, trochlear, and abducens nerve - or cranial nerves III, IV and VI.

First up, the oculomotor nerve has two main motor functions: a somatic motor function and a visceral motor or parasympathetic function, and there are different motor nuclei that control these two functions.

So, the somatic motor function is controlled by the oculomotor nucleus which is located in the midbrain, and the visceral motor function is controlled by the accessory oculomotor nucleus, or Edinger-Westphal nucleus, also located in the midbrain.

The oculomotor nerve innervates four of the six extraocular muscles, namely the superior rectus, medial rectus, inferior rectus and inferior oblique muscle.

Thanks to this cranial nerve, it mainly helps us to direct our gaze superiorly, inferiorly, and medially.

The oculomotor nerve also innervates the levator palpebrae superioris muscle, which lifts the superior eyelid.

Parasympathetic innervation is provided through the ciliary ganglion to the smooth muscle of the sphincter pupillae, which causes constriction of the pupil, and to the ciliary body which produces accommodation for near vision by relaxing the lens and allowing it become more rounded.

Now, the oculomotor emerges from the midbrain, pierces the dura mater lateral to the sellar diaphragm or diaphragm sellae, and then runs through the roof and lateral wall of the cavernous sinus, and the oculomotor nerve enters the orbit through the superior orbital fissure.

At this point, it divides into a superior division to innervate the superior rectus and levator palpebrae superioris muscles, and an inferi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Papulosquamous_and_inflammatory_skin_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5kSrg64xSoWbF6RlP3FmuSdTTtO8SN4p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Papulosquamous and inflammatory skin disorders: Pathology review]]></video:title><video:description><![CDATA[At the dermatology clinic, 9 month old Ethan is brought in due to recurrent skin rashes. According to his mother, he develops red, weeping lesions on his cheeks, chin, forehead, as well as the knees and elbows. His mother said these seemed to be related to the consumption of specific foods, but she couldn’t figure out what kinds. Physical exam reveals multiple erythematous papules with excoriations. Blood work shows increased IgE levels.  On the same day, 68-year-old Marcia presents complaining of a pruritic rash on her wrists and elbows that has persisted for about 8 months. Her medical history is significant for chronic hepatitis C infection. On physical examination, there are multiple, flat-topped, violaceous-colored plaques, on the flexor surfaces of her upper extremities.

Based on the initial presentation, Ethan and Marcia seem to have some form of papulosquamous or inflammatory skin disorder. Okay, first, let’s talk about physiology real quick. Normally, the skin is divided into three main layers, the epidermis, dermis, and hypodermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Above the hypodermis is the dermis, containing hair follicles, nerve endings, glands, blood and lymph vessels. And above the dermis is the epidermis, which contains 5 layers of developing keratinocytes. Keratinocytes start their life at the lowest layer of the epidermis, so the stratum basale or basal layer. As keratinocytes in the stratum basale mature, they migrate into the next layers of the epidermis, called the stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer.
Before we dive into the various skin disorders, there are several high yield terms to describe skin lesions. So, macules are flat, well circumcised lesions up to 1 centimeter in diameter, while patches are similar to a macule but are larger than 1 centimeter. Papu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kidney_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gflhw99eQhC_73i1meGH2IeMTwWt2qXL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kidney histology]]></video:title><video:description><![CDATA[Kidneys are large, bean-shaped organs that are approximately 12 cm long, 6 cm wide, and 3 cm thick in adults. 

The kidneys perform a lot of different functions, such as the excretion and removal of metabolic waste and foreign substances through urine. 

The kidneys also activate vitamin D when needed, and help maintain the balance of fluid volume, pH, blood pressure, and electrolytes in the body. 

The kidneys also secrete important hormones, such as erythropoietin, which increases the production of red blood cells. 

The medial border of each kidney has a concave area called the hilum. This is where the ureter exits the kidney and renal artery, renal vein, and lymph vessels enter and exit the kidney. 

The functional tissue of the kidney, or parenchyma, has an outer renal cortex and inner renal medulla. 

The medulla is organized into cone-like structures called renal pyramids and renal columns in between the pyramids, which are extensions of the renal cortex. 

At the junction between the cortex and medulla are millions of functional units called nephrons. Each nephron can be divided into its major parts: 

The renal corpuscle, proximal convoluted tubule, loop of henle, distal convoluted tubule, and collecting duct.

Each nephron starts with a renal corpuscle, which is a spherical structure in the cortex that has a diameter of about 200 um. 

The corpuscle consists of the glomerulus as well as the surrounding double-layered epithelial capsule called the glomerular or Bowman’s capsule. 

The glomerulus is a bundle or tuft of capillaries that supplies the blood that’s filtered to become a fluid called the glomerular filtrate or ultrafiltrate, which typically contains no blood cells or large proteins. 

The ultrafiltrate initially drains into the capsular or Bowman’s space, which is actually the space in between the two layers that make up Bowman’s capsule. 

The outer layer of the capsule is a parietal layer of flat simple squamous epithelium; and the inn]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eye_conditions:_Inflammation,_infections_and_trauma:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GMghtmznRsiMlJosrijmi_QwTMOf0EcX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eye conditions: Inflammation, infections and trauma: Pathology review]]></video:title><video:description><![CDATA[While doing your rounds, you meet a 4 day old newborn girl, named Caitlyn, who is brought to the emergency department due to redness and swelling of the eyes. Physical examination shows bilateral eye erythema and purulent discharge. The infant was born at home to a mother who received no prenatal care and is unable to provide any medical history. Some days later, 41-year-old Joshua comes to the ophthalmology clinic complaining of black spots and blurry vision that started about two weeks ago. He mentions that the spots go away when he closes his left eye. On examination, visual acuity is 20/100 in the right eye and 20/20 in the left. Fundus examination is pictured. His medical history includes a diagnosis of HIV infection 8 years ago.

Based on the initial presentation, both Caitlyn and Joshua have some form of inflammatory, infectious or traumatic eye condition.  But first, a bit of physiology real quick. If we zoom into the wall of the eye, it is made up of three major layers. There’s a fibrous outer layer that contains the cornea and sclera. The outer surface of the sclera is covered by a mucous membrane, called conjunctiva, which also lines the inside of the eyelids. The middle vascular layer is called uvea and consists of the iris, pupil, choroid, and ciliary body. Finally, the neural layer consists of the retina which helps convert light into neural signals that travel via the optic nerve to the brain for visual processing.
Okay, let’s start with stye, also known as hordeolum, which is a common bacterial infection of the sebaceous glands of the eyelids. For your exams, remember that the most common pathogen is Staphylococcus aureus. Styes present as painful, red, pus-filled lumps and are usually located at the lid margin, in which case they are known as external styes, or under the conjunctival side of the eyelid, also called internal styes. For your exams, keep in mind that for unknown reasons, styes tend to be more common in individu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Risk_factors_for_periodontitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0JDOBJdyQ0iwOqBOcO-j7cfWRwiF90vm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Risk factors for periodontitis]]></video:title><video:description><![CDATA[Periodontal disease refers to a group of inflammatory conditions that affect the tissues around the teeth. 

The mildest form of periodontal disease is gingivitis. 

If left untreated, gingivitis can progress to periodontitis, which can lead to destruction of the supporting structures around the teeth.

Now, etiologic factors in periodontal disease are subdivided into two main groups, primary and secondary etiologic factors. 

The primary, or initiating etiologic factor is the dental plaque or dental biofilm, which is a sticky collection of bacteria, salivary proteins, and dead cells from the oral mucosa. 

On the other hand, secondary, also known as contributing etiologic factors, enhance the ability of dental plaque to cause periodontitis. 

Secondary etiologic factors are further subdivided into local factors, which make the dental plaque more resistant and difficult to remove; and systemic factors, which include conditions like diabetes that could impair the host’s immune response  and increase the risk of periodontitis.

Local factors include calculus, caries, tooth position, anatomical features, iatrogenic factors, and trauma. 

First, let’s focus on calculus, which is defined as a calcified dental plaque. 

Supragingival calculus is located above the gingiva while subgingival is below the gingiva. 

Supragingival calculus is visible upon oral examination and it’s composed of organic and inorganic components. 

Organic components include bacterial cells, salivary proteins, and lipids. 

The inorganic component mainly consists of calcium phosphate. 

In contrast to supragingival calculus, subgingival calculus is not visible upon oral examination and it’s harder to remove. 

Additionally, subgingival calculus is associated with a higher calcium to phosphate ratio and more serum derived proteins. 

Next up is dental caries, also known as tooth decay, which is caused by acid-producing bacteria that can eventually cause tooth demineralization. 

Moreover,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_trials</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nqZRu8mrTdOqkcyBhxvBEJBMRWCE4Akw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical trials]]></video:title><video:description><![CDATA[Clinical trials are scientific research studies that help determine the safety and effectiveness of an intervention. 

This could be a new medication, vaccine, device, procedure, or anything with therapeutic purposes. 

Clinical trials are done on humans, and are often the last step before an intervention is approved for use by the general public.

Now, the main goal of a clinical trial is to find out if the intervention actually works, and for that, there needs to be an experimental group that gets the new intervention and a control group that doesn’t. 

In addition, researchers should eliminate as many external factors as possible, as they could affect the results.

Now, there are multiple ways to design a clinical trial, so let’s go over a couple of them. 

The gold standard is the randomized, controlled clinical trial. 

So as an example, let’s say there’s a new vaccine that’s being developed for a viral epidemic. 

As the participants, we’ll need a group of people who tested positive for the infection. 

Each person will be randomly assigned to either the experimental group who will receive the vaccine, or the control group who will usually receive a placebo. 

Now, if there’s already an effective treatment available for a disease, it would be unethical to give a placebo, so the control group will receive the available treatment instead. 

Now, to limit bias, both the people administering the intervention and the people receiving it won’t know who’s in the control group and who’s in the experimental group, and this is called “double blind.”  

When the people assessing the data also don’t know who’s in what group, it’s a “triple blind”. 

Having placebos and blinded studies will help ensure that any difference between the results of both groups is most likely due to the intervention that’s being tested and not external factors.   

Another type of design is the pre-post study, where an individual will be their own control. 

So for example, to test a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunodeficiencies:_Combined_T-cell_and_B-cell_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6c8UD4PsR3CpZcHIjd-Z1r3AT7K3ELqn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review]]></video:title><video:description><![CDATA[Aurora, an 18 month old girl, is brought to the clinic because of frequent respiratory and ear infections. At first glance, you notice she has some small dilated blood vessels over the sclera of her eyes. Upon physical examination, you also realize that she has a delay in speech, as well as frequent stumbling when walking. Laboratory studies are obtained, showing a low lymphocyte count, low immunoglobulin levels, and high alpha-fetoprotein or AFP. Next comes Mathew, a 16 month old boy that’s brought to the clinic because of a skin rash that appeared on his back since infancy and won’t go away. Mathew’s mother also tells you that he has frequent spontaneous nosebleeds, and has had recurrent respiratory tract infections over the last few months. Laboratory studies are obtained, revealing that Mathew’s platelets are quite small in size and fewer than normal, while the immunoglobulins IgA and IgE are increased.

Based on the initial presentation, both cases seem to have some form of combined B- and T-cell disorder causing immunodeficiency, meaning that their immune system&amp;#39;s ability to fight pathogens is compromised. Combined B- and T-cell disorders are characterized by defects in the development of both B and T cells, which respectively lead to impaired antibody and cellular immune responses. For your exams, the most high yield combined B- and T-cell disorders include severe combined immunodeficiency, ataxia telangiectasia, hyper IgM syndrome, and Wiskott-Aldrich syndrome.

Okay, then! Starting with severe combined immunodeficiency, or SCID for short, which is the most severe form of primary immunodeficiencies. In fact, the immune system is so dysfunctional that it’s considered almost completely absent. 

Now, for your exams, remember that SCID can be caused by mutations in a variety of genes, the most common one codes for the gamma chain of the IL-2 receptor. For your exams, remember that this mutation is X-linked recessive. Okay, now, this]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_superior_mediastinum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RXGcVoz-TMKSuMNgMbEn3wxsSLabufZu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the superior mediastinum]]></video:title><video:description><![CDATA[The mediastinum is the central compartment of the thoracic cavity and lies between the two pulmonary cavities.

It’s covered on each side by the mediastinal pleura and contains all thoracic viscera and structures minus the lungs.

The mediastinum is divided into four parts, of which one is superior and three are inferior.

The superior part is bounded superiorly by the thoracic aperture and extends inferiorly to the transverse thoracic plane, which is a horizontal plane that extends from the sternal angle anteriorly and the junction of T4 and T5 posteriorly.

The transverse thoracic plane separates the superior mediastinum from the inferior mediastinum, and is also an important anatomical landmark representing the bifurcation of the trachea and the beginning and end of the arch of the aorta.

The inferior mediastinum lies between the transverse thoracic plane superiorly, and the diaphragm inferiorly.

It’s further subdivided by the pericardium into anterior, middle and posterior parts, with the pericardium and its contents being in the middle part.

So in this video, let’s focus on the superior mediastinum.

From anterior to posterior, it contains the following structures: the thymus, the great vessels, the inferior continuation of the trachea, the inferior continuation of the esophagus, and the thoracic duct and lymphatics trunks.

Now let’s take a closer look at some of these structures one by one.

So, the thymus is located in the inferior part of the neck and in the anterior part of the superior mediastinum.

It is a glandular structure and lies posterior to the manubrium and extends into the anterior mediastinum.

The thymus is a primary lymphoid organ that plays a huge role in helping our immune cells develop before puberty.

After puberty, however, it undergoes gradual involution and is mostly replaced by fat.

Next up, there are the great vessels.

First we have the veins, which include the brachiocephalic veins and the superior vena cava or S]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fascia,_vessels_and_nerves_of_the_upper_limb</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GqL4dAMjTQuMs_6RWfpnmnUETa_Fjg4j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fascia, vessels and nerves of the upper limb]]></video:title><video:description><![CDATA[The upper limb contains an intricate metro system of blood vessels, muscles, and nerves.

These structures are wrapped up and organized into different compartments by superficial and deep fascia layers, and together they form the multifunctional upper limbs we know and love.

So let’s start with the fascia. You can think of fascia as a pair of thin stockings made of connective tissue that support and bind together different parts of the body, including the lower limbs.

Now, each upper limb actually has two pairs of stockings on top of each other: the superficial fascia, which sits right underneath our skin, and the deep fascia, which is deep to or beneath the superficial fascia, and it sits on top of muscles, organizing them into compartments.

In the upper limb, there are six fasciae to remember. We have the pectoral fascia, the clavipectoral fascia, the axillary fascia, the deltoid fascia, the brachial fascia, and antebrachial fascia.

The wrist and the hand also have fibrous band-like structures called the flexor retinaculum, the extensor retinaculum, and the palmar aponeurosis.

OK, let’s start with the pectoral fascia, which is a broad thin sheath of connective tissue surrounding the pectoralis major muscle, from which it gets its name. Medially, the pectoral fascia is attached to the sternum along with the pectoralis major’s origin.

Superiorly, it attaches to the clavicle, and superolaterally, this fascia passes over this narrow trench called the deltopectoral groove to blend with the deltoid fascia covering the deltoid muscle around the shoulder.

The deltopectoral groove serves as a passageway for the cephalic vein when it is traversing from the arm to enter the lateral aspect of the chest.

Inferiorly, the pectoral fascia spreads downwards and becomes continuous with the fascia of the anterior abdominal wall, while on the lateral side, the fascia curves around the lateral border of the pectoralis major to become continuous with the axillary fasc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_arm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YAB-q7qGS_2p4odsiFbz2ICeRdapfiwN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the arm]]></video:title><video:description><![CDATA[Anatomically speaking, the arm is the part of the upper limb that is between the shoulder and the elbow joint.

It has only one bone called the humerus, and an intricate network of muscles, vessels and nerves distributed around it.

The arm muscles are divided into two compartments separated by the humerus and the medial and lateral intermuscular septae.

The first one is the anterior compartment, and this one houses muscles responsible for elbow flexion. So it’s not a surprise that the anterior compartment is also called the flexor compartment.

Then there’s the posterior compartment. This one houses muscles responsible for elbow extension. So it’s also called the extensor compartment.

These two compartments mainly act on the elbow joint, but some muscles can also act on the glenohumeral joint.

Now, the anterior compartment contains three muscles: the biceps brachii or simply the biceps; the brachialis; and the coracobrachialis muscles. The biceps muscle usually has two heads, a short head and a long head.

The short head attaches to the coracoid process of the scapula and descends anteromedially to the head of the humerus, while the long head attaches to the supraglenoid process of the scapula and descends in the intertubercular or bicipital groove.

It is held in the bicipital groove by the transverse humeral ligament, which extends from the lesser to the greater tubercle of the humerus to turn the groove into a canal for the tendon of the long head.

Both of these heads converge together and attach distally to the tuberosity of the radius, and blend with the fascia of the forearm via the bicipital aponeurosis.

The bicipital aponeurosis is a triangular membranous band that runs across the cubital fossa to blend with the deep fascia covering the flexor muscles on the medial side of the forearm.

The biceps is innervated by the musculocutaneous nerve, and acts on three different joints; the glenohumeral, the elbow joint, and the proximal radi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_pleura</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rg0mI9VSQ4K8WrkarcBiiYBMSHeLrvkb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the pleura]]></video:title><video:description><![CDATA[The pleura is a thin membrane that covers each of our lungs and surrounding pulmonary cavity, and it can be subdivided into two layers, the visceral pleura which intimately adheres to the lungs, and the parietal pleura which lines the rest of the pulmonary cavity.

Between these two pleural layers there’s the pleural cavity, which is normally filled with a thin film of fluid in order to lubricate the pleural surfaces and allow them to slide smoothly over each other during each breath.

Now, on the medial part of each lung, there’s the pulmonary hilum, where the root of the lung passes through.

The root of the lungs is made of structures like the tracheobronchial tree, as well as arteries and veins.

At this level, the visceral and parietal pleura are continuous, making one continuous structure.

To make this easier, you can imagine an underinflated balloon through which you press your fist into, the fist representing the root of the lung and the balloon representing the visceral and parietal pleura.

As you can see, the parietal and visceral pleura are one continuous layer, however they are reflected on different surfaces.

Okay, the visceral pleura covers the entire lung and adheres intimately to all its surfaces, including the ones between the fissures of each lung.

The visceral pleura is continuous with the parietal pleura at the hilum of the lung.

The parietal pleura is thicker than the visceral one, lines the pulmonary cavities and adheres to the thoracic wall, mediastinum and diaphragm.

The parietal pleura actually has four parts: costal, mediastinal, diaphragmatic and cervical pleura.

The costal pleura covers the internal surface of the thoracic wall, from which it’s separated by the endothoracic fascia, a thin layer of loose connective tissue that comes in handy during surgical procedures, making it really easy to separate the lungs from the thoracic wall.

The mediastinal pleura covers the lateral aspects of the mediastinum, which is the spac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bacterial_pneumonia:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dAQVAd0KSlisYsvMZ_ix-twQRY265LF8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bacterial pneumonia: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Neli Singh is an 82-year-old man who arrives at the urgent care clinic with his home health aide. Mr. Singh has a history of cardiac disease, type I diabetes, prostate cancer, and depression.  He was brought to the clinic this afternoon because of a new onset of a productive cough, dyspnea and chest pain. Mr. Singh’s aide tells the triage nurse, “Neli had these same symptoms 2 months ago. I’m worried its pneumonia again.”  

Pneumonia is an infection in the lung tissue caused by microbes, resulting in inflammation. The inflammation brings fluid into the lung tissue, and that extra fluid can make it hard to breathe. 

Now, there are lots of different pneumonia-causing microbes. Usually, it’s caused by viruses and bacteria, but it can also be caused by fungi and a special class of bacteria called mycobacteria. In adults, the most common viral cause of pneumonia is influenza, sometimes just called the flu. In adults, bacterial causes include Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus. There are also more unusual bacteria like Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila, which don’t have a cell wall and are well known for causing an “atypical or walking pneumonia” because they often cause vague symptoms. For example, you might manifest with symptoms of a common cold, and these aren’t severe enough to require you to stay home or be hospitalized. So, you can still be out and about, walking around.  

In individuals with a normal immune system, fungi are a rare cause of pneumonia and often it’s regional - for example, there’s Coccidioidomycosis in California and the Southwest. One special fungal culprit is Pneumocystis jiroveci which is a risk for immunocompromised individuals. Finally, there’s mycobacteria which are slow growing like fungi, hence the “myco” in their name even though they’re still bacteria. The most well-known one is Mycobacterium tuberculosis, also just called TB.  
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pyloric_stenosis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S59NDHFyTs6tixTWTx9Fet0ySt6_cpQb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pyloric stenosis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[In the emergency department, a mother brings in her 3-week-old male infant named Owen Tamm. 

She says that Owen started vomiting with every feeding since two weeks of age, and occasionally he would vomit so forcefully that it sprayed her face. 

Over the past week, he’s been increasingly irritable and fussy, especially after vomiting. But in the last two days, he’s become much more sleepy, and today has been difficult to awaken. 

Diagnostic labs and screenings confirm hypertrophic pyloric stenosis, and Owen is admitted to the Neonatal Intensive Care Unit pending pyloromyotomy.

First, let’s review hypertrophic pyloric stenosis, or HPS. 

This is a gastric outlet obstruction that is the second most common condition requiring surgery in newborns. 

In HPS, babies are born with a normal pylorus, which is the last part of the stomach that consists of a thickened band of smooth muscle. 

This band can contract or relax to allow food to exit the stomach and enter the small intestine. 

But within a few weeks after birth, the pyloric muscle begins to undergo hypertrophy, which is an increase in the size of each cell, and hyperplasia, which is an increase in the overall number of cells. 

Its cause is unknown, but it is more likely due to a combination of genetic and environmental factors, and is about 4 to 5 times more common in males than females, especially first-born males.

As the smooth muscle of the pylorus undergoes thickening and elongation, the pylorus nearly doubles in size, producing an olive-shaped mass felt in the epigastrium just right of the umbilicus. 

This narrows the passageway between the stomach and small intestine. 

If food can’t pass through the pylorus, it quickly starts to build-up, causing gastric distention. 

Eventually, this leads to vomiting that may get more intense over time until it leads to projectile vomiting, where the vomit literally launches out of the infant’s mouth. 

The vomit is non-bilious, meaning it doesn’t contain ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Left-sided_heart_failure:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qfy7q4ioTVS7IpAMSQmOKsGaQpSOHtyb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Left-sided heart failure: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[ Jamal Hendrick is a 63-year-old male client who was admitted to the Medical-Surgical floor yesterday. 

 Mr. Hendrick has a history of chronic left-sided heart failure and hypertension. 

 He was directly admitted by his cardiologist after complaints of shortness of breath, dry cough, and severe fatigue. 

 He states his last hospitalization was around 6 months ago for similar symptoms. 

Heart failure, also called congestive heart failure, is when the heart is unable to pump effectively enough to maintain cardiac output to meet the demands of the body.

Common risk factors for heart failure include uncontrolled hypertension, ischemic heart disease, valvular heart disease, cardiomyopathy, endocarditis, and acute myocardial infarction. 

The onset of heart failure can be acute, which occurs suddenly and resolves in a short period of time, but usually develops slowly over a long period of time and persists as a chronic disease. 

Often an individual can live with chronic heart failure, but then suddenly develop an acute exacerbation. 

Heart failure can be the result of either systolic dysfunction, which is due to inadequate contractility, or diastolic dysfunction, when the heart is unable to relax and fill with blood. 

Heart failure can affect the right side, the left side, or both sides of the heart. 

The left and right sides of the heart are two separate pumping systems, and one side can remain functional for some time even if the other side is failing. 

Most cases of heart failure initially start on the left side, and then eventually progress to include both sides. 

With left-sided heart failure, the left ventricle is unable to pump with enough force to push blood into the aorta and the rest of the body. 

When this happens, the blood remaining in the left side of the heart will back up into the lungs, causing pulmonary problems such as dyspnea, tachypnea, crackles, dry cough, paroxysmal nocturnal dyspnea, pulmonary edema, and pulmonary hypertension]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetic_ketoacidosis_(DKA):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2ZQT2dswRpqAYVIkzLgFMxHqSeeV3rdR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetic ketoacidosis (DKA): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Juanita Perez is a 58-year-old female client with a history of Type 1 diabetes mellitus. 

Mrs. Perez was brought to the Emergency Department (ED) late last night by her spouse, with complaints of severe lethargy, nausea, and a high blood glucose reading at home. 

In the ED, she was found to have a blood glucose reading of 450 mg/dL. 

She was immediately transferred to the Intensive Care Unit, or ICU with the diagnosis of diabetic ketoacidosis.  

Diabetic ketoacidosis or DKA,  is a serious complication of diabetes mellitus. 

It occurs more commonly in type 1 vs type 2 DM because the cause is severe insulin deficiency. 

When insulin levels are low, cells in the body can’t utilize glucose, so fat will be metabolized for energy instead. 

The liver breaks down fat into Ketone bodies and as they build up in the blood, it causes a decrease in pH, leading to acidosis.  

Risk factors for DKA include inadequate insulin administration, concurrent infection or illness, trauma, and injury.

DKA has a very sudden onset and it starts with a severely insufficient amount of circulating insulin. 

If there’s not enough insulin, glucose is unable to enter cells to be used for energy. 

The unused glucose builds up in the blood, causing hyperglycemia. 

At this point the cells are really starving for glucose even though it’s plentiful in the blood. 

So the liver releases glycogen and initiates glycogenolysis, where stored glycogen is broken down into glucose. 

This is accompanied by the release of other counterregulatory hormones - cortisol, growth hormone, and catecholamines - which oppose the effects of insulin and initiate the breakdown of proteins to make additional glucose, a process called gluconeogenesis. 

Blood glucose readings with DKA will typically be anywhere between 300-800 mg/dL.

As glucose levels increase, the renal threshold for glucose resorption is surpassed, which is why we’ll observe polyuria, glycosuria and dehydration caused by the loss of la]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscles_of_the_hand</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gQUSklM7To25w03mi1dECfbKStaIGj2V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscles of the hand]]></video:title><video:description><![CDATA[The hands are the most distal part of our upper limbs, and they’re quite marvelous! 

They’re strong enough to lift heavy boxes, and at the same time delicate and precise enough to thread a needle, or type on a keyboard. 

The diverse range of movements our hands are capable of is made possible by a variety of muscles and their arrangement within the hand.

The hand is composed of intrinsic muscles, which are entirely located within the hand; and extrinsic muscles, which are forearm muscles, but act on the hand and fingers through their long tendons. 

The intrinsic muscles of the hand are covered by the  fibrous  palmar fascia, which divides them into 4 main compartments: the thenar compartment located below the first digit, known as the thumb, the hypothenar compartment located below the fifth digit also known as the little finger, the adductor compartment located in the lateral part of the hand, and finally, the central compartment that’s found in the center of the palm. 

There are also several interosseous compartments between the metacarpals.

The palmar fascia , which is the continuation of the antebrachial fascia in the forearm, forms the palmar aponeurosis centrally. 

The palmar aponeurosis is a strong, thickened portion of the palmar fascia covering the central compartment and overlies the flexor tendons. 

Proximally, the palmar aponeurosis blends with the tendon of palmaris longus and the flexor retinaculum, which if you remember is a transverse ligament spanning over the carpal bones creating the carpal tunnel. 

Distally, the palmar aponeurosis divides into four longitudinal bands that radiate distally to attach to the bases of the proximal phalanges, where they become continuous with the fibrous digital sheaths which enclose flexor tendons going to the digits.  

Within the hand, the medial border of the palmar aponeurosis becomes continuous with the thin hypothenar fascia, which covers the muscles of the hypothenar compartment. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eye_conditions:_Retinal_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XoJ2cYQkSQ60IABf3dbjVRv3TE2anoKW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eye conditions: Retinal disorders: Pathology review]]></video:title><video:description><![CDATA[At the ophthalmology clinic, 71-year-old Zoe comes in. She says that about 4 hours ago, she experienced a sudden flash of light followed by many floaters in her right eye. Her visual disturbances have since progressed to a peripheral loss of vision, and it’s  spreading to the rest of her visual field. Next to her, an 8-month-old male infant named Nirban, is brought in by his father, who is worried because he noticed that Nirban’s eyes appear white in their family pictures. Ophthalmologic examination reveals the absence of red reflex on both eyes. On further questioning, the father tells you that as a child, he had to have his left eye enucleated or removed, but he is unsure as to the exact reason why.

Based on the initial presentation, both Zoe and Nirban have some form of retinal disorder.  But first, a bit of physiology. If we zoom into the wall of the eye, it is made up of three major layers. There&amp;#39;s a fibrous outer layer, which contains the cornea and sclera, and helps shield excess light. The middle vascular layer is called uvea and consists of the iris, pupil, choroid, and ciliary body. Finally, the neural layer consists of the retina, with its own outer pigmented layer, and an inner neural layer that’s composed of photoreceptor cells, which convert light into neural signals that travel via the optic nerve to the brain for visual processing. 

Okay, let’s start with age-related macular degeneration or ARMD for short. This refers to an acquired degeneration of the macula, which is the central area of the retina. It can be divided into dry or non-exudative ARMD, which accounts for the vast majority of cases, and wet or exudative ARMD. Dry ARMD is characterized by yellowish extracellular deposits of waste materials that build up between the Bruch membrane and the retinal pigment epithelium. For your test, remember that these deposits are often known as Drusen. On the other hand, in wet ARMD, there is abnormal neovascularization, meaning that a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_leg</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5cVjLtM6RA62T_WrKpJVV6LZSRW9JhS-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the leg]]></video:title><video:description><![CDATA[The leg, is the region of the lower limb between the knee and the ankle.

It is a tightly packed region consisting of muscles and neurovascular structures.

The leg is organized into three fascial compartments: anterior, lateral, and posterior, which are formed by the interosseous membrane, the anterior intermuscular septum, and posterior intermuscular septum.

The anterior compartment of the leg is also known as the extensor or dorsiflexor compartment, and it’s the area of the body you use to locate the furniture after you turn off the lights.

Ouch! It is bounded anteriorly by the deep fascia of the leg and skin, posteriorly by the interosseous membrane, medially by the lateral surface of the tibia, and laterally by the anterior intermuscular septum and the medial surface of the fibula..

Now, proximally, the deep fascia overlying the anterior compartment is dense, providing part of the proximal attachment of the muscle immediately deep to it, the tibialis anterior.

Distally, the deep fascia presents two band-like thickenings organized as two retinacula.

Retinacula help secure and provide leverage for the tendons of the anterior compartment muscles before and after they cross the ankle joint.

Specifically, the retinacula prevent these tendons from bowstringing anteriorly during movement of the joint.

First, there’s the superior extensor retinaculum, which is a strong, broad band of deep fascia, passing from the fibula to the tibia, proximal to the malleoli.

Second, there’s the inferior extensor retinaculum, a Y-shaped band of deep fascia that attaches laterally to the anterosuperior surface of the calcaneus and medially to the medial malleolus and medial cuneiform. It forms a strong loop around the tendons of the fibularis tertius and the extensor digitorum longus muscles.

The anterior compartment contains four muscles: the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and fibularis tertius which are all dorsiflexors ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_cranial_base</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JX8cYrIeRbK4ucgVx-A3tDJeS56cUr_Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the cranial base]]></video:title><video:description><![CDATA[The cranial base is the most inferior part of the skull.

It consists of the floor of the cranial cavity plus the inferior aspect of the viscerocranium, minus the mandible.

Together with the cranial vault, which is the part of the skull that protects the brain, it contributes to the neurocranium.

Now, the cranial base is a highly irregular surface from both an external and internal view.

So let’s begin with the external surface of the cranial base, which is formed by the maxillary, palatine, vomer, sphenoid, and occipital bones, in the midline; and the zygomatic and temporal bones laterally.

In the most anterior part of the cranial base, there are the alveolar arch and the hard palate.

The hard palate makes up both the roof of the mouth and the floor of the nasal cavity, and it’s made up of the palatine processes of both maxil lary bones and the horizontal plates of both palatine bones behind them.

The maxillary teeth border the hard palate anteriorly and on both sides.

Right behind the incisor teeth there’s the incisive fossa, which has one or more incisive foramina, that allow the nasopalatine nerves and the terminal branches of the sphenopalatine arteries to pass through.

Posteriorly and laterally, on the horizontal plate of each palatine bone, there’s the greater palatine foramen; and right behind it, the lesser palatine foramen through which the greater and lesser palatine nerves and arteries emerge.

Now, superior to the posterior end of the hard palate are the posterior nasal apertures - or choanae - which are also bounded by the body of the sphenoid bones superiorly, the medial pterygoid plates laterally, and the vomer medially.

The choanae allow air to pass from the nasal cavities into the pharynx.

Speaking of which, the vomer is unpaired and located in the midline.

It&amp;#39;s flat and thin, and forms the nasal septum together with the ethmoid bone, to which the vomer articulates superiorly.

Also superiorly, but posterior to the eth]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_larynx_and_trachea</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zMa8HCFARMm0uSSk5GtbEFbJQ4KSTbjA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the larynx and trachea]]></video:title><video:description><![CDATA[The cervical viscera are composed of three layers named after their primary function.

The most superficial layer is the endocrine layer which contains the thyroid and parathyroid glands, then there’s the respiratory layer which contains the larynx and trachea and finally, the deepest layer is the alimentary layer which contains the pharynx and esophagus.

Focusing on the respiratory layer of the cervical viscera, this contains the larynx and trachea that routes air to the lungs, and gives everyone their own unique voice and saying that just made me aware of my own voice on this video recording!

So, let’s start with the larynx which is responsible for voice production and maintaining a patent airway.

The larynx is located in the anterior neck at the level of the bodies of the C3 to C6 vertebrae and connects the inferior part of the pharynx with the trachea. It also contains the vocal cords, or vocal folds, so it’s responsible for voice production.

Now, the larynx has a skeleton which is hardly a skeleton; rather, it’s formed of nine cartilages: thyroid, cricoid and epiglottic cartilages which are single and arytenoid, corniculate and cuneiform cartilages which come in pairs of two.

The thyroid cartilage is the largest cartilage and its superior border lies opposite the C4 vertebra.

It’s formed by two plate-like laminae which unite in the middle to form the laryngeal prominence also known as the Adam’s apple, which is well marked in males and less visible in females.

Superior to this prominence, the laminae diverge to form a V-shaped notch called the superior thyroid notch, and in the middle of the inferior border of the cartilage, a shallow indentation can be found called the inferior thyroid notch.

The posterior border of each lamina projects superiorly as the superior horn and inferiorly as the inferior horn. The superior border and the superior horns attach to the hyoid bone through a membrane called the thyrohyoid membrane.

This membrane has a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Arm,_elbow_and_forearm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1pL8O1ijQhCGfTxDPwUp-JMsSpe704Ql/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Arm, elbow and forearm]]></video:title><video:description><![CDATA[The majority of things we do every day require the use of our arms and forearms. Sometimes we forget how heavily we rely on our arms, and are quickly reminded how important they are when injury occurs. So, let&amp;#39;s take a look at common injuries occurring to the arm and forearm.

Alright, let&amp;#39;s begin by looking at fractures of the humerus, the main bone of the arm. The most common kind are fractures of the surgical neck of the humerus, which occur more frequently in elderly people with osteoporosis who have structurally weaker bones. The cause is usually indirect trauma, like falling on the hand with an extended arm.

Surgical neck fractures can result in damage to nearby structures, such as the axillary nerve causing cutaneous deficits in the proximal lateral arm, as well as damage to the anterior and posterior circumflex humeral arteries.

Next, there are humeral shaft fractures, which are usually caused by direct trauma. Now, remember that the radial nerve passes through the radial, or spiral, groove on the back of the humerus, so a common complication of midshaft humeral fractures is radial nerve injury.

Radial nerve injury results in damage to the extensors of the wrist and potential wrist drop, as well as cutaneous sensation dysfunction of the dorsal hand, forearm, and upper arm. Additionally, the deep brachial artery travels with the radial nerve in the spiral groove and can also be damaged. Finally, distal humeral fractures are a result of trauma to the elbow region, or hyperextension injuries.

In a supracondylar fracture, which is a fracture above the epicondyles, an anteriorly displaced portion of the fractured humerus on the medial supracondylar region could injure the median nerve, resulting in wrist flexion weakness and cutaneous deficits of the anterior 3 and a half digits, as well as the brachial vessels.

An anterior displaced fracture of the lateral supracondylar region could cause damage to the radial nerve, again causing]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peroxisomal_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JknNyw3aTlCnSWFOjm5X3RBaQyCSR15s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peroxisomal disorders: Pathology review]]></video:title><video:description><![CDATA[8 month old Emmanuel is brought to the clinic due to repeated episodes of jerking movements and loss of consciousness over the past few months. His parents are also worried because he feels limp when they lift him up, and his head tends to flop backward or to the side. On physical examination, you notice he has a flat face with a broad nasal bridge, and upon palpation of the abdomen, the liver appears enlarged. Right after him, 17 year old Arletta comes in. She complains that, recently, she has started to have difficulties seeing clearly at night. She also noticed that her skin is unusually dry, and doesn’t seem to improve with moisturizing cream. On physical examination, there are rough scaly patches of skin all over her body. You also notice that both her fourth toes are shorter than normal, and she tells you that they’ve been like that since birth. Finally, you see 32 year old George, who comes in with a 6 month history of progressive fatigue and weight loss. His wife has also recently noticed that, on occasion, he has been slurring his speech. On further questioning, George reluctantly tells you that he has experienced difficulties maintaining an erection. Examination reveals a low blood pressure, along with increased skin pigmentation, mostly around the oral mucosa, palmar creases, and knuckles. 

Based on the initial presentation, Emmanuel, Arletta,, and George all seem to have some form of peroxisomal disorder. But first a bit of physiology real quick. Peroxisomes are cellular organelles that neutralize free radicals, which are molecules with an unpaired electron that can damage the cells by oxidizing lipids, proteins, and even the DNA. When free radicals enter peroxisomes, they get converted by an enzyme called oxidase into hydrogen peroxide or H2O2. But since hydrogen peroxide is still dangerous, there’s another enzyme, called catalase, which safely converts it into water and oxygen. Another thing catalase can do is use that hydrogen peroxide to b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vessels_and_nerves_of_the_gluteal_region_and_posterior_thigh</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Sj96bAyvS6a5014h2jJmuq_CRP24RFND/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vessels and nerves of the gluteal region and posterior thigh]]></video:title><video:description><![CDATA[The gluteal region and posterior thigh contains an abundance of large and small muscles, and coursing through these muscles is a vast network of nerves and vessels. 

These nerves mainly originate from the lumbosacral plexus, whereas the vascular supply derives either directly or indirectly from the internal iliac arteries. 

Ok, so let’s start with the nerves of the gluteal region and posterior thigh. 

Most nerves of the lower limb arise from the lumbosacral plexus, a network of nerves derived from the roots of lumbar and sacral spinal nerves that branch out to form the nerves of the lower limb. 

However, out of all the resulting nerves, the gluteal region and posterior thigh is only supplied by the cluneal nerves, superior and inferior gluteal nerves, the sciatic and pudendal nerves, the posterior cutaneous nerve of the thigh, and nerves to quadratus femoris and to obturator internus.

Let&amp;#39;s start off with the cluneal nerves which innervate the skin of the gluteal region. 

The superior cluneal nerves arise from L1-L3, and supply the skin of the superior buttock. 

The middle cluneal nerve arises from S1-S3 and supplies skin over the sacrum and adjacent area of the buttocks. 

And finally the inferior cluneal nerve is a branch of the posterior cutaneous nerve of the thigh from S2-S3 and supplies skin over the inferior half of the buttocks as far as the greater trochanter. 

Next, there’s the superior gluteal nerve which is formed by the L4, L5, and S1 nerve roots. 

The nerve courses laterally between the gluteus medius and minimus along the deep branch of the superior gluteal artery, and it exits the pelvis through the greater sciatic foramen above the piriformis muscle. 

It then goes on to innervate the the gluteus medius, the gluteus minimus, and the tensor fasciae latae. 

This nerve doesn’t have any sensory function.

The inferior gluteal nerve is formed by the L5, S1, and S2 nerve roots and, much like its brother, it leaves the pelvis t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacologic_adjuncts_to_conventional_periodontal_therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1O0DzgSvT1WxCaXWz5NWM-7mQGKuQqO2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacologic adjuncts to conventional periodontal therapy]]></video:title><video:description><![CDATA[Periodontal disease refers to a group of inflammatory conditions that affect the tissues around the teeth. 

The mildest form of periodontal disease is gingivitis and, if left untreated, gingivitis can progress to periodontitis. 

Now, the primary goal of periodontal therapy is to save the natural dentition and periodontium but also to prevent recurrence of the periodontal disease. 

The conventional treatment is based on mechanical therapy like using curettes to scale and root plane or surgical procedures.  

However, not all patients respond well to conventional therapy, so pharmacological agents can be a useful adjunct in these cases.     

Now, based on the type of delivery, medications used in the treatment of periodontitis can be subdivided into topical, local, and systemic medications. 

The most common topically-delivered medications are antiplaque agents, which are usually delivered in the form of mouthwashes. 

Based on their antimicrobial and antiplaque effect, these agents are subdivided into three generations. 

First-generation agents include fluoride, oxygenating agents, phenolic compounds, quaternary ammonium compounds among other antimicrobials. 

Second-generation agents like chlorhexidine gluconate have prolonged antibacterial activity. 

Finally, we have third-generation agents that interfere with the ability of the bacteria to attach to the teeth. 

The main representative of this group is delmopinol hydrochloride.

Now, switching gears and moving on to local delivery medications, which can be subdivided into oral irrigation and local sustained delivery. 

An oral irrigator is a device that directs a stream of pressurized water or solutions along the gingival margin and between teeth. 

The stream of water disrupts the formation of the dental biofilm and decreases gingival inflammation. 

Oral irrigation is further subdivided into supragingival and subgingival irrigation. 

In supragingival irrigation a tip is placed above the gingival]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/West_Nile_Virus_Infection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/INRxHKh5QeaWCqbgOx5MkiQ1SHSCNSkN/_.jpg</video:thumbnail_loc><video:title><![CDATA[West Nile Virus Infection]]></video:title><video:description><![CDATA[The West Nile virus gets its name from where it was discovered, west of the Nile river in Uganda. 

It primarily causes infection in birds, especially geese and a range of wild birds, although it can also infect other animals like horses. 

The virus affects the nervous system of the animals, causing symptoms that range from weakness and loss of coordination to complete paralysis. 

West Nile virus is a zoonotic virus, which means that it can spread from animals to humans.

The West Nile virus belongs to the genus flavivirus along with a few other viruses like the zika virus and dengue fever virus. 

West Nile virus has a worldwide distribution. 

Before 1999 it was present mainly in Africa, Asia, the Middle East, and some European countries. 

Following an outbreak in New York in 1999, it spread across North America, including all 48 of the contiguous states of the US, and has now also been found in South America and parts of the Caribbean. 

West Nile virus is transmitted primarily by mosquitoes, most often the female Culex species, which usually feed on birds. 

In people, other routes of infection include blood transfusion, organ transplantation, through breast milk and occasionally across the placenta.

The virus has also been found in some tick species, but it is not known if they play a role in passing the virus to susceptible animals or people.

The virus usually causes meningoencephalitis in animals, which is inflammation of the brain along with its protective membranes — the meninges. 

This results in a variety of symptoms including behavioral abnormalities and physical disabilities. 

In horses, common symptoms include discomfort, lameness, staggering, low-grade fever, weakness, inability to stand, muscle fasciculation, anorexia, and inability to swallow, convulsions, and even death. 

Similarly, infected birds also show symptoms like recumbency, uncoordinated movements, and leg and wing paralysis. 

Some birds may also show torticollis, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Florian_Otto:_CEO_and_Co-founder_of_Cedar_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DRn-sPUyTBupAfiJXNsWbbp6Sp_dv9Px/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Florian Otto: CEO and Co-founder of Cedar (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Florian Otto: CEO and Co-founder of Cedar (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Jannine_Versi:_COO_and_Co-Founder_of_Elektra_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GYSryP62SyivXeTVg22BbjpETRuxakpg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Jannine Versi: COO and Co-Founder of Elektra Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Jannine Versi: COO and Co-Founder of Elektra Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._John_Danaher:_Global_President_of_Clinical_Solutions_at_Elsevier_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VIKWYbHvSJC9lKv1dl2SXu6HT7yasBFy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. John Danaher: Global President of Clinical Solutions at Elsevier (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. John Danaher: Global President of Clinical Solutions at Elsevier (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Jeffrey_Burns:_Chief_of_Critical_Care_Med._Boston_Children's_Hospital_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZKBomxkqR-SMKaVwz8ux8KxqQkKXHlNZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Jeffrey Burns: Chief of Critical Care Med. Boston Children&apos;s Hospital (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Jeffrey Burns: Chief of Critical Care Med. Boston Children&apos;s Hospital (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Kathy_Winston:_Dean_of_College_of_Nursing_University_of_Phoenix_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jVEggeC7TIqJTzZd7mY8MRxYS1KqBAcZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Kathy Winston: Dean of College of Nursing University of Phoenix (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Kathy Winston: Dean of College of Nursing University of Phoenix (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Eric_Topol,_MD:_Executive_Vice_President_of_Scripps_Research_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Iai_fGxBSUyQoTkt65-QvVhDRX26oSpc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Eric Topol, MD: Executive Vice President of Scripps Research (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Eric Topol, MD: Executive Vice President of Scripps Research (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Burck_Smith:_Founder_&amp;_CEO_of_StraighterLine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zQZoWSoCQY2OUybcnBD4qnLgTAOW8s_M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Burck Smith: Founder &amp; CEO of StraighterLine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Burck Smith: Founder &amp; CEO of StraighterLine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Sachin_Jain:_President_&amp;_CEO_of_SCAN_Health_Plan_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wo12Lxo3R3eMjdCvXpGg66UVSjeRF-R7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Sachin Jain: President &amp; CEO of SCAN Health Plan (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Sachin Jain: President &amp; CEO of SCAN Health Plan (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Salman_Khan:_Founder_&amp;_CEO_of_Khan_Academy_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hQ93eHTKTuC2-YUEKlrecr4wQMimZ1kG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Salman Khan: Founder &amp; CEO of Khan Academy (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Salman Khan: Founder &amp; CEO of Khan Academy (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bones_of_the_neck</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m3e0axfiQRW_sVnPtN4uYBUqR2mgIAe5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bones of the neck]]></video:title><video:description><![CDATA[The neck is the anatomical region between the base of the cranium superiorly and the clavicles inferiorly and it joins the head to the trunk and limbs, serving as a major conduit for structures passing between them. 

The skeleton of the neck is formed by the cervical vertebrae, the hyoid bone, and the manubrium of the sternum which are part of the axial skeleton, as well as the clavicles which are part of the appendicular skeleton. 

.Alright, so let’s start with the cervical vertebrae, of which there are 7. 

These are the smallest vertebrae, and they form the cervical region of the vertebral column, enclosing the cervical spinal cord and meninges. 

Cervical vertebrae can be typical or atypical, and when it comes to the cervical column, the typical vertebrae are C3, C4, C5 and C6, while the atypical vertebrae are C1, C2 and C7. 

Ok so, all typical vertebrae have a vertebral body, a vertebral arch and seven individual processes. 

The vertebral body is situated anteriorly, and it’s small and longer from side to side than anteroposteriorly. 

It has a concave superior surface and a convex inferior surface. 

These surfaces are the vertebral endplates, which help form the intervertebral joints together with the intervertebral discs and the adjacent vertebra. 

On the superior surface, there’s an elevated superolateral margin called the uncus of the body, or the uncinate process. 

Next, there’s the vertebral arch, which is located posterior to the vertebral body and is formed by two pedicles and two laminae. 

The pedicles are short, thick processes that project posteriorly from the vertebral body to meet the laminae, which are two broad, flat plates of bone, that unite in the midline and complete the vertebral arch. 

The vertebral arch and the posterior surface of the vertebral body form the walls of the vertebral foramen through which the spinal cord and its meninges pass. 

The vertebral foramen is rather large and, in the cervical region, triangular.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscles_of_the_gluteal_region_and_posterior_thigh</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3rdE-rhaS1WDGdVs7yapE6jiRCW5kYL9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscles of the gluteal region and posterior thigh]]></video:title><video:description><![CDATA[When looking at the lower limb from the posterior view, there are two regions that stand out immediately: the gluteal region and the posterior thigh. 

Let’s start with what’s arguably the most popular one of the two and which has been featured in countless pop songs - the gluteal region. 

The gluteal region is situated posterior  to the pelvis and inferior to the iliac crest. 

Laterally it overlies the greater trochanter, and anteriorly, it extends up to the anterior superior iliac spine. 

It also extends from the iliac crest superiorly to the gluteal fold inferiorly. 

The gluteal fold is the crease formed by the inferior aspect of the buttocks and the posterior upper thigh. 

Medially, the region extends to the mid-dorsal line and is called the intergluteal cleft, which is the groove that separates the buttocks from each other. 

Actually, before we move on, let’s review some important landmarks to help you understand this region’s anatomy better. 

First, the posterior sacroiliac ligament is the posterior continuation of the fibrous capsule of the synovial part of the sacroiliac joint, and continues inferiorly with the sacrotuberous ligament. 

The sacrotuberous ligament goes from the posterior surface of the ilium and the lateral surfaces of the sacrum to the ischial tuberosity. 

A similar ligament, called the sacrospinous ligament, passes from the lateral surface of the sacrum and the coccyx to the ischial spine. 

These two ligaments convert the greater and lesser sciatic notches into greater and lesser sciatic foramina. 

Simply put, the greater and lesser sciatic foramina  are passageways, or “doors” for structures leaving the pelvis and entering the gluteal region and vice versa. 

The structures passing through the greater sciatic foramen include the piriformis muscle and the structures that leave the pelvis above it, mostly represented by the superior gluteal vessels and nerve and the structures that leave the pelvis below it - the sci]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_knee_joint</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GJGnmpYAQLOgbNwYGJiQvAY7QWCdbKl7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the knee joint]]></video:title><video:description><![CDATA[The knee joint is a large hinge type of synovial joint, allowing flexion and extension of the lower limb.

The knee joint has three main articular areas: the lateral and medial femorotibial articulations between the lateral and the medial condyles of the femur and tibia, as well as the intermediate femoropatellar articulation between the patella and the femur. Notice that the fibula does not participate in the knee joint!

Ok, now, the articular surfaces of the knee joint are the medial and lateral femoral condyles; the patellar surface of the femur between these two condyles; the articular surface of the patella, which is a plateau with a anteroposterior ridge that fits into the patellar surface known as the trochlear groove; and the articular surfaces of medial and lateral condyles of the tibia, on which the condyles of the femur roll.

Because the knee joint articular surfaces are irregularly shaped and incongruent, knee joint stability heavily relies on tibiofemoral ligaments, and the strength of the surrounding muscles such as the quadriceps.

Now, the knee joint is surrounded by a joint capsule, which has an external fibrous capsule and an internal synovial membrane.

Superiorly, the fibrous capsule attaches to the femur, just proximal to the articular margins of the condyles.

Posteriorly, the fibrous layer encloses the condyles and the intercondylar fossa, and has an opening for the tendon of the popliteus.

Inferiorly, the fibrous layer attaches to the margin of the tibial plateau, except where the tendon of the popliteus crosses the bone.

The quadriceps tendon, patella, and patellar ligament replace the fibrous layer anteriorly, and the fibrous capsule is continuous with the medial and lateral margins of these anterior structures.

Then, the extensive synovial membrane lines all surfaces bounding the articular cavity not covered by articular cartilage, so it can be found attaching to the periphery of the articular cartilage covering both the fem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Joints_of_the_ankle_and_foot</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ggaj5fY6SQKbIppWtjgbOVm-QGC54tkx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Joints of the ankle and foot]]></video:title><video:description><![CDATA[Some of us can agree that we love rock and roll.

However, most of us can also agree that we don&amp;#39;t love it when we step on a rock, and roll our ankles.

How is that for a segue into talking about the ankle?

Alright, enough of the bad opening lines, let’s discuss the joints of the ankle and the foot!

The ankle joint or tibiotalar joint, is a hinge-type synovial joint located between the distal ends of the tibia and the fibula and the superior part of the talus, which are the three main bones of this joint.

The main articular components of this joint are the trochlea and body of the talus, which articulates medially with the medial malleolus of the tibia and laterally with the lateral malleolus of the fibula.

In a nutshell, the tibia and fibula are bound together by the strong tibiofibular ligaments, and, together, their respective malleoli form a bracket shaped socket, which is covered in hyaline cartilage.

This socket is known as a malleolar mortise and is where the pulley-shaped trochlea of the talus fits.

The malleolar mortise is bounded posteriorly by the inferior part of the posterior tibiofibular ligament, superiorly by the articular surface of the tibia, with the medial and lateral walls being the medial malleolus and lateral malleolus respectively.

The joint capsule of the ankle joint is thin anteriorly and posteriorly but is supported on each side by a series of strong ligaments.

Its fibrous layer is attached superiorly to the borders of the articular surfaces of the tibia and the malleoli and inferiorly to the talus.

By contrast, its synovial layer is loose and lines the fibrous layer of the capsule.

Now, the supportive ligaments reinforce the ankle joint.

Laterally, there’s the lateral ligament of the ankle consisting of three completely separate ligaments which help prevent inversion of the ankle.

First, there’s the anterior talofibular ligament that extends anteromedially from the lateral malleolus to the neck of the t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_inferior_mediastinum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xK07k4-kRiif1uBtITyNvJy3SviwWUTW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the inferior mediastinum]]></video:title><video:description><![CDATA[As we know, the mediastinum is divided into the superior mediastinum and the inferior mediastinum.

The superior mediastinum is separated from the inferior mediastinum by the transverse thoracic plane, which is a horizontal plane that extends from the sternal angle anteriorly and the junction of T4 and T5 posteriorly, an important anatomical landmark representing the bifurcation of the trachea and the beginning and end of the arch of the aorta.

The inferior mediastinum lies between the transverse thoracic plane superiorly, and the diaphragm inferiorly, and is further subdivided by the pericardium into anterior, middle and posterior parts.

So first, let’s look at the posterior mediastinum.

It is located anterior to the T5 through T12 vertebrae, posterior to the pericardium and diaphragm, inferior to the transverse thoracic plane and between the parietal pleura of the lungs.

The posterior mediastinum contains the thoracic aorta, thoracic duct and lymphatic trunks, posterior mediastinal lymph nodes, azygos and hemiazygos veins, the esophagus and the esophageal nerve plexus.

The thoracic aorta continues the aortic arch and it begins on the left side of the inferior border of the body of T4, moving downwards in the posterior mediastinum on the left side of T5 through T12 vertebrae.

On its way down, the thoracic aorta is close to the median plane and moves the esophagus towards the right.

The thoracic aorta lies posterior to the root of the left lung, pericardium and esophagus and is surrounded by the thoracic aortic plexus.

Anterior to the inferior border of the T12 vertebra it continues on as the abdominal aorta and enters the abdomen through the aortic hiatus in the diaphragm.

The thoracic duct and azygos vein climb on the right side of the thoracic aorta and accompany it through the aortic hiatus.

The vascular branches of the thoracic aorta are: the esophageal arteries, which supply the esophagus, the bronchial arteries which supply the lungs, the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vessels_and_nerves_of_the_hand</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0kkJIAOKT36niKHpvxiOaKF6RbOx3V7Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vessels and nerves of the hand]]></video:title><video:description><![CDATA[All hands on deck everyone! 

We’re taking a deep dive into the blood supply and nerves of the most mobile and dexterous parts of our musculoskeletal system, the hands. 

Human hands are supplied by an intricate network of blood vessels and nerves, which all work hand-in-hand to deliver the necessary blood supply and coordination in order for the hand muscles to be able to type, draw, suture, climb and everything else hands do.

The hand’s blood supply comes entirely from two main sources: the ulnar and radial arteries, which both originate from the brachial artery. 

Inside the hand, the radial and the ulnar arteries give off numerous  branches and anastomoses, ensuring that working muscles get an uninterrupted blood supply throughout our versatility of movements.

Both the ulnar and the radial arteries enter the hand from the wrist. 

The ulnar artery travels down the medial forearm and enters the hand medally, while the radial artery runs down the lateral forearm and enters the hand  laterally.

Let’s look at the ulnar artery first. 

When entering the wrist, the ulnar artery passes superficiall to the transverse carpal ligament, also known as the flexor retinaculum, and enters the hand through a small tunnel called the ulnar canal, or Guyon’s canal. 

The ulnar canal has a roof, made up by the thickened superficial palmar fascia, a floor made up by the transverse carpal ligament, a medial wall, consisting of the pisiform and pisohamate ligament, and a lateral wall made up by the hook of the hamate. 

The ulnar canal also allows the ulnar nerve to  pass through, medial  to the ulnar artery.

After the ulnar artery reaches the hand, it divides into superficial palmar arch and a deep palmar branch. 

The superficial palmar arch  is the main termination of the ulnar artery and starting in the medial part of the hand it courses towards the lateral part of the hand to anastomose with the superficial  branch of the radial artery. 

Along its course, the super]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_sternoclavicular_and_acromioclavicular_joints</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qN1QH4JDQ2u1iI5YttrBSRZMRcuqj9Rl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the sternoclavicular and acromioclavicular joints]]></video:title><video:description><![CDATA[Joints are structures in which bones meet to either permit movement, or provide stability.

There are plenty of them in our upper limbs.

We’ve got the:sternoclavicular; the acromioclavicular; and the glenohumeral joints in the pectoral girdle; the elbow; the proximal and distal radioulnar joints in the forearm; the wrist joint; and the joints of the hand, which include the carpometacarpal, the intermetacarpal, the metacarpophalangeal, and interphalangeal joints.

So let’s get acquainted with the first two of these joints!

First up, there’s the sternoclavicular joint, which is the only bony articulation attaching the upper limb to the axial skeleton.

It involves the clavicular notch of the manubrium, the medial end of the clavicle, and a small part of the first costal cartilage.

It is a saddle synovial type of joint, named so because the manubrial articulating surface is concave and the clavicular articulating surface is convex, so they fit together the same way that a cowboy sits on his horse’s saddle.

The joint has an articular disc that is firmly attached to the anterior and posterior fibrous joint capsule by the anterior and posterior sternoclavicular ligaments, as well as the interclavicular ligament.

Like any other synovial joint, the articular surfaces of the sternoclavicular joint are covered by the fibrous joint’s capsule which has 4 ligamentous thickenings, simply called ligaments, lined internally by a thin layer of synovial membrane.

The ligaments of the fibrous capsule are the anterior and the posterior sternoclavicular ligaments, which reinforce the joint capsule anteriorly and posteriorly; the interclavicular ligament which strengthens the sternoclavicular joint superiorly; and finally, there is the costoclavicular ligament, which anchors the inferior surface of the medial end of the clavicle to the 1st rib and its costal cartilage, providing stability to the sternoclavicular joint by limiting the elevation of the pectoral girdle.

And]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_popliteal_fossa</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kgkg_Qf8SSe2FtpeeO1dOs_ASxi2RGN9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the popliteal fossa]]></video:title><video:description><![CDATA[The popliteal fossa is the space behind your knee; and even though it may not look like much from the outside, it’s actually a complex region, delimited by muscles and fascia, and it contains a lot of vessels and nerves that pass from the thigh to the leg.

So first, let’s look at the popliteal fossa, which, superficially, resembles a diamond-shaped cavity when the knee is slightly flexed. This means the popliteal fossa has two superior borders and two inferior borders.

So, lets go over these borders; The two superior ones are the superolateral border, delimited by the biceps femoris; and the superomedial border, delimited by the semimembranosus and semitendinosus muscles.

The two inferior borders are the inferomedial border, represented by the medial head of the gastrocnemius muscle, and the inferolateral border, delimited by the lateral head of the gastrocnemius muscle. The popliteal fossa also has a floor and a roof. The roof consists of two layers: the popliteal fascia and skin.

However, things get a bit more complicated with the floor, which has three sections: the bony popliteal surface of the femur superiorly, the posterior aspect of the joint capsule of the knee joint centrally, and the popliteus muscle and fascia covering the popliteus muscle inferiorly.

The popliteal fossa contains the small saphenous vein; the posterior cutaneous nerve of the thigh; the sciatic nerve, which divides into the tibial and common fibular nerves at the superior border; the popliteal arteries and veins along with their branches and tributaries; and the popliteal lymph nodes and lymphatic vessels.

Ok, so now let’s dive in with a little bit more detail, layer by layer. First, there’s the subcutaneous or superficial fascia, which contains the small saphenous vein, the terminal branch of the posterior cutaneous nerve of the thigh, and the medial and lateral sural cutaneous nerves.

Then comes the deep fascia, also called the popliteal fascia which covers and prot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Mediastinum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tK6dakchR9W4UQAVNX_gkNIAT-Ggqh5T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Mediastinum]]></video:title><video:description><![CDATA[We all know how important the heart is, but everyone forgets about the mediastinum, which is the area between the two lungs where the heart actually sits!

The mediastinum doesn&amp;#39;t just house the heart, but many important structures in the thoracic cavity from the superior thoracic aperture down to the diaphragm.

So let&amp;#39;s take a closer look at the clinical conditions that can affect the mediastinum and the structures within it.

First up, there is widening of the mediastinum, which can be seen on a chest x-ray.

Since the mediastinum contains so many structures, each of them can contribute to pathological widening.

It can be observed after a trauma that causes laceration or dissection of the great-vessels, typically the aorta, which can cause hemorrhaging into the mediastinum.

Other times, malignant tumors such as lymphomas can produce massive enlargement of mediastinal lymph nodes and widening of the mediastinum.

Another cause of mediastinal widening is heart hypertrophy due to congestive heart failure.

Now, next up, there’s the esophagus.

The esophagus may have up to four normal anatomic constrictions as it descends, however there are three sites of constriction that can occur specifically in the posterior mediastinum caused by three structures it meets on its way down: two thoracic constrictions with the first being where the esophagus is crossed by the arch of the aorta, and second where it is crossed by the left main bronchus, and one diaphragmatic constriction where it passes through the esophageal hiatus of the diaphragm.

The fourth site of constriction occurs in the cervical region before the esophagus enters the mediastinum, where constriction may be caused by the cricopharyngeus muscle.

At these locations, there’s a slower passage of substances and is where foreign objects that are swallowed are most likely to lodge.

These narrowings can be seen in chest radiographs of a person who underwent a barium swallow study.

Thes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Clavicle_and_shoulder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wx4HXFNUT__dsMWY8YM49DgWRXO6fcom/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Clavicle and shoulder]]></video:title><video:description><![CDATA[Our upper limbs are complex structures. They’ve got bones, muscles, fascia, nerves and blood vessels, and everything in between. Our upper limbs are prone to injury however, and oftentimes, even a small injury can have a huge functional deficit as we are so reliant on our upper limbs in everyday life. One of these commonly injured areas is the shoulder region. 

Ok, so let’s start by taking a look at the injuries of the clavicle. Because of its subcutaneous position, the clavicle is prone to fractures, which are usually the result of direct or indirect trauma. An example of direct trauma is falling directly on the shoulder. Indirect trauma, however, may occur when falling on an outstretched hand, and the force of impact is transmitted through the bones of the forearm and the arm to the shoulder, which can result in a clavicle fracture.  Most of these fractures occur in the middle third of the clavicle, particularly where the middle third meets the lateral third, which is the weakest point of the clavicle. 

So with clavicular fractures, the medial fragment is usually pulled up by the sternocleidomastoid muscles, which can be apparent to the naked eye and palpable. At the same time, the trapezius muscle is having trouble holding the lateral fragment up, because of the weight of the limb, so the shoulder drops. And since the two fragments may glide under each other, the clavicle is also shortened. Additional features may signal complications of a clavicle fracture. For example, if the skin above the fracture seems to be tenting, meaning it looks like a tent, that suggests the fracture may become an open fracture in the future, and warrants surgical stabilization. 

Alright, now, another thing that can happen in this region is an acromioclavicular dislocation,  also called a “shoulder separation”. Just like the name says, the clavicle and acromion process separate, usually because of a direct blow to the shoulder, or a fall landing directly on the shoulder jo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_thyroid_and_parathyroid_glands</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WwXSbeoPQfKpzxlDw9DRNjlLTO_RQLC_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the thyroid and parathyroid glands]]></video:title><video:description><![CDATA[The cervical viscera are composed of  three layers named after their primary function. 

The most superficial layer is the endocrine layer which contains the thyroid and parathyroid glands, then there’s the respiratory layer which contains the larynx and trachea and finally, the deepest layer is the alimentary layer which contains the pharynx and esophagus. 

Let’s focus on the endocrine layer. 

The thyroid gland is the largest endocrine gland in the body and produces two hormones: thyroid hormone and calcitonin. 

It’s located anteriorly in the neck at the level of the C5 to T1 vertebrae and deep to the sternothyroid and sternohyoid muscles. 

It consists of a right and left lobe, located anterolateral to the larynx and trachea. 

These lobes are united over the trachea by a thin isthmus, usually anterior to the second and third tracheal rings, giving it an H-shaped appearance. 

In some people, there is a third lobe called the pyramidal lobe which usually arises from the isthmus and extends  up  to the hyoid bone. 

Now, the thyroid gland is surrounded by a thin fibrous capsule which sends septa deeply into the gland, and this capsule is attached to the cricoid cartilage and the superior tracheal rings by dense connective tissue.

External to the capsule, the visceral portion of the pretracheal layer of deep cervical fascia forms a loose sheath, and between this loose sheath and the fibrous capsule, there’s the superior and inferior thyroid arteries which supply the gland. 

The superior thyroid arteries are usually the first branches of the external carotid arteries and they descend to the superior poles of the gland, then pierce the pretracheal layer of deep cervical fascia and finally divide into anterior and posterior branches which supply mainly the anterosuperior aspect of the gland. 

The inferior thyroid arteries are the largest branches of the thyrocervical trunks and they run superomedially posterior to the carotid sheaths to reach the posteri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antacids:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ozj2mRtuTJ_HRXYlVMphiWniR4yOJp89/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antacids: Nursing pharmacology]]></video:title><video:description><![CDATA[Antacids are acid reducing medications that directly lower the acidity of stomach contents. They are used to treat conditions like gastroesophageal reflux disorder, or GERD, and peptic ulcer disease, or (PUD). 

When combined with antiflatulent medications like simethicone, they also help decrease gas production, which provides comfort and relief to clients experiencing gas or bloating. Antacids can be made up of aluminum, magnesium, calcium or sodium compounds. 

Common antacid medications include: aluminum hydroxide, aluminum hydroxide and simethicone, magnesium hydroxide, magnesium hydroxide and aluminum hydroxide, magnesium trisilicate and aluminum hydroxide, magaldrate, calcium carbonate, calcium carbonate with magnesium hydroxide, and sodium bicarbonate. 

Now when antacids are taken, the medication reacts with gastric acid and results in the production of neutral or low-acidity salts that increase the gastric pH. Additionally, the enzyme pepsin that normally helps digest protein is also inactivated. 

The outcomes of these reactions are a decrease in gastric acidity, enhanced mucosal protection and a reduction of the symptoms associated with GI conditions such as GERD and PUD. 

Antacids can cause several side effects If they are taken for an extended period of time, they may alter aluminum, calcium, sodium and phosphate levels. 

Other general side effects of antacids include belching, constipation, flatulence, diarrhea and gastric distention. 

Since all antacids increase gastric pH and can potentially bind with other drugs, absorption and effectiveness of medications taken along with antacids can be affected. 

For example, they can increase oral absorption of medications that are weak bases, such as quinidine, an antiarrhythmic and anti-parasite medication; and decrease the oral absorption of medications that are weak acids, such as warfarin sodium. 

Also, antacids can chelate, or bond, other medications in the GI tract, resulting in new comple]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_orbit</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tx2EXKDkTniOEcmzbz4Q3VmwSPmK7xhX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the orbit]]></video:title><video:description><![CDATA[To be able to see everything that surrounds us, including this video, we can count on a very special sense organ: the eyes.

The eyes can be easily injured, so each of them is protected by a hard bony structure called the orbit. The orbits also protect the muscles, vessels and nerves of the eyes.

And between each eye and the orbit protecting it, there’s a soft cushion of fat to prevent any friction or damage to the eyes.

Additional protection is ensured by the eyelids, which close and open as needed, and the lacrimal apparatus, which secretes tears to lubricate the eyes.

Now, each orbit is shaped like a pyramid, so they have an apex posteromedially, or towards the inside of the skull; a base anterolaterally, that opens in the facial skeleton; and four walls: superior, inferior, lateral, and medial.

These walls are made up of several bones. The medial wall comprises the ethmoid bone in the center, the lacrimal bone and maxilla - or maxillary bone anteriorly, and the lesser wing of the sphenoid bone posteriorly.

The superior wall - or roof of the orbit - is mainly formed by the orbital part of the frontal bone anteriorly, and a small posterior part by the lesser wing of the sphenoid bone.

The lateral wall is made up of the zygomatic bone anteriorly and the greater wing of the sphenoid bone posteriorly.

Finally, the inferior wall - or floor of the orbit - is formed by the maxillary bone medially, the zygomatic bone laterally, and a tiny part by the palatine bone posteriorly.

In between the two maxillae lies the nasal bone, but it doesn’t contribute to the orbit. Alright now, above the orbit, there’s the supraorbital margin of the frontal bone.

Towards the medial part of the supraorbital margin, the supraorbital nerve and vessels pass through the supraorbital foramen or notch.

Moving onto the inside of the orbit, on the anterolateral part of the roof of the orbit, there’s the lacrimal fossa, a depression in the frontal b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_the_cranial_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aARVlDQJSa_7I-edACZF83nHS6mp3bPO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to the cranial nerves]]></video:title><video:description><![CDATA[The cranial nerves are 12 paired nerves that arise from the brain and travel through foramina and fissures  in the cranium to innervate various structures, primarily in the head and neck. 

Just like spinal nerves, which originate from the spinal cord, cranial nerves originate from the brain, but unlike spinal nerves which are pretty similar to each other - with all of them being mixed nerves - the cranial nerves are a mix and match of motor, sensory and autonomic functions. 

Simply put, some cranial nerves are motor nerves, some are sensory nerves, some are mixed and some carry parasympathetic fibers as well. 

Funnily enough, some of them aren’t even nerves at all. 

The first and second cranial nerves, which are the olfactory and optic nerves, are actually brain projections that belong to the olfactory and optic tracts, but everyone likes to call them cranial nerves so we will too! 

Let’s start by naming the 12 pairs of cranial nerves  in order from rostral, or front of the brain, to the caudal, or back of the brain, on an image of the ventral surface of the brain: 1st Olfactory, 2nd Optic, 3rd Oculomotor, 4th Trochlear, 5th Trigeminal, 6th Abducens, 7th Facial, 8th Vestibulocochlear, 9th Glossopharyngeal, 10th Vagus, 11th Accessory, and 12th Hypoglossal. 

There are many mnemonics out there to help you remember these so choose one that best fits you, but here at Osmosis we like to remember these nerves by saying: 

Oh
Oh
Oh 
To
Touch
And
Feel
Very
Green
Vegetables
A
H!

Now, these nerves don’t all originate from the same place and they enter or exit at different parts of the brain. 

Cranial nerves one and two enter the cerebrum, but most of the cranial nerves enter or exit at various levels of the brainstem. 

Cranial nerves three and four emerge from the midbrain, and it’s worth mentioning that cranial nerve four is the only nerve to arise from the dorsal aspect of the brainstem. 

Cranial nerve five, or the trigeminal nerve, arises from the pons, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_glenohumeral_joint</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yRjp_ei3Su2Q32LqDag9AWdGRZumURQn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the glenohumeral joint]]></video:title><video:description><![CDATA[The glenohumeral joint, also known as the shoulder joint, is a ball and socket type of synovial joint: the ball being the head of the humerus, and the socket being the glenoid cavity of the scapula. 

The shoulder joint is the most mobile joint in our body, and it allows us to do everything from pull ups, to throwing a baseball, and hugging our loved ones!

Let’s take a closer look at our articulating parts here. So, the head of the humerus fits into this shallow glenoid cavity. 

The glenoid cavity is actually so shallow that it only covers one-third of the humeral head. 

Having a shallow glenoid cavity allows for exceptional mobility as the humeral head can rotate freely to allow us an impressive range of motion. 

At the same time, the contour of the glenoid cavity is lined by a fibrocartilaginous rim, called the glenoid labrum, which makes the cavity a little bit deeper, reducing the chance for dislocations.

Like any respectable synovial joint, the glenohumeral joint is covered by a tough, but loose, joint capsule with an internal synovial lining. 

The joint capsule extends from the anatomical neck of the humerus, to the margin of the glenoid. This capsule has two apertures, or passageways. 

The first one is between the tubercles of the humerus, which provides passage for the tendon of the long head of the biceps brachii. 

This tendon then passes in the intertubercular groove covered by a broad fibrous band, called the transverse humeral ligament, which runs from the lesser tubercle of the humerus, to the greater tubercle. 

The second aperture is situated inferior to the coracoid process, and it allows communication between the subtendinous bursa of the subscapularis and the joint’s synovial cavity. 

Speaking of which, there are actually two bursae around the glenohumeral joint, which are basically pockets of synovial fluid. 

There is one between the capsule and the tendon of the subscapularis muscle called the subtendinous bursa of the subscap]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_foot</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nsAut3UvSbqicAer0dn7w_0oQReeLyzk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the foot]]></video:title><video:description><![CDATA[Okay everyone, you are going to get a real kick out of this video, because we&amp;#39;re going to talk about the anatomy of the foot.

The foot can be divided into two main parts - the sole or plantar region, which is the part of the foot contacting the ground, and the dorsum of the foot or the dorsal region, which is the part directed superiorly.

Alternatively, it can be divided into three sections - the hindfoot, containing the talus and calcaneus; the midfoot, containing the navicular, cuboid, and cuneiforms; and the forefoot, which includes the metatarsals and phalanges.

The foot also has two important landmarks - the heel, which is the sole of the foot underlying the calcaneus, and the ball of the foot, which is the sole underlying the heads of the medial two metatarsals.

So let’s talk a bit about the foot’s components. The most superficial elements are skin and fascia, which vary in thickness and strength across the foot, depending on if the area has roles in weight-bearing, ground contact, or compartmentalization.

The skin on the dorsum of the foot is much thinner and less sensitive than the one on the sole. By contrast, the thick skin on the sole is ticklish, hairless, and has numerous sweat glands.

The fascia of the foot can be divided into superficial and deep fascia. The superficial fascia or the subcutaneous fat tissue is loose and deep to the dorsal skin.

It is much more fibrous in the sole and is thicker than in other areas of the foot, making the heel act as a shock absorbing pad.

The deep fascia of the dorsum of the foot is rather thin and continuous proximally with the inferior extensor retinaculum.

It is also continuous with the plantar fascia, the deep fascia of the sole, over the lateral and posterior aspects of the foot

Speaking of which, the plantar fascia on the plantar aspect of the foot helps protect the sole from injury, and supports the longitudinal arches of the foot.

It consists of a thick central part, called t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_anterolateral_abdominal_wall</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/trtgJw1QRpCZ_2tIzAEZXwiZSGO0_7nf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the anterolateral abdominal wall]]></video:title><video:description><![CDATA[The abdominal wall is subdivided into the anterior wall, the right and left lateral walls, and the posterior wall. These walls are musculoaponeurotic, meaning they are composed of muscles and fascial layers, except for the posterior wall which is also made up by the lumbar vertebral column. This musculoaponeurotic wall functions to enclose and protect the abdominal viscera, stabilize and contribute to movements of the trunk, and also increase the intra-abdominal pressure which is needed during urination, defecation, vomiting, and assisting in childbirth.

Now, the anterior and lateral abdominal walls are collectively known as the anterolateral abdominal wall, mainly because the boundary between the two is not distinct. So the anterolateral abdominal wall extends from the thoracic cage down to the pelvis. More specifically, it’s bounded superiorly by the cartilages of the seventh through tenth ribs as well as the xiphoid process, and inferiorly  by the inguinal ligament and superior margins of the anterolateral aspects of the pelvic girdle

The anterolateral wall is composed of many different layers. There’s 12 of them in total. The most superficial layer is the skin, which covers a superficial fatty layer of subcutaneous tissue, or fat, known as Camper fascia, which is a major site of fat storage.  Deep to the Camper fascia, there is a membranous layer of subcutaneous tissue known as Scarpa fascia, which is continuous inferiorly with the superficial perineal fascia, or Colles fascia.  And deep to the superficial fascial layers, there are 3 muscle layers, each covered in a layer of a deep fascia - so  6 layers in total. So right after Scarpa fascia, there’s the superficial investing fascia, followed by the most superficial muscular layer: the external oblique muscle. Then comes the intermediate investing fascia and the internal oblique muscle. And finally, there are the deep investing fascia and the transversus abdominis muscle.Deep to the transversus abdom]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_abdominal_viscera:_Small_intestine</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7kXnxBrYSAezc_Lcv2ZZEF3dQGiQiuNn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the abdominal viscera: Small intestine]]></video:title><video:description><![CDATA[The small intestine is a part of the digestive tract specialized in absorbing nutrients and minerals from the food we eat.

It’s located in the abdominopelvic cavity, and it begins at the pylorus of the stomach and it ends at the ileocecal junction, where it continues with the large intestine.

It has three major components: the duodenum, which can be divided into four parts, the jejunum and the ileum.

Now, when talking about structures of the abdomen we often encounter the terms ‘retroperitoneal’ or ‘intraperitoneal’.

Retroperitoneal is a description for abdominal structures that are only partially covered by peritoneum and lie posterior or behind the abdominal peritoneum, where intraperitoneal means that these structures have invaginated and are completely covered by the visceral peritoneum.

So, of these components, the proximal portion of the first part of the duodenum, in addition to the jejunum and ileum are intraperitoneal, where the distal portion of the first part of the duodenum, in addition to the second, third, and fourth parts of the duodenum are retroperitoneal, and are found posteriorly in the retroperitoneal cavity.

That being said, let’s have a closer look at the duodenum and its four parts.

Overall, the duodenum is shaped like the letter C, curving around the head of the pancreas, and consists of the first, or superior part; second, or descending part; third, or inferior part; and fourth, or ascending part.

The first part lies in the transverse plane and begins anterolaterally to the right of the L1 vertebral body, continuing the pylorus.

The proximal portion of the first part has a segment of the lesser omentum called the hepatoduodenal ligament attached to its superior surface, and the greater omentum attached to the inferior surface.

The proximal 2cm of the first part is also more dilated and freely mobile as it is intraperitoneal with its anterior and posterior surface covered in peritoneum, and is referred to as the ampulla or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Wrist_and_hand</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t9Ia7ernQbKlc_w-TO-YAOSYRJSzxO8I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Wrist and hand]]></video:title><video:description><![CDATA[In everyday life, we rely on our hands for a variety of reasons, from vigorously typing out notes while watching an Osmosis video to playing musical instruments or participating in sports.

Unfortunately, since we use them so much, the hands are quite prone to injury.

Alright, let&amp;#39;s start by looking at distal forearm fractures.

There’s two kinds: Colles fracture, which are a direct result of falling on an extended wrist, and Smith fracture, which results from falling on a flexed wrist, or a direct blow to the posterior forearm.

With Colles fractures, the displaced radial fragment moves posteriorly, or dorsally, and the ulnar styloid process can also become fractured.

Clinically, when the distal radial segment moves dorsally this is called a “dinner fork deformity” because when viewed laterally, the hand and wrist are slightly curved anteriorly making it look like a fork.

With Smith fractures, on the other hand, the displaced distal radial fragment moves anteriorly, or ventrally, which clinically translates as a “garden spade” deformity.

Next, let’s look at carpal bone fractures, of which the most common are scaphoid fractures.

Scaphoid fractures occur as a result of falling on the lateral side of an outstretched hand in abduction.

Clinically, this results in pain and tenderness on the lateral side of the wrist and hand, in a location called the anatomical snuffbox, which is where you can palpate the scaphoid bone between the tendons of extensor pollicis longus on the medial side and extensor pollicis brevis and abductor pollicis longus on the lateral side.

The big problem with these fractures is that because the blood vessels supply the distal part of the scaphoid first then come back and supply the proximal part, a fracture in the middle of this bone disrupts the blood supply.

This can cause avascular necrosis and non union of the proximal fragment of the scaphoid, which is basically when the bone dies off because of lack of blood, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_pharynx_and_esophagus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GstmFjLvQjmxVwarzgX5csM1TReO7xx8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the pharynx and esophagus]]></video:title><video:description><![CDATA[The cervical viscera are composed of three layers based on their main functions.

The most superficial layer is the endocrine layer which contains the thyroid and parathyroid glands, then there’s the respiratory layer which contains the larynx and the trachea, and finally, the deepest layer is the alimentary layer which contains the pharynx and the esophagus.

So, let’s start with the pharynx which also has a respiratory function because it conducts air to the larynx, from where it passes through the trachea and into the lungs.

The pharynx extends from the cranial base to the inferior border of the cricoid cartilage anteriorly and the inferior border of the C6 vertebra posteriorly.

It’s located posterior to the nasal and oral cavities and it extends inferiorly past the larynx, where it continues with the esophagus.

Now, the pharyngeal wall consists of three layers: the buccopharyngeal fascia is the most external layer, covering the pharynx and, inferiorly, it’s continuous with the pretracheal fascia.

Then, there is a muscular layer which has an outer circular part and an inner longitudinal part, and the innermost mucous membrane which has a thick submucosa that contributes to the pharyngobasilar fascia.

Moreover, the posterior wall of the pharynx lies against the prevertebral layer of the deep cervical fascia.

The interior of the pharynx is divided into three parts: the nasopharynx which is located posterior to the nose and superior to the soft palate, the oropharynx which is located posterior to the mouth, and the laryngopharynx which is located posterior to the larynx.

The nasopharynx is the posterior extension of the nasal cavities and communicates with the nose through two paired openings called choanae, which are separated by the posterior end of the nasal septum.

The roof and the posterior wall of the pharynx form a continuous surface that lies inferior to the body of the sphenoid bone and the occipital bone.

On the lateral wall of the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Pleura_and_lungs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HLpqzUXRQN6KeMzhV-JL9R08QPO56me1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Pleura and lungs]]></video:title><video:description><![CDATA[Before you start watching this video, relax, and take a deep breath. 

Think about the air filling up your lungs, which are located on either side of your thoracic cavity. 

Now, we often take breathing for granted because it is under autonomic control, and it’s not until we have trouble breathing when we realize just how important our lungs are. 

There are many conditions that can affect the lungs, which can have a huge impact on our day to day lives. 

Now let’s look at some causes for lung ailments, starting with injuries of the cervical pleura and lung apex. 

Both these structures project through the superior thoracic aperture into the neck. 

So when there’s an injury involving the base of the neck, the lungs and pleural sacs can be injured as well, which can cause a pneumothorax. 

The pleura is also exposed to potential injury in its inferior portion, because it descends below the costal margin in three regions, where a penetrating injury may enter into the pleural sac. 

The first is the right part of the infrasternal angle, the other two parts are the right and left posterior costovertebral angles which are inferomedial to the 12th ribs and posterior to the superior poles of the kidneys. 

So kidney surgery can pose a risk for pleural injury.  

When discussing injuries to the pleura and lungs, it’s important to understand what pleuritic chest pain means. 

Pleuritic chest pain is caused by irritation to the pleura, which results in a classical ‘sharp’, stabbing pain that gets worse when you breathe in, and is exacerbated even further by deep inhalation and exhalation. 

Pleuritic chest pain can have multiple causes, including a pneumothorax, which is when there’s air trapped  within the pleural cavity, or a pleural effusion, when fluid builds up in the pleural cavity. 

Inflammation of the pleura can cause pleuritic chest pain, which is often the result of infection or inflammatory diseases such as rheumatoid arthritis, and may even result in a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_olfactory_(CN_I)_and_optic_(CN_II)_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v35SJYKfRVe1-PRLWoy61SJgTuK32WXq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the olfactory (CN I) and optic (CN II) nerves]]></video:title><video:description><![CDATA[The cranial nerves are made up of sensory fibers, motor fibers, or both, that innervate the majority of structures in the head and neck.

In addition to general sensory and motor innervation, they also transmit unique sensations, via special sensory fibers.

You know these as taste, smell, sight and hearing!

So to stop and smell the roses, but also to see the roses, we need to focus on the Olfactory and Optic nerves, also known as cranial nerves I and II.

So first, there’s cranial nerve I, or the olfactory nerve, which only contains special sensory fibers responsible for the sense of smell.

These fibers transmit olfactory impulses from the olfactory epithelium of the nasal cavity to the brain, where they are perceived as the sense of smell.

Now, the olfactory epithelium is located on each side of the roof of the nasal cavity where the nasal mucosa contains olfactory receptor neurons.

Olfactory receptor neurons are bipolar neurons that each have a dendrite on their apical surface that gives rise to many olfactory cilia, which possess receptors for odorant molecules.

The basal surfaces of these neurons give rise to central processes - or axons - that are collected into bundles to form approximately 20 olfactory nerves on each side, that, together, we call the right and left olfactory nerves.

The fibers pass through small foramina in the cribriform plate of the ethmoid bone, and enter the olfactory bulb in the anterior cranial fossa.

Here, the olfactory nerve fibers synapse on second order neurons, called mitral cells.

The axons of these cells form the olfactory tract, which travels posteriorly to several olfactory areas including the primary olfactory cortex within the temporal lobe.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Median,_ulnar_and_radial_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GPqjkAqPRHyZT6sRkuhb8OhmQjOBrn7V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Median, ulnar and radial nerves]]></video:title><video:description><![CDATA[The median, ulnar and radial nerves course through the forearm and wrist, and they help coordinate the movement of our forearms and hands. 

These nerves, however, are prone to injury because of various causes, and depending on which one of them is injured, that will result in characteristic symptoms that can help us recognize and identify it.

For the median nerve, the clinical manifestations depend on whether the lesion has occurred distally, as in carpal tunnel syndrome, or proximally, as in an anteriorly displaced portion of a medial supracondylar humerus fracture. 

The most common cause of median nerve injury is carpal tunnel syndrome, which is when the tunnel in the wrist through which the median nerve passes becomes narrower and compresses the median nerve. 

This can happen due to repetitive use, like typing on a keyboard, injuries like an anterior lunate dislocation, or associated with conditions such as hypothyroidism, diabetes, or in pregnancy. 

Symptoms of median nerve injury would be pain and paraesthesia in the radial 3 and a half digits, weakness of the first and second lumbrical, thenar atrophy, and weakness of thumb abduction and opposition of the affected hand. 

Specifically,  the recurrent branch of the median nerve is what provides  motor innervation to the thenar muscles of the hand, which are  responsible for abduction, flexion and opposition, so with injuries, people may have issues opposing the thumb, and it may be difficult to perform actions like buttoning up a shirt. 

Damage to the recurrent branch of the median nerve alone causes what is known as ‘ape hand’, which refers to atrophy of the thenar eminence and inability to oppose the thumb.. 

Damage to the entire median nerve at the level or the wrist, or distal median nerve, presents clinically as  a “median claw”. 

Let’s break this down quickly. 

So, the first and second lumbricals are innervated by the median nerve, and the lumbricals normally flex the metacarpophalangea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Axilla</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eyv9xXI9R7aF2ZdaYDLAVMSITJ_0zEjO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Axilla]]></video:title><video:description><![CDATA[The axilla, also known as the armpit, is first and foremost, incredibly ticklish. But from an anatomical standpoint, it’s a key location that contains many important structures that may be damaged, causing significant functional deficits. The axilla is like a train station, where a number of vascular, nervous and lymphatic structures pass between the trunk and the upper limb.

One very important structure is the brachial plexus, which can be divided into five roots, three trunks, six divisions, three anterior and three posterior cords, and five terminal branches. The order can be remembered using the mnemonic “Remember To Drink Cold Beer.” But you may want to wait until the end of the video before you act on that!

Now, an upper brachial plexus injury affects the superior roots, namely spinal nerves C5 and C6, and a classic example of an upper brachial plexus injury is Erb palsy, which can happen in adults as a shoulder trauma that results in an increase in the angle between the neck and the shoulder, or in newborns, when excessive stretching of the neck occurs during childbirth.

The clinical consequences reflect the affected nerves, which are the ones that are derived solely from C5 and C6 roots, namely, the musculocutaneous, axillary, and suprascapular nerves. This causes paralysis of muscles like the biceps brachii, which normally allows forearm flexion and supination, and the infraspinatus and teres minor, so lateral rotation of the arm is affected, as well as the deltoid and supraspinatus muscles, which would usually cause arm abduction but would also be affected. So with superior brachial plexus injuries, the classic finding is a “waiter’s tip position”, which reflects arm adduction and medial rotation, and forearm extension and pronation.

Lower brachial plexus injuries are much more uncommon, and they affect the inferior roots of the brachial plexus, namely C8 and T1. This can happen because of excessive abduction of the arm, aka an increased angl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psychological_sleep_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kqx1Dp4fSjOn1unMC75QRj03QiSMArRm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psychological sleep disorders: Pathology review]]></video:title><video:description><![CDATA[A 31 year old male named Hercules comes to the clinic complaining of excessive daytime sleepiness over the past year, despite getting a regular 7 to 9 hour sleep every night. This has recently started to interfere with his job, since he keeps dozing off at his desk, during meetings, or even while talking on the phone. Hercules is also concerned because he sometimes has very vivid dream-like sensations right before falling asleep, like seeing other people in the room. On further questioning, Hercules also mentions that when he gets really nervous or excited about something, he feels as if he cannot move his legs and might even fall down. Past medical history and physical examination are both unremarkable.

Based on the initial presentation, Hercules seems to have some form of sleep disorder. Many of us can have trouble falling asleep or may sleep too much from time to time, usually because of stress or a temporary illness. But when sleep problems become a regular occurrence and interfere with daily life, that’s a sign of a sleep disorder. For your exams, remember that sleep disorders are usually caused by factors that interrupt the sleep cycle, which is a period of sleep that lasts about 90 minutes and is divided into four stages. The first three stages make up non-REM or NREM sleep, which stands for non-rapid eye movement. So usually during non-REM sleep, our eyes don’t move much or at all. However, keep in mind that the voluntary muscles of the body may still be active. NREM sleep accounts for roughly 80% of the sleep cycle, and across the three stages of NREM, we move from very light sleep during Stage 1, to very deep sleep in Stage 3. This is followed by Stage 4, which is known as rapid eye movement or REM sleep, and accounts for the last 20% of the sleep cycle. During REM sleep, the eyes dart around really fast, and this is where dreaming occurs and memories are consolidated. During REM sleep, the voluntary muscles of the body are paralyzed, probably t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Zinc_deficiency_and_protein-energy_malnutrition:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/InqlXfhjT8KofmT1SI3lvKqYSzuU_GET/_.jpg</video:thumbnail_loc><video:title><![CDATA[Zinc deficiency and protein-energy malnutrition: Pathology review]]></video:title><video:description><![CDATA[A 2 year old girl, named Addae, is brought to the pediatric clinic for a well-child visit. 

She was adopted from Ghana a month ago, and her new parents tell you that they’ve noticed dark patches of flaky skin all over her body. 

Physical examination reveals erythematous plaques on her face, axilla, and groin skin folds, as well as prominent rounded cheeks and a distended abdomen. 

You also notice that both her feet and ankles are swollen, and when you press for a few seconds, a pit remains. 

Finally, upon palpation of the abdomen, the liver appears enlarged. 

You decide to run some blood tests, which reveal that Addae has decreased serum levels of albumin.

Based on the history and initial presentation, Addae seems to have some form of malnutrition, which results from not getting enough nutrients from the diet. 

For your exams, two important conditions associated with malnutrition include zinc deficiency, meaning there’s not enough zinc to meet the body requirements, as well as protein-energy malnutrition, which refers to a lack of energy due to the inadequate intake of protein or total calories, and has two major forms: Kwashiorkor and marasmus.

Okay, let’s begin with zinc deficiency. 

Zinc is a mineral that’s found mostly in poultry, oysters, and fish. 

Normally, it is mainly absorbed in the duodenum and jejunum, and gets transferred via the portal circulation to the liver, where it gets stored. 

So, for your test, note that the liver is the main organ involved in maintaining systemic zinc homeostasis. 

Now, zinc is essential for the function of hundreds of different enzymes.

In addition, zinc is necessary for the formation of specific transcription factors motifs, known as zinc fingers, that bind DNA and regulate the expression of various genes. 

The most high yield one is the gene coding for insulin-like growth factor-1, or IGF-1, which plays a key role in cell growth and proliferation. 

What’s high yield to remember is that this is espec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_brachial_plexus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qFBcXVo8RiW4wLgogu3QVRUDTNC_nJga/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the brachial plexus]]></video:title><video:description><![CDATA[Have you ever fallen asleep with your shoulder in a weird position only to wake up to your arm completely asleep? Or hit the inside of your elbow, or the famous ‘funny bone’, and cause part of your hand to go numb?

This happens when we compress or bang the nerves found in our arms, all of which originate in the brachial plexus. The brachial plexus is a vast network of nerves originating from the anterior rami of C5 to T1, which extends through the axilla into the shoulder, arm, and hand, providing afferent, or sensory, nerve fibers from the skin, as well as efferent, or motor, nerve fibers to the muscles.

Alright, so, the brachial plexus is divided into five roots, three trunks, six divisions, three cords, and five terminal branches. The order can be remembered using the mnemonic. “Remember To Drink Cold Beer.”

Additionally, there are branches that leave the brachial plexus at various points along its length. Since the branches that come off of the roots and trunks are located above the clavicle, they are sometimes called the supraclavicular branches of the brachial plexus.

And since the branches that come off of the cords as well as the terminal branches are located below the clavicle, they are sometimes called the infraclavicular branches of the brachial plexus.

Okay, so starting with the roots, the five roots come from the anterior rami of the last four cervical nerves, C5-C8, as well as the anterior ramus of the first thoracic nerve or T1. These roots usually travel between the anterior and middle scalene muscles along with the subclavian artery.

These five roots give off some branches: the long thoracic nerve, which arises from C5-C7, and gives motor innervation to the serratus anterior muscle, the dorsal scapular nerve from C5, which gives motor innervation to the rhomboid and levator scapulae muscles, and a contribution to the phrenic nerve from C5, which gives motor and sensory innervation to the diaphragm.

At the inferior part of the neck, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_tibiofibular_joints</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9pHA47IbRVSKP2U6u2laG0aKTh2-D6zl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the tibiofibular joints]]></video:title><video:description><![CDATA[Now, everyone knows about the famous hip joint and knee joint, but not many people like to talk about the lesser known tibiofibular joints.

The tibiofibular joints are two joints of the leg, one superior and one inferior.

This doesn&amp;#39;t mean one is better than the other, just that one is lower down!

Right below the knee joint, there are the leg bones, namely the tibia and fibula, which are connected by a superior tibiofibular joint, and an inferior tibiofibular joint, which is a component of the distal tibiofibular syndesmosis, as it is the distal end of the syndesmotic - or fibrous - connection between the tibia and fibula.

These joints have minimal function in terms of movement but play a greater role in stability and weight-bearing.

The superior tibiofibular joint is a plane type of synovial joint, which allows the involved bones to glide over one another to create movement.

This joint is located between the flat articular facet on the fibular head and a similar articular facet situated posterolaterally on the lateral tibial condyle.

As expected, the superior tibiofibular joint is also surrounded by a joint capsule, which attaches to the margins of the articular surfaces of the fibula and tibia.

This joint allows slight gliding movement during dorsiflexion of the foot. The tibiofibular syndesmosis, on the other hand, is a compound fibrous joint.

Basically, it represents the fibrous union of the tibia and fibula by means of the interosseous membrane, which unites the shaft of the bones, and the inferior tibiofibular joint, which unites the distal ends of the bones.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diagnosis_of_periodontitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1l2bjC3JQ4mJcCNINzitj_fkTQSRXj2V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diagnosis of periodontitis]]></video:title><video:description><![CDATA[Periodontal disease refers to a group of inflammatory conditions that affect the tissues around the teeth. 

The mildest form of periodontal disease is gingivitis and, if left untreated, gingivitis can progress to periodontitis. 

Now, the goal of diagnosis is to detect early signs of periodontal disease, treat the condition, and prevent further complications. 

The diagnosis of periodontitis is a systematic process subdivided into several parts, including the patient’s medical and dental history; radiographic evaluation, extraoral examination; intraoral examination; and additional diagnostic tests and procedures.

Let’s start with the medical history which is used to identify systemic factors associated with an increased risk of periodontitis. 

These include systemic conditions, such as diabetes mellitus, pregnancy, and HIV infection; environmental factors, such as stress, smoking, and inadequate nutrition; and the use of medications associated with gingival enlargement, such as phenytoin, nifedipine, and cyclosporine. 

On the other hand, dental history covers important information about the patient’s oral hygiene habits, the regularity of dental visits, previous dental conditions, and current concerns. 

Individuals with periodontitis typically complain of swelling, and bleeding of the gingiva; tooth mobility; and bad breath. 

After the history is taken, the next step is a radiographic evaluation with a full mouth radiographic survey. 

This survey should include periapical radiographs showing the apices of all teeth and appropriate bitewings.

The purpose is to identify and measure the loss of alveolar bone, but also to detect local factors that can complicate the course of periodontitis, such as caries and furcation involvement. 

Now, switching gears and moving on to the extraoral examination, which refers to the evaluation of the temporomandibular joint, the symmetry of the face, and regional lymph nodes. 

This is an important part of the diagnos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Development_of_the_COVID-19_vaccine</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BgSvJTJ2SVSZj5N9eKhE-3SoR-_i_W0x/_.jpg</video:thumbnail_loc><video:title><![CDATA[Development of the COVID-19 vaccine]]></video:title><video:description><![CDATA[It seems like the whole world is holding its breath for the COVID19 vaccine. 

But you might be wondering, how do we even go about making the COVID19 vaccine?

There are two main goals in vaccine development: First, the vaccine needs to be safe to administer to the general population. 

Second, the vaccine needs to be efficacious against the pathogen, for instance a virus. 

There are a couple ways to identify that -  by seeing if it produces a significant immune response to the virus or by seeing if it reduces the chance of getting the disease itself.

Before a candidate vaccine even begins being administered to humans, it goes through extensive animal testing, typically using lab mice. 

In this phase researchers are looking for side effects within the mice, which can range from mild skin irritation at the site of injection, to death.

Researchers also take blood samples from the mice over the next several days to weeks. 

Researchers measure the blood antibody levels of the mice, and specifically look for antibodies being produced that would combat the virus. 

A sufficient number of antibodies being produced after the vaccine is administered is a promising result. 

Sometimes mice are given the virus to see if having the vaccine prevents them from getting the disease. 

If there are no significant negative side effects and there’s evidence of vaccine efficacy, the vaccine can move to clinical trials.

Clinical trials are broken down in three phases, and are designed to measure both the safety of the candidate vaccine and the immune response, just like in mice. 

In all of these phases, humans are given the candidate vaccine, and others are given a placebo with the goal to help make it easier to compare the efficaciousness of the vaccine. 

Healthy adults are usually chosen for these studies because the goal is to ensure that they are least likely to develop a serious problem from the vaccine and so that if they do develop a health issue, it’s most like]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Safety_of_the_COVID-19_vaccines</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Kl7JAa7PTGmPVFW8E5XpF8riSYOO--BL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Safety of the COVID-19 vaccines]]></video:title><video:description><![CDATA[There’s a lot of pressure on researchers and pharmaceutical companies to create a vaccine for COVID-19. 

You might be wondering, how can we be sure that the vaccine will be safe?

To start, this isn’t the first time we’ve made a vaccine. 

There are currently over 50 vaccines covering 26 diseases used within the United States alone. 

Many of the candidate COVID-19 vaccines being tested right now are based on the ideas and technology used to make vaccines that are already approved. 

This is how in the span of just a few months we’ve had so many vaccines enter preclinical and clinical trials. 

Researchers are not starting from scratch. 

In addition, the Food and Drug Administration (also called the FDA) in the United States has given specific guidelines to researchers on how to develop COVID-19 vaccines. 

Once we have a candidate vaccine, researchers subject that vaccine to a gauntlet of animal and clinical trial tests, to ensure that it’s both safe and effective. 

Researchers initially test candidate vaccines on animals first in preclinical trials, and if testing goes well, the candidate vaccine can begin human clinical trials, starting with Phase I, then Phase II, and finally Phase III. 

With each phase, more and more participants are recruited to be vaccinated with the candidate vaccine.

Researchers want to test the vaccine in a large and diverse group of people, to make sure that it’s safe and effective for the whole population. 

Researchers need to test the candidate vaccine in people who differ in age, sex, race, and exisiting health status, like people who have asthma or are pregnant. 

If a candidate vaccine successfully passes Phase III clinical trials, that means researchers are very confident the vaccine will be effective for everyone. 

As of October 1st, 2020, there are 10 COVID-19 vaccines currently in Phase III trials, 13 in Phase II, 17 in Phase I, and 151 in preclinical trials.

That’s a lot of vaccines, but that’s on purpose. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_abdominal_viscera:_Blood_supply_of_the_foregut,_midgut_and_hindgut</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0t8oa4RxRrugsPvTNFZW8A2PRSaewdvg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut]]></video:title><video:description><![CDATA[The gastrointestinal tract is essentially a long tube extending from our mouth to our rectum. We rely on it to eat, break down our food and turn it into well...you get the picture.

Due to its role in breakdown and absorption of nutrients, it is important to understand the different divisions and blood supply of the gastrointestinal tract.

The abdominal section of the gastrointestinal tract develops from three embryological structures called the primordial foregut, midgut and hindgut.

And, in turn, the foregut, midgut and hindgut all derive from the three embryonic germ layers: the endoderm, mesoderm and ectoderm.

The mesoderm is what forms the peritoneum, which either completely or partially lines the organs of the peritoneal cavity including the gastrointestinal tract.

It’s important to understand these different embryological divisions as the foregut, midgut, and hindgut each have their own unique blood supply.

The foregut extends from the esophagus to the duodenum at the level of the major duodenal papilla where the pancreatic and common bile duct insert, and it consists of the esophagus, stomach, the proximal duodenum, as well as the liver, gallbladder, pancreas and spleen.

The midgut extends from the distal portion of the duodenum to the last third of the transverse colon. It consists of the distal duodenum, jejunum, ileum, cecum, appendix, ascending colon and proximal two thirds of the transverse colon.

Finally, the hindgut extends from the distal third of the transverse colon to the anal canal, above the pectinate line. It consists of the distal portion of the transverse colon, descending colon and sigmoid colon and rectum.

Now, remember that organs with the same embryologic origin share the same arterial supply, which primarily comes from the abdominal aorta and its single anterior branches: the celiac trunk for the foregut; the superior mesenteric artery for the midgut; and the inferior mesenteric artery for the hindgut.

The celiac trunk]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Heart</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/px_5rDz9TZq2ZnPDRqb5XAu1Sfy-t1Ex/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Heart]]></video:title><video:description><![CDATA[Have you ever wondered what the secret to someone’s heart is? That&amp;#39;s right, a chest x-ray! All right, so, here at Osmosis we don&amp;#39;t actually have the secret to one’s heart, but we do know how to identify the different medical conditions that can affect the heart.

Let&amp;#39;s start off by identifying the heart borders on a chest x-ray. The heart silhouette is between the lungs, and the right border, made up by the right atrium, as well as the left border, made up by the left ventricle and part of the left auricle, can be clearly seen. Above the left auricle, we can identify the pulmonary artery  and the aortic arch. And in some clinical circumstances, the silhouette sign can be present, which is when the normal heart silhouette of the heart compared to the lungs is lost. More appropriately, you might want to think about it as a “loss of the heart silhouette”. The loss of the heart silhouette only occurs when the pathological process is in direct anatomical contact with the heart. Usually, the middle lobe is seen close to the right border of the heart. So, consolidation in the right middle lobe can also obscure the x-ray silhouette of the right heart border.  

All right, now, even though the heart is protected by the sternum and thoracic cage, it’s still susceptible to injury. During penetrating trauma, like, for example, a stab wound, the right ventricle is the most commonly injured structure because of its anterior position in the chest and the fact that it forms the majority of the anterior surface of the heart, followed by the left ventricle which forms the apex of the heart and may be injured as far laterally as the left midclavicular line at the 5th intercostal space. The atria are less commonly injured than the ventricles. It’s also worth noting that the lungs overlap most of the anterior surface of the heart, so many penetrating injuries to the heart will also result in concurrent lung injury particularly to the parietal pleura.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hand_hygiene_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/p1dy3tSqRg_KsOVKD7haZyP8Rde_6Bpb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hand hygiene (for nursing assistant training)]]></video:title><video:description><![CDATA[When assisting with client care, consistent, proper, and meticulous hand hygiene is the single easiest and most effective practice to reduce the risk of transmission of infection to and from the client. 

Hand hygiene mainly includes handwashing with soap and water and using an alcohol-based hand rub.

Now, depending on your facility’s policy, you may need to perform hand hygiene at different times. 

In any case, it’s important to at least perform hand hygiene upon entering and leaving a client’s room and before and after every contact with a client in general. 

You should also perform hand hygiene before and after applying personal protective equipment, like gloves; after handling any waste; after exposure to items or surfaces that could possibly be contaminated with blood, body fluids, secretions, or excretions; and after contact with non-intact skin, mucous membranes, or wound dressings.

Likewise, remember to perform hand hygiene before and after handling a client’s meal or drink, before coming in the room where clean supplies are maintained, before touching clean clothing or linen, and after helping a client back from the bathroom. 

And, of course, perform hand hygiene upon entering and leaving the facility; before and after drinking, eating, or smoking; before and after putting in contact lenses; before and after doing your make-up or fixing your hair; after picking something off the floor; after using the bathroom; and after coughing, sneezing, or using a tissue.

Now, when practicing hand hygiene, there are some general considerations you need to keep in mind. 

First of all, it’s important to pay special attention to the places where pathogens can easily hide and the places that can be frequently missed, like the back of your hands, between the fingers, and under or around your nails. 

What can help with this is to keep the fingernails short; wear no nail polish, artificial nails, acrylics, or wraps; and remove jewelry, including rings an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Measuring_respiration_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-7cUv_idQk2RgXmHyuyO5wM-SUa2fkZ-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Measuring respiration (for nursing assistant training)]]></video:title><video:description><![CDATA[Breathing, also known as respiration, is how the air moves into and out of the lungs. 

It consists of repetitive cycles of inspiration, which is when air full of oxygen flows into the lungs, and expiration, when the air along with carbon dioxide leaves the lungs. 

In order for this cycle to happen, there are respiratory centers within the brain that control breathing. 

These centers receive information from a group of receptors, known as chemoreceptors, which detect any changes regarding the oxygen and carbon dioxide concentration in the body. 

Now, as a nursing assistant, you need to be able to measure your clients&amp;#39; respiration and determine its characteristics, including the respiratory rate, rhythm, and depth of respiration and whether the respirations are quiet or noisy as well as easy or difficult.

Okay, respiratory rate refers to the number of breaths a client takes in one minute. 

Normal respiratory rate varies among different age groups. 

So, for adults, it’s typically between 12 and 20. 

For adolescents between 12 and 20 years old, normal respiratory rate is 15 to 20. 

For school-aged children between 5 and 12 years old, it’s from 15 to 25. 

For preschoolers from 3 to 5, it’s 22 to 34, while toddlers from 1 to 3 have a normal respiratory rate of 24 to 40. 

Finally, infants under 1 year of age normally have the fastest respiratory rate, which ranges from 30 to 60 breaths per minute. 

Besides age, the respiratory rate can also be influenced by many factors, including physical activity; body temperature; emotions, like anger, fear, or stress; medications; smoking; certain diseases of the heart or lungs; or even the weather! 

A client can also voluntarily choose to increase their respiratory rate or hold their breath and, thus, decrease their respiratory rate. 

So, tachypnea is when the respiratory rate is faster than normal, and this can occur in response to strenuous exercise, fever, pain, anxiety, or specific m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular:_Body_temperature_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S_vsJ3zFSQe2WxKx_iK5mTTyS1aeQocN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular: Body temperature (for nursing assistant training)]]></video:title><video:description><![CDATA[Now, as a nursing assistant, you will need to measure your client’s temperature. 

There are several areas of the body where you can do that, including the oral cavity; the rectum; the axilla, or armpit; the tympanic membrane, or eardrum; and the temporal artery on the forehead. 

Before we discuss how to measure your client’s temperature, we need to cover some definitions. 

Our body is always generating heat through metabolism, and a part of the brain, called the hypothalamus, tries to keep the core body temperature constant like a thermostat. 

When we are febrile, meaning we&amp;#39;ve got a fever, the thermostat is raised higher, and this can be due to an infection, inflammation, or cancer. 

However, body temperature could also be high in hyperthermia, where the thermostat is set at the right temperature, but the body simply can’t get rid of the heat. 

This can be due to an extremely hot environment, excessive exercise, and reduced sweat production. 

In contrast, hypothermia is when body temperature gets too low, and it might be due to exposure to cold for a prolonged period of time, either accidentally or in preparation for a medical procedure.

Starting with an oral temperature: This is an easy and relatively comfortable method. 

A normal oral temperature is between 97.6 to 99.6 degrees Fahrenheit, or 36.5 to 37.5 degrees Celsius, for adults, and 97 to 99 degrees Fahrenheit, or 36 to 37 degrees Celsius, for children. 

But because the mouth is a large space open to the outside environment, this is not a very accurate way to obtain a temperature because the temperature can change significantly. 

So, don’t take an oral temperature if the client has been coughing, sneezing, eating, drinking, smoking, or chewing gum in the past 15 minutes. 

Oxygen therapy with a face mask can also interfere with the results. 

In addition, it&amp;#39;s important to hold the thermometer tightly in their mouth, so you should avoid this method for clients]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular:_Blood_pressure_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2T2wWvw4Qfm-lUrYW-DNLlCvRuOVfH16/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular: Blood pressure (for nursing assistant training)]]></video:title><video:description><![CDATA[As a nursing assistant, you will need to measure your client’s blood pressure. 

Blood pressure refers to the force that the blood exerts on the walls of the arteries. 

Now, a blood pressure measurement has two values. 

The first and the highest is the systolic blood pressure, which is the force that the blood exerts on the walls of the arteries during systole, or when the heart contracts to pump blood through the body. 

The second one is the diastolic blood pressure, which is the pressure on the walls of the arteries during diastole, or when the heart relaxes and refills with blood between heartbeats. 

Now, maintaining normal blood pressure is essential to ensure that tissues around the body are receiving an adequate amount of oxygen and nutrients from the blood. 

If blood pressure gets too low, the brain, heart, and other vital organs might stop functioning normally because they’re not getting enough blood. 

In contrast, blood pressure that is too high, can create a serious problem for the blood vessels and the organs they supply. 

Just like a garden hose that’s always under high pressure, in the long term, blood vessels may develop tiny cracks and tears that can lead to serious problems, like myocardial infarctions, or heart attacks; strokes, or brain attacks; and aneurysms, or bulges of a weakened blood vessel wall. Increased blood pressure can damage small blood vessels, like those seen in the kidney and eyes, leading to kidney failure and vision loss. 

Chronic increased blood pressure also makes it hard for the heart to pump blood out against the increased pressure. 

Over time, the heart gets overworked and this can lead to heart failure.  

There are several factors that can increase or decrease blood pressure. 

The first factor is the cardiac output, which is the total volume of blood the heart ejects in one minute. 

The more blood the heart pumps out, the higher the blood pressure. 

The cardiac output depends mainly on the heart r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integumentary:_Applying_dressings_and_bandages_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xjCv8x4oR0Cs2fK1KtDGGNntRh6SU1yK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integumentary: Applying dressings and bandages (for nursing assistant training)]]></video:title><video:description><![CDATA[Some of the clients you care for will have dressings on their wounds, which are used to protect the wound; absorb wound drainage, or exudate; keep microorganisms from entering the wound; promote comfort, or keep the wound dry during bathing. 

Some dressings can even be used to apply pressure to control bleeding, while others can help remove dead or infected tissue: a process called debridement. 

As a nursing assistant, you will have the opportunity to assist the nurse with applying dressings or bandages, and in the cases where your facility policy allows, you may be asked to apply dressings and bandages for some clients without the nurse’s assistance. 

One of the most common types of dressings you will apply are gauze dressings, which are made of cotton or synthetic material. 

A dry gauze dressing is applied to protect a wound and absorb small amounts of exudate. 

Sometimes a moist-to-dry gauze dressing is applied, which just means that the gauze is moistened first before it’s applied to the wound then a dry gauze is layered on top. 

As the moist dressing dries, it helps with debridement and removal of exudate. 

Gauze dressings are usually secured with tape, which can sometimes irritate the client’s skin,  especially as it is peeled off for dressing changes. 

In cases where the dressing is large and needs to be changed frequently, it can be secured with Montgomery ties, or tape ties, which is when a wide strap is attached to the skin and then tied together over the wound. 

Whenever the dressing needs changing, the ties are untied and then tied again over the new dressing, so no peeling of tape is required! 

If a dressing needs to be secured over a joint, such as a wrist or knee, a bandage made of rolls of webbing, gauze, or stretchy elastic material is wrapped around the dressing. 

Some small wounds, minor burns, or intravenous catheter insertion sites can be covered with a transparent dressing, which is a thin film with an adhesive coating on o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Zellweger_spectrum_disorders_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FGhHwAbTRLOPBxR8RaVhvogCQ0650MiB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Zellweger spectrum disorders (NORD)]]></video:title><video:description><![CDATA[Zellweger spectrum disorders, also called ZSDs, are a group of rare genetic diseases that impair the development of peroxisomes, which are structures found in almost every cell of the body. 

Peroxisomes house enzymes that are responsible for a number of biochemical pathways, including the metabolism of fatty acids and the synthesis of lipids essential for nervous system development. 

A low level of peroxisomes in the body causes visual, auditory, and neurological deterioration as well as liver and kidney dysfunction. 

For this reason, ZSDs are also known as peroxisome biogenesis disorders, or PBDs. ZSDs are named after Dr. Hans Zellweger, who first described the disease in 1964. 

ZSDs were originally characterized as individual diseases of varying severity, however it was later determined that all of these diseases are part of the same disease spectrum.

ZSDs affect many parts of the body. In severe cases, symptoms can present shortly after birth, whereas less severe forms may have symptoms that do not appear until late infancy or childhood.

Infants with severe ZSD often, but don’t always have cranial abnormalities such as flattening of the face, high forehead, widely spaced eyes, broad nose bridge, and an abnormally small jaw. 

The roof of the mouth may be unusually high and narrow, and the fontanelles may feel abnormally large. 

Infants with ZSD may experience deteriorating visual, auditory, and neurological symptoms. 

Visual impairments may include cataracts, glaucoma, and nystagmus. 

Progressive vision loss may manifest as difficulty following objects with the eyes and eyes pointing in different directions. 

Hearing loss may present as a lack of a startle response to loud noises and not turning towards sounds. 

Neurological symptoms may include seizures and delays in developmental milestones like sitting, crawling, or walking. 

Other symptoms include a lack of muscle tone, called hypotonia, and affected children may appear limp and lethargi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eruption_of_primary_and_permanent_dentitions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kr0O3I6OSg6DgETYV6z0ZAb3StGypcU6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eruption of primary and permanent dentitions]]></video:title><video:description><![CDATA[Eruption of teeth is the process by which developing teeth move through the jaw bones and overlying mucosa, to emerge in their respective place within the oral cavity eventually. 

Now, humans are diphyodonts, which means we have two sets of teeth during our lifetime. 

The first set, the primary teeth, also called deciduous teeth, or baby teeth, start erupting at around six months of age. 

And, by about six years of age, the primary teeth fall out and are replaced by a set of permanent teeth that stays with you for the rest of your life.  

Tooth eruption occurs in 3 phases, the pre-eruptive, eruptive, and post eruptive phase. 

The driving force behind the eruption of teeth is still unknown but is thought to be due to a combination of a few factors, which include signals originating from the dental follicle; root formation and elongation, which could drive the tooth in order to acquire space within the jaw; and formation of PDL which provides an occlusal force, aiding in eruption.

Okay, let’s look at all the stages one by one starting with the pre-eruptive phase.  

In this phase, the tooth germs are growing within the jawbones. 

As the bones grow in length, width, and height, more space becomes available for the tooth germs to spread out and grow without affecting each other. 

Lengthening of the jawbones allows the anterior tooth germs to move mesially, or forward, and the molar tooth germs to move distally, or backward. 

At the same time, as the bone widens, the tooth germs move buccally, or outward, and as the height increases, the tooth germs move closer to the surface; that is, the mandibular tooth germs move upwards, and the maxillary tooth germs move downwards.

In this phase, movement of the tooth germ is achieved by two methods - bodily movements and eccentric growth. 

In bodily movement, there is a remodeling of the bony crypts through resorption of bony crypt wall in the direction that the tooth is moving. 

This is followed by depositin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_abdominal_viscera:_Large_intestine</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-6cYx9dnQKuvyY0SetCatsUxThuBsb0s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the abdominal viscera: Large intestine]]></video:title><video:description><![CDATA[The large intestine is a part of the digestive tract specialized in absorbing water from the residual digested food coming from the small intestines, while forming and storing feces until defecation occurs.

The large intestine or colon begins at the ileocecal junction, where it is continuous with the ileum, which is the final part of the small intestine.

There are three main features that distinguish the large intestine from the small intestine - besides the fact that the large intestine has a, well, larger caliber!

First, the large intestine has omental appendices, which present as fatty outgrowths covered by visceral peritoneum.

Second, there are the teniae coli, which are three strips of smooth muscle that run lengthwise from the base of the appendix through the colon and merge at the rectosigmoid junction to form a longitudinal layer around the rectum.

The third and final differentiating feature is that the large intestine has haustra, which are pouch-like bulges of the intestinal wall that form between the teniae when they contract.

The large intestine has several major components: the cecum, appendix, ascending, transverse and descending colon, sigmoid colon, rectum and anal canal.

The cecum is the first part of the large intestine and it receives the terminal ileum, which invaginates into the medial side of the cecum. The cecum lies in the right iliac fossa in the right lower quadrant of the abdomen, and it looks a bit like an intestinal pouch.

It is intraperitoneal, mobile, and doesn’t have its own mesentery. On its posteromedial wall, inferior to the ileocecal junction, the cecum has a blind-ended organ called the appendix, which can vary in length up to and over 10cm.

The appendix is usually retrocecal, meaning behind the cecum, but its position can vary a bit as well. It’s full of lymphoid tissue and its proximal part has attachment to the cecum by a small mesentery called the mesoappendix.

Now, if we open up the large intestine and lo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Superficial_structures_of_the_neck:_Anterior_triangle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SU0jeGmySRSx1xVgibI1HkNYSpyMFoME/_.jpg</video:thumbnail_loc><video:title><![CDATA[Superficial structures of the neck: Anterior triangle]]></video:title><video:description><![CDATA[The neck is the anatomical region between the base of the cranium superiorly and the clavicles inferiorly and it joins the head to the trunk and limbs, serving as a major conduit for structures passing between them.

The neck is divided in two major triangles: anterior and posterior, based mainly on the borders of the sternocleidomastoid, or SCM, and trapezius muscles, as well as other muscular and bony structures found in the neck.

These regions provide a clear location regarding the structures, injuries or pathologies involving the neck. Now, the anterior triangle, like any respectable triangle, has three sides, called boundaries.

The anterior boundary is formed by the median line of the neck, the posterior boundary is formed by the anterior border of the sternocleidomastoid muscle, or SCM for short, and the superior boundary is formed by the inferior border of the mandible.

The triangle has a superficial boundary or a roof formed by subcutaneous tissue containing the platysma, a deep boundary or a floor formed by the pharynx, larynx and thyroid gland and an apex located at the jugular notch in the manubrium.

And if that wasn’t enough, the anterior triangle is further subdivided by the omohyoid and digastric muscles into four smaller triangles: submental, submandibular, carotid and muscular.

The submental triangle sits right below the chin and contains several small submental lymph nodes and small veins that unite to form the anterior jugular vein.

Inferiorly, the submental triangle is bounded by the hyoid body, and laterally by the right and left anterior bellies of the digastric muscles.

The floor is formed by the two mylohyoid muscles which meet in a median fibrous raphe, the apex is located at the mandibular symphysis, and the base is formed by the hyoid bone.

Next, the submandibular triangle contains the submandibular gland, submandibular lymph nodes, cranial nerve XII which is the hypoglossal nerve, mylohyoid nerve and parts of the facial a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Keith_Smith:_Dean_of_Purdue_University_Global_School_of_Health_Sciences_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5rqScUyfQ4OW9QxPOOr-3qOjSsSYkw4s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Keith Smith: Dean of Purdue University Global School of Health Sciences (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Keith Smith: Dean of Purdue University Global School of Health Sciences (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Deep_structures_of_the_neck:_Prevertebral_muscles</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JSJx3sQ8Rwi4V39WSACPjV_1SjGi-Y14/_.jpg</video:thumbnail_loc><video:title><![CDATA[Deep structures of the neck: Prevertebral muscles]]></video:title><video:description><![CDATA[The neck is the anatomical region between the base of the cranium superiorly and the clavicles inferiorly and it joins the head to the trunk and limbs, serving as a major conduit for structures passing between them. 

The neck contains superficial structures, located in the anterior and posterior triangles and deep structures, like the cervical viscera and the prevertebral muscles. 

Now, the prevertebral muscles are deep to the prevertebral layer of the deep cervical fascia and they are divided into anterior prevertebral muscles and lateral prevertebral muscles. 

The anterior prevertebral muscles are located directly posterior to the retropharyngeal space and medial to the neurovascular plane of the cervical plexus, brachial plexus and subclavian artery, and they are represented by longus colli, longus capitis, rectus capitis anterior and anterior scalene muscles. 

Now, the longus colli originates from the bodies of C5 to T3 vertebrae and the transverse processes of C3 to C5 vertebrae. 

It inserts onto the anterior tubercle of the C1 vertebra, the bodies of the C2 to C4 vertebrae and the transverse processes of C3 to C6 vertebrae. 

It’s innervated by the anterior rami of C2 to C6 spinal nerves 

When it contracts bilaterally, it produces flexion of the neck and when it contracts unilaterally it produces rotation to the opposite side. 

Next, there’s the longus capitis, which originates from the anterior tubercles of the transverse processes of  C3 through C6 and inserts onto the basilar part of occipital bone. 

It’s innervated by the anterior rami of spinal nerves C1 through C3 and its contraction results in flexion of the head at the atlanto-occipital joint. 

Next, the rectus capitis anterior originates from the anterior surface of the lateral mass of the atlas, which is the first cervical vertebra, and inserts onto the base of the cranium, anterior to the occipital condyles. 

It’s innervated by branches from the loop between C1 and C2 spinal nerv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Warm_autoimmune_hemolytic_anemia_and_cold_agglutinin_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PYZCSXXuTcmC-E2FGTYfvpcBTdO7B_a1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Warm autoimmune hemolytic anemia and cold agglutinin (NORD)]]></video:title><video:description><![CDATA[Warm autoimmune hemolytic anemia, also called WAHA, and cold agglutinin disease, also called CAD, are autoimmune hemolytic anemias. 

Autoimmune refers to when the body’s immune system mistakenly attacks and destroys healthy cells; hemolytic refers to the destruction of red blood cells; and anemia refers to when the blood does not contain enough healthy red blood cells. 

In WAHA, hemolysis occurs more frequently at body temperature, hence the name “warm.” 

It is the most common autoimmune hemolytic anemia and can occur at any age. 

In CAD, hemolysis occurs more frequently at cold temperatures, hence the name “cold,” usually between 37 to 39oF, or 3 to 4oC. 

Conversely, CAD is less common and generally occurs between 40 to 80 years of age.

The symptoms of both WAHA and CAD vary depending on severity. 

Symptoms often include dizziness, palpitations, shortness of breath, dark urine, pale skin, jaundice, and fatigue. 

In severe cases, individuals may experience chest pain, confusion, fainting, and lethargy, as well as abnormalities in heart rate and blood pressure.

Individuals with WAHA may also develop an enlarged spleen, causing a full feeling in the abdomen. 

Individuals may also develop blood clots that can form in the legs, called deep vein thrombosis, and cause symptoms such as pain, swelling, redness, and warmth in one leg. 

Clots can detach and travel to the lungs, called pulmonary embolism, causing symptoms such as shortness of breath, chest pain, and coughing up blood. 

Individuals with CAD may also experience circulatory symptoms such as cold fingers and toes, and painful bluish or reddish discoloration of the fingers, toes, ankles, and wrists, also called Raynaud phenomenon.

In WAHA and CAD the immune system produces autoantibodies, which in this case are antibodies that target the body’s own healthy immune cells. 

In WAHA, usually IgG antibodies tag the red blood cells  which are  then transported to the spleen to be destroyed. 

In C]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eating_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7uTUA0azQU6i3KT--bMaj7GjSFG4BoxN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eating disorders: Pathology review]]></video:title><video:description><![CDATA[23 year old Adeline is brought to the emergency department by her peers after fainting in the college cafeteria. Upon examination, her pulse is 47/min, and her blood pressure is 89 over 48 mmHg. In addition, her height is 162 cm  or 5 ft 4 in, and she weighs 45.4 kg or 100 lbs. Adeline mentions that she considers herself fat, which is why she’s been trying to lose weight, and admits to purging or making herself vomit whenever she eats a large meal. On further questioning, she tells you that her last menstrual period was more than 3 months ago. You decide to run a urine pregnancy test, which comes back negative. The next day, you see 17 year old Emmanuel, who is brought to the clinic by his mother, who saw him forcibly vomit after lunch. Emmanuel states he has recently been very anxious about the college entrance exam and that he feels like vomiting is the only thing in life that he can control. His vitals show no abnormalities, his height is 185 cm or 6 feet 1 in, and he weighs 72 kg or 158 lbs. Physical examination shows decaying enamel on teeth, as well as thickened skin around the knuckles of his right hand.

Based on the initial presentation, both Adeline and Emmanuel have some form of eating disorder. Eating disorders are mental health disorders in which an individual exhibits abnormal eating behaviors that negatively impact their physical and mental health. They are quite common, especially among young females who struggle with low self-esteem and the social pressure to look a certain way. However, remember that they can affect anybody, regardless of their sex, age, and social background. For your exams, the most common eating disorders include anorexia nervosa, bulimia nervosa, binge eating disorder, and pica.

Okay, let’s start with anorexia nervosa. This is characterized by a constant fear of gaining even the slightest amount of weight, associated with a distorted body image, with individuals often believing that they are overweight, while actuall]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disorders_of_carbohydrate_metabolism:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZY8jvpqzTCmnuQjjnqPo8z2RRtaRg_WO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disorders of carbohydrate metabolism: Pathology review]]></video:title><video:description><![CDATA[A 5 day old newborn infant girl named Emily is brought to the emergency department due to vomiting, diarrhea, and poor feeding. Her mother also mentions that Emily seems to be tired and sleepy all day long. Physical examination reveals bilateral clouding of the lens, along with yellowing of the sclera. Upon palpation of the abdomen, Emily’s liver appears enlarged. Emily’s mother mentions that she lives in a remote area and gave birth at home. You decide to run a urine dipstick test, which comes back negative for sugars, followed by a nonspecific urine test, which shows increased levels of reducing sugars. 
Some days later, you see a 21 year old man of Asian descent named Chris, who’s complaining of repeated episodes of bloating, abdominal cramps, and excessive flatulence that are often associated with watery, frothy stool. He has noticed that his symptoms tend to occur when he eats cheese or ice cream. Upon further questioning, he denies any concomitant diseases or recent gastrointestinal infections. Physical examination is unremarkable.
Okay, based on the history and initial presentation, both Emily and Chris seem to have some form of disorder of carbohydrate metabolism. Carbohydrates are our main source of energy, and can be classified as simple or complex. Simple carbohydrates include monosaccharides, which contain one sugar molecule, like glucose, fructose, and galactose; and disaccharides, where two sugar molecules are linked together. Disaccharides include lactose, which is made up of glucose and galactose, and sucrose, which is formed when glucose links up with fructose. On the other hand, complex carbohydrates include oligosaccharides and polysaccharides, which are respectively short and long chains made up of more than two sugar molecules. 
All right, now, for your exams, the most high yield disorders of carbohydrate metabolism include pyruvate dehydrogenase complex deficiency, galactosemia, disorders of fructose metabolism, and lac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disorders_of_fatty_acid_metabolism:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lcUvCXj3Q2K7Y_MlUTyeDcplT0Wo02Eb/_.png</video:thumbnail_loc><video:title><![CDATA[Disorders of fatty acid metabolism: Pathology review]]></video:title><video:description><![CDATA[Two kids are brought to the clinic by their mothers. The first one’s Dalia, a 2 year old girl. Her mother is concerned because Dalia always seems to be tired and weak, and in general doesn’t eat much. On physical examination of the abdomen, you palpate an enlarged liver. You decide to run a blood test, which reveals that her blood glucose and ketone bodies are decreased, but what really stands out to you is that her carnitine levels are also really low. 

After Dalia, you see Luca, a 3 year old boy who had a brief seizure earlier that day. Luca’s mother tells you that he’s had gastroenteritis for the past few days, so he’s been vomiting and not eating much. You decide to run a blood test, which also reveals low blood glucose and ketone bodies, but unlike Dalia, he has high levels of fatty acyl-carnitine. 

Based on the initial presentation, both Dalia and Luca seem to have some fatty acid metabolism disorder. Now, let’s review fatty acid metabolism real quick. Normally, the body&amp;#39;s main source of energy is the glucose we get from food. When glucose is running low, like with prolonged fasting or exercise, the body is able to obtain energy from stored fats. 

The simplest form of fats are fatty acids, which are grouped by length into short, medium, long, and very long chain fatty acids. Short and medium chain fatty acids are primarily obtained from the diet, while long and very long chain fatty acids can be synthesized from acetyl-CoA by the liver and fat cells. 

Now, keep in mind that acetyl-CoA is usually found in the mitochondrial matrix, whereas the enzymes required for fatty acid synthesis are all in the cytoplasm. For acetyl-CoA to cross the mitochondrial membranes and get to the cytoplasm, it first needs to combine with oxaloacetate to form citrate. Once in the cytoplasm, an enzyme called citrate lyase leaves citrate back into acetyl-CoA and oxaloacetate. This whole process is called the citrate shuttle.

Now, when the body needs some extra e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Drug_misuse,_intoxication_and_withdrawal:_Hallucinogens:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/muJvl-ybS7OaIgWVB7aRqpG4Q8OSA4O3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Drug misuse, intoxication and withdrawal: Hallucinogens: Pathology review]]></video:title><video:description><![CDATA[In the middle of the night, two people are brought to the clinic. First comes 18 year old Kyle and his mother, who&amp;#39;s noticed that lately, Kyle seems to have an increased appetite, and won’t stop laughing or giggling. Kyle adds that he feels like time has stopped and that’s making him a bit anxious. Upon physical examination, Kyle’s eyes are extremely red, he has a heart rate of 105 beats per minute, and a blood pressure of 130 over 90 millimeters of mercury. Next comes 25 year old Matt and his girlfriend Allison, who is very concerned for him. She says that in the past few months, Matt has been very aggressive and violent, and has been frequently getting into fights with strangers for no good reason. Matt interrupts Allyson and tells you that the reason he gets into fights is because some voices in his head tell him so. Upon physical examination, you notice that Matt keeps tapping his feet, and his eyes keep moving from side to side and up and down. In addition, he has a heart rate of 110 beats per minute, and a blood pressure or 135 over 95 millimeters of mercury.

Based on the initial presentation, both Kyle and Matt  seem to have some form of hallucinogen intoxication. Hallucinogens are a class of psychoactive drugs that cause hallucinations, which are distortions of a person’s sensory perception, mood, and thought, as well as enhancement of feelings and introspection. The way they do this isn’t clearly understood, but it involves the interaction of numerous neurotransmitters, including serotonin, dopamine, and glutamate. Now, some high yield hallucinogens include lysergic acid diethylamide or LSD, cannabis or marijuana, MDMA or ecstasy, and phencyclidine or PCP. And in addition to causing hallucinations, they can all cause their own set of unique symptoms that you need to be able to recognize for your exams. In addition to these, they can all cause their own set of unique symptoms that you need to be able to recognize for your exams.

Oka]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fascia,_vessels,_and_nerves_of_the_lower_limb</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QtJ5u5i1QOWvkbUTSqSgvQaLTj2ha62v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fascia, vessels, and nerves of the lower limb]]></video:title><video:description><![CDATA[The lower limb contains an intricate metro system of blood vessels, muscles, and nerves. These structures are wrapped up and organized into different compartments by superficial and deep fascia layers, and together, they form the multifunctional limbs we know as legs.

Let’s begin with fascia, which is... well, what is it anyway? You can think of fascia as a pair of thin stockings made of connective tissue that support and bind together different parts of the body, including the lower limbs.

Now, each lower limb actually has two pairs of stockings on top of each other: the superficial fascia - which sits right underneath our skin - and the deep fascia - which sits on top of the muscles, organizing them into compartments.

Ok, so the superficial fascia - also known as subcutaneous tissue - is located directly deep to the skin and consists of loose connective tissue, with variable amounts of fat. It contains arteries, veins, nerves, lymph vessels and lymph nodes.

Superiorly, the fascia is continuous with the subcutaneous tissue of the anterolateral abdominal wall and buttocks. Inferiorly, at the knee, the superficial fascia loses its fat and blends with the deep fascia but fat is again present distal to the knee, in the subcutaneous tissue of the leg.

Moving on, deep fascia is especially strong and elastic, allowing it to limit the outward expansion of contracting muscles, and act as a barrier to help compress the veins, which in turn, propel blood towards the heart.

The deep fascia can be divided into the deep fascia of the thigh, which is called fascia lata; and the deep fascia of the leg, or the crural fascia. First, the fascia lata is very strong and flexible.

Superiorly, the fascia lata attaches to the inguinal ligament and pubic bone anteriorly, to the iliac crest laterally and posteriorly, and to the sacrum, coccyx, sacrotuberous ligaments, and ischial tuberosity posteriorly.

It also attaches to the membranous layer of subcutaneous tissue of the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Superficial_structures_of_the_neck:_Cervical_plexus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_ozaU3ZwQdSXzbYi1zAHgJEnTGmc7gko/_.jpg</video:thumbnail_loc><video:title><![CDATA[Superficial structures of the neck: Cervical plexus]]></video:title><video:description><![CDATA[The cervical plexus is an important plexus of nerves which provide innervation to the head and neck. This plexus is located anteromedial to the levator scapulae and middle scalene muscles and deep to sternocleidomastoid - or SCM.

Now, the anterior rami of the spinal nerves C1, C2, C3 and C4 form the roots of the cervical plexus, which is an irregular series of nerve loops and the branches that arise from these loops.

Each participating ramus, except the first, splits into ascending and descending branches which unite with branches from neighboring spinal nerves to form the loops.

The superficial branches of the plexus, which initially pass posteriorly are cutaneous, or sensory, branches which innervate the skin, and the deep branches of the plexus, which includes the roots of the phrenic nerve and the ansa cervicalis, pass anteromedially and are motor branches which innervate the muscles of the neck.
The cutaneous branches of the cervical plexus emerge around the middle of the posterior border of the SCM, and they supply the skin of the neck, superolateral thoracic wall, shoulder and scalp between the auricle and the external occipital protuberance.

Now let’s look at the four cutaneous nerves that innervate these areas. There are three nerves branching from the C2 and C3 loop. The lesser occipital nerve, which contains fibers from C2 supplies the skin of the neck and scalp posterosuperior to the auricle.

The great auricular nerve contains fibers from both C2 and C3 and ascends across the SCM to the inferior pole of the parotid gland, where it divides to innervate the skin over - and the sheath surrounding - the parotid gland, the mastoid process, the posteroinferior part of the auricle and an area of skin that extends from the angle of the mandible to the mastoid process.

There is also the transverse cervical nerve which also contains fibers from C2 and C3. It curves around the middle of the posterior border of SCM, passing anteriorly and horizontall]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunodeficiencies:_Phagocyte_and_complement_dysfunction:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MCwR_xI3S9ila4YiftAIlFj7SraubLTy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review]]></video:title><video:description><![CDATA[Alyssa is a 3 week old newborn baby girl that’s brought to the clinic by her parents. They’re a bit concerned because they’ve noticed that Alyssa’s umbilical cord stump hasn’t fallen off yet.

On physical examination, you notice that the stump looks red and swollen, but there’s no pus. You decide to run a blood test, which reveals an increased level of neutrophils.

Finally, you perform flow cytometry, which shows that these neutrophils have reduced expression of CD18.

Next comes Eddie, a 2 year old boy who has a fever that won’t go away after 2 weeks. His parents also mention that he has frequent infections involving the respiratory tract, and he once also had an infection of the knee joint.

Upon physical examination, the first thing you notice is that Eddie has extremely light skin, hair, and eyes. Then, you find swollen lymph nodes all around the body, and you palpate an enlarged liver and spleen.

So again you run some blood tests, but now you find decreased white blood cells, especially neutrophils, and a prolonged bleeding time.

Finally, you do a peripheral and bone marrow smear, which shows abnormally large granules within the white blood cells and platelets.

Based on the initial presentation, both cases seem to have some form of immunodeficiency, meaning that their immune system&amp;#39;s ability to fight pathogens is compromised.

Immunodeficiencies can be classified according to the component of the immune system that is defective.

In this video, we’ll be focusing on phagocyte dysfunction and complement disorders. Okay, let’s start with phagocyte dysfunction.

First we have leukocyte adhesion deficiency, which is an autosomal recessive disorder, meaning that an individual needs to inherit two copies of the mutated gene, one from each parent, to develop the condition.

Normally, when there’s an infection or inflammatory process, as well as for wound healing, chemical signals are released by cells in the affected area, to attract leukocytes s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Implicit_bias</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_T1QVr-6QlSXPy0xlkrL3SU-QbGsb4iW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Implicit bias]]></video:title><video:description><![CDATA[Imagine walking down the road at night. Your gut reaction to seeing a young black man in urban clothing will probably be different than seeing an old white lady pushing a stroller.

These gut reactions occur within milliseconds, before you can consciously assess the situation. So why does this occur? The reason your initial thoughts and feelings might be different in these two situations can be attributed to implicit biases.

An implicit bias is the unconscious attitude and beliefs that affect a person’s feelings, behavior or judgement without their knowledge.

Explicit, or conscious, bias is when someone is aware of their thoughts and emotions towards a specific group. This can be seen in hate speech, discrimination, and sometimes prejudice.

With implicit bias, it gets a little tricky because people are often unaware that their behavior or judgement are being affected since the bias is subconscious.

In healthcare, implicit bias also plays a role and can directly affect healthcare outcomes and patient satisfaction.

Now, implicit biases are formed when you make subconscious generalizations and form stereotypes that attribute certain characteristics with specific groups of people.

This is a cognitive strategy that’s intended to make it faster and easier to make judgements or take action. With enough repeated reinforcement, these can become involuntary habits that are difficult for you to detect.

For example, as a new resident, you might notice that most Latinx patients refuse certain elective surgical procedures. Throughout the years, without you noticing, you gradually stopped discussing these procedures with Latinx patients.

If asked, you would probably say you’re not treating Latinx people any differently than other groups. Implicit bias is more likely to occur in high pressure, time sensitive situations that require a lot of multitasking; something that’s common in many healthcare settings.

In order to better study implicit bias, Harvard developed]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Personality_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mZvgoW5qRc2ZhJfxy0cOyNt9TMuU-j4P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Personality disorders: Pathology review]]></video:title><video:description><![CDATA[28 year old Anna is brought to the emergency department by her roommate, who found her in the bathroom about to cut her wrists. Anna tells you that her boyfriend of two weeks broke up with her today. When asked how she feels, she just utters “empty”. 

She also discloses that she’s been in several intimate relationships that are always amazing in the beginning, but they all end up being disappointing. Upon physical examination, you notice that Anna has multiple scars over her forearms and wrists.

Next, 35 year old Luis presents to the clinic with his girlfriend, who thinks that he is too shy and he would benefit from getting professional help.

Luis mentions that since childhood, he’s always been the “silent” one. He has very few friends, and he avoids hanging out with new people, since he is afraid they will not like him. 

Finally, you see Bella, a 41 year old woman, who comes to the emergency department because she thinks she’s been poisoned by her fiancé. She is certain that he’s been planning to kill her before they get married.

When you ask her why she suspects this or if she has any proof, Bella says that her fiancé has frequently offered to prepare her meals.

She also mentions that she’s afraid she’ll lose her job, because her coworkers have been trying to sabotage her. In addition, Bella doesn’t talk to any of her relatives, because four years ago they forgot her birthday.

Okay, based on the initial presentation, Anna, Luis, and Bella all seem to have a personality disorder.

Now, each of us has a set of personal traits, which are repetitive patterns involving the way we think, feel, act or behave, and perceive ourselves and what surrounds us.

This combined is what makes up a person’s personality. Despite that, we should normally be able to cope with daily circumstances and adapt our personality accordingly.

Now, sometimes these personal traits can interfere with someone’s day-to-day functioning in their personal life, at]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cerebral_vascular_disease:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0536jMRDRx20SIlXvEKuFWueSpe47Zpy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cerebral vascular disease: Pathology review]]></video:title><video:description><![CDATA[At the emergency department, 30-year-old Lydia presents with severe headache and confusion. Clinical examination reveals low grade fever and nuchal rigidity. Past medical history reveals she has polycystic kidney disease. Non-contrast CT reveals blood between the arachnoid and the pia mater. Lydia is treated supportively and sent home. Three days later she suddenly develops a severe headache, vomiting, and confusion. Later that day, 70-year-old Amanda presents with left-sided weakness and numbness, with her foot and leg more affected than her arm. She can speak fluently and understands everything being said to her. Past medical history includes hypertension, hyperlipidemia, and a myocardial infarction last year.  

Based on their presentation, the diagnosis is that both Lydia and Amanda had a cerebral vascular accident, most often referred to as a stroke. A stroke is when there’s a sudden focal neurological deficit due to a part of the brain losing its blood supply. 

Now, to safeguard the brain from hypoxia, the brain has a dual circulation called the circle of Willis, divided into an anterior and posterior circulation. The anterior circulation starts in the neck, where the common carotid artery splits into the external and internal branches. The internal carotid passes through the carotid canal of the temporal bone of the skull and into the cranial cavity. Once inside, the internal carotid artery gives off branches. First are the middle cerebral arteries that supply the lateral portions of the frontal, parietal, and temporal lobes. It’s also important to remember that the middle cerebral arteries supply the two language areas, Broca’s and Wernicke’s. From the initial segment of the middle cerebral arteries, small perforating arteries called lenticulostriate arteries arise to supply a part of the basal ganglia called the striatum, which includes the caudate and putamen, as well as the internal capsule. And that’s something you absolutely mu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Anushka_Gaglani_&amp;_Dr._Abhishek_Nagaraj:_TruBlu_Dentistry_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MMyzw9raTKCxkQbboXNOrVsqTw2Fk4t6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Anushka Gaglani &amp; Dr. Abhishek Nagaraj: TruBlu Dentistry (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Anushka Gaglani &amp; Dr. Abhishek Nagaraj: TruBlu Dentistry (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mandy_Hill:_Director_of_Academic_Publishing:_Cambridge_University_Press_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7mVYDioKRE2PIY3HtdrjbwxFQBiL7_3Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mandy Hill: Director of Academic Publishing: Cambridge University Press (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Mandy Hill: Director of Academic Publishing: Cambridge University Press (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mike_Alkire:_President_of_Premier,_Inc_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CxtKD7d-RUCPcnnaYu0eXeIxSPm6aJqZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mike Alkire: President of Premier, Inc (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Mike Alkire: President of Premier, Inc (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Beth_Bierbower:_Retired_Senior_Executive_at_Humana_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7qlAqmH1TAeHLBCkcSceUCm3TiCjQG9Q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Beth Bierbower: Retired Senior Executive at Humana (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Beth Bierbower: Retired Senior Executive at Humana (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Steven_Scheinman:_President_&amp;_Dean_of_Geisinger_Commonwealth_School_of_Medicine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TlKnmUpzSAC0R2qHG3bXtSWBT82kkH-w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Steven Scheinman: President &amp; Dean of Geisinger Commonwealth School of Medicine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Steven Scheinman: President &amp; Dean of Geisinger Commonwealth School of Medicine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eren_Bali:_CEO_&amp;_Co-Founder_of_Carbon_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c6ogUnwHS1ubIvKLDnEh_4PvTc2XUn6U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eren Bali: CEO &amp; Co-Founder of Carbon Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Eren Bali: CEO &amp; Co-Founder of Carbon Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Josh_Golomb_&amp;_Jeannie_Chen:_Hazel_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yOpNB4ozSWaiamC7vNVGCqrsScOpS7pN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Josh Golomb &amp; Jeannie Chen: Hazel Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Josh Golomb &amp; Jeannie Chen: Hazel Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._George_Daley:_Dean_of_Harvard_Medical_School_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xMGFh3JzTfyFSF-WK2TGy3R-Rom4Akec/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. George Daley: Dean of Harvard Medical School (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. George Daley: Dean of Harvard Medical School (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Atul_Nakhasi:_Physician_&amp;_Policy_Advisor_LA_County_Department_of_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UtjOf3znRdu4VIJBylpCn8mIQ3Sz9ueX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Atul Nakhasi: Physician &amp; Policy Advisor LA County Department of Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Atul Nakhasi: Physician &amp; Policy Advisor LA County Department of Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amy_Compton-Phillips:_CCO_at_Providence_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LDDulmTHSnySYux2llrzljs2R_qrPU04/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amy Compton-Phillips: CCO at Providence Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Amy Compton-Phillips: CCO at Providence Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomical_terminology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v-cFeDv3RauDlDvnFqkFTUOyQoClPwAQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomical terminology]]></video:title><video:description><![CDATA[When someone talks to us, we’re only able to understand them if we know their language. Well… the same thing goes for anatomy!

To study anatomy and communicate among peers, we have to use specialized terminology that helps us describe the structures of the human body, where exactly they’re located, and their relationship to one another.

If I tell you to look at the right-most finger of your hand - which one will it be? Your pinkie? Your thumb? It will depend on the position of your hand and whether you&amp;#39;re looking at the back or the palm. This is why all anatomical descriptions are expressed in relation to one consistent position to eliminate any ambiguity.

Anatomical position is the position that is globally adopted for anatomical and medical descriptions of the human body. Now, let’s describe the position the body is in when we refer to anatomical position.

When a person is in the anatomical position, they are standing straight with their legs close together, their feet parallel to one another, toes directed forward, their arms are down at their sides with the palms of their hands facing forward, and they are keeping their head up and gazing straight forward. All descriptions of the body refer to the position shown here.

Now, if we’re looking at someone in anatomical position, there are four imaginary planes that intersect the body to help us with anatomical descriptions.

First, we have the median plane, which is an imaginary vertical plane going through the body’s midline, over structures such as the nose and belly button, separating the body into right and left halves.

Second, are sagittal planes, which are also vertical planes, but aren&amp;#39;t fixed, meaning that they could be placed anywhere parallel to the median plane, dividing the body into uneven left and right parts. You might also hear the term paramedian plane, which describes a sagittal plane that is near the median plane. 

Next we have frontal planes, also known as corona]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_the_skeletal_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qiQbBtN_RH6JYFCNfHK4M3xASE2Se-X8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to the skeletal system]]></video:title><video:description><![CDATA[What comes to your mind when you hear the word “skeleton”? Maybe last halloween? While you may associate the skeletal system with the dead, it’s actually an integral part of our living bodies.

It is made up of 206 bones that provide form and support, protect the inner organs, and together with muscles, bones also help in performing different types of movements.

Now, our skeleton can be divided into an axial and an appendicular skeleton. Let’s start with the bones of the axial skeleton, which consists of the bones of the head, neck and trunk.

These bones include the skull or the cranium, a small bone in the neck called the hyoid bone, the vertebral column, and the ribs and sternum.

The appendicular skeleton, on the other hand, consists of the bones of the upper and lower limbs.

Now, bones of the axial and appendicular skeletons are further classified based on their shape as long, short, flat, sesamoid, and irregular bones.

Let’s start with long bones, which are tubular in shape, have a long axis and usually two ends that articulate with other bones. An example is the humerus of the upper arm.

Short bones, on the other hand, are cuboidal in shape, and examples include the carpal bones of the wrist.

Next are flat bones, which are flat, thin, and possibly curved bones that usually protect internal organs. An example of flat bones are the cranial bones that protect the brain.

Next are sesamoid bones, which are particularly unique because they lie within tendons.

The largest sesamoid bone is the patella, or the kneecap, which is a triangular bone that covers the anterior side of the knee joint.

Lastly are irregular bones, which are bones that don’t fall into any of these categories, mainly because they have more complex shapes. Examples of irregular bones are the vertebrae which form the spine. 

Ok, now the surface of many bones is rather rough, with many bumps and depressions, called bone markings.

These bone markings allow bones to come in contact]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_the_muscular_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X9n78ZcYTpaQhMVc7a7hfA7zQLy3auY7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to the muscular system]]></video:title><video:description><![CDATA[The human body consists of hundreds of muscles, which come in all different shapes and sizes. Each muscle’s particular structure allows it to perform a specific function.

The muscles are attached to bones or other tissues, to help us maintain position, perform movements and even protect some organs. 

Ok, now muscle tissue is made up of contractile cells, often called muscle fibers. Muscle tissue can be grouped into 3 types; skeletal, cardiac and smooth muscle.

Skeletal muscles connect to the skeleton and other structures like the eyes to help with movement and stability of the body. 

These muscles are voluntary, meaning that we have active control of them to perform movements, like flexing your elbow. 

Cardiac muscle is the muscle tissue that makes up the walls of the heart. These muscles contract in a rhythmic way to pump blood to the whole body and they are involuntary meaning that we can’t consciously control this type of muscle. 

Lastly, is smooth muscle, which mainly lies in the walls of blood vessels and hollow organs. In blood vessels, smooth muscle helps contract the vessel walls to alter their diameter, which helps control blood flow. 

In hollow organs, smooth muscles perform rhythmic contractions called peristaltic contractions, which moves the contents of these organs in one direction, like food in the stomach or small intestine. 

Smooth muscle is also under involuntary control. Alright, now muscles come in a variety of shapes that help serve their specific functions. 

For example, a flat muscle has parallel fibers, and often has a flat sheet-like tendon called an aponeurosis - as is the case for the external oblique muscle covering the abdomen. 

Next is a quadrate muscle, which describes a square muscle with four equal sides. An example of a quadrate muscle is the famous six pack, anatomically called the rectus abdominis, which is a long paired muscle that is divided into square-like portions by bands of connective tissue. 

Pennate m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_the_cardiovascular_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0UpR2_1mQ_ygwOxgqxcflTyOS52GUnwT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to the cardiovascular system]]></video:title><video:description><![CDATA[As a society, we rely on complex transportation networks in order to supply and transport important goods and materials. The same idea goes for the human body.

Here, the circulatory systems form a complex transportation network, which allows movement of important materials, such as oxygen, around the body.

This circulatory system has two divisions: the cardiovascular system and the lymphatic system. Now, let’s get our blood flowing and focus on the cardiovascular system!

The term “cardiovascular” can be broken down into cardio-, meaning heart, and -vascular, meaning blood vessels. So, the cardiovascular system consists of the heart and blood vessels, which together make up the blood transportation network of the body that carries nutrients, oxygen and waste products to and from cells.

The heart is a muscular organ that lies in the chest, and it pumps blood through the network of blood vessels in the body. It’s composed of four chambers: a right and left atrium, as well as a right and left ventricle.

Next are the blood vessels, which are tube-like structures that carry the blood being pumped by the heart. Arteries are the blood vessels that carry oxygen-rich blood away from the heart to supply the body with oxygen and nutrients, and veins carry carbon dioxide-rich blood and waste products from other parts of the body back into the heart.

The blood running through these blood vessels also carry signaling molecules, called hormones, which allow for communication between organs and organ systems.

Lastly, blood helps regulate body temperature. For example, when it&amp;#39;s really cold outside, the blood vessels lying close to the skin constrict to reduce blood flow, saving the heat within the body.

Now, there are two main networks, called the pulmonary and systemic circulation, that allow for blood circulation between the heart and the tissues in our body.

In the pulmonary circulation, oxygen-depleted blood from body tissues runs from the right atriu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_the_lymphatic_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ddWeJv1HTM_BvFIbGaYHzQURR26XCN7k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to the lymphatic system]]></video:title><video:description><![CDATA[The lymphatic system may be the most underrated system of the human body. It protects the body from invaders, maintains the fluid level in the body, and absorbs dietary fat from the intestine.That’s pretty amazing for a system that is really small, sometimes even microscopic! 

Now, the lymphatic system is composed of lymph, lymphocytes, lymphatic vessels and plexuses, lymph nodes and other lymphoid organs. Lymphoid organs are the part of the lymphatic system that are directly involved in the immune system because they produce lymphocytes, as is the case with the thymus and bone marrow and house lymphocytes - and other white blood cells - that are ready to respond to pathogens, as is the case with lymph nodes, the spleen and tonsils.

But we are going to focus on the role of the lymphatic system in returning leaked fluid to the blood, so let’s start by turning our attention to lymph and lymphatic vessels.

Lymph is a clear - or slightly yellow - fluid that is transported through tubes similar to blood vessels, called lymphatic vessels. Now, you may be wondering, where does this lymph come from? Well, it all starts at a network of tiny blood vessels called the capillary beds where nutrient and gas exchange occurs. During this process, around 10% of this fluid is lost and ends up in the extracellular space, which is where the lymphatic system kicks in. This fluid will be taken up first by lymphatic capillaries which are small, porous capillaries throughout the body that form lymphatic plexuses. Once this fluid enters the lymphatic capillaries, it’s called lymph. Now, the small lymphatic capillaries merge to form the next part of the lymphatic system, called lymphatic vessels. Lymphatic vessels drain lymph through lymph nodes and eventually into lymphatic trunks, which drain large regions of the body - like the subclavian trunks that drain the upper limbs. Finally, lymphatic trunks converge to form two bigger channels called lymphatic ducts, specifically the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_the_central_and_peripheral_nervous_systems</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qgBMu7h6S3_qP_thbPvVWXqOTD6eGl8H/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to the central and peripheral nervous systems]]></video:title><video:description><![CDATA[The smell of a morning coffee, the memory of last christmas, and the pain of touching a hot surface. That’s your nervous system at work! 

The nervous system allows each body system to communicate with each other, and monitors internal and external changes to build a proper response that keeps us alive and kicking!

Now, to make things a bit easier, the nervous system is structurally subdivided into two anatomical  components, called the central nervous system, or CNS or short, which consists of the brain and the spinal cord and the peripheral nervous system, or PNS, which consists of the remainder of the nervous system outside of the CNS.

Both the CNS and the PNS are made up of the functional units of the nervous system, called neurons or nerve cells. 

These cells have many parts, with the main part being the cell body, which houses the nucleus of the cell. 

From the cell body arise two types of extensions: dendrites, which are short projections and may be numerous, and an axon, or nerve fiber, which is a single long extension that looks like a thread. 

Now, neurons are special because they’re able to receive and send electrical impulses that allow for communication with other neurons, as well with effector cells, like muscle cells. 

This process starts at the dendrites, which receive electrical signals from other neurons and convey it towards the cell body. Then, the cell body produces an electrical impulse and sends it through its own single axon. 

Many axons are covered with a layer of lipids and proteins that speed up the conduction of these impulses, called the myelin sheath. 

Now, the electrical impulse eventually reaches the distal parts of an axon, called the axon terminals. 

Here, an axon terminal can meet up with a dendrite of another neuron, and this contact site is called a synapse which facilitates the communication between neurons.

Now, there are a few types of neurons that are structurally different from one another. Neurons t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_the_somatic_and_autonomic_nervous_systems</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7rgV0vlFSym62-inh5L338WOQOCS1c4N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to the somatic and autonomic nervous systems]]></video:title><video:description><![CDATA[Whether you’re playing volleyball with friends or just watching TV, your nervous system is always operating, making sure that the right organs function at the right time. The nervous system is structurally divided into two regions, called the central nervous system, or CNS, and the peripheral nervous system, or PNS. The peripheral nervous system can be further subdivided functionally into the somatic nervous system, and the autonomic nervous system. 

Okay, let’s start with the somatic nervous system, which describes a set of nerve fibers  that control voluntary actions and convey sensory information from the skin, skeletal muscles and joints. Somatic sensory fibers allow transmission of sensory information such as touch, pain, temperature, and proprioception. For example, somatic sensory fibers inform our CNS that our cup of coffee is too hot. Then there are somatic motor fibers, which only innervate skeletal muscle and control voluntary actions of the body, like putting the coffee cup back on the table until it cools down. 

On the flip side, the autonomic nervous system controls the involuntary activities within the body. This system consists of visceral motor fibers that carry motor signals to smooth muscle,  such as that found in the intestinal walls that allow for peristalsis to occur, as well as cardiac muscle, and glandular tissue. 

We also have visceral sensory fibers, which are not typically defined as part of the autonomic nervous system, but they act in conjunction with the visceral motor fibers of the autonomic nervous system to control visceral function. Visceral sensory fibers travel with the visceral motor fibers carrying sensory information from the viscera back to the CNS, where visceral motor fibers will act in response to this sensory information. For example, they provide information about things such as the amount of oxygen in your blood, your arterial blood pressure, and the level of distention of your stomach after that big meal! T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_inguinal_region</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A77nrsLkSJaMOwwlBA7WYE88Tr2Boy1n/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the inguinal region]]></video:title><video:description><![CDATA[The inguinal region, sometimes called the groin, is the lower part of the anterolateral abdominal wall. It’s a small area of great importance, as it serves as a passageway for structures such as the spermatic cord, vessels, and nerves to enter or leave the abdominal cavity.

The inguinal region is a compact space, located superior to the thigh, lateral to the pubic tubercle, and inferomedial to the anterior superior iliac spine. 

One important structure in this region is the inguinal ligament, which is a thick fibrous band formed by the inferior border of the external oblique aponeurosis. 

The inguinal ligament extends from the anterior superior iliac spine of the ilium, to the pubic tubercle on the pubic bone. 

Medially, the inguinal ligament’s attachment to the pubis is reinforced by a number of smaller fibrous extensions, including the lacunar ligament and the pectineal ligament. 

The lacunar ligament attaches along the superior pubic ramus and some fibres continue along the pecten pubis as the pectineal ligament. 

The lacunar ligament forms the medial border of the subinguinal space, located inferior to the inguinal ligament. 

Important structures that pass  through this space include the psoas major and iliacus muscles and also the femoral nerve, artery and vein, and the lateral cutaneous nerve of the thigh. 

Now, the most important feature of the inguinal region is the inguinal canal, which is a passage that extends inferomedially through the anterolateral abdominal wall. To better understand the anatomy of this canal, let’s look at how it develops!

In genetically male individuals, the testes begin to develop in the extraperitoneal space of the posterior abdominal wall, and within the first few months each testis descends into the pelvis, pulled by a structure called the gubernaculum, which attaches to the anterolateral abdominal wall - and, later, to the developing scrotum. 

As the testis descends from the abdominal cavity into the scrotum,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_peritoneum_and_peritoneal_cavity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Tq0zEqFIRoWM3vCuKA8FsagPQvKiLUXV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the peritoneum and peritoneal cavity]]></video:title><video:description><![CDATA[At first glance, the peritoneum and peritoneal cavity seem pretty simple, but some aspects, like the peritoneal ligaments, can be a bit confusing. In order to understand them, we need to go way back to their embryological formation.  
Once upon a time, in an amniotic galaxy far far away, the embryonic body cavity is lined with mesoderm. As the fetus is developing, the embryonic body cavity becomes the primordial abdominal cavity and the mesoderm lining it becomes the parietal peritoneum which is a transparent, serous membrane that helps to form a closed sac, called the peritoneal cavity. 

As abdominal organs develop, they protrude into the peritoneum, like pushing your fist into a balloon. Your fist represents the developing abdominal viscera and the balloon represents the parietal peritoneum. As your fist pushes into the balloon it is lined closely by part of the balloon and this represents the visceral peritoneum. So, the visceral peritoneum covers the viscera, while parietal peritoneum lines the internal surface of the abdominopelvic wall; and these two layers are continuous with one another. 
 The parietal peritoneum has the same blood and lymphatic supply and the same nerve supply as the region of the wall it lines, meaning it is sensitive to pressure, pain, heat and cold. The visceral peritoneum, on the other hand, has the same blood, lymphatic, and nerve supply as the viscera it covers, meaning it is sensitive to stretch and chemical irritation. 

Depending on their relationship with the peritoneum, abdominal and pelvic organs can be either intraperitoneal, retroperitoneal, or subperitoneal. 
 Intraperitoneal organs are almost completely covered with visceral peritoneum, but remember they’re not inside the peritoneal cavity. These organs include the stomach, first part of the duodenum, jejunum, ileum, transverse colon, sigmoid colon, liver and spleen.  
Now, the retroperitoneal organs, also known as primarily retroperitoneal, develop posterior to t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_abdominal_viscera:_Esophagus_and_stomach</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-4Z5ZpC3SYmd3KPSdhAJLenrTfmpVa1G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the abdominal viscera: Esophagus and stomach]]></video:title><video:description><![CDATA[Osmosis knows that anatomy can be overwhelming, but hopefully this video on the esophagus and stomach can make it a bit easier, so let&amp;#39;s begin “digesting” this content together! The esophagus and the stomach are part of the upper digestive tract and are involved in the first phases of digestion. We are going to use the pizza we ate for dinner last night as an example to help us explore the pathway of the esophagus and stomach. 

Now, let’s start with the esophagus, which is a muscular tube that carries food from the pharynx to the stomach. We can think about the esophagus as a subway that our food travels in between these two structures. After the pizza we ate has been chewed and swallowed, the muscles of the esophagus help propel the bolus towards the stomach in a wave-like motion called peristalsis. 

The esophagus is made up of two muscular layers: an internal circular layer and an external longitudinal layer. In its proximal or superior third, the external layer consists of striated skeletal muscle, which is under voluntary control, while its distal or inferior third is made up of smooth muscle, which is under involuntary control. 

And as you’d expect, the middle third is a transitional segment that consists of a mix of both types of muscle. The esophagus follows the curve of the vertebral column as it descends through the neck and into the mediastinum. 

Once it reaches the diaphragm, it passes through the esophageal hiatus, just to the left of the median plane at the level of the T10 vertebra, where it  becomes the abdominal esophagus. The abdominal esophagus finishes its journey by becoming continuous with the stomach through the cardial orifice, which is surrounded by the cardiac sphincter. 

It sits left of the midline at the level of the T11 vertebra and designates the esophagogastric junction, which is an important landmark where the mucosa abruptly changes from the stratified squamous epithelium of the esophagus to the simple col]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_abdominal_viscera:_Pancreas_and_spleen</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BPQLxAzzR6eh-IDZ0Q48mW1sRzWoMH5b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the abdominal viscera: Pancreas and spleen]]></video:title><video:description><![CDATA[Both the spleen and the pancreas are visceral organs in the foregut. Don’t get too excited though, that’s where their similarities end. Other characteristics such as the shape and function within the body are quite different. So let’s break them down!

Alright, let’s begin with the spleen, which has a few different important functions. Prenatally, it functions as a hematopoietic organ, which means it makes fetal blood cells. After birth, the spleen is like a hub for lymphocyte proliferation, as well as a recycling center for damaged red blood cells and platelets, and a blood reservoir, from which backup blood can be pumped into circulation after significant hemorrhage. For this reason, we can think of our spleen as our own personal blood bank. 

The spleen is oval in shape and is an intraperitoneal organ. he spleen is an oval-shaped organ located in the left upper quadrant of the abdomen, and it is intraperitoneal. This means that the spleen is entirely enveloped in visceral peritoneum, except at the splenic hilum where the vasculature enters and exits the organ. 

The spleen has an anterior, superior and inferior border. The superior border of the spleen is easily recognizable due to its notched appearance. The outer surface of the spleen can also be divided into two parts; the diaphragmatic surface which is in contact with the concavity of the diaphragm, and the visceral surface that is in contact with the surrounding abdominal viscera. 

Now, let’s break down the anatomical relationships of the spleen with its surrounding structures. The left portion of the diaphragm and the 9th to 11th ribs lie posterior to the spleen, with the diaphragm acting like a barrier between the spleen and the ribs. The stomach lies anterior to the spleen and the two connect at the greater curvature of the stomach via the gastrosplenic ligament. The spleen is lateral to the left kidney and the two are connected via the splenorenal ligament. The gastrosplenic and the splenorena]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_abdominal_viscera:_Liver,_biliary_ducts_and_gallbladder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aWfR2dq0SwOxdx-_388sg8FaSuiV2ECw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the abdominal viscera: Liver, biliary ducts and gallbladder]]></video:title><video:description><![CDATA[The liver is quite an amazing organ, and fact is, the rumors you heard are true - it can actually regenerate itself! If that wasn’t enough, it also plays a major role in digestion, by producing bile, storing energy, detoxifying toxic substances and producing proteins. Let’s get started and look more at the liver along with the other associated organs and structures that help with digestion!

The liver is a large intraperitoneal organ located mostly in the right hypochondriac and epigastric regions of the abdomen, deep to the 7th to the 11th ribs. It sits just to the right of the stomach,  with some of the liver covering its anterior surface. 

It is superior to the duodenum, right side of transverse colon, and right colic flexure. Most of the liver is anterior to the lesser omentum; and it is anterosuperior to the right kidney and adrenal gland. 

The liver has many important functions, including the production of bile to aid in fat digestion, reception and metabolization of absorbed products from digestion, detoxification of toxic substances received from digestion, storage and release of carbohydrates, as well as the production of proteins - primarily plasma proteins such as albumin and clotting factors.

When you look closely, the human liver is actually divided grossly into four parts, referred to as lobes. There is a larger right lobe, which is separated from a smaller left lobe by the falciform ligament. Then comes the caudate as well as the quadrate lobes, which are anatomically included in the right lobe.

Now, the liver is surrounded by potential spaces, which are referred to as hepatic spaces. These spaces usually only contain a small amount of peritoneal fluid, which serves as a lubricant between two membranes in close contact. The hepatic spaces include the right and left subphrenic recesses which are extensions of the peritoneal cavity located on the anterosuperior aspect of the liver, and are separated by the falciform ligament. 

Next is the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_abdominal_viscera:_Kidneys,_ureters_and_suprarenal_glands</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oPBeZRSZQo_qo1kUoKGAtrNWTY2WnvZx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the abdominal viscera: Kidneys, ureters and suprarenal glands]]></video:title><video:description><![CDATA[Looking to learn about the kidneys and their associated organs? Well, “urine” the right place! The kidneys are a pair of bean-shaped abdominal organs, which filter metabolic waste out of the blood in the form of urine. The urine then gets funneled into the urinary bladder by the ureters. Sitting on top of the kidneys, there are the suprarenal glands or adrenal glands. These glands function as a part of the endocrine system by secreting adrenal hormones, which regulate various functions of the body.  

Let&amp;#39;s begin with the kidneys, which are retroperitoneal organs, meaning they lie posterior to the peritoneum. They lie on the posterior abdominal wall, at the level of the T12 to L3 vertebrae, on both the right and the left sides of the vertebral column. The right kidney sits slightly lower than the left one, which helps make space to accommodate the large size of the liver located on that side of the abdomen. 

Now, positioned superior to both kidneys are the suprarenal glands, but they also have a number of different relationships with surrounding organs. Anterior to the left kidney is the spleen, stomach, pancreas, left colic flexure, and jejunum, while the liver, duodenum, right colic flexure and ascending colon lie anterior to the right kidney. The right kidney and liver are separated by the hepatorenal recess, also known as Morisons pouch.  

Posteriorly, both kidneys are associated with the diaphragm, the psoas major, quadratus lumborum and transversus abdominis muscles as well as the subcostal nerve and vessels, and the iliohypogastric and ilioinguinal nerves. The left kidney is also posteriorly associated with the 11th and 12th ribs, while the right is mainly associated with the 12th rib.  

Each kidney has a convex, lateral margin, and a concave, medial margin. On their concave margins, each kidney has a vertical cleft, called the renal hilum, through which renal vessels, nerves, and the ureters enter and exit each kidney.  

At the renal h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_abdominal_viscera:_Innervation_of_the_abdominal_viscera</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iLNyaQUXSJ6efLn5dl5R--u_Q1miNizu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the abdominal viscera: Innervation of the abdominal viscera]]></video:title><video:description><![CDATA[Most of our abdominal organs, also called abdominal viscera, are a part of the digestive system. These include the stomach, the small and large intestine, the liver, gallbladder and pancreas. 

The abdomen is also home to other organs, like the spleen, kidneys, suprarenal glands, and the ureters, which play important roles in other systems. 

All of these organs work involuntarily, so they’re innervated by the autonomic nervous system. And luckily so - can you imagine trying to voluntarily control digesting each vegetable in a salad?!

Ok, now remember that our nervous system is divided into the central nervous system and the peripheral nervous system. 

Functionally, the peripheral nervous system is also divided into two parts. The somatic nervous system controlling the voluntary movement of skeletal muscles, and the autonomic nervous system that controls the involuntary movement of the smooth muscles and also the glands of our organs or viscera. 

Now, the autonomic nervous system is also divided into two parts; the sympathetic, and parasympathetic nervous systems. 

The sympathetic nervous system is our fight or flight response and increases heart rate and breathing rate, while slowing down digestion through reducing peristalsis and constricting blood vessels to the gut to reduce blood flow. 

The parasympathetic nervous system is our rest and digest response and it slows down heart rate, and increases digestion by promoting peristalsis, gland secretion, and dilation of gut vessels for increased blood flow.

Alright, now, press pause, and see if you can tell whether the sympathetic or the parasympathetic nervous system promotes digestion!

Let’s take a deep dive by first looking at the sympathetic nervous system, which consists of the abdominopelvic splanchnic nerves, prevertebral ganglia, the abdominal aortic plexuses and their extensions, the periarterial plexuses. 

Splanchnic nerves mean “nerves for the internal organs,” so they innervate the a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_diaphragm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g7oEPBE_QBua9xc3hK0_l_9GQpqd7KM1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the diaphragm]]></video:title><video:description><![CDATA[The diaphragm is a dome-shaped sheet of skeletal muscle that divides the thoracic cavity from the abdominal cavity. 

That may sound simple, but in fact, the diaphragm is so much more than just a sheet of muscle. In fact, every breath you take is thanks to your diaphragm! 

Ok, so let’s begin by looking at the general structure of the diaphragm. It curves superiorly into right and left domes. 

It has a mobile, central portion known as the central tendon and a peripheral muscular portion that is fixed to the bones, cartilages, and ligaments of the thoracic cage. 

The periphery of the diaphragm can be divided into three parts depending on its specific attachment points. 

The sternal part, attaches to the posterior aspect of the xiphoid process; the costal part attaches to the internal surfaces of the 7th to the 12th ribs and their costal cartilages; while the lumbar part attaches to the medial and lateral arcuate ligaments, the L1 to L3 vertebral bodies and the intervertebral discs in between. 

Now, the diaphragm is the chief muscle for inspiration; meaning that when it contracts, it helps us breathe in. During contraction, the central portion of the diaphragm depresses, increasing the volume of the thoracic cavity, which, in turn, increases the volume in the lungs. 

This makes the intrapulmonary pressure fall below the atmospheric pressure, creating a partial vacuum that allows fresh air to be sucked in! 

On the other hand, expiration is largely passive, meaning the diaphragm relaxes and rises, which decreases the volume of the thoracic cavity, and subsequently increases the intrapulmonary pressure to be above the atmospheric pressure, forcing the air in the lungs to be expelled out. 

The diaphragm also helps with circulation. During contraction, the increased intra-abdominal pressure and decreased intrathoracic pressure helps venous return of blood towards the heart through the inferior vena cava. 

In order to properly perform its functions, the di]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_muscles_and_nerves_of_the_posterior_abdominal_wall</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HC3LQpzdQliIjfD0EfsZi-D3TlW9KS5V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the muscles and nerves of the posterior abdominal wall]]></video:title><video:description><![CDATA[The posterior abdominal wall is a complex area of the body made up of muscles, vessels and nerves that work together to hold abdominal organs in place, adjust our posture, stabilize the hip joint and even flex our thighs on leg day! 

The main paired muscles of the posterior abdominal wall include psoas major, iliacus and quadratus lumborum; and naturally, for those muscles to work properly, they receive innervation from various nerves.

Okay, now let’s take a closer look at these muscles! First up is the psoas major, which is a long, thick muscle that lies lateral to the lumbar vertebrae. It originates superiorly on the transverse processes of the bodies, and adjacent intervertebral discs of the T12 through L5 vertebrae. 

The psoas major passes inferolaterally, deep to the inguinal ligament in order to insert on the lesser trochanter of the femur. Finally, approximately half the population has a psoas minor muscle that sits on the anterior aspect of each psoas major muscle.

Now, the psoas major muscle is covered by the psoas fascia or the psoas sheath, which is attached medially to the lumbar vertebrae and pelvic brim. The psoas sheath is thickened superiorly forming the medial arcuate ligament. 

Inferior to the iliac crest, the psoas fascia is continuous with the part of the iliac fascia that covers the iliacus muscle. 

When acting inferiorly with the iliacus muscle, the psoas muscle flexes and laterally rotates the thigh and when it acts superiorly it causes lateral flexion of the vertebral column. 

When sitting, the psoas muscle acts with the iliacus muscle to flex the trunk. The innervation of the psoas major muscle comes from the anterior rami of the L1, L2 and L3 spinal nerves. 

Next is the iliacus muscle, which is a large triangular muscle that lies lateral to the inferior portion of the psoas major muscle. It originates superiorly on the superior two thirds of the iliac fossa, ala of sacrum, and anterior sacroiliac ligaments. It also inserts]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_vessels_of_the_posterior_abdominal_wall</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QLPkYDWzRPuaqEN50cFEavr5S3mm3T7L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the vessels of the posterior abdominal wall]]></video:title><video:description><![CDATA[The major vessels of the abdomen, including the abdominal aorta and the inferior vena cava, course along the posterior abdominal wall. Branches and tributaries of these vessels help supply and drain the posterior abdominal wall, and the abdominal viscera. Important lymphatic vessels that help with drainage of the lower body are also found in this area. 

Let’s start off with the abdominal aorta, which gives rise to most of the arteries supplying the posterior abdominal wall. It transitions from the thoracic aorta to the abdominal aorta starting at the aortic hiatus, located within the diaphragm, at the level of the T12 vertebra. Then, it descends anterior to the vertebral bodies and ends at the level of the L4 vertebra. 

From superior to inferior, the abdominal aorta has a number of structures associated with it anteriorly. These include the celiac plexus and ganglia, the body of the pancreas, the splenic vein, the left renal vein, the horizontal part of the duodenum and the coils of the small intestine. 

Structures to the right of the abdominal aorta include the inferior vena cava, azygos vein, cisterna chyli, and the thoracic duct. Posteriorly, the left lumbar veins pass behind the aorta to reach the inferior vena cava. 

Now, let’s talk about the various branches that arise from the abdominal aorta. These can be organized in three categories based on the “vascular plane” or direction in which the arteries branch from the abdominal aorta: first, there are paired visceral branches, that travel in the lateral plane; second, there are paired parietal branches, which travel in the posterolateral plane; and third, there are the unpaired visceral branches in the anterior midline plane. 

The paired visceral branches include the middle suprarenal arteries, the renal arteries and the gonadal arteries which supply the suprarenal glands, kidneys, and the testicles or ovaries, based on the biological sex. 

Next up are the paired parietal branches, which include:]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Anterior_and_posterior_abdominal_wall</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d4kib7WgTWq6ZGkliojp3pliS7yXFEIZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Anterior and posterior abdominal wall]]></video:title><video:description><![CDATA[When we think about the clinical conditions affecting the abdomen, we immediately think about injury to organs such as the liver, intestines or stomach. However, there are also many conditions that affect the anterior and posterior abdominal wall, as well as the structures adjacent to them. So let&amp;#39;s get started!

When examining the gastrointestinal system, first, it’s important to do a general inspection of the abdomen which includes looking for scars and incisions which can indicate what surgeries the patient has had in the past. Typically, the location of the abdominal incision indicates what type of surgery the patient has had.

First, there’s the Kocher incision, also called the subcostal incision, which is made parallel and at least 2.5 centimeters below the costal margin in order to avoid the 7th and 8th thoracic spinal nerves. Injury to these nerves results in decreased sensation of the anterior abdominal wall supplied by those respective branches. This type of incision is usually found on the right side and provides access to the gallbladder and biliary ducts, and can be extended towards the left side of the abdomen to access the spleen.

Next up, there are longitudinal incisions, which include midline incisions and paramedian incisions. They can be used in almost all abdominal surgeries, especially exploratory surgeries which are sometimes needed to diagnose uncertain abdominal pathologies. Now, longitudinal incisions provide great exposure of the abdominal viscera and can also be extended as needed.

The midline or median incision is made along any part or length of the linea alba, so from the xiphoid process all the way towards the pubic symphysis. This type of incision is preferred because the linea alba only has small vessels and nerves, so there’s a lower risk of bleeding and nerve damage.

A paramedian incision, which is lateral to the median plane, is made in a sagittal plane and can extend anywhere from the costal margin to the pu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Inguinal_region</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2t0t7-1PQZ_ronKnoFCn9S5uRZaU84Md/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Inguinal region]]></video:title><video:description><![CDATA[The inguinal region, located near the groin, is found in the lower part of the anterior abdominal wall, and it contains several important structures that enter and leave the abdomen. Understanding the anatomy of the inguinal region is important for understanding common clinical conditions such as hernias, and many others! 

Speaking of which, hernias occur when an organ or tissue protrudes through the wall of the muscle or tissue that normally contains it. The majority of hernias occur in the abdominal cavity or the inguinal region, through which subcutaneous fat, abdominal omental fat, or even abdominal viscera can protrude. In order for a hernia to happen, there is typically a weak point along the abdominal wall, such as a weak linea alba, previous surgical interventions that weaken the abdominal wall muscles, or pregnancy. 

First, let’s look at anterior abdominal wall hernias. They can be divided into 4 categories: epigastric, umbilical or periumbilical, spigelian and incisional hernias. Epigastric hernias are caused by a weakened linea alba and are basically defects in the abdominal midline between the umbilicus and the xiphoid process. Then, there are umbilical or paraumbilical hernias, which are hernias through the umbilical ring or around the umbilicus. These are often found in children, because the umbilical ring is weak at birth, but can also be acquired in adults and frequently affect pregnant or obese individuals. 

Spigelian hernias are found along the semilunar lines which are skin folds from the inferior costal margin of the 9th costal cartilage to the pubic tubercles and overly the tendinous insertions of the rectus abdominis muscle, as abdominal tissue can protrude through these areas of tendinous insertions. Finally, an incisional hernia can develop at the site of a prior surgical incision as the muscle and fascia is typically weakened, for example over the surgical site for an appendectomy. 

Hernias can be classified as reducible, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Peritoneum_and_diaphragm</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d2DpdB0qS0eG4Al4QLH-30QjTSKdHS_2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Peritoneum and diaphragm]]></video:title><video:description><![CDATA[The peritoneum is a transparent serous membrane that lines the abdominal cavity and covers the abdominal organs, whereas the diaphragm is a skeletal muscle that separates the thoracic cavity from the abdominal cavity and plays an important role in respiration. 

Understanding the anatomy of these structures allows us to better understand the unique clinical conditions that affect them. 

Let’s start off by reviewing the innervation of visceral and somatic pain in the abdomen. The peritoneum is made up of two continuous layers, the visceral peritoneum and parietal peritoneum. 

The inner visceral layer mainly covers the abdominal organs and has a visceral nerve supply, where the outer parietal layer mainly covers the internal surface of the abdominopelvic walls and has a somatic nerve supply. 

Furthermore, both the visceral and somatic nerve supply of the peritoneum sense pain during different clinical conditions; however, the way in which they sense pain is different. 

The visceral peritoneum is innervated by the autonomic nervous system. When the visceral peritoneum is irritated, pain sensation is detected by visceral afferent fibers which travel with the autonomic nerves, mainly sympathetic nerve fibers, back to the spinal cord. 

Visceral pain is typically sensed as a diffuse, dull pain which is not very well localized, and the pain is often referred to the midline region of the dermatomal areas of the same spinal level as the autonomic nerve supply. 

Typically, pain sensed by the foregut visceral peritoneum is referred to the epigastric region, midgut visceral pain is referred to the umbilical region, and hindgut visceral pain is referred to the hypogastric region. 

Patients who experience visceral pain may also present with nausea, vomiting, or sweating due to activation of the autonomic nervous system. 

On the other hand, the parietal peritoneum has a somatic nerve supply, which is the same as the adjacent abdominopelvic wall in which it lines. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Viscera_of_the_gastrointestinal_tract</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UhkjujeQTISEXu5Gmyjjq4sPTGy-eXdW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Viscera of the gastrointestinal tract]]></video:title><video:description><![CDATA[The gastrointestinal tract runs from the mouth all the way to the anus and contains the esophagus, the stomach, the small and large intestine and the anus. All these structures, like any other part of our body, are prone to injury or disease. 

This video will give you a better understanding of the anatomy of the GI tract and how it relates to the clinical conditions that affect them! 

Let’s start by looking at gastric and duodenal ulcers, which are open lesions in the lining of the stomach or duodenum that lead to inflammation in the gastric or duodenal wall. 

These are often associated with a specific stomach bacteria called H. Pylori, H.Pylori....Helicobacter Pylori. 

Duodenal ulcers are more frequent than gastric ulcers and can be located anywhere along the duodenal wall, classically affecting either the anterior or posterior duodenal wall. If severe enough, ulcers can erode through the duodenal wall, which can cause perforation or gastrointestinal bleeding. 

Anterior wall duodenal ulcers are more prone to perforation into the anterior abdominal cavity, and this can result in a pneumoperitoneum, because air from the gastrointestinal tract enters the abdominal cavity. 

A classic finding on x-ray is free air under the diaphragm indicating a pneumoperitoneum. This can also result in peritonitis, because as duodenal contents leak into the abdominal cavity, they irritate the peritoneum. 

Posterior wall duodenal ulcers can also cause perforation, but more frequently, they cause upper gastrointestinal bleeding. 

That’s because the first part of the duodenum, called the duodenal bulb, is positioned directly anterior to the gastroduodenal artery, so an erosion of the posterior wall can also cause erosion into the gastroduodenal artery resulting in an upper gastrointestinal bleed.

Most gastric ulcers are located at the lesser curvature of the stomach, an area where both the left and right gastric artery can be found perfusing the stomach. 

So, if a gast]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Other_abdominal_organs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/30OfNjFRQeyazSbe1-JvWc9uTK6F5C15/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Other abdominal organs]]></video:title><video:description><![CDATA[The abdominal cavity is home to plenty of organs. Some of them, like the stomach and intestines, are part of the gastrointestinal tract. Other organs, like the liver, gallbladder and pancreas, help with digestion, even though they’re not part of the GI tract itself. And then there are also organs like the spleen, kidneys and ureters, which are part of other important, non gastrointestinal systems. So let’s take a look at the injuries and diseases that can affect these abdominal organs.

First off, we have portal hypertension, which basically means increased pressure in the portal venous system. This is most commonly caused by liver cirrhosis, but can also be caused by vascular obstruction. Some causes of vascular obstruction include portal vein thrombosis, Budd-Chiari syndrome which is thrombosis or compression of the hepatic veins, as well as the parasitic flatworm infection known as schistosomiasis. 

Okay, now, when fibrosis in the liver from cirrhosis obstructs the portal vein, the pressure rises in the portal vein and into its tributaries. This large volume of congested blood flows out from the portal system into the systemic system at the sites of portosystemic anastomoses, also called portocaval anastomoses. 

The first site of portosystemic anastomosis is at the lower esophagus. At this point, the high pressure in the portal system can reach the anastomosis between the left gastric veins and the esophageal veins in the lower esophagus, causing engorged varicose veins which may then go on to rupture and lead to upper gastrointestinal bleeding. 

In more severe cases of portal hypertension, the veins of the anterior abdominal wall, called the epigastric veins, which anastomose with the paraumbilical veins become varicose and look like small snakes radiating from the umbilicus under the skin. This clinical sign is called caput medusae. 

There is another portosystemic anastomosis in the rectum, which in the case of portal hypertension, can lead t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arteries_and_veins_of_the_pelvis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5_go42BoR6CRBf-nfG4V6hgnQPOISkom/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arteries and veins of the pelvis]]></video:title><video:description><![CDATA[The pelvis contains numerous structures, all supplied by the neurovascular structures of the pelvis, including nerves, arteries, veins, and lymph nodes. These structures are found on the posterolateral walls of the pelvic cavity. 

Lymph nodes are usually clustered around the veins, and lymph vessels that come off these nodes ascend parallel to the veins. Let&amp;#39;s focus our attention on the arteries and veins of the pelvis. 

Now, the arteries of the pelvis originate from the abdominal aorta, which is the continuation of the thoracic aorta below the aortic hiatus in the diaphragm. The abdominal aorta gives branches to various organs in the abdomen, then divides at the level of the fourth lumbar vertebra into the right and left common iliac arteries. 

Each artery runs inferolaterally, and ends at the level of the intervertebral disc between L5 and S1 by dividing into the internal and external iliac arteries. Let’s talk about each of those branches. First are the external iliac arteries, which descend on the medial border of a muscle called the psoas major.

After running for a short distance, each external iliac artery gives two branches, called the inferior epigastric and deep circumflex iliac arteries. These branches supply the anterolateral aspect of the abdominal wall. Then, each external iliac artery passes underneath the inguinal ligament to become the femoral artery, which is the main artery that supplies the lower limbs. 

Next are the internal iliac arteries, which are the main arteries of the pelvis, and also supply parts of the gluteal region, medial thigh, and perineum. The branching pattern of the internal iliac arteries is one of the most variable in the body, so in order to identify each branch we must think about the structures they are nourishing. 

Each internal iliac artery runs posteromedially to reach the upper border of the greater sciatic foramen. Then, each internal iliac artery divides into anterior and posterior divisions or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nerves_and_lymphatics_of_the_pelvis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ivmRdue6TEaSyNJabJVS08iQR1eC7xOs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nerves and lymphatics of the pelvis]]></video:title><video:description><![CDATA[The neurovascular structures of the pelvis include nerves, arteries, veins, and lymph nodes. These structures lie on the posterolateral walls of the pelvic cavity. 

Generally the somatic nerves are the most lateral, arteries lie medial to nerves, and veins lie between these two. 

Lymph nodes are usually clustered around the veins, and lymph vessels that come off these nodes ascend parallel to the veins. Now, let&amp;#39;s take a closer look at the lymphatics and nerves of the pelvis specifically. 

Let’s talk about the lymphatic drainage of the pelvis, which follows various major and minor groups of lymph nodes. 

These lymph nodes have variable, sizes, numbers, and locations, and the lymph node clusters’ names are based on the adjacent  structures and nearby blood supply. 

Furthermore, these nodes are all interconnected, so their drainage often overlaps and can vary quite a bit. 

First, there are the inguinal lymph nodes which lie around the inguinal ligament, and they’re divided into superficial and deep inguinal lymph nodes. 

The superficial inguinal lymph nodes receive lymphatic drainage from the superficial lower limb, abdominal wall inferior to the umbilicus, gluteal region and superficial perineal structures such as the distal vagina, vulva and scrotum, and typically drain into the external iliac lymph nodes. 

The deep inguinal lymph nodes receive lymph from the superficial inguinal nodes, as well as the deep portions of the lower limb, the glans clitoris in females or glans penis in males and the distal spongy urethra. These nodes typically drain into the external and common iliac lymph nodes. 

Now, in addition to the inguinal lymph nodes, the external iliac lymph nodes also receive lymph from the anterior superior pelvic viscera, such as the body of the uterus, anterior cervix, and superior bladder. 

Finally, the external iliac lymph nodes drain lymph into the common iliac lymph nodes, which lie around the common iliac artery

Next are th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_urinary_organs_of_the_pelvis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DcZgjOLtTQmzawm5qqQOQnGkTBKMCcg2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the urinary organs of the pelvis]]></video:title><video:description><![CDATA[Urine good hands here at Osmosis, because we care about each other and our learners! Bad puns aside, urine is an important way for us to eliminate waste and it takes quite the journey from the kidneys to the outside world! Let’s look at the path of urine after it leaves the kidneys, and the structures it passes through along its journey. 

After exiting the kidney, urine travels through 3 main structures before leaving the body; the ureters, the urinary bladder and the urethra. 

Let’s start with the ureters, which are paired muscular tubes sitting retroperitoneally that transport  urine from the kidneys to the urinary bladder. The ureters are roughly 30 centimeters long, and have two parts; an upper abdominal part and a lower pelvic part. 

The abdominal part starts at the kidneys, and descends in the abdomen posterior to the peritoneum to reach the pelvic brim. Here, the ureters cross near the bifurcation of the common iliac arteries - where the external and internal iliac arteries begin - and are now referred to as  the pelvic ureters. 

The pelvic ureters run on the lateral walls of the pelvis reaching the ischial spines. Then, each pelvic ureter passes anteromedially to enter the posterior wall of the urinary bladder. Now, the ureter is surrounded by many structures that differ between biologically male individuals and biologically female individuals.

In males, the ureters enter the posterior wall of the bladder superior to the seminal vesicles, which are paired glands that secrete parts of the seminal fluid. Also, the ureters run posterior to the ductus deferens, which are paired tubes that carry sperm from the scrotum to the pelvic cavity. 

The ductus deferens emerges from the inguinal canal and travels to the posterolateral angle of the bladder, where it passes superior to the ureter. In females, the ureters pass medial to the origin of the uterine artery. Then, at the level of the ischial spine, the uterine artery crosses the ureter. Finally, th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_gastrointestinal_organs_of_the_pelvis_and_perineum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HY_vMi9NT0SsRTedLTRvA5lERqO6i0Ef/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the gastrointestinal organs of the pelvis and perineum]]></video:title><video:description><![CDATA[When you eat, food travels over 15 feet before leaving your body! But before it leaves, it has two final stops; the rectum and the anal canal. Let’s explore these gastrointestinal organs of the pelvis and discuss the process of defecation and the structures involved.

The rectum is the terminal chamber of the large intestine that temporarily stores feces before defecation. The rectum joins with the sigmoid colon at the level of S3, forming the rectosigmoid junction.

Then, the rectum courses below in the pelvic cavity, reaching a point anterior and inferior to the tip of the coccyx. Here, the rectum pierces the levator ani muscle to join with the anal canal, forming the anorectal junction.

Let’s think of the pelvis like a bowl. The levator ani muscle acts as the bottom of the bowl to support the structures within the pelvis, especially the rectum.

Another structure that supports the rectum is the anococcygeal ligament which forms a fibrous ridge from the anal canal to the coccyx, acting as an anchor.

The relations of the rectum to the surrounding structures differs between biologically male and biologically female individuals.

In males, the rectum lies behind the fundus of the urinary bladder, the seminal vesicles, the left and right ductus deferens, and the prostate gland. In females, the rectum lies behind the lower end of the uterus and the vagina.

The rectum is a Latin word that means straight, but this is a bit misleading, because the human rectum actually has many flexures.

These flexures include the sacral, the anorectal, and the superior, inferior, and intermediate lateral flexures. The sacral flexure follows the curve of the sacrum and the coccyx, forming an anteroposterior curve with an anterior concavity.

Next is the anorectal flexure, which is a sharp postero-inferior angle at the anorectal junction. This flexure is maintained by a sling-like muscle, puborectalis, which is part of the levator ani muscle group.

When contracted, the pubor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_male_reproductive_organs_of_the_pelvis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NCOrotu7R0SkkpMlHgiT9TiKTWuG5Tww/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the male reproductive organs of the pelvis]]></video:title><video:description><![CDATA[The male reproductive system consists of a number of external and internal organs. The male reproductive organs that lie within the pelvic cavity include the ductus deferens, seminal vesicles, ejaculatory ducts, and prostate. 

These organs are all important in the transportation and protection of sperm cells as they move from the testis to eventually reach the penis. 

Let’s start with the ductus deferens or the vas deferens, which are paired tubes that carry mature sperm from the epididymis to the ejaculatory ducts. 

The ductus deferens begins at the inferior pole of the testis as a continuation of the last part of the epididymis, called the tail of the epididymis. 

Then, it ascends posterior to the testis and medial to the epididymis to enter the spermatic cord, which is a cord-like structure that connects the testes to the abdominal cavity. 

Finally, the ductus deferens penetrates the anterior abdominal wall through the inguinal canal and crosses the external iliac vessels to enter the pelvic cavity. 

Here, the ductus deferens runs along the lateral wall of the pelvis, external to the parietal peritoneum. 

At the posterolateral angle of the urinary bladder, the ductus deferens crosses the ureter, reaching the fundus of the bladder. 

A way to remember the relationship between the ductus deferens and the ureter is the phrase, “Bridge over troubled water” where the ductus deferens is crossing over the ureter which is carrying urine to the bladder. 

At the fundus of the bladder, the ductus deferens lies superior to the seminal vesicle, where it then descends medial to the seminal vesicle, and dilates to form the ampulla of the ductus deferens. 

The ductus deferens then terminates by joining the ducts of the seminal vesicle, forming the ejaculatory ducts.

Now, the arterial blood supply of the ductus deferens comes from the artery of the ductus deferens. 

Typically, this small artery arises from the superior vesical arteries, but may arise from the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_female_reproductive_organs_of_the_pelvis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/874ohANmQzKfKX5TYF8JBJQJSp6oV5D7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the female reproductive organs of the pelvis]]></video:title><video:description><![CDATA[The female reproductive system is made up of external and internal organs. The external organs lie in an area called the vulva, and they include the labia, the clitoris, and the vaginal opening. The internal reproductive organs can be found within the pelvic cavity, and they include the ovaries, which produce the female sex cells, called oocytes, as well as sex hormones estrogen and progesterone; the uterine tubes, which carry the fertilized oocyte to the uterine cavity; the uterus, which houses the growing fetus during pregnancy; and the vagina, which is involved both in intercourse and fetal delivery. 

Now, the ovaries, uterine tubes, and uterus lie within the pelvis and are covered by a double sheet of peritoneum called the broad ligament. This extends from the sides of the uterus to the lateral wall and floor of the pelvis. To visualize the broad ligament, imagine yourself standing with your arms outstretched holding a ball in each hand, your body is the uterus, your arms are the uterine tubes and the balls are the ovaries. Now, a sheet is draped over you and this sheet represents the peritoneum. You can see now how the broad ligament of the uterus is a double fold. Now the broad ligament has three mesenteries; the mesovarium which is associated with the ovaries, the mesosalpinx which covers the uterine tubes and mesometrium which covers the uterus. 

Let’s now look at each of the organs of the female reproductive system starting with the ovaries. The ovaries are the site of egg production, or oogenesis, and also release progesterone and estrogen during the different phases of the menstrual cycle. The ovaries usually sit near the lateral pelvic wall where the broad ligament attaches, and are suspended by a subdivision of the broad ligament called the mesovarium and the suspensory ligament of the ovary, which is a continuation of the mesovarium. 

The ovarian vessels, nerves, and lymphatics pass through this ligament to enter or exit the superolateral ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_perineum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d13MTHzmRFaJHyqsmgTqfm2pT96xtmZH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the perineum]]></video:title><video:description><![CDATA[The perineum is a diamond shaped area and a shallow chamber of the pelvis that lies below the pelvic diaphragm. 

At first glance it may seem like a small and insignificant area but it actually plays a key role in micturition, defecation, intercourse, and delivery by supporting the urinary, gastrointestinal and reproductive organs of the pelvis!

Now, let’s start with the outer surface of the perineum, called the perineal region. This region is shaped like a diamond that extends posterolaterally from the inferior surface of the pubic symphysis, to the ischial tuberosities laterally, bounded by the inferior pubic and inferior ischial rami anterolaterally. 

From the ischial tuberosities, it continues posteromedially to the sacrum and coccyx, bounded by the sacrotuberous ligaments posterolaterally. 

This diamond is divided into two triangles by an imaginary transverse line that extends from the two ischial tuberosities. 

These triangles are called the urogenital triangle, which lies anteriorly, and the anal triangle, which lies posteriorly.

Now, in the middle of the imaginary line that connects the ischiopubic rami lies an irregular mass called the perineal body. 

This mass forms the central point of the perineum, and is a meeting point for many muscles, including the superficial transverse perineal muscles, deep transverse perineal muscles, levator ani, bulbopongiosus, external anal sphincter, and external urethral sphincter muscles.

Alright, now, deep to the skin of the perineal region, there’s the perineal fascia. This fascia has two layers; the superficial perineal fascia, or colle’s fascia, and the deep perineal fascia. 

The superficial perineal fascia also has two layers; a superficial fatty layer and a deep membranous layer. The superficial fatty layer differs between females and males. 

In females, the fatty layer forms the substance of the labia majora, which are the larger folds of the vulva, and the mons pubis, which is the rounded mass tha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_male_urogenital_triangle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H-IIhPK7QeGo04yYeLHVNFCQRnKuv8Zr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the male urogenital triangle]]></video:title><video:description><![CDATA[The diamond shaped perineum is divided into two triangles, the urogential triangle anteriorly and the anal triangle posteriorly. The urogenital triangle differs between males and females. In males, it contains male external genitalia and the perineal muscles. Let’s start with the male external genitalia, which includes the membranous - or intermediate - urethra, the spongy urethra, the scrotum, and the penis. 

The membranous urethra begins at the inferior surface of the prostate gland, called the apex, then it passes through the deep perineal pouch, which houses the deep perineal muscles: the deep transverse perineal muscles and the external urethral sphincter. The deep transverse perineal muscle extends from the medial surface of the ischium to the perineal body. The external urethral sphincter is a circular muscle that surrounds the membranous part of the urethra and compresses it to maintain urinary continence. The deep perineal muscles are innervated by the deep branch of the perineal nerve. 

Now, in the deep perineal pouch, posterolateral to the membranous urethra are a pair of pea-shaped glands called the bulbourethral or Cowper glands. The ducts of these glands cross the deep perineal pouch with the membranous urethra, and terminate by emptying into the proximal part of the spongy urethra. During sexual arousal, these glands secrete mucus-like secretion into the urethra. 

Finally, the membranous part of the urethra extends through the bulb of the penis where it’s continuous with the last part of the urethra, called the spongy urethra. The spongy urethra is located within the corpus spongiosum and extends through the penis to the external urethral orifice. The spongy urethra contains an expansion in the glans penis called the navicular fossa. 

Now, let’s discuss the scrotum, which is a fibromuscular sac that lies posteroinferior to the penis, and inferior to the pubic symphysis. The scrotum contains the testes and associated structures. 

Th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_female_urogenital_triangle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JxLlLkCzQRiRh2dIFhtgc7t9QMes3k51/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the female urogenital triangle]]></video:title><video:description><![CDATA[Anatomy is so much easier when we compartmentalize things! For this reason, the perineum,  can be divided into two triangles, the anterior urogenital triangle and the posterior anal triangle. 

The urogenital triangle can be further divided into a superficial pouch and a deep pouch by a layer of deep fascia called the perineal membrane. In females, the urogenital triangle houses the female external genitalia and the perineal muscles.

Let’s start with talking about the female external genitalia, also called the vulva, which includes the mons pubis, the paired labia majora, labia minora, and the clitoris. As well as deeper structures - the bulbs of the vestibule,  the greater vestibular glands, and the lesser vestibular glands. 

The mons pubis is a rounded, fatty eminence that lies anterior to the pubic symphysis, pubic tubercles, and superior pubic rami. This eminence has a coarse pubic hair that grows after puberty.

Now, from the mons pubis, two folds of skin called the labia majora arise and extend posteriorly towards the anus. These labia meet anteriorly to form the anterior commissure, and posteriorly to form the posterior commissure. 

Also, the labia majora is the termination point of the round ligament of the uterus which is the embryonic remnant of the gubernaculum in females. 

All right, now the labia majora lie on each side of a central depression called the pudendal cleft, which houses the labia minora and the vestibule of the vagina. 

The labia minora are paired hairless folds of skin that contain spongy connective tissue, erectile tissue, and many blood vessels. These labia unite posteriorly to form a fold of skin called the frenulum of the labia minora or the fourchette.  

Anteriorly, each labium divides into medial and lateral folds. The medial folds unite below the clitoris, forming a pointy extension called the frenulum of the clitoris. The lateral folds unite to form a fold of skin called the prepuce or foreskin of the clitoris. This]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Female_pelvis_and_perineum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yypbqCgMRQSqw2IFhthIn19ASve_G4eu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Female pelvis and perineum]]></video:title><video:description><![CDATA[The pelvis lies between the abdomen and the lower limbs, forming the lower part of the trunk.  It supports and contains organs of the gastrointestinal system, the urinary system, and the reproductive system. 

Furthermore, the structure and contents of the pelvis differs between biological male and biological female individuals. 

These anatomic differences are important to understand as they have large clinical implications in biological females for things such as fertility and childbirth. 

So, why don’t we make like a baby and dive into the clinical correlates of the female pelvis and perineum head first! 

Speaking of babies, as cute and adorable as they are, pregnancy and childbirth can lead to a number of complications such as the risk of perineal or pelvic floor injury. 

The pelvic floor holds the pelvic organs in a stable position, and during childbirth the pelvic floor makes every effort to support the fetal head. 

During delivery the fetal head stretches the pelvic floor, frequently resulting in injury to the perineum, levator ani, and ligaments of the pelvic viscera. 

Specifically, injury to the pubococcygeus and the puborectalis muscles of the levator ani often occur. These muscles surround and support the urethra, vagina, and anal canal. 

So injury to these muscles can lead to decreased support for the vagina, bladder, uterus, or rectum. 

Another important structure that can be damaged is the perineal body, which is the fibromuscular center point of the perineum, that serves as an attachment point for structures such as the muscles of the levator ani, fibers from the external urethral sphincter and urethrovaginal sphincter, and the external anal sphincter.  

Damage to the pelvic floor or perineal body can lead to urethral hypermobility and stress urinary incontinence, which is when drops of urine come out when intra abdominal pressure increases. 

Unfortunately, this can occur with coughing, lifting, laughing, and constipation. Also, if ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Male_pelvis_and_perineum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UHuXyorORQuvcU6dm2Ldh8SSTWaV65vb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Male pelvis and perineum]]></video:title><video:description><![CDATA[The pelvis lies between the abdomen and the lower limbs, forming the lower part of the trunk.  It supports and contains organs of the gastrointestinal system, the urinary system, and the reproductive system. 

Furthermore, the structure and contents of the pelvis differs between biological male and biological female individuals. For biological males, there are many clinical conditions that can affect the pelvis and the perineum, and we mean more than just the ones that will make you famous on Youtube or get you on America’s Funniest Home Videos. 

The pelvis is formed by the ilium, ischium, pubis, and sacrum, forming a ring of bones called the pelvic ring. Pelvic bones, like any other bone in the body, are susceptible to injury and subsequent fracture. Fractures of the pelvis usually occur following severe trauma, and this can happen through a variety of mechanisms. 

Fractures can occur in isolation, but since the pelvis is shaped like a bony ring, they tend to occur in two or more areas simultaneously, which means they’re unstable fractures. Think of trying to break a pretzel at only one point! 

Direct trauma, for example a car crash, may fracture susceptible areas such as the pubic rami, the acetabulum, the sacroiliac joints, and the ala of the ilium. Other mechanisms of injury include falling directly on one of the lower limbs, which can force the head of the femur into the pelvic cavity through the acetabulum. These different injuries can damage pelvic structures such as vessels, nerves, and viscera, resulting in a variety of clinical manifestations. 

One classic example is called an open book fracture, where there is pelvic ring disruption due to anterior widening typically at the pubic symphysis. Fracture of the medial portion of the pubic rami can lead to injury of the urinary bladder and urethra, as well as sensory damage to the anterior and medial thigh and motor weakness to the muscles supplied by the femoral nerve. 

Generally, pelvic fractur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bones_of_the_vertebral_column</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oIiszZBYS6_DnAGs1oBofAMhRFe9d1YW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bones of the vertebral column]]></video:title><video:description><![CDATA[The vertebral column, commonly referred to as the spine or spinal column, consists of 33 vertebrae organized in 5 main regions: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal.

The vertebrae come in different shapes and sizes, and they have unique features depending on their region.

Typical vertebrae have a basic structure in common, consisting of a vertebral body, a vertebral arch, and 7 processes: a spinous process, 2 transverse processes, and 2 superior and 2 inferior articular processes.

The vertebral body is the thick, cylindrical, anterior portion of the vertebra, which functions in supporting weight.

As you move down the spine the vertebral bodies become larger, as they bear more weight.

Posterior to the vertebral body, there’s the vertebral arch, which consists of two pedicles and two laminae.

The pedicles are short, thick processes that project posteriorly from the vertebral body to meet the laminae, which are two broad, flat plates of bone, that unite in the midline and complete the vertebral arch.

The space between the walls of the vertebral arch and vertebral body is called the vertebral foramen.

And when you stack all the foramina on top of each other, that forms the vertebral, or spinal, canal, which forms a protective bony case around the spinal cord.

Focusing on the 7 processes of the vertebrae, first we have the spinous process, which extends posteriorly from the midline junction of the laminae and serves as an attachment site for ligaments and muscles.

Next, the left and right transverse processes, they extend posterolaterally from the junctions of the pedicles and laminae, while also serving as important attachment sites for ligaments and muscles.

Finally we have the four articular processes. First there’s the left and right superior articular processes, which project superiorly from the junctions of the pedicles and laminae.

Next are the left and right inferior articular processes, which project inferi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Joints_of_the_vertebral_column</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yQ7WDw35SfmFqNqD0WMazx1XQH2OEehA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Joints of the vertebral column]]></video:title><video:description><![CDATA[The joints of the vertebral column include the joints of the vertebral bodies, the joints of the vertebral arches, the craniovertebral joints, costovertebral joints, and the sacroiliac joints. 

These joints bear the body weight when sitting or standing, and give us the flexibility to do the downward dog in yoga class.    

Let’s start with the joints of the vertebral bodies, which are symphyses or secondary cartilaginous joints - that aid in weight-bearing and provide strength to the vertebral column. 

The articulating surfaces of adjacent vertebral bodies attach to each other by fibrocartilaginous discs called intervertebral discs or IV discs for short, in addition to numerous ligaments. 

The intervertebral discs function as shock absorbers between adjacent vertebrae. 

They also allow for limited movement between adjacent vertebrae, and while the movement between any two vertebrae is minor, the summation of those limited movements throughout the entirety of the vertebral column allow for the large movements of our spine. 

The intervertebral discs consist of two distinct parts, a thick, tough, fibrous outer ring called the anulus fibrosus and a soft gelatinous core called the nucleus pulposus which the anulus fibrosus surrounds. 

The anulus fibrosus is made up of circular layers of fibrocartilage, which  allows the discs to withstand compression. 

Now, the nucleus pulposus provides both flexibility and resilience to the intervertebral discs, where the gelatinous core allows the discs to absorb shock when they’re compressed by vertical forces. 

The nucleus pulposus is avascular, receiving blood via diffusion from vessels at the periphery of the anulus fibrosus and vertebral body.

Now, intervertebral discs are named based on the two vertebrae they lie between. 

For example, the C2-C3 disc is the disc between the C2 and C3 vertebral bodies.

There are 23 intervertebral discs, starting from the C2-C3 disc all the way down to the L5-S1 disc. 

In]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vessels_and_nerves_of_the_vertebral_column</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b0HWIbcRRQy9f2VYesjGYIN2Qca2Vehz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vessels and nerves of the vertebral column]]></video:title><video:description><![CDATA[The vertebral column is important for protecting the spinal cord, as well as providing structural support, flexibility, and range of motion to our bodies. To maintain all of these important functions, our vertebral column requires an adequate blood supply and innervation. 

Alright, let’s start with the arteries of the vertebrae, which arise from various larger, parent arteries depending on the level of the vertebral column. 

In the neck, parent arteries include the vertebral and ascending cervical arteries; In the thorax, the posterior intercostal arteries; 

In the abdomen, they include the subcostal and lumbar arteries. And finally, in the pelvis, parent arteries include the iliolumbar, lateral sacral, and median sacral arteries. 

Now, as these parent arteries cross the external surfaces of the vertebrae, they give rise to  periosteal, equatorial, and spinal branches that directly supply the vertebrae. 

Periosteal branches supply the periosteum, which is a dense layer of connective tissue that surrounds the vertebrae. The equatorial branches supply the vertebral bodies themselves. 

Spinal branches pass through the intervertebral foramina and divide into smaller anterior and posterior vertebral canal branches. 

Anterior vertebral canal branches follow the surface of the vertebral body anteriorly within the vertebral canal. Here, these arteries send nutrient branches that supply the red marrow of the vertebral body. 

Posterior vertebral canal branches follow the vertebral arch posteriorly within the vertebral canal. These branches terminate as radicular arteries that supply the nerve roots, and segmental medullary arteries that supply the spinal cord. 

Finally, both of these branches give rise to ascending,and descending branches that anastomose with spinal canal branches of adjacent levels.

Venous blood drains from the vertebral column through spinal, basivertebral, and intervertebral veins. 

Let’s start with spinal veins, which form plexuses al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscles_of_the_back</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E8iUoeDPT5Ga8wvJvzxSaF17T-mDRvVC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscles of the back]]></video:title><video:description><![CDATA[Here at Osmosis, we support each other - we’ve got each other’s backs. And it turns out, our backs support all of us! Let’s look at the muscles of the back that help maintain our posture and also provide movements of the trunk and upper limb.

The muscles of the back are divided into two major groups: the extrinsic back muscles and the intrinsic back muscles. The extrinsic back muscles include the superficial back muscles, which produce and control upper limb movements, and the intermediate back muscles, which are thought to be involved in respiratory movements. 

The superficial extrinsic back muscles include the trapezius, latissimus dorsi, levator scapulae, and the two rhomboids - rhomboid major and rhomboid minor. 

All these muscles are posterior axioappendicular muscles, which connect the axial skeleton, primarily the vertebral column, to the superior appendicular skeleton, specifically  the pectoral girdle and the humerus. 

The posterior axioappendicular group is divided into two subgroups. The first subgroup consists of two superficial muscles: the trapezius and latissimus dorsi. 

The trapezius is a large triangular muscle that covers the posterior aspect of the neck and the superior half of the back. There are two trapezius muscles in the back, which when seen together, look like a trapezium. 

Proximally, the trapezius originates on the medial third of the superior nuchal line, the external occipital protuberance, the nuchal ligament, and the spinous processes of the C7 to T12 vertebrae. 

Distally, the trapezius inserts on the lateral third of the clavicle, the acromion, and the spine of the scapula. Based on the orientation of its fibers, the trapezius is divided into the descending - or superior - part, the middle part, and the ascending - or inferior - part. 

Contraction of the descending part results in elevation of the scapula, like when shrugging the shoulders. Contraction of the middle part retracts the scapula, and contraction of the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_suboccipital_region</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/phuHLOOoTeG0UAw0yPxZxNVPRHuzEhnD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the suboccipital region]]></video:title><video:description><![CDATA[You may think of the suboccipital region as just ‘the back of the head.’ However, there’s more to it than meets the eye! This region is home to several muscles that assist in various head and neck movements, as well as the vessels and nerves that nourish them. 

The suboccipital region is actually a pyramid shaped muscle compartment located inferior to the external occipital protuberance and deep to the superior part of the posterior cervical region, underlying the trapezius, sternocleidomastoid, splenius, and semispinalis capitis muscles. 

This region has four small paired muscles of which three of them form the boundaries of an area known as the suboccipital triangle. 

Superomedially, the suboccipital triangle is bounded by the rectus capitis posterior major muscle; superolaterally by the obliquus capitis superior muscle and inferolaterally by the obliquus capitis inferior muscle. 

The floor of the suboccipital triangle is formed by the posterior atlanto-occipital membrane and the posterior arch of the atlas, while its roof is formed by the semispinalis capitis muscle. The main inhabitants of the suboccipital triangle are the vertebral artery and the suboccipital nerve. 

Now, let’s take a closer look at the muscles of the suboccipital region. There are four suboccipital muscles which lie deep to the semispinalis capitis muscle. 

First,  there’s the rectus capitis posterior major, which originates on the spinous process of the axis or C2 vertebra and inserts on the lateral part of the inferior nuchal line of the occipital bone. 

Second, there’s the rectus capitis posterior minor muscle, which originates on the posterior tubercle of the posterior arch of the atlas or C1 vertebra. Then it goes on to insert on the medial part of the inferior nuchal line of the occipital bone. 

Third, there’s the obliquus capitis inferior, which originates on the spinous process of the axis - or C2 and inserts on the transverse process of the atlas. 

And finally, the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_vertebral_canal</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rE2OxDLaTQ2KJ8GfAbnl6ONYSkehLWst/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the vertebral canal]]></video:title><video:description><![CDATA[When they say to watch your back, you really should, because there is something pretty important in there called the spinal cord. Now, if you think of a nerve as a road, then the spinal cord is a huge highway. 

It’s a major reflex center and holds many neural tracts that connect the brain to the rest of the body, allowing for important communication to occur. 

The spinal cord starts at the foramen magnum, where it is  continuous with the medulla oblongata, which is the most caudal portion of the brainstem. 

It then extends inferiorly through the vertebral canal.  In adults, it usually ends at the level of the first or second lumbar vertebra. 

In infants, it usually ends at the second or third lumbar vertebra. The tapered end of the spinal cord is called the conus medullaris. 

If we look at a transverse section of the spinal cord, we can see the anterior median fissure that extends along the midline of the spinal cord, anteriorly. Similarly, the posterior median sulcus extends along the midline of the spinal cord, posteriorly. 

The spinal cord can be divided into spinal cord segments. One spinal cord segment gives rise to the anterior and the posterior nerve roots, which come together to form a spinal nerve on each side of the spinal cord. 

There are 31 spinal cord segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. A spinal nerve pair shares its name with the spinal cord segment it arises from. 

So for example, the spinal nerves arising from the C1 spinal cord segment are named the C1 spinal nerves. Logically, the number of paired spinal nerves is the same as the number of spinal cord segments. 

Now, not all regions of the spinal cord are the same size. There are two regions that carry more fibers and are therefore wider, resulting in two spinal cord enlargements. 

The cervical enlargement spans the C4 through T1 segments. The anterior rami of the spinal nerves that arise from most of these segments form the brachial plex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_ascending_spinal_cord_pathways</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fuLkOELjSsaXgm_A4oQU_-u0RquGx16L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the ascending spinal cord pathways]]></video:title><video:description><![CDATA[The spinal cord is like a highway that enables a two-way communication between the brain and other parts of the body. It contains neural pathways, called spinal cord pathways, or simply spinal tracts, which can be either ascending or descending. Both types of tracts are made up of neuronal axons that gather into long columns called funiculi, which are found inside the ventral, lateral and dorsal aspects of the spinal cord. Here, we’ll focus on the ascending tracts, which are sensory pathways, carrying sensory information from the body, like pain, up the spinal cord to the brain. 

Now, let’s start by looking at the anatomy of the spinal cord. Anteriorly, there is a deep midline depression called the ventral median fissure and, posteriorly, there is a more shallow midline depression called the dorsal median sulcus. ​​Each half also has a ventrolateral sulcus, where ventral rootlets leave the spinal cord; and a dorsolateral sulcus, where dorsal rootlets enter the spinal cord. The ventral and dorsal rootlets fuse to form the ventral and dorsal roots, respectively. 

Ventral rootlets and roots carry motor fibers that travel from the spinal cord to different organs and muscles, while their dorsal counterparts - with a sensory ganglion, called the dorsal root ganglion, attached to each dorsal root - carry sensory fibers from organs and receptors throughout the body to the spinal cord. 

Now, on a transverse section, the spinal cord has an area of gray matter shaped like a capital “H” in the middle. The gray matter is subdivided into the gray commissure, which is the strip connecting the two halves of the spinal cord that surrounds the central canal; and the peripheral regions known as horns. 

There are two ventral, and two dorsal horns. Dorsal horns contain neuronal cell bodies that process information received from sensory fibers, entering the spinal cord from the dorsal roots and dorsal rootlets. On the other hand, the ventral horns contain cell bodies of mot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Bones,_joints_and_muscles_of_the_back</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AYPGRuhnQP2rZVb0M7-KIyZfQvScj9S8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Bones, joints and muscles of the back]]></video:title><video:description><![CDATA[The vertebral column is a very complex boney structure with numerous articulating joints and multiple muscles that support it and the vertebral canal. As with any part of our body, all of these structures are prone to injury. If you aren’t familiar yet with what type of injuries, don’t worry, we got your back!

Let’s start with fractures involving the C1 vertebra, or atlas. These fractures are also called Jefferson or burst fractures. As you might remember, C1 is a ring shaped bone that has paired wedge shaped lateral masses connected by thin anterior and posterior arches and a transverse ligament. The C1 vertebra sustains the weight of the cranium, kind of like how the God Atlas of Greek mythology bore the weight of the world on his shoulders.

Now, because the taller side of the lateral mass is directed laterally, when there are vertical forces that compress the lateral masses between the occipital condyles above, and the C2 or axis below, this compressive force drives the two lateral masses of the C1 vertebrae apart, which can lead to fractures in one or both of the anterior or posterior arches. A classic example of this is striking the bottom of the pool with the top of your head when diving. If the force is really strong, it could even rupture the transverse ligament. 

The Jefferson fracture doesn’t necessarily lead to spinal cord injury. This is because the diameter of the vertebral ring actually increases. However, spinal cord injury could happen if the transverse ligament ruptures as well, potentially resulting in the dens of the C2 vertebra, or the odontoid process, compressing on the spinal cord which we will get to shortly.

On a CT-scan, a C1 fracture looks something like this. You can see where the bone has been broken and how the lateral mass shifts laterally. Moving on, the C2 vertebra, or the axis, can also be fractured. C2 is called the axis because it has a bony protrusion called the dens of the axis that fits within the atlas ring,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Vertebral_canal</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fihg6twhQYyXLOU_UqCLboHxTkya-T5D/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Vertebral canal]]></video:title><video:description><![CDATA[Our spinal cord is protected by a strong vertebral canal; however, it’s still vulnerable to a variety of clinical conditions. Being able to recognize and identify these clinical conditions can help us understand the functional deficits that coincide with those conditions, and ultimately allow us to treat them. 

The spinal cord transmits information from both motor neuron branches and sensory neuron branches between the brain and the rest of the body. 

One way we can test whether there is injury to the spinal cord and disruption of these neuronal pathways is eliciting the autonomic tendon reflexes, you know, when the doctor hits your knee with a tendon hammer you automatically kick him? 

This occurs because when you hit the tendon with a tendon hammer, stretch receptors in the muscle tendon send afferent impulses to the spinal cord, through their cell bodies in the dorsal root ganglion, which synapse with alpha motor neurons in the anterior horn. 

These alpha motor neurons then transmit an automatic efferent signal back to the muscle leading to a contraction in the muscle. 

All you have to do is locate the muscle tendon, get the individual to fully relax the muscle, and strike the tendon with a tendon hammer. Testing tendon reflexes can give important information about a patient’s condition. 

Eliciting testing tendon reflexes can tell us if there is damage to a particular nerve route, to an area of the spinal cord or brain, or the general state of a patient’s entire peripheral nervous system which can be affected in things such as diabetes and motor neuron disease. 

Testing tendon reflexes can also help us to determine different myotome levels that may be affected during nerve dysfunction. 

Now remember, a myotome is a group of muscles innervated by a single spinal level, however it is difficult to test a single myotome as each muscle is innervated by multiple spinal levels. 

Therefore, clinically when we test tendon reflexes we are gaini]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Spinal_cord_pathways</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HhDXR_7ERYS4pwjloSD1o77KTSSH-xcL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Spinal cord pathways]]></video:title><video:description><![CDATA[The spinal cord is made up of millions of neurons, whose axons and cell bodies are constantly transmitting information between our brain and the rest of our body. 

In doing so, the spinal cord acts as an amazing information highway, allowing our brain and body to work together to interact with the world around us! 

But what happens when this information highway is disrupted or damaged? Well, injury to the spinal cord leads to a variety of classic clinical conditions with predictable deficits which we will explore in this video, so let’s get to it! 

Okay, before we move on to spinal cord injuries, let’s freshen up our knowledge of the spinal cord itself. Zooming in on a cross-section of the spinal cord, it’s made up of both grey and white matter.  

Grey matter is found in the centre of the spinal cord and has two dorsal or posterior horns that contain sensory neuron cell bodies, and two ventral or anterior horns that contain motor neuron cell bodies. 

Surrounding the grey matter is white matter, which consists of the axons of various neurons. They are organized into tracts that carry information to and from the brain. 

There are four main sensory pathways ascending the spinal column. First, there’s the spinothalamic tract which is divided into two parts. 

The lateral tract carries sensory information for pain and temperature, while the anterior tract carries information for crude touch and pressure. 

Next, there are two dorsal column tracts: the fasciculus gracilis which carries sensory information from the lower trunk and legs, and the fasciculus cuneatus which carries sensory information from the upper trunk and arms. 

These tracts both carry sensations such as two point discrimination, vibration, fine touch and proprioception. Then, there’ s the spinocerebellar tract which has an anterior and posterior part. 

These are ascending pathways from the spinal cord to the cerebellum, and carry proprioceptive information from the body. 

Finally, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Hip,_gluteal_region_and_thigh</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3AA2cLJBTIqHUImiww96PSdDShWnC4EV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Hip, gluteal region and thigh]]></video:title><video:description><![CDATA[At osmosis, we are not too sure where the phrase ‘break a leg’ comes from, but we are pretty sure it is not meant to be taken literally. In this video, we are going to discuss the anatomy behind the clinical conditions affecting the hip, gluteal region, and thigh, and we hope you won&amp;#39;t even break a sweat learning these conditions, let alone a leg!

Let’s start with femoral neck fractures, often simply called hip fractures. They can be classified as intracapsular or extracapsular fractures based on their anatomic location. Intracapsular fractures occur in the region of the femoral head and neck within the joint capsule of the hip, while extracapsular fractures occur outside the fibrous joint capsule, anywhere in the intertrochanteric or subtrochanteric area of the femur. 

Hip fractures are typically caused by mechanical falls or a trauma such as a car crash. And while they can affect anyone, they’re more likely to occur in the eldery, because of associated conditions such as osteoporosis, or Vitamin D and calcium deficiency. The classic presentation of a hip fracture is an individual who presents after a fall, and has an acutely shortened, externally rotated leg on physical examination compared to the contralateral side. This is due to the attachment points and pull of the iliopsoas and gluteus muscles. Other clinical features of a hip fracture include hip or back pain; joint deformity; and inability to bear weight. 

Intracapsular fractures are at risk of avascular necrosis and displacement of the femoral head, whereas extracapsular fractures are less likely to undergo avascular necrosis. See, with an intracapsular hip fracture, the retinacular arteries, branching mainly from the medial circumflex femoral arteries are disrupted, resulting in potential avascular necrosis to the femoral head as the artery within the ligament to the head of the femur isn’t able to ensure adequate blood supply on its own. Conversely, with ext]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Knee</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7M80Tb_KQjqXQoCGq6BSnvFCQC_nsAqq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Knee]]></video:title><video:description><![CDATA[The knee is one of the most complex joints in the human body, and along with the rest of the lower limb there are numerous ligamentous, muscular, and bony structures that are prone to injury. Oftentimes we can injure many of these structures at the same time, but injury to even one of these structures can affect how we walk, dance, or exercise. This video will go over all the relevant anatomy you ‘kneed’ to know in order to understand the clinical conditions affecting the knee. 

First up, let’s discuss the Q angle - where “Q” stands for quadriceps. The Q angle is the angle measured between the femur and the tibia. 

This angle is created by the femur’s diagonal placement within the thigh and by the tibia’s vertical placement in the leg. This angle is typically below 20 degrees and on average is higher in biologic females, and a normal Q angle allows the weight supported by the knee joint to be centered through the middle of the knee, in the knee’s intercondylar region.

When the Q angle increases over the normal range, it can lead to genu valgum or knock knees. With genu valgum, the increase in Q angle shifts the weight bearing center to the lateral compartment of the knee, which increases the quadriceps lateral pull and causes the medial collateral ligament to overstretch. This can cause joint misalignment and a predisposition for articular degeneration in the lateral compartment of the knee and subsequent gait abnormalities. 

To remember the knock knee appearance of genu valgum, think of the ‘g’ as standing for ‘gum’ sticking the knees together! 

Alternatively, when the Q angle is below normal range, a genu varum alignment can occur where the legs angulate away from the midline and create a bow legged appearance. This results in the weight bearing center being shifted through the medial compartment of the knee, stretching the lateral capsule lateral collateral ligament. So this time, there’s joint misalignment and a predisposition to ar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_axilla</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Bbta2LFPSMCRGZDKqSY_LiMIQzy62QHU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the axilla]]></video:title><video:description><![CDATA[I know what you’re thinking: Isn’t the axilla just a fancy name for the armpit?! Well, besides the axilla being notoriously ticklish, it’s also where many important neurovascular structures enter and exit to reach their target locations. 

Think of it like a train station, with many trains passing through enroute to delivering electrochemical signals, blood, and lymphatics to their appropriate destinations. 

Now, let’s start with the boundaries of the axilla. The axilla is located at the junction of the arm and thorax, and connects superiorly to the neck, anteriorly to the pectoral region, inferolaterally to the upper limb, and inferomedially to the thoracic wall. 

The axilla is shaped like a pyramid that has an apex, a base, and four walls. The apex of the axilla is also called the cervico-axillary canal, which is the door between the neck and the axilla. 

The cervico-axillary canal is bounded by the first rib, clavicle, and superior edge of the scapula. The base of the axilla is formed by skin, subcutaneous tissue, and axillary fascia, and forms what is called the axillary fossa, or what we know as the armpit. 

Moving on to the four walls of the axilla, the anterior wall is made up by two muscles: the pectoralis major and pectoralis minor. 

The inferior-most aspect of the anterior wall is called the anterior axillary fold, and it’s formed by the pectoralis major. 

The posterior wall of the axillary is formed mainly by the scapula and overlying subscapularis muscle. 

The inferior aspect of the posterior wall is formed by the teres major and latissimus dorsi muscles, inferiorly forming the posterior axillary fold. The medial wall is formed by serratus anterior muscle that overlies the 1st-4th ribs and intercostal muscles. Finally, the lateral wall is a bony wall formed by the intertubercular sulcus of the humerus. 

Let’s move on to the contents of the axilla. Right below the skin, there’s a lot of fat and connective tissue. If you dissect deeper, y]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_pectoral_and_scapular_regions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1upl4YQFTD_fqTTsCdwMtaX-QnmyzO7M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the pectoral and scapular regions]]></video:title><video:description><![CDATA[The pectoral and scapular regions consist of various structures that include muscles, blood vessels, and nerves; which all act together to make our upper limbs functional. The muscles of the pectoral region are divided into groups based on their locations.

There are axio-appendicular muscles, which extend between the axial and appendicular skeletons; and the scapulohumeral muscles, which specifically connect the scapula to the humerus.

First, let’s take a look at the axio-appendicular muscles, which are divided into two large groups: the anterior and posterior groups of muscles.

The anterior axio-appendicular group is composed of four muscles: the pectoralis major, pectoralis minor, the subclavius, and the serratus anterior.

The pectoralis major is a relatively flat, fan shaped muscle, which covers the upper half of the thorax.

This muscle has two proximal attachments also called heads. The first one is the clavicular head, which attaches proximally to the medial half of the clavicle.

Below it, there’s another much larger part called the sternocostal head, which attaches proximally to the anterior surface of the sternum and the superior six costal cartilages.

Both the clavicular and the sternocostal heads converge distally and then attach to the lateral lip of the intertubercular groove of the humerus.

Superolaterally, the clavicular head of the pectoralis major lies adjacent to the deltoid muscle.

These muscles don’t come completely together, thus creating a narrow gap between them that’s called the deltopectoral groove, which is where the cephalic vein passes.

Additionally, inferolaterally, the sternocostal head of the pectoralis major twists and forms the anterior axillary fold.

The pectoralis major muscle is innervated by two nerves: the lateral pectoral nerve and the medial pectoral nerve.

The lateral pectoral nerve receives fibers from the anterior rami of C5, C6, and C7; and the medial pectoral nerve receives fibers from t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fascia_and_spaces_of_the_neck</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/90z3-j0OTNK4BhsDP8D62xO0QVeQrLsX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fascia and spaces of the neck]]></video:title><video:description><![CDATA[The structures found in the neck are surrounded by a layer of subcutaneous tissue called the superficial fascia, while there are also layers of deep cervical fascia which distribute the structures in the neck into different compartments. 

These fascial layers create different anatomical spaces in the neck, and dictate where an infection may spread if it starts in one of these compartments. 

So, let’s take a look at the different fascia layers of the neck. You can think of fascia as a pair of thin stockings made of connective tissue that support and bind together different parts of the body, including the neck. 

Now, the neck actually has two pairs of stockings on top of each other: the superficial fascia, which sits right underneath our skin, and the deep fascia, which is deep to or beneath the superficial fascia, and it surrounds muscles and viscera organizing them into compartments. 

Ok, so the superficial cervical fascia or the cervical subcutaneous tissue is a layer of fatty connective tissue that lies between the skin and the most superficial layer of deep cervical fascia. 

This fascia is usually thinner than in other regions, especially anteriorly, and it contains cutaneous nerves, blood and lymphatic vessels, superficial lymph nodes and variable amounts of fat. 

Anterolaterally, it contains the platysma, which is a thin sheet of muscle that covers the anterolateral portion of the neck. Inferiorly, the platysma attaches to the deep fascia that covers the superior parts of pectoralis major and deltoid muscles, with its fibers moving superomedially over the clavicle and attaching superiorly to the inferior border of the mandible, and skin and subcutaneous tissues of the lower face. 

The anterior borders of the two platysma muscles join together over the chin and blend with the facial muscles but inferiorly, the fibers remain separated, leaving a gap anterior to the larynx and trachea. 

Deep to the platysma, there are the main cutaneous nerves o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Superficial_structures_of_the_neck:_Posterior_triangle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ywSNnCmqR76l_qrE-WizeTdmQhaD7rZh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Superficial structures of the neck: Posterior triangle]]></video:title><video:description><![CDATA[The neck is the anatomical region between the base of the cranium superiorly and the clavicles inferiorly, joining  the head to the trunk and limbs, and serving as a major conduit for structures passing between them. 

In the neck, there are superficial structures, located in the anterior and posterior triangles, and deep structures, including  the cervical viscera and prevertebral muscles. 

Now, the neck is divided into the anterior and posterior triangles mainly  by the borders of the sternocleidomastoid, or SCM, and trapezius muscles. 

Now, the SCM is a broad, strap-like muscle which has a sternal and a clavicular head. 

The sternal head is rounded and its inferior portion originates from the manubrium of the sternum, while the clavicular head is thick and its inferior portion originates from the superior surface of the medial third of the clavicle. 

The two heads of the SCM are separated inferiorly, forming a superficially visible space called the lesser supraclavicular fossa, which looks like a small triangular depression. 

Superiorly, the two heads of SCM join as they go toward the cranium and  insert on the mastoid process of the temporal bone and the superior nuchal line of the occipital bone. 

The posterior border of this muscle forms the anterior boundary of the posterior triangle. 

When the SCM contracts, it produces movement at either the craniovertebral joints, or the cervical intervertebral joints, or at both. 

So, unilateral contraction of SCM leads to lateral flexion of the neck to the same side, and also rotates the head so your face is turning superiorly towards the opposite side. 

Bilateral contraction of SCM can lead to three different movements: extension of the neck at the atlanto-occipital joint, which makes the chin rise, flexion of the neck which makes the chin approach the manubrium, and extension of the superior cervical vertebrae combined with flexion of the inferior vertebrae which makes the chin thrust forward with he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Deep_structures_of_the_neck:_Root_of_the_neck</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0Xg3uQcQR6OivABn85L4jIclTkeo8XuO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Deep structures of the neck: Root of the neck]]></video:title><video:description><![CDATA[The neck has both superficial and deep structures. But before you stick your neck out and try to guess what the deep structures are, we will just tell you. The deep structures consist of paravertebral muscles and the viscera extending through the superior thoracic aperture at the root of the neck.

When looking at the root of the neck specifically, it joins the neck and thorax, and acts like a passageway for neurovascular structures going from the thorax to the head or upper limb and vice versa. 

It’s located on the cervical side of the superior thoracic aperture, which is formed laterally by the first pair of ribs and their costal cartilages, anteriorly by the manubrium of the sternum and posteriorly by the body of T1 vertebra. 

The root of the neck contains neurovascular structures like the brachiocephalic trunk and the subclavian arteries, as well as veins such as the external and anterior jugular veins and the subclavian vein, and nerves such as the vagus nerve, phrenic nerves and the sympathetic trunks. 

Let’s look at the arteries first. The brachiocephalic trunk is the largest branch of the aorta which arises in the midline from the beginning of the arch of aorta, posterior to the sternal manubrium. 

It’s covered anteriorly by the right sternohyoid and sternothyroid muscles and passes superolaterally to the right and bifurcates posterior to the sternoclavicular joint into the right common carotid artery and right subclavian artery. Now, the right and left subclavian arteries supply each  upper limb and also send branches to the neck and brain. 

Now, while the right subclavian artery arises from the brachiocephalic trunk, the left subclavian artery arises from the arch of the aorta directly, about 1 centimeter distal to the origin of the left common carotid artery. 

Although the two subclavian arteries have different origins, they have the same course in the neck. So, they start posterior to the sternoclavicular joints on either side, and they a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_lymphatics_of_the_neck</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RiJYCLT4Q-_BTVQJaBvUn_nPRuiPxthH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the lymphatics of the neck]]></video:title><video:description><![CDATA[Whenever we go to the doctor&amp;#39;s office with what we think is a respiratory infection, they will often feel for ‘nodes’ in the neck. 

What they are feeling for are the lymph nodes in our neck, which drain the head and neck, and become enlarged when there is an infection. 

Enlarged lymph nodes can also indicate other clinical conditions such as cancers, so by understanding the anatomy of the lymph nodes in the neck and their drainage, this can help with clinical diagnosis! 

So, the lymphatics of the head and neck can be divided in two groups: a superficial group of nodes and a vertical group of deep lymph nodes. 

So, the superficial lymph nodes receive lymph from the scalp, face and neck. 

There are 8 groups of superficial lymph nodes which extend from underneath the chin to the posterior aspect of the head and they are represented by the occipital, mastoid, preauricular, parotid, submental, submandibular, buccal and superficial cervical lymph nodes. 

The occipital lymph nodes are located in the back of the head at the lateral border of the trapezius muscle and collect lymph from the occipital area of the scalp. 

The mastoid lymph nodes are also called retroauricular lymph nodes and they are located posterior to the ear. 

Specifically, they lie on the insertion of the SCM into the mastoid process, and they collect lymph from the posterior neck, upper ear and lateral scalp. 

The preauricular lymph nodes are located anterior to the auricle of the ear and collect lymph from the superficial areas of the face and temporal region. 

The parotid lymph nodes are located superficial to the parotid gland and collect lymph from the lateral side of the face and scalp. 

The submental lymph nodes are located in the submental triangle superficial to the mylohyoid muscle and collect lymph from the chin and lower lip. 

The submandibular lymph nodes are located below the mandible in the submandibular triangle and collect lymph from the face inferior to the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Bones,_fascia_and_muscles_of_the_neck</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LgV_-vGpR32Hs8IwaiHwj6N6S9SiWgoR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Bones, fascia and muscles of the neck]]></video:title><video:description><![CDATA[The neck contains many vital structures, including blood vessels, nerves, and lymphatics, as well as organs like the thyroid and parathyroid glands, parts of the airway like the larynx and trachea, and parts of the digestive tract like the pharynx and esophagus. All these structures are protected by the bones, fascia and muscles of the neck. 

The skeleton of the neck is formed by the cervical spine, the hyoid bone, the manubrium of the sternum, and the clavicles. All of these structures are prone to injuries, so hopefully learning about them in this video won&amp;#39;t be too much of a pain in the neck!  

Let&amp;#39;s get started! First, let’s look at cervical spine fractures. The cervical spine is the most flexible and mobile part of the vertebral column. But that flexibility comes with a price, making the cervical spine vulnerable to injury. Now, cervical spine fractures can be stable, meaning the spinal cord is at minimal to no risk of injury due to the fracture pattern, or unstable, meaning the spinal cord is at a much greater risk of injury due to the fracture pattern.

Let’s take a look at some important types of cervical fractures. Let’s start from the C1, or atlas, vertebra. These fractures are also called Jefferson or burst fractures. As you might remember, C1 is a ring shaped bone that has paired wedge shaped lateral masses connected by thin anterior and posterior arches and a transverse ligament. 

The C1 vertebra sustains the weight of the cranium, kind of like how the God Atlas of Greek mythology bore the weight of the world on his shoulders. Now, because the taller side of the lateral mass is directed laterally, when there are vertical forces that compress the lateral masses between the occipital condyles above, and the C2 or axis below,  this compressive force drives the two lateral masses of the C1 vertebrae apart, which can lead to fractures in either the anterior arch, the posterior arch, or both. 

A classic example of this is strik]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Vessels,_nerves_and_lymphatics_of_the_neck</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qcoCXx7YTRyM8-VKNPAUEcahTYegFFN6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Vessels, nerves and lymphatics of the neck]]></video:title><video:description><![CDATA[The neck is a compact tube, containing many vital structures such as muscles, blood vessels, nerves, and lymphatics, as well as organs of the digestive and the respiratory tract. Now, the neck is like a sheath around these structures - however, it’s still an area prone to various injuries and conditions.

First of all, let’s discuss central venous access, which is when a catheter is placed in a large vein, usually the internal jugular or the subclavian vein. A central access is usually obtained when peripheral access isn’t available, like when an individual is severely hypovolemic, for example. If a patient will need intravenous access for a long period of time for medication delivery, such as chemotherapy, then central venous access is a great option to prevent repeated peripheral IV procedures or for those certain intravenous drugs that cause damage to peripheral veins. It can be used for fluid resuscitation, blood transfusions, central venous pressure monitoring, giving medications, hemodynamic monitoring or plasmapheresis. It can also be used when emergency dialysis is needed.

So first, let’s see how we go about accessing the internal jugular vein for central access. In order to better see the anatomy and maximize the internal jugular vein’s diameter, the individual should be in Trendelenburg position, which means that their head is down at about 15 degrees compared to the rest of the body. If the catheter is placed in the right internal jugular, then the head must be turned towards the left and vice-versa. Usually, for a catheter, the right internal jugular vein is preferred, because it has a more direct path towards the superior vena cava. 

Now there are some important landmarks that we can use to help us identify the internal jugular vein. First, there’s the anterior cervical triangle, which is bordered inferiorly by the clavicle, medially by the sternal head of the sternocleidomastoid muscle and laterally by the clavicular head of the sternocleid]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Viscera_of_the_neck</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J8zcc0eDRMuV-dfOMmI8OXWkSTidRAmy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Viscera of the neck]]></video:title><video:description><![CDATA[The neck houses a number of important anatomical structures and serves as the gateway between our head and body. These structures include major blood vessels and nerves, parts of the respiratory and digestive tract, as well as important endocrine glands such as the thyroid and parathyroid glands. However, the neck is very exposed and vulnerable to injury, and all of these important structures in the neck are susceptible to a variety of clinical conditions. So take a quick moment, stretch out your neck, and let&amp;#39;s get started!

Let&amp;#39;s begin with the thyroid gland. When there is abnormal growth of the thyroid gland, it is called a goiter. When the gland gets big enough, it can be seen as a bulge in the lower part of the neck, and may even extend deep to the sternum. Causes of a goiter include iodine deficiency, autoimmune disorders such as Hashimoto’s thyroiditis and Graves disease, thyroid cancer, or a thyroid cyst. 

The thyroid gland can enlarge anteriorly, posteriorly, inferiorly, laterally, or even substernally, but it won&amp;#39;t enlarge superiorly because of the superior attachments of the overlying sternothyroid and sternohyoid muscles. 

If it enlarges, it has the potential to compress nearby structures such as the trachea, causing difficulty breathing; the esophagus, leading to difficulty swallowing; the recurrent laryngeal nerves, leading to hoarseness; as well as the jugular veins, leading to thrombosis and superior vena cava syndrome in rare cases. 

Another condition that causes swelling of the neck is a thyroglossal duct cyst, which is the most common congenital cyst in the neck. This condition occurs because during development, the thyroid gland actually develops in the floor of the embryonic pharynx in a small area identified as the foramen cecum which is found on the dorsum of the tongue. During development, the thyroid gland migrates from the tongue into the neck passing anterior to the hyoid bone through the thyrog]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscles_of_the_face_and_scalp</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J_qFzqTLSpeTnAsZDtHaLCrHQYO5ew1-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscles of the face and scalp]]></video:title><video:description><![CDATA[Humans make many different facial expressions and they are an extremely important way that we communicate. They let people know when you are happy, like after getting a good mark on an anatomy test, or curious like when you learn something new about the human body. Let’s learn about the muscles responsible for our facial expressions! 

First, let’s start with the scalp which is a layer of skin and subcutaneous tissue that covers the cranium. It extends from the supraorbital margins on the frontal bone to the superior nuchal line on the occipital bone. 

Laterally, it covers the temporal fascia and extends to the zygomatic arches on each side. The scalp is made of five layers, which can be remembered easily as the first letter of each spells out the word SCALP. 

Going in the order from superficial to deep: S stands for skin, C stands for connective tissue, A stands for aponeurosis or epicranial aponeurosis, L stands for loose connective tissue, and P stands for pericranium, which is the periosteum on the external surface of the cranium. 

The first three layers - skin, connective tissue, and the aponeurosis - are connected tightly together, forming a single unit called the scalp proper.

Muscles of facial expression, simply known as the facial muscles are found deep to the skin of the scalp, face, and neck. 

Most facial muscles are attached to bones or fascia on one end, and skin on the other, so that when they contract they create facial expressions. 

All facial muscles originate from the mesoderm of the second pharyngeal arch, along with the facial nerve. During embryological development, a muscular sheet forms and begins to spread over the scalp, face and neck which later forms the facial muscles. 

This spreading carries the branches of the nerve of the second arch with it, which is the facial nerve, or cranial nerve seven. 

So, all facial muscles are innervated by the branches of the facial nerve which are the posterior auricular, temporal, zygomat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nerves_and_vessels_of_the_face_and_scalp</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GONNjxQtRhieXODJ4TRztCieRR_zQ1F7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nerves and vessels of the face and scalp]]></video:title><video:description><![CDATA[The face contains an abundance of small muscles that work together to help us show our emotions. You can thank these muscles for everything your face does, from smiling and frowning to making funny faces in group pictures! 

Naturally, for these muscles to work, there are many tiny nerves, arteries, and veins that supply them. Let’s start off with the sensory innervation of the face. 

Almost all of its sensory innervation is provided by the fifth cranial nerve, also known as the trigeminal nerve, which has three divisions. 

Its superior division is known as the ophthalmic nerve, and it provides sensory innervation for the part of the scalp anterior to the vertex of the head, the forehead, the upper eyelids, the dorsum of the nose and the roof of the nasal cavity. 

The ophthalmic nerve arises from the trigeminal ganglion, leaves the skull through the superior orbital fissure, and enters the orbit, where it gives rise to three branches; the frontal nerve, the nasociliary nerve and the lacrimal nerve. 

So let’s look at them one by one! The frontal nerve runs across the roof of the orbit, and it gives rise to the supraorbital and the supratrochlear nerves. 

The supraorbital nerve exits the orbit through the supraorbital notch and supplies the skin of the anterior part of the scalp, the anterolateral forehead, and the middle of the upper eyelids. 

The supratrochlear nerve exits the orbit lateral to the trochlea and supplies the skin of the anteromedial forehead. 

Next is the nasociliary nerve, which divides into the anterior ethmoidal, the posterior ethmoidal, and the infratrochlear nerves. 

The anterior ethmoidal nerve travels a long way through the nasal cavity, and exits between the nasal bone and the lateral nasal cartilage as the external nasal nerve. 

It supplies sensory innervation to the skin of the dorsum of the nose, the nasal ala, and the nasal vestibule. So, whenever the tip of your nose feels itchy, you know it’s that pesky external nasal ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_infratemporal_fossa</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j1leGkrmQS_QyS4n1lZgzOK-TEqrEbit/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the infratemporal fossa]]></video:title><video:description><![CDATA[The infratemporal fossa, or IT fossa for short, is one of the most important spaces in the head, which acts as a conduit for neurovascular structures entering and exiting the cranial cavity. It contains vital structures such as the maxillary artery and mandibular nerve. 

The infratemporal fossa is an irregularly shaped space located deep and inferior to the zygomatic arch, deep to the ramus of the mandible, and posterior to the maxilla. 

More specifically, the fossa is bounded laterally by the the ramus of the mandible; medially by the lateral pterygoid plate; anteriorly by the posterior surface of the maxilla; posteriorly by the tympanic plate and the temporal bone’s mastoid and styloid processes; superiorly by the inferior surface of the greater wing of the sphenoid, and inferiorly by the attachment of the medial pterygoid muscle close to the angle of the mandible. 

Now, the important structures within the infratemporal fossa include muscles, vessels and nerves. 

The muscles of the infratemporal fossa include the inferior portion of the temporalis muscle, the medial pterygoid and lateral pterygoid muscles. 

Lying either superficial or deep to the lateral pterygoid muscle, there’s the pterygoid venous plexus and the maxillary artery. 

Deep to the lateral pterygoid, the otic ganglion and mandibular nerve or cranial nerve V3  are located inferior to the foramen ovale. 

The mandibular nerve splits within the infratemporal fossa into branches that include the inferior alveolar, auriculotemporal, lingual, buccal, masseteric, and deep temporal nerves. 

Within the infratemporal fossa we also see the chorda tympani nerve, which is actually a branch or cranial nerve seven.

Now let’s take a more in depth look at the different structures within the infratemporal fossa, starting with the vessels. 

First up, the maxillary artery! This artery branches off from the external carotid artery, posterior to the neck of the mandible. 

Then, it courses either deep t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_temporomandibular_joint_and_muscles_of_mastication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ldi8-v0URdu_9jgGu1PyvhvoRBWfrRPd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the temporomandibular joint and muscles of mastication]]></video:title><video:description><![CDATA[Anatomy of the temporomandibular joint and muscles of mastication

Getting into medical school must have been a jaw-dropping moment, but have you ever wondered how it is that your jaw didn’t fall off? You can thank the temporomandibular joint for that!

Now, the temporomandibular joint is a modified synovial hinge joint. So first, just like a hinge joint, it allows for flexion and extension, which translate to elevation…….and depression of the jaw, respectively. Additionally, the TMJ also allows for gliding and rotation. 

The articular components of this joint include the mandibular fossa and the articular tubercle of the temporal bone as the superior surface, and the head of the mandible as the inferior surface. 

Unlike your average hinge joint, the articular surfaces don’t make direct contact here. They are separated by an articular disc, which is attached to the inner surface of the joint&amp;#39;s fibrous capsule. 

The articular disc divides the joint into two parts: the superior articular cavity, which allows the mandible to glide causing protrusion…….and retrusion, and the inferior articular cavity, which allows the hinge movements, elevation or closing of the jaw and depression or opening of the jaw, as well as rotational movements. 

With all of these movements at the temporomandibular joint, there needs to be strong surrounding support so it doesn’t become dislocated. 

This is where ligaments come in handy. The temporomandibular joint is enveloped by the joint capsule and strengthened by one intrinsic and two extrinsic ligaments. 

The intrinsic ligament, called the lateral ligament, is a thickening of the joint capsule and extends from the articular tubercle to the neck of the mandible. 

It strengthens the joint laterally and helps prevent posterior dislocation. The two extrinsic ligaments are the sphenomandibular ligament and the stylomandibular ligament. 

The sphenomandibular ligament extends from the spine of the sphenoid bone to the li]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_tongue</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9De-LH5fSyObd6MhkAfjfrQURVuMBvNr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the tongue]]></video:title><video:description><![CDATA[The tongue is part of what makes these videos possible. Without it, we couldn’t speak! It is also what allows us to enjoy the taste of our favourite foods, and helps us get the occasional pesky bit of food out from between our teeth.  

Now, the tongue is essentially a mass of muscles covered by a mucous membrane, which can contract and relax quickly, allowing the tongue to assume many shapes and positions. 

This is what makes the tongue ideal for speaking by aiding sound formation. The tongue is also involved in taste via taste receptors; it pushes food into the oropharynx during swallowing; it helps with mastication by moving food closer to our teeth; and in oral cleansing.

Looking at things in more detail, the tongue takes up much more space in the mouth than you might realize. It consists of a root, a body and an apex, with the last two being highly mobile. 

The root of the tongue is posterior and slightly vertical, forming the posterior one third of the tongue. It extends from the hyoid, epiglottis, and soft palate, to the mandible. 

The body forms the anterior ⅔ of the tongue, and the apex of the tongue is the most anterior end of the body. 

The entirety of the tongue rests on the mouth’s floor both in the oral cavity and into the oropharynx, with the apex pressing against the lower incisors. 

The tongue also has two surfaces, supero-posterior and inferior, which are separated by the margin of the tongue. 

The supero-posterior surface is the larger of the two and it literally represents the “top” or dorsum of the tongue. The inferior surface or “underside” rests against the floor of the mouth. 

The dorsum of the tongue is characterized by a V-shaped groove called the terminal sulcus. 

The sulcus divides the top of the tongue transversely into a presulcal anterior part in the oral cavity and a postsulcal posterior part situated in the oropharynx. 

The V’s tip points posteriorly to something called the foramen cecum, which represents the remn]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_salivary_glands</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DOMc2U-pQTCHT7A399My-FkbSLWSvYC4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the salivary glands]]></video:title><video:description><![CDATA[Have you ever smelled something so good that your mouth begins to water? Well you can thank your salivary glands for this mouth-watering sensation. The salivary glands, while often overlooked, are a key part of our digestive system. 

There are three main pairs of salivary glands: the parotid, submandibular, and sublingual glands. There are also a few smaller companions called accessory salivary glands, which are sprinkled over the palate, lips, cheeks, tonsils, and tongue.

When it comes to function, salivary glands secrete saliva into the oral cavity. Saliva, as you may know, is a clear, tasteless, and odorless fluid that keeps the mouth’s mucosa hydrated. 

Saliva also helps lubricate food while we chew, making swallowing easier, and it also starts the digestion of starch, because it contains an enzyme called amylase. 

Saliva also acts as ‘nature’s mouthwash’, since it’s rich in antimicrobial compounds such as hydrogen peroxide to keep our mouths clean. Accessory salivary glands have a similar role, except they tend to secrete less saliva.

The parotid glands are the largest of the three paired salivary glands. Superficially, each parotid gland is triangular in shape, where it sits upon the masseter muscle. 

However, most of the parotid gland actually sits in the retromandibular fossa, anteroinferior to the external acoustic meatus, where it is wedged between the the ramus of the mandible and the mastoid process and sternocleidomastoid muscle posteriorly. 

Its apex is situated posterior to - or along - the angle of the mandible, while the base is associated with the zygomatic arch. 

The parotid gland is surrounded by a protective sheath derived from the investing layer of the deep cervical fascia called the parotid sheath. 

Now, a number of structures are closely associated with the parotid gland. First the extracranial portion of the facial nerve passes through the parotid gland and forms the parotid plexus. 

Although it is embedded within the gl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_pterygopalatine_(sphenopalatine)_fossa</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5kPlvvK7RLqwi2ZjGsL_tpnST52xC2GE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the pterygopalatine (sphenopalatine) fossa]]></video:title><video:description><![CDATA[The pterygopalatine fossa, sometimes called the sphenopalatine fossa, is a cavity in our skull that sits behind the maxilla. We are going to think of the pterygopalatine fossa as a house for sale, and talk about its design, location, neighbours, and even the furnishings it comes with.

First, let’s talk about the shape of the house. The pterygopalatine fossa is shaped like an upside down trapezoidal prism and it is situated in a prime location, just posterior to the maxilla. So right off the bat, it makes sense that it’s bounded anteriorly by the posterior aspect of the maxilla! 

Posteriorly, it’s bounded by the pterygoid process of the sphenoid. Medially, the fossa is bounded by the perpendicular plate of the palatine bone whereas laterally it opens into the pterygomaxillary fissure. 

Its roof is formed by the infratemporal surface of the greater wing of the sphenoid bone and it is incomplete as there is an opening into the inferior orbital fissure. Finally, the floor is formed by the pyramidal process of the palatine bone with an opening into the palatine canal.

This means the pterygopalatine fossa’s neighbours include the middle cranial fossa, infratemporal fossa, orbit, nasal cavity, the roof of the oral cavity, and maxillary sinus and the pharyngeal vault . 

Now, the pterygopalatine fossa communicates with its neighbors, aka surrounding structures, through many openings. First, it communicates with the middle cranial fossa through the foramen rotundum, located anteromedially on the sphenoid bone. The foramen rotundum provides passage for the maxillary nerve, which is the second main division of cranial nerve V. 

Another connection to the middle cranial fossa is through the pterygoid canal within the sphenoid bone. The canal provides passage for the nerve and artery of the pterygoid canal. 

The pterygopalatine fossa communicates with the infratemporal fossa through the pterygomaxillary fissure, which transmits the posterior superior alveolar nerv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_nose_and_paranasal_sinuses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xZZrB7xWT1aMVsK--0nXbnypTze6D_s_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the nose and paranasal sinuses]]></video:title><video:description><![CDATA[We use our sense of smell for many things, like smelling cookies baking in the oven, but we also use it to help us taste, like when we take a big bite of those cookies! 

Our sense of smell is thanks to our nose, but actually our nose does much more than just smell. It also provides a passage for air to reach the lungs, and also helps warm and filter that air before it gets down there. Now, let’s see what the nose knows!

Now, the external nose is the part that we see protruding from the midline of our face. Generally speaking, the nose has a pyramidal-shaped structure with two openings called the nares or nostrils. These openings are surrounded laterally by the alae - meaning wings - of the nose, and separated from one another medially by the nasal septum. 

Inside the nostrils is the nasal vestibule, which is lined by skin and small hairs that help filter dust particles from the air that passes through. The dorsum of the nose begins at the root, located between the eyebrows, and slopes downwards to the apex, which is the tip of the nose.

Okay, so our external nose has a skeleton that helps support its structure, made up of hyaline cartilage and bone. The hyaline cartilage is on the more anterior portion of the nose, and provides most of its structure. 

In the midline, there is the cartilaginous part of the nasal septum, or septal cartilage. Two lateral cartilages extend from either side of the dorsal aspect of the septal cartilage. Anteroinferior to these lateral cartilages are the paired alar cartilages that form the apex and part of the nares of the external nose. The alar cartilages are thin and flexible, allowing for dilation or constriction of the nares. 

The bony skeleton gives a base to the nose and includes the nasal part of the frontal bone - located at the root of the external nose - two paired nasal bones, the frontal processes of the maxillary bones, and in the midline, there is a superior and posteroinferior bony part of the nasal septum.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_external_and_middle_ear</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e9h-5WkmRzCGD53dV3BWJpq5SDWud12d/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the external and middle ear]]></video:title><video:description><![CDATA[The ear is made up of three parts: the external, middle, and inner ear. Together, these structures help process air vibrations as sound, and this helps us enjoy our favourite music, as well as alert us of potential threats. Now, while the inner ear also plays a role in balance, the main role of the external and middle ear is to transfer and amplify sound to the inner ear with the help of the three smallest bones in the body: the auditory ossicles. 

Let’s start with the external ear, which is by far the most common anatomical spot to hang earrings from. The external ear is actually a complex structure made of the auricle, also called the pinna; and the external acoustic meatus. 

Now, let’s take a closer look at the auricle, which is the part of the external ear that surrounds the opening of the external acoustic meatus, and funnels soundwaves towards the external acoustic meatus. It is made of irregularly shaped cartilage covered with skin. The elevated outer rim of the auricle is the helix. The smaller elevated rim parallel to the helix is called the antihelix. The depression in the middle of the auricle is called the concha. Right next to the concha, there’s the opening of the external acoustic meatus. Inferior to the concha, there’s the lobule of the auricle. And finally, anterior to the opening, there’s an elevation called the tragus. 

The next part of the external ear is the external acoustic meatus, which is an S-shaped canal that extends from the concha, through the temporal bone, to the tympanic membrane.  The entire canal is covered with skin, and is divided into a lateral third, made of cartilage, and a medial two-thirds, made of bone. 

Now, at the end of the external acoustic meatus, there’s the thin, oval tympanic membrane, more commonly known as the eardrum, which separates the external ear from the middle ear. When sound waves hit the tympanic membrane, it vibrates and transfers the vibration to the three auditory ossicles of the middle ea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_inner_ear</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iBAXv8FZSU2Wx6S8i-rf6xqURbaur3jG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the inner ear]]></video:title><video:description><![CDATA[How is it you can listen to your favorite song, close your eyes, dance, and not fall on your face? Well, there is a little thing called the inner ear that contains the vestibulocochlear organ which gives you the ability to perceive sounds and maintain your balance. 

The inner ear is found in the petrous part of the temporal bone between the middle ear laterally, and the internal acoustic meatus medially. It is a small and important area which houses the irregularly shaped vestibulocochlear organ, which kind of looks like a snail shell attached to a few bony rings. 

Now, the inner ear contains the bony labyrinth and the membranous labyrinth. The bony labyrinth is connected to the middle ear by two windows. The oval window is found on the lateral wall of the vestibule and is covered by the base of the stapes, while the round window is found at the base of the cochlea and is covered by the secondary tympanic membrane. 

The bony labyrinth, within the otic capsule, is filled with perilymph and is made of a series of cavities which are the vestibule, the semicircular canals, and the cochlea. Suspended within the bony labyrinth, there’s the membranous labyrinth, which is basically a series of sacs and ducts filled with endolymph. 

The membranous labyrinth is organized into the utricle and saccule within the vestibule, the three semicircular ducts and their membranous ampullae, and the cochlear duct within the cochlea. 

Let’s take a look at the structures responsible for balance, which are the semicircular canals, on the one hand, and the utricle and saccule, on the other hand. There are three semicircular canals, an anterior, posterior, and lateral canal, oriented in the three different planes of space. 

Each canal contains a dilated end called the ampulla that contains an area of sensory epithelium called the ampullary crest. This is lined with tiny hair cells that pick up information about rotational movements of the head in the plane of the duct within w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Skull,_face_and_scalp</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P4U4wE-zQMqCJuySxB_t73GkTeu4QAWU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Skull, face and scalp]]></video:title><video:description><![CDATA[The head is one of the most complex parts of our body. Besides having an abundance of muscles, nerves and blood vessels, it protects our brain and houses various facial structures. In this video, we’ll go through a variety of conditions that can affect the skull, face, and scalp. This might not be the easiest subject to learn about, but you’ll see that it’s nothing to get a headache over! 

First, let’s discuss the bones of the skull that make up the cranial vault, which as a group are also called the calvaria. We’ll start from the very beginning of their development. See, the flat bones that make up the skulls of neonates have gaps between them and these gaps are covered by fibrous membranes. These membrane-covered gaps between the bones are called fontanelles. The anterior fontanelle is a large diamond-shaped area found at the junction of the sagittal suture, coronal sutures and frontal suture.  

In adults, this point where the sutures eventually come together is called the bregma. The anterior fontanelle is bordered by the frontal bone anteriorly and two parietal bones posteriorly.  By 18 months of age, the bones fuse together and the anterior fontanelle closes. The posterior fontanelle is a triangular shaped membrane found at the junction of the lambdoid sutures and sagittal suture. In adults, this point is called the lambda. The posterior fontanelle is bordered by the two parietal bones anteriorly and the occipital bone posteriorly. The posterior fontanelle usually closes during the first few months of life and is no longer palpable by the end of the first year.

By palpating fontanelles before they close, bone growth and development of the skull can be assessed. How fontanelles look is also important from a clinical standpoint. For example, a depressed fontanelle can indicate dehydration, while a bulging fontanelle can signal increased intracranial pressure.

Now, let’s move on to bone fractures, and to start let&amp;#39;s remember an intersection ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Temporal_regions,_oral_cavity_and_nose</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mgUvr1CDTxGygPVtbfmd4Y4uTYKuGydh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Temporal regions, oral cavity and nose]]></video:title><video:description><![CDATA[The face is made up of a large network of nerves, vessels, muscles, and other structures which are susceptible to disease. In particular, there are many clinical conditions that affect the temporal region, oral cavity, and nose. Understanding the anatomy of these areas can help us better understand the clinical presentation, complications and management of these conditions. So let’s get face to face with our… well, face! 

First up, the parotid gland. Remember that the facial nerve enters the parotid gland to form the parotid plexus and give rise to the temporal, zygomatic, buccal, marginal mandibular, and cervical branches. However, these branches don&amp;#39;t actually innervate the gland but just pass through it to exit at its borders. The auriculotemporal nerve, which is a branch of the mandibular nerve, courses superficially to the gland and is responsible for general sensation of the gland. Additionally, parasympathetic innervation from the glossopharyngeal nerve travels with the auriculotemporal nerve to innervate the parotid gland. 

Now, understanding these anatomical relationships is also important when it comes to surgery to the parotid gland, as the majority of salivary gland tumors occur within the parotid gland which are often surgically removed. During parotid gland surgery, the surgeon needs to identify, dissect, and isolate the facial nerve and its branches with great care, so that there’s no damage to them. See, if the nerve or one of its branches is damaged, that causes paralysis of some or all facial muscles on that side. The auriculotemporal nerve also requires special care to avoid damaging it during surgery, because during healing the nerve can go on to reinnervate into the sweat glands of the overlying skin. So instead of salivating when eating or thinking about food, this reinnervation causes excessive sweating and redness of the cheek during the normal parasympathetic response. This condition is called Frey syndrome.

Now let’s m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_cranial_meninges_and_dural_venous_sinuses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/etHHIPV3RbC5y8ZxywICU2PfSiCw_lru/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the cranial meninges and dural venous sinuses]]></video:title><video:description><![CDATA[The brain and spinal cord are covered by the meninges, which are three layers or membranes of connective tissue that not only protect the brain and spinal cord, but also form a framework for vessels and venous sinuses. Just think of this as the brain needing three layers of blankets when going to bed at night to make sure it is extra cozy and secure! These three layers, from superficial to deep, are the dura mater, arachnoid mater, and pia mater. 

The dura mater is a tough, thick, fibrous external meningeal layer. Deep to the dura mater is the thin arachnoid mater. The dura and arachnoid mater are separated from each other by a potential space called the subdural space. Deep to the arachnoid mater is the pia mater. The pia mater is a delicate vascular layer that is intimately adhered to the brain, covering the gyri and extending along the different sulci and fissures. Together, the arachnoid and pia mater are collectively known as the leptomeninges. Between the arachnoid mater and pia mater is the subarachnoid space, also known as the leptomeningeal space, which is a true space between the arachnoid and pia mater which contains cerebrospinal fluid or CSF for short, as well as major vessels, and cranial nerves. 

Okay, let&amp;#39;s dive in and take a closer look at the dura mater, which is the thickest, outermost meningeal layer. The dura mater itself is further divided into two layers. 

The first, more superficial, layer is called the endosteal layer, or periosteal layer of the dura mater. It is located on the interior surface of the skull bones and ends at the foramen magnum. The endosteal layer does not continue with the dura mater of the spinal cord, but instead becomes continuous with the periosteum on the external aspect of the skull bones. Between the endosteal layer of the dura mater and the skull bones, there lies a potential space called the extradural, or epidural space, which is not a natural space, but may become a pathological space during]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_ventricular_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PhY_5y52RKmKL8AtnKoTbTncREOeUc45/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the ventricular system]]></video:title><video:description><![CDATA[An adult human brain weighs about 1.5 kgs, but we don’t really feel it weighing us down! 

That’s because the brain is cushioned by cerebrospinal fluid or CSF, which can be found within brain cavities called ventricles. 

These cavities are involved in the production, transport and removal of CSF, and they are connected to each other. So, as a whole they are often referred to as the ventricular system of the brain.

CSF doesn’t only fill the ventricles, but also the subarachnoid space, which surrounds the brain and spinal cord. This way, CSF cushions and protects the brain from head trauma, and it also provides buoyancy so that the brain doesn’t compress blood vessels and cranial nerve roots against the cranium. It also provides protection against sudden intracranial pressure changes. 

CSF can also transport nutrients for nervous tissue, 

as well as remove metabolic waste products. 

It can also transport hormones, and

influence the brain&amp;#39;s excitability by regulating its ionic composition.  .

Now, the ventricular system consists of four ventricles: two lateral ventricles, the third ventricle and the fourth ventricle. 

CSF flows from the lateral ventricles through the left and right interventricular foramina, also called the foramina of Monro, to the third ventricle. 

From here, it passes through the cerebral aqueduct to reach the fourth ventricle. CSF can then flow caudally into the central canal of the spinal cord. 

The fourth ventricle also has two lateral apertures, called the foramina of Luschka, 

and a median aperture, called the foramen of Magendie, both of which allow CSF to reach the subarachnoid space.

The lateral ventricles are the largest. They occupy both cerebral hemispheres, and they’re present all four lobes, This is best seen on coronal sections of the brain, 

cutting through the frontal lobe, 

the parietal lobe, and temporal lobes, 

and finally the occipital lobe. 

On a mid-sagittal section of the brain, you can see t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_cerebral_cortex</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7rA8SSMFS0Gij0bkeAPFVt7uQJqPyoaL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the cerebral cortex]]></video:title><video:description><![CDATA[Now, we know what you are thinking. Don’t worry, here at Osmosis we are not telepathic, but by watching this video on the cerebral cortex, we know you have the brain on your mind, so let’s get to it! 

The human central nervous system basically consists of the spinal cord and the brain, which includes the cerebrum, diencephalon, cerebellum, and brainstem. 

Taking a closer look at the cerebrum, it consists of two nearly symmetrical halves, called the cerebral hemispheres, and the basal ganglia, also referred to as basal nuclei. Furthermore, each cerebral hemisphere is divided into four main lobes, the frontal, parietal, temporal, and occipital, as well as what has become to be known as the fifth lobe, the insula, or insular cortex. 

If we were to cut through the cerebral hemispheres in the coronal plane, which means transecting from left to right and dividing the brain into rostral and caudal divisions, we would see the cerebral cortex. This is the outermost area of the cerebral hemispheres, and is composed of gray matter containing billions of nuclei, or neuronal cell bodies. 

A cell body and its dendrites, along with its axon and synaptic terminal, collectively make-up a structure called a neuron. Neurons thus allow for information processing and communication with other neurons within the nervous system. The gray matter gets its name from its dark appearance during gross inspection. 

Deep to the gray matter is the subcortical white matter, which is made up of myelinated axons connected to the nuclei of the gray matter. White matter gets its name because the myelination of the axons gives this area a white appearance on gross inspection. 

The largest white matter tract is the corpus callosum, which sends signals between the two cerebral hemispheres essentially connecting them together. 

Found throughout the subcortical white matter are further collections of gray matter masses containing neuronal cell bodies referred to as the basal gangli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_diencephalon</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RA7vWxT7SHGO8cURD8zIpjDQSB2ahZqa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the diencephalon]]></video:title><video:description><![CDATA[Our central nervous system is made up of the cerebrum, the cerebellum and the brainstem, which continues inferiorly with the spinal cord. The cerebrum consists of two cerebral hemispheres, which have an external cerebral cortex made up of nuclei which form the gray matter and deep to that, the white matter consisting of axons.  

Embedded within the white matter, there are the basal ganglia, or basal nuclei. Removing them reveals a part of the brain hidden between the hemispheres, called the diencephalon. Together, the cerebrum and diencephalon form the forebrain, or prosencephalon. The diencephalon connects the cerebrum superiorly with the midbrain of the brainstem inferiorly. 

On a mid-sagittal section through the brain, we can see the cavity of the third ventricle and the diencephalon around it. The two major parts of the diencephalon are the thalamus, which lies more dorsally, and the hypothalamus, which lies more ventrally.  

There are actually two thalami, one on each side, flanking the lateral aspect of the space created by the third ventricle. Between the left and right thalami there’s a bridge of gray matter that connects them, called the interthalamic adhesion, or connection. The hypothalamus forms the inferior part of the lateral wall and the floor of the third ventricle. Between the thalamus and the hypothalamus there’s the hypothalamic sulcus, which separates them. The diencephalon contains two endocrine glands as well: the posterior lobe of the pituitary gland, below the hypothalamus, and the pineal gland, near the caudal end of the thalamus. 

Okay, let’s take a closer look at the thalamus first, which is an egg-shaped structure made of gray matter that contains neuronal cell bodies. The thalamus is connected with almost all parts of the central nervous system, like the brainstem and the cerebral cortex, enabling it to influence many different processes in the brain. In fact, the thalamus is a part of almost every sensory pathway, where it]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_limbic_system</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SmT4V9rNTMynTXKeYWsRXr_lSu_qnSUT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the limbic system]]></video:title><video:description><![CDATA[The limbic system consists of several parts within the telencephalon, also known as the cerebrum; the diencephalon, which includes the thalamus and hypothalamus; and the midbrain. 

The term “limbic” means “border” in latin, so this system’s name originated from its location at the border between the telencephalon and diencephalon. 

One way to remember the limbic system is to think of the word HOME; Homeostasis, Olfaction, Memory, Emotion. 

This is because limbic system structures are involved in olfaction, or smell, in the regulation of emotions, like anger and fear, and other behaviors, like aggression and sexual behaviour. 

Memory formation and the recollection of those memories are supported by the limbic system, and It can even influence responses of the autonomic nervous system, like cardiovascular or gastrointestinal functions. 

To easily recall some of the functions, you can remember the famous 5 F’s, which are: Feeding, Fleeing, Fighting, Feeling and...Fornicating, the last one being, really, just a fancy word for Sex.

Structures that are included in the limbic system include the: hypothalamus, olfactory cortex, hippocampal formation, amygdala, subcallosal area, cingulate gyrus, parahippocampal gyrus, mammillary bodies and the basal forebrain. 

Let’s take a closer look at each of them, starting with the hippocampal formation, which is crucial for converting short-term memory into long-term memory, shipping those memories into other cortical regions for long-term storage and assisting in retrieval of memories when needed. 

It is also involved in spatial orientation, which is the ability to identify the position of our body relative to the objects around us. 

The hippocampal formation consists of the hippocampus, the dentate gyrus, subiculum and entorhinal cortex.

Now, on a mid-sagittal section of the brain, the hippocampal formation is hidden within the medial temporal lobe. 

It lies posterior to the amygdala and spreads caudally all the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_basal_ganglia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QGAVGzOpRUOYiB1wpWCElaXbQDCO48rh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the basal ganglia]]></video:title><video:description><![CDATA[Generally speaking, our central nervous system is made up of three parts; the cerebrum, the cerebellum, and the brainstem. The cerebrum consists of two nearly symmetrical halves called the cerebral hemispheres, and deep within these hemispheres lie the basal ganglia. 

On a coronal or axial section of the brain, the outermost area represents the cerebral cortex, which is made up of gray matter that consists of billions of neuronal cell bodies. The axons that are connected to these cell bodies create the white matter of the brain, which is the innermost area. 

One prominent white matter fiber bundle is the internal capsule, which is like a highway that allows signals, and thus information, to flow to and from the cerebral cortex. On both sides of the internal capsule, we can see areas of subcortical gray matter that form the basal ganglia. 

The basal ganglia are very important for providing a feedback mechanism to motor cortices for initiation and control of voluntary movements. So, for example, you want to write your name on a piece of paper. 

First, you plan the movements using your prefrontal cortex, and that sends a signal to the motor cortex as well as the basal ganglia. The basal ganglia now help the motor cortex prepare for, and initiate the action. The result is that you position your arm so that you can start writing. 

Then, the basal ganglia ensure that your hand movements are as precise and executed as planned, and while doing so, they also maintain your posture. In addition to this, the basal ganglia can help you learn new procedural motor skills, like riding a bicycle.

The basal ganglia are a collection of nuclei that include the caudate nucleus, the putamen, the globus pallidus externus and the globus pallidus internus. These nuclei have highly complex connections with other parts of the central nervous system, like the cerebral cortex, the thalamus and the brainstem. But the two most important structures that are closely related to the b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_cerebellum</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5UmsS8WIQMiBlRtkicY_hpntT5SBW_vo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the cerebellum]]></video:title><video:description><![CDATA[The word cerebellum translates to little brain. Not because it’s the brain of a tiny animal or baby, but rather because of the fact that the cerebellum looks like a smaller version of the human cerebrum. 

Very simply, the cerebellum assists with coordinating and adjusting voluntary movement. It plays a major role in posture, balance, maintenance of muscle tone and coordinating skilled voluntary motor activities - things like riding a bicycle, or for the more adventurous, walking a tightrope! 

In order for the cerebellum to undertake these functions, it has to be in constant communication with the cerebral cortex. It also receives and sends signals to many other structures in the central and peripheral nervous systems, processing information about current movement and positional states in order to help refine, correct and improve the motion. 

Now, the cerebellum sits in the posterior part of the cranium, called the posterior cranial fossa, and it is covered by the tentorium cerebelli, which separates the cerebellum from the occipital and temporal lobes of the brain. Anterior to the cerebellum lies the fourth ventricle, pons, and medulla oblongata.

Just like the cerebrum, the cerebellum consists of two hemispheres. These two hemispheres are connected by a narrow ridge in the middle called the vermis. From an inferior view, parallel to the vermis, there are two distinguishable lobules called the cerebellar tonsils.

The cerebellum can be divided into three lobes; the anterior lobe, the posterior lobe, and the flocculonodular lobe. From a superior view, we can identify the anterior lobe, functionally referred to as the spinocerebellum, which is responsible for the regulation of muscle tone and adjusting on-going movements. Posterior to the anterior lobe is the V shaped primary fissure. 

From a superior view, and posterior to this primary fissure, is the posterior lobe, functionally referred to as the cerebrocerebellum, or pontocerebellum, which contains t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_brainstem</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fXdAxaqeQHGLAfIFTWv3vGyeRrq44JsH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the brainstem]]></video:title><video:description><![CDATA[Our central nervous system is made up of the cerebrum, the cerebellum, the brainstem and the spinal cord. The brainstem is a trunk-like part that sits in the posterior cranial fossa and connects the spinal cord inferiorly with the forebrain superiorly. 

The brainstem can be divided into three parts. From caudal to rostral these parts are: the medulla oblongata, the pons and the midbrain. 

The brainstem is made up of white and gray matter. The white matter contains many ascending and descending fibers that act like a highway, allowing information to travel to and from the spinal cord and the higher parts of the central nervous system. 

Scattered amongst the white matter tracts, there are islands of gray matter that consist of neuronal cell bodies, many that are the nuclei associated with cranial nerves. 

Some of these collections of nuclei serve as centers for life sustaining reflexes, like those involved with breathing and our heartbeat, others coordinate states of alertness or arousal, while others mediate motor activities and relay sensory information.

First, let’s look at the medulla oblongata, specifically its ventral aspect. Right in the middle, there is the anterior median fissure. 

On either side of it, there are two bumps called the pyramids, which contain axons of the corticospinal, or pyramidal, tract. 

Before entering the spinal cord, these fibers cross over to the opposite side, forming the decussation of the pyramids. 

Lateral to each pyramid, there are two oval bumps called the olives. They contain the inferior olivary nuclei, which have rich connections to the cerebellum and are involved in motor coordination and learning.

Now, on the dorsal aspect of the medulla oblongata, it’s visible that the rostral medulla contains the inferior part of the fourth ventricle, a space filled with cerebrospinal fluid, or CSF. 

Across the floor of the fourth ventricle, spreading transversely, there are the striae medullaris, which are raised s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_white_matter_tracts</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YXJ0kriTSMWgS7ONBqersO7CRLS9w2db/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the white matter tracts]]></video:title><video:description><![CDATA[Our central nervous system consists of three major parts, the cerebrum, the cerebellum, and the brainstem. The largest part is the cerebrum, which consists of two nearly symmetrical halves called the cerebral hemispheres. 

If we were to cut through the cerebral hemispheres in the coronal plane, we would see that the outermost area is the cerebral cortex, which consists of gray matter that contains billions of neuronal cell bodies. 

Deep to the gray matter is the subcortical white matter, which is made up of myelinated axons that are extensions of the neuronal cell bodies, allowing them to send and receive signals. 

The term white matter is used because the myelination of the axon fibers gives this area a white appearance on gross inspection. 

Axon fibers can be divided into three main groups - commissural fibers, association fibers, and projection fibers - depending on the target of the axons. 

The cerebral commissural fibers connect the left and right cerebral hemispheres and consist of the corpus callosum, the anterior commissure, the posterior commissure, and the hippocampal commissure. 

Association fibers connect different regions within the same hemisphere and they include the U-fibers, uncinate fasciculus, cingulum bundle, arcuate fasciculus, superior longitudinal and inferior longitudinal fasciculi, and the occipitofrontal fasciculus. 

Finally, projection fibers connect the cerebral cortex with more caudal structures in the central nervous system, like the thalamus, brainstem, and spinal cord. 

These ascending and descending projection fibers all travel in a structure called the internal capsule, which has five parts that we will explore later!

Okay, first, let’s cover the cerebral commissural fibers. Starting with the corpus callosum, which means tough body in latin, this is the largest white matter structure in the brain. It sends signals between the two cerebral hemispheres and connects them together at the same time.

If we make a mid s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_blood_supply_to_the_brain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k91n_SbMTXOfYlb2WzSy822mSD618QNh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the blood supply to the brain]]></video:title><video:description><![CDATA[The human brain is one of the most important and sophisticated organs of the human body. In fact, every minute, it receives about 15% of the total blood pumped by the heart to our entire body! Cerebral circulation is a complex circulatory system, formed by the two internal carotid arteries, the two vertebral arteries, and their branches. The terminal branches of both the internal carotid arteries and the vertebral arteries lie in the subarachnoid space, which is a space between two meningeal layers called the arachnoid mater and pia mater. Anatomoses between these two arteries and their branches give rise to the Circle of Willis, which is a system of vessels at the base of the brain that helps to ensure adequate blood flow to this vital organ. 

Let’s start off with the internal carotid arteries, or ICAs, which are the terminal branches of the common carotid arteries, and form the anterior part of the cerebral vascular system. The ICAs ascend on both sides of the neck to reach the base of the skull, where they enter a passageway in the petrous part of the temporal bone, called the carotid canal. Within the carotid canal, the ICA is close to venous plexuses as well as the carotid plexuses of sympathetic nerves. Within the canal, each ICA turns 90 degrees anteromedially, then another 90 degrees superiorly to exit the carotid canal and enter the cranial cavity. 

Inside the cranial cavity, the ICA runs through the cavernous sinus, which is, in fact, a dural venous sinus. So the ICA, an artery, actually runs through a sinus filled with venous blood!  Within the cavernous sinus, the ICA travels alongside the abducens nerve, and lies in proximity to the oculomotor nerve, the trochlear nerve and the ophthalmic and maxillary divisions of the trigeminal nerve. Then, the ICA emerges from the cavernous sinus and divides into the anterior cerebral artery, the middle cerebral artery and several smaller branches. 

To simplify this complex course, the ICA can be divided]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Cerebral_hemispheres</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9j9DNkArS6u8R1xfB7j7dvM0QIaEN074/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Cerebral hemispheres]]></video:title><video:description><![CDATA[The cerebral hemispheres are two symmetrical halves of the brain that contain billions of neurons and their connections, forming an amazing network of cells which help govern our everyday actions. These cerebral hemispheres consist of the cerebral cortex, subcortical white matter, and gray matter masses called the basal ganglia found throughout the subcortical white matter. Due to the complexity of our brains, the clinical conditions affecting our cerebral hemispheres lead to a variety of abnormal and strange symptoms, so understanding the anatomy of the cerebral hemisphere is crucial in understanding these conditions. 

Let’s start with lesions of the cerebral cortex, which is the superficial gray matter of our brains containing billions of neurons responsible for processing information. Depending on which part of the cortex these lesions occur in, it can cause different clinical manifestations. 

First, there are lesions of the prefrontal cortex, which is an area responsible for the makeup of a person’s personality and governs social behaviour. So, prefrontal cortex lesions cause frontal lobe syndrome which generally result in personality changes, and can specifically cause problems with planning, initiative, judgment, and social behaviour. Individuals have difficulty making decisions, and may become impulsive and aggressive. Individuals can also exhibit socially unacceptable behavior, where they no longer restrain from saying or doing inappropriate things, and may also no longer care about their clothing and appearance.

Injury to the prefrontal cortex may also contribute to the reemergence of primitive reflexes, such as the grasp reflex, suckling reflex, and groping reflex. Bilateral damage of the prefrontal cortex may lead to incontinence, gait apraxia, and can even lead to akinetic mutism, where awake individuals lack the will or motivation to move or speak, but will follow you with their eyes in response to noise.  

Next up, the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Cerebellum_and_brainstem</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/naNfAnF8RNKfs0len68cEH71Qb_LdJrs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Cerebellum and brainstem]]></video:title><video:description><![CDATA[The cerebellum, which is  latin for ‘little brain’, is a part of the brain that plays a major role in posture, balance, maintenance of muscle tone and coordination of skilled voluntary motor activities. The brainstem, on the other hand, is a trunk-like structure that connects the higher parts of the central nervous system with the spinal cord and serves as a center for life sustaining reflexes, such as breathing and our heartbeat. Injury and disease to these parts of our brain can result in a variety of complex neurological problems, which can even have life threatening consequences. 

First off, let’s look at lesions of the cerebellum, which can be caused by a variety of things such as stroke, space occupying lesions, infections, or drug toxicities. Remember that the cerebellar cortex can be divided into three functional regions that are positioned longitudinally: the lateral zone; the intermediate or paravermal zone; and the median or vermal zone. 

One type of lesion is a lateral lesion of the cerebellum, which affects the lateral and intermediate zone of the cerebellum and their associated cerebellar nuclei, which impairs voluntary movements of the extremities. Think Lateral lesions affect Lateral structures! The lateral zone assists in motor planning, and the intermediate zone has been shown to control muscles of the distal parts of the limbs, particularly the hands and feet. 

Clinically, lateral cerebellar lesions can cause ipsilateral limb ataxia, meaning loss of coordination of the limb on the same side as the lesion. This can manifest as: intention tremor, which are involuntary, trembling movements that occur with voluntary targeted movements; dysmetria, which is when individuals overshoot or undershoot an intended position of the extremities for example during the finger to nose test; dysdiadochokinesia which is the inability to perform fast alternating movements; a loss of balance with a tendency to fall to the same side as the lesion, and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cranial_nerve_pathways</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CM5i6uvBSA_V0UiTe4a24EzFQnWeyg1u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cranial nerve pathways]]></video:title><video:description><![CDATA[Not only are there 12 cranial nerves with unique functions, each cranial nerve also has its own unique pathway from where it begins to where it ends. All this information can surely make your brain explode, but we are going to break it down for you! 

Simply put, cranial nerves connect centrally to cranial nerve nuclei which is where cranial motor nerves begin, or where cranial sensory nerves terminate. Remember, nerve fibers leaving the brain are considered efferent fibers, where nerves fibers entering the brain are considered afferent fibers. These centrally located nuclei contain the cell bodies of motor and sensory neurons of the cranial nerves, and the nuclei are where these neurons will synapse with the neurons of higher brain centers such as the thalamus and cerebral cortex. 

So essentially, these nuclei act as a pit stop for the exchange of signals travelling between higher brain centers such as our cerebral cortex, to all of the structures our cranial nerves go on to innervate, ultimately facilitating the function of the cranial nerves. This is important as the cranial nerves will carry different types of motor and sensory information, so the nuclei help organize all this information. 

In short, cranial nerves can carry two types of motor information, the first being somatic and branchial motor information, and the second being visceral motor or parasympathetic motor information. Then there are the three types of sensory information, the first being somatic sensory information, the second is visceral sensory information, and the third is special sensory information. So, we used the analogy before that cranial nerve pathways are like highways, so let’s talk about these highways and how they transmit the information carried along cranial nerves from the brain centrally to our head, neck, and body peripherally.  

Let’s begin by talking about the cranial nerves that carry somatic motor fibers and branchial motor fibers, which eventually go on to in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_trigeminal_nerve_(CN_V)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yLQog3sCS9eALP1bghEfrn5ySbiCyNUO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the trigeminal nerve (CN V)]]></video:title><video:description><![CDATA[When it comes to the trigeminal nerve, or CN V, tri means three, so right off the bat, you can tell that the trigeminal nerve has three major branches: the ophthalmic nerve, or V1, the maxillary nerve, or V2, and the mandibular nerve, or V3. 

The ophthalmic and the maxillary nerves only have sensory functions, while the mandibular nerve has both sensory and motor functions. 

So, the trigeminal nerve is in charge of sensation for the face, mouth, nasal cavity and dura mater of the cranial cavity, and also of motor functions like biting and chewing. 

In addition to motor and sensory fibers, postganglionic parasympathetic fibers join many of the branches of the trigeminal nerve to reach their final destination; so the branches of the trigeminal nerve serve as a pathway for parasympathetic innervation. 

Now, the trigeminal nerve emerges from the lateral aspect of the pons by a large sensory root and a small motor root. 

The large sensory root mainly consists of cell bodies of the pseudounipolar neurons that make up the sensory trigeminal ganglion, which sits within a dural recess lateral to the cavernous sinus, called the trigeminal cave. 

When the ophthalmic, maxillary, and sensory component of the mandibular nerves detect a signal from their sensory nerve endings, the pseudounipolar neurons that make up these nerves transmit their signal through the trigeminal ganglion as first order neurons in the pathway, to synapse in the different trigeminal nuclei located along the brainstem. 

The cell bodies of these pseudounipolar nerves are located in the trigeminal ganglion, similar to how the dorsal root ganglions hold the cell bodies for the sensory pseudounipolar neurons of the body. 

After synapsing in the trigeminal nuclei, the second order neurons cross the medial plane at the level of the pons and ascend as the trigeminal lemniscus to synapse again in the contralateral thalamus to third order neurons.  

These third order neurons then travel through t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_facial_nerve_(CN_VII)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fN4B76UjT5SOW-h491LICUSnQwmtjuSP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the facial nerve (CN VII)]]></video:title><video:description><![CDATA[Humans can make thousands of expressions with their faces, and this is possible thanks to the 7th cranial nerve, also known as the facial nerve. 

The facial nerve does much more than just control our facial expressions though, it also plays an important role in salivating, sensation for some parts of the skin,  and it’s even involved in the perception of taste! 

The facial nerve has many functions including somatic sensory, special sensory, branchial motor, and visceral or parasympathetic motor innervation. 

Parasympathetic innervation travels with the facial nerve to glands such as the lacrimal glands, nasal glands, palatal mucosal, and submandibular and sublingual salivary glands. 

It provides special sensory innervation to the anterior two thirds of the tongue; as well as somatic sensory innervation for a small portion of skin at the ear and external tympanic membrane. 

Now, where did the facial nerve come from? The facial nerve actually originates from a structure that begins to appear when we are about the size of a poppy seed, known as the second pharyngeal arch. 

Remember, the pharyngeal arches are 6 embryological structures, of which only 5 eventually develop into the muscles, arteries, bones and cartilage of the head and neck. 

Many structures are derived from the second pharyngeal arch, such as the lesser horn of the hyoid bone, the styloid process, the stylohyoid ligament, and the stapes. 

Importantly, the stylohyoid muscle, the posterior belly of the digastric muscle, the stapedius muscle and the muscles of facial expression are also derived from the second arch, which means they are all innervated by the facial nerve.

Now, the upper motor neuron of the branchial motor pathway for the facial nerve starts from the motor cortex, and its axons travel through the internal capsule to eventually reach the facial motor nucleus located in the ventrolateral part of the pons, where it synapses with the pathway’s lower motor neuron. 

The lower m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_glossopharyngeal_nerve_(CN_IX)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vgu1IQsiRF6SNCWzC1T7sE-aSmq0Bdeh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the glossopharyngeal nerve (CN IX)]]></video:title><video:description><![CDATA[The glossopharyngeal nerve is the ninth cranial nerve and it has several roles. From helping us taste a freshly picked strawberry on the back of the tongue through its special sensory role, to keeping the carotid sinus in the loop about blood pressure variations through its visceral sensory component, as well as providing branchial motor innervation to a muscle in the pharynx and parasympathetic innervation to the parotid gland. 

It may also receive somatic sensory information from a tiny part of skin on the external ear, but this isn’t important to remember. This nerve is working four - sometimes five - jobs, and doing them all really well! 

But now, where did the glossopharyngeal nerve come from? The glossopharyngeal nerve actually originates from a structure called the third pharyngeal arch that forms during intrauterine life, when the embryo is roughly the size of a poppy seed. 

Remember that the pharyngeal arches are 6 embryological structures, of which only 5 eventually develop into the muscles, arteries, bones and cartilage of the head and neck. 

Now, the third pharyngeal arch is less complex than the first two arches and gives rise to only a few structures such as the common carotid artery, the proximal portion of the internal carotid artery, the lower body and the greater horn of the hyoid bone and the stylopharyngeus muscle.

All of these structures are innervated by the nerve of the third pharyngeal arch, which is the glossopharyngeal nerve. 

So let’s take a closer look at the roles of this nerve. First up, there’s the special sensory component, that picks up taste information from the taste buds located in the posterior one-third of the tongue. 

This pathway starts with special sensory fibers in the tongue, that travel via lingual branches of CN IX to the inferior glossopharyngeal, or petrosal, ganglion which contains the cell bodies of these  first order neurons, in the jugular foramen. 

Then, the fibers enter the cranial cavity and rea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_spinal_accessory_(CN_XI)_and_hypoglossal_(CN_XII)_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aLAonkBdSJ6xhEKaqulAsz3eT1KAFTH2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the spinal accessory (CN XI) and hypoglossal (CN XII) nerves]]></video:title><video:description><![CDATA[The spinal accessory nerve, or the eleventh cranial nerve, and the hypoglossal nerve, or the twelfth cranial nerve, are two purely motor cranial nerves that innervate muscles in the neck, as well as the tongue. 

Specifically, the spinal accessory nerve provides somatic motor innervation to the sternocleidomastoid and trapezius muscles, while the hypoglossal nerve provides somatic motor innervation to almost all the muscles of the tongue.

Let’s start with the spinal accessory nerve. The somatic motor pathway of the spinal accessory nerve starts in the cerebral cortex. Then, the axons travel to the spinal accessory nucleus, which is located in the cervical spinal cord, specifically in the posterolateral aspect of the anterior horn. 

The axons travel through the rootlets from the first five or six cervical segments of the spinal cord and form the spinal accessory nerve. The spinal accessory nerve ascends through the foramen magnum, enters the posterior cranial fossa, and then exits through the jugular foramen. 

It continues its journey down along the internal carotid artery and runs deep to the sternocleidomastoid muscle, which it supplies. Then, it emerges from the sternocleidomastoid muscle through its posterior border, and continues inferiorly in the posterior triangle of the neck to reach and supply the trapezius muscle through multiple branches. 

The spinal accessory nerve is located superficially in the posterior triangle of the neck, and you can identify it using two landmarks: one third of the way down from the posterior border of the sternocleidomastoid muscle and one third of the way up from the anterior border of the trapezius muscle. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Olfactory_(CN_I)_and_optic_(CN_II)_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uBmZLi7TTdur_Zqxqa_cpqr5R5uaaWVV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Olfactory (CN I) and optic (CN II) nerves]]></video:title><video:description><![CDATA[It&amp;#39;s time to stop and smell the roses! Or... perhaps stop and see the clinical correlates of cranial nerve 1 and cranial nerve 2? Common sayings aside, this video will focus on the olfactory nerve, or cranial nerve 1, which allows us to experience smells, and your optic nerve, or cranial nerve 2, which allows us to see the world around us. Both of these nerves are prone to injury along their pathways, so knowing their anatomy can help us locate the different types of lesions that affect these nerves and understand why they are prone to injury. 

Let’s start with the olfactory nerve. The olfactory nerve consists of chemoreceptors found in the nasal mucosa, and their axons make up rootlets that project through the cribriform plate of the ethmoid bone. These rootlets then synapse in the olfactory bulb, which rests on top of the cribriform plate, and this thin bony plate makes up the roof of the nasal cavity. 

Fast acceleration and deceleration movements, such as a high impact car crash, can cause shearing and tearing of these rootlets as they travel through the cribriform plate. Head trauma, such as a direct blow to the nose, can also fracture the thin cribriform plate, putting the olfactory nerve at risk of injury. The fracture can injure both the rootlets passing through it, or the bulb resting on top of it. 

Fracture of the cribriform plate can sometimes present with cerebrospinal fluid rhinorrhea, which is cerebrospinal fluid leaking from the nose - not to be confused with an ordinary runny nose from a cold! Damage to the olfactory nerve can cause anosmia, which means loss of smell. As smell is extremely important in the perception of taste, most individuals with anosmia actually complain of loss of taste. Clinical testing of anosmia is usually not performed, and diagnosis is made by asking the individual if they’ve lost their sense of taste or smell. 

One clinical condition that is associated with dysfunction of the olfactory nerve ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Trigeminal_nerve_(CN_V)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N2pqrDLtQDeQLd_CkyIPlir0RL2kx4PB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Trigeminal nerve (CN V)]]></video:title><video:description><![CDATA[The trigeminal nerve is the fifth cranial nerve. It provides both sensory and motor functions, while also serving as a highway for parasympathetic innervation. 

This is the nerve that allows you to feel wonderful things, like the kiss of your partner, 

or a summer breeze on your face, 

but also less pleasant things, like a dentist drilling into your teeth. 

Luckily, understanding the anatomy and distribution of the trigeminal nerve can help us better diagnose and manage several conditions - and it even makes going to the dentist less painful! 

First off, let’s remember some important anatomical features of the trigeminal nerve. The trigeminal nerve has three divisions: the ophthalmic or V1, the maxillary or V2, and the mandibular division or V3. 

Through its branches, the trigeminal nerve supplies sensory innervation to the skin of the entire face, the mucosa of sinuses, as well as the nasal, and oral cavities. It also carries the sensory fibers for taste which go on to travel with the chorda tympani branch of cranial nerve VII, or the facial nerve. 

The trigeminal nerve also carries parasympathetic innervation to the ciliary body and sphincter pupillae, the lacrimal gland, the nasal glands, palatal salivary glands, and the parotid, submandibular, and sublingual glands., though these parasympathetic fibres originally arise from other cranial nerves.

Finally, the trigeminal nerve supplies motor innervation to the muscles of mastication. And if all that wasn’t enough, the trigeminal nerve is also involved in the corneal reflex, also known as the blink reflex, which causes involuntary blinking when the cornea is stimulated to protect the eye from foreign bodies, like a pesky grain of sand getting in your eye. 

In this reflex, the trigeminal nerve is the sensory or afferent pathway, while the facial nerve serves as the motor or efferent pathway. Talk about a jack of all trades!

So with that in mind, you can see why trigeminal nerve injuries can cause]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Facial_(CN_VII)_and_vestibulocochlear_(CN_VIII)_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oMdNCBAuT5Wn6L134b9_3MirSNKSwnbN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Facial (CN VII) and vestibulocochlear (CN VIII) nerves]]></video:title><video:description><![CDATA[The facial nerve is all about supplying those facial muscles and allowing for the whole range of facial expressions that they create. But don’t just judge a nerve by its face; ‘cause that’s not all it can do! The facial nerve is also involved in salivating, secreting tears, and it even plays a role in taste. 

On the other hand, the vestibulocochlear nerve is the cranial nerve that helps you hear your favorite song, so then you can use your facial nerve to smile when you hear it.  And it also plays a role in balance, so you can dance along without tipping over! Understanding the anatomy of the facial and vestibulocochlear nerves is important, as damage to these nerves can cause significant impairments when it comes to facial expression, hearing and balance, among several other functions! 

Let’s start with the general anatomy of the facial nerve. Remember that there are two facial nerves, one on each side, and each of them is primarily responsible for providing motor innervation to the muscles of facial expression. The facial nerve also innervates the stapedius muscle in the middle ear; gives parasympathetic innervation to the lacrimal glands, nasal glands, palatal mucosal, submandibular, and sublingual salivary glands; and also carries the special sensory information of taste from the anterior two-thirds of the tongue and the palate. 

It is also involved in the corneal reflex, also known as the blink reflex, which causes involuntary blinking when the cornea is stimulated to protect the eye from foreign bodies like sand. In this reflex, the trigeminal nerve is the sensory or afferent pathway, while the facial nerve serves as the motor or efferent pathway. 

Now, the clinical presentation of facial nerve damage is called facial nerve palsy. If the entire facial nerve is damaged, all of its functions are affected. Without motor innervation, facial muscles become weak or impaired. This means the affected individual will have trouble when trying to smile, fro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Glossopharyngeal_(CN_IX),_vagus_(X),_spinal_accessory_(CN_XI)_and_hypoglossal_(CN_XII)_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wTlLxqjkRd_Jxtpal2KiOmjqQP6e_QWr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Glossopharyngeal (CN IX), vagus (X), spinal accessory (CN XI) and hypoglossal (CN XII) nerves]]></video:title><video:description><![CDATA[The glossopharyngeal, vagus, spinal accessory, and hypoglossal nerves, also known as cranial nerves IX, X, XI, and XII, respectively, all combine to carry sensory, motor, and parasympathetic innervation to the pharynx, larynx, tongue, and many other regions. Injury of these nerves can affect important functions like swallowing, the gag reflex, breathing, and even cardiac output. Now, we know that cranial nerves can be a hard pill to swallow, but soon you’ll see that by knowing the anatomy and the important functions of these nerves, the clinical presentations and the management of these injuries isn’t so difficult to understand.

First, let’s discuss bulbar palsy, which refers to a unilateral lower motor neuron lesion of cranial nerves IX, X, XI and XII, and it’s caused by a lesion in the medulla that affects the nucleus ambiguus and the hypoglossal nucleus. Symptoms are associated with impaired function of the affected nerves. For example, if the glossopharyngeal nerve is damaged, this causes difficulty with swallowing. Other common symptoms include nasal regurgitation, slurred speech, and difficulty speaking. Also, reflexes like the gag reflex and jaw jerk are usually absent.

Pseudobulbar palsy, on the other hand, refers to a bilateral upper motor neuron lesion of cranial nerves XI, X, XI and XII, caused by more supra nuclear proximal damage to motor fibers somewhere between the cortex and the medulla leading to an upper motor neuron injury. The symptoms are similar to bulbar palsy, however, the gag reflex and jaw jerk are usually overactive, which if you remember, is indicative of an upper motor neuron lesion. 

Next, let’s discuss jugular foramen syndrome, which refers to a collection of symptoms that arise when cranial nerves IX, X, and XI, which all pass through the jugular foramen, are damaged in that area. Any obstructions or lesions, most commonly tumors in the area, but also trauma or an abscess, can damage these cranial nerves and cause jugular]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mood_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EIx1IOryQAOYVsIT8RTlQb1uQuiONYLU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mood disorders: Pathology review]]></video:title><video:description><![CDATA[54 year old Liam presents to the clinic because of a persistent feeling of sadness, ever since he got divorced and his former wife moved out with their son, five months ago. 

Liam mentions that he doesn’t enjoy anything anymore, not even listening to his favorite songs. 

However, he does briefly cheer up every time his son visits him. 

Upon further questioning, Liam admits to gaining a lot of weight recently, and feels like he can’t stop eating. 

When you ask Liam about his sleep habits, he tells you that he often sleeps more than 13 hours a night, but still feels tired when waking up. 

Next to him, 25 year old Elfie is brought to the clinic by her father, who is worried that Elfie has not slept much for the past 5 days, but still seems overly energetic. 

Her father is also furious because two days ago Elfie maxed out her credit cards shopping for clothes.

Elfie interrupts him to say that nobody understands her, because she’s more intelligent than everyone on this planet! 

Then, Elfie starts pacing around the room as she continues to speak rapidly and jumps from one topic to another. 

She denies experiencing any psychotic symptoms, like hearing or seeing things that others don&amp;#39;t. 

Finally, Elfie also mentions that she hasn&amp;#39;t stopped going to work or interacting with her colleagues these past five days. 

Okay, based on the initial presentation, both Liam and Elfie seem to have some form of mood disorder. 

Many of us can have days when we feel sad or overly happy. 

But with mood disorders, these emotional variations can become impossible to control, sometimes even to the point where they interfere with day-to-day activities like working, studying, eating, and sleeping. 

Now, the main risk factors seem to include having a family history or experiencing a personal trauma. 

However, the underlying cause is poorly understood; for your exams, what you need to remember is that there’s usually an imbalance of the neurotransmitters s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Trauma-_and_stress-related_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VP-Xp0O4S0SlKJW0hCYNT2OBTTuWSUFC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Trauma- and stress-related disorders: Pathology review]]></video:title><video:description><![CDATA[A 31 year old female named Amelia comes to the mental health clinic complaining of trouble sleeping due to vivid nightmares recounting an armed bank robbery she witnessed 4 months ago. 

Ever since that event, she has avoided going to crowded places that remind her of the bank, to the point where she had to give up her job at the mall. 

Suddenly, your phone starts ringing and Amelia jumps from her seat. You apologize, and she then mentions that this happens whenever she hears sudden or loud noises.

Okay, based on the initial presentation, Amelia seems to have some form of trauma or stress-related disorder. 

Many individuals at some point in their lives experience trauma, which can be thought of as a distressing event that causes an overwhelming amount of stress, exceeding one’s ability to cope or process the emotions caused by that experience. 

Trauma can be caused by one single event, such as a serious car crash or sexual assault or abuse; or can last for a more prolonged period of time, such as experiencing poverty, neglect during early childhood, or military combat. 

Most of the time, with support from loved ones, individuals are able to recover from a traumatic experience. 

Unfortunately, some individuals may develop trauma and stress-related disorders, where traumatic experiences lead to symptoms like flashbacks, nightmares, and anxiety, all of which can interfere with day-to-day activities like working, studying, eating, and sleeping. 

Now, the underlying cause of trauma and stress-related disorders is poorly understood; but what you need to remember is that individuals affected usually have altered levels and response to stress hormones like adrenaline and cortisol. 

For your exams, the most high-yield trauma and stress-related disorders are post-traumatic stress disorder, acute stress disorder, and adjustment disorder. Okay, let’s start with post-traumatic stress disorder, or PTSD for short. 

This usually occurs in individuals who have eit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amnesia,_dissociative_disorders_and_delirium:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZXxcDleSTaO2xSb_cnyqomC9R8yAUUQN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amnesia, dissociative disorders and delirium: Pathology review]]></video:title><video:description><![CDATA[78 year old Joanne is brought in by her son, who is worried because Joanne seems to forget things all the time. 

You start by introducing yourself, and then explain to Joanne the reason she’s in the hospital. 

You then ask her a few things about herself. 

She looks confused and tells you that she used to be a Broadway singer before retiring and she has travelled all around Europe. 

Her son tells you she used to work as a sales woman and she’s never been to Europe in her entire life. 

A few minutes later, Joanne asks her son where they are and who you are. 

On physical examination, you notice a strong alcoholic odor, so her son reluctantly tells you that Joanne has a history of chronic alcohol abuse. 

Next to her, a 66 year old man is also brought to the hospital, after being found by the police wandering in the streets, with a battered suitcase. 

He doesn’t seem to know his name, location, or where he was going, and stares blankly when you ask him anything.

The only thing he is able to tell you is that he is going on a business trip. 

When you contact his relatives, they tell you that his name is Matthew, and that he was recently fired from his job. 

Physical examination is unremarkable.

Based on the initial presentation, both Joanne and Matthew  seem to have some form of amnesia, dissociative disorder, or delirium.

Okay, starting with amnesia, this can be categorized into two types. 

The first type is anterograde amnesia, which refers to an inability to form new memories, often forgetting what happened hour to hour. 

The second and probably most high yield type of amnesia is retrograde amnesia, and it refers to an inability to recall old memories. 

As a result, they may completely forget important people or moments in their life, which can cause anxiety for the individual experiencing retrograde amnesia, as well as their friends and family. 

Both anterograde and retrograde amnesia can be caused by acute and chronic conditions. 

Acute cau]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Schizophrenia_spectrum_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zo2KAMAHSAK3ORCXBFDu3hpASHK2m2JV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Schizophrenia spectrum disorders: Pathology review]]></video:title><video:description><![CDATA[A 32-year-old male named Bert is brought to the psychiatric clinic by his concerned mother, who thinks that Bert’s behavior has changed over the past 9 months. Upon further questioning, Bert’s mother reveals that he has been isolating himself, and stopped calling or visiting his family and friends. Bert says that he must stay at home because some aliens have been trying to control his mind. On physical examination, Bert appears disheveled, has poor eye contact with others, and shows little facial expression. You decide to order a toxicology screen, which comes back negative.  

Some days later, you see a 52-year-old female named Akuchi, who is brought by her concerned husband to the psychiatric clinic. Akuchi’s husband explains that she started to act strange 2 months ago when they were at the funeral of her best friend. Upon further questioning, Akuchi explains that the funeral was fake because she saw her best friend watching her from a black sedan.  

Additionally, her husband says that every time they come home, Akuchi is looking for microphones and cameras throughout the house because she thinks that someone is trying to kill them.  

Her husband concludes that, except for these non-bizarre thoughts, she seems functional for the most part of the day. Just like with Bert, you decide to order a toxicology screen, which comes back negative. 

Okay, based on the initial presentation, both Bert and Akuchi seem to have some form of schizophrenia spectrum disorder. These are a group of conditions, including schizophrenia, that are characterized by difficulty thinking clearly, making good decisions, distinguishing reality from imagination, and behaving appropriately, sometimes even to the point where they interfere with day-to-day activities like working, studying, eating, and sleeping. Now, the main risk factors for developing a schizophrenia spectrum disorder seem to include having a family history, experiencing a personal trauma, or heavy use of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malingering,_factitious_disorders_and_somatoform_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u7AJK4MaRx6eZH8XetN_X-hkTHKUMa3W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malingering, factitious disorders and somatoform disorders: Pathology review]]></video:title><video:description><![CDATA[A 5 year old girl named Celia is brought to the emergency department by her mother due to a sudden episode of loss of consciousness. 

You decide to run some blood tests, which reveal low glucose levels. 

After glucose administration, Celia fully recovers. 

You admit her to the hospital to do exhaustive studies to start looking for a cause of her hypoglycemia. 

The tests all come back normal, so you decide to discharge Celia. 

The next morning, Celia has another unexplained episode of hypoglycemia, so you decide to check her blood insulin levels, which are found high, while her C-peptide levels are slightly low. 

Some days later, 32 year old Sofia presents to the emergency department. 

Sofia is complaining of severe chest pain that has been going on for the past couple hours, and she is certain that she is having a heart attack. 

According to the hospital records, she has presented to the emergency department with similar symptoms 7 times within the past 12 months. 

And each time, cardiac evaluation was normal. 

Upon examination, both cardiac auscultation and ECG are normal. 

Sofia becomes frustrated and storms out of the hospital demanding a second opinion. 

Based on the initial presentation, both Celia and Sofia have some form of malingering, factitious, or somatic symptom and related disorders. 

What all these have in common is that the affected individual claims to have physical or psychological symptoms that aren’t explained by any known physical or mental disorder.

Okay, starting with malingering, this is when individuals are intentionally faking or exaggerating their symptoms in order to achieve some secondary gain or external goal. 

This may include getting money, housing, time off from work, access to medications, or even escaping jail time. 

In other words, they’re conscious or aware of their specific motivation. 

For your exams, remember that these individuals are typically uncooperative, meaning that they demand an extensive wor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Childhood_and_early-onset_psychological_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hl9QJavPS-2uQwdCxKcCIaPUT-C0XaEE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Childhood and early-onset psychological disorders: Pathology review]]></video:title><video:description><![CDATA[A 16 year old female, named Tayla, comes to the clinic because she’s been feeling urges to repeatedly blink her eyes, shake her head from side to side, or clear her throat. Tayla notes that she is able to suppress the urge for a while, but she eventually loses control of her actions. This all started a little over a year ago, and Tayla is under distress because her classmates often tease her about it. During the conversation, she suddenly utters an inappropriate curse word, and immediately goes on to say that she doesn’t know how that came out of her mouth. Physical examination reveals no neurological deficits and she shows normal cognitive skills for her age.

Okay, based on the initial presentation, Tayla seems to have some form of childhood or early-onset psychological disorder. These include several psychological conditions that typically have their onset during childhood, although some of these disorders may last into adulthood. As a consequence, these disorders can interfere with how the affected person functions independently in society, and impair everyday activities like working, studying, eating, and sleeping, as well as have an impact on their families. 

For your exams, the most common childhood or early-onset psychological disorders are separation anxiety disorder, selective mutism, oppositional defiant disorder, conduct disorder, disruptive mood dysregulation disorder, tourette syndrome, and child abuse. 

Let’s begin with separation anxiety disorder. That happens when separation from someone that the child is very attached to, like a parent, causes overwhelming or excessive fear and anxiety. In some cases, this can reach the point where it may lead to factitious physical complaints so that individuals can stay home and miss school. To be diagnosed as separation anxiety disorder, this needs to last for at least four weeks or more. Bear in mind, though, that this can be considered normal behavior until the age of 3 or 4. 

Now, treatment inclu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psychiatric_emergencies:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ux-y_B4sTpaZPOsV6Qj9oMGCS-6RD-R7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psychiatric emergencies: Pathology review]]></video:title><video:description><![CDATA[A 53 year old male named Noah is brought to the emergency department by his son, who found him with an empty bottle of fluoxetine in his hand. His son mentions that Noah was recently diagnosed with depressive disorder. Upon physical examination, you realize that Noah has a body temperature of 38.9 degrees Celsius, or 102.02 degrees Fahrenheit, and a blood pressure of 162 over 95 millimeters of mercury. In addition, Noah’s pupils appear dilated, and his muscles are very stiff. Finally, neurological examination reveals that Noah has overactive reflexes. Later that day, a 34 year old female named Amelia is brought to the emergency department by her husband. He explains that Amelia has a medical history of schizophrenia, and a few days back she took multiple doses of haloperidol. Upon physical examination, Amelia’s body temperature is 38.7 degrees Celsius or 101.66 degrees Fahrenheit, and her blood pressure is 170 over 100 millimeters of mercury. Similarly to Noah, Amelia has muscle stiffness, but neurological examination reveals diminished reflexes.

All right, now, both Noah and Amelia seem to have some form of psychiatric emergency, which is when a psychiatric condition becomes life-threatening and requires prompt treatment. For your exams, some high yield psychiatric emergencies include suicide attempts, serotonin syndrome, acute dystonia, neuroleptic malignant syndrome, tyramine-induced hypertensive crisis, and delirium tremens.

Now, a very relevant psychiatric emergency, not only for your exams, are suicide attempts. Suicide is when someone takes their own life intentionally. Now, many suicide attempts can be prevented by keeping an eye out for red flags or risk factors, which can be easily remembered with the memory trick SAD PERSONS. The first S here stands for sex, as suicide tends to be more common among males. Next, A stands for age, so remember that suicide is more common among young adults and the elderly. For your exams, you should know tha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Drug_misuse,_intoxication_and_withdrawal:_Stimulants:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LCEeJtGAQYa7ETQTBH_BtZ6nS2meSG7B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Drug misuse, intoxication and withdrawal: Stimulants: Pathology review]]></video:title><video:description><![CDATA[In the middle of the night, a 25 year old female, named Sylvie, comes to the emergency department complaining of retrosternal chest pain that began a couple of hours ago. Earlier that night, she was at a party, where she and her friends consumed alcohol. 

Upon further questioning, Sylvie reveals that she also consumed an illicit drug. She is otherwise healthy, has no history of cardiac disease, and does not take any medications. 

On physical examination, Sylvie is sweating profusely. In addition, her pupils are dilated, and the nasal septum is atrophic. 

Vital signs reveal a temperature of 100 degrees Fahrenheit or 37.7 degrees Celsius, a heart rate of 110 beats per minute, and a blood pressure of 160 over 90 millimeters of mercury. 

Some days later, you meet a 36 year old male, named Hunter, who comes in due to recurrent headaches associated with trouble concentrating and irritability. 

Hunter adds that he feels like he can’t stop eating, and as a consequence, he’s gained about 3 kilograms, or about 7 pounds, over the last two weeks. 

When you ask about his habits, Hunter admits to smoking 2 packs of cigarettes daily for the last 10 years, but stopped smoking about two weeks ago. 

Based on the initial presentation, both Sylvie and Hunter seem to have a form of stimulant intoxication or withdrawal. 

Stimulants are a group of substances that, when consumed, typically lead to increased activity in the body and brain. 

Stimulants include legal substances like caffeine, nicotine, and some amphetamines that can be prescribed for medical treatment; as well as illegal substances, such as cocaine and other amphetamines like MDMA. 

Now, for your exams, remember that excessive intake of stimulants may result in stimulant intoxication, which can cause several non-specific symptoms, including being more awake, alert, and energetic, having an elevated mood, and a decreased appetite. 

However, they also come with some undesirable symptoms like anxie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Drug_misuse,_intoxication_and_withdrawal:_Other_depressants:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JdeM85nHRTuPixU0PGKFq8SmQyyl0Fv4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Drug misuse, intoxication and withdrawal: Other depressants: Pathology review]]></video:title><video:description><![CDATA[A 28-year-old male named Frank is brought to the emergency department unconscious after being found by his roommate in their apartment. On physical examination, Frank is unresponsive, his breathing is slow, and he has pinpoint pupils. In addition, both his arms are covered in what looks like multiple needle tracks. Vital signs reveal a heart rate of 60 beats per minute, a respiratory rate of 7 breaths per minute, and a blood pressure of 90 over 60 millimeters of mercury. 

A few days later, a 14-year-old female named Sarah is brought to your office by her worried mother. Sarah has been experiencing headaches that have increased in frequency over the past 6 months. Upon further questioning, the mother reveals that Sarah sometimes appears confused, with a clumsy gait, and has been sleeping less lately. On physical examination, you notice that Sarah&amp;#39;s skin is dry and irritated around the mouth, and she has sores on the lips. You ask to have a private talk with Sarah, during which she admits to having sniffed glue and spray paint once or twice with a friend over the past few months.

Based on their initial presentation, both Frank and Sarah seem to have some form of depressant drug abuse, which specifically has led Frank to intoxication, while Sarah is experiencing withdrawal from it. Now, depressants are a class of drugs that depress bodily functions by reducing the activity of various excitatory neuronal pathways in the brain. Some high yield depressants include alcohol, as well as opioids, barbiturates, benzodiazepines, and inhalants like spray paints and glue.

For your exams, remember that intoxication with a depressant can result in various symptoms, including mood elevation, a decrease in anxiety, and behavioral disinhibition, which refers to a disregard for social rules that leads to inappropriate, impulsive, or even aggressive behavior. Another high yield fact is that depressants can lead to sedation, and even central nervous system or C]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disorders_of_amino_acid_metabolism:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HxCNV7SUTR6PI0wpYrT1X6DcS-WHR20X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disorders of amino acid metabolism: Pathology review]]></video:title><video:description><![CDATA[A 6 month old infant girl named Joanna is brought to the emergency department by her mother. She’s concerned because, over the past couple of weeks, Joanna has been having repetitive episodes of sudden and rapid jerking movements associated with loss of consciousness. Upon physical examination, you notice that her sweat and urine has a musty odor, and that her head circumfernce is smaller compared with other babies of the same age and sex. Joanna’s mother mentions that she lives in a remote area and gave birth at home. Next to her, 17 year old Andreas comes in with left calf pain and swelling, which has been gradually increasing over the past few weeks. On further questioning, Andreas also mentions he has recently started to experience blurry vision, and has scheduled an appointment with his ophthalmologist. He has no history of immobilization, trauma or malignancy, and does not smoke or use recreational drugs. On physical examination, Andreas is unusually tall and thin, with long arms and legs, and long fingers. When you look into his eyes, you also notice that both his lenses have a partial dislocation down and inward.
Okay, based on the initial presentation, both Joanna and Andreas seem to have some form of amino acid metabolism disorder. But first a bit of physiology real quick. Amino acids are the building blocks of proteins, and we have 20 of them. Now, all of them are made of a nitrogen group, a carbon skeleton, and a side chain that is unique to each amino acid. When amino acids are metabolized, the nitrogen is formed into a toxic compound called ammonia, which is sent to the liver. In liver cells, ammonia goes through a series of enzymatic reactions, known as the urea cycle, to be converted into the less toxic urea. Once urea is formed, it can go into the bloodstream and get excreted by the kidneys. Now, another way for liver cells to get rid of ammonia is to recycle it back to amino acids. For your exams, the most important recycling pa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glycogen_storage_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yJNaNc-BTNK-khN0in1dK4Z7Sb6Fom2P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glycogen storage disorders: Pathology review]]></video:title><video:description><![CDATA[5-year-old Manthos is brought to the emergency department by his mother due to recurring episodes of losing consciousness, accompanied by sweating and pallor. Manthos’ mother also mentions that symptoms tend to be worse when he wakes up, and decreases after meals. Physical examination reveals fat, rounded cheeks, relatively thin extremities, and a protuberant abdomen. Upon palpation of the abdomen, the liver is found to be enlarged. Laboratory studies are obtained, showing a glucose level of 40 milligrams per deciliter or 2.2 millimoles per liter, a triglyceride level of 200 mg/dl or 5.1 mmol/L, and a lactic acid level of 3.1 milligrams per deciliter or 0.34 millimoles per liter. Some days later, 3-month-old Becca is brought to the office by her parents, who complain that she’s been having problems feeding. Based on her history, Becca has also failed to reach the appropriate motor and cognitive developmental milestones. Physical examination reveals reduced muscle tone, and echocardiography shows an enlarged heart.
Based on the initial presentation, both Manthos and Becca seem to have some form of glycogen storage disease. Okay, but first a bit of physiology. Glycogen is made up of a main chain, where glucose molecules are linked by alpha 1,4 glycosidic bonds, and multiple branches, each of which is connected to the main chain by alpha 1,6 glycosidic bonds. When glucose enters the cells, it is turned into glucose-6-phosphate, which can either be used to make ATP through glycolysis or turn into glycogen. This process is called glycogenesis and occurs mainly in liver and muscle cells. To do that, an enzyme called phosphoglucomutase turns glucose-6-phosphate into glucose-1-phosphate, which is then converted into UDP-glucose by UDP-glucose pyrophosphorylase. UDP-glucose is then attached by glycogen synthase to a glucose residue at the end of the glycogen branch, forming an alpha 1,4 glycosidic bond. Finally, the glycogen-branching enzyme adds branches by c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fat-soluble_vitamin_deficiency_and_toxicity:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7HL64znXSxK982OyW457Tq8rRFGnd8KH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fat-soluble vitamin deficiency and toxicity: Pathology review]]></video:title><video:description><![CDATA[At the clinic, 32 year old Naya comes in with bilateral hip pain. She exercises regularly and has not changed anything in her routine recently. She mentions that she has recently also started to experience blurry vision, and has scheduled an appointment with her ophthalmologist. In addition, she mentions that her skin is unusually dry, which hasn’t improved with moisturizing cream. She takes several tablets of cod liver oil supplements daily. Physical examination reveals an enlarged liver and spleen. Next to her, 2 year old Lorenzo has been brought to the clinic by his mother for a yearly pediatric checkup. He was diagnosed with chronic kidney disease about one year ago in Italy. They then migrated to the United Kingdom. On examination, there is lateral bowing of the legs, as well as beading of the ribs along the anterior side of the chest. 

Based on the initial presentation, both Naya and Lorenzo seem to have some form of fat- soluble vitamin deficiency or toxicity. Fat- soluble vitamins include vitamins A, D, E, and K. Just like all vitamins, they need to be attained by diet. So, inadequate dietary consumption can be the cause of their deficiency. In a test question, some big clues are that the affected individuals often come from lower income countries or have an eating disorder like anorexia nervosa. Now, in the small intestine, fat- soluble vitamins are absorbed along with dietary fats, which means that anything affecting fat absorption can also affect the absorption of fat-soluble vitamins. Fat malabsorption typically presents with steatorrhea, meaning fatty, greasy, floating, voluminous, and terribly smelling stools. But a deficiency of fat-soluble vitamins might be the only clue you get for that. Now, causes of fat malabsorption can be broadly divided into two major groups: digestive disorders where the food can’t be broken down in the intestinal lumen, and absorption defects where the intestinal mucosa can’t take in the nutrients. 

For your]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Water-soluble_vitamin_deficiency_and_toxicity:_B1-B7:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SU3-QD6tR5SPLhgeY2onOS5FTs_ibyGc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review]]></video:title><video:description><![CDATA[82 year old Henry presents to the clinic with his daughter, who is really worried that he is not eating proper meals, but he refuses any help. She mentions that Henry has been living alone since his wife died, about two years ago. Upon physical examination, you notice that Henry is severely underweight; in addition, his tongue is swollen, and he has some scaling and painful lesions on his lips and at the corners of his mouth. 

Next to him, 60 year old Beth is brought to the clinic by her son because she’s had several episodes of diarrhea for the past few weeks. Her son also mentions that Beth has started forgetting things, and that she has a history of chronic alcohol abuse. On physical examination, you notice multiple rough and scaly skin lesions in Beth&amp;#39;s face, neck, and limbs. 

Based on the initial presentation, both Henry and Beth seem to have some form of water- soluble vitamin deficiency or toxicity. Water-soluble vitamins include the B-complex vitamins and vitamin C. And just like all vitamins, they need to be derived from food, and inadequate dietary consumption can result in deficiency. So, in a test question, look for individuals who come from lower income countries, are at an advanced age, engage in chronic alcohol abuse, or have an eating disorder like anorexia nervosa.

Okay, now, another high yield fact is that water-soluble vitamins get easily excreted in the urine. On the other hand, fat-soluble vitamins get stored in fat cells. And that’s why the water-soluble vitamin toxicity, also known as hypervitaminosis, is much less common than that of fat-soluble vitamins. Keep in mind that hypervitaminosis can indeed occur when there’s excess intake of vitamin supplements, highly fortified foods, or medications containing a vitamin derivative.

Okay, now in this video, we’re gonna be focusing on the water-soluble vitamins B1 through B7! Let’s start with vitamin B1, also known as thiamine, which is mainly found in whole grain cereals and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Water-soluble_vitamin_deficiency_and_toxicity:_B9,_B12_and_vitamin_C:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I_bs4tBIQliyW3wtpj8rJ_6qSbSzDIKt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Water-soluble vitamin deficiency and toxicity: B9, B12 and vitamin C: Pathology review]]></video:title><video:description><![CDATA[35 year old Emily comes to the clinic because she’s been experiencing tingling and numbness in both hands and feet. Emily also mentions that she’s been following a vegan diet for the past 12 years, but she’s never taken any vitamin supplements. You immediately decide to run a blood test, which reveals that Emily has elevated levels of both homocysteine and methylmalonic acid. In addition, a peripheral blood smear shows megaloblasts and hypersegmented neutrophils. 

Next comes 38 year old Joseph, who’s complaining about the fact that his gums are swollen and bleed easily. On further questioning, Joseph tells you that he’s been homeless for several years. Upon physical examination, you notice that he is underweight, and has multiple bruises, especially on his legs. You decide to take a look at his scalp, and find tiny red spots associated with small twisted hairs that look like corkscrews.

Based on the initial presentation, both Emily and Joseph seem to have some form of water- soluble vitamin deficiency or toxicity. Water- soluble vitamins include the B-complex vitamins and vitamin C. And just like all vitamins, they need to be derived from food, and inadequate dietary consumption can result in deficiency. So, in a test question, look for individuals who come from lower income countries, are at an advanced age, engage in chronic alcohol intake, or have an eating disorder like anorexia nervosa.

Okay, now, another high yield fact is that water-soluble vitamins get easily excreted in the urine. On the other hand, fat-soluble vitamins get stored in fat cells. And that’s why their toxicity, also known as hypervitaminosis, is much less common than that of fat-soluble vitamins, which instead get stored in fat cells. Keep in mind that hypervitaminosis can indeed occur when there’s excess intake of vitamin supplements, highly fortified foods, or medications containing a vitamin derivative.

Okay, now in this video, we’re gonna be focusing on the water-soluble vita]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bias_in_performing_clinical_studies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8z10p0F3RSyH_Z9rZurDcG7sQf_rA5_5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bias in performing clinical studies]]></video:title><video:description><![CDATA[Clinical studies are a type of scientific research study performed on human volunteers, or participants, to help determine the safety and effectiveness of a therapeutic intervention, such as a new medication, vaccine, device, or procedure. 

Now, systematic errors due to inaccuracy in clinical studies might result in bias, which refers to an incorrect conclusion about the effects of the therapeutic intervention. 

This conclusion may result in an inaccurate representation of the relationship between an exposure and an outcome, which means that the clinical study lacks internal validity. 

In addition, these results can’t be applied to the general population, which means that they lack external validity. 

There are different types of biases that can occur while performing clinical studies, including the recall bias, measurement bias, Hawthorne effect, procedure bias and observer- expectancy bias. 

Starting with recall bias, which is common in case control studies. These are a type of retrospective clinical study that compares the history of two groups of people. 

One group includes those that have a certain outcome, called cases, and the other group includes those that don’t have a certain outcome, called controls; to see if they’ve been exposed to different things that may have led to or protected from the outcome. 

Now, recall bias means there can be a difference in the accuracy or completeness of the data retrieved between the cases versus the controls, and this could lead to an over- or underestimation of the exposure. 

One reason for recall bias is that individuals in the case group remember exposures differently than those that are in the control group. 

For example, individuals with skin cancer might be more likely to recall using a tanning bed multiple times, since they know that tanning beds are a risk factor for skin cancer. 

On the other hand, individuals without skin cancer might recall using a tanning bed fewer times than they actually d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bias_in_interpreting_results_of_clinical_studies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nRQa3A0RQIOOw-lNFZi_KYFITwao_PTX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bias in interpreting results of clinical studies]]></video:title><video:description><![CDATA[Clinical studies are a type of scientific research study performed on human volunteers, or participants, to help determine the safety and effectiveness of a therapeutic intervention, such as a new medication, vaccine, device, or procedure.

Now, systematic errors due to inaccuracy in clinical studies might result in bias, which refers to an incorrect conclusion about the effects of the therapeutic intervention. 

This conclusion may result in an inaccurate representation of the relationship between an exposure and an outcome, which means that the clinical study lacks internal validity. 

In addition, these results can’t be applied to the general population, which means that they lack external validity. 

Now, while interpreting the results of a clinical study, there are different types of biases that can occur, including the confounding bias, lead-time bias, and length-time bias.

Starting with the confounding bias, this can occur when there’s an independent factor, known as confounder, that is related to both the exposure and the outcome. 

And this can result in an over- or underestimation of the observed association between the exposure and the outcome. 

For example, if a clinical study is trying to figure out if there’s an association between obesity and colorectal cancer, the association might be distorted by the consumption of carcinogenic products like red and processed meat, if obese participants also happen to consume larger amounts of red and processed meat than nonobese participants. 

To prevent confounding bias from distorting the results, confounders simply need to be identified and eliminated. Potential confounders can be identified by conducting multiple, repeated studies. 

Confounding bias can also be reduced in crossover studies, where participants are paired to themselves and act as their own controls. 

The ideal method, though, to reduce confounding bias is randomization, where each person is randomly assigned to one of the study gro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cytoskeleton_and_elastin_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K2UcAvzsQeyzLEjZhbcHbJPlQI65SDrv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cytoskeleton and elastin disorders: Pathology review]]></video:title><video:description><![CDATA[A 10 year old male, named Thomas, is brought to the clinic by his father because of a persistent fever, as well as a productive cough with dark, foul-smelling sputum. Upon further questioning, his father states that, since birth, Thomas has had multiple bouts of sinusitis and pneumonia, which required antibiotics. Upon chest auscultation, you realize that the heart sounds are heard on the right side of the chest! You then decide to order a chest X ray, which reveals that Thomas’ heart is in fact located on the right side of the chest! Finally, you get a CT scan, which reveals abnormally dilated airways. 

Right after Thomas, you meet Sara, a 17 year old female who comes into the clinic complaining that her joints frequently slip out of place. On physical examination, her height is at the 90th percentile and weight at the 60th percentile for her age. In addition, you notice that her fingers and toes are abnormally long. Upon chest auscultation, you hear a diastolic murmur in the aortic area. 

Based on the initial presentation, Thomas seems to have some sort of a cytoskeletal disorder, whereas Sara most likely has an elastin-related disorder.

Okay, before we start with cytoskeletal disorders, here’s a bit of physiology real quick! The cytoskeleton is an intracellular network of proteins, which allows each cell to maintain its shape, but also to move, contract, divide, and absorb or secrete molecules. Now, one of the protein structures in the cytoskeleton is microtubules. These are tiny hollow rods found at the base of cilia, which are hair-like structures on the surface of epithelial cells lining the respiratory and reproductive tracts. 

Specifically, each cilium has microtubules arranged in a 9+2 pattern, meaning there are 9 microtubules doublets on the periphery, as well as two single central microtubules. 

Now, in between the microtubules, there’s the dynein arm ATPase protein, which uses ATP to make microtubules slide past each other. This causes the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Purine_and_pyrimidine_synthesis_and_metabolism_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7AryM2LRSW2JR0mdqp51VeLnRnazThhX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Purine and pyrimidine synthesis and metabolism disorders: Pathology review]]></video:title><video:description><![CDATA[Three kids are brought to the clinic by three very concerned mothers. 

The first one’s Carl, a 10 month old boy that, according to his mother, is always sick with bronchitis and diarrhea. 

On physical examination, you notice that Carl is quite small for his age. 

Laboratory studies are obtained, showing an absolute lymphocyte count of 2,000 cells per cubic millimeter. 

A sputum culture reveals that Carl’s bronchitis is caused by a fungal infection by Pneumocystis jirovecii. 

Next comes Mark, a 2 year old boy with aggressive and self-destructive behavior, such as constantly biting his lips, tongue, and fingers. 

In addition, Mark doesn’t seem to be able to walk or speak a word. 

His mother tells you that her younger brother, so Mark’s uncle, was diagnosed with a rare disease that caused mental retardation, and she’s worried Mark may have it too. 

Upon physical exam, you notice some orange sand-like deposits in his diapers. 

Laboratory studies show elevated levels of uric acid in his blood. 

Finally, you see Laura, a 4 month old girl with a history of anemia that was diagnosed some days after birth. 

Since then, Laura has been on a bottle-feeding regimen with folate and vitamin B12 supplementation; however, her anemia is not getting any better. 

On examination, you notice cloudy urine that left some residues on Laura’s diaper, so you ask for a urinalysis. 

Results revealed that the residues are orotic acid crystals.

Based on the initial presentation, all three cases seemed to be due to purine and pyrimidine metabolism disorder. 

But first, a bit of  biochemistry review. 

Normally, each nucleotide can be broken down into a sugar that’s either a deoxyribose in DNA or a ribose in RNA, followed by one to three phosphate groups, and a nucleobase, which can be either a purine or a pyrimidine. 

There are two purine bases, adenine and guanine; and three pyrimidine bases, cytosine, thymine, and uracil. 

Now, the nucleoside based on adenine and ribos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eye_and_ear_histology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kV7-xzFPTdiTzN-wx6V-9ywqSzKmaIvM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eye and ear histology]]></video:title><video:description><![CDATA[Special senses, such as vision, smell, hearing, and balance are senses that use specialized organs and sensory receptors in order to convey information about a person’s surroundings to the central nervous system. 

This video will focus on the eyes, which are the sensory organs responsible for vision; and the inner ears, which are the sensory organs responsible for both hearing and balance.

The eyes are complex and highly developed photosensitive organs. 

Each eye has three concentric layers or tunics that make up the outer portion of the eye. 

The tough external fibrous layer is made up of both the sclera and transparent cornea. 

The vascular layer consists of the pigmented iris, choroid, &amp;amp; ciliary bodies. 

And the innermost sensory layer is formed by the retina. 

The optic nerve transmits the signal from the retina to the cerebrum. 

Even at low magnification, we can see that the inner portion of each eye is split into two main chambers by the lens: the aqueous chamber and vitreous chamber. 

The aqueous chamber is filled with a clear fluid called aqueous humor, and the vitreous chamber contains a gelatinous and transparent connective tissue called the vitreous body. 

Let’s first take a closer look at the outer fibrous layer or tunic. 

The cornea covers the anterior 1/6th of the eye and can be further divided into five sub-layers. 

Starting from the surface of the cornea is the corneal epithelium, then the bowman membrane, stroma, descemet’s membrane, and corneal endothelium along the inner surface. 

The corneal epithelium is made of non-keratinized stratified squamous epithelium that stains darker than the remaining layers.  

Bowman membrane is composed of collagen fibers and has a thickness between 7-12 µm. 

When stained with hematoxylin and eosin it can be difficult to identify, but it has a more solid pink appearance when compared to the underlying stroma. 

The stroma is the thickest layer of the cornea and is made of collagen f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuroendocrine_tumors_of_the_gastrointestinal_system:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uTqk8x3BSDqkjJu3qc_IaK-HSYKppQYz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuroendocrine tumors of the gastrointestinal system: Pathology review]]></video:title><video:description><![CDATA[A 27 year old female named Clara comes to the clinic complaining of abdominal pain and watery diarrhea, which started three months ago. Since then, Clara has also noticed that from time to time, the skin of her face and neck suddenly turns red and feels warm, especially when she drinks alcohol or gets angry. On clinical examination, you notice that both Clara’s legs and feet look swollen. Next, you run a urine test which shows an increased level of 5-hydroxyindoleacetic acid. You then decide to order a CT scan, which reveals a large mass in the appendix, along with several smaller masses involving the liver. Some days later, you see a 65 year old male named William, who came in complaining of heartburn and abdominal pain for the past few months. He also states that his stools are often greasy and foul-smelling. Upon further questioning, William mentions that lately he’s lost around 15 kilograms or 33 pounds, although he hasn’t been exercising or dieting at all. The first thing you do is run a blood test, which reveals a serum gastrin level of 1400 picograms per milliliter. Then, you decide to perform an upper gastrointestinal endoscopy, during which you observe multiple ulcers in the stomach, duodenum, and jejunum.

Okay, based on the initial presentation, both Clara and William seem to have some form of neuroendocrine tumor of the gastrointestinal system. These tumors arise from neuroendocrine cells, which are most abundant in the epithelial layer of gastrointestinal tract. Other common locations are the thyroid gland with medullary thyroid cancer, the lungs, where small cell carcinoma can occur, and the medulla of the adrenal gland, which can give rise to pheochromocytoma. 

Neuroendocrine cells get their name from the fact that they’re activated like neurons, since they can receive input from neurotransmitters released by other neurons, but they respond like endocrine cells by releasing hormones into the bloodstream. In a test question, neuroendocr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heme_synthesis_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rmXY4s6mSkG_krCZFCOs1EVaRSGk4Uh5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heme synthesis disorders: Pathology review]]></video:title><video:description><![CDATA[18 year old Christopher is brought to the emergency room by his best friend Paul after suddenly getting abdominal cramps at a party. Cristopher goes to the restroom while you ask Paul a few questions. Paul tells you that Cristopher was behaving strangely at the party, and adds that it was his first time drinking alcohol. When Christopher comes back from the restroom, he tells you that his urine had a reddish color. Unfortunately, his family history is unknown, since he was adopted at a very young age. Next to him, there’s 45 year old Magdalene, who developed skin blisters on her hands and forearms after spending the day having some alcoholic cocktails on the beach. Upon further questioning, Magdalene mentions that her urine had a strange tea color earlier. You decide to take a look at her past medical history, which reveals that Magdalene had hepatitis C a few weeks ago.  

Based on the initial presentation, both Christopher and Magdalene seem to have some form of heme synthesis disorder. Heme synthesis disorders are associated with hereditary or acquired deficiencies of enzymes that are involved in the heme synthesis pathway. But first let’s go over the heme synthesis pathway really quick! It’s important to remember that heme synthesis occurs in the liver, where heme is used in the cytochrome P450 enzyme system, as well as in the bone marrow where heme is used to synthesize hemoglobin. Now, heme synthesis begins in the mitochondria, where succinyl CoA binds to glycine via aminolevulinic acid or ALA synthase to produce aminolevulinic acid or ALA. Remember, this is the rate-limiting step for heme synthesis, meaning that it’s the slowest step in the pathway, and it requires vitamin B6, or pyridoxine, as a cofactor. What’s also high yield is that this step is stimulated by low levels of heme, while it’s inhibited by elevated levels of heme, as well as glucose and hemin, which is an oxidized form of heme that contains ferric iron or Fe3+ with chloride. Okay, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_transfusion_reactions_and_transplant_rejection:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bSdQar3ST5qdrgfGHnje2ITaSTGp0FOq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood transfusion reactions and transplant rejection: Pathology review]]></video:title><video:description><![CDATA[35 year old Adam is brought to the emergency department by an ambulance after being involved in a motor vehicle crash. Upon examination, you notice that he is significantly bleeding from his thigh, so you decide to give him a blood transfusion. Five minutes later, he develops shortness of breath, one episode of nonbloody vomiting, and a diffuse rash with erythematous borders starts to appear all over his body. Also, his blood pressure drops to 60 over 40 millimeters of mercury. Some days later, you see 50 year old Jack, who’s complaining of fever, malaise, and a decreased production of urine for the past two days. On further questioning, Jack tells you that he underwent a kidney transplantation one month ago. Upon examination, you realize that he has a high blood pressure of 150 over 80 millimeters of mercury. You decide to perform a biopsy of his transplanted kidney, which reveals a dense lymphocytic infiltrate.

Okay, based on the initial presentation, Adam seems to have some form of blood transfusion reaction, which includes any adverse event that occurs following blood transfusion. Jack, on the other hand, seems to be experiencing some form of transplant rejection, which is when the immune system of the recipient attacks the transplanted organ or graft. 

All right, let’s start with blood transfusion reactions. For your tests, there are six blood transfusion reactions that you need to be aware of, including anaphylactic or allergic transfusion reaction, acute hemolytic transfusion reaction, delayed hemolytic transfusion reaction, febrile nonhemolytic transfusion reaction, transfusion-related acute lung injury, and transfusion-associated circulatory overload. 

Let’s begin with the anaphylactic or allergic transfusion reaction. It is a type I hypersensitivity reaction mediated by the recipient’s IgE antibodies against plasma proteins like immunoglobulins found in transfused blood. Initially, the proteins in the donor’s plasma will be recognized by ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunodeficiencies:_T-cell_and_B-cell_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c6jznnSvQ4GELMXTNhG_5W8CTluge4Jy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunodeficiencies: T-cell and B-cell disorders: Pathology review]]></video:title><video:description><![CDATA[Gaia, a 6 year old girl, is brought to the clinic by her parents because she’s been having diarrhea and abdominal cramps for the past few weeks. 

When you ask about her clinical history, her parents tell you that Gaia was diagnosed with celiac disease a few years back; however, they point out that she&amp;#39;s stopped consuming any food products that may contain gluten altogether. 

You decide to first run stool tests, which reveal the presence of the parasite giardia lamblia. 

In addition, Gaia’s parents tell you that she has a history of asthma and allergic rhinitis, so you also order an immunoglobulin test, which shows low IgA and increased IgE levels in her blood. 

Next comes Joe, a 10 year old boy that’s brought to the clinic because he fell and broke his arm. 

Upon physical examination, you notice a red, weeping rash on his scalp.

You also notice that there’s a skin abscess on his leg that lacks any surrounding warmth and redness. 

Joe’s parents tell you that he develops abscesses like that all the time.

You order an immunoglobulin test for Joe too, which reveals increased IgE but normal IgA levels.

Based on the initial presentation, both cases seem to have some form of immunodeficiency, meaning that their immune system&amp;#39;s ability to fight pathogens is compromised. 

Immunodeficiencies can be classified according to the cell of the immune system that is defective, into B cell and T cell disorders, which respectively lead to a deficiency in humoral or antibody-mediated and cell-mediated immune responses. 

Let’s begin with B cell disorders, starting with Bruton or X-linked agammaglobulinemia, or XLA for short. 

This is caused by a mutation in the BTK gene, which is found on the X chromosome. 

XLA is an X-linked recessive condition, so it almost exclusively manifests in biological males because they have only one X chromosome. 

On the other hand, biological females have two X chromosomes, so even if they have a defective ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bacterial_and_viral_skin_infections:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8IyTEEs4SaWbymczrehFVkQpQJqgOm2i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bacterial and viral skin infections: Pathology review]]></video:title><video:description><![CDATA[At the clinic, 10-year-old Quentin is brought by his parents after an episode of dark-colored urine. Upon examination, his blood pressure is high and you notice that the area around his ankles appears swollen. His parents also mention that last week, Quentin developed multiple vesicles with a honey-colored crusting around his nose and mouth. You decide to perform a urinalysis test, which reveals there’s blood in the urine with red blood cell casts, as well as higher than normal levels of protein. 

Later on that same day, 70-year-old Claudio presents to the emergency department complaining of severe pain in his genital area that started about a week ago. On examination, you notice severe scrotal swelling, a purplish rash, and palpable crepitus in the perineal area. Claudio also appears lethargic, and has a fever and low blood pressure. Upon further questioning, Claudio mentions that he had surgery for varicocele about two weeks ago. Past medical history reveals that in his 40s, Claudio was diagnosed with diabetes mellitus, which he has not been controlling properly. You decide to order a swab culture, which comes back positive for anaerobic bacteria and Streptococcus pyogenes. 

Based on the initial presentation, both Quentin and Claudio seem to have some form of skin infection. 

Okay, first, let’s go over some physiology. Normally, the skin is divided into three main layers, the hypodermis, dermis, and epidermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Above the hypodermis is the dermis, which contains hair follicles, nerve endings, glands, blood vessels, and lymphatics. And above the dermis is the epidermis, which contains five layers of developing keratinocytes. 

Keratinocytes start their life at the lowest layer of the epidermis, so the stratum basale or basal layer. As keratinocytes in the stratum basale mature, they migrate up into the next layers of the epidermis, called the stratum spino]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Viral_exanthems_of_childhood:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H4yrHcgMT2qr8UQrJaqEB3rzSR6ihAvr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Viral exanthems of childhood: Pathology review]]></video:title><video:description><![CDATA[A 1 year old boy named Adam is brought to the pediatric clinic by his mother, who is concerned because Adam developed a pink skin rash that began in the trunk and has now spread to the extremities. 

On physical examination, the rash appears to be maculopapular. Upon further questioning, she recalls that Adam had a high fever for the past few days, and the rash appeared after the fever went down. 

Next you see Rose, a 9 year old girl who came in with her father, due to a very itchy rash all over her body. Her father claims that the rash started 2 days ago after having a mild fever, and that several of Rose’s schoolmates also have the same rash. 

Upon physical examination, you notice that the rash involves her face, trunk, and extremities, and presents with different types of lesions, including papules, vesicles, and crusts.

Now, based on the initial presentation, both Adam and Rose seem to have a viral exanthem of childhood, which is a group of eruptive skin rashes caused by viral infection and usually affect children. 

Generally, viral exanthems can be macular, papular, maculopapular, or vesicular. A macular rash has macules, which are up to 5 mm in diameter, and completely flat, meaning that you can’t feel them if you run your finger over them. 

On the other hand, a papular rash has papules, which are raised bumps that are up to 1 cm in diameter. And a maculopapular has both macules and papules. 

Finally, a vesicular rash has vesicles, which are up to 5 mm in diameter, and look like clear blisters filled with fluid. Viral exanthems of childhood include varicella; hand-foot-mouth disease; roseola infantum; measles; rubella; and erythema infectiosum.

Alright, now one of the most common viral exanthems is varicella, more commonly referred to as chickenpox. It is caused by the varicella-zoster virus, or VZV for short, which is a DNA virus, and is also known as human herpesvirus 3 or HHV-3, as it belongs to the Herpesviridae family. 

Now, this is a hi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_musculoskeletal_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6v_LeGWNTdSZXwrrqp74qEzKRISToR9X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric musculoskeletal disorders: Pathology review]]></video:title><video:description><![CDATA[A 13-year-old boy named Lucas comes to the clinic for right knee pain, which gets worse when he is running, jumping, or climbing stairs. Upon further questioning, Lucas mentions that he plays basketball for his school team, and recently, he started training more intensely for an upcoming tournament. On physical examination, you are able to move his hip in all directions with no resistance or pain, but you notice that his right knee has a more prominent tibial tubercle, which is also tender to the touch.  

Some days later, a 4-year-old girl named Sophia is brought to the clinic by her parent. Earlier that day, Sofia’s older sibling was swinging her by the arms. Since then, Sofia has been experiencing pain in her right arm when she tries to move it. On physical examination, you notice that Sophia is holding her arm by her body, and cries when you try to move it. You decide to quickly hyperpronate her arm, after which Sophia becomes able to use her arm again without pain.  

Okay, both Lucas and Sophia seem to have some form of a pediatric musculoskeletal condition, meaning a condition that commonly affects the muscles, bones, or cartilage of individuals younger than 18 years. For your tests, the most high-yield pediatric musculoskeletal disorders include developmental dysplasia of the hip, Legg-Calvé-Perthes disease, slipped capital femoral epiphysis, Osgood-Schlatter disease, patellofemoral syndrome, radial head subluxation, and a variety of bone fractures.  

Okay, let’s start with developmental dysplasia of the hip, or DDH, which is also known as congenital hip dysplasia. In DDH, the femoral head dislocates out of the acetabulum during development in utero. For your exams, it’s important to keep in mind that this is more common in twin or multiple pregnancies, where the fetuses have to share the space within the uterus, which may put a lot of pressure on them; as well as in firstborns, because the mother’s uterus is not as stretched out; o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disorders_of_sex_chromosomes:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yom7eFlVRvKYhVlHOLNPNjspReaJ-u-Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disorders of sex chromosomes: Pathology review]]></video:title><video:description><![CDATA[Noam, a 33 year old male, comes to the clinic after trying to conceive a baby with his wife for more than a year, with no luck. Noam is very thin and quite tall. Upon physical examination, you notice that his testes are smaller than normal, and he has enlarged breast tissue. In addition, Noam doesn’t seem to have much facial and pubic hair. You decide to run a blood test, which reveals that Noam’s testosterone and inhibin B levels are decreased, while gonadotropin and estrogen are increased. In addition, you perform a karyotype analysis on his cells and find 47 chromosomes, among which there’s two X chromosomes and one Y chromosome. 

Next, you see Hadas, a 17 year old girl who’s worried because she hasn’t gotten her first menstrual period yet. The first thing you notice is that Hadas is quite short for her age. Upon physical examination, she has a webbed neck, a broad chest, and poorly developed breasts with widely spaced nipples. In addition, you notice her ring fingers are very short. A blood test shows low estrogen levels and high gonadotropins, and a karyotype analysis reveals only 45 chromosomes, with one X chromosome.

Okay, based on their presentation, both Hadas and Noam seem to have some sort of disorder of sex chromosomes. Now, humans typically have 23 pairs of chromosomes, so 46 total; out of which 22 pairs are autosomal, and 1 pair consists of sex choromosomes, which can be X or Y. Generally, an individual with two X chromosomes, or 46,XX is considered to be genetically female. However, only one X chromosome gets expressed and the other is inactivated through a process called X inactivation or lyonization, becoming a Barr body. On the other hand, an individual with one X and one Y chromosome, or 46,XY is genetically male. And since there’s only one X chromosome to begin with, there’s generally no Barr body. 

Now, individuals with sex chromosome disorders have aneuploidy, meaning that there’s a missing or extra sex chromosome. Most often, this]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disorders_of_sexual_development_and_sex_hormones:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4EhG1ZnXTP6oZqGGXt8d8UIrSKe8y7m3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disorders of sexual development and sex hormones: Pathology review]]></video:title><video:description><![CDATA[Clay, a 17 year old male arrives at the clinic after noticing that he’s not developing like his friends. On further questioning, Clay mentions that he was born without a sense of smell. Upon physical examination, you notice that he has no facial or body hair, and that his external genitals are small and underdeveloped for his age. You decide to run a blood test, which shows low levels of the hormones GnRH, LH, FSH, and testosterone. Finally, you order a semen analysis, which reveals a low sperm count. 

Next comes Jessie, a 13 year old girl, and her concerned mother, who’s noticed that Jessie has started to develop some masculine features, such as a deeper voice and excess body hair growth. A blood test shows increased testosterone levels and low dihydrotestosterone, so you decide to perform a karyotype test, which reveals 46 chromosomes, with one X and one Y chromosome. 

Okay, now based on their initial presentation, both Clay and Jessie seem to have some form of disorder of sexual development and sex hormones.

But first, let’s go over some terminology! On the one hand, we all have a genotypic sex, which is determined by our karyotype or set of chromosomes. Generally, there are two sex chromosomes; those who have X and Y sex chromosomes are typically considered genetically males, while those who only have X chromosomes are typically considered genetically females. On the other hand, phenotypic sex is determined by the primary sexual characteristics, so the genitalia and gonads, as well as the secondary sexual characteristics, such as breast and muscle development, as well as body hair and fat distribution. 

The development of primary and secondary sexual characteristics is generally under control of the hypothalamic-pituitary-gonadal axis. First, the hypothalamus secretes gonadotropin-releasing hormone, or GnRH for short, which goes to the anterior pituitary to stimulate the release of gonadotropic hormones, which are luteinizing hormone or LH, and fol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexually_transmitted_infections:_Vaginitis_and_cervicitis:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zTf2rnCeSkW9yTgmtqZYVQVWQGOilhh3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sexually transmitted infections: Vaginitis and cervicitis: Pathology review]]></video:title><video:description><![CDATA[A 26 year old female named Anna comes to the clinic one day with complaints of painful and more frequent urination, as well as pain during sexual intercourse, and increased vaginal discharge for the past 5 days. Upon further questioning, Anna tells you that she’s had multiple sexual partners lately. On physical examination, there&amp;#39;s purulent vaginal discharge. You obtain a discharge sample with a swab and perform a Gram stain, which reveals the presence of gram-negative diplococci bacteria within neutrophils. You prescribe her a combination of azithromycin and ceftriaxone. 

A year later, Anna comes back with similar complaints, but this time she also has a fever; and lower abdominal pain that worsens when she moves. Upon further questioning, Anna reveals that she’s had two more episodes of vaginal infections over the past year, but she didn’t seek medical attention. On physical examination, you notice that Anna has a fever, and when you perform a gynecological exam, movement of the cervix elicits pain. 

Now, based on the initial presentation, Anna seems to have vaginitis or cervicitis caused by a sexually transmitted infection, or STI for short. STIs are mainly transmitted from person to person during sexual contact through body fluids, such as vaginal secretions, semen, or blood. The ones most at risk of contracting an STI are sexually active individuals, particularly those who have unprotected sex or multiple sexual partners. But, it’s important to note that sexually transmitted infections can also be transmitted via contact with skin or mucous membranes, including eyes, mouth, throat, and anus. And that’s a high yield fact!

Now, STIs that may cause vaginitis and cervicitis include chlamydia, which is caused by Chlamydia trachomatis; gonorrhea, which is caused by Neisseria gonorrhoeae; and trichomoniasis, caused by Trichomonas vaginalis.

Now, let’s begin with Chlamydia trachomatis, which is a gram-negative obligate intracellular bacteriu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/HIV_and_AIDS:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_0aMK6I5TUiHahzG5HdHEi5RRm6xdJ_s/_.jpg</video:thumbnail_loc><video:title><![CDATA[HIV and AIDS: Pathology review]]></video:title><video:description><![CDATA[Two people come to the infectious disease clinic. The first one’s David, a 42 year old man who has a fever, associated with a cough and difficulty breathing. David mentions that he’s HIV-positive, so you decide to run a blood test, which reveals an alarming T cell count of 180 cells / mm3. You immediately ask for a chest X-ray, which shows gray hazy-looking areas in both lungs. Next comes Charles, a 32 year old man. Charles was referred to the clinic by his dentist, who detected white plaques on both sides of his tongue. When you try to scrape the plaques with a tongue depressor, you realize that they can’t be removed. Upon further questioning, Charles tells you that lately he’s been losing a ton of weight, although he hasn’t been exercising or dieting at all. You decide to ask for an HIV-1/2 antigen/antibody immunoassay, which turns out positive.
Okay, now both David and Charles have HIV, which stands for human immunodeficiency virus. HIV specifically targets the cells of our immune system, leading to progressive immunodeficiency, which is when the immune system begins to fail gradually. Ultimately, affected individuals can develop AIDS, or acquired immunodeficiency syndrome. What’s important to note is that AIDS puts at increased risk of certain opportunistic infections or tumors that a healthy immune system would usually be able to fend off.

Now, HIV can be transmitted via certain bodily fluids from an infected person, including blood, genital fluids like semen or vaginal discharge, and breast milk. However, HIV is not present in saliva, sweat, urine, or feces. Now, to contract the infection, these bodily fluids need to come into direct contact with a healthy person&amp;#39;s blood, broken skin, or mucosal surfaces. 

The most common means of transmission is horizontal via sexual intercourse, especially via male-to-male transmission, but also male-to-female and female-to-male transmissions can occur, while female-to-female transmission of HIV is quite]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_TORCH_infections:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8283_IyYT9aQqcQXlWkbPbxcRwCL7dZ2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital TORCH infections: Pathology review]]></video:title><video:description><![CDATA[At the clinic, two mothers came in with their babies. The first baby is an 11 month old girl called Cecile, who is brought by her parents, who are immigrants, for a routine visit. You immediately noticed that she doesn’t react when you call her name, as if she can’t hear you at all. Upon eye examination, you find that Cecile has bilateral clouding of the lens. Then, upon cardiac auscultation, you hear a continuous rumbling murmur. Upon further questioning, Cecile’s mother tells you that, during the first trimester of pregnancy, she developed a rash that mainly involved her head and neck, as well as swollen lymph nodes behind the ears. 

After Cecile, comes a 6 month old baby boy named Arthur with his mother, who is concerned because Arthur has developed multiple purple marks on his skin. Upon physical examination, you noticed that Arthur has an unusually large head for his age. Then, on fundoscopy, his eyes show white and yellow scars that look like cotton. You decide to order a CT scan of the brain, which reveals scattered calcifications. Upon further questioning, Arthur’s mother admits to handling her cat’s litter while she was pregnant, despite her doctor’s advice against it. 

All right, now both Cecile and Arthur seem to have a congenital TORCH infection. TORCH is an acronym that stands for infections caused by Toxoplasma gondii; Other agents, such as syphilis, parvovirus B19, varicella zoster virus, and listeria; then there’s Rubella; Cytomegalovirus, and finally Herpes simplex virus-2 or HSV-2. 

All these infections are lumped together because they can be vertically transmitted, which means that a pregnant individual can transmit the infection to their child either before birth via the placenta, or during and after birth via blood, body fluids, or breast milk. 

Now, keep in mind that TORCH infections may share some non-specific signs and symptoms, including delayed growth, and hepatosplenomegaly or enlarged liver and spleen, which can lead to jaun]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Apnea,_hypoventilation_and_pulmonary_hypertension:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qpd5lLEqQKq_6B5PRMGAd0d9R6_Eyd4j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Apnea, hypoventilation and pulmonary hypertension: Pathology review]]></video:title><video:description><![CDATA[Joseph, a 42 year old man comes to the clinic because he’s been waking up many times at night, which makes him very sleepy during the day. 

His partner also complains that Joseph has always snored but recently it’s louder than ever. 

On physical examination he has a  BMI of 35 kilograms per square meter, and has a blood pressure of 140 over 90 millimeters of mercury. 

You decide to conduct a sleep study, which reveals a very low partial pressure of oxygen. 

Later, a 35 year old woman called Robin also comes to the clinic. 

She tells you that, lately, she’s been experiencing shortness of breath and fatigue. 

Robin is quite worried, and mentions that she has a congenital heart defect. 

On physical examination, she has a mean pulmonary arterial pressure of 28 millimeters of mercury. 

You decide to perform an electrocardiogram or ECG test, and a chest X-ray, which show that Robin has right ventricular hypertrophy.

Based on the presentation, both cases seem to have some respiratory disease, associated with some cardiovascular issues. 

Now, for your exams, some important conditions include sleep apnea, obesity hypoventilation syndrome, and pulmonary hypertension. 

So, let’s begin with sleep apnea! 

This is when a person, during their sleep, experiences recurrent and intermittent episodes in which they stop breathing for more than 10 seconds. 

In addition, since fresh air is not getting into the lungs, individuals with sleep apnea will have nocturnal hypoxia. 

This puts the body under stress, which in turn responds by releasing epinephrine. 

Now, the recurrent epinephrine surges have several effects. 

Firstly, this wakes up the person so that they can breathe again. 

This causes disrupted sleep, which in turn leads to somnolence or sleepiness during the day or while awake. 

Secondly, the body tries to compensate for the hypoxia by increasing the amount of red blood cells, or erythrocytes, available to carry the oxygen in blood to our tissues. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-biologic_disease_modifying_anti-rheumatic_drugs_(DMARDs)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hnILb7xkTJKNFCNnQCDBdy_WTWuUSvUH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-biologic disease modifying anti-rheumatic drugs (DMARDs)]]></video:title><video:description><![CDATA[Disease-modifying anti-rheumatic drugs, or DMARDs for short, are a group of medications primarily used to modify or slow down the progression of rheumatoid arthritis. Now, there are two types of DMARDs, biologic DMARDs, which are developed from microorganisms, animals, or humans, and non-biologic DMARDs, which are chemically synthesized in the laboratory. In this video, we’ll particularly focus on the non-biologic DMARDs.

Alright, first let’s talk about physiology eal quick. During the S phase of the cell cycle, the cell performs DNA replication. DNA is composed of a sequence of deoxyribonucleotides and each deoxyribonucleotide is made out of a phosphate group, a five-carbon sugar like deoxyribose, and a nucleobase, which can be either a pyrimidine like cytosine, or thymidine, or a purine like adenine or guanine. Now, pyrimidine synthesis starts when folic acid, or vitamin B9, from our diet, is converted into dihydrofolate or DHF. DHF then gets converted by an enzyme called dihydrofolate reductase or DHFR into tetrahydrofolate, or THF. 

THF acts as a mediator and accepts a methyl group from the amino acid serine, becoming 5,10-methyl-THF. This methyl group is then used by an enzyme called thymidylate synthetase, which transfers it to dUMP or deoxyuridine monophosphate, turning it to dTMP or deoxythymidine monophosphate. dTMP then through a series of reactions eventually turns into thymine. And at that point, we’re all set to make DNA. 

At the same time, purine synthesis starts with the amino acids glutamine, aspartate, and glycine, together with bicarbonate and formate, which is the anion derived from formic acid. These undergo a ten-step pathway and the result is inosine monophosphate, or IMP, which is a precursor to adenine and guanine. And at that point, we’re all set to make DNA.

Okay, now, rheumatoid arthritis or RA for short is a chronic, progressive, inflammatory disorder that affects synovial joints and, sometimes, other parts of the body like ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_overdoses_and_toxicities:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/olsbw9g1SlKZ_uqlIdq8Zf7zQQyGNbO-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication overdoses and toxicities: Pathology review]]></video:title><video:description><![CDATA[A 19 year old young man named Cameron is brought to the emergency room by his father, who found Cameron vomiting next to a half-empty bottle of aspirin. Cameron tells you that he has a headache and is hearing a weird ringing noise. You decide to perform a blood test, which reveals that Cameron has metabolic acidosis. 

Later that day, 32 year old Adaline presents in the emergency room due to nausea, vomiting, and slurred speech. Adaline reports that she has the flu and has been taking ibuprofen for the last couple of days. You notice that Adaline is very thirsty, and she also keeps going to the restroom to urinate. Her history reveals that she was diagnosed with bipolar disorder a few years ago, and is currently under treatment with lithium. 

Based on their history and presentation, both Cameron and Adaline seem to have some type of medication overdose or toxicity. An overdose refers to taking too much of a substance, and can result in toxicity, which refers to how harmful that substance can be to the body. 

Now, let’s go over some pharmacology basics. The therapeutic index, or TI for short, is a quantitative measurement of a drug’s dosing and its safety. For your exams, you should know that the TI is calculated as the ratio of the median toxic dose or TD50, which is the dose that causes a toxic response in 50% of the population, over the median effective dose or ED50, which is the dose that causes a therapeutic effect in 50% of the population. 

Now, if the test question gives you a median lethal dose or LD50 for short instead of TD50, don’t panic! These two can be used interchangeably in the formula, but keep in mind that TD50 refers to human clinical trials, while LD50 refers to animal studies, and is defined as the dose that causes death in 50% of tested animals. 

The important thing to note here is that medications with a wide therapeutic index are safer, since their toxic dose is much higher than their effective dose. On the flip si]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Environmental_and_chemical_toxicities:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x8wfhJ-STGye8XRcJOMUXM02QW6SqtOs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Environmental and chemical toxicities: Pathology review]]></video:title><video:description><![CDATA[Kristen is a 47 year old female who showed up at the ER due to vomiting and diarrhea. Kristen works as a farmer, and tells you that her symptoms started right after she sprayed her crops with insecticides using her bare hands. On clinical examination, her pupils appear constricted. And a few minutes later, Kristen has a seizure. 

Next comes Federico, a 9 year old boy who is brought to the ER by his parents after accidentally consuming a bottle of insecticide. His parents mention that he complained of stomach ache, and had repeated episodes of vomiting and diarrhea. Upon clinical examination, you first notice that Federico&amp;#39;s breath has a characteristic garlic-like odor. 

Lastly, you see Richard and Lucy, a 60 year old couple that arrived at the ER, both complaining of a dull headache and nausea. They seem confused, but they mention that their symptoms started more or less at the same time, while they were both relaxing next to the fireplace. Upon clinical examination, you realize that their skin looks cherry red, so you decide to run a blood test, which reveals high carboxyhemoglobin levels.

Based on their history and presentation, all cases seem to have some form of environmental and chemical toxicity. Toxicity refers to the extent of poisoning or damage to the body due to exposure to a toxic substance. For your exams, the most high yield toxic substances include acetylcholinesterase inhibitors; methanol and ethylene glycol; heavy metals, including arsenic, iron, lead, and mercury; cyanide and carbon monoxide; as well as methemoglobin, which is an endogenous substance that can become toxic at high levels. 

Let’s start with acetylcholinesterase inhibitor poisoning. Okay, normally, acetylcholinesterases are enzymes that break down the neurotransmitter acetylcholine, so that it can’t activate the cholinergic receptors in the peripheral and central nervous system. And there are two types of cholinergic receptors, called muscarinic and nicotinic re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_vestibulocochlear_nerve_(CN_VIII)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bq29edZfRQeuC7re9qMfQNgpReWLOPXV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the vestibulocochlear nerve (CN VIII)]]></video:title><video:description><![CDATA[Do you know that feeling when you listen to your favorite song and you start dancing along? Well, you can thank the eighth cranial nerve for that! CN eight, or the vestibulocochlear nerve, transmits special sensory information, related to balance and hearing, from the inner ear to the brain. 

The vestibulocochlear nerve emerges laterally at the cerebellopontine angle, which is the junction between the pons, medulla and cerebellum. Once it emerges from the cerebellopontine angle, it enters the internal acoustic meatus where it separates into its two branches: the cochlear nerve and the vestibular nerve. The cochlear nerve carries information about hearing, and the vestibular nerve carries information about movements of the head which aids in balance. 

Now, let’s look at the pathway of sensory information, starting with the auditory pathway. This begins in the cochlea, which is a bony tube that spirals on itself, resembling the shape of a snail shell. 

If we uncoil this structure and look within it in cross-section, there are three fluid-filled cavities called the scala vestibuli, the cochlear duct, and the scala tympani. The scala vestibuli is connected to the middle ear through the oval window, and contains perilymph. The cochlear duct is filled with endolymph, and houses the organ of Corti, which is our organ of hearing and contains our hearing receptors, or hair cells. Finally, the scala tympani is connected to the middle ear through the round window, and it also contains perilymph. 

The auditory pathway does begin in the cochlea, but first the sound waves have to get from the outside world to the cochlea and this requires the help of some very small structures. The sound vibrations first travel through the external ear and vibrate the tympanic membrane which sends a cascade of vibrations through the ossicles in the middle ear which eventually transmit these vibrations against the oval window. 

When these vibrations hit the oval window, they transfe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Monitoring_fluid_intake_and_output_(for_nursing_assistant_training)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IoepsQjpQm6KfHL4FooQjX9HRnqPAVfr/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Monitoring fluid intake and output (for nursing assistant training)]]></video:title><video:description><![CDATA[Normally, the amount of total body water should be balanced through the ingestion and elimination of water: ins and outs. To ensure this balance, as a nursing assistant, you may need to track and record all fluid intake and output on an intake and output sheet, commonly known as an I&amp;amp;O sheet. This is particularly important for certain groups of clients, like those on special fluid orders, including “encourage fluids” and “restrict fluids;” those who are at risk of developing dehydration, or losing too much body fluid, which impairs normal body functions; or those who might develop edema where swelling occurs in tissues due to excess fluid build up. High risk of dehydration exists for those who may not be drinking an adequate amount of fluids throughout the day or those who might be losing too much due to receiving certain medications, like diuretics, or through vomiting, diarrhea, bleeding, burns, excessive sweating, fever, or vigorous exercise. Common signs include dry mouth, excessive thirst, and dark urine. Likewise, clients at risk of developing edema include those receiving intravenous fluids or those with heart or kidney disease, where the body has trouble eliminating excess fluid. The fluid builds up and causes swelling, especially in the lower extremities. Nursing assistants should check with nurses in charge of the client and the nursing plan of care to find out if the clients intake and output should be monitored. So, every time one of these clients receives or loses fluids in any way, the exact volume can be recorded. These volumes are then totaled at the end of every shift and then at the end of a 24-hour period. 

Okay, so for fluid intake, you’ll need to count anything the client drinks, including water and beverages as well as all foods that are liquid at room temperature, like ice cream, gelatin, sherbert, pudding, custard, ice chips, and popsicles. The nurse will also measure the fluids provided through intravenous therapy, entera]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cranial_nerves_rap</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YdVKelEhQWuAqnMik9WusTOLRiC8m_21/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cranial nerves rap]]></video:title><video:description><![CDATA[Hey man, what&amp;#39;s up?

Yo, I was just calling about the cranial nerves test we have next week.

Yeah, what about it? You ready for it?

Nah, man; I find it so hard trying to remember all 12 nerves!

Yeah, I get that. Have you tried Osmosis?

What, put a textbook to my head and hope it diffuses into my brain?

No, man...Does that work?

I don&amp;#39;t think so, I don&amp;#39;t feel anything.

Well, I mean Osmosis, they&amp;#39;re people who help med students learn! They make videos, yeah.

How much can you learn from a video?

You&amp;#39;d be surprised. Check this out!

Where is that music coming from?

Just listen closely:

Number one, the first piece in this whole gallery

Enjoy your favorite food without a sole calorie

Well it makes sense to me and I’m not talkin’ salary

The nerve pickin’ particles out is the olfactory

Number 2, let me get you up to speed with a synopsis

the nerve that I do all my seeing with is the optic

Passin’ through the pupil, light’s sent into the retina

Your eye will spy exactly where I’m going on this topic

But that’s not the only one controlling the eye, this

nerve: Number Three’s the one contracting the iris

If we’re speakin’ ciliary this is your controller

Or keep your eyes rollin with the oculomotor

If lights are movin’ up and down like a copier

What nerve is lettin’ your eyes follow? The trochlear

It’s Number Four, but it’s got a singular mission

Ironic that a purpose is prevent double vision

“The brain and the spinal cord

connecting like a circuit board,

to send signals from all of the above

Axons and dendrites

reading different stimuli

and store memories for learning or for love.”

Number Six, a sight nerve’s got you lookin’ left and right,

Like you’re crossing the street, or when you write and you read

or, if ya lookin’ to sneak, or following somebody serving

The abducens movin’ your eyes, like they’re swerving

Now back to number five, you thought I skipped one?

Nah, take V and make i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Collagen_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ssnn4vmKTKGs77MGO8h9awGrRz6hxww7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Collagen disorders: Pathology review]]></video:title><video:description><![CDATA[A 5 year old male, named Mateo, is brought by his father to the emergency department for right thigh pain. Past medical history reveals multiple fractures following minor traumas. Upon further questioning, Mateo’s father states that Mateo has been experiencing progressive hearing loss. On physical examination, you notice that Mateo’s scleras appear bluish in color. You then decide to order an X-ray, which shows a fracture of the right femur. 

Later that day, you see  Mary, an 18 year old female, who comes in complaining of left shoulder pain after she tripped during a basketball game. She mentions that she&amp;#39;s had multiple joint dislocations since childhood, including two elbow dislocations in the past year. Mary has also noticed that her skin is “stretchy” when pulled, and seems to bruise easily. You then order an X-ray, which reveals anterior dislocation of the left shoulder. 

Based on the initial presentation, both Mateo and Mary seem to have some form of a collagen disorder. So let’s first start with a bit of physiology real quick! What’s high yield for your exams is that there are five major types of collagen. Type I collagen is mainly found in the skin, sclera, teeth, bones, tendons, and ligaments. Type II collagen is abundant in cartilage. Type III collagen is mainly present in the walls of blood vessels, as well as hollow organs, like the intestines and the uterus. Type IV collagen is found in the basement membrane of the glomeruli of the kidneys, as well as the lens of the eyes, and cochlea of the inner ears. Finally, there’s type V collagen, which is found in cell surfaces, hair, and placenta, as well as in places where type I collagen is found.

Now, collagen synthesis starts when the collagen genes get transcribed from DNA to mRNA, which gets translated into an alpha chain of amino acids, which mostly consists of repetitive sequences of glycine, proline, and lysine. Some of these proline and lysine residues will then need to get hydrox]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pericardial_effusion_and_cardiac_tamponade:_Nursing_process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NXiSwttaRVmQsMVVPO51ycs5TceMtJfI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pericardial effusion and cardiac tamponade: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Lydia Smith is a 42-year-old female client with a history of metastatic breast cancer currently being treated with radiation therapy. 

She presents with shortness of breath and chest pain while at the radiation therapy clinic this morning. 

She states she started having intermittent chest pain two days prior that feels like heavy pressure under her sternum. 

Her radiation treatment is postponed temporarily, and her oncologist sends her for several cardiac tests including a chest x-ray, electrocardiogram or ECG, and an echocardiogram, to determine the cause of her symptoms. 

Her cardiac test results confirm a large pericardial effusion, and she is directly admitted by her oncologist to a telemetry unit pending pericardiocentesis.

When extra fluid builds up in the pericardial cavity, it is known as pericardial effusion, which can then develop into cardiac tamponade depending on how much extra fluid there is and how quickly it accumulates. 

Cardiac tamponade puts pressure on the outside of the heart restricting its movement. 

As a result, the heart is unable to pump normally, causing compromised cardiac functioning and resulting in decreased cardiac output.

The heart sits inside a two-layered pouch called the pericardium. 

Within this pouch there is the pericardial cavity which is filled with a small amount of fluid that lets the heart slip around as it beats. 

Typically, there is approximately 15 to 50 milliliters of fluid in the pericardial cavity at any given time.

The pericardial cavity can stretch to accommodate a gradual accumulation of fluid without immediate adverse effects. 

When fluid accumulates gradually, the pericardium can hold as much as 1.5 liters of fluid before tamponade sets in. 

In contrast, if there is a rapid buildup of fluid, even as little as 100 milliliters, does not allow the pericardial cavity to stretch and can compress the heart, leading to cardiac tamponade.

A rapid accumulation of fluid can occur as a result of tra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aortic_aneurysm:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fM1-vYDlTTm2dnF91BpFk4eYTpSD2M9b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aortic aneurysm: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[David Carter is a 65-year-old male client who arrives at the Primary Care Clinic for his annual follow-up appointment. 

He is a current smoker and has a history of hypertension and atherosclerosis. 

He was diagnosed with 4.0 cm asymptomatic abdominal aortic aneurysm last year. 

Mr. Carter brought in his blood pressure machine from home, and he tells the front desk staff he is feeling anxious about his appointment today. 

The aorta is a large elastic artery that carries blood from the left ventricle of the heart, down through the thorax and abdomen. 

The artery wall consists of three layers: the tunica intima, tunica media, and the tunica adventitia, which are composed of smooth muscle, elastic fibers and collagen which give the artery strength and elasticity. 

If an area of weakness develops along the aorta, a dilation or bulge forms, called an aneurysm. 

Aortic aneurysms are described according to their location, shape, size, and whether they involve all or part of the artery wall. 

So, if the aneurysm forms within the abdominal cavity, it’s called an abdominal aortic aneurysm, or Triple-A. 

Likewise, if the aneurysm is found within the thorax, or chest, it’s called a thoracic aortic aneurysm, or T double-A. 

Finally, a thoracoabdominal aortic aneurysm, or T triple-A involves both the thoracic and abdominal aorta. 

Aortic aneurysms come in two basic shapes. 

A circular dilation that involves the entire circumference of the aorta is called a fusiform aneurysm. 

In contrast, a saccular aneurysm is formed when there’s only a localized outpouching, like a bubble on the side of the aorta. 

Both fusiform and saccular aneurysms are classified as true aneurysms because they involve all three layers of the aortic wall. 

In cases where there’s only a partial disruption of the artery wall, it’s called a false, or pseudoaneurysm.

In general, an aneurysm that measures between 3 and 4.4 centimeters is considered a small aneurysm; medium aneurysms have a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_obstructive_pulmonary_disease_(COPD):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W2a4ry2nTQ2rJl5EWNTt7ZrCTO6n0QTS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic obstructive pulmonary disease (COPD): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[James Robyn is a 67-year-old male client who was brought to the emergency department, or ED, with a 3-day history of exertional breathlessness, wheezing, fatigue, and a worsening productive cough. 

He states he has been having increased difficulty with normal day to day activities such as eating, talking and going up the stairs. 

He has a history of cigarette smoking, two packs per day, since he was 25 years old. 

However, he quit smoking a year ago after being diagnosed with chronic obstructive pulmonary disease, or COPD. 

COPD, or chronic obstructive pulmonary disease, is a type of lung disease where chronic inflammation causes damage to the lungs and obstructs airflow. 

It’s usually caused by inhalation of toxic substances, like tobacco smoke, or occupational pollutants like dust and silica. 

In some people an autosomal dominant disorder called alpha-1 antitrypsin deficiency results in breakdown of the lung parenchyma by an enzyme called elastase.  

COPD is characterized by long-term inflammation of the bronchial tubes, referred to as chronic bronchitis, and alveolar destruction, referred to as emphysema. 

Most people diagnosed with COPD have elements of both chronic bronchitis and emphysema. 

Chronic inflammation of the bronchial tubes in COPD causes a hypersecretion of mucus by the respiratory goblet cells. 

The mucus then forms a plug that obstructs the airways causing air trapping, and it also causes chronic productive cough. 

Obstruction of the bronchi can also cause exertional dyspnea, which can progress to resting dyspnea, fatigue, wheezing and chest tightness. 

Destruction of the alveolar sacs impairs gas exchange, resulting in hypoxemia and hypercapnia. 

Loss of elastic recoil causes collapse of the airways during exhalation, trapping the air and dilating the airspaces. 

To make breathing easier, they often use  the tripod position, where they sit up and lean forward with their hands on their knees. 

They may use pursed lip breat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastroesophageal_reflux_disease_(GERD):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8yznkk8pRjOpD2MceW6yJ14vTdq7LUsh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastroesophageal reflux disease (GERD): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Frank Green is a 52-year-old male client who presents to the clinic for his annual physical.  

During his visit, he reports having heartburn pain during the day and being awakened from it at night. 

He says for the past several months he has occasionally taken cimetidine, a Histamine H2 Receptor Antagonist, or H2RA, to treat his heartburn. 

But over the past month he needed to take it every evening, and it no longer relieves his discomfort. 

Gastroesophageal reflux disease, or GERD, occurs when there is an abnormal backflow of gastric contents into the esophagus, which then irritates the esophageal lining. 

Normally, food travels from the mouth, down the esophagus, and into the stomach where a band of smooth muscles called the lower esophageal sphincter, or LES, keeps the food from moving back up the esophagus. 

In GERD, however, the gastric contents will flow back, or reflux, into the esophagus. 

GERD is a common gastrointestinal disorder with an estimated prevalence of 17 to 28% in the US population.

The risk for GERD increases with factors that decrease the LES tone so it is not as effective in protecting the esophagus from gastric contents. 

For example, certain medications like nitrites and calcium channel blockers decrease LES tone and increase the risk of reflux. 

A hiatal hernia, where part of the stomach bulges through the diaphragm, allows gastric contents to pool below the esophagus where it can reflux more easily. 

On the other hand, gastric contents can be forced past the LES with conditions that put pressure on the stomach, like obesity and pregnancy, and actions like coughing, vomiting, and heavy lifting, which increase intra-abdominal pressure. 

Reflux is also more likely to happen within an hour of eating or when lying down after a meal. 

Lastly, alcohol, tobacco, caffeine and spicy foods tend to trigger reflux.

Now, when the esophageal lining is exposed to the acidic gastric contents it produces symptoms like heartburn and p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hiatal_hernia:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PeizbwDtS1mdlGen6Ac85iz-Qu_GuDzj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hiatal hernia: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Mary Fowler, aged 68, presents to the emergency department, or ED, with vomiting and abdominal pain and distention. 

Mary has a history of a paraesophageal hiatal hernia with symptoms of gastroesophageal reflux disease, or GERD, which she normally manages with lifestyle modifications and acid-reducing medications. 

Her symptoms worsened over the last 2 days, and she has been unable to keep food or liquid down over the last 24 hours.  

Mary is diagnosed with a large incarcerated paraesophageal hiatal hernia, confirmed with an abdominal X-ray and computerized tomography, or CT scan. 

She will be cared for in the ED while she awaits surgical repair of her hernia.

A hiatal hernia occurs when part of the stomach moves up, or herniates, into the chest through the hiatus, which is the opening in the diaphragm for the esophagus as it enters the abdominal cavity. 

Underneath the diaphragm, the esophagus then connects with the stomach to form the gastroesophageal junction and the lower esophageal sphincter, or LES, a ring of muscles that opens to allow food and liquids into the stomach and closes to keep gastric contents from coming back up through the esophagus.

There are two main types of hiatal hernias. 

The most common type is a sliding hernia, where the gastroesophageal junction slides up and down through the hiatus. 

Less common are paraesophageal hernias, where parts of the stomach roll up through the hiatus, forming a pocket next to the esophagus. 

The risk of developing a hiatal hernia increases if the diaphragm is weakened from trauma, abdominal surgery, or smoking. 

Likewise, anything that increases pressure inside the abdomen, like coughing, obesity, pregnancy, straining, or heavy lifting increases the risk of hernia development. 

The risk also increases with age due to age-related widening of the hiatus, or in those who are born with an unusually large hiatal opening. 

Because hiatal hernias can interfere with the function of theLES, signs ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_tract_infections_(UTI):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZJbE41tdQBW1ArMgzXeBZBMASve2Hf8Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary tract infections (UTIs): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Alejandra Ramirez is a 38-year-old female who presents to urgent care reporting that she has been experiencing painful urination, and has needed to urinate more frequently and urgently than normal over the past two days. 

Ms. Ramirez has a history of type 2 diabetes mellitus. 

She is sexually active with no history of sexually transmitted infections. 

A urinary tract infection, or UTI, happens when the urinary tract which is made up of upper urinary tract, consisting of the kidneys and the ureters, and the lower urinary tract, bladder, prostate, and the urethra, becomes infected by pathogenic microorganisms. 

UTIs are most often caused by an ascending bacterial infection. 

Esherichia coli, or E. coli accounts for 75 to 95 percent of all urinary tract infections while other bacteria such as Klebsiella pneumoniae, Staphylococcus saprophyticus, or Proteus mirabilis are also common causes of infection.

Once the bacteria enter the urinary tract, they multiply and colonize the urinary tract, causing inflammation. 

Inflammation of the urethra, or urethritis, results in dysuria, which is a symptom of pain or burning during urination. 

Inflammation of the bladder, or cystitis, leads to edema of the bladder wall, which can result in suprapubic pain, which is pain felt in the lower abdomen near the bladder, a feeling of bladder fullness, and a need to urinate frequently and urgently. 

Bacteria in the urine, or bacteriuria, often results in cloudy, foul smelling urine, while damage to the bladder mucosa can cause blood in the urine, referred to as hematuria. 

If bacteria ascend further to the upper urinary tract, pyelonephritis, or inflammation of the ureters and kidneys, can occur, producing pain in the side of the back, or flank pain, also called costovertebral angle, or CVA, tenderness, along with manifestations of a systemic response to the infection, such as fever, chills, nausea and vomiting.

Complications of UTIs include scarring and narrowing of the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Benign_prostatic_hyperplasia_(BPH):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LFxndb5MTc2IVyHOBOrpEH1IQESG-hRo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Benign prostatic hyperplasia (BPH): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Martin Lewis is a 68-year-old client who presented to his community health clinic complaining of recurring trips to the bathroom, a frequent urge to urinate, and a weak urine stream that dribbles. 

His family physician completed an assessment of his symptoms including a digital rectal exam. 

A diagnosis of benign prostatic hyperplasia or BPH is suspected. 

The physician ordered several laboratory tests including a basic metabolic panel, prostate specific antigen, and urinalysis to help confirm the diagnosis. 

After completing these tests, Martin returns to the clinic two weeks later for a follow-up appointment. 

Benign prostatic hyperplasia, or BPH, is a condition where noncancerous cells in the prostate gland increase in number, enlarging the prostate. 

This condition is common in men over 50 and is often considered a normal part of aging. 

By the age of 60 around 50% of men develop BPH, and over 90% have it by the age of 85. 

Other risk factors for developing BPH include obesity, sedentary lifestyle, and family history of BPH. 

The exact cause of BPH is not well understood, but current understanding is that environmental and genetic factors play a role along with the influence of the sex hormones tesosterone, dihydrotestosterone, or DHT, and estrogen.  

Whatever the cause, the hyperplastic growth of prostatic smooth muscle and epithelial tissue enlarges the prostate which then compresses the urethra, obstructing the flow of urine.

BPH can be asymptomatic, but when symptoms are present, they include lower urinary tract symptoms, such as urinary urgency, hesitancy, which is trouble initiating urination, a weak urine stream, dribbling and straining to urinate, and nocturia. 

These symptoms significantly impair quality of life.

If the bladder isn&amp;#39;t emptied completely it can eventually cause kidney damage and even lead to kidney failure if not treated. 

Also, the stasis of urine in the bladder increases the chance of kidney stones formi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Smoke_inhalation_injury:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bNfTVwbaRuOKk6QgGEXYTO2fS76GMDV5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Smoke inhalation injury: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Janine Jones is a 35-year-old female who was brought to the emergency department, or ED, by ambulance after being trapped in her home during a fire. 

Firefighters responded when a neighbor noticed smoke coming from Janine’s home. 

Janine appears alert and oriented but she is unsure how long she was stuck in her home. 

She presents with coughing, shortness of breath, and a hoarse voice. 

She is admitted to the intensive care unit or ICU, with smoke inhalation injury.  

Smoke inhalation injuries occur when the airways or lungs are damaged from inhaling heat, irritant particulates, or toxic chemicals present in smoke. 

The most common scenario involves being in a house fire or other enclosed space during a fire. 

Now, there are some factors that may put an individual at risk for an inhalation injury during a fire. 

Non-modifiable risks include age, in particular young children and the elderly, as well as those with physical or mental disabilities. 

These factors can make it harder for the individual to stop a fire, or escape from it. 

In addition, having an underlying lung disorder increases the risk of harm from smoke inhalation. 

On the other hand, modifiable risk factors include being in a building without functioning smoke detectors, or being under the influence of alcohol or drugs during a fire.

Now, once the smoke is inhaled into the airways, it can cause three main types of airway injury. 

The first type is thermal injury, which is when the heat from the smoke burns the epithelium lining the airway. 

The second type of injury comes from particulates and chemicals that can irritate and cause direct damage to the airway. 

And third, smoke inhalation can cause asphyxiation, where oxygen availability and use by the tissues is impaired.

The signs and symptoms associated with a smoke inhalation injury typically depend on the duration and extent of exposure, and how far the inhaled smoke travels down the airways. 

First there’s upper airway i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pressure_injury:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Cr5dXK_OQL2iZXiy9oZzHvXqR7KqLfFr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pressure injury: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Joann Mercer is a 78-year-old female client who resides in a skilled nursing facility. 

Mrs. Mercer has a history of osteoarthritis and hip fracture. 

She needs assistance to walk, and spends most of her time in bed or sitting in her wheelchair. 

The certified nursing assistant, or CNA, who is taking care of Mrs. Mercer informs you of redness and a shallow ulcer that developed on her sacrum. 

You are concerned that Mrs. Mercer has developed a pressure injury.

Pressure injuries, also known as decubitus ulcers, involve damage to the skin or underlying tissue that result from prolonged pressure. 

Now, pressure injuries usually appear over bony prominences, especially the sacrum, followed by the heels, since these areas have the thinnest subcutaneous tissue between the bone and the skin. 

So the prolonged pressure causes a reduced blood flow to that tissue area, resulting in tissue hypoxia and ischemia, and ultimately leading to necrosis and ulceration.

Most often, pressure injuries develop in clients who aren’t moving about, like those on chronic bedrest or consistently in a wheelchair. 

Other factors that can increase the risk for skin injury are thinning of skin and subcutaneous tissue due to advanced age as well as dry skin and thin subcutaneous tissue due to inadequate nutrition and hydration; and prolonged contact to skin irritants like sweat, urine, and feces. 

Other important risk factors for pressure injuries are conditions that may impair blood flow, such as heart and lung disease and diabetes mellitus. 

Clients should be assessed for the risk of developing a pressure injury using a validated assessment tool like the Braden Scale. 

This scale looks at six criteria, which include sensory perception, moisture, activity, mobility, nutrition, and friction or shear. 

The lower the score, the higher the risk of injury. 

Nutritional assessments can be used to assess the likelihood of injury as well as healing. 

With non-healing injuries, labo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Asthma:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/krBVpBrFR9C8n6Jhg2MIymorT3qXJb0r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Asthma: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Megan Fitzpatrick is a 29-year-old woman with a history of asthma who was brought to the emergency department, or ED, by a friend after having trouble breathing which was not resolved with the use of her inhaler.  Megan presents with wheezing, shortness of breath, and chest tightness. She is able to speak in short sentences but frequently pauses to breathe. She appears anxious and states her asthma has never felt this awful before.  

Asthma is a chronic inflammatory disease of the airways characterized by bronchial hyperresponsiveness and airflow obstruction. Although the specific causes of asthma are ultimately unknown, it’s thought to be caused by a combination of genetic and environmental factors.  

Asthma symptoms are often initiated by an environmental trigger. The triggering substance can differ from person to person, but some common ones include air pollution, like cigarette smoke and car exhaust, as well as allergens like dust, pet dander, cockroaches, and mold. Medications like aspirin and beta-blockers have also been known to trigger symptoms in some individuals with asthma. Lastly, cold, dry air or exercise can also trigger asthma in some individuals.   

Inhaling a triggering substance can initiate what is known as an asthma exacerbation or attack. The triggering substance travels down the airways to the bronchioles, which are composed of cartilage, smooth muscle, and a mucosal lining containing mucus-secreting goblet cells. Immune cells such as mast cells and basophils, are stimulated to release chemical mediators such as histamine and leukotrienes that cause the smooth muscle in the bronchioles to spasm, known as a bronchospasm, and cause the goblet cells to produce an abundance of mucus.  

Together, bronchospasm and mucus obstruct the airway, making it difficult to breathe, and leading to symptoms such as coughing, chest tightness, dyspnea, and wheezing, which is a high-pitched whistling sound that usually happens during exhalation. Over ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronary_artery_disease_(CAD)_&amp;_angina_pectoris:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NImFgHgeSWCBohwQkmtg3jaUQGaH8WM_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronary artery disease (CAD) and angina pectoris: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Dwayne Harris is a 52 year old African American male client presenting to the cardiac catheterization lab to undergo a percutaneous coronary intervention, also known as PCI. 

Mr. Harris has a diagnosis of coronary artery disease, chronic stable angina, hyperlipidemia, and is a current smoker with a 20 pack year history. 

Because his angina is no longer responding to treatment, his cardiologist recommended PCI for Mr. Harris. 

Coronary artery disease, or CAD, is the narrowing or obstruction of coronary arteries. 

This narrowing is caused by atherosclerosis, a lipid containing plaque that accumulates on artery walls. 

Over time, the plaque build up reduces myocardial perfusion and causes ischemia as the demand for oxygen exceeds the supply. 

Myocardial ischemia leads to a type of chest pain called angina, which can be either stable or unstable. 

Stable angina usually occurs when atherosclerotic plaque is fixed to the artery wall and occludes at least 75 percent of the coronary artery, whereas with unstable angina, the plaque ruptures and almost completely occludes the artery lumen. 

The clinical presentation helps to differentiate stable and unstable angina using the acronym OPQRST. 

O stands for onset, which for stable angina is during activity or emotional stress, due to increased oxygen demand, whereas for unstable angina, onset can be sudden or even at rest. 

P is for palliation. Stable angina is relieved by re st or vasodilators like nitroglycerin, whereas unstable angina is not relieved. 

Q stands for the quality of pain, which often involves pressure, crushing, squeezing, or tightness. Pain is more severe with unstable angina. 

R stands for radiation of pain, because it often radiates to the shoulders, arms, jaw, neck, or back. 

S is for site, which is deep, substernal, and sometimes hard to localize, meaning the client is unable to point to the site of pain with a single finger. 

T stands for time. With stable angina, pain can last 15 s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anxiety_disorders,_phobias_and_stress-related_disorders:_Pathology_Review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EJP7k-RoRSOpyFzl5TU_VMWXR7iX_fUC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anxiety disorders, phobias and stress-related disorders: Pathology Review]]></video:title><video:description><![CDATA[19 year old Anastasia comes to the emergency department convinced that she’s about to die from a heart attack. 

It all started as soon as she entered the lecture hall to take her final exam for college, when she began sweating and feeling light-headed. 

Within 5 minutes, this quickly progressed to being unable to breathe and experiencing a stabbing chest pain. 

She denies the use of illicit substances or alcohol and has no personal or family history of cardiovascular or pulmonary disease. 

Her mother, who’s by her side, mentions that Anastasia has had five similar episodes in the past six months, all while preparing for her exams. 

Anastasia adds that she wants to quit college, because she is afraid an attack will happen again and she won’t be able to make it. 

Upon examination, her ECG is normal, and on a blood test, D-dimer is negative, and cardiac enzymes remain normal after 6 hours. 

The next day, you see 43 year old Olivia, who is brought to office by her husband, who thinks she needs help. 

They constantly get into fights because Olivia wants everything in the house to be sparkling-clean and organized in a very specific way. 

She always blames him for leaving contaminated fingerprints around the house and moving items from their proper place. 

She then goes on to clean up for hours and even loses sleep over it

When you ask Olivia about these behaviors, she says that she understands they are irrational and wishes she could stop them, but she just can’t.

Okay, based on the initial presentation, both Anastasia and Olivia seem to have some form of anxiety or obsessive-compulsive disorder. 

Many of us experience fear or anxiety during stressful times, which is perfectly normal and can actually be beneficial, since it helps set the body on high-alert. 

Now, fear is the emotional response to an imminent threat or danger, and can cause a fight or flight response when your life is threatened. 

For your exams, make sure you can differentiate fea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cerebrotendinous_xanthomatosis_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m5rm5H6VQK6jNnZllCoyhpA2Qty0A_4y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cerebrotendinous xanthomatosis (NORD)]]></video:title><video:description><![CDATA[Cerebro refers to the brain, tendinous refers to the tendons, and xanthoma refers to fatty deposits. 

Cerebrotendinous xanthomatosis, also called CTX, is a rare genetic disorder caused by alterations  in the CYP27A1 gene that adversely affect the body’s ability to convert  cholesterol to the bile acids chenodeoxycholic acid and cholic acid. 

This results in the accumulation of abnormal disease-causing compounds and leads to fatty deposits, or xanthomas, in the brain and tendons as well as other parts of the body.

The symptoms and progression of CTX may differ greatly from person-to-person with symptoms that can range from mild to severe and that can appear from infancy through adulthood. 

Among infants, the disease may first present as chronic diarrhea that remains unchanged despite treatment, or as seizures, often called infantile spasms. 

Infants with CTX may develop cholestatic liver disease where bile can stagnate in the liver, causing symptoms such as jaundice, and liver enlargement. 

Another symptom in children may include juvenile cataracts that can manifest as difficulty following objects with the eyes, eyes pointing in different directions, or cloudiness over the eye’s lens. 

Neurological symptoms can appear in childhood or later in life  and may include cognitive impairment such as difficulty with memory, concentration, and reasoning. 

Other symptoms may include epilepsy and spasticity, causing difficulties in movement and speech. 

Adolescents may display behavioral changes such as agitation, aggression, and depression and may also experience hallucinations and suicidal thoughts. 

In early adulthood, tendinous xanthomas may appear where fatty bumps or nodules form around the elbows, hands, knees, and heels. 

If the disease remains untreated and continues to progress, affected individuals may become wheelchair bound and continued neurological decline may lead to early dementia. 

CTX is also linked to atherosclerosis, osteoporosis, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_and_nerve_supply_of_the_oral_cavity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vSMYBvD9Rw6C0c18hdXKJ-VBRRuIMm-4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood and nerve supply of the oral cavity]]></video:title><video:description><![CDATA[The oral cavity or mouth, though quite small, is supplied by a dense network of nerves and blood vessels. 

The nerve supply comes from the branches of six cranial nerves, namely - the trigeminal nerve, facial nerve, glossopharyngeal nerve, vagus nerve, and the hypoglossal nerve, whereas the blood supply comes from the branches of the external carotid artery and the veins drain into the internal and external jugular veins. 

First off, let&amp;#39;s start with the arteries. 

The arterial supply comes from the external carotid artery branches - the lingual artery, facial artery, and the maxillary artery. 

The lingual artery is the second branch of the external carotid artery and arises at the level of the greater cornu of the hyoid bone. 

It runs upwards and medially till it reaches the greater cornu and then dips downwards, beneath the posterior belly of digastric and stylohyoid muscles, creating a loop over the hypoglossal nerve. 

The lingual artery then ascends almost vertically upwards to reach the tongue&amp;#39;s inferior surface and continues as its terminal branch, the deep lingual artery, which supplies the anterior two-thirds of the tongue. 

The lingual artery gives off four branches: the suprahyoid artery, the dorsal lingual artery, the deep lingual artery, and the sublingual artery. 

The suprahyoid artery runs along the hyoid bone and supplies the omohyoid, sternothyroid, and thyrohyoid muscles. 

The dorsal lingual artery supplies the posterior one-third of the tongue, soft palate, palatoglossal fold, lingual tonsil, epiglottis. 

The deep lingual artery supplies the tongue’s ventral surface. 

The sublingual artery supplies the sublingual salivary gland, the genioglossus, geniohyoid and mylohyoid muscles, and the mandible.

Second, the facial artery arises from the external carotid artery at the level of the angle of the mandible, just above the lingual artery. 

It then takes an S-shaped course deep to the posterior belly of diga]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cemento-osseous_dysplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/66AZYJx0TLuPxcK3e1hpItn4TICzwHkN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cemento-osseous dysplasia]]></video:title><video:description><![CDATA[Hi! My name is Mark Mintline, and I am an oral and maxillofacial pathologist. And I would like to talk to you today about cemento-osseous dysplasia. 

Cemento-osseous dysplasia is a non-neoplastic fibro-osseous lesion of the tooth-bearing regions of the jaws. It is the most common benign fibro-osseous lesion of the gnathic bones and is often diagnosed by dentists clinically. Typically, these lesions are non-expansile, but florid cases are an exception. Cemento-osseous dysplasia is most common in black females, but can be found in other races and ethnicities. 

Traditionally, cemento-osseous dysplasia is divided into three variants based on anatomic location. Periapical cemento-osseous dysplasia which is associated with mandibular anterior teeth, focal cemento-osseous dysplasia which is associated with a single tooth or site, and florid cemento-osseous dysplasia which has multifocal or multiquadrant involvement. 

Ideally, cemento-osseous dysplasia is identified based on clinical and radiographic features. Most periapical and florid cases are diagnosed without a biopsy. However, features of focal cemento-osseous dysplasia may be less specific. Radiographic examination of cemento-osseous dysplasia is essential. Lesions can be radiolucent, mixed, or radiodense depending on maturity.

Here is an example of periapical cemento-osseous dysplasia with increased calcifications. The lesions are associated with vital teeth and the lesions are well-defined with a radiolucent rim. Occasionally, radiolucent lesions are mistaken for odontogenic inflammatory lesions and clinicians unfortunately, endodontically treat that. To reiterate, cemento-osseous dysplasia is associated with vital teeth. 

Focal cemento-osseous dysplasia is associated with a single site. Over time, the lesion shows increased density as it matures. Serial radiographs are incredibly helpful to diagnose and monitor lesions. Once a case of periapical or focal cemento-osseous dysplasia has been establishe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intraoral_biopsy_techniques</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/33Y110DHQWKq6sPXVA6xAUWVTb_T-fbE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intraoral biopsy techniques]]></video:title><video:description><![CDATA[Hi! My name is Mark Mintline, and I am an oral and maxillofacial pathologist. And I would like to talk to you today about how to perform intraoral biopsies of vesiculobullous lesions. My goal is to talk to you a little bit about biopsy techniques and the laboratory testing of blistering diseases so that your comfort level for performing biopsies goes up.

Pemphigoid and pemphigus are rare autoimmune blistering diseases that often first present in the mouth. 

Unfortunately, often there are delays in diagnosis. On average, it takes 6-10 months for a person with pemphigus vulgaris to get a final diagnosis. And patients with pemphigus vulgaris or mucous membrane pemphigoid see an average of 5 healthcare providers before getting a final diagnosis.

Biopsies can quicken diagnosis times and save lives.

When taking a biopsy, our goal is to obtain a representative tissue sample with intact epithelium. For blistering diseases, both conventional H&amp;amp;E histology and direct immunofluorescence (DIF) are needed.

Pemphigus vulgaris is an acquired autoimmune disease that leads to intraepithelial separation.

Mucous membrane pemphigoid is a chronic autoimmune disease that results in subepithelial separation.

When taking a biopsy to evaluate for pemphigus and pemphigoid it is important to: 1) sample from a representative site, 2) not damage the tissue, and 3) appropriately transport the specimen.

In order to obtain a piece of representative intact epithelium, we should biopsy adjacent or perilesional to an active or new blister.

Biopsies of bullae, erosions, and ulcers will likely not yield intact epithelium and therefore will be non-diagnostic for the pathologist.

A biopsy of an ulcer will lead to a non-diagnostic specimen.

In general, two punch biopsies are preferable: one punch for H&amp;amp;E and one punch for DIF.

Punch biopsies are less likely to tear tissue and are less technique-sensitive than shave or larger biopsies.

You may choose to divide one b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endodontic_disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6clQUtoySdq1Dq_XpRajbuDBTJSRdDkH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endodontic disease]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Endodontic disease through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ryan_Padrez:_Medical_Director_of_The_Primary_School_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i4SF9qcEQHuYU2-7JLss5gt-TLyIkjxO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ryan Padrez: Medical Director of The Primary School (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Ryan Padrez: Medical Director of The Primary School (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chuck_Cairns:_Dean_&amp;_Sr_VP_of_Medical_Affairs,_Drexel_College_of_Med._(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BBLzY4VlQ-m4VrJUuc0BBMfMRbmCrcmN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chuck Cairns: Dean &amp; Sr VP of Medical Affairs, Drexel College of Med. (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Chuck Cairns: Dean &amp; Sr VP of Medical Affairs, Drexel College of Med. (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Samir_Malik:_Executive_Vice_President_of_Genda_Telepsychiatry_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tmpCDJ3GSaGfBjYDWB4knsLXSQy9tXef/_.jpg</video:thumbnail_loc><video:title><![CDATA[Samir Malik: Executive Vice President of Genoa Telepsychiatry (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Samir Malik: Executive Vice President of Genoa Telepsychiatry (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Marlene_Icenhower:_Senior_Risk_Specialist_at_Coverys_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l0HdJLxzSLCuI2wEESSFvg_fQsut7TqG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Marlene Icenhower: Senior Risk Specialist at Coverys (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Marlene Icenhower: Senior Risk Specialist at Coverys (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Marcus_Osborne:_Senior_VP_of_Walmart_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_NOdXW9-TV29U2rqUnK-KG09QJu-M2rg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Marcus Osborne: Senior VP of Walmart Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Marcus Osborne: Senior VP of Walmart Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/David_Fischel:_CEO_of_Steriotaxis_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xHcqaq81Q-ykfPgH0kfvWwPmQniDknQ_/_.jpg</video:thumbnail_loc><video:title><![CDATA[David Fischel: CEO of Steriotaxis (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of David Fischel: CEO of Steriotaxis (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Shantanu_Nundy:_Chief_Medical_Officer_at_Accolade_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EBXR-om3R0SLEBCltzZcMiWwQjSlZliT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Shantanu Nundy: Chief Medical Officer at Accolade (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Shantanu Nundy: Chief Medical Officer at Accolade (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Mark_Schuster:_Dean_&amp;_CEO,_Kaiser_Permanente_Bernard_J._Tyson_S.O.M._(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/B29vdxfGTf6607ng7UWdY01bSbGRrD-O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Mark Schuster: Dean &amp; CEO, Kaiser Permanente Bernard J. Tyson S.O.M. (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Mark Schuster: Dean &amp; CEO, Kaiser Permanente Bernard J. Tyson S.O.M. (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Glenn_Geelhoed:_Founder_of_Mission_to_Heal_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_faOdvD-R8CcodaerW9JD-ShQGaiV9k7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Glenn Geelhoed: Founder of Mission to Heal (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Glenn Geelhoed: Founder of Mission to Heal (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alex_Frommeyer:_CEO_of_Beam_Dental_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cXR2ksaUR6qcEyv9lQfmV12ZSxKQ0dI9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alex Frommeyer: CEO of Beam Dental (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Alex Frommeyer: CEO of Beam Dental (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eric_Kinariwala:_Founder_and_CEO_of_Capsule_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C2M5I8eiSl_ryDlxpMbgJyFzTv_q7kjx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eric Kinariwala: Founder and CEO of Capsule (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Eric Kinariwala: Founder and CEO of Capsule (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sara_Miller:_Sr._Director,_Quality_Improvement_Institute_at_MedIQ_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cFe-pKd_RtKRIhbRve4ozqtES1abE-r7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sara Miller: Sr. Director, Quality Improvement Institute at MedIQ (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Sara Miller: Sr. Director, Quality Improvement Institute at MedIQ (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Thomas_Rebbecchi:_Medical_Advisor,_National_Board_of_Medical_Examiners_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M63uAr12ShyG1rrWOX5HO6X3SgGVrvYX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Thomas Rebbecchi: Medical Advisor, National Board of Medical Examiners (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Thomas Rebbecchi: Medical Advisor, National Board of Medical Examiners (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kang-Xing_Jin:_Head_of_Health_at_Facebook_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rbOixvg2TFuITOzQOEcnplYITTelML3A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kang-Xing Jin: Head of Health at Facebook (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Kang-Xing Jin: Head of Health at Facebook (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eve_Cuny:_Director_Environmental_health_&amp;_Safety,_University_of_the_Pacific_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sHon9rJqR_qO3NWl5TiwbEZkTrivqdT4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eve Cuny: Director Environmental health &amp; Safety, University of the Pacific (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Eve Cuny: Director Environmental health &amp; Safety, University of the Pacific (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Brian_Radbill:_Chief_Medical_Officer_at_Mount_Sinai_Morningside_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OgGPxXsMRgycOTIbF8IKck4LQGGxJsOT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Brian Radbill: Chief Medical Officer at Mount Sinai Morningside (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Brian Radbill: Chief Medical Officer at Mount Sinai Morningside (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Standards_of_care_for_COVID-19_patients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/as1i97OLQLqo3NfgeOrd_68lSvaNrGFh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Standards of care for COVID-19 patients]]></video:title><video:description><![CDATA[Significant progress has been made on how to care for COVID-19 patients, and treatment recommendations continue to evolve. 

In this video we present the current guidelines and recommendations from the United States National Institute of Health, or NIH, COVID-19 Treatment Guidelines Panel as of January 2021. 

An individual’s treatment heavily depends on the patient’s health condition as well as the resources available to the health care team, so health care professionals should follow local policies and use their clinical judgement on a case-by-case basis.

Patients with mild symptoms from COVID-19 should be advised to treat the disease like any other bad cold. 

Patients should rest, drink fluids, and can take over the counter medications to manage symptoms like fever and congestion. 

Healthcare providers should encourage patients to isolate themselves, including isolating within a specific part of their home to avoid contact with other household residents.

In November 2020, the United States Food and Drug Administration or FDA, issued Emergency Use Authorization to allow bamlanivimab or casirivimab plus imdevimab to be given to outpatients who are at high-risk for serious infection, such as people with cancer, type 2 diabetes, and pre-existing heart conditions like heart failure. 

Bamlanivimab and casirivimab plus imdevimab are laboratory manufactured monoclonal antibodies designed to fight COVID-19 by preventing the virus from entering the host cells. 

To date, the NIH panel does not have enough information to make a recommendation for or against using these drugs for COVID-19 patients with mild symptoms, and these drugs can only be given through emergency use authorization or as part of a clinical trial. 

Drug supply may also be limited depending on a provider’s location and administration should be  prioritized for those with the highest risk. 

Bamlanivimab and casirivimab plus imdevimab are not recommended for patients who are hospitalized as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19_vaccines:_What_healthcare_providers_need_to_know</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zAHzs_5DRSKWiOPlrLHUFTJPTNaIk9QR/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19 vaccines: What healthcare providers need to know]]></video:title><video:description><![CDATA[As of early January 2021, the United States has begun Phase 1 of the COVID-19 vaccine rollout. 

This video will help health care providers get up to date on key information  regarding the vaccines.

National guidelines are recommending prioritizing giving the vaccine to the public according to a person&amp;#39;s status as an essential worker and their risk of becoming ill from COVID-19. 

Based on these criteria, they have identified different categories/segments. 

The first category, called Phase 1a, is where residents of long-term care facilities and front-line healthcare workers, including first responders will be vaccinated, [22]. 

Next is Phase 1b, where essential workers and adults aged 75 and over will be vaccinated [22]. 

In Phase 1c, adults aged 65 and over, as well as patients at high-risk for severe COVID-19 infection caused by pre-existing health conditions will be vaccinated.

In Phase 2, everyone 16 years of age or older who hasn’t received a vaccine will be eligible to receive one. 

These national recommendations continue to evolve and may change over time, however, it’s ultimately up to each state to decide how vaccines will be distributed.

Currently there are two vaccines approved by the FDA for use in the United States. 

The first is BNT172b2. 

It was created by BioNTech, Fosun Pharma, and Pfizer and is colloquially called the “Pfizer vaccine”. 

It’s an mRNA vaccine that must be stored long-term in -112 to -76 fahrenheit, or -80 to -60 celsius. 

MRNA vaccines differ from traditional vaccines as they cause our body to manufacture the spike protein of the virus we’re trying to protect against, instead of introducing remnants of the virus itself. 

Once thawed and diluted, vials can be stored in a refrigerator for 6 hours. 

Initially, these vials were reported to hold 5 doses per vial, however, it has been discovered each vial contains 6 usable doses and official documentation has been updated. 

People receiving this vaccine sho]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Larry_Benz:_President_and_CEO_of_Confluent_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eVKi8hmKS2mKBkOyXkEUJ-iPSmuP6pP3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Larry Benz: President and CEO of Confluent Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Larry Benz: President and CEO of Confluent Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Applying_sterile_gloves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RTHyZSbvR1uj3NnpCh4e1UzDRGW2LKtL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Applying sterile gloves]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Applying sterile gloves through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maintaining_an_airway</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-JQMFAghScuCeg3kC88YWEVfRBqB3BIt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Maintaining an airway]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Maintaining an airway through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Venipuncture_for_blood_sampling</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bZWZwF3xSii0cErL_Vp6ag6ER2qVp8Of/_.jpg</video:thumbnail_loc><video:title><![CDATA[Venipuncture for blood sampling]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Venipuncture for blood sampling through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Removing_an_intravenous_line</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i14r6XPnRRG9gdlbskG-CuhfReG1u9vg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Removing an intravenous line]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Removing an intravenous line through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardioversion</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OxRQXaf8QIyiSyjqUEv9kRF4Q3u_NCId/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardioversion]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Cardioversion through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chelsea_Clinton:_Vice_Chair_of_the_Clinton_Foundation_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c88Gg02-T86e3Xua287F-O_aRPaJCAMM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chelsea Clinton: Vice Chair of the Clinton Foundation (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Chelsea Clinton: Vice Chair of the Clinton Foundation (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19_vaccine_hesitancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4Yg-xEQwRGWQtVuUUveYDVTKTXOe3bAT/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19 vaccine hesitancy]]></video:title><video:description><![CDATA[Vaccine hesitancy has become a significant health concern, and is defined by the World Health Organization as “a delay in acceptance or refusal of vaccination despite availability of vaccination services” 

Vaccine hesitancy is a complex issue, and its causes are unique to each individual. 

While vaccine hesitancy has been an ongoing public health issue for years, the rapid development of vaccines in response to the COVID-19 pandemic has exacerbated the issue. 

A survey by Fisher et al. in September 2020 revealed 11% of people in the United States plan to decline the COVID-19 vaccine, with another 32% of people undecided if they’d accept the vaccine. 

With such a large percentage of the population being hesitant to vaccination, it’s imperative healthcare providers initiate and maintain an open dialog about vaccination with patients.

Patients are often willing to have a discussion about vaccination, even if they are hesitant to receive a vaccine. 

When beginning a dialog on vaccines with patients, always ensure you frame the discussion in a positive, non-confrontational light. 

Be respectful and truly understand the person’s perspective. Do they feel worried? Do they feel suspicious? 

These are legitimate feelings that warrant a conversation about safety and the process of how vaccines get made and evaluated before they’re given to patients. 

Even if the patient decides not to be vaccinated, it is important to maintain a strong healthcare provider-patient relationship so that you can continue to engage them over time. 

The more opportunities you have to engage them, the more likely  a skeptical patient may be to change their mind and decide to become vaccinated.

Patients are the ultimate decision makers on whether they’ll be vaccinated or not. 

Your role as a healthcare provider is to be a resource to them. 

Reinforcing this with the patient will help build trust and a strong clinician-patient relationship. 

Highlight that both of you have shar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Venous_thromboembolism_(VTE):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qJ3qzP2CTXSSVvUlxaRzLTogSWy_64oy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Venous thromboembolism (VTE): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Renata Gutierrez is a 34-year-old woman who came to the Emergency Department, or ED, with her partner, because of shortness of breath, chest pain, and coughing up blood-tinged sputum. The triage nurse informs you that Ms. Gutierrez delivered a healthy full-term baby by cesarean section one week ago. She has no other significant past medical history.  

Venous thromboembolism, or VTE, refers to a clot that starts in a vein.  

Specifically, a pulmonary embolism, or PE, occurs when an embolus, which is a small mass that could be a blood clot, fat, or even an air bubble, becomes lodged in the pulmonary artery and obstructs the pulmonary circulation. Most often the embolus is a blood clot associated with deep vein thrombosis, or DVT, which is when a clot forms in a large vein, usually in the leg or pelvis. The clot can break off and travel up the inferior vena cava to the right atrium, into the right ventricle, and finally into the pulmonary artery. This causes decreased blood flow to the lung tissue and impaired oxygenation. 

Factors that increase the risk of a pulmonary embolism are summarized in Virchow triad, which include slowed blood flow, or venous stasis, hypercoagulation, meaning the blood is more likely to form clots, and damage to the endothelial lining of a blood vessel. Venous stasis can occur because of prolonged immobility like during a severe illness or after surgery, when an enlarged uterus compresses the nearby veins during pregnancy, or due to long-haul travel. Hypercoagulability can be caused by clotting disorders, use of oral contraceptives, smoking, and it occurs normally during pregnancy. And lastly, damage to the endothelial cell lining of a blood vessel can be the result of trauma or surgery.  

Signs and symptoms of a pulmonary embolism depend on the size and location of pulmonary artery blockage. Even a small blockage impairs blood from getting into the lungs to pick up oxygen. Impaired oxygenation may cause a sudden onset of dyspne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Post-COVID_syndrome:_Mental_health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ct3StmLlQFCqpmZ0aLHM6WmSSTaQ0iB_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Post-COVID syndrome: Mental health]]></video:title><video:description><![CDATA[Neuropsychiatric symptoms appear to be common with COVID-19 patients. 

One recent study suggests COVID-19 patients have an increased chance of developing a new mental health illness within 90 days of diagnosis, compared to other illnesses such as influenza. 

Patients who were admitted into intensive care are particularly susceptible to developing mental health issues. 

For example, one study found up to 22% of patients who were admitted to a hospital for COVID-19, developed symptoms of anxiety or depression, and up to 38% of patients admitted to intensive care developed the same symptoms. 

Other psychological symptoms that patients may experience include confusion, insomnia, decreased memory retention and poor concentration. 

Critically ill patients also appear to be susceptible to developing post-traumatic stress disorder, or post-intensive care syndrome.

Healthcare providers have been particularly at risk for psychological distress during the pandemic, particularly health care professionals who spend a significant amount of time in direct contact with patients, who have been quarantined, and those whose workplaces don’t have sufficient personal protective equipment. 

Healthcare providers who face social stigma because of their profession, who don’t receive sufficient time off, or who do not receive clear communication from superiors may also need extra psychological support. 

Studies of healthcare workers in both China and Italy revealed that almost 50% of healthcare workers experienced traumatic distress during the pandemic, up to 25% experienced depression, up to 20% experienced anxiety, and up to 8% experienced insomnia. 

In Canada, almost 50% of healthcare workers indicated they needed psychological support during the pandemic. 

Healthcare workers can decrease their likelihood of developing psychological distress by getting regular physical exercise, seeking psychotherapy services, talking with colleagues or support groups, or practicing me]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Post-COVID_syndrome:_Heart,_lungs_and_clotting</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/etvzQiA6TkaJW-DTOeC4b0BURHGDcua9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Post-COVID syndrome: Heart, lungs and clotting]]></video:title><video:description><![CDATA[Now that we’re a year into the COVID-19 pandemic, we’re beginning to have an understanding of the lasting long-term effects the disease has. 

Prolonged symptoms have colloquially been called long COVID, and those who are experiencing these symptoms are colloquially called long haulers. 

Long COVID may also be referred to as long-term COVID, chronic COVID, or post COVID syndrome, as no official term has been established yet.

It’s important to remember research on COVID-19 and its prolonged effects on the body have only just begun, and to date we cannot draw any firm conclusions on the long-term effects of the disease. 

The studies we highlight here represent only initial findings, and should be taken with a grain of salt.

To begin, we are discovering that long-term complications from COVID-19 are fairly common. 

In October of 2020, the United Kingdom’s National Institute for Health Research announced 10 to 20% of people who contracted COVID-19 continue to have symptoms or complications of COVID-19 one month after diagnosis. 

One study in Italy suggested 87% of patients infected with COVID-19 continued to have persistent symptoms 60 days after their initial symptoms began.

With the rising number of people experiencing long-term COVID-19 symptoms, the British National Institute for Health and Care Excellence, also called NICE, has categorized three unique stages of COVID-19 recovery. 

The acute COVID-19 stage is the period of recovery within 4 weeks after diagnosis. 

The ongoing COVID-19 stage lasts 4 to 12 weeks after diagnosis, and the long COVID stage lasts over 12 weeks after diagnosis. 

Fatigue is the most common symptom that appears to continue to persist after COVID-19 infection. 

A study in Ireland found over half of all patients continued to have persistent symptoms of fatigue 10 weeks after initial diagnosis, regardless of how severe their initial symptoms were.

Cardiopulmonary issues such as shortness of breath, cough, and chest pain a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19_mutant_variants_and_herd_immunity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ufx4MaCiToOzu7bXwBK7HPTXSlmRtmMs/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19 mutant variants and herd immunity]]></video:title><video:description><![CDATA[By now, you’ve likely heard about the new variant strains of COVID-19 that are circulating around the world. 

There are a number of concerns with these new strains, as they may make it easier to spread COVID-19 to others, and they may increase the severity of COVID-19 illness. 

This video aims to explain what is known about the different strains and how they may affect achievement of herd immunity.

All viruses mutate. As more people get infected with a virus, the virus has more opportunities to multiply and there are more chances that a mutation may occur. 

A mutated virus can be considered a new strain when the virus has enough mutations to make it distinct from the original virus. 

So, often new strains appear in places with uncontrolled outbreaks. 

The new strains can become a problem when the mutation gives the virus an advantage, such as making it easier to quickly spread or increasing the infection severity.

For each of the COVID-19 variant strains, it’s likely the mutations took place within a single patient who was infected with the virus for a long period of time.

Most relevant COVID-19 mutations affect the spike protein, which is a protein located on the outside of the virus that can bind to the host cell, helping the virus enter the cell. 

The genetic code for the spike protein is within the “conserved” region, meaning the spike protein tends to be consistent across each new generation of the virus. 

Most of the developing vaccines have been targeting proteins on the viruses, one of which is the spike protein, so alterations in the spike protein may make vaccines somewhat less effective.

As of early March 2021, there are three clinically important strains of COVID-19: B.1.1.7, also called the UK strain, B.1.351, also called the South African strain, and P.1, also called the Brazilian strain. 

While there are a number of other strains that exist, these three strains are clinically important because they potentially may be more contagi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_compartment_syndrome:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y0kQRUjaTe6VS7PxKf8Gu3_9Sgu_MWsh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute compartment syndrome: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Huang Li is a 26-year-old male client who presents to the emergency department, or ED. While snowboarding this morning, Mr. Li sustained a nondisplaced transverse fracture in his right tibial shaft. A cast was applied in the ED, and he was discharged home with a prescription for the opioid analgesic acetaminophen with codeine for pain. Mr. Li came back to the ED six hours later stating his pain is unbearable with a rating of 10/10. He says the pain medication isn’t helping at all, and it feels like there are pins and needles in his leg under the cast. The ED team urgently begins evaluating Mr. Li for acute compartment syndrome.

Acute compartment syndrome is a serious condition in which there’s a rapid increase in the pressure within an enclosed compartment that contains muscles, nerves, and blood vessels, surrounded by a layer of fibrous connective tissue, called fascia. Since the fascia is not elastic it can’t stretch much. So when the pressure within these compartments rises, normal blood flow can be cut off, leading to tissue damage due to hypoxia and ischemia.

The most common cause of acute compartment syndrome is bleeding within the compartment. This typically occurs with long bone fractures, like the tibia, as well as penetrating injuries. Any limb compression, like from a crush injury or severe contusion, can also lead to acute compartment syndrome. Other causes are severe circumferential burns, which can lead to tissue edema. Finally, another potential cause can be reperfusion injury in clients who experience prolonged tissue hypoxia, where a sudden restoration of blood supply can result in massive inflammation and edema.

Now, there are also some factors that may put the client at an increased risk of acute compartment syndrome, such as experiencing severe trauma, penetrating injury, motor vehicle crash, or burn injury. Acute compartment syndrome can also occur in clients who receive massive amounts of intravenous fluids, which may extravasate a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Appendicitis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vMTJsh9BRzawhIRD2SaLuQa8QA_dYKp-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Appendicitis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[16-year-old Manny Correa is admitted to the pediatric inpatient unit from the urgent care clinic.  

Manny’s father George brought him to the clinic after Manny experienced pain around his belly button for the past 24 hours. 

An abdominal ultrasound confirmed an inflamed appendix.  Manny is scheduled for an appendectomy today. 

Appendicitis is a condition where the appendix, a finger-like projection that hangs off of the cecum of the large intestine, becomes obstructed and inflamed. 

Appendicitis can be caused by lymphoid hyperplasia, where overgrown lymphoid follicles obstruct the appendix, or when a hard lump of stool called a fecalith, a tumor, or even parasites like pinworms cause an obstruction, resulting in appendicitis. 

Appendicitis is more common in the second and third decades of life, with the highest incidence between the ages of 10 and 19. 

It is more common in men than in women.

Now, when the appendix becomes obstructed, mucosal secretions and the bacteria that normally live in the appendix build up inside, causing the appendix to expand and press against the visceral nerve fibers, resulting in pain that is often felt in the periumbilical area. 

Multiplication of bacteria inside the appendix leads to inflammation, which is accompanied by fever, anorexia, nausea, and sometimes vomiting. 

Eventually, the appendix starts to irritate the nearby parietal membrane lining the walls of the abdominal cavity, causing the pain to intensify and migrate to the right lower quadrant, an area known as McBurney’s point, which is located 1.5 to 2 inches from the navel to the anterior superior iliac spine. 

Palpating McBurney’s point and quickly releasing pressure will demonstrate rebound tenderness, and the person may show guarding, where their abdominal muscles tense up when pressed in an attempt to avoid pain. 

Rovsing&amp;#39;s sign is elicited if pressure over the person’s left lower abdominal quadrant causes pain in the right lower abdominal qu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atopic_dermatitis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q2wZHIHHRqaZzu6tXHfJqtj1Q9GxKu2Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atopic dermatitis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Kameron Jones is a 2-year-old male who presents to your pediatric clinic accompanied by his mother. 

Mrs. Jones explains that Kameron has developed a red rash on his scalp, cheeks, and chest that has gotten worse over the past week. 

Yesterday, she noticed that some of those areas of skin looked red and developed cracks that began to ooze. 

She says Kameron has been scratching at his chest constantly, and he’s been more irritable, since the rash appeared. 

The pediatrician diagnoses atopic dermatitis, and Kameron will begin treatment today. 

Atopic dermatitis, also known as eczema, is a chronic inflammatory skin disease that occurs most frequently in children, ages five and under, but may also affect adults, especially those with a predisposition towards allergic diseases, including asthma, allergic rhinitis, and conjunctivitis.

Now, the exact cause of atopic dermatitis is not fully understood, however it seems to be a mix of skin barrier abnormalities and dysfunction in the immune system. 

In regards to skin barrier abnormalities, atopic dermatitis is associated with a mutation in the filaggrin gene. 

Filaggrin is a protein that binds to keratin and contributes to the formation of the skin barrier, so individuals with atopic dermatitis have a slightly porous skin barrier, which sets them up for allergens or microbes to get under the skin. 

In regards to dysfunction in the immune system, atopic dermatitis is associated with atopy, which is a genetic predisposition to develop allergies due to an increased inflammatory response to triggers, such as allergens or irritant substances. 

There are some risk factors for atopic dermatitis. 

Unfortunately, some of them are non-modifiable, including younger age, atopy, family history, and mutations in the filaggrin gene. 

On the other hand, modifiable risk factors include contact with triggers, including allergens like pollen, mold, or animal dander, as well as a certain kind of soap or detergent, or an i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexually_transmitted_infections:_Warts_and_ulcers:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cNJsaSnhQeKjC7OoBVGHyxFCQWGCeZhy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sexually transmitted infections: Warts and ulcers: Pathology review]]></video:title><video:description><![CDATA[A 35 year old female named Rae comes to the clinic one day with complaints of multiple verrucous skin lesions that have appeared over the anogenital region. Upon further questioning, Rae tells you that her husband also developed the same lesions over the same region a few weeks ago, but hasn’t seeked medical attention. On physical examination, you notice that the skin lesions are soft and flesh-colored, and have a unique cauliflower-like appearance. You decide to perform a biopsy of the lesion, which reveals the presence of multiple vacuolated epithelial cells with enlarged, irregular nuclei. 

A few days later, a 30 year old male named Mark comes to the clinic concerned about a painful ulcer that recently developed in his genital region. Upon further questioning, he mentions that he’s sexually active, but doesn’t always use protection. On examination of the genital region, you notice that the ulcer is covered by exudate; in addition, Mark has inguinal lymphadenopathy, which is tender. You obtain a sample of the exudate and order a gram staining, which shows gram-negative, rod-shaped bacteria arranged in parallel strands. 

Now, based on the initial presentation, Rae has warts, while Mark has ulcers, and both cases seem to be caused by a sexually transmitted infection, or STI for short. 

STIs are mainly transmitted from person to person during sexual contact through body fluids, such as vaginal secretions, semen, or blood. The ones most at risk of contracting an STI are sexually active individuals, particularly those who have unprotected sex or multiple sexual partners. But, it’s important to note that sexually transmitted infections can also be transmitted via contact with skin or mucous membranes, including eyes, mouth, throat, and anus. And that’s a high yield fact!

Now, a common STI that may cause warts, called condylomata acuminata, is caused by human papillomavirus, or HPV. 

On the other hand, STIs that may cause ulcers include genital herpes, cau]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Drug_misuse,_intoxication_and_withdrawal:_Alcohol:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EFAR461iR22XPW8w7SGVmSYPRumLeZBE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Drug misuse, intoxication and withdrawal: Alcohol: Pathology review]]></video:title><video:description><![CDATA[Two individuals are brought into the emergency department, one night. One is 28 year old Brian who was brought in by his friend with complaints of altered consciousness and vomiting. 

The friend recalls that Brian had a habit of binge drinking on weekends. On examination, he was disoriented, and had slurring of speech, loss of coordination, and nystagmus. 

The second is 2 year old Michelle who’s brought by the mother who reported a seizure episode an hour ago. 

Upon further questioning, the mother reveals that Michelle was born 2 months prematurely, was always crying and irritable, and was slow in reaching developmental milestones. 

On examination, Michelle has reduced height and weight, a small eye opening, smooth philtrum, and thin lips. A neurological exam shows reduced muscle tone and coordination. 

When you obtain a more focused history regarding the mother&amp;#39;s pregnancy, she reported drinking 3-5 glasses of wine each night during the 1st and 2nd trimester.

Okay, both Brian and Michelle’s symptoms are due to alcohol. Alcoholic drinks contain the chemical ethanol, which mainly acts in two ways in the brain, one, it acts as an agonist to GABA, which is the brain’s major inhibitory neurotransmitter; and two, it acts as an antagonist of glutamate, which is an excitatory neurotransmitter. 

Both these actions produce an overall inhibitory action on the brain’s neuronal circuits. Now, ethanol’s effects vary based on the blood alcohol concentration, or BAC, which is the percentage of ethanol in a given volume of blood. 

At a blood alcohol concentration of 0.0 to 0.05%, ethanol produces a relaxed and happy feeling, along with slurred speech and some difficulty with coordination and balance. 

At a blood alcohol concentration of 0.06 to 0.15%, there is increased impairment to speech, memory, attention, and coordination, and some individuals can get aggressive and even violent. 

Complex tasks like driving can become dangerous, which is why it is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Oculomotor_(CN_III),_trochlear_(CN_IV)_and_abducens_(CN_VI)_nerves</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4YwXg9fXSq289DlUcSpDMTiXQCKqWTWc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves]]></video:title><video:description><![CDATA[In order to move our eyes and see the world around us, like watching this osmosis video, we rely on the control of our extraocular muscles which are primarily innervated by three cranial nerves; cranial nerve III, or the oculomotor nerve, cranial nerve IV or the trochlear nerve, and cranial nerve VI or the abducens nerve. These cranial nerves allow us to move our eyes in various directions, and also help to govern certain reflexes of the eyes. Injury to these cranial nerves can lead to a number of problems involving the eye, so understanding their anatomy can help us better understand the clinical consequences of these conditions!

First up, let’s discuss damage to the oculomotor nerve, also called oculomotor nerve palsy. The oculomotor nerve carries both motor and parasympathetic fibers which can be injured either individually or together. When looking at the anatomy of the oculomotor nerve, the parasympathetic fibers are found in the peripheral or superficial portion of the nerve, and the motor fibers are found in the central or deep portion of the nerve. This is significant as more external compression may only affect the parasympathetic fibers, where lesions of central nerve fibers might only affect the motor fibers. Remember, Motor is Middle, and Parasympathetic is Peripheral.

Now, if the motor fibers of the oculomotor nerve are damaged, that results in ophthalmoplegia, meaning impaired function of the four extraocular muscles innervated by the oculomotor, which are the superior, medial and inferior rectus, and the inferior oblique muscles. When these four muscles are impaired, that leaves the two other extrinsic eye muscles unaffected, so their actions are now left unopposed. This means the lateral rectus pulls the eye laterally, and the superior oblique pulls it inferiorly and laterally. Individuals with this type of injury present with the ipsilateral eye in a characteristic ‘down and out’ position. When the individual tries to look in any other d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Carbon_monoxide_poisoning:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/guFiDnk8QiCFvKjzNEEm73yISs67pkMK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Carbon monoxide poisoning: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Emma Rogers is a 12-year-old female brought to the ED by paramedics. Emma’s mother Faye called emergency services when she went to Emma’s room to wake her up and noticed she was lethargic, confused and unable to stay awake. The paramedics found Emma in her basement bedroom which was adjacent to a hot water heater. Carbon monoxide poisoning is suspected. 

Carbon monoxide poisoning occurs when there’s a buildup of carbon monoxide in the blood. CO is produced from the burning of fuels that contain carbon, such as charcoal, oil, coal, wood and kerosene. It is known as the “silent killer” because it’s odorless, tasteless, and colorless.  

Some classic scenarios where CO poisoning can occur include: an individual that’s been in a fire and has inhaled smoke; someone in a poorly ventilated area with a running vehicle, fireplace, or faulty gas stove or hot water heater; or if they live in an old building with a defective heating system. An individual may also be chronically exposed to CO, and that’s common in smokers, automobile workers, and people working in certain industries.  

Now, there are some factors that may put an individual at risk for CO poisoning. Non-modifiable risks include age, in particular young children and the elderly, as well as those with physical or mental disabilities.  

These factors can make it harder for the individual to stop or escape from the situation where CO is being produced. In addition, cigarette smoking and having an underlying lung disorder increases the risk of harm from CO poisoning.  

On the other hand, modifiable risk factors include being in a building without functioning CO detectors, or being under the influence of alcohol or drugs. 

Now, once CO is inhaled, it makes its way into the bloodstream. The affinity of hemoglobin for CO is about 240 times more than its affinity for oxygen, so CO will competitively bind to hemoglobin, forming carboxyhemoglobin, or COHb, and the oxygen carrying capacity of blood decreases. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cirrhosis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uRzkDBckSYOijq7NGwp8OOJVSt_BDz0s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cirrhosis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Rita Davis is a 55-year-old African American woman with a history of cirrhosis from chronic hepatitis C infection. 

Today, Rita is visiting the clinic for concerns about increased abdominal distention, loss of appetite, and fatigue.  

Cirrhosis is a condition in which the liver, a large organ in the right upper quadrant of the abdomen, becomes irreversibly scarred from chronic inflammation. 

Because the liver has many functions related to digestion, metabolism, detoxification, and production of important molecules the body needs, damage to the liver can have widespread impact on a person’s health.

Let’s look at some of the contributing factors for chronic liver inflammation. 

One of the most common modifiable risk factors is long-term alcohol use. 

On the other hand, non-modifiable risk factors for cirrhosis include viral hepatitis, autoimmune hepatitis, and other autoimmune disorders, including primary biliary cholangitis and primary sclerosing cholangitis, which can cause liver injury through progressive scarring of the bile ducts. 

Liver injury can also occur from non-alcoholic fatty liver disease, in which fat cells build up in the liver. 

Genetic disorders like hemochromatosis and Wilson’s disease can cause inflammation from accumulating elements like iron or copper in the liver, whereas alpha-1 antitrypsin deficiency creates malformed proteins that become stuck in the liver.

The liver is highly regenerative, meaning that after injury it replaces injured tissue with regenerative nodules. 

These nodules are colonies of liver cells, or hepatocytes, surrounded by collagen-rich scar tissue. 

This causes the smooth liver tissue to become bumpy and stiff. 

Over time, inflammation causes bands of scar tissue to form between nodules. 

As the scar tissue grows, it compresses the network of blood supply in the liver. 

This leads to increased venous pressure and portal hypertension, which occurs as blood backs up into the portal vein. 

Now, higher]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epiglottitis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/598tb81zRsCkIgcYJWBRmAOqQDmUWnhd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epiglottitis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Eve Vu is a 5-year-old female who is brought to the emergency room, or ED, by her mother with reports of a sore throat and fever. 

According to her mother, Eve has been irritable, refuses liquids, and when Eve started drooling, she brought her in as soon as she could. 

Eve is triaged quickly for suspected epiglottitis.

Epiglottitis, also called supraglottitis, is inflammation of the epiglottis, which is a flap of cartilage located behind the tongue, and its surrounding tissues. 

Epiglottitis typically occurs in children between 2 and 5 years of age, but can occur from infancy to adulthood. 

Males are more at risk than females, and those who are immunocompromised are more at risk as well. 

The most common causes used to be Haemophilus influenzae type b, but this has become less common thanks to an increase in childhood vaccination. 

Streptococcus pneumoniae and Staphylococcus aureus are now the most common causes in the US.  

Epiglottitis can also be caused by viral and fungal infections, or by non-infectious causes like smoke inhalation, hot foods or liquids, and foreign bodies.

In bacterial epiglottitis, the initial symptoms include sore throat and a sudden onset of high fever. 

This can happen much quicker in children compared to adults.  

When the epiglottis and nearby tissue become infected, inflammation and edema develops.  

As the epiglottis swells up, it can fold backwards and act like a ball valve that obstructs the airways during inhalation.  

The swelling of the nearby tissue makes matters worse by narrowing the airways. 

In children, this will lead to the 3 Ds; Distress or anxiety,  Dysphagia, or difficulty swallowing, and Drooling due to the inability to swallow.  

Airway obstruction can also cause turbulent airflow resulting in an inspiratory stridor which sounds like a high pitched whistling. 

The voice also becomes muffled so it sounds like they have a hot potato in their mouth when they speak. 

The work of breathing is incr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epistaxis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PUqsQbhUQpKAFYuP4R4snF2XQEi0fRV8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epistaxis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Ethan Porter is a 10-year-old student who was brought to the school nursing office by his gym teacher with a nosebleed. 

Ethan was newly diagnosed with von Willebrand disease, and about 5 minutes ago, his nose suddenly started bleeding while he was running the track outside in gym class.  

Epistaxis, or nose bleed, is caused by ruptured blood vessels in the nasal mucosa. 

Up to 90% of epistaxis is anterior epistaxis where bleeding occurs in the anterior nasal cavity and the blood typically comes out of the nares. 

Posterior epistaxis occurs in the superior or posterior nasal cavity so the blood usually goes down the throat.  

In the anterior nasal cavity, numerous arteries in the face connect together to form the Kiesselbach’s plexus, also known as Little&amp;#39;s area. 

This blood vessel rich area is located on the nasal septum and is covered by a thin mucus membrane that offers little protection so dryness, irritation or even minor trauma, like nose picking, can lead to bleeding. 

An intranasal mass and foreign bodies can also be causes. 

The most common sign is visible bleeding, usually from one nostril. 

After having the person gently blow their nose to clear blood clots, the nasal cavity is typically assessed with a light source and a nasal speculum to look for signs of active bleeding, excoriation, or scabbing.  

Posterior epistaxis occurs further back in the nose, and the most common site is where blood vessels come together in the lateral wall of the nasal cavity to form the Woodruff’s plexus. 

Since it’s located deeper in the nasal cavity, more severe head and nasal trauma can cause this type of epistaxis. 

It is more serious than anterior epistaxis because the bleeding is often more severe and blood can go down the pharynx, esophagus and trachea. 

If blood goes down the trachea it can cause coughing and hemoptysis, while swallowing blood can cause nausea, vomiting and hematemesis.  

If bleeding occurs frequently it could even lead]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Foreign_body_aspiration_&amp;_upper_airway_obstruction:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GX97DeCfR_GGlMuF2CYeAOVjSHCteAr5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Foreign body aspiration and upper airway obstruction: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Ali Jafari is a 11-month-old male brought to the emergency department, or ED, by his parents, who state that Ali was playing on the floor when he started to cough and choke. 

They rushed him to the ED when Ali’s coughing got worse and started to have trouble breathing. 

Ali is being treated for upper airway obstruction due to foreign body aspiration. 

The upper airway consists of the nasal cavity, paranasal sinuses, pharynx, and larynx. 

Any mass or edema in these regions can cause partial or complete obstruction.  

One common cause is upper respiratory tract infections like croup, laryngitis, and epiglottitis which are typically caused by viruses, and can lead to inflammation which can cause edema and obstruction of parts of the upper airway. 

Allergens like dust, pollen and pet dander can cause mild reactions like rhinitis and sinusitis where nasal discharge and congestion can lead to obstruction. 

More severe reactions like anaphylaxis can occur when there’s severe allergic reactions to things like peanuts or shellfish. 

This can lead to angioedema, which is a rapid and severe swelling of the mucosa, leading to obstruction. 

Trauma that causes airway obstruction can include direct trauma like a car crash or gunshot wound which can collapse parts of the airway or cause bleeding that obstructs the airway. 

Congenital anomalies include conditions like laryngomalacia which is an anomaly of the laryngeal tissues that causes a partially obstructed airway. 

Finally, foreign body aspiration occurs when a foreign object, like a nut, coin, or small toy gets lodged in the airway. 

It can happen to anyone, but occurs most commonly in young children who have a smaller airway diameter than adults. 

They also like to explore by placing objects in their mouth and are easily distracted during eating which can increase risk of aspiration. 

Children younger than 2 usually don’t have molars yet, so they are unable to grind their food into smaller more managea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gout:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BQmdxgpDRSuDglz9DLJ78hVDQneQShUQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gout: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Hubert Symanski is a 49-year-old male client with a history of Type 2 diabetes mellitus who presents to the clinic today with severe pain in the big toe of his right foot. 

He explains that when he woke up this morning his toe was red, swollen and felt like it was on fire. He denies any recent injury to his toe or foot. 

Walking around the house and putting on shoes is very painful, and the only shoes he can comfortably put on are sandals. 

He reports that he had an episode of gout a year ago, confirmed by joint aspiration, and he is concerned that this may be another episode. 

Gout is an inflammatory disease in which urate crystals deposit in a joint and cause damage. 

Typically, the underlying cause is hyperuricemia, or too much uric acid, also known as urate, in the blood. 

Uric acid is a natural waste product of purines, which are one of the building blocks of DNA and RNA. 

Once produced, uric acid circulates in the bloodstream before it is filtered out and excreted by the kidneys to the urine.  

Now, hyperuricemia is associated with several risk factors. 

An important risk factor is overproduction of purines, which is most common with increasing age, male sex, obesity, and alcohol use. 

Overproduction of purines can also occur with increased consumption of purine-rich foods such as shellfish, alcohol, anchovies, and red meat, as well as high-fructose corn syrup containing beverages such as sodas. 

Hyperuricemia can also result when cells die at a faster than normal rate, resulting in increased breakdown of purines into uric acid, for instance as a result of chemotherapy, radiation treatment, as well as recent trauma or surgery. 

In addition, some individuals have a genetic predisposition to developing hyperuricemia, so an important risk factor is family history. 

Finally, hyperuricemia can also occur when there’s reduced excretion of uric acid by the kidney, which can result from dehydration, diabetes, chronic kidney disease, and medicati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertension:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NmkwzJCbTCmfKZroUmeJptTzT6SkXrFg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertension: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Jada Williams is a 55-year-old African American female who presents to her primary care office. 

At her visit one month ago, her blood pressure was 150/94 mmHg. 

She was diagnosed with stage 2 hypertension and started on blood pressure medication. 

Hypertension, commonly referred to as high blood pressure, is a very common condition, impacting about 1 billion people around the world. 

Blood pressure is classified in five categories: normal, elevated, stage 1, stage 2, and hypertensive crisis. 

Blood pressure is considered normal when the systolic blood pressure is more than 90 mmHg but less than 120 mmHg and the diastolic blood pressure is more than 60 mmHg but less than 80 mmHg. 

When the systolic blood pressure is between 120 and 129 mmHg and the diastolic blood pressure is less than 80 mmHg, the blood pressure is said to be elevated. 

Stage 1 hypertension is between 130 and 139 mmHg on the systolic side, and between 80 and 89 mmHg on the diastolic side. 

Stage 2 hypertension is defined as anything that is 140 mmHg or higher on the systolic side and 90 mmHg or higher on the diastolic side. 

Hypertensive crisis is present when the systolic blood pressure is over 180 mmHg or the diastolic blood pressure is over 120 mmHg.

Now, there are also two types of hypertension, primary hypertension, which accounts for about 90 percent of hypertension cases, and secondary hypertension, which is much less common. 

Primary hypertension has no known underlying cause, but it is thought to be due to the interaction of environmental and genetic factors affecting the cardiovascular and renal systems. 

Several risk factors contribute to primary hypertension. 

For example, nonmodifiable risk factors include advanced age, biological male sex, a family history of hypertension, diabetes mellitus, and African American or Hispanic ethnicity. 

Modifiable risk factors include a sedentary lifestyle, obesity, smoking, excess sodium and alcohol consumption, and stress. 

O]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meningitis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YjOynYtNQ8W7Dli9qvkuSEBxTuOvEOVB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meningitis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Alejandro Delgado is a 19-year-old college student who was brought to the emergency department, or ED, by his roommate with a report of a sudden onset of headache, confusion and fever. 

He has a petechial rash on his arms and chest. 

The lesions don’t blanch, and Alejandro says they appeared a few hours before he came to the ED. 

Alejandro has no known allergies or comorbidities, and he is not aware that he’s been exposed to someone who is sick. 

The ED physician performed a targeted neurological examination which showed nuchal rigidity. 

Kernig and Brudzinski signs were negative. 

A lumbar puncture and blood draw were completed and sent to the lab for analysis, Gram stain and culture. 

Alejandro was then transferred to the inpatient unit for treatment and continued monitoring.

Meningitis refers to inflammation of the meninges, which are three protective membranes that cover the brain and spinal cord. 

From outside to inside they’re the dura mater, arachnoid mater, and pia mater, with cerebrospinal fluid, or CSF for short, in the space between the arachnoid and pia. 

Now, meningitis can be caused by any pathogen that can infect the meninges, such as viruses, bacteria, fungi, and parasites. 

The most common and life-threatening type is bacterial meningitis. 

There are two routes that bacteria can use to reach the meninges. 

The most common route is hematogenous spread, which is when bacteria enter the bloodstream and move through the blood brain barrier to reach the meninges. 

The second way is by direct spread from a nearby infected structure, like the skull, spine, or sinuses. 

Bacterial meningitis is more common in clients at the extremes of age, such as children younger than 5 years old or adults who are older than 60, as well as those who have other conditions, such as diabetes, HIV, cirrhosis, chronic kidney disease, malignancy, cystic fibrosis, or a history of splenectomy. 

Other important risk factors include nearby infections, such ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Laryngotracheobronchitis_(LTB)_&amp;_croup:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0r-AB4SDQOa4iRI4lROQzC2lRAqw24XQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Laryngotracheobronchitis (LTB) and croup: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Two year old Sara Little is brought to the Emergency Department, or ED, by her mother. 

She has a high-pitched, barking cough that started in the evening and worsened throughout the night.  

Mrs. Little explains that Sara has had “cold symptoms” for about 3 days. 

She initially had a runny nose and slight cough but began running a fever yesterday. 

She hasn’t been eating or drinking well and seems more anxious and difficult to soothe at night. 

When Mrs. Little noticed wheezing, she called the pediatrician who directed her to bring Sara to the ED. 

Upon arrival, Sara has a barking cough, inspiratory stridor, and a respiratory rate of 42 per minute. 

Sara will be treated for laryngotracheobronchitis, or LTB, also known as croup. 

Croup is an inflammation of the upper airway, typically caused by a virus, such as parainfluenza, adenovirus, influenza A or B, or respiratory syncytial virus, or RSV.  

Cases of croup are seen seasonally, most often in late fall and early winter. 

It affects children ages 3 months to 6 years and is most common in boys and in children where there is a family history of croup or recurrent croup. 

Croup is spread through airborne respiratory droplets, saliva and physical contact with an infected person or contaminated surface. 

The droplets enter the body, initially infecting the nasal passages and pharynx, subsequently spreading to the larynx, trachea and bronchi. 

The infection causes inflammation, edema and mucus secretion, leading to narrowing of the subglottic area, which is composed of the lower part of the vocal cords and the upper trachea. 

Not only is this area the narrowest portion of a child’s upper airway, but it has a complete ring of cartilage around it which doesn’t expand. 

When the airway becomes significantly narrowed, it results in hoarseness, a harsh high-pitched sound during inspiration referred to as inspiratory stridor, and a distinctive seal-like barking cough. 

Nasal flaring, substernal, subco]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Methicillin-resistant_Staphylococcus_aureus_(MRSA):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LrWCsysLTc_G2DZpvK_Qj0q-SkKfUjx7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Methicillin-resistant Staphylococcus aureus (MRSA): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Elias Moore, a 17-year-old African American male, who is on his school’s wrestling team who developed a red, painful sore on the upper left side of his thigh. 

At first it looked like a spider bite, but the next day it began to swell and formed a bump filled with pus. 

He showed it to his mother who took him to the pediatrician’s office where he was diagnosed with community-acquired methicillin-resistant Staphylococcus aureus, also known as CA-MRSA.

MRSA is a strain of Staphylococcus aureus, or staph for short. 

It’s often referred to as a superbug due to its resistance to the widely-used beta lactam antibiotics such as penicillins, cephalosporins, and carbapenems. 

This is because MRSA has the mecA gene that allows the bacteria to produce proteins that are more difficult for the medications to bind to, and it also codes for the beta lactamase enzyme which can break these medications down. 

Unfortunately, due to the misuse and overuse of antibiotic treatment by both clinicians and patients, MRSA has become more common in recent years. 

The two types are healthcare-associated MRSA, or HA-MRSA, and community-associated MRSA, or CA-MRSA. 

HA-MRSA infections are a leading cause of infection in hospitals due in part to the fact that it creates biofilms that colonize medical devices like catheters, endotracheal tubing, and surgical instruments. 

On the other hand, CA-MRSA occurs when there’s been no exposure to the healthcare setting and it can affect healthy individuals. 

CA-MRSA is primarily transmitted from direct or indirect contact and can either asymptomatically colonize or cause an active infection. 

Risk factors for developing an active infection include chronic illnesses like kidney disease, diabetes, or malignancies; activities that could cause damage to the skin, like contact sports and intravenous drug use; living in crowded or unsanitary conditions like army barracks or prisons; and those with HIV or using immune suppressing medications l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myocardial_infarction_(MI):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/glCxMWXVTZSdCkGfOxUhbY1oQjGYPXiE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myocardial infarction (MI): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Miguel Garcia is a 60-year-old Hispanic male with a history of hypertension who was brought to the emergency department, or ED, for chest pain. 

The pain began two hours ago and he states it feels like an elephant is sitting on his chest. 

The physician just confirmed with an electrocardiogram, or ECG, that Mr. Garcia is experiencing a STEMI, which stands for ST segment elevation myocardial infarction. 

The team is acting swiftly to prepare him for an emergent percutaneous coronary intervention, known as a PCI.  

A myocardial infarction, also known as an MI or heart attack, refers to the death of cardiac muscle tissue from prolonged ischemia. 

Risk factors include being over 40 years old or male; having diabetes mellitus, dyslipidemia, hypertension, or a family history of MIs; smoking tobacco; obesity; a sedentary lifestyle; and eating a high fat diet. 

The most common cause of MI is atherosclerosis. This is when lipid containing plaque builds up in the coronary arteries.

When the coronary artery is occluded, blood and oxygen supply cannot meet the demands of the myocardium, causing ischemia. 

This leads to angina, or a type of chest pain. Angina can either be stable or unstable. 

Stable angina is provoked by activities that increase oxygen demand, such as exercise, lasts up to 15 minutes, and is relieved by rest or vasodilators like nitroglycerin. 

This is because the occlusion limits blood flow while the oxygen demand of the myocardium increases, but when demand decreases or if the artery becomes dilated, the pain resolves

On the other hand, unstable angina can occur without exertion or even at rest, persists longer than 15 minutes, is a more severe pain than stable angina, and is not relieved by rest or vasodilators. 

This is often due to the plaque rupturing which causes platelets to attach to the plaque, forming a thrombus. 

The result is a more severe reduction in coronary blood flow than what occurs in stable angina, so it doesn’t resol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rheumatic_heart_disease:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/le0v4tpeQRiG2ZotDEbmxxmjQ_eW25wu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rheumatic heart disease: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Saanvi Kumar is a 17-year-old female client who recently immigrated from India. Saanvi has a history of recurrent rheumatic fever with the last episode resolving 10 years ago. Lately, Saanvi noticed she feels more tired than usual and started feeling short of breath during gym class, so her pediatrician referred her to a cardiologist for further evaluation. The cardiologist ordered an echocardiogram, a chest X-ray, and an electrocardiogram, or ECG, and Saanvi is diagnosed with rheumatic heart disease.

Rheumatic heart disease is a complication of rheumatic fever, which is a delayed multisystemic inflammatory condition that typically occurs two to four weeks after a strep throat infection. Strep throat is caused by bacteria called Streptococcus pyogenes, which is often referred to as group A beta hemolytic streptococcus or GAS for short. Not everyone who has strep throat will develop rheumatic fever, but it’s important to note that children between the age 5 and 15 are at a higher risk.

Rheumatic fever arises because Streptococcus pyogenes has a bacterial protein that mimics the structure of some proteins in the human body. So, when the immune system produces antibodies against the bacterial protein, these antibodies also end up targeting our own tissue.  The heart is one of the major organs affected but others include the joints, skin, and brain. Once bound to human proteins, these antibodies activate nearby immune cells, which induce an inflammatory response that leads to tissue destruction and fever.

Now let’s focus on the inflammation of the heart, which is also known as carditis. Clients with rheumatic fever typically develop pancarditis, which is the inflammation of all three layers of the heart: endocardium, myocardium, and pericardium. But, if a client repeatedly experiences attacks of rheumatic fever, chronic inflammation of the heart can lead to leaflet damage and valvular lesions. This condition is called rheumatic heart disease and it&amp;#39]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eye_injury:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9Pn1EU7aR9KmdJY_66pGeR8vR8_O_Z5M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eye injury: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Kevin Stackhouse is a 25-year-old-male construction worker who presents to  the emergency department, or ED, after sustaining an injury to his eye when a panel of glass shattered during installation. Mr. Stackhouse reports he experienced sharp pain followed by vision loss in his right eye. Upon arrival to the ED, he was found to have swelling and lacerations in the periorbital area, as well as pain and decreased eye movement. The on-call ophthalmologist performs a slit lamp examination and fundoscopy, which reveals 2 small glass fragments present in the eye, along with a corneal laceration. Mr. Stackhouse is given a tetanus booster and is taken to the operating room, or OR, for surgical removal of the fragments and repair of the corneal laceration.

Penetrating eye injuries occur when the eye is pierced by a sharp object, such as pencils, screwdrivers, nails, knives, as well as or high velocity flying fragments like those from fireworks and other explosions.

Now, there are some factors that may put the client at risk for penetrating eye injuries. Modifiable risk factors include occupations that have exposure to sharp objects, such as construction workers, mechanics, or being in the military. On the other hand, a non-modifiable risk factor is male gender, and that’s probably because males are more likely to have high risk occupations. Another non-modifiable risk factor is age, in particular children are at increased risk of penetrating eye injuries, since they can be careless  or less coordinated when playing. 

Generally, signs and symptoms of penetrating eye injury may include eye pain, redness, and blurred or impaired vision, as well as photophobia or light sensitivity, and epiphora or excessive tearing. Now, the extent of the penetrating eye injury depends on its depth. So, first, there’s eyelid laceration, which is a skin cut on the eyelid. Next, if the penetrating object makes it to the cornea, it may result in corneal abrasion, which is a superficia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glaucoma:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1LjBpqP-QPGKm8LAn7vKX65tQOK9_2lE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glaucoma: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Mrs. Barbara Yao is a 67-year-old female client who was brought by her husband to the emergency department, or ED, with reports of blurred vision, eye pain, a severe headache, and nausea for the past two hours. She states that she sees red halos around lights and you notice her eyes appear red. The ED physician diagnoses her with acute angle-closure glaucoma. 

Glaucoma refers to a group of eye conditions that are associated with increased pressure in the eye, referred to as intraocular pressure, or IOP. But, before we proceed with glaucoma, first, let’s take a look at a cross-section of the eye. On one side of the lens, we have anterior and posterior chambers filled with the fluid aqueous humor; while on the other side, we have the vitreous body filled with the gel-like vitreous humor. Now, the aqueous humor is secreted by the ciliary epithelium into the posterior chamber, and from here, it flows through the pupil to the anterior chamber. Next, from the anterior chamber, the fluid drains out of the eye through the trabecular meshwork, into the Sclemm’s canal, and eventually into the aqueous veins. Controlled production and drainage result in normal intraocular pressure, which typically ranges from 10 to 20mmHg. 

Now, in glaucoma, drainage of aqueous humor is restricted. As a result, the aqueous humour builds up and pushes against the vitreous body.  This causes intraocular pressure to rise which eventually leads to damage to the optic nerve and the retina. Depending on whether or not the angle between the iris and the cornea is obstructed, glaucoma can be defined as open- or closed-angle. 

In open-angle glaucoma, which is also known as wide-angle glaucoma, the angle between the cornea and the iris is not obstructed but the trabecular meshwork is. This is the most common type of glaucoma and Black individuals, those with advanced age, or a family history are at a higher risk. Now, open-angle glaucoma can be primary, where the cause is unknown, or se]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_kidney_injury_(AKI):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c8TyZzPcQYatdRezQoOah5rBTHykNRnl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute kidney injury (AKI): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[You are assigned to take care for Maurice Jones, a 58-year-old Black male, who sustained a back injury several weeks ago while cleaning out his garage, and since then he’s been taking ibuprofen three to four times each day for pain. Mr. Jones has a history of hypertension for which he takes the angiotensin II receptor blocker, or ARB, losartan, though he says sometimes he forgets to take it. He also takes the proton pump inhibitor, or PPI, omeprazole, for gastrointestinal reflux disease, or GERD. He presented to his primary care provider, or PCP, with fatigue, headache, lower extremity edema, and decreased urine output. 

His vital signs were oral temperature 99.0 F or 37 C, heart rate 98 beats per minute, respiratory rate 20 breaths per minute and blood pressure 148/96mmHg. Labs were ordered which showed BUN  28 mg/dL, creatinine 2.4 mg/dL, sodium 124 mEq/L, and potassium 5.3 mEq/L. Arterial blood gas analysis revealed pH 7.25, PCO2 32, PO2 85, HCO3 30. Urine specific gravity is 1.010. Mr. Jones was admitted to the medical unit with a diagnosis of acute kidney injury, or AKI. 

Acute kidney injury, or AKI for short, refers to a sudden decrease in kidney function over hours or days. As a result, the kidney’s ability to manage fluid, electrolyte, and acid-base balance is impaired, and there’s decreased excretion of waste products, such as urea and creatinine, which build up in the blood.

There are some factors that can put an individual at risk for AKI. Unfortunately, many of them are non-modifiable factors that decrease kidney function over time, such as advanced age, diabetes mellitus, autoimmune diseases, certain cancers, uncontrolled hypertension, and heart, liver, or kidney disease. Some modifiable risk factors include exposure to nephrotoxic agents, such as certain antibiotics, heavy metals, or chemotherapy or being exposed to iodinated IV contrast dye during radiology procedures.

Now, the causes of AKI can be classified into prerenal, intrarenal, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gorlin_syndrome_(Gorlin_Syndrome_Alliance)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PX5OGuZkTQaSW2XZFteV0A5mQTiTxkrD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gorlin syndrome (Gorlin Syndrome Alliance)]]></video:title><video:description><![CDATA[Gorlin syndrome is a rare genetic disorder that affects approximately 1 in  31,000 people worldwide. 

At the most basic level, people with Gorlin syndrome have an increased lifetime risk of tumors, both cancerous and non-cancerous, in nearly any organ of their body. 

The most common tumor experienced is a skin cancer  called basal cell carcinoma, so  the disease is also known as basal cell carcinoma nevus syndrome. 

Because of the rarity of the disease, your doctors might not recognize or know much about Gorlin syndrome. 

Medical care may be delayed or compromised if it is not identified, so it is important for people with Gorlin syndrome and their family members to learn about the syndrome and be able to effectively manage care. 

Gorlin syndrome is caused by a defect in a gene that suppresses tumors in a person’s body. 

Genes are like instructions for cells. Every cell has two copies of each gene. We inherit one gene from each parent. 

Sometimes, we inherit a mutated gene from one parent, and sometimes a gene mutates on its own. 

If one gene is mutated then the other gene can suppress tumor growth on its own to a degree. 

This means that if a person with Gorlin syndrome has only one broken copy of a tumor suppressing gene in each cell, they may have some features of the disease. 

If any cell in their body develops a second mutation that affects the working copy of  the tumor suppressing gene, then the cell has no way to prevent itself from replicating out of control.

The cells will begin to pile up into a mass, and a tumor will form. 

People with Gorlin syndrome usually have tumor growth at some point in their lives, but how many develop, at what age and which organs are affected is variable. 

There are three genes known to cause Gorlin syndrome: PTCH1, PTCH2 and SUFU. 

Genetic testing may identify which defect you have. 

The specific gene that is altered can affect which manifestations and symptoms you experience. 

A genetic counsellor ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peptic_ulcer_disease_(PUD):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4dr0Gn7YSieT6tU8yZM3ZLqSQS67di4b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peptic ulcer disease (PUD): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Paola Salazar is a 56-year-old hispanic female client admitted to your unit after an esophagogastroduodenoscopy, or EGD, revealed a bleeding gastric ulcer which was controlled by thermal coagulation. 

Her recent history includes intermittent upper abdominal pain, and a recent weight loss of five pounds because of nausea and decreased appetite. 

After experiencing an episode of hematemesis, her primary care physician, or PCP, ordered an EGD. 

A biopsy taken during the procedure is negative for Helicobacter pylori, or H. pylori  for short.

Her other health problems include fatigue and chronic back pain.  

Peptic ulcer disease, or PUD, is an erosion of the lining of the gastrointestinal, or GI tract, most commonly in the proximal duodenum and stomach. 

The lining of the GI tract is made of four layers, the mucosa, which is the innermost layer, followed by the submucosa, muscularis, and serosa. 

Cells in the mucosa secrete harsh gastric juices, like hydrochloric acid and pepsin, which help digest food. 

Normally the mucosa is protected from self-digestion due to tightly joined epithelial cells that resist penetration, and by prostaglandins that stimulate secretion of a protective layer of mucus and bicarbonate. 

When the gastric juices overcome these protective mechanisms and damage the gastric lining, a peptic ulcer develops.

Sometimes PUD is asymptomatic, but often the exposure to irritating gastric juices can cause  burning epigastric pain. 

Typically, pain from gastric ulcers increases 15-30 minutes after a meal, while pain from duodenal ulcers increases 2-3 hours after a meal and at night. 

Other common symptoms include bloating, abdominal fullness, and nausea.  

If the erosion extends down to the muscularis level it can damage blood vessels resulting in an upper GI bleed, hematemesis, or melena, when blood passes through the lower GI tract, producing a dark, tarry stool. 

Anemia from extensive blood loss causes symptoms like fatigue, pallor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Poisoning:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u7Sw55R6TeCWrx5wljjW9uYDQPiINvD6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Poisoning: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Gabriel Hernandez is an 18 month old male who was brought to the emergency department, or ED, by his father. 

Mr. Hernandez stated that he put Gabriel down for a nap in his room, and about an hour later he found Gabriel sitting in the kitchen with an empty bottle of children’s acetaminophen in his hand. 

The 120mL bottle was previously about three-fourths full.  

Mr. Hernandez immediately called the poison control hotline and was instructed to bring Gabriel to the ED. 

Poisoning occurs when a person eats, drinks, or breathes in a harmful substance that can cause illness or death. 

Poisoning can be intentional or purposeful, which is most common in clients who are suffering from a terminal illness or mental health issues; and unintentional or accidental, which typically occurs when a client is accidentally exposed to a chemical spill or aerosolized toxin, or when they ingest a substance without knowing it is dangerous, or finally, when they accidentally overdose on their prescribed medications. 

This may occur when a client forgets that they already took their daily dose, or they take two medication brands that contain the same active ingredient. 

Most cases of accidental poisoning involve children who ingest over-the-counter medications for pain, fever, cough, and cold and flu. 

The most common ones include acetaminophen, since it is found in many over-the-counter products, and its maximum daily adult dose is only 4 grams; as well as NSAIDs, like ibuprofen; and cough syrups. 

Other important causes of accidental poisoning include ingestion of supplements, like multivitamins or iron; as well as cleaning and disinfectant chemicals, such as bleach, soap solution, and window cleaners. 

Less commonly, children might ingest essential oils or plants, like mushrooms, tobacco, or marijuana. 

Now, there are some risk factors that can increase the risk of poisoning. 

The first one are extremes of age, since toddlers are more likely to put unknown objects ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stroke:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_3Ew6Cs5QR2U0X4XuDDVgGrbSSuBaFca/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stroke: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Russell King is a 70-year-old male client who experienced an embolic stroke in his left middle cerebral artery. His wife says she found Russell slumped in his recliner, unable to get up. She noticed that his face looked like it was drooping on one side, and his speech was slurred. She called an ambulance, and he was brought to the emergency department, or ED, and was quickly diagnosed with a stroke and treated with thrombolytic therapy. After Russell recovered in the stroke unit, he was transferred to an inpatient rehabilitation facility where he will undergo rehabilitation therapy.

A stroke is when there’s a sudden neurological deficit because part of the brain loses its blood supply. There are factors that may put an individual at risk for stroke. Unfortunately, many of them are non-modifiable, including older age; male sex; history of prior stroke; and family history of stroke. On the other hand, modifiable risk factors include uncontrolled hypertension, dyslipidemia, diabetes, heart disease like atrial fibrillation, as well as obesity, lack of physical activity, diet high in saturated fats, and smoking or using drugs like cocaine or amphetamines.

Okay, now there are two main types of stroke: an ischemic stroke, in which a blocked artery reduces blood flow to the brain, and a hemorrhagic stroke, in which an artery in the brain breaks and creates a pool of blood that damages the brain. In this video, we are going to focus on ischemic strokes, which are much more common. Now, most ischemic strokes are caused by thrombosis, meaning that a clot forms over an atherosclerotic plaque. This is when a buildup of fat and cholesterol forms within a cerebral artery and starts to obstruct its blood flow. Another mechanism for ischemic stroke is an embolism. This happens when an embolus, which is a piece of blood clot or fatty deposit, breaks off from an atherosclerotic plaque from an artery outside the brain, most often from the heart or neck. The embolus then tra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gonorrhea_&amp;_chlamydia:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Phnwg2V2Q4qOnvO_DlZaeeDdRbyE5XZG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gonorrhea and chlamydia: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Chad Davis is a 22-year-old male who presents to the health department’s sexually transmitted infection clinic with symptoms of painful urination and urethral discharge for the past two days. He states his girlfriend was recently diagnosed with chlamydia, and they are sexually active. He uses condoms sporadically and he’s worried he also has chlamydia.   

Gonorrhea and chlamydia are among the most common sexually transmitted infections, or STIs, in the United States in both men and women. Now, gonorrhea is caused by a gram-negative bacterium called Neisseria gonorrhoeae; while chlamydia is caused by a gram-negative bacterium called Chlamydia trachomatis. Both infections are transmitted during sexual contact through sexual fluids, such as vaginal secretions or semen, so they often occur together, primarily affecting genital organs. However, it’s important to note that these infections can also be transmitted via contact with skin or mucous membranes, including eyes, mouth, and anus.

Risk factors associated with gonorrhea and chlamydia can be subdivided into two main groups. Behavioral risk factors include having unprotected sexual contact, as well as new or multiple sexual partners. On the flip side, individual risk factors include young age, between 15 and 24 years old, since they’re more likely to have new or multiple sexual partners, as well as having a history of prior sexually transmitted infections, and HIV positive status. 

Most often, gonorrhea and chlamydia cause asymptomatic infection. However, symptomatic clients can present with mucopurulent discharge from the vagina or penis, as well as dysuria or pain and burning during urination, and urinary frequency. In males, gonorrhea and chlamydia can infect the urethral mucosa, causing inflammation known as urethritis. Sometimes the infection can spread to the prostate, resulting in prostatitis. Also, it can cause inflammation of the epididymis, or epididymitis, and cause symptoms such as testicular ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Trigeminal_neuralgia:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vVn3mzX0TF_LzHFDJItavxlOS1WsV4cE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Trigeminal neuralgia: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[For the past three weeks, Eliza Fitter, aged 65, has been experiencing excruciating painful attacks on the right side of her face several times each day. The pain is often triggered while eating, drinking, and brushing her teeth. Eliza presents to her physician’s office where she is diagnosed with trigeminal neuralgia.

Trigeminal neuralgia, also known as tic douloureux, is a neuropathic pain condition that involves the trigeminal or fifth cranial nerve, which supplies sensory information to the skin and mucous membranes of the face, as well as motor information for the muscles of mastication. And because of that, pain can often be triggered by chewing, brushing the teeth, shaving, or even just smiling! 

Now, the exact cause of trigeminal neuralgia is not well known, but it’s thought to be associated with vascular compression of the trigeminal nerve root. Some risk factors include female sex, increased age, and family history, as well as disorders like hypertension, multiple sclerosis, a brainstem tumor, an aneurysm, or a previous stroke.

Now, the main symptom of trigeminal neuralgia is a sudden, excruciating, sharp, pain, similar to an electric shock. Typically, the pain is unilateral and involves the lower face, from the corner of the mouth to the jaw, although in some clients it can also involve the area around the nose, cheek, and above the eye. The pain occurs in paroxysmal attacks that generally last from a few seconds up to 2 minutes, and may recur after just  minutes, as often as a hundred times per day! As a consequence,trigeminal neuralgia can be incapacitating and interfere with the client’s daily activities like eating, sleeping, or communicating. In the long term, the pain could be so unbearable that it may lead to mental health disorders like depression, and some clients may even consider suicide.

Diagnosis of trigeminal neuralgia mainly relies on history, since neurological examination is typically normal. There’s no specific laboratory o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tonsillitis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zaARzMx8Q4CqMfWJ1xfAnU4xQk_Q3dG5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tonsillitis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Mason Taylor is a 22-year-old male college student who presents to the college health clinic  with a two-week history of a sore throat and a   subsequent decrease in oral intake due to pain with swallowing. He reports a very painful sore throat, fatigue and feeling feverish. 

Tonsillitis is an inflammation of the palatine tonsils, which are two lymphoid organs located in the oropharynx. Tonsillitis is sometimes accompanied by adenoiditis, which refers to inflammation of adenoid tonsils in the nasopharynx, as well as pharyngitis, which is an inflammation of the throat or pharynx.

Tonsillitis is most often caused by a viral infection. Common viruses that cause tonsillitis include rhinovirus, adenovirus, and respiratory syncytial virus, or RSV. Other important viral causes of tonsillitis include coronaviruses, human immunodeficiency virus or HIV, and Epstein-Barr virus or EBV, which causes infectious mononucleosis. 

On the flip side, one of the most common causes of tonsillitis is bacterial infection from group A streptococcus. This is why bacterial tonsillitis is commonly referred to as strep throat.

Now, the main risk factor for tonsillitis is being between the age of 5 and 15 years of age. Other risk factors include being in crowded environments where pathogens can be transmitted from person to person, and not practicing good hand hygiene. In addition, tonsillitis occurs more commonly during winter and early spring. Finally, clients who don’t get properly treated for bacterial tonsillitis, like those who don’t complete an antibiotic course, are more likely to develop it again later.

Now, symptoms of tonsillitis depend on the underlying cause. Symptoms of viral tonsillitis include a low grade fever, cough, rhinorrhea or runny nose, and sneezing. On the other hand, bacterial tonsillitis tends to present with more severe symptoms, such as a high grade fever, sore throat, as well as dysphagia or difficulty swallowing, and odynophagia or painful swallowing]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Benjamin_Young:_Head_of_Global_Medical_Directors_VllV_Healthcare_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/szGn54f-ROe_zERoE_JEjJ6iSaizjaJq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Benjamin Young: Head of Global Medical Directors VllV Healthcare (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Benjamin Young: Head of Global Medical Directors VllV Healthcare (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Laura_Turner:_Executive_Director_of_the_Student_Doctor_Network_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zy35-MUQR6WMx1CJen53vQEUQ4_kh1sy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Laura Turner: Executive Director of the Student Doctor Network (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Laura Turner: Executive Director of the Student Doctor Network (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Scott_Shaw:_CEO_of_Lincoln_Tech_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/16iN-HmaR7We_F05fGQH8c5jTmaAH2y5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Scott Shaw: CEO of Lincoln Tech (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Scott Shaw: CEO of Lincoln Tech (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Rich_&amp;_Dr._Smith-Coppes:_Rasmussen_University_Nursing_Program_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/huoltANkQqKN12gQZI8Ql16rQVqV5Tag/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Rich &amp; Dr. Smith-Coppes: Rasmussen University Nursing Program (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Rich &amp; Dr. Smith-Coppes: Rasmussen University Nursing Program (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Jay_Feldstein_&amp;_Dean_Miller:_Philadelphia_College_of_Osteopathic_Medicine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U63Y_wN0TwWRp5tbuCQ1hXFKT1KIny5X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Jay Feldstein &amp; Dean Miller: Philadelphia College of Osteopathic Medicine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Jay Feldstein &amp; Dean Miller: Philadelphia College of Osteopathic Medicine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Vivian_Lee:_President,_Health_Platforms_at_Verily_Life_Sciences_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4iBIUFEETGSVg5us2nohV4EEQomo52_L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Vivian Lee: President, Health Platforms at Verily Life Sciences (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Vivian Lee: President, Health Platforms at Verily Life Sciences (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Peter_Buckley:_Dean,_Virginia_Commonwealth_University_School_of_Medicine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k5SZB4D5Q_Wn5P1SG94uH-2uQsWbZIF9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Peter Buckley: Dean, Virginia Commonwealth University School of Medicine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Peter Buckley: Dean, Virginia Commonwealth University School of Medicine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Sophia_Yen:_CEO_of_Pandia_Health_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Xw0iVTaNR3uvalWXjuq0z3NmSamLbvJW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Sophia Yen: CEO of Pandia Health (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Sophia Yen: CEO of Pandia Health (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Omar_Dawood:_Chief_Medical_Officer_at_Calm_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G1DoTQtmRpylQPq0e559MuiIQyO3XT25/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Omar Dawood: Chief Medical Officer at Calm (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Omar Dawood: Chief Medical Officer at Calm (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Mia_Finkelston:_Medical_Director_of_Amwell_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R-psKHfCSuy5elcAe7hj0lXbQ1etac3b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Mia Finkelston: Medical Director of Amwell (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Mia Finkelston: Medical Director of Amwell (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._John_Whyte:_Chief_Medical_Officer_of_WebMD_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v3SdeEZnTHKOqfKwrpmFZDvsRGSRZ7Wn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. John Whyte: Chief Medical Officer of WebMD (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. John Whyte: Chief Medical Officer of WebMD (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eric_Larsen:_President,_Advisory_Board_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lEWeGbjPTMSF_7ldrc-D4SBFQbqD53GU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eric Larsen: President, Advisory Board (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Eric Larsen: President, Advisory Board (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Daniel_Kraft:_Founder_of_Exponential_Medicine_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yPiRa4-mQ3CJ37d4J2BSnK1nQQaCQbQ6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Daniel Kraft: Founder of Exponential Medicine (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Daniel Kraft: Founder of Exponential Medicine (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Omar_Ishrak:_Former_CEO_of_Medtronic_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jwGaiDkCR9u6ZddSfeEb7k4XRemn89a9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Omar Ishrak: Former CEO of Medtronic (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Omar Ishrak: Former CEO of Medtronic (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Alister_Martin:_Founder_of_VotER_(Raise_the_Line)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jYILNarOSJuEJiLzH9Aw53WGT-uvtY8M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Alister Martin: Founder of VotER (Raise the Line)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Alister Martin: Founder of VotER (Raise the Line) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypothyroidism:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AIkV8BNDTeaXU6Nap6r3RUMMTNqAg0eG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypothyroidism: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Blythe Callaghan is a 71-year-old female client who presents to the primary care clinic with fatigue, weight gain, and constipation. She also reports feeling cold and depressed and has spent the past few days in bed. After an examination by her physician and a review of laboratory results, Blythe is diagnosed with primary hypothyroidism.
Hypothyroidism is a condition in which the thyroid gland produces and releases low amounts of thyroid hormones. Now, hormonal production is normally regulated by the hypothalamus, which is located at the base of the brain. When the hypothalamus detects low blood levels of thyroid hormones, it releases thyrotropin-releasing hormone, or TRH for short. TRH then stimulates the anterior pituitary gland to release thyroid-stimulating hormone, or TSH, which in turn stimulates hormone production by the thyroid gland, a butterfly-shaped gland located in the neck.
The thyroid gland is made up of thousands of thyroid follicles, which release two iodine-containing thyroid hormones, triiodothyronine or T3, and thyroxine or T4, into the bloodstream. These hormones then get picked up by nearly every cell in the body. Once inside the cell, T4 is mostly converted into T3, which is the active form. T3 speeds up the cell&amp;#39;s basal metabolic rate by stimulating protein synthesis, and burning up more energy in the form of sugars and fats. Other effects of thyroid hormones include increasing the cardiac output, stimulating bone resorption, as well as heat production and activating the sympathetic nervous system, which is responsible for our &amp;#39;fight-or-flight&amp;#39; response.
Now, hypothyroidism occurs when there&amp;#39;s low levels of thyroid hormones, which causes a slowing down of metabolic processes. Hypothyroidism is usually either primary, secondary, or tertiary.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Local_musculoskeletal_injuries:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZFUfrcg0R-_C3-1NvOAOvOJmSUieBIm3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Musculoskeletal injuries: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Liam Warner is a 24-year-old male who is dropped off at the urgent care clinic with right ankle pain and swelling.  This morning Liam was running in a 10K run when  his foot landed on an uneven surface, injuring his ankle. He says “My foot didn’t land right and I could feel it rolling  inward. I wasn’t able to finish because I could barely walk.”  While in the clinic, an ankle X-ray series rules out a bone fracture, and a grade 2 sprain is suspected.  

Local musculoskeletal injuries mainly include conditions that affect bones, joints, muscles, and ligaments. The most common ones include bone fractures; joint dislocations; muscle or tendon strains; and finally, ligament sprains. Now, sprains typically occur when the physical force applied to the joint exceeds the elasticity of the surrounding ligaments. And this is particularly common in ankle injuries, when there’s incorrect positioning of the foot at landing, like when a person is walking or running on an uneven surface; or they fall and twist their ankle; another frequent scenario involves jumping and awkwardly landing on their foot; or being stepped on during a sports game.

Now, there are two main types of ankle sprains. Lateral sprains are the most common ones and they are typically caused by forced inversion of the foot. In other words, a person’s sole rotates inwards or medially, but too much, eventually damaging the ligaments located on the outer side of the joint. On the other hand, medial sprains are caused by forced eversion of the foot, meaning a sole rotates outwards or laterally, eventually damaging the medial ligaments. 

Alright, there are some factors that can put a person at risk for ankle sprains. Modifiable risk factors include wearing inappropriate footwear, having poor athletic condition, not warming up before training, and fatigue from overtraining or intense physical activity. On the other hand, non-modifiable risk factors include being male between the ages of 15 to 24, or being f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatitis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aIsZc3vsQiivffvOw8tCyZI5TOyOmtYn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatitis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Tonya Abbott is a 43-year-old female client with a history of chronic alcohol use who presents to the emergency department with severe epigastric pain rated 9/10 along with nausea and vomiting.  An abdominal CT scan confirms pancreatic enlargement and edema and Tonya is admitted to the Progressive Care Unit to be treated for acute alcohol-induced pancreatitis.      

Acute pancreatitis refers to the sudden inflammation and destruction of the pancreas. The pancreas is a long, skinny gland located in the upper abdomen, or the epigastric region, behind the stomach. It plays an endocrine role, since it has scattered islets of Langerhans that produce and secrete hormones like insulin and glucagon into the bloodstream. However, the vast majority of the pancreas also plays an exocrine role, since it has acinar cells that produce and secrete pancreatic juice, which contains digestive enzymes like trypsin, amylase, and lipase, into the duodenum to help digest food. In acute pancreatitis, the pancreas is destroyed by its own digestive enzymes, a process called autodigestion. 

Now, acute pancreatitis can result from pancreatic duct obstruction, which can be caused by gallstones, tumors, or parasites. Other causes include genetic diseases like cystic fibrosis, or acinar cell injury caused by alcohol, certain medications like some antibiotics or cortico-steeroids, as well as viral infections like paramyxovirus, autoimmune diseases like lupus,  ischemia, abdominal trauma, or even medical procedures like endoscopic retrograde cholangiopancreatography or ERCP. All of these potential causes may allow the digestive enzymes produced by the acinar cells to be released and activated within the pancreas before they reach the digestive tract. As a result, there’s pancreatic tissue destruction, which ultimately triggers an inflammatory response. This can cause blood vessels to become leaky, causing fluid to collect around the pancreas, which leads to parenchymal edema. Ultimatel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anxiety_disorders:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zom6BxcDRpC0GpG0ucofkNllR5uYhds0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anxiety disorders: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Georgia Ryan is a 22-year-old female client who presents to her college campus clinic with a report of an inability to sleep and difficulty concentrating for the past 9 months. Georgia says that lately she’s been self-isolating from fellow students and that she has stopped attending her classes the past few days. After a review of Georgia’s medical history and current symptoms, the advanced practice registered nurse, or APRN, diagnoses Georgia with generalized anxiety disorder.

Anxiety is the anticipation of a future threat or stressful situation with an uncertain outcome, and is often associated with feelings of fear, worry, and nervousness, which causes avoidant behaviors. Anxiety disorders are a group of disorders in which these feelings are disproportionate to the stressful situation, and can be accompanied by physical and psychological symptoms that are so severe as to interfere with day-to-day activities. The most common anxiety disorders include generalized anxiety disorder, panic disorder, and phobia-related disorders.

Now, the underlying cause of anxiety disorders is poorly understood, but it seems to be related to an imbalance of the neurotransmitter GABA. The main risk factors for anxiety disorders include having a family history of an anxiety disorder or experiencing a personal trauma. Other risk factors include having other mental health disorders, having medical conditions like hyperthyroidism or pheochromocytoma, and using or experiencing withdrawal of substances like alcohol or cocaine.

Anxiety disorders typically present with symptoms like excessive fear, worry, and nervousness that interfere with day-to-day activities, but there are slight variations between the different anxiety disorders. Clients with generalized anxiety disorder may experience restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and trouble sleeping. These symptoms persist for at least 6 months. 

On the other hand, panic disorder]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperthyroidism:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r-6MDAQpRk2-yqwODnkH6zPiScyWk4YB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperthyroidism: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Suzanne Benoit is a 45-year-old female client who presents to her primary care clinic with a report of insomnia, anxiety, and unintentional weight loss. She states she hasn’t felt like herself for the past few weeks, and reports occasional episodes of heart palpitations and hand tremors that she initially thought might be manifestations of panic attacks. After an examination by her physician and a review of laboratory results, Suzanne is diagnosed with primary hyperthyroidism.  

Hyperthyroidism is a condition in which the thyroid gland produces and releases excess thyroid hormones. Now, hormonal production is normally regulated by the hypothalamus, which is located at the base of the brain. When the hypothalamus detects low blood levels of thyroid hormones, it releases thyrotropin-releasing hormone, or TRH for short. TRH then stimulates the anterior pituitary gland to release thyroid-stimulating hormone, or TSH, which in turn stimulates hormone production by the thyroid gland, a butterfly-shaped gland located in the neck. The thyroid gland is made up of thousands of thyroid follicles, which release two iodine-containing thyroid hormones, triiodothyronine or T3, and thyroxine or T4, into the bloodstream. These hormones then get picked up by nearly every cell in the body. Once inside the cell, T­4 is mostly converted into T3, which is the active form, and it can exert its effect. T3 speeds up the cell’s basal metabolic rate by stimulating protein synthesis, and burning up more energy in the form of sugars and fats. Other effects of thyroid hormones include increasing the cardiac output, stimulating bone resorption, as well as heat production and activating the sympathetic nervous system, which is responsible for our ‘fight-or-flight’ response.

Now, hyperthyroidism occurs when there’s too much thyroid hormone, leading to a hypermetabolic state, in which cellular reactions are happening faster than normal. Hyperthyroidism is usually either primary or seconda]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hydrocephalus:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tnx8lc9tSPu_nl1WwF4z2BcVSQqFhxKs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hydrocephalus: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Ishaan Mondal is a 5 week old male who presents with an increased head circumference, vomiting, and irritability. His mother, Ziva, reports that while Ishaan appears hungry, he has difficulty suckling when attempting to breastfeed. After an appointment with his pediatrician, Ishaan is directly admitted to the neonatal intensive care unit, or NICU, for monitoring and treatment of hydrocephalus. 

Hydrocephalus refers to the excessive buildup of cerebrospinal fluid, or CSF, within the brain. The CSF helps provide cushion and protection, as well as metabolic fuel for the brain. Now, the brain has two lateral ventricles, as well as the third and fourth ventricles, which are all interconnected, and each one contains a structure called a choroid plexus. The choroid plexus is made up of ependymal cells, which produce the CSF that can drain down to the fourth ventricle. From there, the CSF enters the subarachnoid space, and gets reabsorbed by arachnoid granulations into the dural venous sinuses, which are pools of venous blood. Finally, the CSF and venous blood are drained together out of the skull and into the internal jugular vein. Now, since the skull is such a rigid structure, the volume of the brain, CSF, and blood must be constant and in balance. So, with hydrocephalus, the increased CSF volume causes the four ventricles to enlarge and intracranial pressure to rise, which can compress and damage brain structures.

Now, there are two types of hydrocephalus. Noncommunicating, or obstructive hydrocephalus, is caused by an obstruction of the CSF flow anywhere along its path. This can be caused by a brain tumor, cyst, or by congenital causes, like cerebral aqueduct stenosis. On the other hand, communicating, or nonobstructive hydrocephalus is most often caused by decreased CSF reabsorption. This occurs when there’s inflammation or obstruction of the arachnoid granulations, which can be caused by infections, such as meningitis, as well as subarachnoid hemorrhage. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Candidiasis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1RWRxyqoQXC7zVvRMeSOX1grROCeankN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Candidiasis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[27-year-old Olivia Hartman presents to the gynecology clinic with complaints of vulvar itching,  white, clumpy vaginal discharge, and painful intercourse. She reports that she recently completed antibiotic therapy to treat an urinary tract infection. After a sample of the vaginal discharge is tested, the gynecologist diagnoses Olivia with candidiasis and antifungal treatment is prescribed.  

Now, candidiasis is a fungal infection caused by Candida species, most commonly Candida albicans. Candida albicans makes part of the normal human microbial flora, so it’s typically present in low numbers on the skin and mucous membranes, most notably the vaginal mucosa in females. Now, candidiasis occurs when there’s overgrowth of Candida albicans which disrupts the normal microbial flora. Most often, candidiasis affects the female reproductive organs, therefore it’s often referred to as candida vulvovaginitis. However, other frequent locations for Candida infection include the mouth, esophagus, and moist and warm areas of the skin, like groins or armpits. 

One of the most common risk factors for Candida overgrowth is recent antibiotic use, since it kills off some important bacteria that are also part of the normal microbial flora, which means that there’s normally less competition for Candida to thrive. Other important risk factors include having diabetes mellitus, being immunocompromised, or taking corticosteroids, all of which can lead to a weakened immune system that can’t keep Candida under control. Finally, there’s increased risk of candidiasis in those who use hot tubs, as well as those with intrauterine devices, implanted prosthetic devices or high estrogen levels, which can be due to combined oral contraceptive use, estrogen therapy, or pregnancy, since all these factors favor Candida overgrowth.

The most important clinical feature of candidiasis is a thick, white, odorless vaginal discharge, that looks like cottage cheese. Additionally, clients can present]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_insipidus:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I5Ha7TACSriNjDNfrO4mElU6TjmMzUEx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes insipidus: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Harvey Nguyen is a 30-year-old male client who suffered a traumatic brain injury during a skiing accident 4 months ago. 

He presents to his primary care physician, or PCP, with a report of  increased thirst, increased urine output, and frequent nighttime urination. 

He says he doesn’t go anywhere without a water bottle and always needs to know where the restroom is when he is away from home. 

He says that he is tired all the time because he has to make frequent trips to the bathroom during the night. 

His laboratory results are serum sodium 147 mEq/L; serum glucose 100 mg/dL; serum osmolality 312 mOsm/kg; urine specific gravity 1.001; and urine osmolality 248 mOsm/kg.  

His PCP refers him to an endocrinologist who admits Harvey to the medical unit for a water deprivation test which confirms the diagnosis of central diabetes insipidus. 

Diabetes insipidus is a condition characterized by excessive water loss through urine because the kidneys don’t reabsorb enough water. 

Now, the primary hormone that regulates water reabsorption and balance in the body is ADH, also called vasopressin. 

ADH is normally produced by the hypothalamus and is stored in the posterior pituitary, which are both located within the brain. To do this, the hypothalamus contains osmoreceptors, which are able to sense the osmolality of the blood. 

The normal blood osmolality value is between 285 and 295 mOsm/kg. Now, when a person is dehydrated, osmolality increases, so osmoreceptors sense this and, in response, stimulate the pituitary to release the stored ADH into the blood. 

ADH then travels to the kidneys to decrease water excretion in urine, and increase water reabsorption back into the blood, which ultimately helps restore normal blood osmolality. 

In addition, osmoreceptors trigger the sensation of thirst. After the person drinks water, the osmolality returns to normal, and ADH secretion stops.  

There are four types of diabetes insipidus. The first type is central diabe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_mellitus_(DM):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7C4xo1nTSUiDXzHrb2kgw6guQcGnxpLa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes mellitus (DM): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Harold Owl is a 63-year-old male client with a history of type 2 diabetes who is referred to the endocrinology clinic by his primary care provider for evaluation.  

Mr. Owl takes the biguanide metformin and sulfonylurea glyburide to manage his diabetes, but his latest hemoglobin A1c, or HbA1c test, was 8.9% and he has recently developed numbness in his feet. 

In diabetes mellitus, commonly just called diabetes, the body has trouble moving glucose from the blood into the tissue cells. 

As a result, cells starve for energy despite having high blood glucose levels, which is called hyperglycemia. 

Normally, high blood glucose stimulates the pancreatic beta cells to produce and secrete the hormone insulin, which in turn reduces blood glucose by stimulating the uptake of glucose into the cells. In diabetes, the blood glucose stays high because insulin’s function is impaired.

There are two main types of diabetes. In type 1 diabetes, there’s autoimmune destruction of the pancreatic beta cells, so they can’t produce and secrete insulin.

The exact cause of type 1 diabetes is unknown, but it’s thought to have a genetic and environmental component, and risk factors include personal or family history of type 1 diabetes, as well as celiac disease, and thyroid disease. 

The onset is usually abrupt, generally appears before the age of 30, and is most often diagnosed during childhood or puberty.

On the other hand, in type 2 diabetes, the pancreas is able to produce and secrete insulin, but the tissue cells tend to be insulin resistant, meaning they are unable to respond well to insulin stimulation. 

Type 2 diabetes is associated with risk factors, like male sex, increasing age, or having a first degree relative with type 2 diabetes, a body mass index or BMI over 25, a sedentary lifestyle, or a cardiovascular disease like hypertension. 

With type 2 diabetes, the symptoms usually begin after the age of 45, and gradually worsen over a few months.

Classic sympt]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Syndrome_of_inappropriate_antidiuretic_hormone_(SIADH):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0IA_ZkVkRCOErg8lVUKfCEjuQ7ilpsrI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Syndrome of inappropriate antidiuretic hormone (SIADH): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Jamal Hashim is a 68-year-old male client who presents to his primary care provider’s office along with his wife, Admira. 

Jamal was recently diagnosed with depression and has been taking the selective serotonin reuptake inhibitor, or SSRI, sertraline, for the past 3 weeks. 

Today, Jamal reports that he’s been experiencing intermittent forgetfulness, headache, lethargy, muscle weakness, and decreased urine output. 

Laboratory results showed a serum sodium level of 124mEq/L. His SSRI is discontinued and Jamal is admitted to the medical unit for continued monitoring and treatment of syndrome of inappropriate antidiuretic hormone.

Syndrome of inappropriate antidiuretic hormone secretion, or SIADH for short, is a condition where the body produces too much of the hormone ADH, also called vasopressin, leading to decreased blood osmolality, which refers to the concentration of dissolved particles like sodium and other electrolytes. 

The normal blood osmolality value is between 285 and 295 milliOsmoles per kilogram. 

Now, ADH is the primary hormone that regulates fluid balance in the body, and is normally produced by the hypothalamus and stored in the posterior pituitary, which are both located within the brain. 

To do this, the hypothalamus contains osmoreceptors, which are able to sense the osmolality of the blood. 

When a person is dehydrated, for example, osmolality increases, so osmoreceptors sense this and, in response, stimulate the pituitary to release the stored ADH into the blood. 

ADH then travels to the kidneys to decrease water excretion in urine, and increase water reabsorption back into the blood, to help restore normal blood osmolality. 

In addition, osmoreceptors trigger the sensation of thirst. After the person drinks water, the osmolality returns to normal, and ADH secretion stops.

Okay, now SIADH can have several important causes. The first one is paraneoplastic syndrome, where a tumor outside the brain secretes ADH. This is especial]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_incontinence_-_Stress:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cynunzqORr_HIILoQfE-5S3KQ2GG0XYx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary incontinence - Stress: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Heidi Anderson is a  60-year-old female who presents to her primary care clinic with reports of urine leakage when she sneezes, coughs and during exercise. 

Her symptoms started one year ago, and she started wearing a panty liner which she changes several times each day.  

Mrs. Anderson has had two vaginal births and one cesarean section. She has been very embarrassed about her incontinence and has finally gathered the courage to seek treatment. 

Urinary incontinence is the loss of bladder control, meaning that urine leaks involuntarily, causing both social and hygienic problems. 

There are five major types of urinary incontinence. So, when there is a sudden urge to urinate that is difficult to delay, that’s urge incontinence, also known as an overactive bladder. 

Overflow incontinence occurs when the pressure from a bladder that gets too full causes urine to leak out. 

This can be caused by problems associated with urinary retention like spinal cord injuries or an enlarged prostate. 

Functional incontinence happens when either a physical, cognitive, or environmental problem makes it hard to reach the bathroom in time, like with mobility problems or dementia. 

There is also a type of mixed incontinence, which is a combination of two or more types of incontinence, usually urge incontinence and stress incontinence. 

Stress incontinence is the most common type of incontinence. It occurs when urine leaks out because of increased intraabdominal pressure, like when coughing, sneezing, laughing, and during physical exercise. 

Stress incontinence is usually caused by weakened pelvic floor muscles, which are a group of muscles that support the bladder, uterus, vagina, and bowel. 

Pregnancy and childbirth are the most common causes of a weakened pelvic floor, especially with multiple pregnancies or trauma caused by vaginal deliveries assisted by instruments like forceps. 

The risk also increases during menopause because decreased estrogen causes atrophy ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemophilia:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M31fNnnVSfOANLLqaYN15kIKQvS7F5Y1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemophilia: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[James West is a 14-year-old male client with a history of hemophilia type A. He was brought to the emergency department, or ED, by his grandmother, Mrs. West, after falling off his skateboard. 

James states that he was wearing a helmet and protective pads over his elbows and knees but that he fell onto his buttocks while learning a new skateboarding trick. 

He says that it hurts to sit down or bend his left leg at the hip. Hemophilia is a group of genetic bleeding disorders caused by deficiencies in various coagulation factors. 

Normally, after a tissue injury, there’s an immediate constriction of the blood vessel to limit the amount of blood flow and loss. 

After that, platelets start adhering to the injured vessel wall to form a plug, and the coagulation cascade is activated. 

First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver, and usually these are inactive and just floating around the blood. 

The coagulation cascade starts when one of these proteins gets activated. This active protein then activates the next clotting factor, and so on. 

Now, the coagulation cascade can get started in two ways. The first way is called the extrinsic pathway, and it starts when tissue factor gets exposed by the injury of the endothelium. 

The tissue factor turns inactive factor VII into activated factor VIIa. Together, the tissue factor and the newly formed factor VIIa form a complex that turns factor X into active factor Xa. 

Factor Xa, with factor Va as a cofactor, turns factor II, also called prothrombin, into factor IIa, also called thrombin. 

Thrombin then turns factor I or fibrinogen, into factor Ia or fibrin, which precipitates out of the blood at the site of injury. 

On the other hand, the intrinsic pathway starts when platelets near the blood vessel injury activate factor XII into factor XIIa. 

Next, factor XIIa activates factor XI to factor XIa, which further activates factor IX to factor IXa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leukemia:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Kfs3XY3KTbGXD1J4glYHQFaXR8Sw0sPf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leukemia: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Taylor Oscar is a 64-year-old male who presents to the clinic with a 3-week history of extreme fatigue, bruising, and flu-like symptoms. 

Laboratory findings reveal a white blood cell count of 18,000/mm3 with 40 percent blasts, hemoglobin 12.6 g/dL, and platelets 112,000/mm3. 

A bone marrow biopsy and aspirate is performed, which confirms a diagnosis of acute myeloid leukemia or AML. 

Taylor is emergently admitted to the hematology oncology unit to begin treatment for AML.

Leukemia refers to a group of cancers that can occur when there’s uncontrolled proliferation of non-functional white blood cells, or WBCs, in the bone marrow.  

This differentiates leukemias from lymphomas, which can also arise from WBCs, but they typically form solid tumors in lymphatic tissue, such as lymph nodes, thymus, or spleen.

Leukemias are grouped by how quickly the disease develops. Acute leukemia develops very quickly, over days to weeks, so the WBCs don’t mature at all, and usually remain in the earlier “blast” form. 

On the other hand, chronic leukemia develops slowly, over many months or years, so the non-functional WBCs have time to mature partially. 

Now, leukemias can be further grouped based on the cell type involved. Myeloid leukemias are caused by proliferation of cells from the myeloid cell line, such as monocytes or granulocytes, which include eosinophils, basophils, and neutrophils. 

On the other hand, lymphoid leukemias are caused by the proliferation of cells from the lymphoid line, which includes B- and T- cells. 

So overall, there’s acute myeloid leukemia, or AML; and acute lymphoblastic leukemia, or ALL; as well as chronic myeloid leukemia, or CML; and chronic lymphocytic leukemia or CLL.

Now, leukemias are thought to be caused by mutations in the precursor blood cells in the bone marrow, leading to uncontrolled proliferation. 

There are certain risk factors that have been identified for developing these mutations. 

These include exposure to ioniz]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anaphylaxis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5Ck4oppzRxycLBrg72-wdqZMTq_TtY4S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anaphylaxis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Jocelyn Williams is a 18-year-old female client with a history of severe peanut allergy who is brought to the emergency department, or ED, via paramedics after accidentally eating a cookie that contained peanuts.  

After a few bites she felt a tingling sensation in her mouth and lips and her tongue started to swell. She could not find her EpiPen, so her roommate called 911. 

Upon arrival to the ED, the paramedic reports that Jocelyn’s face was flushed and swollen at the time of their arrival; she had generalized hives, tachypnea, and labored respirations. 

Her initial vital signs were tympanic temperature 98.7 F or 37 C, heart rate 126 beats per minute, respiratory rate 32 breaths per minute with audible wheezing, blood pressure 96/60, and SpO2 87% on room air. 

They administered one dose of epinephrine IM per protocol, and placed her on a non-rebreather mask at 10L/min.    

Anaphylaxis is a severe allergic reaction that affects multiple organ systems and can be life-threatening. 

Now, allergic reactions typically happen when the immune system overreacts and starts targeting harmless antigens that don’t cause any problems for most people. 

These include antigens found in certain foods like peanuts, eggs, and shellfish, as well as venom from insect bites or bee stings. 

Other antigens include certain medications, such as antibiotics like penicillin, as well as NSAIDs, or streptokinase, which is used as a thrombolytic therapy. 

In addition, some clients can develop allergic reactions when exposed to latex or radiocontrast agents used for imaging techniques like a CT scan or MRI.

Now, let’s say a person gets stung by a bee for the first time. So the first time these antigens enter the body, they get picked up and recognized by immune cells, called dendritic cells. 

These then activate other immune cells, the T lymphocytes, which in turn stimulate B lymphocytes to secrete IgE antibodies into the bloodstream. 

IgEs then bind to the surface of mast c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lyme_disease:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8j8Q72P0T4WA9xs6lrvHMkUgStKcXycU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lyme disease: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Jacob Myers is a 32-year-old male who presents to his primary care provider after discovering a painless bulls-eye looking rash on his thigh that has gotten bigger over the past three days. 

He also reports symptoms of fatigue, fever, chills, muscle aches along with joint pain and stiffness that started three days after he returned from a week-long camping trip. 

The provider suspects that Jacob has Lyme disease. Lyme disease is an infectious disease that’s caused by a bacterial species called Borrelia, most often Borrelia burgdorferi. 

The Borrelia species are all spirochetes, which means that they are long, thin, and spiral-shaped.

Now, Lyme disease is a zoonotic disease, meaning that it can infect a wide range of animals, including deer, cattle, and rodents, but it isn’t known to spread directly from animals to humans, but instead it needs a vector, meaning some sort of intermediate organism to spread from the animal to the human. 

In Lyme disease, the vector is the Ixodes tick, which is often found in wooded areas, thick brush, marshes, and tall grass. 

Now, the transmission of Lyme disease starts when the Ixodes tick feeds on the blood from an infected animal host. 

If this tick then feeds on the blood from a human, it will transmit the bacteria with their saliva. 

Once the bacteria is in a human&amp;#39;s bloodstream, it can disseminate to distant tissues, particularly the skin, joints, and heart, causing inflammation and damage.

Now, there are some factors that may put a client at risk of Lyme disease, such as outdoor activities in wooded or grassy areas, like hiking and hunting, as well as some occupations like landscaping, farming, and railroad work. 

The risk is also increased when clients wear clothing that exposes the skin. In addition, Lyme disease is more common during spring and summer, as ticks typically prefer warm temperatures.

Now, symptoms of Lyme disease can progress through three stages. The first is called the early local]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperbilirubinemia:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HSGLA6SsRrikNKgL9WpXTgKlSEyrB-30/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperbilirubinemia: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Charlotte Simpson is a 4-day-old female born by spontaneous vaginal delivery at 36 weeks of gestation, weighing 6 pounds, 11 ounces, or 3034g. 

At the time of discharge, Mrs. Simpson, G1P1, was breastfeeding well and Charlotte had no evidence of jaundice. 

Two days later Mrs. Simpson brings Charlotte to the pediatrician’s office. She reports that Charlotte had been spending less time suckling during feedings and would fall asleep after nursing only a couple of minutes. 

She says that Charlotte has been less active, and has had just one stool per day for the past two days. She also noticed that the whites of her eyes have developed a yellowish tinge. 

A total serum bilirubin, or TSB, of 18.2 mg/dL confirms a diagnosis of hyperbilirubinemia and Charlotte is admitted to the pediatric unit for phototherapy. Hyperbilirubinemia refers to the increase in total serum bilirubin levels. 

This often results in the deposition of bilirubin in the skin, sclera, and mucous membranes, causing a yellowish pigmentation known as jaundice.

Now, there are some risk factors that can make hyperbilirubinemia more likely to occur. 

These include gestational diabetes, an ABO blood group or Rh incompatibility between mother and baby, as well as preterm birth before 37 weeks, low birth weight below 1,500 grams, and being of East Asian race. 

Other factors that increase the risk of hyperbilirubinemia include genetic disorders like glucose-6-phosphate disease, as well as birth injuries like bruising or cephalohematoma, which is when blood accumulates under the scalp caused by pressure during labor.

Now, there’s two types of bilirubin: unconjugated and conjugated. Unconjugated or indirect bilirubin is a waste product that results from the breakdown of red blood cells. 

Unconjugated bilirubin is later linked or conjugated with glucuronic acid to produce conjugated or direct bilirubin, which can be excreted as bile by the liver into the small intestines. 

So, what’s causing the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Placenta_previa:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iqV7gUVIRL_7KT-K19o_aO2VSvGOYY_g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Placenta previa: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[30-year-old Sofia Ortiz, G5 T4 P0 A0 L4, is brought to the emergency department, or ED, by her sister with painless vaginal bleeding at 34 weeks of gestation. 

She says that during the last 4 weeks she has experienced intermittent spotting and that she came to the ED because the bleeding has suddenly become bright red and much heavier. 

Sofia has had routine prenatal care for all of her pregnancies, and each of her babies were delivered by cesarean section. 

She has no known allergies, an uncomplicated medical history, and her only medications are prenatal vitamins.  

A focused assessment reveals active vaginal bleeding, an absence of uterine contractions and a baseline fetal heart rate, or FHR, of 150 beats per minute. 

Sofia is transferred to the labor and delivery unit for monitoring. The placenta is a temporary organ that develops in the uterus during pregnancy, and it represents a lifeline connecti on between mother and fetus. 

It provides oxygen and nutrients to a growing fetus, and also removes waste products from its blood. 

Normally, the placenta implants in the upper uterus. Placenta previa occurs when the placenta implants in the lower part of the uterus and partially or completely covers the opening of the cervix, referred to as the cervical os. 

Now, the exact reason why placenta previa occurs is still unknown, but there are some factors that can increase the risk for it. 

The first risk factor is multiple gestation, in which the uterus must accommodate either more than one fetus with a larger placenta, or more than one placenta, each containing one fetus, which increases the risk of implantation near or over the cervical os. 

Additionally, abnormalities of the uterus, such as uterine fibroids, can prevent the normal implantation of an embryo. 

Also, previous uterine surgical interventions can cause uterine scarring and make the uterine lining less hospitable for implantation, which encourages implantation further down in the uterus]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Placental_abruption:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4DrHeXL0Rla47xYrWTTW0bk6SgaajB0f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Placental abruption: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Maria Beam, G2 T0 P0 A1 L0 at 36 weeks of gestation, is a 38-year-old female client who presents to the emergency department with pain in her lower back and uterus. 

Maria has a history of smoking and hypertension and she has had no prenatal care for this pregnancy. 

Uterine palpation reveals a distended, tender and rigid uterus. Scant vaginal bleeding is present. 

Maria is sent to the labor and delivery unit for further assessment and observation.

Placental abruption, also referred to as abruptio placentae is a medical emergency where there’s premature detachment of all or part of a normally implanted placenta from the uterine wall, resulting in hemorrhage. 

Placental abruption can be classified as complete or partial, depending on the degree of detachment from the uterine wall; as well as apparent or concealed, depending on whether the hemorrhage is seen or not. 

This usually happens after about 20 weeks of gestation and affects about 1% of pregnancies worldwide.

Now, the placenta is a temporary organ that forms where the embryo attaches to the uterine wall, and its job is to permit gas and nutrient exchange between the mother and the fetus. 

Detachment is usually caused by degeneration of the uterine arteries that supply blood to the placenta, often due to a chronic disease process in the placenta.

The most important risk factors for this include chronic problems like hypertension or smoking. 

Also use of certain illicit drugs, like cocaine and methamphetamine can increase the risk of abruption. 

Other risk factors include multiple gestation, maternal age over 35 years, preeclampsia or eclampsia, polyhydramnios, as well as a history of multiparity or previous abruption. 

Finally, experiencing acute events like blunt trauma to the abdomen from a car crash or fall may increase the risk of placental abruption.

Most often, placental abruption presents with dark or bright red vaginal bleeding, which is accompanied by symptoms like abdominal pain]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prolapsed_umbilical_cord:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Slt3SnacSL6SsAA6WzUm1CMASMKtdUSK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prolapsed umbilical cord: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Tao Wang, G3T2P0A0L2 at 39 weeks of gestation, is a 36-year-old female client who is admitted to the labor and delivery unit after she started having contractions every 5 minutes, each lasting 60 seconds. 

Ms. Wang’s obstetric history is uncomplicated and her first two children were born by spontaneous vaginal delivery. 

She has no medical issues impacting this present pregnancy.  A prolapsed umbilical cord is a rare but life-threatening obstetric emergency that occurs when the umbilical cord is abnormally positioned between the fetal presenting part and the cervix. 

Normally, the fetal presenting part is its head, which during vaginal delivery descends through the birth canal first, followed by the upper body, and finally, the lower body, umbilical cord and placenta. 

Now, the umbilical cord is a soft, tortuous bundle of blood vessels that is attached to the umbilicus of the fetus and connects to the center of the placenta. 

The umbilical cord contains one vein that carries oxygenated blood and nutrients from the placenta to the fetus, as well as two arteries that carry deoxygenated blood and waste from the fetus to the placenta, and the urachus that drains the fetus’s urinary bladder.  

Now, when the umbilical cord prolapses, it presents either ahead of the fetal presenting part, which is called an overt prolapse, or alongside the presenting part, referred to as an occult prolapse. 

As a result, during vaginal delivery, the descending fetus compresses the umbilical cord, resulting in a decreased blood and oxygen supply to the fetus, which can cause fetal hypoxia.

Now, a prolapsed umbilical cord does not always have a clear cause, but there are some factors that may increase the risk of developing cord prolapse. 

Nonmodifiable risk factors include maternal age of 35 or older, multiparity, multiple gestation, and polyhydramnios, as well as male sex, noncephalic fetal presentation, placenta previa,  premature rupture of membranes, preterm labor, an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eating_disorders:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RGqnaByqQiCBcDiY_DP2yaBbS6_58d1v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eating disorders: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Lily Truitt is a 22-year-old female client with a history of anorexia nervosa who is admitted to the medical psychiatric unit following signs of malnourishment at an outpatient clinic appointment. 

Over the last two weeks, Lily has expressed increasing concern about the way she looks. She feels that she is overweight and has been anxious about being seen in class and at social events.

She discloses that she has been restricting her intake and that she hasn’t eaten anything in 2 days.

Eating disorders are mental health disorders characterized by abnormal eating behaviors that can negatively impact a client’s physical and mental health. 

They are quite common, especially among young females, usually between 12-25 years of age. However, they can affect anybody, regardless of their sex, age, and social background. 

The most common eating disorders include anorexia nervosa and bulimia nervosa.

Now, the exact cause of eating disorders is not well known, but they seem to be tied to both biological and environmental risk factors. 

Biological risk factors include genetics and family history for an eating disorder, as well as associated mental health disorders like anxiety or obsessive compulsive disorder. 

In addition, anorexia nervosa is thought to be associated with dysfunction in neural systems implicated in regulatory self-control and reward, which seems to be caused by a deficiency in neurotransmitters like serotonin and dopamine. 

On the other hand, environmental risk factors include the psychosocial pressure to have a socially-defined “ideal body,” and having careers that promote weight loss, like modeling or sports, as well as experiencing childhood trauma, bullying, and loneliness, as well as stress and big life transitions or changes.

Symptoms vary according to the specific eating disorder. Anorexia nervosa is characterized by a constant fear of gaining weight, associated with a distorted body image, with individuals often believing that they ar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fractures:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MhyCZLDwTQGFwgUximHe3hjkRLiMwoOx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fractures: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Malaya Tanglao is a 15-year-old female who presented to the ED with her father, Ulan, after being unable to bear weight on her left lower extremity following a skiing accident. 

X-ray confirms that she sustained a closed transverse midshaft fracture to her left tibia that is displaced with resulting soft tissue injury. Malaya is now being admitted to the pediatric orthopedic unit for pain management and preparation for surgical intervention.

A fracture is defined as a complete or partial break in a bone, which occurs when the physical force applied to the bone is stronger than the bone itself. Most often, this occurs due to trauma associated with a fall, sports injury, or motor vehicle crash. 

Fractures may also result from overuse during repetitive activities, such as running or jumping. Finally, some conditions, such as osteoporosis or cancer, can weaken the bones and cause spontaneous fractures. There are some factors that can put an individual at risk for fractures. 

Modifiable risk factors that may weaken the bones include low vitamin D, smoking, alcohol, and glucocorticoid use; while nonmodifiable risk factors include increasing age, as well as congenital disorders like osteogenesis imperfecta, and malabsorption problems that may impair the ability to absorb important nutrients for bone health, like calcium and vitamin D.

Now, most commonly, we talk about closed or simple fractures, which occur when the bone breaks, but the overlying skin remains intact. On the other hand, open or compound fractures occur when the fractured ends pierce through the overlying skin. 

There are many different types of fractures, such as greenstick fractures, which occur when one side of the bone breaks, while the other side of the bone bends. Impacted fractures occur when a piece of one bone gets wedged into another bone.

Comminuted fractures are where the bone breaks into multiple fragments. Finally,  in spiral fractures, the fracture line follows the projection ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rheumatoid_arthritis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L3Ye5TF1Qr2F_l_OIIr7VcUcSvS8OXk7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rheumatoid arthritis (RA): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Clara Reed is a 44-year-old female client who presents to the rheumatology clinic after being referred by her primary care physician. For the past several weeks, she has been having pain, stiffness and swelling in both hands along with stiffness in her body that is worse in the morning. She has also been feeling fatigued and her appetite has decreased.

Alright, so rheumatoid arthritis is a chronic, autoimmune, inflammatory disorder that mostly affects the joints, but can also involve other organ systems like the skin and lungs. This condition is typically triggered by an interaction between genetic and environmental factors. Rheumatoid arthritis tends to run in families and it’s been associated with the HLA-DR4 gene.  Other risk factors include being female, middle aged, and obese.  Finally environmental factors like infections, smoking, and   exposure to asbestos and silica are also linked to the disease.

A person with the HLA–DR4 gene, might develop rheumatoid arthritis after getting exposed to something in the environment like cigarette smoke or a specific pathogen. These environmental factors can cause modification of the proteins in our body and turn them into antigens that trigger the immune system to produce specific autoantibodies against them. 

The first antibody  is called rheumatoid factor, or RF, and targets modified IgG antibodies; whereas the second antibody is called anti-cyclic citrullinated peptide antibody or anti-CCP, and targets citrullinated proteins, like citrullinated collagen II. 

Next, these antibodies and immune cells enter the circulation and reach joints. Here, immune cells release inflammatory cytokines that induce inflammation and stimulate synovial cells to proliferate. Increased number of synovial and immune cells in the joint creates a pannus, which is a thick synovial membrane with granulation tissue. 

Over time, the cytokines released in the pannus start to damage the articular cartilage, leaving the underlying ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parkinson_disease:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IteaS7x-RYmbqjiP-SJA9oPPTi2aqEF-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parkinson disease: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Michael Desante is a 67 year old male with a history of Parkinson disease. His daughter has been his primary caregiver since his diagnosis, however, as Michael’s disease progressed, Michael moved into a long-term care center for further support.

Parkinson disease, or PD for short, is a progressive neurological disease that affects movement. Most often, the cause of PD is unknown, but there are some factors that can increase the risk. 

Non-modifiable risk factors include increasing age, with a mean age of onset of 57 years; as well as male sex; and having a family history of PD. 

On the other hand, modifiable risk factors include exposure to toxins like pesticides, and a history of head trauma. Now, in PD there’s degeneration of the dopamine-producing neurons in the substantia nigra of the basal ganglia. 

Normally, the substantia nigra helps initiate movements, but also fine tunes the way that movements happen. When these neurons die, the first symptom is a resting tremor, which is an involuntary shaking that presents at rest and decreases with movement. 

Most often, resting tremor affects the hands, which is called a “pill-rolling” tremor because it looks like someone is rolling a pill between their thumb and index finger.

Over time, resting tremor can also involve the feet, tongue, and jaw. In addition, the client can experience bradykinesia, or slowness of voluntary movement. 

A more severe form of bradykinesia is akinesia, which is when they become unable to initiate a voluntary movement. For instance, the client may feel like their legs freeze up when trying to walk. 

Another typical symptom is “cogwheel” rigidity, which is a type of stiffness characterized by a series of catches or stalls as a person’s arms or legs are passively moved by someone else. 

And because of rigidity of facial muscles, some clients with PD may have a mask-like facial expression, as well as difficulty speaking, chewing, and swallowing. 

As a result, food, fluid, or s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchiolitis_&amp;_respiratory_syncytial_virus_(RSV):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ATFj6u-KSeWblenwAFOPSx8cQCG1W5aA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchiolitis and respiratory syncytial virus (RSV): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Charlie Santos is a 2-month-old male who is brought to urgent care by his mother. She says that he has had a runny nose and an axillary temperature of 100.4 F, or 38 C, for the past two days.

This morning she noticed that he seemed to need to work harder to breathe, and she tells you he has been fussy and not feeding well. She also mentions that he attends daycare, and recently many of the children have been sick with similar symptoms. 

Based on Charlie’s clinical presentation and history, an infection with respiratory syncytial virus, or RSV, is suspected. The respiratory tract is divided into two parts; the upper airway, which consists of the nasal cavity, paranasal sinuses, pharynx, and larynx; and the lower airway, which consists of the trachea, bronchi, bronchioles, alveoli, and lungs. 

Inflammation of the bronchioles, which are the smallest airways of the lungs, is known as bronchiolitis. It commonly occurs during the colder months, so fall, winter, and early spring, and it’s most often caused by the respiratory syncytial virus, or RSV for short. 

Other causes include viruses like adenovirus, parainfluenza virus, or rarely from bacteria like Mycoplasma pneumoniae. Now, the most important risk factor for bronchiolitis is young age, since it mostly affects children under 2 years of age, with infants less than 3 months being at the highest risk. 

Other risk factors include premature birth, attending crowded places like daycare, or having older siblings who can catch it in school. Finally, some underlying conditions may increase the risk of bronchiolitis, including chronic lung disease, congenital heart disease, or being immunocompromised.

Transmission of RSV typically occurs from direct contact with respiratory droplets when an infected person talks, sneezes, or coughs. These droplets can then land in the mouths or noses of people nearby, or be inhaled into their lungs. 

The virus can also survive on surfaces for a few hours, so it’s possible to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Conjunctivitis:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AkvDt1I7TgWmGJGOI74zjZ6URzWwbbus/_.jpg</video:thumbnail_loc><video:title><![CDATA[Conjunctivitis: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Leilani Flores is a 3-year-old client who was brought to the primary care clinic by her father,  Alvin.  Yesterday, Leilani’s older sister was diagnosed with bacterial conjunctivitis, and was started on antibiotic eye drops. 

Today, Alvin is concerned that the infection has spread to Leilani.  He reports that she woke up with her right eye crusted shut with yellow drainage and she has been rubbing the eye frequently.  

Conjunctivitis, commonly known as pink eye, refers to the inflammation of the conjunctiva, which is the clear membrane that covers the sclera and the inner surface of the eyelids, in response to an infection, allergen, or irritant. 

As a result there’s dilation of conjunctival blood vessels, which typically causes the eye to look pink or red. So, there are two main causes of conjunctivitis, infectious and non-infectious. 

Infectious conjunctivitis can be further divided into viral and bacterial conjunctivitis. Viral conjunctivitis is the most common one and is typically caused by adenovirus, but can be also due to herpes simplex virus or varicella-zoster virus. 

On the other hand, bacterial conjunctivitis is most often caused by Staphylococcus Aureus, Streptococcus pneumoniae, or Haemophilus influenzae, but less commonly, it can also be caused by Neisseria gonorrhoeae, or Chlamydia trachomatis. 

Both viral and bacterial conjunctivitis are highly contagious, and spread through direct hand-to-eye contact with contaminated objects, or with an infected person’s secretions like tears or eye discharge. 

So, the main risk factors include close contact with someone who has conjunctivitis, as well as attending crowded places like schools or daycare. 

Other factors that increase the risk of conjunctivitis include poor hand hygiene and improper use of contact lenses. There’s also non-infectious conjunctivitis, which includes allergic and irritant conjunctivitis. 

Allergic conjunctivitis is usually caused by airborne allergens, like p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Reye_syndrome:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/faI-jqDPQxypmiycXs_6hNo3SMSWEa2A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Reye syndrome: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Gabriella Jones is a six-year-old girl who was brought to the emergency department by her mother. Mrs. Jones states that for the past 24 hours Gabriella has become increasingly lethargic with rapid breathing and has been vomiting for the past two days. 

Mrs. Jones adds that about one week ago, Gabriella had influenza and her pediatrician recommended acetaminophen if Gabriella developed a fever. 

Mrs. Jones didn’t have any acetaminophen on hand, so she gave Gabriella two doses of aspirin instead after Gabriella developed a fever. Gabriella is admitted to the pediatric intensive care unit, or PICU, with a probable diagnosis of Reye syndrome. 

Reye syndrome is a rare but life-threatening condition that occurs in children younger than 18 years of age that take salicylate-containing medications like aspirin to treat a viral illness, especially influenza and varicella. 

It is characterized by hepatic encephalopathy, where a liver dysfunction results in a buildup of toxic substances that causes brain dysfunction. 

Now, the exact cause of Reye syndrome is not fully understood, but it’s thought that the use of salicylate medications may inhibit some important enzymes within the liver cells, or hepatocytes, leading to liver malfunction.

Now, hepatocytes have a variety of fundamental functions. First off, they play a key role in breaking down fatty acids to generate ATP, which is the main energy source for the body, via their metabolic powerhouses, the mitochondria. 

Another important function of hepatocytes is the detoxification of harmful substances like medications, and byproducts of metabolism like ammonia, which is converted by hepatocytes into urea, to be excreted by the kidneys. 

Hepatocytes are also involved in the production of most coagulation factors for blood clotting. Finally, hepatocytes are involved in the regulation of blood glucose.

In Reye syndrome, the malfunctioning hepatocytes are no longer able to perform their functions, such as p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chickenpox_(Varicella):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZMbLOs-7Q9_OfqhbSPer6qPKRIK7dDVA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chickenpox (Varicella): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[15-month-old Lillian Becker presents with a vesicular rash to her trunk and arms, itchiness, and fever. Onset of symptoms occurred after being picked up from daycare 2 days ago. 

After being brought in to the pediatric clinic by her father, Ray, Lillian is diagnosed with chickenpox. Varicella, more commonly referred to as chickenpox, is an infectious disease caused by the varicella-zoster virus, or VZV for short, also known as human herpesvirus 3 or HHV-3 for short. 

This is a highly contagious airborne virus, meaning it’s transmitted from person to person through respiratory droplets; for example, when a person sneezes or coughs. 

But the virus can also be transmitted by direct contact with the skin or oral mucosa of an infected person. Because of that, an important risk factor for varicella involves going to crowded or poorly ventilated public places, such as day-care centers, as well as being immunocompromised.  

Now, once a person inhales the virus-containing droplets, these travel down the respiratory mucosa, and the virus starts replicating in the epithelial cells. This is called the incubation period, where the client is asymptomatic, and lasts 14 to 21 days. 

Then, the virus gets picked up by nearby immune cells and gets transported to a nearby lymph node, so the client may start to experience prodromal symptoms, such as fever, headache, and malaise. 

Prodromal symptoms are more likely in clients over the age of 10, and more severe in adults. About 36 to 48 hours later, the immune cells reach the skin and release the virus. At this point, clients typically develop skin lesions, usually involving the scalp, face, and trunk.

Initially, skin lesions appear as flat, red, and very itchy spots called macules. Over time, macules become elevated and progress into papules, and then into small fluid-filled vesicles. 

Within 1 to 2 days, these vesicles begin to crust over and form scabs. After 5 days the scabs fall off, typically without leaving a sca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peripheral_venous_disease_(PVD):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0ojEzAPgQj6mp5Zvu_qCpE8KTp6oHHsG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peripheral venous disease (PVD): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Muriel Diallo is a 45-year-old female client with a history of peripheral venous disease and obesity. She is referred to the vein clinic by her primary care provider for treatment of a chronic, non-healing leg ulcer in her right lower extremity.

Peripheral venous disease, or PVD for short, is characterized by an obstruction or defect of the veins, and most often affects the legs. Normally, veins drain blood from peripheral organs and tissues towards the heart, and they have one-way valves to prevent backflow. 

In PVD, veins are either obstructed by a blood clot or embolus, are weak or dilated, or there’s valvular insufficiency, so blood ends up leaking backward and pooling in the lower legs, leading to venous hypertension.

Risk factors for PVD include female sex, increasing age, sedentary lifestyle, obesity, and pregnancy. Other important risk factors for PVD include associated conditions like heart failure, varicose veins, and having a history of trauma or surgery. 

Finally, another risk factor for PVD involves standing or sitting with the legs crossed for long periods of time. Okay, now clients with PVD often report pain in the legs, swelling, and a sensation of heaviness. 

Fluid and red blood cells can leak out of the small veins and capillaries and into the surrounding tissues, causing edema and inflammation in the lower extremities. As the red blood cells break down in the tissue, they release hemosiderin, which eventually causes the skin to take on a brownish discoloration. 

Moreover, as normal subcutaneous tissue is replaced by fibrous tissue, the skin becomes thick, leathery, and itchy. This will cause the skin to become more vulnerable to ulceration and painful sores, most often above the medial malleolus.

Clients with PVD may also develop some serious complications. First off, clients may develop chronic non-healing sores and ulcers, which pose a risk for infection and pain. 

In addition, pooling of blood can increase the risk of blood cl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pelvic_inflammatory_disease_(PID):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j3sPoyEYSUSw_GCKGwnaQBiOQWiBJ978/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pelvic inflammatory disease (PID): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Margarita Salvador is a 25-year-old female client who presents to her gynecologist’s office with a report of lower abdominal pain, a fever of 101°F or 38.3°C, chills and thick, yellow foul smelling vaginal discharge. 

She states her symptoms began three days ago. A pelvic examination is positive for cervical motion tenderness and right-sided adnexal tenderness. A transvaginal ultrasound visualizes a 4 cm right-sided tubo-ovarian abscess. 

A vaginal swab was sent for laboratory analysis to check for chlamydia and gonorrhea. Ms. Salvador is diagnosed with pelvic inflammatory disease, or PID, and will be admitted to the medical surgical unit for treatment.

Pelvic inflammatory disease, or PID for short, is an infection of the upper female reproductive system, which includes the uterus, fallopian tubes, and ovaries. 

Most often, PID develops from a bacterial infection that begins in the vagina or cervix, such as sexually transmitted infections, or STIs, like chlamydia, caused by Chlamydia trachomatis, and gonorrhea, caused by Neisseria gonorrhoeae. 

Another cause of PID can be bacterial vaginosis, which refers to the infection of the vagina due to overgrowth of bacteria like Gardnerella vaginalis, which are normally present in low numbers in the vaginal flora. 

Occasionally, PID can be caused by other forms of bacteria introduced in the reproductive tract during surgery, abortion, or even childbirth. Now, PID is typically caused by only one type of bacteria, but in some clients, the infection can become polymicrobial, meaning the original infection makes it easier for other bacteria to settle into the reproductive tract.

Risk factors associated with pelvic inflammatory disease can be subdivided into two main groups. Modifiable risk factors include having unprotected sexual contact, as well as new or multiple sexual partners. 

On the other hand, non-modifiable risk factors include being under the age of 35, since they’re more likely to have new or multip]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_cancer:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RW_Zi_SnQcGxgFaw4DtQtiwdSTeZ0c6o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breast cancer: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Linda Davis is a 54-year-old female client recently diagnosed with ductal carcinoma in situ, or DCIS. Because Ms. Davis’s mother had breast cancer, she was concerned when she felt a painless lump in her left breast during her monthly self breast exam. 

A mammogram shows linear and branching areas of microcalcifications, so a percutaneous core needle biopsy is performed. Pathology reveals pleomorphic, high-grade nuclei, areas of central necrosis in the ducts without invasion of the basement membrane, and ER+/PR+/HER2- cells. 

Ms. Davis presents to the oncology office for consultation. Breast cancer is the uncontrolled growth of epithelial cells within the breast tissue. It is the second most common cancer worldwide, and is also the second leading cause of cancer deaths in females, but on rare occasion, it may affect males. 

Now, the female breasts are typically made up of glandular tissue, which consists of lobes containing numerous milk-producing lobules with a network of lactiferous ducts that transport milk to the nipple during lactation.

On the other hand, male breasts have ducts and some may have a few lobules that don’t produce milk. Now, this glandular tissue is surrounded by stroma, which is made of adipose and fibrous connective tissue. 

Located throughout the breasts are blood vessels, as well as lymphatic vessels that mainly drain into a group of lymph nodes in the axilla.

Alright, now, most breast cancers are adenocarcinomas originating from the ducts or lobules, and can be categorized by whether or not they have invaded surrounding tissue. 

Non-invasive, also called in situ, breast cancers are confined to the ducts, called ductal carcinoma in situ, or DCIS for short, or lobules, called lobular carcinoma in situ, or LCIS for short. 

Some non-invasive breast cancers can become invasive breast cancers, which infiltrate the basement membrane and spread to surrounding tissue where they can reach the blood and lymphatic vessels, ultimate]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tumor_lysis_syndrome_(TLS):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rHD8DE3NR56_ySz5yluYkoUmSwCGGqHE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tumor lysis syndrome (TLS): Nursing Process (ADPIE)]]></video:title><video:description><![CDATA[Michael Wheatley is a 24-year-old male client who presents to the emergency department or ED, with muscle cramps in both legs, joint pain in his knees, hips, shoulders and wrists, as well as lethargy and nausea.

He mentions that he was recently diagnosed with non-Hodgkin’s lymphoma, for which he received his first dose of chemotherapy in an outpatient oncology clinic yesterday.

The ED physician orders IV fluids at a rate 200 mL/hour and admits Michael to the inpatient oncology unit for further evaluation and treatment.

Tumor lysis syndrome, or TLS, is an oncologic emergency that’s characterized by severe metabolic and electrolyte abnormalities. This most often occurs as a complication during treatment of hematological malignancies, like leukemia and lymphoma, with chemotherapeutic medications that rapidly kill large numbers of tumor cells. 

Rarely, TLS can also occur spontaneously with tumors that have a high proliferative rate or a large tumor burden, prior to any treatment. Regardless, the end result is a massive release of intracellular contents during lysis, of tumor cells into the bloodstream. 

This results in hyperkalemia, which can interfere with electrical activity in the heart, brain, and nerves. In addition, there’s hyperuricemia, and the excess uric acid can form crystals that deposit in the tiny kidney tubules, resulting in acute kidney injury. 

Finally, there’s hyperphosphatemia, and the excess phosphate can bind to the calcium in the blood, forming a complex, leading to hypocalcemia, which can also interfere with electrical activity in the heart, brain, and nerves. 

Moreover, these phosphate-calcium complexes can also form crystals that deposit in the kidney tubules, contributing to the development of acute kidney injury.

Now, there are some factors that may put the client at risk of TLS, such as older age, and having a large tumor burden, which can be evidenced by the presence of a very high white blood cell count, and high lactate d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Seizure_disorder:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hWr77uKwSmmeD4ZQw3a0MiT5Q4CQkyEa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Seizure disorder: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Francisco Bernard is an 18-year-old male client who was brought to the emergency department, or ED, after his father witnessed him suddenly go rigid, lose consciousness, and fall to the floor. 

His arms and legs immediately began to jerk rapidly, then slow and eventually stop. Afterwards, Francisco was confused and lethargic with no memory of what happened.

Upon arrival in the ED Francisco was awake but disoriented. He was transferred to the neurological unit where he was diagnosed with epilepsy. A seizure is a sudden event that occurs due to abnormal, excessive, and synchronous firing from neurons in the brain. 

This manifests as a change in the client&amp;#39;s level of consciousness, body movements, sensation, or autonomic functions, that usually last for a few seconds or minutes. 

Seizures can be triggered by stress, tiredness, and lack of sleep. High fever, especially in young children, as well as infections like meningitis, encephalitis, or brain abscess, can also result in seizures. 

Also, withdrawal of certain substances like alcohol, cocaine, benzodiazepines and barbiturates may cause seizures. During pregnancy, seizures can be provoked by eclampsia, which occurs in the setting of high blood pressure. 

Now, epilepsy is when a client has two or more seizures separated by at least 24 hours. A very important risk factor for epilepsy is family history. 

Epilepsy can also be caused by brain damage due to traumatic brain injury or stroke, as well as brain tumors. Other causes include congenital diseases like Sturge-Weber Syndrome, metabolic disorders like phenylketonuria, as well as neurodegenerative diseases such as Alzheimer’s disease. 

In many cases, however, the cause of epilepsy is unknown.Right before having a seizure, clients may experience neurological symptoms called auras, which present with subtle muscle movements called automatisms, such as chewing, lip smacking, or rapid blinking. 

Some clients may also report smelling unusual odo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sickle-cell_disease:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o2WU3pEHQYO3F6094fpD3rf9QgGG6ATW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sickle cell disease: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Darnell Tyler is a 24-year-old Black male client with a history of sickle cell disease who presents to the emergency department, or ED, with a report of sudden, severe pain, rated a 9/10 that started late last night in his back, hands and feet. 

He says he has been nauseous and vomiting for the last few days. After blood is drawn for culture, IV fluids and antibiotics are started. Then Darnell is admitted to the medical unit for further treatment and evaluation. 

Sickle cell disease is a group of genetic conditions that affect hemoglobin, which can cause red blood cells to take the shape of a sickle or crescent. As a result, these red blood cells are more fragile and can be destroyed more easily, which can cause anemia.

Normally, red blood cells are able to carry oxygen from the lungs to peripheral tissues because they  contain hemoglobin A, or HbA for short. Now, hemoglobin A is made up of two α-globin and two β-globin peptide chains, giving red blood cells a characteristic flexible biconcave shape that allows them to travel easily through blood vessels. 

With this in mind, sickle cell disease is caused by a mutation in the HBB gene, which almost always results in the 6th amino acid of beta globin being a valine instead of glutamic acid. 

As a result, two normal α-globin and two mutated β-globin peptide chains give rise to an abnormal hemoglobin called hemoglobin S for sickle, or HbS for short. 

Now, under normal conditions, HbS is also able to carry oxygen quite well. However, under conditions such as hypoxia, acidosis, or dehydration, HbS forms long chains within the red blood cells. 

This ultimately distorts the red blood cells into a rigid and fragile crescent shape that looks like a sickle. Now, sickle cell disease is autosomal recessive, so both parents must pass the mutated HBB gene to their child, so they will be homozygous for HbS. 

This is especially common in individuals whose ancestors came from Sub-Saharan Africa, as well as Sout]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peripheral_arterial_disease_(PAD):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_ERF54UhRnOUZhQl0rZiFb9ISfSUl1qK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peripheral arterial disease (PAD): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Mike Craig is a 68-year-old male client who is referred to the vascular clinic by his primary care provider, or PCP.  Mr. Craig has a history of type 2 diabetes, hypertension, and dyslipidemia, and he’s been experiencing intermittent leg pain in his lower legs while taking walks with his dog.  

An ankle-brachial index, or ABI, is performed which confirmed a diagnosis of peripheral artery disease, or PAD. Peripheral arterial disease, or PAD for short, is the progressive narrowing of the arteries that supply peripheral tissues and organs, so basically all arteries except for the heart and brain. 

As a result, there’s reduced blood supply to these tissues, which ultimately become ischemic. There are some factors that may put an individual at risk for PAD. 

Non-modifiable risk factors include increasing age, male sex, and having a family history of PAD. On the other hand, modifiable risk factors include smoking, obesity, and having a sedentary life, as well as predisposing conditions like diabetes, dyslipidemia, and hypertension.

The most common cause of PAD is atherosclerosis, which is a buildup of fatty and fibrous material just under the inner lining of a blood vessel, forming a plaque. 

This buildup usually happens over the course of years. Eventually, the lumen of the vessel becomes so narrow that it results in reduced perfusion to the tissue it tends to supply. 

PAD can be worsened by an embolism. This happens when an embolus, which is a piece of blood clot or fatty deposit, breaks off from an atherosclerotic plaque from an upstream artery, and gets lodged in a narrower peripheral artery, blocking its blood flow.

Now, in most cases PAD affects the arteries supplying the legs. When less blood gets to the muscle tissue in the legs, that tissue becomes ischemic, causing a type of cramping pain that is often referred to as intermittent claudication. 

Initially though, when the client’s  at rest, there’s enough blood to meet the tissue’s demands, so t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Frostbite:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8JdZBrQkRKuFzEFrj4G33h__StyQzS1g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Frostbite: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Christine Lee is a 46-year-old woman who presents to your emergency department after changing a flat tire in the cold with her bare hands. The temperature outside was around 29 degrees F, or minus 1.7 degrees C. Ms. Lee is concerned about her hands and fingers. She says that her fingers feel numb and tingly. Her fingertips are pale and cool, while her knuckles are red, warm, and swollen. The physician diagnoses Ms. Lee with frostbite.

Frostbite is defined as a severe localized injury that occurs when a part of the body such as hands, feet, and face, is exposed to temperatures below 31 degrees F or minus 0.5 degrees C. It typically occurs within 30 minutes where the skin is exposed to low temperatures and windy weather.

Normally, our body responds to low temperatures by constricting small blood vessels close to the skin. This way, it prevents loss of heat by shifting the warm blood from the extremities to internal organs. As a result, the exposed skin becomes pale, cold, and numb; and a person starts to experience a tingling and aching sensation. Next, low temperatures cause intracellular and extracellular fluids to freeze and form small ice crystals that give the tissue a firm, solid feel. Furthermore, these ice crystals directly damage the surrounding tissue and vascular endothelial cells. And, if the exposure to low temperatures continues, blood vessels can lose their vascular tone, eventually causing the pooling of blood and changing the skin color from pale to purplish.

Now, when the affected part of the body is rewarmed, the blood flow is restored and reperfusion injury occurs. In reperfusion injury, damaged blood vessels leak fluid into surrounding tissue, eventually causing edema. At this point, the skin develops a blotchy appearance. The blotchy skin can be followed by fluid-filled blisters, which most commonly occurs in the next 24-48 hours. At the same time, damaged blood vessels initiate platelet aggregation, eventually causing thrombosis and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Age-related_physiological_changes:_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T3rnym_VRcmNPLd4HdZMa99jQwm-2Reu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Age-related physiological changes: Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Matilda Nowell is a 78-year-old female client with a history of depression and osteoarthritis, who presents to the primary care clinic today with a report of frequent and prolonged episodes of constipation along with bloating and abdominal pain. Mrs. Nowell lives alone and has no family close by, and she struggles to afford nutritious food due to her limited income. 

Age-related physiological changes include all changes that normally occur in the body over time with aging. First, let’s start with the integumentary system, which undergoes changes in collagen and elastin that eventually cause the skin to lose elasticity, become thinner, and develop wrinkles over time, while the hair becomes gray, thinner, and may fall out, which may lead to baldness. On the flip side, the muscular system atrophies over time, which often leads to a decrease in physical strength; while the skeletal system progressively loses bone mass and density, which typically leads to a gradual decrease in height, and can result in osteopenia or osteoporosis, therefore bones might break more easily, while joints may degenerate and develop arthritis.

Cardiovascular age-related changes generally involve progressive degeneration of the heart, while the valves and large arteries become stiffer, ultimately causing hypertension or decreased cardiac output upon exertion. On the other hand, changes of the respiratory system mainly involve the alveoli, which may lose their architecture and elasticity, which leads to a decreased lung capacity; in addition, there’s decreased mucociliary action and diminished cough reflex, so airway clearance is ultimately impaired.

The urinary system is affected by functional changes that decrease the filtration capacity of the kidneys; in addition, the bladder capacity is decreased, as there’s instability of the detrusor muscle and decreased sensation of bladder fullness, which combined result in urinary frequency or even incontinence; while the reproductive syst]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperosmolar_hyperglycemic_state_(HHS):_Nursing_Process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZB3ZLkNsQoyeDesYjG_xpuZRQ_yF7SGL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperosmolar hyperglycemic state (HHS): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Malcolm Johnson is a 68-year-old male client with a history of poorly controlled type 2 diabetes mellitus who recently recovered from viral pneumonia. 

Over the past few days, he has felt more thirsty than usual, has been urinating frequently, and has felt fatigued. 

This morning his son, Kyrone, noticed his father seemed confused, so he checked Mr. Johnson’s blood sugar and the reading was 685 mg/dL. 

Kyrone promptly brought Mr. Johnson to the emergency department. Lab results revealed elevated serum glucose, elevated serum osmolarity, and negative serum ketones. 

Mr. Johnson is being admitted to the medical intensive care unit for hyperosmolar hyperglycemic state. 

Hyperosmolar hyperglycemic state, or HHS for short, is a metabolic complication of diabetes mellitus, more often in type 2 than type 1 diabetes. 

HHS occurs when the blood glucose levels go really high, over 600 mg/dL, which leads to extremely increased urination, or polyuria. 

This ultimately causes severe dehydration, resulting in a blood osmolarity of over 320 mOsm/kg. 

Now, osmolality is the concentration of dissolved particles in the blood, and one of the major particles is glucose. 

Normally, blood glucose levels should be lower than 100 mg/dL while fasting for over 8 hours, and lower than 140 mg/dL 2 hours after eating; so normal blood osmolality is maintained between 285 and 295 mOsm/kg. 

Glucose is a polar molecule, which means it cannot passively diffuse across cell membranes, so it needs insulin to regulate its membrane transport into the cells. 

As a consequence, when it is increased, it remains in the blood vessels and causes a hyperosmolar state that draws water into the blood. 

As a result, water begins to leave the body’s cells and enter the blood vessels, leaving the cells relatively dry and shriveled. 

The excess of water within blood vessels is eliminated via urination, which leads to polyuria and severe total body dehydration. 

Now, HHS mainly occurs in client]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bile_synthesis_disorders_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dfOzYInzQzSMyFxVDTpWafjgRrKph_zY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bile synthesis disorders (NORD)]]></video:title><video:description><![CDATA[Bile acid synthesis disorders, or BASDs, are a group of rare disorders characterized by defects in the creation or synthesis of bile acids. Bile acids are molecular compounds made in the liver that have many functions including stimulation of bile flow in the liver and  triggering bile to enter the intestines to facilitate absorption of fat and fat soluble vitamins. 

Cholesterol is a key ingredient in making bile acids. So, when bile acids are not formed properly, the abnormal intermediate compounds produced because of a block in the bile acid production pathway, build up within the body and cause liver injury that can lead to progressive liver failure. 

Due to failure to produce normal  bile acids, there is often a reduced ability to take up fat soluble vitamins from food, with associated growth failure.

Most signs and symptoms of bile acid synthesis disorders begin in infancy or early childhood with some cases not recognized until adolescence or adulthood. 

Because of the build-up of  toxic products in the liver, patients may experience yellowing of their skin or eyes, failure to thrive and growth deficiency, as well as an enlarged liver or spleen.  

Since the normal bile acids are not present in bile, people may experience diarrhea or pale colored stools. People with a BASD may also have vitamin deficiencies, due to their inability to absorb fat and fat soluble vitamins. 

As a result, they experience symptoms such as vision problems due to lack of vitamin A, rickets due to vitamin D deficiency,  and blood clotting problems due to lack of vitamin K. 

Sometimes the lack of vitamin E or the buildup of cholesterol-like substances can result in neurological diseases which progress throughout childhood or adulthood. 

Without treatment, BASDs may lead to life-threatening conditions including scar tissue formation on the liver, high blood pressure in the major vein of the liver, abdominal swelling, and eventually liver failure.

Bile synthesis is a mult]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/PhytonadioneVitamin_K1:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2xfkbYMWRD6ZGtn5E7CQ9QYmQSOGsZj0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Phytonadione (Vitamin K1): Nursing pharmacology]]></video:title><video:description><![CDATA[Vitamin K1, is a fat-soluble vitamin that helps regulate the process of blood coagulation. Vitamin K is found in abundance in green leafy food, like spinach, kale, and chard; and it’s also produced by the gastrointestinal microbial flora. 

Neonates are particularly susceptible to vitamin K deficiency because breast milk is low in vitamin K. 

In addition, there is an absence of gastrointestinal flora at birth that synthesize vitamin K. Moreover, the newborn&amp;#39;s immature liver is less able to produce coagulation factors.

Now, vitamin K deficiency results in impaired coagulation cascade and blood clotting formation. This can potentially lead to hemorrhage, or vitamin K deficiency bleeding or VKDB for short, which is a condition previously known as hemorrhagic disease of newborn. 

VKDB is most likely to occur between days 1 and 7 of life; by day 7, most healthy newborns start producing their own vitamin K. 

Vitamin K deficiency in newborns can be prevented by giving phytonadione, also known as vitamin K1, which is the most active form of vitamin K. 

Phytonadione is administered intramuscularly in the newborn setting, typically within one hour after birth. 

Once administered, phytonadione acts as a cofactor to an enzyme found in the liver called gamma glutamyl-carboxylase, which converts the inactive forms of coagulation factors II, VII, IX, and X into their active forms.

Now, IM administration phytonadione to a newborn may have potential side effects. The most common ones include pain and erythema at the injection site, as well as a skin rash or urticaria.

Other potential side effects include hypersensitivity reactions, as well as hyperbilirubinemia, which is more likely to occur in premature infants.

Before administering phytonadione to a newborn, there are a number of nursing considerations to keep in mind. 

First, educate the newborn’s family about why the medication is needed. Explain how during the first week of life, newborns are at ris]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oxytocin:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VJf1592gQEaQVzKSGQKFuNyNRJKKihtx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oxytocin: Nursing pharmacology]]></video:title><video:description><![CDATA[Oxytocin is a peptide hormone released by the posterior pituitary that causes uterine muscle contraction during labor. It’s also responsible for the milk let-down reflex where milk is ejected during breastfeeding. 

It’s commonly used to induce labor or help strengthen uterine contractions to facilitate delivery. After delivery of the placenta, it’s used to treat uterine atony, prevent postpartum hemorrhage and to manage incomplete or inevitable spontaneous abortion.

Okay, a synthetic version of oxytocin is used clinically. To induce labor or strengthen contractions, it’s administered via IV.  

After reaching the uterus, it will activate receptors on smooth muscle cells and trigger calcium ion release from the sarcoplasmic reticulum. 

This increase in intracellular calcium will cause the muscle to contract harder with increased frequency and duration in order to help with the delivery. 

When used postpartum, the uterine contractions will squeeze intrauterine vessels to slow or stop postpartum hemorrhage.  

Now, when oxytocin is administered as a nasal spray it causes contraction of the myoepithelial cells around milk-containing alveoli in the breasts. This will squeeze the milk into the lactiferous ducts where it could be ejected during lactation. 

The main adverse effects of oxytocin are related to uterine hyperstimulation, where there’s too much contraction. This could cause painful contractions, and lead to uterine rupture and hemorrhage. It could even restrict placental blood flow, resulting in abnormal fetal heart rate patterns. 

Other side effects include nausea, vomiting, hypertension, cardiac arrhythmias and amniotic fluid embolism. With prolonged use, it could have an effect similar to antidiuretic hormone and increases water retention. This is particularly dangerous since it could cause water toxicity and result in coma or even death. 

Oxytocin is contraindicated or used with caution when vaginal delivery could increase the risk of compli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neonatal_eye_prophylaxis:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r_j_OcxDSymFmHB1I-m-RDpwQG_lv-If/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neonatal eye prophylaxis: Nursing pharmacology]]></video:title><video:description><![CDATA[Neonatal eye prophylaxis refers to the use of medication to prevent ophthalmia neonatorum, which is an eye infection that is most commonly caused by Neisseria gonorrhoeae or Chlamydia trachomatis. 

These bacteria are usually transmitted during vaginal delivery as the baby passes down an infected birth canal, but intrauterine infection of the fetus may also occur after rupture of membranes. 

Now, ophthalmia neonatorum typically presents as conjunctivitis, with eye redness, edema, and purulent discharge within 2 to 5 days of life, and while some infections can be mild, untreated infections with Neisseria gonorrhoeae are notorious for their ability to creep onto the cornea, resulting in blindness. So, neonatal eye prophylaxis is mostly aimed at preventing gonococcal ophthalmia neonatorum.

Now, in the past, neonatal eye prophylaxis involved the use of the chemical silver nitrate. Ironically, it was later discovered that silver nitrate itself damaged the conjunctiva, resulting in chemical conjunctivitis.

Currently, the primary medication used in neonatal eye prophylaxis for Neisseria gonorrhoeae is erythromycin, which is a macrolide antibiotic, and is given to all newborns in the form of an ophthalmic ointment within the first hour of life.

Now, once administered, erythromycin acts by entering into the bacterial cell and binding to the 50S subunit of bacterial ribosomes. As a result, the ribosome is stopped in its tracks and the synthesis of proteins is inhibited. The absence of necessary proteins prevents the bacterial cell from growing and replicating.

Ophthalmic erythromycin administration is rarely associated with side effects, which include mild eye irritation and redness.

Okay, ophthalmic erythromycin is administered within one hour after birth to allow time for bonding and breastfeeding. Before administration, be sure to confirm that informed consent has been obtained from the baby’s parents or guardians.

Reassure them that the medication is a st]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prostaglandins:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UhyR1oEhSGu5gKOKvd4SDFOiTeG56IqU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prostaglandins: Nursing pharmacology]]></video:title><video:description><![CDATA[Prostaglandins are a group of molecules released by most cells in the body that can have effects on different tissues and organs, including the uterus, where they cause cervical ripening  and uterine muscle contraction. 

Prostaglandins include dinoprostone, also referred to as PGE2, and misoprostol, also referred to as PGE1. Dinoprostone is a naturally occurring prostaglandin E2 that comes in the form of a gel for endocervical administration, or vaginal insert administered intravaginally. 

Dinoprostone is typically used to facilitate labor by inducing cervical ripening, to induce abortion in the second trimester, or to evacuate the uterus when there’s a spontaneous abortion or intrauterine fetal death, as well as to manage a benign hydatiform mole. 

Misoprostol, on the other hand, is a synthetic prostaglandin E1 analog that can be administered intravaginally and sometimes orally for cervical ripening. 

It is also used to control postpartum hemorrhage, for treatment of incomplete or missed abortion, and to induce abortion when administerd with mifeprostone, a progestrone agonist.

Once administered, prostaglandins stimulate secretion of collagenase in the cervix, which degrade collagen. 

This increases the relative amount of water, which softens the cervix which facilitates cervical ripening. It also triggers an increase of intracellular calcium, which causes the smooth muscle cells in the uterus to contract with increased strength, frequency and duration. 

The main side effects of prostaglandins are related to uterine hyperstimulation, where there’s too much contraction. 

This could cause painful contractions, and lead to uterine rupture and hemorrhage. It could even restrict placental blood flow, resulting in abnormal fetal heart rate patterns. 

Other side effects include nausea, vomiting, diarrhea, and diaphoresis. Finally, some serious but luckily rare side effects include cardiac arrhythmias, disseminated intravascular coagulation, and amniotic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ergot_alkaloids:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SdHVImyDTGqCreBrhjNwJFf_R0qlIu12/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ergot alkaloids: Nursing pharmacology]]></video:title><video:description><![CDATA[Ergot alkaloids are a group of medications produced by the fungus Claviceps purpurea. Ergot alkaloids, or simply ergots, include methylergonovine, which can be used to prevent or treat postpartum hemorrhage. 

Other ergots include ergotamine, which can be used to treat severe migraines, as well as bromocriptine, which can be used to treat Parkinson disease.

Now, ergot alkaloids have similar structure to the neurotransmitters norepinephrine, serotonin, and dopamine. As a result, they can act as antagonists on alpha-adrenergic receptors on smooth muscle cells, as well as agonists of serotonin and dopamine receptors, mainly found in the brain. 

In particular, methylergonovine primarily acts on alpha-adrenergic receptors on the uterus, increasing the tone, and rate of uterine rhythmic contractions, as well as inducing vasoconstriction. 

For this reason, methylergonovine can be administered intramuscularly, and less frequently orally or intravenously, usually after delivery of the placenta to decrease bleeding, and promote uterine involution. 

Typically, methylergonovine is used as second-line after safer medications like oxytocin have failed to control the bleeding. However, methylergonovine may cause significant side effects. 

The most common ones include gastrointestinal symptoms like nausea or vomiting, as well as abdominal pain and diarrhea. Another important side effect is related to uterine hyperstimulation, where there’s too much contraction, and may result in uterine tetany. 

Some clients may develop allergic reactions, such as a skin rash or swelling of the face, lips, or tongue; or present with headaches, dizziness, vertigo, and tinnitus. 

Cardiovascular effects are mainly associated with intravenous administration, and include hypo- or hypertension, Raynaud phenomenon, palpitations, angina, and arrhythmias. 

Ergot toxicity may cause ergotism, which mainly presents with nausea, vomiting and dyspnea; in addition, hypoperfusion of the limbs may]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inhaled_mast_cell_stabilizers:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QgtdfNE9SkufTqILRpZlZcB3QfWdwkoS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mast cell stabilizers - Inhaled: Nursing pharmacology]]></video:title><video:description><![CDATA[Mast cell stabilizers are a group of medications that help reduce inflammation and are typically used in allergic conjunctivitis, as well as allergic rhinitis and asthma, which is an obstructive lung disease characterized by reversible narrowing of the airways. 

Now, these allergic conditions are usually triggered by an environmental factor like air pollutants, cigarette smoke, exercise or stress. 

These factors cause a type of immune cells called mast cells, to release various inflammatory chemical mediators like histamine and leukotrienes, triggering an excessive inflammatory response. 

Okay, now cromolyn is the only mast cell stabilizer that is used in clinical practice, and depending on the affected area, it can be administered as eye drops for allergic conjunctivitis; by a metered spray pump intranasally for allergic rhinitis; or as a nebulizer solution for asthma. 

Alright, so once administered, mast cell stabilizers work by stabilizing the mast cell membrane, preventing the release of inflammatory mediators. This way, mast cell stabilizers produce a mild anti-inflammatory effect at the site of inflammation. 

However, compared to other anti-inflammatory medications like inhaled corticosteroids, mast cell stabilizers don’t work fast enough for treatment of acute asthmatic attacks. 

In addition, they have a very short duration of action, which is why they’re only used for maintenance therapy in clients with mild asthma, or as prophylaxis right before known exposure to a trigger. 

Okay, now generally, mast cell stabilizers are very safe and well-tolerated. Some uncommon side effects when inhaling cromolyn can include cough, hoarseness, and bitter taste. Additionally, clients may also experience mild burning or stinging upon instillation into the eyes and nose.

Before preparing to administer cromolyn for asthma, allergic rhinitis or allergic conjunctivitis, perform a baseline assessment, including current symptoms, vital signs, and lung sounds, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Analgesics_for_obstetrics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JV-avhawRfWUjyuvD2FjN0WiTR2UXWTO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Analgesics for obstetrics: Nursing pharmacology]]></video:title><video:description><![CDATA[Analgesics are medications used to relieve pain, and can be used for various reasons in obstetrics, such as during pregnancy to manage headaches, back, or pelvic pain during delivery to help reduce pain from uterine contractions, cervical stretching, and vaginal distension; as well as following vaginal delivery for perineal lacerations, and following cesarean delivery for pain at the incisional site.

Commonly used analgesics in obstetric settings include acetaminophen, which is mainly used during pregnancy; as well as systemic analgesics like opioids and regional analgesics like local anesthetics, which are typically used once the client goes into labor. 

However, other analgesics like NSAIDs, such as ibuprofen, should be avoided during pregnancy, since they can cause fetal harm, including fetal renal impairment, oligohydramnios, and premature closure of the fetal ductus arteriosus.

Now, opioids can be full opioid agonists like fentanyl and remifentanil; and partial opioid agonists like butorphanol and nalbuphine; whereas regional anesthetics include bupivacaine and ropivacaine.

Now, in general, analgesics act by blocking neurons that transmit pain sensations. Opioids act on opioid receptors called the mu, kappa, and delta receptors. These receptors are typically  located on the pre- and post-synaptic membranes of the pain-conducting neurons in the spinal cord and brain. 

Now, opioids are primarily given orally, intramuscularly, and intravenously. When opioids bind to their receptors, they result in a decreased sensitivity to pain by increasing the pain threshold and altering pain transmission. 

On the other hand, regional anesthetic medications act by reversibly blocking sodium channels on the neurons and prevent the transmission of pain. 

Regional anesthetics can either be injected locally into the pudendal nerve area, called a pudendal anesthesia or nerve block, to numb the lower vagina, vulva, and perineum, which is often used in the repair of e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antidepressants_-_Tricyclic_antidepressants_(TCAs)_&amp;_monoamine_oxidase_inhibitors_(MAOIs):_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yvArFRZQRASM5_kKWhTbDVa-RHawCb_o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antidepressants - Tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs): Nursing pharmacology]]></video:title><video:description><![CDATA[Antidepressants are medications primarily used to treat major depressive disorder, which is a condition associated with a persistent feeling of sadness and loss of interest in everyday activities. 

Even though the exact cause of major depressive disorder is still unknown, there&amp;#39;s some evidence that suggests that it’s related to low levels of neurotransmitters called monoamines, which include serotonin, norepinephrine, and dopamine. 

In this video, we’re going to cover two of the main classes of antidepressants: tricyclic antidepressants and monoamine oxidase inhibitors.

First, let’s focus on tricyclic antidepressants or TCAs for short, which can be further subdivided into tertiary or non-selective TCAs, like amitriptyline, imipramine, and clomipramine; and secondary or selective TCAs, such as desipramine and nortriptyline. 

Now, tricyclic antidepressants are taken orally, and once absorbed into the bloodstream, they travel to the brain. Here, TCAs inhibit the reuptake of serotonin and norepinephrine. 

As a result, their free levels within the synaptic cleft are increased right away, although the effect of TCAs alleviating symptoms of depression is not evident for a few weeks. 

Other indications for TCAs include phobic, panic, obsessive-compulsive, and anxiety disorders; neuropathic pain; as well as migraine prevention. 

Now, even though TCAs are very effective in the treatment of depression, they can also act on other receptors, so they’re not considered as the first line therapy due to their side effects.

Blockade of muscarinic receptors results in anticholinergic side effects, such as dry mouth, blurred vision, tachycardia, urinary retention, and constipation. 

On the other hand, blockade of alpha-1 adrenergic receptors may cause orthostatic hypotension; whereas blockade of histamine receptors may result in sedation. 

Moreover, TCAs may also block GABAA receptors, which normally send inhibitory neuronal signals, so by blocking these in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchodilators:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vOYn0pO1STOuWwcrNMkiWrUARsC3148l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchodilators: Nursing pharmacology]]></video:title><video:description><![CDATA[Bronchodilators are a group of medications that help breathing by keeping the airways dilated. That being said, they are typically used in obstructive lung diseases, like asthma and chronic obstructive pulmonary disease, or COPD for short, where clients suffer from narrowing and obstruction of the airways. 

Asthma is characterized by chronic inflammation in the lungs, as well as asthma exacerbations or attacks, where certain triggers, such as viruses, allergens, stress, aspirin or other NSAIDs and exercise, lead to reversible bronchial smooth muscle spasms and mucus production, both of which make it hard to breathe. As a result, clients experience symptoms like dyspnea, wheezing, chest tightness, and coughing. 

On the other hand, in COPD, there’s chronic inflammation and fibrosis in the lungs, most commonly due to smoking. As a result, the airways become irreversibly obstructed and the lungs are not able to empty properly, which leaves air trapped inside the lungs. As a result, clients experience symptoms like dyspnea and a productive cough. 

Now, COPD generally refers to a group of progressive lung diseases that includes chronic bronchitis and emphysema. These two differ in that chronic bronchitis is defined by long-term inflammation of the bronchial tubes, whereas emphysema is defined by destruction and enlargement of the alveoli. 

Although the airway obstruction in COPD is irreversible, bronchodilators can often help prevent the complete closure of the airway during expiration, which provides mild symptomatic relief.  

Now, based on their mechanism of action, bronchodilators can be broadly divided into three main groups; β2-agonists; anticholinergics; and methylxanthines. 

The effect of all these medications is bronchial smooth muscle relaxation, which in turn results in dilation of the narrowed airways and improved air flow. 

In particular, β2-agonists, like albuterol and salmeterol, come in an aerosolized form, and can be taken via metered dose]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Angiotensin-converting_enzyme_(ACE)_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sFnWSZyVQJqsFC7igNHQi-BnTJuCaZWW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Angiotensin-converting enzyme (ACE) inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Angiotensin converting enzyme inhibitors, or ACE inhibitors for short, are a group of medications that help decrease blood pressure and are typically used to treat hypertension or heart failure, but they can be also administered to clients who have recently had a myocardial infarction.

Now, ACE inhibitors usually end in “-pril”, and include enalapril, lisinopril, ramipril, benazepril, and captopril. 

Most of these medications are taken orally, but there’s one ACE inhibitor called enalaprilat that can be administered intravenously for hypertension or severe heart failure when oral treatment isn’t practical. However, it’s not recommended for acute heart failure or myocardial infarction.

Alright, ACE inhibitors work by inhibiting the action of an enzyme called angiotensin-converting enzyme, or ACE for short, preventing it from converting angiotensin I into its active form angiotensin II. Angiotensin II causes blood vessels to constrict, which increases the blood pressure. 

In addition, it stimulates the adrenal glands to release aldosterone, which increases reabsorption of sodium and water in the kidneys. This results in increased blood volume, which also contributes to increased blood pressure. 

So once ACE inhibitors are administered, there’s less angiotensin II in the bloodstream, which decreases vasoconstriction, as well as decreased aldosterone release by the adrenals, leading to natriuresis, or excretion of sodium along with water by the kidneys. In this way, ACE inhibitors effectively lower the blood pressure. 

Now, the most common side effects of ACE inhibitors are mild and nonspecific, such as a headache, dizziness, and fatigue. However, many clients also complain of a constant, dry, irritating cough. 

That’s because normally, ACE also breaks down bradykinin, so when the client takes ACE inhibitors, bradykinins accumulate, and they’re thought to induce the cough reflex. In fact, this is a common reason for quitting ACE inhibitors and switching]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Angiotensin_II_receptor_blockers_(ARBs):_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9BBaXVP3SWm9kw6zeD2wv8OqT4qkeBwk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Angiotensin II receptor blockers (ARBs): Nursing pharmacology]]></video:title><video:description><![CDATA[Angiotensin II receptor blockers or ARBs for short, are a group of medications that help decrease blood pressure and are typically used to treat hypertension or high blood pressure, and heart failure.

Now, ARBs usually end in “-sartan,” like candesartan, valsartan, irbesartan and losartan, and are taken orally.

Alright, ARBs work by binding to angiotensin II receptors on vascular smooth muscles and the adrenal glands, which prevents angiotensin II from binding. 

Normally, when angiotensin II binds to these receptors on blood vessels, it causes them to constrict, which increases the blood pressure. 

On the other hand, in the adrenal glands, angiotensin II stimulates the release of aldosterone, which increases reabsorption of sodium and water in the kidneys. 

This results in increased blood volume, which also increases blood pressure. Once ARBs are administered, angiotensin II can’t bind to angiotensin II receptors, which decreases vasoconstriction, as well as aldosterone release by the adrenals. 

This causes natriuresis, or excretion of sodium along with water by the kidneys. In this way, ARBs effectively lower the blood pressure. 

However, ARBs can also cause some side effects. The most common ones are mild and nonspecific and include headache, dizziness, and drowsiness. 

ARBs have also rarely been associated with the development of angioedema, which is a fluid accumulation and swelling of the eyes, lips, tongue, pharynx, and glottis, and can be life threatening. 

Other side effects include hypotension, tachycardia, and hypoglycemia. Finally, ARBs decrease potassium excretion in the urine, and this could lead to hyperkalemia, so it’s important for clients who are taking ARBs to avoid taking potassium supplements and salt substitutes that contain potassium.

As far as contraindications go, as a boxed warning, ARBs and other medications with a similar mechanism of action are contraindicated during pregnancy, since they may cause fetal injury. 

Fina]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leukotriene_modifiers:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0BRufS1CRxm-7BdZQvIxNQ5dTZq33akP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leukotriene modifiers: Nursing pharmacology]]></video:title><video:description><![CDATA[Leukotriene modifiers are a group of medications that help breathing, so they are typically used to manage nasal congestion and inflammation associated with allergic rhinitis, as well as to manage narrowing and obstruction of the airways in obstructive lung diseases, such as asthma. 

Asthma is characterized by chronic inflammation in the lungs, as well as asthma exacerbations or attacks, where certain triggers, such as viruses, allergens, stress, aspirin and exercise, lead to reversible bronchial smooth muscle spasms and mucus production, both of which make it hard to breathe. As a result, clients experience symptoms like dyspnea, wheezing, coughing, and chest tightness.

Now, leukotriene modifiers act by decreasing the action of leukotrienes, which are inflammatory molecules produced and released by certain immune cells, such as mast cells, to trigger an inflammatory response. 

Once released, leukotrienes bind to leukotriene receptors located on the bronchial smooth muscles, causing them to contract, as well as on the mucous glands to increase mucus secretion. In addition, leukotrienes increase blood vessel permeability, which results in fluid leakage and edema. 

Now, leukotriene modifiers can be classified into two groups, based on their mechanism of action. On the one hand, leukotriene receptor antagonists, such as montelukast and zafirlukast, bind to and block leukotriene receptors on the airways, preventing leukotrienes from binding. 

On the other hand, leukotriene synthesis inhibitors, such as zileuton, inhibit the enzyme that produces leukotrienes. 

Now, regardless of the exact mechanism, the net effect is decreased leukotriene action, leading in turn to decreased smooth muscle contraction in the airways, decreased mucus secretion, and decreased inflammation. 

Alright, now unlike other medications that are used for asthma, leukotriene modifiers are typically administered orally and have slower onset of action, which is why they are only used a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inhaled_corticosteroids:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4jhmsKv3T5aK0qSdSDs6IGtWToCVrYxm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Corticosteroids - Inhaled: Nursing pharmacology]]></video:title><video:description><![CDATA[Inhaled corticosteroids are medications that improve breathing by decreasing lung inflammation. They are primarily used in clients with persistent asthma, meaning those who have asthmatic symptoms more than 2 days per week. Asthma is characterized by chronic inflammation in the lungs, as well as asthma exacerbations or attacks, where certain triggers, such as viruses, allergens, stress, aspirin or other NSAIDs and exercise, lead to reversible bronchial smooth muscle spasms and mucus production, both of which make it hard to breathe. As a result, clients experience symptoms like dyspnea, wheezing, chest tightness, and coughing. Inhaled corticosteroids help decrease the frequency of symptoms and prevent exacerbations. Inhaled corticosteroids can also be used in clients with chronic obstructive lung disease, or COPD, to prevent exacerbation and slow the progression of the disease.

Now, commonly used inhaled corticosteroids include fluticasone, beclomethasone, budesonide, and mometasone. These medications are typically used as maintenance therapy to help control the underlying lung inflammation, and are often combined with inhaled bronchodilators, such as long acting beta-2 agonists like salmeterol, which provide immediate relief of symptoms by inducing airway smooth muscle relaxation. 

Now, once in the lungs, inhaled corticosteroids enter the respiratory epithelial cells and  suppress the expression of certain genes that code for inflammatory proteins. This leads to decreased movement of inflammatory and immune cells into the bronchi and lungs, as well as decreased production and release of inflammatory mediators like histamine and leukotrienes. As a result, there’s reduced airway inflammation and edema, as well as decreased mucus production, which ultimately leads to airway dilation and improved air flow. 

Because they work on the gene level, inhaled corticosteroids may need days or even weeks to demonstrate effectiveness. That&amp;#39;s why they are onl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lung_surfactants_&amp;_antenatal_corticosteroids:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-koElwIuQA69LuIampcAiD4UTdKe7WR_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lung surfactants and antenatal corticosteroids: Nursing pharmacology]]></video:title><video:description><![CDATA[Lung surfactants are lipoproteins produced and secreted by type II pneumocytes lining the lung alveoli to keep them from collapsing when air is exhaled. 

The production of surfactants typically begins at around week 26 of gestation, and reaches sufficient levels by week 35. So, preterm babies born before that don&amp;#39;t produce enough lung surfactants. 

As a consequence, their alveoli collapse, leading to neonatal respiratory distress syndrome. To prevent this, preterm babies are administered exogenous lung surfactants.

Commonly used exogenous lung surfactants include beractant, which is a bovine lung derivative; calfactant, which is a calf lung derivative; and poractant alfa, which is a porcine lung derivative. 

Exogenous surfactants are usually administered directly into the newborn’s airways through an endotracheal, or ET tube, or via less invasive surfactant administration or LISA for short, such as nebulized surfactant preparations, laryngeal masks, and intratracheal instillation.

Once administered, lung surfactants form a film that coats the inner walls of the alveoli. This film decreases the surface tension, which helps maintain the alveolar shape by preventing the inner walls from sticking to each other and collapsing during expiration. 

Now, before birth, corticosteroids like betamethasone and dexamethasone can be administered to promote fetal lung maturation. This is also known as antenatal corticosteroid therapy, and it is usually administered intramuscularly to pregnant clients at 24 to 33 weeks and 6 days of gestation who are expected to go into preterm labor. 

Administration of antenatal corticosteroids reduces the risk of respiratory distress syndrome in premature babies.  Also, it has been shown to have other benefits too, including a reduced risk of neonatal mortality; sepsis; intraventricular hemorrhage, or bleeding in the brain; and necrotizing enterocolitis, a serious intestinal condition affecting premature babies. 

Once ad]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tocolytics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mtGyu8E4TMqb4qCTWLLIkLW1QLiKRZGR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tocolytics: Nursing pharmacology]]></video:title><video:description><![CDATA[Tocolytics are a group of medications that suppress uterine contractions. For that reason, tocolytics are typically used to prolong pregnancy and delay birth after preterm labor starts before 34 weeks of gestation. Delaying labor is usually done to transfer the client to a higher health care facility if needed, or to administer medications that improve fetal outcomes, such as corticosteroids, which promote fetal lung maturation.

Now, the most commonly used tocolytics are magnesium sulfate, calcium channel blockers like nifedipine, beta2-agonists like terbutaline, and NSAIDs like indomethacin.

When tocolytics are administered, they cause smooth muscle relaxation in the uterus via various mechanisms. Both magnesium sulfate and calcium channel blockers like nifedipine block calcium channels, which inhibits the entry of calcium ions into uterine smooth muscles and thus decreases their contractility. In addition to its tocolytic effect, magnesium sulfate also has a neuroprotective effect on the preterm brain, which is more susceptible to injury. On the other hand, beta2-agonists bind to beta2-receptors located on the surface of smooth muscle cells, ultimately leading to a decrease in the level of intracellular calcium and decreasing their contractility. Finally, NSAIDs inhibit the enzyme cyclooxygenase, which normally helps to produce prostaglandins. As a result, there’s a decrease in prostaglandin levels, which ultimately results in relaxation of the uterine smooth muscle.

Now, tocolytics can cause several maternal and fetal side effects. Side effects of magnesium sulfate include nausea, flushing, and headache. In addition, magnesium sulfate toxicity can lead to respiratory depression, cardiac arrest, as well as neurological side effects like altered mental status, reduced deep tendon reflexes, and muscle weakness. Now, magnesium sulfate may have side effects on the fetus. As it relaxes the muscles, some babies who are exposed to magnesium can present with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rho(D)_immune_globulin:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QaMZJpTvRWKJHnGFbMlzPwBUQWuJA9F0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rho(D) immune globulin: Nursing pharmacology]]></video:title><video:description><![CDATA[RhO (D) immune globulin, or RhIG for short, is a biological class of medications primarily used in the management of Rh-negative pregnancies, which occur when the client has Rh-negative blood, while the fetus has Rh-positive blood. 

The first Rh-negative pregnancy is usually not associated with complications, but in the following pregnancies, this Rh incompatibility can cause severe, life-threatening fetal complications. 

What happens is that during delivery of the first Rh-negative pregnancy, some of the baby’s red blood cells can get into the client’s circulation. 

Now, since the mother has Rh-negative red blood cells, her immune system recognizes the baby’s Rh-positive red blood cells as foreign, and triggers the production of anti-Rh antibodies. 

At first, the mother produces IgM antibodies, which are too big to cross the placenta, therefore there are no complications during the first pregnancy. 

But, over time, the mother develops IgG anti-Rh antibodies, which are smaller. As a result, if another Rh-negative pregnancy occurs, these preformed IgG antibodies are able to cross the placenta and destroy the fetal Rh-positive red blood cells. 

This process is called Rh isoimmunization, and ultimately causes hemolytic disease of the fetus and newborn, or HDFN for short. 

In order to prevent Rh isoimmunization, all pregnant clients with Rh-negative blood should be given RhO (D) immune globulin, which can be administered intramuscularly.

Once RhO (D) immune globulin is administered, it suppresses the mother’s immune response and antibody formation against the fetus. 

In fact, if the mother receives RhO (D) immune globulin within 72 hours postpartum, the chances of Rh isoimmunization drop to 1 or 2%. 

Moreover, if the mother receives RhO (D) immune globulin at 28 weeks of gestation, and then again within 72 hours after the delivery, the chance of developing Rh isoimmunization becomes less than 1%! 

Unfortunately, RhO (D) immune globulin is not effect]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antipsychotics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n7x96K14SFuV4426pMwYHtXfS1KodfvH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antipsychotics: Nursing pharmacology]]></video:title><video:description><![CDATA[Antipsychotics are medications mainly used to treat schizophrenia and other psychotic disorders, such as psychosis, acute mania, delirium, bipolar disorders, and obsessive-compulsive disorders. Antipsychotics are most often administered orally, but some can also be sublingual or transdermal, or injected intramuscularly, intravenously, or subcutaneously.

Once administered, they travel to the brain and block dopamine D2 receptors in the mesolimbic pathway, thereby helping alleviate some psychotic symptoms. Now, there are two main groups of antipsychotics: the first-generation or typical antipsychotics, and the second-generation or atypical antipsychotics.

Typical antipsychotics can be further classified as high-potency or low-potency medications. High-potency antipsychotics include medications such as haloperidol, trifluoperazine, and fluphenazine. These medications have a high affinity for dopamine receptors, meaning they require lower doses to achieve their therapeutic effect. On the flip side, low-potency antipsychotics include medications such as thioridazine and chlorpromazine. 

These medications have less affinity for dopamine receptors, therefore they require larger doses to achieve the same therapeutic effect as high-potency antipsychotics.

On the other hand, second generation, or atypical antipsychotics, include medications such as clozapine, olanzapine, quetiapine, risperidone, and ziprasidone. In addition to blocking dopamine D2 receptors, atypical antipsychotics also work by blocking serotonin 5-HT2A receptors in the mesocortical pathway. Another atypical antipsychotic is asenapine, which is administered sublingually or transdermally, to prevent clients from “cheeking” their medication; that’s when a client pretends to swallow their medication, but instead keeps it hidden between the teeth and the cheek.

Now, antipsychotics are not selective to the dopamine receptors in the mesolimbic pathway, meaning that they can also block dopamine recept]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anxiolytics_&amp;_sedative-hypnotics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SxvFeb3tSA63zUjiXNl9hOXgTZu3psAF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anxiolytics and sedative-hypnotics: Nursing pharmacology]]></video:title><video:description><![CDATA[Anxiolytics and sedative-hypnotics are medications that act as central nervous system depressants that reduce tension and induce calm or sleep, and are primarily used to relieve anxiety, as well as insomnia. 

It’s important to note that the preferred medications for the long-term management of anxiety are typically selective serotonin reuptake inhibitors, or SSRIs for short, due to their low abuse potential and dependence. 

But, medications that can be used for the short-term management include benzodiazepines, barbiturates, and miscellaneous anxiolytics.

First, let’s start with benzodiazepines. These medications are usually taken orally, but some of them can also be administered intravenously, intramuscularly, subcutaneously, sublingually, or even rectally. 

Now, based on the overall duration of action, benzodiazepines can be subdivided into three main groups. 

The first group includes short-acting benzodiazepines, which typically end in -azolam, such as alprazolam and midazolam; the second group covers intermediate-acting benzodiazepines that end in -azepam, like lorazepam and clonazepam; and finally, the third group includes long-acting benzodiazepines that also end in -azepam, such as diazepam.

In addition to treating anxiety and insomnia, benzodiazepines are also indicated for treatment for status epilepticus, where a person has ongoing or multiple seizures for over 5 minutes. 

Other important indications include preoperative sedation, induction of general anesthesia sedation for mechanical ventilation, and alcohol withdrawal syndrome.

Now, benzodiazepines work by binding to GABAA receptors, increasing the frequency at which they open up to let chloride ions into the cell. The influx of negatively charged chloride ions makes the neuron less responsive to stimuli. 

Now, benzodiazepines can cause side effects like headache, sedation, and dizziness; as well as blurred vision and dry mouth. 

Also, despite being a central nervous system depressan]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nitrates:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hw13JeoGR02kzNK9qtwEBe6uRRe9EOED/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nitrates: Nursing pharmacology]]></video:title><video:description><![CDATA[Nitrates are medications that come under the umbrella of a larger group called vasodilators, which dilate the walls of blood vessels. Nitrates are primarily used to treat angina pectoris, which is pain caused by reduced blood flow to the heart muscle; as well as hypertension, and heart failure. 

More recently, they’ve also been approved for the topical treatment of anal fissures. The most commonly used nitrates include nitroglycerin, isosorbide dinitrate, and isosorbide mononitrate. 

Out of these, nitroglycerin has a rapid and short-lasting action, so it is typically given through rapidly absorbable routes like sublingual, oral spray, or intravenously, to treat acute anginal pain or hypertension; or as transdermal patches or topical ointments for long-term prevention. Nitroglycerin can also be administered rectally for the treatment of anal fissures.

On the other hand, isosorbide dinitrate and isosorbide mononitrate have a longer duration of action and are typically administered orally as tablets or sustained-release capsules, which makes them useful for the long-term prevention of angina pectoris, or to treat clients with heart failure.

Once absorbed into the blood, nitrates quickly get converted into their active form, called nitric oxide. Nitric oxide diffuses to the smooth muscle cells of both veins and arteries, causing wall relaxation and vasodilation. 

The result of venous vasodilation is peripheral blood pooling, which in turn decreases the return of venous blood to the heart. 

This way, nitrates predominantly reduce preload, which is the pressure that stretches the heart as it fills with blood from venous return. 

At the same time, arterial vasodilation lowers the systemic vascular resistance, which will also reduce the afterload, or the pressure that the heart must work against to eject the blood. 

Ultimately, by reducing preload and afterload, nitrates reduce the amount of work the heart has to do, eventually decreasing the heart’s oxyge]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mood_stabilizers:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xKZgq5rBQUqu0CM5yGErfKtNSyG4qAkt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mood stabilizers: Nursing pharmacology]]></video:title><video:description><![CDATA[Mood stabilizers are medications used to treat bipolar disorder, which is a mental health condition characterized by dramatic shifts in emotions, mood, and energy levels. 

In other words, a person with bipolar disorder can alternate from extreme lows to extreme highs, so mood stabilizer medications can help smooth out these mood swings. 

Now, the first-line mood stabilizer is lithium, but other medications can also be used, including antiepileptics, such as carbamazepine, valproic acid, and lamotrigine; and antipsychotics, like olanzapine.

Now, lithium is taken orally, and it’s rapidly absorbed by the gastrointestinal tract. Once absorbed, it travels to the brain and regulates the release of neurotransmitters through an unclear mechanism. 

In particular, lithium seems to inhibit the release of norepinephrine and dopamine, while it increases the production of serotonin and alters the sodium-potassium ion transport in neurons, as well as in muscle cells.

It’s important to note that lithium has boxed warning for toxicity because it has a narrow therapeutic index, meaning that small variations in its blood concentrations can result in serious side effects and toxicity.

The most common causes of lithium toxicity include increased lithium dosage; decreased renal elimination, which is especially common in clients with kidney problems or hyponatremia; and the use of medications that can affect renal clearance, such as NSAIDs, ACE inhibitors, and diuretics.

Now the most important side effects of lithium toxicity include thirst, lethargy, slurred speech, and muscle weakness, as well as gastrointestinal side effects, such as nausea, vomiting, and diarrhea. 

In addition, individuals may develop seizures, hyperreflexia or overactive reflexes, and ataxia, which refers to a lack of coordination and muscle control.

Another important side effect of lithium therapy is nephrogenic diabetes insipidus, which is characterized by polyuria or the production of large quan]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antidepressants_-_SSRIs_and_SNRIs:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3qW_aPY1QRCG0EJNcYAbReuURJ6D_X7S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antidepressants - SSRIs and SNRIs: Nursing pharmacology]]></video:title><video:description><![CDATA[Antidepressants are medications primarily used to treat major depressive disorder, which is a condition associated with a persistent feeling of sadness and loss of interest in everyday activities. 

Even though the exact cause of major depressive disorder is still unknown, there&amp;#39;s some evidence that suggests that it’s related to low levels of neurotransmitters called monoamines, which include serotonin, norepinephrine, and dopamine. 

In this video, we’re going to cover two of the main classes of antidepressants: selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors.

First, let’s focus on selective serotonin reuptake inhibitors, or SSRIs for short, such as fluoxetine, fluvoxamine, sertraline, paroxetine, citalopram, and escitalopram. 

SSRIs are taken orally, and once absorbed into the bloodstream, they travel to the brain. Here, SSRIs inhibit the reuptake of serotonin. 

As a result, free levels of serotonin within the synaptic cleft are increased right away, although the effect of SSRIs alleviating symptoms of depression are not evident for a few weeks. 

Other indications for SSRIs include anxiety disorders like obsessive-compulsive disorder, or OCD; post traumatic stress disorder, or PTSD; panic disorder and phobias; as well as eating disorders like bulimia.

On the other hand, serotonin-norepinephrine reuptake inhibitors, or SNRIs, include duloxetine, venlafaxine, desvenlafaxine, and levomilnacipran. 

SNRIs are also taken orally, and once they reach the brain, they inhibit the reuptake of both serotonin and norepinephrine, increasing their levels in the synaptic cleft. 

Other indications for SNRIs besides major depressive disorder include generalized anxiety disorder and neuropathic pain.

Now, the brain has different types of serotonin receptors besides the ones involved in depression. Some of them mediate functions like mood, sleep, appetite, or sexual function. 

So, some side effects of SSRIs and SNRI]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Direct-acting_vasodilators:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/75vSVAUZRcmnkXP2p_ECcDUIRvGK7bWX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Direct-acting vasodilators: Nursing pharmacology]]></video:title><video:description><![CDATA[Direct-acting vasodilators are a class of antihypertensive medications that are used for severe refractory hypertension, malignant hypertension, and hypertensive emergencies. These medications include hydralazine, which can be administered orally, intravenously, and intramuscularly; minoxidil, which can be administered orally or topically; and sodium nitroprusside, which is given intravenously.

Once administered, direct acting vasodilators rapidly work on the vascular smooth muscle cells by preventing the increase of intracellular calcium concentration. 

As a result, direct acting vasodilators prevent vasoconstriction and promote vasodilation, leading to a reduction in the total peripheral resistance and blood pressure. 

Keep in mind that hydralazine and minoxidil mainly work on arterioles, while sodium nitroprusside works on both arterioles and venules. 

Now, since direct acting vasodilators tend to work rapidly, they can result in sudden vasodilation and hypotension. This may lead to side effects, including dizziness, headache, reflex tachycardia, palpitations, and edema. 

Other side effects include nausea, vomiting, and gastrointestinal distress. So to counteract side effects like reflex tachycardia and edema, direct acting vasodilators can be used in combination with beta-blockers or diuretics, but under close monitoring for adverse effects. 

Now, through an unclear mechanism, hydralazine may trigger a lupus-like syndrome, which can involve multiple organs. Clients may experience severe malaise, myalgia, arthralgia, pericarditis, and hepatosplenomegaly, and upon blood tests, they may present with leukopenia, thrombocytopenia, and positive autoantibodies. 

What’s important to keep in mind is that hydralazine-induced lupus-like syndrome mainly affects clients who take higher doses for a prolonged period of time, and can be reversed upon discontinuation of hydralazine.

Regarding minoxidil, an important boxed warning is that it can cause pericardia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_to_treat_Alzheimer_disease:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0vqlCvBpT72-_8nQSspBEpFeRNmkpKK5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for Alzheimer disease: Nursing pharmacology]]></video:title><video:description><![CDATA[Alzheimer disease is the most common cause of dementia, and although there’s no cure, certain medications can be used to help mitigate some of the symptoms and improve the client’s quality of life. 

Now, these medications can be broadly divided into two classes; acetylcholinesterase inhibitors and NMDA receptor antagonists.

Starting with acetylcholinesterase inhibitors, these include rivastigmine, galantamine, and donepezil. Acetylcholinesterase inhibitors are taken orally, while rivastigmine can be taken in the form of a transdermal patch as well as orally. 

Once absorbed into the bloodstream, they travel to the brain. Here, they inhibit the enzyme acetylcholinesterase, which normally breaks down the neurotransmitter acetylcholine. 

As a result, acetylcholine builds up in the synaptic cleft, causing increased and prolonged effects. And since there&amp;#39;s some evidence suggesting that Alzheimer disease is related to low levels of acetylcholine in the brain, acetylcholinesterase inhibitors can help improve symptoms.

However, increased acetylcholine levels can also cause cholinergic side effects like miosis, blurred vision, headaches, dizziness, and drowsiness. 

At the same time, in the airways, acetylcholine triggers bronchoconstriction and increases bronchial secretions, which can manifest with dyspnea and a persistent cough. 

In the cardiovascular system, acetylcholine slows down the heart rate and reduces blood pressure, which can result in bradycardia, heart block, hypotension, and even cardiac arrest. 

In the gastrointestinal tract, these medications can cause increased motility and secretions, leading to nausea, vomiting, cramps, diarrhea, increased salivation, and involuntary defecation, or even gastrointestinal bleeding. 

Finally, in the urinary tract, acetylcholine stimulates the bladder muscles and sphincter relaxation, which may cause a sense of urgency. 

As far as contraindications go, acetylcholinesterase inhibitors should be used]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_to_control_airway_secretions:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xt5biMxcQSKgQ2F0DutZzkpbSc6Q9drt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications to control airway secretions: Nursing pharmacology]]></video:title><video:description><![CDATA[There are certain medications that can be used to control airway secretions, which refers to the mucus secreted by the respiratory tract epithelium. 

These medications are typically used when the airway secretions are either too much or too thick to be coughed out normally. They can broadly be divided into 4 classes; nasal decongestants, expectorants, mucolytics, and antitussives.

The most commonly used nasal decongestants include sympathomimetic medications like oxymetazoline and pseudoephedrine, and corticosteroids like fluticasone and mometasone; and can be administered orally or intranasally. 

Nasal decongestants are usually used to treat a congested, or stuffy, nose, such as from allergic rhinitis. They act by constricting the blood vessels in the nasal mucosa, which ultimately reduces the local tissue edema and shrinks the congested mucosa; while corticosteroids also help decrease inflammation.

Nasal decongestants can lead to side effects like anxiety, tremors, insomnia, hypertension, and increased blood glucose. Prolonged use of decongestants, typically for more than 48 hours, may lead to rebound nasal congestion once the decongestant is stopped. 

Additional side effects specific to corticosteroid nasal decongestants include a bad taste after administration, and dryness of the nasal mucosa following continuous use.

Nasal decongestants should be used with caution in clients with hypertension, cardiac disease, hyperthyroidism, or diabetes mellitus, due to their adverse effects on blood pressure and blood glucose.

On the other hand, commonly used expectorants include guaifenesin, usually given orally in the form of cough syrups; while common mucolytics include acetylcysteine and dornase alfa, which are usually given orally or by nebulizer. 

Expectorants and mucolytics are used to relieve chest congestion due to infections like the common cold; chronic obstructive pulmonary disease, asthma, and cystic fibrosis. 

Both classes of medications]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diuretics_-_Osmotic_&amp;_carbonic_anhydrase_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KqxZdpQcRdSeLcGVjYagYjnqRuS4u903/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diuretics - Osmotic and carbonic anhydrase inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Diuretics, also called water pills, are medications that act on the kidneys to increase diuresis, or the production of urine, to help excrete more water from the body. 

Diuretics act on the kidneys’ basic unit, the nephron, to induce salt and water excretion. Zooming into the nephron, it’s made up of a glomerulus, which filters the blood. 

The filtered content goes through the renal tubules, which have four parts the proximal convoluted tubule; the U-shaped loop of Henle, with a thin descending, a thin ascending, and a thick ascending limb; and finally, the distal convoluted tubule; and the collecting duct, which drain the urine out of the kidneys.

In this video, we’re going to cover two of the main classes of diuretics, osmotic diuretics and the carbonic anhydrase inhibitors.

Okay, the main osmotic diuretic is mannitol, which is a sugar alcohol that can be administered intravenously. After administration, mannitol travels through the bloodstream and attracts water out of the cells it encounters along the way. 

Eventually, mannitol and the extra water reach the kidneys and get secreted by the glomerulus into the renal tubule. 

Inside the tubules, mannitol increases the osmolality of the tubular fluid, which makes water stay inside the tubules to be excreted rather than be reabsorbed. Ultimately, both mannitol and water are excreted in the urine.

Osmotic diuretics are primarily used to lower intraocular pressure in glaucoma, or to lower intracranial pressure, such as following head trauma or neurosurgery. 

In addition, mannitol can also be used to help excrete harmful substances that may otherwise build up in the body. Examples include myoglobin from the breakdown of muscles, and hemoglobin from the breakdown of red blood cells. 

Now, an important side effect is that mannitol also pulls water from cells into the extracellular space, which could worsen edematous conditions like heart failure and pulmonary edema. 

In addition, as more water gets pul]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Laxatives:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A-2sk3YBRDqtOIBAEqrEYNqaT7S_XJ4q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Laxatives: Nursing pharmacology]]></video:title><video:description><![CDATA[Laxatives are a group of medications that help the passage of stool, and are used to relieve constipation. Now, based on their mechanism of action, laxatives can be broadly divided into four main groups: osmotic laxatives, stimulant laxatives, bulk-forming agents, and emollients or stool softeners. 

Most of these medications are taken orally, but some of them can also be given rectally in the form of enemas or suppositories, to cleanse the bowels before procedures like colonoscopies or surgeries.

Starting with osmotic laxatives, these include saline laxatives, such as magnesium hydroxide, magnesium citrate, and sodium phosphate salts; and indigestible sugars and alcohols, like lactulose and polyethylene glycol. 

Both saline laxatives and indigestible sugars and alcohols are not well absorbed or digested, so they draw more water out of the intestinal cells and into the lumen via osmosis. 

This increases intestinal motility, called peristalsis, which pushes the stool through the gastrointestinal tract and also helps mix the stool with water.

Moving on to bulk-forming agents, these include methylcellulose, polycarbophil, and psyllium. Now, these medications can’t be digested by the enzymes in our gastrointestinal tract, so they remain in the intestinal lumen and end up getting incorporated into the stool. 

As a result, bulk-forming agents work by drawing in more water, making the stool swell up into a soft, bulky mass, which is easier to pass, while also stimulating peristalsis.

Next are stimulant laxatives like bisacodyl, and senna. These medications are also known as irritant laxatives, since they work by irritating the nerve endings in the large intestinal walls. 

As a result, these medications stimulate smooth muscle contraction; thereby increasing intestinal peristalsis. 

Finally, emollient laxatives or stool softeners mainly include docusate, are more effective in preventing rather than treating constipation. 

Docusate is a surfactant, which m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Histamine_H2_antagonists:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gNC0iVU7Qra2oviLCTMpjn-JTaKs7yB8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Histamine H2 antagonists: Nursing pharmacology]]></video:title><video:description><![CDATA[Histamine H2-receptor antagonists, also called H2 blockers, are medications that help reduce the production of gastric acid. 

Because of that, they can be used to treat peptic ulcers; gastroesophageal reflux disease, or GERD; and Zollinger-Ellison syndrome, which is a rare condition caused by gastrin-secreting tumors. In addition, histamine H2-receptor antagonists can be used to prevent stress-induced ulcers. 

These medications include cimetidine, which can be administered orally, intravenously, and intramuscularly; famotidine, which is given orally or intravenously; and nizatidine, which is given orally.

Now, gastric acid is secreted by the parietal cells, which have different membrane receptors that modulate their activity. One of them is the H2 histamine receptor. 

Normally, the stomach is protected from the acidic environment by the mucus secreted by foveolar cells, and the esophagus is protected by the lower esophageal sphincter, which prevents gastric acid from coming back up. 

When some of these mechanisms fail, the person can develop peptic ulcers or gastroesophageal reflux disease. 

Histamine H2-receptor antagonists block H2 receptors so histamine can’t bind them, which decreases gastric acid secretion, and in turn mitigates the harmful effects of gastric acid in these disorders.

Generally, histamine H2-receptor antagonists are safe medications. However, they may cause some side effects, since H2 receptors are not only located in the stomach. 

So, in the brain, some side effects include headaches, dizziness, somnolence, confusion, and hallucinations. 

In the skin, these medications may cause pruritus and a rash; while cardiovascular side effects include hypotension and cardiac dysrhythmias. 

Histamine H2-receptor antagonists may lead to sexual side effects like decreased libido and impotence; as well as gastrointestinal side effects like diarrhea or constipation. 

In addition, histamine H2-receptor antagonists reduce the production of g]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antidiarrheals:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8mgXwojaSb_88V0IMuZvuBRVQ2W4MnV2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antidiarrheals: Nursing pharmacology]]></video:title><video:description><![CDATA[Antidiarrheals are a group of medications that are used to treat diarrhea, which is characterized by loose, watery stool, or an increased frequency of bowel movement. 

Now, based on their mechanism of action, antidiarrheals can be broadly divided into four main groups: opiates and opiate-related agents, somatostatin analogues, adsorbents, and bulk-forming agents.

Let’s start with opioids like loperamide, diphenoxylate, difenoxin, and paregoric. These are taken orally and work by stimulating the opioid receptors found in the intestinal wall, which decreases peristalsis or bowel movement. 

The slowed transient time allows for increased absorption of fluid and electrolytes into the fecal mass.

Next, there are somatostatin analogues, such as octreotide. This can be administered orally, subcutaneously, intramuscularly, or intravenously, and it’s mostly used to treat diarrhea associated with certain tumors or chemotherapy. 

The way octreotide works is by binding to somatostatin receptors and mimicking somatostatin’s effects. 

These include inhibiting hormone release by the pancreas and gastrointestinal tract, as well as slowing down peristalsis and decreasing the secretion of fluid and electrolytes into the bowel lumen.

Moving on to adsorbents, these include bismuth subsalicylate, and are taken orally. Once in the intestinal lumen, bismuth subsalicylate has protective properties, since it can coat the walls of the intestines, as well as antimicrobial properties, since it can kill causative bacteria.

 In addition, bismuth subsalicylate has antisecretory actions, so it helps reduce how much fluid is secreted into the bowel lumen.

Finally, bulk-forming agents include methylcellulose, polycarbophil, and psyllium. Now, these medications can’t be digested, so they remain in the intestinal lumen and end up getting incorporated into the stool. 

As a result, bulk-forming agents work by absorbing water, making the stool swell up into a bulky mass. In addition, b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Calcium-channel_blockers:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Xwripd-xQMm-CFKe1VrTbq9WTfSFhpCl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Calcium-channel blockers: Nursing pharmacology]]></video:title><video:description><![CDATA[Calcium channel blockers are medications that are primarily used to treat cardiac arrhythmias, hypertension, and angina pectoris. Calcium channel blockers are used to a lesser extent for prophylaxis of migraines and for symptomatic treatment of Raynaud phenomenon, which is caused by reduced blood flow in tiny peripheral vessels. Finally, calcium channel blockers also relax uterine smooth muscle, which is useful to prevent premature uterine contractions, and this can help delay preterm labor. 

Now, calcium channel blockers can be administered orally or intravenously, and are divided into two main groups, dihydropyridines and non-dihydropyridines. Dihydropyridines include amlodipine, nicardipine, nifedipine, felodipine, and clevidipine, which have a more potent action on the blood vessels, specifically the arterioles, than the heart. As a result, they’re preferred to treat hypertension. Another dihydropyridine is nimodipine, which has the added benefit of being able to cross over the blood-brain barrier. So, it can be used to prevent or treat cerebral vasospasm caused by an aneurysmal subarachnoid hemorrhage. 

On the other hand, non-dihydropyridines include verapamil and diltiazem, which have a more potent action on the heart than the blood vessels. Verapamil is highly selective for cardiac calcium channels; and, thus, is mainly used to treat angina pectoris and arrhythmias. Diltiazem is equally good at blocking both cardiac and vascular calcium channels, and so it’s effective in hypertension and arrhythmias. 

Now, once administered, calcium channel blockers block voltage-gated calcium channels, and they act by decreasing the amount of calcium entering the cell.  

Normally, calcium is required for the contraction of both the cardiac muscles and the vascular smooth muscles. So, the decreased calcium reduces the muscle’s ability to contract, ultimately relaxing them.  

Now, calcium channel blockers relax vascular, particularly arterial, smooth muscles, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Treatment_for_Helicobacter_pylori:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w4xkfbFIRM6rFNMYnybQMmE-TeuavRH0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Treatment for Helicobacter pylori: Nursing pharmacology]]></video:title><video:description><![CDATA[Helicobacter pylori, or H. pylori for short, is a bacterium that can cause inflammation of the stomach lining; and can result in peptic ulcers. 

The recommended treatment for H. pylori typically involves using a triple- drug therapy regimen, including a proton pump inhibitor or PPI like omeprazole, and two antibiotics, which include clarithromycin plus either metronidazole or amoxicillin. 

If triple-therapy fails, clients can be given quadruple-therapy regimen, which again includes a proton pump inhibitor, as well as a mucosal protective agent like bismuth subsalicylate, and the antibiotics metronidazole and tetracycline. 

Treatment for H. pylori is usually administered orally, but clients with bleeding peptic ulcers can be given intravenous treatment.

Once administered, proton pump inhibitors act on the parietal cells in the stomach by binding to and inhibiting the H+/K+-ATPase, or proton pumps. 

These pumps are involved in the secretion of gastric acid by exchanging potassium ions from the lumen with hydronium from the cells. As a result, proton pump inhibitors ultimately decrease gastric acid secretion. 

On the other hand, antibiotics help eradicate the bacterial infection through different mechanisms of action. Clarithromycin is a macrolide antibiotic, which works by binding to the 50S subunit of the ribosome, stopping protein synthesis and bacterial replication. 

Metronidazole works by generating free radicals, which can damage various bacterial structures, including DNA, and ultimately cause bacterial cell death. 

Amoxicillin is a beta-lactam penicillin, which works by inhibiting cell wall synthesis in bacteria, leading to bacterial death. And tetracycline acts by binding to the 30S subunit of the bacterial ribosome, ultimately stopping protein synthesis and bacterial replication.

Finally, bismuth subsalicylate forms a protective coating over ulcerated tissue, and also increases the production of mucus, prostaglandins, and bicarbonate. In ad]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Proton_pump_inhibitors_(PPIs):_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_Az3nNAgT4Klk14hjmPECaGCRtK3C4-L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Proton pump inhibitors (PPIs): Nursing pharmacology]]></video:title><video:description><![CDATA[Proton pump inhibitors, or PPIs for short, are medications used to treat conditions like peptic ulcers, gastroesophageal reflux disorder or GERD, and Zollinger-Ellison syndrome, which is caused by a gastrin-secreting tumor that leads to excess gastric acid secretion which then results in peptic ulcers. 

Proton pump inhibitors are also included in the combination treatment against H. pylori, since they have a weak antibacterial effect.

Now, proton pump inhibitors usually end in “-prazole”, and include medications that are administered orally, like omeprazole, lansoprazole, dexlansoprazole, rabeprazole; as well as medications available intravenously, like pantoprazole and esomeprazole. 

Once administered, proton pump inhibitors act on the parietal cells in the stomach by binding to and inhibiting the H+/K+-ATPase or proton pumps. 

These pumps are involved in the secretion of gastric acid by exchanging potassium ions from the lumen with hydronium from the cells. As a result, proton pump inhibitors ultimately decrease gastric acid secretion. 

Side effects of proton pump inhibitors are uncommon, but can include headaches, dizziness, fatigue, and blurred vision, as well as dry mouth, increased thirst, and hiccups. 

In addition, some clients may experience gastrointestinal disturbances, such as increased or decreased appetite, nausea, abdominal pain, constipation, or diarrhea. 

Also, prolonged acid suppression can decrease the absorption of iron, calcium, magnesium, and vitamin B12, or cobalamin. 

When the gastric juices are less acidic, it also allows ingested pathogens, like Clostridioides difficile, to survive and invade the gastrointestinal tract. 

Therefore, clients treated with proton pump inhibitors are more susceptible to gastrointestinal infection; this is also associated with an increased risk of microaspiration and lung colonization, leading to pneumonia. Other side effects may include a skin rash, and osteoporosis.

Now, as far as contraindic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eosinophilic_esophagitis_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mlPCzrXxSnSUZDANoX26VSgOTnmvGhhO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eosinophilic esophagitis (NORD)]]></video:title><video:description><![CDATA[Eosinophilic esophagitis, or EoE, is a chronic food allergy associated digestive disorder in which people have large numbers of eosinophils in the esophagus. Eosinophils are a type of white blood cell that play many roles within the immune system and are involved in allergic reactions. 

Signs and symptoms of eosinophilic esophagitis can vary quite a bit, and are frequently the same as those for gastroesophageal reflux disease, also known as GERD. 

These symptoms are caused by increased inflammation and swelling within the esophagus, and include trouble swallowing, food getting stuck in the throat, nausea, vomiting, poor growth in childhood, weight loss, stomach pain, poor appetite, and malnutrition.

The increase in eosinophils in the esophagus can be caused by a number of things, particularly hypersensitivity reactions or changes to the expression of certain genes. 

The hypersensitivity reactions involved are a form of allergic reaction after exposure to a food or environmental allergen. When certain cells come in contact with the allergen they signal other cells, most commonly eosinophils, to accumulate and get activated in the esophagus. 

The first exposure to an allergen may take time to create a response. However, some cells remember that allergen to more quickly react to future exposures. 

Therefore, the more a person is exposed to allergens which trigger a hypersensitivity reaction, the more eosinophils will be present.

Additionally, changes to gene expression appear to play a role in increasing the number of eosinophils in a person with EoE. 

A primary gene involved in people with EoE is CCL26 which encodes for eotaxin-3. Eotaxin-3 is a protein that triggers increased eosinophil production and the gene is often overexpressed, meaning it is used to make more proteins than usual in people with eosinophilic esophagitis. 

When eotaxin-3 makes more proteins, those proteins trigger more eosinophils to be recruited to the esophagus, consequently r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antihistamines:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CIMpIetiQS6tYhsrftX4nBBcRDGSkrkS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antihistamines: Nursing pharmacology]]></video:title><video:description><![CDATA[Antihistamines are medications that can be used for a variety of conditions, such as alleviating symptoms of a common cold, to decrease motion sickness, and they can occasionally be used to help induce sleep. 

But the primary use of antihistamines is to alleviate symptoms of allergic conditions, such as allergic rhinitis, allergic conjunctivitis, and urticaria, as well as as an adjunctive therapy for anaphylaxis, which is a severe systemic allergic reaction. 

Now, these allergic conditions are usually triggered by an environmental factor, like pollen, which causes mast cells to release inflammatory mediators like histamine, triggering a widespread response. 

When acting on the brain, histamine promotes wakefulness. In the bronchi, histamine causes smooth muscle contraction, leading to bronchoconstriction, while in blood vessels, it causes smooth muscle relaxation, resulting in vasodilation. 

In addition, histamine increases vascular permeability, allowing fluid to accumulate in the airways, which increases nasal and bronchial secretions.

Now, antihistamines can be administered orally, topically, and injected intravenously or intramuscularly. 

Once administered, they block the histamine H1 receptors, preventing histamine from binding and triggering its effects on target organs. 

There are two main groups of antihistamines: first generation antihistamines include chlorpheniramine, diphenhydramine, hydroxyzine and promethazine, while second generation antihistamines include loratadine, fexofenadine, cetirizine, and levocetirizine.

Now, peripherally, both generations of antihistamines can block H1 receptors in the bronchi, resulting in bronchodilation, which improves airflow, while in the blood vessels of the skin, they cause smooth muscle contraction, which leads to vasoconstriction, in turn decreasing localized flushing; in the capillaries, they decrease vascular permeability, reducing edema; in mucous membranes, they reduce nasal and bronchial secre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiemetics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M1Iol1AJTiydpBm9Qa_0uBaGRZqbsN-R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiemetics: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiemetics are a group of medications that are used to treat nausea and vomiting. These include ondansetron, metoclopramide, aprepitant, prochlorperazine, and promethazine, as well as antihistamines like diphenhydramine, and cannabinoids, such as dronabinol.

Let’s start with ondansetron, which can be administered  orally, intravenously, and intramuscularly. Once administered, ondansetron acts as a 5-HT3 receptor antagonist peripherally by decreasing vagal nerve stimulation, but it is also a very powerful central acting antiemetic blocking an area in the brain called chemoreceptor trigger zone, or CTZ for short. 

Ondansetron is primarily used to control nausea and vomiting after surgical anesthesia, as well in individuals undergoing chemotherapy or radiotherapy. 

Next, metoclopramide can be administered orally, intranasally, intravenously, and intramuscularly, and subcutaneously. Once administered, it acts by blocking dopamine receptors in the CTZ. 

As a result, the levels of dopamine decrease, preventing nausea and vomiting after surgical anesthesia as well as chemotherapy-induced nausea and vomiting. 

Okay, another antiemetic is aprepitant, which can be given orally, as well as intravenously in the form of fosaprepitant. Once administered, it acts as a neurokinin receptor antagonist that blocks neurokinin-1, or NK-1, receptors in the CTZ, and thus, it can be used to prevent chemotherapy-induced nausea and vomiting. 

Alright, moving onto prochlorperazine, which is a phenothiazine, and can be given orally, rectally, intravenously, and intramuscularly. Phenothiazines block dopamine receptors in the CNS and they’re mostly used as antipsychotics. 

However, most phenothiazines also have antiemetic effects, and in fact, prochlorperazine is used solely as an antiemetic. The mechanism of the antiemetic effects is complex. 

They’re primarily due to the blockage of D2 receptors in the CTZ, as well as due to anticholinergic and antihistamine effects. Prochlo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Analgesics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pBiAosMUTbmBvVdj2TzRDmiMQ-qpjqoq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Analgesics: Nursing pharmacology]]></video:title><video:description><![CDATA[Analgesics, also commonly known as painkillers, are medications primarily used to relieve pain, such as a headache, muscle and neuropathic pain, as well as pain related to trauma and fractures. 

Analgesics can be subdivided into two main groups: non-opioid analgesics, and opioid analgesics. Keep in mind though that there are a number of other medications that primarily serve other purposes, but can be used as analgesics. 

These medications include antidepressants like amitriptyline, anticonvulsants like gabapentin, and corticosteroids like dexamethasone, as well as local anesthetics like lidocaine. 

Now, let’s start with non-opioid analgesics, which include non-steroidal anti-inflammatory drugs or NSAIDs, and acetaminophen. NSAIDs inhibit the enzyme cyclooxygenase or COX, both in the central nervous system and peripheral tissues. 

Now, there are two types of COX enzymes. The first one is called COX-1, which is indirectly involved in platelet aggregation, production of protective mucus in the stomach and vasodilation of the renal vasculature. 

On the flip side, COX-2 is only active in inflammatory cells and vascular endothelium during inflammation, and is involved in the production of small pro-inflammatory compounds like prostaglandins. 

Now, a very commonly used NSAID is acetylsalicylic acid, often referred to as aspirin, which is taken orally. On the other hand, non-aspirin NSAIDs can be further classified as non-selective COX inhibitors that act on both COX-1 and COX-2, like ibuprofen, naproxen and ketorolac; and selective COX-2 inhibitors, like celecoxib. 

Non-aspirin NSAIDs are most often administered orally, but some can also be given intramuscularly, intravenously, topically, or rectally.

Now the most important side effects of NSAIDs include gastrointestinal problems, such as gastritis, gastric ulcers, or even bleeding, and that’s a boxed warning! 

Additionally, chronic use of NSAIDs can impair normal blood flow in the kidneys and may incre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_antispasmodics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bPP_VW_2QoGZCro6nmI4N8U8TD6RFjzV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antispasmodics (GU): Nursing pharmacology]]></video:title><video:description><![CDATA[Urinary antispasmodics are medications that can be used to reduce involuntary contractions or spasms of the detrusor muscle, which is a wall of smooth muscle that surrounds the bladder. These spasms cause a sudden and frequent urge to urinate, and could result from conditions like urge incontinence or overactive bladder, as well as from a urinary tract infection or injury.

The most commonly used urinary antispasmodics include antimuscarinic medications like tolterodine, flavoxate, and oxybutynin, as well as beta-3 adrenergic agonists like mirabegron, which can be administered orally or topically. The way these work is by inhibiting the effects of the parasympathetic nervous system on the detrusor muscle, causing it to relax.

Now, side effects commonly associated with urinary antispasmodics include headaches, dizziness, and drowsiness. In addition, clients may experience dry eyes and blurry vision, as well as dry mouth and dry skin. Some clients may also have tachycardia, nausea, vomiting, constipation, urinary retention, as well as anxiety and restlessness. Finally, the most severe side effects of urinary antispasmodics include hyperthermia, confusion, and delirium. 

As far as contraindications go, urinary antispasmodics should not be given to clients with intestinal or urinary obstruction, as well as those with hypertension or cardiovascular disease. Another contraindication is narrow angle glaucoma, since these medications can worsen the obstruction of aqueous humor drainage. Finally, urinary antispasmodics are contraindicated in clients with myasthenia gravis.

Okay, when caring for your client with an overactive bladder who is prescribed a urinary antispasmodic, first obtain a baseline assessment of your client’s urinary symptoms, such as frequency, urgency, nocturia, and the degree of incontinence they are experiencing. Then, assess your client’s vital signs. Finally, review their laboratory test results, specifically BUN, creatinine, kidney functi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skeletal_muscle_relaxants:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pIl6VUkYT-uHV2I-toT7S4bARKSvxG_Q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skeletal muscle relaxants: Nursing pharmacology]]></video:title><video:description><![CDATA[Skeletal muscle relaxants are medications that reduce muscle contraction, so they are primarily used to relieve both acute or chronic muscle spasms and spasticity. 

Muscle spasms are sudden and involuntary muscle tightness or contractions, and are most often caused by muscle fatigue or injury. 

On the other hand, muscle spasticity is a sustained muscle spasm associated with decreased dexterity that originates from the central nervous system, which can occur due to damage to the nerves that coordinate muscle activity, and can also be seen with chronic neurological disorders, such as multiple sclerosis and stroke; as well as in cerebral palsy and spinal cord damage.

Now, skeletal muscle relaxants can further be divided into centrally-acting and direct-acting muscle relaxants. Centrally-acting muscle relaxants include cyclobenzaprine, methocarbamol, metaxalone, chlorzoxazone, tizanidine, baclofen, carisoprodol, and orphenadrine. 

Other medications can also act as centrally-acting muscle relaxants, such as benzodiazepines, but they’re most commonly used as anxiolytics, sedatives, or anticonvulsants. On the other hand, direct-acting muscle relaxants include dantrolene.

All of these medications can be taken orally. Additionally, methocarbamol can also be administered intravenously or intramuscularly, while dantrolene can be given intravenously, and baclofen can be given intrathecally.

Once administered, centrally-acting muscle relaxants act on the neurons of the central nervous system or CNS to interfere with muscle reflexes and decrease the skeletal muscle tone. 

Although the exact mechanism by which they act is poorly understood, the site of action of some of these medications is known. 

Cyclobenzaprine and methocarbamol primarily act on the brainstem and the spinal cord neurons. Carisoprodol and chlorzoxazone block the nerve conduction in the descending reticular formation in the brain, which is responsible for maintaining muscle tone and posture. 

T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatic_enzyme_replacements:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0VFDU_GgSWCVpq0BSmzSNfV8S3_hSeo6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatic enzyme replacements: Nursing pharmacology]]></video:title><video:description><![CDATA[Pancreatic enzyme replacement therapy is the administration of digestive enzymes that are normally produced by the pancreas to digest food. Pancreatic enzyme replacement is primarily used in conditions that result in pancreatic enzyme deficiency, such as cystic fibrosis, chronic pancreatitis, pancreatic duct obstruction like by tumors, and surgeries like pancreatectomy. Additionally, it can be used in conditions that cause insufficient secretion of pancreatic enzymes, such as gastric and intestinal resection surgeries. 

The main pancreatic enzyme replacement available is pancrelipase, which can be administered orally, immediately before or with a meal or snack. Now, the medication is covered with an enteric coat that protects them from gastric acid, so they can safely reach the duodenum. Once there, the tablet coat dissolves in the alkaline environment and releases the replacement enzymes, which perform the function normally accomplished by pancreatic enzymes. These include amylase, proteases, and lipase. Amylase digest carbohydrates into smaller units of glucose molecules. On the other hand, proteases include trypsin and chymotrypsin, which break down proteins into amino acids. Finally, lipase digests lipids like triglycerides into glycerol and fatty acids. These smaller molecules are then absorbed across the intestinal cells into the bloodstream. 

Now, pancreatic enzyme replacement therapy is generally safe and well tolerated. However, some clients may experience gastrointestinal side effects like abdominal pain, nausea and vomiting, flatulence, constipation, or diarrhea. Pancreatic enzyme replacement can also affect blood glucose level, so these clients should undergo frequent blood glucose monitoring. Other side effects include headaches, ear pain, nasal congestion, and a cough. Less common side effects include dizziness, epistaxis, gallstones, and pruritus, such as pruritus ani due to irritation of the skin around the anus.

Pancreatic enzyme r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_glycosides:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hh300S9rRvGIz3hG4mHZOv9JRYmHefSu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac glycosides: Nursing pharmacology]]></video:title><video:description><![CDATA[Cardiac glycosides, also called digitalis glycosides, are medications derived from the foxglove plant, Digitalis purpurea. They are commonly used for the treatment of atrial arrhythmias, such as atrial flutter and atrial fibrillation, which are caused by rapid, uncoordinated contractions of the atria. In addition, cardiac glycosides can be prescribed for congestive heart failure when other medications fail. 

Now, the most commonly used cardiac glycoside is digoxin, which can be given orally, intravenously, and intramuscularly. Once administered, digoxin works by reversibly inhibiting the sodium-potassium ATPase located in the cell membrane of cardiomyocytes. Normally the sodium-potassium ATPase pumps three sodium ions out of the cell for every two potassium ions that it pumps in, and to do this, it consumes one ATP molecule for energy. When the sodium-potassium ATPase is inhibited by digoxin, sodium builds up inside the cell. This interrupts the sodium-calcium exchanger on the cell membrane, which normally pumps one calcium ion out in exchange for three sodium ions. As a result, digoxin causes calcium to build up within cardiomyocytes, allowing the cardiac muscle fibers to contract more efficiently, which leads to an increase in the force of the heart’s contractions and cardiac output. In turn, the increase in cardiac output increases the renal blood flow and urine output, which also helps reduce peripheral edema. 

Digoxin also stimulates the vagus nerve, which provides the parasympathetic supply to the heart, and reduces the conduction velocity through the AV node. These two effects combined result in a decreased heart rate. But because parasympathetic innervation is much richer in the atria, these effects mainly involve the atria. 

Now, a major drawback is that digoxin has a very narrow therapeutic window, which means that small variations in its blood concentration can easily cause toxicity. Some common side effects of digoxin that can indicate toxic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombolytics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-trkudhWT-y0ER_XP4i-HpXtR-SLTPPp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombolytics: Nursing pharmacology]]></video:title><video:description><![CDATA[Thrombolytics, also called clot busters, are medications that break up clots, and are used for the short-term emergency management of thrombotic conditions, such as myocardial infarction, pulmonary embolism, ischemic stroke, and thrombosis of prosthetic heart valves and stents. 

Now, thrombolytics are usually derived from enzymes involved in fibrinolysis, or the gradual degradation of the fibrin mesh. These include alteplase, reteplase, and tenecteplase, which are  derived from tissue plasminogen activator, or tPA, through recombinant DNA technology, and act locally at the clot site.

Thrombolytics are given intravenously. Once in the blood, they act on a protein produced by the liver called plasminogen, and convert it into its active form called plasmin. 

These medications directly bind to fibrin proteins in the clot and preferentially act on plasminogen trapped in the fibrin mesh, also called fibrin-bound plasminogen. The resulting plasmin then acts as a protease and cuts the fibrin into smaller pieces. 

This allows the trapped red blood cells and platelets to float away, dissolving the clot.The main side effect of all thrombolytics is undue bleeding from other sites, including the injection site, gastrointestinal bleeds, and hemorrhagic stroke. 

In severe cases, thrombolytic-associated bleeding can be treated with medications like aminocaproic acid, which acts by binding to plasminogen and plasmin, ultimately inhibiting their action on fibrin. 

If aminocaproic acid fails, other transfusion products can be administered, such as platelets or coagulation factors in the form of fresh frozen plasma. 

In addition, thrombolytics, when given following a myocardial infarction, can precipitate an abnormal cardiac rhythm, or a reperfusion arrhythmia, which is usually benign. Other side effects include hypersensitivity reactions like anaphylaxis, nausea, vomiting, and fever.

Due to the risk of bleeding, thrombolytics are contraindicated in clients with activ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gallstone-dissolving_agents:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RLV6ohT7TmmW9MvUFrWDHmm7QnqVmVHF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gallstone-dissolving agents: Nursing pharmacology]]></video:title><video:description><![CDATA[Gallstone-dissolving agents are medications used to treat cholelithiasis, more commonly known as gallstones, as an alternative for clients who can’t or prefer not to undergo surgery to remove them, as well as for treatment of clients with primary biliary cirrhosis, and to prevent gallstones in obese clients who are rapidly losing weight, such as after bariatric surgery.

Gallstone-dissolving agents include ursodiol, also known as ursodeoxycholic acid, or UDCA for short, as well as chenodiol, also known as chenodeoxycholic acid, which are bile acids that can be taken orally. 

Now, once gallstone-dissolving agents are administered, their mechanism of action is not totally clear, but they primarily seem to act on the intestines by reducing cholesterol absorption, as well as on the liver by reducing the secretion of cholesterol into bile.

As a result, gallstone-dissolving agents help change the composition of bile, which facilitates bile flow, and ultimately dissolves gallstones.

Unfortunately, the decreased intestinal absorption of cholesterol can cause gastrointestinal side effects, such as abdominal pain, dyspepsia, nausea, vomiting, and diarrhea. 

In addition, clients taking gallstone-dissolving agents may experience headaches, dizziness, weakness, tachycardia, back pain, and may develop alopecia, a skin rash, or pruritus. 

Some clients may present with respiratory side effects like infection or cough; as well as urinary side effects, such as a frequent urge to urinate, as well as difficult, burning, or painful urination, and even bloody or cloudy urine. Finally, chenodiol has a boxed warning for hepatotoxicity, so it requires monitoring for liver function.

As far as contraindications go, gallstone-dissolving agents should not be given to clients with calcified, radiopaque, or radiolucent gallstones, as well as in clients with complete biliary obstruction, unremitting acute cholecystitis, cholangitis, or gallstone pancreatitis. Finally, chenodiol is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_for_thyroid_disorders:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7zPVBCwwReOzeE24JywPFHjGQX6kjdwy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for thyroid disorders: Nursing pharmacology]]></video:title><video:description><![CDATA[Thyroid disorders can be broadly divided into two categories which are on opposite ends of a spectrum: hypothyroidism, which describes a decrease in the thyroid hormones; and hyperthyroidism, which describes an increase in the thyroid hormones. 

Now, thyroid hormones include triiodothyronine, or T3 for short, and thyroxine, or T4, and both contain iodine. The synthesis of these hormones is stimulated by another hormone, called thyroid stimulating hormone or TSH for short, which is released by the pituitary gland.

Okay, so on one side of the spectrum, there’s hypothyroidism. This is treated with thyroid hormone replacement therapy, which involves medications to replace the reduced thyroid hormones. 

These medications include levothyroxine, which is a synthetic form of T4, and liothyronine, which is a synthetic form of T3.

Both of these medications may be given orally or intravenously, and levothyroxine can be administered intramuscularly too. 

Once administered, they bind to intracellular thyroid hormone receptors in tissue cells to mimic the actions of thyroid hormones, such as increasing the metabolic rate, body temperature and cardiac output.

Now, the most common side effects of thyroid hormone replacement therapy include headaches, insomnia, nervousness, as well as weight loss, excessive sweating, and heat intolerance. 

Some clients may also experience cardiovascular side effects, such as tachycardia, palpitations, and even cardiac arrest.

Alright, now contraindications of thyroid hormone replacement therapy include thyrotoxicosis or a high level of thyroid hormones, as well as in clients with adrenal insufficiency, and those who had a recent myocardial infarction. Also, as a boxed warning, these medications should not be used as obesity treatment.

Now, on the other side of the spectrum, there’s hyperthyroidism. This is treated with antithyroid agents like methimazole and propylthiouracil, which are administered orally. 

Once administered, the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oxygen_therapy:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0gLZQGcHRgSkbcMEdX-Zd5UmTHmoAA6p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oxygen therapy: Nursing pharmacology]]></video:title><video:description><![CDATA[Oxygen therapy is the delivery of supplemental oxygen to treat hypoxia, which is when there is not enough oxygen to meet the needs of the body. 

Hypoxia can be caused by various lung diseases that interfere with its ability to properly absorb oxygen, such as pneumonia, chronic pulmonary obstructive disease, or COPD for short, and sleep apnea; as well as blood disorders like various types of anemia, where the red blood cells are not able to carry enough oxygen to meet the body’s demands. 

Oxygen also acts as a potent pulmonary vasodilator and thus, it can be helpful in clients with heart problems like heart failure, where the heart has trouble pumping enough blood to meet the body’s demands. 

Now, various delivery devices can be applied to administer oxygen therapy. The most common choice is the nasal cannula, which typically is used to deliver oxygen at 1 to 6 liters per minute. 

This consists of two prongs that are placed into the nostrils, and a band of tubing wraps around the cheeks and behind the ears to keep it in place. A nasal cannula is easy to apply and is less intrusive, so the client can eat, drink, and talk freely. 

Bear in mind that nasal cannulas are not ideal for clients who breathe through their mouths, or those who require high oxygen concentrations. In these cases, the preferred choice is usually a face mask that covers the client’s nose and mouth. 

There’s a variety of face masks, ranging from simple ones used to deliver oxygen at 6 to 12 liters per minute, to face masks connected with reservoir bags, used to deliver oxygen at 10 to 15 liters per minute. 

These include partial-rebreather masks, which consist of a simple face mask and a bag storing exhaled air and pure oxygen. Every time the client inhales, they breathe in oxygen and exhale air from the bag as well as an amount of room air. 

With non-rebreather masks, only oxygen from the bag is breathed in, while exhaled air escapes through holes on the sides of the mask. Venturi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Beta-adrenergic_blockers:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fU5tY1L8Qvy70dRjSB56Uz7BT8ef0ZR9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Beta-adrenergic blockers: Nursing pharmacology]]></video:title><video:description><![CDATA[Beta-adrenergic blockers, or just beta blockers, are a group of medications that are mainly used to treat cardiovascular conditions like hypertension, coronary artery disease and its manifestations like angina pectoris and myocardial infarction, as well as heart failure and arrhythmias. Beta blockers can also be used to treat essential tremor, glaucoma, and as prophylactic treatment of migraine attacks.

Now, beta blockers work by blocking beta receptors, of which there are three types, known as beta 1, which are mainly found in the heart and kidneys; beta 2, found in the lung bronchioles as well as the arteries of skeletal muscles; and beta 3, found in adipose tissue. 

So beta blockers are classified into two main groups; nonselective and selective. Nonselective beta blockers can block both beta 1 and beta 2 receptors, and include nadolol, propranolol, pindolol, and sotalol. 

On the other hand, selective beta blockers only block beta 1 receptors, and include atenolol, metoprolol, carvedilol, and nebivolol. So keep in mind that all beta blockers end in -lol, (which is pretty funny) and they can be administered orally, intravenously, or even via the ophthalmic route. 

Once administered, beta blockers block beta receptors, thereby preventing the catecholamines norepinephrine and epinephrine from binding and activating them. As a result, beta blockers decrease the sympathetic nervous system response. 

Now, the main therapeutic effects of beta blockers come from the blockade of beta 1 receptors in the heart, which decreases heart contractility and slows the conduction through the atrioventricular or AV node. This helps decrease the heart rate, which ultimately decreases the cardiac output. 

In addition, the blockade of beta 1 receptors in the kidneys decreases the release of renin, which stimulates the adrenal glands to release aldosterone, which in turn acts on the kidneys to induce water and sodium reabsorption. So with beta blockers, there will be less]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Keratolytics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1-WwIg4cS7Gj8GB9eyLYeX2zQEuzap0n/_.jpg</video:thumbnail_loc><video:title><![CDATA[Keratolytics: Nursing pharmacology]]></video:title><video:description><![CDATA[Keratolytics are a group of medications used to treat rough or scaly skin, which can be caused by a variety of skin conditions, such as mild to moderate acne, seborrheic keratosis, warts, dandruff, psoriasis, and skin hyperpigmentation as a result of other conditions like eczema.

Now, commonly used keratolytics include salicylic acid, pyrithione zinc, coal tar, retinoids like tretinoin and acitretin, and alpha-hydroxy acids, like glycolic and lactic acid. 

These medications are applied topically on the skin, while retinoids can also be taken orally. Once administered, keratolytics primarily work by softening and shedding of the stratum corneum, which is the outer layer of the skin, decreasing the skin’s thickness and improving its moisture. 

Unfortunately, this shedding of the stratum corneum may result in side effects, such as skin irritation, which can manifest as erythema, as well as a burning, itching or tingling sensation. 

In addition, retinoids often cause dry eyes and mouth, chapped lips, and skin peeling. Finally, retinoids and alpha-hydroxy acids cause photosensitivity, so clients must avoid exposure to sunlight.

As far as contraindications go, keratolytics should not be used on open wounds or any areas of burnt, cut, irritated or scraped skin. In addition, sensitive areas such as near the eyes or mouth should also be avoided. 

Acitretin has an important boxed warning for hepatotoxicity. Finally, retinoids have a very important boxed warning for pregnancy.

Now, when your client is prescribed a keratolytic, first ask them about the onset and duration of their symptoms. Then, assess the affected area of skin, making note of its type and location, as well as the presence of drainage. 

In addition, be sure to assess the affected skin for open areas, as well as problems like burns, cuts, and irritated or scraped skin. 

Lastly, if a female client is prescribed a retinoid, be sure to confirm a negative pregnancy test before administering the medication. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiepileptics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mT0g67xnRUWLLPIKuCfXbteVTQSf2PHE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiepileptics: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiepileptics, also known as anticonvulsants, are medications primarily used to treat epilepsy, as well as generalized or partial seizures. On rare occasions, these medications can be used to treat mood disorders. 

Now, the most commonly used antiepileptics can be subdivided, based on their mechanism of action, into four main groups: sodium channel blockers, calcium channel blockers, GABA inhibitors, and GABA analogues. 

In addition, other medications can be used as antiepileptics, including barbiturates like phenobarbital and benzodiazepines like diazepam, which are primarily used as anxiolytics and sedative-hypnotics.

Now, let’s focus on sodium channel blockers first. These medications work by blocking voltage-gated sodium channels, eventually inhibiting excitatory neurons from firing action potentials. 

Decreased activity of excitatory neurons results in the reduction and alleviation of seizures. Sodium channel blockers include hydantoins, iminostilbene derivatives, valproate derivatives, and lamotrigine.

First, let’s focus on hydantoins. These medications include phenytoin, which can be administered orally or intravenously; and its prodrug, fosphenytoin, which can be administered intravenously or intramuscularly. 

Common side effects of these medications include headaches, dizziness, visual disturbances, such as blurred vision, nystagmus, and diplopia, as well as gingival hyperplasia. 

Some clients might experience hypersensitivity reactions like Stevens-Johnson syndrome and toxic epidermal necrolysis, as well as drug reactions with eosinophilia and systemic symptoms or DRESS for short.

In addition, these medications can cause hepatotoxicity, as well as impaired metabolism of vitamin D, which can result in osteomalacia. 

Moreover, these medications can impair the absorption of folic acid and vitamin B12; this can lead to hematologic side effects, often referred to as blood dyscrasias, such as agranulocytosis, leukopenia, thrombocytopenia, and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diuretics_-_Thiazide_&amp;_thiazide-like_diuretics,_loop_diuretics,_&amp;_potassium_sparing_diuretics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/paPLHy3sSL_pDvvBgahz-UvHQ6Cmo1pJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diuretics - Thiazide, thiazide-like, loop, and potassium-sparing diuretics: Nursing pharmacology]]></video:title><video:description><![CDATA[Diuretics, also called water pills, are medications that act on the kidneys to increase diuresis, or the production of urine, to help excrete more water from the body. Therefore, they are generally used to treat hypertension, as well as edema caused by fluid overload conditions, such as  heart failure and pulmonary edema, as well as renal diseases like nephrotic syndrome, and hepatic diseases like cirrhosis. Diuretics are most often administered orally, but some of them can also be administered intravenously.

Once administered, these diuretics act on the kidneys’ basic unit, the nephron, to induce electrolyte and water excretion. 

Zooming into the nephron, it’s made up of a glomerulus, which filters the blood. The filtered content goes through the renal tubules, which have four parts: the proximal convoluted tubule; the U-shaped loop of Henle, with a thin descending, a thin ascending, and a thick ascending limb; the distal convoluted tubule; and the collecting duct, which drain the urine out of the kidneys.

Now, the main classes of diuretics include thiazide and thiazide-like diuretics, loop diuretics, and potassium sparing diuretics.

Okay, starting with thiazide diuretics and thiazide-like diuretics, which have a slightly different structure but act in the same way. Available thiazide diuretics include chlorothiazide and hydrochlorothiazide, while examples of thiazide-like diuretics are chlorthalidone and indapamide. 

 Now, once administered, thiazide and thiazide-like diuretics act on the distal convoluted tubule, which has a sodium-chloride transporter that reabsorbs one sodium and one chloride ion together from the tubule. Thiazide diuretics block this transporter, which inhibits the reabsorption of sodium and chloride ions. And since water follows sodium, there will be more water molecules in the lumen as well, so more urine is produced. 

Now, thiazide and thiazide-like diuretics are the first-line treatment of hypertension. However, these medic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eye_anesthetics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z-ZWRJSqR3CWKr2rtabanepTSaCai32Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eye anesthetics: Nursing pharmacology]]></video:title><video:description><![CDATA[Ophthalmic or eye anesthetics are medications used to induce a temporary loss of corneal sensation, including pain, and can be used for various reasons in ophthalmology, such as during comprehensive eye exams, and during brief ophthalmic procedures, like removal of foreign objects or corneal sutures, as well as surgery for cataracts or glaucoma.

Now, commonly used eye anesthetics include proparacaine hydrochloride and tetracaine hydrochloride. 

These medications are applied topically in the form of eye drops, and the way they work is by reversibly blocking sodium channels on the sensory neurons of the cornea. As a result, eye anesthetics prevent the transmission of corneal sensation.

Unfortunately, eye anesthetics can result in side effects, such as loss of the corneal blink reflex, and blurred vision. 

In addition, clients may experience photophobia, dry, red eyes, and a stinging or burning sensation. There are no known contraindications for the use of eye anesthetics.

Alright, when preparing to assist with administering an eye anesthetic, start by assembling the sterile local anesthetic field. 

Ensure that all medications are labeled with name, strength, amount, and expiration date, and that ocular solutions are separated from those not used intraocularly. Lastly, be sure to verify which eye has been prescribed the eye anesthetic.  

Next, let your client know that the eye anesthetic will help decrease their pain and discomfort during the procedure. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oral_antidiabetic_medications_-_Biguanides_and_thiazolidinediones:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cziPZU7kQ7OjqPFzcyKF27yPQLi6OUfl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oral antidiabetic medications - Biguanides and thiazolidinediones: Nursing pharmacology]]></video:title><video:description><![CDATA[Biguanides and thiazolidinediones are medications primarily used to treat type 2 diabetes mellitus. Type 2 diabetes is characterized by insulin resistance, which is when tissue cells have trouble responding to insulin in order to use glucose from the blood. 

As a result, tissue cells starve for energy despite having high blood glucose levels, which is called hyperglycemia.

Now, the most commonly used biguanide is metformin, whereas commonly used thiazolidinediones are medications that end with the suffix -glitazone, like pioglitazone and rosiglitazone. These medications can be taken orally. 

Once administered, they decrease insulin resistance by increasing insulin sensitivity, and thus, the uptake of glucose by muscle and fat cells. 

In addition, these medications inhibit gluconeogenesis, or glucose production in the liver. The combination of these two mechanisms ultimately leads to a decrease in blood glucose.

Alright, now the good news about biguanides and thiazolidinediones is that they never cause hypoglycemia when used alone as monotherapy. 

However, both groups have several other side effects. Clients taking biguanides can often present with gastrointestinal disturbances, such as anorexia, nausea, vomiting, and diarrhea. 

In addition, they might experience dizziness, fatigue, and a characteristic bitter or metallic taste. As a boxed warning, biguanides can lead to lactic acidosis, which can be a life-threatening complication. 

Lastly, prolonged use of biguanides decreases absorption of vitamin B12 and folic acid, which can cause deficiency. 

On the other hand, thiazolidinediones can increase the risk of fractures, and can also lead to bladder cancer. 

Thiazolidinediones also have a boxed warning for heart failure, while only rosiglitazone has a boxed warning about an increased risk of myocardial infarction.

As far as contraindications go, both biguanides and thiazolidinediones should not be used in clients with hepatic disease, as well as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastric_mucosal_protective_agents:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Pob1anosRFiHNf7A05RlmGbhQQS8glf-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastric mucosal protective agents: Nursing pharmacology]]></video:title><video:description><![CDATA[Mucosal protective agents are medications that protect the mucosal lining of the stomach from gastric acid, and are used to treat conditions like peptic ulcers, NSAID-induced ulcers, and gastroesophageal reflux disorder or GERD. 

Mucosal protective agents are also used as a part of the combination treatment against the bacterium H. pylori. Now, these medications can be broadly divided into three classes; prostaglandin analogues, sucralfate, and bismuth compounds.

Starting with prostaglandin analogues, these include misoprostol, which is a synthetic analog of prostaglandin E1 that can be taken orally. 

Once administered, misoprostol stimulates the production of gastric mucus, as well as bicarbonate, which helps neutralize the gastric acid. 

At the same time, misoprostol acts directly on the parietal cells of the stomach to decrease their secretion of gastric acid. 

Common side effects of prostaglandin analogues include stomach cramps and diarrhea. Other side effects may include diaphoresis, headaches, cardiac arrhythmias, and thrombotic events.

As a boxed warning, prostaglandin analogues are contraindicated during pregnancy, since they can induce abortion. They should also be avoided by clients of childbearing age that do not use contraception. 

In addition, prostaglandin analogues must be used with caution in clients with glaucoma, cardiovascular disease, respiratory disease like asthma, and hepatic or renal disease, since they can exacerbate these conditions.

Next is sucralfate, this is taken orally. The way it works is by forming a protective barrier over the ulcer, which prevents damage by gastric acid. 

In addition, similarly to prostaglandin analogues sucralfate also stimulates mucosal protective mechanisms and bicarbonate production.

Now, sucralfate contains aluminum hydroxide, which can inhibit smooth muscle contraction in the gastrointestinal tract, leading to side effects like constipation. Other side effects include headaches, dizziness]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_oral_cavity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TxmudKRaQqC0sx2S84zADRMURIqKzMgw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the oral cavity]]></video:title><video:description><![CDATA[When you’re eating a slice of pizza, the first place food enters is the oral cavity and it is actually where digestion starts. Here, we get to taste the pizza and form a bolus of food to swallow for further digestion in the gut. Many structures work together to chew and swallow like the lips, teeth, and palate, so let’s explore them!

Now, the oral cavity itself is divided into the oral vestibule and the oral cavity proper. The vestibule is the compartment between the anterior and lateral aspects of the teeth and gingiva and the posterior and medial aspects of the lips and cheeks. 

Moving further inside is the oral cavity proper, bounded by the dental arches anteriorly and laterally, and the palate superiorly. The oral cavity proper is mainly occupied by the tongue.

Now let’s get back to that slice of pizza. To eat it, first you open your mouth, and the opening through which the food enters is called the oral fissure. 

Once the pizza’s inside the oral cavity, you use the lips, which act like valves, to keep the oral fissure closed and the food inside while you’re chewing. The lips, and the muscles within it, also help us exhale through the mouth, whistle, speak, or kiss. 

Now, the lips extend from the nasolabial sulci and the nares to the mentolabial sulcus, which is just inferior to the lips, but not all of its surface looks the same. 

The most remarkable feature is the part we’re actually used to calling “lips”: a thin, hairless, reddish skin, called the transitional zone, because it represents the transition between the skin of the face and the inner labial mucosa. 

The vermillion border is the outer edge of our lips that marks the limit between the skin of the face and the transitional zone. 

Finally, in the upper lip, is the philtrum which is a groove superior to the lips that extends from the midline of the vermilion border to the nasal septum.

Now, the lips get their blood supply mainly from branches of the external carotid arteries. Specifi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemostatics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TT7j0dLDRzqjgyH2dXlAlXj_TKiJT6rQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemostatics: Nursing pharmacology]]></video:title><video:description><![CDATA[Hemostatics are medications used to induce hemostasis, which is a physiological process that results in clot formation to prevent or stop a hemorrhage. 

Primary hemostasis first starts when platelets are activated and aggregate to form a platelet plug at the site of an injured blood vessel. 

Next, secondary hemostasis starts with the coagulation cascade, when clotting factors become consecutively activated to ultimately activate prothrombin into thrombin. 

The activated thrombin then cleaves fibrinogen into fibrin, which binds with other fibrin proteins to form a fibrin mesh that reinforces the platelet plug. 

Now, when the tissue has healed, the endothelial cells produce an enzyme called tissue plasminogen activator, or tPA, which in turn converts plasminogen into its active form plasmin. 

Plasmin then acts as a protease by cutting fibrin into smaller pieces, called fibrinolysis, and ultimately dissolving the clot.

Now, the most commonly used hemostatics include antifibrinolytics, such as aminocaproic acid and tranexamic acid, and vitamin K analogues like phytonadione, which can be administered orally, intravenously, intramuscularly, or subcutaneously; as well as topical hemostatic agents, such as gelatin, microfibrillar collagen, bovine thrombin, and human fibrin sealant, which are applied topically. 

Let’s first focus on antifibrinolytics, which work by inhibiting the conversion of plasminogen to plasmin, which ultimately prevents fibrinolysis. 

Now, aminocaproic acid is primarily used as prophylaxis to prevent bleeding after cardiac surgeries, like coronary artery bypass surgery, or CABG, as well as to prevent bleeding in clients with cirrhosis, in which the liver is unable to synthesize clotting factors, and to prevent recurrence of subarachnoid hemorrhage. 

Some side effects of aminocaproic acid include malaise and muscle weakness, bradycardia, hypotension, as well as injection site reactions.

 Less commonly, aminocaproic acid can cause gas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oral_antidiabetic_medications_-_Sodium-glucose_co-transporter-2_(SGLT-2)_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TESawmNGSyKR60oYaX7Ziv_bRS6-1YSW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oral antidiabetic medications - Sodium-glucose co-transporter-2 (SGLT-2) inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Sodium-glucose transporter 2 or SGLT-2 inhibitors are medications used to treat type 2 diabetes mellitus, which is characterized by insulin resistance; this is when tissue cells have trouble responding to insulin in order to use glucose from the blood. 

As a result, tissue cells starve for energy despite having high blood glucose levels, which is called hyperglycemia. Now, SGLT-2 inhibitors include canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin. All SGLT-2 inhibitors end in -gliflozin, and they are taken orally. 

Once administered, SGLT-2 inhibitors travel to the proximal convoluted tubules in the kidneys, where they block the sodium-glucose transporter or SGLT-2, which facilitates the reabsorption of 90% of glucose from renal tubules. 

As a result, SGLT-2 inhibitors lead to an increased excretion of glucose in urine, known as glycosuria, which ultimately lowers blood glucose levels. 

Now, all this glucose in the urine may favor microbial growth. For that reason, the most common side effects of SGLT-2 inhibitors are urinary tract infections, particularly yeast infections. 

In addition, the decreased reabsorption of glucose in the renal tubules leads to an increase in the urine osmolality, causing more water to be lost in urine too. 

This can result in urinary frequency and polyuria, as well as renal impairment or even failure; this is especially likely to affect clients who also take medications like diuretics, ACE inhibitors, ARBs, or NSAIDs, and could result in dehydration and orthostatic hypotension. 

Other dangerous side effects of SGLT-2 inhibitors include hyperkalemia and euglycemic ketoacidosis. Some clients on SGLT-2 inhibitors may also present with reduced bone density, which increases the risk of fractures. 

Finally, canagliflozin can increase the risk of lower limb amputation; while dapagliflozin and ertugliflozin may increase the risk of necrotizing fasciitis of the perineum.

Now, SGLT-2 inhibitors are contraindicated i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oral_antidiabetic_medications_-_Alpha-glucosidase_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MqBDy-n2RDugalwy1IxxrqkeSQOiG9Y5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oral antidiabetic medications - Alpha-glucosidase inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Alpha-glucosidase inhibitors are medications primarily used to treat type 2 diabetes mellitus, and have an unlabeled use for type 1 diabetes mellitus as an adjunct to insulin. 

Now, type 2 diabetes mellitus is characterized by insulin resistance, which is when tissue cells have trouble responding to insulin to use glucose from the blood, while in type 1 diabetes mellitus, there’s no insulin at all. 

As a result, tissue cells starve for energy despite having high blood glucose levels, which is called hyperglycemia.

Now, alpha-glucosidase inhibitors include medications like acarbose and miglitol, which can be taken orally. 

Once administered, these medications act  in the small intestine, where they inhibit the enzyme alpha-glucosidase, which helps digest complex carbohydrates into simple carbohydrates, such as glucose, that can be absorbed through the lining of the intestine and into the blood. 

As a result, alpha-glucosidase inhibitors delay the absorption of ingested carbohydrates, ultimately leading to a smaller rise in blood glucose.

Unfortunately, the undigested carbohydrates remain within the intestines and are digested by intestinal bacteria. 

Because of that, clients taking alpha-glucosidase can often present with gastrointestinal side effects, such as abdominal pain, flatulence, and diarrhea. In addition, acarbose may lead to hepatic injury, while clients on miglitol may develop a skin rash.

As far as contraindications go, alpha-glucosidase inhibitors should not be given to clients with gastrointestinal conditions like inflammatory bowel disease, or IBD for short, as well as ileus, colonic ulceration, or intestinal obstruction. 

Alpha-glucosidase inhibitors are also contraindicated in clients experiencing diabetic ketoacidosis, or DKA for short. 

In addition, these medications inhibitors should be avoided during pregnancy, unless strictly necessary, and are contraindicated while breastfeeding. 

Finally, alpha-glucosidase inhibitors shoul]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oral_antidiabetic_medications_-_Dipeptidyl_peptidase-4_(DPP-4)_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OA21diSYRtSTSwoWBFzO1aeCRIiZ4ATP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oral antidiabetic medications - DPP-4 inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Dipeptidyl peptidase-4 inhibitors, or DPP4 inhibitors for short, are medications used to treat type 2 diabetes mellitus. Type 2 diabetes mellitus is characterized by insulin resistance, which is when tissue cells have trouble responding to insulin in order to use glucose from the blood. 

As a result, tissue cells starve for energy despite having high blood glucose levels, which is called hyperglycemia. Now, commonly used DPP4 inhibitors are sitagliptin, saxagliptin, linagliptin, and alogliptin. All of them end with the suffix -gliptin, which makes them easy to recognize!

DPP4 inhibitors are taken orally. Once administered, these medications inhibit the enzyme DPP4, which normally destroys the hormone incretin. 

As a result, DPP4 inhibitors increase the levels of incretin, which in turn increases insulin secretion and decreases glucagon secretion. The end result is a reduction in glucose production by the liver, and thus a reduction in blood glucose levels.

Now, the most common side effects of DPP4 inhibitors include headaches, nausea, vomiting, and diarrhea or constipation, as well as mild infections of the upper respiratory or urinary tract. 

In addition, they can increase the risk of hypoglycemia, pancreatitis, and acute renal failure. Less frequently, DPP4 inhibitors can cause life-threatening side effects, such as anaphylaxis, angioedema or Stevens Johnson syndrome.

As far as contraindications go, DPP4 inhibitors should not be used in clients with a history of pancreatitis, hypoglycemia, and angioedema. 

They should also be avoided in clients with a history of diabetic ketoacidosis, or DKA for short, which is an acute life-threatening complication of diabetes. 

Finally, precautions should be taken during pregnancy and breastfeeding, as well as in elderly clients, and those with other endocrine, hepatic, or renal disorders.

Now, if a client with type 2 diabetes is prescribed a DPP4 inhibitor like sitagliptin, be sure to review their most recent]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-insulin_injectable_antidiabetic_drugs_-_Glucagon-like_peptide-1_(GLP-1)_agonists_&amp;_amylinomimetics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x0M-XhrgQaCQIkcnLvALB2FRR3yCNRd1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-insulin injectable antidiabetic drugs - GLP-1 agonists and amylinomimetics: Nursing pharmacology]]></video:title><video:description><![CDATA[Glucagon-like peptide-1 or GLP-1 receptor agonists, and amylin mimetics, are two classes of medications that are primarily used to treat type 2 diabetes mellitus, but can also be used in type 1 diabetes as adjunct to insulin therapy. 

Now, type 1 diabetes occurs when the pancreas is unable to produce enough insulin to maintain normal blood glucose levels. On the other hand, type 2 diabetes mellitus is characterized by insulin resistance, which is when tissue cells have trouble responding to insulin in order to use glucose from the blood. 

As a result, tissue cells starve for energy despite having high blood glucose levels, which is called hyperglycemia. Okay, so GLP-1 receptor agonists include albiglutide, exenatide, liraglutide, semaglutide, and lixisenatide; these medications are also known as incretin mimetics, since they act by mimicking an incretin hormone that’s released by intestinal cells in response to a meal, ultimately stimulating a decrease in blood glucose levels. 

On the other hand, the only amylin mimetic is pramlintide, which mimics a hormone called amylin that’s secreted by the pancreatic beta cells together with insulin after a meal to help decrease blood glucose levels. 

Notice that both medication classes end with -tide, and are administered through subcutaneous injections. Once administered, both GLP-1 and amylin agonists have several mechanisms of action. First, they act on the stomach to slow gastric emptying, which leads to a delay in the delivery and absorption of glucose in the intestines. In addition, these medications can affect the hypothalamus to suppress the appetite. 

In the pancreas, they suppress the secretion of glucagon, preventing it from increasing gluconeogenesis, or glucose production by the liver. Finally, GLP-1 agonists also stimulate pancreatic beta cells to secrete insulin in a glucose-dependent manner, meaning that secretion of insulin is proportional to the amount of glucose ingested. 

This is why GLP-1 a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Iron_preparations:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0Bu0nJgxTuO5yI3JAK0cmtT4Tu67nD45/_.jpg</video:thumbnail_loc><video:title><![CDATA[Iron preparations: Nursing pharmacology]]></video:title><video:description><![CDATA[Iron preparations are medications that contain iron, and can be used to treat iron deficiency anemia. This is defined as a state of low red blood cells or hemoglobin in the blood, which could result from nutritional iron deficiency, chronic kidney disease, blood loss or hemorrhage, and during pregnancy or breastfeeding, in which there’s an increased demand for iron and for red blood cells production.

Most often, iron preparations can be given orally, such as ferrous sulfate, ferrous gluconate, and ferrous fumarate. 

In clients who don&amp;#39;t tolerate oral iron preparations for their side effects or because of gastrointestinal malabsorption, iron preparations can be given intravenously, such as iron sucrose and ferumoxytol, as well as intramuscularly, such as iron dextran.

Now, most of the iron in oral preparations is lost with stool, while some of it is stored inside the intestinal cells as ferritin. 

When the body’s iron demand increases, active transport channels shuttle this stored iron to the blood, where it binds to its carrier protein, transferrin. 

On the other hand, intravenous and intramuscular iron preparations bypass intestinal absorption and go straight to the blood. 

Regardless of the route of administration, once iron is in the blood, it can then be stored inside macrophages as ferritin, or transported to various tissues like the bone marrow, where it’s used for hemoglobin synthesis, and ultimately for red blood cell production. 

Now, the main side effects of oral iron preparations include metallic taste, temporary staining of teeth enamel as well as gastrointestinal symptoms such as nausea, vomiting, abdominal pain, flatulence, constipation, and dark stools. 

In addition, oral iron preparations may impair the absorption of other medications, such as with antacids, tetracyclines, and quinolones. 

On the other hand, intravenous and intramuscular iron preparations may cause staining of the skin around the injection site, as well as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oral_antidiabetic_medications_-_Sulfonylureas_&amp;_meglitinides:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FXONjfDSQhK-0WVhDlXYq2HtTWaDKIzI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oral antidiabetic medications - Sulfonylureas and meglitinides: Nursing pharmacology]]></video:title><video:description><![CDATA[Sulfonylureas and meglitinides are medications used to treat type 2 diabetes mellitus. Type 2 diabetes is characterized by insulin resistance, which is when tissue cells have trouble responding to insulin in order to use glucose from the blood. As a result, tissue cells starve for energy despite having high blood glucose levels, which is called hyperglycemia. 

Now, sulfonylureas can be classified into first and second generation and are easy to recognize because they all have the suffix “–ide” and include glimepiride, glipizide and glyburide. On the other hand, meglitinides have the suffix “-glinide” and include repaglinide and nateglinide.  

Okay, now both sulfonylureas and meglitinides are given orally and once administered, they both act on the pancreas by inhibiting ATP-sensitive potassium channels on the membrane of pancreatic beta cells. As a result, these medications initiate a cascade of events that stimulate the pancreatic beta cells to secrete more insulin, ultimately leading to a decrease in blood glucose levels. 

The most common side effects of both classes of medications are hypoglycemia and weight gain. Other notable side effects of sulfonylureas include hepatotoxicity, leukopenia, and thrombocytopenia; while meglitinides commonly cause nausea, diarrhea, and indigestion.   

As far as contraindications go, both sulfonylureas and meglitinides should not be used in clients with type 1 diabetes mellitus, or those experiencing diabetic ketoacidosis or DKA, since these medications will be ineffective in patients with no pancreatic beta-cell function. In addition, some of these medications should be used with caution during pregnancy and breastfeeding, as well as in children or elderly clients. Final precautions for these medications include hepatic or renal disease. 

Alright, if a client with type 2 diabetes is prescribed an oral antidiabetic medication, such as a sulfonylurea or meglitinide, be sure to review their most recent laboratory test]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Topical_corticosteroids:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RpRDzupYTSqVSvKHJVvx0a3gR2Wlwg0E/_.jpg</video:thumbnail_loc><video:title><![CDATA[Corticosteroids - Topical: Nursing pharmacology]]></video:title><video:description><![CDATA[Corticosteroids, also commonly known as steroids, are a group of anti-inflammatory medications used to treat a variety of conditions in almost all healthcare fields! 

In this video, we’re going to focus on topical corticosteroids used for dermatological conditions, including psoriasis, eczematous rashes, lichen sclerosus, bullous pemphigoid, and pemphigus foliaceus. 

They can also be used to relieve the symptoms of urticaria or pruritic lesions, such as those caused by allergic reactions, insect bites, or poison ivy.

Alright, now topical corticosteroids can be classified according to their potency into low, intermediate, or high potency. 

Low potency corticosteroids include hydrocortisone; while intermediate potency corticosteroids include triamcinolone and certain betamethasone formulations; and finally, high potency corticosteroids include stronger betamethasone formulations and clobetasol. 

Most of the topical corticosteroids are available in different formulations, including ointments, creams, gels, or lotions. 

Once applied to the skin, topical corticosteroids reduce inflammation locally by acting on glucocorticoid receptors of skin cells and white blood cells, ultimately decreasing their production of inflammatory mediator molecules, such as prostaglandins and leukotrienes, as well as increasing their production of anti-inflammatory molecules.

In addition, topical corticosteroids cause local vasoconstriction of cutaneous blood vessels, which also helps reduce inflammation. Common side effects of topical corticosteroids include stinging, itching, and skin irritation with the first few applications. 

Over time, they may lead to impaired wound healing and collagen formation, as well as skin atrophy, stretch marks, telangiectasia, and easy bruising. Prolonged use can also cause facial dermatoses like acne, rosacea, and perioral dermatitis. 

Additionally, they can increase the risk of developing skin infections, as well as alter the appearance of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Topical_antibiotics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b04kMvrBRUeK54ebq0jZmezKR2aUjknI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Topical: Nursing pharmacology]]></video:title><video:description><![CDATA[Topical antibiotics are medications used to prevent or treat infections in damaged skin, including burns, wounds, cuts, or scrapes, as well as surgical incisions. 

Some of the most commonly used topical antibiotics include bacitracin-polymyxin B, as well as mafenide acetate, and silver sulfadiazine. 

These are non-prescription antibiotics that are applied locally in the form of an ointment. Once applied, they prevent infections by interfering with bacterial growth and proliferation. 

In terms of side effects, topical use of bacitracin-polymyxin B usually doesn’t cause any adverse reactions, but some clients may present with mild skin irritation or urticaria. 

On the other hand, mafenide can cause mild skin irritation and a burning sensation. Less frequent but more severe side effects include hypersensitivity reactions leading to urticaria, as well as swelling of the face, lips, tongue, or throat. 

Mafenide can also cause metabolic acidosis, and some clients with G6PD deficiency have developed fatal hemolytic anemia with disseminated intravascular coagulation.

Lastly, silver sulfadiazine can leave a temporary black discoloration skin, and can cause a burning sensation, a skin rash like erythema multiforme, or even skin necrosis. 

Finally, systemic absorption of silver sulfadiazine has also been associated with severe hypersensitivity reactions, such as Stevens-Johnson syndrome and toxic epidermal necrolysis, as well as leukopenia, and interstitial nephritis.

Topical antibiotics should be used with caution during pregnancy and breastfeeding, as well as in clients with a history of other skin conditions, such as eczema, and viral skin infections like herpes, varicella, or shingles. 

In addition, prolonged use of topical antibiotics is not recommended, since it can result in bacterial or fungal superinfection. 

Finally, mafenide should also be used with caution in clients with G6PD deficiency, as well as pulmonary or renal disease.

Okay, when your c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Topical_antifungals:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FomIl82XSpumwXTp3HqcjqiiSrK9VuU3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antifungals - Topical: Nursing pharmacology]]></video:title><video:description><![CDATA[Topical antifungals are medications used to treat cutaneous fungal infections, which are conditions that affect the skin, hair, and nails, and can be caused by a variety of fungi, such as Candida albicans or dermatophytes.

The most commonly used topical antifungals include nystatin, tavaborole, ciclopirox, and azoles like ketoconazole, miconazole, econazole, and efinaconazole. These medications are applied topically on the affected skin, in the form of ointments, creams, gels, or foams.

Once administered, topical antifungals work by disrupting and damaging the fungal cell membranes, ultimately resulting in a fungistatic action, meaning that they stop fungal growth, or a fungicidal action, meaning they kill the fungi.

As far as side effects go, topical administration of antifungals can cause the development of a skin rash, as well as itching, and burning of the skin area. 

Additionally, some clients may present with serious hypersensitivity reactions, such as Stevens-Johnson syndrome. Fortunately, there are no major contraindications for the use of topical antifungals.

Alright, when caring for a client that is prescribed a topical antifungal medication like ketoconazole, first assess the affected skin area, making note of the presence of moist, red patches, papules, pustules, and discharge, as well as itching, burning, and pain. Then, review recent laboratory test results, including results from skin scrapings.

Next, be sure to teach your client how the prescribed medication can help treat their cutaneous fungal infection. Remind them that the medication is for topical use only, and not for ophthalmic, oral, or vaginal use. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ophthalmic_anti-inflammatories_&amp;_anti-infectives:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UuO7jIPiQqql0ZNMRWjHhnVbRCyB8Y2B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ophthalmic anti-inflammatories and anti-infectives: Nursing pharmacology]]></video:title><video:description><![CDATA[Commonly used ophthalmic medications can be broadly divided into two categories: anti-inflammatories and anti-infectives. Ophthalmic anti-inflammatories are a group of medications that are used to treat inflammatory eye conditions, such as allergic conjunctivitis, non-infectious uveitis, and to treat eye inflammation after an ophthalmic procedure.

In contrast, ophthalmic anti-infectives are used to treat infectious eye conditions caused by bacteria, fungi, or viruses. These conditions include infectious conjunctivitis, uveitis, blepharitis, keratitis, and endophthalmitis. 

A hordeolum or stye, which is a common bacterial infection of the sebaceous glands of the eyelids, is also treated with ophthalmic anti-infectives. Finally, ophthalmic anti-infectives can also be used in clients with corneal ulceration to prevent infection.

Okay, starting with ophthalmic anti-inflammatories, they can be broadly classified into five groups: NSAIDs, which include diclofenac, flurbiprofen, ketorolac, and nepafenac; as well as corticosteroids, which include dexamethasone and prednisolone; antihistamines, such as emedastine and epinastine; and mast cell stabilizers, including cromolyn and nedocromil. 

Finally, a combination of antihistamines and mast cell stabilizers can be used, such as azelastine, epinastine, ketotifen, and olopatadine.

These medications are applied topically in the form of eye drops or ointments. Once applied, they control the eye inflammation by decreasing the number of inflammatory cells, and inhibiting the production and effects of inflammatory mediator molecules, such as histamines or prostaglandins.

Unfortunately, ophthalmic anti-inflammatories can cause side effects, such as headaches, increased intraocular pressure, thinning of the cornea, and a delay in corneal healing. In addition, clients may experience a stinging or burning sensation when the medication is applied. 

Finally, prolonged use of these medications has also been associated with]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mydriatics_&amp;_cycloplegics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IaQ5sdt7QWeXJBEOxygrLWqlQWatj9mb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mydriatics and cycloplegics: Nursing pharmacology]]></video:title><video:description><![CDATA[Mydriatics and cycloplegics are a group of medications that have various indications for use in ophthalmology, such as during eye exams or ophthalmic surgical procedures. 

Mydriatics cause mydriasis, or pupil dilation; whereas cycloplegics cause cycloplegia, or paralysis of the muscles that are responsible for accommodation to focus on nearby objects.

Commonly used mydriatics include adrenergic agonist medications, such as epinephrine and phenylephrine, while some medications that act as both mydriatics and cycloplegics include antimuscarinic medications, such as atropine, cyclopentolate, homatropine, scopolamine, and tropicamide. 

These medications are applied topically in the form of eye drops, or ophthalmic ointments. Once applied, these medications work by blocking acetylcholine from binding to cholinergic receptors. 

Mydriatic effects can involve stimulation of the iris dilator muscle, which dilates the pupil; or inhibition of the iris sphincter muscle, which constricts the pupil, or both. 

On the other hand, cycloplegic effects result in paralysis of the ciliary muscle of the eye, leading to a loss of accommodation of the lens to focus on nearby objects.

Unfortunately, mydriatics and cycloplegics can result in side effects, such as dry eyes, blurred vision, and photophobia. Less frequently, they might be absorbed systemically, and clients may experience confusion and drowsiness, as well as dry mouth, flushing, tachycardia, hypertension, and constipation.

Finally, the only contraindication for mydriatics and cycloplegics is that they should not be used in clients with narrow-angle glaucoma.

Okay, if a client with ophthalmic injury is prescribed a mydriatic and cycloplegic medication before an ophthalmologic procedure, start by assembling the sterile field and ensure the mydriatic and cycloplegic medication, as well as any other medications used in the procedure, are labeled with name, strength, amount, and expiration date. 

Before administrat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_for_antidiuretic_hormone_(ADH)_disorders:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X0YNU9yxT6i-d_UhQhpxtwxCShqFcj37/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for antidiuretic hormone (ADH) disorders: Nursing pharmacology]]></video:title><video:description><![CDATA[Antidiuretic hormone, or ADH for short, is the primary hormone that regulates fluid balance in the body, and is normally produced by the hypothalamus and stored in the posterior pituitary, which are both located within the brain. 

Now, ADH disorders arise when the pituitary releases too much or too little of it. These disorders include diabetes insipidus, which results from a decrease in ADH; and syndrome of inappropriate ADH secretion, or SIADH for short, which results from an increased secretion of ADH.

Okay, so on one end of the spectrum, there’s ADH deficiency, which causes diabetes insipidus. This disorder is treated with ADH replacement therapy, which involves medications like vasopressin, which is a synthetic form of ADH, and desmopressin, which is a vasopressin analogue.

Both medications can be administered subcutaneously. In addition, vasopressin can be administered intramuscularly, and desmopressin can be administered orally, intranasally, or intravenously. 

Once administered, these medications act on the kidneys by mimicking the actions of ADH, ultimately promoting the reabsorption of water at the distal convoluted tubule and collecting duct.

Now, these medications may cause side effects like headache, lethargy, and flushing. Other important side effects include nausea, vomiting, heartburn, and abdominal cramps. 

In addition, clients who take vasopressin may present with urticaria and vertigo. These medications also cause vasoconstriction, resulting in cardiovascular side effects. Clients on vasopressin may experience chest pain, and even myocardial infarction. 

On the other hand, clients taking desmopressin may develop hypertension, tachycardia, and palpitations. In addition, desmopressin may cause anaphylactic reactions. Finally, desmopressin can lead to water intoxication and hyponatremia, which can cause seizures and fatal brain dysfunction. 

Alright, now these medications are contraindicated in hyponatremia, and that’s a boxed warni]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiplatelet_agents:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/30b5MSRsS06O6VwYxRXOomJLTR_-Y-00/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiplatelet agents: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiplatelet agents are medications that are mainly used to treat and prevent thromboembolic events like ischemic stroke, transient ischemic attack, and coronary artery disease or myocardial infarction, as well as in clients who underwent cardiac valve replacement or coronary angioplasty, or those with peripheral artery disease.

Now, antiplatelet medications act by preventing the activation of platelets to form a blood clot. When platelets are activated, they start binding to each other. 

In addition, they release various activating substances, such as thromboxane A2 and adenosine diphosphate or ADP, to activate other platelets and make them express a new surface receptor called glycoprotein IIb/IIIa or GPIIb/IIIa. 

These receptors help platelets bind to circulating proteins called fibrinogen, which helps link various platelets together. 

When platelets attach to the same fibrinogen protein, they are linked together. This allows platelets to rapidly aggregate at the site of injury and form a platelet plug, which is a primary clot that can help stop the bleeding.  

Based on their mechanism of action, antiplatelet medications can be divided into four groups. These include NSAIDs like acetylsalicylic acid, often referred to as aspirin; ADP receptor antagonists like clopidogrel, prasugrel, and ticagrelor; phosphodiesterase inhibitors like dipyridamole and cilostazol; and glycoprotein IIb/IIIa inhibitors like abciximab, tirofiban, and eptifibatide.

Aspirin is given orally and works by irreversibly inhibiting the enzymes found within the platelets called cyclooxygenase or COX-1 and COX-2. These enzymes are involved in the production of molecules like thromboxane A2, as well as prostaglandins. 

So, in the presence of aspirin, platelets don’t produce thromboxane A2, resulting in impaired platelet plug formation. Moreover, since aspirin binds to the COX enzymes irreversibly, its actions last for the entire lifespan of the platelets, which is typically about ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticoagulants_-_Heparin:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A9Yvuf8TSC2Yc5J7-MhEdpHgSZejVdtm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticoagulants - Heparin: Nursing pharmacology]]></video:title><video:description><![CDATA[Anticoagulants are medications that work by interfering with the functional clotting factors in the coagulation cascade, and are used to prevent the formation of thrombi, or blood clots, and are used to prevent or treat thromboembolic events, such as deep vein thrombosis, pulmonary embolism, ischemic stroke, transient ischemic attack, coronary artery disease or myocardial infarction.  

They&amp;#39;re also used in clients with coagulation disorders, including antiphospholipid syndrome and disseminated intravascular coagulation; as well as in clients who underwent cardiac valve replacement or coronary angioplasty; and during surgical procedures like cardiopulmonary bypass, percutaneous coronary intervention, extracorporeal membrane oxygenation, and in clients undergoing dialysis. 

Among the most important anticoagulants are heparins. These include unfractionated heparin, which is derived from porcine sources, and can be administered intravenously or subcutaneously; as well as low molecular weight heparins or LMWHs, which are synthetic analogs of certain portions of the heparin molecule. These include enoxaparin, dalteparin, and tinzaparin, and are given subcutaneously. 

Once administered, heparins work by binding to and enhancing the activity of antithrombin III, which is an anticoagulant protein synthesized by the liver. Antithrombin III normally binds to and inhibits Factor Xa and Factor IIa, also known as thrombin, thus making them unavailable to participate in the coagulation cascade. Antithrombin III also inhibits factors VII, IX, XI, and XII, although with much less affinity. Ultimately, heparins stop the formation of the primary clot.  

Now, unfractionated heparin is usually used in immediate and short-term anticoagulation because it has a rapid onset of action, usually within seconds, and a short half-life. Additionally, unfractionated heparin doesn&amp;#39;t cross the placental barrier, making it the anticoagulant of choice during pregnancy. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_cholinergic_agents:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HMuZXwVzSHeIsbECwpt83uCkRniOG0xC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholinergic therapy (GU): Nursing pharmacology]]></video:title><video:description><![CDATA[Urinary cholinergic agents are a group of medications that can be used to treat urinary retention, which refers to the inability of a client to empty their bladder completely, or sometimes even at all. The most commonly used cholinergic agent is bethanechol.

Bethanechol can be administered orally, and it works on the bladder as a muscarinic agonist, ultimately stimulating the contraction of the detrusor muscle, which is a wall of smooth muscle that surrounds the bladder.

Unfortunately, clients taking a cholinergic agent may experience increased urinary frequency and urgency. Additional side effects commonly associated with cholinergic agents include headache, dizziness, blurred vision, and lacrimation. 

Clients may also develop a skin rash, urticaria, flushing, and diaphoresis. 

In addition, clients may experience hypersalivation, abdominal cramps, nausea, vomiting, diarrhea, and fecal incontinence. Some clients may also have bronchoconstriction, which can lead to dyspnea or asthma. 

The most severe side effects of cholinergic agents include hypotension, bradycardia, as well as reflex tachycardia, and even arrhythmias or cardiac arrest. Finally, cholinergic toxicity can be managed with the antidote atropine, which blocks muscarinic receptors.

As far as contraindications go, cholinergic agents should not be given to clients with genitourinary or gastrointestinal obstruction, as well as those with severe hypotension, bradycardia, or coronary artery disease. 

Additional contraindications include asthma or COPD, as well as parkinsonism or seizures. 

Finally, cholinergic agents should be used with caution during pregnancy and breastfeeding, as well as in children younger than 8 years, and in clients with hypertension. 

Now, when a client with urinary retention is prescribed a cholinergic agent like bethanechol, first ask them about their urinary symptoms; this includes hesitancy, an intermittent or slow stream of urine, and if they feel their bladder i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stimulant_medications_used_to_treat_attention-deficit_hyperactivity_disorder_(ADHD):_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5o25u1LlQ_W-CUpgKvPNam9ZRomeK6Cc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stimulant medications for attention-deficit hyperactivity disorder (ADHD): Nursing pharmacology]]></video:title><video:description><![CDATA[Attention Deficit Hyperactivity Disorder, or ADHD for short, refers to a range of behaviors characterized by inattention, hyperactivity, and impulsivity. Now, pharmacological treatment of ADHD can involve several medication groups, the main ones being central nervous system or CNS stimulant medications. 

Additional medication groups that can be used to treat ADHD include norepinephrine reuptake inhibitors, such as atomoxetine; and alpha 2 adrenergic agonists, like guanfacine. 

Finally, adjuvant medications include antidepressants, such as serotonin-norepinephrine reuptake inhibitors like venlafaxine, and tricyclic antidepressants, like imipramine; as well as antipsychotics, such as risperidone. 

Alright, now CNS stimulants include amphetamine, dextroamphetamine, lisdexamfetamine, and methylphenidate. All of them are taken orally, while methylphenidate can also be applied transdermally. 

Once administered, these medications are absorbed into the bloodstream, and travel to the brain. Here, they work at the synaptic cleft by inhibiting the reuptake of the neurotransmitters norepinephrine and dopamine. 

This results in an increased concentration of these neurotransmitters within the synaptic cleft, subsequently increasing focus and attention while decreasing impulsivity. 

Now, it’s important to note that CNS stimulants are highly addictive, therefore they have a boxed warning for potential abuse and dependence. In addition, these medications can often cause side effects like hyperactivity, irritability, insomnia, anorexia, and weight loss. 

Also, clients often develop tachycardia and palpitations, while some may present hypertension or even arrhythmias; in fact, some of these medications have a boxed warning for serious cardiovascular disease, such as myocardial infarction, and even sudden death. 

Finally, some clients may also experience headaches, dizziness, tremors, and on rare occasions, CNS stimulants can cause seizures. 

Now, CNS stimulants are ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticoagulants_-_Warfarin:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8leBCMyORrOmDhT-C5iYhUpJRaG2I8we/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticoagulants - Warfarin: Nursing pharmacology]]></video:title><video:description><![CDATA[Anticoagulants are medications that work by interfering with the function of clotting factors in the coagulation cascade, preventing the formation of thrombi, or blood clots. These medications are used to prevent or treat thromboembolic events, such as deep vein thrombosis, pulmonary embolism, ischemic stroke, transient ischemic attack, coronary artery disease or myocardial infarction. 

They&amp;#39;re also used in clients with coagulation disorders, including antiphospholipid syndrome and disseminated intravascular coagulation; as well as in clients who underwent coronary angioplasty or cardiac valve replacement; and during surgical procedures like cardiopulmonary bypass, percutaneous coronary intervention, extracorporeal membrane oxygenation, and in clients undergoing dialysis.

One of the most important anticoagulants is warfarin, which is given orally, and works as a vitamin K antagonist. 

Normally, vitamin K is used by the liver as a cofactor for the synthesis and activation of the clotting factors II, VII, IX, and X, as well as the anticoagulant proteins C and S. During this process, the active form of vitamin K, called vitamin K hydroquinone, is converted into vitamin K epoxide, which is then recycled back into vitamin K hydroquinone by another enzyme called epoxide reductase. 

Warfarin antagonizes the function of vitamin K by inhibiting the epoxide reductase enzyme and preventing vitamin K hydroquinone from getting recycled. As a result, there’s no synthesis and activation of the clotting factors II, VII, IX, and X, but also the anticoagulant proteins C and S. Out of all the vitamin K-dependent proteins, protein C has the shortest half-life so it is the first to be depleted in clients taking warfarin. This results in an initial period of hypercoagulation before the anticoagulant effect kicks in. To prevent this, bridging anticoagulation with LMWH is usually prescribed for a short period while starting warfarin therapy.

Now, the main side effec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Biologic_agents:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oVSR3B8yS0iD7ve7XTB0TSQLQueknQIJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Biologic agents: Nursing pharmacology]]></video:title><video:description><![CDATA[Biologic agents are a group of medications used to treat various inflammatory conditions, including rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, psoriasis, and Crohn’s disease. 

Now, biologic agents can be broken down into two main classes: tumor necrosis factor, or TNF blockers, which include etanercept, infliximab, and adalimumab; and interleukin inhibitors, which include interleukin- 1 or IL-1 inhibitors, like anakinra, interleukin- 6, or IL-6 inhibitors, like tocilizumab, and interleukin- 17A, or IL-17A inhibitors, like secukinumab.

These biologic agents are administered subcutaneously, and as their names suggest, the way they work is by inhibiting their respective inflammatory cytokines, so TNF, IL-1, IL-6, or IL-17A, ultimately preventing them from attaching to their receptors. 

As a result, these medications help suppress the immune response in clients with inflammatory conditions. 

Now, clients on biologic agents might develop a skin rash or injection site reactions, such as erythema, mild pain, and discomfort. 

A major side effect of biologic agents is bone marrow suppression, which can put the client at increased risk of infection. 

In fact, most TNF blockers have a boxed warning for the development of severe infections, such as tuberculosis, as well as lymphoma and other neoplastic diseases. 

Additionally, TNF blockers have been associated with headaches and demyelination of the nervous system, as well as myocardial infarction, heart failure, stroke, hypotension, and some clients may develop hypersensitivity reactions, such as Stevens Johnson syndrome or toxic epidermal necrolysis. 

In contrast, interleukin inhibitors might lead to arthralgia and gastrointestinal disturbances, such as nausea, vomiting, or diarrhea.

As far as contraindications go, biologic agents should be used with caution during pregnancy and breastfeeding, as well as in children and elderly clients. 

In addition, they are contraindicated in clie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_affecting_the_parathyroid_glands:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jFviwRfESWaUURyrTs93FOLpTgGe1BRf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications affecting the parathyroid glands: Nursing pharmacology]]></video:title><video:description><![CDATA[Parathyroid disorders affect the parathyroids, which are four small glands located on the thyroid gland. Now, the parathyroid glands produce parathyroid hormone, or PTH for short, in response to low levels of calcium in the bloodstream. So parathyroid disorders include hypoparathyroidism, which is characterized by a decrease in PTH, and hyperparathyroidism, which is characterized by an increase in PTH.

Let’s start with hypoparathyroidism, which is treated with the active form of vitamin D3 called calcitriol, which can be given orally or intravenously, as PTH replacement therapy. Once administered, calcitriol acts by binding to PTH receptors and mimicking the actions of PTH. These include promoting the absorption of calcium from the gastrointestinal tract, as well as promoting the reabsorption of calcium from renal tubules, and to a certain extent, releasing calcium from bones into the bloodstream. As a result, calcitriol causes an increase in blood calcium levels. This medication can also be given to treat secondary hyperparathyroidism or hypocalcemia associated with chronic kidney disease, as well as pseudohypoparathyroidism.

Now, the most common side effects of calcitriol include headache and drowsiness, as well as a dry mouth and a metallic taste. Clients can also experience abdominal pain, anorexia, nausea, vomiting, diarrhea or constipation. Calcitriol may also cause blurred vision and photophobia, as well as myalgia and arthralgia. Other important side effects include hypertension, arrhythmias, hypercalcemia, pancreatitis, and anaphylactic reactions.

Alright, now contraindications of calcitriol include hypercalcemia, hyperphosphatemia, and vitamin D toxicity, while precautions should be taken in clients with cardiovascular disease and renal calculi, as well as during pregnancy and breastfeeding.

In contrast, hyperparathyroidism is treated using calcitonin, which can be administered subcutaneously, intramuscularly, and intranasally. Once admi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiglaucoma_medications:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6QK3jtRRTo2wJmCQCs6hA81ZQTyJ2xSO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiglaucoma medications: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiglaucoma medications are used to treat glaucoma, which refers to a group of eye conditions in which drainage of aqueous humor out of the eye is restricted, causing an increased intraocular pressure.

Now, antiglaucoma medications can be divided based on their mechanism of action into two classes: those that decrease aqueous humor production, and those that increase aqueous outflow. 

Medications to decrease aqueous humor production include beta-adrenergic blockers, like timolol, levobunolol, and betaxolol; and carbonic anhydrase inhibitors, like brinzolamide and acetazolamide. 

On the other hand, medications to improve aqueous outflow include prostaglandin analogs, like latanoprost and bimatoprost; and cholinergic agents, like pilocarpine. 

Additionally, some medications can work by both decreasing the production and increasing the outflow of aqueous humor, including alpha-adrenergic agonists like brimonidine and apraclonidine. Finally, acute cases can be treated with osmotic diuretics, like mannitol. 

After administration, osmotic diuretics act as hyperosmotic agents by creating an osmotic gradient that attracts water out of the eyes and into the blood, to rapidly decrease intraocular pressure. 

Almost all medications are administered as eye drops, with the exception of acetazolamide and mannitol, which can be administered orally and intravenously.

Alright, now the most common side effects of antiglaucoma eye drops include blurred vision, eye redness, stinging, and itching following application. 

In particular, beta-adrenergic blockers cause neurological side effects like headache, depression, hallucination, and sleep problems, like insomnia and nightmares. 

Other side effects include hypotension, decreased cardiac output, and bradycardia, as well as bronchospasm leading to cough or dyspnea. 

On the other hand, carbonic anhydrase inhibitors may cause neurologic side effects, such as dizziness, drowsiness, and fatigue. 

Carbonic anhydrase inhi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-biologic_disease-modifying_antirheumatic_drug_(DMARD)_therapy:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l7JLUqQbQsGB-KPxm9IAf2V8RhiCfiDl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Non-biologic disease-modifying antirheumatic drug (DMARD) therapy: Nursing pharmacology]]></video:title><video:description><![CDATA[Nonbiologic disease modifying antirheumatic drugs, or DMARDs for short, are a group of medications primarily used to treat rheumatoid arthritis. The most commonly used ones are methotrexate, sulfasalazine, leflunomide, and hydroxychloroquine. Now, in addition to rheumatoid arthritis, most of these medications have other indications. So, methotrexate can be used to treat psoriasis and certain cancers. Sulfasalazine is also indicated for ulcerative colitis. Finally, hydroxychloroquine can be also used to treat malaria and systemic lupus erythematosus.  

Now, nonbiologic DMARDs can be administered orally, subcutaneously, intramuscularly, and intravenously. Once administered, they mainly work by inhibiting the immune response and suppressing inflammation.  

However, nonbiologic DMARDs can cause some notable side effects, such as bone marrow suppression, which can lead to conditions like anemia and leukopenia; as well as severe skin reactions and stomatitis, or painful mouth sores. Other general side effects include gastrointestinal disturbances, such as anorexia, nausea, vomiting, and diarrhea. In addition, the immunosuppressive effects of these medications can lead to an increased risk of developing infections and certain cancers. 

More specifically, methotrexate can also lead to pulmonary fibrosis, hepatotoxicity, and nephrotoxicity.Next, sulfasalazine can result in hypersensitivity reactions like anaphylaxis and orange discoloration of the urine; while important side effects of leflunomide include heart palpitations, hepatoxicity, and interstitial lung disease.  

Finally, hydroxychloroquine’s most common side effects are vision problems due to corneal or retinal damage. In addition, some clients may also experience neurological side effects, such as seizures, as well as cardiovascular side effects like heart failure, QT prolongation, and torsade de pointes.  

As far as contraindications go, these medications should not be used during pregnancy.   

Met]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_descending_spinal_cord_pathways</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ehSsVr4XShKQ0WKIBaLdjRz0QW6QCQ_g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the descending spinal cord pathways]]></video:title><video:description><![CDATA[The spinal cord is like a highway that enables two-way communication between the brain and the rest of the body. It contains neural pathways, called spinal cord pathways or tracts, which either ascend or descend depending on the information they are carrying. Both types of tracts are made up of neuronal axons that gather into long columns which are found inside the ventral, lateral and dorsal aspects of the spinal cord. The descending tracts are the motor pathways that tell various muscles in the body to contract, like when lifting a heavy weight.

Now, let’s start by looking at the anatomy of the spinal cord. Anteriorly, there is a deep midline depression called the ventral median fissure and, posteriorly, there is a more shallow midline depression called the dorsal median sulcus.  Each half also has a ventrolateral sulcus, where ventral rootlets leave the spinal cord; and a dorsolateral sulcus, where dorsal rootlets enter the spinal cord. The ventral and dorsal rootlets fuse to form the ventral and dorsal roots, respectively Ventral rootlets and roots carry motor fibers that travel from the spinal cord to different organs and muscles, while their dorsal counterparts - with a sensory ganglion, called the dorsal root ganglion, attached to each dorsal root - carry sensory fibers from organs and receptors throughout the body to the spinal cord. 

Now, on a transverse section, the spinal cord has an area of gray matter shaped like a capital “H” in the middle. The gray matter is subdivided into the gray commissure, which is the strip connecting the two halves of the spinal cord that surrounds the central canal; and the peripheral regions known as horns. There are two ventral, and two dorsal horns. Dorsal horns contain neuronal cell bodies that process information received from sensory fibers, entering the spinal cord from the dorsal roots and dorsal rootlets. On the other hand, the ventral horns contain cell bodies of motor neurons, with motor fibers,exiting t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Aminoglycosides:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9hVj9xNdS__b27NbQJIm9oCSQkyoHXUb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Aminoglycosides: Nursing pharmacology]]></video:title><video:description><![CDATA[Aminoglycosides are a class of antibiotics used to treat severe systemic infections caused by aerobic, Gram negative bacteria, such as Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and the Enterobacter species. 

Additionally, aminoglycosides can be effective against certain Gram positive bacteria when used in combination with cell-wall inhibitors, like penicillins or cephalosporins. 

Now, aminoglycoside antibiotics used to treat bacterial infections include streptomycin, amikacin, gentamicin, tobramycin, and neomycin. These medications are poorly absorbed in the gastrointestinal tract, so they are primarily administered intramuscularly or intravenously. 

Streptomycin and amikacin can be used in the treatment of mycobacterial infections. Gentamicin can also be applied topically to treat eye or ear infections; while tobramycin can be given topically to treat eye infections, or in a nebulized form to treat Pseudomonas infections in clients with cystic fibrosis. 

Neomycin can be given orally to treat hepatic encephalopathy and before colorectal surgeries to act directly in the intestinal bacterial flora and reduce the risk of infection after surgery.

Aminoglycosides are powerful bactericidal antibiotics that work by binding to the 30S subunit of the bacterial ribosome. As a result, these medications disrupt bacterial protein synthesis and ultimately kill the bacteria. 

Since aminoglycosides need to enter the bacteria in order to be effective, they may be given alongside an antibiotic that inhibits bacterial cell wall synthesis, such as beta-lactams, to facilitate access of the aminoglycoside across the cell wall.

Regarding side effects, one thing to keep in mind is that aminoglycosides have a significant post-antibiotic effect, meaning that their bactericidal activity persists for a period of time even after the antibiotic is stopped. 

In addition, although aminoglycosides are very effective antibiotics, they also have a high risk of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiprotozoals:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ktzCLQboR1GYSUFjgdv2UFNSSGCPaxIh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiprotozoals: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiprotozoals are a group of medications used to treat protozoal infections, such as giardiasis, trichomoniasis, or intestinal amebiasis.

The most commonly used antiprotozoals are atovaquone, tinidazole, benznidazole, pyrimethamine, and nitazoxanide, which can be taken orally; as well as pentamidine that can be administered by nebulizer, intramuscularly, or intravenously. 

Once administered, antiprotozoals act on protozoa by blocking DNA synthesis, preventing them from reproducing, and ultimately killing them.

Side effects typically include headaches, dizziness, peripheral neuropathy, ataxia, and loss of coordination. Some clients may also develop a skin rash or urticaria. 

In addition, antiprotozoals may often cause gastrointestinal disturbances, such as an unpleasant mouth taste, nausea, vomiting, diarrhea, and cramping. 

Moreover, these medications can disrupt the normal intestinal flora, so clients might develop bacterial or fungal superinfections. 

Finally, some of these medications can be associated with hematologic abnormalities, such as leukopenia, anemia, or thrombocytopenia; while tinidazole has a boxed warning for increasing the risk of developing malignancy.

Now, antiprotozoals are contraindicated during pregnancy and breastfeeding, while precautions should be taken with children and elderly clients. 

In addition, these medications should also be used with caution in clients with hematologic or central nervous system disorders, as well as in those with cardiac, renal, or hepatic disease, and alcoholic beverages should be avoided.

Okay, when caring for a client with giardiasis who has been prescribed tinidazole, first obtain a baseline of your client’s symptoms, such as fatigue, stomach pain and cramping, as well as stool characteristics and frequency. 

Then, assess for signs of dehydration, such as decreased urine output, dark yellow urine, or decreased skin turgor. 

Lastly, review their most recent laboratory test results, includin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_and_learning_disorders:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KY7c_l-bQimuPg7sHXSJr8DcSXCGPW3m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developmental and learning disorders: Pathology review]]></video:title><video:description><![CDATA[A 9 year old male, named Yama, is brought to the clinic by his mother, who is concerned about Yama’s behavior. She explains that his teacher has repeatedly complained about yama constantly disrupting the class and interrupting his classmates. In addition, Yama also seems to struggle paying attention to his teacher and constantly forgets to do his assignments. At home, Yama seems to find it hard to sit still, and often disregards anything his parents tell him. Yama’s mother estimates this behavior started about 8 months ago, and she thought it would just be a phase. During the visit, you notice that Yama seems restless and is constantly grabbing objects around him.

Okay, based on the initial presentation, yama seems to have some form of developmental and learning disorder. Now, everyone develops at slightly different paces, but almost everyone hits the same general developmental milestones and learns the same sets of skills at about the same time. These are things like language and communication, socializing, cognitive skills like problem solving, and physical milestones like walking, crawling, and fine motor skills, all of which all progress as the brain develops. 

If one of these doesn’t develop as scheduled, it may be described as a type of developmental and learning disorder. 

These include several psychological conditions that typically have their onset during childhood, although some of these disorders may last into adulthood. As a consequence, these disorders can interfere with how the affected person functions independently in society, and impair everyday activities like working, studying, eating, and sleeping, as well as have an impact on their families. 

For your exams, the most high yield developmental and learning disorders are autism spectrum disorder, rett syndrome, intellectual disability, specific learning disorder, and attention deficit hyperactivity disorder. 

Okay, let’s start with autism spectrum disorder. For your exams, remember t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Eye</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9fQ7uDbxSeq8o93MhIL18D-5QtSWbd0t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Eye]]></video:title><video:description><![CDATA[The eyes enable us to see trees of green, red roses too… and basically everything in the wonderful world around us. From an anatomical perspective, the eyes are sensory organs, and they’re protected by a hard bony casing called the orbit, and shielded from the outside environment by softer tissues like the eyelids. Unfortunately, all of these structures are prone to various diseases - but luckily, understanding eye anatomy can help us recognize and treat these conditions!  

Let’s start with the eyelids. Remember that they’re controlled by a muscle called the orbicularis oculi, which is a ring of muscles with two different parts that are arranged in circumferential bands around the orbit. The outer and thicker ring is the orbital part, while the thinner part that lies nearer to the eyelids is known as the palpebral part. The orbicularis oculi muscles are innervated by the facial nerve, and when they contract, they bring the eyelids together to close the eye for protection. So with a facial nerve lesion, the function of the orbicularis oculi muscle is affected, which impairs the muscle’s ability to close the eyelids. First, this means that blinking and moisturizing the front of the eye with lacrimal secretions is impaired, so the cornea can dry out. Then, there is also the added risk of foreign bodies entering the eye due to impaired blinking, for example sand blowing into our face during a windstorm. Abrasions and infections can then result which can ultimately lead to corneal ulceration. 

Now, the eye can also be subject to infection even if the eyelids are working properly. One of the most common ones is hordeolum - usually referred to as a “stye”. This is an abscess of the eyelid, typically presenting as localized erythematous and painful swelling on the eyelid. A hordeolum can be external, which is when it arises from either the gland of Zeis or the gland of Moll which both secrete sebum in the eyelash follicle on the margin of the eyelid. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Ear</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-JQmCRVESHC9Sl8-oMqu-Y-zTaWkJgsP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Ear]]></video:title><video:description><![CDATA[The ear has many roles, from hearing and maintaining balance, to showing off jewelry and piercings. But just like the rest of our body, there are a variety of conditions that can affect them, so understanding the anatomy of the ear can help us better understand the clinical conditions that affect it! 

Let’s start with the auricular hematoma, also known as a cauliflower or boxer’s ear. You may have guessed from its name - this condition is most common in professional boxers and wrestlers. Boxer’s ear is a deformity caused by blunt trauma to the auricle, in which blood accumulates between the perichondrium and auricular cartilage, resulting in a hematoma. If left undrained, fibrosis can develop in the overlying skin which causes deformity of the auricle. This results in the auricular deformity known as the cauliflower or boxer’s ear. 

Next up, let&amp;#39;s look at ear pain. The ear receives cutaneous innervation from multiple nerves of the head and neck which makes it prone to referred pain. This is called secondary otalgia, which means that the ear perceives pain when the primary issue is in another anatomical site. 

Now, the majority of the external auditory canal innervation comes from the auriculotemporal nerve, which is a branch of the trigeminal nerve. It provides sensory innervation to the anterior portion of the preauricular skin, anterior auricle, and the anterior portions of the external auditory canal. Conditions such as dental infections, maxillary sinusitis, as well as temporomandibular joint disease can cause referred pain in these parts of the ear. 

Along with the auriculotemporal nerve innervating the ear, a small auricular branch of the vagus nerve and parts of the glossopharyngeal nerve go on to innervate a small portion of the posterior external auditory canal and tympanic membrane. As these two nerves also innervate portions of the pharynx and larynx, pathologies irritating these areas can be referred to the ear. Examples ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Leg_and_ankle</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2GfgDz5VRa_nPE-E9tuoNN1bTeKQn97k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Leg and ankle]]></video:title><video:description><![CDATA[When it comes to the clinical correlates of the leg and ankle, there is so much more than just rolling our ankle or banging our shin bone. There are a variety of clinical conditions that affect these structures, and it&amp;#39;s not until these conditions occur that we remember the importance of our lower limbs. So we hope you get a kick out of this video learning the clinical conditions affecting the leg and ankle! 

First up, let’s discuss tibial nerve injury. The tibial nerve is the medial and larger branch of the sciatic nerve, and it often splits from the common fibular nerve at the apex of the popliteal fossa, eventually dividing into the medial plantar nerve and lateral plantar nerve which provide motor and sensory information to the foot.

Tibial nerve injuries can occur either proximally, at the popliteal fossa, or distally at the tarsal tunnel which is more common. Injury at the popliteal fossa is rare as the nerve is protected deep within soft tissue at this level. Mechanisms that may cause injury at the popliteal fossa are deep penetrating trauma, knee surgery, compression from a tumor or a Baker&amp;#39;s cyst, and posterior knee dislocation. 

An injury at the popliteal fossa affects the innervation of both the lower leg and the foot. Individuals can present with weakness in plantarflexion, inversion, and toe flexion of the foot, due to decreased innervation to the muscles in the deep compartments of the lower leg. Additionally, those affected can present with their foot in a calcaneovalgus position, or more simply in dorsiflexion and eversion. Injury at this level also impairs innervation to the intrinsic muscles of the foot and can also cause paresthesia to the sole of the foot. 

On the other hand, there are distal tibial nerve injuries, most commonly at the tarsal tunnel. Distally the tibial nerve passes through the tarsal tunnel, between the medial malleolus and calcaneus deep to the flexor retinaculum. Injury at the tarsal t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Foot</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6RiDxP9ORgyF11v7AJfnuhjPRAaOGBLm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Foot]]></video:title><video:description><![CDATA[The foot is the most distal part of our lower limbs - and while it represents only a small part of the body, its unique structure allows for walking, running, and dancing, but is also an unfortunate vulnerable point for being tickled. 

Laughing aside, let&amp;#39;s kick off this video which will focus on the clinical conditions affecting the foot. 

First, let&amp;#39;s talk about plantar fasciitis. Plantar fasciitis describes inflammation of the deep plantar fascia, also called the plantar aponeurosis. The deep plantar fascia is a thick, pearly-white band of tissue that attaches to the medial process of the calcaneal tuberosity and extends to the toes and supports the medial longitudinal arch of the foot. 

Excessive training, particularly those who frequently run, jog, or walk, 

can cause repetitive microtrauma.  

This leads to inflammation of the plantar fascia particularly at its attachment point to the calcaneus. 

Additionally, individuals who undergo high impact exercise like jumping in volleyball or frequently train in bare feet may also experience plantar fasciitis. 

Risk factors for plantar fasciitis include obesity, prolonged standing or working on hard surfaces, and pes planus, which is “flat feet” defined by the loss of the medial longitudinal arch of the foot where it contacts the ground

Diagnosis of plantar fasciitis is often clinical, and it commonly presents in middle aged adults. Individuals typically present with unilateral or bilateral heel pain that is worse in the morning and after prolonged rest, and gradually lessens with activity. 

The pain is typically palpated over the medial process of the calcaneal tuberosity, 

but can be felt along the length of the sole of the foot, 

while pain can also be felt on passive dorsiflexion of the toes. 

Heel spurs often coexist with plantar fasciitis, but it is also unclear whether they can cause plantar fasciitis, or represent a secondary response to an inflammatory]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Anterior_blood_supply_to_the_brain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3ALpauKzQ4yBInaDmwG0n-giQX2_O1Q_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Anterior blood supply to the brain]]></video:title><video:description><![CDATA[Your brain is awake and working hard all day, every day, even when you’re sleeping! So it makes sense that it needs a lot of oxygen and energy, which is why it is well supplied from several major arteries. The circulation of the brain can ultimately be divided into the anterior and posterior circulation, and understanding their anatomy can help us understand the clinical consequences and management of various issues that can arise! So let’s delve into the anterior circulation of the brain!

Remember that the anterior circulation supplies the anterior portion of the brain, and comes from the internal carotid arteries which divide into the anterior and middle cerebral arteries. The anterior circulation then connects to the posterior circulation through the posterior communicating arteries. The posterior circulation comes from the vertebral arteries, which combine to form the basilar artery. Together, the connection between the anterior and posterior circulation form the circle of willis, which is an anastomotic network of arteries at the base of the brain which ensure adequate blood flow to the brain, even in cases where part of this circulation becomes occluded! However, there are still instances where obstruction of these arteries and their branches disrupts blood flow to the brain, causing a stroke, which can lead to irreversible neuronal damage.

Now, a stroke can be classified as either ischemic or hemorrhagic. Ischemic strokes are much more common, and they happen because of an acute blockage of one of the blood vessels supplying the brain. Ischemic strokes can be thrombotic, embolic or hypoxic. A thrombotic stroke occurs when there’s a blood clot in the artery, formed directly at the site of infarction, which typically occurs because of a ruptured atherosclerotic plaque. An embolic stroke, on the other hand, is where an embolus from another part of the body travels to the site of infarction to cause obstruction. For example, with atrial fibrillation, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_clinical_correlates:_Posterior_blood_supply_to_the_brain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hOByoVpARSutITB7BchUpsHLTRuJXYgQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy clinical correlates: Posterior blood supply to the brain]]></video:title><video:description><![CDATA[Blood supply to the brain can be divided into an anterior and a posterior circulation. The posterior circulation supplies the cerebellum, brainstem, occipital lobes, and inferomedial temporal lobes, and comes from the vertebral arteries.  The vertebral arteries combine to form the basilar artery, which eventually divides into the posterior cerebral arteries. The posterior circulation then connects to the anterior circulation through the posterior communicating arteries. Remember that the anterior circulation comes from the internal carotid artery which divides into the anterior and middle cerebral arteries. Together, the connection between the posterior and anterior circulation form the Circle of willis, which is an anastomotic network of arteries at the base of the brain that ensure adequate blood flow even in cases where part of this circulation becomes occluded! However, there are still instances where obstruction of these arteries and their branches can disrupt blood flow to the brain, so understanding their anatomy and what parts of the brain they nourish can help us better understand the clinical manifestations and management. 

When blood flow to the brain is obstructed, that causes a stroke, which can be either ischemic or hemorrhagic. Ischemic strokes can be caused by thrombi, emboli, and hypoperfusion injuries, with the latter most commonly affecting the watershed areas of the brain. Hemorrhagic strokes, on the other hand, occur when there is a bleed within the brain tissue called an intracerebral or intraparenchymal hemorrhage, or a bleed in the subarachnoid space called a subarachnoid hemorrhage. The posterior circulation of the brain is susceptible to all of these, and the clinical signs and symptoms depend on which artery is occluded.

Let’s look at the vertebral arteries first, starting with the subclavian steal phenomenon. This is when the vertebral artery on the same side as an occluded, or blocked subclavian artery “steals” blood from the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Penile_conditions:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/omO825KEQ1GJtSiHTBs0TyrWRSaRbAD7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Penile conditions: Pathology review]]></video:title><video:description><![CDATA[Jacob is a 32 year old male who comes to the emergency department because of a painful, sustained erection, which has lasted five hours now. Upon further questioning, Jacob tells you that he takes antidepressant medications. You immediately order a penile arterial blood gas analysis, which reveals decreased concentration of oxygen, increased concentration of carbon dioxide, and decreased arterial pH. 

Next you see Tafari, a 55 year old male of African descent. Tafari is worried because he developed a lesion on the glans penis about six months ago, and it won’t go away. Upon physical examination, you notice that the lesion looks bright red and has well-defined borders. Finally, you decide to perform an excisional biopsy to remove and analyze the lesion.

Okay, based on the initial presentation, both Jacob and Tafari seem to have some form of penile condition. 

Now, the penis is made of three long cylindrical bodies: the corpus spongiosum that surrounds the penile urethra, and the two corpora cavernosa that are made of erectile tissue. The corpora cavernosa are wrapped in a fibrous coat called the tunica albuginea, and each corpus cavernosum is made up of blood-filled spaces called the cavernosal spaces. These spaces are lined with endothelial cells surrounded by smooth muscle. Running down the center of each corpus cavernosum is a large artery called the deep artery, which gives off smaller arteries that supply the cavernosal spaces. Next, blood gets drained from these spaces by small emissary veins, which drain into the deep dorsal vein. This vein then carries the blood back into the systemic circulation. 

Now, for your exams, some high yield penile conditions you must absolutely remember include Peyronie disease, priapism, and squamous cell carcinoma of the penis.

Let’s start with Peyronie disease, which refers to an abnormal curvature of the penis. For your exams, make sure you don’t confuse this disease with a penile fracture, where penile injury ma]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testicular_and_scrotal_conditions:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pPO5H_eYRMyQc9yZGpBCu0tqSHq7wXyD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Testicular and scrotal conditions: Pathology review]]></video:title><video:description><![CDATA[In the middle of the night, a 16 year old male named Shane is brought to the emergency department by his parents after waking up with severe pain in his right scrotum. Shane does not recall any traumatic events prior to the onset of his symptoms. On physical examination, the scrotum appears swollen; in addition, you notice that the pain is worsened with elevation of the scrotum, and stroking of the right inner thigh does not result in elevation of the right testis. 

Later that day, you meet a 28 year old male called Elias, who comes in for a fertility evaluation. Elias and his wife have been trying to conceive for two years without success. Recently, Elias has also noticed an enlargement and a feeling of pressure in his left scrotum. On physical examination, you palpate a mass along the spermatic cord that feels like a “bag of worms”. 

Based on the initial presentation, both Shane and Elias seem to have some form of testicular and scrotal condition. Now, for your exams, remember that the testes begin their development in the abdominal cavity, within the peritoneum. During the third trimester of pregnancy, the testes usually begin to descend into the pelvis via the inguinal canal, and ultimately settle in the scrotum. This needs to occur because sperm can&amp;#39;t survive at body temperature, and that’s a high yield fact! 

Now, as the testes gradually migrate, a peritoneal outpouching called the processus vaginalis forms, and pulls the layers of the anterolateral abdominal wall with it into the developing scrotum. The testes then follow the processus vaginalis into the scrotum. After the testes have descended to the scrotum, the processus vaginalis closes up. Within the scrotum, each testis remains partially covered by an extension of the peritoneum, which forms a serous layer called the tunica vaginalis. The only part that’s not covered by the tunica vaginalis is where the testes are attached to the epididymis and spermatic cord. 

Now, the epididymis]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_of_the_vagus_nerve_(CN_X)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DmheOqk2Sa29--oXx-sH6nwWR4WJ9WCn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy of the vagus nerve (CN X)]]></video:title><video:description><![CDATA[The vagus nerve is the tenth cranial nerve, and its name comes from the latin word vagary, which means indefinite or wandering. 

This actually reflects its wide distribution seeing as the vagus nerve is the most extensively distributed cranial nerve; in fact, it innervates structures all the way from the head and neck to parts of the digestive tract! 

The vagus nerve has multiple functions such as somatic, visceral and special sensory innervation, as well as somatic and visceral motor innervation.

Now, the vagus nerve emerges from the lateral medulla through a group of rootlets that join and leave the cranium through the jugular foramen along with cranial nerves 9 and 11, or the glossopharyngeal and spinal accessory nerves. 

Both left and right vagus nerves leave the cranium through the jugular foramen on their respective sides, and penetrate the carotid sheath. 

Then, they descend within the carotid sheath, posterior to the common carotid artery and medial to the internal jugular vein. From here, each vagus nerve takes a different course as they enter the thorax. 

The right vagus nerve crosses the right subclavian artery anteriorly, runs posterior to the superior vena cava and descends posterior to the right main bronchus to contribute to the cardiac, pulmonary and esophageal plexuses. 

When it reaches the lower part of the esophagus, it forms the posterior vagal trunk and then enters the abdomen through the esophageal hiatus of the diaphragm. 

The left vagus nerve, on the other hand, enters the thorax between the left common carotid artery and the left subclavian artery and descends on the aortic arch. 

Then, it runs posterior to the left main bronchus, contributing to the cardiac pulmonary and esophageal plexuses, and finally it continues to form the anterior vagal trunk,  and enters the abdomen through the esophageal hiatus.

 In the abdomen, the vagal trunks terminate by dividing into branches that contribute to various plexuses which supply ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiarrhythmics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x9us5mibScOTg8kqy_9sODlRQduCPKKb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiarrhythmics: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiarrhythmics, also called antidysrhythmics, are a class of medications that help control arrhythmias or abnormal heartbeats, such as supraventricular tachycardia, ventricular tachycardia and ventricular fibrillation.

In general, antiarrhythmics act by altering electrical conduction pathways through the heart, and can be administered orally, intravenously, or intramuscularly. Now, based on their mechanism of action, they can be divided into four main classes. 

Class I antiarrhythmics are sodium channel blockers that inhibit sodium influx into cardiac cells, and can be further subdivided into three groups depending on how they affect conduction and repolarization. Class IA antiarrhythmics, such as quinidine and procainamide, act by slowing conduction and prolonging repolarization. Class IB, like lidocaine and mexiletine, also act by slowing conduction, but they shorten repolarization. And class IC, such as flecainide and propafenone, prolong conduction but have no effect on repolarization. 

Next, class II antiarrhythmics are beta-blocker medications, and include propranolol, esmolol, sotalol, and acebutolol. These medications act by preventing the catecholamines norepinephrine and epinephrine from binding and activating them; ultimately decreasing heart contractility and slowing the conduction through the atrioventricular or AV node. 

Moving onto class III antiarrhythmics, these are potassium channel blockers. The most important drug in this class is amiodarone, which acts by inhibiting potassium efflux from cardiac cells, ultimately prolonging repolarization and action potential duration. 

Finally, class IV antiarrhythmics are calcium channel blockers, and include verapamil and diltiazem. These medications block calcium influx into cardiac cells, which ultimately helps decrease heart contractility and slow conduction velocity. 

Unfortunately, antiarrhythmics can have several side effects. First of all, they can surprisingly cause arrhythmias! Addit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Insulin:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0TcQf76VRPSjjh9X7MSG1Mg7RdmLmqr7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Insulin: Nursing pharmacology]]></video:title><video:description><![CDATA[Insulin is a medication used to treat clients with diabetes mellitus. Now, there are two main types of diabetes mellitus. Type 1 diabetes mellitus arises when the pancreas is unable to produce insulin in order to maintain normal blood glucose levels. 

On the other hand, type 2 diabetes mellitus is characterized by insulin resistance, which is when tissue cells have trouble responding to insulin in order to use glucose from the blood; as a result, tissue cells starve for energy despite having high blood glucose levels, which is called hyperglycemia. 

Insulin is also used in the management of gestational diabetes, diabetic complications, like diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic coma, as well as in hyperkalemia. 

Now, there are five main categories of insulin based on their onset of action and duration of effect. These include rapid-acting, short-acting or regular, intermediate-acting, long-acting, and ultra long-acting insulins. 

All categories of insulin can be given subcutaneous injection or through an insulin pump, while the short-acting insulin can also be given intravenously. 

Now the short-acting, or regular, insulin starts working 30 minutes after administration, with a peak effect at 2 to 3 hours, and can last between 6 to 8 hours. 

Next, there’s rapid acting insulins which include insulin aspart, lispro, and glulisine. These medications begin working within 5 to 15 minutes of administration, with a peak effect at 30 minutes, and may last for 3 to 5 hours. Another rapid acting insulin is inhaled insulin, which can only be used as an adjunct to therapy with injected insulins, and never by itself. 

Next up is the intermediate-acting insulin, known as neutral protamine hagedorn or NPH insulin. NPH insulin only becomes active around 1 to 2 hours after administration, with a peak effect after 4 hours, and lasts for 16 to 24 hours.  

Moving on, we have the long-acting insulins, which include insulin glargine and detemir.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antihyperlipidemics_-_Fibrates:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g7NTZTNhSgSEFEeeZlzTLvSnTseGylMk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antihyperlipidemics - Fibrates: Nursing pharmacology]]></video:title><video:description><![CDATA[Antihyperlipidemics are medications used to treat clients with dyslipidemia, which refers to increased blood levels of lipids, such as cholesterol and triglycerides. In addition, they’re indicated to treat clients with coronary artery disease and prevent myocardial infarction. Antihyperlipidemics include different classes of medications, among which some of the most commonly used are fibrates.

Now, fibrates include gemfibrozil and fenofibrate, which are administered orally. Once absorbed into the bloodstream, fibrates work by activating an intranuclear receptor called PPARα, or peroxisome proliferator-activated receptor alpha, a major regulator of lipid metabolism.

When activated by fibrates, PPARα causes adipose tissue cells to produce more lipoprotein lipase, increasing lipolysis and lowering triglyceride levels. 

Fibrates also increase the synthesis of HDL, which is sometimes referred to as “good” cholesterol; however, they aren’t very effective at decreasing the levels of low-density lipoproteins or LDL, which is sometimes referred to as “bad” cholesterol. 

Therefore, they can be combined with other antihyperlipidemics, such as statins, to treat clients with mixed dyslipidemia, where both triglyceride and cholesterol levels are elevated.

Okay, the most common side effects of fibrates include gastrointestinal disturbances like dyspepsia and diarrhea. In addition, fibrates decrease the conversion of cholesterol into bile acid, which promotes the formation of gallstones, potentially leading to serious side effects like cholelithiasis and pancreatitis. 

Clients taking fibrates may also develop a skin rash, urticaria, and pruritus. Fibrates can also cause rhabdomyolysis, and the risk increases when combined with medications like certain statins or colchicine. 

Fatigue, dizziness and headache are also common, especially with fenofibrate. Finally, clients taking gemfibrozil may develop pancytopenia and eosinophilia.

Now, fibrates are contraindicated i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Plant_extracts_for_chemotherapy:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FbVWdMx7SAK9D3Z1yvxdk5zCTqG-oeSo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Plant extracts for chemotherapy: Nursing pharmacology]]></video:title><video:description><![CDATA[Plant extracts used for chemotherapy are medications obtained from plants that can be used to treat various types of cancer, including leukemia and lymphoma, as well as rhabdomyosarcoma, neuroblastoma, and Wilms’ tumor.

These medications can be broadly divided into vinca alkaloids, which includes vinblastine, vincristine, and vinorelbine; taxanes, which include docetaxel and paclitaxel; podophyllotoxins, such as etoposide and teniposide; as well as retinoids like bexarotene; and angiogenesis inhibitors like thalidomide.

All of these medications can be administered intravenously, and etoposide can be taken orally too. Once administered, these medications stop the replication of the rapidly dividing cancer cells, and ultimately cause their death.

Unfortunately, plant extracts also act on healthy rapidly dividing cells, including those in the skin, bone marrow, and gastrointestinal tract. As a result, these medications can often cause several side effects, such as alopecia, skin rash, and photosensitivity, as well as nausea, vomiting, diarrhea, constipation, and even gastrointestinal bleeding. 

Additionally, some clients may experience vesication, phlebitis, and there’s a boxed warning for extravasation, which can cause tissue necrosis. 

A very dangerous complication is tumor lysis syndrome, where rapidly killing large numbers of tumor cells results in severe metabolic and electrolyte abnormalities. Another very important side effect is myelosuppression, which can lead to pancytopenia.

In fact, vinorelbine, docetaxel, and paclitaxel have a boxed warning for severe neutropenia; while taxanes and podophyllotoxins have a boxed warning for bone marrow suppression, as well as hypersensitivity reactions, such as Stevens Johnson syndrome, toxic epidermal necrolysis, and anaphylaxis. 

Plant extracts can also cause hepatotoxicity, which is a boxed warning for taxanes. On the other hand, vincristine and vinorelbine can also cause neurotoxicity, which may result ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antihyperlipidemics_-_Statins:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-x43U0i7RIiv31mCGmPB_eVrQoO0fGwo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antihyperlipidemics - Statins: Nursing pharmacology]]></video:title><video:description><![CDATA[Antihyperlipidemics are medications used to treat clients with increased blood levels of lipids, like cholesterol, by decreasing the levels of low- density lipoproteins or LDLs, which is sometimes referred to as “bad” cholesterol; and to an extent, antihyperlipidemics can also decrease blood triglycerides. 

In addition, they’re indicated to treat clients with coronary artery disease and prevent myocardial infarction. 

Antihyperlipidemics include different classes of medications, among which some of the most commonly used are HMG-CoA reductase inhibitors, also called statins. 

Statins include simvastatin, rosuvastatin, atorvastatin, lovastatin, and pravastatin, which are administered orally. 

Once absorbed into the bloodstream, statins travel to the liver, where they inhibit the enzyme HMG-CoA reductase. As a result, there’s a decrease in cholesterol synthesis. This also causes hepatic cells to increase the number of LDL receptors on their surface. 

This facilitates the uptake of cholesterol-rich LDLs, and VLDLs to a smaller degree, which provides a moderate decrease in triglyceride level. So ultimately, statins help lower overall lipid levels.

Luckily, statins are very well tolerated. The most common side effects include gastrointestinal symptoms like abdominal cramps, diarrhea or constipation, flatulence, heartburn, and nausea. 

Especially with rosuvastatin, clients can develop a skin rash, and may experience headache and dizziness. Other side effects include blurred vision, cataracts, fatigue, and insomnia. 

Some of the more serious side effects of statins include myalgia, and rhabdomyolysis, or muscle breakdown. 

Next, although rare, statins can cause hepatotoxicity, especially in clients who already have a hepatic disease. Finally, simvastatin and atorvastatin can cause pancreatitis, while rosuvastatin can cause renal failure, and pancytopenia.

As far as contraindications go, statins are teratogenic, so they should be avoided during pregnancy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Cyclic_lipopeptides:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0BuKFmNHQgi7D_G6Ogwh3vfKRtC2lV3Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Cyclic lipopeptides: Nursing pharmacology]]></video:title><video:description><![CDATA[Cyclic lipopeptides are a new class of antibiotics used to treat complicated infections caused by gram-positive bacteria like Staphylococcus epidermidis, Staphylococcus haemolyticus, and Staphylococcus aureus, especially the methicillin-resistant type called MRSA, as well as Streptococcus agalactiae, Streptococcus pyogenes, and Enterococcus faecalis. 

It is also used in bacteremia caused by Staphylococcus aureus, and infective endocarditis caused by MRSA. 

Currently, there is only one approved medication in this class, called daptomycin, which is given intravenously or intrathecally. 

Once administered, it works by binding to the bacterial membrane and perforating it, creating holes that leak ions, causing rapid depolarization. 

This ultimately leads to inhibition of bacterial DNA, RNA, and protein synthesis, which in turn results in bacterial cell death.

Common side effects of daptomycin include headache, dizziness, insomnia, and hypo- or hypertension. 

Clients might also experience gastrointestinal side effects, such as abdominal pain, nausea, vomiting, and diarrhea. 

In addition, daptomycin may disrupt the healthy intestinal flora, which can allow certain bacteria like Clostridioides difficile to survive and overgrow within the gastrointestinal tract, rarely but potentially leading to Clostridioides difficile infection or CDI for short. 

Other side effects include pain or burning with urination, as well as skin manifestations like rash, itching, and pallor, while some clients may also experience numbness and tingling from peripheral neuropathy. 

Other serious side effects include eosinophilic pneumonia, nephrotoxicity, anemia, myopathy and rhabdomyolysis with or without renal failure, and hypersensitivity reactions like angioedema or anaphylaxis.

Now, daptomycin should be used with caution during pregnancy and breastfeeding, as well as in children and elderly clients. 

Precaution should be taken in clients with eosinophilic pneumonia, as well]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Metronidazole:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lbNS9go6RWy8aLwPOCSuwgBnQZi1a_G-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Metronidazole: Nursing pharmacology]]></video:title><video:description><![CDATA[Metronidazole is an antibiotic used to treat many conditions caused by anaerobic bacteria or protozoans. Some bacterial infections include septicemia, endocarditis, and infections involving bone, joint, and the lower respiratory tract. 

For these bacterial infections, metronidazole is administered intravenously. Metronidazole is also used to treat rosacea, for which it’s administered topically. 

Finally, metronidazole is also used orally or topically to treat bacterial vaginosis; and it is used to treat protozoal infections, including amebiasis, trichomoniasis, and giardiasis, for which it’s given orally.

Now, once administered, metronidazole gets inside anaerobic bacteria and protozoans, and produces free radicals, which damage the pathogen’s DNA. 

Without the DNA as a template, the pathogen can’t synthesize any more nucleic acids like DNA or mRNA, and will ultimately die.

Common side effects of metronidazole include headache, dizziness, and gastrointestinal disturbances like abdominal cramps, anorexia, nausea, vomiting, and diarrhea. 

In addition, metronidazole may allow certain bacteria like Clostridioides difficile to survive and invade the gastrointestinal tract, rarely but potentially leading to Clostridioides difficile infection or CDI for short. 

In high doses, or with prolonged treatment, it can cause a reddish urine, and neurological effects, such as seizures, confusion, and peripheral neuropathy can be seen; as well as aseptic meningitis, when given intravenously. 

Other serious side effects include bone marrow suppression, which may result in leukopenia and thrombocytopenia. 

Some clients on metronidazole may also develop a skin rash, urticaria, and phlebitis at the injection site, as well as severe hypersensitivity reactions like Stevens Johnson syndrome and toxic epidermal necrolysis. Metronidazole also has a boxed warning for carcinogenic potential. 

Other side effects include irritability, insomnia, blurred vision, dry mouth, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Enhancing_communication_and_rapport-building</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bfKc1m6AT6OON4AaE68wPbIJQzqIhL5W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Enhancing communication and rapport-building]]></video:title><video:description><![CDATA[Providing safe, quality care requires effective communication between you, your co-workers, and your clients. Communication is the process where information is exchanged between a sender and a receiver. 

Now, communication can be verbal or nonverbal. Verbal communication uses language to deliver information and that could be written or spoken. 

Another type of verbal communication is sign language, which involves the use of hand and body gestures or signs that represent specific letters and words. 

On the other hand, nonverbal communication uses facial expressions, tone of voice, and body movements and gestures to convey a message. 

This type of communication tends to be more subtle, so you need to be alert to your clients’ nonverbal behaviors. 

For example, a client’s facial expressions or strained voice may indicate that they’re in pain even when they do not express pain verbally.

Alright, communication is a two-way process between a sender and a receiver and has four basic parts. 

First, the sender creates a message that contains the information they want to deliver to another person. 

The information should be relevant, organized, concise, and clear. Remember to avoid medical jargon when talking to clients and their family members. 

For example, instead of saying to your client, &amp;quot;Please void now, so I can ambulate you,” saying, &amp;quot;I&amp;#39;ll help you to the bathroom, so you can use the toilet before we go for a walk,&amp;quot; will send a clearer message. 

Second, the sender delivers the information to the receiver, which could be directly face-to-face or indirectly through memos, emails, and telephone calls. 

Face-to-face communication allows for non-verbal cues to take place, while indirect methods of communication don&amp;#39;t. 

Whether communicating directly or indirectly, use simple and common words instead of the more complex ones and make sure to speak clearly and at an appropriate volume. 

If the information]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assisting_with_conflicts</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fT0KVET5Q_GgRe2JlzK06-sjQuiUWvKK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assisting with conflicts]]></video:title><video:description><![CDATA[We all have our own interests, opinions, and beliefs, so it is possible to find ourselves occasionally disagreeing with other people. Sometimes, these disagreements can lead to conflict. 

Conflict is a clash that can result from differences in the interests, ideas, or viewpoints among people. Conflict can arise when one person can’t understand or accept another person’s opinions or beliefs, when someone misunderstands the words or actions of another person, or when one person’s wants or needs contend with another’s. 

Regardless of the source, conflict can be common in the workplace. Conflict is especially common in the healthcare setting because emotions often run high. 

Clients are sick and often in pain and afraid, their family members may feel helpless or upset, and healthcare team members often feel stressed or overwhelmed by their demanding work. 

Conflicts can arise due to a host of possible reasons, including but not limited to work schedules, delegated tasks, amount of work, or quality of care. 

Conflicts can be between two healthcare team members, a healthcare team member and a client, a healthcare team member and a client’s family member, or even two clients. 

Regardless of the reason or the people involved, conflict is uncomfortable for everyone: It can make for an uneasy workplace, compromise the quality of client care, and have a negative impact on the safety and well-being of clients. So, it must be prevented as much as possible.  

Now, if you find yourself in a conflict, be sure to behave professionally and calmly take the appropriate steps to resolve the conflict quickly and effectively.

First, remember it&amp;#39;s important to do your best to prevent conflict from happening in the first place. Practicing good communication with your co-workers and adhering to professional standards of conduct can go a long way in preventing conflict. 

When conflict does happen, try to resolve any conflict as soon as possible to keep the conflict from growing into an even bigger problem.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Culture_and_diversity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tL0yIBdjSn2BcaX-BzuEU6NTQN_mbjiG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Culture and diversity]]></video:title><video:description><![CDATA[As a nursing assistant, you are constantly communicating with your clients while you take care of them. Communication can be verbal, when using spoken language, and nonverbal, when using body language, like gestures, facial expression, and touch. 

Communication may be challenging when working with clients who have different cultural backgrounds. The clients might speak different languages, making verbal communication harder, or they might misinterpret nonverbal messages because their culture gives those nonverbal cues different meanings.

To prevent miscommunication, make sure you are familiar with the client’s care plan as it contains cultural guidelines for you to be aware of. 

Show an interest in your clients’ and their friends’ and family’s culture by learning more about it and knowing how to approach them. 

Remember to be a professional and avoid judging others by respecting their beliefs and values that might be different from yours. 

You should be self-aware of your own biases that you bring to the care environment and avoid making generalizations or stereotyping people from different cultures.

When working with clients that might not speak the same language as you as their primary language, make sure you are speaking calmly, slowly, and clearly in a normal tone. 

Use short and simple phrases and try to notice if your client recognizes some of the words. Repeating what you said in a different way can be helpful, too. 

Don’t raise your voice and avoid using slang or complex medical terms. In everyday communication, a very helpful tool could be a picture board with two languages, where your client can point to the picture of what they are trying to say. 

Avoid using a client’s family member to translate because they could misunderstand the medical terms and give false information. 

Therefore, it is always better to use an interpreter that your agency provides. This way, you will be sure that everything is translated correctly.

During client ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maintaining_dignity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eBbKJjJkTsisBJz-LhD_XgvQTiaC_rDw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Maintaining dignity]]></video:title><video:description><![CDATA[Dignity means being and feeling worthy of respect, and it’s a basic right of all human beings, regardless of their race, culture, disabilities, or socioeconomic situation. As a nursing assistant, there are a few things you should keep in mind to help clients maintain their dignity. 

First off, remember that clients are people with identities, so avoid calling them by their room numbers. Instead, ask them how they would like to be addressed. 

Some people prefer the use of Mr. or Mrs. but not everyone so, always address them in the way that they prefer. Don’t call them by their first name or nickname unless they ask you to. Finally, you should keep it professional and never call a client “honey” or similar names.

Next, be sure to show compassion and empathy. Be sure to let your clients know you care. You can do so using your body language, like with a gentle tap on the shoulder, as well as by keeping eye contact, smiling, and nodding your head while they’re speaking to you. 

In addition, be patient and take the necessary time to listen to your clients and answer their questions. Finally, try to help them with small tasks, like getting a glass of water or their glasses, and ask if they need anything else. 

Remember to help clients meet their basic needs while supporting their independence. Firstly, make sure clients are getting enough food and water and assist them with their meals if necessary. 

Some individuals may need additional assistance, such as intravenous infusion of fluids and nutrients. Next, make sure that your clients get enough quality rest and sleep by providing a quiet, comfortable, and safe environment. 

Also, encourage your clients to stay active and do some physical activity, like walking, if possible. If a client can’t move, you can help them by providing passive range of motion. 

Finally, assist clients with toileting and elimination as well as personal hygiene, grooming, and getting dressed. 

Now, keep in mind that some of these]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abuse,_mistreatment,_and_neglect</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R5yV_arXRm_Qgc5ErKcOyvFTQKaxocuB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abuse, mistreatment, and neglect]]></video:title><video:description><![CDATA[Abuse and mistreatment mean treating somebody else with cruelty or violence on purpose and often repeatedly. Abuse is a violation of the criminal law; therefore, it’s punishable. 

Now, abuse can involve actively doing something bad to harm another person, but it can also involve failing to do something good, like giving proper care to someone that needs you to meet their basic needs, such as nourishment, hydration, or toileting needs, and this is also known as neglect. 

A type of neglect is abandonment, which means withdrawing help or care from someone who needs it. As a nursing assistant, leaving your facility before the end of your shift without permission or sleeping at work instead of providing care are examples of abandonment. 

It can seem hard to imagine that healthcare workers who choose to come to work each day and care for others are at risk for abusing their own clients. 

However, although there is no excuse for any type of abuse, mistreatment, or neglect, situations where a client requires a great deal of care can lead to exhaustion, frustration, and potential abuse. 

As a nursing assistant, if you ever find yourself overwhelmed with your care responsibilities, remember to reach out to your supervisor to find the support you need to continue providing safe, quality care to your clients.

The main types of abuse include physical, psychological, sexual, and financial abuse. Physical abuse involves using force to cause physical harm or pain to someone else’s body. 

This includes hitting, slapping, pushing, pinching, or even shaking a client. Signs of physical abuse include bruising; red marks on the skin; fractures; or even broken objects, like eyeglasses. 

On the other hand, psychological abuse, also called emotional abuse, involves using words or actions that cause emotional harm or fear, such as treating clients without respect, insulting or humiliating them, or threatening them with physical harm or abandonment. 

Signs of psychological ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ethical_principles_and_legal_aspects_of_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TBVXAR0_RT6SPFcFPk6meqGqRs6e7_l-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ethical principles and legal aspects of care]]></video:title><video:description><![CDATA[Ethics is a moral code of rules that dictates what is right and wrong and guides our behavior accordingly. In other words, we usually act a certain way because we believe it is the right thing to do. 

On the other hand, a law involves legal rules that are dictated by the state or a governmental body to protect basic human rights. 

In other words, the law tells us what we legally can or can’t do, and failing to obey these laws can result in punishment. 

When providing care as a nursing assistant, you must always make sure your conduct is both ethical and legal. 

Now, each profession has its code of ethics, which dictates ethical principles that guide the standards of behavior and professional practice. 

The goal of the code of ethics is to guide conduct and practice and to help professionals make the right decisions when ethical issues arise. 

The general ethical principles that apply to every healthcare worker are beneficence, nonmaleficence, justice, autonomy, fidelity, and confidentiality. 

Beneficence means doing good for your clients, taking care and treating them with respect and taking consideration of their dignity. On the other hand, nonmaleficence means to avoid causing any harm to your client. 

Now, justice means you must treat all clients equally and fairly, regardless of their race, culture, disabilities, or socioeconomic situation. 

Autonomy means respecting your client’s right to make their own decisions. Fidelity means acting with honesty, loyalty, and integrity to earn your client’s trust. 

Finally, confidentiality means maintaining a client’s privacy by keeping sensitive issues a secret unless your client gives you permission to share them.

Alright, now onto the legal aspects of care. The law can be classified as criminal or civil. The criminal law involves the relationship with society in general. 

Acts that violate criminal laws are called crimes and include abuse, stealing, and murder. People that commit a crime can be punis]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hand_hygiene</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hIu2SDfiSPWRjL0pRh0Ipp8vT0uvrajx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hand hygiene]]></video:title><video:description><![CDATA[When assisting with client care, consistent, proper, and meticulous hand hygiene is the single easiest and most effective practice to reduce the risk of transmission of infection to and from the client. Hand hygiene mainly includes handwashing with soap and water and using an alcohol-based hand rub.

Now, depending on your facility’s policy, you may need to perform hand hygiene at different times. In any case, it’s important to at least perform hand hygiene upon entering and leaving a client’s room and before and after every contact with a client in general. 

You should also perform hand hygiene before and after applying personal protective equipment, like gloves; after handling any waste; after exposure to items or surfaces that could possibly be contaminated with blood, body fluids, secretions, or excretions; and after contact with non-intact skin, mucous membranes, or wound dressings.

Likewise, remember to perform hand hygiene before and after handling a client’s meal or drink, before coming in the room where clean supplies are maintained, before touching clean clothing or linen, and after helping a client back from the bathroom. 

And, of course, perform hand hygiene upon entering and leaving the facility; before and after drinking, eating, or smoking; before and after putting in contact lenses; before and after doing your make-up or fixing your hair; after picking something off the floor; after using the bathroom; and after coughing, sneezing, or using a tissue.

Now, when practicing hand hygiene, there are some general considerations you need to keep in mind. First of all, it’s important to pay special attention to the places where pathogens can easily hide and the places that can be frequently missed, like the back of your hands, between the fingers, and under or around your nails. 

What can help with this is to keep the fingernails short; wear no nail polish, artificial nails, acrylics, or wraps; and remove jewelry, including rings and brac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_used_to_treat_hepatic_encephalopathy:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8WikpmZ4Q2iNiW29-tQ9Cm92QDekPnLd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for hepatic encephalopathy: Nursing pharmacology]]></video:title><video:description><![CDATA[Hepatic encephalopathy refers to a life-threatening condition characterized by liver dysfunction, so the liver is unable to metabolize toxic substances, like ammonia, which is mainly produced in the gastrointestinal tract by the bacterial flora. As a result, these toxic substances can build up and travel to the brain, ultimately causing brain dysfunction. These clients can present with symptoms like insomnia or hypersomnia, mood changes, asterixis or flapping tremor, confusion, and even coma.

The two medications most commonly used to treat hepatic encephalopathy include lactulose, which is an osmotic laxative; and rifaximin, which is an antibiotic.

Okay, so lactulose is an indigestible and non-absorbable synthetic sugar that can be given orally or rectally. Once administered, lactulose gets broken down by the intestinal bacterial flora into lactic acid and short-chain fatty acids like acetic acid. These acidic metabolites partially dissociate to release hydrogen ions, which convert the ammonia generated into ammonium ions that get excreted in the stools.

Additionally, since lactulose is indigestible and non-absorbable, it stays in the lumen and pulls out water from the intestinal cells via osmosis. This lubricates the stool and helps it move faster through the gastrointestinal tract, leaving less time for the ammonia to be produced or absorbed.

Now, common side effects of lactulose include abdominal cramps, bloating, and flatulence, due to the production of methane by the intestinal bacteria that break down lactulose. In addition, lactulose can cause diarrhea, which can further lead to dehydration and electrolyte disturbances, such as hypernatremia and hypokalemia; and severe cases may result in arrhythmias. Finally, lactulose should be used with caution in clients with intestinal obstruction. Additional precautions should be taken during pregnancy and breastfeeding, as well as in elderly or debilitated clients, and in those with diabetes mellitus, as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Debridement_agents:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Uk_x0PsUQRqQqPCw3w9R4Q2nQUKbrjdn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Debridement agents: Nursing pharmacology]]></video:title><video:description><![CDATA[Debridement agents are a group of medications that are used to remove debris or dead tissue from a burn, ulcer, or wound, which helps promote healing and decrease the risk of infection. 

Some commonly used debridement agents include collagenase, and a combination medication containing trypsin, balsam peru, and castor oil. These medications come in the form of ointments that are applied topically on the skin. 

Once applied, collagenase is an enzyme that acts by breaking down collagen in non-viable tissue, and helps in forming granulation tissue, which contains healthy cells that fill up the dead tissue from the wound and fight off infections. 

Similarly, sutilain breaks down proteins of the intercellular matrix, which fills the spaces between neighboring skin cells. This allows the cells of the outer skin layers to shed, which is known as desquamation. 

Finally, trypsin activates an enzyme called metalloproteinase, which breaks down the intercellular matrix, making it easier for skin cells to slough off; while balsam peru stimulates blood flow to the wound area, as well as castor oil, which prevents the breakdown of healthy skin cells. 

Additionally, both balsam peru and castor oil help prevent wound infection by inhibiting bacterial and fungal growth in the skin. 

Unfortunately, debridement agents may cause side effects, such as skin irritation, which can manifest as pain, erythema, as well as a burning, itching, or a tingling sensation. 

Luckily, there are no contraindications for the use of debridement agents. 

If a client with a necrotic wound is prescribed a debridement agent, first review their medical record for any health conditions that could affect healing, such as impaired mobility, impaired circulation to the wound site, deficient nutrition, or conditions like diabetes mellitus. 

Then, perform a baseline assessment of the affected area, noting the location, and size, measuring length, width, and depth of the wound, and the amount of nec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anthelmintics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PSdpa4K1RBaetHH6GWClzW-aTXKIWNr5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anthelmintics: Nursing pharmacology]]></video:title><video:description><![CDATA[Anthelmintics are a group of medications used to treat intestinal and systemic parasitic worm infections, such as those caused by pinworms, tapeworms, and intestinal flukes.

The most commonly used anthelmintics include albendazole, thiabendazole, ivermectin, praziquantel, diethylcarbamazine, and pyrantel. These medications are taken orally.

Once administered, anthelmintics act in parasitic worms by disrupting metabolic pathways that are required for their normal functioning, ultimately killing the worm.

As far as side effects go, these are typically very few and limited to the duration of treatment. So, clients might experience headaches, drowsiness, dizziness, and weakness. 

In addition, anthelmintics may often cause gastrointestinal disturbances, such as anorexia, nausea, vomiting, diarrhea, and cramping. Finally, some clients may develop a skin rash or urticaria.

Now, anthelmintics are contraindicated during pregnancy and breastfeeding. Additional precautions should be taken in clients with severe diarrhea, malnourishment, and hepatic or renal disease. 

Alright, when a pediatric client is diagnosed with a pinworm infection caused by Enterobius vermicularis, they can be prescribed an anthelmintic medication, like albendazole. 

Before administering the medication, be sure to perform a focused assessment, including their current weight and a description of their symptoms, such as the presence of erythema or excoriation, itching in the perianal area, a report of restless sleep due to itching during the night, as well as irritability and loss of appetite. 

Then, review their most recent laboratory test results, including CBC, renal and hepatic function tests. Lastly, review the results of the cellophane tape test confirming the presence of pinworm eggs. 

Then, explain to the client and caregiver that pinworms are a common intestinal infection, especially in children, and assure them that albendazole is effective in treating the infection. 

In addit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antispasmodics_(GI_spasms):_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q2pViEO2SnC7TvsZdyPQHnEVQFaswEtW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antispasmodics (GI): Nursing pharmacology]]></video:title><video:description><![CDATA[Gastrointestinal antispasmodics are medications used to treat spasms of the gastrointestinal tract muscles, which can occur in diseases like irritable bowel syndrome, or IBS for short, biliary colic, and pancreatitis.

The most commonly used gastrointestinal antispasmodics include antimuscarinic medications like dicyclomine, which can be administered orally, as well as hyoscyamine, which can be given orally and sublingually.

Once administered, these medications bind to the muscarinic receptors on gastrointestinal smooth muscles. As a result, they block acetylcholine from binding to these receptors, which ultimately decreases smooth muscle contraction and relieves the spasm.

Now, gastrointestinal antispasmodics may cause anticholinergic side effects, such as blurred vision, dry mouth, decreased sweating, urinary retention, and constipation. Some clients may also present with headaches, dizziness, and tachycardia.

Now, contraindications of gastrointestinal antispasmodics include severe ulcerative colitis, stenosing peptic ulcer, paralytic ileus, gastrointestinal obstruction, and toxic megacolon. 

In addition, these medications are contraindicated in clients with closed- or narrow-angle glaucoma, myasthenia gravis, cardiovascular disease, prostatic hypertrophy, and bladder obstruction. 

Finally, gastrointestinal antispasmodics should be used with caution during pregnancy and breastfeeding, in elderly clients, as well as in clients with hypertension, and hepatic or renal disease.

Okay, if a client with irritable bowel syndrome or IBS is prescribed a gastrointestinal antispasmodic like dicyclomine, first perform a baseline assessment, including vital signs, fluid intake and output, and gastrointestinal status. 

Be sure to make note of their current IBS symptoms, such as diarrhea, abdominal pain, or bloating, as well as stool characteristics and frequency. 

Then, review recent laboratory test results, specifically renal and hepatic function; and diagnost]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Trimethoprim_&amp;_sulfonamides:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NnxQdJe9SvS_H8SDu4i2ZDf0QnaBAoyR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Trimethoprim and sulfonamides: Nursing pharmacology]]></video:title><video:description><![CDATA[Trimethoprim and sulfonamides are antibiotics that are typically administered in combination as trimethoprim-sulfamethoxazole, or TMP-SMX for short. 

TMP-SMX is most commonly used to treat acute and simple urinary tract infections or UTIs, acute otitis media, traveler&amp;#39;s diarrhea, and shigellosis. But it’s also effective in treating pneumonia and sinus infections caused by Streptococcus pneumoniae and Haemophilus influenzae. 

It’s the first line therapy for the treatment and prevention of Pneumocystis jirovecii infections, which are caused by a yeast-like fungus that can affect immunocompromised people. Finally, it’s effective against Methicillin-Resistant Staphylococcus aureus, or MRSA. 

Trimethoprim-sulfamethoxazole is most often given orally, and for serious infections and Pneumocystis jirovecii pneumonia, it can be administered intravenously. 

Now, sulfonamides can also be used alone as sulfadiazine orally to treat infection by Toxoplasma gondii, or as silver sulfadiazine, which is administered topically in clients with second and third-degree burns to help prevent and treat wound sepsis.

Now, once administered, these medications act to inhibit the synthesis of folate, also known as folic acid or vitamin B9, which is necessary for the synthesis of DNA and RNA. As a result, they interfere with bacterial DNA and RNA synthesis, which ultimately kills the bacteria.

Typically, topical silver sulfadiazine is very well tolerated and doesn’t cause many side effects. The most common is agranulocytosis. Others include skin necrosis, erythema multiforme, skin discoloration, burning sensation, rashes, and interstitial nephritis. 

On the flip side, the list of side effects for oral sulfadiazine, as well as trimethoprim-sulfamethoxazole, is larger. Luckily, the most common ones are mild and include gastrointestinal disturbances like nausea, vomiting, and abdominal pain. 

Now, in some cases, trimethoprim-sulfamethoxazole can disrupt the normal intesti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acetylcholinesterase_inhibitors_to_treat_myasthenia_gravis:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UZUePgX8QbO8hI1KpAftJZ1vSQC9Adl4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acetylcholinesterase inhibitors for myasthenia gravis: Nursing pharmacology]]></video:title><video:description><![CDATA[Myasthenia gravis is an autoimmune disorder caused by antibodies that bind to and destroy acetylcholine receptors on the surface of skeletal muscle cells, resulting in fatigue and muscle weakness due to impaired muscle contractions. 

Although there’s no cure, certain medications, called acetylcholinesterase inhibitors, can be used to help mitigate some of the symptoms and improve the client’s quality of life.

Now, the most commonly used acetylcholinesterase inhibitors for myasthenia gravis are neostigmine and pyridostigmine. These medications can be administered orally, intravenously, or intramuscularly, while neostigmine can be also given subcutaneously to children. 

Once absorbed into the bloodstream, acetylcholinesterase inhibitors travel to the skeletal muscles and inhibit the enzyme acetylcholinesterase, which normally breaks down the neurotransmitter acetylcholine. 

As a result, these medications cause acetylcholine to build up in the synaptic cleft, causing its cholinergic effects to be increased and prolonged. 

This helps counteract the effect of acetylcholine receptor antibodies, and ultimately results in improved muscle strength and contraction.

However, increased acetylcholine levels can also cause cholinergic side effects, such as miosis, blurred vision, headaches, dizziness, and drowsiness. 

At the same time, in the airways, acetylcholine triggers bronchoconstriction and increases bronchial secretions, which can lead to dyspnea and a persistent cough.

In the cardiovascular system, acetylcholine reduces blood pressure and slows down the heart rate, which can result in hypotension, bradycardia, heart block, and even cardiac arrest. 

In the gastrointestinal tract, these medications can cause increased motility and secretions, leading to increased salivation, nausea, vomiting, cramps, diarrhea, and involuntary defecation; 

and in the urinary tract, acetylcholine stimulates the bladder muscles and sphincter relaxation, which may cause a s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunosuppressants_to_treat_autoimmune_diseases:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hUpwHIlbRMuoeyCCUx6IYxnqQveusBDz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunosuppressants for autoimmune diseases: Nursing pharmacology]]></video:title><video:description><![CDATA[Autoimmune diseases occur when the immune system mistakenly attacks various tissues and organs around the body, such as in systemic lupus erythematosus and rheumatoid arthritis. 

Often there are periods of illness, called flares, and periods of remission during which there are few or no symptoms. Unfortunately, autoimmune diseases can’t be cured, but their symptoms can be treated with a variety of systemic immunosuppressant medications. 

Okay, immunosuppressants to treat autoimmune diseases include corticosteroids like prednisone or dexamethasone, monoclonal antibodies like belimumab, immunomodulators like azathioprine, antimetabolites like methotrexate, and antimalarials like hydroxychloroquine. 

These medications can be taken orally, or injected as intravenously, intramuscularly, or less commonly, subcutaneously. Once administered, immunosuppressants primarily work by blunting the inflammatory process so that it can’t cause damage to healthy tissues, and preventing or limiting the severity of flares.

Unfortunately, some of these medications can also increase the risk of side effects like bone marrow suppression, which can lead to anemia, thrombocytopenia, and leukopenia, as well as increased risk for infections. Some clients may also experience drowsiness, fatigue, and gastrointestinal disturbances, such as anorexia, nausea, vomiting, and diarrhea. 

Also, if administered by injection, they can cause infusion or injection site reactions. Now, corticosteroids can also lead to symptoms of hypercortisolism, such as acne, mood changes, muscle weakness, hyperglycemia, and weight gain, predominantly in the trunk and face, respectively termed buffalo hump and moon facies. 

Additionally, prolonged use of corticosteroids can increase the risk of osteoporosis and pathological fractures. 

On the other hand, belimumab can often cause headaches, depression, insomnia, and some clients may even experience suicidal ideation. Clients on azathioprine may develop alo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Oxazolidinones:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xYmZ1sEVTqqMpE0emcDNlKwkSxeVK-aV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Oxazolidinones: Nursing pharmacology]]></video:title><video:description><![CDATA[Oxazolidinones are a class of antibiotics used to treat a wide range of infections caused by gram positive bacteria, such as Streptococcus spp, Staphylococcus spp, including methicillin-resistant Staphylococcus aureus or MRSA for short, and Enterococci spp, including vancomycin-resistant Enterococci or VRE, and other strains resistant to other classes of antibiotics. 

Additionally, oxazolidinones can be effective against mycobacteria and certain anaerobic bacteria, such as Fusobacterium spp, Prevotella spp, Porphyromonas spp, Bacteroides spp, and Peptostreptococcus spp.

Alright, the most commonly used oxazolidinones include linezolid and tedizolid. These medications can be administered orally or intravenously. 

Once administered, oxazolidinones target the bacterial 50S ribosomal subunit, which inhibits protein synthesis. As a result, these medications have a bacteriostatic effect, meaning they stop bacterial growth.

Side effects of oxazolidinones include headaches, dizziness, and insomnia; as well as optic neuropathy, which can lead to vision loss, but is usually reversible; and peripheral neuropathy, which can manifest as numbness, tingling, or weakness in the arms and legs, and is typically irreversible. 

Some clients may also experience changes in tongue color and taste, as well as gastrointestinal disturbances like nausea, vomiting, and diarrhea. 

In addition, oxazolidinones may disrupt the normal intestinal flora, which can allow certain bacteria like Clostridioides difficile to survive and overgrow within the gastrointestinal tract, rarely but potentially leading to Clostridioides difficile infection or CDI for short. 

A very serious side effect of oxazolidinones is reversible bone marrow suppression, which can result in anemia, leukopenia, and thrombocytopenia. 

Clients taking oxazolidinones may also develop lactic acidosis, as well as hypersensitivity reactions, such as Stevens Johnson syndrome or anaphylaxis. 

In addition, one of the most]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vaccines:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XbJ84qWNQYCnaAZODaUrWf1nQyeJ2qDH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vaccines: Nursing pharmacology]]></video:title><video:description><![CDATA[Vaccines are biological products designed to protect humans from potentially serious infections caused by various kinds of pathogens. 

Most vaccines are routinely administered to clients as part of a vaccination schedule; while other vaccines are only given to certain populations, such as chronically ill clients or those travelling to foreign countries. 

Now, there are five main types of vaccines: live attenuated, inactivated, subunit, toxoid vaccines, and mRNA vaccines. 

Live attenuated vaccines contain pathogens that have been weakened in the laboratory. As a result, these weakened pathogens are no longer able to cause infection, but are still able to trigger a protective immune response. 

These vaccines are used to protect against influenza with the live attenuated influenza vaccine or LAIV for short; as well as measles, mumps, and rubella, called the MMR vaccine, and can also include varicella zoster, also known as the MMRV vaccine; other live attenuated viruses include vaccines for rotavirus, smallpox, and yellow fever. 

On the other hand, inactivated vaccines use a pathogen that has been killed in the laboratory, so it is no longer able to replicate or cause infection, but is still able to trigger a protective immune response. 

These include vaccines against Hepatitis A, or HAV vaccine, as well as against polio, called the Salk vaccine or inactivated polio vaccine or IPV, and against rabies, or the rabies vaccine. 

Another important inactivated vaccine is again for influenza with the inactivated influenza vaccine or IIV for short. 

Next, subunit, recombinant, and polysaccharide vaccines contain just the portion of the pathogen that stimulates the immune response, such as a viral protein, DNA, or sugar. 

Some of these vaccines are combined with proteins to form conjugated vaccines, which elicit a much stronger and longer lasting immune response. 

These vaccines are used to protect clients against Haemophilus influenzae type B, or HiB vaccine]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nervous_system:_Seizures_and_strokes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DXk88zinQk_lykZHBjJAMOsmSxiLv8Sm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nervous system: Seizures and strokes]]></video:title><video:description><![CDATA[The nervous system can develop several types of disorders, which can affect the clients you care for. The disorders can cause different problems depending on their cause and the area of the nervous system involved 

One of the most common nervous system disorders is stroke, also known as cerebrovascular accident or brain attack. This is when the brain gets damaged due to being deprived of oxygen- rich blood. 

There are two main types of stroke: an ischemic stroke, which occurs when there’s a blockage of an artery, and a hemorrhagic stroke, which occurs when an artery in the brain leaks into the brain tissue.  

Now, most ischemic strokes are caused by thrombosis, meaning that a clot forms over an atherosclerotic plaque. 

This is when a buildup of fat and cholesterol forms on the inside of a blood vessel in the brain known as cerebral blood vessels and starts to obstruct arterial blood flow. 

Another mechanism for ischemic stroke is an embolism. This happens when a blood clot breaks off from an atherosclerotic plaque from an artery outside the brain, breaks loose, and travels to the brain where it gets lodged in a cerebral artery. 

Factors that can increase the client&amp;#39;s risk for having a thrombotic or embolic stroke include anything associated with atherosclerosis, like smoking, hypertension, or high blood pressure; diabetes; and a diet high in saturated fat. 

Now, sometimes a small clot can block a cerebral artery for a short period of time before dissolving, restoring normal blood flow. 

So, if it self-resolves within 24 hours, usually within minutes to hours, it’s called a transient ischemic attack, or TIA for short. The main risk factor for a TIA is atherosclerosis.

All right, now in hemorrhagic strokes, a  cerebral blood vessel ruptures and bleeds out, creating a pool of blood that increases pressure within the brain. 

In addition, less oxygen-rich blood is flowing downstream to the cells that need it. The main risk factor for hem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Macrolides:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pZQH21SRQZ_QS2QUe-QZCvoPTjSq7UY9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Macrolides: Nursing pharmacology]]></video:title><video:description><![CDATA[Macrolides are a class of antibiotics used to treat a wide range of infections caused by gram-positive and gram-negative bacteria. These medications include erythromycin, azithromycin, and clarithromycin. 

All can be administered orally to treat mild to moderate bacterial infections of the respiratory, gastrointestinal, and genitourinary tracts; erythromycin can also be given intravenously, and azithromycin has an ophthalmic formulation to treat bacterial conjunctivitis.

Now, once administered, macrolides target the bacterial 50S ribosomal subunit in order to inhibit protein synthesis. As a result, these medications have a bacteriostatic effect, meaning they stop bacterial growth. 

They’re also considered broad spectrum antibiotics, as they’re active against most gram-positive bacteria and moderately active against some gram-negative bacteria.

Typically, macrolides are well tolerated, and rarely cause side effects. The most common ones can include headaches, a skin rash, and gastrointestinal disturbances like diarrhea, abdominal pain, nausea, and vomiting. 

In addition, macrolides may disrupt the normal intestinal flora, which can allow certain bacteria like Clostridioides difficile to survive and overgrow within the gastrointestinal tract, rarely but potentially leading to Clostridioides difficile infection or CDI for short. 

Some clients on macrolides may also develop vaginitis and candidiasis, and if they’re used for a prolonged time, they can also lead to ototoxicity and hearing loss. 

Now, more serious side effects include a prolonged QT interval, ventricular arrhythmias like torsade de pointes, and hepatotoxicity, potentially leading to hepatitis. 

They can also cause seizures, and rare but serious hypersensitivity reactions like angioedema, Stevens-Johnson syndrome, and toxic epidermal necrolysis. 

Finally, regarding specific side effects, erythromycin can cause esophagitis, while azithromycin can rarely cause thrombocytopenia; while c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Polymyxins:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zolKGRXoRtKTpwaUys3g_YjdT4OfjNhS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Polymyxins: Nursing pharmacology]]></video:title><video:description><![CDATA[Polymyxins are an older class of antibiotics, which are nowadays used as a last resort to treat bacterial infections when other antibiotics are either contraindicated or ineffective. 

These medications affect susceptible gram-negative bacteria such as Escherichia coli, Pseudomonas aeruginosa, Klebsiella spp., and Shigella spp. 

There are two approved medications in this class: polymyxin B and polymyxin E, also known as colistin. Both are available for intramuscular and intravenous use. 

Additionally, polymyxin B can be given intrathecally, as an ophthalmic formulation, as well as by inhalation.

Once administered, polymyxins work by binding to the bacterial membrane and disrupting it, which ultimately leads to bacterial cell death.

Now, polymyxins can cause serious side effects like neurotoxicity and nephrotoxicity. In fact, that’s a boxed warning for polymyxin B! 

Clients with neurotoxicity might experience facial flushing, drowsiness, dizziness, ataxia, and paresthesia. Sometimes, neurotoxicity can cause respiratory paralysis. 

On the other hand, nephrotoxicity may present with a low urine output, albuminuria, cellular casts in the urine, and azotemia. 

Finally, specific side effects associated with intravenous administration of polymyxins include fever, rash, and itching; while side effects of intrathecal polymyxin B use include headaches and neck stiffness.

Regarding contraindications, polymyxins should not be used during pregnancy and breastfeeding, as their safety hasn&amp;#39;t been established. 

These medications should be used cautiously in elderly clients, as well as in those with neuromuscular disease like myasthenia gravis, and in clients with renal disease. 

Finally, polymyxins should not be combined with other neurotoxic or nephrotoxic medications, such as aminoglycosides. And again, that’s a boxed warning for polymyxin B! 

Also, polymyxins shouldn&amp;#39;t be used with general anesthetics and neuromuscular blocking agents, such]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Why_you_should_learn_by_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1WB2eqq5Q4K3cXRGPRKD930pQ-ytFs_m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Why you should learn by Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Why you should learn by Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Post-mortem_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L5kmpkuHTIacvkl3mAGgGh8QTZ6D32_o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Post-mortem care]]></video:title><video:description><![CDATA[As a nursing assistant, sometimes you might be present when one of your clients dies. In this case, you should let the nurse know right away if you think the client has died. You could be asked to document the absence of vital signs and the time. 

In addition, death needs to be legally confirmed by a physician or nurse authorized to pronounce the person’s death. The time of death appears on the individual’s death certificate. 

Now, after death has been determined, you need to assist the nurse in giving post-mortem care. Post-mortem care is how the client’s body is cared for after their death. 

Sometimes, cultural or religious beliefs can dictate how the body should be cared for. Post-mortem care is crucial in order to maintain respect and dignity of the person who has died and to keep the body in proper alignment. 

This is important to do before rigor mortis sets in, which is the stiffening of skeletal muscles, and it occurs within two to four hours after death. 

Once this happens, it’s difficult to reposition the body. One more thing to keep in mind is that gas trapped in the GI tract can be released when repositioning or moving the body, leading to sighs or moans coming from the deceased client. 

This is a natural process, and there’s no need to be afraid. Sometimes, an autopsy needs to be done in order to confirm the cause of the individual’s death. An autopsy is the examination of the individual’s organs and tissues after death. 

When performed, medical devices, like tubes, drains, catheters, and IV lines, should not be removed. When an autopsy will not be performed, all these devices can be removed as part of post-mortem care. 

Before anything else, the skin needs to be cleaned of mucus, urine, feces, or other fluids. That’s because bodily fluids may be infectious, even after death. 

Then, the body is placed in proper alignment before rigor mortis sets in. To best assist with post-mortem care, you need some information from the nurse. 

First]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Comfort_care_for_the_dying_person</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fUvozNRHQmKjxLg_4e05T4FzRy2sh-5Q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Comfort care for the dying person]]></video:title><video:description><![CDATA[Caring for a dying client can be challenging, and your own personal feelings about death can affect the care you provide. If you have fears about death and have not yet come to terms with the idea of dying, you may be unconsciously reducing the quality of care you provide.

For instance, you may avoid spending a lot of time in the room of a dying client because you’re afraid they might want to discuss death. 

Also, you might check in on them less frequently than other clients because you don’t want to become attached to your client. These are normal fears, especially for a new nursing assistant. 

It can be helpful to share your concerns with the nurse as well as to discuss it with a clergy member or a mental health counselor in order to explore your own feelings and beliefs about death. 

A person can die suddenly. However, sometimes, there are warning signs that death is near and that it will occur in the next minutes, hours, or days. 

So, being able to recognize signs and symptoms that death is near will help you know what type of care your clients need. 

Signs of impending death include abnormal vital signs due to a slowing down of blood circulation and include decreased blood pressure and a rapid and weak pulse. 

The skin can appear pale; cyanotic, meaning blue; cool or warm; and mottled. Next, they could have irregular, shallow breaths, called Cheyne-Stokes respiration. 

They could also have heavy and noisy breathing, called a death rattle, which is caused by saliva building up in the back of the throat. 

As death approaches, the digestive system will also slow down, and the person can experience nausea, vomiting, abdominal distention, or fecal impaction or incontinence. 

They may also refuse food or water, leading to dry mouth. The urine output also decreases, and the person may have urinary incontinence. 

As the nervous system becomes affected, they may also lose their muscle tone, and this makes it difficult for them to reposition themselv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spiritual_and_cultural_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/chBEtk6cSBq3BRuXwXQFfXyrRLWBpf1b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spiritual and cultural care]]></video:title><video:description><![CDATA[Holistic care means providing care for the person as a whole, rather than just their disease or symptoms. 

This is based on the fact that each person is unique and complex, made up of physical, psychological, social, cultural, and spiritual parts, which all need to be considered to provide safe, effective care for your clients.

Now, culture refers to a set of beliefs, values and/or traditions that are the norm for a group of people. 

People who have the same culture may come from the same background, they may speak the same language, or they may have the same race or ethnicity. 

An important factor to recognize is that culture is not the same as race; while culture refers to the thinking and behavior of a person, race is usually based on parts of the person’s visible features, like skin color, facial features, hair texture, and body frame. 

Finally, there&amp;#39;s religion and spirituality. Religion is closely linked with a person&amp;#39;s culture and represents organized, ritualistic spiritual beliefs and forms of worship. 

Not every client will be part of a specific religion. On the other hand, spirituality refers to the person&amp;#39;s beliefs about the meaning and purpose of life and is something that exists in all people, regardless of their religion. 

Each client&amp;#39;s plan of care should include information about their cultural and religious practices. Κnowing about these will help you provide effective care.

Interestingly, culture, religion, and spirituality also influence how people see health, illness, and death. 

For example, some cultures consider that illness occurs when the body is exposed to either excess heat or excess cold. 

It’s believed that heat and cold are elements that exist in things like food, air, herbal medicine, organs, and diseases. 

So, if the person has a “hot” condition, like fever or sore throat, cold is used to treat it. Conversely, if the person has a “cold” condition, like joint pain, heat would be ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_health_and_illness</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bZsbq_dfTWiUbW5lg65xySpJT9qieJlK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mental health and illness]]></video:title><video:description><![CDATA[Mental health refers to our cognitive, emotional, and behavioral mental well-being as well as our ability to manage everyday stress, which can happen when there&amp;#39;s a change in a person&amp;#39;s life, such as contracting an illness, starting a new job, or losing a loved one. 

It’s normal to feel stressed out sometimes, but a person who is mentally healthy is able to cope with it and return to a state of mental well-being. 

Now, mental illness refers to a disease that affects mental health and the ability to manage stress. Mental illness can have a variety of different causes. 

Some mental illnesses can run in families and be inherited. Others can result from substance abuse. 

Finally, some mental illnesses may be the consequence of a person’s environment, such as cultural factors or experiencing a traumatic event. 

As a nursing assistant, you will encounter clients with different types and degrees of mental illness, such as anxiety, obsessive compulsive disorder, posttraumatic stress disorder, depression, bipolar disorder, schizophrenia, substance use disorder, and even suicidal tendencies. 

You will be in a position to listen to and observe your clients, report signs and symptoms of mental illness, and to support them with their daily activities.

Let’s start with Anxiety, which is a feeling of worry, apprehension, or unease in response to an imminent or uncertain event. 

Symptoms of anxiety include restlessness, trouble sleeping, fatigue, appetite changes, irritability, or even increased heart rate or blood pressure. 

Now, it’s totally normal to experience a little bit of anxiety every now and then, but having feelings of anxiety too much or too often can become a mental illness and affect our daily activities; this is known as an anxiety disorder. 

Anxiety disorders also include phobias and panic disorder. Phobias refer to an excessive fear of a specific thing or situation and can become very disabling for the affected person. 

T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Orthotic_and_prosthetic_devices</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JlI1rxzjRgynhV0tSxQ0lHZZSZeKt0qb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Orthotic and prosthetic devices]]></video:title><video:description><![CDATA[Supportive devices are used to strengthen, support, and protect parts of the body; while prosthetics are artificial devices meant to replace parts of the body. 

Both play an important role in rehabilitating clients with disability, so they can achieve the highest level of function possible.  

It’s important for you to recognize these and understand how they function as you may be asked  to care for clients using these devices.

Let’s start with supportive, or orthotic devices, sometimes called orthoses. Often, people think orthotics only refer to shoe inserts that help with foot problems, but they include a wide variety of devices that support the numerous joints in the body. 

The most diverse types are braces, which are worn around a joint to limit its movement, offer support, or reduce load on the joint. 

Some, like prophylactic knee braces, are used to prevent injuries; others are used to relieve symptoms, like wrist braces that can help with carpal tunnel syndrome. 

Some, like ankle or shoulder braces, are worn after surgery or injuries to help the joint remain in place during the healing process. 

Support devices are also used to try and immobilize a joint, such as a soft or hard cervical collar. Splints are kind of like braces in that they also limit movement. 

They are generally only used after an injury or surgery in the short term, while some braces can be worn indefinitely.  

While orthotic devices provide support for existing body parts, prosthetics act as artificial replacements for them. 

Some are functional, like a prosthetic leg, which can help the client walk; but others, like prosthetic eyes, are for cosmetic purposes only. 

A specialist called a prosthetist will design and fit the prosthesis, but the rehabilitation process often involves other disciplines. 

For example, physical therapists will help the client learn to walk with their new prosthetic leg, while occupational therapists can help them learn how to perform daily tas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_safety:_Hazards</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RhRMDCWETSqtwbRn1Tk6hLh_RLmqD0C9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace safety: Hazards]]></video:title><video:description><![CDATA[As a nursing assistant, you need to know how to prevent hazards in your healthcare facility that could pose risk of injury to you, your co-workers, and clients. 

We will be talking about some of these hazards, which include falls, entrapment, chemical injuries, and electrical shock. Alright, let’s start with falls. 

Falls are the most common type of accident in healthcare facilities; they can lead to fractures, like hip fractures, and head injuries, which could be life-threatening. 

There are a few factors that increase the client’s risk of falls. These risk factors can be related to the client and their condition or to the healthcare settings. 

Okay, so one risk factor that increases a client’s risk of falls is the age of the client, where the older the client is, the higher their risk of falling. Another factor is the client’s mental status, where they could be experiencing confusion or delirium. 

Other risk factors include medical conditions that cause muscle weakness or musculoskeletal problems; dizziness; and orthostatic hypotension, which is when the client’s blood pressure falls when they move from a sitting position to a standing position.

Also, the client’s risk for falls increases if they need to rush to the bathroom often due to issues like urinary incontinence. 

Finally, there are certain medications that increase the risk of falls, such as sedatives and anesthetic drugs, which affect the client’s mental status, and antihypertensive medications that lower the blood pressure.

Now, healthcare setting or facility risk factors that increase the risk of falls include a bed left in a high position; lack of bedrail use; and tubes, bags, and catheters attached to the client. 

Other facility risk factors include inadequate lighting; lack of grab bars, like in hallways or stairways; and wet or slippery floors.

Also, the use of canes, wheelchairs, and crutches that do not properly fit the client, like a cane that&amp;#39;s too lo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Restraints</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V71u61Q2Rx_rtbf6IsGlKxsdSXCPRfHh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Restraints]]></video:title><video:description><![CDATA[Restraints are sometimes needed to temporarily help keep clients and the people around them safe. The purpose of a restraint is to restrict a client’s freedom of movement or to prevent a client from reaching certain parts of their body. 

Some common uses for restraints include preventing agitated or aggressive clients from harming themselves or others and preventing confused or disoriented clients from interrupting ongoing therapy, like removing medically necessary tubes or catheters from their bodies. 

Sometimes, restraints are used as a last resort to keep clients from falling and harming themselves. Now, there are two types of restraints: physical and chemical. 

Physical restraints are devices that are attached to or near a client’s body that restrict the client’s freedom of movement or their ability to access certain parts of their body; these cannot be easily removed by the client. 

Physical restraints attached to a client’s body are commonly applied to the chest or waist or joints, such as the wrists, elbows, or ankles. 

Physical restraints near a client’s body may be attachments to chairs, side rails on a bed, or even tightly tucked sheets. Additionally, restricting access to other rooms or areas of a facility is also considered a type of physical restraint. 

Chemical restraints are medications, such as sedatives or tranquilizers, that are not a standard treatment for a medical or psychological condition. 

These medications restrict a client’s freedom of movement or their ability to access certain parts of their body by altering a client’s mood or behavior. 

Chemical restraints are used to help calm anxious, agitated, or physically combative clients to protect them and those around them from harm.

Now, there are a variety of types of physical restraints. Vest and jacket restraints are applied to the chest and help keep a client confined to a bed or chair. They can also be used to restrain physically combative clients. 

Wrist restraints are]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Measuring_respiration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JosSqR_sTjKqjOZnrUsEWTzCTOSb00_F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Measuring respiration]]></video:title><video:description><![CDATA[Breathing, also known as respiration, is how the air moves into and out of the lungs. It consists of repetitive cycles of inspiration, which is when air full of oxygen flows into the lungs, and expiration, when the air along with carbon dioxide leaves the lungs. 

In order for this cycle to happen, there are respiratory centers within the brain that control breathing. 

These centers receive information from a group of receptors, known as chemoreceptors, which detect any changes regarding the oxygen and carbon dioxide concentration in the body. 

Now, as a nursing assistant, you need to be able to measure your clients&amp;#39; respiration and determine its characteristics, including the respiratory rate, rhythm, and depth of respiration and whether the respirations are quiet or noisy as well as easy or difficult.

Okay, respiratory rate refers to the number of breaths a client takes in one minute. Normal respiratory rate varies among different age groups. 

So, for adults, it’s typically between 12 and 20. For adolescents between 12 and 20 years old, normal respiratory rate is 15 to 20. 

For school-aged children between 5 and 12 years old, it’s from 15 to 25. For preschoolers from 3 to 5, it’s 22 to 34, while toddlers from 1 to 3 have a normal respiratory rate of 24 to 40. 

Finally, infants under 1 year of age normally have the fastest respiratory rate, which ranges from 30 to 60 breaths per minute. 

Besides age, the respiratory rate can also be influenced by many factors, including physical activity; body temperature; emotions, like anger, fear, or stress; medications; smoking; certain diseases of the heart or lungs; or even the weather! 

A client can also voluntarily choose to increase their respiratory rate or hold their breath and, thus, decrease their respiratory rate. 

So, tachypnea is when the respiratory rate is faster than normal, and this can occur in response to strenuous exercise, fever, pain, anxiety, or specific medicatio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_clients_with_developmental_and_intellectual_disabilities</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6uT01rhoT7_Ff2xiP4C_UkI-R1u3H0sa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for clients with developmental and intellectual disabilities]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Caring for clients with developmental and intellectual disabilities through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_clients_with_delirium_or_dementia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BntbwImMT06pe83sFtlPn6-fTaiiajVP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for clients with delirium or dementia]]></video:title><video:description><![CDATA[As a nursing assistant, you will be caring for clients that have either delirium or dementia. You need to be familiar with these diseases and what you can do to provide the best care to your clients. 

Both delirium and dementia lead to a decline in various mental functions, including memory, thinking, language, behavior, mood, and personality. Delirium has a sudden onset, while the onset of dementia is gradual. 

Delirium occurs as a consequence of an underlying condition, like an infection, medication toxicity, a recent surgery, or serious illness, and signs and symptoms often fluctuate, meaning they come and go. 

On the other hand, dementia is caused by structural changes in the brain; it progressively gets worse over time. Delirium can last hours or weeks, and it is reversible when the underlying cause is addressed promptly.

Okay, let’s take a closer look at delirium, which is a medical emergency and must be recognized and treated promptly. 

As a nursing assistant, you might notice your client isn’t their usual self, which could signal the onset of delirium.

You might notice client behaviors, like disorientation, where they don&amp;#39;t know where they are or what day it is, or they might have difficulty concentrating. 

Their level of activity will often fluctuate between agitated, angry, and aggressive to being drowsy, withdrawn, and depressed. 

Their speech may not make sense; they could experience hallucinations, which means they see, hear, or even smell things that are not actually real but are very real to them; or they could experience delusions, where they believe things that are not true.

Now, there are some general considerations to keep in mind when caring for a client with delirium. First, it’s really important to keep your client safe. 

Check the nurse and client’s care plan for interventions, such as creating a calm environment by reducing environmental noise; reorienting the client to person, place, time, and procedures; and ens]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integumentary:_Emptying_closed_drains</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EZdUppj7S1ezHUGyvIbv-9eaQg2VecVY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integumentary: Emptying closed drains]]></video:title><video:description><![CDATA[Now, as a nursing assistant, you may help provide care to clients that have some type of wound drain. You can be asked to empty a closed drain system or monitor wound drainage, meaning that you’ll have to check the amount as well as the characteristics of the fluid, including its color, clarity, and odor. 

That’s important to make sure that the wound is healing properly and that there isn’t any complication, like a wound infection. 

Before we talk about how to assist with wound drains, we need to go over what wound drainage and drains are. Throughout the course of healing, many wounds normally generate plenty of fluid; this is known as drainage. 

Depending on the type and dimensions of the wound as well as the presence of an infection or bleeding, the type and amount of drainage may vary. 

There are four types of wound drainage: serous drainage, which is thin and clear; sanguineous drainage, which is bright red blood; serosanguineous drainage, which is basically thin and clear but also has a red or pink color; and purulent drainage, which is thick and yellow, green, tan, or brown in color.

If drainage is left to build up inside the wound, it could lead to tissue swelling, which will disrupt the process of healing. 

Therefore, if the amount of drainage produced is large, a healthcare professional should usually insert a wound drain, which would channel that fluid out of the wound. 

Now, there are two main types of wound drain systems: open and closed. An example of an open drain system is the Penrose drain, which consists of a soft, rubber tube that lets fluid flow out of the surgical site and directly onto a dressing or gauze bandage. 

A sterile pin is often attached to the outer portion of the drain to keep the tubing from slipping back into the wound. 

However, the thing with these drainage systems is that they allow pathogens to easily sneak into the wound and possibly lead to an infection. In contrast, a closed drain system uses a vacuum to wi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integumentary:_Applying_abdominal_binders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fWPX_TbDSiuoDR7KT2dyAsY5SvO0s8m7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integumentary: Applying abdominal binders]]></video:title><video:description><![CDATA[As a nursing assistant, you may help provide care to clients who are recovering after surgery. These clients often need to have an abdominal binder applied, which is a wide band of elastic or cotton material that fits around the abdomen and does a variety of things. 

It helps keep dressings and bandages in place and speed up wound and incision healing; it also supports muscles, relieves pain, promotes deep breathing, and minimizes swelling and fluid buildup. 

Now, when applying an abdominal binder to a client, there are some common care tips you need to remember. First of all, it’s important to choose the right size of the abdominal binder for the client, because if it’s too big, it will not be effective and might even slip off. 

If it’s too small, it might irritate the skin underneath or cause trouble with breathing or blood flow. If there are any tubes or wound drains, be sure they are not kinked or compressed, so they can drain freely. 

Be sure to check under the binder regularly and observe the condition of the skin. Observe the surgical dressings, too. 

Also, ensure that the client is comfortable at all times and doesn’t experience any pain, discomfort, or feeling of pressure. 

Before applying an abdominal binder to a client, check with the care plan and the nurse to find out the type and size of the binder you should use. 

You should also find out if the nurse has any concerns about the client you should know about. You can then gather the supplies you’ll need, including gloves, gauze bandages, and the abdominal binder. Remember to also practice hand hygiene before putting on clean gloves. 

Start by raising the bed to a height that’s comfortable to work with. Lock the wheels and lower the bed rail on the side you’ll be working on. 

Assist the client into a comfortable supine position with the knees somewhat flexed, and then, help the client roll away from you facing the raised bed rail. 

Fold or roll the far ends of the binder toward the mi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Basic_care_needs_and_activities_of_daily_living</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bztgF12MQmKUwW3iUHkgAiBkQ7qmvx-0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Basic care needs and activities of daily living]]></video:title><video:description><![CDATA[We all have needs, and your client is no exception. A need is a necessary component in order to survive and maintain physical and mental health. Most people are able to fulfill their own needs. 

However, experiencing an illness, an accident, or advanced age can prevent them from doing so. As a nursing assistant, you need to recognize and assist these clients. 

Abraham Maslow, a well-known American psychologist, listed the needs in order of priority, and that list is referred to as Maslow’s Hierarchy of Needs. 

It’s often presented in the shape of a pyramid with the lower-level, or fundamental, needs at the bottom and the higher-level needs at the top. 

Remember, a person’s lower-level needs have to be fulfilled before they try to achieve higher-level needs. At the bottom of the pyramid are the physiological needs, such as oxygen, water, food, shelter, and rest. These needs must be met for a person to stay alive. 

Now, above them, there’s safety. In a healthcare environment, clients often feel uncomfortable or unsafe. Make sure to help them feel secure by explaining to them all procedures and listening to their concerns. 

Next is the need for a sense of love and belonging. This need is usually fulfilled by family, friends, and, in the case of a client, their team of healthcare providers. 

Then, moving higher in the pyramid, there’s self-esteem, which is the sense of self-worth, or self-respect. 

When a person loses the ability to take care of himself, for example, due to a neurological disorder such as Parkinson disease, they might lose their self-esteem. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integumentary:_Applying_dressings_and_bandages</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2ST4YV4pTEWF7MgGrG3LrzYJSUqYm6bU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integumentary: Applying dressings and bandages]]></video:title><video:description><![CDATA[Some of the clients you care for will have dressings on their wounds, which are used to protect the wound; absorb wound drainage, or exudate; keep microorganisms from entering the wound; promote comfort, or keep the wound dry during bathing. 

Some dressings can even be used to apply pressure to control bleeding, while others can help remove dead or infected tissue: a process called debridement. 

As a nursing assistant, you will have the opportunity to assist the nurse with applying dressings or bandages, and in the cases where your facility policy allows, you may be asked to apply dressings and bandages for some clients without the nurse’s assistance. 

One of the most common types of dressings you will apply are gauze dressings, which are made of cotton or synthetic material. A dry gauze dressing is applied to protect a wound and absorb small amounts of exudate. 

Sometimes a moist-to-dry gauze dressing is applied, which just means that the gauze is moistened first before it’s applied to the wound then a dry gauze is layered on top. 

As the moist dressing dries, it helps with debridement and removal of exudate. Gauze dressings are usually secured with tape, which can sometimes irritate the client’s skin,  especially as it is peeled off for dressing changes. 

In cases where the dressing is large and needs to be changed frequently, it can be secured with Montgomery ties, or tape ties, which is when a wide strap is attached to the skin and then tied together over the wound. 

Whenever the dressing needs changing, the ties are untied and then tied again over the new dressing, so no peeling of tape is required! 

If a dressing needs to be secured over a joint, such as a wrist or knee, a bandage made of rolls of webbing, gauze, or stretchy elastic material is wrapped around the dressing. 

Some small wounds, minor burns, or intravenous catheter insertion sites can be covered with a transparent dressing, which is a thin film with an adhesive coating on one s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endodontic_Diagnosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SwHJQaWjT2WQVU2HySP1ZOJLTR6KTNle/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endodontic Diagnosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Endodontic Diagnosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Periodontal_attachment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l_8Fs7WmRgKCJdRDnKgC0SvrRpCL3Usr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Periodontal attachment]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Periodontal attachment through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Plaque-induced_periodontal_disease_diagnoses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zDZFl14IRY2kel0QU3X_HJ9OSCKo32cq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Plaque-induced periodontal disease diagnoses]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Plaque-induced periodontal disease diagnoses through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intraoral_Biopsy_Techniques_for_Pemphigus_&amp;_Pemphigoid</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U9G6wgxVR56x7t84wRpYG31EQM_mvGqe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intraoral Biopsy Techniques for Pemphigus &amp; Pemphigoid]]></video:title><video:description><![CDATA[Hi! My name is Mark Mintline, and I am an oral and maxillofacial pathologist. And I would like to talk to you today about how to perform intraoral biopsies of vesiculobullous lesions. My goal is to talk to you a little bit about biopsy techniques and the laboratory testing of blistering diseases so that your comfort level for performing biopsies goes up.

Pemphigoid and pemphigus are rare autoimmune blistering diseases that often first present in the mouth. 

Unfortunately, often there are delays in diagnosis. On average, it takes 6-10 months for a person with pemphigus vulgaris to get a final diagnosis. And patients with pemphigus vulgaris or mucous membrane pemphigoid see an average of 5 healthcare providers before getting a final diagnosis.

Biopsies can quicken diagnosis times and save lives.

When taking a biopsy, our goal is to obtain a representative tissue sample with intact epithelium. For blistering diseases, both conventional H&amp;amp;E histology and direct immunofluorescence (DIF) are needed.

Pemphigus vulgaris is an acquired autoimmune disease that leads to intraepithelial separation.

Mucous membrane pemphigoid is a chronic autoimmune disease that results in subepithelial separation.

When taking a biopsy to evaluate for pemphigus and pemphigoid it is important to: 1) sample from a representative site, 2) not damage the tissue, and 3) appropriately transport the specimen.

In order to obtain a piece of representative intact epithelium, we should biopsy adjacent or perilesional to an active or new blister.

Biopsies of bullae, erosions, and ulcers will likely not yield intact epithelium and therefore will be non-diagnostic for the pathologist.

A biopsy of an ulcer will lead to a non-diagnostic specimen.

In general, two punch biopsies are preferable: one punch for H&amp;amp;E and one punch for DIF.

Punch biopsies are less likely to tear tissue and are less technique-sensitive than shave or larger biopsies.

You may choose to divide one b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Incident_reports:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KmY_KCr0SPqazW1pfRSJ-O41TFC7OmnL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Incident reports: Nursing]]></video:title><video:description><![CDATA[Nurse Kevin has just started his lunch time rounds on the unit. As he approaches room 3B, he’s shocked to see his client, Mrs. Baron, laying on the floor. Nurse Kevin moves quickly to reach Mrs. Baron, and immediately assesses the situation. 

“Mrs. Baron, are you alright?”. “Oh, I’m just fine”, she says, “I fell out of bed trying to reach my meal tray.” After ensuring Mrs. Baron’s safety and collecting information from her about what happened, it’s time for Nurse Kevin to complete an incident report:

Incident reports, or sometimes called incident reporting, unusual occurrence report, or variance report; is a commonly used term to describe safety event reporting. A safety event can occur when evidenced-based best practice isn’t followed, resulting in harm or potential harm to a client. 

Some examples of safety events include accidental needlesticks, falls, medication errors which are the number one cause of incidents, defective systems or equipment failure, missing client belongings and hospital acquired infections. Usually, an incident report is generated from the healthcare worker, like a Nurse Kevin for example, that was either involved in the incident or witnessed it. 

Now, incident reports are an important safety communication tool, and the ultimate goal of this type of reporting is to provide risk management and healthcare administration with information that can help them identify areas that are most prone to error. 

For example, if a risk manager recognizes there’s an increase of reports about clients falling out of bed, this can indicate problems with things like bed safety, client monitoring, or the call light system. 

With the data collected, risk managers, hospital administration and staff can further research the events and help develop best practices to prevent those events from occurring in the future. 

While many facilities encourage and support the reporting of incidents, it’s essential that they also have a solid plan in place for f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Emotional_and_mental_health_needs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/np6TSjpZRbmxgJpWA0-pnk1IQ-a-zaAH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Emotional and mental health needs]]></video:title><video:description><![CDATA[As you care for your clients, you will often assist them to meet their emotional and mental health needs as they deal with the stress of illness, hospitalization, changes in their ability to care for themselves, and other personal and family issues. 

Understanding how stress and coping affects your client&amp;#39;s emotional and mental health will help you give the best care possible for your clients.

Now, everyone has felt overwhelmed or stressed at some point in their life. Stress is a physical or mental factor that causes tension emotionally or physically. 

This can be due to external factors, like having to adapt to major life changes, or internal factors, like having an illness.  Many people learn to use certain activities to relieve stress and feel better. 

These are called coping mechanisms, which are specific activities people purposefully decide to engage in to relieve stress. 

Some people have healthy coping mechanisms, like jogging, spending time with friends, singing, or meditating, while others may rely on smoking, overeating or undereating, nail biting, or abusing alcohol or illicit drugs. 

While these alternative coping mechanisms may relieve stress temporarily, they can increase the risk of both physical and mental health problems.  

While coping mechanisms are conscious and deliberate reactions to stress, defense mechanisms are our natural, often unconscious, reactions to stress that try to protect us from emotional trauma. 

Compensation is when we try to make up for a loss by filling the void with something else positive. 

For example, someone struggling with loneliness after a divorce might volunteer at an animal shelter.

Conversion is when emotions manifest as, or are changed into, physical symptoms. For example, someone who is emotionally upset complains of chest pain or difficulty breathing.

Denial is refusing to accept or believe something that is true or the feelings associated with it, especially if the truth is frighte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Types_of_personal_protective_equipment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-EbWYmqCTRKNfSY8YF6yeJZWS3GZ9wLV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Types of personal protective equipment]]></video:title><video:description><![CDATA[When assisting with client care, personal protective equipment, or PPE for short, should be used to avoid transmission of infection to and from the client. 

This includes wearing non-sterile gloves, a gown, a mask, goggles, or a face shield as needed. The PPE needed depends on the type of the procedure, the client, and the risk for exposure to body fluids. Okay, let’s take a closer look at the components of PPE, starting with non-sterile gloves. 

These should be used every time there is a risk for exposure to blood, all types of body fluids, secretions, and excretions, as well as open skin lesions or rashes; mucosal surfaces, such as when providing perineal care; and possibly contaminated items, such as soiled clothing and linens or contaminated surfaces. 

Now, when wearing non-sterile gloves, there are some general considerations for you to follow. First of all, the gloves must be intact without any holes, so make sure you don’t tear them when putting them on. 

Long and rough fingernails or rings can also tear the gloves. Also, be sure that they fit properly, meaning that they’re not too loose or too tight, and cover your wrists. 

In case you or the client is sensitive to latex, use gloves that are from a different material, such as vinyl. It is also important to use a different pair of gloves for every client and for every procedure. 

Also, when caring for a client, change gloves when moving from a contaminated site of their body, such as the perineum, to a site that’s cleaner. 

Also, remove contaminated gloves when you need to touch a commonly used item or surface, such as a light switch, door handle, or faucet. 

Always consider the outside of the gloves as contaminated and the inside as clean. Now, when removing the gloves, turn the inside out and dispose of them safely. 

Afterwards, don’t forget to wash your hands before putting on gloves and after removing them. Moving onto waterproof gowns. These usually open at the back and will cover you ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Putting_on_and_removing_personal_protective_equipment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iWpHWDI4RfqGPLvVmkUjC_eLRWyMcShJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Putting on and removing personal protective equipment]]></video:title><video:description><![CDATA[When assisting with client care, personal protective equipment, or PPE for short, should be used to avoid transmission of infection to and from the client. 

PPE should be used when there’s risk of exposure to blood; all types of body fluids, secretions, and excretions; open skin lesions or rashes and mucosal surfaces; and possibly contaminated items or surfaces. Now, the PPE you need to wear can vary from situation to situation. 

This includes wearing non-sterile gloves, a waterproof gown if there’s a possibility that your clothes might get contaminated, protective mask or respirator to protect you from inhaling microbes through your nose or mouth, and goggles or a face shield for procedures where splashes of body fluids are likely not all the pieces are needed in every situation

Now, there are some general considerations that must be undertaken by the nursing assistant when putting on or removing PPE. First, don’t forget to wash your hands before putting on PPE and after removing it. 

Keep in mind that PPE items can come in various sizes, so make sure you pick the right size. Remember to check that your PPE is intact and without any damage before putting it on. 

If your gloves get torn or become heavily contaminated, take them off, wash your hands, and put a new pair on. 

Once you have your PPE on, be sure to keep your hands away from your face and avoid touching surfaces unnecessarily. 

Finally, PPE should be used only once so remember to change all PPE between clients. Make sure you remove PPE at the doorway before leaving the client’s room, except for the mask or respirator.

Let&amp;#39;s get started. The first item we put on is the gown, which can be disposable or non-disposable. 

The opening of the gown should be at the back while, at the front, the gown should fully cover your torso from the neck to knees as well as the entirety of the arms. Make sure your gown is securely fastened to your body with the drawstrings snug.

The next step is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Standard_and_transmission-based_precautions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vIzBvbUJRkyoSUtzpCrQf-mURpeAB2V6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Standard and transmission-based precautions]]></video:title><video:description><![CDATA[When assisting with client care, a set of protective practices should be applied to prevent the transmission of infection to and from the client. 

These include standard precautions which are used for any client, at any time, in any situation and transmission-based precautions for clients with a diagnosed or suspected infectious condition.

Okay, let’s start with standard precautions. So, every time there’s a risk for exposure to blood, all types of body fluids, secretions, and excretions other than sweat, as well as open skin lesions or rashes, mucosal surfaces, and possibly contaminated items or surfaces, make sure to utilize personal protective equipment, or PPE for short. 

This includes wearing gloves, a waterproof gown if there’s a possibility that your clothes get contaminated, and protective mask, goggles, or a face shield for procedures where splashes of body fluids are likely. 

When moving from a contaminated area to a clean body area, remember to change your gloves and wash your hands thoroughly. 

If there’s no access to water or soap and your hands aren’t visibly dirty, you can also use an alcohol-based sanitizer. Remember to still wash your hands afterwards as soon as you can.

Do the same after touching any surfaces in or out of the care setting. Now, in the case of unexpected contact with blood or any body fluids, wipe up any spills, disinfect the area with a facility-approved cleaning product, and practice hand hygiene right away. 

In any case, before leaving the client’s room or moving on to another client, remove all your personal protective equipment and practice hand hygiene.

Next, to limit the potential transmission of respiratory infections, standard precautions include wearing a mask when caring for clients with suspicious signs or symptoms, like cough. 

It’s also important to instruct these clients to keep at least a 1 meter, or 3 feet, distance between themselves and others or to otherwise wear a mask. 

Clients should also r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Waldenstrom_macroglobulinemia_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/skkNE4GqT76oqKHwujMCDbqnS-GZWdQE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Waldenstrom macroglobulinemia (NORD)]]></video:title><video:description><![CDATA[Waldenstrom macroglobulinemia is a rare type of blood cancer that affects a specific type of white blood cell called B lymphocytes, which normally produce immunoglobulins like IgM. 

This disease leads to high numbers of these cells in the bone marrow, which is located at the spongy center of some bones; as well as in lymphatic tissues, like the spleen and lymph nodes. 

The increased number of B lymphocytes results in the production of high levels of IgM. This can ultimately cause the blood to become very thick, almost jelly-like, which prevents the normal, smooth blood flow throughout the body.

Some of the signs and symptoms of Waldenstrom macroglobulinemia are caused by blood flow changes. 

Damage to small blood vessels can lead to bleeding, and this is especially common in areas of the body with delicate blood vessels, like the nose and gums. 

If there’s involvement of the retina, the inner lining of the eye, individuals may present with impaired or blurred vision. 

Accumulation of B lymphocytes in the bone marrow can lead to anemia, which occurs when there aren’t enough red blood cells to deliver sufficient oxygen to body tissues. 

As a result, individuals may experience fatigue and weakness. Patients may also experience tingling in the extremities, like fingers and toes. 

Lastly, the immunoglobulins tend to accumulate in the lymph nodes, spleen, and liver, making these organs enlarge.

B lymphocytes develop in the bone marrow. As they become more mature, they leave the bone marrow and move into the blood and lymphatic tissues. 

Mature B lymphocytes produce specific proteins called antibodies, also known as immunoglobulins or Ig for short, which circulate around the body and help identify and fight off infections. 

There are a few types of antibodies, one of which is IgM. Since it is the largest of the antibodies, it’s considered a macroglobulin. 

In Waldenstrom macroglobulinemia, B lymphocytes do not function properly. They abnormally divide]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/NGLY1_deficiency_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z03UB9pjT3GIvDzOwoLG4M0ZQWCpJt23/_.jpg</video:thumbnail_loc><video:title><![CDATA[NGLY1 deficiency (NORD)]]></video:title><video:description><![CDATA[NGLY1 deficiency is a rare genetic disorder affecting multiple parts of the body due to a deficiency of the enzyme N-glycanase. 

Enzymes are proteins which help speed up chemical reactions in the body and N-glycanase speeds up the removal of sugar chains from proteins. 

Without this process, proteins do not function normally and misshaped ones may accumulate. NGLY1 deficiency is a chronic condition that presents during infancy and early childhood.

NGLY1 deficiency has a number of characteristic symptoms, although the specific symptoms a patient experiences are often unique to the individual. 

Most infants and children with NGLY1 deficiency do not grow or develop as expected. Symptoms may include low birthweight, a smaller than expected head circumference, and missing developmental milestones, such as walking or talking. 

Intellectual disability is also common. Many affected individuals have motor problems including shaking and uncontrollable movements, which can range from slight tremors while trying to do fine motor skills like writing, to an uncontrolled sometimes painful jerky movement. 

Skeletal abnormalities may also occur such as small hands or feet, frequently broken bones, uneven shoulders or hips, difficulty standing up straight, and dislocated joints. 

Some patients develop seizures which can start as early as two months of age. Individuals with NGLY1 deficiency often will not produce tears when crying. 

This in turn may cause other complications, such as scarring and ulcers in the eyes, painful or irritated eyes, and poor vision. Lastly, liver problems may arise in children with NGLY1 deficiency.

NGLY1 deficiency is caused by changes or  mutations in the NGLY1 gene, and follows an autosomal recessive inheritance pattern. 

This means that both copies of the NGLY1 gene must be mutated for an individual to have the disorder. The mutated NGLY1 gene causes the N-glycanase enzyme to be dysfunctional or be completely absent. 

N-glycanase’s r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Recurrent_pericarditis_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b_hXV6LxSwu7Q6KM51eSOtyUSk2GgjEJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Recurrent pericarditis (NORD)]]></video:title><video:description><![CDATA[Recurrent pericarditis is a disease characterized by recurring episodes of swelling or inflammation of the fluid filled sac surrounding the heart, the pericardium. 

Pericarditis is considered recurrent when an episode occurs at least four to six weeks after the end of a previous episode. 

Each episode may last days to weeks and be followed by a period of time with  no symptoms between episodes.

The main symptom of a pericarditis episode is a sharp chest pain that increases when taking deep breaths and lying down. 

Pain may decrease when bending forward and may spread to the neck, upper back, or shoulders. 

Other symptoms include shortness of breath, fever, tiredness, not feeling well, and a feeling that the heart is beating too hard or fast. 

Symptoms of a recurrent pericarditis episode are usually similar to, but less severe than, the first episode. If the pericarditis becomes severe, blood flow throughout the body may decrease. 

This decreased blood flow may make symptoms more intense, and may cause new symptoms such as dizziness, confusion, nausea, clammy moist skin, feet swelling, and loss of consciousness.

Anything that can cause pericarditis can also cause recurrent pericarditis. Most often this includes autoimmune diseases such as systemic lupus erythematosus or rheumatoid arthritis, but may also be caused by metabolic disorders such as kidney failure, and rare inflammatory diseases like familial Mediterranean fever. 

Recurrent pericarditis can also be caused by pericardial infections from viruses, drugs that target the pericardium, cancer, heart attacks and  cardiac surgery.

All of these causes result in damage to pericardial tissue. In response to the pericardial injury, the body’s immune system begins to repair the tissue, causing swelling and inflammation in the area. 

This inflammation may expand to surround the lungs leading to chest pain and difficulty breathing. The inflammation can also cause blood vessels around the heart to bec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Classical_homocystinuria_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LNTpgwj5Txu0ddRjrNnMb5hdQ3uIT2Z3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Classical homocystinuria (NORD)]]></video:title><video:description><![CDATA[Classical homocystinuria also called cystathionine beta-synthase, or CBS, deficiency is characterized by too much of the amino acid homocysteine in the blood and urine. 

Amino acids are the building blocks of proteins, and proteins are needed for proper growth and development of our bodies. Enzymes are a type of protein in the body which help speed up chemical reactions. 

CBS deficiency usually occurs when there is a problem with one of the enzymes involved in converting the amino acid methionine into the amino acid cysteine, resulting in a buildup of methionine and homocysteine and decreased production of cysteine.

This build up of methionine and homocysteine amino acids can cause a wide range of symptoms which vary by severity and age. 

Infants experience generalized symptoms such as slow growth and weight gain, as well as possible developmental delays. After age three, more specific symptoms begin to appear. 

Symptoms in the eyes may include the lenses of the eye dislocating or becoming cloudy, severe nearsightedness, and quivering of the iris. 

Other symptoms may include vision loss from damage to the primary nerve that sends signals from the eye to the brain, severe headache or eye pain from increased pressure in the back of the eye, and blurry vision or “floaters” in the field of vision from retinal damage.

Skeletal abnormalities also occur, with people affected by the condition characteristically having long, lanky limbs, and knees that bend towards each other when standing up straight. 

The arch of the inside of the foot may be high, with the majority of the foot not touching the ground. The chest may also stick out more than usual or cave inward. 

Older individuals with CBS deficiency tend to experience a decrease in bone density, making it easier for their bones to fracture.

Blood clots can also form at any age, causing the most serious complications of CBS deficiency depending on the location of the clot. 

These complications include ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cyclic_vomiting_syndrome_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HKjdl6OJRg25Q4ItFJT9RLIQQ520ErBm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cyclic vomiting syndrome (NORD)]]></video:title><video:description><![CDATA[Cyclic vomiting syndrome, or CVS for short, is a disorder characterized by recurrent or cyclic episodes of severe nausea and vomiting. CVS can occur at any age, but is typically more common and severe in children.

Episodes of nausea and vomiting may last for a few hours to several days. They generally have sudden onset, resolve for a period of time, and are similar each time. 

In some people, especially adults, nausea and vomiting may continue between episodes,but the intensity is far less severe than during episodes. 

Episodes may occur a few times a year or as frequently as several times a month. Episodes may return like clockwork, and monthly episodes are common. They can occur at times of stress, or be apparently random.

During an episode, vomit can be bilious, appearing green or yellow. Children may experience bouts of projectile vomiting as frequently as four or more times per hour, which can potentially lead to dehydration and electrolyte imbalances, involving sodium and potassium. 

Episodes can also be associated with severe abdominal pain, retching, and diarrhea, as well as decreased appetite and weight loss. 

Some individuals may also experience migraine-like symptoms, like headaches and sensitivity to light and sound, as well as fever, dizziness, a lack of energy, and pallor. 

In severe cases, an individual can become incapacitated and unable to walk or talk until the episode resolves. The exact cause of CVS is still unknown, but it seems to have many contributing factors. 

The nervous system is thought to play a role. Nerves deliver messages throughout the body, including between the brain and gut, to coordinate functions.

Most individuals with CVS have migraines or a family history of migraines. In fact, CVS is sometimes called “abdominal migraine”.

Gastrointestinal motility may also  have a role. The gastrointestinal tract has a layer of smooth muscles, which normally help push food, liquid, and gas from the esophagus down to the re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Emergency_care:_Medical_emergencies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MQtxATUASRCcsQ6vf_-PQeZoSSG6QpUm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Emergency care: Medical emergencies]]></video:title><video:description><![CDATA[Medical emergencies are conditions that endanger an individual&amp;#39;s life or threaten to leave permanent disability; they require immediate medical care. 

As a nursing assistant, you need to know how to recognize these life threatening situations and follow your facility’s policy to provide proper care and first aid until help arrives. Let’s go over some of the most common medical emergencies.

Heart attack, also known as myocardial infarction or MI, is a condition that develops when an artery that supplies the muscular wall of the heart gets blocked by a blood clot, stopping the normal blood flow. 

The part of the muscle that is supplied by the affected artery is now deprived  from the oxygen and starts to die, losing its ability to contract. 

Smaller damage can decrease the heart’s ability to pump out blood, while extensive damage can lead to cardiac arrest.

Signs and symptoms of a heart attack include severe chest pain that feels like pressure or squeezing, and the pain can radiate to the left arm, neck and jaw, back, or stomach. 

Your client could also have an increased heart rate; shortness of breath; cold, pale, and sweaty skin; nausea; and fear of death.

If you recognize these signs and symptoms, assist your client to lie down and elevate the head to facilitate breathing. Because time is of the essence, immediately call the nurse and activate the emergency medical services system. 

While waiting for the help, try to calm your client down, monitor vital signs, and be ready to provide basic life support if needed.

Now stroke, also known as a brain attack or cerebrovascular accident, CVA for short, is similar to a heart attack, but this time, parts of the brain get cut off from the blood supply. 

There are two types of stroke: hemorrhagic stroke, where a blood vessel in the brain ruptures and bleeds into the brain, and ischemic stroke, where a blood vessel gets obstructed by a blood clot, stopping the blood flow. 

In both types, brain ce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Introduction_to_vital_signs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yfgiz768QQ2bIu8HtdySWeNuQyi4awTJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Introduction to vital signs]]></video:title><video:description><![CDATA[The commonly measured vital signs include body temperature; blood pressure; heart rate, also called pulse; and respiratory rate. Pain is often considered a vital sign and is measured along with the others. 

Measuring vital signs is a crucial component in taking care of a client’s health. Vital signs help assess the general physical health of a person, provide clues to possible diseases, and help monitor the progress of the client’s health status. 

Normally, vital signs are measured and interpreted by a nurse. However, as a nursing assistant, you will be asked to measure vital signs, and so you will need to know how to measure them.

Vital signs are typically measured at certain times. First, vital signs are measured when you encounter the client for the first time during the admission process or during the initial home care visits. 

This will provide the client’s baseline and can be used to compare with future measurements. Usually, vital signs are measured every shift. Clients who are ill, like those in hospitals, need their vital signs measured every few hours. 

You will even find some severely ill clients attached to machines that monitor their vital signs continuously. 

On the other hand, clients such as those in long-term care facilities, may have their vital signs measured only a couple days each week. 

The client’s plan of care will specify how often the client’s vital signs need to be taken, so make sure you check that as well.

Next, vital signs are often measured when the client is receiving medications; during nursing interventions; and before, during, and after medical procedures, such as surgical operation. 

This is because such procedures may cause significant stress to the client that may result in a significant change in the vital signs. So, it is important to take measurements, document them, and report to the nurse. 

You should also measure vital signs after an incident, like a fall; when you notice changes in the client’s status ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Pulse_oximetry</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q5Rp8WMQQfOSQICMWZH7jkmwR4Ogv89E/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Pulse oximetry]]></video:title><video:description><![CDATA[As a healthcare professional, you will help provide safe care to patients who have or are at risk for hypoxemia, or low levels of oxygen in the blood. These patients require pulse oximetry, or pulse-ox for short, which is a non-invasive, easy, and pain-free method of measuring the percentage of hemoglobin that’s saturated with oxygen. This is known as the saturation of peripheral oxygen or SpO2 for short. A normal SpO2 usually indicates that the amount of oxygen travelling through the bloodstream to the tissues is enough to meet the needs of the body. 

Now, a pulse oximeter consists of a probe, which is attached by a cable to a pulse oximeter. The probe has a light source on one side and a photodetector, or sensor, on the other side.  

So, when it gets clipped onto a body part, two different wavelengths of light shine through the tissues on one side, and on the other side, the sensor detects how much of each wavelength has been absorbed by the arterial blood in the tissues. The principle is that, when hemoglobin is bound to oxygen, it absorbs a different wavelength of light than when it is not bound to oxygen, so the percentage of hemoglobin bound to oxygen can be calculated by the device.  

Now, there are several types of probes, depending on the site where they can be placed. The most commonly and easily used ones are digit probes, which can fit onto a finger or a toe. There are also earlobe probes, which attach to the patient’s ear. Less commonly, if the digits or earlobes are inaccessible, a pulse oximetry probe can be applied across the forehead and secured with a headband. Both earlobe and forehead probes tend to be more accurate than digit probes in cases when blood flow to the extremities is compromised or if the patient moves their hands or feet frequently, creating motion artifacts.  

There are also sensor pads that can be used on several different sites, including an adult&amp;#39;s nose bridge and a newborn&amp;#39;s palms or soles.  

No]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Measuring_peak_expiratory_flow_rate</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4iR_x2WsQmqSEoWAovDC2YRIRMaCdOw6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Measuring peak expiratory flow rate]]></video:title><video:description><![CDATA[Peak expiratory flow rate, or PEFR for short, is the fastest and the hardest someone can exhale after a full inspiration. 

This can be used to measure the client’s ability to push air out of their lungs and, thus, measure the amount of obstruction in the airways of clients with certain respiratory conditions, like asthma. 

This is essential to determine how open their lungs are, if their treatment is working properly, and if they need a dose adjustment or even a new medication.

Measurement of PEFR is performed with a special portable handheld device called a peak flow meter. 

This is made up of a mouthpiece attached to a numbered scale with a small arrow that moves as the client blows air out, indicating the speed of airflow measured in liters per minute.

Now, before you start assisting a client with measuring PEFR, here are some general considerations. 

Clients that are experiencing pain, motor function impairments, and people with dementia or other cognitive impairments might be unable to measure PEFR independently. Those who can, should perform PEFR measurements at home or in a healthcare facility. 

Measurements are done regularly at certain times, such as first thing in the morning and last thing at night, before or after using asthma medications, or when experiencing symptoms of an asthma exacerbation, like shortness of breath, cough, or wheezing.

When assisting a client with their PEFR test, first make sure the client is standing erect if they’re able. 

The arrow should be set on the zero mark and a clean, disposable mouthpiece should be attached to the device. 

Instruct the client to inhale through the mouth by taking a deep breath and placing their lips tightly around the mouthpiece, keeping their tongue away from the opening. 

Then, the client should exhale as fast and forcibly as possible. This process should be repeated twice more. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Oxygen_therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E86_vKbJRGmH3Lxk8XVkzuXjS5GdBSZw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Oxygen therapy]]></video:title><video:description><![CDATA[Oxygen therapy is the delivery of extra oxygen to those with conditions that cause hypoxemia, when oxygen levels in the blood are low; and hypoxia, which is when there is not enough oxygen at the tissue level to meet the needs of the body.  

This includes patients with diseases that interfere with the lungs’ ability to absorb oxygen, like pneumonia, chronic bronchitis, emphysema, and pulmonary fibrosis; blood problems, like anemia, where the blood doesn&amp;#39;t carry enough oxygen; and heart problems, like heart failure, where the heart has trouble pumping blood around the body.  

Now, oxygen is considered a medication, so an order is needed. 

An oxygen setup consists of an oxygen source and a delivery device. There are several sources for oxygen therapy. With a wall outlet, oxygen is delivered into each patient room from a central supply.  

In contrast, an oxygen tank contains oxygen gas under pressure and is typically portable, so it can be carried along as the patient moves. However, this should be moved very carefully; if the tank tips over and the valve breaks open, pressurized oxygen can burst out forcefully and result in severe trauma. Oxygen tanks have a gauge that shows how much oxygen is left. There are also liquid oxygen systems which store oxygen as a liquid at very cold temperatures and then convert it to a gas for use. They are used either for bulk storage of oxygen for a hospital system or can be portable for home use for patients with high oxygen needs, where having a compact way to storge large amounts of oxygen is helpful.  

Finally, oxygen concentrators pull in air from the atmosphere and selectively remove nitrogen to deliver air that is about 90 to 95% oxygen to the patient. These devices are easy to use and can deliver an unlimited amount of concentrated oxygen as long as they have a power supply. One caveat is that some units are designed to only deliver up to 5 liters of oxygen per minute, and so those aren’t a good fit for ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Mechanical_ventilation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XNuGiUYYTjmeUxaJokwwbJsvQuyOUC8p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Mechanical ventilation]]></video:title><video:description><![CDATA[As a nursing assistant, you will help provide safe care to clients with mechanical ventilation. This is when a machine reduces or even takes over the work of breathing from clients who find it difficult or impossible to do so without help.

The use of mechanical ventilation can range from short to long term and from care in a healthcare facility to home care.

Okay, now, mechanical ventilation can be “invasive” or “noninvasive.” Invasive mechanical ventilation involves the insertion of an artificial airway. An artificial airway is basically a tube that gets placed in the trachea.

One example of this is an endotracheal tube, which is a tube that gets inserted through the mouth and down past the pharynx and larynx into the trachea.

Another is a tracheostomy tube, which is inserted directly through an opening made in the skin of the neck, called a tracheotomy.

Typically, both types of tubes have an inflatable balloon that forms a seal against the tracheal wall. Tracheostomy tubes are also kept in place with a collar or ties wrapped around the client’s neck.

Now, the thing with endotracheal tubes is that because they go through the pharynx and larynx, the client won’t be able to speak, drink, or eat anything via the mouth, which can be extremely uncomfortable for the client.

If mechanical ventilation is required for a long period of time, a tracheostomy tube might be preferred over an endotracheal tube.

Endotracheal tubes can be used only temporarily, for a few weeks, but tracheostomy tubes can be used permanently, such as for clients whose larynx has been surgically removed due to cancer or those with paralyzing conditions that require them to stay on a ventilator permanently.

Now, tracheostomy tubes allow the client to take food or fluids normally through the mouth. Speaking with a tracheostomy tube in place has also been made possible through one-way speaking valves, such as the Passy-Muir valve.

This valve opens as the client breathes in and closes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocrine:_Blood_glucose_testing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YjdKI_frSCKXLFuu7iq6I8X6QwGlCETo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocrine: Blood glucose testing]]></video:title><video:description><![CDATA[Blood glucose testing is a procedure used to measure a client&amp;#39;s blood glucose level using a small portable device called a glucometer. 

It requires a drop of capillary blood most commonly obtained from a finger and takes a few seconds to show results. 

This is especially important for people with diabetes mellitus type 1 and type 2 as well as gestational diabetes. 

Regular blood glucose testing evaluates effects of medications, diet, and exercise to keep blood glucose levels under control. 

This will prevent future complications like vision impairment, kidney and nerve damage, and cardiovascular disease.

As a nursing assistant, you might be asked to help test a client’s blood glucose, so here are some general considerations. 

First, check to see if the procedure is within your authorized duties and follow facility policies and/or protocols. Also, make sure to familiarize yourself with the type of glucose meter used at your facility. 

Next, the clients might have thickened, damaged, edematous, or inflamed areas of skin, so you should ask the nurse to determine the most appropriate site for a puncture. 

Some need testing only once a day, while others might need it more than once and at specific times, like before meals or drug administration. 

Clients who have coagulation disorders or take drugs that can alter bleeding time might take longer to stop the bleeding after the procedure. 

Be sure to check with the nurse and the plan of care to determine how often a client needs their blood glucose checked and what’s the normal range for the client.

Now, before you perform blood glucose testing, gather the necessary supplies including gloves, lancet device, antiseptic swab, washcloth, cotton or gauze, and glucometer and strips; make sure you read the instructions on how to use a glucometer because some steps might differ depending on a manufacturer. 

For the procedure, make sure your client is comfortably sitting or lying in bed in the semi-Fo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Oropharyngeal_suctioning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ad6JWnUgTrCLh-AhdjLl5qOARgm3CTXq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Oropharyngeal suctioning]]></video:title><video:description><![CDATA[Oropharyngeal suctioning is a procedure used to remove secretions from the oral cavity and pharynx. Secretions can block the trachea and obstruct the normal airflow, which can lead to an insufficient oxygen supply. 

Normally, clients cough to remove these secretions, but some individuals are too weak or cannot cough, so these clients require suctioning to clear the airway. 

Generally, the nursing assistants should alert the nurse if they think a client requires suctioning. They can assist the licensed nurse in oropharyngeal suctioning by gathering the required supplies.

Now, common signs and symptoms that suggest that a client may require suctioning include difficulty coughing up secretions and swallowing, decreased consciousness, visible secretions that obstruct the airflow, vomitus in the mouth, and noisy breath sounds. 

This procedure is also used in individuals who have had oral surgeries; mouth trauma; or cerebrovascular injuries, like a stroke that results in drooling and impaired swallowing. 

Finally, oropharyngeal suctioning is used to provide oral hygiene and prevent infection in individuals that have impaired swallowing or artificial airway.

Now, the suction catheter used for oropharyngeal suctioning is a rigid, bent, and plastic catheter called the Yankauer suction catheter, or Yankauer tip. 

A Yankauer suction catheter is transparent, which lets you see the secretions and fluids being suctioned out. 

The standard type of Yankauer catheter has a bulb tip with one large and several smaller openings. 

The bulb tip prevents trauma to the oral cavity, while smaller openings provide suctioning even if the large opening is blocked. Switching gears and moving on to the supplies you need to gather for the procedure. 

This includes clean gloves; mask and goggles, or face shield; bath towels, cloth, or disposable paper drape; disposable cup or washbasin; and tap water or normal saline. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assistive_devices_for_ambulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Okc69aFRRjSMQTQOuXX33uJ6QwCoD-rz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assistive devices for ambulation]]></video:title><video:description><![CDATA[Assistive devices for ambulation, or just ambulation devices, are tools used to aid in walking.  The most common types include walkers, canes, and crutches. 

You need to know when each of these are appropriate and assess if the patient is using them correctly. 

Remember that a patient’s ambulation device is ordered to fit them specifically, kind of like glasses, so they should not be shared with other patients.  

Let’s start by looking at walkers. These are movable, lightweight devices that consist of a metal frame, 2 hand grips, and 4 legs. 

Walkers provide great stability due to their wide base, so they are great for people who can bear weight on their feet but have trouble walking due to weakness of the legs or balance issues. 

When assessing the proper fit of a patient’s walker, make sure that the hand grips are at the patient’s waist level. Check the legs because they should have non-slip tips like a rubber cover. 

To use a walker, the patient should stand straight while holding the hand grips. When moving forward, they lift it up and move it another 6-10 inches in front of them and set it down. 

Because many patients have difficulty lifting a walker, many models now have wheels on the front legs. However, these are prone to rolling forward, so brakes are usually built in. 

So, when the patient is going to stand for a while, make sure the brakes are locked. Using the walker as support, they should move one leg forward and then the other. Once balance is reestablished, repeat the process. 

Next up, we have canes. These are also movable, lightweight devices made of a strong material like wood or metal. Canes consist of a handle, a shaft, and legs. 

There are single leg, triple leg or quad leg canes, and the ones with multiple legs provide more stability but are also more cumbersome. 

Canes are used by patients who could bear weight but have weakness in one of their legs, like a stroke patient or those with paralysis in one leg. 

Crutches and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assisting_with_ambulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vTiUsdP_SrSS1uh8hiXBrhfrT4WTDIj-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assisting with ambulation]]></video:title><video:description><![CDATA[Ambulation means “walking,” and your client might need to ambulate to get to places or may need to do it to prevent atrophy, which is when muscles waste away from prolonged bed rest. 

Other health problems from long-term immobility include decreased cardiovascular and pulmonary functions, poor digestion, pressure ulcers, contractures, urinary problems, and many others. So, even if they require assistance, clients are encouraged to ambulate frequently.  

Before we talk about ambulation assistance, here are some general considerations. Explain to the client how far you’ll be walking and how you will assist them. 

Check if they need an ambulation device, like a cane or walker. If a device is needed, check to see if it’s functional. Make sure the route is not slippery and that there are no obstacles. 

Make sure IV lines and poles are free from tangles and that the IV pump is unplugged from the wall and has enough battery to last during ambulation. Make sure they’re properly dressed and wearing non-skid footwear. 

During ambulation, encourage them to walk normally without shuffling or sliding. You might need an additional assistant if the person’s unbalanced, weak, or not cooperative.

Finally, and most importantly, be sure not to leave the client’s side at any time during the process.  

Now, before getting a resting person to stand and walk, you need to get them into a sitting, or “dangling,” position, where they sit erect with their feet dangling off the side of the bed. 

The main reason for this is to protect against falling. One common cause of falls is orthostatic hypotension, where blood rushes into the legs as the person shifts into an upright position, causing a drop in blood pressure and decreased blood flow to the brain. 

It can result in dizziness or even fainting, especially in the elderly. If you have the person stand in this condition, it could lead to falls, so having them sit in the dangling position will help their body adjust without t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Transferring_clients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8CiWZpGiR4aMmcS-YSTk_IX0ReS8WsXP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Transferring clients]]></video:title><video:description><![CDATA[Transfer is defined as the process of moving a person from one surface to another one. Clients that typically require a nursing assistant’s help with transferring include those who are weak or paralyzed, have recently had surgeries, or are injured. 

The most common hospital transfers include bed to wheelchair transfer, wheelchair to bed, bed to stretcher, and vice versa. 

Regardless of the type of transfer, you should always keep in mind some safety measures to protect yourself and your clients. 

Plan the transfer and explain the procedure to the client.  Adjust the bed height to a comfortable level for work and lower the side rails if they are up. 

When using wheelchairs, don’t forget to line up the front swivel wheels with the back wheels when transferring clients. 

As far as clothing measures go, a person&amp;#39;s clothing should fit them well, while their shoes must provide a good grip and have non-skid soles. 

During the transfer, clients should always lead with their stronger side, but they should not hold onto you around your neck. Instead, they can use your arm or the arm of the chair for support. 

Don’t put your hands under the client’s arms to support them because, if they fall, this can lead to more injuries. 

Protect yourself by using correct body mechanics, and most importantly, spread your feet shoulder-width apart and keep your back straight!

Now let’s focus on a transfer belt, also called a gait belt! When your client is unable to sit, stand up, or walk, you can use a transfer belt to make the whole process easier and safer. 

When used to help a person walk, this belt is usually made from canvas, nylon, or leather with a buckle at the end. Some belts also have loops that the caregiver can hold onto. 

The transfer belt is put around the client’s waist, and it can be used to maintain the stability of the client, reposition individuals in chairs and wheelchairs, and assist with ambulation. 

It’s important to note that these ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Repositioning_clients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RVaMNeZWQkiKlOJClWhMs_8JRHmpGrVU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Repositioning clients]]></video:title><video:description><![CDATA[Most clients will reposition themselves when they get uncomfortable from staying in the same position for too long. 

However some people, like those in a coma, in a hip or full body cast, or recovering from surgery, will need your assistance. In addition, many clients will need to be repositioned for procedures or other activities.  

Now, you’ll need to know the different procedures when moving a client into different positions,  but there are a few things to keep in mind for all of them. 

If the person is large, confused, or non-cooperative, you might need to ask for assistance. Be sure to check for tubes and drains, so you don’t accidently pull them out. 

Make sure the wheels on the bed or wheelchair are locked and hand rails on the bed are lowered. Check to see if the client is properly covered for their modesty. 

Be sure to use good body mechanics. Stand with your feet spread shoulder-width apart and knees slightly bent to protect your back. 

Be gentle and do not lift them by their limbs. When moving someone with a cast that’s still wet, try to use only the palms of your hands. 

This will help spread the force over a larger area and prevent deforming the cast before it can dry. 

For immobile clients resting in the supine position, first reposition them to a lateral position, then back to the supine position, and finally the lateral position on the other side. 

Remember everyone needs to reposition at least once every two hours to prevent complications, like pressure ulcers and contractures, and some will need to be moved more frequently. 

When you’re done, check that their clothing and the bedsheets are not tangled and replace any pillows you moved. 

When moving someone towards one side of the bed for easier access during a procedure, first make sure the bed is raised to a height that’s comfortable for you to work with. 

Make sure the head of the bed is flat. Slide your hands under their head and shoulders to move their upper body gent]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Condom_catheters</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dcdLaI0PT5WOSsKJGVnC5UbCTxKCz_XP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Condom catheters]]></video:title><video:description><![CDATA[A condom catheter, also known as external urinary catheter or urinary sheath, consists of a flexible sheath that fits over the penis, much like a condom, and is connected to tubing that lets urine flow to a drainage bag. 

This provides a safe and non-invasive way to commonly manage urinary incontinence or involuntary loss of urine in biological males. 

Condom catheters should be changed on a daily basis. Now, before we talk about how to apply or remove a condom catheter, here are some general considerations. 

First, ask the nurse to tell you what catheter size to use. That’s important because if it’s too small, it may compress or traumatize the urethra, restricting the flow of urine or blood. 

And if it’s too large, it could leak or slip off. Clip the hair at the base of the penis or put on a hair guard before applying the catheter to prevent hairs from getting in the catheter. 

You also need to check the type of the condom catheter used. Some of them are held in place by a self-adhesive coating on their inside, while  others need an external strap of elastic tape. 

Remember to close the room’s door and bedside curtain and respect the client’s privacy. Before beginning the procedure, unclip the tubing from the bedsheet from the bed linens or the client’s leg, if there is any. 

Once you are finished replacing the condom catheter, secure the tubing again and make sure that it doesn’t have any kinks and that the condom is not twisted because that will obstruct urine flow. 

You also need to ensure that the drainage bag is placed below the level of the bladder to prevent the urine from flowing back into the bladder. 

Okay, so, you’re removing a condom catheter, and reapplying a new one. First, cover the over-bed table with paper towels. 

Then fill the wash basin with water and check that the temperature is comfortably warm. Place the basin together with soap, towels, and washcloths on the over-bed table. 

Ensure that the wheels on the bed are locked ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Urinary_catheters_and_routine_indwelling_catheter_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8H7PpWUCRUOGXYdT_4_Zx_EOS5_C56mi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Urinary catheters and routine indwelling catheter care]]></video:title><video:description><![CDATA[A urinary catheter is a tube that goes into the bladder that drains urine. This is commonly used in a variety of situations, like before, during, or after an operation, in order to keep the bladder empty. It’s also used to monitor the amount of urine produced by people with urinary incontinence, in those with wounds or pressure ulcers that need to be protected from contact with urine, or to collect sterile urine samples. 

Catheter care is essential for preventing urinary tract infections since an indwelling catheter is a pathway for bacteria to move up from the perineum into the bladder. This is important because, during normal urination, the urine flow acts as a natural way to “flush” bacteria out of the urinary tract.

Now, the most common types of urine catheters are straight, indwelling, and suprapubic catheters. Both straight and indwelling catheters are inserted into the bladder through the urethra, but the difference is that a straight catheter is removed once the urine is drained, while an indwelling urinary catheter, also called the Foley catheter or retention catheter, remains in the bladder and lets the urine drain continuously into a drainage bag. 

With the suprapubic catheter, “supra-” means above and “pubic” refers to the pubic bone, so it is inserted into the bladder through a surgical incision made above the pubic bone. 

Let’s focus on the indwelling catheter. This consists of a soft balloon that is inflated inside the bladder to keep the catheter from slipping out and a length of tubing, which connects the catheter with a drainage bag for collecting urine. 

Indwelling catheters may have two or three lumens. In double-lumen indwelling catheters, one is for urine drainage and the other is used to inflate the balloon. In triple-lumen indwelling catheters, the additional lumen is used to regularly deliver irrigation fluid into the bladder. This can help prevent blood clots from forming, which is important in certain cases, like after a pro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Removing_indwelling_catheters</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-argHE92SXe1296s0Zb6t4rfTzG8er4Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Removing indwelling catheters]]></video:title><video:description><![CDATA[An indwelling urinary catheter is also called the Foley catheter or retention catheter. It is a tube that goes through the urethra into the bladder where it remains, allowing urine to drain continuously into a drainage bag. It consists of a balloon that can be inflated inside the bladder to keep the catheter from slipping out, a long tubing, and the drainage bag that collects urine.  

Before we talk about how to remove an indwelling catheter, here are some general considerations. Before beginning the procedure, ask the nurse to tell you the exact amount of water that had been used to inflate the balloon and check the port on the balloon catheter, which will tell you the recommended volume used to inflate the balloon. 

It’s important to remove all the water; otherwise, a partially inflated balloon could cause trauma to the urethral wall during the removal. Close the room’s door and bedside curtain and respect the client’s privacy. 

Keep in mind that using an indwelling catheter can lead to decreased muscle tone and temporary urinary incontinence after the catheter is removed. Finally, inform the client that it’s normal to experience some burning sensation and decreased urine volume the next time they void.  

All right, so first, gather the supplies you’ll need including gloves, a bath blanket, a disposable bag, and the correct sized syringe as directed by the nurse. Confirm this size is correct by double-checking the number stated on the balloon port of the catheter. 

Start by making sure that the wheels on the bed are locked and the side railings on the working side are down. Lower the head of the bed so that the bed is flat and at a comfortable working height. 

Next, put your gloves on and cover the client with a bath blanket, exposing only the genital area. Ask them to open their legs and bend their knees, if they can. If not, help them to do so. Unclip the catheter tubing from the bedsheet. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Bladder_and_bowel_training</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hj8IdsAJR3q-_wp_zxlPckOYQJi_EHEa/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Bladder and bowel training]]></video:title><video:description><![CDATA[Most clients are able to hold their urine and feces until they make it to the bathroom or until a receptacle like a bedpan or a urinal is provided. However, some clients have urinary or fecal incontinence, meaning they have involuntary loss of urine or feces. This is particularly uncomfortable for the client because their clothes and bedsheets get soiled and smell foul. It’s important that you know how to assist them. 

Let’s start with urinary incontinence. There are several types of urinary incontinence. Urge incontinence is when someone has a sudden urge to urinate followed immediately by involuntary urination. This usually results in frequent urination, especially at night. Urge incontinence can occur after a bladder infection, which can cause the muscle of the bladder to spasm leading to unintentional urination. 

Stress incontinence is when urine leaks out when pressure inside the abdomen increases. Often, the problem is a weakened sphincter muscle. When the intra abdominal pressure increases, like when you sneeze, cough, laugh, or bear down, the pressure inside the bladder also increases and urine leaks out through the weakened sphincter.  

Overflow incontinence is when the bladder can’t empty normally, so the urine builds up until it overflows or leaks out. This can be due to a blockage of the urethra caused by a tumor or an enlarged prostate. Weakened muscles in the bladder wall can also cause this type of incontinence since they can’t push all the urine out when voiding. This type of incontinence results in a weak or intermittent urinary stream or hesitancy, where it takes awhile for the urine to begin to flow. 

Reflex incontinence happens when damage to the nervous system disrupts normal bladder functions. Various conditions, like spinal cord injuries, Parkinson disease, and multiple sclerosis, as well as procedures, such as prostatectomy or hysterectomy, can damage parts of the nervous system involved with the urination reflex. As a result, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Performing_urine_testing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s56bf5b9RxyKVi6G4U9azVu1SvStuCM7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Performing urine testing]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Genitourinary: Performing urine testing through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Tracheostomy_suctioning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IxsE2922RQ2KGdOeAQAtKUaMRvqdBfWB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Tracheostomy suctioning]]></video:title><video:description><![CDATA[Tracheostomy suctioning is a procedure used to remove secretions from the trachea in individuals with tracheostomy tubes. A tracheostomy tube is an alternative airway for breathing that is inserted through a hole made on the neck and trachea into the tracheal lumen. Tracheostomy tubes are used to bypass an upper airway obstruction; to prevent aspiration; and enable easier suction of tracheal secretions, which can block the normal airflow and lead to an insufficient oxygen supply. 

Generally, nursing assistants should alert the nurse if they think a client requires suctioning. They can assist with tracheostomy suctioning by gathering the required supplies. Now, common signs and symptoms that suggest that a client may require suctioning include a non-productive cough, increased heart and respiratory rate, noisy breathing, shortness of breath, visible secretions, and the presence of coarse breathing sounds or rattling lung sounds. 

Now, there are two types of suction catheters used for tracheostomy suctioning. The first one is a one-time use catheter with a control port, which comes in a sterile kit along with sterile gloves and connecting tubing. This catheter is sterile, which minimizes the risk of infection; it’s transparent, which lets the nurse see the secretions and fluids being suctioned out; and it has the thumb control port, which enables  suction control. One-time use suction catheters typically have a tip with a single opening and come in various sizes. 

For clients who require mechanical ventilation, a closed, or in-line, suction catheter can be used without disconnecting the mechanical ventilator; they are typically used in intensive care units. These catheters are wrapped by a sterile plastic sleeve, so sterile gloves are not necessary. Instead, the nurse can use the regular, or clean, gloves.

Switching gears and moving on to the supplies. If this procedure is within your authorized duties and facility policy and you’re assigned to gather su]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Incentive_spirometry</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MkhjxuqqSyyHIJuGNOfcyP6aS_mopdmZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Incentive spirometry]]></video:title><video:description><![CDATA[Incentive spirometry is a respiratory exercise to help clients improve their lung expansion, prevent fluid and mucus from collecting in the lungs, and reduce the risk of developing respiratory complications, like pneumonia and atelectasis. 

It is especially important for people with underlying lung diseases, those who are overweight or have other chronic diseases, as well as those recovering from surgery. 

Incentive spirometry is performed with a special device called an incentive spirometer, which is made up of a mouthpiece attached to a breathing tube that connects to an air chamber with an adjustable volume indicator. 

Flow oriented incentive spirometer uses balls to indicate volume, while the volume oriented spirometer uses pistons. Now, before you start, here are some general considerations. 

Clients that are experiencing pain, motor function impairments, and people with dementia or other cognitive impairments might be unable to perform incentive spirometry exercises. 

Those who can, should do incentive spirometry 5-10 times every hour while awake. After performing the test, people sometimes feel dizzy and out of breath for a short period of time.  

When performing incentive spirometry, first make sure the client is in the sitting or the most erect position possible, ideally in the high-Fowler’s position. 

Set the volume indicator at the target volume level. Ask them to exhale completely through the mouth. 

Then, tell them to place their lips tightly around the mouthpiece and inhale through the mouth by taking a slow, deep breath. As they inhale, you’ll see the piston or balls rise inside the air chamber. 

This shows how deeply the client can inhale. Maximal inspiration is the volume reached when they cannot inhale any more. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Chest_physiotherapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aT833oVEQa2eTLNpnhr3u4r8TSKWiqG_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Chest physiotherapy]]></video:title><video:description><![CDATA[Chest physiotherapy, or simply CPT, is a technique that can be performed by certain healthcare workers for people suffering from diseases that impair mucus clearance, such as chronic obstructive pulmonary disease, bronchitis, and cystic fibrosis. 

The goal of CPT is to help the client clear excessive mucus secretions from the lungs in order to prevent complications, like mucus plugs, infections, and atelectasis. 

Before performing this procedure, be sure this is within your scope of practice and is allowed by your facility&amp;#39;s policy. 

To start, first gather the supplies you’ll need, including gloves, face shield, and gown for you and pillows for the client’s comfort. 

In addition, keep suction machine equipment available to assist in clearing airway secretions in case the client’s ability to cough and clear their airway is ineffective. 

Make sure you know if the client is feeling weak, anxious, or in pain. CPT must be scheduled according to the client’s needs and daily routine and activities. 

Individuals in pain can take analgesics 20 minutes before beginning CPT. Each CPT session usually lasts between 20 and 40 minutes which can be very exhausting, so try to schedule it between rest periods. 

Avoid performing CPT around 1 to 2 hours before and after meals. The best times to perform CPT are in the morning to clear secretions that may have accumulated over night as well as at night to clear the lungs before bedtime. 

Frequency of CPT varies for each client from just once daily to as frequent as every 2 hours. This will depend on each client’s needs and capabilities as well as the healthcare professional orders, so make sure to check the nurse charts.

Now, CPT includes postural drainage, percussion, vibration, and shaking. It involves a lot of touching, so before you begin, make sure you always explain to the client where and how you’ll be touching.

Postural drainage involves placing the individual in different positions for 10 to 15 ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory:_Collecting_a_sputum_specimen</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WDzGYR8wQ_6-y1Ue0uUBUHeuQZ_WP6LG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory: Collecting a sputum specimen]]></video:title><video:description><![CDATA[Sometimes, the clients you care for may have respiratory complaints. A healthcare provider may order a sputum specimen for a client they suspect may have a respiratory infection, such as pneumonia or other respiratory illnesses, like lung cancer. 

A nurse may delegate collection of the sputum specimen to a nursing assistant. A sputum specimen is simply a sample of sputum from a particular client. 

Sputum, sometimes referred to as “phlegm,” is made up of mucus as well as some other respiratory secretions that can be coughed up, or expectorated, from the lungs, bronchi, and trachea. 

If a client is coughing or spitting up blood, or sputum that contains blood, that’s called hemoptysis, where “hemo-” refers to blood, and “-ptysis” refers to spitting up. 

Now, before collecting a sputum specimen, there are a few things you should keep in mind and a few supplies you’ll need to gather and prepare. 

Coughing up or spitting up mucus into a cup can be both uncomfortable and embarrassing for a client. 

So, it’s important you ensure client privacy and comfort as much as possible throughout the duration of the procedure. 

Be sure you’re collecting sputum, which is produced in the respiratory tract, and not saliva or spit, which is produced in the mouth. 

The supplies you’ll need are clean gloves, a small cup of water, an emesis basin, a sterile specimen container with its lid, facial tissues, disinfectant wipes, client identification labels, the laboratory requisition form, and a small biohazard plastic bag. 

All right, first, wash your hands, put on some clean gloves, and greet the client. Identify them using two identifiers: usually their full name and birth date, being sure to check that information against the client’s identification bracelet, labels, and laboratory requisition form. 

Next, provide the client with a small cup of water to rinse their mouth in order to clear away any microbes that may be present in their mouth; ask them to spit into an emes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular:_Body_temperature</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9s1pmWkYQZ6h8nvKqFpeYNvkRW6qkU-c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular: Body temperature]]></video:title><video:description><![CDATA[Now, as a nursing assistant, you will need to measure your client’s temperature. There are several areas of the body where you can do that, including the oral cavity; the rectum; the axilla, or armpit; the tympanic membrane, or eardrum; and the temporal artery on the forehead. 

Before we discuss how to measure your client’s temperature, we need to cover some definitions. 

Our body is always generating heat through metabolism, and a part of the brain, called the hypothalamus, tries to keep the core body temperature constant like a thermostat. 

When we are febrile, meaning we&amp;#39;ve got a fever, the thermostat is raised higher, and this can be due to an infection, inflammation, or cancer. 

However, body temperature could also be high in hyperthermia, where the thermostat is set at the right temperature, but the body simply can’t get rid of the heat. 

This can be due to an extremely hot environment, excessive exercise, and reduced sweat production. 

In contrast, hypothermia is when body temperature gets too low, and it might be due to exposure to cold for a prolonged period of time, either accidentally or in preparation for a medical procedure.

Starting with an oral temperature: This is an easy and relatively comfortable method. A normal oral temperature is between 97.6 to 99.6 degrees Fahrenheit, or 36.5 to 37.5 degrees Celsius, for adults, and 97 to 99 degrees Fahrenheit, or 36 to 37 degrees Celsius, for children. 

But because the mouth is a large space open to the outside environment, this is not a very accurate way to obtain a temperature because the temperature can change significantly. 

So, don’t take an oral temperature if the client has been coughing, sneezing, eating, drinking, smoking, or chewing gum in the past 15 minutes. Oxygen therapy with a face mask can also interfere with the results. 

In addition, it&amp;#39;s important to hold the thermometer tightly in their mouth, so you should avoid this method for clients who a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular:_Pulse</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VgOSDVD-RJGkIACS6LvhLoMIQRukD0FB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular: Pulse]]></video:title><video:description><![CDATA[With every heartbeat, the heart creates a wave, or pulse, that’s sent to arteries all over the body in order to deliver oxygenated blood to our organs and tissues. 

As a nursing assistant, you need to be able to obtain a pulse and determine its characteristics, including the pulse rate, rhythm, and amplitude, or character. 

Okay, you can calculate the pulse rate by counting the number of pulses in one minute. This is actually equal to the heart rate, or the number of times the heart beats per minute. 

Normal pulse rate varies among different age groups. So, for those 12 years of age or older,  it’s typically between 60 and 100. For school-aged children between 5 and 12 years old, it’s 75 to 110. 

For preschoolers from 3 to 5, it’s 80 to 120, while for toddlers from 1 to 3, have a normal pulse rate of 80 to 130. 

Finally, infants under 1 year of age normally have the fastest pulse rate, which ranges from 120 to 160 beats per minute. 

Besides age, the pulse rate can also be influenced by many factors, including physical activity; body temperature; emotions, like anger, fear, or stress; medications; or even the weather! 

So, tachycardia is when the pulse rate is faster than normal, and this can occur in response to strenuous exercise, fever, pain, anxiety, or specific medications. 

In contrast, bradycardia means that the pulse rate is too slow and can be due to heart problems or various medications.

Another important characteristic is the pulse rhythm, which is normally regular, meaning that the intervals between the beats are equal. 

In an irregular rhythm, also known as arrhythmia, the beats do not follow an even tempo and some of them might even be skipped. 

Arrhythmia can be a result of heart problems or a complication of a heart attack or heart surgery. It can also be caused by problems with the balance of electrolytes, such as potassium, in the blood.

Then, there’s the pulse amplitude, or character, which refers to how strong, forceful,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular:_Applying_antiembolic_stockings_and_sequential_compression_devices</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tFFytQVXTySm9V02oejT1L9fQ7OKicDp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular: Applying antiembolic stockings and sequential compression devices]]></video:title><video:description><![CDATA[Αs a nursing assistant, you will be asked to apply antiembolic stockings and sequential compression devices, or SCDs, in clients that are at risk for deep vein thrombosis, or DVT, such as those who are recovering from a major surgery or have heart and circulatory problems. Make sure you know how they work and how to apply them. 

But first thing’s first: In deep vein thrombosis, deep vein refers to veins that run between the muscles as opposed to superficial veins that you can see on the surface and thrombosis refers to blood clot formation. 

So a DVT is a blood clot in one of those deep veins, and it typically involves the deep veins of the lower legs or thighs. An individual with DVT will often complain of rapid swelling, redness, and pain on the lower leg. 

The bad news is that it can lead to life threatening conditions, such as pulmonary embolism where a broken off piece of the clot called an embolus travels to the lungs and causes respiratory problems. 

Alright, antiembolic stockings and SCDs can be used to prevent DVTs. They both work by exerting pressure on the veins of the lower legs, promoting blood return to the heart instead of pooling in the legs. 

Thus, they decrease the risk for blood clots. Now, antiembolic stockings look similar to conventional stockings, but they are much more elastic. They can extend from the foot to the calf or thigh level. 

They can provide different levels of pressure, so it&amp;#39;s important to make sure the ones prescribed for the client aren&amp;#39;t so tight that they cut off blood circulation but also not too loose because they won’t promote blood return to the heart. 

They also leave an opening over or under the toes which can be used by the health care team to check blood circulation in the lower leg as well as the color and the temperature of the skin. 

Now, sequential compression devices are plastic sleeves that wrap around the client’s legs and consist of multiple compartments that are connected t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular:_Blood_pressure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wsz2narASQC7iaw56aN_eSd3SOuniOxM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiovascular: Blood pressure]]></video:title><video:description><![CDATA[As a healthcare professional, you will need to measure your patient’s blood pressure. Blood pressure refers to the force that the blood exerts on the walls of the arteries. Now, a blood pressure measurement has two values.  

The first and the highest is the systolic blood pressure, which is the force the blood exerts on the walls of the arteries during systole, or when the heart contracts to pump blood through the body. The second one is the diastolic blood pressure, which is the pressure on the walls of the arteries during diastole, or when the heart relaxes and refills with blood between heartbeats.  

Now, maintaining normal blood pressure is essential to ensure that tissues around the body are receiving an adequate amount of oxygen and nutrients from the blood.  

If blood pressure gets too low, the brain, heart, and other vital organs might stop functioning normally because they’re not getting enough blood.  

In contrast, blood pressure that’s too high can create a serious problem for the blood vessels and the organs they supply. Just like a garden hose that’s always under high pressure, in the long term, blood vessels may develop tiny cracks and tears. 

This can lead to serious problems like myocardial infarctions, or heart attacks; strokes, or brain attacks; and aneurysms, or bulges of a weakened blood vessel wall.  

Increased blood pressure can damage small blood vessels, like those seen in the kidney and eyes, leading to kidney failure and vision loss.  

Chronic increased blood pressure also makes it hard for the heart to pump blood out against the increased pressure. Over time, the heart gets overworked, and this can lead to heart failure.  

There are several factors that determine what a person’s blood pressure is at any given time. The first factor is the cardiac output, which is the total volume of blood the heart ejects in one minute. The cardiac output depends on the heart rate, or the number of times the heart beats per minute, and th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary:_Collecting_a_urine_specimen</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P2lE6j06RUW0swtGKWbCwMcsQwi33ZYk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary: Collecting a urine specimen]]></video:title><video:description><![CDATA[Urinalysis includes physical examination of the urine, testing of urine, and examination of the urine under a microscope. 

It can be used to diagnose and monitor various conditions, including kidney disorders; urinary tract infections; and systemic diseases, such as diabetes. 

Now, for the routine urinalysis, a random urine specimen is required, which means that urine can be collected any time during the day without any special measures. 

When the client is suspected to have a UTI, or urinary tract infection, it’s important to do a clean catch specimen. 

“Clean catch” refers to cleaning the perineum and the skin on the genitalia to clear away any microbes on the skin that could contaminate the urine sample. 

The sample should be taken  midstream, meaning it should be collected from the middle of the urine flow. 

This way, the first and last portion of the urine that’s more likely to contain bacteria from skin are not collected. 

A properly collected clean catch specimen will help make sure any bacteria found in the urine specimen came from inside the urinary tract. 

Now, before we review the details of collecting a urine specimen, here are some common care tips. 

Based on facility policies, a nursing assistant can collect a urine specimen under the supervision of and at the direction of a licensed nurse who will provide you with instructions. 

Always confirm the client’s identity to make sure the procedure is performed on the right person. Make sure that the specimen container is labeled with the client’s name and room number, as well as the date and time the specimen was collected. 

At all times, respect the client’s privacy and modesty by remembering to close the doors and window covers, and ensuring the client is properly covered. 

Okay, now, when collecting a urine specimen, first, gather the supplies you’ll need, including: gloves, paper towels, a specimen container, a collection device, toilet tissue, and a biohazard transport bag. 

You ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/GI/GU:_Routine_ostomy_care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pGxvsJ6xSgiPONEb8VaDiHR2Sm2bmgNE/_.jpg</video:thumbnail_loc><video:title><![CDATA[GI/GU: Routine ostomy care]]></video:title><video:description><![CDATA[An ostomy is a surgically created opening used to connect an internal organ to the abdominal wall, through which waste products, like intestinal contents, are eliminated. 

The opening that can be seen on the body surface is called a stoma, and it’s usually connected to an ostomy pouch, also called a bag or appliance, where stool and flatus collect. 

An ostomy can be permanent or temporary, and it can be necessary because of fecal incontinence, an intestinal tumor, bowel trauma, and a bowel inflammatory disease. 

In these circumstances, part or all of the intestine is removed, and the remaining part of the intestine is brought up through the abdominal wall to allow for elimination of waste products. 

Now, depending on how much bowel is removed, an ostomy can be either an ileostomy or a colostomy. With an ileostomy, a part of the small intestine is connected to the abdominal wall. 

An ileostomy can be permanent when the entire large intestine is removed or temporary when it’s done to allow the large intestine to heal after trauma or surgery.  

With a colostomy, only part of the large intestine is removed, and the remaining part is connected to the abdominal wall. 

Remember that, normally, in the small intestine, the nutrients are pretty liquid because most of the water is reabsorbed in the large intestine. 

So, with an ileostomy, the feces are liquid, and they flow at a fairly constant rate. With a colostomy, on the other hand, feces have a different consistency depending on the location of the colostomy. 

So, if nearly all the large intestine was removed and the colostomy is near the beginning, feces are more liquid. If the colostomy is near the end of the digestive tract, feces are more solid. Like ostomies, ostomy appliances also come in different shapes and sizes. 

There are drainable appliances, also called “open-end” appliances which are sealed with a clip or a Velcro-type system at the bottom, so they can be drained and reused. 

Then there ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal:_Administering_an_enema</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3ezVSkbuTUWbSvj5GZZv7LfbSueoGurs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal: Administering an enema]]></video:title><video:description><![CDATA[An enema is when fluid is inserted into the rectum and lower colon, and that’s usually done to stimulate the elimination of feces from the rectum. 

So, an enema can be performed to treat constipation (which is when people have trouble voiding their bowels) or a fecal impaction (which is when the feces form a dry, hard mass in the rectum and can’t be eliminated by the person). 

Another reason for using an enema is to clean the rectum and lower the colon before a diagnostic or surgical procedure.

Enemas can be classified depending on their purpose or their composition. So in the first category, there are cleansing enemas, which are used to clean the colon of feces entirely. 

Then there are oil-retention enemas, which are lubricating enemas that soften the feces in order to make them easier to eliminate. 

Third, there are medicated enemas, which contain medication that can be prescribed for a variety of reasons, like lowering serum potassium levels for example. 

Depending on their composition, the different types of enemas include tap water; normal saline; Harris Flush and carminative, which help with gas elimination; soap suds; and oil-retention enemas, which is an oil-based solution.

Now before we go into the procedural details of administering an enema, here are some come common care tips. Always double-check the client’s ID to make sure the procedure is performed on the right person. 

Based on the facility’s policies, a nursing assistant can administer an enema under the supervision and at the direction of a licensed nurse, who will direct you on the type of enema, the amount of solution, and any other special instructions. 

The client should empty their bladder before the procedure to make sure there are no accidents.  It’s important that there’s a vacant bathroom nearby or a bedpan or bedside commode if the client has mobility problems. 

You should also close the bed curtains and door, and keep the person covered as much as possible for privac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastrointestinal:_Collecting_a_stool_specimen</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PTmp-vCyRfq_mzgvYnDEgJVxSjOQavs3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastrointestinal: Collecting a stool specimen]]></video:title><video:description><![CDATA[The primary functions of the gastrointestinal system are digestion, which is breaking down food that we eat into nutrients; absorption, which is getting those nutrients into the bloodstream; and excretion, which is getting rid of digestive waste as feces. 

The gastrointestinal system is made of hollow, connected organs that make up a canal, called the gastrointestinal tract, as well as a couple of accessory organs that are not part of the canal but play an important role in the food digestion process.

Alright, from top to bottom, the gastrointestinal tract starts with the mouth, then the esophagus, the stomach, the small intestine, the large intestine, and ends with the anus.

Digestion starts after food ingestion, which is putting food into the mouth. The first step is mastication, which is chewing on food to physically break it into small chunks. 

This process is also referred to as mechanical digestion. During mastication, the tongue mixes food with saliva secreted from salivary glands. 

Saliva contains some chemical substances, called enzymes, which start breaking down chemical bonds between food molecules. 

This process is called chemical digestion, and it continues at different levels of the gastrointestinal tract as food moves along. 

As mastication goes on, we get a food-saliva mixture, called a bolus, which is ready to be swallowed. Swallowing takes place through a muscular tube, called the esophagus. 

To move this food bolus along, muscles of the esophagus contract and produce a wave-like movement that pushes food downward into the stomach. This movement is called peristalsis, and it also continues throughout the GI tract. 

When the food arrives in the stomach, it mixes with gastric juice consisting of acid and gastric enzymes, which turns the food bolus into a pulpy soup, called chyme, made of much smaller food particles. 

Next, chyme moves to the first part of the small intestines, called the duodenum, where bile secreted by the liver ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medical_and_surgical_asepsis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NN9g47XQT4Kmjn0hfGK8bw7ITViPo-d6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medical and surgical asepsis]]></video:title><video:description><![CDATA[With asepsis, sepsis refers to infection, while the prefix “a” means “the absence of.” In other words, asepsis is defined as the absence of pathogens. Now, there are two basic types of asepsis: medical asepsis and surgical asepsis. 

Medical asepsis, which is also known as “clean technique,” are practices that kill some microorganisms to prevent them from spreading. On the flip side, surgical asepsis, which is also known as “sterile technique,” includes practices that completely kill and eliminate microorganisms.

Let’s start with medical asepsis which includes sanitization, antisepsis, and disinfection. Sanitization refers to cleaning practices and techniques that physically remove microorganisms. These include hand washing and cleaning of clients’ personal equipment, clothing, and linens. 

Now, there are several things that you should know in order to maintain a sanitary environment. The most important one is hand hygiene which includes hand washing and use of hand sanitizer. 

Always wash your hands before meals, after using the bathroom, and before and after any contact with your clients. Don’t forget to wash your hands after touching your own or your client’s body fluids, such as urine, feces, blood, saliva, vomitus, or genital discharge. 

Next, when coughing or sneezing, always cover your nose and mouth with a tissue or your elbow. Teach your clients to do the same. 

Next up are personal items. Each client should have their own soap, cups, toothbrushes, and towels. Personal equipment should be regularly cleaned to prevent the growth of microorganisms. 

Also, when cleaning the room and objects, make sure to not stir up the dust. In other words, avoid shaking dirty linens, and use a moistened cloth or mop to wipe dust. 

When disposing dirty linens to laundry bins, keep them away from your uniform. This way, you will prevent the contamination of your uniform, and subsequently, you will prevent the spread of microorganisms. 

Also, regularly empty t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Cephalosporins:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mjDAWJnlTdOvseHEo2kgLjbOQquw-ynk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Cephalosporins: Nursing pharmacology]]></video:title><video:description><![CDATA[Cephalosporins are a large group of broad-spectrum antibiotics, which can be used to treat a wide variety of bacterial infections, including meningitis, pneumonia, urinary tract infections, and sepsis. These antibiotics get their name from Cephalosporium acremonium, a fungus from which they are derived.

Now, cephalosporins belong to beta-lactam antibiotics, which means they have a beta-lactam ring in their core, and they mainly work by disrupting the synthesis of the peptidoglycan layer, a major component of bacterial cell walls. This weakens the bacterial cell wall, ultimately killing the bacteria.

Now, cephalosporins are typically classified into five generations, each being used to treat certain types of bacterial infections. 

First-generation cephalosporins include cephalexin, which is administered orally; cefadroxil, which is administered orally and intravenously; and cefazolin, which is given intravenously and intramuscularly. 

In general, first-generation cephalosporins are effective against most gram-positive bacteria, such as Staphylococci and Streptococci species; as well as some gram-negative bacteria like Escherichia coli, Proteus mirabilis, and Klebsiella pneumonia. 

So, first-generation cephalosporins are used to treat respiratory tract infections, urinary tract infections, some skin infections; and bone and joint infections. They can also be given as surgical antibiotic prophylaxis, to prevent infections from spreading to deeper tissues during surgical operations.

Next, second-generation cephalosporins include cefaclor and cefprozil which are administered orally; as well as cefotetan and cefoxitin, which are given intravenously and intramuscularly; and cefuroxime, which is given orally and intravenously. 

Compared to the first generation, second-generation cephalosporins are less effective against Staphylococcus species. Instead, they are more effective against certain types of gram-negative bacteria, such as Haemophilus influenzae, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amenorrhea:_Pathology_review</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zvz8RscgR6Os_67c5AfatFzyTkuenEPf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amenorrhea: Pathology review]]></video:title><video:description><![CDATA[Two people come to the clinic one day. First you see Ana, a 17 year old teenage girl. Ana comes with her mother, who’s worried because Ana hasn’t had her first period yet. 

Upon physical examination, you notice that Ana is quite short for her age. In addition, she has a wide neck, broad chest, and poorly developed breasts with widely spaced nipples. You decide to perform a blood test, which reveals low estrogen levels and high FSH and LH. 

Next, comes María, a 25 year old female who’s concerned because she hasn’t had her period for nine months now. 

She’s sexually active, so the first thing you do is ask for a pregnancy test, which comes up negative. 

When asked about physical activities, she refers to going for a 2-hour run every single day, plus swimming and then tennis on weekdays. 

Regarding her diet, she’s very strict when it comes to avoiding fatty foods. On physical examination, you realize that María is underweight, and a blood test reveals low levels of estrogen, LH, and FSH. 

Okay, now both Ana and María have amenorrhea, which is generally defined as the absence of menstruation in females of reproductive age. 

Now, for menstruation to happen, an individual must have a regular female reproductive anatomy and sexual development, which is normally under control of the hypothalamic-pituitary-gonadal axis. 

First, the hypothalamus secretes gonadotropin-releasing hormone, or GnRH for short, which goes to the anterior pituitary to stimulate the release of gonadotropic hormones, which are luteinizing hormone or LH, and follicle-stimulating hormone or FSH. 

LH and FSH then stimulate the gonads to produce sex hormones; in females, LH and FSH stimulate the ovaries to secrete estrogen and progesterone, which are responsible for the female primary sexual characteristics. 

These are the changes necessary for reproduction, including menstruation, ovulation, and uterine development. 

LH and FSH are also responsible for the development of secondary sex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_stenosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7fy_NTWQSWqR79KYjGgRlotmT2Kb8bsQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary stenosis: Nursing]]></video:title><video:description><![CDATA[The heart can be divided into a right and left side. The right side of the heart is responsible for pumping poorly oxygenated blood to the lungs, and the left side of the heart is responsible for pumping highly oxygenated blood out to the entire body. 

Now, there are conditions that can affect the right side’s ability to pump effectively. These conditions, or heart defects, obstruct or decrease pulmonary blood flow, which ultimately leads to inadequately oxygenated blood. 

These types of heart defects are primarily congenital, which means they were present at birth. Such defects include pulmonary stenosis, tetralogy of Fallot and tricuspid atresia. 

Pulmonary stenosis, sometimes called pulmonic stenosis, occurs when there is narrowing of the pulmonic valve. 

Though little is known about what causes it, genetic and environmental factors may play a role in its development. 

Now, the narrowing of the valves obstructs normal blood flow through the pulmonary artery. This means less blood is making its way to the lungs. 

Depending on the severity of the disease, this could cause no symptoms at all, like in mild cases; or dyspnea, fatigue and syncope in moderate cases; and cyanosis in severe cases. These symptoms also tend to worsen with exertion. 

In moderate to severe cases of pulmonary stenosis, the right ventricle muscle can enlarge. 

This happens because the right ventricle has to work harder to pump blood past the stiff, narrowed valve, and the harder that muscle has to work, the bigger it becomes. 

This is known as hypertrophy. Now, a bigger ventricle muscle doesn’t mean a stronger pump. In fact, a hypertrophied ventricle actually doesn’t pump as effectively. 

And over time, it can no longer pump enough blood to meet the body’s demand; we call this “heart failure.” 

So this means even less blood is getting to the lungs and the symptoms associated with pulmonary stenosis worsen, coupled with new symptoms of right sided heart failure; like jugular]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antivirals_for_influenza:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9m4OcA-8R5yqZt0AarAsYiSMSfO0fMH4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antivirals for influenza: Nursing pharmacology]]></video:title><video:description><![CDATA[The influenza virus causes seasonal influenza,  commonly called “the flu”, which is one of the most common infectious diseases. There are several antiviral medications that can be used either in the prevention of influenza for high-risk clients, or in the acute treatment of severe cases of influenza.

Alright, so, the most commonly used antivirals for influenza include neuraminidase inhibitors, such as oseltamivir, peramivir, and zanamivir; as well as endonuclease inhibitors like baloxavir marboxil. 

Also, there are additional antivirals that are currently not recommended, including adamantanes, such as amantadine and rimantadine. Most of these antivirals are taken orally, except for peramivir, which is given intravenously, and zanamivir, which comes in a powder form that is inhaled by mouth.

Once administered, each class of antiviral act through a different mechanism of action. Neuraminidase inhibitors, as their name implies, bind and inhibit the viral enzyme neuraminidase, thereby preventing the release of new viruses. 

Endonuclease inhibitors, on the other hand, inhibit, you guessed it, a viral enzyme called endonuclease, ultimately stopping the transcription of viral RNA. Finally, adamantanes act by inhibiting the viral protein M2, which prevents viruses from replicating inside the host cell. Ultimately, all of these antivirals help stop viral replication and the release of new influenza viruses.

However, these medications also come with side effects. Luckily, these are usually mild, and they mainly refer to gastrointestinal disturbances, such as nausea, vomiting, stomach pain, and diarrhea. 

Less commonly, antiviral medications for influenza can cause neuropsychiatric symptoms, such as delirium, delusions, and hallucinations. In addition, some clients can develop serious hypersensitivity reactions, such as Stevens-Johnson syndrome, toxic epidermal necrolysis, and erythema multiforme. Finally, clients taking zanamivir can present with bronchospasm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Fluoroquinolones:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lxol1ZNfQQ2HmZRUNWgBbvLmQsKZDNWN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Fluoroquinolones: Nursing pharmacology]]></video:title><video:description><![CDATA[Fluoroquinolones are a group of broad spectrum antibiotics, which can be used to treat a wide variety of bacterial infections. These include eye infections like bacterial conjunctivitis; chest infections like Tuberculosis or pneumonia; gastrointestinal infections like shigellosis; urinary tract infections or UTIs; genital infections like gonorrhea; and bone and joint infections. 

They are very effective against several gram negative organisms like Enterobacteriaceae spp., Haemophilus spp., Legionella spp., Neisseria spp., Moraxella spp., and even Pseudomonas spp. and gram positive bacteria like Streptococcus pneumoniae. 

Now, there are four generations of fluoroquinolones, but among all of them only a few are commonly used. They are ciprofloxacin, levofloxacin, moxifloxacin, norfloxacin and ofloxacin. These medications can be administered both orally or intravenously, while ciprofloxacin and ofloxacin are also available in otic formulations, and ofloxacin and moxifloxacin are available as ophthalmic solutions.

Once administered, fluoroquinolones have a bactericidal effect by inhibiting a bacterial enzyme called DNA topoisomerase, also known as DNA gyrase, which is essential for bacteria to loosen up the tight coilings of DNA for the replication process. As a result, when DNA gyrase is inhibited by fluoroquinolones, bacterial DNA replication comes to a halt, ultimately killing the bacteria.

However, fluoroquinolones may cause side effects like central nervous system disturbances, including headache and restlessness, as well as dizziness, confusion, depression, nightmares, insomnia, and some may even present with seizures. 

Often, fluoroquinolones may also cause gastrointestinal disturbances like abdominal cramps, nausea, vomiting, diarrhea, and flatulence, as well as pancreatitis and hepatotoxicity.  In addition, fluoroquinolones may disrupt the normal intestinal flora, which can allow certain bacteria like Clostridioides difficile to survive and overg]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Weight_loss_medications:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wQU_RWivT9qnh3dkNv_EAMh0R36W6qdV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Weight loss medications: Nursing pharmacology]]></video:title><video:description><![CDATA[Weight loss medications can be used for the short-term management of obesity, and include anorexiants, sympathomimetic medications, lipase inhibitors, glucagon-like peptide-1 or GLP-1 receptor agonists, as well as opioid antagonists combined with atypical antidepressants.

Starting with anorexiants, the most commonly used are benzphetamine and diethylpropion, which are taken orally. These medications are believed to decrease appetite by stimulating the release of dopamine and norepinephrine in the satiety center of the brain, which is located in the hypothalamic and limbic areas. As a result, these neurotransmitters ultimately increase the feeling of satiety and decrease the perception of hunger.

Then, there are sympathomimetic medications, among which the most commonly used one for weight loss is phentermine, which is taken orally. Once administered, phentermine is absorbed into the bloodstream, and travels to the brain. 

Here, it works at the synaptic cleft by inhibiting the reuptake of the neurotransmitters dopamine and norepinephrine. This results in an increased concentration of these neurotransmitters within the synaptic cleft, ultimately decreasing the perception of hunger.

Moving on, lipase inhibitors include orlistat, which is taken orally. This medication acts  in the gastrointestinal tract by inhibiting the absorption of fats, causing them to get excreted in the feces.

Next are GLP-1 receptor agonists, which are primarily used as oral antidiabetic medications, and mainly include liraglutide that is administered through subcutaneous injection. The way liraglutide works is by acting on the stomach to slow gastric emptying. This leads to an increase in the feeling of satiety after eating. In addition, this medication can act in the brain to suppress appetite. 

Finally, weight loss medications include opioid antagonists like naltrexone, which is generally combined with an atypical antidepressant, namely bupropion. These medications are taken to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Tetracyclines_&amp;_glycylcyclines:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zXnktCvxSOSZgrAm-ldPTZWQRZaObKQg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Tetracyclines and glycylcyclines: Nursing pharmacology]]></video:title><video:description><![CDATA[Tetracyclines are a group of broad-spectrum antibiotics, which were originally derived from soil-dwelling Streptomyces bacteria. 

These medications can be used to treat a wide variety of bacterial infections, including central nervous system infections like meningitis, respiratory infections like community-acquired pneumonia, gastrointestinal infections like cholera, skin conditions like acne, and genitourinary infections like chlamydia and syphilis.

In addition, tetracyclines can be used to treat rare infections like rocky mountain spotted fever, anthrax, lyme disease, and tularemia. 

Tetracyclines are very effective against gram-positive bacteria like Bacillus anthracis and Clostridium spp, as well as some gram-negative bacteria like Shigella spp, Escherichia coli, Rickettsia spp, Borrelia burgdorferi, Helicobacter pylori, and Neisseria meningitidis, and finally some atypical bacteria like Mycoplasma pneumoniae, Chlamydia trachomatis, Vibrio cholerae, and Francisella tularensis.  

However, some of these bacteria developed resistance against tetracyclines in time. So as a solution, tetracyclines were modified into a newer generation of antibiotics called glycylcyclines. These are commonly used in complicated skin infections and intra abdominal infections. 

Glycylcyclines are very effective against some gram-positive bacteria like Streptococcus pyogenes, Clostridium perfringens, both methicillin susceptible and methicillin resistant Staphylococcus aureus; and gram-negative bacteria like Klebsiella pneumoniae. 

Now, according to the duration of action and half-life, tetracyclines are divided into two groups. Short acting tetracyclines, like tetracycline itself, have a half-life of around 8 hours, while long acting ones like doxycycline and minocycline have a half-life of 16 to 22 hours. 

These medications can be administered both orally or intravenously. On the other hand, glycylcyclines are only administered intravenously. The main drug in this]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunoglobulins:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aqTI_oGpT3Sz7xHhjw25L5SjTj_6IO-F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunoglobulins: Nursing pharmacology]]></video:title><video:description><![CDATA[Human immunoglobulin therapy contains a mixture of immunoglobulins, also called antibodies, derived from the plasma of healthy donors. 

Immunoglobulin therapy is used in a variety of health conditions, including treatment of immune deficiencies, prophylaxis of infectious diseases, and management of various inflammatory or autoimmune diseases, such as Kawasaki disease, idiopathic thrombocytopenic purpura, and Guillain-Barré syndrome. 

Immunoglobulin products primarily contain IgG antibodies, as well as small amounts of IgM and IgA antibodies. 

There are three routes of immunoglobulin administration: intravenous, more commonly known as IVIG, subcutaneous, or SCIG, and intramuscularly, or IMIG. 

Other examples of commonly used immunoglobulins include the hepatitis B immune globulin, or HBIG, which is administered to clients after exposure to the hepatitis B virus; the tetanus immunoglobulin, or TIG, which is used primarily for prophylaxis of tetanus infection in clients with traumatic, puncture, or contaminated wounds; and the botulism immune globulin, or BIG, which is used to treat infant botulism caused by toxin type A or B. 

Additionally, a specific immunoglobulin called RhO (D) immune globulin, or RhoGAM, is given to Rh-negative clients during pregnancy in order to prevent Rh immunization against their Rh-positive fetus. 

Once administered, immunoglobulins act just like natural antibodies; so they recognize a specific antigen, bind to it so that the immune system can eliminate it, as well as modulating the immune response. 

This can be helpful to fight off infections, as well as to prevent the immune system from attacking the body’s own cells in autoimmune disorders. 

One thing to keep in mind is that immunoglobulins offer passive immunity, which is temporary and only lasts for as long as the antibodies persist, usually a few weeks to months.

Now, the most common side effects of immunoglobulin therapy are headaches and local injection site reacti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antivirals_for_herpesviruses:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eS-I54C8TUWecpVw6MCB2xIITjOeVrvt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antivirals for herpesviruses: Nursing pharmacology]]></video:title><video:description><![CDATA[Herpesviruses are a family of DNA viruses that include herpes simplex virus or HSV types 1 and 2, varicella-zoster virus or VZV, cytomegalovirus or CMV for short, Epstein-Barr virus or EBV, and human herpesvirus or HHV 6, 7, and 8. 

Certain herpesvirus infections can be treated with a class of antiviral medications called guanosine analogs, which include medications that end in the suffix -clovir. 

The main drugs used to treat herpes infections include valacyclovir, valganciclovir, and famciclovir, which are given orally, as well as acyclovir and ganciclovir, which can also be administered topically or intravenously in addition to orally.

Once administered, guanosine analogs act by inserting into the replicating viral DNA. As a result, viral DNA synthesis is halted, ultimately stopping viral replication.

Now, clients taking guanosine analogs may experience headache and nausea. These medications can also cause a skin rash, pruritus, nephrotoxicity, and hypersensitivity reactions like Stevens-Johnson syndrome and angioedema. 

Acyclovir and valacyclovir can cause neurological side effects, including agitation, tremors, confusion, and myoclonus; more rarely, clients can develop hallucinations, and even encephalopathy or seizures. 

Acyclovir and valacyclovir can also lead to  thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome. Acyclovir can also cause pain or phlebitis at the injection site when given intravenously. 

On the other hand, famciclovir can cause menstrual changes and hepatotoxicity. Finally, valganciclovir has boxed warnings for hematologic toxicity, carcinogenesis, impaired fertility, and fetal toxicity.

Now, regarding contraindications, guanosine analogs should be used with caution during pregnancy and breastfeeding, and in clients with neurologic, hepatic, or renal disease. 

Acyclovir and valacyclovir should also be used cautiously when there’s an electrolyte imbalance or dehydration. 

In addition, acyclovir should not b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacokinetics_-_Elimination:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NYnfSZ4qQpC-Q9bk8mnY8UPtRYijBWNT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacokinetics - Elimination: Nursing pharmacology]]></video:title><video:description><![CDATA[Pharmacokinetics refers to the movement and modification of a medication inside the body. So once the medication is administered, first it has to be absorbed into the circulation, then distributed to various tissues throughout the body, metabolized or broken down, and finally, eliminated or excreted in the urine or feces. 

You can remember this with the acronym ADME; which stands for Absorption, Distribution, Metabolism, and Elimination.

Okay, now let’s focus on elimination, which is the process of removing medications and their metabolites from the body through excretion. 

This is done primarily by the kidneys, through glomerular filtration, meaning that certain medications can be filtered out as the blood flows through the glomerulus. 

In addition, as the filtrate makes its way through the renal tubules, other medications from the peritubular capillaries get actively secreted into the tubular lumen, while others are passively reabsorbed into the blood. 

Ultimately, the medications that are filtered, secreted, and not reabsorbed, end up being excreted from the body via urine. 

Aside from the kidneys, medications can also be eliminated through the gastrointestinal or GI tract. 

So orally administered medications that do not get absorbed along the GI tract are directly passed in feces. 

On the other hand, some medications undergo a process of enterohepatic circulation, when a medication is transferred by the liver into the bile. 

After that, bile carrying the medication is released into the GI tract, where the medication can be reabsorbed, entering the portal circulation, to ultimately return to the liver. 

At this point, the process of enterohepatic circulation occurs again, and the liver transfers the medication back into the bile to be secreted into the GI tract, until it’s ultimately eliminated from the body through the feces. 

Lastly, small amounts of certain medications can be cleared out of the body through the lungs as we exhale air, as w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mastocytosis_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CaMalIXXSR6hw1qEZkRnpZYTTJywPw6X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mastocytosis (NORD)]]></video:title><video:description><![CDATA[Mastocytosis, or clonal mast cell disease, is a rare disorder that leads to increased numbers of incorrectly functioning mast cells. 

Mast cells are a kind of white blood cell that have many roles in the immune system, including allergic reactions. 

There are two main categories of mastocytosis. In cutaneous mastocytosis, the mast cells accumulate only in the skin. 

In systemic mastocytosis, mast cells also accumulate in other tissues, like the liver, spleen, lymph nodes, gastrointestinal tract, and, most commonly, bone marrow. 

Generally, the signs and symptoms of mastocytosis are similar to an allergic reaction. They can range between categories and from mild to life-threatening. 

Some examples are pain, flushing, malaise, headaches, memory and concentration difficulties, stomach aches, production of more than the usual amount of gastric juices, abdominal discomfort, nausea, bloating or diarrhea, and anaphylaxis which is a severe allergic reaction that can be deadly.

Now, within each main category of mastocytosis, there are additional forms. Their distinction can be based on more specific signs and symptoms. 

For example, in the most common form of cutaneous mastocytosis, lesions appear on the skin’s surface as brownish, flat or elevated spots. 

They may be surrounded by Darier’s signs, which are areas of skin that become red and itchy when scratched or rubbed. 

In the rarest form, lesions aren’t present but the skin is rougher and thicker. Itching and blistering may also occur in individuals who are less than one year old.

Some skin changes may be present in systemic mastocytosis, but these forms also involve dysfunction in other tissues. 

Blood cell production in the bone marrow may decrease and bones may soften and weaken. In addition to liver dysfunction, swelling or enlargement of the liver, spleen or lymph nodes may occur. 

In aggressive systemic mastocytosis, liver function may be lost and in advanced mastocytosis, other blood disorder]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heart_defects_that_decrease_pulmonary_blood_flow_-_Nursing_considerations_&amp;_client_education:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tSMLlqltSYCqKew4A7lpLefXTUiX50tF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heart defects that decrease pulmonary blood flow - Nursing considerations &amp; client education: Nursing]]></video:title><video:description><![CDATA[Nursing considerations when caring for clients with heart defects that decrease pulmonary blood flow include monitoring and managing tissue perfusion, maintaining adequate gas exchange, monitoring cardiac output, preventing infection, maintaining adequate nutrition, decreasing the client’s risk for injury and providing reassurance and education to the client and family. 

Now, when monitoring and managing tissue perfusion, keep a close eye on the client’s hemoglobin and hematocrit levels. 

Low H&amp;amp;H levels can indicate poor oxygenation. It’s also important to create a calm and soothing environment since causing the client to become upset or cry can result in a hypercyanotic spell. 

Should that happen, place the client in a knee-to-chest position or if they are an older child, assist them to a squatting position. 

The healthcare provider will likely prescribe oxygen to meet the body’s demands, and morphine for its sedative effects, during these times. 

Also, be sure to provide education and anticipatory guidance to the parents, guardians or caregivers about how to manage hypercyanotic spells. 

Limiting activity and maintaining the client’s airway are helpful nursing interventions to promote adequate gas exchange. 

And, thoughtful planning on carrying out your nursing care can help allow ample time for the client to rest. 

Additionally, monitoring the client’s electrolyte levels closely will help you to determine if acidosis is present and needs to be corrected.   

Decreased cardiac output is a potential complication for clients with heart defects that decrease pulmonary blood flow, so continuous monitoring of vital signs, like heart rate, blood pressure and respiratory rate, must be performed. 

Also, assess for signs of heart failure, which may include peripheral edema and abdominal distention. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tetralogy_of_Fallot:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ex6Dv2HWQNaus8z8UOEBxnuaTmOMdDan/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tetralogy of Fallot: Nursing]]></video:title><video:description><![CDATA[Tetralogy of Fallot, or ToF, is the most common congenital heart defect. Similarly to pulmonary stenosis, the cause of ToF is unknown, but genetic factors likely play a role in its development. ToF consists of four different defects. 

These defects include pulmonary stenosis, right-ventricular hypertrophy, VSD and an overriding aorta, which happens when the aorta is displaced and blood from both sides of the heart is able to flow through it. 

In some clients a fifth defect, ASD, may be present. Since all of these factors can lead to right to left shunting of blood, ToF can also be classified as a cyanotic heart condition. 

Now, the direction of the shunting in ToF isn’t always right to left. In this condition, it depends on the severity of the obstructive defects and the pressure difference between pulmonary vascular resistance and systemic resistance. 

Pulmonary vascular resistance is the amount of force exerted against blood flow from the pulmonary artery to the left atrium; and systemic resistance is the amount of force exerted on circulating blood by the vasculature of the body. 

So if the pulmonary vascular resistance is greater than systemic resistance, blood will shunt from right to left. 

But, if the systemic resistance is greater than pulmonary vascular resistance, blood will shunt from left to right. 

In this situation, excess oxygenated blood from the left ventricle will shunt over to the right ventricle through that VSD. 

These clients are at risk for developing pulmonary congestion since all this extra blood volume shunting over to the right side will make its way to lungs.

Now, symptoms can vary broadly in different clients, some with just mild symptoms, while others can have a much more severe experience. The wide difference in symptoms is directly related to how much blood gets oxygenated. 

These symptoms of ToF can be present at birth, and the infant may appear cyanotic, like in right to left shunting scenarios; or acya]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tricuspid_atresia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XaVCX9L0QUazGQfxRILXBV5fQBuNELAO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tricuspid atresia: Nursing]]></video:title><video:description><![CDATA[Tricuspid atresia, also known as pulmonary atresia, is a term used to describe an under-developed or absent tricuspid valve. 

Tricuspid atresia is a congenital condition who’s cause isn’t well understood, and is not as common as the other heart defects that obstruct or decrease pulmonary blood flow. 

The tricuspid valve is located between the right atrium and right ventricle, allowing blood from the atrium to flow down into the ventricle.  Without it, blood can’t flow normally on this side. 

And, if there’s no alternate route to direct the blood flow, there would be virtually no blood in the right ventricle available to be pumped to the lungs for oxygenation. 

This can also result in an underdeveloped, or hypoplastic, right ventricle. In order to maintain vital blood flow, an alternate route must be present. 

Luckily, additional defects that present with this disorder; an ASD, patent foramen ovale, or PFO, and a VSD; provide a substitute route for the blood that would otherwise be trapped on the right side.

So, blood from the right atrium flows through the ASD or PFO to the left atrium, eventually making its way down to the left ventricle then out through the aorta; and blood from the left ventricle flows through the VSD into the right ventricle, eventually making its way through the pulmonary artery then to the lungs. 

However, it’s important to note that all of this leads to mixing of poorly oxygenated and highly oxygenated blood. 

Cyanosis, tachycardia, heart murmur and dyspnea are the most common early manifestations of tricuspid atresia, often noted at birth; while older children can exhibit signs of chronic hypoxemia, like clubbing of fingers and toes, as a result of long-term desaturated blood circulating in the body. 

Though tricuspid atresia can be discovered during a prenatal ultrasound, diagnosis can be made through physical exam and diagnostic tests, like ECGs, echocardiogram, chest x-ray, cardiac catheterization, MRI of the heart and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_used_to_treat_acne_vulgaris:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/p2FTBdKjQtq2ybltuu-PxqQpSI_rcX-V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for acne vulgaris: Nursing pharmacology]]></video:title><video:description><![CDATA[Acne vulgaris is a common skin disorder characterized by raised, red bumps that occur when hair follicles get clogged by particles like dead skin cells or oil, and it primarily occurs on the face, neck, chest, and back. 

Although the exact cause of acne is not completely understood, there are a few main factors that are known to contribute to acne formation. 

These include keratin plugs that block the opening of the hair follicle; increased sebum released by sebaceous glands, which sometimes occurs in response to increased androgen production during puberty; and overgrowth of bacteria like Cutibacterium acnes that trigger local inflammation.  

Acne vulgaris can be categorized into different types based on specific characteristics. Mild acne usually consists of comedones, while moderate acne usually consists of pustules, and severe acne usually consists of cysts and nodules. 

Depending on the severity and location of acne, there are various medications that can be used to treat acne. 

These include topical medications, such as keratolytics like salicylic acid, azelaic acid, and benzoyl peroxide, vitamin A derivatives like tretinoin and adapalene, and topical antibiotics like erythromycin or clindamycin; as well as systemic medications, such as oral antibiotics like the tetracyclines tetracycline and doxycycline, oral retinoids like isotretinoin, and hormonal agents like spironolactone or oral contraceptives containing a combination of estrogen and progestin. 

Okay, now let’s dive deeper into the different classes of medications, starting with topical agents. 

Keratolytics include salicylic acid, azelaic acid, and benzoyl peroxide, and once administered, they primarily work by softening and shedding the stratum corneum, which is the outer layer of the skin. 

As a result, keratolytics help decrease the skin’s thickness and improve its moisture. Next, vitamin A derivatives include tretinoin and adapalene, and they work by blunting the inflammatory proc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antimetabolites:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8JcuMA-3R5uhy_NFF4G_gieETROup_hv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antimetabolites: Nursing pharmacology]]></video:title><video:description><![CDATA[Antimetabolites are medications used primarily for cancer treatment. They are most effective against hematologic malignancies, like leukemia, lymphoma, and myelodysplastic syndrome; but they can also be effective against solid tumors, like breast cancer, head and neck cancer, and osteosarcoma. 

Based on the specific substance with which they interfere, antimetabolites can be classified into folic acid analogs, like methotrexate, which can be administered orally, subcutaneously, intramuscularly, intravenously, or intrathecally; pyrimidine analogs, like fluorouracil, which can be administered topically or intravenously, and cytarabine, which can be administered subcutaneously, intravenously, or intrathecally; purine analogs, like mercaptopurine, taken orally, as well as cladribine and fludarabine, administered intravenously; and ribonucleotide reductase inhibitors, such as hydroxyurea, which can be administered orally or intravenously.

Okay, the reason antimetabolites are effective for cancer treatment is that they disrupt DNA synthesis. 

They do that either by mimicking folic acid, or nucleobases, such as pyrimidines and purines; or by inhibiting enzymes that are involved in the pathway, such as adenosine deaminase and ribonucleotide reductase. 

As a result, they stop DNA replication and cell proliferation, eventually leading to cancer cell death. Unfortunately, this action can also increase the risk of serious side effects. 

All antimetabolites can cause bone marrow suppression, but this is only a boxed warning for methotrexate, cladribine, fludarabine and hydroxyurea. 

Bone marrow depression can lead to leukopenia and an increased risk of infections, thrombocytopenia and an increased risk of bleeding, as well as anemia. 

Some clients can also experience gastrointestinal disturbances, such as anorexia, nausea, vomiting, and diarrhea. 

GI toxicity is actually a boxed warning for methotrexate, and also more common with fluorouracil, cytarabine and me]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antimalarials:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nHIKQX4uSMugprw6HzlCeXbaTyiugLZZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antimalarials: Nursing pharmacology]]></video:title><video:description><![CDATA[Antimalarials are a group of medications primarily used in the prevention and treatment of malaria, which is caused by Plasmodium spp, a protozoan parasite transmitted by certain Anopheles mosquitoes. In addition, some antimalarials can also be used to treat amebiasis and some autoimmune disorders like systemic lupus erythematosus and rheumatoid arthritis.

The oldest medication of this group is quinine, but its derivative chloroquine is most often used because it has fewer side effects. Other antimalarials include hydroxychloroquine, mefloquine, primaquine, pyrimethamine, and a combination of atovaquone and proguanil. If Plasmodium is resistant to antimalarial therapy, antibiotics like doxycycline, tetracycline, and clindamycin can be used.

Antimalarials are administered orally. Once administered, they work in various ways. Chloroquine, quinine, pyrimethamine, atovaquone, and proguanil all inhibit parasitic DNA synthesis; pyrimethamine, in particular, also inhibits protein synthesis. 

Mefloquine and hydroxychloroquine affect the function of lysosomes in the parasitic cell. Finally, primaquine affects the mitochondria of the parasite.

Antimalarials can cause a number of side effects, most commonly of the gastrointestinal tract such as nausea, vomiting, cramps, and anorexia. In addition, clients can develop alopecia, a skin rash, photosensitivity, and hypersensitivity reactions like Stevens-Johnson syndrome and drug reaction with eosinophilia and systemic symptoms or DRESS for short. 

Some clients taking antimalarials may also experience neurological side effects, such as headaches, nightmares, and even seizures; and mefloquine has a boxed warning for causing adverse neuropsychiatric reactions like anxiety, depression, hallucinations, and suicidal ideation. 

Now, clients on antimalarials can often develop blurred vision and difficulty focusing due to damage to the cornea, while chloroquine and hydroxychloroquine can cause irreversible retinopathy. Quin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Glycopeptides:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8JQtnDOoRlqm3Q8N0VndHCSFRBamriVU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Glycopeptides: Nursing pharmacology]]></video:title><video:description><![CDATA[Glycopeptides are antibiotics primarily used to treat skin infections such as erysipelas, cellulitis, wound infections, and skin abscesses caused by gram-positive bacteria. 

Additionally, some glycopeptides can be used to treat staphylococcal enterocolitis, gastrointestinal Clostridioides difficile infection, joint or bone infections, and other serious infections like pneumonia, endocarditis, bacteriemia, and septicemia. 

Glycopeptides work well against Staphylococcus epidermidis, Staphylococcus agalactiae, Staphylococcus aureus, especially the methicillin-resistant type called MRSA, as well as Streptococcus pneumoniae, Streptococcus pyogenes, and vancomycin susceptible Enterococcus faecalis. 

There are four medications in this group: vancomycin, telavancin, dalbavancin, and oritavancin. All glycopeptides are administered intravenously, while vancomycin can also be given orally. 

Once administered, glycopeptides inhibit bacterial cell wall synthesis by interfering with peptidoglycan polymerization and cross-linking, ultimately causing bacterial cell death.

Common side effects of glycopeptides include ototoxicity, injection site reactions, and gastrointestinal disturbances like nausea, vomiting, and diarrhea. 

In some cases, glycopeptides can disrupt the healthy intestinal flora and allow resistant bacteria to overgrow, which may result in superinfection, such as Clostridioides difficile infection or CDI for short. For treatment, CDI and staphylococcal enterocolitis are the only indications for oral vancomycin. 

Some glycopeptides can also cause side effects like prolonged QT interval, arrhythmias, and peripheral edema. Clients taking glycopeptides can also develop anaphylactic reactions. Other serious side effects include nephrotoxicity, which is a boxed warning for telavancin! 

Some clients taking glycopeptides may also develop hematologic side effects like leukopenia and eosinophilia; while vancomycin can also cause immune thrombocytopenia and ne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Penicillins:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hr7otKOPQsGLC0a2z8fMkSGbQ8iJUIX_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Penicillins: Nursing pharmacology]]></video:title><video:description><![CDATA[Penicillins are antibiotics that got their name from the Penicillium mold, from which they were originally extracted. They belong to the pharmacological group of beta-lactam antibiotics, because they have a beta-lactam ring in their structure. Penicillins are used to treat a wide range of infections, including streptococcal infections, like pharyngitis, tonsillitis, scarlet fever, and endocarditis; as well as pneumococcal infections; staphylococcal infections; diphtheria; anthrax; and syphilis. 

Now, to build their cell walls, bacteria need an enzyme called DD-transpeptidase, or penicillin binding protein, or PBP for short. Penicillins, like all beta lactam antibiotics, bind to this enzyme thanks to their beta-lactam ring, and prevent it from working.  

Now, some bacteria have developed resistance to beta lactam antibiotics. The most notable is Staphylococcus aureus, which has developed an enzyme called beta-lactamase or penicillinase, that breaks down the beta-lactam ring within the antibiotic, rendering it ineffective. 

So, penicillins are further classified into four groups: basic penicillins, broad-spectrum or aminopenicillins, penicillinase-resistant or antistaphylococcal penicillins, and extended-spectrum or antipseudomonal penicillins. 

Basic penicillins include penicillin V, which is given orally, and penicillin G, which is administered intramuscularly or intravenously. In addition, there’s a specific penicillin G called penicillin G benzathine, which is a long-acting penicillin that’s only administered intramuscularly. These are quite effective against common gram-positive bacteria, so they’re used to treat upper respiratory infections, otitis media, pneumonia, rheumatic fever, erysipelas, skin and soft-tissue infections, and STIs like syphilis. However, they don’t work well against most gram-negative bacteria. 

On the other hand, broad spectrum penicillins include amoxicillin, which is given orally, and ampicillin, which is administered oral]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chloramphenicol:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vElhqQbfRDmuo8lw1rdYlJrxS7Gh-Y-7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chloramphenicol: Nursing pharmacology]]></video:title><video:description><![CDATA[Chloramphenicol is a broad spectrum antibiotic that is active against both gram-positive and gram-negative bacteria. 

However, due to its severe toxicity, chloramphenicol is no longer used as the first medication of choice in most countries with access to safer antibiotics; instead, this medication is typically used when other antibiotics are ineffective or contraindicated.

Nowadays, chloramphenicol is most often used intravenously, and since it readily crosses the blood-brain barrier, it may be used to treat bacterial meningitis in clients who have major hypersensitivity reactions to penicillin. 

Additionally, it can be considered for the treatment of serious rickettsial infections, such as typhus and Rocky Mountain spotted fever.

Once administered, chloramphenicol has a bacteriostatic effect by reversibly binding to the 50S subunit of the bacterial ribosome, thereby inhibiting bacterial protein synthesis, and ultimately stopping bacterial growth.

Now, chloramphenicol may cause side effects like gastrointestinal disturbances, such as nausea, vomiting, and diarrhea. 

Additionally, it has a boxed warning for blood dyscrasia, including fatal aplastic anemia, hypoplastic anemia, and bone marrow suppression, and it can increase the risk of developing superinfections. 

Other side effects of chloramphenicol include severe metabolic acidosis; as well as neurotoxicity, which can manifest as optic neuritis or peripheral neuropathy. 

Finally, infants lack a hepatic enzyme involved in the metabolism of chloramphenicol, so the medication may accumulate in their body until it reaches toxic levels. 

As a result, administering chloramphenicol to infants can lead to gray syndrome, which presents with anemia and cyanosis. 

In severe cases, there may also be vomiting, hypothermia, limp body, cardiovascular collapse, and eventually death if not treated promptly.

Now, as far as contraindications go, chloramphenicol is not recommended for use during pregnancy, breas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Platinum-based_agents:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vZ7jWUwBR7WEA4DtKAC2pfP2RjKWfkyr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Platinum-based agents: Nursing pharmacology]]></video:title><video:description><![CDATA[Platinum-based agents, sometimes called platins, are medications that are mainly used to treat cancer. 

Broadly speaking, they are part of the bigger “alkylating-like agents” category, and they are primarily used in the treatment of solid tumors, like colon, rectum, lung, ovarian, uterus, testicular, and bladder cancer.

Now, the most commonly used platins include cisplatin, carboplatin and oxaliplatin, which are administered intravenously. 

Once administered, platins act as cell-cycle phase nonspecific agents, which means they work by causing damage to the DNA of rapidly dividing cancer cells in all phases of the cell-cycle, ultimately causing their death. 

There are three ways they do this. First, they can attach an alkyl group to one of the DNA bases of cancer cells. 

Repair enzymes recognize there’s something wrong, so they jump in to replace the alkylated bases and cause DNA fragmentation, which eventually results in DNA damage and cancer cell death. 

The second mechanism is the crosslinking of DNA, which means the alkylating agent links two DNA bases together, forming cross-bridges. 

Cross-linking prevents DNA from being separated for essential cell processes, like replication or transcription, eventually resulting in cancer cell death and stopping the multiplication of cancer cells. 

Cisplatin and carboplatin employ both these mechanisms to exert their antineoplastic effect, while oxaliplatin only seems to act through crosslinking of DNA. 

Additionally, cisplatin and carboplatin also act through a third mechanism, which is to inhibit the enzymes involved in cell replication and multiplication.

Unfortunately, platinum-based agents also act on healthy rapidly dividing cells, including those in the skin, bone marrow, and gastrointestinal tract. 

As a result, these medications can often cause several side effects, such as alopecia, skin rash, and photosensitivity, as well as nausea, vomiting. Vomiting is actually a boxed warning for cisplatin ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_for_respiratory_syncytial_virus_(RSV):_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l8p8Zw02QoakHoYsF94a-SVnTNuUe0x-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for respiratory syncytial virus (RSV): Nursing pharmacology]]></video:title><video:description><![CDATA[Respiratory syncytial virus, or RSV for short, is an enveloped RNA virus that causes the cells lining the respiratory tract to merge, forming a large multinucleated cell called syncytia. RSV commonly affects the lower respiratory tract of young children, causing bronchiolitis. 

Initially, bronchiolitis often resembles the common cold, but in some cases, it can also progress to atelectasis, or airway collapse, which causes severe symptoms such as wheezing, dyspnea, and even apnea in young infants.

There are two main classes of medication used in the treatment of RSV infection; these include monoclonal antibodies like palivizumab, and antiviral medications like ribavirin.

Starting with palivizumab, this medication is administered via intramuscular injection and is given for prevention, during the winter months, to infants at high risk for RSV, including prematurely-born infants, and to those with chronic lung disease or congenital heart disease. 

Now, palivizumab is a monoclonal antibody that targets the fusion protein on the surface of RSV. The fusion protein helps the virus fuse to the host cell membrane and enter it, also facilitates the fusion between infected cell membranes, resulting in syncytium formation. 

So by neutralizing the fusion protein, palivizumab prevents RSV from infecting the host cells and forming syncytia. 

Common side effects of palivizumab include injection site reactions like pain, redness, and swelling. Some clients may also present with fever, chills, and myalgia. 

Other side effects include nausea, vomiting, dyspnea, and hypersensitivity reactions like skin rashes, pruritus, angioedema, and even anaphylaxis. 

Additionally, palivizumab can also cause thrombocytopenia, which can result in easy bruising or bleeding.

Now, palivizumab should be used with caution in children with thrombocytopenia and other bleeding disorders due to increased risk of bleeding. 

Additionally, palivizumab should be used with caution when com]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_stimulants:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T7asOp19R1yZe9STupGJz37TTbeuoaXJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory stimulants: Nursing pharmacology]]></video:title><video:description><![CDATA[Respiratory stimulants are a group of medications that can be administered to clients with asthma, chronic obstructive pulmonary disease or COPD for short, or respiratory depression; as well as to treat apnea of prematurity. 

Respiratory stimulants include doxapram, which is administered intravenously, as well as certain phosphodiesterase enzyme inhibitors, also known as methylxanthines, such as caffeine, theophylline, and aminophylline, which are most often taken orally, but they can also be given intravenously. 

Once administered, these medications primarily work on the brainstem and medulla by stimulating the respiratory center, and thus act as respiratory stimulants. 

In addition, methylxanthines can also act on the lungs by inhibiting the phosphodiesterase enzyme, and ultimately cause bronchodilation.

Side effects commonly caused by respiratory stimulants include muscle tremors, agitation, anxiety, irritability, and insomnia. Clients might also experience gastrointestinal disturbances like nausea, vomiting, and diarrhea. 

These drugs may also cause hypertension, heart palpitations, tachycardia, and ECG abnormalities. 

In addition, theophylline has a very narrow therapeutic window, meaning it&amp;#39;s very easy to overdose, and can cause arrhythmias or seizures. 

Finally, administering high doses of caffeine to premature infants can lead to intracranial hemorrhage.

As far as contraindications go, respiratory stimulants are contraindicated in clients with severe arteriosclerosis, symptomatic cardiovascular disease, and moderate to severe hypertension.  

Respiratory stimulants should also be avoided in clients with a history of seizures, as well as hepatic or renal disease. 

Additional precautions should be taken during pregnancy and breastfeeding. Regarding interactions, theophylline and phenytoin should not be used together, as they decrease each other’s effects. 

Finally, theophylline should not be combined with beta blockers, beta adrene]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alpha-2_adrenergic_agonists:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RLx_mqc_Q4SJXLuTV6T0pzMlRnSg99xQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alpha-2 adrenergic agonists: Nursing pharmacology]]></video:title><video:description><![CDATA[Alpha-2 adrenergic agonists are medications that oppose the effects of the sympathetic nervous system, ultimately decreasing smooth muscle contraction. 

These medications include clonidine, guanfacine, and methyldopa, which can be administered orally, and clonidine also transdermally, to treat hypertension. 

In addition, clonidine can also be used orally to treat attention deficit hyperactivity disorder, or ADHD for short, and less frequently, through epidural infusion for pain management in cancer. 

Finally, methyldopa can also be administered intravenously to treat hypertensive crises. Once administered, alpha-2 adrenergic agonists act in the brainstem. 

Normally, neurons in the brainstem carry signals to the spinal cord nuclei, where they synapse and release norepinephrine to stimulate the sympathetic nervous system. 

This triggers the fight or flight response, which results in smooth muscle contraction, in turn leading to an increase in the heart rate and blood pressure, as well as decreasing gastrointestinal motility and urination by contracting the sphincters. 

Now if we zoom into this synapse, we can see that some of the norepinephrine turns around and binds to alpha-2 adrenergic receptors. 

This inhibits further release of norepinephrine and serves as a mechanism of negative feedback control. 

So, alpha-2 adrenergic agonists work by stimulating these receptors, therefore blocking the downstream sympathetic response, and ultimately decreasing blood pressure.

Some common side effects include nausea, vomiting, constipation, and dry mouth. Some clients may also experience bradycardia, while clonidine can also cause rebound hypertension when stopped abruptly, as well as CNS depression. 

On the other hand, guanfacine and methyldopa can also cause orthostatic hypotension and sedation. 

In addition, methyldopa can also cause granulocytopenia, thrombocytopenia, and hemolytic anemia, as well as hepatotoxicity and hepatic necrosis.

As far as contr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Beta_lactam_&amp;_beta_lactamase_inhibitor_combinations:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W5owTiBpSlqJjxuoPCA1ZA8NT7S2_WrE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Beta lactam and beta lactamase inhibitor combinations: Nursing pharmacology]]></video:title><video:description><![CDATA[Beta-lactams are a group of antibiotics that contain a beta-lactam ring in their structure that is essential for the antibacterial activity of antibiotics like penicillins and cephalosporins. However, over time, due to their widespread use, some bacteria have acquired resistance by developing enzymes called beta-lactamases. For this reason, some beta-lactam antibiotics are often combined with a class of medications known as beta-lactamase inhibitors in order to treat infections caused by beta-lactam-resistant bacteria like Haemophilus influenzae, methicillin-sensitive Staphylococcus aureus, Bacteroides fragilis, Proteus spp., Escherichia coli, Klebsiella spp., and Acinetobacter spp. Additionally, cephalosporin-containing combinations are effective against Pseudomonas aeruginosa.

Now, beta-lactam/beta-lactamase inhibitor combinations typically contain either a penicillin or a cephalosporin combined with a beta-lactamase inhibitor. Commonly used penicillin beta-lactamase inhibitor combinations include amoxicillin-clavulanate, which is given orally; ampicillin-sulbactam, which is given intramuscularly and intravenously; and piperacillin-tazobactam, which is given intravenously. Commonly used cephalosporin beta-lactamase inhibitor combinations include ceftazidime-avibactam, which is given intravenously; and ceftolozane-tazobactam, which is given orally.

Once administered, beta-lactam antibiotics act by inhibiting bacterial cell wall synthesis, which kills the bacteria. However, in resistant bacteria, the beta-lactamase enzyme binds to the beta-lactam ring within the antibiotic and breaks it down, thus inactivating the antibiotic. This is where the beta-lactamase inhibitors come into play, by binding to the beta-lactamase enzymes in the bacteria. As a result, beta-lactamase inhibitors prevent the beta-lactamase enzyme from inactivating the beta-lactam antibiotic. As a result, the antibiotics are left free to go about their job of killing the bacteria.

The be]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glucocorticoids_&amp;_mineralocorticoids:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U8x3-hn5T6urBWM0w5gfjWVLQMaWYKIV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glucocorticoids and mineralocorticoids: Nursing pharmacology]]></video:title><video:description><![CDATA[Glucocorticoids and mineralocorticoids are endogenous hormones normally produced by the adrenal glands. In clients with impaired adrenal function, these hormones can be administered as replacement therapy.

Synthetic glucocorticoids, also commonly known as corticosteroids, are medications that can be used in clients with decreased adrenal function, such as in adrenal insufficiency; this is also known as Addison disease, and specifically occurs when the adrenal glands don&amp;#39;t make enough endogenous glucocorticoids, so these clients need hormone replacement therapy with synthetic glucocorticoids. In addition, glucocorticoids are used in the treatment of numerous inflammatory conditions, such as asthma, rheumatoid arthritis, and inflammatory bowel disease, as well as  preventing organ rejection in transplant recipients.

Alright, now, based on the duration of action, synthetic glucocorticoids can be classified into three groups. The first group are short-acting glucocorticoids, such as cortisone and hydrocortisone. Cortisone needs to be converted into hydrocortisone in the liver in order to be active, so it can only be taken orally; while hydrocortisone can be given orally, intravenously, intramuscularly, and topically. The second group are intermediate-acting glucocorticoids, which include prednisone, prednisolone, and methylprednisolone. Prednisone can only be taken orally; while prednisolone can be administered orally, intravenously, or topically; and methylprednisolone can be given orally, intravenously, intramuscularly, or injected intra-articularly. The third and final group are long-acting glucocorticoids, which include betamethasone and dexamethasone. Both of these medications can be taken orally, intravenously, intramuscularly, or intra-articularly. In addition, betamethasone is also available for topical use.

Once administered, glucocorticoids act by binding to intracellular glucocorticoid receptors and then migrating into the nucleus to mod]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Antimycobacterials:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7OI9CZGGRfGSo5lWRwWt5E4cRTqBG77r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Antimycobacterials: Nursing pharmacology]]></video:title><video:description><![CDATA[Antimycobacterials are medications used to treat infections caused by the mycobacterium species. These include tuberculosis, caused by Mycobacterium tuberculosis; leprosy, also known as Hansen’s disease, caused by Mycobacterium leprae; and non-tuberculous lung infections caused by Mycobacterium avium complex or MAC, which includes Mycobacterium avium, Mycobacterium chimaera, and Mycobacterium intracellulare.

Antimycobacterial drugs can be divided into two broad categories. We have the first-line antimycobacterials, which are the standard initial therapy; and the second-line antimycobacterials, used when the first-line drugs aren’t suited, like when they have contraindications, they have failed to treat the infection, or with multi-drug resistant tuberculosis. 

The first-line antimycobacterials include isoniazid or INH for short, which is administered orally or intramuscularly; as well as streptomycin or SM, which is given intravenously or intramuscularly;  rifampin or RIF, which is given orally and intravenously; and rifapentine or RPT, ethambutol or EMB, and pyrazinamide or PZA, all of which are given orally. 

On the other hand, the second-line antimycobacterials include bedaquiline, cycloserine, ethionamide, rifabutin, and aminosalicylic acid all of which are administered orally; as well as capreomycin which is administered intravenously or intramuscularly; and amikacin which can be administered intravenously, intramuscularly, or by inhalation. These medications are mainly used for treating active mycobacterial infections, except rifabutin, which is preferred as preventive treatment against Mycobacterium Avium complex in clients with advanced HIV infection, who are severely immunocompromised. Finally, antimycobacterials also include leprostatic medications, such as dapsone, which is administered orally to treat leprosy.

Now, antimycobacterials have different mechanisms of action by targeting various mycobacterial structures. Isoniazid, ethambutol, am]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_products:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ebawSYmHS0__1SdGJhV5HWPHSrONtCK8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood products: Nursing pharmacology]]></video:title><video:description><![CDATA[Blood products are natural components of blood that can be transfused as adjuncts or replacement therapy. They can be used in conditions that increase the risk of bleeding, like thrombocytopenia, platelet dysfunction, or clotting factor deficiencies, as well as symptomatic anemia, and for hypovolemic shock that is secondary to trauma or severe bleeding.

Now, there are different types of blood products, depending on what they contain. Whole blood contains red blood cells, white blood cells, platelets, and plasma. On the other hand, some clients may be transfused with specific blood components. This includes packed red blood cells, or PRBCs for short, which are red blood cells that have been almost completely separated from platelets and plasma; as well as platelet transfusions, and fresh frozen plasma. In addition, specific components can be extracted from plasma, such as albumin, as well as cryoprecipitate, a blood product that contains clotting factors.

Now, the blood for these blood products can be taken from clients themselves, or from a different person. In autologous transfusion, the blood is taken from the client before a scheduled procedure, so that their own blood is reinfused later on. A specific type of autologous transfusion is called intraoperative blood salvage, or cell salvage, and it refers to a retrieval of blood that has been suctioned or drained during surgery from the client’s body cavities, joint spaces, or other closed body sites. The blood is reused and reinjected into the client after it’s been washed or filtered. Another possible blood source is allogenic transfusion, in which case the blood is derived from a compatible donor in terms of ABO and Rh(D) blood group.

Now, all blood products are administered through an intravenous transfusion, and work by replacing the blood components that are missing or dysfunctional. Whole blood transfusions replace all blood components, so they’re indicated to restore severe blood loss. Packed re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disease-modifying_therapy_for_multiple_sclerosis:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1EOC6UbGQw68UmVluVO05W-9SCKHbEcQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disease-modifying therapy for multiple sclerosis: Nursing pharmacology]]></video:title><video:description><![CDATA[Multiple sclerosis, or MS for short, is a chronic and progressive demyelinating disease of the central nervous system. Myelin is the protective sheath that surrounds the axons of neurons, allowing them to quickly send electrical impulses. In MS, demyelination happens when the immune system inappropriately attacks and destroys the myelin. As a result communication between neurons breaks down, ultimately leading to various sensory, motor, and cognitive problems. Although there’s no cure for MS, disease-modifying therapy can be used to help slow the disease progression, as well as mitigate some of the symptoms, and ultimately improve the client’s quality of life.

Now, disease-modifying therapy for MS includes monoclonal antibodies and immunomodulators. The most commonly used monoclonal antibodies for MS include rituximab, natalizumab, ocrelizumab, and alemtuzumab, which are administered intravenously. On the other hand, immunomodulators for MS include dimethyl fumarate, teriflunomide, and fingolimod, which are administered orally, as well as glatiramer and recombinant human interferon beta-1a and interferon beta-1b, which can be injected intramuscularly or subcutaneously.

Once administered, these medications blunt the inflammatory process, which ultimately helps reduce the severity and frequency of relapses or exacerbation of multiple sclerosis.

Unfortunately, these medications can cause side effects like bone marrow suppression, which can result in anemia, thrombocytopenia, leukopenia, and an increased risk for infections. In fact, for alemtuzumab, that’s a boxed warning, with an increased risk of developing fatal infections, autoimmune effects, and malignancy. 

Clients on disease-modifying therapy may also experience drowsiness, fatigue, nausea, vomiting, and diarrhea. These medications may also result in hypersensitivity reactions, such as injection site reactions, Stevens-Johnson syndrome, toxic epidermal necrolysis, and anaphylaxis, while alemtu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sympathomimetic_medications:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Dag6Su1JTPOE76tx-FkaoxKYTQy-3pZp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sympathomimetic medications: Nursing pharmacology]]></video:title><video:description><![CDATA[Sympathomimetics are medications that mimic the effect of endogenous catecholamines, like norepinephrine and epinephrine. As a result, these medications activate the sympathetic nervous system, which in turn triggers the fight or flight response, ultimately increasing the heart rate and blood pressure, as well as slowing down digestion. This response maximizes blood flow to the muscles and brain.  

Now, sympathomimetic medications include dobutamine, dopamine, norepinephrine, epinephrine, and isoproterenol. All of them are administered intravenously, while isoproterenol can also be given intramuscularly, and epinephrine can also be administered intramuscularly, as well as through endotracheal tube or inhalation.

Once administered, sympathomimetic medications act by stimulating adrenergic receptors. Now, there are two main groups of adrenergic receptors: the alpha receptors, and beta receptors. Alpha adrenergic receptors are mainly located on the walls of blood vessels of the skin, as well as the gastrointestinal and genitourinary systems, and when stimulated, they cause vasoconstriction and decreased blood flow to these tissues. 

On the other hand, beta receptors have two main subtypes: beta-1 and beta-2. Beta-1 adrenergic receptors are mainly located in the heart, and when activated, they increase the heart rate and contractility, which helps pump out more blood. On the other hand, beta-2 adrenergic receptors are found on smooth muscle cells in the walls of blood vessels supplying skeletal muscles and the brain, so their activation leads to vasodilation and increased blood flow to these tissues; and in the lungs, they cause bronchodilation. 

Each type of adrenergic agonists stimulate these receptors to a different degree, which makes them useful to treat different conditions. But in general, all of them activate beta-1 receptors, so they all increase heart contractility, helping in the treatment of conditions where the cardiac output is decreased.

No]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Lincosamides:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZKyrNCGyTfaQ8RRAjYx-9f_hRSasHTAL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Lincosamides: Nursing pharmacology]]></video:title><video:description><![CDATA[Lincosamides are a class of antibiotics used to treat severe infections caused by gram positive and anaerobic bacteria. The lincosamide family of antibiotics includes both clindamycin and lincomycin, however, lincomycin has been widely replaced by clindamycin in almost all of its uses.

Now, clindamycin is most often used to treat skin and soft tissue infections caused by staphylococci and streptococci. It can be active against community-acquired strains of methicillin resistant Staphylococcus aureus, or MRSA for short, an increasingly common cause of cutaneous infections. Additionally, clindamycin is indicated for the treatment of anaerobic infections caused by Bacteroides species and other anaerobes that often participate in mixed flora infections. 

Consequently, it is often used in combination with cephalosporins or aminoglycosides to treat penetrating wounds of the abdomen and gut, infections originating in the female reproductive tract, and lung abscesses. 

Finally, clindamycin may be used for the prophylaxis of endocarditis in clients with underlying valvular heart disease, as well as to treat Pneumocystis jirovecii pneumonia in clients with HIV infection.

For the treatment of systemic infections, clindamycin can be administered orally or by intravenous or intramuscular injection. Additionally, clindamycin can be used topically for the treatment of acne and rosacea, as well as intravaginally for the treatment of bacterial vaginosis.

All right now, once administered, clindamycin targets the 50S ribosomal subunit of the bacteria, thereby inhibiting protein synthesis and ultimately limiting the growth of bacteria. Although clindamycin has a primarily bacteriostatic effect, it can also act as a bactericidal antibiotic at higher concentrations. 

Since clindamycin tastes extremely bitter, it is not commonly prescribed to children. The most common side effects of clindamycin include gastrointestinal disturbances like nausea, vomiting, diarrhea, and abd]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antivirals_for_Hepatitis_B_&amp;_C:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BHZpnISgSxq7-_2M7qfvmN6wR6a20fyJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antivirals for hepatitis B and C: Nursing pharmacology]]></video:title><video:description><![CDATA[Viral hepatitis is the inflammation of the liver caused by hepatitis viruses A, B, C, D, or E. Out of these, chronic hepatitis caused by hepatitis B virus, or HBV, and hepatitis C virus, or HCV, can be treated with antiviral medications. 

Now, chronic HBV infection can be treated with a class of antiviral medications called NRTIs, which include nucleotide reverse transcriptase inhibitors like adefovir and tenofovir, as well as nucleoside reverse transcriptase inhibitors like entecavir; these medications are administered orally. 

On the other hand, chronic HCV infection can be treated with antiviral medications that target different components of the virus, so they’re typically used in combination; these include nucleotide polymerase inhibitors like sofosbuvir, as well as nucleoside analogues like ribavirin, both of which are taken orally. 

Finally, there’s a third class of medications that can be used to treat both chronic HBV and HCV; these include interferons like peginterferon alfa-2a, which is administered by subcutaneous injection.

Now, once administered, all of these antivirals have a different mechanism of action. NRTIs used to treat hepatitis B act by inserting into the replicating viral DNA. As a result, viral DNA synthesis is halted, ultimately stopping viral replication. On the other hand, medications used to treat hepatitis C work in different ways, inhibiting different viral proteins or enzymes required for viral replication. Interferons, on the other hand, induce the innate antiviral immune response that helps kill off cells that are infected by the virus.

Now, clients taking NRTIs for hepatitis B infection can have side effects. All these medications come with a boxed warning for severe, acute hepatitis exacerbations on discontinuation of therapy. These medications also cause lactic acidosis, which is a boxed warning for adefovir and entecavir, as well as severe hepatomegaly with steatosis; and a risk for individuals with concurrent HIV]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/First_Responders_First_-_Barriers_to_accessing_mental_health_services</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ap1QyLyFSSSk9KJ78NK0yBU0QnWSF1P1/_.jpg</video:thumbnail_loc><video:title><![CDATA[First Responders First - Barriers to accessing mental health services]]></video:title><video:description><![CDATA[Unlike most medical diagnoses, mental health disorders like anxiety and depression are more subjective and appear invisible and intangible. But like other medical disorders, mental health can affect all aspects of life and can worsen if poorly managed. The psychosocial well-being of healthcare workers can have a drastic effect on their ability to respond to crises and can also directly impact their ability to respond to client outcomes. Here are the common barriers to accessing mental health services and some suggestions to overcome them.

The most common barrier involves the stigma associated with seeking mental health services. Often, culture and community impact the perception of seeking mental health services as some cultures perceive it as a socially unacceptable topic. As a result, seeking mental health services often brings up difficult emotions like fear, shame, and guilt. Often, the fear of being judged can prevent individuals from seeking the help they need. Many healthcare workers have concerns that seeking mental health services could adversely affect their careers and lead to decreased confidence from superiors or teammates. This reluctance to seek support can lead to further isolation, thereby exacerbating mental health disorders. It’s important to recognize the impact of mental health issues and take the necessary steps to address them. Practice self-care and engage in healthy coping strategies to help prevent stress from mounting, potentially leading to more significant problems. Find and engage in support groups like the Frontline Nurses WikiWisdom Forum and Compassionate Listening Circles. Often, these support systems can help you normalize and recognize the need for mental health services and reduce the stigma around seeking help.

Other barriers include the lack of available and appropriate mental health services. There’s a shortage of mental health professionals in the US, and some nurses living in rural areas may find that there are f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/First_Responders_First_-_Building_resilience_in_nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rh5nSOUzTxmXVgUIVLVYltbERgKAzeUw/_.jpg</video:thumbnail_loc><video:title><![CDATA[First Responders First - Building resilience in nursing]]></video:title><video:description><![CDATA[Burnout, stress, and compassion fatigue are common factors that contribute to dissatisfaction in the nursing profession, especially in high-intensity units like emergency, pediatric, and intensive care. A method to combat these factors is to support the cultivation of resilience in nurses.

Resilience helps us navigate through trying times, from getting past small mistakes to finding our way through crises. It is the ability to face challenges directly in a positive manner, allowing you to recover, adapt, and thrive despite failures and setbacks. Resilience is not an inherent trait, it is a skill that can be learned and built up over time through strategies that promote  self-care, self-confidence, and a positive mindset.

Nurse leaders and managers are responsible for establishing a healthy work environment as the well-being of any healthcare team is directly related to patient safety and quality of care. This includes recognizing and applying strategies to foster resilience among nursing staff.

Here are seven strategies to strengthen nurse resilience.

The first is facilitating social connections by supporting the development of interpersonal relationships between nurses, who are often the only people that really understand the contextual realities of the profession. Events like debriefing sessions, potluck dinners, and holiday crafts allow nurses to develop social support groups to bond and share experiences. Team-building activities like outdoor and community events can help nurses build a sense of camaraderie. These can be done adjacent to work times, to accommodate the competing demands of work/life balance. Facilitating social connections helps strengthen teamwork and establish support systems to reduce stress and improve mental well-being.

Next involves promoting positivity by helping nurses develop a positive mindset. This can include implementing activities like practicing gratitude at the end of meetings or conducting random acts of kindness f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/First_Responders_First_-_Institutional_management_and_logistics_stressors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2ujT1xfKRaauohkFBVbhPL0MT_GeMS7_/_.jpg</video:thumbnail_loc><video:title><![CDATA[First Responders First - Institutional management and logistics stressors]]></video:title><video:description><![CDATA[A number of workplace stressors that likely affect you daily are caused by management and employment logistics. Constant exposure to these stressors, or constantly feeling stressed, can negatively affect your resilience, well-being &amp;amp; mental health.

You all, as floor and charge nurses, nurse educators, and nursing managers are leaders in your units and heavily influence the real and perceived stressors. Resilient leadership can prevent stressors from affecting staff, but they can also become a stressor for staff too. Three negative management styles that have been studied in healthcare environments are passive leadership, abusive supervision, and over-controlling leadership.

Passive leadership is inactive, choosing to be non-participatory for both positive and negative situations in the workplace. These leaders may do nothing to address a nurse who consistently does not return from break on time. This type of leadership can reduce team effectiveness and create negative attitudes amongst nursing staff, leading to stress.

Abusive supervision is leadership that is hostile towards nurses and can include consistent or occasional verbal or non-verbal behaviors, such as discrediting a nurse’s judgment, displaying overtly rude behaviors, imposing overly critical or patronizing comments, or subjecting a nurse to embarrassing situations in front of others. For example, these leaders may disclose a clinical error a nurse made on shift, and shame the nurse in an email thread with other staff members. This type of leadership causes stress and anxiety, reduces self-esteem, decreases job performance, and fosters fear and resentment towards leaders.

Overcontrolling leadership restricts a nurse’s autonomy and decision-making ability, often due to previous perceived mistakes. For example, if you mislabelled a blood sample, an over-controlling leader may begin to observe and comment on your performance regularly across several of their clinical procedures. This t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/First_Responders_First_-_Stress_relieving_activities</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lhnFqtKdTz2MYOXdO6SG0MFUTSyTrnv8/_.png</video:thumbnail_loc><video:title><![CDATA[First Responders First - Stress relieving activities]]></video:title><video:description><![CDATA[Stress is a part of everyday life, and paying careful attention to the body can prevent stress from mounting. Healthcare providers meet unique challenges, especially in the face of disasters like the COVID-19 pandemic. Often, it’s easy for self-care to fade into the background as demands increase. However, taking small, conscious, and actionable steps every day can make a positive impact on life and work.

Here are some tips to support healthy stress levels and manage self-care, stress, mental well-being, and interpersonal connections.

Self-care activities help support your body’s physiological needs and keep it recharged. First, stay hydrated by keeping a water bottle nearby. This could be at your station or in the break room. Hydrating with water can limit sugar intake and prevent sugar-related energy crashes. Second, allow your body to slow down, especially during meals. This brief pause can provide a mental break and promote proper digestion. Third, recharge your body with enough sleep to recover and repair itself. When getting inadequate sleep, take naps or close your eyes for five to ten minutes to allow the body and mind to rest before moving to the next task. Planning for adequate sleep is particularly important in planning for shift work. Fourth, maintain good posture and focus on extending the spine when walking or sitting. This relieves tension and improves focus. Finally, avoid substances that can impair judgment like tobacco, alcohol, and other drugs as these can be harmful and prevent the body and mind from restoring balance.

Follow these steps to reduce the burden of stress on the body. First, identify personal warning signs of stress and recognize their triggers. These can include increased heart rate, difficulty concentrating, negative emotions such as irritability, anxiety, or sadness, and social conflicts. Use these signs to help guide breaks throughout the day. Second, recognize moments that can cause mental or emotional distress and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/First_Responders_First_-_Stressors_for_nurses_outside_the_workplace</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wBsuoABnQ4ehiloHWemcGdedQqO_pnFQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[First Responders First - Stressors for nurses outside the workplace]]></video:title><video:description><![CDATA[There are a number of stressors that can occur daily outside the workplace that can impact a nurse’s ability to work within the workplace. Constant exposure to these stressors, or constantly feeling stressed, can negatively affect a nurse’s mental health.

For example, Briana is a nurse manager at a pediatric specialty clinic. When COVID-19 hit, many policies at childcare centers changed. Children were often sent home at the first possibility of illness, putting a lot of stress on Briana to figure out childcare. She and her co-workers worked to save PTO days in anticipation of when schools or childcare centers closed, and while not an ideal or permanent solution, this allowed Briana and her co-workers to be prepared for challenges ahead. This situation isn’t unique to COVID-19. Nurses often work long hours throughout their careers and arranging childcare can be stressful. Coordinating work schedules with parents or extended family can be tricky, and using professional childcare services can be expensive, particularly for single-parent households. In some cases, it may not be possible to pay for professional childcare, and you may need to make career decisions, such as moving to an outpatient unit with shorter working hours, to accommodate your family circumstances.

Besides childcare, there will likely be a number of other financial stressors you may face. The cost of living in some cities may be higher than expected, making it difficult to live within your planned budget in an area close to work. Combined with long shift work schedules, long commutes could further increase childcare costs while also decreasing available time to spend with family and raise children. All of these stressors can weigh heavily on a natural caregiver. If you’re experiencing any of these stressors, talk with your family and friends and see if any creative solutions can be arranged, such as a friend picking up your children from school and supervising them on workdays, and you ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/First_Responders_First_-_Red_flags_of_stress</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cmrgJJXMQiWRlR8-e4mCJLoAS66Qth0R/_.jpg</video:thumbnail_loc><video:title><![CDATA[First Responders First - Red flags of stress]]></video:title><video:description><![CDATA[Stress is the body’s response to any disturbances in the body and may take the form of emotional, physiological, behavioral, and cognitive stressors. Stress in small amounts is good as it can provide motivation and endurance to overcome challenges. However, stress in excessive amounts or for prolonged periods can have a damaging effect on the body. These stressors often occur from concerns related to finances, job performance, relationships, and health. When crisis situations arise, such as disasters, these stressors can compound and overlap. During the COVID-19 pandemic, Erik, an ICU nurse, was caught between anxiety about bringing the infection home, especially to his pregnant wife and unborn child, and working more as needed to support his clients and teammates. Like many others, he made the difficult decision to isolate and live separately. The loss of the physical presence of loved ones, as well as other stressors, can intensify and build upon one another. Prolonged stress can increase anxiety and depression, and can lead to panic attacks, heart disease, diabetes, or suicide. In these periods of prolonged or excessive stress, it is crucial to recognize the body’s warning signs of impending stress and seek support from colleagues, family, or professionals to intervene as soon as possible. These signals reveal that the body is struggling and needs help.

So, what are the warning signs of stress? In general, common signs can present themselves in four areas. First are emotional indicators and often present as negative emotions. These may include feeling irritable, angry, or frustrated in social situations. Experiencing emotions like anxiety, fear, guilt, or sadness are also common. Other signs include feeling disconnected from others, losing interest in daily activities, or feeling numb and unable to feel joy or sadness. 

Second are physiological indicators and can include physical distress symptoms like headaches, stomachaches, diarrhea, muscle tension]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/First_Responders_First_-_Physical,_mental,_&amp;_emotional_toll_of_stress</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VjTxlX5iQ8mBUWoX6ViIukQKQLaIsNRg/_.jpg</video:thumbnail_loc><video:title><![CDATA[First Responders First - Physical, mental, &amp; emotional toll of stress]]></video:title><video:description><![CDATA[Any disturbance of the human body, such as temperature changes, infections, emotional responses, or any of the situations described in other course modules can produce a stress response. Regardless of the source of the disturbance, the body responds to different types of stressors similarly.

In some cases, stress can be positive as it helps people overcome challenges. These are often short-term stressors, like responding to sudden loud noises, that activate the fight-or-flight response through the sympathomedullary pathway or SAM. A stress trigger causes the hypothalamus to send action potentials, or messages, to the adrenal medulla, stimulating the release of epinephrine and norepinephrine. This causes a temporary increase in heart rate, blood pressure, and blood glucose as well as bronchiole dilation. Nutrients like blood, glucose, and oxygen get redirected to essential organs like the brain, heart, and skeletal muscles. Usually, people experience a pounding heart, faster breathing, sweaty palms, and trembling hands.

Though short-term stress is helpful, long-term stress can become detrimental. Prolonged stress involves the interaction between the hypothalamus, pituitary, and adrenal glands, also called the hypothalamic-pituitary-adrenal or HPA axis, and initiates a cascading hormonal response. The hypothalamus secretes corticotropin-releasing hormone, triggering the anterior pituitary gland to release adrenocorticotropic hormone, signaling the adrenal glands to release aldosterone and cortisol. Aldosterone increases blood volume and blood pressure. Cortisol increases blood glucose, facilitates the breakdown of proteins and fats, and temporarily suppresses the body’s immune response. 

Chronic exposure to stressors like financial difficulties, career concerns, relationship problems, and deadlines can lead to persistent elevations in heart rate, blood pressure, and blood glucose, eventually leading to health problems like heart disease and diabetes. Cont]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/First_Responders_First_-_Stressors_for_nurses_when_working_with_clients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/p6yi6OGHSz6DkTjVakhFI015R7y5A3zV/_.jpg</video:thumbnail_loc><video:title><![CDATA[First Responders First - Stressors for nurses when working with clients]]></video:title><video:description><![CDATA[There are a number of stressors that affect nurses every day while providing care to clients. Constant exposure to these stressors, or constantly feeling stressed can negatively affect a nurse’s mental health.

Some of the most common causes of stress for nurses are related to nurses having insufficient time. Nurses are often overloaded with too many tasks during their shift, managing several tasks at once, and unable to give the proper attention needed for each task. When a nurse is focusing on a task such as writing progress notes or performing a clinical procedure, they are frequently interrupted with questions or are asked to reprioritize their tasks. Nurses also feel they don’t have enough time or emotional energy to give proper emotional support to clients or their families when they need it most. There’s always a clock ticking, and nurses know that every moment they spend documenting progress notes, or getting tasks done before the end of their shift means less time with clients.

In addition to feeling stressed by not having enough time, nurses face a number of stressors caused by the health care and nursing environment. As a client’s needs change, a nurse may need to call for another health provider, such as a physician, medical imaging technician, or respiratory therapist. Health care providers are usually busy with a number of responsibilities, and sometimes it can be hard for the nurse to get a hold of the teammate they need, adding high stress especially if communicating an urgent or time-sensitive situation. 

Other situations that can add stress to a nurse include: nurses completing tasks outside their comfort zone or outside their scope of practice, witnessing the death of a client, consoling the family of a recently diagnosed or deceased client, and working with violent clients.

Nurses often experience most or all of these stressors on a regular basis, and prolonged exposure can take a toll on the nurse’s mental and physical health. If yo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacokinetics_-_Absorption:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3a3lfnUlTSCNoTXjtSP4uEw4T6y_t6dy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacokinetics - Absorption: Nursing pharmacology]]></video:title><video:description><![CDATA[Pharmacokinetics refers to the movement and modification of a drug or medication inside the body. Once a medication is administered, it’s first absorbed into the circulation, then distributed to various tissues throughout the body, metabolized or broken down, and finally, eliminated or excreted in the urine or feces. This process can be broken down into four components with the acronym ADME; which stands for Absorption, Distribution, Metabolism, and Elimination.

Now, the first step of pharmacokinetics is absorption, which refers to the process of how a medication goes from the site of administration to the bloodstream. To do so, the medication may need to cross one or more cell membranes; and this can occur via passive transport, which requires no energy, or active transport, which requires energy in the form of ATP.  

With passive transport, the medication goes down its concentration gradient, so from an area of higher concentration to an area of lower concentration. There are two types of passive transport: passive diffusion and facilitated diffusion. 

Passive diffusion allows small, lipid-soluble, and nonpolar medications to freely move across the membrane. Facilitated diffusion, on the other hand, allows larger, water-soluble, and polar medications to move across the membrane through transport proteins like channels and carrier proteins. 

Now, some medications need to be transported through active transport against their concentration gradient, so from an area of lower concentration to an area of higher concentration. This can be achieved with specific carrier proteins that use ATP as an energy source to pump medications against their gradient.

Now, the rate of the absorption, or how quickly this process occurs, as well as the extent of the absorption, or how much of that medication reaches the bloodstream, can be affected by several factors. One of them is the pH of the environment where absorption takes place. 

Okay, so most medications are eit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_to_treat_growth_hormone_disorders:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nsKjQgzdSdKneZ4PXJ0RTGujSLaHk9Cy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for growth hormone disorders: Nursing pharmacology]]></video:title><video:description><![CDATA[The pituitary gland is a small gland located at the base of the brain, and it produces, stores, and releases various hormones that control other endocrine glands. One of these is growth hormone, and disorders can arise when the pituitary produces too much or too little of it. Okay, so on one end of the spectrum, there’s growth hormone deficiency, which can occur in disorders like hypopituitary dwarfism, as well as Prader-Willi syndrome, Turner syndrome, and acquired immunodeficiency syndrome or AIDS-related wasting or cachexia.

Growth hormone deficiency is treated by replacing it using a recombinant human growth hormone, called somatropin. This medication can be injected subcutaneously or intramuscularly. Once administered, it stimulates the proliferation of cartilage cells at the epiphyseal or growth plate of long bones, which results in bone growth.

Now, the most common side effects of somatropin include skin reactions at the injection site, as well as headache, flu-like symptoms, fatigue, weakness, and aggressive behavior. Some clients may experience gastrointestinal symptoms, such as nausea, vomiting, and pancreatitis. In addition, it may cause hypercalciuria, glucose intolerance, and ketosis, as well as endocrine side effects, such as hypothyroidism, and hypoadrenalism. Lastly, some clients may develop antibodies against growth hormone.

All right, now contraindications of somatropin include those with closed growth plates and in clients with neoplasms, acute respiratory failure, and those affected by Prader-Willi syndrome with obesity or sleep apnea. Finally, somatropin should be used with caution during pregnancy and breastfeeding, as well as in newborns or elderly clients, and those with diabetes mellitus or hypothyroidism. On the opposite end of the spectrum, we have disorders characterized by an excess of growth hormone, including acromegaly, which affects adults, and gigantism, which affects children.

Both disorders are treated using agents t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antitumor_antibiotics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VIIalVTYQkaqw7TKswrob8msQwCdUfTY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antitumor antibiotics: Nursing pharmacology]]></video:title><video:description><![CDATA[Antitumor antibiotics are chemotherapeutic agents used to treat various cancers, including leukemia, lymphoma, soft tissue sarcoma, osteosarcoma, as well as solid tumors, such as breast, bladder, ovarian, and lung cancers. Antitumor antibiotics include bleomycin, dactinomycin, mitomycin, as well as anthracyclines such as daunorubicin, doxorubicin, idarubicin, and epirubicin.

These medications are primarily given intravenously, but bleomycin can also be administered intramuscularly. Once administered they act as cell cycle nonspecific agents, which means they target cells in all phases of the cell cycle. The exception is bleomycin, which specifically goes for cells in the G2 phase. Now, the way they work is twofold: first, these medications disrupt protein synthesis in target cells; and second, they bind to DNA, causing its fragmentation. Ultimately, this stops the rapidly dividing cancer cells from replicating and eventually causes their death.  

Unfortunately, antitumor antibiotics also act on rapidly dividing healthy cells in our body, like those in the bone marrow, skin, and gastrointestinal tract. So antitumor antibiotics, with the exception of bleomycin, can all cause bone marrow suppression, which is a boxed warning for all anthracyclines as well as mitomycin. Bone marrow suppression can lead to anemia, leukopenia, increasing the risk of infections, and thrombocytopenia, increasing the risk of bleeding. Moreover, they can all cause alopecia, as well as gastrointestinal toxicity, which can manifest as nausea, vomiting, diarrhea or stomatitis. 

Another important thing to remember is that all these medications are vesicants, which means they can cause blistering and tissue damage if they leak from the administering site into neighboring tissues; and this is actually a boxed warning for all anthracyclines. Other important side effects include pulmonary toxicity, which can occur with bleomycin, dactinomycin and mitomycin, and cardiotoxicity cardiac tox]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Angiogenesis_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kkt6sYlkQoam2HSFjFq5nXcBR8_9YFFY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Angiogenesis inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Angiogenesis inhibitors are medications mainly used to treat cancers like non-small cell lung cancer, cervical cancer, metastatic colorectal cancer, metastatic renal cell carcinoma, and recurrent glioblastoma. In addition, these medications can be used to treat macular degeneration.

The most commonly used angiogenesis inhibitor is bevacizumab, which is a monoclonal antibody that’s administered intravenously for cancer treatment, and intravitreal for macular degeneration. Once administered, bevacizumab acts by binding to the protein human vascular endothelial growth factor, or VEGF for short, which helps promote angiogenesis, meaning the formation of new blood vessels throughout the body. So, bevacizumab inhibits the activity of VEGF, ultimately reducing the progression of cancer or macular degeneration.

Now, bevacizumab may often lead to side effects, such as headaches, dizziness, or syncope. In addition, some clients may present with injection-site infusion reactions or exfoliative dermatitis. Other common side effects include abdominal pain, anorexia, nausea, vomiting, or diarrhea. 

Clients on bevacizumab may also develop heart failure, hypertension, and venous thromboembolism; as well as thrombocytopenia, leukopenia, and increased risk of infections. Additional side effects include dyspnea, epistaxis, hemoptysis, and vaginal bleeding. Finally, bevacizumab can potentially cause gastrointestinal perforation and bleeding, as well as wound dehiscence.

Regarding contraindications, bevacizumab should be used with caution in clients with serious bleeding or hypertensive crisis, and it should not be used 28 days before and after surgery, since it can interfere with wound healing.  In addition, bevacizumab should be used cautiously during pregnancy and breastfeeding, as well as in children and elderly clients. Other precautions include clients with cardiovascular or thromboembolic disease.

Okay, when caring for a client prescribed bevacizumab for recurrent ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticoagulants_-_Direct_thrombin_inhibitors_&amp;_factor_Xa_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rfRfmEIrQPypdc66lb5Lvm3RSBSiJ9Mp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticoagulants - Direct thrombin and factor Xa inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Anticoagulants are medications used to prevent the formation of thrombi, or blood clots, and they’re used to prevent or treat thromboembolic events, such as deep vein thrombosis, pulmonary embolism, ischemic stroke, transient ischemic attack, coronary artery disease or myocardial infarction. 

They&amp;#39;re also used in clients with coagulation disorders, including antiphospholipid syndrome and disseminated intravascular coagulation; as well as in clients who underwent coronary angioplasty or cardiac valve replacement; and during surgical procedures like cardiopulmonary bypass, percutaneous coronary intervention, extracorporeal membrane oxygenation, and in clients undergoing dialysis.

Now, anticoagulants work by interfering with the normal function of clotting factors involved in the coagulation cascade. One of the most important factors is factor X, which gets activated into Xa, and in turn activates factor II, also known as prothrombin, into factor IIa or thrombin. Thrombin further activates factors I, V, VIII, IX, and XIII. Factor I, also known as fibrinogen, is activated to form factor Ia, or fibrin, which binds to other fibrin proteins to form a crosslinked fibrin mesh. 

Factor V gets activated and acts as a cofactor for factor X, while factor VIII acts as a cofactor for factor IX, and factor XIII helps fibrin form crosslinks. Ultimately, the fibrin mesh allows platelets to rapidly aggregate at the site of injury and form a platelet plug, which is a primary clot that can help stop the bleeding. So, based on the mechanism of action, some of the most important anticoagulants include direct thrombin inhibitors and factor Xa inhibitors.

Direct thrombin inhibitors include desirudin, bivalirudin, and argatroban, which are given intravenously; as well as dabigatran, which is given orally. Once administered, direct thrombin inhibitors act by reversibly binding to thrombin in the circulation and those already attached to a forming clot and inhibitin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medications_used_to_treat_migraines:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v6ihunP2SuySBoMo_9wKsVdQTbWgFdG8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medications for migraines: Nursing pharmacology]]></video:title><video:description><![CDATA[Migraines are a specific type of pounding or pulsating headache that’s typically localized to one side of the head, and is often associated with additional symptoms like photophobia, phonophobia, nausea, or even vomiting. As preventative therapy, some clients may take beta blockers like metoprolol, antiepileptics like topiramate, or tricyclic antidepressants like amitriptyline. 

On the other hand, acute treatment of migraines involves managing the symptoms with abortive agents, which can be broadly divided into four classes; ergot derivatives, triptans, ditans, and calcitonin gene-related peptide or CGRP receptor antagonists, which are also used as preventive therapy.

Starting with ergot derivatives, these include ergotamine and dihydroergotamine. Ergotamine can be administered in sublingual tablets, while dihydroergotamine can be injected intramuscularly or intravenously, or used as a nasal spray. Once administered, ergot derivatives work by binding to serotonin and alpha-adrenergic receptors on the blood vessels in the brain, causing them to constrict. And that helps decrease the pain because vasodilation of these blood vessels seems to be a trigger for pain receptors, causing the migraine in the first place. 

However, ergot derivatives not only cause vasoconstriction of the blood vessels in the brain, but also blood vessels all around the body, which can cause hypertension. Vasoconstriction of coronary blood vessels in the heart can also bring about a type of chest pain called angina, which, in severe cases, can get complicated with arrhythmias or even myocardial infarction. At the same time, ergot derivatives stimulate serotonin receptors in the vomiting center of the brain, so they can trigger nausea, vomiting, or gastrointestinal disturbances. Itching of the skin, as well as leg weakness, numbness, tingling and muscle pain in arms and legs are also common side effects.

Ergot derivatives also stimulate contraction of the smooth muscles of the uter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antihyperlipidemics_-_Miscellaneous:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7ixL5N03QOeAQwWgxIzWPL67Tr_EhwiX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antihyperlipidemics - Miscellaneous: Nursing pharmacology]]></video:title><video:description><![CDATA[Antihyperlipidemics are medications used to treat clients with dyslipidemia, which refers to increased blood levels of lipids, such as cholesterol and triglycerides. In addition, they’re indicated to decrease the risk of cardiovascular events. Antihyperlipidemics include different classes of medications, including niacin, also known as vitamin B3 or nicotinic acid; PCSK9 inhibitors, like alirocumab and evolocumab; and omega-3 fatty acids, like icosapent and fish oil.

Let’s start with niacin, which is taken orally. Once administered, it works by inhibiting the enzyme lipoprotein lipase in adipose tissue, which decreases the release of free fatty acids into the bloodstream. As a result, there’s less fatty acids available for the liver to produce triglycerides. For that reason, niacin is primarily used to treat hypertriglyceridemia. LO1-LO3

Now, a common side effect is “niacin flush,” which leads to a red, flushed face, and pruritus. Clients may also experience headaches, dizziness, insomnia, and paresthesia or a sensation of pins and needles, as well as gastrointestinal side effects, including abdominal pain, nausea, vomiting, diarrhea, or flatulence. Other side effects include hyperglycemia, hyperuricemia, and hepatitis with increased blood transaminases. 

Niacin is contraindicated in clients with active hepatic disease or peptic ulcer disease, as well as in those with arterial hemorrhage. Caution should be taken during pregnancy and breastfeeding, as well as in clients with cardiovascular disease, diabetes, or gout. Additional precautions should be taken in clients with hepatic or renal impairment, as well as in those who consume large amounts of alcohol.

Next, we have PCSK9 inhibitors, like alirocumab and evolocumab, which are monoclonal antibodies administered via subcutaneous injection. Once administered, these medications target the PCSK9 protein that’s normally secreted by liver cells and binds to LDL receptors on the cell’s surface, causing them ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacokinetics_-_Distribution:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XusNIZfuQ96tK6QT2_UVepkJQzWLPhrO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacokinetics - Distribution: Nursing pharmacology]]></video:title><video:description><![CDATA[Pharmacokinetics refers to the movement and modification of a medication inside the body. Once a medication is administered, it first has to be absorbed into the circulation, then distributed to various tissues throughout the body, metabolized or broken down, and finally, eliminated or excreted in the urine or feces. This process can be broken down into four components with the acronym ADME; which stands for Absorption, Distribution, Metabolism, and Elimination.

Now, we’re going to focus on the second step of pharmacokinetics, so distribution, which refers to the process of how an absorbed medication moves from the bloodstream to body tissues. Now, each organ and body tissue receives different amounts of medications; and the rate of the distribution - or how quickly this process occurs - as well as the extent of the distribution - or how much of that medication reaches a body tissue - can be affected by several factors. 

One such factor is blood supply to different tissues. Μedications are more rapidly distributed to body tissues that receive large amounts of blood supply, like the brain, liver, kidneys, and spleen; and less rapidly to the tissues with lower blood supply, like the GI tract, skin, adipose tissue, and bones. 

However, some tissues like the brain have an additional filter or barrier, known as the blood-brain barrier, which is a highly selective membrane that strictly regulates which substances are able to cross. The blood-brain barrier consists of tight junctions that seal off the endothelial cells lining the capillaries in the brain. In addition, the blood-brain barrier is surrounded by a basement membrane and astrocytes, which further strengthen it. As a result, the blood-brain barrier is able to prevent the entry of large, water-soluble molecules or pathogens that are floating around in the blood, while letting in water, oxygen, glucose, and smaller, lipid-soluble molecules. 

Similarly, the size and polarity of a medication affects its]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Carbapenems_&amp;_monobactams:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O8yUshdHQ3iN4W6DfTV6-ddcRke386y6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Carbapenems and monobactams: Nursing pharmacology]]></video:title><video:description><![CDATA[Carbapenems and monobactams are beta-lactam antibiotics, which means that they have a characteristic beta-lactam ring in their structure. However, due to their widespread use, some bacteria have acquired resistance to many beta-lactams by developing enzymes called beta-lactamases, which latches on to the beta-lactam ring and degrades the antibiotic. For this reason, carbapenems and monobactams have a slight modification in their beta-lactam ring structure, which makes them less susceptible to beta-lactamases. 

Now, carbapenems can be used to treat serious infections, such as complicated appendicitis, peritonitis, soft-tissue infections, bacterial meningitis, as well as gynecological infections, pyelonephritis, and bacteremia. Carbapenems have a wide range of action against gram-positive bacteria like methicillin-sensitive Staphylococcus aureus, Streptococcus pneumoniae, and group A beta-hemolytic streptococci; and gram-negative bacteria like Enterococcus faecalis, Pseudomonas aeruginosa, Klebsiella spp, Neisseria spp, and Acinetobacter spp. 

On the other hand, monobactams are only useful in the treatment of gram-negative bacterial species, and are primarily used to treat clients with cystic fibrosis who have pulmonary Pseudomonas aeruginosa infections.

Starting with carbapenems, the most commonly used ones include doripenem, ertapenem, meropenem, as well as meropenem-vaborbactam, a combination of meropenem  and vaborbactam, a beta-lactamase inhibitor, which further increases the spectrum of activity, and imipenem-cilastatin, a combination of carbapenem and the dipeptidase inhibitor cilastatin which prevents imipenem from being broken down, prolonging its antibacterial effect. Now, all of the carbapenems are administered intravenously, and ertapenem can also be given intramuscularly. 

Moving on to monobactams, the only medication in this group is aztreonam, which is only given via inhalation. Once administered, carbapenems and monobactams work by bindin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiretrovirals_for_HIVAIDS_-_Protease_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_TwlSWzlTJKSTVxruAG62HCJSfOpNtGe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiretrovirals for HIV/AIDS - Protease inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiretrovirals are medications used to treat infections caused by retroviruses. This is a group of RNA viruses that includes human immunodeficiency virus, or HIV, which can cause acquired immunodeficiency syndrome, or AIDS. Now, antiretrovirals include different classes of medications, among which some of the most commonly used are protease inhibitors.

Okay, so protease inhibitors, or PIs for short, are a class of antiretroviral medications with a characteristic suffix “-navir” in their drug names. Important protease inhibitors include indinavir, nelfinavir, saquinavir, atazanavir, fosamprenavir, tipranavir, darunavir, ritonavir, and a combination of ritonavir/lopinavir. All these medications are taken orally.

Once administered, protease inhibitors work by binding and inhibiting the viral enzyme HIV protease, which plays a major role in maturation of newly replicated viruses. The result is the formation of immature viruses, which are unable to continue infecting host cells.

Now common side effects associated with most protease inhibitors are fatigue, headache, and gastrointestinal side effects, such as diarrhea, nausea, and vomiting. Protease inhibitors can also cause hypersensitivity reactions, such as skin rashes, Stevens-Johnson syndrome, toxic epidermal necrolysis, and sometimes anaphylaxis. 

They can also cause metabolic issues, such as insulin resistance, hyperglycemia, as well as hyperlipidemia, and hepatotoxicity. Some protease inhibitors may also lead to cushingoid fat redistribution, which typically involves peripheral wasting, along with truncal obesity, and the development of a fat pad on the base of the neck. 

Clients taking protease inhibitors may also develop serious side effects, such as hemorrhage, especially in clients with a preexisting bleeding disorder called hemophilia; as well as an excessive inflammatory response called immune reconstitution syndrome, that can also cause flare-ups of a previously known infection like tuberculo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacokinetics_-_Metabolism:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j3ot2P0PS8C-fY5lKs-tdNcLSy2srrdc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacokinetics - Metabolism: Nursing pharmacology]]></video:title><video:description><![CDATA[Pharmacokinetics refers to the movement and modification of a drug or medication inside the body. So once the medication is administered, it first has to be absorbed into the circulation, then distributed to various tissues throughout the body, metabolized or broken down, and finally, eliminated or excreted in the urine or feces. This process can be broken down into four components with the acronym “ADME”, which stands for absorption, distribution, metabolism, and excretion. 

In this video, we’re going to focus on metabolism, which refers to the conversion, or biotransformation, of a medication. In most cases, metabolic reactions act by turning an active medication into a less active metabolite, as well as turning lipid soluble medications into a more water soluble metabolite, which can be eliminated more easily from the body, mainly via the urine or feces. Some other medications, though, are administered in an inactive form, also known as a prodrug, that needs to be metabolized into its active form before it can be effective. 

All right, now most metabolic reactions take place in the liver; although certain medications can be metabolized by other tissues and organs, including the lungs, kidneys, skin, and walls of the small intestine.

After a medication is taken orally, it is absorbed from the walls of the small intestine and transported into the liver via the portal vein. Once in the liver, hepatic enzymes work on the medication to metabolize it; this process is known as first-pass metabolism or first-pass effect, and is responsible for breaking down most medications, as well as converting certain prodrugs into their active metabolites. For example, enalapril, an ACE inhibitor used to treat hypertension, gets converted into its active metabolite, enalaprilat, in the liver. Similarly, codeine, a weak opioid, is converted by hepatic enzymes into morphine, which is more effective for pain management. 

As a result of first-pass metabolism, certain medica]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alkylating_agents:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YvZTkhEzTSOpPlAm-sX1oWJBTRGqG2Z-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alkylating agents: Nursing pharmacology]]></video:title><video:description><![CDATA[Alkylating agents are medications that are mainly used to treat cancer. They are effective against hematologic malignancies, such as leukemia, lymphoma, and multiple myeloma, as well as solid tumors, like breast, ovarian, uterus, lung, and bladder cancer.

The most commonly used alkylating agents are nitrogen mustards like cyclophosphamide, bendamustine, and ifosfamide; nitrosoureas like carmustine, lomustine, and streptozocin; triazenes, such as dacarbazine and temozolomide; and other alkylating agents, including busulfan and procarbazine.

Alkylating agents are cell-cycle phase nonspecific, which means they work by causing damage to the DNA of cancer cells in all phases of the cell-cycle, ultimately leading to cancer cell death. There are two primary ways they do this. First, they can attach an alkyl group to one of the DNA bases of cancer cells. Repair enzymes recognize there’s something wrong, so they jump in to replace the alkylated bases and cause DNA fragmentation, which eventually results in DNA damage and cancer cell death. 

The second mechanism is the crosslinking of DNA, which means the alkylating agent links two DNA bases together, forming cross-bridges. Cross-linking prevents DNA from being separated for essential cell processes, like replication or transcription, eventually resulting in cancer cell death and stopping the multiplication of cancer cells.

In terms of side effects, all alkylating agents can cause gastrointestinal toxicity, which can manifest as anorexia, vomiting, stomatitis or diarrhea; and tumor lysis syndrome, which is when a lot of cancer cells are killed rapidly and that can cause metabolic disturbances. There’s also a risk of damaging other rapidly- dividing, non-cancerous cells, like hair cells, skin cells, and the germ cells in the gonads, which can cause alopecia, rashes and infertility. 

All alkylating agents can also cause bone marrow suppression, leading to decreased platelets and increased risk of bleeding, d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Western_University_-_Oral_Ulcers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YJ7nWEnNRECG0bSgv3y8WWcGQXaHD9nU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Western University - Oral Ulcers]]></video:title><video:description><![CDATA[Oral ulcerations are lesions in the mouth with loss of surface epithelium. There are several causes of oral ulcers, often indicated by their name. For instance, a traumatic ulceration is an ulcer developed after an injury. Other common types of ulcers include the aphthous ulcer; non-specific ulcer; traumatic ulcer with stromal eosinophilia, or TUGSE; and herpetic ulceration. Across all types, there is no difference in prevalence by gender. But, the general prevalence, location, and age vary by etiology.

Typically, an oral ulceration appears as a well-defined, slightly depressed lesion with an erythematous or reddish to yellow center. Sometimes, the yellowish center represents a thick fibrinopurulent membrane that is a mix of acute inflammation and fibrin. This membrane can be removed by applying pressure. The ulcer may also have an irregular white halo with rolled borders. Although these features are common, other clinical features vary by type.

Aphthous ulcers or canker sores are the most common mucosal pathosis, found in 20% of adults with about 80% experiencing these ulcers before age 30. Aphthous ulcers only occur on the unattached oral mucosa, unlike herpetic ulcers or cold sores which occur on the attached oral mucosa. Most aphthous ulcers are related to stress, as often reported by patients. Yet, some individuals will suffer recurrences, termed recurrent aphthous stomatitis. Researchers believe it may be caused by T cell dysfunction leading to mucosal breakdown or the presence of microorganisms.

A traumatic ulceration is caused by an injury that cuts the epithelial surface below the basal cell layer. Sources of trauma include ill-fitting dentures, hard foods like crusty bread and chips, biting injury, irritation from chemicals in toothpastes or rinses, and burns from hot foods or drinks. It is often associated with an underlying inflammatory response. TUGSE is a subtype defined by the presence of many eosinophils. Although its etiology is presume]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_Skills:_Abdominal_Assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WjDLgWrQQW2MA2Cbrdi73zrYQBmLA3fF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical Skills: Abdominal Assessment]]></video:title><video:description><![CDATA[Hello! This video covers how to do an abdominal assessment. In a normal examination you’d do everything on this list, but to keep things concise this video will focus on the steps in blue and will also cover: special populations like infants, children, and the elderly; and include a summary.

Meet Fred. Before we go into inspecting his abdomen, let’s make sure that he’s comfortable. Fred’s already emptied his bladder and we’ve kicked up the heat a notch in the room. Let’s put a pillow under his knees, too. Fred, do you have any abdominal pain we should know about? Let’s leave those areas till last.

Fred’s abdomen is flat, but if it were a little rounded that would be ok too. It’s pretty symmetrical, as well. If we ask Fred to breathe in and hold his breath, there are no bumps or bulges, nor is there any muscle separation.

The umbilicus, navel, or belly button isn’t red or swollen, and the skin is nice and smooth. Overall, Fred looks well: he’s comfortable and breathing normally; but what if he didn’t?

His abdomen could be scaphoid, where it caves in, that usually indicates malnutrition. It could be also protuberant, where it sticks out, which may be caused by excess fat or ascites. There could be bulges, like a hernia. The skin could be a little yellow or green, suggesting jaundice, or there could be areas of discoloration following bruising. Veins might be sticking out due to malnutrition or cirrhosis, or you might see striae - stretch marks - which could be due to rapid growth, pregnancy, cirrhosis, or Cushing syndrome.

Now let’s auscultate Fred’s abdomen. Percussion and palpation stimulate peristalsis, so we always auscultate the abdomen first. With the diaphragm endpiece, gently hold the stethoscope against Fred’s skin.

Let’s start in the right lower quadrant. Bowel sounds are most common here, and sound like high-pitched gurgling, every few seconds. You don’t have to hear sounds in each quadrant. As long as there are some sounds somewhere with pa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_skills:_Medication_administration_-_Giving_transcutaneous_medication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JbQ037hVSHOql95LrSOwbyChQKmGBaBw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical skills: Medication administration - Giving transcutaneous medication]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical skills: Medication administration - Giving transcutaneous medication through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clinical_skills:_Patient_controlled_analgesia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ah8Uf9XdQryKFy7Eym57J3X9TqWkL30P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clinical skills: Patient controlled analgesia]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Clinical skills: Patient controlled analgesia through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dr._Sharon_Goldfarb:_Raise_the_Line_faculty_award_winner</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AB9g6K-5QfKE5FCois4UI2cgT5a01Kp_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dr. Sharon Goldfarb: Raise the Line faculty award winner]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dr. Sharon Goldfarb: Raise the Line faculty award winner through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dispelling_Next_Generation_NCLEX_misinformation_with_Dr._Sharon_Goldfarb</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IsBN2vdyR8aPyyNAC2_1beH0QeGowkc_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dispelling Next Generation NCLEX misinformation with Dr. Sharon Goldfarb]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Dispelling Next Generation NCLEX misinformation with Dr. Sharon Goldfarb through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_Thrive_Using_the_New_Osmosis_Nursing_Navigation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cpDriwglR5KSNz3ngr_SUOAAQ4ypKV9h/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to Thrive Using the New Osmosis Nursing Navigation]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to Thrive Using the New Osmosis Nursing Navigation through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_be_a_Good_Nurse!</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qtg2e1JhSE_M38gev7pC45oDST6Zw1sE/_.jpg</video:thumbnail_loc><video:title><![CDATA[How to be a Good Nurse!]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to be a Good Nurse! through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alpha-1_blockers:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DSW8S5keRJSRtlbmPGdbVa8eSDChkxkG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alpha-1 adrenergic blockers: Nursing pharmacology]]></video:title><video:description><![CDATA[Alpha-1 adrenergic blockers are medications that oppose the effects of the sympathetic nervous system, ultimately decreasing smooth muscle contraction. Hence, these medications can be used to treat hypertension and benign prostate hyperplasia, and include prazosin, terazosin, and doxazosin, which are administered orally.

Normally, the sympathetic nervous system triggers the fight or flight response by secreting catecholamines, which activate alpha-1 adrenergic receptors on the different organs. This results in smooth muscle contraction, in turn leading to an increase in the heart rate and blood pressure, as well as decreasing gastrointestinal motility and urination by contracting the sphincters. 

So, once administered, alpha-1 adrenergic blockers bind and inhibit these alpha-1 adrenergic receptors. As a result, alpha-1 blockers cause vasodilation, which in turn decreases blood pressure. In the urinary tract, they help relax the sphincters, which helps relieve the symptoms of benign prostate hyperplasia by decreasing the urine outflow obstruction.

Now, since alpha-1 receptor inhibition causes vasodilation, common side effects include orthostatic hypotension and reflex tachycardia, especially after the first dose; as well as palpitations and edema. Other side effects include anxiety, CNS depression, and blurred vision. 

Often, clients may also experience dizziness, headaches, and drowsiness, as well as nausea, diarrhea or constipation, urinary frequency, incontinence, and impotence. Rarely, these medications may lead to priapism. Finally, clients taking doxazosin may develop arrhythmias or hepatitis.

There are no major contraindications for alpha-1 blockers, but they must be used cautiously in pregnancy, breastfeeding, children, and elderly clients. In addition, prazosin and terazosin should be used with caution in clients with prostate cancer, and doxazosin in those with hepatic disease. Finally, these medications may have dangerous interactions with v]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antihyperlipidemics_-_Bile_acid_sequestrants_&amp;_cholesterol_absorption_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VbH1ZAv1QsiJC-nWTj2pO4sCQF_sryvb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antihyperlipidemics - Bile acid sequestrants and cholesterol absorption inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Antihyperlipidemics are medications used to treat increased levels of lipids in the blood, like cholesterol, particularly low density lipoprotein, or LDL cholesterol; as well as triglycerides. Therefore, they’re also indicated in coronary artery disease therapy. Antihyperlipidemics include different classes of medications, among which are bile acid sequestrants, like cholestyramine, colesevelam and colestipol, as well as cholesterol absorption inhibitors like ezetimibe. All of them are administered orally.

Once administered, bile acid sequestrants, which are positively charged molecules, bind to the negatively charged bile acid in the intestine, preventing it from being reabsorbed. In turn, the liver compensates by increasing the production of bile salts, which uses up a lot of cholesterol. To get more cholesterol from the rest of the body, the liver increases uptake of LDLs, lowering its levels in the blood. The downside is that this also increases endogenous cholesterol and triglyceride synthesis.

And then cholesterol absorption inhibitors work by blocking a transport protein that mediates cholesterol absorption in the small intestine. This medication is mainly used to treat high levels of LDL and is typically used in combination with other lipid lowering agents like statins.

Common side effects of bile acid sequestrants include gastrointestinal disturbances, mostly constipation, abdominal pain, bloating, and nausea; and they can decrease absorption of fat soluble vitamins such as A,D,E and K; and with decreased vitamin K absorption, increased bleeding risk can ensue. Similarly, all bile acid sequestrants can decrease the absorption and effect of fat-soluble medications like digoxin, oral contraceptives and warfarin. Side effects of ezetimibe include headache, arthralgias, and myalgias; and rarely, rhabdomyolysis.

As far as contraindications go, bile acid sequestrants shouldn’t be used in clients with complete biliary obstruction or hypertriglyceride]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiretrovirals_for_HIVAIDS_-_Integrase_strand_transfer_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x9AlGzacTr66iOXcaAbz_UYmRtqgs-4x/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiretrovirals for HIV/AIDS - Integrase strand transfer inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiretrovirals are medications used to treat infections caused by retroviruses. This is a group of RNA viruses that includes human immunodeficiency virus, or HIV, which can cause acquired immunodeficiency syndrome, or AIDS. Now, antiretrovirals include different classes of medications, among which some of the most commonly used are integrase strand transfer inhibitors. 

Okay, so integrase strand transfer inhibitors, or INSTIs for short, end in the suffix “-gravir”. This class of antiretrovirals includes raltegravir, dolutegravir, elvitegravir, and bictegravir, which comes in combination with antiretrovirals from the class of nucleoside and nucleotide reverse transcriptase inhibitors or NRTIs, namely emtricitabine and tenofovir.

Integrase strand transfer inhibitors are taken orally. Once administered, they work by blocking the action of the viral enzyme integrase, which allows the virus to insert and integrate its genome into the host’s cell DNA. As a result, blocking this process prevents the virus from multiplying, which halts the infection.

Now, common side effects of integrase inhibitors include headache, insomnia, and gastrointestinal side effects, such as nausea, vomiting, and diarrhea, as well as elevated liver enzymes. In addition, clients taking these medications can develop hypersensitivity reactions, as well as excessive inflammatory response called immune reconstitution syndrome, that can also cause flare-ups of a previously known infection like tuberculosis. Now, some integrase strand transfer inhibitors can have specific side effects. Raltegravir and dolutegravir can cause hyperglycemia, while raltegravir can also cause rhabdomyolysis, and dolutegravir may cause acute liver failure. Finally, clients on elvitegravir can also develop acute liver failure, and may experience depression and suicidal ideation.

Regarding contraindications for integrase inhibitors, precautions should be taken during pregnancy and breastfeeding, as well as in chil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiretrovirals_for_HIVAIDS_-_NRTIs_&amp;_NNRTIs:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lSHXNKQmQcqGBU5-JtOCWJ5BSmm2SJz5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiretrovirals for HIV/AIDS - NRTIs and NNRTIs: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiretrovirals are medications used to treat infections caused by retroviruses. This is a group of RNA viruses that includes human immunodeficiency virus, or HIV, which can cause acquired immunodeficiency syndrome, or AIDS. Now, antiretrovirals include different classes of medications, among which some of the most commonly used are nucleoside reverse transcriptase inhibitors, or NRTIs, and non-nucleoside reverse transcriptase inhibitors, or NNRTIs. NRTIs include zidovudine, didanosine, stavudine, lamivudine, abacavir, and emtricitabine. On the other hand, NNRTIs include efavirenz, delavirdine, nevirapine, rilpivirine, and etravirine. 

Both NRTIs and NNRTIs are taken orally, while the NRTI zidovudine can also be administered intravenously. Once administered, these medications inhibit the viral enzyme reverse transcriptase. More specifically, NRTIs compete with naturally occurring nucleosides and bind to the viral RNA chain. On the other hand, NNRTIs directly bind to and inhibit the reverse transcriptase. Ultimately, both NRTIs and NNRTIs prevent this enzyme from reverse-transcribing the viral RNA into proviral DNA, thus interfering with viral replication.

Unfortunately, clients taking NRTIs or NNRTIs may experience a wide range of side effects, and many of them can be serious. These medications often cause fever, headache, dizziness, insomnia, and anxiety or depression, as well as asthenia and peripheral neuropathy. Gastrointestinal side effects like nausea, vomiting, diarrhea, anorexia, constipation and abdominal pain are also common, as well as myalgia, arthralgia, and dyspnea or cough. Although more rarely, they can lead to hepatotoxicity and hypersensitivity reactions, such as Stevens-Johnson syndrome and toxic epidermal necrolysis. All NRTIs can also cause lactic acidosis, hepatomegaly, and steatosis, which is a boxed warning for zidovudine, didanosine, stavudine, and emtricitabine. In addition, zidovudine, didanosine, and stavudine can cause bone m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacodynamics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gs5ii33USjOGY6ISX4YHcQM0Ri_JxPW6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacodynamics: Nursing pharmacology]]></video:title><video:description><![CDATA[Pharmacodynamics refers to the mechanisms and effects of a medication within the body. Or more simply, it’s what medications do to the body and how they do it. 

Now, medications bind to receptors, which are specialized proteins found inside the cell or on its surface, to cause a change in the cell’s activity that ultimately creates a physiological effect. When a medication binds a receptor and mimics the body’s own chemical messengers, like hormones and neurotransmitters, to produce a desired response, it&amp;#39;s called an agonist. So, an agonist is like a key that fits into a lock, causing it to open. There are also medications that are partial agonists. Like agonists, they fit into the lock, but not as well, so they produce a weaker response. Lastly, there are antagonists, which bind to a receptor and block it so it can’t be bound to and activated by other medications or the body’s own chemical messengers. So, it’s like a key that can’t turn the lock, and may even get stuck in the lock. 

An example of an agonist is morphine, which primarily binds to mu receptors, and less so kappa receptors, to mimic the body’s endogenous opioid peptides, to produce an analgesic effect. In contrast, pentazocine is a partial agonist, so it produces a less powerful analgesic effect. On the other end of the spectrum, naloxone is an opioid antagonist that blocks the effects of opioid peptides.

Now, after a medication binds to a receptor, there are additional factors that determine how the body will respond, including the dose of the medication, its efficacy, and its potency. So, let’s draw a graph, to show the relationship between the dose, on the x axis, and the response on the y axis. What we get is an S-shaped curve, called the dose-response curve, which has three phases. At first, in phase 1, the curve is more or less flat; that’s because the dose of the medication is too low, so not enough receptors bind to the medication to cause a significant response. As the do]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunomodulators:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mtULdUo3T1uQOOgdouE7rlLyTtK6XNRD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunomodulators: Nursing pharmacology]]></video:title><video:description><![CDATA[Immunomodulators are medications that modify the body’s immune response. According to their main effect, immunomodulators can be subdivided into immunostimulants, which are used to enhance the immune response against a specific pathogen or cancer cell; and immunosuppressants, which include monoclonal antibodies used in the targeted treatment against certain types of cancer; and tyrosine kinase inhibitors used for diseases such as leukemias and gastrointestinal tumors.

Now, let’s begin with immunostimulants, which include interferons and interleukins, among other agents. Interferon medications mimic the effects of natural interferons, which are tiny proteins released by virally infected cells.  As their name implies, they “interfere” with viral replication, thereby helping cells fight off viral infections. Additionally, they inhibit tumor growth and enhance the immune response. 

Interferon medications can be administered subcutaneously or intramuscularly, and they include interferon alpha-2b, which can be used for the treatment of disorders like hairy cell leukemia or AIDS-related Kaposi sarcoma, as well as interferon beta-1a and interferon beta-1b, which can be used for the treatment of relapsing multiple sclerosis. 

Moving on, interleukins are tiny signaling proteins that are similar to interferons; they communicate between cells to stimulate cellular immunity, inhibit tumor growth, and increase the production of platelets. One medication called aldesleukin is a human recombinant interleukin 2 agent, which means it acts like interleukin 2 would, promoting the proliferation and activity of various types of lymphocytes.  Aldesleukin is administered intravenously, and can be used for treatment of metastatic melanoma or metastatic renal cancer. 

However, overstimulation of the immune system can also cause side effects. Interferons, for example, can all cause neurotoxicity, which leads to side effects from headache and fatigue to anxiety, depression and, r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hormones_&amp;_hormone_modulators_for_cancer_treatment:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yZmPeuZnQK_NgpmyxD-nvTc0Rqi_BzTI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hormones and hormone modulators for cancer: Nursing pharmacology]]></video:title><video:description><![CDATA[Hormones and hormone modulators are a group of medications that suppress the function of specific hormones, which slows or stops the growth of hormone-dependent cancers, such as breast, endometrial, and prostate cancers. They can also be used to ease the symptoms caused by certain types of cancer, such as brain or renal cancers.

Now, hormones and hormone modulators can be broadly classified as sex hormones; antiestrogens; aromatase inhibitors; antiandrogens; and gonadotropin-releasing hormone analogs.

Now, some commonly used sex hormones include hydroxyprogesterone, which is administered intramuscularly or subcutaneously for advanced uterine adenocarcinoma; as well as medroxyprogesterone, and megestrol, which are taken orally for endometrial or breast cancer. Once administered, these medications work by suppressing the pituitary gland from releasing gonadotropins, so follicle-stimulating hormone or FSH for short, and luteinizing hormone or LH. As a result, gonadotropins aren’t available to stimulate  sex hormone production by the gonads, which ultimately delays the growth of sex hormone-dependent tumors.

There are also antiestrogens, which include selective estrogen receptor modulators, or SERMs for short, such as tamoxifen, raloxifene, and fulvestrant. These medications are administered orally, and work by blocking estrogen receptors on cancer cells, which delays the growth of estrogen-dependent tumors. 

Similarly, there’s aromatase inhibitors, which include anastrozole, letrozole, and exemestane. These medications are administered orally, and act by blocking the production of estrogen, which ultimately also helps limit the growth of estrogen-dependent tumors. 

Next are antiandrogens, which include flutamide, apalutamide, and bicalutamide. These medications are also administered orally, and they block androgen receptors on cancer cells, ultimately stopping the growth of androgen-dependent tumors like prostate cancer. 

Finally, gonadotropin-releasing]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiretrovirals_for_HIVAIDS_-_CCR5_antagonists,_fusion_inhibitors,_&amp;_attachment_inhibitors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c6lHcAIiQ0Ol1N-GijuowW50RUWQX_lU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiretrovirals for HIV/AIDS - CCR5 antagonists, fusion inhibitors, and attachment inhibitors: Nursing pharmacology]]></video:title><video:description><![CDATA[Antiretrovirals are medications used to treat infections caused by retroviruses. This is a group of RNA viruses that includes human immunodeficiency virus, or HIV, which can cause acquired immunodeficiency syndrome, or AIDS. Now, antiretrovirals include different classes of medications, such as CCR5 antagonists, fusion inhibitors, and attachment inhibitors.

The only medication of the CCR5 antagonist class is maraviroc. It is administered orally in combination with other antiretroviral medications for adult clients infected with an HIV strain that’s resistant to other antiretrovirals. Once administered, maraviroc works by blocking the CCR5 coreceptor on the CD4+ T cells, which is used by the CCR5-tropic HIV to enter these cells. Unfortunately, if the virus uses a CXCR4 coreceptor instead of CCR5, this medication will have no therapeutic effect.

Common side effects of maraviroc include dizziness, fever, cough, abdominal pain, and a skin rash or hypersensitivity reactions, such as Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug rash with eosinophilia with systemic symptoms or DRESS. In addition, maraviroc can cause serious side effects like upper and lower respiratory tract infections or pneumonia, bronchospasm, and cardiac ischemia. 

Clients might also experience visual disturbances, as well as orthostatic hypotension, and gastrointestinal disturbances like dyspepsia, diarrhea, or constipation. Some clients on maraviroc may experience musculoskeletal side effects like joint pain or muscle cramps, and an excessive inflammatory response called immune reconstitution syndrome, that can also cause flare-ups of a previously known infection like tuberculosis. Finally, maraviroc has a boxed warning for hepatotoxicity!

Regarding contraindications, maraviroc is contraindicated in clients with impaired renal function. Precaution should be taken during pregnancy and breastfeeding, as well as with children or elderly clients. Additionally, maraviroc sh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Other_antineoplastics:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OcSgfrXGSEWZr-M_BITFwjxwQwyOTMPP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Other antineoplastics: Nursing pharmacology]]></video:title><video:description><![CDATA[Antineoplastic agents are medications used to treat cancer. Except for the usual antineoplastics, there are other medications that can be also used to treat various forms of cancer, particularly acute lymphoblastic leukemia or ALL, ovarian cancer, and cutaneous T-cell lymphoma. 

Other antineoplastics that are commonly used include asparaginase, and pegaspargase, which are given intramuscularly or intravenously to treat acute lymphoblastic leukemia, as well as altretamine, which is taken orally to treat ovarian cancer. Then there’s azacitidine, a medication that can be administered orally, intravenously or subcutaneously to treat myelodysplastic syndrome or acute myeloid leukemia; hydroxyurea, which is administered orally in clients with chronic myeloid leukemia or head and neck cancer; and irinotecan, which is administered intravenously to clients with metastatic colorectal cancer.   

Once administered, what asparaginase and Pegaspargase do is break down asparagine, which is a non-essential amino acid, into aspartic acid and ammonia. Cancer cells can’t synthesize asparagine themselves, so this impairs their protein synthesis, ultimately stopping cellular processes and causing apoptosis. 

On the other hand, the way altretamine works is not perfectly clear, but it could damage cancer cells by crosslinking of DNA, which means the agent links two DNA bases together, forming cross-bridges. Cross-linking prevents DNA from being separated for essential cell processes, like replication or transcription, eventually resulting in cancer cell death and stopping the multiplication of cancer cells. 

Next, azacitidine causes damage to double stranded DNA during cell replication, while hydroxyurea and irinotecan inhibit enzymes involved in DNA synthesis, ultimately stopping cancer cell division. Irinotecan in particular belongs to a group of medications called topoisomerase I inhibitors, so it inhibits this enzyme to eventually cause double stranded DNA breaks and hal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psoriasis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K44fnNBBQoygAvlo1ShIAKycSqiB_nZ7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psoriasis: Nursing]]></video:title><video:description><![CDATA[Psoriasis is a chronic autoimmune disease that primarily causes skin inflammation, and is typically characterized by well circumscribed erythematous patches topped with white silvery scales.

Now, let’s go over some physiology. Normally, the skin is divided into three layers, the epidermis, dermis, and hypodermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Just above the hypodermis is the dermis, which contains hair follicles, nerve endings, glands, blood vessels, and lymphatics. And just above the dermis is the epidermis, which itself has multiple cell layers that are composed of developing cells called keratinocytes. 

Keratinocytes start their life at the lowest layer of the epidermis, called the stratum basale, or basal layer, which continually divide and produce new keratinocytes. As keratinocytes in the stratum basale begin to mature, they migrate into the next layers, called the:stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer. 

As new keratinocytes push up into the stratum corneum, older dead cells are sloughed off forming skin flakes or dandruff. In this way, the thickness of the epithelium remains constant, with a regulated turn-over of keratinocytes.

Now, there isn’t a single cause of psoriasis, but rather it’s a multifactorial disease, with a combination of genetic predisposition and environmental risk factors and triggers; these include stress, traumatic insults, infection, and obesity, smoking, alcohol use, and taking certain medications like antimalarials or lithium.

Regardless of what triggers the disease, there’s an abnormal inflammatory process that causes dilation of the blood vessels at the border between the dermis and epidermis. This attracts immune cells, which infiltrate into the epidermis, causing chronic damage to the skin. 

As a result, keratinocytes begin to proliferate excessiv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cervical_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i_efNTziSBmKqGe3VGu7-CtuTYmRYWau/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cervical cancer: Nursing]]></video:title><video:description><![CDATA[Cervical cancer is a malignant tumor that originates in the cervix, and is one of the most common types of cancer.

All right, now let’s go over some anatomy and physiology. The cervix is the lower part of the uterus, and can be divided into two sections; the inner part is called the endocervix, which is a narrow canal that leads into the uterus; while the outer part is called the ectocervix, and it sticks out into the vagina. 

Zooming in, the endocervix is lined by mucus-secreting simple columnar epithelial cells. Conversely, the ectocervix is continuous with the vagina and is lined by stratified squamous epithelial cells. The area where the two epithelia meet is called the transformation zone, and it is where there is a change from columnar cells to squamous cells, called the squamocolumnar junction. The exact location of the squamocolumnar junction will change or shift depending on the age of the individual, as well as changes in the size of the uterus during menstruation. 

Now, cervical cancer can arise due to a variety of causes and risk factors. Most cervical cancers are caused by human papillomavirus, or HPV for short. Specifically, high-risk HPV strains such as 16 and 18 are responsible for more than half of all cervical cancers. Since HPV is a sexually transmitted infection, the risk of developing cervical cancer is higher in clients who engage in unprotected sex or who have multiple sexual partners. Additional risk factors include early age at first sexual intercourse, smoking, having a compromised immune system, obesity, long-term use of oral contraceptive pills, as well as having a family history of cervical cancer.

Now, it’s important to note that not all HPV infections result in cervical cancer. In fact, the immune system is able to fight off most HPV infections so they don’t cause any serious harm. When that doesn’t happen, though, the virus inserts itself into the immature squamous cells of the transformation zone, leading to changes in ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_kidney_disease_(CKD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PLANhaP8SCWFCPtOjTNg5SK-RymV5yEp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic kidney disease (CKD): Nursing]]></video:title><video:description><![CDATA[Chronic kidney disease, or CKD for short, is a condition characterized by a slow and progressive decrease in kidney function, with a glomerular filtration rate, or GFR, of less than 60 mL/minute that develops over a minimum of three months.

Now, let’s take a closer look at how the kidneys work. We can think of the kidneys as the body’s natural blood filter. Their main function is to clear blood of metabolic wasteful substances and toxins by excreting them through urine. In addition, they secrete important hormones, and are essential in regulating the acid-base balance, pH, blood pressure, and electrolyte levels in the body. 

Within each kidney, there are millions of tiny functional units called nephrons, which consist of a renal corpuscle and a set of renal tubules. The renal corpuscle is where blood filtration occurs, and it includes the glomerulus, a tiny bundle of capillaries, and the Bowman’s capsule, a cup-shaped structure that surrounds the glomerulus. 

As blood flows through the glomerulus, water and small solutes dissolved in the blood are filtered into the Bowman’s capsule, creating an ultrafiltrate of blood. This filtrate then travels through the renal tubules, where urine is ultimately produced and modified according to the body’s necessities. The rate at which renal filtration takes place is called glomerular filtration rate, or GFR for short, and it is one of the main measures of kidney function. In a healthy adult, the estimated GFR is around 100-120 mL/min, and this value decreases slowly in all of us as we grow older.

All right, now, several conditions can speed up the rate at which GFR deteriorates, increasing the risk of developing CKD. In the United States, the leading causes of CKD are diabetes mellitus and hypertension, both of which are more common in elderly clients. Less common causes include renal artery stenosis, glomerular diseases, polycystic renal disease, tubulointerstitial diseases, and systemic disorders, like lupus or a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Migraines:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NrUOQJO9ROys6eLwYolV6zaSSlyrQemh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Migraines: Nursing]]></video:title><video:description><![CDATA[Migraines are a specific type of recurrent headache that’s characterized by moderate to severe pulsating or throbbing pain, which is typically localized to one side of the head, and can be very disabling.

Okay, first, a bit of physiology. The cells that make up our brain are called neurons, and have three main parts, the dendrites, cell body, and axon. The dendrites are little branches that receive signals from other neurons, and carry them to the cell body, which has all of the neuron’s main organelles. The cell body then transmits the signal through the axon, which ultimately releases neurotransmitters in order to send the signal along to the dendrite of another neuron. Depending on the signal, the result is either the excitation or inhibition of that neuron.

Now, normally, throughout the body, there are special neurons that act as pain receptors, called nociceptive nerve fibers. When these neurons detect a painful stimulus, they send a signal that conveys the feeling of pain to the brain. The brain itself does not have pain receptors, but it can detect signals from pain receptors of nearby tissues in the head and neck, such as the blood vessels, muscles, and the meninges covering the brain. 

Although the underlying cause of migraines isn’t well understood, it seems to be related with neuronal hyperexcitability, where neurons respond excessively to a signal. The main risk factors include family history, an age between 25 and 55 years, and being assigned female at birth. Other risk factors include obesity, depression, and emotional or physical stress. In addition, migraine attacks are often associated with specific triggers, such as bright or flickering lights; loud noises; physical exertion; lack of sleep; weather changes; cigarette smoke; foods like chocolate or cheese, alcohol, especially red wine, as well as some food additives and the artificial sweetener aspartame; and medications like oral contraceptives. In young individuals, migraine attacks c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7xCpSeDqRjCngu660INZb0qJTg2izLh-/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19: Nursing]]></video:title><video:description><![CDATA[COVID-19 is a highly contagious disease that predominantly affects the respiratory tract. This disease is caused by the SARS-CoV-2 virus, which is a type of coronavirus. It’s a single-stranded RNA virus with a crown of protein spikes that stick out on the outer surface. The name can be broken down as follows: SARS is for severe acute respiratory syndrome; CO is for corona, VI is for virus, D is for disease, and 19 is for 2019, the year it was first identified. 

Now, let’s quickly review the respiratory tract, which can be divided into two regions: the upper respiratory tract and lower respiratory tract. The upper respiratory tract includes the nose, nasal cavity, the oral cavity, pharynx, epiglottis, larynx, and the upper part of the trachea; while the lower respiratory tract includes the lower part of trachea, and the lungs containing the bronchi, bronchioles, alveolar ducts, and finally the alveoli.  

Alveoli are tiny air-filled sacs where most gas exchange occurs, so as we breathe, the inhaled oxygen moves from the alveolar sacs into the blood, while the carbon dioxide moves from the blood into the alveolar sacs to be exhaled. 

Okay, so COVID-19 is caused by the SARS-CoV-2 virus entering the respiratory tract. The virus is most often spread from person to person through tiny, aerosolized particles and larger droplets, which are expelled when an infected individual talks,  sneezes,  or coughs. The droplets can ultimately reach the respiratory tract of another person when they’re inhaled, or land on their eyes, nose, or mouth. Since the droplets don’t travel far, they tend to settle on surfaces, so, less frequently, the virus can be transmitted indirectly when an individual touches a contaminated surface and then, prior to washing their hands, they touch their eyes, nose, or mouth.  

On the other hand, aerosolized particles can remain suspended in the air for longer periods and travel further distances, so they can cause infection when they’re in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Influenza:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zeUbMhx1QAK3Z-d6gwdIQZwVR_aAR7vn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Influenza: Nursing]]></video:title><video:description><![CDATA[Influenza, commonly known as the flu, is a highly contagious respiratory disease caused by the influenza virus. There are three types of the influenza virus that can infect humans: influenza types A, B, and C. Influenza types A and B are responsible for the annual regional flu epidemics, or the flu season, which is when cases of influenza rise, and spans from about September to April, with peaks around December to February. On the other hand, influenza C may lead to mild illness, but not epidemics or pandemics. 

Now, let’s quickly review the respiratory tract, which can be divided into two regions: the upper respiratory tract and lower respiratory tract. The upper respiratory tract includes the nose, nasal cavity, the oral cavity, pharynx, epiglottis, larynx, and the upper part of the trachea; while the lower respiratory tract includes the lower part of trachea, and the lungs containing the bronchi, then the bronchioles, onto the alveolar ducts, and finally into the alveoli. 

These tiny air-filled sacs are the body’s primary sites of oxygen and carbon dioxide gas exchange. The gases move across the alveolar-capillary membrane, with oxygen moving from the alveolar sacs into the blood, and carbon dioxide moving from the blood into the alveolar sacs to be exhaled. This allows for a consistent oxygen supply to carry out bodily functions and to maintain the proper blood pH level.

Now, the influenza virus invades the respiratory tract and uses it to spread the infection. The flu is typically transmitted from person to person via respiratory droplets or, in some instances, aerosolized particles that are expelled from the respiratory tract of an infected individual. These droplets can be propelled a few feet into the air when talking, coughing, or sneezing, and can then land in the eyes, nose, or mouths of people nearby, or get inhaled into the lungs. Less frequently, the virus is transmitted indirectly when an individual touches a contaminated surface and then]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoporosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xc-A2QKGRSqDTFwRcqDUOPUxTAGde7Be/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteoporosis: Nursing]]></video:title><video:description><![CDATA[Osteoporosis is a chronic condition in which the bones gradually lose density or mass, becoming porous. This eventually leads to a decrease in bone strength, making the bones fragile and more prone to fracture with minimal trauma, or even spontaneously. 

Now, most bones in the body have a  dense external layer called compact bone; and a softer internal layer called spongy or trabecular bone, which normally consists of trabeculae and pores resembling a honeycomb. At first glance, a bone may appear inert and unchanging, but it’s actually a very dynamic tissue. In general, a bone is replaced with new cells every three to ten years in a process called bone remodeling, which has two steps: bone resorption, when specialized cells called osteoclasts break down bone, and bone formation, which is when another type of cells called osteoblasts form new bone. 

Now, one of the main components of bones is calcium. For that reason, bone remodeling is highly dependent on blood calcium levels, which, in turn, are kept in the normal range by a balance between parathyroid hormone, or PTH, calcitonin, and vitamin D, as well as sex hormones. PTH is produced by the parathyroid glands in response to low blood calcium, and it increases bone resorption to release calcium from bones into the bloodstream. Vitamin D promotes calcium absorption in the gut, so it also increases blood calcium, promoting bone formation and decreasing bone resorption. On the other hand, calcitonin is produced by the thyroid gland in response to high blood calcium, so it opposes the action of PTH, therefore promoting bone formation and calcium deposition, while decreasing bone resorption. Finally, sex hormones like estrogen and androgens play a role by inhibiting bone resorption.

Now, there’s no specific cause of osteoporosis, but several risk factors that can accelerate bone mass loss. Modifiable risk factors include hormonal imbalances like hypogonadism or hyperthyroidism, malnutrition or dietary]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharyngitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Tla7VW2mQomDEW0MegKWfy7ZSAafDnzX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharyngitis: Nursing]]></video:title><video:description><![CDATA[Pharyngitis, more commonly known as sore throat, is an inflammatory disease of the pharynx, or the back of the throat, and it’s most often caused by an invading pathogen like a virus or bacteria, and rarely by fungi.

Now, let’s quickly review a bit of anatomy and physiology of the respiratory tract. When we breathe in, air enters the respiratory tract through the nose or mouth, respectively into the nasal and oral cavities, and then into the pharynx. At each side of the back of the throat, there is a pair of structures called adenoids and tonsils, which are small clumps of lymphoid tissue that act as the body&amp;#39;s first line of defense that swallow harmful foreign particles and pathogens that enter through the nose or mouth. The lower part of the pharynx is continuous with the larynx or the voice box. Now, the pharynx also connects the oral cavity to the esophagus. So, at the top of the larynx sits a spoon-shaped flap of cartilage called the epiglottis, which acts like a lid that seals the airway off while eating or drinking, so that anything we consume can only go one way, down the esophagus and towards the stomach. In contrast, during breathing, the epiglottis stays open, so that air can make its way into the larynx, and then continue its journey through the trachea, or windpipe, towards the lungs.

Zooming in, the epithelium lining respiratory tract consists of goblet cells that release mucus, which is sticky and contains enzymes to help trap and destroy harmful foreign particles and pathogens; as well as columnar epithelial cells that have hair-like projections called cilia, which work to sweep the harmful particles up and out of the airways. In addition, the epithelial layer that lines the pharynx is actually thicker than elsewhere in the respiratory tract, as it has to protect the tissues from any harmful particles from the air we breathe in, as well as from anything we consume. 

Okay, so pharyngitis is caused by any harmful particle that man]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Impetigo:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c50orpxXSC2IWQrPHybUZdWMSNm7ZFRE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Impetigo: Nursing]]></video:title><video:description><![CDATA[Impetigo is a superficial and highly contagious bacterial skin infection, most often affecting young children between the ages of 2 and 5 years, and is more common during warm, humid months of the year.

Alright, let’s go over some physiology. Normally, the skin surface is colonized by a huge number of microorganisms that make up the normal skin flora. This flora consists mostly of bacteria, such as Staphylococcus epidermidis, as well as certain fungi, such as Candida albicans. The normal skin flora is typically non-pathogenic, meaning that these microorganisms don’t cause any disease. In fact, they are often beneficial, since they serve as a physical and competitive barrier that helps prevent pathogenic microorganisms from invading and infecting the skin. 

Now, impetigo is a bacterial skin infection that’s typically caused by Gram positive pathogenic bacteria like Staphylococcus aureus or Streptococcus pyogenes. In addition, there’s an increasing number of impetigo cases caused by antibiotic-resistant strains, such as methicillin-resistant Staphylococcus aureus or MRSA for short, as well as gentamicin-resistant Staphylococcus aureus. 

Typically, the infection is transmitted from person to person through direct contact with skin lesions. Less frequently, the infection can be transmitted indirectly when a client touches a contaminated surface, such as clothing or bed linens. Common places where impetigo spreads include daycare centers, nursing homes, or schools. 

Now, risk factors that can disrupt the normal skin flora include living in a warm, humid climate, as well as having poor hygiene, and underlying conditions like diabetes or a weakened immune system. Additional risk factors that can allow these bacteria to invade the skin include having previous damage due to insect bites, minor trauma, abrasions, or skin conditions like eczema or psoriasis. 

Now, the infection can be classified as primary impetigo when it occurs on intact skin, or secondary imp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypoparathyroidism:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cAYLqyXxQOmQ60HxaObm9q-1TpiQH3C1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypoparathyroidism: Nursing]]></video:title><video:description><![CDATA[Hypoparathyroidism is a condition characterized by low blood parathyroid hormone, or PTH for short, which ultimately results in hypocalcemia, or low blood calcium levels, as well as hyperphosphatemia, or high blood phosphate levels. 

Now, PTH is produced by four small glands called the parathyroid glands. These glands lie in the neck, being stuck to the back surface of the thyroid gland. The main function of PTH is keeping the levels of calcium within the normal range. For example, when calcium levels are low, PTH boosts bone resorption, which causes the release of calcium and phosphate from the bone into the bloodstream. In addition, PTH activates vitamin D, which in turn increases calcium and phosphate absorption from the gut. PTH also stimulates calcium reabsorption and phosphate excretion from the kidney. On the other hand, high calcium levels cause the secretion of PTH to fall, which increases the deposition of calcium in bones and the excretion of calcium by the kidneys.

Alright, now hypoparathyroidism can be caused by anything that damages the parathyroid glands. The most common cause is iatrogenic where surgery or radiation therapy for another condition also injures the parathyroid glands. Thyroidectomy is a good example since when a part of the thyroid is removed, the parathyroids will often be removed or damaged also. Hypoparathyroidism may also be caused by autoimmune destruction mediated by autoantibodies. Next, there are the functional causes like hypomagnesemia where the parathyroid glands will function poorly when magnesium level is low. However the glands are not damaged, so when hypomagnesemia is corrected, the hypoparathyroidism will resolve. Finally, hypoparathyroidism can be idiopathic, meaning that the cause is unknown. 

Now, risk factors of developing hypoparathyroidism include neck surgery or radiation therapy; and serious injury to the neck, like during a car crash or by strangulation; as well as a family history of parathyroid d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hematopoietic_growth_factors:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EjB5WvXHRJ6BqJLbofp5yJJNSMOupRXo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hematopoietic growth factors: Nursing pharmacology]]></video:title><video:description><![CDATA[Hematopoietic agents are medications used to increase the production of different types of blood cells including white blood cells, red blood cells, and platelets. They are mainly used in disorders that decrease the levels of specific blood cells,  but they are also used after treatments like chemotherapy, or radiation therapy, that suppresses the bone marrow.    

Now, hematopoietic growth factors act like analogs or synthetic versions of the various physiological growth factors produced by the body. These include granulocyte colony-stimulating factor or G-CSF, granulocyte-macrophage colony-stimulating factor or GM-CSF,  thrombopoietin agents, and erythropoietin stimulating agents or ESAs. 

Let’s start with G-CSF analogs, which include filgrastim and pegfilgrastim. These medications can be administered intravenously and subcutaneously and work by increasing the production of neutrophils in the bone marrow. So they’re used to reduce the risk of infections on account of low neutrophil counts, which can be associated with  leukemia, myelofibrosis, or severe, chronic neutropenia. 

Another indication is for clients undergoing treatments that inhibit neutrophil production, like chemotherapy or radiation therapy for solid tumors or hematologic malignancies, as well as those receiving bone marrow transplantation. Finally, G-CSF analogs can be used in hematopoietic stem cell transplantation, where progenitor cells are mobilized from the bone marrow by G-CSF, and then collected from the peripheral blood.

The most commonly reported side effects of G-CSF analogs are nausea and bone pain, resulting from the high production of new neutrophils in the bone marrow. Other side effects include fever, fatigue, skin rashes, coughing, dyspnea or chest pain. Less commonly, alopecia or hypertension can also occur, as well as diarrhea or severe hypersensitivity reactions. Very rarely, G-CSF analogs might cause the spleen to become enlarged and rupture. In clients with sickle c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pneumothorax_&amp;_hemothorax:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jE-HGQZuSye05hVzibUscINqS7CdmS0l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pneumothorax and hemothorax: Nursing]]></video:title><video:description><![CDATA[Pneumothorax and hemothorax are conditions that affect the pleural space surrounding the lungs. When air leaks into this space, it’s called a pneumothorax; whereas when blood fills this space, it’s called a hemothorax.

Now, let’s quickly review the anatomy and physiology of the pleural space. The lungs are lined with a membrane called the visceral pleura, while the chest cavity is lined with the parietal pleura. The thin space between these two membranes is called the pleural space. The pressure within the pleural space is negative, meaning it’s below atmospheric pressure. Now, the lung tissue’s elastic recoil applies a constant force that tries to contract the lungs, kind of like a stretched out rubber band. To prevent the lungs from shrinking, the negative pleural pressure around the lungs pulls the lung parenchyma outwards and counteracts the elastic recoil. 

When a person inhales, the alveolar pressure becomes lower than the atmospheric pressure, which allows the air to enter the lungs. During exhalation, the alveolar pressure becomes greater than the atmospheric pressure, letting air move out of the lungs. However, at all times, the pleural pressure will remain lower than both the atmospheric pressure and the alveolar pressure, which helps prevent the lung from completely collapsing. Now, if pneumothorax or hemothorax occur, this physiological function of the pleural space gets disrupted. 

Pneumothorax is categorized as either open or closed, depending on its cause. An open pneumothorax is caused by an opening in the chest wall that allows air to enter the pleural cavity from outside the body. A common type is traumatic pneumothorax due to a penetrating injury like a knife wound. 

On the other hand, a closed pneumothorax results from an injury to the lungs that allows air to escape into the pleural space. This could be due to a traumatic cause, such as a broken rib from blunt damage piercing the lung, or an iatrogenic cause where a central venous ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diarrhea:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2p0ZvhFdQF2vSDy7qnk0qXZJQDm02I2k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diarrhea: Nursing]]></video:title><video:description><![CDATA[Diarrhea is a condition where loose or watery stools are discharged from the intestines more frequently than normal, so more than three times in 24 hours. Now, based on its duration, diarrhea can be classified as acute, if it lasts for 2 weeks or less; persistent, if it lasts for more than 2 weeks but less than 30 days; and chronic if it lasts for more than 30 days.

Okay, let’s focus on the physiology of the intestines, which include the small intestine, as well as the large intestine or colon, and the rectum. The small intestine is the longest portion of the gastrointestinal tract, and it’s the main site for food digestion and absorption of most nutrients, such as amino acids, fatty acids, monosaccharides, vitamins, and minerals, as well as water. 

The food that is not digested and absorbed travels to the large intestine, where the remaining nutrients and water are absorbed, and the stools are formed. From the large intestine, stools travel down to the rectum, and are eliminated from the body through the anus. 

Moreover, the intestines contain a variety of non-pathogenic bacteria, which form the healthy intestinal flora, and aid with food digestion, as well as with the prevention of intestinal invasion by pathogenic bacteria and other microorganisms.

Now, based on the cause, diarrhea can be defined as infectious or non-infectious diarrhea. As its name implies, infectious diarrhea is caused by pathogenic microorganisms, which include: bacteria, most commonly Salmonella spp, and Shigella spp, as well as Escherichia coli, Vibrio cholerae, and Clostridioides difficile; as well as viruses, such as adenoviruses, norovirus, and rotavirus; and protozoa, such as Giardia lamblia and Entamoeba spp. 

On the flip side, non-infectious diarrhea can be subdivided into three main groups. The first group is when diarrhea occurs as a side effect of medications that can disrupt the intestinal flora, such as antibiotics. The second group is food intolerance, li]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Guillain-Barré_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UAe0wyX2RsCcIspVw9de12XvSKGgyEh4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Guillain-Barré syndrome: Nursing]]></video:title><video:description><![CDATA[Guillain-Barré syndrome, or GBS for short, is a rare but potentially serious autoimmune disease characterized by acute demyelination and degeneration of the peripheral nerves, which ultimately leads to muscle weakness and even paralysis.

Now, let’s quickly review the anatomy and physiology of the peripheral nervous system, which includes all of the neurons that extend beyond the brain and the spinal cord. Neurons are made up of three main parts, the dendrites, cell body, and axon. The dendrites are little branches that receive nerve impulses, or signals from other neurons, and carry them to the cell body, which has all of the neuron’s main organelles. 

The cell body then transmits the nerve impulse through the axon to the next neuron in the series. 

The axons are surrounded by myelin, which is a fatty protective sheath that also helps speed up that impulse. This myelin is produced by Schwann cells, which are a group of cells that support neurons. 

For peripheral nerves, the cell body can either be located in the spinal cord, and this is called a spinal nerve; or the brain, which is called a cranial nerve.

Alright, so Guillain-Barré syndrome is caused by demyelination of the peripheral nerves. The underlying cause of this demyelination isn’t clear, but there are some known risk factors and triggers, such as a recent bacterial infection, like Campylobacter jejuni and Mycoplasma pneumoniae, as well as a viral infection, like cytomegalovirus and Epstein-Barr virus, and in rare cases, clients may also develop Guillain-Barré syndrome soon after getting a vaccine, such as the flu vaccine.

Okay, now these bacteria and viruses don’t directly damage the myelin sheath. Instead, it’s thought that they have antigens on their surface that look similar to the lipids in the myelin sheath, 

so immune cells and antibodies can mistakenly attack and destroy the myelin sheath surrounding peripheral nerves. As a result, nerve impulses become slow and sluggish, and ultima]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholecystitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W9mYWxdrTi6IWdL-aciO3qUzSka0j87I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholecystitis: Nursing]]></video:title><video:description><![CDATA[Cholecystitis refers to inflammation of the gallbladder, which is a small, pear-shaped organ located beneath the liver.

Now, let’s quickly review some anatomy and physiology. The biliary tree is made of the liver, gallbladder, and bile ducts. The liver is in charge of producing bile, which is mostly made up of bile salts and acids, cholesterol, phospholipids, proteins, bilirubin and small amounts of various other compounds, like water, electrolytes, and bicarbonate. 

Then, bile flows out of the liver through the hepatic ducts towards the gallbladder, where it’s stored. Now, eating fatty foods stimulates the cells in the small intestine to secrete cholecystokinin into the bloodstream. Cholecystokinin, in turn, stimulates the gallbladder contraction, causing it to release bile through the cystic duct and then the common bile duct.

Finally, the common bile duct joins the pancreatic duct, forming the ampulla of Vater, which is surrounded by the sphincter of Oddi. This sphincter acts as a one way valve that allows bile and pancreatic juice to be drained into the duodenum, but prevents backflow from the duodenum into the pancreatic and common bile ducts. Once in the duodenum, bile acts as a fat emulsifier, which essentially helps to digest lipids from food into small micelles, making them easier to absorb.

Now, cholecystitis is caused by biliary stasis, meaning that the bile flow is impaired. Depending on the underlying cause, cholecystitis can be classified as calculous or acalculous. The most common type is calculous cholecystitis, where biliary stasis is caused by cholelithiasis, or a gallstone, obstructing the cystic duct. On the other hand, in acalculous cholecystitis, biliary stasis is caused by gallbladder dysfunction, leading to impaired gallbladder emptying in the absence of gallstones; most often, this occurs due to ischemia of the gallbladder, mainly in hospitalized clients who are critically ill.

Risk factors for cholecystitis include cholelithi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diverticular_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gQ6QCMoETaC_mzXlTBG4ZsaAQ_atq8o8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diverticular disease: Nursing]]></video:title><video:description><![CDATA[Diverticular disease is a condition characterized by the formation of diverticula, which are small pouch-like protrusions that form along the walls of a hollow structure, most commonly, the large intestine. Having multiple diverticula in the colon is called diverticulosis. And if one or more of these diverticula become inflamed, that’s called diverticulitis.

Now, let’s zoom into the wall of the intestine, which is made up of four layers. The outermost layer is called serosa or adventitia. Next is the muscular layer, which contracts to move food through the bowel. After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. And finally, there’s the inner lining of the intestine called the mucosa; which surrounds the lumen of the gastrointestinal tract and comes into direct contact with digested food.

Now, there isn’t a single cause of diverticular disease, but rather it’s a multifactorial disease, meaning that there’s a combination of genetic predisposition and environmental risk factors. These include age over 40 years old, consuming a diet low in fiber and high in fatty foods or red meat, being obese, and having a sedentary lifestyle. Other risk factors include smoking, alcohol use, and taking certain medications, like NSAIDs.

All right, now, regardless of the cause, there’s an increase in the pressure inside the colon. This pressure pushes on the mucosa and submucosa until they bubble out through weak spots along the wall, like where a blood vessel penetrates the muscle layer of the intestine. These blood vessels can get weaker and rupture, leading to gastrointestinal bleeding. In addition, bacteria and undigested food may get stuck inside these protrusions, and cause infection within the intestinal wall. 

Diverticulitis can in turn lead to serious complications, including bowel obstruction, as well as the formation of an abscess, which is a pocket of infected pus. Some clients may d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genital_warts:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/41cudRuCRDqDFLz_rnlGHXklS4uHgDHE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genital warts: Nursing]]></video:title><video:description><![CDATA[Genital warts, also known as condylomata acuminata or anogenital warts, are benign but highly contagious skin growths, typically around the genital or anal area. 

Now, let’s go over some physiology. The outermost layer of the skin is called the epidermis, and it has multiple cell layers that are composed of developing epithelial cells. The innermost layer, called the basal layer, contains basal cells, which continually move up in the epidermis and  divide and replicate to form new cells that replenish it. As these cells move up, they mature, become flatter, and lose their ability to replicate. Ultimately, when the cells reach the top layer, they are shed from the epithelium, so that a new generation of cells can come in and take their place. 

Now, genital warts occur due to infection of the basal cells caused by human papillomavirus, or HPV for short, which is one of the most common sexually transmitted infections, or STIs. HPV is a large family of DNA viruses with over 100 strains; specifically, genital warts are most commonly caused by HPV strains 6 and 11, which are considered to be low-risk because they typically cause benign growths. On the other hand, high-risk HPV strains 16 and 18 have a high risk of causing malignant growths, including cancer of the cervix, anus, and penis, as well as cancer of the upper respiratory tract. 

Now, HPV infection is typically spread through direct skin-to-skin contact with an infected client, and there is a higher risk in clients who engage in unprotected sex or who have multiple sexual partners. Additional risk factors include early age at first sexual intercourse, smoking, or having a compromised immune system. Finally, pregnant clients are at risk of transmitting HPV to their baby during labor.

Normally the basal cells are well protected underneath all the other epidermal layers. However, if there are micro-abrasions or cuts in the epidermis, HPV can gain access to the basal cells and infect them. Once that hap]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Buerger_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Od9ZVdC-R9Gvm8QzfUhhoXOJSJmnCVFS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Buerger disease: Nursing]]></video:title><video:description><![CDATA[Buerger disease, also called thromboangiitis obliterans, is a peripheral vascular condition characterized by inflammation of small and medium-sized arteries and veins of the extremities. This inflammation is recurrent, segmental, and non-atherosclerotic, meaning that it’s not caused by atherosclerosis. 

All right, let’s go over some physiology. There are three major types of blood vessels: arteries, veins, and capillaries. Normally, blood flows from large arteries into medium and then small arteries called arterioles, which in turn, carry the blood to capillary beds. All arterial vessels have three layers: from outside in, there’s tunica externa or the adventitia layer, which has loose connective tissue; then the tunica media or the media layer, which contains some elastic tissue and smooth muscle that allow the arteriole to dilate or constrict in response to local conditions; and finally, the endothelium, which consists of a single layer of endothelial cells on top of a layer of connective tissue, called lamina propria. 

The endothelial cells maintain blood flow by preventing blood cells from reaching the underlying lamina propria. If their continuity is disrupted, blood cells may come up against coagulation factors in the lamina propria. This initiates a coagulation cascade that leads to the formation of a blood clot, which in turn blocks the blood flow. 

Now, the arterioles deliver oxygen-rich blood into a network of capillaries, called the capillary bed. Here, oxygen and nutrients pass to tissue cells, which will then return carbon dioxide and wastes back into the capillary bed. These capillaries will then merge to form the smallest veins, called the venules. The structure of these venules is similar to that of arterioles but with thinner walls that contain less smooth muscles. Eventually, these venules drain blood into medium veins, which then drain into large veins that deliver the blood straight back to the heart. 

All right, now the exact cause]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Syphilis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vBAQFE1VQ1qc62vk_46bf4zrRHeAAN_2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Syphilis: Nursing]]></video:title><video:description><![CDATA[Syphilis is a sexually transmitted infection or STI, that primarily affects the skin and mucous membrane of the external genitalia, and over time disseminates throughout the body, ultimately causing serious damage to the cardiovascular and nervous systems.

Now, syphilis is caused by a spirochete or spiral-shaped bacteria called Treponema pallidum. This infection is mainly transmitted from person to person during sexual contact through body fluids, such as vaginal secretions, semen, or blood, and it can also be transmitted via contact with skin or mucous membranes, including eyes, mouth, throat, and anus. The main risk factors for contracting syphilis include having vaginal, anal, and oral unprotected sex, as well as having multiple or anonymous sexual partners.

Pregnant clients can also transmit the infection to their fetus, either via the placenta, which may result in spontaneous abortion, fetal death, or poor fetal growth; or during childbirth, causing congenital syphilis.  

Now, syphilis has four stages: primary, secondary, latent, and tertiary. The first stage as soon as the client gets infected is called primary syphilis or early localized stage, in which the bacteria start replicating at the contact site, most often the skin and mucous membrane of the external genitalia. After 10 to 90 days from the initial infection, clients typically develop a lesion called chancre, which contains a high number of replicating bacteria and is highly contagious. Now, the chancre typically heals on its own within 3 to 6 weeks, but during this time, the bacteria manage to disseminate to nearby lymph nodes and into the bloodstream. 

This leads to the second stage, called secondary syphilis, also called the dissemination stage, which can occur about 2 to 10 weeks after the chancre develops. This dissemination results in a generalized rash that self-resolves within 4 to 12 weeks. 

At this point, the disease enters a dormant stage called latent syphilis, which can las]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mood_disorders:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oMXTqrDFRj6GomZwrZHxOw1qQNSL7psL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mood disorders: Nursing]]></video:title><video:description><![CDATA[Mood disorders are mental health conditions that affect a client’s emotional state, which can range from depression or extreme sadness to mania or excessive excitement. 

Now, let’s go over some physiology. Emotions are processed in a series of steps in different parts of the brain linked together into the emotion processing network. This network includes structures such as the prefrontal cortex, the cingulate cortex, the amygdala, the hippocampus, and the basal ganglia. 

The neurons in these structures communicate through neurotransmitters like dopamine, serotonin, and norepinephrine, which are released from one neuron and bind to receptors of another neuron to modulate its activity. Dopamine is essential to modulate functions like learning, emotion, and reward mechanisms. Serotonin is involved in the regulation of mood, sleep, appetite, and libido. Finally, norepinephrine is involved in mood, focus, attention, and sleep.

Okay, so mood disorders are thought to be caused by neurotransmitter imbalances in the brain. Risk factors for mood disorders include genetic predisposition; personal or family history of a mood disorder; history of trauma or psychosocial stressors; substance misuse; age under 40; being assigned female at birth; and giving birth; among many others.

Now, the mechanisms underlying the pathology of mood disorders are poorly understood, but there seems to be abnormal neurotransmitter release or receptor availability. As a result, communication between neurons in the emotion processing network is impaired. Neurotransmitters can either be decreased, leading to reduced neuron activation and depression; or they can be increased, leading to excessive neuron activation and mania.

So mood disorders can have a spectrum of clinical manifestations that may cause significant impairment at school, work, or social life. On one end of the spectrum, there’s depression, where the main clinical manifestations can be summarized with the mnemonic SIG E CAP]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Erysipelas_&amp;_cellulitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9z87eXwIQS2DlArtzMgGPJhJRLS_SMd2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Erysipelas and cellulitis: Nursing]]></video:title><video:description><![CDATA[Erysipelas is a superficial bacterial skin infection that involves the upper dermis, whereas cellulitis is a deeper bacterial skin infection involving the deeper dermis and subcutaneous tissues.

Okay, let’s go over some physiology. Normally, the skin is divided into three layers, the epidermis, dermis, and hypodermis. 
The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle. Just above the hypodermis is the dermis, which contains hair follicles, nerve endings, glands, blood vessels, and lymphatics. And just above the dermis is the epidermis, which itself has multiple cell layers that form the external skin surface.

Now, normally, the skin surface is colonized by a huge number of microorganisms that make up the normal skin flora. This flora consists mostly of bacteria, such as Staphylococcus epidermidis, as well as certain fungi, such as Candida albicans. The normal skin flora is typically non-pathogenic, meaning that these microorganisms don’t cause any disease. In fact, they are beneficial, since they serve as a physical and competitive barrier that helps prevent pathogenic microorganisms from invading and infecting the skin.

Now, both erysipelas and cellulitis are typically caused by Gram positive pathogenic bacteria. For erysipelas, the most common causative bacterium is Streptococcus pyogenes, also called group A β-hemolytic Streptococcus; whereas cellulitis is usually caused by Streptococcus pyogenes or Staphylococcus aureus. 

Risk factors that can allow these bacteria to invade the skin include having previous damage due to insect bites, minor trauma, abrasions, or skin conditions like eczema, as well as previous skin infections like impetigo or a history of cellulitis. 

Additional risk factors include older age, obesity, diabetes mellitus, arteriovenous insufficiency, lymphatic obstruction, and immunocompromised clients.
Now, erysipelas occurs when pathogenic bacteria find a way to invade the skin and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperparathyroidism:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b7QtAIltTD_qaaYByfS_2vcMRbCLYCah/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperparathyroidism: Nursing]]></video:title><video:description><![CDATA[Hyperparathyroidism is a condition characterized by an increase in blood levels of the parathyroid hormone, or PTH for short, which ultimately results in hypercalcemia, or high blood calcium levels, as well as hypophosphatemia, or low blood phosphate levels.

Now, PTH is produced by four small glands called the parathyroid glands. These glands lie in the neck, being stuck to the back surface of the thyroid gland. The main function of PTH is keeping the levels of calcium within the normal range. For example, when calcium levels are low, PTH boosts bone resorption, which causes the release of calcium and phosphate from the bone into the bloodstream. In addition, PTH activates vitamin D, which in turn increases calcium and phosphate absorption from the gut. PTH also stimulates calcium reabsorption and phosphate excretion from the kidney. On the other hand, high calcium levels cause the secretion of PTH to fall, which increases the deposition of calcium in bones and the excretion of calcium by the kidneys.

Alright, now based on the underlying cause, hyperparathyroidism may be classified into three types. First is primary hyperparathyroidism, which is caused by congenital hyperplasia, parathyroid tumor or cancer, and neck radiation or trauma. Next is secondary hyperparathyroidism, which happens as a compensatory response to a condition outside the parathyroid glands that’s causing hypocalcemia, including vitamin D deficiency, chronic kidney disease, and PTH-secreting carcinomas of the lung and kidneys. Finally, there is tertiary hyperparathyroidism, which can happen in clients who had long standing secondary hyperparathyroidism, in which the parathyroids have been producing high levels of PTH for so long that they undergo hyperplasia, or enlargement, and stop responding to feedback from calcium levels in the blood. As a result, the parathyroids become permanently overactive, independently of blood calcium levels. 

Now, risk factors of developing hyperparathyr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atelectasis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qQV72PTBRA_dWoQMbBqB6883TqKiJ94G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atelectasis: Nursing]]></video:title><video:description><![CDATA[Atelectasis is a condition where the alveoli in a lung subsegment or the entire lung collapse, inhibiting gas exchange.

Now, let’s quickly review the lower respiratory tract, which includes the lower part of the trachea, and the lungs containing the bronchi, bronchioles, alveolar ducts, and finally the alveoli. Alveoli are tiny air-filled sacs where most gas exchange occurs, so as we breathe, the inhaled oxygen moves from the alveolar sacs into the blood, while the carbon dioxide moves from the blood into the alveolar sacs to be exhaled. The walls of alveoli are coated in surfactant, an oily secretion that reduces surface tension at the alveolar air interface and prevents the walls of the alveoli from sticking to each other.

Alright, now the causes of atelectasis can be classified as obstructive and non-obstructive. Obstructive atelectasis is the most common and results from obstruction of the bronchi between the alveoli and the trachea. This prevents gas from moving into the alveoli, so they collapse. Causes of obstructive atelectasis include foreign objects, tumors, retained secretions and mucus plugs. In non-obstructive atelectasis, there’s something pressing on the lungs, which results in the alveoli being physically compressed. Some causes can include large pleural effusions and chest trauma. Non-obstructive atelectasis can also be caused by the lack of surfactant, which might be encountered in premature newborns. Now, risk factors for atelectasis include premature birth, lifestyle factors, such as smoking and obesity, lung diseases like COPD, asthma, cystic fibrosis, and bacterial infections. Other risk factors include anything leading to hypoventilation like spinal cord injuries, sedation from recent surgery, especially with general anesthesia; as well as pain, and prolonged immobility. Lastly, there’s increased risk of developing atelectasis for clients who have chest wall abnormalities, such as scoliosis, rib fractures, or other trauma.

Al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Raynaud_phenomenon:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T0M6lrZtT3CKp36faoAzn5gBSwy_OpaY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Raynaud phenomenon: Nursing]]></video:title><video:description><![CDATA[Raynaud phenomenon is a peripheral vascular condition characterized by vasoconstriction of arterioles near the skin, most often of the fingers and toes, which makes them turn white, then blue, and then red.

Okay, now let’s quickly review some anatomy and physiology. Normally, blood flows from large arteries into medium and then small arteries called arterioles, which in turn carry the blood to capillary beds. All arterial vessels have three layers: from inside out, there’s the endothelium; then the media layer, which contains smooth muscle; and finally the adventitia layer, which has loose connective tissue, as well as vasa vasorum or vessels that supply the artery, and nervi vasorum or nerves that innervate the artery and help regulate vasoconstriction via contraction of the smooth muscle in the media layer. 

Now, some nerves in the skin function as thermoreceptors, which sense changes in temperature and then send signals up through the spinal cord to the hypothalamus, which is at the base of the brain. The hypothalamus serves as the body’s thermostat and coordinates the body’s response to temperature changes through the sympathetic and parasympathetic nervous systems. 

Normally, there’s a lot of heat energy in the blood that gets lost from skin to the environment. So, when the hypothalamus gets the signal that we’re cold, it stimulates the sympathetic nervous system, which in turn signals the nervi vasorum to trigger vasoconstriction in certain body areas, such as the skin, resulting in a reduction of blood flow. That shunts blood away from the skin and towards the body’s core or organs, where less heat energy is lost. On the other hand, when we’re hot, the hypothalamus stimulates the parasympathetic nervous system, which ultimately leads to vasodilation in skin to dissipate the heat.

Now, Raynaud phenomenon is caused by abnormal and exaggerated vasoconstriction in skin. When this occurs alone and is not associated with any other disease, i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sudden_infant_death_syndrome_(SIDS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OVPevDsTQg2_aA31hno-8Lr9R9WJTfEk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sudden infant death syndrome (SIDS): Nursing]]></video:title><video:description><![CDATA[Sudden infant death syndrome, or SIDS, which is also known as cot death, or crib death, refers to the sudden death of an otherwise healthy infant during their first year of life, where no cause of death is identified, even after thorough investigation with an autopsy. SIDS has actually become the leading cause of death in infants between one month and 1 year of age. 

Now, there’s no known cause of SIDS, but there are a number of risk factors that seem to correlate with getting SIDS. These mainly have to do with how an infant sleeps, so they include sleeping face down or on the side, under soft or loose bedding like a blanket, pillows, or stuffed toys, and on a soft sleep surface like a couch or chair. Sleeping with parents, or other children or pets, as well as overheating have also been shown to increase the risk for SIDS. 

There is also a higher incidence of SIDS among babies two to three months old, those who have been assigned male at birth, as well as among formula-fed babies, those born prematurely or with low birth weight, and those with a family history, so with a sibling that died of SIDS, or history of apnea. In addition, infants of Hispanic, Native American or African descent have the highest rates of SIDS, while infants of Asian descent have the lowest rates of SIDS. 

Risk factors related to the pregnancy include complications like  placenta previa, placental abruption, or premature rupture of membranes. Other pregnancy-related risk factors include receiving little or no prenatal care, being a teenager or young age, and smoking or substance use during the pregnancy, as well as after birth, exposing the baby.  Lastly, alcohol consumption is also thought to be a risk factor because there are more cases of SIDS during weekends, the holidays, and other times of year when drinking is included in celebrations. 

Now, although the pathophysiology is unclear, there are some theories as to how SIDS occurs. One such theory is the triple-risk model, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocarditis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z0ahoRTPRx2u3Wv65hdXjacSS6uwaP9U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocarditis: Nursing]]></video:title><video:description><![CDATA[Endocarditis refers to inflammation of the inner layer of the heart, called the endocardium. Okay, but first, a bit of anatomy and physiology. The heart wall is made of three layers: the outer layer is the epicardium, the middle layer is the myocardium, and the inner layer is the endocardium. These layers line the four heart chambers, which are the two atria and two ventricles. The endocardium also lines the heart valves at the end of each chamber. 

First, there are two atrioventricular valves, the mitral or bicuspid valve on the left, and the tricuspid valve on the right. The atrioventricular valves prevent blood from returning to the atria after filling the ventricles. And second, there are two semilunar valves called the aortic valve at the left, and the pulmonary valve at the right. The semilunar valves prevent blood from returning to the ventricles after being pumped out.

Okay, so depending on its cause, endocarditis can either be infective, or less frequently, non-infective. Infective endocarditis is most often caused by bacteria like Staphylococcus aureus or Staphylococcus epidermidis, which can be found in the skin, and may enter the bloodstream during surgical procedures, or through an infected intravenous catheter, skin wounds, or intravenous drug use. 

Another common bacterial cause is Streptococcus viridans, which can be found in the mouth and may enter the bloodstream during a dental procedure. Additionally, Streptococcus gallolyticus is normally found in the intestinal flora; so when there’s colorectal bleeding, like with colorectal cancer, these bacteria can migrate into the bloodstream. On the other hand, Enterococci are a part of the normal urogenital flora, and can enter the bloodstream via genitourinary catheterization or surgery. 

Less frequently, infective endocarditis can be caused by the HACEK organisms, which include the bacteria Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella. Finally, infective endocardi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antirejection_immunosuppressants:_Nursing_Pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s5kt6s4bQ2SOXvA2HZN0y2wcTEK-xt2G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antirejection immunosuppressants: Nursing pharmacology]]></video:title><video:description><![CDATA[Antirejection immunosuppressants are medications used to prevent organ rejection after a transplant, which can occur when the recipient’s immune system attacks the transplanted organ. These medications are also used to prevent graft-versus-host disease, or GvHD for short, which can occur after a bone marrow transplant. GvHD is similar to transplant rejection but works the other way around, so it’s the donor or graft T cells that reject the recipient or host; and as a result, the recipient can develop life-threatening inflammation involving various organs.

Now, based on their primary mechanism of action, antirejection immunosuppressants can be classified into several groups. The first group covers inhibitors of transcription, and the main representatives here are cyclosporine and tacrolimus; the second group includes inhibitors of nucleotide synthesis, like mycophenolate; while the third group covers inhibitors of growth factor signal transduction, such as sirolimus. Finally, the fourth group includes DNA alkylating agents, like cyclophosphamide. These medications are primarily administered orally or intravenously, and once administered, all immunosuppressants ultimately suppress and disrupt the inflammatory process and prevent the progression of the disease.

Unfortunately, these medications can also increase the risk of side effects like myelosuppression; development of new infections; or reactivation of previous infections, such as hepatitis B. Some immunosuppressants, like tacrolimus and mycophenolate, have a boxed warning for the development of certain cancers, especially lymphoma and skin cancer. 

Other important side effects include hepatotoxicity, cardiotoxicity, as well as teratogenic effects. Some clients might experience vomiting, nausea, hyperglycemia, and menstrual irregularities, or may develop a skin rash, alopecia, and hypersensitivity reactions like anaphylaxis. Lastly, cyclosporine has a boxed warning for systemic hypertension and nephro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Altered_level_of_consciousness_(LOC):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I0Pp0FtISg6YXy6v9TBo0-HaR8auJydm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Altered level of consciousness (LOC): Nursing]]></video:title><video:description><![CDATA[An altered level of consciousness is characterized as a decreased wakefulness, awareness, or alertness, and includes a range of categories like hyperalert, delirious, lethargic, and comatose.

Now, let’s quickly review the physiology of consciousness. Normal consciousness is composed of alertness and awareness while awake, as well as arousal or the ability to be woken up from sleep. Consciousness and arousal are believed to be regulated by the reticular activating system, which is a network of neurons that’s located in the brainstem. Normally, these neurons ultimately act by activating parts of the brain cortex involved in wakefulness, attention, behavior, and thinking.

So, altered levels of consciousness can have many causes and risk factors, which can be broadly categorized as structural, metabolic, infectious, toxic, or other. Structural causes include cerebral edema, increased intracranial pressure, stroke, or traumatic brain injury; while metabolic causes include dehydration, hypo- or hyperthermia, hypo- or hyperglycemia, hypo- or hypernatremia, hypoxia, hypercapnia, or uremic encephalopathy. Infectious causes include meningitis, encephalitis, or sepsis. Toxic causes include carbon monoxide, alcohol, or medications, such as opiates, salicylates, barbiturates or benzodiazepines. Lastly, other causes include syncope, seizures, sleep deprivation, serious illness, sensory impairment, or intense pain. 

The underlying pathology leading to an altered level of consciousness depends on the cause. Some cases seem to be associated with dysfunction or damage of the reticular activating system; while other cases seem to result from direct dysfunction or damage to the brain, as well as reduced delivery of oxygen or glucose. Ultimately, neural activity is disrupted, leading to impaired wakefulness and attention, and sometimes even altered behavior and thinking.

So the typical clinical manifestations may have gradual or sudden onset, and include clouded consciousn]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Liver_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6Mol7gXnT5yb9PeCfnLFuImPT2O9SVfI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Liver cancer: Nursing]]></video:title><video:description><![CDATA[Liver cancer is a malignant tumor that can originate in the liver or, more frequently, spread to the liver from another organ.

Now, let’s go over some anatomy and physiology, The liver is a large, solid organ located in the right upper quadrant of the abdomen, which has several functions, including the production of bile, cholesterol, and certain blood proteins like albumin and clotting factors, as well as helping with glucose and fat metabolism, drug metabolism, and detoxification to eliminate harmful substances like alcohol. 

To be able to carry out these functions, the liver needs to have a rich blood supply, and there are two main sources. One source is the hepatic portal vein, which carries deoxygenated venous blood from the intestines and spleen into the liver to be filtered and detoxified before entering the systemic venous system. On the other hand, the hepatic artery supplies the liver with oxygenated arterial blood from the systemic arterial system.

So, liver cancer can arise due to chronic tissue damage from a variety of factors. Modifiable risk factors include prolonged exposure to harmful substances like alcohol, high fat or carbohydrate diet, as well as obesity and smoking. 

On the other hand, non-modifiable risk factors include having a chronic liver disease, such as cirrhosis or chronic hepatitis B or C infection; genetic disorders like hemochromatosis or alpha-1 antitrypsin deficiency; as well as family history, older age, and being assigned male at birth. 

Now, liver cancer can be either primary or secondary. Primary liver cancer occurs when the malignant tumor originates in the liver, the most common type being hepatocellular carcinoma. On the other hand, secondary liver cancer occurs when a malignant tumor originates in another organ, and then manages to metastasize or spread through blood and ultimately settle in the liver. And because of the liver’s rich blood supply, the majority of liver cancer cases are actually secondary, mos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rib_fracture:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1vBba7cwSaujTpDcl-3MC8LNQseW3D5E/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rib fracture: Nursing]]></video:title><video:description><![CDATA[Rib fractures happen when one or more ribs break, and usually result from direct trauma or repetitive injury.  

Now, there are 12 ribs on each side of the chest, with each rib attaching posteriorly to the thoracic vertebrae, and ending anteriorly as costal cartilage. There are three types of ribs: true, false, and floating ribs. The first seven pairs of ribs are true ribs, and they attach directly to the sternum through costal cartilages. The 8th, 9th, and 10th pairs of ribs are false ribs, and they attach indirectly to the sternum through the costal cartilage of the 7th rib. The last two pairs of ribs are called floating ribs because they don’t attach to the sternum at all. 

Now, the ribs form the side component of the thoracic cage, which provides support and protection for the thoracic structures, such as the heart, lungs, and blood vessels. Other functions of ribs include increasing or decreasing the thoracic volume to facilitate breathing, in addition to providing attachment points for muscles.

The main cause of rib fractures is direct trauma to the chest, which can be caused by falls, child abuse, and car crashes. Rib fractures can also be caused by repetitive chest trauma, which might be due to recurrent cough or engagement in certain sports, such as golf or tennis. 

Risk factors for rib fractures include modifiable ones, such as osteoporosis, engagement in contact sports, and malignant bone tumors involving the ribs; as well as non-modifiable ones, such as advanced age.

Regardless of the cause, fractures typically happen in ribs four through ten, and can be associated with several complications. A fractured rib that’s sharp, splintered, or displaced may damage or pierce nearby organs and tissues, such as the pleura or lungs, leading to pneumothorax, which is when there’s air from the injured lung leaking into the pleural cavity, and that doesn’t allow the lung on that side to expand properly. This may lead to atelectasis or collapse of th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Detached_retina:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-4-xKo9oQrG6oK0Uqxgs3Zk4SA6eWlwl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Detached retina: Nursing]]></video:title><video:description><![CDATA[Retinal detachment occurs when the neurosensory layer of the retina is separated from the underlying retinal pigment epithelium, resulting in fluid accumulation between the two layers. 

Okay, but first, a bit of physiology. The eye is made up of three major layers. There&amp;#39;s a fibrous outer layer, which contains the cornea and sclera. The middle vascular layer is called uvea and consists of the iris, pupil, choroid, and ciliary body. Finally, the neural layer consists of the retina, with its own outer pigmented layer, and an inner neural layer that’s composed of photoreceptor cells, which convert light into neural signals that travel via the optic nerve to the brain for visual processing. 

Now, there’s two kinds of photoreceptors: rods, which are great for seeing in low light conditions but only offer black and white vision; and cones, which are less sensitive but can detect different colors. So, there’s an oval spot in the middle of the posterior retina, called the macula, that has a depressed spot called the fovea at its center. The fovea contains the highest concentration of cones and is the part of the retina that offers the highest visual acuity.

Now, if we take a closer look at a cross-section of an eye, we can see that it’s split into three different chambers: anterior, posterior, and vitreous. The anterior chamber includes the area from the cornea to the iris. The posterior chamber is a really narrow space between the iris and the lens. Finally, the much larger vitreous chamber includes the space between the lens and the back of the eye. Now, both the anterior and posterior chambers are filled with a clear watery fluid called aqueous humor, while the vitreous chamber is filled with a clear but thicker fluid called vitreous humor.

Now, the cause of retinal detachment can be rhegmatogenous or non-rhegmatogenous. The most common type is rhegmatogenous, which happens when a tear or hole causes a break in the retina, which allows vitreous flu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Irritable_bowel_syndrome_(IBS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1pHE247ISYOuuuExxAmDOZzVTfif98a4/_.png</video:thumbnail_loc><video:title><![CDATA[Irritable bowel syndrome (IBS): Nursing]]></video:title><video:description><![CDATA[Irritable bowel syndrome, or IBS for short, is a condition characterized by irregular intestinal motility. Based on the associated symptoms it can fall into three groups: IBS - C, which is associated with constipation; IBS - D, which is associated with diarrhea; IBS - M, which is mixed, meaning that it is associated with alternating bouts of constipation and diarrhea; and IBS unclassified, meaning the IBS can’t be classified into one of the other subtypes.

All right, now, let’s zoom into the wall of the intestine, which is made up of four layers. The outermost layer is called serosa or adventitia and is a connective tissue that binds the intestine to the surrounding structures. Next is the muscular layer, which houses three smooth muscle layers. These muscles contract and relax in a rhythmic way to produce wave-like movements of the intestines, called peristalsis, which propel the food down the gastrointestinal tract. The contractions of these muscles are controlled by a mini nervous system that lies within the walls of the intestines. Typically, this system works on its own, but it is also affected by the sympathetic and parasympathetic nervous systems. 

After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. And finally, there’s the innermost layer, called the mucosa, which consists of simple columnar epithelium spanned by goblet cells. This mucosa forms invaginations called colonic crypts or glands.

Now, there isn’t a single cause of irritable bowel syndrome, but rather it’s a multifactorial disease, meaning that there’s a combination of risk factors and dietary triggers. These include genetic predisposition and family history, as well as an age below 50, or being assigned female at birth. Additional risk factors include gastrointestinal conditions, such as previous gastrointestinal infections, alterations in the fecal microflora, hypersensitivity of visceral receptors in the wall of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Carpal_tunnel_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CzRbuYpZQYySL4HHMBpWsM-4SxqmCIUb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Carpal tunnel syndrome: Nursing]]></video:title><video:description><![CDATA[Carpal tunnel syndrome is a condition in which the median nerve is compressed inside the carpal tunnel of the wrist, causing pain and tingling in the hand. 

Let’s start with a bit of  anatomy and physiology. The carpal tunnel is a rigid canal in the wrist, created by a sheet of fibrous tissue forming its roof, and the carpal bones forming the floor.  The tendons of forearm muscles run through this canal, as well as the median nerve. The median nerve supplies motor, sensory, and autonomic innervations to the thumb, index, and middle fingers, in addition to the palmar aspect of the ring finger. 

Alright, now the cause of carpal tunnel syndrome is not clear, but there are a number of risk factors, including jobs and activities that involve repetitive movement of the wrist, such as musicians, carpenters, excessive cell phone use, and certain sports, such as golf, tennis, or racquetball. Median nerve compression is generally more common in clients who are assigned females at birth since they tend to have a smaller carpal tunnel. Hormonal imbalance, which can occur during the premenstrual period, pregnancy, and menopause,  can also increase the risk for carpal tunnel syndrome. Other risk factors include conditions that may cause swelling inside the carpal tunnel, including diabetes mellitus, peripheral vascular disease and rheumatoid arthritis, as well as acromegaly, which is when excessive growth hormone causes excessive growth in the adult bones and tissues, which can narrow the carpal tunnel. 

Regardless of what triggers carpal tunnel syndrome, pathology-wise, there’s increased pressure inside the carpal tunnel, which results in obstruction of venous outflow. This leads to fluid moving from the blood vessels and into the carpal tunnel, which increases the pressure even more, ultimately causing median nerve compression.

In terms of clinical manifestations, clients with carpal tunnel syndrome typically present with pain and paresthesia in the thumb, in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Retinoblastoma:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K0ZajUVFQbqY_O196nYk2-fLS9KW6gXz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Retinoblastoma: Nursing]]></video:title><video:description><![CDATA[With retinoblastoma, retino- refers to the retina of the eye and -blastoma means arising from embryonic tissue. So, retinoblastoma describes a malignant tumor of the retina that arises from embryonic retinal cells; and it typically affects children younger than 5 years of age.

Now, let’s quickly review the physiology of the retina, which is a thin layer of nerve cells that lie at the back of the eye. This layer houses blood vessels, as well as nerve cells called photoreceptors, which receive light and convert it into neural impulses. These impulses are then directed to the visual cortex of the brain, where they get translated into images.

Now, the cause of retinoblastoma is rooted in genetics, specifically, inactivation mutations of a tumor suppressor gene called RB1, which can be the result of an inherited germline mutation or a spontaneous mutation. Spontaneous mutations means that both RB1 mutations occur spontaneously in the somatic cells of the individual, and typically cause retinoblastoma in only one eye. On the other hand, inherited mutations usually cause multiple tumors in both eyes. 

Lastly, risk factors for retinoblastoma include advanced paternal age, family history of retinoblastoma or a known RB1 gene mutation in one parent, paternal exposure to radiation, in addition to maternal exposure to diesel or gasoline exhaust during pregnancy. 

Now, the pathology of retinoblastoma starts with mutations to the RB1 gene, which cause unregulated growth of retinal cells. Over time, these cancerous cells form a tumor in the retina, which can then invade nearby structures. Left untreated, retinoblastoma can metastasize to the brain, opposite eye, lymph nodes, bone, bone marrow, and to the liver. Other complications of retinoblastoma include blindness, retinal detachment, and secondary tumors, which are typically sarcomas.

Typically, the clinical manifestations of retinoblastoma start by the age of one year in cases of bilateral involvement, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Jaundice:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vcfCxVVlSv_96edSS4-N1el2QJCPD6vO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Jaundice: Nursing]]></video:title><video:description><![CDATA[Jaundice, also called icterus, is characterized by yellowish discoloration of the skin, mucous membranes, and the sclera, due to the deposition of bilirubin.

Now, let’s go over some physiology. Bilirubin is a yellowish pigment that’s normally found in bile, and is produced in the liver by breaking down hemoglobin from red blood cells. 

Normally, red blood cells have an average lifespan of 120 days. When red blood cells get old or damaged, they travel to the spleen, where they are broken down to release hemoglobin. The hemoglobin is degraded into unconjugated or indirect bilirubin, which is then released into the bloodstream. 

Unconjugated bilirubin then travels to the liver, where it gets taken up by hepatocytes. These cells bind a molecule called glucuronic acid to the unconjugated bilirubin, forming conjugated or direct bilirubin. Then, the hepatocytes use this conjugated bilirubin, as well as cholesterol and phospholipids, to produce bile. Then, bile is secreted by the liver through the hepatic bile ducts towards the gallbladder, where it’s stored. 

Now, when food reaches the stomach, the gallbladder secretes bile through the cystic and common bile duct into the duodenum. The bile then mixes with the food to help digestion while traveling along the intestines. 

Ultimately, upon reaching the colon, the colonizing bacteria convert bile’s conjugated bilirubin into urobilinogen. Most of that urobilinogen gets reabsorbed into the blood and travels to the kidneys, where it gets excreted into the urine, giving it its distinct yellow color. 

The urobilinogen that remains in the colon gets further converted by colonizing bacteria to stercobilinogen, which is excreted into the feces, giving the distinct brown color. 

Alright, now the causes of jaundice can be classified as hemolytic or prehepatic, hepatocellular or intrahepatic, and obstructive or posthepatic. Hemolytic jaundice is caused by hemolysis or breakdown of red blood cells; which occurs in condit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pleurisy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nXcQhSQzSf6IQSIdoWCFPYMMQsGc5foi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pleurisy: Nursing]]></video:title><video:description><![CDATA[Pleurisy, also known as pleuritis, refers to the inflammation of the pleura, which is the membrane that covers the lungs.

First, let’s quickly review some anatomy and physiology. Remember that the pleura is a serous membrane that consists of two layers: the visceral pleura, which sticks to the surface of the lungs; and the parietal pleura, which lines the inside of the chest wall. Between these two layers is the pleural space, which contains 20 to 25 milliliters of pleural fluid. This lubricating fluid reduces friction between the two pleural layers, which allows them to slide over each other during respiration, as the lungs expand with inhalation and then relax with exhalation. Finally, it’s worth mentioning that the parietal pleura also has pain receptors, called nociceptors, with innervation coming from the intercostal nerves and fibers from the phrenic nerve that also innervates the diaphragm.

Now, the most common cause of pleurisy is a viral infection caused by the influenza virus, which causes the flu. Less frequently, pleurisy can be caused by a parainfluenza virus, adenovirus, coxsackieviruses, cytomegalovirus, Epstein-Barr virus, or respiratory syncytial virus. Pleurisy can also be caused by bacterial infections, such as pneumonia from Streptococcus pneumoniae, or tuberculosis; as well as fungal infections such as coccidioidomycosis or histoplasmosis. 

Other causes and risk factors include pulmonary conditions like pneumothorax or pulmonary embolism, as well as autoimmune diseases like systemic lupus erythematosus or rheumatoid arthritis; cardiovascular diseases like myocardial infarction and myocarditis; and cancers, including pleural lymphoma or metastatic pleural tumors. Other causes and risk factors of pleurisy include chest trauma, surgery, and medications like hydralazine. 

Alright, so the pathology of pleurisy starts with inflammation of the visceral and parietal pleura, which causes them to become swollen, limiting their movement.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Otitis_media:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CImIYMTxS0CvxSD2vGO3LTvzRJ_ZazFN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Otitis media: Nursing]]></video:title><video:description><![CDATA[Otitis media refers to inflammation or infection of the middle ear, and can be classified as acute when it lasts less than three weeks, or chronic when it lasts longer.

Let’s start with some anatomy and physiology. The middle ear is a cavity that lies within the temporal bone, just behind the tympanic membrane. It houses three small bones called ossicles, which transmit sound waves from the tympanic membrane to the inner ear. The middle ear communicates with mastoid air cells, which are air filled cavities within the mastoid part of the temporal bone. In addition, it communicates with the nasopharynx through the Eustachian tube, which allows air to ventilate the middle ear and normalizes the pressure of the middle ear with the atmospheric pressure.

All right, now otitis media is typically caused by viral infections like respiratory syncytial virus, rhinovirus, adenovirus, and coronavirus; or bacterial infections like Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. 

Risk factors for otitis media include having a cold or upper respiratory infection, chronic sinusitis, and allergies. Other risk factors include dysfunction or anatomic abnormalities of the Eustachian tube, as well as barotrauma, where injury is caused by changes in air or water pressures. Also, children are at higher risk of otitis media, since their Eustachian tubes are shorter and more horizontal, making it harder for fluid to drain out of the ear and easier for bacteria to climb up into the middle ear. Lastly, exposure to tobacco smoke increases the risk of otitis media because it impairs the Eustachian tube’s mucociliary function, making respiratory infections more likely. 

So the pathology of otitis media occurs when the infection triggers an inflammatory process that obstructs the Eustachian tube. This results in impaired ventilation of the middle ear, which in turn traps secretions and favors bacterial growth. In addition, the pressure inside the middle e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Perinatal_depression:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vaquo398Q8iNBWTyXi-TfN1YQFOTdNcd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Perinatal depression: Nursing]]></video:title><video:description><![CDATA[Perinatal depression, also known as major depressive disorder with peripartum onset, and previously known as postpartum depression, is a type of depressive disorder that most often occurs during pregnancy or during the four weeks following delivery.
Now, let’s quickly review the physiology of some hormonal fluctuations that take place in the perinatal period. During pregnancy, the placenta releases a couple of hormones, including human placental lactogen, estrogen, and progesterone; while the pituitary gland releases prolactin, among others. All these hormones travel through the bloodstream to their specific areas of action to regulate specific body functions. During labor, the pituitary gland secretes another hormone called oxytocin, which stimulates uterine muscle contractions to facilitate delivery. Once the baby’s delivered,  these hormones start rapidly decreasing. 

Now, the exact cause of perinatal depression isn’t understood, but it’s likely related to changes in hormone levels, as well as an imbalance of GABA, serotonin, dopamine, and glutamate. All of these  are neurotransmitters that help regulate mood, reward-motivated behavior, appetite, and sleep. These changes come along with the emotional and physical stress that can accompany the birth of a child. Now, the main risk factors for perinatal depression seem to include having a family or personal history of  trauma, such as sexual abuse, as well as a history of depression, premenstrual syndrome, or premenstrual dysphoric disorder. Clients who are younger than 25; single; or who have an unwanted pregnancy; as well as those who struggle with stressful life events before or after delivery; have inadequate social or financial support;  those who smoke; or have difficulty breastfeeding, also seem to be at an increased risk.

So, pathology-wise, the exact mechanism that leads to perinatal depression is not clear. It is thought that clients who develop perinatal depression have an increased sensi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tuberculosis_(TB):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bUt_cnZvRYCg6bcofNgZE2-lSl_fVeKQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tuberculosis (TB): Nursing]]></video:title><video:description><![CDATA[Tuberculosis or TB for short is an infectious disease that primarily affects the respiratory tract, and is caused by Mycobacteria spp., such as Mycobacterium tuberculosis.

Now, let’s quickly review the respiratory tract, which can be divided into two regions: the upper respiratory tract and lower respiratory tract. The upper respiratory tract includes the nose, nasal cavity, the oral cavity, pharynx, epiglottis, larynx, and the upper part of the trachea; while the lower respiratory tract includes the lower part of trachea, and the lungs containing the bronchi, bronchioles, alveolar ducts, and finally the alveoli. Alveoli are tiny air-filled sacs where most gas exchange occurs, so as we breathe, the inhaled oxygen moves from the alveolar sacs into the blood, while the carbon dioxide moves from the blood into the alveolar sacs to be exhaled.

Now, TB is caused by Mycobacteria spp. settling in the bronchioles and alveoli. The majority of TB cases are caused by Mycobacterium tuberculosis. However, it can rarely be caused by Mycobacterium bovis, Mycobacterium africanum, and Mycobacterium microti. These bacteria are transmitted from person to person via respiratory droplets. This happens when a person with active TB talks, sneezes, or coughs, spreading droplets that may then be inhaled by others nearby. 

Risk factors for TB include close contact with an infected individual, as well as living in crowded areas, working in a healthcare facility, having limited access to healthcare, not being vaccinated, experiencing homeless, and alcohol or IV drug abuse.

In addition, children and immunocompromised individuals are at higher risk for TB; these include clients with HIV, cancer, malnutrition, diabetes, elderly clients, or those taking immunosuppressant medications like corticosteroids.

Now, there are various stages of TB infection. Primary tuberculosis occurs when an individual is exposed to mycobacteria for the first time. These bacteria can make their way to the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lung_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MQfjN_BsQXaydP5wl4G3ptMcTU2HaB94/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lung cancer: Nursing]]></video:title><video:description><![CDATA[Lung cancer is a malignant tumor that primarily originates in the lungs, or less frequently can originate in another organ and spread to the lungs through metastasis. Unfortunately, lung cancer is one of the most common and aggressive types of cancer. 

Alright, now the lungs are these paired organs in the chest containing a collection of tubes and passages called the airways, which include the bronchi, then the bronchioles, the alveolar ducts, and finally the alveoli. The airways are lined by several types of epithelial cells that serve multiple functions.  

These include columnar epithelial cells that have hair-like projections called cilia, which work to sweep foreign particles and pathogens up and out of the airways. Another type, called goblet cells, secrete mucin to moisten the airways and trap foreign pathogens. There are also club cells, sometimes called Clara cells, that secrete glycosaminoglycans to protect the bronchioles, and neuroendocrine cells that secrete hormones into the blood.  

So, lung cancer occurs when any of these epithelial cells acquire mutations, which can arise due to a variety of risk factors. Environmental risk factors include exposure to toxins like tobacco smoke, air pollution, asbestos, coal dust, radon gas, or ionizing radiation. There are also some genetic risk factors, where few clients are genetically predisposed to develop lung cancer even without the presence of environmental risk factors. 

So, once an epithelial cell becomes mutated and cancerous, it starts dividing uncontrollably, forming a tumor mass. As the tumor keeps growing, new blood vessels also develop via angiogenesis to supply it. Eventually, cancerous cells start invading neighboring tissues and may even spread to nearby lymph nodes or metastasize to distant organs, such as the brain, bones, or liver. 

Now, there are two main types of lung cancer, non-small cell and small cell. Non-small cell lung cancers account for most lung cancers, and there’s dif]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuroblastoma:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DQMsgExPQDmrNUoudQahm8cMSMCbYwBo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuroblastoma: Nursing]]></video:title><video:description><![CDATA[Neuroblastoma is a malignant tumor composed of neural crest cells, which are embryonic nerve cells. In fact, neuroblastoma is the most common extracranial cancer in infants, and it’s only rarely seen in children over five years old.

But let’s review some basic physiology first. During embryonic development, special cells called neural crest cells start migrating along the spine. In the thoracic region of the spine, neural crest cells differentiate into the neurons of the sympathetic chain, lying on either side of the entire spinal cord. In the lumbar region, neural crest cells differentiate into the cells of the adrenal medulla, the inner part of the adrenal gland that sits atop the kidneys. Together, the sympathetic chain and adrenal medulla form the sympathetic nervous system, connecting the brain and central nervous system to various organs including the heart and blood vessels.

When an individual is under stress, the sympathetic nervous system releases norepinephrine, and the cells of the adrenal medulla release norepinephrine and epinephrine. These hormones bind to receptors in various tissues like the blood vessels, the heart, and the lungs. After the stress is over, and the hormones are no longer needed, they are broken down into metabolites to be eliminated from the body.

Although the exact cause of neuroblastoma remains unknown, several non-modifiable risk factors have been recognized. These include family history of neuroblastoma and genetic mutations in the MYCN oncogene, the ALK fusion oncogenes, and mutations in tumor suppressor genes, like the PHOX2B gene.

Alright, now, regardless of the risk factor, in neuroblastoma, some neural crest cells in the sympathetic chain or adrenal medulla don’t differentiate properly during fetal development. And these cells ultimately go on to form a tumor, most commonly in the adrenal medulla, or other areas of the sympathetic chain. When any type of neuroblastoma forms, cells in the surrounding tissue]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hirschsprung_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_h0TgcfiQVO45_hO6_gCUyXbT96Sijcq/_.png</video:thumbnail_loc><video:title><![CDATA[Hirschsprung disease: Nursing]]></video:title><video:description><![CDATA[Hirschsprung disease is a congenital condition in which neural ganglia or clusters of nerves from segments of the colon are missing, which ultimately leads to a blocked colon, causing it to enlarge. This is why sometimes it’s also referred to as intestinal aganglionosis or just congenital megacolon.

Okay, so the intestines move the waste through the bowels in one direction only, via coordinated wave-like smooth muscle contractions called peristalsis. This is controlled by the autonomic nervous system, which is divided into two parts; the sympathetic, and the parasympathetic nervous systems. The sympathetic nervous system is our fight or flight response and increases heart rate, while slowing down digestion through reducing peristalsis. On the other hand, the parasympathetic nervous system is our rest and digest response and it slows down heart rate, and increases digestion by promoting peristalsis.

Now, if we look closely at the intestinal smooth muscle layer, it’s actually composed of a circular and a longitudinal muscle layer. Within these layers are two plexuses, or networks of nerves made up of ganglia, which are clusters of individual parasympathetic ganglion cells. First there’s the myenteric plexus, also known as Auerbach’s plexus, which when activated, primarily causes smooth muscle relaxation. The myenteric plexus connects with the submucous plexus, or also known as Meissner’s plexus, which is buried in the submucosa and is responsible for helping to control blood flow and epithelial cell absorption and secretion. 

Now, these two nerve plexuses are formed during early stages of fetal development when a group of fetal cells called neural crest cells start differentiating into neuroblasts. Around week 4 of development, these neuroblasts start migrating from the mouth towards the anus. Around week 8, they get to the proximal colon of the gut, and pass through the distal colon, and around week 12 they finally reach the rectum. Two specific genes th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myasthenia_gravis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fgmbz-KSSvmnFf6mawIGFcOVRtiBKgka/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myasthenia gravis: Nursing]]></video:title><video:description><![CDATA[Myasthenia gravis is a chronic, progressive autoimmune disease caused by antibodies that bind to and destroy neuromuscular communication, where nerves send impulses to trigger skeletal muscle contraction. Over time, this results in fatigue and muscle weakness due to impaired muscle contractions. 

Now, to better understand myasthenia gravis, let&amp;#39;s review the normal physiological process of muscle contraction that occurs at cellular level. Muscle contraction is initiated at the neuromuscular junction, which is basically a connection between the axonal end of a motor neuron and a skeletal muscle fiber. So, the end of the neuron is called the presynaptic membrane, while the muscle cell is called the postsynaptic membrane. 

Now, to trigger muscle contraction, the axonal end of the motor neuron releases the neurotransmitter acetylcholine, also called ACh, at the neuromuscular junction. Acetylcholine then binds to the nicotinic acetylcholine receptors present on the muscle cell membrane. The binding of acetylcholine to its receptor activates a chain reaction within the muscle cell, which ultimately results in voluntary muscle contraction.

Now, myasthenia gravis is caused by autoantibodies that target the neuromuscular junction. In a minority of cases, this occurs as a paraneoplastic syndrome, where an underlying cancer like thymoma or bronchogenic carcinoma can result in the production of autoantibodies. However, in the majority of cases, myasthenia gravis does not have a clear underlying cause. Clients at risk are those who are assigned female at birth in their 20s and 30s, or  clients assigned male at birth in their 60s and 70s.

So, in myasthenia gravis, the client&amp;#39;s own B cells generate autoantibodies, setting in a type II hypersensitivity reaction. These autoantibodies specifically bind with the postsynaptic acetylcholine receptor, or AChR for short, in 90% of clients, or sometimes target the muscle-specific tyrosine kinase receptors, or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatic_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QcbJdbufQpSsLMPHmmqlSGlYS4iK6yfS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatic cancer: Nursing]]></video:title><video:description><![CDATA[Pancreatic cancer is a malignant tumor arising in the pancreas. Unfortunately, it’s one of the most aggressive types of cancer, so most clients have a poor prognosis. 

Now, let’s quickly review some anatomy and physiology. The pancreas is located in the abdomen, right behind the stomach, and it consists of four main parts, the head, neck, body, and tail. Now, the pancreas is a mixed exocrine and endocrine organ. Its exocrine glands produce digestive enzymes like amylase and lipase, which are released through the pancreatic duct into the duodenum; while its endocrine glands produce hormones like insulin and glucagon, which are released into the blood to help regulate our metabolism and blood glucose. 

Okay, so pancreatic cancer can rarely arise from endocrine glands, called neuroendocrine tumors; and more commonly from exocrine glands, which is called pancreatic adenocarcinoma. So, pancreatic adenocarcinoma occurs when a cell from the exocrine pancreas acquires mutations, which can arise due to a variety of risk factors. Modifiable risk factors include smoking, excessive alcohol consumption, chronic pancreatitis, diabetes mellitus, obesity, and diet high in processed meat; while non-modifiable risk factors include older age, being assigned male at birth, family history, and genetic predisposition due to inherited gene mutations like BRCA or PALB2. 

Once a pancreatic cell becomes mutated and cancerous, it starts dividing uncontrollably, forming a tumor mass. Most often, tumors originate in the head of the pancreas, and less frequently, in the body or tail of the pancreas. Now, as the tumor keeps growing, new blood vessels also develop via angiogenesis to supply it. Eventually, cancerous cells start invading neighboring tissues, such as the bile duct, duodenum, or stomach; and may even spread to nearby lymph nodes or metastasize to more distant organs, such as the liver.

Initially, clients with pancreatic cancer may experience symptoms like fatigue and we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Macular_degeneration:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vm5YbX2GS0_axXKcokqv-yhbTZKPwg5w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Macular degeneration: Nursing]]></video:title><video:description><![CDATA[Macular degeneration is an eye condition in which the part of the retina that is responsible for clear vision, called the macula, degenerates. This causes blurred or reduced central vision, and is typically related to aging. There are two main types of macular degeneration: dry or nonexudative, which is the most common one; and wet or exudative.

Okay, but first, a bit of physiology.  If we zoom into the wall of the eye, it is made up of three major layers. There&amp;#39;s a fibrous outer layer, which contains the cornea and sclera, and helps shield excess light. The middle vascular layer is called the uvea and consists of the iris, pupil, ciliary body, and choroid. Finally, the neural layer consists of the retina, with its own outer pigmented layer, and an inner neural layer that’s composed of photoreceptor cells, called rods and cones, which convert light into neural signals that travel via the optic nerve to the brain for visual processing.

Now, there’s an oval spot in the middle of the posterior retina, called the macula, which contains the highest concentration of cones and is the part of the retina that offers the highest visual acuity.

Alright, now, even though the exact cause of macular degeneration is still unknown, several risk factors have been identified. Modifiable risk factors include smoking, diabetes, hypertension, and hyperlipidemia, whereas non-modifiable risk factors include aging and a family history of macular degeneration. 

Now, let’s look at the pathology of macular degeneration. Dry macular degeneration typically develops slowly over time and is characterized by yellowish extracellular deposits of waste materials, known as drusen, that build up between the choroid and the retinal pigment epithelium. On the other hand, in wet macular degeneration, which develops rapidly, there is abnormal neovascularization, meaning that abnormal blood vessels grow from the choroid behind the retina and can leak intravascular fluid or blood. 

In]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoarthritis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b673zkwyTr2_iyCEF7-A6-YtSN2qMb0l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteoarthritis: Nursing]]></video:title><video:description><![CDATA[Osteoarthritis, also known as degenerative joint disease, is a chronic, non-inflammatory condition characterized by gradual wear and tear of joint cartilage and underlying bone followed by inadequate repair. In fact, it is the most common type of arthritis overall.

Now, let’s go over some anatomy and physiology. Joints can be classified into three main groups based on their structure and range of movement. Fibrous or synarthrodial joints, like the joints between the bones of the skull, generally don’t move at all. On the other hand, cartilaginous or amphiarthrodial joints, like the joints of the spine, allow for some movement. Finally, synovial or diarthrodial joints, like those of the wrist, elbow, shoulders, hips, knees, and ankles, are freely movable. 

Now, zooming in, the bones of healthy synovial joints are connected via a fibrous capsule that is continuous with the periosteum, which is the outer layer of bones. The fibrous capsule has an inner lining called the synovial membrane; this membrane consists of connective tissue and specialized cells that remove debris and produce synovial fluid, which is a viscous fluid found inside the joint capsule to lubricate the joint. In addition, the bones are covered with a layer of articular cartilage, which is a type of connective tissue with a lubricated surface that acts like a protective cushion for bones to smoothly glide against. 

Now, the main cause for osteoarthritis seems to be the daily stress applied to synovial joints throughout an individual’s lifetime, especially to weight-bearing joints like those of the hip, knee, and ankle. This is why the biggest risk factor for osteoarthritis is age, especially after 50 years; alongside obesity, joint overuse or injury, and altered walking patterns, which can increase joint stress. 

Other risk factors include a family history of osteoarthritis; being assigned female at birth; and having associated medical conditions, such as metabolic disorders like diabete]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteomyelitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r-hsaC2lQ0iLI3Qg9V2e8OYCTGmmRNKw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteomyelitis: Nursing]]></video:title><video:description><![CDATA[Osteomyelitis is an inflammation of the bone and its associated structures, and it typically results from an infection. Osteomyelitis can be acute, when symptoms last up to one month; or chronic, when symptoms last more than one month. 

Now, normally, the bones’ surface is covered by a dense layer of connective tissue called the periosteum, and it&amp;#39;s where the muscles, tendons, and ligaments are attached.  Beneath the periosteum, there’s a dense external layer called compact bone. This consists of many tiny cylinders known as osteons, which form the structural and functional units of bones. Each osteon is composed of concentric layers of collagen and hydroxyapatite surrounding a central canal called the Haversian canal, which contains the nerves and blood vessels that supply the osteon. In the center of the bone, there’s the medullary canal, a hollow space lined by a honeycomb- looking structure called the spongy or cancellous bone. This is made of crosslinking tiny roads called trabeculae, which make bones resistant to mechanical stress so that they can bear weights without caving in. The spaces in the spongy bone are occupied by the bone marrow, which is the site of blood cell production.

Now, the most common cause of osteomyelitis is an infection with Staphylococcus aureus, which is a round-shaped bacterium that normally lives on the skin. Other bacteria that can cause osteomyelitis include Mycobacterium tuberculosis, Pseudomonas aeruginosa,  Streptococcus spp., Salmonella spp., and Pasteurella spp. Less commonly, osteomyelitis might also be caused by viruses, parasites, and fungi. 

Risk factors for osteomyelitis can be grouped into local and systemic ones. Local risk factors include trauma and open wounds. Systemic risk factors, on the other hand, include having a weak immune system, which can be because of an HIV infection, as well as poor circulation, which could be due to uncontrolled diabetes or peripheral vascular disease. Bac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pyelonephritis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yJ7lRXsGSmCQehpO1nAq5FdWT0qAz338/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pyelonephritis: Nursing]]></video:title><video:description><![CDATA[Pyelonephritis is an ascending urinary tract infection that causes inflammation of the kidneys and the renal pelvis. 

Alright, let’s quickly review the anatomy and physiology of the urinary tract. The kidneys are bean-shaped organs located behind the peritoneum on either side of the vertebral column, just below the rib cage. Now, the kidneys are composed of the renal parenchyma and a collecting system. The renal parenchyma is the solid, functional part of the kidneys, where blood is filtered and urine is produced. This urine is then drained into the renal pelvis, which then narrows to form the ureter, and transports urine to the bladder. Ultimately, urine exits the bladder through another structure called the urethra.  

Now, pyelonephritis is most often caused by bacterial infection; and the most common bacteria are Escherichia coli. Other potential bacteria include Proteus species, Enterobacter species, Enterococcus species, and Klebsiella species, as well as Pseudomonas aeruginosa. Less frequently, pyelonephritis is caused by Staphylococcus species, Salmonella species, and fungi like Candida species. 

One of the main risk factors for pyelonephritis is urinary stasis or retention. This occurs when the bladder is not able to completely empty, and can be associated with prolonged bed rest or paralysis, or with obstruction of the urinary tract. Obstruction can be caused by structural abnormalities like strictures; kidney stones or tumors; and scarring from pelvic radiation or surgery, recurrent infections, or traumatic injuries. 

Another important risk factor for pyelonephritis is urinary reflux, which refers to the backflow of urine from the bladder to the ureters or kidneys. This can be caused by structural abnormalities, like narrowing in the bladder neck or urethra, or an abnormal ureter valve that stays open even when the bladder is full, allowing backflow of urine. Other causes of urinary reflux include bladder stones, bladder tumors, and benign pr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prostate_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ULR_XFVSSmqJG6bhJsCbJeI6Trug9d1h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prostate cancer: Nursing]]></video:title><video:description><![CDATA[Prostate cancer is a malignant tumor that originates in the prostate gland and is the most common cancer and the second most common cause of cancer death among clients assigned male at birth. 

Now, let’s quickly review the anatomy and physiology of the prostate gland. The prostate is a small gland that sits under the bladder and in front of the rectum. It can be divided into four zones. The peripheral zone, which is the outermost posterior section and is the largest of the zones, containing about 70% of the prostate’s glandular tissue. Moving inward, the central zone contains about 25% of the glandular tissue. Then there is the transitional zone, which contains around 5% of the glandular tissue, and lastly is the periurethral zone, surrounding the prostatic urethra. 

Now, the prostate gland secretes the prostatic fluid, which is a slightly alkaline, milky fluid that has nutrients that nourish the sperm, enhance its movement, and help it survive in the acidic environment of the vagina. To do that, the prostate cells rely on stimulation from androgens for survival, such as testosterone produced by the testes.

All right, now prostate cancer is typically caused by a genetic mutation in a prostate cell, such as a mutation in breast cancer genes 1 and 2, also known as BRCA1 and BRCA2 genes. These mutations may arise from a variety of risk factors. Non-modifiable risk factors include advanced age, having a family history of prostate cancer, as well as being Black. On the other hand, modifiable risk factors include obesity, a diet high in animal fat and low in fiber and vegetables, and long-term exposure to ionizing radiation or certain chemicals, such as benzene and toluene.

So, once a prostate cell becomes mutated and cancerous, it starts dividing uncontrollably, forming a tumor mass. Early on, prostate cancer cells depend heavily on androgens for survival, but eventually, the cancer cells mutate and find a way to keep multiplying without relying on androgen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glomerulonephritis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ibiKSagJRY_G7Ih35SplL5oIQQqBVT8H/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glomerulonephritis: Nursing]]></video:title><video:description><![CDATA[Glomerulonephritis refers to inflammation of the glomeruli. It can be primary when the disease starts in the glomeruli, or secondary, when the glomeruli are affected by systemic disease. It can also be acute, when symptoms develop suddenly and resolve with treatment; or it can be chronic if acute disease is not treated, or when the disease process develops slowly, leading to irreversible failure of the kidneys.  

First, let’s quickly review some kidney physiology! Remember that the nephron is the functional unit of the kidney, and its role is to filter waste products and water from the blood. Each nephron is made up of a renal corpuscle and a set of renal tubules, which are, in order: the proximal convoluted tubule, loop of Henle, distal convoluted tubule and finally, collecting ducts which drain urine into the renal papillae and eventually empty into the renal pelvis. 

The renal corpuscle is made up of the glomerulus, which is a bundle of capillary loops, and Bowman’s capsule, which surrounds the glomerulus. Now, blood enters the glomerulus through the afferent arteriole, then moves inside the glomerulus, where glomerular filtration occurs. Then, the remaining blood exits the glomerulus through the efferent arteriole. Now, the glomerular capillary wall is a semi-permeable membrane with three layers: the endothelium, which is the inner layer; the basement membrane; and the epithelium, which is the outermost layer. 

For filtration to occur, the endothelial and epithelial cells that line the capillary wall are separated by small pores that filter water and small particles from the blood and into the Bowman capsule. Only small particles are filtered from the blood and never proteins, since they are larger molecules. Also, normally, there aren’t any red blood cells in the urine. For glomerular filtration to occur, the hydrostatic pressure created by the blood pressure needs to be greater than opposing forces, such as the tubular filtrate and oncotic pressur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amblyopia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JmtNnkenTCqsDBd5OmdaY1_fTDOnTlt1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amblyopia: Nursing]]></video:title><video:description><![CDATA[Amblyopia is a condition in which there’s reduced vision in one eye due to abnormal visual development. Amblyopia is commonly referred to as lazy eye, because the affected eye is weaker and often wanders inward or outward.

First, let’s quickly review the physiology of vision. Visual development begins during the first days of life, when the newborn starts receiving visual stimuli from the external world. This helps maturation of the visual pathways connecting the eyes and brain, until they reach maturity at about 4 years of age.

Okay, now, the visual pathways begin in the eye. If we zoom into the wall of the eye, there&amp;#39;s an outer fibrous layer, which contains the cornea and sclera, and helps control the focus and entry of light. So the light that passes through the cornea is directed to the lens, which in turn collects light arrays and focuses them into the retina at the back of the eye. The retina houses photoreceptors that translate light into electrical impulses, which are then carried by the optic nerve into the visual cortex of the brain. Finally, the visual cortex processes the impulses coming from both eyes, and fuses them into one clear image.

Now, the causes of amblyopia include any condition that interferes with normal visual development, such as strabismus, or an abnormal alignment of the eyes; astigmatism, which is when light doesn’t focus properly on the retina, causing blurry vision;  as well as refractive errors, like near- or farsightedness, and differences in visual acuity between the two eyes. Other causes include eye trauma; ptosis, which is drooping of the upper eyelid; congenital cataract, which is clouding of the eye lens; as well as corneal opacities and eyelid hemangioma. These conditions can also be considered risk factors for amblyopia, along with a family history of amblyopia, premature birth, and neurodevelopmental disorders  .

Now, the pathology of amblyopia usually starts when one of the eyes does not co]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colorectal_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ICq5lAPNTvmzGorDK3ZOB2DSSKOTvbBB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colorectal cancer: Nursing]]></video:title><video:description><![CDATA[Colorectal cancer is a malignant tumor that originates in the large bowel, so the colon or the rectum, and is one of the most common types of cancer.

All right, now, the colon has four parts, called the ascending colon, which runs up on the right side of the abdomen; the transverse colon, which runs across the upper part of the abdomen; the descending colon, which runs down the left side of the abdomen; and finally the sigmoid colon, which is the S-shaped part that joins the rectum. 

Let’s zoom into the wall of the large intestine, which is made up of four layers. The outermost layer is called serosa or adventitia. Next is the muscular layer, which contracts to move food through the bowel. After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. And finally, there’s the innermost layer, called the mucosa, which consists of simple columnar epithelium spanned by goblet cells. This mucosa forms invaginations called colonic crypts or glands.

Now colorectal cancer occurs when any of these epithelial cells acquire a mutation in the adenomatous polyposis coli or APC genes, which are tumor suppressor genes, meaning that they suppress the growth of tumor cells. This mutation leads to the formation of a small polyp, also called early adenoma. Later on, these polyps may develop further mutations, such as KRAS or p53 gene mutations, leading to the development of colon cancer.

Mutations may arise due to a variety of risk factors. Modifiable risk factors include smoking, obesity, and a diet high in processed meat, and excessive alcohol intake. On the other hand, nonmodifiable risk factors include age above 40, family history of colorectal cancer or colorectal polyps, in addition to hyperinsulinemia and inflammatory bowel disease, including Crohn disease and ulcerative colitis. 

So, once an epithelial cell becomes mutated and cancerous, it starts dividing uncontrollably, forming a tumor mass. As the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urticaria:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ITB_2xMQTPOSpGOoIODbYd3DSQ2ICohN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urticaria: Nursing]]></video:title><video:description><![CDATA[Urticaria, also commonly known as hives, is a skin reaction characterized by wheals, which are raised, pruritic areas that are erythematous or red with central pallor and clearly defined borders.

Now, let’s quickly review the physiology of skin reactions. The skin is the outer barrier that protects the body from any external threat like pathogens or antigens. To do this, the skin has a thick outer layer called epidermis, which in turn consists of multiple cell layers. Below the epidermis, there’s a deeper layer called the dermis, which is mostly made of connective tissue, and contains structures like hair follicles, nerve endings, and blood vessels. Within the dermis, there’s also a special type of immune cell called mast cells, which serve as a first line of defense to trigger an immune response when they sense an external threat.

Now, urticaria is typically caused by exposure to allergens, such as pollen, pet dander, dust, bee stings, latex, and food like shellfish and nuts, as well as certain medications like antibiotics or NSAIDs. Other common causes include viral, bacterial, or parasitic infections.

Less frequently, urticaria can be caused by stress, exercise, sweat, exposure to extreme temperatures or sunlight, as well as vibration, friction, or pressure against the skin. Finally, urticaria can also be idiopathic, meaning that the cause is unknown. 

Risk factors for developing urticaria include having allergies or a family history of allergies or urticaria; as well as frequent infections, stress, cold or heat exposure, taking certain medications, and having an autoimmune disease like lupus.

Okay, the underlying pathology of urticaria is a type I hypersensitivity reaction. So, the first time a client is exposed to an allergen, the immune system reacts by producing allergen-specific IgE antibodies, which in turn bind to the surface of mast cells in the skin and mucosa. If the client is exposed to that same antigen again, the IgEs allow mast cells ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_respiratory_distress_syndrome_(ARDS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/32_w2ee_R1_lTeCD_46q0ZDNQ7Wg0OrS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute respiratory distress syndrome (ARDS): Nursing]]></video:title><video:description><![CDATA[Acute Respiratory Distress Syndrome, or ARDS, is a type of severe respiratory condition characterized by severe lung inflammation and noncardiogenic pulmonary edema. As a result, there’s decreased lung compliance, leading to hypoxemia and respiratory failure.

Now, let’s quickly review the respiratory tract, which can be divided into two regions: the upper respiratory tract and lower respiratory tract. The upper respiratory tract includes the nose, nasal cavity, the oral cavity, pharynx, epiglottis, larynx, and the upper part of the trachea; while the lower respiratory tract includes the lower part of the trachea, and the lungs containing the bronchi, bronchioles, alveolar ducts, and finally the alveoli.

Alveoli are tiny air-filled sacs where most gas exchange occurs, so as we breathe, the inhaled oxygen moves from the alveolar sacs into the blood, while the carbon dioxide moves from the blood into the alveolar sacs to be exhaled. Now, the alveoli are lined by two types of alveolar epithelial cells, called pneumocytes. The vast majority are type I pneumocytes, which allow oxygen and carbon dioxide to pass through them. There are also type II pneumocytes scattered around which produce surfactant, an oily secretion that coats the alveoli and prevents their collapse.

Now, ARDS is not a primary lung disease, rather it arises as a complication of a systemic injury that causes widespread inflammation which results in damage to the alveolar-capillary membranes within the lung. So, the most common underlying cause of ARDS is sepsis, which causes inflammation in response to an infection. This infection is most often bacterial, but some cases can be associated with viral infections, such as COVID-19. But other injuries include trauma, severe burns, near-drowning, acute pancreatitis, massive blood transfusions, aspiration of gastric contents, and toxic smoke inhalation, as well as vaping-related injury. The list basically includes any serious injury that direc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ovarian_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eO-cGitDSiSqNlaAsWvFfDxyTji1a1Dp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovarian cancer: Nursing]]></video:title><video:description><![CDATA[Ovarian cancer is a malignant cell growth that begins in the ovaries or the fallopian tube. It is often bilateral and spreads quickly to nearby organs through direct extension, to abdominal organs through abdominal seeding, and to distant organs through the blood and lymphatic vasculature.

Now, let’s recap the anatomy and physiology of the ovaries, which are paired almond-shaped organs that lie within the pelvic cavity, on each side of the uterus. The functions of the ovaries include producing and releasing oocytes through the process of oogenesis, in addition to producing estrogen and progesterone, which are responsible for maintaining pregnancy, growth, and development in assigned females at birth. 

Now, let’s look at the microscopic structure of the ovaries. Each ovary is lined by a simple squamous epithelium called the germinal epithelium, which is then covered by a thick connective tissue capsule called the tunica albuginea. The inside of the ovary is divided into two zones: cortex and medulla. The cortex houses small sacs of oocytes and supporting cells called the ovarian follicles, which are embedded in the outer layer of a unique type of connective tissue called the ovarian stroma.

Now, the exact cause of ovarian cancer is unknown, but there’s typically a genetic mutation in a cell of the ovary or the fallopian tube, such as a mutation in breast cancer genes 1 and 2, also known as BRCA1 and BRCA2 genes. 

These mutations may arise from a variety of risk factors. Nonmodifiable risk factors include middle or older age, family history, early menarche, late menopause, a history of polycystic ovarian syndrome or PCOS, endometriosis, breast, or colon cancer. 

On the other hand, modifiable risk factors include smoking, obesity, hormone replacement therapy, and ovarian hyperstimulation from infertility treatments like in vitro fertilization, as well as pelvic inflammatory disease, nulliparity, and first pregnancy at an older age. 

Now, all these risk ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meniere_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xqn3s6H7RMazZAhtpFoIcYhjTza0XBI5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meniere disease: Nursing]]></video:title><video:description><![CDATA[Ménière disease is a progressive condition that affects the inner ear, and can lead to episodes of vertigo, tinnitus, and hearing loss. 

Now, the ear is composed of three main parts. The first part is the outer ear, which includes the visible part of the ear, called the pinna or auricle, as well as the ear canal. The second part is the middle ear, which is a tiny chamber that houses even tinier ear bones. And the third part is the inner ear, sometimes called the labyrinth, which can be further divided into three parts. The central part is the vestibule, which is connected to the other two other parts; the semicircular canals, towards the back, which play a role in balance, and the cochlea, towards the front of our head, that deals with hearing.

Now, the cochlea is the part involved in hearing, and is lined by small hair cells and filled with fluid called endolymph. When sound reaches the cochlea, the endolymph vibrates, causing the hair cells to vibrate. As a result of this vibration, the small hair cells fire off electrical signals conveying sound to the brain, allowing for the processing of hearing. On the other hand, the semicircular canals are involved with balance. These canals are also lined by hair cells and filled with endolymph. So, when the head moves, the endolymph inside the canals sloshes in one direction and makes the hair cells move, causing them to fire off an electrical signal conveying the direction and speed of the head movement. This signal is then carried to the brain, allowing for the processing of balance. 

Now, the cause of Ménière disease is unclear, but risk factors seem to include genetic predisposition and family history; a viral infection or autoimmune reaction involving the inner ear; and abnormal flow or resorption of endolymph, which can be due to an obstruction or congenital malformation of the inner ear. 

Okay, so in Ménière disease there’s excessive accumulation of endolymph in the inner ear, which is known as endolym]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Strabismus:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IbzO632yS9SbCei1bbaevZ7GQP6VgcnF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Strabismus: Nursing]]></video:title><video:description><![CDATA[Strabismus is a common condition characterized by misalignment of the eyes due to a lack of eye muscle coordination. Strabismus can present occasionally or constantly, and is commonly referred to as crossed eyes or squint. 

Let’s start with some basic anatomy and physiology. Eye movement is controlled by the six extraocular muscles, which include four rectus muscles and two oblique muscles. The rectus muscles are the superior rectus, which moves the eye upwards; the inferior rectus, which moves the eye downwards; the medial rectus, which moves the eye medially; and the lateral rectus, which moves the eye laterally. The last two are the superior and inferior oblique muscles, which control the rotation of the eyeball. 

These extraocular muscles are innervated by cranial nerves that arise directly from the brain. More specifically, the abducens nerve, or cranial nerve VI, innervates the lateral rectus muscle; the trochlear nerve, or cranial nerve IV, innervates the superior oblique; and lastly, the oculomotor nerve, or cranial nerve III, innervates the rest of the extraocular muscles. Typically, control of eye movement should have developed completely by 4 months of age. 

Now, strabismus can be caused by problems involving the brain centers controlling eye movements, the cranial nerves that supply the muscles, or less commonly, the muscles themselves. This includes cranial nerve palsy, which is characterized by impaired function leading to weakness or even paralysis of the innervated muscle; as well as cerebral palsy, head trauma, or strokes. Strabismus can also be caused by sensory deviation due to eye conditions like refractive errors, cataract, retinal detachment, or retinoblastoma. Less frequently, strabismus has congenital causes, such as Down syndrome. Finally, when the cause is unknown, strabismus can also be idiopathic. 

These conditions can also be considered risk factors for strabismus, along with family history, thyroid disease, neuromuscu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cushing_syndrome_&amp;_Cushing_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PMy57uhbQ6mmo1ViIl95IoksQ6a5nh_z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cushing syndrome and Cushing disease: Nursing]]></video:title><video:description><![CDATA[Cushing syndrome is an endocrine disorder characterized by elevated cortisol levels in the blood. It can result from excessive production of cortisol from the adrenal cortex; or it can be iatrogenic, from the administration of glucocorticoid medications for a prolonged period of time. In some cases, elevated cortisol levels are secondary to an ACTH-secreting pituitary adenoma, which is called Cushing disease.

Now, let’s quickly review the anatomy and physiology of cortisol production. Normally, the hypothalamus, which is located at the base of the brain, secretes corticotropin-releasing hormone, known as CRH, which stimulates the pituitary gland to secrete adrenocorticotropic hormone, known as ACTH. ACTH then travels to the paired adrenal glands, one on top of each kidney, where it specifically targets cells in the adrenal cortex. 

The adrenal cortex is the outer part of the adrenal gland and is subdivided into three layers: the zona glomerulosa, the zona fasciculata, and the zona reticularis. In the zona fasciculata, ACTH stimulates cortisol secretion. Cortisol is a glucocorticoid, and it’s involved in a number of things such as maintaining glucose levels, blood pressure, and the suppression of the inflammatory and immune response. Additionally, it can also influence things like mood and memory, as well as degrade collagen and connective tissue within the tissues. 

Now, to make sure that these actions work for the benefit of the body, and not against it, free cortisol levels have to stay within the normal range. To do that, the body uses negative feedback, which means that high levels of cortisol make the hypothalamus and pituitary gland secrete less CRH and ACTH, respectively. This ultimately results in decreased stimulation of the zona fasciculata, so cortisol levels go down. Finally, bear in mind that cortisol secretion has a circadian rhythm, so cortisol levels are normally higher in the morning and at their lowest around midnight.

Okay, now,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ur2GWdZyRwyXfanGsVGSVzHQSauxZJ7F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis: Nursing]]></video:title><video:description><![CDATA[Hepatitis refers to an inflammation of the liver due to infection or injury, and it’s often self-limiting, but some cases can result in extensive liver damage.

Now, let’s quickly review some anatomy and physiology. The liver is a large, solid organ located in the right upper quadrant of the abdomen, which has several functions, including the production of bile, cholesterol, and certain blood proteins like albumin and clotting factors; as well as helping with glucose and fat metabolism; detoxification through medication and alcohol metabolism; and it also plays a big role in bilirubin metabolism.

Now, hepatitis can be caused by a viral infection, called viral hepatitis, or other kinds of injury, in which case it’s called non-viral hepatitis. 

The more common one is viral hepatitis, which is caused by hepatitis viruses A, B, C, D, or E. Hepatitis A virus is usually transmitted through the fecal-oral route, through contaminated food or water, or through person-to-person contact; and risk factors include living or working in nursing homes, daycare centers, and living in or traveling to countries with poor access to clean water, sanitation, and hygiene; as well as sexual contact with an infected individual. 

Next, we have hepatitis B, C, and D viruses, which are primarily transmitted through blood and other body fluids; so the main risk factors include intravenous drug use, blood transfusions, hemodialysis, and working  as a healthcare professional; as well as high-risk sexual behavior, such as having multiple partners or not using protection. 
Hepatitis B can also be transmitted vertically to the baby before or after birth. 

Of note, the hepatitis D virus can’t cause an infection in the absence of hepatitis B virus. So the most important risk factor for a hepatitis D infection is a hepatitis B infection. 

Lastly, hepatitis E is transmitted through the fecal-oral route, mostly through consuming contaminated food or water.

On the other hand, non-viral hep]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endometriosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gd4vk1tfRS2N2QLvYAm6pqlrRwS-Z-bW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endometriosis: Nursing]]></video:title><video:description><![CDATA[Endometriosis gets its name from the endometrium, which lines the inside of the uterine cavity. With endometriosis, there is ectopic endometrial tissue, which means endometrium can be present in other parts of the body, like the ovaries or fallopian tubes, or even as far as the lungs! Also, with endometriosis, the ectopic tissue behaves just like regular endometrium would, and it undergoes cyclic changes in response to the menstrual cycle. 

Now, let’s look at the overall anatomy and physiology of the uterus. Remember that the uterine wall is comprised of three layers: the endometrium, which is the innermost, mucosal layer, and  is itself made up of a basal layer, and a functional layer; the myometrium, which is the strong smooth muscle that gives the uterine wall its thickness; and the perimetrium, which is the outermost layer, and it’s basically a continuation of the peritoneal lining. 

Now, during each menstrual cycle, an egg is released from the ovaries at ovulation, and estrogen and progesterone levels increase. Estrogen thickens the functional layer of the endometrium to prepare it for implantation. If there is no fertilization, hormone levels drop, and the functional layer sloughs off, and is eliminated along with a small amount of blood during menstruation. And after menstruation, the cycle repeats itself all over again! 

Okay, now, the exact cause behind endometriosis is still unknown, but there are few theories that try to explain this phenomenon. One such theory is retrograde menstruation, which suggests that during menstruation, some blood and endometrial cells could flow backwards into a fallopian tube and implant into the nearby pelvic tissues. 

Next, there is the benign metastases theory, which suggests that endometrial cells can travel to distant organs like the heart or lungs through lymph and blood, while some theories blame it on genetics, immunity and abnormal hormonal patterns. In addition to these proposed causes, there are some ri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypersensitivity_reactions_-_Type_II:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yOMUoikxRFSonJkU5B3M_YI1QRGCfY_e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypersensitivity reactions - Type II: Nursing]]></video:title><video:description><![CDATA[A hypersensitivity reaction is an overreaction to a foreign antigen which then causes serious damage to the body’s tissues. There are four types of hypersensitivity reactions: type I is immunoglobulin E, or IgE mediated; type II is mediated by antibodies that activate cellular cytotoxicity, type III is mediated by immune-complexes, and type IV is a delayed T cell mediated hypersensitivity reaction. A type II, or cytotoxic, hypersensitivity reaction occurs when IgG or IgM antibodies bind to an antigen on the surface of a cell and cause other immune cells and complements to attack it, leading to the cell’s destruction.

Let’s start by discussing the physiology of the humoral immune response. The humoral immune response is the part of the immune system that provides protection against invading pathogens by utilizing antibodies designed to specifically target certain antigens. It all begins in the bone marrow, where undifferentiated hematopoietic stem cells differentiate into various types of  white blood cells, including T and B lymphocytes, or T and B cells, for short. 

When a pathogen, like a bacteria or virus enters the body, it runs into antigen-presenting cells, or APCs. APCs like macrophages or dendritic cells, then engulf and digest the pathogen and the fragments are then presented on the APC’s surface via proteins called major histocompatibility complex class II, or MHC II. Now these fragments serve as antigens which are any thing that could trigger an immune response.  So the APCs present these antigens to T helper cells which have T-cell receptors, or TCRs, that recognize the antigen. These T helper cells will go on to activate specific B cells which causes them to transform into plasma cells that could produce antibodies against the specific antigen. 

Antibodies called IgM and IgG are produced and they can attach to the antigens on the bacteria or virus that activates the complement system. Complements are a group of proteins, named C1 throu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aspergillosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9mubzPnXRgma1hAr0AjVQePrTDa32LAb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aspergillosis: Nursing]]></video:title><video:description><![CDATA[Aspergillosis is an infection caused by a fungus called Aspergillus, most commonly Aspergillus fumigatus, that typically affects the respiratory system. There are three types of aspergillosis; chronic, which is the most common; allergic; and invasive, which is the most severe.

Now, let’s quickly review the physiology of how the immune system fights off fungal infections. This is typically accomplished by white blood cells, which are part of the innate immune system. When a pathogen enters the body, the innate immune system reacts quickly. Some of the first cells on the scene include phagocytic cells like macrophages which essentially eat the pathogen. In response, they send out signals, such as beta-d-glucan, to activate other cells like neutrophils to surround and kill the pathogen. These combined, non-specific innate immune responses kill most fungal pathogens before they can spread around the body. 

Now, the cause of aspergillosis is being exposed to the Aspergillus fungus. This fungus is  ubiquitous, and particularly loves damp areas, older buildings, moist soil, and damp woods and leaves, so working in construction or farm jobs in these areas puts a client at higher risk for developing an Aspergillus infection. 

Additionally, risk factors for severe aspergillosis include being immunocompromised because of AIDS or neutropenia; long-term term steroid use; or anti-rejection medications after a transplant. Also, chronic lung disease like COPD, asthma, TB, and cystic fibrosis put clients at increased risk. 

Okay, now, the pathology of aspergillosis typically begins when a person inhales Aspergillus spores which then land in the respiratory tract, particularly the lungs. If the client’s immune system doesn’t properly clear the infection, then the spores are able to grow into fungi and spread throughout the lungs. When clients are severely immunocompromised, the infection can spread to the brain, heart, kidneys, or skin at which point it is considered in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sarcoidosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P5D-ELqmTf_vZcNMsISHWzifTbG-9bIy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sarcoidosis: Nursing]]></video:title><video:description><![CDATA[Sarcoidosis is a chronic, multisystemic disease characterized by the formation of non-caseating, meaning non-necrotizing granulomas, which are nodules of chronically inflamed tissue in the lungs and lymph nodes. Less commonly, these granulomas can accumulate in the heart, kidneys, joints, eyes, liver, spleen, and skin.

Now, let’s quickly recap the physiology of the immune system. So, normally, the cells of the immune system are ready to spot and destroy any foreign pathogens that could harm the body. Some cells that help with this are called macrophages. When these cells come in contact with a pathogen, they latch onto it and then engulf or swallow it. The macrophage then breaks down the pathogen, presents a piece of it, called an antigen, to its surface, and carries it to a lymph node. That’s where macrophages find other immune cells called T-helper lymphocytes, which recognize and bind to the antigen, and start proliferating. 

Proinflammatory cytokines, or signaling molecules, like tumor necrosis factor alpha, or TNF-ɑ for short, are then released by macrophages to help activate the helper T-cell and it begins to divide or proliferate. The new T-cells leave the lymph node and start secreting other cytokines that recruit more immune cells like additional T-cells and macrophages. 

Okay, now, the exact cause behind sarcoidosis is still unknown, but there are several risk factors that can be grouped into modifiable and non-modifiable ones. Modifiable risk factors include exposure to mold, silica, or pesticides, whereas non-modifiable risk factors include age between 20 and 60 years, being assigned female at birth, and family history of pulmonary sarcoidosis. Clients who are of Black race or Northern European descent are also at a higher risk of developing pulmonary sarcoidosis.

Now, the pathology of pulmonary sarcoidosis starts with an antigen entering the body. This antigen gets picked up by macrophages, which secrete cytokines that attract other i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Increased_intracranial_pressure_(ICP):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DsGimV6lTgug9P2jPQrs01VWSqyYcTif/_.jpg</video:thumbnail_loc><video:title><![CDATA[Increased intracranial pressure (ICP): Nursing]]></video:title><video:description><![CDATA[Increased intracranial pressure is a potentially life-threatening condition characterized by increased pressure within the skull. 

First, let’s take a look at the physiology of intracranial pressure or ICP, which is how much pressure there is within the cranium and spinal column, and it plays an important role in how much oxygen gets to the brain. ICP, which is normally between 7 and 15 mmHg, is determined by the cerebral perfusion pressure or CPP, which is the amount of force available to deliver blood to the brain. CPP is defined as the difference between the mean arterial pressure, or MAP and the ICP.

Now, when it comes to regulating ICP, remember that the mature skull is a rigid structure that can’t expand. So, to maintain a normal ICP, there must be a balance between the volumes of its contents, including brain tissue, cerebrospinal fluid or CSF, and blood supplying the brain. As a result, if there’s an increase in the volume of any one of these three, there should be a compensatory decrease in the other two, which is known as the Monroe-Kellie hypothesis. Normally, the volume of the brain remains relatively stable, so ICP can be regulated by changes in CSF and blood volume. When needed, CSF production can be decreased or reabsorption can be increased to help bring ICP back to normal. Similarly, cerebral blood volume can be decreased either by cerebral vasoconstriction or increasing the venous blood drainage out of the skull. 

Finally, it’s worth noting that cerebral blood vessels are lined by highly selective endothelial cells that only allow certain substances to pass into the interstitial fluid surrounding the neurons. This is commonly referred to as the blood-brain barrier, and it helps protect the neurons from pathogens, some immune cells, different products of metabolism as well as some medications that can be found in the systemic circulation. 

So, increased ICP can be caused by an increased volume within the skull. An increase in brain tis]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_contusion:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hvDUz22iQ02tJSqSMa2kAzSXQcq7E6b7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary contusion: Nursing]]></video:title><video:description><![CDATA[Pulmonary contusion is a lung injury that develops after chest trauma, and is characterized by interstitial hemorrhage that inhibits gas exchange.

Now, let’s quickly review the lower respiratory tract, which includes the lower part of the trachea, and the lungs containing the bronchi, bronchioles, alveolar ducts, and finally the alveoli. Alveoli are tiny air-filled sacs that are surrounded by tiny blood vessels, called capillaries. 

If we zoom in even more, we can see a tiny space between the alveolar wall and the capillary wall, called the interstitial space, which normally contains a small amount of interstitial fluid. And that’s where most gas exchange occurs, so as we breathe, the inhaled oxygen moves through the alveolar membrane, the interstitial space, and the capillary membrane to reach the blood, while the carbon dioxide moves from the capillaries through the interstitial space and into the alveolar sacs to be exhaled.  

Now, the alveoli are lined by alveolar epithelial cells, called pneumocytes. The vast majority are type I pneumocytes, which allow oxygen and carbon dioxide to pass through them. There are also type II pneumocytes scattered around which produce surfactant, an oily secretion that coats the alveoli and prevents their collapse. 

The main cause of pulmonary contusion is direct blunt trauma to the chest. Risk factors for pulmonary contusion typically include car crashes, falls from heights, child abuse, and sport injuries. Clients who serve in the military are also at an increased risk of pulmonary contusions, due to blast injuries from explosives.

Okay, let’s look at what happens when the force from the chest injury reaches the lung parenchyma. Well, first, there’s tearing of the alveolar and capillary membrane, which causes blood and interstitial fluid to leak into the alveolar space, preventing gas exchange. At the same time, immune cells start producing pro-inflammatory cytokines which trigger inflammation and edema of th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myocarditis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bczcF7eaSFOqDx8HCdPYf5H5QdG6DpgE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myocarditis: Nursing]]></video:title><video:description><![CDATA[Myocarditis refers to the inflammation of the heart muscle, called the myocardium.

Okay, but first, a bit of anatomy and physiology. The heart wall is made of three layers: the outer layer is the epicardium, the middle layer is the myocardium, and the inner layer is the endocardium. 

So, the myocardium is a muscular layer that consists of cells called cardiomyocytes, which relax so that the heart can be filled with blood during diastole, and then contract to pump the blood out of the heart during systole. 

Contraction of the cardiomyocytes is controlled by the pacemaker cells in the sinoatrial or SA node, which generates electrical signals that get sent out through the conduction system  in the heart.

Now, most cases of myocarditis are caused by a viral infection, such as Coxsackie A or B virus and parvovirus B19; but can also be caused by a bacterial infection, like Streptococcus pyogenes or Borrelia burgdorferi, which causes Lyme disease; a fungal infection, such as Candida or Aspergillus; or a parasitic infection, like Trypanosoma cruzi, which causes Chagas disease. 

Myocarditis can also be caused by autoimmune disease, such as systemic lupus erythematosus or polymyositis, where the immune system attacks its own tissues, including the myocardium. 

Other causes of myocarditis include toxins like carbon monoxide poisoning, radiation therapy in the chest, and certain medications like sulfonamides, or chemotherapeutic medications, such as anthracycline and doxorubicin. Finally, some cases of myocarditis are idiopathic, meaning the cause is unknown.

Okay, regardless of the cause, the pathological outcome is acute damage to the cardiomyocytes. This in turn activates the immune system, causing the release of cytokines and oxygen free radicals. This results in severe inflammation, and even cardiomyocyte death, which impairs the heart’s ability to contract. Once the causative agent gets cleared out, the inflammation typically resolves, and myocardial cont]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypersensitivity_reactions_-_Type_I:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v1ewddcPQf2xyZsDKdO7YUA1QtSoWSm3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypersensitivity reactions - Type I: Nursing]]></video:title><video:description><![CDATA[A hypersensitivity reaction is an overreaction to a foreign antigen which then causes serious damage to the body’s tissues. There are four types of hypersensitivity reactions: type I is immunoglobulin E, or IgE mediated; type II is mediated by antibodies that activate cellular cytotoxicity, type III is mediated by immune-complexes, and type IV is a delayed T cell mediated hypersensitivity reaction. Type 1 hypersensitivity reactions, or IgE-mediated reactions, are an immediate immune response where the IgE antibody responds to an antigen, causing acute inflammation.

Let’s start by looking at the physiology of the immune response. A food allergen or pathogen  enters the body and runs into antigen-presenting cells, or APCs. APCs like macrophages or dendritic cells, then engulf and digest the allergen and the fragments are then presented on the APC’s surface via proteins called major histocompatibility complex class II, or MHC II. Now these fragments serve as antigens which are any thing that could trigger an immune response.  So the APCs present these antigens to  T helper cells which have T-cell receptors, or TCRs, that recognize the antigen. In response, the T helper cells will signal B Cells to transform into plasma cells that will start producing antigen specific IgE antibodies. 

These antibodies bind to other immune cells like mast cells and basophils and prep them to fight off the allergen in future encounters. This process is called priming or sensitization.  So the next time the food allergen shows up, the mast cells armed with the IgE antibodies will use them to attach to the antigens on the allergen. When two or more of the antibodies on the mast cell bind to the antigen, it  will cause the mast cell to degranulate and release various proinflammatory molecules. One of these is histamine which causes vasodilation, and increases blood vessel permeability. This increases blood flow to the area and lets other immune cells, like macrophages, get to the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombocytopenia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QWCkMEfbRAqqqgq06OZ7aDvgReCY6Q-4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombocytopenia: Nursing]]></video:title><video:description><![CDATA[Thrombocytopenia is when there’s a low number of platelets, also known as thrombocytes, in the blood.  Normally, there are between 150,000 and 450,000 thrombocytes per microliter of blood; while in thrombocytopenia, this number goes below 150,000 cells per microliter. Remember that platelets are involved in blood clotting, so with thrombocytopenia, clients have an increased risk of bleeding. 

But let’s start with some basic physiology of platelets, which form in the bone marrow. Although often called cells, platelets are actually small fragments of megakaryocytes, which themselves derive from hematopoietic stem cells, that give rise to all types of blood cells. After they’re formed, platelets leave the bone marrow to enter the bloodstream, and almost 50% of them are stored in the spleen, while the remaining keep circulating through the vascular system. 

Now, when there’s any kind of damage to a blood vessel, circulating platelets aggregate to form a platelet plug at the site of the injury. This process is also known as primary hemostasis, and it’s followed by secondary hemostasis. During secondary hemostasis, clotting factors come into play one after another, eventually cleaving the fibrinogen into fibrin, which forms a protein mesh. This protein mesh is like a giant net that wraps around the platelet plug and reinforces it, stopping the bleeding.

Now, based on the cause, thrombocytopenia can be subdivided into three main groups. The first group covers conditions associated with impaired platelet production, such as inherited thrombocytopenia; viral infections, like HIV and HCV infections; folate and vitamin B12 deficiencies; and aplastic anemia. Aplastic anemia is typically associated with bone marrow suppression, and it’s characterized by decreased production of platelets as well as red and white blood cells.  

The second group covers thrombocytopenias caused by increased platelet destruction or consumption, which are further subdivided into non-immu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hufVUYr1TiuntD2Gj6TmB0HRQvihxwMq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal cancer: Nursing]]></video:title><video:description><![CDATA[Renal cancer is a malignant tumor that arises from the cortex, pelvis, or the calyces of the kidneys. The most common type of renal cancer is renal cell carcinoma, which forms from the cells lining the proximal convoluted tubules of the kidney. 

All right, let’s quickly review some kidney physiology! We can think of the kidneys as the body’s natural blood filter. Their main function is to clear blood of metabolic wasteful substances and toxins by excreting them through urine. In addition, they secrete important hormones, and are essential in regulating the acid-base balance, pH, blood pressure, and electrolyte levels in the body. 

So, if we take a cross-section of the kidney, there is an outside rim, known as the renal cortex, and an inner portion, which is the renal medulla. The cortical tissue extends towards the medulla, forming renal columns that divide the medulla into pyramidal-shaped structures called the renal pyramids. The tips of the pyramids, called the renal papilla, project into minor calyces which join together to form major calyces which funnel into the renal pelvis. Urine collects in the renal pelvis and then heads out of the kidney through the ureter.

Now, within the cortex and the medulla there are millions of tiny functional units called nephrons, which consist of a renal corpuscle and a set of renal tubules. The renal corpuscle is made up of the glomerulus, a tiny bundle of capillaries, and the Bowman’s capsule, which is a cup-shaped structure that surrounds the glomerulus. So, blood gets filtered through the glomerulus, and then travels through the renal tubules, which are, in order: the proximal convoluted tubule, loop of Henle, distal convoluted tubule and finally, collecting ducts which drain urine into the renal papillae and eventually empty into the renal pelvis. 

Now, the exact cause of renal cancer is often unknown, but there’s typically a genetic mutation in a cell of the cortex, pelvis or calyces, such as a mutation i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_immunodeficiency_virus_(HIV)_&amp;_acquired_immunodeficiency_syndrome_(AIDS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-TzaerWOSACezZdeXb0f6pGuS52OmJd2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS): Nursing]]></video:title><video:description><![CDATA[Human immunodeficiency virus, or HIV for short, is a retrovirus that targets the body’s immune system. Over time, HIV infection can lead to acquired immune deficiency syndrome or AIDS for short, making clients more vulnerable to other infections and certain tumors that a healthy immune system would usually be able to fend off. 

All right, let’s quickly review some physiology. The immune system consists of white blood cells that protects us from pathogens, and destroys tumor cells. Now, the immune system has two main branches that work together, and include the innate and the adaptive immune responses. 

So, the first is the innate immune response, which involves non-specific cells like neutrophils and macrophages that act as first-responders, as well as dendritic cells, which then activate the adaptive immune response. This response is highly specific, and is mediated by cells called lymphocytes, which include T and B cells. T cells can be further divided into CD4+ and CD8+ T cells. CD4+ T cells are also known as T helper cells, because they interact with dendritic cells, and in turn help activate the rest of the lymphocytes. On the other hand, CD8+ T cells, also known as cytotoxic T cells, are in charge of cell-mediated immunity, where they attack abnormal cells. Finally, B cells mediate a type of adaptive response, called humoral immunity, by secreting antibodies that bind to and destroy specific antigens.

Now, HIV infection is primarily caused by contact with certain bodily fluids from an infected person, such as blood, semen, vaginal and anal secretions, and breast milk. However, HIV is not present in saliva, sweat, urine, or feces.

The main risk factors for contracting HIV include having unprotected sex, especially anal sex, as well as having multiple or anonymous sexual partners. Other risk factors include using intravenous drugs, especially sharing needles, or unsterile cutting or piercing, as well as accidental needlesticks, and transfusing bloo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Encephalitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IDX6pYrQToaCHLmSxvirF2FATeuaRqwE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Encephalitis: Nursing]]></video:title><video:description><![CDATA[Encephalitis is the inflammation of the brain, also known as the cerebrum, which can also involve the meninges, cerebellum, and brainstem.

Let’s start by looking at the physiology of the nervous system, which is divided into the central and peripheral nervous system. The central nervous system includes the brain and spinal cord, while the peripheral nervous system includes all the nerves that connect the central nervous system to the muscles and organs. The brain is divided into the cerebrum, which consists of the two cerebral hemispheres, the cerebellum, which sits down at the base of the skull, and the brainstem, which is located right in front of the cerebellum.

Now, the brain is protected from the rest of the body by three meningeal layers. From outside to inside, these are the dura mater, arachnoid mater, and pia mater. Between the arachnoid and pia mater there’s the subarachnoid space, which houses the cerebrospinal fluid. The cerebrospinal fluid is a clear, watery liquid that cushions the brain from impact and bathes it in nutrients.

Zooming in, the cells that make up our brain are called neurons and they receive and send electrical impulses to one another. Now, neurons need a lot of oxygen and nutrients to function properly, so the brain has a rich blood supply. But for any nutrients to enter and leave the brain, they have to go through the tightly regulated blood-brain barrier. This refers to the endothelial cells in the blood vessels of the brain which are so tightly bound to one another that they only allow certain molecules to slip through them.

Now, in most cases, encephalitis is caused by a virus, such as herpes simplex virus, or HSV for short; enteroviruses, like echovirus and coxsackie virus; West Nile virus; rabies; mumps; and measles. Varicella zoster virus and cytomegalovirus can also cause encephalitis, particularly in immunocompromised clients. Less commonly, encephalitis can be caused by bacteria, fungi, or parasites. Very rarely,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cystic_Fibrosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OdE_EkSKSziFEpy4o4JIa3-cTiyiRLXa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cystic fibrosis: Nursing]]></video:title><video:description><![CDATA[Cystic fibrosis is an inherited, chronic and progressive condition characterized by dysfunction of the exocrine glands, primarily in the respiratory, gastrointestinal, and reproductive systems. 

First, let’s quickly review some physiology. Exocrine glands are found throughout the body, and their main function is to secrete products like sweat from the skin; as well as saliva, gastric or pancreatic juices, and bile from the gastrointestinal tract; in addition to mucus to protect the respiratory, gastrointestinal, and reproductive systems, as well as seminal fluid from the prostate. 

Now, zooming in, the exocrine glands consist of cells that secrete their products containing substances like water, ions, and enzymes into a ductal system. To do so, these cells have a special transporter protein called cystic fibrosis transmembrane conductance regulator protein, or CFTR for short. This protein pumps chloride ions out of the cell in order to help draw water out, forming those products and thinning them out, as needed for secretion.

Alright, so the main cause of cystic fibrosis is a mutation in the CFTR gene, which codes for the CFTR protein. This mutation is inherited with an autosomal recessive pattern, meaning that an individual needs to inherit one mutated gene from each parent to develop the condition. Thus, the main risk factor for cystic fibrosis is family history. In addition, another risk factor seems to be race and ethnicity, being more prevalent among individuals of white race. 

Now, the pathology of cystic fibrosis develops because the mutated CFTR protein can’t insert into the cell membrane. As a result, exocrine cells can’t pump chloride ions out, so water doesn’t get drawn in, and the secretions are left overly thick. This can affect various organs in different ways. 

In the respiratory tract, the thick mucus traps pathogens but can’t be swept up and out by cilia. As a consequence, these pathogens are able to remain in the lungs and keep repli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adaptive_immune_response:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s8oE7vYUQXOsh0Xezm6EjQX9RxCak-gt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immune response - Adaptive: Nursing]]></video:title><video:description><![CDATA[Immunity is the ability of the body to fight pathogens, like viruses, bacteria, and fungi; but, also, foreign substances, like toxins and chemicals. Now, the immune system consists of two main branches: innate immunity and adaptive immunity. Innate immunity is the first line of immunity, that we are born with; it is fast, meaning that it responds within several minutes to hours; it’s non-specific, therefore it does not differentiate one pathogen from another; and finally, it’s short-lived, meaning it does not retain the memory of previous infections. On the flip side, adaptive immunity is the second line of defense, that is acquired throughout life; it is slower and takes time to respond; but it’s also specific, so it recognizes different pathogens; and long-term, so it doesn’t forget a previous exposure to a pathogen.

Now, let&amp;#39;s cover the physiology of the adaptive immune response, which can be further subdivided into active and passive adaptive immunity.

In the active adaptive immune response, antibodies are produced by the client’s own immune system, following exposure to a particular antigen. In this case, two mechanisms can be employed: the humoral response, where antibodies are secreted by B cells; and the cell-mediated response which is carried out by T cells. Both B and T cells are a type of white blood cell called lymphocytes, and they’re produced in the bone marrow. B cells are called “B” cells because they  mature in the bone marrow, while T cells are called “T” cells because they mature in the thymus. 

Now, when mature B cells leave the bone marrow they’re still naive, meaning they haven’t been exposed to an antigen yet; so they usually circulate around in the blood or find their way to the lymph nodes or spleen.  Once they encounter an antigen, they become memory B cells, or plasma cells, which secrete specific antibodies against the antigen. 

Now T cells usually mature and differentiate into either helper T cells, or cytotoxic T ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholelithiasis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7Njfz0EdRW2sUvoqx8SjmNfUQU6-2dRI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholelithiasis: Nursing]]></video:title><video:description><![CDATA[Cholelithiasis refers to the presence of gallstones, or calculi, in the gallbladder as a result of precipitation of bile components, such as cholesterol and bilirubin.

Now, let’s quickly review some anatomy and physiology of the hepatobiliary system, which is made of the liver, gallbladder, and bile ducts. The liver is in charge of producing bile, which is mostly made up of bile salts and acids, cholesterol, phospholipids, proteins, bilirubin and small amounts of various other compounds, like water, electrolytes, and bicarbonate. 

Then, bile flows out of the liver through the hepatic ducts 
towards the gallbladder, where it’s stored. Now, eating fatty foods stimulates the cells in the small intestine to secrete cholecystokinin into the bloodstream. 

Cholecystokinin, in turn, stimulates the gallbladder contraction, causing it to release bile through the cystic duct, then the common bile duct, and ultimately into the duodenum. Once in the duodenum, bile acts as a fat emulsifier, which essentially helps to digest lipids from food into small micelles, making them easier to absorb. 

Now, gallstone formation is caused by precipitation of bile components, such as cholesterol and bilirubin, respectively leading to the formation of cholesterol gallstones and pigment gallstones. 

That being said, the main risk factors for cholesterol gallstones include being assigned female at birth, pregnancy, and oral contraceptive pills are associated with higher estrogen levels, which then increases cholesterol synthesis in the liver. Other common risk factors include obesity and a high cholesterol diet; as well as increasing age, especially after 40. These can be remembered by the 3 Os for stooones, so ovulating, obesity, and older. 

Next, anything affecting the terminal ileum, like Crohn’s disease, or ileal resection, can reduce the reabsorption of bile acids into the circulation and back to the liver, increasing the risk of cholelithiasis. 
In addition, gallbladder stas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Head_injury:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y8zMLaukRf6uOOuV8TKUd5qoQECg1GXI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Head injury: Nursing]]></video:title><video:description><![CDATA[Head injury describes any trauma to the structures and tissues in the head, including the scalp, skull, blood vessels; and when it causes brain damage, it’s called a traumatic brain injury, or TBI for short. 

First, let’s review some anatomy and physiology. The skull has two components: the cranium and facial bones. The cranium is the bony casing that houses and protects the brain. It is lined by the meninges, which are three protective membranes that wrap around the brain and spinal cord. These three layers are the innermost pia mater, the arachnoid mater in the middle, and the outermost dura mater. Between the arachnoid and the pia mater lies the subarachnoid space, which is a thin space filled with cerebrospinal fluid that helps to cushion the brain. So within all these structures, you’d think that the brain should be pretty safe from minor trauma or injuries. 

Alright now, head injuries can be caused by a variety of mechanisms, including contact head injuries, acceleration-deceleration injuries, and penetrating injuries. Contact head injuries occur when a client hits their head on a hard surface, like when falling down the stairs; or receives a violent blow or jolt to the head, such as when getting hit in boxing, or getting tackled in a football game. On the other hand, acceleration-deceleration injuries happen when the brain bounces around inside the cranium, like when a fast moving car hits a tree and stops suddenly. The bouncing of the brain inside the skull causes damage to the brain on the site of impact, called coup injury. In addition, the recoil force directs the brain the other way to strike the opposite side of the skull, resulting in another contusion called contrecoup injury. Lastly, head injuries can be caused by penetrating injuries, such as a knife or gunshot wounds.  

Risk factors for getting a head injury include engaging in high-risk activities like motor racing, rock climbing, sky-diving, or bungee jumping. Additionally, these typ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Toxic_shock_syndrome_(TSS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A58dFgicTpOiinMik4q5W44LSPeZt7HY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Toxic shock syndrome (TSS): Nursing]]></video:title><video:description><![CDATA[Toxic shock syndrome, or TSS, is an acute condition caused by a bacterial infection. TSS can be life threatening, as it involves multiple organ systems. 

TSS is caused by the immune response to bacterial toxins produced by Staphylococcus aureus or Group A Streptococcus species, like Streptococcus pyogenes.

The most widely recognized risk factor for developing TSS is improper use of tampons during menstruation, but some contraceptive methods, such as a sponge or diaphragm, can also pose a risk. However, TSS can also present in other settings such as soft tissue infections, post-surgical infections, burns, or retained foreign objects such as nasal packing and dialysis catheters. 

Now, let’s look at the pathophysiology of TSS. For example, TSS can happen when a tampon or a contraceptive device is left in the vagina for too long. 

During menstruation, menstrual blood accumulates and provides a good medium for the bacteria to grow on. 

Both Staphylococcus aureus and Streptococcus pyogenes produce exotoxins that are able to cross the vaginal mucosa through a mucosal break or via the uterus and enter the bloodstream. 

For Staphylococcus aureus, the main culprit is called toxic shock syndrome toxin 1, or TSST 1 for short. That should be easy to remember! Streptococcus pyogenes, on the other hand, has an M protein in its structure that can overstimulate the immune system, causing TSS. 

Alternatively, bacteria can also grow in infected tissues such as wounds or burns, and from there, they enter the bloodstream. 

Once in the bloodstream, these toxins over activate some immune cells called T cells, which further leads to the overactivation of cytokines and inflammatory cells. 

The end result of this is a massive systemic inflammatory response, which can cause capillary leakage, meaning fluid leaks out of the capillaries as well as severe end-organ failure, including liver dysfunction and renal failure, as well as acute respiratory distress syndrome and impair]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nephrotic_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fZEwisN9TxiHaZBjP50TJfAjS6m-Q8Xz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nephrotic syndrome: Nursing]]></video:title><video:description><![CDATA[Nephrotic syndrome is a disorder  characterized by a constellation of signs and symptoms caused by conditions that affect the tiny glomeruli in the kidneys, resulting in excessive loss of protein through urine, called proteinuria. 

First, let’s quickly review some kidney physiology! Remember that the nephron is the functional unit of the kidney, and its role is to filter waste products and water from the blood. Each nephron is made up of a renal corpuscle and a set of renal tubules, which are, in order: the proximal convoluted tubule, the loop of Henle, the distal convoluted tubule and finally, the collecting ducts which drain urine into the renal papillae and eventually empty into the renal pelvis. The renal corpuscle is made up of the glomerulus, which is a bundle of capillary loops, and Bowman’s capsule, which surrounds the glomerulus. Now, blood enters the glomerulus through the afferent arteriole, then inside the glomerulus, glomerular filtration occurs. Then, the remaining blood exits the glomerulus through the efferent arteriole. The glomerular capillary wall is a semi-permeable membrane with three layers: the endothelium, which is the inner layer; the basement membrane; and the epithelium, which is the outermost layer. For filtration to occur, the endothelial and epithelial cells that line the capillary wall are separated by small pores that filter water and small particles from the blood and into the Bowman capsule. Only small particles are filtered from the blood and never proteins, since they are larger molecules. Also, normally, there aren’t any red blood cells in the urine. For glomerular filtration to occur, the hydrostatic pressure created by the blood pressure needs to be greater than opposing forces, such as the tubular filtrate and oncotic pressure, which is the pressure of proteins. The final product of filtration is called filtrate or primary urine, which will flow through the Bowman capsule into the proximal convoluted tubule. 

Ok, n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Laryngeal_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3mWZRK1LRqqXA7I7A41HmKQNQI_idfMn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Laryngeal cancer: Nursing]]></video:title><video:description><![CDATA[Laryngeal cancer is a malignant tumor that originates from the larynx, which is the part of the throat used for swallowing and talking. 

First, let’s quickly review the anatomy and physiology of the larynx, which is located in the upper portion of the neck between the pharynx and the trachea. Now, the larynx can be divided into three main parts. The upper part, or the supraglottis, is located below the base of the tongue and includes the epiglottis, which closes off during swallowing, preventing food and liquids from entering the airway. 

Next is the middle part, or glottis, which contains the vocal cords. When these are closed, air pressure builds up below them, causing them to vibrate and produce sound when we speak. Finally, the lower part, or subglottis, extends between the vocal cords and the start of the trachea. 

Now, the larynx is lined with a stratified squamous epithelium which then transitions into a pseudostratified ciliated columnar epithelium. This contains goblet cells, which produce mucus to trap small foreign particles; as well as columnar cells, which have cilia, or tiny little hair-like projections that move mucus up the respiratory tract so it can be coughed out.

All right, now, laryngeal cancer occurs when any of these epithelial cells acquire mutations, which can arise due to a variety of risk factors. Modifiable risk factors include exposure to irritants, such as tobacco smoke, alcohol, asbestos, coal dust, and ionizing radiation. Other modifiable risk factors include obesity, infection with human papillomavirus, or HPV, as well as a history of gastrointestinal reflux disease, where acid from the stomach goes all the way up the esophagus into the pharynx. From there, the acid can contact and irritate the larynx. As for non-modifiable factors, few clients with a family history of laryngeal cancer are genetically predisposed to develop this type of cancer even without the presence of environmental risk factors.

So, chronic ex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pleural_effusion:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-a_hJ7EcS-evt51H9qorP3isR86XEbXl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pleural effusion: Nursing]]></video:title><video:description><![CDATA[Pleural effusion is a condition in which excess fluid accumulates in the space between the visceral layer and parietal layer of the pleura, called the pleural space. 

Normally, this space contains 20 to 25 milliliters of fluid that provides lubrication, allowing the two pleural layers to slide over each other during breathing. This pleural fluid forms as a filtrate from pleural blood vessels. At the same time, it is drained into the lymphatic vessels, and this allows for regular renewal of the fluid.

Now, pleural effusion is typically caused by increased production or impaired drainage of the pleural fluid. Depending on the cause, the excess fluid in pleural effusion can be protein-poor, called transudate, or protein-rich, called exudate. 

Transudate, also called hydrothorax when it involves the pleural space, forms when too much fluid starts to move from the pulmonary capillaries into the pleural space, either because of increased hydrostatic pressure or decreased oncotic pressure within the pulmonary capillaries. So increased hydrostatic pressure occurs usually in the context of heart failure, where the heart can’t pump blood effectively, so it backs up into the pulmonary vessels, leading to pulmonary hypertension; ultimately, the high pressure forces fluid out of the pulmonary capillaries and into the pleural space. On the other hand, decreased oncotic pressure can be caused by cirrhosis, which leads to decreased hepatic production of plasma proteins like albumin; or nephrotic syndrome, where renal filtration of blood is impaired, so the proteins are lost in urine. 

On the other hand, exudate forms when there’s increased permeability of the pulmonary capillaries, which allows fluid, immune cells, and large proteins, along with lactate dehydrogenase or LDH,  to leak out of the capillaries and into the pleural space. This can be caused by trauma, malignancy, such as lung cancer, inflammatory conditions like pancreatitis, and systemic lupus erythematos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypopituitarism:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cXeGNtxrRASPcYvn7ZaW7Ep7R_u8iFvI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypopituitarism: Nursing]]></video:title><video:description><![CDATA[With hypopituitarism, hypo- means low and pituritism refers to the pituitary gland. So hypopituitarism describes an excessive decrease or absence of the pituitary hormones. Now, hypopituitarism comes in two flavors: selective hypopituitarism, meaning only one pituitary hormone is deficient, and this is the more common scenario; and panhypopituitarism, a rare situation when all pituitary hormones are deficient, which can be life threatening.

Now, the pituitary is a small, pea-sized gland at the base of the brain.  Specifically, the pituitary gland sits in the sella turcica, a small bony cavity in the sphenoid bone. This is really just a fancy way to say “behind the nose!” Above the pituitary gland, there’s the optic chiasm, and laterally, there are the cavernous sinuses.   Now, let’s quickly review some anatomy and physiology.

The pituitary gland is made up of an anterior lobe and posterior lobe. The anterior lobe, also called the adenohypophysis, contains endocrine cells that produce tropic hormones, which in turn control the secretion of hormones from other endocrine glands or influence a response in target tissues. These include thyroid stimulating hormone, or TSH; adrenocorticotropic hormone, or ACTH; growth hormone, or GH; the gonadotropins, namely follicle stimulating hormone, or FSH, and luteinizing hormone, or LH; prolactin. Additionally, a smart part of the pituitary gland that can be considered part of the anterior lobe secretes melanocyte stimulating hormone, or MSH. 

So for the anterior lobe, TSH stimulates thyroid hormone production, which, in turn, increases the basal metabolic rate in all cells. Next, ACTH stimulates adrenal cortisol production, which, in turn, has plenty of effects around the body, such as regulating glucose metabolism, blood pressure, and electrolyte balance, and immunity. 

Then there’s GH, which stimulates the growth and development of various body tissues, and it also causes release of insulin like growth factor 1 or ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polycystic_kidney_disease_(PKD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Mk4FvrT3QrOAwcDy4jA4IxmLTeuOsGGO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polycystic kidney disease (PKD): Nursing]]></video:title><video:description><![CDATA[With polycystic kidney disease, poly- means multiple and cystic refers to fluid-filled sacs. So, polycystic kidney disease describes a condition in which fluid-filled sacs form in the kidney. There are three types of polycystic kidney disease: infantile polycystic disease, which appears in infancy or childhood; adult polycystic disease, which appears in adulthood; these first two conditions are inherited. The third type is not inherited, and is therefore called acquired polycystic disease.

First, let’s quickly review the anatomy and physiology of the kidneys. These organs are made up of an outer cortex and an inner medulla. The cortical tissue extends towards the medulla, forming renal columns that divide the medulla into pyramidal-shaped structures called the renal pyramids. Now, the cortex and the medulla house the functional units of the kidney, called the nephrons, which filter the blood and create urine. 

This urine drains from the tips of renal pyramids to the minor calyces, which then drain into the major calyces. The major calyces then merge to form the renal pelvis, which drains urine into the ureters. The two ureters carry urine to the urinary bladder, which is a pelvic organ that stores urine. 

During urination, urine passes from the bladder to the urethra and to the outside of the body. The kidneys can also produce hormones, such as renin and erythropoietin. Renin raises blood pressure when it falls below normal, while erythropoietin stimulates red blood cell production from the bone marrow. 

Now, the causes of polycystic kidney disease depends on the type of disease. Infantile polycystic disease is caused by a mutation of the polycystic kidney and hepatic disease gene, or PKHD1 gene for short. This type is inherited in an autosomal recessive pattern, meaning that the individual needs to receive one gene mutation from each parent to have the disease, so it’s also known as autosomal recessive polycystic kidney disease, or ARPKD. 

On the oth]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rupture_of_diaphragm:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/od_2nbk2SpWRSJI38olIp-k5QI6mMtvF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rupture of diaphragm: Nursing]]></video:title><video:description><![CDATA[Diaphragm rupture refers to tears of the diaphragm, mostly caused by blunt or penetrating trauma to the abdomen. 

Now, let’s quickly recap the anatomy and physiology of the diaphragm, which is a dome-shaped sheet of skeletal muscle that divides the thoracic cavity from the abdominal cavity. It curves superiorly into right and left domes, or hemidiaphragms, with the liver lying just beneath the right dome. It has a mobile, central portion known as the central tendon and a peripheral muscular portion that is fixed to the bones, cartilages, and ligaments of the thoracic cage. 

Now, the diaphragm is the chief muscle for inspiration; meaning that when it contracts, it helps us breathe in. During contraction, the central portion of the diaphragm depresses, increasing the volume of the thoracic cavity, which, in turn, increases the volume in the lungs. This makes the intrapulmonary pressure fall below the atmospheric pressure, creating a partial vacuum that allows fresh air to be sucked in!  The diaphragm also helps with circulation. During contraction, the increased intra-abdominal pressure and decreased intrathoracic pressure help with the venous return of blood towards the heart through the inferior vena cava.

Now, the most common cause of diaphragm rupture is penetrating injury to the thorax or the abdomen, like a knife or gunshot wound, which can pierce through the diaphragm. 

Less commonly, diaphragm rupture can be caused by blunt abdominal trauma, such as a motor vehicle crash, which causes a sudden increase in intra-abdominal pressure, causing the diaphragm to rupture. This rupture is far more common on the left hemidiaphragm compared to the right hemidiaphragm, which is protected by the liver.

Okay, let’s look at what happens when there’s a tear in the diaphragm. First, abdominal organs, like the stomach or bowel, may herniate or pass through the diaphragm tear.  These abdominal organs increase the intrathoracic pressure and push against the lung, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cutaneous_fungal_infections:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hOF1CfiyS36sQh-qYPA4Xe18SCOkO27h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cutaneous fungal infections: Nursing]]></video:title><video:description><![CDATA[Cutaneous fungal infections, also known as mycoses, are common and superficial infections caused by fungi invading the skin and its appendages, which include the hair, scalp, and nails. 

Now, let’s review some physiology. Normally, the skin surface is colonized by a huge number of microorganisms that make up the normal skin flora. This flora has a healthy balance that consists mostly of bacteria, such as Staphylococcus epidermidis, as well as low amounts of certain fungi, such as Candida albicans, Malassezia, and dermatophytes like Trichophyton. These microorganisms are typically non-pathogenic, meaning that they don’t cause any disease. In fact, they are beneficial, since they serve as a physical and competitive barrier that helps prevent pathogenic microorganisms from invading and infecting the skin.

Okay, so cutaneous fungal infections are typically caused by a disruption of the healthy balance of the skin flora. Now, clients can develop different infections based on the causative fungus. The most common ones include candidiasis, which is caused by an overgrowth of Candida albicans; as well as tinea or pityriasis versicolor, which is caused by Malassezia furfur; and tinea infections, which are caused by a variety of dermatophyte fungi. 

Risk factors of fungal infections include medications like antibiotics or glucocorticoids, poor personal hygiene, as well as warm and humid environments, in addition to close contact with animals, such as dogs, cats, cows, and goats. Additional risk factors include obesity, diabetes mellitus, and being immunocompromised; as well as high estrogen levels due to oral contraceptive use, estrogen therapy, or pregnancy. 

So, cutaneous fungal infections occur when the healthy balance of the skin flora gets disrupted, which may allow the fungi in the skin to overgrow. In most cases, a healthy immune system is able to notice and stop this, keeping the fungi under control. However, in some cases, fungi manage to persist, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_edema:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y4wzZcY6THirIRS0VnP4KXYnTumN08_u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary edema: Nursing]]></video:title><video:description><![CDATA[Pulmonary edema refers to the buildup of fluid in the lungs; and this can be further classified as cardiogenic pulmonary edema, which occurs as a result of heart disease; and noncardiogenic pulmonary edema, which usually occurs in the presence of damaged pulmonary capillaries.

To understand pulmonary edema, first, let’s quickly review the lower respiratory tract, which includes the lower part of the trachea, and the lungs containing the bronchi, bronchioles, alveolar ducts, and finally the alveoli. Alveoli are tiny air-filled sacs that are surrounded by tiny blood vessels, called capillaries. 

Zooming in even more, we can see a tiny space between the alveolar wall and the capillary wall, called the interstitial space, which normally contains a small amount of interstitial fluid. And that’s where most gas exchange occurs. 

So, each time we breathe in, the inhaled oxygen moves through the alveolar membrane, the interstitial space, and then through the capillary membrane to reach the blood, which is brought back through the pulmonary veins into the left heart and further into the systemic circulation. 

On the other hand, carbon dioxide is carried from the right heart, through pulmonary arteries, into the lungs, where it diffuses  from the capillaries through the interstitial space and into the alveoli, and then gets breathed out.

Now, cardiogenic pulmonary edema is caused by inadequate pumping of the heart, which usually occurs because of left-sided heart failure, ventricular arrhythmias, myocarditis, myocardial infarction, or valvular disorders, as well as severe hypertension and cardiomyopathy. 

On the flip side, noncardiogenic pulmonary edema can be caused by damage to the lungs, which can occur because of pulmonary infections; acute respiratory distress syndrome, or ARDS for short; sepsis; pneumonia; as well as inhalation of toxic substances or aspiration of gastric contents. Other important conditions associated with noncardiogenic pulmonary edema ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia_-_Aplastic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zimg3JRZSX639ukV9gfENfoGR9KW5Sg7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia - Aplastic: Nursing]]></video:title><video:description><![CDATA[Aplastic anemia is a condition characterized by pancytopenia, meaning decreased production of all blood cell lines, so red and white blood cells, as well as platelets. This condition can be inherited, when it occurs because of genetic mutations, as well as acquired, when it occurs because of external factors.

Let’s start by looking at the physiology of blood cell production, or hematopoiesis. This process starts in the bone marrow, which is the innermost portion of bone, where hematopoietic stem cells reside. These serve as progenitor cells for all the different cell types found in the blood, including white blood cells, which primarily function as the defense mechanism against infections; as well as red blood cells, which are essential to carry oxygen to the tissues; and platelets, which play a key role in blood clotting. 

Now, hematopoietic stem cells reach their final, mature form, when they receive the appropriate signals in the form of specific growth factors or stimulating factors. One of these growth factors is called erythropoietin, or EPO. This is a hormone released by the kidneys, that tells hematopoietic stem cells to differentiate into red blood cells. Another important factor is the granulocyte colony-stimulating factor, or G-CSF, which is produced by various cells and tissues, including the bone marrow itself, and it stimulates the production of a specific group of white blood cells called neutrophils. Finally, there’s thrombopoietin, a hormone produced by the liver and kidneys, which stimulates platelet production.

Alright, now the causes of aplastic anemia can be inherited or acquired. The most common cause of inherited aplastic anemia is Fanconi’s anemia, a rare genetic disorder characterized by progressive bone marrow failure. 

On the other hand, acquired causes of aplastic anemia include any other factor that leads to suppression or destruction of the bone marrow, including other conditions like an autoimmune disease, or undergo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Biliary_atresia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2wEZ4HAnQbOuuY-h07Q00y-6S5q6E0Ja/_.jpg</video:thumbnail_loc><video:title><![CDATA[Biliary atresia: Nursing]]></video:title><video:description><![CDATA[Biliary atresia refers to the  obstruction or total absence of bile ducts, which results in an impaired bile flow from the liver into the gallbladder and small intestine. 

Let’s start with some basic anatomy and physiology of the liver and gallbladder. Liver cells produce bile, which helps digest fats in the intestines. 

The bile flows from the liver into the right and left hepatic ducts which merge to form the common hepatic duct. The common hepatic duct is where the cystic duct opens. The cystic duct functions like a two way street, allowing the passage of bile from the liver to the gallbladder, where it’s stored in between meals; while at the same time allowing bile to pass from the gallbladder, into the common bile duct, which is the part of the bile duct below the opening of the cystic duct. 

Remember that the gallbladder, is a pear-shaped hollow organ found beneath the liver that stores and concentrates the bile. 

So, after a high-fat meal, the gallbladder contracts and pushes the bile through the cystic duct, down the common bile duct, and into the duodenum, to help with digestion. 

Afterwards, some of the bile is excreted through feces, giving them their characteristic color, while some is reabsorbed into the blood and then eliminated through urine. 

Now, the exact cause of the biliary atresia is still unknown. Some theories suggest that genetic mutations can result in the abnormal fetal development of the biliary system; while others propose that biliary atresia results from some sort of inflammation of the bile ducts. The ultimate cause of this inflammation is not fully known, but it’s thought to occur because of perinatal exposure to viruses or toxic substances. This inflammation causes destruction of the bile ducts, eventually impairing bile flow from the liver. 

No matter what the cause is, important risk factors that have been associated with biliary atresia include being assigned female at birth, as well as black or Asian race. 

Next]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Schizophrenia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KiMdgWdnTu_1KSfVJ6uP886eQPi7M4HH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Schizophrenia: Nursing]]></video:title><video:description><![CDATA[Schizophrenia is a psychiatric condition caused by imbalanced dopamine levels in the brain.  It’s characterized by disturbances in perception, thinking, behavior, and emotions. 

Alright, now let’s cover some basics of brain anatomy and physiology. Neurons communicate with each other through neurotransmitters.

Some, like glutamate, are excitatory neurotransmitters, meaning they cause neurons to fire. Some, like GABA, are inhibitory neurotransmitters and prevent a neuron from firing.

Finally, there are some like dopamine that could be excitatory or inhibitory depending on what neurons they act upon.

Dopamine is a neurotransmitter that’s primarily found in 4 main dopaminergic pathways of the brain; the mesolimbic pathway, which controls motivation and desire; the mesocortical pathway, which helps regulate emotions; the nigrostriatal pathway, which helps control voluntary movements; and lastly, the tuberoinfundibular pathway, which releases dopamine to limit the secretion of prolactin.

Now, the exact cause why schizophrenia occurs is still not fully understood; but, some theories suggest that it’s due to a combination of neurotransmitter imbalances in the brain, and anatomical brain changes due to  genetic and environmental factors during early brain development. 

Now, the main risk factors for developing schizophrenia include genetic predisposition, having a family history of schizophrenia; perinatal complications like infections, hypoxia, living in urban areas; as well as exposure to toxins; and the use of substances, especially cannabis, LSD, and methamphetamines.

Now, the mechanisms underlying the pathology of schizophrenia are poorly understood, but there seems to be abnormal levels of dopamine, particularly in the mesolimbic and mesocortical pathways. So, high levels of dopamine in the mesolimbic pathway result in positive symptoms, while low levels of dopamine in the mesocortical pathway cause negative symptoms.

Another contributor to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypersensitivity_reactions_-_Type_III:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hnIaGznBSYCzu-nKHxYXEmT3QYmBZR8a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypersensitivity reactions - Type III: Nursing]]></video:title><video:description><![CDATA[A hypersensitivity reaction is an overreaction to a foreign antigen which then causes serious damage to the body’s tissues. There are four types of hypersensitivity reactions: type I is immunoglobulin E, or IgE mediated; type II is mediated by antibodies that activate cellular cytotoxicity, type III is mediated by immune-complexes, and type IV is a delayed T cell-mediated hypersensitivity reaction. A type III hypersensitivity reaction occurs when antibodies attach to soluble antigens and form antibody-antigen complexes that float around the blood vessel, causing tissue damage depending on where they end up.

Let’s start by discussing the physiology of the humoral immune response. The humoral immune response is the part of the immune system that provides protection against invading pathogens by utilizing antibodies designed to specifically target certain antigens. It all begins in the bone marrow, where undifferentiated hematopoietic stem cells differentiate into various types of  white blood cells, including and T lymphocytes, or B and T cells, for short.

When a pathogen, like a bacteria or virus enters the body, it runs into antigen-presenting cells, or APCs. APCs like macrophages or dendritic cells, then engulf and digest the pathogen, and the fragments are then presented on the APC’s surface via proteins called major histocompatibility complex class II, or MHC II. Now these fragments serve as antigens that can trigger an immune response.  So the APCs present these antigens to T helper cells which have T-cell receptors, or TCRs, that recognize the antigen. 

These T helper cells go on to activate specific B cells which causes them to transform into plasma cells that could produce antibodies against the specific antigen. 

Antibodies called IgM and IgG are produced and they can attach to the antigens on the bacteria or virus, creating an antigen-antibody complex.  Next, the complement system activates, which is a group of different proteins named C1 thro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testicular_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yMEu8kcoTIGCIbvPiJap8mYKSO_kHVH4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Testicular cancer: Nursing]]></video:title><video:description><![CDATA[Testicular cancer is a rare form of cancer that can affect one or both testicles or testes. However, when it occurs, it’s usually in individuals assigned male at birth that are between 15 to 44 years old.

Let’s start with some anatomy and physiology. The testes are a pair of reproductive organs located inside the scrotum that hangs under the base of the penis, and are mainly responsible for producing testosterone and sperm cells. On a cross-section, each testicle has septa that partition it into lobules. Each lobule contains up to four seminiferous tubules, where sperm is synthesized from germ cells. These seminiferous tubules are lined up by specialized epithelial cells that contain Sertoli cells which envelopes and supplies nutrients to developing spermatocytes. Outside the tubules are Leydig cells, which produce and release testosterone.

Although the exact cause behind testicular cancer is unknown, there are risk factors that can contribute to the development of testicular cancer. Such risk factors include Klinefelter syndrome; cryptorchidism, which means undescended testes; hypospadias, which is when the  urethra opens underneath the tip of the penis; as well as having a past history of testicular anomalies, cancer, or radiation in the genital area; having HIV or AIDS;  frequent marijuana use; and maternal exposure to pesticides or exogenous estrogen during pregnancy. 

Now, when it comes to pathology, testicular tumors occur when cells in the testicle start to divide uncontrollably, and the end result is either a benign or a malignant tumor. Malignant tumor cells can spread to nearby tissue and even to other organs via the bloodstream or lymphatic system.  The most common type of metastases are to the abdominal lymph nodes; but distant metastases to the lungs, liver, bones and brain can also occur. Now, based on the type of testicular cells that are involved, testicular cancers are broadly classified into two groups. First, there are germ cell tumor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cataracts:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rr-2c0nySP_xicuYpczlOe1YRb6jFoXd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cataracts: Nursing]]></video:title><video:description><![CDATA[Cataracts refer to an eye condition in which the normal transparent eye lens becomes cloudy. This distorts the image projected onto the retina and causes cloudy vision.

Okay now, let’s go over some physiology. Normally, the lens is a transparent biconvex structure that lies behind the iris, dividing the anterior and posterior segments of the eye. The lens is held in place by the ciliary processes, which are tiny projections from a structure called the ciliary body. The ciliary body also controls the degree to which the lens becomes flatter or rounder. And this in turn bends the light entering the eye to focus images onto the retina. If we zoom into the lens, we’ll see that it’s composed of three layers: the capsule, cortex, and nucleus. The nucleus is made up of concentric layers of transparent proteins called crystallins. 

Now, cataracts are caused by the opacification or clouding of the lens. When this occurs at birth, it&amp;#39;s called congenital cataracts. So, risk factors for congenital cataracts include congenital infections, such as toxoplasmosis and rubella, as well as genetic conditions, such as trisomy 13, which causes Down syndrome, Wilson’s disease, in which extra copper is stored in the body tissues, and myotonic dystrophy, which is characterized by progressive muscle weakness and loss.  Other risk factors for congenital cataracts include inborn errors of metabolism, like galactosemia, which is a hereditary condition that impairs the conversion of galactose to glucose in newborns.

Now, cataracts can also develop later in life, in which case it&amp;#39;s acquired. Acquired cataracts are often associated with advanced age, usually above 60, smoking, excessive alcohol use, penetrating eye trauma, and infections. Other risk factors for acquired cataracts include exposure to UV light, prolonged use of medications like glucocorticoids, and diabetes mellitus.

Regardless of the cause, the pathological outcome is a change in the structure and c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preeclampsia_&amp;_eclampsia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ofTJh65CTyKyVD6zh5bVR_N1RzKJPYR1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preeclampsia and eclampsia: Nursing]]></video:title><video:description><![CDATA[Preeclampsia is a pregnancy-specific condition characterized by new-onset hypertension and proteinuria after 20 weeks of gestation or during the postpartum period in a previously normotensive client; while eclampsia is when a client with preeclampsia develops generalized seizures. These two conditions differ from gestational hypertension, which simply refers to new onset of hypertension during pregnancy, without proteinuria or seizures.

Now, let’s quickly review the physiology of blood pressure regulation during pregnancy. There are three key factors to keep in mind: cardiac output, which is the amount of blood that the heart pumps out to the systemic circulation in a minute; intravascular volume, which is the amount of blood in the client’s circulation; and peripheral vascular resistance, which is the resistance of blood flow in peripheral arteries, and is regulated via vasoconstriction or vasodilation as needed. 
Remember that in pregnant clients, the cardiac output and intravascular volume increase, but the peripheral vascular resistance decreases. 

That’s because during pregnancy, there’s a relative decrease in the response to vasoconstrictor molecules, like angiotensin II, and there are also higher levels of vasodilator molecules, like prostacyclin PGI2. As a result, blood vessels dilate more to accommodate the increased blood volume, and this keeps blood pressure in the normal range, below 120 over 80 mmHg.

This increased blood volume can come in pretty handy, especially since the placenta needs a lot of blood. Remember that the placenta is a temporary organ that develops in the uterus during pregnancy, and connects the pregnant client with the fetus. The way this works is that a type of endometrial arteries called the spiral arteries dilate during pregnancy, and open into the placenta to form little pools of blood. On the fetal end, the umbilical vein connects to the placenta and also opens into those pools. This way the umbilical vein can get nu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bell_palsy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mxB-a9vaSJ_nzfn8w0rICm4pR82f_9mY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bell palsy: Nursing]]></video:title><video:description><![CDATA[Bell palsy is a condition characterized by weakness or paralysis of the muscles on one side of the face, that’s caused by damage to cranial nerve VII, which is the facial nerve. 

Now, let’s quickly review the anatomy and physiology of facial innervation. The 12 pairs of cranial nerves are peripheral nerves, also called lower motor neurons, that emerge from the brain or brainstem. The seventh cranial nerve is the facial nerve, which emerges from the brainstem, 

and then enters the temporal bone where it travels through the facial canal. The facial nerve then exits the skull through a tiny hole called the stylomastoid foramen. 

From there, it branches off to innervate different facial muscles that control facial expression ipsilaterally, so on the same side. The facial nerve also innervates the lacrimal glands, as well as the sublingual gland and submandibular salivary glands, and the mucous membranes of the nose, mouth, and nasopharynx. In addition, the facial nerve also carries sensory information about taste from the anterior ⅔ of the tongue. Finally, the facial nerve innervates the stapedius muscle in the ear, which helps dampen loud noises. 

If we look back, the facial nerve receives information from a region of the brain called the motor cortex, which has upper motor neurons that send information to the brainstem nuclei of the facial nerve, and then the facial nerve gives rise to two lower motor neurons, one to innervate the lower side of the face, and one for the upper side. Now, the lower motor neuron that innervates the upper side of the face receives information from both sides of the motor cortex, so both from an upper motor neuron coming from the ipsilateral side, as well as an upper motor neuron coming from the contralateral or opposite side that crosses in the midline. On the other hand, the lower motor neuron that innervates the lower side of the face only receives information from the contralateral motor cortex, so from an upper motor neu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Paget_disease_of_bone:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7Re8f9KCQBCaTMZbs_u9cooMSeC2LfYS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Paget disease of bone: Nursing]]></video:title><video:description><![CDATA[Paget disease of bone is a disorder in which there’s a lot of bone remodeling that happens in some regions of the bone. Typically, there’s excessive bone resorption followed by disorganized and excessive bone growth, leading to skeletal deformities, fragile bones, and potential fractures. Paget disease of bone can affect a single bone or several bones, and most often, it involves the skull, spine, pelvis, arms, and legs.

Now, let’s quickly review the physiology of bones.Normally, the surface of the bones is covered by a dense layer of connective tissue called the periosteum, and it&amp;#39;s where the muscles, tendons, and ligaments are attached.  

Beneath the periosteum, there’s a dense and tough external layer called compact bone or cortical bone composed of collagen and hydroxyapatite which contains calcium and phosphate. 

In the center of the bone, there’s the medullary canal, a hollow space lined by a honeycomb- looking structure called the spongy or cancellous bone. The spaces in the spongy bone are occupied by the bone marrow, which is the site of blood cell production.

At first glance, a bone may appear inert and unchanging, but it’s actually a very dynamic tissue. In general, a bone is replaced with new cells every three to ten years in a process called bone remodeling, which has two steps: bone resorption, when specialized cells called osteoclasts break down bone, and bone formation, which is when another type of cells called osteoblasts form new bone. 

The exact cause of Paget disease of bone is unclear, with some theories suggesting that it can get triggered by infections like the measles virus, and is linked to genetic mutations. 
Risk factors include being assigned male at birth, age over 40, family history of Paget disease, Caucasian race, or northern European descent. 

The pathology of Paget disease has three phases, called lytic, mixed, and sclerotic phases. Phase one is the lytic phase, and that’s where osteoclasts increa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thalassemia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HvIEG1_LQ6evf-2Q0cUgSdYaT-ifSuc0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thalassemia: Nursing]]></video:title><video:description><![CDATA[Thalassemia refers to a set of genetic disorders characterized by mutations in the hemoglobin gene. This impairs the function and number of red blood cells, ultimately causing anemia. There are two primary types of thalassemia: alpha thalassemia and beta thalassemia, both of which can have minor or major versions.

Now, let’s quickly review the physiology of red blood cells and hemoglobin. Red blood cells, or RBCs are small, round cells that are responsible for delivering oxygen and removing carbon dioxide throughout the body. They are produced in the bone marrow, in a process called erythropoiesis; then, they move around the blood for about 120 days and finally, they are destroyed by the spleen, in a process called hemolysis. 

Now, inside each RBC, there are millions of hemoglobin molecules. Hemoglobin is a compound protein made up of heme and globin. Specifically, adult hemoglobin is made up of four globin chains, two alpha and two beta, and each of these proteins contains a heme group in the  middle. 

Heme is a ring-shaped structure, and it’s the home of one iron ion that can attach to oxygen. So at the end of the day, it’s hemoglobin that makes it possible for RBCs to perform their main role, which is oxygen transport. Finally, when red blood cells are destroyed, the heme is further broken down in the liver into bilirubin, which is subsequently excreted, while the iron is stored in the liver for future use. 

Now, thalassemias are caused by an inherited DNA mutation in the genes that code for the hemoglobin alpha or beta subunits. So, clients at higher risk of thalassemia include those with a positive family history; as well as people from ethnic groups with a higher prevalence of thalassemia, like those originating from the area around the Mediterranean sea,  the Middle East, India, Pakistan and Africa. Now, pathology-wise, thalassemia starts with a genetic mutation in the genes for the alpha or beta globins, that’s inherited in an autosomal recessi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_insufficiency_(Addison_disease):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jnFjhxl4Tmiitnnx722huvtYTqiAhPol/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenal insufficiency (Addison disease): Nursing]]></video:title><video:description><![CDATA[Adrenal insufficiency is an endocrine disorder that happens when the adrenal gland doesn’t produce enough hormones, particularly mineralocorticoids like aldosterone, glucocorticoids like cortisol, and androgens like testosterone. It’s called “primary” when the underlying problem is localized to the adrenal gland itself, which can develop either acutely or chronically, and the chronic form is also known as Addison disease. On the other hand, it’s called “secondary” when the pituitary gland doesn’t stimulate the adrenals enough to ensure adequate cortisol production.

Now, let’s quickly review the anatomy and physiology of the adrenal glands. There are two adrenal glands, one above each kidney, and each one has an inner layer called the medulla and an outer layer called the cortex. Zooming in, the cortex is further subdivided into three more layers, namely the zona glomerulosa, zona fasciculata, and the zona reticularis. And each of their functions can be easily remembered by thinking of the mnemonic Salt, Sugar, and Sex. 

So, the outermost layer is the zona glomerulosa, which secretes aldosterone. Aldosterone is part of a hormone system called the renin-angiotensin-aldosterone system. Together, these hormones decrease potassium levels, increase sodium levels, and increase blood volume and blood pressure. 

The middle layer is the zona fasciculata, and the cells there make the hormone cortisol as well as other glucocorticoids. The hypothalamus, which is an almond-size structure which sits at the base of the brain, releases corticotropin-releasing hormone, or CRH for short, which acts on the pituitary gland, a pea-sized structure sitting just underneath the hypothalamus. In response, the pituitary gland sends out adrenocorticotropic hormone, or ACTH for short, which stimulates the zona fasciculata to secrete more cortisol. 

Now, cortisol is involved in a number of things such as maintaining glucose levels, blood pressure, suppression of the inflammatory and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hearing_impairment_&amp;_otosclerosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5FZpdqkQRQOEJtq4ETCp2kzeS5agH0bO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hearing impairment and otosclerosis: Nursing]]></video:title><video:description><![CDATA[Hearing impairment refers to partial or total loss of hearing. There are three types of hearing loss: conductive hearing loss, which occurs when there’s an obstruction of sound wave transmission; sensorineural hearing loss which occurs when the inner ear or auditory nerve is damaged; and mixed hearing loss which is a combination of the two.  

Let’s start with the normal physiology of hearing. The ear is made up of three parts: the external, middle, and inner ear, all of which help process air vibrations as sound. The main role of the external and middle ear is to transfer and amplify sound, while the inner ear also plays a role in balance. Let’s start with the external ear, which is by far the most common anatomical spot to hang earrings from. The external ear is actually a complex structure made of the auricle, also called the pinna; and the external acoustic meatus. Now, at the end of the external acoustic meatus, there’s the thin, oval tympanic membrane, more commonly known as the eardrum, which separates the external ear from the middle ear. When sound waves hit the tympanic membrane, it vibrates and transfers the vibration to the middle ear. 

The middle ear, also called the tympanic cavity, is a tiny chamber found in the petrous part of the temporal bone, and it houses the three auditory ossicles, called the malleus, incus and stapes, which are the three smallest bones in the body. These ossicles create a chain that connects the tympanic membrane to the oval window to transfer and amplify air vibrations into the inner ear to be processed as sound. Now, the inner ear contains the bony labyrinth, which contains cavities filled with perilymph, and the membranous labyrinth, which is made of sacs and ducts suspended in the bony labyrinth. 

A part of the inner ear called the cochlea contains the sensory cells for hearing. Now, sound waves travel from the air, through the ear canal, and hit the tympanic membrane, causing it to vibrate. The vibrations are ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neutropenia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X7tHW0HjQpyPPvH0k8wVIZzaSOSgUTCd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neutropenia: Nursing]]></video:title><video:description><![CDATA[Neutropenia refers to an abnormally low number of neutrophils in the blood. Normally, neutrophil count ranges from 2500 to 7500 neutrophils per microliter, but with neutropenia, it’s usually less than. 1500 neutrophils per microliter of blood. Remember that neutrophils are a subtype of white blood cells that fight off bacterial and fungal infections, so with neutropenia, individuals are at higher risk of developing these infections. 

Let’s start with some basic physiology of neutrophils. These cells are created in the bone marrow, from hematopoietic stem cells, which give rise to all types of blood cells. Now, once neutrophils are formed, they leave the bone marrow and enter the bloodstream, where they have an important role in the innate immune response against bacterial and fungal pathogens. Specifically, they fight foreign pathogens by phagocytosis, which is a process of ”ingesting” them into the cell. And next, they digest them inside the cell!

Ok, now, neutropenia can be caused by conditions like infections, when neutrophils are used up faster than they can be produced; as well as autoimmune conditions like systemic lupus erythematosus, which is associated with increased neutrophil destruction. Alternatively, neutropenia can occur because of inefficient bone marrow production, which can be seen in hematologic conditions like aplastic anemia or leukemia. Finally, neutropenia can occur  because of an infection that weakens the immune system, such as AIDS; or as a side effect of some medications, including antibiotics like carbapenems and cephalosporins;  and chemotherapeutic agents, which are medications used to treat cancer.

Now, with fewer neutrophils in the blood, the immune system can’t fight infections effectively, and this results in recurrent infections. The most common bacterial infections are caused by Staphylococcal, Streptococcal, and E. coli species, while the most common fungal infection is caused by Candida albicans. Finally, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiomyopathy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NhfSBseZRHuJSGijM_5EXgXKR__tTz16/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiomyopathy: Nursing]]></video:title><video:description><![CDATA[Cardiomyopathies are a group of diseases of the myocardium, which is the muscle layer of the heart wall. The three main types are dilated cardiomyopathy, which is the most common one; as well as hypertrophic, and restrictive cardiomyopathy. 

Now, let’s quickly review some anatomy and physiology. The heart wall is made of three layers: the outer layer is the epicardium; the middle and thickest layer is the myocardium, which contracts in a rhythmic way to pump blood; and the inner layer is the endocardium. These layers line the four heart chambers, so the two atria and two ventricles, which are separated by the heart valves at the end of each chamber. First, there are two atrioventricular valves, the mitral or bicuspid valve on the left, and the tricuspid valve on the right. The atrioventricular valves prevent blood from returning to the atria after filling the ventricles. And second, there are two semilunar valves called the aortic valve at the left, and the pulmonary valve at the right. The semilunar valves prevent blood from returning to the ventricles after being pumped out. 

Okay, when it comes to the causes of dilated cardiomyopathy, there are many potential causes, which include genetic mutations; cardiotoxic agents, such as alcohol, cocaine, lead, as well as chemotherapeutic  medications like doxorubicin and trastuzumab. Dilated cardiomyopathy can also be caused by infections such as human herpesvirus 6, cytomegalovirus, or Lyme disease; nutritional deficiencies, like lack of thiamine; and metabolic disorders, like hyperthyroidism. Sometimes, dilated cardiomyopathy can also be related to pregnancy, called peripartum cardiomyopathy.

Next up is hypertrophic cardiomyopathy, which is most commonly caused by mutations in genes coding for components of the cardiac muscle cells. These mutations are typically inherited in an autosomal dominant fashion. On a side note, it’s important to distinguish hypertrophic cardiomyopathy from “athlete’s heart”, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Secondary_immunodeficiency_disorders:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9xLzzsxwRya6Cpd2KAYVxhRVS76FRm-J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunodeficiency disorders - Secondary: Nursing]]></video:title><video:description><![CDATA[Secondary immunodeficiencies are acquired disorders that occur as a result of some extrinsic factor affecting the immune system. 

Let’s start with some immune system physiology. The immune system consists of white blood cells that protect us from pathogens, like viruses, bacteria, and fungi; but, also, foreign substances, such as toxins and chemicals, and destroy abnormal cells, such as those that might develop into cancer. 

Now, the immune system consists of two main branches: innate immunity and adaptive immunity. The innate immune response involves non-specific defense mechanisms, meaning they don’t differentiate one pathogen from another. These include complement proteins and cells like phagocytes and natural killers; as well as dendritic cells, which activate the adaptive immune response. The adaptive immune response is highly specific, meaning that it recognizes different pathogens and is mediated by cells called lymphocytes, which include T and B cells. 

T cells can be further divided into CD4+ and CD8+ T cells. CD4+ T cells are also known as T helper cells, because they interact with dendritic cells, and in turn help activate the rest of the lymphocytes. On the other hand, CD8+ T cells, also known as cytotoxic T cells, are in charge of cell-mediated immunity, where they attack abnormal cells. Finally, B cells mediate a specific adaptive response, called humoral immunity, by secreting antibodies that bind to and destroy extracellular antigens. These antibodies can be classified into several classes, including IgA, IgG, IgM, and IgE.

Now, there are several causes of  secondary immunodeficiency, including calorie and protein malnutrition; adverse environmental conditions, like UV light, extreme cold, or high altitude; surgery and trauma; and medications, such as glucocorticoids, chemotherapy, and immunosuppressive agents used to treat autoimmune disorders or to prevent organ transplant rejection. 

Additionally, secondary immunodeficiency can be a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypersensitivity_reactions_-_Type_IV:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lh3qqMFVSdCNqB42WbKWbM3BQyCDgt1A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypersensitivity reactions - Type IV: Nursing]]></video:title><video:description><![CDATA[A hypersensitivity reaction is an overreaction to a foreign antigen or against its own tissue which then causes serious damage to the body’s tissues. There are four types of hypersensitivity reactions: type I is immunoglobulin E, or IgE mediated; type II is mediated by antibodies that activate cellular cytotoxicity, type III is mediated by immune-complexes, and type IV is a delayed T cell mediated hypersensitivity reaction.  A “cell mediated reaction” is not dependent on antibodies, which makes it different from the other 3 types. It’s called a delayed reaction because it usually takes 48 to 72 hours to recruit enough T cells and cause the reaction.

Let’s start by discussing the physiology of T cells. T cell precursors originate in the bone marrow but they migrate to the Thymus to mature; which is why they’re called T cells. In the thymus, they differentiate into many different types of T cells; this include T helper cells, and cytotoxic T cells, or killer T cells.  Let’s talk about helper T cells first. 

When a pathogen enters the body,  APCs like macrophages or dendritic cells, then engulf and digest the pathogen and the fragments are then presented on the APC’s surface via proteins called major histocompatibility complex class II, or MHC II. Now these fragments serve as antigens which are any thing that could trigger an immune response.  So the APCs present these antigens to naive T helper cells which have never been exposed to antigens.  The T helper cells will recognize the antigen with their T cell receptors or TCRs, and mature. They will then release cytokines that enhance the immune response.  One of these is interleukin 2 which causes the T cell and other T cells to proliferate.  Other cytokines can attract immune cells like macrophages and neutrophils to the area, and they can also cause the blood vessel walls to become leaky, allowing these additional immune cells to reach the tissue where that pathogen is located.  

Now, another type of T ce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thermoregulation_:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OKseFH98RbaTfhZPy11-18u-T7CT3OVi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thermoregulation : Nursing]]></video:title><video:description><![CDATA[Thermoregulation is the body’s ability to balance between heat gain and heat loss, thus maintaining a stable internal temperature of around 36 to 37.5° C or 96.8 to 99.5° F.  This range is considered normal body temperature but it’s actually the average across the population. Normal body temperature can vary depending on the time of day, age of the individual, activity level, and many other factors. This normal body temperature is maintained by four mechanisms: neural and vascular control; heat production; heat loss; and behavioral control. 

Okay, let’s discuss the physiology of these four mechanisms, starting with neural and vascular control. If we zoom into the brain, there&amp;#39;s a region called hypothalamus. The hypothalamus acts like a thermometer.  It has thermoreceptors that monitor the body’s internal, or core, temperature; and it also receives information about the peripheral temperature from the thermoreceptors in the skin. 

Now, the hypothalamus is also the body’s thermostat, because it controls the internal temperature “set point” and when the core temperature deviates from the set point, the hypothalamus will signal the rest of the body to increase or decrease the body temperature and bring it back to the set point. So, on a hot summer day, the hypothalamus senses the core body temperature is getting too high and responds by initiating mechanisms like sweating and dilating skin blood vessels, resulting in body heat loss. On the flip side, on a cold winter day, the hypothalamus senses that the core body temperature is getting too low, and in turn, activates mechanisms like shivering which generates heat, and vasoconstriction in the skin that prevents heat loss. 

Now normally the set point is 36 to 37.5° C or 96.8 to 99.5 °F;  however, when the person has a fever, the hypothalamus can adjust the thermostat, raising the set point to a higher temperature. The body responds by increasing the core temperature to the new set point, which is he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autoimmunity:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UvUtxV2CS1u_v4JVGr8njQWlR5i4m59r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autoimmunity: Nursing]]></video:title><video:description><![CDATA[Autoimmunity is when the immune system perceives the body’s own cells or proteins as foreign antigens and triggers an immune response resulting in organ damage or systemic inflammation.

Let’s start by looking at how the body would normally prevent autoimmunity. Now, the immune response can be classified as innate and adaptive, and the latter is the main culprit with autoimmunity. See, the adaptive immune system is made up of B and T lymphocytes, also called B and T cells. Each lymphocyte only targets a specific pathogen, so you would have some lymphocytes that will only attack E. coli  and some lymphocytes that only attack the influenza virus. This is called a specific immune response. 

Now, the reason B and T cells can recognize specific pathogens is because each cell has B or T cell receptors that only bind to a specific antigen, and they need to come in contact with one of these antigens in order to activate. Usually, an antigen presenting cell, or an APC, like a macrophage or dendritic cell brings the antigen to the lymphocytes and causes them to activate. This will cause clonal expansion, meaning the activated lymphocyte will quickly proliferate, creating an army of lymphocytes that also targets the same antigen. If the lymphocyte is a B cell, it will start creating antibodies against the antigen. If the lymphocyte is a T helper cell, it can help activate other lymphocytes like B cells, or it could call cells like macrophages and neutrophils to the pathogen to destroy it.      

Now, the B and T cell receptors are generated randomly, but there are so many lymphocytes in the body that it’s likely some will target whatever pathogen enters the body. The downside is this random process inevitably leads to lymphocytes with receptors to self antigens. To ensure these lymphocytes do not attack other healthy cells in the body, there are processes called central and peripheral tolerance. 

In central tolerance, APCs constantly bring different self peptides t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia_-_Macrocytic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W2eOTcQBQECBzkeH-RFKMHOxQG_tUig6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia - Macrocytic: Nursing]]></video:title><video:description><![CDATA[Megaloblastic anemia, also called macrocytic anemia, is a condition where large, structurally abnormal, immature red blood cells, or RBCs, are produced by the bone marrow.

First, let’s look at the physiology of red blood cell production, or erythropoiesis. This process takes place in the bone marrow, where a stem cell differentiates into an erythroblast, which starts synthesizing hemoglobin. This is a protein that’s able to bind and carry oxygen. 

Erythroblasts then lose their nucleus and differentiate into immature RBCs, called reticulocytes. These immature cells are released from the bone marrow into the bloodstream, to ultimately become mature RBCs, called erythrocytes. 

Now, RBCs normally have a limited lifespan, of 120 days, so they require continuous replacement through erythropoiesis. To do so, the body needs important vitamins and minerals, including vitamin B12, also known as cobalamin, and vitamin B9, better known as folic acid or folate; these vitamins are used for the synthesis of DNA, which is essential for cell division and maturation. 

Now, these vitamins are primarily obtained from a balanced diet that includes all types of foods. Once ingested, food passes through the gastrointestinal tract, where nutrients are slowly absorbed. Some nutrients, such as vitamin B12, require a specific carrier protein like intrinsic factor, which is produced by gastric parietal cells, to be absorbed into the circulation.

Alright, so megaloblastic anemia is most often caused by a deficiency in vitamin B12 or folate. Now, vitamin B12 deficiency can be caused by impaired gastrointestinal absorption or decreased dietary intake. Impaired absorption may have a number of risk factors, including medications that interfere with absorption such as proton pump inhibitors, H2 receptor blockers, or metformin; a lack of intrinsic factor, which could be caused by gastrectomy, gastric bypass surgery, or autoimmune gastric atrophy, which results in pernicious anemia. Gas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skin_cancer_-_Basal_cell_carcinoma,_squamous_cell_carcinoma,_&amp;_melanoma:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZITGmj_jQyOXOlQyQMrJhfyVQO_kvEYX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skin cancer - Basal cell carcinoma, squamous cell carcinoma, and melanoma: Nursing]]></video:title><video:description><![CDATA[Skin cancer is the growth and proliferation of abnormal cells in the skin, and the most common types include basal cell carcinoma, squamous cell carcinoma, and melanoma.

Let’s start with the anatomy and physiology of the skin, which is divided into three main layers: the hypodermis, dermis, and the epidermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle and acts as a cushion that protects underlying tissues from trauma. Above the hypodermis is the dermis, containing hair follicles, nerve endings, as well as sweat glands, and blood vessels. And just above the dermis is the epidermis, which itself has multiple cell layers that are composed of developing cells called keratinocytes.

Now, keratinocytes start their life at the lowest layer of the epidermis, called the stratum basale or basal layer. As keratinocytes in the stratum basale mature, they migrate into the next layers of the epidermis, called the stratum spinosum, stratum granulosum, stratum lucidum, and finally, the stratum corneum, which is the uppermost and thickest epidermal layer. Now, the stratum basale also contains the melanocytes, which produce a pigment called melanin, that gives each individual their skin color. At the same time, melanin acts as a natural sunscreen, because its protein structure dissipates, or scatters UVB light.

So, the cause of skin cancer is mutations in skin cells, which can arise due to a variety of factors. The most important environmental risk factor is excessive UV radiation exposure, either from the sun or sunlamps and tanning booths. In general, light skinned clients are considered to be at a higher risk of developing skin cancer, and the risk increases with cumulative sun exposure over time. Other risk factors include exposure to occupational chemical carcinogens, like arsenic or coal tars; and the presence of premalignant skin lesions. These include actinic keratosis, which might develop into squamous cell ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hip_fractures:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xeRgF8g7R5axO5gAoNDKGXpZTr6cKCq8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hip fractures: Nursing]]></video:title><video:description><![CDATA[Hip fractures are fractures that occur in the upper third of the thigh bone, called the femur. These fractures can be grouped into two types: intracapsular fractures, which are fractures that happen within the capsule of the hip joint; and extracapsular fractures, which are fractures that happen outside the capsule. One of the most common sites for a hip fracture is at the femoral neck and this is a type of intracapsular fracture. 

Now, the hip joint, also called the acetabulofemoral joint, is a ball and socket joint formed between the acetabulum of the hip bone and the head of the femur. The articulating bones are covered by hyaline cartilage and a joint capsule, which is reinforced on the outside by strong ligaments. This makes the joint strong and stable, allowing it to connect the free bones of the lower limb to the pelvic bones. The hip joint allows multiaxial movements, but is also important for weight-bearing and providing stability. 

 Now, intracapsular fractures are caused by trauma and osteoporosis. Low bone mass due to osteoporosis causes the bones to become more fragile, making them more prone to breaking. Because of this, intracapsular fractures are also called fragility fractures, because they typically occur after minimal trauma, like falling from a chair. On the other hand, extracapsular fractures are typically caused by severe direct trauma, like a car crash. 

Risk factors for hip fractures include old age, which can lead to falls, being assigned female at birth, and having a family history of osteoporosis.

Now, the main blood supply for the femoral head comes from the lateral femoral circumflex artery that travels along the femoral head. This artery is often compromised during a hip fracture which can cause complications like avascular necrosis of the femoral head. Furthermore, reduced blood flow means slower healing which leads to longer periods of immobility and hospitalization. This increases the risk of developing thrombotic ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Innate_immune_response:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CuNCG3aHT2K_Kei0a72BMtQkRUegJzed/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immune response - Innate: Nursing]]></video:title><video:description><![CDATA[Immunity is the ability of the body to fight pathogens, like viruses, bacteria, and fungi; but, also, foreign substances, like toxins and chemicals. Now, the immune system consists of two main branches: innate immunity and adaptive immunity. Innate immunity is the first line of immunity, that we are born with; it is fast, meaning that it responds within several minutes to hours; it’s non-specific, therefore it does not differentiate one pathogen from another; and finally, it’s short-lived, meaning it does not retain the memory of previous infections. On the flip side, adaptive immunity is the second line of defense that is acquired throughout life; it is slower and takes time to respond; but it’s also specific, so it recognizes different pathogens; and long-term, so it doesn’t forget a previous exposure to a pathogen.

Now, let&amp;#39;s cover the physiology of the innate immune system, which can be further subdivided into anatomic, physiologic, and cellular components. Anatomic components include physical barriers, like skin and mucous membranes, while physiologic components include additional mechanisms like the microflora found in different parts of the body, like the skin, gut and reproductive organs; or the low stomach pH. 

The cellular components of innate immunity include several types of white blood cells, all of which are produced in the bone marrow from hematopoietic stem cells which give rise to all blood cells. 

First up, there’s phagocytes, like neutrophils, macrophages and dendritic cells, and these are immune cells that digest pathogens in a process called phagocytosis. There are some key differences between them. 

First up, neutrophils are circulating immune cells, so they are normally found in the blood. In fact, they’re the most numerous type of white blood cell in the blood! Microscopically, they also have a multi-lobed nucleus, which is why they’re also called polymorphonuclear neutrophils, or PMN for short. They’re also granulocyte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_mononucleosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pfoObNGdRjiR1RD_cnsNtU2vTMONkxND/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious mononucleosis: Nursing]]></video:title><video:description><![CDATA[Infectious mononucleosis, or simply mono, is a highly contagious, but self-limiting viral infection caused by the Epstein-Barr virus. Infectious mononucleosis is typically seen in young clients and adolescents and is often referred to as “the kissing disease” because the Epstein-Barr virus primarily spreads through saliva.

First, let’s quickly review the physiology of normal immune response, which is subdivided into innate and adaptive immunity. Innate immunity consists of natural barriers, like skin and mucous membranes; natural killer cells, which help fight virus-infected and tumor cells; and phagocytes, such as macrophages, neutrophils, and dendritic cells. 

Now, when a pathogen, like a virus, reaches a person’s mouth, breaches the mucosal barrier, and enters the body, the innate immune system reacts quickly. The first cells on the scene are macrophages and neutrophils, which directly fight the pathogen. At the same time, they also secrete small molecules called cytokines to increase the permeability of local blood vessels and message other immune cells that there’s an active fight in the body. Additionally, cytokines induce the production of acute inflammatory proteins and cause systemic effects, such as fever. 

Simultaneously, dendritic cells engulf and digest the pathogen, eventually presenting small fragments of it on their surface. At this point, the adaptive immune system, which relies on B and T lymphocytes, comes to the rescue. Specifically, T helper cells recognize these fragments and help activate B lymphocytes, primarily in pharyngeal lymph tissue, tonsils, and regional cervical lymph nodes. Once stimulated, B cells start to produce antibodies, which circulate throughout the body and bind to pathogens, eventually enabling cytotoxic T lymphocytes and NK cells to recognize and destroy them.

The most common cause of infectious mononucleosis is the Epstein-Barr virus, also known as human herpesvirus 4 or HHV-4. This is a small DNA virus that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rubella_(German_measles):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tjpcx9w8TCedhNvPOK-jReeJQRGksUa8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rubella (German measles): Nursing]]></video:title><video:description><![CDATA[Rubella, also known as German measles or the 3-day measles, is a mild viral childhood infection caused by the Rubella virus and is usually associated with malaise, fever, rash, and lymphadenopathy. Thanks to vaccination, there are fewer cases of rubella, but in some parts of the world where the population is not immunized, it’s still possible to see outbreaks.

Now, the cause of rubella is infection with the Rubella virus, which is an RNA virus that has recently been reclassified to the Matonaviridae family from the Togaviridae which it originally belonged to. Important risk factors for rubella include immunodeficiency; being unvaccinated or incompletely vaccinated; coming in contact with an infected person; and finally, living in or traveling to an endemic area.

Moving on to pathology. Rubella virus is an airborne virus, meaning it spreads via small virus-containing droplets that get flung in the air when an infected person coughs or sneezes.  If another person breathes in these droplets, or they get in contact with infected surfaces and then touch their mouth, nose, or eyes, they can become infected. 

Once the virus enters the body, it binds to a specific receptor on the membrane of epithelial cells in the nasopharynx and enters the cell. Inside the cell, the virus replicates, creating new viral particles, which leave the cell and enter surrounding lymphatic and blood vessels, eventually reaching regional lymph nodes where they replicate once again. From here, the virus enters blood vessels again, and spreads throughout the body, making its way into various bodily fluids like urine, cerebrospinal fluid, and synovial fluid of joints. Important complications of rubella infection include polyarthritis and polyarthralgia. 

Now, the virus can also cross the placenta during pregnancy, causing congenital rubella syndrome, or CRS for short, in the fetus. The risk of CRS is highest when the pregnant individual gets rubella during the first trimester. Infection]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Legal_blindness:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NiqNJwegSvGTIzmtLcOqPwM5TVqie8nd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Legal blindness: Nursing]]></video:title><video:description><![CDATA[Legal blindness is defined as having a central visual acuity of 20/200 or less in the better-seeing eye, or having a peripheral visual field of 20 degrees or less. So, many people who are legally blind in some sense can still see, but they have severe visual impairment.

First, let’s quickly review the physiology of vision. Okay, now, the visual pathways begin in the eye. If we zoom into the wall of the eye, there&amp;#39;s an outer fibrous layer, which contains the cornea and sclera, and helps control and focus the entry of light. So the light that passes through the cornea is directed to the lens, which in turn collects light arrays and focuses them into the retina at the back of the eye. The retina houses photoreceptors that translate light into electrical impulses, which are then carried by the optic nerve into the visual cortex of the brain. Finally, the visual cortex processes the impulses coming from both eyes, and fuses them into one clear image.

Now, common causes of legal blindness include eye conditions like cataracts, age-related macular degeneration, glaucoma, diabetic retinopathy, eye infections like trachoma, or it can be congenital. Lastly, the cause of legal blindness may also be idiopathic or unknown. Risk factors for legal blindness include being assigned female at birth or over the age of 50, as well as having a systemic disease like diabetes mellitus, or undergoing eye surgery.

Okay, so the pathology of legal blindness can have two main origins. On the one hand, it can originate from abnormalities or damage involving a structure within the eye, such as the lens or retina. If any of these structures isn’t properly functioning, the eye is not able to perceive light and images, and thus fails to translate it to electrical impulses for the brain. 

On the other hand, the eye might be fine, but a part of the central nervous system, such as the optic nerve or the brain, can be affected. As a result, either the optic nerve is unable to car]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rubeola_(Measles):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-FbLtroWRiytbUq4AezltgOyQjGOZYzv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rubeola (Measles): Nursing]]></video:title><video:description><![CDATA[Rubeola, also known as measles, is a highly contagious viral childhood exanthem caused by the measles virus, and it’s usually associated with a triad of cough; coryza, meaning the inflammation and swelling of the nasal mucosa; and conjunctivitis, followed by a rash that progresses from head to toe. Thanks to vaccination, there are fewer cases of measles, but in some parts of the world where the population is not immunized, outbreaks are still possible.

Let’s start by discussing the physiology of the immune response to a viral infection. 
After a foreign antigen, like a virus, enters the body, it runs into antigen-presenting cells, like macrophages and dendritic cells, by whom it is engulfed and digested into fragments. These antigen fragments are then presented on their surface and recognized by T helper cells, a type of T lymphocytes that activate B lymphocytes to produce antibodies against that antigen. Next, these antibodies bind to any affected cell that expresses the antigen on its surface, eventually enabling natural killer or NK cells and cytotoxic T cells to easily recognize and destroy them. Furthermore, these natural killer cells enhance the inflammatory response by producing cytokines that recruit neutrophils, macrophages, and mast cells. 

Now, the cause of measles is measles virus, which is an RNA virus that belongs to the Morbillivirus genus and Paramyxoviridae family. Important risk factors for measles include immunodeficiency; being unvaccinated or undervaccinated; coming in contact with an infected person; vitamin A deficiency; pregnancy; and living or traveling to an endemic area.

Now moving on to pathology. Measles is an airborne virus, meaning it spreads via small virus-containing droplets that get flung in the air when an infected client coughs or sneezes. If another client breathes in these droplets, or they get in contact with infected surfaces and then touch their eyes or mouth, they can become infected. Once the virus enters the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Roseola_(Exanthem_Subitum):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tXQ9GvurS-yB25aAXiJDLqarQWSdRS9e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Roseola (Exanthem subitum): Nursing]]></video:title><video:description><![CDATA[Roseola, also known as roseola infantum, exanthem subitum, or sixth disease, is a self-limiting, viral exanthem, most commonly caused by human herpesvirus 6, or HHV-6. Roseola is typically seen in children between the ages of six months and two years, and it’s characterized by a fever that may exceed 104 F or 40 C.

Let’s start by discussing the physiology of the immune response with a focus on T lymphocytes. It all begins in the bone marrow where undifferentiated hematopoietic stem cells begin to differentiate into different types of white blood cells. Some of these cells migrate to the thymus where they become mature T cells, also known as T lymphocytes. These cells defend us against intracellular viruses, fungi, and tumor cells and are responsible for long-term immunity. 

Now, after a foreign antigen enters the body, it runs into antigen-presenting cells, like macrophages and dendritic cells, which engulf the foreign antigen and digest it into fragments. These antigen fragments are then presented on their surface and recognized by T helper cells, which help activate B cells to produce antibodies against that antigen. Next, these antibodies bind to any affected cell that expresses the antigen on its surface, eventually enabling natural killer, or NK cells, and cytotoxic T cells to easily recognize and destroy them.

Now, the most common cause of roseola is human herpesvirus 6, or HHV-6 for short, which is a small DNA virus that belongs to the Herpesviridae family. Less commonly, roseola can also be caused by enteroviruses and adenoviruses, as well as human herpesvirus 3 and 7. Important risk factors for developing roseola include age between 6 and 24 months and immunosuppression.

Now moving on to pathology. HHV-6 is an airborne virus, meaning it spreads via small virus-containing droplets that get flung in the air when an infected client coughs or sneezes. If an individual inhales these droplets or they come in contact with infected surfaces and then t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kawasaki_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yqrpJHKhRkipPfSiJI3Dkxq7TAaq1Fb5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kawasaki disease: Nursing]]></video:title><video:description><![CDATA[Kawasaki disease is a condition associated with acute inflammation of medium-sized arteries; and it’s typically seen in children between the ages of 6 months and 5 years.

First, let’s cover some basic physiology  of arteries. There are three main types of arteries: large arteries, like the aorta; medium arteries, like the coronary arteries that supply the heart; and finally, small arteries. 

Now, each artery consists of three layers: from outside in, there’s the tunica adventitia, which has loose connective tissue; then the tunica media, which mainly contains smooth muscle cells but also some elastic tissue; and finally the tunica intima, or endothelium, which consists of a single layer of endothelial cells on top of a layer of connective tissue, called lamina propria.

The exact cause of Kawasaki disease remains unknown, but some sources suggest that it might be triggered by an infection or autoimmune process. The most important risk factors associated with Kawasaki disease include being below 5 years of age, being assigned male at birth, and having Asian or Pacific Islander ancestry.

Now let’s look at the pathology of Kawasaki disease.  Typically the client’s immune system is activated to fight off an infection. Then, for reasons we still don’t understand, the immune cells like neutrophils, macrophages and even B cells and T cells start attacking the endothelial lining of medium sized blood vessels, most commonly the coronary arteries of the heart. Now, these cells cause inflammation within the artery which damages the endothelial lining. They can even invade into the tunica media where they destroy the elastin and collagen fibers that make up the arterial wall.  

Now, Kawasaki disease can cause serious life-threatening cardiovascular complications.  First, damage to the endothelium exposes collagen and tissue factors in the tunica media, which can trigger coagulation. Clots forming on the arterial wall reduce blood flow to heart tissue, causing isch]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_gestation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2Dcgcf0mQrGoAS0qrMPAV78jTxW7zEEO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple gestation: Nursing]]></video:title><video:description><![CDATA[Multiple gestation or multifetal pregnancy describes pregnancy with more than one fetus at a time. The most common type of multiple gestation is twin pregnancy, meaning a pregnancy with two fetuses. 

All right, now let’s quickly review the physiology of fertilization, starting with the ovaries, which are the paired female gonads. Each month, they release one mature egg, also called oocyte, which is the female gamete. After leaving the ovaries, the egg enters the fallopian tube and reaches the widest part of it, called the ampulla of the fallopian tube. This is where the few sperm that have made it this far after ejaculation surround the egg; and of them, a single sperm succeeds in entering the egg and fertilizing it, forming the zygote. 

The zygote then makes its way through the fallopian tube in order to reach the uterus; and at the same time, it undergoes mitosis, meaning it divides over and over again into smaller cells called blastomeres. When there are 32 blastomeres, the fetus is called a morula. At about day four after fertilization, a fluid cavity appears inside the morula to form the blastocyst, which contains an inner and outer group of cells. About six or seven days after fertilization, the blastocyst reaches the uterus and implants in the inner lining of the uterus, called the endometrium. 

Now, multiple gestation typically happens when the ovaries release more than one oocyte in a particular month, and more than one sperm ends up fertilizing them; one for each. This gives rise to dizygotic twins, also called fraternal or non-identical twins; because the two zygotes develop individually. Alternatively, multiple gestation can occur when the zygote divides into two separate zygotes shortly after fertilization. This situation gives rise to monozygotic, also called identical twins. 

Now, multiple gestation differs between monozygotic and dizygotic twins. With monozygotic twins, if the division of the zygote in two happens at the morula stage, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypospadias_&amp;_epispadias:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u_z1-eSARwOEAOK51_CCky8IQ1qhiywF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypospadias and epispadias: Nursing]]></video:title><video:description><![CDATA[Hypospadias and epispadias are congenital conditions associated with an abnormal position of the urethral opening. In hypospadias, the urethral opening is located along the underside of the penis, on its ventral surface; while in epispadias the urethral opening is positioned along the upper side of the penis, on its dorsal surface.

First, let’s cover some basic physiology and embryology of the male external genitalia. Around the 8th week of pregnancy, the testes start to produce testosterone, which is an androgen responsible for masculinization of the external genitalia. So, in the genital tubercle, urogenital sinus, urogenital folds, and labioscrotal swellings, testosterone is converted to a more potent form called dihydrotestosterone or DHT for short. 

Dihydrotestosterone elongates the genital tubercle in the cranial direction, meaning towards the future head, into a primitive phallus, which represents the precursor of the future penis. In the urogenital sinus, it stimulates the formation of the bladder, prostate, bulbourethral glands, and the part of the urethra outside of the penis. On the flip side, in the urethral folds, it stimulates the formation of the ventral shaft of the penis and the penile urethra. Finally, dihydrotestosterone makes the urethral folds and the labioscrotal swellings fuse on the midline in order to form the ventral shaft of the penis, the penile urethra and the scrotum, respectively.

Now, the exact cause of hypospadias and epispadias is still unknown, but some theories suggest they might be associated with abnormal levels of androgens and estrogens. Important risk factors for hypospadias include family history, genetic mutations, maternal age over 35 years, maternal hypertension or diabetes, and maternal exposure to tobacco smoke or pesticides.

Additionally, clients with some congenital conditions have a higher incidence of hypospadias than others. These include inguinal hernia; which occurs when an internal organ, like inte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock_-_Septic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PH-maPl4STKkbxgxjLlXCP4uST6X5FDY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock - Septic: Nursing]]></video:title><video:description><![CDATA[Shock is a life-threatening condition that occurs when body organs don’t receive enough oxygen and nutrients for them to function properly. Shock can be grouped into four types based on the cause: hypovolemic, cardiogenic, obstructive, and distributive shock. And septic shock is a type of distributive shock that occurs secondary to sepsis, which is when the body mounts an excessive inflammatory response because of an infection. 

Now, to understand distributive shock, let’s quickly review the physiology of blood vessels, which contain smooth muscle in their walls. When the smooth muscle relaxes, it increases the diameter of blood vessels, called vasodilation. On the other hand, when smooth muscle contracts, that decreases the diameter of blood vessels, called vasoconstriction. 

The contraction and relaxation of smooth muscle is primarily controlled by the sympathetic nervous system, which normally maintains a partial constriction, generating enough force to keep blood moving through the circulatory system. The sympathetic system stimulation can increase or decrease to keep up with the body’s needs. Increased sympathetic stimulation of the blood vessels causes vasoconstriction, which leads to increased mean arterial pressure, or MAP for short. Vasoconstriction, when the total blood volume is constant, raises blood pressure and allows blood to flow faster through the blood vessels. 

In contrast, vasodilation is typically caused by decreased sympathetic stimulation, in addition to inflammatory cytokines and histamine, which decrease mean arterial pressure. So, vasodilatation, when blood volume is constant, lowers the blood pressure and slows down the blood flow through the blood vessels.

Alright, now the main cause of septic shock is infections, particularly those caused by gram positive bacteria, like Staphylococcus aureus, Streptococcus pneumoniae or Enterococcus species, and gram-negative bacteria, like Escherichia coli. In addition to bacteria, in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infertility:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KVMkZ6sITRmK8yN8QE3AUX6UR2y7IQnw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infertility: Nursing]]></video:title><video:description><![CDATA[Infertility is defined as the inability to conceive after 12 months of regular, unprotected sexual intercourse in couples of reproductive age. Infertility can affect one or both partners, or, in some cases, no cause can be found in either partner, in which case it’s termed unexplained infertility.

Now, let’s go over some anatomy and physiology when it comes to conceiving. The female gonads are called ovaries, which are paired reproductive organs that produce sex hormones, namely estrogen and progesterone; as well as gametes, called oocytes, in the process known as oogenesis. 

These functions are an integral part of the menstrual cycle, which usually lasts around 28 days and can be divided in two phases. First, there’s the follicular phase, during which estrogen rises, and the oocytes mature until ovulation, which typically occurs on day 14 of a 28 day cycle. 

During ovulation, the mature oocyte is released in the fallopian tube and it can possibly be fertilized by a male gamete, called a sperm. If fertilization occurs, the fertilized egg travels down the Fallopian tube and implants into the uterine lining, so pregnancy occurs.

If fertilization doesn’t occur, ovulation is followed by the luteal phase, during which progesterone rises and peaks, and then hormone levels gradually decrease until menstruation occurs, and the cycle starts all over again. 

The menstrual cycle is primarily controlled by two pituitary hormones: luteinizing hormone or LH for short, and follicle-stimulating hormone or FSH for short; but a normal concentration of several other hormones, including thyroid hormones, cortisol and prolactin, is needed for the menstrual cycle to unfold optimally. 

On the other hand, the male gonads are called testicles, or testes, which are also paired reproductive organs that lie in the scrotum. The testes produce the sex hormone testosterone, and they’re also where spermatogenesis, or the development of sperm, happens. Just like oogenesis, spermatog]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pericarditis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4L7Nq0-FRAOHHhI01jU47K9VQ__GIL4c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pericarditis: Nursing]]></video:title><video:description><![CDATA[Pericarditis refers to inflammation of the pericardium, which is a thin, fibro-elastic sac that surrounds the heart and the roots of the great vessels, cushioning them, and preventing friction during each heartbeat. 

Let’s start with a bit of physiology. The pericardium has two layers: an outer fibrous layer, known as the parietal pericardium; and an inner serous layer, called the visceral pericardium. The visceral pericardium is continuous with the parietal pericardium, so they form an enclosed space called the pericardial cavity. Within it, there’s serous pericardial fluid, that is secreted by visceral pericardium cells and drained by parietal pericardial cells and lymphatics, in order to maintain a normal volume of about 5 to 20 mL. The pericardial fluid cushions the heart from any kind of external jerk or shock, and also acts as a lubricant to reduce friction with each heartbeat. The pericardium also fixes the heart to the mediastinum, preventing it from twisting, so that blood circulation through the great vessels doesn’t get cut off. 

Now, pericarditis is caused by inflammation of the pericardium, and most cases are idiopathic, meaning that there’s no identifiable cause. When the cause is identified, it’s usually an infection, most commonly a virus, such as Coxsackie B virus or echovirus. Less frequently, pericarditis can be caused by bacteria like Streptococcus pneumoniae or Staphylococcus aureus; as well as fungi like Histoplasma capsulatum and Candida spp. 

On the other hand, non-infectious causes of pericarditis include Dressler syndrome, also known as postmyocardial infarction syndrome, which is an immune response triggered by antigens released by dying heart cells, and occurs several weeks after myocardial infarction. Another non-infectious cause of pericarditis is uremia, which is when blood levels of urea get really high, usually due to kidney failure. The high levels of urea irritate the visceral pericardium cells, leading them to secrete]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cerebral_palsy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LeOn0yhUQ2_1t6yJV3KBKYuwSQSVUEaY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cerebral palsy: Nursing]]></video:title><video:description><![CDATA[Cerebral palsy refers to a group of non-specific disorders that are typically related to movement, coordination, and posture, caused by abnormal brain development and function. 

First, let’s review some anatomy and physiology of the nervous system, which is divided into the central nervous system, including the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the muscles and organs. 

So, when the brain wants a muscle to contract, like dorsiflexing the foot, the motor cortex sends a signal through the upper motor neurons which carries the information down the spinal cord and then through a lower motor neuron in the peripheral nervous system to the muscles fibers in the foot, causing it to move.  

Between the lower motor neuron and the muscle fiber is a space called the neuromuscular junction. The lower motor neurons have voltage-gated calcium channels in their membranes. Whenever they receive an electrical impulse from the brain, these channels open up and let calcium inside. The increased intracellular calcium concentration triggers the release of the  neurotransmitter acetylcholine into the neuromuscular junction. Acetylcholine goes from the neuron over to receptors on muscle cell membranes, causing voluntary muscle contraction. 

Now, there isn’t a single cause of cerebral palsy, but rather it’s a multifactorial disease, meaning that there’s a combination of factors that can be either antenatal or postnatal, based on whether they occur before or after birth. 

During these periods of early development, the brain is highly susceptible to damage. Typically, the most common factors that increase the risk of  cerebral palsy during the antenatal period include congenital brain malformations; intrauterine infection; chromosomal abnormalities; intrauterine growth restriction; multiple gestation; preeclampsia, or new onset hypertension and proteinuria during pregnancy; as w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Atrial_fibrillation_(Afib):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Lbl_A7qrR7CR5c_RufhJLV7DR7O57dRK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Atrial fibrillation (Afib): Nursing]]></video:title><video:description><![CDATA[Atrial fibrillation, sometimes called Afib for short, is the most common cardiac arrhythmia which occurs when the atria contract way faster than normal, and in a disorganized manner. As a result, the atria have a quivering, or twitching movement that can’t pump blood into the ventricles efficiently. 

Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. 

From the atrium, electrical activity goes to the atrioventricular, or AV node, where impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.  

From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles, causing them to depolarize. This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG. 

Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the pause between ventricular depolarization and repolarization is represented by the ST segment. Sometimes, immediately after the T wave, there’s a U wave, which represents late repolarization of the ventricles. 

Okay, now, atrial fibrillation is typically caused by any kind of structural damage to the heart, or any damag]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postoperative_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0WfM-IjGQuSGwYDmR7OkeWr2Q6a38Mj8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postoperative care: Nursing]]></video:title><video:description><![CDATA[Postoperative care is the management of a client’s health during the postoperative period. This begins right after the surgical procedure is complete, and lasts until the client is discharged from the healthcare facility. Postoperative care promotes the client’s recovery after surgery by managing pain, supporting oxygenation and cardiovascular stability, maintaining fluid balance, providing wound care, monitoring bowel function, assisting with mobility, and preventing complications. 

Postoperative care typically begins when the client is transferred from the operating suite to the postanesthesia care unit, or PACU for short. How long they’re being cared for in this setting depends on the client’s health status, the type of procedure, and the type of anesthesia, as well as the rate of progression to alertness and hemodynamic stability. The goal of this phase of care is to stabilize the client for transfer to the next level of care, which could be an intensive care unit or another inpatient care unit; as well as being discharged home in the case of ambulatory surgery. In order for clients to transition to a different level of care, they should meet certain criteria such as responding easily to stimuli, having stable vital signs, and adequate pain control. 

Now, the most common complications during the postoperative period include pain, hemorrhage, hypothermia, and infections at the site of the surgery, called surgical site infection, or SSI for short, as well as wound dehiscence and evisceration. There can also be respiratory complications, like airway obstruction, laryngospasm, pneumonia, atelectasis, and pulmonary embolism. 

Cardiovascular complications can also occur, such as hypotension, hypertension, and dysrhythmias. Clients can also develop nervous system complications, including delirium and delayed emergence from anesthesia. 

On the other hand, gastrointestinal complications include postoperative nausea and vomiting, constipation, postoperative ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lymphoma_-_Hodgkin_&amp;_non-Hodgkin:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JYZOxo7dQjimYPnCQmHs64qzS1aWJFI9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lymphoma - Hodgkin and non-Hodgkin: Nursing]]></video:title><video:description><![CDATA[Lymphoma is a tumor derived from lymphocytes, specifically B-cells and T-cells, which are white blood cells that mainly live in lymph nodes and move through the blood and the lymphatic system. Lymphomas can be broadly grouped into two categories; Hodgkin and non-Hodgkin lymphomas. Hodgkin lymphomas tend to spread in a contiguous manner, meaning they spread to nearby lymph nodes, but rarely involve extranodal sites. In contrast, non-Hodgkin lymphomas can sometimes spread non-contiguously, and can involve extranodal sites like the skin, gastrointestinal tract, and brain.

Now, let’s quickly review the anatomy and physiology of the lymphatic system. The lymphatic system protects the body from invaders, maintains the fluid level in the body, and absorbs dietary fat from the intestine. It is composed of lymph, lymphocytes, lymphatic vessels and plexuses, lymph nodes, and other lymphoid organs, such as the thymus, the bone marrow, the spleen, and the tonsils. The lymph is a clear, or slightly yellow, fluid that is transported through tubes similar to blood vessels, called lymphatic vessels. Lymphatic vessels drain lymph through lymph nodes and eventually into lymphatic trunks, which drain large regions of the body, like the subclavian trunks that drain the upper limbs. 

Lymphatic trunks converge to form two bigger channels called lymphatic ducts, specifically the right lymphatic duct and the thoracic duct. Now, as lymph travels through lymphatic vessels, it encounters lymph nodes which filter the lymph and check to see if there are any foreign invaders the body needs to attack. In the case of an invader, the lymphocytes react and initiate an immune response. Typically, lymph nodes lie close to each other, forming groups that may lie superficial or deep within the body, such as the cervical lymph nodes, the mediastinal lymph nodes, and the axillary lymph nodes.

Although the exact cause of lymphoma remains unknown, several risk factors have been established]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemorrhagic_stroke_-_Intracranial_hemorrhage_(ICH)_&amp;_subarachnoid_hemorrhage_(SAH):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eRligGwaSoaDfZscTPw542LXRqO2mPdu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemorrhagic stroke - Intracranial hemorrhage (ICH) and subarachnoid hemorrhage (SAH): Nursing]]></video:title><video:description><![CDATA[Stroke, also known as cerebrovascular accident or brain attack, is when the brain gets damaged due to being deprived of oxygen-rich blood. There are two main types of stroke: ischemic stroke, which occurs when there’s a blockage of an artery, and hemorrhagic stroke, which occurs when an artery in the brain leaks into the brain tissue.

First, let’s discuss the anatomy and physiology of the brain, which has three main parts called the cerebrum, cerebellum, and brainstem. The cerebrum is the most obvious part of the brain and it’s divided into two cerebral hemispheres, each of which has four lobes, called the frontal, temporal, parietal, and occipital lobe. The frontal lobe controls eye and voluntary movement. There’s also a specific region of the frontal lobe called Broca’s area, which controls speech production. Next, there’s the temporal lobe, which plays an important role in long-term memory formation, and recognition of faces, scenes, and speech. The temporal lobe also has an area called Wernicke’s area, which is in charge of understanding spoken and written language. Both Broca’s and Wernicke’s areas are located in the dominant hemisphere, meaning the left hemisphere for right-handed people, and right hemisphere for left-handed people. Finally, the parietal lobe is responsible for sensory perception; while the occipital lobe plays an important role in visual processing. 

Now, the cerebellum helps with muscle coordination and balance; while the brainstem refers to the part of the central nervous system that connects the brain with the spinal cord. Within the brainstem, descending motor fibers from the left and right cerebral hemispheres decussate, meaning they cross over to the opposite side, and eventually make their way down to the spinal cord. This makes it so that the right cerebral hemisphere controls muscles on the left side of the body and vice versa. The brain stem also contains the nerve cell bodies of cranial nerves, as well as cardiovas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Birth-related_procedures:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fti8N38JS6aWZ6v5Y-wMk0wqRoCZfLBb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Birth-related procedures: Nursing]]></video:title><video:description><![CDATA[Labor, also called childbirth, is a physiologic process during which the fetus and placenta are expelled from the uterus. 
The most common form of delivery is vaginal, meaning that the baby passes through the vaginal canal. 
However, some deliveries require the assistance of healthcare providers in the form of birth-related procedures. These procedures include, labor induction and augmentation, assisted vaginal delivery, sometimes called operative vaginal delivery, and episiotomy. 

Now, let’s discuss induction and augmentation of labor, which are artificial methods that start the labor process. One method is cervical ripening, which is used to ripen or soften the cervix so that it’s more likely to dilate with uterine contractions. Cervical ripening can be done pharmacologically or mechanically. 

With pharmacological cervical ripening, prostaglandin E2, also known as dinoprostone, is most commonly used. It comes in the form of intravaginal gel, intracervical gel, or timed-release vaginal insert. Prostaglandin E1, also known as misoprostol, can also be used for cervical ripening, but it’s an off-label use. One setback of using prostaglandins for cervical ripening is that it also increases the contractility of the uterus, and can even result in tachysystole, or excessively frequent uterine contractions, so both the uterine activity and the fetal heart rate must be monitored when prostaglandin E2 is in place. When it comes to contraindications of cervical ripening, these include previous cesarean birth and major uterine surgery. 

For mechanical cervical opening, there are two methods. The first can be done using a trans-cervical balloon catheter. A trans-cervical catheter is inserted through the internal cervical os, or cervical opening, and the balloon is inflated. Then, the balloon is retracted down against the cervical os. This creates direct pressure and induces release of endogenous prostaglandins. 

On the other hand, membrane stripping involves the d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_process:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OdBs-AjXRkK52N1AEtEgcdcYTuCUD5AX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory process: Nursing]]></video:title><video:description><![CDATA[The inflammatory process, or simply inflammation, is an innate, nonspecific, immediate, defensive mechanism that helps protect the body against infections and injuries. 

The goal of inflammation is to respond to the stimuli and restore balance. Often, this includes eliminating the cause of tissue injury, clearing out necrotic or dead cells, and starting tissue repair. 

There are three main types of inflammation: 
acute inflammation, which lasts several days; subacute inflammation, which lasts from 2 to 6 weeks; and finally, chronic inflammation, which can last for months or even years.

The inflammatory process can be caused by external triggersand internal triggers. External triggers include pathogens, such as bacteria, viruses, and fungi; but also environmental triggers like allergens, toxins, and irritants. On the other hand, the most important internal trigger is cellular injury.

Let’s start with a bit of physiology. The body responds to a trigger with two distinct mechanisms; the vascular response and the cellular response. First, let’s focus on the vascular response.

The vascular response involves changes to the microcirculation in the capillaries, arterioles, and venules. The initial response is transient vasoconstriction of local blood vessels, followed rapidly by vasodilation, caused by nitric oxide released from endothelial cells as well as other chemical mediators. Vasodilation increases blood flow to the site of injury, causing redness and warmth. Next, there’s increased permeability of the capillaries, which makes a protein-rich fluid, called inflammatory exudate, to leak into the interstitial space. Less proteins in the capillaries means there’s a decrease in capillary osmotic pressure; and, at the same time, more proteins in the interstitial space cause an increase in interstitial osmotic pressure. This osmotic pressure imbalance draws even more fluid from the capillaries into the interstitial space, resulting in local swelling.     

Du]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Types_of_leadership:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qWTcg8m4RLq94LRRGiKUYre_SYG5qY_1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Types of leadership: Nursing]]></video:title><video:description><![CDATA[Nurse Natasha works on the medical unit at a hospital and has noticed many of her nurse colleagues are not following the hospital policy to complete change-of-shift reports at the clients’ bedsides. Instead, they’re being done in the hallways or at the nurse’s station. Nurse Natasha knows that the policy exists because bedside reporting helps to reduce errors and increases communication and collaboration between the nurse and the client. She speaks to the unit manager and says, “I’d like to create a Bedside Reporting Team made up of other nurses on the unit to help solve the change-of-shift reporting issue we are experiencing.” Nurse Natasha will use what she has learned about types of leadership to determine how to lead this new team. 

A leader influences a person or group of people to change behavior or actions in order to accomplish a goal. Leadership comes from a desire to make things better, bring people or groups together, improve communication, and work to achieve goals. A manager, on the other hand, is a particular kind of leader that concentrates on achieving the goals of an organization like decreasing costs or improving employee satisfaction. A manager is often placed in a position of authority within an organization. Therefore, a manager may act as a leader but a leader does not necessarily have to be a manager. Leaders who are not in an official position of authority are called ‘informal leaders’. 

In nursing, leadership is crucial for solving problems, providing safe, effective, and cost-effective client care, and for promoting the health of clients and communities. In fact, every nurse can serve as a leader. 

Just a few examples of nurse leaders include a nurse practitioner coordinating with a pharmacist to avoid drug interactions for a client, a nurse manager enforcing safe staffing ratios for a hospital unit, a community health nurse speaking to policy-makers to lobby for better access to public transportation and healthy food in the co]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Erythema_infectiosum_(Fifth_disease):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U4XFVaQXQlKotuvzsOtJopbARYGc0Zpn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Erythema infectiosum (Fifth disease): Nursing]]></video:title><video:description><![CDATA[Erythema infectiosum, also known as fifth disease, is a common and highly contagious, self-limiting viral exanthem, or eruptive skin rash, caused by the human parvovirus B19. Erythema infectiosum is typically seen in children between the ages of five and fifteen years, and it’s characterized by a distinctive facial rash with a “slapped cheek” appearance.

Let’s start by discussing the physiology of the immune response. It all begins in the bone marrow, where undifferentiated hematopoietic stem cells begin to differentiate into different types of white blood cells. Some of these cells migrate to the thymus where they become mature T cells, also known as T lymphocytes, which defend us against intracellular viruses, fungi, and tumor cells. Additionally, they are responsible for long-term immunity. 

Now, after a foreign antigen enters the body, it runs into antigen-presenting cells, like macrophages and dendritic cells, by whom it is engulfed and digested into fragments. These antigen fragments are then presented on their surface and recognized by T helper cells, which help activate B cells to produce antibodies against that antigen. Next, these antibodies bind to any affected cell that expresses the antigen on its surface, eventually enabling natural killer or NK cells and cytotoxic T cells to easily recognize and destroy them.

Now, the cause of erythema infectiosum is human parvovirus B19, which is a small DNA virus that belongs to the Erythroparvovirus genus and Parvoviridae family. Important risk factors for developing erythema infectiosum include age between five and fifteen years, late winter to early summer season, being in daycare, coming in contact with an infected individual, living in crowded living conditions, and immunodeficiency.

Okay, moving on to pathology. Human parvovirus B19 is primarily an airborne virus, meaning it most often spreads via small virus-containing droplets that get flung in the air when an infected client coughs or sne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fetal_development:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VZRYkkE2TtKRlcaXZuptHsaxTS6oXftk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fetal development: Nursing]]></video:title><video:description><![CDATA[Prenatal development usually lasts 38 to 40 weeks, and it can be subdivided into three main stages. The first stage, called the preembryonic stage, starts with conception and ends with implantation, lasting for 2 weeks. The second stage, or the embryonic stage, lasts from the third week through the eighth week, and it’s when the embryo develops until it becomes a fetus. The last and the longest stage of prenatal development is called the fetal stage, and it lasts from the ninth week until birth. Now, these stages are calculated based on fertilization age, meaning how much time has passed since the last ovulation, when the fertilization of the oocyte by the sperm took place. On the other hand, gestational age is measured from the first day of the mother’s last menstrual period, so it’s usually 2 weeks longer than fertilization age. 

Let’s start with the preembryonic stage, which covers the first two weeks in development. This stage starts with conception, more specifically, with fertilization; this is when a sperm meets the egg in the fallopian tube and they fuse, forming the zygote. The zygote then makes its way through the fallopian tube in order to reach the uterus; and at the same time, it undergoes mitosis, meaning it divides over and over again into smaller cells called blastomeres. When there are 32 blastomeres, the fetus is called a morula. Next, a fluid cavity appears inside the morula to form the blastocyst. Eventually, the blastocyst reaches the uterus and implants in the inner lining of the uterus, called the endometrium. 

Next comes the embryonic stage, which lasts from the beginning of the third week of gestation to the eighth week. The first major change in this phase is that the embryo develops its three primitive germ layers; the ectoderm, the mesoderm, and the endoderm, so it starts looking like 3 pancakes on top of one another. And throughout the embryonic phase, these three layers give rise to all the organs and tissues of the embryo. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_myeloma:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P57jyFJURtCMrnGD99G5D5_ySTGE2xek/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple myeloma: Nursing]]></video:title><video:description><![CDATA[Multiple myeloma, also called plasma cell myeloma, is a condition in which there’s a malignant proliferation of plasma cells in the bone marrow. This further affects the bones and eventually destroys them. 

First, let’s look at the physiology of the bone marrow and plasma cells. The main function of the bone marrow is to transform hematopoietic stem cells into all types of blood cells, like red blood cells, platelets, and white blood cells, which include lymphocytes. Plasma cells, specifically, develop from  B-lymphocytes, or B-cells, which are key cells of the adaptive immune response. In the bone marrow, B-cells mature and acquire a set of diverse B-cell receptors. Afterwards, they are sent to the lymphoid tissue, like the lymph nodes and the spleen, where they encounter various antigens. By meeting different types of antigens, B-cells are activated and specialize into antibody-secreting plasma cells that are able to fight off infections. 

Now, the cause of multiple myeloma is still unknown.  However, some evidence suggests that genetic abnormalities in oncogenes, which are genes involved in the uncontrolled proliferation of cancer cells, can play a role in the development of multiple myeloma. 

However, there are some known risk factors for developing multiple myeloma, which include age above 60 years old; a past medical or family history of plasma cell tumors; exposure to radiation or organic chemicals, like benzene, herbicides and insecticides; as well as some professions with increased exposure to environmental toxins, like firefighters. Finally, viral infections that impair the immune system, like an HIV infection, are also a risk factor for multiple myeloma. 

Okay, now let’s look at the pathology of multiple myeloma, which starts with excess production of abnormal plasma cells in the bone marrow. These abnormal plasma cells produce monoclonal antibodies, called M proteins, which are ineffective at fighting off infections.  Some of the M pro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_gestational_age:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E30a7ZhCT7Wcm6WwDxv7GLhFTt2Aj8Z2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of gestational age: Nursing]]></video:title><video:description><![CDATA[Gestation refers to the period between conception and birth, which typically lasts for 40 weeks. On the other hand, gestational age is a term used to describe a newborn based on their physical and neuromuscular characteristics. An accurate gestational age is obtained in order to provide the basis for planning care, both prenatally, meaning before birth; or postnatally meaning after birth. 

First, let’s focus on prenatal assessment of gestational age, which is typically determined by the length of pregnancy after the first day of the mother’s last menstrual period, expressed in weeks and days. A much more accurate way to estimate gestational age is to use ultrasound to evaluate the size of the embryo or fetus by measuring the crown rump length or CRL for short. The CRL refers to the distance from the top of the head, or crown, down to the bottom of the buttocks, or rump. An ultrasound can be also used to measure the size of specific fetal parts, such as the cranium, abdomen, and long bones.

On the other hand, postnatal assessment is primarily determined using a scoring system called the New Ballard Score. The New Ballard Score assesses the infant’s maturity by evaluating neuromuscular and physical characteristics, where the scores for each characteristic can range from  -1 to 5. Higher scores indicate a more mature gestational age, and lower scores indicate a less mature gestational age. In general, the gestational age assessment is most accurate if done within the first 48 hours after birth.

Alright, there are 6 components of neuromuscular maturity, which include posture, square window, arm recoil, popliteal angle, scarf sign, and heel to ear. Let’s start with posture, which looks at the amount of flexion of the arms, knees, and hips, as well as the degree of hip adduction or abduction. The healthcare provider places the infant in the supine position, and observes the posture when the infant is quiet and comfortable. More mature infants have a norm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Atrial_flutter_(Aflutter):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3fM7t7zPQKmdk-BlexuAlJ4TQuKXtDD6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Atrial flutter (Aflutter): Nursing]]></video:title><video:description><![CDATA[Atrial flutter, or AF for short, is a type of tachyarrhythmia, where tachy means fast, and arrhythmia means irregular rhythm. So AF is a fast, abnormal heart rhythm that causes poor, inefficient atrial contractions, which can affect the heart’s ability to pump blood. It’s called flutter because of its identifiable recurring, regular, sawtooth-shaped flutter waves that can be seen on an ECG.  

Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. 
Then, the impulse is conducted through the atrium, creating the P wave on an ECG. 

And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles.

 From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.  

From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles, causing them to depolarize. 

This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG. 

Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the pause between ventricular depolarization and repolarization is represented by the ST segment.
 Sometimes, immediately after the T wave, there’s a U wave, which represents late repolarization of the ventricles. 

N]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physiologic_changes_-_Pregnancy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FHaLXVaZTDKl-teMZW5DzYy2SJyBVgX9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physiologic changes - Pregnancy: Nursing]]></video:title><video:description><![CDATA[Physiological changes in pregnancy include all adaptations of the human body that occur in response to a developing fetus. These changes are essential for fetal survival and are primarily caused by high levels of estrogen and progesterone in the body.

First, let’s cover the most important signs and symptoms of pregnancy, which can be subdivided into three main groups: presumptive, probable, and positive. Presumptive signs and symptoms include amenorrhea, or the absence of menstruation; increased breast size and breast tenderness; nausea and vomiting; as well as increased urinary frequency; and quickening, meaning the fluttering sensation caused by fetal first movements. 

Probable signs of pregnancy include a positive pregnancy test, uterine enlargement, and irregular uterine contractions, which are often referred to as Braxton Hicks contractions. Other important probable signs include the Goodell’s sign, or the softening of the cervix that occurs after 4 gestational weeks; the Hegar’s sign, which indicates the softening of the lower uterine segment that occurs after 6 gestational weeks; and finally, the Chadwick’s sign, which describes the blue to purple discoloration of vulvar, vaginal, and cervical mucous membranes. Just like Hegar&amp;#39;s sign, Chadwick&amp;#39;s sign also appears after 6 weeks of gestation.

Another important probable sign is ballottement. Here, an examiner places a finger inside the vagina and pushes the lower segment of the uterus, indirectly pushing the fetus to go upwards. Once displaced, the fetus returns to its previous position causing an impact on the uterine wall. This impact can be felt on the examiner’s finger. 

Finally, we have positive signs of pregnancy, which include active fetal movements, detection of fetal heart rate, and ultrasound detection of the fetus.

Now, let’s look at the physiological changes that impact the cardiovascular system, which must adapt in order to accommodate the needs of an enlarging uteru]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Components_of_the_birth_process:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XjhxmeXoSHWYq7MYH3SrXswpTsONk8Bh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Components of the birth process: Nursing]]></video:title><video:description><![CDATA[The main components of the birth process refer to the factors that interact with each other during childbirth. These components are grouped into 4Ps: power, which refers to uterine contractions and maternal pushing efforts; passage, which refers to the maternal pelvis that the baby passes through during labor; passenger, which refers to the fetus and placenta; and psyche, which refers to the client’s psychological status during labor. 

Now, let’s look at each of these components, starting with power. Involuntary uterine contractions are the primary force of labor that dilate and efface the uterine cervix, after which maternal pushing efforts kick in. The descending fetus puts pressure on the vaginal wall and the rectum, which triggers the urge to push. These pushing efforts aid uterine contractions to push the fetus through the maternal pelvis. 

The next P stands for passage, namely the maternal soft tissues, like the cervix, as well as the pelvis.  Now, during labor, the cervix dilates and effaces, meaning it gets wider and thinner, to allow for an easier passage of the fetal head. 

The pelvis is divided by an imaginary line called the pelvic brim into the upper or false pelvis, and the lower or true pelvis. The true pelvis is divided into the pelvic inlet above; the pelvic cavity in the middle; and the pelvic outlet below. Now, the right and left sides of the maternal pelvis are connected by cartilage called the symphysis pubis. During pregnancy, a hormone called relaxin increases, which softens joints, including, the symphysis pubis, which helps it to widen somewhat during childbirth to help accommodate the fetal head. 

Overall, the shape of the pelvis can be classified into 4 types: the wider, more open gynecoid pelvis; the narrower android pelvis; the narrow and elongated anthropoid pelvis; and the wide but shallow platypelloid pelvis. The pelvic shape, as well as the diameters of the pelvic inlet and outlet, can influence how easily the fetus can]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neonatal_respiratory_distress_syndrome_(NRDS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T0KebCIwR4uDAgP6rUL2wxr8Tx29Uc94/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neonatal respiratory distress syndrome (NRDS): Nursing]]></video:title><video:description><![CDATA[Neonatal respiratory distress syndrome is a respiratory condition caused by deficiency of lung surfactant. It most commonly affects preterm infants, meaning those born before 37 weeks. However, the risk is much higher for those born before the 28th week. The disorder is characterized by alveolar collapse, and noncardiogenic pulmonary edema, which can lead to hypoxemia and respiratory failure. 

Alright, now let’s quickly review the physiology of the respiratory system. Alveoli are tiny air-filled sacs where most gas exchange occurs, so as a person breathes, the inhaled oxygen moves from the alveolar sacs into the blood, while the carbon dioxide moves from the blood into the alveolar sacs to be exhaled. During intrauterine life, the alveoli are filled with fetal lung fluid, which expands the lungs and allows them to develop properly. By 24 to 25 weeks of gestation, surfactant production starts. 

This is an oily secretion that coats the interior of the alveoli and reduces surface tension to prevent their collapse. Surfactant typically builded up to an adequate level by 34 to 36 weeks of  gestation, but more surfactant can also be released during labor and immediately after birth to enhance the transition from fetal to neonatal life. Additionally, with labor approaching, the amount of fetal lung fluid starts decreasing as it gets absorbed from the alveoli into the interstitial space.

Now, at birth, several, mechanical, thermal, and sensory factors stimulate newborns to take the first breath. This allows them to force out the remaining fetal lung fluid and get air to enter the lungs. Infants crying also helps raise the pressure inside the chest, allowing more fluid to exit the lungs. Complete absorption of fetal lung fluid may take several hours after birth.

Okay, now the main cause of neonatal respiratory distress syndrome is insufficient production of lung surfactant, which can be due to premature birth or an abnormal pulmonary surfactant B gene, whi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Group_B_streptococcus_(GBS)_infection_in_pregnancy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MNKUDS-dT5_tIW_Q7hVNu3-aSY_wZcVx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Group B streptococcus (GBS) infection in pregnancy: Nursing]]></video:title><video:description><![CDATA[Group B streptococcus or GBS for short, is a common bacterium called Streptococcus agalactiae. It is a Gram positive, facultative anaerobe bacteria, meaning it can survive in both aerobic and anaerobic environments. This makes it suited to colonize the gastrointestinal and genitourinary tract; and in healthy, immunocompetent adults, it typically doesn&amp;#39;t cause any symptoms. However, in fetuses and newborns, it can cause infections that can lead to major and sometimes fatal complications.

Now, the main cause of GBS infection in pregnancy is when the bacteria colonizes the mother’s genitourinary tract and then gets passed on to the fetus during pregnancy or labor. Common risk factors associated with GBS infection in pregnancy include previous pregnancy with GBS infection, obesity, or Black ethnicity. Finally, preterm delivery, rupture of membranes of more than 18 hours, and vaginal delivery, also increase the risk of newborn GBS infection.

Now, pathology-wise, when GBS colonizes the genitourinary tract, it can ascend into the uterus and infect the fetal membranes, namely the chorion and amnion, causing chorioamnionitis. With chorioamnionitis, the infection can spread to the fetus, causing fetal distress or even intrauterine death. Another consequence is premature rupture of membranes and premature delivery. 

On the other hand, GBS can get passed on to the infant during labor when the bacteria is aspirated into the fetal airways. This can cause pneumonia or neonatal sepsis. Alternatively, bacteria from the blood can cross the blood-brain barrier and migrate into the cerebral spinal fluid, causing neonatal meningitis. Meningitis can lead to neurologic sequelae like sight or hearing loss and cerebral palsy. Unfortunately, all three of these conditions can lead to death in some newborns. 

Clinically, GBS infections during pregnancy are often asymptomatic. However, an intrauterine infection can cause non-specific symptoms like fever and bacteriuria, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fetal_circulation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-qUxYhX3S065OyfB4JcbQb3eRD_adVNj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fetal circulation: Nursing]]></video:title><video:description><![CDATA[Fetal circulation involves the delivery of oxygen and nutrients from the placenta to the fetus and the transport of waste products from the fetus to the placenta, in order for them to be eventually eliminated by the mother’s body. 

Fetal circulation has some unique features because the fetal lungs are not involved in gas exchange and there are three fetal shunts, which redirect the blood to ensure the highest oxygenated blood reaches the heart and brain, while redirecting blood away from the nonfunctional fetal lungs. 

Now let’s first review the physiology of the umbilical cord that connects the fetus to the placenta, which takes on the role of exchanging oxygen, carbon dioxide, nutrients, and wastes. The cord houses two umbilical arteries and one umbilical vein. The umbilical vein provides the path for oxygenated blood to flow from the placenta to the fetus, while the umbilical arteries carry deoxygenated blood back to the placenta. 

Now, oxygenated blood first flows through the umbilical vein and to the fetal liver, and here, the circulation divides as it meets the first fetal shunt called the ductus venosus. At this point, most of the blood passes through the ductus venosus and flows directly into the inferior vena cava. Meanwhile, the remaining blood perfuses the liver and then meets up with the rest of the blood in the inferior vena cava. Together, this blood flows into the right atrium of the fetal heart. 

In the fetal heart, the pressure on the right side is higher than on the left side of the heart. This is because the fetal lungs are filled with fluid and the arteries are tightly constricted, so the pressure in the fetal lungs is high,  leading to increased pressure in the right side of the heart.

This pressure difference allows a majority of the oxygenated blood in the right atrium to pass through the second shunt, called the foramen ovale, which is an opening between the two atria. 

This shunt allows most of the blood to bypass the lungs a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock_-_Hypovolemic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/imHmW_KvRiGx5OqsQHL4dVk-QiK6xSgf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock - Hypovolemic: Nursing]]></video:title><video:description><![CDATA[Hypovolemic shock is a life-threatening condition characterized by a decrease in intravascular volume in the cardiovascular system, which becomes insufficient to support adequate perfusion of the body tissues.

Now, let’s talk about the physiology of the cardiovascular system, which consists of the heart and blood vessels. The main job of the heart is to pump oxygenated and nutrient-rich blood through the arteries to the body tissues, and receive deoxygenated blood through the veins and pump it to the lungs to pick up more oxygen. 

For this to be possible, there are three key factors to keep in mind: the cardiac output, which is the amount of blood pumped out by the heart per minute; the intravascular volume, which is the amount of blood in the client’s circulation; and the peripheral vascular resistance, which is the resistance of blood flow in peripheral arteries. 

Normally, oxygen is delivered to the tissues because there’s enough pressure in the cardiovascular system to push blood through the body; so, blood pressure has a major effect on the amount of blood that reaches tissues and organs. For the most part, blood pressure is regulated by changes in peripheral vascular resistance and cardiac output, so that if one of them decreases, the other increases to try to compensate.

So, hypovolemic shock is caused by a significant decrease of intravascular volume, and can be classified as hemorrhagic and non-hemorrhagic. Hemorrhagic shock is the most common, and it’s usually caused by severe bleeding from postpartum hemorrhage, gastrointestinal bleeding, or traumatic injuries. On the other hand, non-hemorrhagic hypovolemic shock can be caused by anything that results in significant fluid loss, such as vomiting or diarrhea; renal losses, such as excessive diuresis in diabetic ketoacidosis or diabetes insipidus; excessive sweating, like in hyperthermia or hyperthyroidism; or third-spacing, which includes anything that causes intravascular fluid to shift into ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pertussis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZKrbPwcNRBKu3tzoIsEV6tiiTRaqdN4S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pertussis: Nursing]]></video:title><video:description><![CDATA[Pertussis, also known as whooping cough, is an acute respiratory infection caused by the bacteria Bordetella pertussis. The disease is characterized by paroxysmal cough, meaning fits of sudden and periodic cough, as well as abundant respiratory secretions. It can affect people of all ages, but it can be particularly severe, and even life threatening in children younger than 6 months. 

Now, the respiratory tract consists of the upper and lower airways, as well as the lungs. The tiniest branches of the lower airways, called the bronchioles, end with the alveolar sacs, which are lined by a thin membrane that allows gas exchange to occur. 

Now, the respiratory system is equipped with defense mechanisms against potential pathogens. For example, the upper and lower airways are lined with ciliated epithelial cells that sweep pathogens that make their way inside, to be expelled back out through the nose or mouth. At the same time, the lungs have plenty of immune cells, like macrophages, that react when a pathogen makes its way in by producing cytokines that attract more immune cells. These immune cells destroy and dispose of the invading pathogen. 

Okay, now, pertussis is an infection caused by a gram-negative bacillus, called Bordetella pertussis. Risk factors for acquiring infection include pregnancy, close contact with an infected individual and lack of immunization or underimmunization. 

Pathology-wise, pertussis is transmitted by airborne contagious droplets. After inhalation, the bacteria adheres to the epithelial cells of the upper respiratory tract and the nasopharynx. Once attached, it produces toxins that damage the local tissues, causing inflammation and edema of the respiratory tract. This results in abundant secretions of the respiratory tract.  In addition, some of the toxins can also paralyze the cilia, thus preventing the bacteria and the mucus secretion from being cleared. All this mucus irritates the trachea, causing fits of violent coughing.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pregestational_conditions:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/30VhO3xlRgWNLZhY-C4OsCu8TvuUzgO6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pregestational conditions: Nursing]]></video:title><video:description><![CDATA[Pregestational conditions are chronic medical problems that are present from before pregnancy and can pose a risk to the mother or the fetus during pregnancy. They include diabetes mellitus, thyroid problems, and certain cardiac conditions, as well as asthma.

Alright, now let’s quickly go over each of these conditions, starting with diabetes mellitus, which  is when the body has trouble moving glucose from the blood into the cells, so blood glucose levels are constantly high. There are two main types of diabetes: type 1 diabetes, which is when the body doesn’t make enough insulin; and type 2 diabetes, which is when the body makes enough insulin, but the cells are insulin resistant, meaning they don’t respond to insulin by taking glucose in. 

Next, there are thyroid problems, which can be split into hyper- and hypothyroidism. Hyperthyroidism occurs where there’s excess thyroid hormones, and this is generally caused by overproduction from the thyroid gland. Conversely, hypothyroidism is typically caused by an immune attack targeting the thyroid gland, causing destruction and inflammation, which results in low circulating thyroid hormones. Thyroid hormones are important because they increase the rate of metabolism in all cells, so they make us think, move, and talk faster, and they also increase heat generation. They also activate the sympathetic nervous system, the part of the nervous system responsible for the ‘fight-or-flight’ response, increasing cardiac output. 

Third, there are cardiac conditions, which can be either congenital or acquired. Common congenital heart defects include atrial septal defect, or ASD; ventricular septal defect, or VSD; and patent ductus arteriosus, or PDA. On the other hand, acquired conditions that can complicate pregnancy include rheumatic heart disease; valvulopathies, which are caused by a defect in one or more of the four valves of the heart; and cardiomyopathies, which are disorders affecting the heart muscle, called th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ectopic_pregnancy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0nZCNLHeR5K53Ptc2BOuPb_PRYG21QPG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ectopic pregnancy: Nursing]]></video:title><video:description><![CDATA[An ectopic pregnancy is a pregnancy that occurs somewhere other than in the uterine cavity, most commonly in one of the fallopian tubes.

Alright, now let’s quickly review the physiology of fertilization, starting with the ovaries, which are the paired female gonads. Each month, they release one mature egg, also called oocyte, which is the female gamete. After leaving the ovaries, this egg enters the fallopian tube and reaches the widest part of it, called the ampulla of the fallopian tube. This is where the few sperm that have made it this far after ejaculation surround the egg; and of them, a single sperm succeeds in entering the egg and fertilizing it, forming the zygote. The zygote then makes its way through the fallopian tube in order to reach the uterus; where it implants in the endometrium, also called the uterine lining. At the same time, the endometrial tissues react to a surge in progesterone released from the ovaries, and engorges with blood and fluids, to become a cozy home for the future embryo.

Now, the cause of an ectopic pregnancy in any given client is often unknown, but there are several risk factors. These include cigarette smoking; a history of pelvic inflammatory disease; conception by in-vitro fertilization; gynecologic surgery; current use of intrauterine devices; tubal ligation; or a previous ectopic pregnancy. All of these factors contribute to the formation of scar tissue within the fallopian tube, which in turn prevents the progress of the embryo into the uterus, causing it to attach to the tube itself.

Now, pathology-wise, in the vast majority of ectopic pregnancies, the embryo does not complete its journey to the uterus and implants in the fallopian tube, and this is called a tubal pregnancy. However, there are also ovarian ectopic pregnancies, in which case, the egg never leaves the ovary; as well as abdominal ectopic pregnancies, when the egg is “lost” to the abdominal cavity following ovulation, instead of entering the fal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Decision-making:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BnXe6bc-TuCY8eAyt-hCUTtORYSqs-tD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Decision-making: Nursing]]></video:title><video:description><![CDATA[Nurse Alma is the charge nurse on a medical surgical unit. During today’s shift, the unit is understaffed by one nurse who was unable to come in due to illness, and Nurse Alma has just received notification that her unit will be receiving an unexpected client admission. Nurse Alma needs to decide which nurse should admit and care for the new client. She will use her decision-making skills to determine the best client assignment. 

Decision-making is the process of making the best choice based on available evidence for a scenario. Thoughtful decision-making is important to determine what the most beneficial or least harmful option is for the people who it impacts. So Nurse Alma will consider all of her options and the evidence available to her to make the best decision for her team.

Now, when decision-making, a model that you can use to guide your process is the DECIDE model, which stands for: Define, Establish, Consider, Identify, Develop, and Evaluate. 

The “D” in DECIDE is for Defining the problem. This sounds simple but it can be a multi-step process when evaluating larger issues and includes determining barriers to the desired outcome. So, Nurse Alma’s problem is that there is a new client admission on the way and her barrier is that she does not have an adequate number of nursing staff to accommodate the admission. 

The “E” stands for Establishing the criteria you’ll base your decision on, or how you will measure the success of your decision. To do this, you can ask yourself three guiding questions: “What do I want to achieve with this decision?’”; “What do I want to preserve?”; “What problems do I want to avoid?” As Nurse Alma completes this step of decision-making, she decides she would like to achieve a safe client assignment, preserve her staff’s confidence in her, and avoid increasing staff stress. 

Next, the “C” stands for Consider, which means you should consider all of the potential courses of action. When Nurse Alma Considers, she determi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Managing_conflict:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3S3WY0PeRiGEAx-RJCAAr-ajT0m1xddU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Managing conflict: Nursing]]></video:title><video:description><![CDATA[Nurse Matt works on a medical surgical unit at a hospital and is caring for a client who requires a sterile, moist-to-dry dressing change. As Nurse Matt gathers the materials for the dressing change, a travel nurse named Monica approaches him and says, “You’re grabbing the wrong supplies, Matt. In the hospital I come from, we change the dressings differently and everyone here seems to be doing it wrong!” Nurse Matt is aware that Nurse Monica has upset several staff members by telling them to complete dressing changes the way she has been taught. Nurse Matt recognizes this difference in opinion has caused a conflict on the unit and decides to speak directly to Nurse Monica about this. He will use conflict resolution techniques to determine the best course of action. 

A conflict occurs when a person experiences a disagreement in values or beliefs within themselves or with other people. Conflicts can occur between any member of the healthcare team, such as nurses, nursing students, and physicians, as well as clients and their family members. 

In today’s complex healthcare environment, resolving conflicts, such as the one between Nurse Matt and Nurse Monica, is important in order to provide optimal client care and facilitate healthcare team performance.

Alright, conflict can be categorized into three main types: intrapersonal, interpersonal, and organizational. Intrapersonal conflict occurs within oneself and is a result of a person being confronted with ways of thinking which are different from what they are used to. An example of intrapersonal conflict would be a nurse having conflicting feelings when asked to work an extra shift. The nurse must balance feeling obligated to help the unit and also the need for self-care and rest. 

Interpersonal conflict happens when two or more individuals disagree about a topic. This is what is happening between Nurse Matt and Nurse Monica and is the most common type of conflict. 

Lastly, organizational conflict is when]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bladder_tumors:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E4P5n77tQWCgCMOD495H7x3lRc6owZj2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bladder tumors: Nursing]]></video:title><video:description><![CDATA[Bladder tumors are growths arising from various tissue layers of the bladder wall. Malignant bladder tumors include urothelial carcinoma, which is the most common type, as well as squamous cell carcinoma and adenocarcinoma, among others, and these tumors can spread to surrounding tissues and organs. 

In contrast, benign bladder tumors, including urothelial papilloma, leiomyoma, fibroma, and hemangioma, are less common, and stay localized to the bladder.

Okay, let’s quickly review some anatomy and physiology. 

The urinary bladder is a hollow visceral organ that’s basically a reservoir for holding urine. Let&amp;#39;s zoom into the wall of the urinary bladder which is made up of four layers. The outermost layer is called serosa, or adventitia. Next is the muscular layer, which contracts to allow urine to pass down into the urethra. After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. And finally, there’s the innermost layer, called the mucosa, which consists of a special type of epithelial cells, called urothelial cells.  

Now, the exact cause of bladder tumors is unknown, but there’s typically a genetic mutation in one of the cells of the bladder. These mutations may arise from a variety of risk factors. 
Nonmodifiable risk factors include age above 55 years, family history of bladder tumors, being assigned male at birth, and white race. 

On the other hand, modifiable risk factors include exposure to toxic substances, most importantly tobacco use, or industrial dyes, radiation, medications like cyclophosphamide, as well as obesity. Damage to the bladder from chronic urinary tract infections or recurrent kidney stones also increases the risk for bladder tumors.

Okay, so the pathology of bladder tumors begins once a cell of the bladder wall becomes mutated and starts dividing uncontrollably, forming a tumor. The most common type of benign bladder tumor is urothelial papilloma, which]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Herpes_zoster:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xLTeRzqRTXa0dYA22Hzz9rkBTByX6mfO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Herpes zoster: Nursing]]></video:title><video:description><![CDATA[Herpes zoster, also known as shingles, is a painful, blistering rash on a localized area of the skin that is caused by the reactivation of the varicella zoster virus, or VZV. This virus initially causes a disease called varicella, or chickenpox, and can lay dormant in nervous ganglia around the body for many years before reactivation.

Now, let’s quickly recap the physiology of the nervous system, which is divided into the central nervous system, including the brain and spinal cord, and the peripheral nervous system, which includes all the nerves that connect the central nervous system to the skin, muscles, and organs.

Peripheral nerves that originate from the brain are called cranial nerves, and they’re in charge of motor and sensory innervation of the head and neck. A specific cranial nerve, called cranial nerve V, or the trigeminal nerve, is responsible for the sensation in the face. Its sensory neurons create a nerve cell cluster called the trigeminal ganglion, located in the bones on the side of the face between the eyes and ears. 

Another cranial nerve, cranial nerve VII, also known as the facial nerve, innervates the muscles of the face. 

The peripheral nerves originating from the spinal cord are called the spinal nerves. Each nerve is formed by a dorsal and a ventral root. Ventral roots contain neurons that carry motor innervation from the spinal cord to the muscles. Sensory information, like touch, temperature, pain, and pressure from the skin and other tissues travel through 1st order sensory neurons, in the dorsal root ganglion near the spinal cord, then through the dorsal root, and into the spinal cord, where it synapses with the 2nd order neurons. Now, each spinal nerve is in charge of the sensation of a specific area of the skin, called a dermatome.

Now, herpes zoster is caused by the varicella zoster virus, also known as human herpesvirus 3 or HHV-3 for short, which is a DNA virus that belongs to the family of Herpesviridae. Important ri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Newborn_adaptation_to_extrauterine_life:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PDqo2Ru_RVuLon6oct-pDjb0S9KkfXbM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Newborn adaptation to extrauterine life: Nursing]]></video:title><video:description><![CDATA[During intrauterine life, the placenta supplies the fetus with oxygen and nutrients essential for its growth and development. After birth, this supply ceases, the infant has to adapt to the extrauterine environment. The main changes during this adaptation period include those of the respiratory and cardiovascular system. 

Now, in order to understand the changes that take place during transition to extrauterine life, let’s review some key differences between fetal and newborn circulation. Remember that during intrauterine life, the fetal lungs are not functional in terms of gas exchange. Instead, they are filled with fluid, and the arteries in the lung are constricted, resulting in high vascular resistance in the lungs. Because of this high pressure, relatively little blood reaches the lungs. Because no gas exchange occurs in the lungs, the fetus needs to get oxygen from the placenta. 

Now, there are three fetal shunts to help divert most of the blood away from the lungs, while maximizing the delivery of oxygenated blood to key organs like the brain and heart.  First is the ductus venosus that connects the umbilical vein to the inferior vena cava, thus allowing most of the oxygenated blood to bypass the liver and travel up to the heart. Next is the foramen ovale in the atrial septum, that allows blood from the right atrium to flow directly into the left atrium. This allows oxygenated blood to bypass the non-functional lungs and get pumped to the rest of the body instead by the left ventricle. The last shunt is the ductus arteriosus which connects the pulmonary artery to the aorta and also helps bypass the lungs. 

The liver and lungs still receive enough blood to keep their tissue healthy and growing, but the three shunts allow large quantities of blood to bypass them and help the fetus optimize its limited oxygen and nutrient supply. 

Now, toward the end of gestation, the fetal lungs start to prepare for extrauterine life. First, there’s increased produ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preterm_labor:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QwzFM_qFTw2YZrCT6PboRbxaQtq8nOqo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preterm labor: Nursing]]></video:title><video:description><![CDATA[Labor refers to uterine contractions and cervical changes that lead to childbirth, and this usually occurs between 37 and 42 weeks of gestation. So preterm labor is when labor occurs before 37 weeks gestation.

Okay, now, let’s start by looking at the physiology of labor, also called parturition. This process starts with the release of uterotropins like estrogen which makes the uterine smooth muscles more responsive to stimulation. The stimulation comes from uterotonic compounds like oxytocin and prostaglandin which can induce labor by causing uterine smooth muscle contraction.  These contractions are initially mild, short, and far apart, and progress to stronger, longer lasting contractions that are about 3 to 5 minutes apart. The contractions pull back on the tissue of the cervix, causing the membrane to efface and the cervix to dilate. 

Now, even though there are several conditions associated with preterm labor, the exact cause isn’t always clear. Stress is one common cause as it can lead to increased prostaglandin production and induce labor early on. This stress can be psychosocial, as well as biological, like when there’s an infection. Certain bacteria can also release toxins that either stimulate uterine contraction or erode the fetal membranes, causing premature rupture of the membranes. 

The strongest risk factor for preterm labor is previous preterm labor and birth. Other risk factors include polyhydramnios, meaning excessive amniotic fluid, or oligohydramnios, which is too little amniotic fluid; any structural abnormality of the uterus; in vitro fertilization; multiple gestation; and a history of elective pregnancy termination. Preterm labor is more common in clients with a low socioeconomic status,  lack of prenatal care, or if there is heavy alcohol consumption, cocaine use or heroin use, during pregnancy. 

Now, whatever the cause, preterm labor before the 34th week of gestation is associated with significantly increased morbidity and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Scoliosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-HG5n8HWSnqpv8d89SAdG89rRluJNjgs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Scoliosis: Nursing]]></video:title><video:description><![CDATA[Scoliosis refers to 3-dimensional deformity of the spine, that includes a rotational and lateral, or sideways curvature of the spine that resembles an “S” or a “C” shape. Scoliosis can be idiopathic, or without known causes; congenital, or present from birth; and neuromuscular, which occurs because of some other neuromuscular condition.

First, let’s quickly review some anatomy and physiology of the spine. The bony spine, also known as the vertebral column, is made of vertebrae, and there are intervertebral discs that sit  between adjacent vertebrae. These fibrocartilaginous structures act as a shock-absorbing apparatus of the spinal cord. 

Now, there are 33 vertebrae, which are organized in 5 main regions: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal. Now, the cervical and the lumbar regions slightly curve inward, creating the physiologic lordosis of the spine. On the other hand, the thoracic and the sacral regions normally curve backward, which is often referred to as physiologic kyphosis. Together, the vertebrae create a bony canal that houses the spinal cord and surrounding meninges. 

So, the most important functions of the spine include protection of the spinal cord and support of the head and body weight. The spine also provides the attachment of the rib cage and neighboring muscles; and allows great flexibility and motion of the trunk.

Now, based on the cause, scoliosis can be divided into three main types: idiopathic, congenital, and neuromuscular. Idiopathic scoliosis is the most common type, meaning there’s no identifiable cause. On the other hand, congenital scoliosis develops due to abnormal intrauterine development of the spine, and is present at birth. The last one is neuromuscular scoliosis, which is associated with conditions that affect the neuromuscular system. These include cerebral palsy, muscular dystrophy or atrophy, as well as spinal cord tumors and myelomeningocele, which is when the spinal cord and the surro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polycythemia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PlI5wIIUS1Gaa9q0BxXQm3SdQ9ygrHGR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polycythemia: Nursing]]></video:title><video:description><![CDATA[Polycythemia is a condition associated with an increased number of circulating red blood cells or RBCs for short. 

Polycythemia can be primary, meaning there&amp;#39;s a spontaneous increase in the production of red blood cells; or secondary, when another condition causes increased production. 

First, let’s cover some basic physiology of blood cells, starting with RBCs. When we breathe in, air flows through the nasal cavity, pharynx, and larynx, down into the trachea. From here, the air reaches the lungs, where RBCs pick up oxygen and transport it to the peripheral tissues, where they release it. 

After releasing oxygen, the RBCs pick up carbon dioxide. 

Carbon dioxide is a waste product of cellular metabolism, 

which is then transported back to the lungs, 

and eventually eliminated through the air that we breathe out. 

Additionally, red blood cells have an important role in maintaining the acid-base balance in the body. 

The production of red blood cells starts in the bone marrow, where the hematopoietic stem cells reside. 

In order to proliferate and reach their mature form, hematopoietic cells require stimulation by specific growth factors. One of these factors is a hormone called erythropoietin, produced by kidneys. Once produced, erythropoietin enters the blood and travels to the bone marrow, where it signals hematopoietic cells to differentiate into red blood cells. 

Moreover, if there’s tissue hypoxia or low levels of oxygen in peripheral tissues, the kidneys can increase the production of erythropoietin, therefore ramping up the production of red blood cells. 

Finally, the other two groups of blood cells include white blood cells, which primarily defend the body from foreign pathogens; and platelets, which have a key role in blood clotting and hemostasis.

Now, primary polycythemia, also known as polycythemia vera, is a chronic myeloproliferative disorder caused by an acquired mutation of the JAK2 gene, which codes for a protein that pr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Herniated_intervertebral_disc:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ykqLKDrGTKutEBsyK5y5C0JHRnO_kYyU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Herniated intervertebral disc: Nursing]]></video:title><video:description><![CDATA[A herniated intervertebral disc refers to a bulging or protrusion of part of the intervertebral disc, which is rubbery cushion between the vertebrae of the spine. Herniated intervertebral discs are one of the most common causes of back pain. 

First, let’s quickly review some anatomy and physiology. The bony spine, also known as the vertebral column, consists of 33 vertebrae that provide support for the head and protect the spinal cord. 
Between the vertebrae are the intervertebral discs, which are fibrocartilaginous structures that provide stability, allow spinal motion, and absorb shocks along the spinal column. 

They have a central part called the nucleus pulposus, which is composed mostly of water, but also proteoglycans and some collagen. It provides volume for the disc, absorbs shock, and helps distribute weight and pressure evenly between the vertebrae. The tougher, outer part is called the annulus fibrosus, which is composed mostly of collagen fibers, but also some water and proteoglycans. It provides stability and protects the central nucleus pulposus.

Finally, there’s an anterior longitudinal ligament, which runs down the anterior surface of the vertebrae, and a posterior longitudinal ligament, which is much narrower and attached to the posterior surface of the vertebral bodies, and the intervertebral bodies.

Now, the spinal cord travels through the spinal canal and stops at the second lumbar vertebra. Here it ends in a cone, called conus medullaris. Since the spinal cord is shorter than the spinal canal, the nerves of the lumbar, sacral, and coccygeal regions have to travel down the spinal canal to reach their corresponding openings. In doing so, they form a nerve bundle below the spinal cord called the cauda equina.

Now, the main cause for herniated discs seems to be the daily stress applied to the spine throughout a client’s lifetime. Less commonly, herniated intervertebral discs can be caused by spinal trauma, connective tissue disorders,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1wVPVMJQQL239L6t1__2jiXwR92nSiJm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal cancer: Nursing]]></video:title><video:description><![CDATA[Esophageal cancer is a malignant tumor that originates in the mucosa of the esophagus. There are two types of esophageal cancer, squamous cell carcinomas and adenocarcinomas.

Alright, now, the esophagus is a hollow tube that allows food to pass through from the pharynx to the stomach. And at both ends is a sphincter or a bundle of muscles that can block off or open the esophagus. The upper esophageal sphincter relaxes to allow food to pass through. The lower esophageal sphincter contracts to prevent acid reflux from the stomach.

Let’s zoom into the wall of the esophagus, which is made up of four layers. The outermost layer is a fibrous layer called the adventitia, and unlike the rest of the gastrointestinal tract, this layer does not contain a serosa. Next is the muscular layer, which contracts to move food through the esophagus.  After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. And then, there’s the innermost layer, called the mucosa, which comes into direct contact with food, and protects the esophageal wall from friction. The mucosa also has three layers of its own: a layer made of stratified squamous epithelium; a layer of connective tissue called the lamina propria, and a layer of muscle cells called the muscularis mucosae. Finally, at the lower esophageal sphincter, the esophageal mucosa joins the columnar gastric epithelium to form the gastroesophageal junction.

Alright, now, esophageal cancer occurs when epithelial cells in the mucosa acquire mutations that let them grow and divide out of control. Typically these are mutations in proto-oncogenes which result in a promotion of cell division, or mutations in tumor suppressor genes which result in a loss of inhibition of cell division. 

Now, mutations may arise due to a variety of risk factors. Risk factors for both squamous cell carcinoma and adenocarcinoma include age over 60 years, being assigned male at birth, asbestos ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia_-_Iron-deficiency:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gFuVT0wTQv2_B2sg5ElkNuomT6yDDx27/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia - Iron-deficiency: Nursing]]></video:title><video:description><![CDATA[Iron deficiency anemia is a common condition that occurs when there are decreased iron stores in the body, which is essential for the production of hemoglobin in red blood cells, or RBCs for short.

Now, let’s quickly discuss the physiology of RBC production, or erythropoiesis. This process takes place in the bone marrow, where a stem cell differentiates into an erythroblast, which starts synthesizing hemoglobin, which is a protein that’s able to bind and carry oxygen. Erythroblasts lose their nucleus and differentiate into immature RBCs, called reticulocytes. These immature cells are released from the bone marrow into the bloodstream, to ultimately become mature RBCs, called erythrocytes. Now, RBCs have a limited lifespan of 120 days, so they require continuous replacement through erythropoiesis. 

To do so, the body needs important vitamins and minerals, including iron, which is an essential component of hemoglobin. Now, iron is primarily obtained from a balanced diet that includes all types of foods. Once ingested, food passes through the gastrointestinal tract, where nutrients are slowly absorbed. Some nutrients, such as iron, are best absorbed in acidic environments like the proximal duodenum, where gastric acid lowers the pH, in order to absorb iron into the circulation.

Alright, now iron deficiency anemia can be caused by decreased dietary intake, decreased gastrointestinal absorption, increased body demand, or increased loss. The most common cause of iron deficiency is a decreased intake of iron-rich foods, such as red meat, beans, and leafy greens; risk factors include poor nutritional status from practicing strict diets, chronic alcohol use, and experiencing homelessness, abuse, or neglect. 

On the other hand, decreased gastrointestinal absorption of iron can occur due to decreased stomach acid production; risk factors include taking certain medications, such as proton pump inhibitors like omeprazole or H2 blockers like cimetidine; as well as u]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Legal_issues:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D7Atc1JdQ76uwws9S3AxJP7vQvSRL6W3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Legal issues: Nursing]]></video:title><video:description><![CDATA[Nurse Abe works in the emergency department and has noticed that one of the other nurses, Nurse Brynn, hasn&amp;#39;t been scanning the medication and client wristband barcodes prior to administering medications. Nurse Abe knows barcode scanning is a way to help prevent medication errors and so he questions Nurse Brynn who states, “I know the hospital policy says we’re supposed to scan medication barcodes, but I keep forgetting to do it. Don’t worry Abe, I still check the medications so I know they’re safe to give.” What Nurse Abe has witnessed is a potential nursing legal issue.

As a nurse, you are legally responsible for your actions when caring for clients. It is important to understand the legal issues that nurses can face in order to avoid potential consequences like disciplinary action by your employer, loss of credentials or certification, loss of your nursing license, and even criminal charges or jail time. 

To recognize legal issues in nursing, it is important to appreciate how legal terms, like liability and tort, guide professional nursing practice.  Liability means that someone is responsible for some wrongdoing according to the law. Another important term is tort, which is a wrongful act or omission against another person or their property that causes injury or harm. Torts are the most common source of legal liability for nurses. So if one of Nurse Brynn’s clients experiences harm from a medication error, Nurse Brynn could be held liable in a court of law for the tort of failure to use the medication scanning system. 

Alright, torts can be classified as intentional or unintentional. Intentional torts are deliberate acts against a person or their property that cause harm, such as battery or assault. Battery is when a person physically harms another person, like a slap or kick, and assault is when a person threatens to hurt another person causing fear.  

An intentional tort can also occur if there is a lack of informed consent for procedure]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Motivational_interviewing_(MI):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z5oOqFlLSneMOFPlWOpuSU2MRMi6srIk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Motivational interviewing (MI): Nursing]]></video:title><video:description><![CDATA[Nurse Joe works in a community health clinic where he regularly cares for Mr. Anand who has type 2 diabetes and hypertension. During the past several visits, Nurse Joe has encouraged Mr. Anand to stop smoking by teaching him the risks of smoking and also providing him with educational material on ways to quit. During the clinic visit today Mr. Anand says, “I really want to quit smoking but it just feels impossible.” Nurse Joe recently learned about motivational interviewing and decided to use this technique today with Mr. Anand. 

Motivational interviewing is a client-centered strategy that can be used to encourage clients to change a behavior that can be harmful to their health. It’s based on intrinsic motivation which is when a person engages in a behavior because it is personally rewarding to them. So, by using motivational interviewing, Nurse Joe can help Mr. Anand to identify personal goals that are meaningful for him to achieve so he feels more motivated to make a behavioral change. 

Motivational interviewing can be very effective when working with clients who need assistance making lifestyle changes, especially those clients who may feel ambivalent about making a change. Ambivalence is when your client feels uncertain or unmotivated to take the steps needed to produce behavioral change. Nurse Joe recognizes Mr. Anand is showing signs of ambivalence when Mr. Anand goes on to say, “I know I should quit smoking, but I really enjoy it.” 

Motivational interviewing can take some practice but there are three acronyms you can use to guide you, including, RULE, PACE, and OARS.

Let’s start with RULE which can help you remember the four guiding principles of motivational interviewing: Resist, Understand, Listening, and Empower. When using motivational interviewing with your client, the “R” in RULE stands for resist. This means it’s best to resist using the righting reflex, which is where you impose your solution about what they should do. Motivational inter]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Interprofessional_teamwork:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AOTzV_RNTFq1CZd7TTqjxEJ9R1auKe9s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Interprofessional teamwork: Nursing]]></video:title><video:description><![CDATA[Nurse Dara works in the surgical step-down unit where she has been assigned to care for Ms. Hart who experienced abdominal wound dehiscence 4 days ago after surgery for hernia repair, and is scheduled to be discharged today. Ms. Hart reports that she has trouble getting out of bed by herself and she tells Nurse Dara, “I’m really nervous about having to care for this wound at home.” Nurse Dara will work as part of the interprofessional healthcare team to assure that all Ms. Hart’s needs are met prior to her discharge. 

Now, interprofessional teams are groups of healthcare professionals working together to provide effective, client-centered care. This could include everyone from doctors and nurses, to pharmacists and therapists, dieticians, psychologists, technologists and technicians, to social workers and care managers. The members of the team will depend on the specific needs of the client. 

Interprofessional teams require interprofessional collaboration so the team can work together to create and carry out a healthcare plan that treats the client as a whole person. This will help prevent communication breakdown,reduce errors, improve efficiency of care delivery, and cut down healthcare costs.

Okay, there are 4 core competencies for effective interprofessional teamwork. First, there are  values and ethics for interprofessional practice, which means that team members should appreciate each team member’s contribution to the team in order to create shared values, such as a commitment to patient-centeredness, as well as safer, more effective care. 

Next are roles and responsibilities for collaborative practice, which means that team members should understand their own role and the roles of others so everyone can best apply their skills to meet the needs of the client. Then, there’s interprofessional communication, which emphasizes the need for open and effective communication between team members and with the client. And finally, team-based practice compe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Poliomyelitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BBYdEkwnRe6_cS8uk8dYU39WRuGilXhF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Poliomyelitis: Nursing]]></video:title><video:description><![CDATA[Poliomyelitis is a highly contagious viral infection that leads to severe nerve injury. It is caused by the poliovirus, which moves from the gut to the central nervous system. This can cause irreversible paralysis, breathing difficulties, and even death. 

Let’s start with a quick review of the physiology of the upper gastrointestinal system, which consists of the mouth, pharynx, esophagus, stomach, and the first part of the small intestine, called the duodenum. 

Now, let’s zoom into the wall of the gastrointestinal tract, which is made up of four layers. The outermost layer is called serosa or adventitia. Next is the muscular layer, which contracts to move food through the bowel. After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. And finally, there’s the innermost layer, called the mucosa, which consists of a layer of epithelium covering the lamina propria. 

The epithelium acts as a physical barrier that prevents harmful pathogens from entering the body. Additionally, the lamina propria houses immune cells, like dendritic cells and macrophages, that react to harmful pathogens. Additionally, round accumulations of lymphatic cells, called Peyer’s patches, can sometimes be found in the mucosa of the duodenum.

Now, the main cause of poliomyelitis is the poliovirus, which is an RNA virus that belongs to the Enterovirus genus, and the Picornaviridae family. Important risk factors for poliomyelitis include immunodeficiency; age below 5, being unvaccinated or undervaccinated; and finally, living in poor sanitary conditions, or traveling to an endemic area.  

Alright, now the pathology of poliomyelitis starts with acquiring the virus through the fecal-oral route through contaminated water or food. In some cases, it could also be transmitted through droplets produced by a sneeze or cough. 

Once in the gastrointestinal tract, the virus binds to receptors on the membrane of epithelial cells]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Therapeutic_communication:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GoWEJ0nCSBCaknmrSBKeofBdQiaM7Pzu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Therapeutic communication: Nursing]]></video:title><video:description><![CDATA[Nurse Rose works in an outpatient mental health clinic and has noticed that one of the clients, Gabriella, is visibly upset and sitting by herself away from the other clients. Nurse Rose says, “Gabriella, what’s wrong? Is something bothering you?” Gabriella rolls her eyes and shakes her head stating, “I just want to be left alone.” Nurse Rose is formulating a response when Gabriella stands up and yells, “Why don’t you go and talk to one of the other patients? You like them better anyway!” Nurse Rose is surprised by the increase in intensity of Gabriella’s emotions and does not understand what she is referring to. Nurse Rose will use what she has learned about therapeutic communication to determine how best to handle this situation. 

Communication is the process of sending and receiving information between two or more people. One type of communication that is used by many disciplines, including nurses, is therapeutic communication. Therapeutic communication is a type of communication where information between clinicians and clients is exchanged in order to collaborate effectively and promote the physical and psychological well-being of clients. Therapeutic communication is crucial to the formation of client-centered relationships, which can foster trust and respect, especially for clients experiencing emotional distress, like Gabriella.

Another use of therapeutic communication is de-escalation, which is a goal of communication when escalation occurs. Escalation refers to an increase, or rise in intensity, during an interpersonal interaction. This is what is occurring between Nurse Rose and Gabriella. Nurse Rose can recognize Gabriella’s emotions are escalating when she stands up and yells. When faced with an escalating interaction, it is important for the nurse to de-escalate the situation. De-escalation occurs when a person reduces the intensity of a conflict. One way to do this is through therapeutic communication.

There are two main types of communica]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cryptorchidism:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EEeYxlyBTeKJz-XEbTOlKtGVR8qNWkDF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cryptorchidism: Nursing]]></video:title><video:description><![CDATA[Cryptorchidism, also known as undescended testis, is a condition characterized by partial or abnormal descent of one or both testicles into their normal position within the scrotal sac. Cryptorchidism is commonly seen in neonates, and, in most cases, it spontaneously resolves during the first year of life.

First, let’s cover some basic physiology of testicular descent. Initially, during intrauterine development, testes develop in the abdomen.Here, each testicle is anchored to the labioscrotal swelling, which is the future scrotum, by a fibrous cord called the gubernaculum

Between the 7th and 12th week of fetal development, the gubernaculum shortens, eventually pulling the testicles down toward the inguinal canal, where they usually stay until the 7th month of intrauterine development. Finally, during the last month of pregnancy,the testes descend into the scrotum. The process is controlled by an androgen hormone called testosterone. Once in the scrotum, the testes have an adequate environment for normal sperm production, also known as spermatogenesis, which starts at puberty. 

Finally, during fetal development, a small cremasteric muscle develops within the gubernaculum. The main function of this muscle is to retract the testicle toward the inguinal canal when the outside environment is not suitable for testes, like, for example, when it’s too cold.  

Now, the exact cause of cryptorchidism remains unknown. Some theories suggest that cryptorchidism may occur due to gubernaculum abnormalities, while others connect this condition with androgen deficiency. Cerebral palsy and conditions associated with abdominal wall defects, like Prune-Belly syndrome, can also result in cryptorchidism. Important risk factors for cryptorchidism include family history, as well as birth-related risk factors, such as preterm birth; and low birth weight. 

Additionally, clients with some congenital conditions have a higher incidence of cryptorchidism than others. These inc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Precocious_puberty:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mxQrUExFTlCuC_fcm259in8xS4Oghaqp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Precocious puberty: Nursing]]></video:title><video:description><![CDATA[Puberty is the natural process of sexual maturation where an individual becomes sexually mature. When puberty begins too early, it’s called precocious puberty, and this generally means puberty has started before the age of 8 in those assigned female at birth, and 9 in those assigned male.  

Let’s start with some physiology. Puberty is normally under the control of the hypothalamus-pituitary-gonadal axis. It begins when the hypothalamus starts releasing gonadotropin-releasing hormone, or GnRH for short, which travels to the nearby pituitary gland to stimulate the release of two gonadotropin hormones into the blood. These are luteinizing hormone, or LH, and follicle-stimulating hormone, or FSH. These two hormones then signal the ovaries and testes to release sex hormones, mostly estrogen and progesterone in those assigned females at birth, and testosterone in those assigned males at birth. 

The increase in sex hormones triggers the maturation of the sex organs and the development of secondary sexual characteristics, including the appearance of facial and pubic hair, breast development, and voice changes, among others. Now, on average, puberty begins around age 10 and a half  in those assigned female at birth, and 11 and a half in those assigned male. Generally speaking, puberty lasts for about 4 years, but this can vary quite a lot depending on factors such as race, genetic background, and geographical region.

Okay, precocious puberty can occur because of central factors that involve the brain, hypothalamus, and pituitary gland; or because of peripheral causes that involve the ovaries, testicles, or adrenal glands. So, common causes of central precocious puberty include brain tumors or brain trauma. Most of the time, however, there’s no identifiable cause, and it’s simply called idiopathic central precocious puberty, and it’s influenced by factors like when a parent began puberty, as well as an individual&amp;#39;s weight. 

Conversely, causes of periphe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_arterial_hypertension_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gq_ZFJJAROae_4KjhxHdngP-TlGh6Dj5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary arterial hypertension (NORD)]]></video:title><video:description><![CDATA[Pulmonary arterial hypertension, or PAH, is a rare disorder characterized by high blood pressure in the blood vessels of the lungs, specifically the pulmonary arteries. The pulmonary arteries are blood vessels that carry blood from the right side of the heart through the lungs. So, when pulmonary arterial pressure rises, blood backs up into the right side of the heart, eventually leading to right-sided heart failure. PAH more commonly occurs in middle-aged, biological females. 

Individuals with PAH initially experience symptoms like difficulty breathing, fatigue, weakness, chest pain, dizziness, and syncope, or loss of consciousness. As the disease progresses, signs of complications may start appearing, including hemoptysis, or coughing up of blood; and hoarseness due to compression of a nerve in the chest by an enlarged pulmonary artery. Eventually, untreated individuals end up in right heart failure, which causes abnormal fluid collection all over the body, resulting in edema, or swelling of the face and lower limbs; ascites, or fluid collecting in the abdomen, liver enlargement , raised jugular venous pressure, and in the end stages - cyanosis, or abnormal bluish discoloration of the skin due to low blood oxygen levels.

PAH is most often idiopathic, which means that the cause is unknown. Occasionally, PAH can be a heritable disorder due to mutations in genes such as the BMPR2 gene. Without this gene working, there&amp;#39;s excessive proliferation, or rapid reproduction of the smooth muscle cells in blood vessels. Another cause of PAH is connective tissue disorders like scleroderma, which damage the endothelial layer of the pulmonary arteries, leading to a release of vasoconstricting substances, causing tightness and narrowing of the blood vessels, such as endothelin 1, thromboxane, and serotonin, as well as smooth muscle hypertrophy, or enlargement. Other causes of PAH include congenital heart disease with left-to-right shunts and portal hypert]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fresenius_-_Hemodiafiltration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VUnw_HwNT529e-ZmXjiQ5pxUQqGpOhG1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fresenius - Hemodiafiltration]]></video:title><video:description><![CDATA[Hemodiafiltration, or HDF, is a renal replacement modality that combines diffusion and convection to improve removal of molecules in the middle molecular weight range versus hemodialysis. Like hemodialysis, blood and dialysate flow in opposite directions in the dialyzer, cleaning the blood of toxins and excess fluid.

While diffusion allows solutes to passively filter through a high-flux dialyzer down a concentration gradient from blood to dialysate, convection uses pressure to actively “drag” larger, potentially uremic molecules, such as Beta-2-microglobulin, across the dialyzer into the ultrafiltrate. During an HDF treatment, approximately 20-30% of the plasma water is removed by ultrafiltration.

The convection volume, or total ultrafiltration volume, consists of the substitution volume plus the net ultrafiltration volume for fluid removal. The substitution volume is the amount of replacement fluid infused into the patient’s blood line to maintain fluid balance. This fluid must be sterile and nonpyrogenic. In high volume HDF, a large volume of plasma water is ultra filtered and must be replaced.

In online HDF, potable water undergoes extensive treatment with carbon filters, reverse osmosis, and sterilizing ultrafilters, with one ultrafilter being installed into the circuit before the site of infusion. This allows delivery of sterile, non-pyrogenic fluid to the patient and use of online substitution fluid, instead of saline, for priming, infusion, or as a bolus administration.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mumps_(Parotitis):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eMh2msAbQdCKuqTaM4WZwu9dS2SClTwg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mumps (Parotitis): Nursing]]></video:title><video:description><![CDATA[Mumps is a highly contagious, systemic viral infection caused by the mumps virus and is usually associated with fever, swelling and inflammation of the parotid glands, or parotitis. Thanks to vaccination, there are fewer cases of mumps, but in some parts of the world where the population is not immunized, it’s still possible to see outbreaks.

Let’s start by discussing the physiology of the immune response. Now, after a foreign antigen enters the body, it runs into antigen-presenting cells, like macrophages and dendritic cells, which ingest it and break it into fragments. These antigen fragments are then presented on their surface and recognized by T helper cells, which help activate B cells to produce antibodies against that antigen. These antibodies will then bind to the pathogen and attract other immune cells to attack it.  

Now, the cause of mumps is the mumps rubulavirus, or just mumps virus. This is an RNA enveloped virus that belongs to the Paramyxoviridae family. 

Important risk factors for mumps include immunodeficiency; being unvaccinated or undervaccinated; coming in contact with an infected person; and traveling or living in an endemic area.

Moving on to pathology. Mumps virus is an airborne virus, meaning it spreads via small virus-containing droplets that get flung in the air when an infected client coughs or sneezes. 

If another client breathers in these droplets, or they get in contact with infected surfaces and then touch their mouth, they can become infected. 

Once the virus enters the body, it enters epithelial cells that line the nasopharynx where they replicate. The new viruses are released to infect other nearby cells. 

Some of the mumps virus is picked up by the macrophages and dendritic cells, and carried to the local lymph nodes.

The virus continues to replicate inside the lymph node and mucus membrane and eventually, they’ll get into the bloodstream where they can spread to other organs throughout the body. 
The salivary gl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Zika_virus:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BrmJ8yCSSG2ECusl0v_UuB-PTZao3hE-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Zika virus: Nursing]]></video:title><video:description><![CDATA[Zika fever, also known as Zika disease, Zika infection, or just Zika, is an infectious disease caused by the Zika virus. This is a vector-borne infection that is transmitted by the bite of an infected Aedes mosquito.

Let’s start by discussing the physiology of the immune system, which is subdivided into innate and adaptive immunity. Innate immunity consists of natural barriers, like skin and mucous membranes; natural killer cells, which help fight virus-infected and tumor cells; and phagocytes, such as macrophages, neutrophils, and dendritic cells. 

When a pathogen breaches the natural barriers and enters the body, the innate immune system reacts quickly. Some of the first cells on the scene are macrophages and neutrophils, which directly fight the pathogen. At the same time, they also secrete small molecules called cytokines to increase the permeability of local blood vessels and message other immune cells that there’s an active fight in the body. Additionally, cytokines induce the production of acute inflammatory proteins and cause systemic effects, such as fever. 

Simultaneously, dendritic cells engulf and digest the pathogen, eventually presenting small fragments of it on their surface. At this point, the adaptive immune system, which relies on B and T cells, can come to the rescue. Specifically, T helper cells recognize these fragments and help activate B cells, which eventually produce antibodies.  

These antibodies circulate throughout the body and bind to affected cells that express the antigen on their surface, thereby enabling NK cells and cytotoxic T cells to recognize and destroy them.

The cause of Zika fever is the Zika virus, which is a small single-stranded RNA virus that belongs to the Flaviviridae family. 

The most important risk factor for getting Zika fever is traveling to or living in endemic parts of the world where Zika fever is highly present. These include Central and South America, the Caribbean, Africa, as well as south and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock_-_Obstructive:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ex0gVR1ESsalWynD9oOGAS5vTd6citJX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock - Obstructive: Nursing]]></video:title><video:description><![CDATA[Obstructive shock is a life-threatening condition that develops when a mechanical obstruction prevents the heart from filling properly or pumping enough blood through the cardiovascular system. This reduces the amount of oxygenated blood that reaches the tissues, causing acute hypoperfusion and tissue hypoxia.

Alright, let’s go over the physiology of the cardiovascular system, which consists of the heart and blood vessels. The heart pumps out blood to the body’s organs and tissues with each heartbeat, which consists of two phases: systole, which is when the heart contracts and pumps the blood out; and diastole, which is when the heart relaxes and fills with blood. The stroke volume, meaning the amount of blood pumped out by the heart in a single heartbeat, is influenced by the cardiac contractility, preload, and afterload. Contractility is how strongly the heart is contracting during systole. Preload is how much the heart’s smooth muscle is stretched at the end of diastole, and this is mainly dependent upon how much blood is filling the heart. The more they&amp;#39;re stretched the more force they can generate during contraction, kind of like a rubber band. Afterload refers to the resistance that the heart must overcome to pump out blood during systole, and this is affected mainly by peripheral vascular resistance under non-pathological conditions. This is mainly determined by the vasodilation and vasoconstriction of blood vessels. If we multiply the stroke volume by the heart rate we’ll get the cardiac output, which is the amount of blood pumped out by the heart in one minute, and it’s the main measure of the heart’s function. 

Okay, now obstructive shock is caused by an obstruction that prevents the heart from filling properly with blood during diastole, thus decreasing preload, or pumping blood out during systole, which increases afterload. One of the most common causes of obstructive shock is cardiac tamponade, where blood or fluid builds up in the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Smallpox:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5EzUN7VMQ5S3QWGyGpSbMDxCTdulEsUY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Smallpox: Nursing]]></video:title><video:description><![CDATA[Smallpox is a very contagious and potentially fatal viral disease caused by Variola virus and is usually associated with fever, malaise, headache and back pain followed by a characteristic rash. Thanks to vaccination, smallpox is the first human infectious disease that was successfully eradicated worldwide in 1980.

Let’s start by discussing the physiology of the immune response. It all begins in the bone marrow, where undifferentiated hematopoietic stem cells begin to differentiate into different types of white blood cells. Some of these cells migrate to the thymus where they become mature T cells, also known as T lymphocytes, which defend us against intracellular viruses, fungi, and tumor cells. Additionally, they are responsible for long-term immunity. 

Now, after a foreign antigen enters the body, it runs into antigen-presenting cells, like macrophages and dendritic cells, by whom it is engulfed and digested into fragments. These antigen fragments are then presented on their surface and recognized by T helper cells, which help activate B cells to produce antibodies against that antigen. Next, these antibodies bind to any affected cell that expresses the antigen on its surface, eventually enabling natural killer or NK cells and cytotoxic T cells to easily recognize and destroy them. Furthermore, these natural killer cells enhance the inflammatory response by producing cytokines that recruit neutrophils, macrophages, and mast cells.

Okay, the cause of smallpox is Variola virus, which is a large DNA virus that belongs to the Orthopoxvirus genus and the Poxvirus family. Important risk factors for contracting smallpox, before it was eradicated, included close contact with an infected client or contaminated surfaces, infancy, older age and immunodeficiency. Nowadays, clients with occupational exposure, such as laboratory researchers that study Variola virus, health care workers, first responders, and military personnel can also be at risk. It’s import]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Managing_change:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q3R2a9HKQpGLp7bwire8ZtbmT3SPefqS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Managing change: Nursing]]></video:title><video:description><![CDATA[Nurse Jack is the manager of an outpatient surgical clinic. This clinic has just announced that some traditional telephone communication between healthcare team members will now take place through an instant messenger application on the computer. Nurse Manager Jack recognizes that there is some resistance within the nursing staff about this change so he speaks to the unit charge nurse, Nurse Taylor. Nurse Manager Jack says, “The other staff nurses respect your opinion, so I’m wondering if you can assist with the transition by adopting the change to act as an example for the rest of the staff.” 

Nurse Taylor responds, “I know that instant telehealth communication between clinicians can improve continuity of care and client safety; I’d be happy to help!” Nurse Manager Jack and Nurse Taylor will work together with the other staff nurses to manage this change. 

Change is a complex process that involves making an alteration or modification to something that already exists. Change can be planned or unplanned, also known as first order and second order change, respectively. Planned, or first order change, is a deliberate and organized process which has the goal of making improvements over time, such as transitioning to an instant messaging communication system. On the other hand, unplanned, or second order change, is usually unanticipated. This type of change involves completely disrupting how things are normally done in order to adapt quickly to developing situations. An example of this is when healthcare facilities had to quickly implement COVID-19 precautions during the onset of the pandemic. 

Okay, so whether a change is planned or unplanned, it’s important to understand the change process so change can be effectively managed. One way to approach planned change is to break it into 3 stages: unfreezing, moving, and refreezing. 

Just as you would defrost a frozen meal before cooking it, change must go through the initial step of unfreezing, which is when in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Omphalocele_&amp;_gastroschisis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l0Hsv4KrQ3a1rIyx4xbTdguBSl6MWTeg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Omphalocele and gastroschisis: Nursing]]></video:title><video:description><![CDATA[Omphalocele and gastroschisis are both congenital abdominal wall defects. An omphalocele is an umbilical ring defect where the abdominal contents, such as the gastrointestinal tract or liver, can protrude into an external peritoneal sac. Alternatively, in gastroschisis, the abdominal contents slip outside the abdomen without a sac.

Alright, let’s quickly review the physiology of the development of the abdominal wall. From the outside in, the abdominal wall is formed by the skin, superficial fascia, muscles, the deep fascia, and the parietal peritoneum which lines the abdominal cavity. During the third to fourth week of fetal development, the embryo starts to change shape from a flat, three-layer disc to something more shaped like a cylinder, a process called embryonic folding. In the horizontal plane, the two lateral folds eventually come together and close off at the midline, except for at the umbilicus, where the umbilical cord connects the fetus to the placenta. This folding allows for the formation of the gut within the abdominal cavity. 

During around the sixth week of development, the liver and intestines grow really quickly, and because the abdominal cavity is still pretty small, there’s limited space, which causes the midgut to herniate through the umbilical ring into the umbilical cord, and this happens normally. At about week 10, though, the abdominal cavity typically has grown enough to allow the midgut to come back from the umbilical cord.

Now, the causes of omphalocele and gastroschisis are mostly unknown, but they are associated with certain conditions or environmental exposures. Omphaloceles are associated with genetic and chromosomal abnormalities such as Trisomy 13, 18, or 21, or Beckwith-Wiedemann syndrome which is a genetic condition where the infant grows larger than normal. Meanwhile, gastroschisis is rarely associated with genetic conditions but instead is related to fetal exposure to nitrosamines in tobacco and cyclooxygenase inhi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stages_of_labor:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BydBsLBTQDi6Iw6ug8nnI2vkTOC-3A_X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stages of labor: Nursing]]></video:title><video:description><![CDATA[Labor is the process at the end of pregnancy during which the baby passes through the birth canal. It occurs spontaneously, usually between 37 and 42 weeks of pregnancy. Labor involves a series of continuous and progressive contractions of the uterus, as well as dilatation and thinning of the cervix. 

Now, let’s look at the physiology of labor, which is made up of the first, second, third, and fourth stage. 

The first stage of labor begins with the onset of true labor and ends when the cervix is 100% effaced, or thinned and shortened, and fully dilated at 10 centimeters. Now, the first stage can further be subdivided into a latent phase, an active phase, and a transitional phase. 

The latent phase starts with the beginning of regular contractions, which usually start out as mild, and then increase in frequency, duration, and intensity. Cervical dilation progresses from 0 to 3 cm and effacement progresses from 0% to 40%. 

Also during this phase, the fetal membranes usually rupture spontaneously, if they haven’t ruptured already. 

The length of the latent phase is typically much longer in nulliparous individuals, meaning those who have never previously given birth, then for multiparous individuals, who have previously given birth.

Next, during the active phase, the frequency, duration, and intensity of contractions continues to increase, and the rate of cervical dilatation and effacement accelerates, expanding from 4 to 7 cm, along with an effacement of 40% to 80%.

The fetus starts to descend, and is usually between stations − 2 to 0. Remember that the fetal stations represent the number of centimeters that the fetal presenting part is above or below the ischial spines of the maternal pelvis; so essentially, they measure fetal descent through the birth canal. 

Finally, during the transition phase, the frequency, duration, and intensity of contractions continues to increase, cervical dilation progresses from 8 to 10 cm, effacement progresses from 80% ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Evidence-based_practice_(EBP):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Db4nb4RSRtmM0wN6PLPtXbBgSFGk38d4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Evidence-based practice (EBP): Nursing]]></video:title><video:description><![CDATA[Nurse Jamaal works at a long-term care facility and has noticed that the average number of catheter-associated urinary tract infections, or CAUTIs, has been increasing each month.  Nurse Jamaal speaks to Nurse Jenny, another staff nurse, about the increased incidence of CAUTIs and asks about the facility policy for catheter care. Nurse Jenny replies, “We clean urinary catheters once per day here. It’s how we’ve always done it.” 

Nurse Jamaal knows that CAUTIs can negatively affect client health and be very costly to healthcare institutions so he wonders if a more frequent cleaning schedule, such as twice per shift, would be more effective than once per shift over the span of one month. In order to address this question, Nurse Jamaal decides to implement evidence-based practice, called EBP. 

EBP is a process which addresses a clinical problem by using the best evidence available to implement practice changes. The goal of EBP is to improve client outcomes and overall quality of care. 

The foundation of EBP in healthcare is research, which is a systematic process of validating, refining and generating  knowledge. Research and EBP work hand in hand to guide nurses in making effective and appropriate decisions using clinical judgment. In order to try to find a solution to decrease the rate of CAUTIs within the facility, Nurse Jamaal should use EBP. 

EBP is a systematic process which includes seven steps, which are numbered zero to six: Cultivating a spirit of inquiry, asking the question, searching and collecting evidence, appraising the evidence, integrating the evidence, evaluating the outcomes, and disseminating the outcomes. Following this step-by-step approach ensures that you obtain the strongest available information to improve client care. 

Step Zero is cultivating a spirit of inquiry. You can do this by noticing the potential for improvements in safety or care, and always questioning clinical practice instead of accepting what you have been taught]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disseminated_intravascular_coagulation_(DIC):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6U1HdkgySr_JgyrWRIj50W4vRJGfn2O6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disseminated intravascular coagulation (DIC): Nursing]]></video:title><video:description><![CDATA[Disseminated intravascular coagulation, or DIC for short, is a rare but life-threatening condition. It is characterized by accelerated clotting within blood vessels, which in turn leads to increased consumption of platelets and clotting factors, which can ultimately result in uncontrollable bleeding. 

Now, let’s quickly review the physiology of clotting, also known as the coagulation cascade, which is activated in response to an injury to limit the bleeding. So normally, when a tissue and its blood vessels are injured, the circulating platelets are activated locally and aggregate to form a temporary plug at the site of injury. The platelet plug then starts attracting circulating clotting factors, which starts off the coagulation cascade, ultimately resulting in the formation of fibrin, which in turn builds a tightly connected mesh that stabilizes the platelet plug. Lastly, in order to avoid excessive clotting, a protein called plasmin balances off the clotting process by breaking down the fibrin mesh and ultimately dissolving the clot through a process called fibrinolysis. 

Now, DIC is caused by the presence of an underlying disorder that triggers uncontrolled activation of the coagulation cascade.  

The most common cause is sepsis. Other causes include cancer, serious trauma, and obstetric complications, such as a placental abruption or amniotic fluid embolism.  

In addition, DIC can be caused by a severe immune reaction, which can be triggered by an incompatible blood transfusion, organ transplant rejection, or toxins like snake or spider venom. 

Now, the pathology of DIC develops when a severe disorder or immune reaction triggers massive systemic activation of the coagulation cascade, resulting in widespread clot formation intravascularly, hence the name disseminated intravascular coagulation. These clots can then go on and block small and midsize vessels, causing ischemia or necrosis of the involved tissue. Additionally, this widespread clotting l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperemesis_gravidarum:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XN3OuXZ_Q0SGiE_FdQ2Pdg4uQqqISC9w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperemesis gravidarum: Nursing]]></video:title><video:description><![CDATA[Nausea and vomiting of pregnancy, or morning sickness, is a common sign of pregnancy. However if there’s more severe and persistent nausea and vomiting it is called hyperemesis gravidarum. This disorder can be dangerous to the mother and fetus if left untreated. 

First, let’s quickly review some relevant physiology during pregnancy. There are several hormonal changes, like increased estrogen and progesterone, as well as increased levels of human chorionic gonadotropin, or beta-hCG for short. These changes ensure the normal progression of pregnancy, and also contribute to some maternal physiological changes, such as relaxation of smooth muscles in various parts of the body. 

This leads to decreased motility in the gastrointestinal tract so there’s a delay in the movement of food through the stomach and intestines. In addition, relaxation of the lower esophageal sphincter allows stomach acid to reflux up the esophagus. This can cause “heartburn” and sometimes nausea. Due to these changes, many pregnant mothers experience “morning sickness” which is mild and episodic nausea that can appear, despite its name, at any time of the day. It typically starts as early as 5-6 weeks of gestation and ends at 16 to 20 weeks. This is considered a physiological process during pregnancy and is harmless to the mother and fetus.

Now, the cause of hyperemesis gravidarum is not fully understood, but it’s thought that some people produce increased levels of estrogen, progesterone and especially beta-hCG or they respond to the increased levels of these hormones more severely. 

Some risk factors for hyperemesis gravidarum include conditions that cause an additional increase of beta-hCG levels, like multigestational pregnancy and gestational trophoblastic disease. Other risk factors include being pregnant for the first time, called primigravida, white race, as well as a family history of hyperemesis gravidarum, which suggests a genetic component. Those with a personal history o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shoulder_dystocia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/quinai_mQle4OukG3ssfZjp4TaixotCB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shoulder dystocia: Nursing]]></video:title><video:description><![CDATA[Shoulder dystocia is an obstetrical emergency that can occur during vaginal delivery, and it refers to when the fetal shoulders can’t progress past the maternal pubic bone after the fetal head has been delivered. This usually requires additional obstetrical maneuvers to deliver the baby safely. 

Let’s start by looking at the anatomy and physiology of the birth canal during delivery, starting with the pelvis, made up of the sacrum and the paired hip bones, each of which is made up of the ilium, ischium and pubic bones. The anatomy of the female bony pelvis differs from the male bony pelvis, in that it’s wider and flatter in shape and has a wide pubic arch, which helps with vaginal delivery. Usually, the female pelvic inlet is about 12cm in an antero-posterior diameter, and 13cm in a transverse diameter.  

Now, remember that the bisacromial diameter, meaning the distance between the outermost parts of the fetal shoulders, is usually between 12 and 15 centimeters. Because of that, the fetal shoulders typically enter the pelvis at an oblique angle, and the posterior shoulder, meaning the one facing the back of the birth canal, is usually a little ahead. Following external rotation of the fetal head, the anterior shoulder can usually glide under the symphysis pubis in order to be delivered. 

Now, shoulder dystocia is usually caused by discrepancy between fetal shoulders and maternal bony pelvis. So, risk factors for shoulder dystocia include maternal factors, which can be remembered with the acronym SAP-DOE. This stands for small pelvic inlet; advanced age; prior history of shoulder dystocia or large infants; gestational or pregestational diabetes, obesity, and excessive maternal weight gain. The main risk factor related to the fetus is fetal macrosomia, or a fetus that’s larger than normal. Finally, there are risk factors related to the labor process, which include a prolonged second stage of labor, abnormal labor progress, and labor induction. Now, patholo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Crisis_intervention:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/id_gItx9TNGfswHAGEgpmEvMRqqWTeDT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Crisis intervention: Nursing]]></video:title><video:description><![CDATA[A crisis is a sudden, temporary, overwhelming emotional reaction caused by a stressful event perceived as a threat. Crisis intervention is a short-term management method used by health professionals in clients who are experiencing a crisis.

Now, there are three main types of crises: developmental, situational, and existential crises. Developmental crises are predictable and expected occurrences during life. Common examples of developmental crises include graduation, new job, marriage, the birth of a child, and retirement. Situational crises are unpredictable random and unexpected events. Common examples of situational crises include severe illness, job loss, unwanted pregnancy, divorce, and the death of a loved one. Finally, existential crises are usually related to one’s life&amp;#39;s meaning, purpose, and freedom. One common example of existential crisis occurs when an older person reflects on their life and accomplishments only to feel unfulfilled and dissatisfied.

Now, regardless of the type of crisis, there are typically four main phases. During the first phase, the client encounters a stressful situation or a precipitating event that disrupts their psychological balance and causes discomfort and anxiety. As a result, the client activates problem-solving and coping mechanisms to resolve the crisis. 

If the client fails to resolve the crisis, they enter the second phase. During the second phase, discomfort and anxiety continue to rise, and the client starts perceiving this stressful situation as a threat, resulting in it affecting their daily function and quality of life. Since problem-solving and coping mechanisms have failed, the client switches to a trial and error method, which uses various mechanisms in an attempt to resolve the crisis. 

But, if the trial and error method fails, the client enters the third phase, which is associated with further negative impact on their daily function, severe panic, and even physical symptoms, such as sweati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disaster_management:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/52HLzJuSTzSYMIsRqrzuY5HPS1iAJ00z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Disaster management: Nursing]]></video:title><video:description><![CDATA[Nurse Judy is working in the pediatric intensive care unit when she feels the ground start to shake beneath her feet. She looks around at the faces of her colleagues on the unit who appear confused and a bit afraid. The shaking lasts 10 seconds and then the unit clerk asks, “Was that an earthquake?” Nurse Judy responds, “I’m not sure. I’ve never been in an earthquake before.” Within minutes, the charge nurse is notified that there has been an earthquake and that the disaster management plan has been initiated. 

A disaster, or mass casualty event, is when illnesses or injuries exceed the resources or capabilities of a healthcare facility or a community. Disaster management, also called emergency preparedness and response, is the planning and actions taken by the healthcare team to decrease the potential for harm during a disaster. 

Now, disasters can be categorized as both internal and external. An internal disaster takes place within the facility and can include fires, hurricanes, explosions, violence in the facility, or loss of critical utilities like water or electricity. These types of disasters may require evacuation of the facility.

On the other hand, external disasters occur outside of the facility. These disasters can be natural or man-made. Natural disasters include weather-related events such as hurricanes, tornadoes, earthquakes, like at Nurse Judy’s hospital, or pandemics. Man-made disasters, also called technologic disasters, include events like a nuclear reactor malfunction or terrorism which can include nuclear, biologic, or chemical sources of terrorism. At times, special considerations, like decontamination and containment, must be taken for nuclear, biologic, or chemical disasters. In some cases, a disaster can be considered both internal and external, like when a hurricane results in loss of critical utilities at a hospital and also casualties in the community. 

Most healthcare facilities have their own disaster management plan which ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_-_Conducting_a_literature_review:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rHYj_kfPR-WVURG3QRXyHHjnSYWXRXq2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research - Conducting a literature review: Nursing]]></video:title><video:description><![CDATA[Nurse Marin works in a cardiac catheterization lab. Last week, a client experienced a major bleed from the puncture site after leaving the cath lab. This is the third bleeding event in the past month. Nurse Robin, who also works in the lab, asks “I wonder if there is something we can do differently to prevent bleeding in this client population?” Nurse Marin agrees and proposes that the healthcare team begin a quality improvement study on how to prevent bleeding in the post-catheterization period. As a first step in this research study, Nurse Marin will perform a literature review to learn more about best practice in the post-catheterization client.

Literature is any written document like a newspaper, magazine, scientific journal, or book. A literature review is done when a researcher wants to compile all of the literature that currently exists on a topic to answer a research question or problem. This is sometimes called the ‘state of the science.” A literature review is often done as one of the first steps of a research study or it can be published alone as a summary of what is known about a topic.

Now, literature can be classified in a few different ways. First, you can categorize literature as either theoretical or empirical. Theoretical literature discusses the application of a theory to practice. Types of literature that fall into this category are theories and theoretical models. Nurse Marin finds a source that describes how the Theory of Self-Care could be applied in the post-catheterization period. Empirical literature, on the other hand, includes sources that use direct or indirect observation, like quantitative and qualitative research. Nurse Marin finds an example of empirical literature when she comes across a quantitative research study showing that clients on anticoagulants during pre-cardiac catheterization were more likely to have post-catheterization bleeding.

Next, literature sources are categorized as either primary or secondary. Prima]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infant_of_a_diabetic_mother_(IDM):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sJmCgB01QSmdEmvNVmoQgmw3RYasl1wJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infant of a diabetic mother (IDM): Nursing]]></video:title><video:description><![CDATA[Infants of mothers with diabetes, or IDMs for short, have a higher risk of developing fetal and neonatal complications, including growth abnormalities, respiratory distress, and metabolic complications, in addition to preterm delivery.

Alright, let’s take a look at the physiology of glucose metabolism during pregnancy. During fetal development, all of the nutrients the fetus receives come directly from the mother&amp;#39;s blood through the placenta. Glucose is the primary source used by the fetus for growth and development. Fetal insulin reduces blood glucose by binding to insulin receptors embedded in the cell membrane. When activated, the insulin receptors allow glucose to be transported into the cell, thereby moving glucose from the blood and into the tissues. During pregnancy, hormones released by the placenta increase the mother’s body’s resistance to insulin, resulting in higher levels of maternal blood glucose. These metabolic changes allow the fetus to receive a steady supply of glucose necessary for fetal growth and development.

Now, diabetes occurs when the body’s ability to produce or respond to the hormone insulin is impaired, resulting in higher blood glucose levels. Diabetes in pregnancy can be either pregestational, which is where diabetes is diagnosed before pregnancy; or gestational, which is where mothers without previously diagnosed diabetes have high blood glucose levels during pregnancy, especially during their third trimester. The risk of fetal and neonatal complications increases with higher maternal glucose levels or BMI.   

Now, pathology-wise, poor glucose control at the time of conception and during the first trimester can interfere with organogenesis in the embryo, resulting in major birth defects and spontaneous abortions early in pregancy; and this most common with pregestational diabetes, because blood glucose is more likely to be elevated around the time of conception and during the first trimester when the fetal organs]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_hemorrhage:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4KXihKPATgWi9lK72PTKhilcSzetsj_C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postpartum hemorrhage: Nursing]]></video:title><video:description><![CDATA[Postpartum hemorrhage or PPH is an obstetrical emergency which occurs when there is any significant loss of blood after delivery of a baby. Now, some blood loss is expected during childbirth, but PPH is when the blood loss during the first 24 hours exceeds 500 mL after vaginal birth or 1000 mL after cesarean delivery. Significant bleeding in the first 24 hours after delivery is called early or primary postpartum hemorrhage, while late or secondary postpartum hemorrhage occurs 6 weeks to 12 weeks after birth. 

Okay, let’s start with some physiology. So, after delivery, the uterus tends to regress back to its normal size and resume its pre-pregnancy position by the sixth week, a process known as involution. Immediately after the delivery of placenta, the smooth muscles of the uterus continue to contract and squeeze down on the placental arteries where they are attached to the uterine wall, causing them to clamp them shut and reduce uterine bleeding. 

There are also some physiological changes that occur during pregnancy that begin to change back to pre-pregnancy levels in the postpartum period. For example, during pregnancy there is increased blood plasma volume in relation to red blood cell mass. As a consequence, maternal hemoglobin and hematocrit are usually relatively low during pregnancy, since the same amount of red blood cells are circulating in a higher volume of blood. After delivery, through increased diuresis or urine production, and increased diaphoresis or sweat production, blood volume returns to normal in about 6 to 12 weeks, and hemoglobin, and hematocrit levels normalize in 4 to 6 weeks. Likewise, during pregnancy, plasma fibrinogen and other pro-coagulant factors increase, and they stay elevated until 4 to 6 weeks following delivery. 

The most common causes of postpartum hemorrhage can be divided into two groups; the early causes and the late causes. The early causes can easily be remembered as the 4 Ts: Tone, Trauma, Tissue, and Thrombin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Enuresis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YzIHWp4fTmKx8grqAXPOaPO_SvyaTRmw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Enuresis: Nursing]]></video:title><video:description><![CDATA[Enuresis refers to involuntary urination in children who have passed the age of toilet training, which is typically around 5. Enuresis is more commonly known as “bedwetting,” and this is called nocturnal enuresis if it happens mainly at night, or diurnal enuresis if it mainly happens during the day. Primary enuresis is defined as involuntary urination in a client who has never developed bladder control. Secondary enuresis refers to involuntary urination in a client who’s already developed bladder control. 

Okay, first, let’s cover some basic physiology of urine production and excretion. Kidneys filter the blood to produce urine in a process that is controlled by several hormones, including vasopressin, which is also known as antidiuretic hormone, or ADH for short.  ADH  is produced by the hypothalamus and stored in the posterior pituitary. Now, when a person is thirsty or dehydrated, the posterior pituitary releases ADH into the blood, which then travels to the kidneys to increase water reabsorption, subsequently decreasing urine production. More ADH is released during the night to prevent urination until the morning. 

Now, once the kidneys filter the blood, they produce urine that is passed through ureters down into a hollow, muscular organ called the bladder. The bladder’s main function is to store urine, and as the urine accumulates, the walls of the bladder start to stretch, subsequently stretching the specialized nerve cells located in the bladder wall. Once stretched enough, these nerve cells send a signal through the spinal cord to the pontine micturition center in the brainstem and activates the micturition reflex. As a result, the bladder contracts to push out urine, while the internal and external urethral sphincters relax to let the urine out. Ultimately, this results in micturition or urination. 

Now, until the 12th month of life, infants have no voluntary control over urination. Between the 12th and 18th month, they develop some control, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Basic_electrocardiogram_-_Normal_sinus_rhythm_(NSR):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g1dX_ua6St2aIzFjxcQmEAIfRte9HcfT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Electrocardiogram (ECG) - Normal sinus rhythm (NSR): Nursing]]></video:title><video:description><![CDATA[An electrocardiogram, commonly referred to as an ECG, is a routine noninvasive diagnostic test that uses electrodes placed on the skin to provide a graphic representation or picture of cardiac electrical activity. The standard ECG, is also known as a 12-lead resting ECG because it has 12 leads or sets of electrodes. These include six limb leads, which are placed on the arms and legs, and six precordial leads, which are placed around the chest. Keep in mind that a 12 lead ECG only uses 10 electrodes. That&amp;#39;s because the chest electrodes record one lead each, while the limb detectors, together, actually record 6 leads.

Now, let’s quickly review the electrophysiology of the heart. The cardiac conduction system is made up of specialized myocardial cells that can create and send an electrical impulse, also called an action potential. These cells have many special features, including automaticity, meaning they can generate an impulse by themselves; conductivity, meaning they can carry the impulse to other cells; and contractility, which is the ability to shorten the length of their fibers, causing a contraction. 

The way it goes is that the electric impulses begin in the sinoatrial or SA node, which is located at the junction of the superior vena cava and right atrium. The SA node is considered the pacemaker of the heart and spontaneously and rhythmically produces impulses at 60 to 100 beats per minute. The impulse then moves quickly through the atrial muscle causing depolarization. When the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. Meanwhile, the impulse lands at the atrioventricular or AV node, which lies at the lower back section of the septum that separates the right and left atria. Conduction velocity or the speed at which the impulse is propagated slows way down in the AV node. This allows time for the atria to contract while the ventricle fills. From the AV node, the depolarization wave]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neurological_assessment_-_Neonate:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hXC_7K_7SSC_kkg7dacSNk-GQLSQMngN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neurological assessment - Neonate: Nursing]]></video:title><video:description><![CDATA[Newborn neurological assessment is a part of the thorough evaluation of the newborn that’s performed within 24 hours after birth. The goal is to confirm normal neurological status and early detection of treatable conditions and conditions that might affect their development.

Begin your assessment by observing the infant&amp;#39;s posture and muscle tone. A healthy term infant will be flexed and have good muscle tone; the cry will be strong; and the motor activity will be spontaneous and symmetrical. 

Problems such as  prematurity; birth injury; exposure to opioids; or problems like hypoglycemia or sepsis are associated with abnormal assessments that include  limp, floppy muscle tone; asymmetrical motor activity; jitteriness; or a weak, high-pitched cry.

Let’s start with normal newborn reflexes. During the assessment, the strength and symmetry of the infant’s reflexive responses are evaluated. It&amp;#39;s important to note that some reflexes are normally present at birth, but they should disappear by a specific age. If they persist beyond that age, it could indicate a neurological issue that requires further investigation.  

First, let’s focus on the Babinski reflex. The Babinski reflex is induced by lightly stroking the lateral aspect of the sole of the foot. Normally, the infant responds by hyperextending the big toe back and upwards while spreading the other toes. Normally, the Babinski reflex disappears eight to nine months after delivery. 

Moving on to the Moro reflex. This reflex is sometimes called the startle reflex, because it is often seen in response to a loud noise. When assessing the Moro reflex, lift the infant up a few inches, and then suddenly lower them. 

Alternatively, you can withdraw the hand that’s supporting the head, allowing the head to fall back into your hand. Normally, the infant responds by extending their arms outward and opening their hands. There may also be a slight extension of the neck. This is followed by flexion ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Systemic_lupus_erythematosus_(SLE):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DKg1yQKATDKKJdYhocuZYCqUTq2tW6HJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Systemic lupus erythematosus (SLE): Nursing]]></video:title><video:description><![CDATA[Systemic lupus erythematosus, or simply SLE or lupus, is a chronic autoimmune disease that affects multiple systems, mainly the skin, joints, and serous membranes. 

SLE is progressive, meaning that it gets worse over time with alternating periods of remission and exacerbation. A less common type of lupus particularly affects the skin, called cutaneous lupus erythematosus, or CLE for short. Clients with this condition eventually develop a full-blown SLE over time.

Now, let’s quickly recap the physiology of the immune system, which protects the body from harmful agents. This can be done with the aid of immune cells, including macrophages and lymphocytes. 

So, let’s imagine that a foreign particle enters the body, it will be faced by macrophages, which swallow this harmful agent and break it down, leaving a small particle called an antigen. The macrophage then presents this antigen on its surface for another type of immune cells to recognize, called T lymphocytes. Types of T lymphocytes include cytotoxic T lymphocytes, which fight against intracellular pathogens and cancer cells by initiating cell death; as well as T helper cells, which activate another type of lymphocytes, called B lymphocytes. 

Once activated, B lymphocytes can differentiate into plasma cells or memory cells. Plasma cells produce antibodies. These bind to antigens found on the surface of the pathogen, producing immune complexes. 

So, an antibody tags the pathogen for other immune cells to recognize. In contrast, memory cells monitor the body for the same antigen, and when the pathogen visits the body again, these cells convert to plasma cells, and start producing antibodies to fight this pathogen even faster than the first exposure. 

During development, the immune cells learn how to skip the antigens found on the surface of body cells and not react to them, called self-tolerance. This is the main function of another type of T lymphocytes, called regulatory T cells, which sup]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_designs:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0m3sFksdSwSGgy-jRrKnA7YORomNdmjB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research designs: Nursing]]></video:title><video:description><![CDATA[Nurse Ian works as a school nurse, and has noticed that many students visiting the nurse’s office have been reporting vague symptoms such as headache, fatigue, and upset stomach. However, after assessing them, Nurse Ian isn’t able to identify a specific cause. It seems, though, that the students generally tend to feel better after sitting quietly in the office for a few minutes and then are ready to return to class. Nurse Ian wonders if the symptoms are related to stress and decides to conduct a literature review to better understand if implementing stress reduction techniques helps to lower nurse office visits. As Nurse Ian reviews the literature, he discovers different kinds of research designs that address the topic. 

Okay, so research is a systematic process of validating, refining, and generating knowledge. It is used by nurses and other members of the healthcare team to answer questions that come up when caring for clients. When conducting research, a research design is chosen, which is the overall strategy used to organize the study in order to answer the research question. The two broad approaches to research design are quantitative and qualitative. There are also mixed-method designs, which combine both quantitative and qualitative into one research study.

First, let’s look at quantitative research designs, which are systematic and objective. These studies primarily use numerical and statistical data, which can come from formal experiments, surveys, clinical trials, information from existing data sets, or questionnaires.

Now, quantitative research designs include descriptive, correlational, experimental, and quasi-experimental designs. Descriptive research is used to understand more about a population or phenomenon. It often answers a “What is?” type of question, like the article Nurse Ian finds that answers the question “What are the characteristics of students who visit the school nurse?” 

Next, there’s correlational research, which shows th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Common_discomforts_of_pregnancy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rlfELp61ReCjFb1JGOekRzsWTNyM-96V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Common discomforts of pregnancy: Nursing]]></video:title><video:description><![CDATA[Common discomforts of pregnancy refer to all temporary symptoms and changes that pregnant clients experience as their babies grow and develop within the uterus. The most common discomforts of pregnancy include nausea, vomiting, heartburn, backache, round ligament pain, urinary frequency, constipation, hemorrhoidal disease, varicose veins, and finally, leg cramps. 

First, let’s start with nausea and vomiting which is often attributed in part to pregnancy hormones. It typically occurs in the morning and as a result, is often referred to as morning sickness. Nausea and vomiting are some of the earliest discomforts of pregnancy and can be worsened by fatigue, cooking smells, and fried, greasy, or spicy food. 

Now, morning sickness should not be confused with hyperemesis gravidarum, which is a condition that also occurs during pregnancy that’s characterized by severe vomiting that interferes with the client’s daily life. It could also result in weight loss, dehydration, electrolyte imbalance and may require hospitalization, IV fluids and antiemetics. 

Management of nausea and vomiting includes eating small and frequent, high protein meals, maintaining hydration, eating slowly, and avoiding odors or other factors that can trigger nausea. Increasing intake of vitamin B6 can also be helpful, as well as consuming beverages containing ginger, like ginger ale or ginger tea.

Next up is heartburn or pyrosis. Now, the esophagus and the stomach are separated by a muscular valve called the lower esophageal sphincter, which prevents the reflux of stomach contents back into the esophagus. Early in pregnancy, hormonal changes lead to a decreased tone of the lower esophageal sphincter, thereby allowing the stomach contents to reach the esophagus and cause heartburn. Later in pregnancy, the growing fetus can directly exert pressure on the stomach, causing the stomach contents to move back into the esophagus. 

Management of heartburn includes eating small, frequent meals a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Necrotizing_enterocolitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2Odj55NtRYan2ui3w83Z2OUhQTuoQ-1J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Necrotizing enterocolitis: Nursing]]></video:title><video:description><![CDATA[Necrotizing enterocolitis or NEC for short, is an inflammatory condition of the gastrointestinal tract characterized by mucosal damage and necrosis of the gastrointestinal wall. This is an urgent condition primarily seen in preterm infants.

Now, let’s cover some basic physiology and histology of the 4 main gastrointestinal layers. The outermost layer is called the adventitia or serosa and it’s thin and fibrous. Next up is the muscularis externa which is made up of smooth muscle cells located in the outer longitudinal layer and in the inner circular layer. These layers work together to move food forward via peristalsis which is a series of coordinated wave-like contractions. 

The next layer is the submucosa, which consists of dense connective tissue that contains blood vessels, lymphatics, and nerves. Finally, the innermost layer is called the mucosa, which secretes mucus and digestive enzymes but also absorbs nutrients from the gastrointestinal lumen. 

The intestines also contain a variety of non-pathogenic bacteria that make up a healthy intestinal flora. These aid with food digestion as well as protect the intestine from pathogenic microorganisms by out competing them. However, the fetus develops in a sterile environment, so their gastrointestinal tract is also sterile. Beneficial bacteria can only start colonizing their gastrointestinal tract during delivery and will continue after birth.

Now, the exact cause of necrotizing enterocolitis remains unknown, but some theories suggest that it’s associated with bacterial invasion of the gastrointestinal wall. Several risk factors have been associated with necrotizing enterocolitis, including prematurity, and low birth weight. 

Another risk factor for necrotizing enterocolitis is formula-feeding, possibly due to the loss of protective components of breastmilk, such as oligosaccharides, lactoferrin, and cytokines. Other important risk factors include genetic predisposition and the use of antibiotics.

Now,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spontaneous_abortion:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-KxUbjkuT0KXkXUdF7bHaOAJRQSIdISA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spontaneous abortion: Nursing]]></video:title><video:description><![CDATA[Spontaneous abortion, commonly referred to as a miscarriage, is the loss of pregnancy by natural causes before a gestational age where the fetus can live outside the uterus. This is generally classified as any time before 20 weeks of gestation or when the fetus is 500 grams or 1.1 pounds, or less. Loss of pregnancy at 20 weeks gestation and beyond is called stillbirth or fetal death. Three types of spontaneous abortion include incomplete, complete, and missed. 

Now let&amp;#39;s quickly review the physiology of gestational development. First, fertilization takes place in the ampulla of one of the two fallopian tubes, which is a muscular passageway where the egg moves from its starting position in the ovaries to the uterus. After about 6 to 8 days, the zygote begins implanting into the uterus. During the first four weeks of pregnancy, the four fetal membranes develop. These are the chorion and the amnion, as well as the yolk sac and the allantois. Of these, the allantois gets incorporated into the umbilical cord, the amnion becomes the amniotic sac, the chorion contributes to the development of the placenta, while the yolk sac eventually shrinks and disappears. Now, the placenta, along with two umbilical arteries and one umbilical vein, is the main exchange point between the pregnant individual and the developing fetus throughout pregnancy. This serves as an exchange point between the pregnant individual and the fetus.These structures allow for an exchange between the pregnant individual and the fetus, where nutrients and oxygen rich blood pass to the fetus, and waste products pass from the fetus.

Alright, now, there are many causes for a spontaneous abortion, the most common of which is a fetal chromosomal disorder. Often, this chromosomal disorder is a trisomy where the fetus has 3 copies of a specific chromosome instead of 2. Certain trisomies like, 16 and 22, are incompatible with life. A spontaneous abortion can also occur because of maternal c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_bowel_disease_-_Crohn_disease_&amp;_ulcerative_colitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xJVn0i6IQPuDroct2_BqBQm1TE2wa8fH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory bowel disease - Crohn disease and ulcerative colitis: Nursing]]></video:title><video:description><![CDATA[Inflammatory bowel disease or IBD is a condition characterized by chronic gastrointestinal tract inflammation due to autoimmune reactions, as well as systemic symptoms like fatigue, fever, and unintentional weight loss. There are two types of IBD, Crohn disease and ulcerative colitis.

The gastrointestinal tract consists of a long tube, where food travels through, which runs from the mouth to the anus. 

Now if we zoom into a cross-section of the gastrointestinal tract, the walls are typically lined by the same four layers of tissue. From the inside out, there’s the mucosa, which absorbs nutrients and secretes mucus and digestive enzymes; the submucosa, a dense layer of tissue that contains blood vessels, lymphatics, and nerves; the muscularis externa, which contracts to move food through the bowel; and the outermost layer is either the adventitia or the serosa, and faces the abdominal or peritoneal cavity.

So when we eat a big meal, the food travels from the mouth, down the pharynx and esophagus, to reach the stomach, which has a handful of glands that secrete hydrochloric acid and pepsin to help digest the food, now called a bolus. 

Then the bolus passes towards the small intestine, or small bowel, made of the duodenum, jejunum, and ileum, where nutrients are absorbed.  Examples are  - monosaccharides, amino acids, fatty acids, electrolytes, minerals, vitamins, and water. 

To increase the surface for absorption, the mucosa in the small intestine has lots of tiny ridges and grooves, each of which has little finger-like projections called villi. And in turn, each villus is covered in tiny little microvilli. Then, whatever isn’t absorbed travels to the large intestine, made of the cecum, colon, rectum, and anal canal. 

Here, there are trillions of bacteria, collectively called the gut microbiome, which help produce essential B and K vitamins.  Now, in the large intestine, a little more water and electrolytes are absorbed to finally form the feces that a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developing_a_research_problem_&amp;_hypothesis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nLYN0g3hRoSV_EIKjLXxEvdcQIWaodd0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developing a research problem and hypothesis: Nursing]]></video:title><video:description><![CDATA[Nurse Jory works in the community health clinic. In the past year, there’s been an increase in the number of clients not showing up for their appointments and Nurse Jory wants to understand why. 

Research is a systematic process of validating, refining, and generating knowledge. It is used by members of the healthcare team, such as nurses, to answer questions that come up when caring for clients. 

A research problem is a specific area of knowledge that needs further investigation and it is sometimes phrased as a question. Nurse Jory wants to understand more about situations that impact clinic attendance, so they use the question, “What reasons do clients give for not keeping their scheduled appointments at the community health clinic?” 

Next, the research purpose is generated from the research problem. The research purpose is a single sentence that explains what you are looking to learn by completing the research study. So, Nurse Jory’s research purpose is “The purpose of this research study is to explore barriers to appointment attendance.” 

After the research problem and purpose statement comes the research hypothesis, by identifying the research variables. Research variables are the concepts that are measured, manipulated, or controlled in a study. Oftentimes, researchers want to know how one variable affects another variable. For example, a researcher may want to know how daily exercise impacts blood pressure. 

Now, there are different types of variables to consider, including independent variables, dependent variables, extraneous variables, confounding variables, and demographic variables. First are the independent and dependent variables. So, let’s go back to the exercise and blood pressure example. The independent variable is not affected by the other variables, so in this case, the amount of exercise you get does not depend on blood pressure, so it’s independent.  The dependent variable will change based on other variables in the study, in thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Ventricular_fibrillation_(Vfib):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dc-HId3ASa2uqUAz5Bm-gHauS8yNUPCe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Ventricular fibrillation (Vfib): Nursing]]></video:title><video:description><![CDATA[Ventricular fibrillation or V-fib for short is a life-threatening condition, which occurs when the ventricular muscle fibers start firing impulses from multiple foci in a totally disorganized manner. As a result, instead of a single, coordinated contraction, there is quivering of the ventricles.

Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.  

From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles, causing them to depolarize. This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG. Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the pause between ventricular depolarization and repolarization is represented by the ST segment. Sometimes, immediately after the T wave, there’s a U wave, which represents late repolarization of the ventricles. 

Okay, now back to ventricular fibrillation, which can be caused by disruption to normal heart muscle conductiv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_&amp;_development_theories:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3LSRcl3_Ts2r2RSt93T76it3Q3u28ufR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development theories: Nursing]]></video:title><video:description><![CDATA[Growth involves physical changes in height and weight and appearance of the body, while development refers to a change in functional ability, such as cognitive, motor, and psychological aspects of the client. Growth and development start from the time of conception and progress until a person dies. Growth and development theories provide a framework to understand this wide array of changes, and they help healthcare providers plan individualized care for clients based on their stage of development, and to provide anticipatory guidance for parents and caregivers.

Major growth and development theories include biophysical developmental theory by Gesell,  psychosocial development theory by Erikson; cognitive development theory by Piaget; moral development theory by Kohlberg; and finally, the psychoanalytic development theory by Freud.

OK, let’s start with Gesell&amp;#39;s theory of biophysical development, which focuses on physical growth, and promotes the idea that every child has unique growth patterns that are influenced by an interaction between genes and the environment. 

It also states that even from early prenatal life, growth occurs in a cephalocaudal and proximodistal manner. Cephalocaudal growth means that the head and brain develop first and then progress towards the feet, while proximodistal growth means that the central body parts, like the heart, develop before distal parts like arms and legs. 

Erikson&amp;#39;s theory of psychosocial development focuses on the psychosocial aspects of human development, such as personality, thinking, and behavior. Erikson described eight stages of psychosocial development, from infancy to adulthood, during each of which a client experiences opposing conflicts that need to be resolved in order for development to be successful.

The first stage occurs from birth until one year of age, and is characterized as trust vs mistrust. During this stage, the infant needs physical comfort and a reliable and sensiti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Flail_chest:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5ItI1M1BSdCauRB4GTkE_uc-SXyHJjmM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Flail chest: Nursing]]></video:title><video:description><![CDATA[Flail chest is a serious condition, often caused by severe blunt chest trauma. It occurs when multiple consecutive ribs are fractured, creating a separate, free floating section of ribs and connecting tissue that moves out of sync with the rest of the chest during breathing. 

First, let’s quickly look at the anatomy and physiology of the thoracic cage. The thoracic cage is made up of 12 pairs of ribs and the sternum, which together create the shape of the chest wall and protect thoracic structures, such as the heart, lungs, and blood vessels. 

Now, the key muscles involved in breathing are the intercostal muscles, which are located between each set of ribs, and the diaphragm, which covers the whole bottom of the thoracic cage. When a person inhales the diaphragm contracts, moving downward and the intercostal muscles contract to move the rib cage out. This increases the volume while decreasing pressure in the thoracic cavity. The change in pressure pulls air down into the lungs. In contrast, when a person exhales the diaphragm and intercostal muscles relax which decreases the volume, while increasing pressure in the thoracic cavity. This makes air move out of the lungs.

Now, the main cause of a flail chest is blunt trauma to the chest, which can be caused by falls, abuse, car crashes, crush injuries, or even cardiopulmonary resuscitation.

Risk factors for a flail chest include modifiable ones, such as intoxication, and practicing contact sports; as well as non-modifiable ones, such as advanced age, and being assigned male sex at birth.

Okay, now, the pathology of a flail chest begins when a blunt trauma causes three or more ribs to fracture in two or more places, or when there’s bilateral detachment of ribs from the sternum. This creates a segment of the ribs that is not mechanically attached to the rest of the chest wall, As a result of these two pathologies, the chest moves in a paradoxical or uncoordinated fashion. This means that when the pers]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physiologic_changes_-_Postpartum:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5T1qn-DuRlC1ONEM0pmHMDOITGuSFYzx/_.png</video:thumbnail_loc><video:title><![CDATA[Physiologic changes - Postpartum: Nursing]]></video:title><video:description><![CDATA[The postpartum period, also known as puerperium, is defined as the first six weeks after delivery. Physiologic changes during the postpartum period include the reversal of changes that occurred during pregnancy. Moreover, these changes are primarily caused by a rapid drop in estrogen and progesterone.

Now, after delivery, a client usually loses 4500 to 5800 grams or 10 to 13 lb, which covers the weight of the fetus, amniotic fluid, and the placenta. The weight loss starts immediately after delivery and continues over the next several months due to normalization of blood volume and  increased caloric expenditure from milk production. 

Okay, let’s focus on reproductive changes, starting with the uterus. After delivery, the uterus begins to return to its nonpregnant state of size and position, a process called uterine involution. As soon as the placenta is delivered, uterine muscle fibers constrict uterine blood vessels, preventing a life-threatening condition called postpartum hemorrhage. Uterine contractions, often referred to as afterpains because they cause sharp pain in the lower abdomen, continue during the postpartum period to further aid uterine involution. Now, clinicians can track the progress of involution by palpating the top part of the uterus, called the fundus. At about 12 hours after delivery, the fundus can be palpated at 1 cm above the umbilicus. After that, it normally descends by about 1 centimeter, or 1 fingerbreadth, per day, until it reaches the pelvic cavity by the 14th day. 

Now, let’s take a look at vaginal discharge after birth, called lochia. There are three types; lochia rubra, lochia serosa, and lochia alba. Lochia rubra refers to the dark red vaginal discharge that is present for the first 3 days. It consists of blood, small blood clots, decidua, and mucus. As the bleeding reduces, the volume of vaginal discharge reduces, and lochia rubra transforms into lochia serosa. 

Lochia serosa refers to the thin, red to brown vaginal ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Neonate:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZdOSKWIeTcq_j2cA5k4cisjHQ3yjYLYw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Neonate: Nursing]]></video:title><video:description><![CDATA[The physical assessment of a newborn is an ongoing process to monitor the newborn’s adaptation to extrauterine life, and to identify problems that need immediate intervention. At the same time, the assessment considers factors such as the prenatal history; any complications during the pregnancy, labor, and birth; the type of anesthesia or analgesia used during birth; if any neonatal resuscitation measures were needed; and the newborn’s gestational age.

Let’s start by looking at the newborn’s vital signs. First, the apical pulse is auscultated. It’s a good idea to assess this first, when the infant is in a quiet state, and before any other assessments which could agitate them. A newborn’s heart rate normally varies between 120 and 160 beats per minute, but it can rise to 180 beats per minute when the infant is crying or drop as low as 80 to 90 beats per minute when in deep sleep. A consistently high or low heart rate should be investigated.

Next up is the newborn’s respirations. Respirations are usually irregular, and there may be occasional 5 to 20 second pauses; so they are counted for a full minute for accuracy. A normal respiratory rate is between 30 to 60 breaths per minute. You’ll notice that the abdomen will rise and fall with each respiration; this is normal, because newborns tend to use their diaphragm to breathe more than their intercostal muscles. A respiratory rate of more than 60 breaths per minute could signal problems like cold stress, congenital heart defects, or infection; while a respiratory rate less than 30 breaths per minute could be associated with central nervous system depression.

Then, the temperature is measured, which normally ranges between 97.7° F and 99.5° F, or 36.5° C and 37.5° C. The axillary temperature is the preferred method of measurement, because it is easily accessed and is a close estimate to the newborn’s core temperature

Blood pressure is not routinely measured in well newborns, except when there are murmur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diphtheria:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QMEeFqicRzO9WaQ081veaBDtTP2yAvj8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diphtheria: Nursing]]></video:title><video:description><![CDATA[Diphtheria is a toxin-mediated bacterial infection that typically affects the upper respiratory tract, and less commonly, the skin.

Now, let’s quickly review a bit of the anatomy and physiology of the upper respiratory tract, and skin. Starting with the upper respiratory tract, this is made up of the nose, nasal cavity, oral cavity, pharynx, epiglottis, larynx, and the upper part of the trachea. 

So, when we breathe in, air enters the respiratory tract through the nose or mouth, respectively into the nasal cavity and oral cavity, and then into the pharynx. At each side of the pharynx, there is a pair of structures called adenoids and tonsils, which are small clumps of lymphoid tissue that act as the body&amp;#39;s first line of defense that swallow harmful foreign particles and pathogens that enter through the nose or mouth. The lower part of the pharynx is continuous with the larynx, which is connected through the trachea, or windpipe, with the lungs. 

Zooming in, the epithelium lining respiratory tract consists of goblet cells that release mucus, which is sticky and contains enzymes to help trap and destroy harmful foreign particles and pathogens; as well as columnar epithelial cells, that have hair-like projections called cilia, which work to sweep the harmful particles up and out of the airways. 

Moving on to the physiology of the skin, this is divided into three main layers: the hypodermis, which is made of fat and connective tissue, the dermis, which contains hair follicles, sweat glands, nerve endings, and blood vessels, and finally, the epidermis. The epidermis itself has multiple layers of squamous or flat epithelial cells.

Alright, now, diphtheria is caused by the gram-positive bacillus bacteria called Corynebacterium diphtheriae. Important risk factors for developing diphtheria include immunodeficiency; being unvaccinated or undervaccinated; coming in contact with an infected client; and finally, living in crowded or unsanitary conditions ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psychosocial_changes_-_Pregnancy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1ulgJhz7SC_NscfvkSNXJ2B_T_Cqca2i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psychosocial changes - Pregnancy: Nursing]]></video:title><video:description><![CDATA[Psychosocial changes during pregnancy include the rollercoaster of emotions that parents experience from the moment they find out about the pregnancy to the moment they accept that they are going to be parents all the way up to birth. During this period, the nurse should support the client and the client’s partner and help promote a healthy outcome. 

Now, during the first trimester, clients typically feel uncertainty because they are not sure if they are actually pregnant. Some may respond to uncertainty by talking to friends or family and looking for signs and symptoms of pregnancy. Others might use over-the-counter pregnancy tests, while others might seek professional help from a healthcare provider. 

Once the pregnancy is confirmed, they may experience a feeling of ambivalence or internal conflict. Particularly if it&amp;#39;s their first pregnancy, they may begin to worry about the added responsibility and life changes that come with having a child. But, with time, ambivalence usually gives way to acceptance of their new reality. 

Next comes self-focus, meaning they start focusing on themselves and the effects the pregnancy symptoms. At this point, pregnancy symptoms, such as nausea and fatigue begin to present. At the same time, hormonal changes in the body can trigger mood swings that can range from being extremely happy to irritability and even sadness. 

Finally, they might experience changes in their sexuality, which can vary based on their individual cultural or religious beliefs. So, some clients might notice a rise in their sexual interest or a fall due to the pregnancy symptoms, particularly nausea and breast tenderness. 

During the first trimester, nurses can assist their clients by reassuring them about these normal changes and by suggesting ways they can cope with the discomforts of pregnancy, as well as any psychological stress they are experiencing.

Once the client enters the second trimester, they have more physical evidence of pre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_-_Sampling:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vm9ngkXxTn2OoquEFGDj420DSL2x1uBZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research - Sampling: Nursing]]></video:title><video:description><![CDATA[Nurse Beth works in a large outpatient pediatric practice that cares for many clients diagnosed with a variety of illnesses. She noticed that of the children diagnosed with COVID-19, a substantial number of them are reporting long-term symptoms, like headaches. So, she develops a research study to better understand the number of pediatric clients diagnosed with COVID-19 who are experiencing headaches 6 months or more following their initial COVID-19 diagnosis. As she begins to develop her study, Nurse Beth uses what she knows about population sampling so the right participants are included in the study. 

Okay, so research is a systematic process of validating, refining, and generating knowledge. It is used by nurses and other members of the healthcare team, to answer questions that come up when caring for clients. 
Now, the population is an entire group, with certain shared characteristics, that the researcher wants to study. Characteristics of a population can include but are not limited to physical traits, like height or eye color; diagnoses like hypertension or chronic kidney disease; or shared experiences, like taking an online course or receiving outpatient intravenous antibiotics. 
These characteristics, often referred to as sampling criteria, determine what or who will be studied. 

Sampling criteria can be divided into two categories, inclusion criteria, or characteristics belonging to individuals that will be studied, and exclusion criteria, or characteristics of individuals that will not be studied. In Nurse Beth’s study, children who are patients in pediatric clinics in Beth’s area who are under the age of 18, and who’ve been diagnosed with COVID-19 will meet the study’s inclusion criteria; whereas, children who have not been diagnosed with COVID-19 will be excluded. 

In most research, it’s impossible to study an entire population; Nurse Beth can’t possibly study every single child in the United States diagnosed with COVID-19! Therefore, a sam]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Ventricular_tachycardia_(Vtach):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XDphXQd1RQyAjCtM017e8oXUSTmy3y6j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Ventricular tachycardia (Vtach): Nursing]]></video:title><video:description><![CDATA[Arrhythmias are irregular heartbeats that occur due to any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse, which can affect the heart’s ability to pump blood throughout the body. 

Ventricular tachycardia, or simply V-tach, is a type of tachyarrhythmia, where a point in the ventricles fires abnormal signals, causing the heart to beat faster than normal, at a rate of 150 to 250 beats per minute. Ventricular tachycardia can be paroxysmal, meaning that it presents as three or more beats that are self-limiting; or sustained, meaning that it lasts for at least 30 seconds.

Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.  From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to 

the right and left ventricles, causing them to depolarize. This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG. Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Asystole:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Mf8-jGRaSkGBfQAnxvEmaLxLSgGsV61T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Asystole: Nursing]]></video:title><video:description><![CDATA[Cardiac arrest occurs when the heart suddenly stops pumping blood throughout the body. There are two types of cardiac arrest, asystole or cardiac flatline, and pulseless electrical activity, or PEA for short. Asystole is the most common type and refers to the total absence of electrical and mechanical activity of the heart. On the other hand, PEA occurs when there is electrical activity in the heart, but the cardiac muscle is unresponsive to stimulation; therefore, there’s no mechanical activity of the heart and pulse.

Now, let’s cover some physiology of the cardiac conduction system. The cardiac conduction system is made up of specialized myocardial cells that can create and transport electrical potential, also called an action potential. These cells have many special features, including automaticity, meaning that they can generate an impulse, excitability, which is the ability to respond to a stimulus by creating an electrical impulse, conductivity meaning they can carry the impulse to other cells, and contractility, which is the ability to shorten the length of their fibers, causing a contraction. 

Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial node or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. From the atrium, electrical activity goes to the atrioventricular node, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.  From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bund]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Quality_&amp;_safety:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mEkdfSj3TACs1J5khIGsbYV7Sravt7ju/_.jpg</video:thumbnail_loc><video:title><![CDATA[Quality and safety: Nursing]]></video:title><video:description><![CDATA[Nurse Kendra works in the pediatric intensive care unit and is caring for Jonah who is being treated for cellulitis. While preparing to administer Jonah’s medications, Nurse Kendra accidentally reconstitutes the prescribed antibiotic with a 0.45% saline solution instead of the 0.9% normal saline as ordered. As Nurse Kendra spikes the bag, she notices the error and returns to the medication room. Nurse Kendra knows that if she had not noticed the medication error, it could have led to serious consequences for her client. Because of this near-miss event, Nurse Kendra decides to begin a quality improvement initiative on her unit to prevent errors like this from happening in the future.

Quality and safety are closely related concepts in healthcare. Quality is how well health services achieve the desired outcomes for a client or population. Safety refers to protecting clients from risk and harm while they’re receiving care. So, safety can be considered a component of quality. When Nurse Kendra discovered the medication error, she identified a safety issue because administering the medication as she prepared it would have resulted in client harm. If that had occurred, the quality of Jonah’s care would also be compromised since providing safe care is part of quality care. 

Now, quality and safety are highly regulated and monitored within healthcare institutions. Two of the major regulatory bodies include the Centers for Medicare and Medicaid Services and The Joint Commission. 

The Centers for Medicare and Medicaid Services is a national organization that collects data on quality measures, for example the percentage of their hypertension clients whose blood pressure is adequately controlled. These data points are used to ensure that all healthcare organizations receiving Medicare and Medicaid funding are compliant with current standards when providing care. 

The Joint Commission is an independent, non-profit organization that develops standards of safety as a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Suicide:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HyqHCjfeQ6KGbAbI8X4vUkiNT_KxQABe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Suicide: Nursing]]></video:title><video:description><![CDATA[The word suicide comes from the Latin word suicidim, which literally means the act of ending one’s own life. A suicidal attempt is an attempt to end one’s own life that results in survival; while suicidal ideations are thoughts about suicide. 

First, let’s cover some basic physiology of the brain, which contains several types of neurons, including serotonergic neurons, which release serotonin; dopaminergic neurons, which release dopamine; and noradrenergic neurons, which release norepinephrine. Overall, all these neurotransmitters, as well as several others and various factors like home and social environment, to name a few, play a key role in the delicate balance of mental functions, and influence things like memory, behavior and mood, amongst others. 

Now, let’s switch gears and move on to risk factors, which can be easily remembered with the memory trick: SAD PERSONS. The first S here stands for sex, as suicide tends to be more common among those assigned male at birth. Next, A stands for age, since suicide is more common among young adults and the elderly. D is for depressive disorder, which is a mental health condition that causes a persistent feeling of sadness, associated with a loss of interest in everyday activities like hobbies. Then P stands for previous suicide attempts, which is the most important risk factor for suicide. E stands for excessive use of alcohol or substances, which causes clients to be more impulsive, and take risks they normally wouldn’t take, like driving recklessly. R is for rational thinking loss in psychosis, a severe mental health disorder that can impair thought and emotions, to the point where clients lose touch with reality. The next S is for sickness, which refers to chronic non-psychiatric diseases, like end-stage cance
r. O stands for organized plan, which is when the client has a specific method for suicide in mind. Next, N stands for no social support, meaning that they have no friends or family to turn to d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Small_for_gestational_age_(SGA)_infant:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bhMvqDuZRfqZxNpHs2nBkVNDRNeR15zN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Small for gestational age (SGA) infant: Nursing]]></video:title><video:description><![CDATA[Small for gestational age or SGA for short, is a term used to describe an infant whose weight is below the 10th percentile for gestational age. In other words, this is an infant who weighs less than 90% of infants of the same gestational age. 

SGA infants can be born prematurely, at term, or at post term, and they may also have experienced intrauterine growth restriction, or IUGR for short. It’s important to note, though, that not all IUGR infants end up being SGA.

Now, first, let’s cover some basic physiology. Gestation refers to the period between conception and birth, which typically lasts for 40 weeks. During these 40 weeks, the embryo, and later fetus, grows and develops within the uterus. On the other hand, gestational age is a term used to describe a newborn based on their physical and neuromuscular characteristics. 

Now, based on the gestational age and the infant’s birth weight, we can determine birth weight percentiles. The birth weight percentile helps us evaluate the infant’s intrauterine growth and development, which is considered normal when the value is between the 10th and 90th percentile. 

For example, an infant weighing around 3350 grams is within the 40th percentile, and is considered appropriate for gestational age, or AGA. On the other hand, an infant weighing around 2700 grams is within the 3rd percentile, and therefore SGA. Finally, an infant weighing around 4200 grams is within the 95th percentile and is considered large for gestational age, or LGA for short.

Now, moving on to causes. Some SGA infants can be genetically predisposed to be physiologically small; while others can have impaired fetal development due to some other fetal or maternal condition. 

Now, factors that increase the risk of impaired fetal development can be classified as fetal or maternal. Starting with fetal risk factors, these include genetic abnormalities, multiple gestation, as well as congenital infections, which are grouped under the acronym TORCH. T ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_sclerosis_(MS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c9EZUkkZSAKeCkzkLJ9Nmt3PQ7qhL53S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple sclerosis (MS): Nursing]]></video:title><video:description><![CDATA[Multiple sclerosis or MS is an autoimmune degenerative nerve disorder that causes demyelination of the nerve fibers of neurons in the brain and the spinal cord. This demyelination occurs when the body&amp;#39;s own immune system inappropriately attacks and gradually destroys the myelin sheath, slowing down the communication between neurons.

Let’s start by looking at the physiology of neurons. Remember that neurons are the cells of the brain and spinal cord that transmit electrical signals throughout the central nervous system and the body. These signals are transmitted as nerve impulses, which move across a branch of the neuron called axon, which is covered by a protective myelin sheath. The role of this sheath is to speed up the transmission of electric impulses, allowing information to travel quickly from one neuron to another in order for us to perceive sensations and perform movements. 

Just like other autoimmune diseases, the exact cause of MS is unknown, but it is linked to both genetic and environmental factors. Multiple sclerosis typically affects clients between the ages of 20 and 40, and genetic risk factors include a family history of MS, clients assigned female at birth, as well as genes that encode a specific type of immune molecule, called HLA-DR2, which is used to identify and bind to foreign molecules. Environmental risk factors might include infections, smoking, and living in a colder climate, as well as vitamin D deficiency. This is an interesting one, because it might help explain why the rates of multiple sclerosis are higher among the clients living at higher latitudes, compared to the clients living closer to the equator where there’s a lot more sunlight.

Together, these genetic and environmental factors trigger the activation of the body’s own immune cells that enter the CNS, target the myelin and cause widespread inflammation. As inflammation progresses, it gradually damages the axons as well. This impairs the transmission ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_-_Data_analysis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K7RhBBOtS3CYp6BdJax2rnumTNuSVRCF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research - Data analysis: Nursing]]></video:title><video:description><![CDATA[Nurse Luis works in urgent care and a staff nurse named Katie brought it to Luis&amp;#39; attention that the nurses there don’t always introduce themselves when assuming care for clients. She said, “I’ve noticed that sometimes the nurses at our urgent care forget to introduce themselves when going into a client’s room. I find myself forgetting to do this too, I wish there was something that would remind us to do it more consistently.” After speaking to several other nurses, Nurse Luis decided to do a research study focused on the use of pop-up reminders for nurses to introduce themselves each time they access a client’s electronic health record. Nurse Luis collected quantitative data by using a survey that asked clients to document the number of times the nurse introduced themselves when they entered their room, and qualitative data by interviewing nurses about their experience with the introduction reminder. Now it is time for Nurse Luis to analyze all the data he’s collected. 

Data analysis is the systematic process of applying different techniques to describe and evaluate information that the researcher has collected. Data analysis can be one of the most exciting steps of the research process since the researcher is finally able to find answers to their research question! Whether your study is quantitative, qualitative, or a mixture of both, you will use data analysis techniques to understand the findings. All right, there are different ways to analyze data, depending on the type of data that was collected. Quantitative research analyzes numerical data through descriptive and inferential statistics. Descriptive statistics allow researchers to describe, organize, and summarize characteristics of data. For example, Nurse Luis included descriptive statistics about the number of years the participants in his study have been a nurse, and this could help bring more insight into the study findings. 

On the other hand, inferential statistics allow resea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Premature_ventricular_contractions_(PVCs):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dpcQPBrTTCKuVMqwfHMXufc4QGWMD9bz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Premature ventricular contractions (PVCs): Nursing]]></video:title><video:description><![CDATA[Premature ventricular contractions, or simply PVCs, are a type of arrhythmia, where an extra beat starts in a point in the ventricles, causing the ventricles to contract earlier than normal in the cardiac cycle. Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles.

From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.  From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles, causing them to depolarize. This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG.

Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the pause between ventricular depolarization and repolarization is represented by the ST segment. Sometimes, immediately after the T wave, there’s a U wave, which represents late repolarization of the ventricles. Now, the 3 main causes of premature ventricular contractions are enhanced automaticity, triggered activity, and reentry.  Now, automaticity is the property of cells in the SA node, AV node, Bundle o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physiology_of_lactation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SWYmTr9cQku0cTheFIKJbFdNSz__vVvt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physiology of lactation: Nursing]]></video:title><video:description><![CDATA[Lactation describes the process of milk production and secretion from the breasts; and it also refers to the period of time during which the mother is breastfeeding.  

Let’s start by reviewing the physiology of the breasts. The breasts contain mammary glands responsible for lactation in biological females. Mammary glands are made up of 12 to 20 lobes, each of them containing many smaller lobules. These smaller lobules have grape-like clusters of alveoli that contain mammary secretory epithelial cells, the milk producing cells of lactation. These alveoli, lobules and lobes are connected through a network of ducts called the lactiferous ducts and eventually form a unique lactiferous duct for each lobe which opens independently to the areola to drain the milk produced during lactation. Each lactiferous duct has a dilated portion deep to the areola called the lactiferous sinus in which there’s a small drop of milk that accumulates or remains in a nursing mother, which becomes expelled from the areola when compressed during feeding. 

During pregnancy, the placenta releases progesterone, estrogen, and human placental lactogen, while the pituitary gland releases prolactin. Now, these hormones work together to promote the development of breast tissue by increasing the number and size of the alveoli and the development of the lactiferous ducts.  

Prolactin also stimulates milk production and during the later stages of pregnancy, the breasts produce an early version of breast milk called colostrum which is a thick yellowish fluid rich in immune cells and antibodies and high in protein. However, during this stage, high levels of progesterone and estrogen inhibit significant milk production to prevent wasting milk before the baby is born.  

When the baby is delivered and the placenta is removed, the level of progesterone and estrogen decrease and milk production ramps up. 2 to 5 days after birth, the breasts start producing larger quantities of transitional milk w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preterm_infant:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J5QdZAUUSBqtcmRqoJ2HTl4NTpOKouat/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preterm infant: Nursing]]></video:title><video:description><![CDATA[A preterm infant is born before 37 completed weeks of gestation. Classification of prematurity can be based on gestational age, so a late preterm infant is born between 34 weeks and 36 weeks and 6 days of gestation; a moderate preterm infant is born between 32 weeks and 33 weeks and 6 days of gestation;a very preterm infant is born less than 32 weeks of gestation; and an extremely preterm infant is born before 28 weeks of gestation. 

Preterm infants can also be classified by birth weight. A low birth weight infant weighs less than 2500 grams; a very low birth weight infant weighs less than 1500 grams; and an extremely low birth weight infant weighs less than 1000 grams.

Let’s start with some basic physiology. Gestation refers to the period between conception and birth, which typically lasts for 40 weeks. During these 40 weeks, the embryo, and later fetus, grows and develops within the uterus. 

Normally, every infant born between the 37th and 42nd week of gestation is considered a term infant, so an infant born before the 37th week is considered preterm. 

Now, based on the gestational age and the infant’s birth weight, we can determine birth weight percentiles. Furthermore, birth weight percentiles help us evaluate the infant’s intrauterine growth and development, which is considered normal when the value is between the 10th and 90th percentile. 

For example, an infant born at 40 weeks of gestation that weighs around 3350 grams is within the 40th percentile. In other words, this baby is appropriate for gestational age. On the other hand, an infant born at 40 weeks of gestation that weighs around 2700 grams is within the 3rd percentile, and therefore small for gestational age. Finally, an infant born at 40 weeks of gestation that weighs around 4200 grams is within the 95th percentile and is considered large for gestational age.

Now, the cause of preterm birth can be medically indicated, when there are maternal, fetal, and placental complications such a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Large_for_gestational_age_(LGA)_infant:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v1sf314ZQ3aeU-hnnRoPMxIFSICJd2Cp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Large for gestational age (LGA) infant: Nursing]]></video:title><video:description><![CDATA[Large for gestational age or LGA for short, is a term used to describe an infant, whose weight is over the 90th percentile for gestational age. In other words, the infant weighs more than 90% of infants of the same gestational age. 

Large for gestational age is not a synonym for macrosomia, which is a term used to describe an infant&amp;#39;s birth weight over 4000 grams regardless of gestational age. Infants who are LGA can be preterm, term, or postterm.

Now, first, let’s cover some basic physiology. 

Gestation refers to the period between conception and birth, which typically lasts for 40 weeks. During these 40 weeks, the embryo, and later fetus, grows and develops within the uterus. 

On the other hand, gestational age is a term used to describe a newborn based on their physical and neuromuscular characteristics.

Now, based on the gestational age and the infant’s birth weight, we can determine birth weight percentiles. 

The birth weight percentile helps us evaluate the infant’s intrauterine growth and development, which is considered normal when the value is between the 10th and 90th percentile. 

For example, an infant weighing around 3350 grams is within the 40th percentile, and is considered appropriate for gestational age, or AGA. On the other hand, an infant weighing around 2700 grams is within the 3rd percentile, and therefore SGA. Finally, an infant weighing around 4200 grams is within the 95th percentile and is considered large for gestational age, or LGA for short.

Ok, now, when it comes to causes, some LGA infants can be genetically predisposed to be physiologically large; while others have impaired fetal development due to some other fetal or maternal condition. 

Important risk factors can be either fetal or maternal risk factors. 

A fetal risk factor is male sex. Also, LGA infants are more common in Asian, Black, and Hispanic ethnic groups. 

Maternal risk factors include diabetes mellitus, large stature; obesity or excessive weight]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrapartum_assessment_-_Uterine_activity:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fjbWc1d7Q_eCdZQRg8i-uuCeRdaICRlK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intrapartum assessment - Uterine activity: Nursing]]></video:title><video:description><![CDATA[The intrapartum period refers to the time of pregnancy from the onset of labor to delivery of the newborn and the placenta. During this period, the uterus contracts to provide the main force necessary for delivery. So intrapartum assessment of uterine activity refers to assessing the frequency, duration, and intensity of these contractions. Of note, the assessment of the fetus during labor is always interpreted relative to uterine activity.  

First, let’s go over the physiology of the uterus, which is a pear-shaped, hollow, muscular organ that protects and nurtures the fetus, but also promotes its delivery during labor. The superior part of the uterus is called the fundus, the middle part is the body and the bottom, cylindrical portion is the cervix. Zooming in, the uterus has three layers: the outer serosal layer, or perimetrium; the middle muscular layer, or myometrium; and the inner mucosal layer, or endometrium. 

The myometrium consists of smooth muscle fibers, which can tighten to produce uterine contractions in response to certain hormones, like oxytocin. Now, the number of oxytocin receptors in the myometrium are low during most of the pregnancy, but they increase dramatically during the third trimester, reaching the greatest concentration during active labor. The oxytocin receptors, especially those in the fundus, respond to oxytocin by promoting rhythmic synchronized endometrial contractions from the fundus towards the cervix, causing  dilation and effacement, or thinning of the cervix, as well as pushing the fetus through the birth canal. Normal uterine activity during labor involves 5 contractions or fewer in a 10 minute period, averaged over 30 minutes. Between contractions, the uterus relaxes to allow adequate blood flow to the placenta and fetus. 

Now, let’s switch gears and go through some types of dysfunctional labor. First up, is tachysystole, which is defined as more than 5 contractions in a 10 minute period, averaged over 30 minutes.T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_-_Data_collection:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pvpHiZ4AR1q8VTvHKXAbhDudQ3OLkQw_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research - Data collection: Nursing]]></video:title><video:description><![CDATA[Nurse Jenna works in the imaging department at a local hospital. She noticed that clients who are scheduled for MRIs report high stress levels when compared to clients scheduled for other diagnostic testing, such as X-ray and CT scans. Nurse Jenna asks the nurse researcher, Nurse Chad, about this observation and he says, “How about we research stress levels in clients scheduled for MRIs compared to CT scans and X-rays? I’d be happy to assist you in the data collection process!” Nurse Jenna and Nurse Chad plan to measure stress levels in a sample of clients scheduled for MRIs, CT scans, and X-rays at their hospital by collecting interview data as well as biological data through measuring cortisol levels in the participant’s saliva. They will use what they know about data collection to gather both types of information.

Okay, so research is a systematic process of validating, refining, and generating knowledge. Data are pieces of information collected during research. Nurses use data all the time to care for clients and communities. Data can be as simple as a single blood glucose level to determine an insulin dose for a client, or as complex as international vaccine statistics to guide vaccination education campaigns. In addition to informing practice, data is also important in research. In research, data collection is done by systematically gathering data to be used to answer a research question and advance knowledge around a specific topic. 

Now, when conducting a research study, researchers can either use existing data, such as information contained in medical records, or they collect new data, like Nurse Jenna, who is collecting information on stress levels in clients scheduled for MRIs. New data can be collected in several ways, like through observation, such as watching clients for signs of stress; self-reporting, such as through interviews or surveys about stress; or through physiological data, like collecting saliva for cortisol samples which is a m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock_-_Cardiogenic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zWLPf95USc_MMSIOUUYmET2wQFqyAxvb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock - Cardiogenic: Nursing]]></video:title><video:description><![CDATA[Cardiogenic shock is a life-threatening condition where the heart is unable to pump enough blood to the rest of the body due to cardiac dysfunction. This leads to acute hypoperfusion and hypoxia of the tissues and organs, despite the presence of an adequate intravascular volume in the cardiovascular system. 

Alright, let’s go over the physiology of the cardiovascular system, which consists of the heart 

and blood vessels. The heart pumps out blood to the body’s organs and tissues with each heartbeat, which consists of two phases: systole, which is when the heart contracts and pumps the blood out; and diastole, which is when the heart relaxes and fills with blood. The stroke volume, meaning the amount of blood pumped out by the heart in a single heartbeat, is influenced by the cardiac contractility, preload, and afterload. Contractility is how strongly the heart is contracting during systole. Preload is how much the heart’s smooth muscle is stretched at the end of diastole, and this is mainly dependent upon how much blood is filling the heart. The more they&amp;#39;re stretched the more force they can generate during contraction, kind of like a rubber band. Afterload refers to the resistance that the heart must overcome to pump out blood during systole, and this is affected mainly by peripheral vascular resistance under non-pathological conditions. This is mainly determined by the vasodilation and vasoconstriction of blood vessels. If we multiply the stroke volume by the heart rate we’ll get the cardiac output, which is the amount of blood pumped out by the heart in one minute, and it’s the main measure of the heart’s function. 

Okay, cardiogenic shock can be caused by any condition that prevents the heart from pumping enough oxygenated blood, thus affecting the cardiac output. The most common causes involve damage to the heart tissue. The most important is acute myocardial infarction where ischemia and necrosis of cardiac tissue impairs its ability to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Informatics:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VqjyTAaQSxu3uu6K7t7XjebeSGKklF0W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Informatics: Nursing]]></video:title><video:description><![CDATA[Nurse Kofi works in the emergency department at a small rural hospital and has noticed that several incident reports have been filed within the last month regarding medication errors. After investigating further, he found that several of the medication errors were related to inaccurate or incomplete documentation of medication administration. For example, Nurse Amy administered an extra dose of an antihypertensive medication to a client, causing them to become hypotensive. When Nurse Kofi speaks to Nurse Amy about this, she says, “I looked at the paper chart, but the previous documentation was illegible, so I couldn’t tell that the medication had already been given!” Nurse Kofi brought these issues to the hospital administration team and recommended improving informatics by switching to a computerized clinical information system from paper records. After reviewing the incident reports, the hospital administration team decides to switch to an electronic health record for the facility. 

Okay, so healthcare informatics is a type of informatics used to support clinical decision making by using data to improve the safety and effectiveness of healthcare delivery. An example of the use of healthcare informatics is the electronic health record, or EHR. EHR which is used by different members of the healthcare team to document, store, and view client data like client notes, vital signs, and medication. Okay, so many facilities use a clinical information system, or CIS. A CIS is a large, computerized management system that allows for secure storage and retreival of client information, which is used by nurses and other healthcare team members to plan, implement, and evaluate care. A CIS facilitates timely and effective access to information which can enhance the quality of client care as well as improve workflow processes. So, there can be many components to a CIS. 

The EHR for example, is a very common one. An advantage of EHRs is the ability for different members ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemolytic_disease_of_the_fetus_&amp;_newborn:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W0SzicgRR_qsDjHdms0AeiETTNWmzaeH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemolytic disease of the fetus and newborn: Nursing]]></video:title><video:description><![CDATA[Hemolytic disease of the fetus and newborn, also called erythroblastosis fetalis, is an immune-mediated condition in which the red blood cells of the fetus or newborn are hemolyzed, or destroyed by the mother’s antibodies. Let’s start by looking at the physiology of blood groups. The most common blood group classification is based on the ABO and the Rh system. These systems are based on the presence or absence of certain glycoproteins on the surface of red blood cells. The ABO system relies on the presence or absence of type A and B glycoproteins on RBCs.  So people with the A blood type have type A glycoproteins; people with B blood type have type B glycoproteins; people with type AB, intuitively, have both; and people with the O blood type have neither type of glycoproteins on their RBCs. The immune system produces antibodies against the glycoproteins that are missing from the surface of the individual’s erythrocyte. That’s why people with type A blood have antibodies to type B blood, and those with type B blood have antibodies to type A blood. People with blood type AB don’t have antibodies to type A or type B blood;  whereas people with type O blood have antibodies to both A and B glycoproteins.

Next, the Rh classification looks at whether or not the Rhesus factor, or “Rh” factor for short, is present on RBCs. If this factor is present on their red blood cells, that makes the blood type Rh positive; whereas if it’s absent, the blood type is Rh negative. People that are Rh positive can receive both Rh negative or Rh positive blood since they do not have antibodies against the Rh glycoprotein. But if an Rh negative person receives Rh positive blood, they could develop a hemolytic transfusion reaction. Having said that, Rh antibodies require prior exposure to Rh positive RBCs. So, someone who doesn’t have Rh antibodies, won’t have a transfusion reaction the first time they’re exposed to Rh positive blood. However, they develop anti-Rh antibodies, so if t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intestinal_obstruction:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WxYr0U3lR6ih8OnzzIrCJxUASt2NdJy2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intestinal obstruction: Nursing]]></video:title><video:description><![CDATA[Intestinal obstruction is when the normal flow of contents moving through the small or large intestine is interrupted, causing problems with nutrient and fluid absorption and waste elimination. Okay, first, let’s recall the physiology of the intestinal tract. The small and large intestines are tube-shaped structures through which the partially digested food, fluid and air pass through. After the intestines absorb the nutrients and fluid, the stool is formed and passed further until excreted.

Let’s zoom into the wall of the intestine, which is made up of four layers. The outermost layer is called serosa or adventitia, that faces the abdominal or peritoneal cavity. This is the space between the abdominal wall and abdominal organs that is lined with peritoneal membrane and contains a small amount of serous fluid. Next is the muscular layer, which contracts to move food through the bowel, and this is called peristalsis. After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. And finally, there’s the innermost layer, called the mucosa, which contains the epithelial lining, facing the lumen, that enables nutrients and fluid absorption.

The causes of bowel obstruction can be either mechanical or functional; and the latter is also called ileus. Mechanical obstruction is caused by actual blockages in the small or large intestine, and it can be defined as partial or complete, as well as simple or strangulated. Partial obstruction is when gas or liquid stool can pass through the point of narrowing, while with complete obstruction, nothing is able to pass through. Now, there’s also simple mechanical obstruction, which is when the obstructed segment of the intestine maintains its blood supply, and strangulated mechanical obstruction, which is when blood supply has been compromised. On the other hand, functional causes disrupt peristalsis, so even without a blockage, food, liquids and gas do]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_-_Critical_appraisal:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vY_Q6hT7TzuD9vowfjF28lYoSMCFrddQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research - Critical appraisal: Nursing]]></video:title><video:description><![CDATA[Nurse Greg works in an oncology unit where several clients have asked him about the connection between diet and cancer. He’s been working with a dietician who told him that she has seen great results in reducing incidence rates of hypertension and diabetes in clients who follow a plant-based diet.This gives Nurse Greg an idea. He wonders, “Will a plant-based diet also be effective in reducing incidence rates of cancer?” He decides to review the literature to better understand how plant-based diets affect cancer rates. He completes a literature search and is now moving on to the next step which is critical appraisal of the literature. 

A literature review is when a researcher compiles all of the literature that currently exists on a topic. This is sometimes called the “state of the science.” Once the literature search is complete, the researcher must critically appraise each of the sources. This is an organized, step-by-step process that evaluates each source using standardized criteria. It is an important step in research because it helps the researcher understand what is known about a topic and if that information is reliable. To do a critical appraisal, the researcher will choose criteria to judge both the content and quality of each source.   

First comes appraising for content, also known as inclusion criteria, which includes things like topic, year of publication, or even the type of source. Usually, the researcher will exclude sources that do not meet their inclusion criteria before analyzing the sources for quality. This saves time, because eliminating sources means there are less to evaluate for quality later. For example, Nurse Greg found 100 sources about plant-based diets and cancer during his search so he needs to determine if those sources match the criteria of what he is studying.  He decided to exclude all sources older than five years because the data they contain might be outdated. That leaves him with 50 sources. Then, he excluded any s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Failure_to_thrive_(FTT):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fdindbZWRBCSZBweXdJPpDahQDyM-eVz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Failure to thrive (FTT): Nursing]]></video:title><video:description><![CDATA[Failure to thrive, or FTT for short, refers to inadequate growth, typically seen in infancy and childhood. This can happen because of an underlying disorder, insufficient caloric intake, or sometimes a mixture of both! Let’s start by looking at the physiology of pediatric growth. A child’s growth is monitored by several parameters, including weight, length or stature, and head circumference, based upon what is considered typical for a given age. This is done by plotting a child’s growth parameters on growth charts which show the percentile of the child on each parameter compared to a large representative population. These charts are standardized by the Centers for Disease Control and Prevention or CDC. Separate charts are available for those assigned male and female at birth. For infants between 0 and 36 months, the growth charts used are length for age and weight for age, head circumference for age, and weight for length. Finally, between 2 and 20 years of age, the standard charts include stature for age and weight for length and body mass index or BMI for age.

Now, the causes of failure to thrive can be classified into three broad categories; organic, non-organic, and mixed causes. Organic causes are those that result from an underlying disorder interfering with bodily functions necessary for growth and development such as nutrient intake, absorption, and metabolism. Such disorders include gastroesophageal reflux; celiac disease, which is when absorption in the small intestine is impaired; nephrotic syndrome, which is when the kidneys leak too many proteins in the urine; cystic fibrosis, which is a genetic condition that affects pancreatic enzyme secretion; as well as genetic syndromes like Down syndrome, or congenital malformations like hypertrophic pyloric stenosis or cleft lip and palate.  

Non-organic causes result from external factors, particularly an insufficient calorie intake which initially affects weight and later on can affect stature.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_-_Ethics:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NT-UNcLjQjK6j9YWs4zxFl7ISy6VCEw3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research - Ethics: Nursing]]></video:title><video:description><![CDATA[Debbie is a client who’s being discharged from the hospital after having a portable chest tube placed following a spontaneous lung collapse. Before leaving, Debbie is approached by Nurse Randy, a nurse researcher, who says, “I’m conducting a study to learn about peoples’ experience being discharged home with a chest tube. Would you be interested in participating?” Debbie says, “I’m not sure, I’m a little worried about my personal information being shared with strangers.” Nurse Randy informs Debbie of the ethical considerations of his study and explains how he plans to protect each participant’s human rights, including privacy. After listening to Nurse Randy, Debbie agrees to participate in the study and Nurse Randy obtains informed consent from her. 

Okay, so research is a systematic process of validating, refining, and generating knowledge; and ethics refers to moral principles that guide a person’s behavior and choices, like deciding between right or wrong. When conducting a study, researchers should adhere to principles of  research ethics by following ethical principles which protect human rights, such as Nurse Randy obtaining Debbie’s informed consent by explaining the purpose of the study; how Debbie would participate in the study; any possible risks or benefits of the study; and giving her the choice whether or not to participate in the study. When research ethics are not upheld, research misconduct occurs. 

Research misconduct is intentional behavior in research that is considered unethical. There are several historical incidences of research misconduct which served as catalysts in the formation of the ethical codes and guidelines which direct ethical research today. One example is the Tuskegee syphilis study. In this study, which lasted from 1932 to 1972, researchers observed the effect of untreated syphilis in Black men. The participants were examined by doctors, but never administered penicillin, even though it became standard treatment in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_-_Dissemination:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hkH87vDiQJGKDmQOf6LM7Y5eTjOwHcbg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research - Dissemination: Nursing]]></video:title><video:description><![CDATA[Nurse Jeong works in a large cardiac rehabilitation center and just completed a mixed-methods research study on the prevalence of depression in clients diagnosed with heart failure. Through use of a quantitative survey, he found that depression occurred in 20% of the study’s participants. Nurse Jeong’s qualitative data supported his survey results by uncovering themes such as, “overwhelming fatigue” and “loss of independence.” Nurse Jeong brings the results of his study to the nurse researcher, Sonia, who says, “I see you’re now ready to share these important findings with the healthcare community! I would be happy to help guide you in this process.” Nurse Jeong and Nurse Sonia will use what they know about disseminating research findings to communicate Nurse Jeong’s research findings with a larger audience. 

Okay, so dissemination is when a researcher communicates the findings of their research with others. In nursing research, findings can be shared with physicians, policy makers, fellow researchers, community leaders, as well as other nurses, with the goal of enhancing knowledge and promoting quality care in a particular discipline. However, it usually takes some time before research findings will result in an actual effect on clinical practice. One way to disseminate research findings is through a research report, or a written description of a completed study. By documenting study findings in a research report, nurses and other healthcare professionals can access and share this information efficiently and effectively. 

A research report generally contains four main sections: introduction, methods, results, and discussion. First, the introduction is where the background, significance and aim of the research question is identified along with any gaps in the existing literature. For example, Nurse Jeong’s introduction included his research aim: to describe the prevalence of depression in clients with heart failure. In addition, the introduction can also]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cesarean_birth:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bmsZDEyVRGmeAt-kRjqU4UI5S765fcxw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cesarean birth: Nursing]]></video:title><video:description><![CDATA[Cesarean birth is when the fetus is delivered through a surgical incision in the abdominal wall and the uterus.This type of delivery is preferred if a vaginal delivery could compromise the fetus, the mother, or both; or if the delivery of the fetus needs to be accomplished urgently. Other times, a cesarean delivery can also be performed on maternal request. Maternal indications can include heart disease; preeclampsia, which is when hypertension is associated with proteinuria; placental problems such as placenta previa or placental abruption; cephalopelvic disproportion, where the maternal pelvis is too small for the fetal head to pass through; active genital herpes simplex virus infection that can be transmitted to the fetus during vaginal birth; and previous uterine surgeries, such as previous cesarean birth due to risk of uterine rupture at the scar site. Fetal indications can include abnormal fetal heart rate tracings; malpresentation, such as breech or transverse lie; prolapsed umbilical cord; as well as congenital malformations or intrauterine infections. Some other fetal-related risk factors include fetal macrosomia, and multiple gestation, such as twin pregnancies. 

Let’s switch gears now and go through the process of cesarean birth. The first step is preparation of the client for the procedure. This includes routine preoperative laboratory tests, such as complete blood count, blood typing and screening; continuous fetal monitoring; and administration of prophylactic antibiotics. A wedge is placed under one hip to reduce uterine compression of the aorta and inferior vena cava, and to promote placental blood flow. A urinary catheter is placed to help empty the bladder. Then, the anesthesiologist administers regional anesthesia, like an epidural, or combined spinal-epidural anesthesia. If cesarean birth is performed as an emergency procedure, then general anesthesia can be chosen as it can be administered much quicker. Lastly, sterile abdominal skin ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Defense_mechanisms:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gx82-9N9QxOJTdV4pND5O3pSSCOWP09s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Defense mechanisms: Nursing]]></video:title><video:description><![CDATA[Defense mechanisms are conscious or unconscious psychological processes that individuals can use to protect themselves from anxious, inconvenient, or unpleasant feelings and thoughts. These mechanisms can be classified as adaptive, intermediate, or maladaptive depending on how much they help or harm an individual or the people in their lives. 

Let’s start with the adaptive, also known as healthy or mature defense mechanisms, which include altruism, sublimation, humor, and suppression.

With altruism, an individual will provide help to others to help relieve feelings of anxiety. So for example, a billionaire makes a large donation to a hospital. So they can either derive gratification from doing the good deed itself, or from the responses from the receiver or others, such as having a hospital wing named after them. Altruism shouldn’t be confused with self-sacrificing behavior, where they deny their own needs or interests in order to help others.

With sublimation, the person replaces strong and suppressed impulses, such as sexual or aggressive ones, with an activity that is considered more socially acceptable and constructive. So for example, a person who’s very angry about his boss can channel that energy through physical labor or contact sports such as boxing. 

Next, humor is commonly used to express uncomfortable feelings, lighten up stressful situations, and relieve tension. An example of using humor as a defense mechanism is when someone trips when entering the room. Feeling embarrassed, they say, “ ’” 

Finally, there’s suppression. This is where the individual consciously forces negative and undesirable feelings, ideas, and impulses out of their awareness.  An example of suppression would be a student being angry with their roommate about leaving dirty dishes in the sink. Since they need to study for a big exam, they stop thinking about the dishes and focus on studying instead. In this case, suppression is useful for allowing them to focus on more ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Workplace_violence:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1PfhiIucREum5JKKmnucIlPkQAycBAVX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Workplace violence: Nursing]]></video:title><video:description><![CDATA[Workplace violence is an undesired consequence that can sometimes occur when working with people in stressful situations such as in healthcare settings. Workplace violence can range from threats, harassment, intimidation, and verbal abuse to physical assaults that could even result in homicide. Now, there are four major types of violence that nurses might face in their work environment. The most common type is violence that’s perpetrated by a client that’s receiving care from the nurse. This can also include family members or friends of the client the nurse is interacting with. 

Then there’s worker-on-worker violence, also known as bullying or lateral violence, where the perpetrator and the nurse work together. There is also violence that can occur from personal relationships, where the nurse has an existing exterior relationship with the perpetrator. This could include acts of domestic or intimate partner violence that are committed in the healthcare setting.  Finally, there’s violence that’s associated with criminal intent. This is where the violence is carried out during the commission of a crime in the healthcare setting, which can include, trespassing, robberies, active shooters, and terrorism.

Now, violent behavior can occur anywhere on a hospital, but there are some high-risk areas, such as psychiatric units and the emergency department. Other risk factors that can lead to violence include working with individuals under the influence of drugs or alcohol, or who have a history of violence or certain psychiatric disorders. The risk is also greater when working alone or when the unit is understaffed. The environment of the workplace can also result in some violent behaviors. This includes poor environmental design, lack of security, long wait times, and uncomfortable waiting rooms. 

Other risk factors include, lack of staff training on personal safety and de-escalation techniques, lack of institutional violence prevention programs or policies, as we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postterm_infant:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xEkH_H8JSI6ndc_50-GnETgwQ_6H8TC3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postterm infant: Nursing]]></video:title><video:description><![CDATA[A postterm infant is any infant born after 42 weeks of gestation. A postterm infant could be small for gestational age or SGA; appropriate for gestational age or AGA; or large for gestational age or LGA. A postterm infant can also be dysmature, which means they have experienced wasting of subcutaneous fat and muscle. Let’s start with some basic physiology. Gestation refers to the period between conception and birth, which typically lasts for 40 weeks. During these 40 weeks, the embryo, and later fetus, grows and develops within the uterus. Normally, an infant comes to the world after 40 weeks of gestation, but every infant born between the 37th and 42nd week is considered a term infant. An infant born after the 42nd week is called a post-term infant. 

Now, based on the gestational age and the infant’s birth weight, we can determine birth weight percentiles. Furthermore, birth weight percentiles help us evaluate the infant’s intrauterine growth and development, which is considered normal when the value is between the 10th and 90th percentile. For example, an infant born after 40 weeks of gestation that weighs around 3350 grams is within the 40th percentile. In other words, this baby is appropriate for gestational age, or AGA. On the other hand, an infant born after 40 weeks of gestation that weighs around 2400 grams is below the 10th percentile, and therefore small for gestational age, or SGA. Finally, an infant born after 40 weeks of gestation that weighs around 4200 grams is on the 95th percentile and is considered large for gestational age, or LGA.

Now, most commonly, the cause of postterm birth is unknown. The most important risk factors for postterm birth include obesity; first pregnancy or previous postterm pregnancies; and advanced maternal age. Genetic factors also influence postterm birth. Switching gears and moving on to pathology. The fetus will continue to receive a normal supply of oxygen and nutrients and growth will continue unchecked, as l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_promotion_&amp;_illness_prevention:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9aon_AwITyC8r1rEFR4EKBQVQIuHASbK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health promotion and illness prevention: Nursing]]></video:title><video:description><![CDATA[Yousef is a community health nurse who’s volunteering at a free medical clinic. One of the clients who comes to the clinic is a 53-year-old construction worker, named Ben, who states, “I want to be tested for diabetes.” Nurse Yousef notes that Ben is moderately overweight, has a patch over his left eye, and is a current smoker. Nurse Yousef asks Ben to elaborate on why he wants to be tested for diabetes, and Ben responds, “I haven’t been going to the gym as much, so I’ve gained some weight. My dad has diabetes, so I want to make sure I don’t have it.”

Nurse Yousef says, “Thank you for sharing, Ben. I’d be happy to get you screened for diabetes today. I think it would be a good idea for us to discuss some other aspects of your health too. I can’t help but notice you have a patch over your eye.” Ben nods in agreement and says, “Yeah, I went blind in my left eye about a year ago after a work accident. The doctor said there’s nothing they can do.” Nurse Yousef will use what he knows about health promotion and illness prevention to care for Ben.

Okay, so the concepts of health promotion and illness prevention are closely related since they both affect a client’s wellbeing and quality of life. Health promotion refers to activities that protect health and enhance an individual’s existing level of wellness, such as regular exercise and eating a balanced diet. On the other hand, illness prevention involves actions that can reduce an individual’s exposure to risk factors, which are things that increase the likelihood of developing an illness, disease, or trauma. Examples of illness prevention are high blood pressure screenings or wearing a helmet when riding a bike.

Although risk factors don’t cause an illness directly, they increase the chance of developing one and they can be categorized into modifiable and non-modifiable factors. Modifiable risk factors are ones that can be altered by lifestyle practices and behaviors, like drinking enough water or not texting]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock_-_Anaphylactic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/auonpTk1TLWxyeXr0YdtaHZRTxuaosS-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock - Anaphylactic: Nursing]]></video:title><video:description><![CDATA[Shock is a life-threatening condition that occurs when body organs don’t receive enough oxygen and nutrients to function properly. Shock can be grouped into four types based on the cause: hypovolemic, cardiogenic, obstructive, and distributive shock, which can be further divided into septic, anaphylactic, and neurogenic shock. Now, to understand anaphylactic shock, let’s quickly review the physiology of blood vessels, which contain smooth muscle in their walls. When the smooth muscle relaxes, it increases the diameter of blood vessels, called vasodilation. On the other hand, when smooth muscle contracts, the diameter of blood vessels decreases, called vasoconstriction. 

The contraction and relaxation of smooth muscles are primarily controlled by the sympathetic nervous system, which normally maintains a partial constriction, generating enough force to keep blood moving through the circulatory system. The sympathetic system stimulation can increase or decrease to keep up with the body’s needs. Increased sympathetic stimulation of the blood vessels causes vasoconstriction and increases peripheral vascular resistance. Vasoconstriction, when the total blood volume is constant, raises blood pressure and allows blood to flow faster through the blood vessels. In contrast, vasodilation is typically caused by decreased sympathetic stimulation, in addition to inflammatory cytokines and histamine, which decrease peripheral vascular resistance. 

So, vasodilation, when blood volume is constant, lowers the blood pressure and slows down the blood flow through the blood vessels.Okay, now the main cause of anaphylaxis and anaphylactic shock is a systemic allergic reaction to an external trigger, which can be medications, insect bites, or food, for example, nuts. Important risk factors include certain comorbidities such as older age, asthma and other respiratory disorders like chronic obstructive pulmonary disease; or cardiovascular disease. 

Now, let’s talk about pathol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Palliative_&amp;_hospice_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v9HpgDp1QVemS3cK-pMdgo45SLCzkCpr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Palliative and hospice care: Nursing]]></video:title><video:description><![CDATA[Nurse Sumara works in an oncology unit at a hospital. She has been caring for a client named Monique during her chemotherapy treatment for stage IV breast cancer. Monique has been experiencing pain, nausea, fatigue, and decreased appetite due to the treatment, so the oncologist initiates palliative care to better manage her symptoms. Over the next 30 days the palliative care provides symptom relief for Monique, however, the cancer isn’t responding to treatment and continues to progress. Monique’s oncologist plans a meeting with Monique, her family, and Nurse Sumara to discuss Monique’s options. The oncologist discusses Monique’s disease progress and then says, “Your options are to continue palliative care and cancer treatment or consider hospice. This decision is totally up to you and your healthcare team will support you no matter what you decide.” 

Palliative care is a type of specialized care that focuses on managing symptoms for those with serious illnesses to reduce suffering and maintain quality of life. This includes treatment for a wide range of symptoms like pain, depression, constipation, and insomnia. Palliative care is often provided together with curative treatment, like surgery or chemotherapy in Monqiue’s case. 

On the other hand, hospice care is also focused on supportive care and symptom management but without treating the actual disease. Hospice care is usually reserved for clients with six months or less to live who have no options for curative treatment or have chosen not to pursue treatment. 

Okay, so both palliative and hospice care are ways of providing holistic care for clients with a serious or life-threatening medical condition with the goal of helping them and their families to achieve the best quality of life. Palliative and hospice care teams are multidisciplinary, and can include physicians, social workers, case managers, nutritionists, spiritual advisors, and nurses.

Nurses who provide care for clients receiving palliativ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Charge_nurse_as_a_leader:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7n_w-8rpSoOZyo_WwBi5N37SS42IGLy6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Charge nurse as a leader: Nursing]]></video:title><video:description><![CDATA[Nurse Jeehae is the charge nurse during night shift on a respiratory unit. Around midnight, Nurse Jeehae receives a call from Nurse Henry in the Emergency Department who says, “I’ll be sending up three admissions to you in 30 minutes. I’m sorry but we need to clear beds to make room for more clients.” Nurse Jeehae says, “I understand; we’ll make it work.” After ending the call, Nurse Jeehae informs the staff nurses who will be taking the new client admissions and learns that these rooms haven’t been cleaned and aren’t ready for new clients yet. Just as Nurse Jeehae is about to call the housekeeper, she sees one of the newly admitted clients already being wheeled into the unit by a nursing assistant. The client’s family member appears angry and states, “I demand to speak to the manager of this unit. We’ve been in the ED for 6 hours and my brother’s IV is bleeding!” Nurse Jeehae recognizes that there are several issues requiring her immediate attention, therefore, she’ll use her leadership skills to manage this situation as the charge nurse. 

A charge nurse is a nurse who is responsible for the management and leadership of a group of staff during a specified period of time or a shift. The charge nurse oversees operations on their unit such as supporting and training staff in their area, organizing nurse-client assignments, and  resolving conflict. If there’s an issue the charge nurse can’t resolve, they&amp;#39;ll bring it to the nurse manager. In some cases, the charge nurse also provides direct care to clients in addition to the other charge nurse duties. Another important responsibility for charge nurses is collaboration. The charge nurse collaborates with a variety of individuals within the healthcare environment to facilitate safe client care and unit processes. First, the charge nurse interacts with nurses and may serve as a role model or resource for them, especially novice nurses. The charge nurse may also act as a liaison between the staff and the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ethics:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ypDXOy7RRn6ky6gTtjmen5mNT-6E2o1U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ethics: Nursing]]></video:title><video:description><![CDATA[Nurse Hailey works in the intensive care unit. During today’s shift, she is assigned to care for Mr. Lee, a client with diabetes who was hospitalized for ketoacidosis. Mr. Lee is on an insulin drip to help control his blood glucose. During the change of shift report, Nurse Hailey is reviewing the insulin titrations with Nurse James who cared for Mr. Lee the night before. While they are looking over the documentation Nurse Hailey notices a potential error and says, “It seems like there was a protocol error. Mr. Lee’s insulin dose was increased but the blood glucose was never checked.” Nurse James responds, “Oh no! I don’t know how I could have made this mistake.

Nurse Hailey tries to comfort Nurse James by saying, “It’s okay. He’s fine now so at least there were no adverse effects from the error.” Nurse James agrees, “You’re right. No need to make this a big deal. Let’s keep it to ourselves.” Nurse Hailey knows that any medication error should be reported to the charge nurse immediately but she doesn’t want to get her friend, Nurse James, in trouble. She is feeling conflicted about what to do and is experiencing an ethical dilemma.

Ethics are moral principles that guide a person’s behavior and choices. Since ethics are determined by social standards, they are referred to as being externally driven, meaning they are not decided by any single person. Ethics help us to figure out what is “right” and what is “wrong.” Usually, ethical principles are not written down; they are considered common knowledge within a community. For example, stealing is considered “wrong” for most people. But professional groups, like doctors and nurses, often have a more formal, written summary of ethical guidelines. This is called a code of ethics and is used to inform the moral decision making of those in the group.

So for Nurse Hailey, she is having an ethical dilemma. She doesn&amp;#39;t want to betray her co-worker, Nurse James. But ethically, she knows that lying, or withho]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_research_process:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EGO4t9e0QAGfLqoXdooWXuXxT_yLimpg/_.jpg</video:thumbnail_loc><video:title><![CDATA[The research process: Nursing]]></video:title><video:description><![CDATA[Nurse Miguel works in a physical rehabilitation facility. One of his clients, who has chronic back pain related to a car accident, mentions, “I feel so much better since starting yoga. It’s made a big difference in my pain!” Nurse Miguel realizes this isn’t the first client who has mentioned yoga has improved their pain, so he wonders, “How can I know if yoga is an effective treatment for chronic, trauma-related back pain?” 

He decides to develop a research project to better understand how yoga affects back pain. Before he develops his study, he reviews some of the basic principles of research to better understand the steps of the research process.

Okay, so research is a systematic process of validating, refining, and generating knowledge. It can be used to answer questions that are encountered when providing care, like “What kind of diet is best for a client with heart disease?” or “What types of exercise help reduce joint pain in arthritis clients?” 

The first step in the research process is to identify a research problem. A research problem is   sometimes referred to as a “gap” in knowledge. It is a specific issue, often identified by nurses in their everyday clinical practice that needs further investigation, 

Gaps can address specific issues with client care that don’t already have a clear answer. This can be because there is not enough research demonstrating significance of a practice or there has been limited application to practice. 

Nurse Miguel couldn’t find any information on the impact of yoga for the treatment of chronic back pain caused by trauma. He recognizes this is a gap in the literature that he might be able to investigate with a research study. 

The next step is to complete a literature review. To complete a literature review, the researcher will carefully search through scientific databases in order to find sources on their research topic. The goal of the literature review is to develop a comprehensive understanding of what is c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Research_-_Levels_of_measurement:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZTSKesQiS4qWsKp0rSjlrjMcQ2a-U97K/_.jpg</video:thumbnail_loc><video:title><![CDATA[Research - Levels of measurement: Nursing]]></video:title><video:description><![CDATA[Nurse Remi works in a rehabilitation unit where the majority of clients he cares for are recovering from total hip or knee replacement surgery due to osteoarthritis. Nurse Remi is interested in conducting a research study to determine the predisposing characteristics of clients diagnosed with osteoarthritis in his unit, but first must complete a literature review to gather a list of these characteristics. Nurse Remi shares his idea with the unit manager, Nurse Sharron, saying, “There are so many risk factors for osteoarthritis, how do I categorize them all?” Nurse Sharron says, “In research, there are rules for organizing data called levels of measurement, and I can help you manage these.” So Nurse Remi and Nurse Sharron went about using levels of measurement to categorize the risk factors associated with development of osteoarthritis. Okay, so levels of measurement, also called scales of measurement, tell you how variables are recorded in research. Variables are concepts that are measured, manipulated, and controlled in a study. Understanding the levels of measurement helps you to correctly measure the concept of interest, and then use the appropriate statistics to analyze your data.

There are four levels of measurement which include nominal, ordinal, interval, and ratio. First, there is nominal, or categorical measurement. Nominal data is organized into categories that are exclusive, exhaustive, and unranked data. For example, when assessing marital status, a participant cannot say they are both single and married; they must choose one exclusive category or the other. In addition, marital status can’t be ranked, like being single is not better or worse than being married. Nominal data is exhaustive too, meaning they include all possible variations of the attribute that’s being measured. For example, when you flip a coin, you must either get heads or tails. You can also use nominal measurement when collecting data on the participants,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Heart_blocks:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tWnMtycuR4_2YhbxOdmV29naS9_54myX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Heart blocks: Nursing]]></video:title><video:description><![CDATA[Arrhythmias are irregular heartbeats that occur due to any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse, which can affect the heart’s ability to effectively pump blood throughout the body.  

Now a heart block, or atrio-ventricular block, occurs when there is delay or disturbance in the conduction of cardiac electrical impulse from the atria to the ventricles. There are three types of atrio-ventricular block or AV block, for short: first degree AV block, second degree AV block which is further divided into Mobitz type I and Mobitz type II, and lastly, third degree AV block.

The cardiac conduction system is made of specialized myocardial cells that create and transport electrical potential which play a role in regulating heart rate and rhythm. They possess automaticity which is the ability to generate an impulse, excitability or the ability to respond to a stimulus by initiating stimulus, conductivity or the ability to send that impulse, and contractility or the ability to shorten fiber length.

Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.

From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Premature_atrial_contractions_(PACs):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MqBEOQR0TVeYHtFe-WyWhSq8QNeHkO1X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Premature atrial contractions (PACs): Nursing]]></video:title><video:description><![CDATA[Arrhythmias are irregular heartbeats that occur due to any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse, which can affect the heart’s ability to pump blood throughout the body. Premature atrial contractions, or simply PACs, are a type of arrhythmia, where an extra beat starts in a point in the atrium other than the sinoatrial node, and causes the atria to contract earlier than normal in the cardiac cycle. 

Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.  From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles, causing them to depolarize. This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG. Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the pause between ventricular depolarization and repolarization is represented by the ST segment. Sometimes, immediately after the T wave, there’s a U w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Sinus_tachycardia_&amp;_sinus_bradycardia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GIT1OhaBTvus2sWA2GxmgDR1ToahNmnH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Sinus tachycardia and sinus bradycardia: Nursing]]></video:title><video:description><![CDATA[Arrhythmias are irregular heartbeats that occur due to any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse, which can affect the heart’s ability to effectively pump blood throughout the body.   

In sinus tachycardia and sinus bradycardia,  the electrical impulse originates where it should, in the sinoatrial node, but the node fires either too fast or too slow.  The cardiac rhythm is normal, meaning the beats are spaced evenly apart, but in sinus tachycardia the heart rate is more than 100 beats per minute, while in sinus bradycardia, it is less than 60 beats per minute. 

Now, the cardiac conduction system is made up of specialized myocardial cells that can create and transport electrical potential, also called an action potential. These cells have many special features, including automaticity, meaning that they can generate an impulse; excitability, which is the ability to respond to a stimulus by creating an electrical impulse; conductivity meaning they can carry the impulse to other cells; and contractility, which is the ability to shorten the length of their fibers, causing a contraction. 

Let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat.  

The normal electrical activity of the heart starts in the sinoatrial node or SA node, which is considered the pacemaker of the heart. 

Then, the impulse is conducted through the atria, causing depolarization and creating the P wave on an ECG. When the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles.   

From the atria, the impulse goes to the atrioventricular node, or AV node, where the impulse propagation speed slows way down. The interval from the atrial depolarization to just before ventricular depolarization  is the PR interval on an ECG. This delay allows the atria to contract while the ventri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arrhythmias_-_Supraventricular_tachycardia_(SVT):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w1uU7195T6_0aN_gjEr29ljmR76aasVh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arrhythmias - Supraventricular tachycardia (SVT): Nursing]]></video:title><video:description><![CDATA[Supraventricular tachycardia, or SVT for short, is an arrhythmia where the heart beats faster than normal, meaning over 100 bpm, but most clients with SVT have a heart rate between 151 and 220 bpm. The cause of the tachyarrhythmia must originate from above the ventricles and this could be from the myocytes of the atrium or part of the heart’s conduction system. The most common type is called paroxysmal SVT, or PST where there’s sporadic attacks that start and stop suddenly. 

Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. 

From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.  From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles, causing them to depolarize. 

This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG. Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the pause between ventricular depolarization and repolarization is represented by the ST segment. Sometimes, immediately after the T wave, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arterial_embolism:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JnJwC3pETTmR7SvVbwhqZ6N-RrCu9jwd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arterial embolism: Nursing]]></video:title><video:description><![CDATA[Arterial embolism occurs when some material lodges in an artery, subsequently causing a sudden interruption of arterial blood supply to parts distal to the occlusion. The most common types of arterial embolism include thromboembolism, which occurs when a blood clot, or thrombus, breaks loose, becoming an embolus; and atheroembolism, which occurs when cholesterol crystals from an arterial plaque break loose and enter the circulation.

Alright, let’s cover some basics of physiology. There are three major types of blood vessels: arteries, veins, and capillaries. Normally, blood flows from large arteries into medium and then small arteries called arterioles, which in turn deliver oxygen-rich blood into a network of capillaries, called the capillary bed. Here, oxygen and nutrients pass to tissue cells, which will then return carbon dioxide and wastes back into the capillary bed. These capillaries will then merge to form the smallest veins, called the venules. Eventually, these venules converge to form small veins, which then drain into medium superficial veins. Next, these superficial veins drain blood into medium deep veins, which continue to converge, forming large veins that eventually drain back into the right side of the heart. From here, venous blood goes into the lungs, where it gets oxygenated. 

Now, let&amp;#39;s zoom in and take a closer look at the arterial wall, which consists of three layers: from outside in, there’s tunica externa or the adventitia layer, which has loose connective tissue; then tunica media or the middle layer, which contains some elastic tissue and smooth muscle that allow the artery to dilate or constrict in response to local conditions; and finally the endothelium, which consists of a single layer of endothelial cells on top of a layer of connective tissue, called lamina propria. The endothelial cells maintain blood flow by preventing blood cells from reaching the underlying lamina propria. Additionally, endothelial cells exp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_heart_defects_-_Acyanotic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bbrAFqfBTvqSRg0okSzno2BWQ0el8cNJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital heart defects - Acyanotic: Nursing]]></video:title><video:description><![CDATA[Congenital heart defects are cardiac conditions and anomalies that are present at birth. These are usually divided into two categories; aycanotic or cyanotic, based on the presence or absence of cyanosis, which means bluish discoloration of the skin. Congenital heart defects that don’t cause cyanosis are known as acyanotic heart defects. The main types of acyanotic heart defects are ventricular septal defect, or VSD for short, which is the most common one, in addition to atrial septal defect, or ASD, patent ductus arteriosus, or PDA, and coarctation of the aorta.  

Now, let’s quickly recap the anatomy and physiology of fetal circulation. During fetal life, the lungs are filled with fluid and have high vascular resistance, so they don’t participate in gas exchange. Instead, the placenta serves as the organ of gas exchange, as well as delivering nutrients and removing metabolic wastes from the fetus.  

So, oxygenated blood flows from the uterine arteries into the placenta, where oxygen passes through the capillaries and into the umbilical vein.  

Then, part of the blood reaches the fetal liver, whereas about half of it bypasses the liver by a shunt called the ductus venosus, which diverts the oxygenated blood into the inferior vena cava, which has deoxygenated blood from the lower body.  

Then, this blood flows into the right atrium and further mixes with deoxygenated fetal blood coming from the brain and upper body through the superior vena cava. Most of this mixed blood then moves through a small flap called the foramen ovale directly into the left atrium, into the left ventricle, and through the ascending aorta into the systemic circulation, supplying oxygen to the brain and upper body, as well as the lower body. 

The rest of the blood from the right atrium flows into the right ventricle, and into the pulmonary arteries. A small amount of this blood moves into the pulmonary circulation and perfuses the lung tissue, but most of it is shunted]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_heart_defects_-_Cyanotic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yc4lgnxlQ_SdeC5zA9Y88MfISFK16g7P/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital heart defects - Cyanotic: Nursing]]></video:title><video:description><![CDATA[Congenital heart defects are cardiac conditions and anomalies that are present at birth. These are usually divided into two categories based on the presence or absence of cyanosis, which means bluish discoloration of the skin. The main types of cyanotic heart defects are tetralogy of Fallot, or ToF for short, which is the most common one; in addition to transposition of great vessels, or ToGV; tricuspid atresia; as well as persistent truncus arteriosus, or PTA; and total anomalous pulmonary venous return, or TAPVR. 

Now, let’s quickly recap the anatomy and physiology of fetal circulation. During fetal life, the lungs are filled with fluid and have high vascular resistance, so they don’t participate in gas exchange. Instead, the placenta serves as the organ of gas exchange, as well as delivering nutrients and removing metabolic wastes from the fetus.  

So, oxygenated blood flows from the uterine arteries into the placenta, where oxygen passes through the capillaries and into the umbilical vein.  

Then, part of the blood reaches the fetal liver, whereas about half of it bypasses the liver by a shunt called the ductus venosus, which diverts the oxygenated blood into the inferior vena cava, which has deoxygenated blood from the lower body.  

Then, this blood flows into the right atrium and further mixes with deoxygenated fetal blood coming from the brain and upper body through the superior vena cava. Most of this mixed blood then moves through a small flap called the foramen ovale directly into the left atrium, into the left ventricle, and through the ascending aorta into the systemic circulation, supplying oxygen to the brain and upper body, as well as the lower body.  

The rest of the blood from the right atrium flows into the right ventricle, and into the pulmonary arteries. A small amount of this blood moves into the pulmonary circulation and perfuses the lung tissue, but most of it is shunted through the ductus arteriosus back into the aort]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shock_-_Neurogenic:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zqKh86xvRpyATilQa3uCqh8RSnOpWAHy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shock - Neurogenic: Nursing]]></video:title><video:description><![CDATA[Shock is a life-threatening condition that occurs when the organs don’t receive enough oxygen and nutrients to function properly. Shock can be grouped into four types based on the cause: hypovolemic, cardiogenic, obstructive, and distributive shock. Neurogenic shock is a type of distributive shock where damage to the brain or spinal cord causes dysregulation of the cardiovascular system, leading to decreased heart rate and vasodilation, which eventually leads to impaired tissue perfusion. 

Now, to understand the neurogenic shock, let’s quickly review the physiology of blood vessels, which contain smooth muscle in their walls. When the smooth muscle relaxes, it increases the diameter of blood vessels, called vasodilation. On the other hand, when smooth muscle contracts, the diameter of blood vessels decreases, called vasoconstriction. 

The contraction and relaxation of smooth muscles are primarily controlled by the sympathetic nervous system, which normally maintains a partial constriction, generating enough force to keep blood moving through the circulatory system. The sympathetic system stimulation can increase or decrease to keep up with the body’s needs. Increased sympathetic stimulation of the blood vessels causes increased heart rate and vasoconstriction, which increases peripheral vascular resistance. Vasoconstriction, when the total blood volume is constant, raises blood pressure and allows blood to flow faster through the blood vessels. In contrast, decreased heart rate and vasodilation is typically caused by decreased sympathetic stimulation, in addition to inflammatory cytokines and histamine, which decrease peripheral vascular resistance. So, vasodilatation, when blood volume is constant, lowers the blood pressure and slows down the blood flow through the blood vessels.

Now let’s switch gears and look at the causes of neurogenic shock. This type of shock is primarily caused by trauma to cervical or upper thoracic segments of the spinal c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Valvular_heart_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7jiJDTDCQu2loSpVRhoOd6E_QdK0uPXi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Valvular heart disease: Nursing]]></video:title><video:description><![CDATA[Valvular heart disease refers to damage or defect involving one or more heart valves, and it can be divided into stenosis or narrowing of the valvular orifice; as well as regurgitation or insufficiency, and prolapse, in which the valvular leaflets fail to close adequately. 

Now, let’s go over some anatomy and physiology. If we take a look at a cross-section of the heart. Here, we can see the outer layer called the epicardium; the middle layer called the myocardium, and finally, a very thin inner layer called the endocardium.  

Now, the endocardium folds over the heart openings, forming the valvular leaflets that separate the heart chambers, so the atria and ventricles.  

There are two atrioventricular valves; the mitral valve separates the left atrium from the left ventricle, while the tricuspid valve separates the right atrium from the right ventricle.  These valves are connected to the papillary muscles,  and chordae tendinae of the heart.  

So when the heart is relaxed during diastole, they are open, enabling the ventricles to fill up with blood. On the flip side, when the heart contracts during systole, the valves close, thereby preventing the blood flow from the ventricles back into the atria.  

Then, there are two semilunar valves; the aortic valve separates the left ventricle from the aorta, while the pulmonary valve separates the right ventricle from the pulmonary artery.  

Now, in contrast to the atrioventricular valves, the semilunar valves close after ventricular contraction during systole, when the heart starts to relax in diastole, thereby preventing the backflow of the blood from the arteries into the ventricles. 

Alright, so valvular heart disease is caused by damage or defects involving one or more heart valves.Rheumatic fever, which is a delayed inflammatory condition that typically occurs  two to four weeks after a strep throat infection from Streptococcus pyogenes, also referred to as group A beta hemolytic streptococcus or GAS fo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperpituitarism:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wARweonnSGShlhvoN5Kz0mP1SCuNICNa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperpituitarism: Nursing]]></video:title><video:description><![CDATA[With hyperpituitarism, hyper- means high, and pituritism refers to the pituitary gland, which is a small, pea-sized gland at the base of the brain that’s made of an anterior lobe, an intermediate lobe and a posterior lobe. So hyperpituitarism describes an excessive secretion or production of one or more of the pituitary hormones, typically those produced by the anterior pituitary. 

The anterior lobe, also called the adenohypophysis, contains endocrine cells that produce tropic hormones, which in turn control the secretion of hormones from other endocrine glands or influence a response in target tissues. These include thyroid stimulating hormone, or TSH; adrenocorticotropic hormone, or ACTH; growth hormone, or GH; the gonadotropins, namely follicle stimulating hormone, or FSH, and luteinizing hormone, or LH; prolactin.

So, TSH stimulates thyroid hormone production, which, in turn, increases the basal metabolic rate in all cells. Next, ACTH stimulates adrenal cortisol production, which, in turn, has plenty of effects around the body, such as regulating glucose metabolism, blood pressure, electrolyte balance, and immunity. 

Then there’s GH, which stimulates the growth and development of various body tissues, and it also causes release of insulin like growth factor 1, or IGF1, from the liver and skeletal muscles, which mediates the effects of GH on target tissues. Finally, prolactin stimulates lactation during breastfeeding; while FSH and LH influence the function of gonads. All of these hormones are regulated via negative feedback. This means that when a gland, say, the thyroid, secretes more thyroid hormones, this will inhibit TSH levels, in order to maintain the thyroid hormone levels within a normal range. 

The posterior lobe, on the other hand, contains hormone-secreting nerve endings extending down from the hypothalamus. The posterior lobe secretes antidiuretic hormone, also called vasopressin or simply ADH, which regulates fluid volume in the body b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_atresia_&amp;_tracheoesophageal_fistula:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NyOa_dr4S-mOXm61VmV4f-KoTTmRrEBS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal atresia and tracheoesophageal fistula: Nursing]]></video:title><video:description><![CDATA[Esophageal atresia and tracheoesophageal fistula are congenital gastrointestinal anomalies where the esophagus and trachea don’t separate normally during development. Because these two organs develop together and eventually separate, the two conditions often occur together.

Let’s now quickly review the normal development of the esophagus and trachea. They both form from the primitive foregut between weeks 4 and 6 of intrauterine development. Afterwards, they are separated by the tracheoesophageal septum, which divides the foregut into the laryngotracheal tube at the anterior side and the esophagus at the posterior side. Eventually, the laryngotracheal tube develops into the larynx and the trachea, while the esophagus elongates and connects to the stomach.

Now, the exact cause of both esophageal atresia and tracheoesophageal fistula isn’t known, but it has been suggested that environmental factors, along with genetic factors play an important role in their development.

However, there are some risk factors associated with both these conditions. They include prenatal factors, such as maternal use of alcohol and smoking, uncontrolled diabetes mellitus, increased maternal age or exposure to drugs like methimazole and diethylstilbestrol. Risk factors unrelated to maternal ones include chromosomal anomalies, like trisomy 13, 18 or 21 and VACTERL syndrome, which is associated with spinal, anal, heart, tracheoesophageal fistulas, kidneys and limb anomalies.

Now let’s switch gears and look at the pathology of these conditions. With esophageal atresia, the esophagus fails to elongate and connect to the stomach around week 4 of intrauterine development. So essentially, there’s a proximal esophagus that ends in a blind pouch; and a distal esophagus, which ends right above the diaphragm. This is commonly associated with a tracheoesophageal fistula, which is a connection between the trachea and either the proximal, the distal or both parts of the esophagus. 

Based o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dialysis_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U5e3XXpORFCJ9ldDqYfHxxj4TIqV3dZi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dialysis care: Nursing]]></video:title><video:description><![CDATA[Dialysis is a type of kidney replacement therapy that removes toxic byproducts of protein metabolism, like urea, uric acid, and creatinine; waste products from the blood; as well as excess fluid. Additionally, through dialysis, electrolyte levels and acid-base imbalances can be corrected. There are two types of dialysis: hemodialysis and peritoneal dialysis. Now, let’s review some renal physiology. Each kidney is made up of millions of tiny functional units called nephrons, each of which consist of a renal corpuscle and the renal tubules. The renal corpuscle is where blood filtration happens, and it’s made up of the glomerulus, which is a tiny bundle of capillaries and the Bowman’s capsule, which is a cup-shaped structure surrounding the glomerulus. Blood flows through the glomerulus and then water and small solutes are filtered into Bowman’s capsule, creating an ultrafiltrate of blood. Then this ultrafiltrate goes through the renal tubules, where electrolytes and water can be secreted or reabsorbed. 

In addition, they are important in regulating acid-base balance. The kidneys also clear blood of metabolic wasteful substances and toxins. Finally, what leaves the tubules becomes the urine, which flows into the bladder and is excreted during micturition. Okay, now, let’s look at some situations when dialysis is indicated. Most often, clients who require dialysis have end-stage chronic kidney disease, which means the kidneys have lost almost all their function. In this case, both hemodialysis and peritoneal dialysis are adequate long-term options. However, there are some urgent conditions that benefit from dialysis, and hemodialysis is usually preferred in these situations. These clients also usually have associated acute kidney injury. 

Indications for urgent dialysis include pulmonary edema unresponsive to conventional treatment; life-threatening hyperkalemia, when potassium levels are over 6.5 mEq/L and there are associated electrocardiographic abnormali]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epididymitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iHjPcV0aTiqBvV9oPU1HtSvSSJ2lfc0W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epididymitis: Nursing]]></video:title><video:description><![CDATA[Epididymitis is an inflammation of the epididymis that most commonly affects young, sexually active clients assigned male at birth under 35 years of age. It is usually characterized by unilateral pain and swelling in the scrotum. First, let’s recall the anatomy and physiology of the epididymis, which is a tubular, comma-shaped structure curving superiorly and posteriorly around the testes. The epididymis collects and stores the sperm cells produced by the testicle until they are mature and capable of fertilization. During ejaculation, sperm leave the epididymis and travel via ductus, or vas deferens, to the prostate gland, where it enters the urethra to be expelled outside of the body. The urethra is also the way urine is excreted from the body, but during ejaculation, the bladder sphincter right above the prostate contracts and prevents urine from mixing with sperm.

Now, the causes of epididymitis often vary with age. The most common cause of epididymitis in clients younger than 35 is a sexually transmited infection or STI, especially from bacteria like Neisseria gonorrhoeae and Chlamydia trachomatis. The most common cause of epididymitis in older clients and children, is an urinary tract infection or UTI with bacteria from the gastrointestinal tract, such as Escherichia coli. Less common causes of epididymitis include; viruses, such as mumps virus, as well as non-infectious causes, including trauma and irritation, medications like amiodarone, and autoimmune disease.In addition, there are also certain risk factors for developing epididymitis. Non-modifiable risk factors include being aged 20 to 39 years old and having congenital abnormalities of the genitourinary tract. Modifiable risk factors, on the other hand, include increased sexual activity, multiple sexual partners, and anal or unprotected intercourse. Other modifiable risk factors include urinary retention, which could be due to benign prostatic hyperplasia, or prostatitis; as well as engagi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_&amp;_urinary_calculi:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ciR0OqOYTDOM4L3xrZcI_K89SASL5sN3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal and urinary calculi: Nursing]]></video:title><video:description><![CDATA[Nephrolithiasis and urolithiasis refer to the presence of stones, also known as calculi, in the kidney and the urinary tract, respectively. Stones form when solutes in the urine precipitate out and crystallize. 
Depending on which solute precipitates to form the stone, there are five main types of stones: calcium oxalate, calcium phosphate, struvite, uric acid, and cystine stones.

Now, let’s quickly review some anatomy and physiology of the urinary tract, which is made of the kidneys, ureter, bladder, and urethra. The kidneys are in charge of producing urine, which is made up of water and solutes.

 The process starts with glomerular filtration in the renal corpuscle, which is made up of the glomerulus and the Bowman’s capsule. As blood flows into the glomerulus, water, electrolytes like sodium, and other small particles in the blood like creatinine, urea nitrogen, and glucose, pass through the endothelial lining of the capillaries and into Bowman&amp;#39;s space. 
Large proteins and red blood cells however, aren’t filtered. 
Now, the next steps, which include tubular reabsorption and secretion, take place in the renal tubules, which are surrounded by the peritubular capillaries. Here, water and solutes get passed back and forth between the filtrate in the lumen of the renal tubule and the blood in the peritubular capillaries. 

Finally, urine is drained into the renal pelvis, which then narrows to form the ureter, and transports urine to the bladder. Ultimately, urine exits the bladder through the urethra.

Now, nephrolithiasis and urolithiasis are caused by the increased concentration of certain solutes in the urine. This can happen if there’s an increase in the solute, which could be calcium with oxalate or phosphate, leading to the formation of calcium stones; magnesium, ammonia, and phosphate, leading to struvite stones, as well as uric acid forming uric acid stones and cystine, forming cystine stones. Alternatively, there could be a decrease in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_retention:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2iqMw5KIRgaCIBQalSBWrBLGS1SBt_7B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary retention: Nursing]]></video:title><video:description><![CDATA[Urinary retention is a condition characterized by the inability to completely empty the urinary bladder. 

Okay, let’s quickly review some anatomy and physiology. The urinary bladder is a hollow organ that lies behind the pubic bones and pubic symphysis, and it’s superior to the prostate in individuals assigned male at birth or anterior to the vagina in individuals assigned female at birth. 

The bladder has a strong wall that’s made up of a urothelium that’s capable of stretching and expansion; as well as a smooth muscle layer called the detrusor muscle, which is able to relax or contract, as needed. 

During urination, the bladder empties urine into a muscular tube called the urethra, which extends from the neck of the bladder, or the internal urethral sphincter, to the external urethral sphincter, and carries urine to pass outside our body. 

In individuals assigned male at birth, the urethra is long and typically measures about 18 to 22 centimeters. On the other hand, in individuals assigned female at birth, the urethra is short - only about 4 centimeters long. 

Now, let’s quickly explain the physiology of urination. First, the urine is formed in the kidneys and passes down into the urinary bladder. As the bladder progressively fills with urine, the urothelium expands and the detrusor muscle relaxes. 

When the bladder is almost full, the nerves in the bladder wall send impulses to the micturition center at the brainstem. This activates the micturition reflex, which causes involuntary relaxation of the internal urethral sphincter and contraction of the detrusor muscle, allowing urine to pass down into the urethra. Fortunately, there’s another sphincter that lies just below the internal sphincter, called the external urethral sphincter, which is controlled voluntarily. So, when the individual is ready to urinate, they can voluntarily relax their external sphincter, allowing urine to pass outside the body, and emptying the bladder completely. 

Now, the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Primary_immunodeficiency_disorders:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1zBGSPJhR6qOJwZ_7rIUQYz5Q12Q0dJ8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunodeficiency disorders - Primary: Nursing]]></video:title><video:description><![CDATA[Primary immunodeficiency disorders are a diverse group of conditions that affect one or more elements of the immune system, leading to increased vulnerability to infection, autoimmune manifestations, and several types of cancer. All right, let’s quickly review some physiology. The immune system consists of white blood cells that protect us from pathogens like viruses, bacteria, and fungi, as well a foreign substances, such as toxins and chemicals, and destroy abnormal cells, such as those that might develop into cancer. Now, the immune system consists of two main branches: innate and adaptive. The innate immune response involves non-specific defense mechanisms, meaning that they do not differentiate one pathogen from another. These include complement proteins and cells like phagocytes and natural killers; as well as dendritic cells, which then activate the adaptive immune response. 

The adaptive response is highly specific, meaning that it recognizes different pathogens and is mediated by cells called lymphocytes, which include T and B cells. T cells can be further divided into CD4+ and CD8+ T cells. CD4+ T cells are also known as T helper cells, because they interact with dendritic cells, and in turn help activate the rest of the lymphocytes. On the other hand, CD8+ T cells, also known as cytotoxic T cells, are in charge of cell-mediated immunity, where they attack abnormal and infected cells. Finally, B cells mediate a specific adaptive response, called humoral immunity, by secreting antibodies that bind to and destroy extracellular pathogens. These antibodies can be classified into several classes based on their structure and function, including IgM, IgA, IgD, IgG and IgE. Now, primary immunodeficiencies are a group of over 130 disorders that result from genetic defects in one or more elements of the immune system, including antibodies, T cells, complement components, and phagocytes. 

Unlike secondary immunodeficiencies, which are acquired and typical]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Scleroderma:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-XPs1tZLTxmURXb9LGPBiCYSRTSS6O9j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Scleroderma: Nursing]]></video:title><video:description><![CDATA[Scleroderma is a connective tissue disease characterized by chronic inflammation, sclerosis, and fibrosis of the skin, blood vessels, and internal organs. There are two types of scleroderma: localized or limited scleroderma, which is more common and typically involves the skin of the face and fingers; and systemic or diffuse scleroderma, which is less common but more severe, as it tends to involve the internal organs too. Let’s start by reviewing the physiology of connective tissue, which is the most abundant tissue type in the body. It provides structural support and protection throughout the body. This tissue houses the most abundant proteins in the body, called collagen, which are large, strong fibers that add elasticity to the connective tissue and helps it in bearing tensile force. Now, the exact cause of scleroderma is still unknown, with some experts suggesting there’s an inflammatory response against the connective tissue. This is often associated with the presence of autoantibodies, namely anticentromere antibodies in localized disease, and topoisomerase-1 antibodies in systemic disease. 

Risk factors of scleroderma include being assigned female at birth, in addition to environmental or occupational exposure to coal, plastic, and silica dust. On the other hand, risk factors for localized scleroderma include ages below 40 and white race, whereas risk factors for systemic scleroderma include ages between 30 and 50 and black race. The pathology of scleroderma starts with an inflammatory response that mainly attacks the connective tissue of the skin, blood vessels, and in some cases even internal organs. This causes an increase in the production of collagen fibers, which leads to progressive connective tissue damage and fibrosis. As a result, there’s progressive sclerosis of the skin, as well as microvascular abnormalities and occlusion, and disruption of the normal function of internal organs, mainly the heart, lungs, kidneys, and gastrointestinal t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sjögren_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JFjf_s7rQnGYCbtGMTKHhgPaR1i0OZeM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sjögren syndrome: Nursing]]></video:title><video:description><![CDATA[Sjogren syndrome is an autoimmune disease in which the immune system targets and attacks various exocrine glands, most commonly the lacrimal glands and the salivary glands.

Alright, now let’s quickly review the physiology of exocrine glands, which are found throughout body organs. These glands release various substances into a ductal system, which in turn carries these substances to an epithelial surface. Two particular examples of exocrine glands are salivary and lacrimal glands. 

Now, there are three main pairs of salivary glands, called major salivary glands, which include the parotid, submandibular, and sublingual glands. 

There are also a few smaller companions called minor salivary glands, which are sprinkled over the palate, lips, cheeks, tonsils, and tongue. When it comes to function, salivary glands secrete saliva into ducts that open in the oral cavity. Saliva contains enzymes that begin the digestion process, lubricates, and protects the mucosal surfaces of the mouth, in addition to preventing bacteria from forming dental cavities or caries. 

On the other hand, lacrimal glands are paired exocrine glands located within the orbital cavity, just above the lateral angle of the eye. These glands secrete tears, which lubricate and nourish the surface of the eyes, help wash away debris, and act as a protective barrier against foreign particles, like pollen or dust.

The exact cause for Sjogren syndrome is unknown, but it seems to be related to both genetic and environmental factors. Sjogren syndrome typically affects clients over the age of 40, and risk factors include a family history of Sjogren syndrome, clients assigned female at birth, white or black race, as well as HLA genes that encode specific types of immune molecules, called HLA-DRW52, HLA-DQA1, or HLA-DQB1, which normally identify and bind to foreign molecules. 

Environmental risk factors mainly include viral and bacterial infections of the exocrine glands, as well as being diagnosed wi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acne:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9R0NSVe_QcGeaT_ytLLatSqRRnGmxpSS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acne: Nursing]]></video:title><video:description><![CDATA[Acne is a common skin condition in which pores of the skin become blocked by ingrown hair, oil, dead skin cells, or bacteria. It is often linked to hormonal fluctuations in teenagers and young adults, and can sometimes persist into adulthood. Let’s start by quickly reviewing the physiology of the skin. The skin has three main layers: epidermis, dermis, and hypodermis or subcutaneous tissue. The epidermis is the outer layer of the skin that houses cells filled with melanin pigment and keratin, called keratinocytes. Right beneath the epidermis, there’s the dermis, which is a layer of connective tissue that contains the blood vessels and nerves of the skin. Additionally, the dermis also houses epidermal appendages, which are structures that originate from the epidermis but extend into the dermis, such as hair follicles and sebaceous glands. 

Hair follicles are the living structures of hairs, which are surrounded by a layer of keratinized tissue called the hair shaft. This shaft extends through the epidermis to open into tiny pores on the surface of the skin. Additionally, the sebaceous glands produce oil or sebum under the influence of androgen hormones. Then, it pumps this oil through small ducts that open into the hair shaft at the junction between the epidermis and the dermis. Finally, the dermis is lined on the inside by the subcutaneous tissue, which is a fatty connective tissue that functions in insulation and temperature regulation. All right, so the main cause of acne is blockage of the tiny pores of the skin by dead skin cells, bacteria, and overproduction of sebum by sebaceous glands. When it comes to risk factors of acne, these can be modifiable or non-modifiable. Modifiable risk factors include stress, using oily skin products, steroid use, excessive exposure to sunlight, and repetitive friction or pressure on the skin. 

For non-modifiable risk factors, these include family history of acne, as well as younger ages and hormonal changes in pu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Animal_&amp;_snake_bites:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_iM4H14uSteauo0UG-0tEII_SuqtTb9h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Animal and snake bites: Nursing]]></video:title><video:description><![CDATA[Bites can be caused by a wide variety of animals, including dogs, cats, and small rodents, like hamsters or squirrels; as well as wild animals, such as snakes. Perhaps more surprisingly, bites can also be caused by humans! 

Let’s start by looking at the anatomy and physiology of the skin. The skin is made of the epidermis, which is an outer layer that acts as a protective barrier against the environment; the dermis, which primarily contains blood vessels and nerve endings; and the hypodermis, which is a layer of connective tissue that provides structural support to the skin. 

The skin also contains several immune cells which are responsible for phagocytizing invading pathogens, such as those that may have broken through the epidermis via a cut, scrape, or bite wound. When activated, immune cells release inflammatory molecules, like cytokines and histamine, which attract more immune cells to the site of injury. In addition, the release of cytokines causes capillaries to get larger and become more permeable, allowing plasma proteins and fluid to leave the circulation. Ultimately, all of these factors contribute to the classic signs of inflammation: heat, pain, redness, and swelling. 

Now, the most common animal bites are from dogs, followed by cats and small rodents, like squirrels or rats. In particular, dog bites account for up to 90% of all animal bites, and they typically affect children under the age of 10. On the other hand, cat bites are less common and tend to occur more frequently in adult clients. 

Finally, snake bites are a major hazard in certain areas of the world, including Southeast Asia, sub-Saharan Africa, and Latin America, as well as certain parts of the United States, depending on the species. Most snake bites occur in forested areas, but also in regions of high density of snake population, typically farming regions where grain attracts rodents that, in turn, attract snakes. There are two main venomous snake families: the Elapids]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Burn_injury:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/35USzeLLRYyBSD5kYtUuGWG9QCG3YqtS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Burn injury: Nursing]]></video:title><video:description><![CDATA[Burn injuries are a type of acute wound where the skin and tissue underneath are damaged by exposure to heat, extreme cold electricity, chemicals, or radiation. 

Okay, first, let’s talk about physiology. The skin is the outer barrier that protects the body from excessive water loss, as well as any external threat like pathogens. The skin is divided into three main layers, the hypodermis, dermis, and epidermis. The hypodermis is made of fat and connective tissue that anchors the skin to the underlying muscle and acts as a cushion that protects underlying tissues from trauma. Above the hypodermis is the dermis, which is made of proteins like collagen that provides structural support, as well as elastin that provides flexibility. The dermis also contains hair follicles, nerve endings that collect sensory information, as well as sweat glands, and blood vessels, which help regulate body temperature. And just above the dermis is the epidermis, which itself has multiple cell layers that are composed of developing cells called keratinocytes. 

Now, the skin has this special ability to repair itself when damaged. To do that, there are three main processes: reepithelialization, granulation, and wound retraction. Reepithelialization describes the resurfacing of damaged skin by new skin cells. If the damage is too great to be fixed only by reepithelialization, granulation and wound retraction come into action. Granulation is the process of forming granulation or scar tissue, which contains new blood vessels and fibroblasts. These fibroblasts form new connective tissue and have the ability to contract, pulling the edges of the wound together in a process called wound retraction. 

Okay, burn injuries can be classified based on the cause. The most common cause are thermal burns, which can result from scalds from hot liquids or steam, from open flames, such as from house fires, or by direct contact when a hot object like oven doors or cookware is touched. Less comm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Folliculitis,_carbuncles,_&amp;_furuncles:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zdVFf4A3T92yVwdXaqAb2GsiT3Kh3i62/_.jpg</video:thumbnail_loc><video:title><![CDATA[Folliculitis, carbuncles, and furuncles: Nursing]]></video:title><video:description><![CDATA[Folliculitis is a superficial bacterial infection of the hair follicles, while furuncles, or boils, are deeper infections of the hair follicles and the surrounding tissue, and carbuncles are groups of two or more furuncles. They are usually caused by bacteria, but viruses, fungi, and parasites may also cause the infection.

Okay, let’s go over some physiology. Normally, the skin is divided into three layers, the epidermis, dermis, and hypodermis. The epidermis is the thin outermost layer of skin, the dermis is the thicker layer that lies below that, and the hypodermis is the lowest layer that’s made of fat and connective tissue and anchors the skin to the underlying muscle.

Now, hair, along with nails and skin glands, are considered skin appendages  that help with regulating body temperature and protection from the environment. Hair is found on nearly every part of skin except the palms of the hands, soles of the feet, and the lips. 

Every strand of hair is composed of the shaft, root, and bulb that sits in a pouch-like structure called the hair follicle. Next is the epidermal tissue that dips down into the dermis, and is associated with other structures like apocrine glands, sebaceous glands, the arrector pili muscle, and nerve receptors. Inside the bulb lies the hair matrix which serves as the active site of hair growth and gives hair its color.

Now, normally, the skin surface is colonized by a huge number of microorganisms that make up the normal skin flora. This flora consists mostly of bacteria, such as Staphylococcus epidermidis, as well as certain fungi, such as Candida albicans. The normal skin flora is typically non-pathogenic, meaning that these microorganisms don’t cause any disease. In fact, they are often beneficial, since they serve as a physical and competitive barrier that helps prevent pathogenic microorganisms from invading and infecting the skin and its appendages.

Now, folliculitis, furuncles and carbuncles are all typically ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Herpes_simplex_virus_(HSV):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5uAU9iZNT6_o_rh2WZf8ofa7Q8qX2jZ_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Herpes simplex virus (HSV): Nursing]]></video:title><video:description><![CDATA[Herpes simplex is a highly contagious infection caused by herpes simplex viruses. There are two types of herpes simplex virus. Herpes simplex virus 1, HSV-1, tends to cause infections above the waist, typically affects the lips, and that’s called herpes labialis; while HSV-2 tends to cause infections below the waist, involving the genitals, and that’s herpes genitalis. 

During the primary infection, both types also infect nearby sensory neurons and travel up their axon to sensory ganglia where they can lay dormant for life causing recurrent infections from time to time. 

Okay first, let’s quickly review the physiology of the nervous system. The central nervous system consists of the brain and spinal cord, while the peripheral nervous system includes all the nerves that connect the central nervous system to the skin, muscles, and other organs.

Cranial nerves are peripheral nerves that originate from the brain, and they’re mostly in charge of motor and sensory innervation of the head and neck. 

A specific cranial nerve, cranial nerve V, is the trigeminal nerve and it’s responsible for the sensation in the face. Its sensory neurons create a nerve cell cluster called the trigeminal ganglion, located in the bones on the side of the face between the eyes and ears. 

On the flip side, the peripheral nerves that originate from the spinal cord are called the spinal nerves. 

Each nerve is formed by a dorsal root that contains sensory information, like touch, temperature, pain, and pressure from the skin and other tissues, 
and a ventral root that contains neurons that carry motor innervation from the spinal cord to the muscles. 

Alright now, an important risk factor associated with both types of herpes simplex is having multiple sexual partners. 

Additionally, specific risk factors for HSV-1  include coming in contact with another person’s saliva, most commonly through kissing or sharing drinks; playing contact sports, like wrestling; and sharing cosmetics. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Insect_stings_&amp;_bites:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UALqF7RqTS253_qcir-qzeW9SHS2aoSC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Insect stings and bites: Nursing]]></video:title><video:description><![CDATA[Insect stings and bites are relatively common injuries; the difference between them is that stings happen when an insect introduces toxic venom into someone&amp;#39;s body, often as a self-defense mechanism; whereas bites happen when an insect pierces someone’s skin in order to feed on their blood.

Let’s start by looking at the anatomy and physiology of the skin. The skin is made of the epidermis, which is an outer layer that acts as a protective barrier against the environment; the dermis, which primarily contains blood vessels and nerve endings; and the hypodermis, which is a layer of connective tissue that provides structural support to the skin. 

In addition to being a physical barrier against the external environment, the skin harbors several types of immune cells that participate in the body’s immune response. Normally, the immune system recognizes and acts against pathogens that cause disease, but in some clients, it can overreact and start targeting harmless molecules that don’t cause any problems for most people, including certain foods, medications, as well as the venom or saliva of some insects.

Now, insect stings are caused by stinger insects of the Hymenopteran family, which includes bees, wasps, hornets, yellow jackets, and fire ants; as well as other animals like spiders and scorpions. On the other hand, insect bites are most commonly caused by insects that feed on the host&amp;#39;s blood to survive, and these include mosquitoes, chiggers, bedbugs, lice, and ticks. 

Since many insects only sting when provoked, risk factors for getting stung include disturbing the animals, such as stepping on a bee-hive, for example. Additionally, insect stings and bites are more likely to happen in clients who spend a lot of time outdoors, especially those who live in warmer climates or near wetlands and forested areas with lots of wood, bushes, and tall grass. Other risk factors include collecting insects as a hobby and not using protective clothes o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediculosis_&amp;_scabies:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VmKj_8EMSwW-sNslhQk6LWMgRXaqAG5b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediculosis and scabies: Nursing]]></video:title><video:description><![CDATA[Pediculosis and scabies are both parasitic skin disorders. Pediculosis is an itchy infestation of the lice in hairy parts of the head or body, while scabies is a skin infection caused by an infestation of mites called Sarcoptes scabiei.

Let’s start by looking at the anatomy and physiology of the skin. The skin is made of the epidermis, which is an outer layer that acts as a protective barrier against the environment; the dermis, which primarily contains blood vessels and nerve endings; and the hypodermis, which is a layer of connective tissue that provides structural support to the skin.  Hair follicles begin in the dermis, and hair grows out of these follicles in most body areas. The visible part of the hair is called the hair shaft.

Now, pediculosis is caused by different lice species: head lice called Pediculus humanus capitis; body lice, or Pediculus humanus; and pubic or crab lice, called Phthirus pubis. Meanwhile, scabies is always caused by Sarcoptes scabiei.

One of the largest risk factors for contracting pediculosis or scabies is having close contact with an affected individual. This commonly happens among children in school, especially head lice. Other risk factors for pediculosis include sharing personal items, like brushes or towels, as well as having sexual intercourse with an affected individual. Risk factors for scabies include living in an institutionalized setting, like prison or a long-term care facility, or being a refugee or unhoused.

Now let’s switch gears and look at the pathology of pediculosis. This condition starts after direct contact with a person who is infected with lice, or indirect contact through sharing personal items. Next, the female lice lays eggs in the hair shaft, and then the growing and adult lice suck blood from the individual’s skin. Saliva and fecal matter from the lice leads to inflammation and itching. 

Scabies is almost always transmitted by direct physical contact. The female mites burrow into the outer l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amputation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RZUuag8eTuC2KDJM-raibwdVS_uPrRYO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amputation: Nursing]]></video:title><video:description><![CDATA[Amputation is when an extremity is separated from the rest of the body. This most often involves a limb or a part of it like a digit, but can also involve a portion of the nose or ears.

Now, the causes of amputation may include trauma, such as a motor vehicle crash or power tool injuries. Amputation can also be performed surgically to prevent or manage a condition, such as tissue death and gangrene, which can be caused by peripheral vascular diseases or neurological conditions like diabetic neuropathy, infections like osteomyelitis, thermal injuries, cancer, and congenital limb disorders.

All right, so in terms of classification, limb amputations may occur above a joint, such as the elbow, called above elbow amputation or AEA for short, or the knee, called above knee amputation, also known as, AKA; as well as below a joint, such as below elbow amputation or BEA for short, or the knee, called below knee amputation or BKA. Amputation can even happen through a joint, which is called disarticulation.

Now, undergoing an amputation carries a risk for certain complications. The most common one is local or wound pain; as well as neuroma, which is a tender thickening of a nerve stump in the scar region after amputation, so upon palpation, clients experience sharp shooting pain. Another type of pain in amputation is known as phantom limb, in which the client may perceive unpleasant sensations like tingling or even sharp pain in the limb that has been amputated. In addition, clients may develop contractures, where the affected tissues like skin, muscles, and ligaments become stiff and fibrous, leading to restrictions of movement. 

Other complications include local infections of the amputation stump, most often caused by bacteria colonizing the skin, like Staphylococcus species; and if not treated in time, local infections can lead to sepsis. Another very serious complication from amputation is hemorrhage, which can either occur immediately if a major blood vessel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Muscular_dystrophies_-_Duchenne_&amp;_Becker:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xazyNP6UQfGSyVAiSZ1bdw7lQGWFegka/_.jpg</video:thumbnail_loc><video:title><![CDATA[Muscular dystrophies - Duchenne and Becker: Nursing]]></video:title><video:description><![CDATA[Muscular dystrophies are a group of genetic disorders characterized by progressive muscle degeneration and weakness. There are several types of muscular dystrophies, but the two most common ones are Duchenne and Becker muscular dystrophy. All right, let’s review some anatomy and physiology. The muscular system consists of skeletal or striated muscles, which are attached to bones and contract under voluntary control; as well as smooth muscles found in the walls of hollow organs, and cardiac muscles, which are only found in the heart, and both of which function under involuntary control. Now, a protein, called dystrophin, is normally found on the membrane of muscle cells, primarily skeletal and cardiac, where it provides mechanical support and stabilization. 

Now, both Duchenne and Becker muscular dystrophies are caused by mutations in the gene that codes for the dystrophin protein. In Duchenne muscular dystrophy, dystrophin is completely absent; whereas in Becker muscular dystrophy, there is some dystrophin present, but it does not function properly. Now, Duchenne and Becker muscle dystrophies are X-linked recessive genetic disorders, so they occur almost exclusively in those assigned male at birth. This is because the dystrophin gene is located in the X-chromosome. So, let’s say a mother has 1 mutated and 1 normal chromosome. She passes down one of the mutated X chromosomes down to her daughter, the father passes down a normal X chromosome, so the daughter is still able to produce functional dystrophin. However, if the mother passes the mutated chromosome to her son and the father passes down a Y chromosome, which doesn’t have the dystrophin gene, the son will not be able to produce functional dystrophin and will develop the disease. 

In this case the mother didn’t have the disease, so they&amp;#39;re an “asymptomatic carrier. ”Now, pathology-wise, the lack of the dystrophin protein in muscle cells causes them to be fragile and easily damaged. Intracell]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Juvenile_idiopathic_arthritis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vXlydASARz6NJIdSgCTzF1meS3mo0lGc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Juvenile idiopathic arthritis: Nursing]]></video:title><video:description><![CDATA[Juvenile idiopathic arthritis, previously known as juvenile rheumatoid arthritis, is an inflammatory disease that occurs in children and young adolescents under the age of 16. 

Alright first, let’s start by reviewing some immune system physiology. So when an antigen enters the body, it comes in contact with a type of immune cells called antigen presenting cells, or APCs. These include macrophages, dendritic cells, and even naive B cells. The APCs will engulf and digest the pathogen then present fragments on their surface. Another type of immune cells, called T helper cells, then recognize the antigen, causing them to activate and proliferate; this results in an army of T helper cells that release cytokines, including interleukin 1, interleukin 6, and tumor necrosis factor, or TNF for short. These cytokines are signalling molecules that attract other immune cells to the site. These cells can be part of the adaptive immune system, like cytotoxic T cells, or killer T cells; or part of the innate immune system, like neutrophils and natural killer, or NK cells. In addition, T helper cells can also trigger another type of immune cells called B cells to secrete antibodies against the antigen. 

Finally, after the immune response ends, some immune cells, called memory cells, survive and can remember an antigen, allowing them to activate a quicker immune response to that antigen in the future. 

Okay, as the term idiopathic suggests, the exact cause of juvenile idiopathic arthritis is unknown. However, several risk factors have been identified. These include genetic factors, like having a particular HLA subtype called HLA-B27; being assigned female at birth; as well as antibiotic use during infancy and childhood. On the bright side, some possible protective factors have also been identified, including having been breastfed.

Now, while the exact mechanism of the disease is unknown, it is believed that an environmental factor triggers an atypical autoimmune re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amyotrophic_lateral_sclerosis_(ALS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EY21ycdkTwu5KWenNFseLUjUQWSN-R0t/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amyotrophic lateral sclerosis (ALS): Nursing]]></video:title><video:description><![CDATA[Amyotrophic lateral sclerosis or ALS, also called Lou Gehrig’s disease, is a progressive neuromuscular disease characterized by damage and degeneration of the upper motor neurons in the brain, as well as the lower motor neurons in the spinal cord.

Now, let’s quickly go over the physiology of the neuromuscular system, which includes muscles and the motor neurons serving them to ultimately trigger voluntary muscle contraction. 

When we want to perform a movement, the motor cortex of the brain sends electrical impulses through an upper motor neuron. In turn, this neuron travels down the lateral corticospinal tract cord, until it reaches a second neuron, called the lower motor neuron, which relays the electrical impulses. Then, the lower motor neurons give rise to the peripheral nerves that carry the electrical impulses directly to the desired muscle fibers, which ultimately contract.

Now, the exact cause of ALS is unknown, with some evidence suggesting the cause to be excessive levels of the neurotransmitter glutamate, which can cause neurons to become overexcited, leading to damage and even death. In addition, between five to ten percent of ALS cases have a mutation in the C9ORF72 gene, suggesting that the disease can be inherited.

Risk factors of ALS can be grouped into modifiable and nonmodifiable risk factors. Modifiable risk factors include smoking and participating in military wars, especially in Gulf wars, where individuals are often exposed to traumatic injuries and the inhalation of chemicals and metals.

On the other hand, non-modifiable risk factors include white race, being assigned male at birth, in addition to age between 40 and 60 years, and family history.

The pathology of ALS starts with the degeneration of upper and lower motor neurons in the brain and the spinal cord respectively. This weakens the ability of neurons to transmit electrical impulses, and leads to progressive degeneration of muscles, a process called amyotrophy. As a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epidural_&amp;_subdural_hematoma:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3-nLMvRLQW2CGhe9CRZD4l6VRUaOh4WH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epidural and subdural hematoma: Nursing]]></video:title><video:description><![CDATA[Intracranial hemorrhage or ICH for short, refers to bleeding inside the skull. Types of intracranial hemorrhage include epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intracerebral bleeding. Now, epidural hematoma is the collection of blood in the epidural space, which is the space between the dura mater and inner surface of the skull. In contrast, subdural hematoma is the collection of blood in the subdural space, meaning between the dura mater and the arachnoid mater.

Let’s start by looking at the physiology of the meninges. This is a membrane that wraps around the brain and protects it from the outside environment. It’s made up of three meningeal layers. From outside to inside, these are the dura mater, arachnoid mater, and pia mater. Between the arachnoid and pia mater there’s the subarachnoid space, which houses the cerebrospinal fluid. The cerebrospinal fluid is a clear, watery liquid that cushions the brain from impact and bathes it in nutrients. 

Now, the dura mater consists of an external and an internal layer. The external layer of the dura mater adheres tightly to the inner surface of the skull, so the epidural space is only a virtual space in the cranium, meaning the space isn’t appreciable unless pathology is present. 

Between the external layer of the dura mater and the inner surface of the skull, there are meningeal arteries that supply meninges. The internal layer of the dura mater lies above the arachnoid mater, the two are separated by the subdural space. The subdural space plays a major role in venous blood drainage in the brain. The dura mater also forms dural venous sinuses which carry the venous blood from the brain. These sinuses are connected to the veins outside of the cranium by bridging veins.

Okay, let’s move onto epidural and subdural hematoma. The most common cause of epidural hematoma is rupture of the meningeal artery. This is often caused by blunt head trauma from falls or car crashes. The most commo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Huntington_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q5UsktjrTDG_Zdy41K3KwD8NT_GZ5jOh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Huntington disease: Nursing]]></video:title><video:description><![CDATA[Huntington disease, or HD for short, is a rare hereditary progressive neurodegenerative condition that’s characterized by motor, psychiatric, and cognitive problems. Okay, first, let’s focus on some anatomy and physiology of the brain; specifically, the basal ganglia, which are a collection of nuclei  located deep in the brain. These structures help initiate, fine-tune, and complete voluntary movements. To do this, the basal ganglia receive information from the cerebral cortex, and respond by sending information to the thalamus through two pathways: the direct pathway, which is excitatory; and the indirect pathway, which is inhibitory. And there are two main neurotransmitters involved in these pathways: the excitatory neurotransmitter glutamate, and the inhibitory neurotransmitter GABA. A third neurotransmitter, called dopamine, can play both an excitatory and inhibitory role. By using the excitatory and inhibitory pathways, the basal ganglia controls what signals the thalamus sends to the motor cortex, which results in the initiation of voluntary movement. 

Now, Huntington disease is caused by a mutation of the HTT gene, which is located on chromosome 4 and is responsible for the synthesis of the huntingtin protein. This mutation is inherited through the autosomal dominant pattern, meaning that one affected copy of a gene is enough to cause the disease. In other words, a person with Huntington disease has a 50% chance of passing on the affected gene to their child, so the most important risk factors are a family history of Huntington disease. The pathology of Huntington disease results from the mutated HTT gene, which codes for a defective huntingtin protein. This defective protein aggregates in the neurons of the basal ganglia, ultimately causing cell death, especially of GABAergic inhibitory neurons. As the disease progresses over time, more neurons continue to die, and eventually, the basal ganglia undergoes significant atrophy. At the same time, ther]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intracranial_aneurysm:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3LjeJS5_QyKawJuWD7h0YwUhSROwbcz-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intracranial aneurysm: Nursing]]></video:title><video:description><![CDATA[Aneurysms are abnormal dilations in a blood vessel that form in weakened areas of the blood vessel walls. Aneurysms can happen to any blood vessel in your body, including the cerebral vessels, in which case they’re called intracranial or cerebral aneurysms.

Alright, let’s go over some physiology. There are three major types of blood vessels: arteries, veins, and capillaries. Normally, blood flows from large arteries into medium and then small arteries called arterioles, which in turn carry the blood to capillary beds. 

All arterial vessels have three layers: from outside in, there’s tunica externa or the adventitia layer, which has loose connective tissue, and sometimes, ‌vasa‌ ‌vasorum‌ ‌or‌ ‌vessels‌ ‌that‌ ‌supply‌ ‌the‌ ‌artery; then tunica media or the media layer, which contains some elastic tissue and smooth muscle that allow the arteriole to dilate or constrict in response to local conditions; and finally the endothelium, which consists of a single layer of endothelial cells on top of a layer of connective tissue, called lamina propria. 

Alright, now the main cause of intracranial aneurysms is weakness in the walls of cerebral blood vessels, which can be due to injury to the blood vessel wall. Sometimes this is from trauma, or it could be due to another pathological process. Bacterial or fungal infections can cause aneurysms, in which case they are known as mycotic aneurysms. Genetic disorders, like Ehlers-Danlos and Marfan syndromes, impairs the body’s ability to synthesize connective tissue proteins like fibrillin or collagen, which lead to weakened blood vessel walls and result in aneurysm formation.

In terms of risk factors for intracranial aneurysms, modifiable ones include hypertension, atherosclerosis, and cigarette smoking, as well as alcohol and cocaine use. Now, non-modifiable risk factors include age between 40 and 60, family history of aneurysms or stroke, and being assigned female at birth. Clients with polycystic kidney disease, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physiology_of_pain:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2C_WL2DsRgWFpvLER6hgzJG2QSquNT32/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physiology of pain: Nursing]]></video:title><video:description><![CDATA[Pain is an unpleasant physical or emotional experience that occurs in response to actual or potential tissue damage. Depending on the cause and duration, pain can cause suffering and decreased quality of life. As a symptom, pain is one of the most common reasons that bring clients to healthcare facilities. First, let’s look at the four main mechanisms involved in the physiology of pain, which are transduction, transmission, perception and modulation. Transduction is the process through which a pain-inflictive stimulus is converted into a biological signal. This stimulus can be mechanical, like pinching someone; chemical, like a strong acid causing chemical damage to the skin; or thermal, like spilling hot coffee on your lap. Now, these situations cause the damaged tissue, and in the case of inflammation, nearby immune cells to release molecules that can trigger pain like serotonin, histamine, prostaglandins, bradykinin, and substance P.

These will activate special pain receptor cells called nociceptors and cause them to fire off an action potential. Think of this as a message that tissue injury has occurred. Now, after the action potential has been generated, the second step begins, which is transmission of the action potential from the site of injury to the cortex of the brain. The nociceptors are first order neurons and they relay the action potential to the dorsal horn of the spinal cord where they synapse with a second order neuron. The second order neuron carries the message up to the brainstem and thalamus where they synapse with a third order neuron.  The third order neuron is responsible for carrying the message to the cortex for processing. Once the message reaches the cortex, specifically the somatosensory cortex, the next step called perception begins. This is where you consciously perceive pain and its characteristics like location, intensity, and what makes the pain better or worse.

Different regions of the somatosensory cortex correspond to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spinal_cord_injury_(SCI):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rlTTePy8QZygp6yGiEp3pdmUTB_lrcd1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spinal cord injury (SCI): Nursing]]></video:title><video:description><![CDATA[A spinal cord injury refers to any damage to the spinal cord, or the bundle of nerves protruding from the bottom of the spinal cord, called cauda equina. Now, let’s quickly review some anatomy and physiology. The spinal column consists of 33 vertebrae organized in 5 main regions: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 5 coccygeal. Together, the vertebrae create a bony canal that houses the spinal cord and surrounding meninges. The spinal cord is a bundle of nerve fibers that serves as a highway for information to travel between the brain and the rest of the body. This information is transmitted by highly specialized spinal tracts that carry motor information down the spinal cord to the body, and sensory information from the body up to the brain. The spinal cord travels through the spinal canal, and stops at the second lumbar vertebra.  Here it ends in a cone, called conus medullaris. Since the spinal cord is shorter than the spinal canal, the nerves of the lumbar, sacral and coccygeal regions have to travel down the spinal canal to reach their corresponding openings. In doing so, they form a nerve bundle below the spinal cord called the cauda equina. Now, spinal cord injuries can have a number of different causes. In younger clients, most spinal cord injuries are caused by a motor vehicle crash; penetrating trauma, like a gunshot or a stab wound in the back; or recreational injuries, like those caused by impact sports or diving in shallow waters. 

In older clients, though, spinal cord injuries are most often caused by severe falls, such as falling from a ladder; as well as medical conditions, including large tumors, infections, or degenerative diseases of the spine, like a protruding intervertebral disk or osteophytes. Risk factors for developing a spinal cord injury include engaging in high-risk behaviors, such as not wearing safety equipment when playing sports, speeding, and diving in shallow waters. Lastly, clients with a history of bone or ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Delirium:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fju0aZsnQjyNdTex0JCIBa1LQlq7CLnV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Delirium: Nursing]]></video:title><video:description><![CDATA[Delirium is a sudden, waxing and waning decline in various mental functions, including memory, thinking, language, behavior, mood, and personality. 

Let’s start by looking at the anatomy and physiology of the brain, which has three main parts, called the cerebrum, which consists of the two cerebral hemispheres, the cerebellum, which sits down at the base of the skull, and the brainstem, which is located right in front of the cerebellum. 

Zooming in, the cells that make up our brain are called neurons. Neurons are composed of a cell body, which contains all the cell’s organelles, and nerve fibers that extend out from the neuron cell body. These nerve fibers are either dendrites that receive signals from other neurons or axons that send signals along to other neurons.

Neurons communicate with each other through neurotransmitters, such as acetylcholine, dopamine, norepinephrine, and glutamate. 

Now, the brain is responsible for various mental functions, including memory, language, personality, visuospatial function, concentration, executive function, and praxis, which is the ability to carry out complex motor activities.

Okay, now, delirium usually occurs as a consequence of an underlying condition, which can include infections, medication toxicity, particularly with the use of sleep medications or aminoglycosides, and electrolyte imbalances. 

Other causes include severe stress, pain, sleep deprivation, dehydration, or malnutrition. Delirium can also occur after a recent hospitalization, surgery, or use of mechanical ventilation, as well as after trauma. 

Now, risk factors for developing delirium include advanced age; being assigned male at birth, and personal or family history of delirium. Clients with dementia or psychiatric disorders, such as depression and schizophrenia, are also more likely to develop delirium. Finally, delirium is more common in clients with underlying medical conditions, such as heart failure, cancer, and diabetes, as well ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dementia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GBUcup58SUGOaed1GcJiToR-RtKlj28M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dementia: Nursing]]></video:title><video:description><![CDATA[Dementia is a neurological condition, caused by structural changes in the brain, and characterized by a progressive decline in mental functions, including memory, thinking, language, behavior, mood, and personality. 

There are several types of dementia and Alzheimer disease is by far the most common type, followed by vascular dementia, frontotemporal dementia, and Lewy body dementia. 

Let’s start by looking at the anatomy and physiology of the brain, which has three main parts, called the cerebrum, which consists of the two cerebral hemispheres, the cerebellum, which sits down at the base of the skull, and the brainstem, which is located right in front of the cerebellum. Each of the cerebral hemispheres is made of the frontal lobe, parietal lobe, temporal lobe, and occipital lobe.

Zooming in, the cells that make up our brain are called neurons. They’re composed of a cell body, which contains all the cell’s organelles, and nerve fibers that extend out from the neuron cell body. These nerve fibers are either dendrites that receive signals from other neurons or axons that send signals along to other neurons. Neurons communicate with each other through neurotransmitters, such as glutamate, GABA, and dopamine. 

Now, the brain is responsible for various mental functions, including memory, language, personality, visuospatial function,  concentration, executive function, and praxis, which is the ability to carry out complex motor activities.

Okay, now, causes of dementia can be classified into reversible and irreversible ones. Reversible causes can be controlled and possibly cured with the right treatment. Some common examples of this include infectious conditions, like syphilis and HIV; dietary deficiencies, especially vitamin B12 deficiency; and hormone imbalances, such as thyroid problems. Irreversible causes cannot be cured and include Alzheimer disease, which is by far the most common cause of dementia; vascular dementia, which is the second mo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thermoregulation_-_Neonate:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y-VXwyXzRLu-khsgYTxNC50SRbmg8Drg/_.png</video:thumbnail_loc><video:title><![CDATA[Thermoregulation - Neonate: Nursing]]></video:title><video:description><![CDATA[Thermoregulation is the ability to balance between heat loss and heat production with the goal of maintaining a steady core temperature. Neonatal thermoregulation is different from that of children or adults for several reasons, including the neonatal predisposition to heat loss, and their unique means of generating heat on account of their brown adipose tissue, or BAT for short. Now, let’s look at the physiology of neonatal thermoregulation. There are some ways a neonate produces and conserves heat in order to keep their internal temperature within a normal range.  First, neonates conserve heat when exposed to cooling by assuming a flexed position, which helps to decrease the amount of surface area exposed to the external environment. Okay, heat can be lost in four ways: by radiation, conduction, evaporation and convection. Heat loss by radiation is the transfer of heat from the body to another object without touching it. So, if the baby’s bed is next to a cold window, the baby’s body heat can quickly be transferred from the baby toward the cold window. Heat loss by conduction is the transmission of heat from the body to another object by touching it. So if the baby is weighed on a cold scale, the baby will lose heat as it is transferred to the scale. Next is convection, where heat is carried away by cooler air.

This happens when the baby leaves the cozy warm uterus and enters a cooler, drafty outside world, and the baby’s body heat is transferred to the environment by air currents. Lastly, evaporation is the loss of heat by transferring liquid into gas, which can happen when moisture from the skin and lungs evaporates and turns to vapor. Immediately after birth, babies can lose a lot of heat through the evaporation of amniotic fluid. Now, when a neonate is exposed to excessive cooling, or cold stress, a cascade of events occur in an attempt to maintain a stable temperature. First, peripheral and central neurosensors send signals to the hypothalamus, whi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Biology_of_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Mq4Pb1P6SyaoeGWPGRWpjenETpW6Ybbu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Biology of cancer: Nursing]]></video:title><video:description><![CDATA[Cancer is a group of malignant conditions characterized by uncontrolled and unchecked cell division and growth. Now, cancer can involve any organ in the body, with the most common ones being breast cancer, prostate cancer, lung cancer, and colorectal cancer, in addition to melanoma, leukemia, and lymphoma. 

Now, let’s quickly review the physiology of cell division and growth, which takes place as a cell cycle in multiple phases: G1, S, G2, and M. During the G1 phase, the cell grows and prepares for DNA replication. In the S phase, the cell doubles its DNA content through DNA replication. This is followed by the G2 phase, during which the cell produces proteins and cellular components to be used in the next phase, called the M phase. Here, the cell divides through mitosis to produce two identical daughter cells. 

Now, there are two types of genes that control the cell cycle, called tumor suppressor genes and proto-oncogenes. Tumor suppressor genes suppress uncontrolled cell division by preventing cells from entering the S phase; whereas proto-oncogenes stimulate cell division by encoding proteins involved in regulating the cell cycle.

Now, the main cause of cancer is gene mutation, or changes to the DNA sequence. These changes can be inherited from a parent, called germline mutations, or acquired throughout the client’s life, called somatic mutations. In addition, there’re epigenetic mutations, where tumor suppressor genes can be methylated and thus silenced, while proto-oncogenes can be unmethylated to activate their expression. 

Mutations may arise due to a variety of risk factors. Non-modifiable risk factors include advanced age, in addition to personal or family history of cancer. On the other hand, modifiable risk factors include smoking, alcohol, obesity, excessive sun exposure, and certain occupations, as well as exposure to carcinogens, which are typically grouped into chemical, radiation, and viral carcinogens.

Chemical carcinogens include ben]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bone_tumors:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hXm0gujrQJCIkhqJdxOp02y2TzuTXATU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bone tumors: Nursing]]></video:title><video:description><![CDATA[Bone tumors are abnormal growths in the bone that can be broadly classified into benign and malignant. Benign bone tumors stay localized to the bone, and include osteochondroma, giant cell tumor of bone, osteoblastoma, osteoid osteoma, and enchondroma.

In contrast, malignant bone tumors can spread to surrounding tissues and organs. They are further classified as primary malignant tumors, which originate from bone cells, and include osteosarcoma, chondrosarcoma, and Ewing sarcoma; and secondary or metastatic tumors, which originate from other sites in the body, most commonly breast, lung, or prostate; and travel to the bones via lymphatic or blood vessels.

Okay, let’s start by looking at the physiology and anatomy of the bones. Normally, the bones’ surface is covered by a dense layer of connective tissue called the periosteum, and it&amp;#39;s where the muscles, tendons, and ligaments are attached. Beneath the periosteum, there’s a dense external layer called compact bone; and a softer internal layer called spongy or trabecular bone, which normally consists of trabeculae and pores resembling a honeycomb. 

Now, looking at a long bone, like the femur, it has two epiphyses, which are at the ends that contribute to joints with other bones and are mostly made up of trabecular bone. Between the two epiphyses, is the diaphysis or bone shaft, made up mostly of cortical bone, and a central hollow space, known as the medullary cavity. Bone marrow occupies both the medullary cavity and the spaces in the spongy bone of the epiphysis, which is the site of blood cell production. 

Now, in children and adolescents, there’s an additional narrow portion between the epiphysis and the diaphysis called the metaphysis, which is mostly made of trabecular bone. The metaphysis contains the growth plate, a cartilaginous tissue that actively grows during childhood. By adulthood, the growth plate has ossified and fused with the diaphysis and the epiphysis, becoming a mature bone.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brain_tumors:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u164x93eSRSu6wpbFj_Gl3ACR0y3PtJw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brain tumors: Nursing]]></video:title><video:description><![CDATA[Brain tumors are abnormal growths that can be broadly classified into primary tumors, which originate from cells within the nervous system, and secondary or metastatic tumors originating and spreading from cells outside the nervous system.

Okay, let’s start by looking at the physiology of the nervous system, which is divided into the central nervous system, that includes the brain and spinal cord, while the peripheral nervous system includes all the nerves that connect the central nervous system to the muscles and organs.

Zooming in, the brain is made up of different types of cells. 	First, there are neurons, which receive and send electrical impulses to one another. Then there are neuroglial cells, which help support and protect the brain, and can be classified into astrocytes, which are the most abundant, as well as ependymal cells, microglia, and oligodendrocytes.

Astrocytes have long processes with enlarged terminal ends that surround blood vessels of the brain as part of the blood-brain barrier. so that only certain molecules can slip through. Astrocytes also help provide nourishment to neurons, and recycle neurotransmitters. Next are ependymal cells, which line up the ventricles of the brain, and produce CSF. Then, microglia are the immune cells of the central nervous system. Lastly, there are oligodendrocytes, which have cellular processes that wrap themselves around axons to form a myelin sheath. In the peripheral nervous system, the myelin sheath is similarly formed by another type of cells, called Schwann cells. Additionally, there are cells that secrete hormones into circulation. These cells are found in the pituitary gland, located at the base of the brain. 

Some brain cells have a limited ability to be replaced, especially after injury, and they do it by having undifferentiated stem cells, called neural stem cells and glioblasts, which activate and mature into neurons or neuroglia, respectively.

Now, brain tumors occur when any of these c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastric_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fEtoWq__SUSWnomRp1ZOlq1bSCuwStAK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastric cancer: Nursing]]></video:title><video:description><![CDATA[Gastric cancer is a malignant tumor that originates in the stomach, and is one of the most common types of cancer. First, let’s recall the physiology of the stomach. The stomach is a hollow, J-shaped organ of the digestive system that stores food, mixes it with gastric juices and empties it into the small intestine. It is divided into four parts, called the cardia, the fundus, the body and the pylorus. Now, let’s zoom into the wall of the stomach, which is made up of four layers. The outermost layer is called serosa or adventitia, and it faces the abdominal or peritoneal cavity. 

This is the space between the abdominal wall and abdominal organs that is lined with peritoneal membrane and contains a small amount of serous fluid. Next layer is muscularis, which contracts to stir the food and move it further into the guts. After that is the submucosa, which consists of a dense layer of tissue that contains blood vessels, lymphatics, and nerves. And finally, there’s the innermost layer, called the mucosa, which consists of a simple columnar epithelium that forms many invaginations, called gastric pits, which connect to gastric glands. The gastric glands are composed of cells that produce gastric acid, which helps break down food and inactivate ingested bacteria; mucus, which protects the mucosa from the gastric acid; enzymes, which break down proteins; and intrinsic factor, which is a protein necessary for vitamin B12 absorption.

Now, the exact cause of gastric cancer is unknown, but there is usually a genetic mutation in a cell of the gastric mucosa. These include mutations in a tumor suppressor gene, which results in loss of inhibition of cell division, or a proto-oncogene, which stimulates cell division. And these mutations can be hereditary, meaning that the client inherits the mutation from one of their parents, or non-hereditary, also known as sporadic, which occur de novo or spontaneously. Whatever the cause is, the chance of developing gastric cancer ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Contraception_-_Barrier_methods:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V4iVfBSGStuRTU3t28Pd1m1CT-azxwLm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Contraception - Barrier methods: Nursing]]></video:title><video:description><![CDATA[Barrier methods of contraception are reversible methods that can be used to prevent pregnancy. They get their name because they act as a “barrier” that prevents the sperm from getting into contact with the egg. They can be further classified as chemical or mechanical barriers, both of which prevent the sperm from entering the cervix.

Alright, now let’s quickly review the physiology of fertilization, starting with the ovaries, which are the paired female gonads. Each month, they release one mature egg, also called oocyte, which is the female gamete. After leaving the ovaries, this egg enters the fallopian tube and reaches the widest part of it, called the ampulla of the fallopian tube, where it can be fertilized by a sperm.

Sperm, on the other hand, is produced continuously by the testicles, and during intercourse, the penis releases it into the vagina. In order to reach the oocyte, sperm must cross the vagina, as well as the external cervical os, or opening, the endocervical canal, the internal cervical os, and the uterine cavity, to finally reach the fallopian tube, where one of them can finally fertilize the oocyte, so that a zygote is formed. The zygote then starts dividing and travels to the uterine cavity, where it can implant and develop into a fetus. 

With this in mind, barrier contraceptives can act on several levels to prevent a sperm from meeting the oocyte. Let’s look at chemical barrier contraceptives first, namely spermicides. These are available as foams, foaming tablets, suppositories, vaginal films, creams, and gels. They contain chemical compounds like nonoxynol-9 or octoxynol that act like a surfactant, disrupting the sperm’s cell membrane, so the neck of the sperm detaches from the head, reducing mobility and causing cell death. So spermicides live up to their name by essentially killing sperm before they can enter the cervix. Overall, this method is about 80% effective as a contraceptive. 

The advantage of spermicides is that they’r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Contraception_-_Hormonal_methods:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rn32d_IcQPSYCMLTwUfzc9rrRs20Rlsh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Contraception - Hormonal methods: Nursing]]></video:title><video:description><![CDATA[Contraception or birth control refers to various methods that prevent pregnancy, and they can range from devices to medications and different procedures. Hormonal methods are some of the most popular means of contraception that can be used. They contain different concentrations of estrogen and progestin or sometimes progestin alone and are available as pills, injections, combined oral pills, vaginal rings, skin patches, as well as subcutaneous or intrauterine implants.

Now, to understand hormonal methods of contraception, let’s start by having a look at the ovaries, which are the gamete and hormone producing organs in individuals assigned female at birth. The ovaries contain ovarian follicles, which house the female gametes, called oocytes. Ovarian follicles also secrete the hormones estrogen and progesterone, which have a key role in the menstrual cycle and ovulation. Hormone production, as well as ovulation, which refers to the release of an oocyte each month, is under the control of the hypothalamus and the pituitary gland, way up in the brain.

See, the hypothalamus secretes gonadotropin releasing hormone, or GnRH, which tells the pituitary to secrete follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH. FSH stimulates the maturation of a dominant ovarian follicle each month during the follicular phase of the menstrual cycle, which goes from the first day of menstruation until day 14 of an average 28 day cycle. As the dominant follicle matures, it secretes more and more estrogen, which acts as a negative feedback signal, meaning it tells the pituitary to secrete less FSH, as well as LH, since there’s so much estrogen around. That is how it goes until day 14, which is when ovulation occurs.

Now, right before ovulation, estrogen levels increase past a critical point, and they become a positive feedback signal. This basically translates to the pituitary as enough estrogen has been produced for ovulation to occur. In turn, the pituitary s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Contraception_-_Natural_methods:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ThuyF-SiTrGJBtTGEqJY74pcSZKCdtq3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Contraception - Natural methods: Nursing]]></video:title><video:description><![CDATA[Natural methods of contraception, also referred to as fertility awareness or periodic abstinence methods, are contraception methods that use certain physiologic cues to predict ovulation, and determine the time when fertilization is most likely to occur. Knowing this can be used either to increase the likelihood of becoming pregnant or to avoid it. Natural methods of contraception include the calendar method, standard day’s method, basal body temperature method, the cervical mucus method, the sympto-thermal method, lactational amenorrhea, and finally, coitus interruptus. 

All right, now, let’s go over the physiology of the ovaries, which are the gamete and hormone producing organs in clients assigned female at birth. The ovaries contain ovarian follicles, which house the female gametes, called oocytes. Ovarian follicles also secrete the hormones estrogen and progesterone, which have a key role in the menstrual cycle and ovulation. Hormone production, as well as ovulation, which refers to the release of an oocyte each month, is under the control of the hypothalamus and the pituitary gland, way up at the base of the brain.

So, the hypothalamus secretes gonadotropin releasing hormone, or GnRH, which tells the pituitary to secrete follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH. FSH stimulates the maturation of a dominant ovarian follicle each month during the follicular phase of the menstrual cycle, which goes from the first day of menstruation until day 14 of an average 28 day cycle. As the dominant follicle matures, it secretes more and more estrogen, which acts as a negative feedback signal, meaning it tells the pituitary to secrete less FSH and LH. That is how it goes until day 14, which is when ovulation occurs. 

Now, right before ovulation, estrogen levels increase past a critical point, and they become a positive feedback signal. This basically tells the pituitary that enough estrogen has been produced for ovulation to occur. In]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anthrax:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vqWkdofTSjeZEgUyeJZssgefT3OltmpB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anthrax: Nursing]]></video:title><video:description><![CDATA[Anthrax is a zoonotic disease caused by Bacillus anthracis, which is a Gram positive, rod-shaped bacterium, which primarily enters the body through the skin, lungs, gastrointestinal tract, and through direct injection. Infection with Bacillus anthracis is associated with high mortality.

Now, first, let’s cover some basic physiology of the skin. The most superficial layer of the skin is the epidermis, which is in close contact with the outside world and primarily serves as a protection from foreign pathogens. Next up is the dermis, which is made up of connective tissue that contains blood vessels, lymphatics, nerve endings, as well as immune cells, like macrophages and dendritic cells. These cells represent innate immunity and they are first on the scene when a pathogen breaches the skin and enters the body. Finally, the deepest layer of the skin is called hypodermis and is primarily made up of adipose tissue.

Now, let’s switch our focus to the anatomy of the respiratory tract. When we breathe in, the air flows through the nasal and oral cavity into the pharynx and larynx, down into the trachea or windpipe. Next, the trachea splits into two main stem bronchi that enter the lungs and branch into smaller bronchi, which further give rise to smaller conducting and respiratory bronchioles, and finally alveolar ducts. Alveolar ducts open up into alveolar sacs, which are small grape-like groups of alveoli where the gas exchange takes place. Within the alveoli, there are immune cells called alveolar macrophages, which help clean the alveolar space from foreign substances but also fight pathogens that make it to the lungs. 

Finally, let’s cover the basic histology of the gastrointestinal tract, starting with the outermost layer, which is called the adventitia or serosa. Next up are the muscularis externa and the submucosa; and finally, the innermost layer is called the mucosa. Moreover, the mucosa secretes mucus, digestive enzymes, and absorbs nutrients from]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chest_tube_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o04Doq1QSPqmdWpkLowGafWkTsy0yzU6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chest tube care: Nursing]]></video:title><video:description><![CDATA[A chest tube can be used to remove air, fluids, or blood from the pleural space; to prevent air or fluid from reentering the pleural space; and to reestablish intrapleural and intrapulmonary pressures after surgery or trauma, in order to re-expand the lungs. A chest tube can also be inserted into the mediastinum after open heart surgery to drain fluid from the pericardial sac. Now, let’s quickly review the physiology of the pleura, which is a two-layered serous membrane that covers the lungs. The first layer of the pleura adheres to the surface of the lungs, called visceral pleura, whereas the second layer lines the chest wall, and it’s called the parietal pleura. Between these two layers there’s the pleural space, which is typically filled with a small amount of serous fluid that prevents friction between the two layers while breathing. 

Moreover, let’s look at the physiology of breathing, which consists of two stages: inspiration and expiration. Inspiration is an active process, meaning that it requires muscles such as the diaphragm and the intercostal muscles to contract, which increases the intrathoracic volume and lowers the intrapulmonary pressure below the atmospheric pressure. This pressure gradient makes air flow from a high pressure area, meaning the atmospheric air, to a lower pressure area; so air is pulled inside the lungs. On the other hand, expiration is a passive process, meaning that it doesn’t require muscle contraction. That’s because the lungs have a special feature called elastic recoil, meaning they have a tendency to return to their normal size after being expanded. This allows the lungs to deflate after inspiration, decreasing the intrathoracic volume and increasing the intrathoracic pressure. 

This process passively pushes the air from the area of higher pressure, which is the lungs, to the area of lower pressure, which is the atmosphere.Now, one end of the chest tube is typically inserted through the rib cage into the pleural sp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tracheostomy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A6hzeCM8QTWmYvE1KR5VU6oPSG6WrUK7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tracheostomy: Nursing]]></video:title><video:description><![CDATA[A tracheostomy is a type of artificial airway consisting of a small, plastic tube that’s inserted through a surgically created opening, or stoma, in the anterior neck, known as a tracheotomy.  

Typically, a tracheostomy is placed when a patient can’t keep their own airway open. It can be placed urgently when intubation by other means isn’t possible, or as a planned procedure, if the patient requires long-term airway assistance. 

Now, patients with a tracheostomy typically have a short tube that protrudes from the anterior of their neck, which is usually stabilized with a flange and ties that encircle the neck.  

Many tracheostomy tubes have an outer cannula, which keeps the airway patent, and an inner cannula, which can be disposable or non-disposable and is removed for cleaning.  

The tube may or may not be connected to a mechanical ventilator or another source of oxygen; and depending on the type of tracheostomy tube your patient has, they may or may not be able to talk. 

Okay, so tracheostomy tubes come in various sizes and configurations. First, tubes can be cuffed, meaning there is a balloon that can be inflated to provide a leak-proof connection; or uncuffed, where there is no balloon.  

Cuffed tubes are typically used short-term because they occlude the upper trachea and pharynx, and the pressure exerted can compress tracheal capillaries, limit blood flow, and predispose the patient to tracheal necrosis.  

On the other hand, uncuffed tubes are used for patients with long-term tracheostomies to decrease the risk to surrounding tissues. 

It’s also important to note that tracheostomy tubes can be fenestrated or non-fenestrated. A fenestrated tube has a hole on its dorsal surface, which helps promote spontaneous breathing.When patients have a fenestrated, cuffed tracheostomy tube, the cuff can be deflated and inner cannula removed,  

This allows air to pass from their lungs through the opening in the tube,  enabling them to breathe spontaneousl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchopulmonary_dysplasia_(BPD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O6Qo35fXT3GAHW5LFBnC-yDtTsCAtniY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchopulmonary dysplasia (BPD): Nursing]]></video:title><video:description><![CDATA[Bronchopulmonary dysplasia, or BPD, also known as neonatal chronic lung disease, is an iatrogenic respiratory disease most commonly affecting preterm newborns that results from lung injury and disrupted lung development.

Now, let’s quickly review the respiratory tract, which can be divided into two regions: the upper respiratory tract and lower respiratory tract. The upper respiratory tract includes the nose, nasal cavity, the oral cavity, pharynx, epiglottis, larynx, and the upper part of the trachea; while the lower respiratory tract includes the lower part of the trachea, and the lungs containing the bronchi. These are lined by pseudostratified ciliated columnar epithelium. This contains goblet cells, which produce mucus to trap small foreign particles; as well as columnar cells, which have cilia, or tiny little hair-like projections that move mucus and foreign particles up the respiratory tract. The bronchi gradually branch into bronchioles, which give rise to the alveolar ducts, and finally the alveoli. Alveoli are tiny air-filled sacs that are surrounded by tiny blood vessels, called capillaries. 

If we zoom in even more, we can see a tiny space between the alveolar wall and the capillary wall, called the interstitial space. And that’s where most gas exchange occurs, so as we breathe, the inhaled oxygen moves through the alveolar membrane, the interstitial space, and the capillary membrane to reach the blood, while the carbon dioxide moves from the capillaries through the interstitial space and into the alveolar sacs to be exhaled.  Now, the alveoli are lined by alveolar epithelial cells, called pneumocytes. The vast majority are type I pneumocytes, which allow oxygen and carbon dioxide to pass through them. There are also type II pneumocytes scattered around which produce surfactant, an oily secretion that coats the alveoli and prevents their collapse. 

Alright, now the cause of BPD is multifactorial, and is often due to positive pressure ventila]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preoperative_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/280hGHOSTgOqpB5NP6H67jeDTI6IO8Oe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preoperative care: Nursing]]></video:title><video:description><![CDATA[Preoperative care is the preparation and management of a client during the preoperative period, which is the time period between the decision to perform a surgery and the beginning of the surgical procedure. All right, so the first step of preoperative care starts with the surgeon, with a registered nurse as witness, obtaining informed consent from the client. Then comes the client’s history, asking about current medications, especially the high risk ones like anticoagulants; as well as alcohol intake; cigarette smoking; illicit drug use; in addition to a personal or family history of complications from anesthesia;also allergies; or chronic illnesses, such as hypertension, diabetes, and anemia. 

Clients should also be assessed for risk factors of obstructive sleep apnea since this condition can interfere with breathing when the client is under general anesthesia. The risk factors are summarized with the STOP-BANG mnemonic that stands for snoring history, tiredness during the day, observed breathing cessation during sleep, high blood pressure, in addition to a body mass index of higher than 35 kg/m2, age over 50 years, as well as neck circumference larger than 40 centimeters, and gender assigned male at birth. This is typically followed by diagnostic studies as needed like electrocardiogram or ECG; as well as imaging studies. In addition, clients should obtain the indicated laboratory tests, such as a complete blood count or CBC, coagulation profile, blood typing, and pregnancy test as needed. Lastly, the preoperative care is wrapped up with the client&amp;#39;s education, in order to prepare them for the surgical procedure and let them know what to expect after the procedure.

Okay, let’s look at the nursing care you’ll provide to a client during the preoperative period. Your priority goals of care include preparing the client for surgery, establishing a baseline assessment, and providing psychosocial support. Begin preparing your client for surgery by r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Cardiac:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x-TuDTITSXGLgUpAMrsn9AwNS42L_Eae/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Cardiac: Nursing]]></video:title><video:description><![CDATA[Geriatrics is the branch of medicine that deals with the physiology and psychology of aging, as well as the diagnosis and treatment of diseases affecting older clients. Now, aging affects various organ systems, one of which is the cardiovascular system. All right, now let&amp;#39;s  start by reviewing the physiology of the cardiovascular system, which consists of the heart and the blood vessels. The heart is a muscular pump that sits in the middle of the chest cavity, between the two lungs, and on top of the diaphragm. Now, let’s take a closer look at the inside of the heart, which consists of four chambers and four valves. Deoxygenated blood coming from the superior vena cava and inferior vena cava enters the right atrium, and then passes through the tricuspid valve into the right ventricle. The right ventricle pumps the blood out the pulmonary valve and into the pulmonary arteries which carry the blood to the lungs. Here, the blood gets oxygenated and is then sent back to the left atrium, which moves the blood through the mitral valve and into the left ventricle. 

Finally, blood in the left ventricle gets pumped out through the aortic valve out to the aorta, which branches into smaller arteries to supply tissues around the body. Okay, so, blood moves around the heart as it alternates between systole, a period of contraction and emptying of the heart chambers, and diastole, a period of relaxation and filling. The heart’s contractions also create pressure in the arteries, so systolic blood pressure is the pressure in the arteries when the heart is contracting and squeezing out blood, and diastolic blood pressure is when the heart is filling up with more blood. Now, the heart&amp;#39;s contractions are regulated by its conductive system, which consists of a group of specialized cells that are capable of transmitting electrical signals. The main component of this system is the sinoatrial or SA node, also known as the pacemaker of the heart. This node init]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Gastrointestinal:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j69O1AaGT4KbtVJgkdz0MYlkQ_6pthXP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Gastrointestinal: Nursing]]></video:title><video:description><![CDATA[Geriatrics is the branch of medicine that deals with the physiology and psychology of aging, as well as the diagnosis and treatment of diseases affecting older clients. Now, aging affects various organ systems, one of which is the gastrointestinal system. All right, let’s start by reviewing the physiology of the gastrointestinal system, which is primarily responsible for mechanical and chemical digestion of food; absorption of nutrients; and finally, excretion of waste as feces. From top to bottom, the gastrointestinal tract starts with the oral cavity, then the esophagus, the stomach, the small intestine, the large intestine, and ends with the anus. First, let’s start with the oral cavity, which plays an important role in breaking down food. As a person ages taste buds atrophy and decrease in number, resulting in decreased ability to taste salty, sweet, bitter, sour and umami. This can decrease enjoyment of food, so poor eating habits and nutritional deficiencies could develop. 

Many elderly clients also have periodontal disease, which refers to disease that affects the gum, or gingivae, and the underlying bones that support the teeth. The mildest form of periodontal disease is gingivitis, where just the gums are inflamed. If left untreated, gingivitis can progress to the more severe disease called periodontitis, where both gum and bones are affected and can eventually result in tooth loss.  Additionally, with aging, the production of saliva by salivary glands decreases, which can lead to xerostomia or dry mouth, and this can also contribute to gingivitis and tooth decay. Elderly clients without teeth, or clients who have poorly fitting dentures, often find it hard to chew food. These clients tend to avoid certain hard to chew foods, which can eventually result in poor nutrition. Now, moving on to the esophagus, which is a part of the gastrointestinal system that propels the food from the pharynx down into the stomach. The esophagus and the stomach are s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Integumentary:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jO-2WKlgRNuEo-llbwzt0zi4Sj_i9X90/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Integumentary: Nursing]]></video:title><video:description><![CDATA[Geriatrics is the branch of medicine that deals with the physiology and psychology of aging, as well as the diagnosis and treatment of diseases affecting older clients. Now, aging affects various organ systems, one of which is the skin, also known as the integumentary system. 

Alright, now let&amp;#39;s start by reviewing the physiology of the integumentary system, which is the outer barrier that protects the body from excessive water loss, as well as any external threat like trauma or pathogens. The skin is divided into three main layers, the hypodermis, dermis, and epidermis. The hypodermis, also known as the subcutaneous layer of the skin, is made of fat and connective tissue that anchors the skin to the underlying muscle, and acts as a cushion that protects underlying tissues from trauma. Above the hypodermis is the dermis, containing collagen and elastin fibers, nerve endings, sweat and sebaceous glands, as well as blood and lymphatic vessels. Just above the dermis is the epidermis, which has multiple cell layers that are composed of developing cells called keratinocytes, which are flat pancake-shaped cells that are named for the keratin protein that they’re filled with. 

Keratinocytes start their life at the basal layer, also called the stratum basale, which is made of a single layer of stem cells that continually divide and produce new keratinocytes. This layer also contains the melanocytes, which produce a pigment called melanin, that gives each individual their skin color, and acts as a natural sunscreen. Now, as keratinocytes mature, they migrate into the next layers of the epidermis, called the stratum spinosum, and then into the stratum granulosum. Keratinocytes in this layer begin the process of keratinization, which is the process where the keratinocytes flatten out and die, and in the process they begin to create the epidermal skin barrier. 

Keratinization leads to development of the stratum lucidum layer which is made up of translucent,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Medications:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o7RBgDrfS2C8J97_GuOvWMoJQKWEdkcJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Medications: Nursing]]></video:title><video:description><![CDATA[Medication considerations in the geriatric population refers to the fact that, as we age, the body undergoes changes. As a result, medications must be used with caution, taking into account both age-related and client-specific changes.

Alright, now when a medication is administered to the body, the body reacts to that drug in various manners, and the study of these reactions is called pharmacokinetics. Pharmacokinetics includes four main elements: absorption, distribution, metabolism, and elimination. Absorption describes how a medication moves from the site of administration to the blood, whereas distribution is the movement of the medication from the blood to body tissues. Conversely, metabolism deals with the biotransformation of medications, which happens mainly in the liver. On the other hand, elimination studies how the body gets rid of the medication or its metabolites, which typically happens in the kidneys. Now, pharmacodynamics involves how a medication affects the body, including the timing of the medication’s onset, peak effect, and duration, as well as interactions with certain receptors. 

Now, aging affects each of these elements differently. For example, the rate of absorption in older clients is slower, due to decreased blood flow to the stomach, slower gastric emptying, and decreased acid production, as well as a decrease in the surface area of the small bowel. This means that medications need more time to reach their peak effect. The bioavailability though, which is the percentage of medication that reaches the blood, doesn’t differ with age. As for distribution, with age, body water, serum albumin, along with lean body mass, tend to decrease, in contrast with fat storage which generally goes up. This causes water-soluble medications to have lower volume of distribution, and fat-soluble medications to have higher volume of distribution, in addition to high proportion of free or active metabolites of the medication. When it comes to meta]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Respiratory:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aCq5YvQXShqBaYCp-ZsgKOq3TfuoOVdL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Respiratory: Nursing]]></video:title><video:description><![CDATA[Geriatrics is the branch of medicine that deals with the physiology and psychology of aging, as well as the diagnosis and treatment of diseases affecting older clients. Now, aging affects various organ systems, one of which is the respiratory system. All right, now let&amp;#39;s start by reviewing the physiology of the respiratory tract, which can be divided into the upper respiratory tract and lower respiratory tract. The upper respiratory tract includes the nose, nasal cavity, the oral cavity, pharynx, epiglottis, larynx, and the upper part of the trachea; while the lower respiratory tract includes the lower part of the trachea, and the lungs, which contain the bronchi, bronchioles, alveolar ducts, and finally the alveoli. 

Most of the respiratory tract is lined with a pseudostratified ciliated columnar epithelium, which contains goblet cells that produce mucus to trap small foreign particles; as well as columnar cells, which have cilia, or tiny little hair-like projections, that move mucus up the respiratory tract so it can trigger the cough reflex, and get coughed out. The cough reflex is also controlled by the central and peripheral nervous systems. Now, let’s follow air as it passes through the respiratory tract. First, it enters the nose, which humidifies and warms that air, before sending it to the pharynx. From the pharynx, air passes through the epiglottis, and enters the larynx. Next is the trachea, which ends at the carina by bifurcating into the right and left main bronchi, which get inside the lungs, where they gradually branch into smaller bronchi, and bronchioles. These bronchioles have smooth muscles in their walls that allow them to constrict or dilate in response to certain stimuli. 

Bronchioles carry the air into alveolar ducts, and finally the alveoli, which are tiny sacs responsible for gas exchange between the air and the blood. Alveoli also have elastic recoil, which gives them the ability to stretch and rebound with each breath.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Sensory:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7ZsZE77LQnKxDqe0xzZ3vzSLT5qBKMAh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Sensory: Nursing]]></video:title><video:description><![CDATA[Geriatrics is the branch of healthcare dealing with both the physiology and psychology of aging, as well as the diagnosis and treatment of diseases affecting older adults. As we age, the body undergoes various changes, such as a decline in the function of the sensory system, which gathers information about our surroundings and what’s happening inside our bodies. The sensory system includes touch, vision, hearing, taste, and smell. Age-related changes in the sensory system can impact many aspects of a client’s quality of life, and thus must be taken into consideration when caring for elderly clients. 

First, let’s start with touch. Tactile receptors are nerve endings that pick up sensory information when something comes in contact with your skin, like when you’re holding a pen. This sensation is then sent through sensory neurons to the spinal cord and eventually to the brain. Now, some parts of your body, like the tips of the fingers, are more sensitive to touch because they have more tactile receptors than other areas, like your back. 

Now, with aging, the blood flow to nerve endings, the spinal cord, and even some parts of the brain can decrease, which causes a decreased sensation of touch. Additionally, chronic conditions, like diabetes mellitus, can affect small blood vessels that supply nerve endings and further affect sensation, particularly in distal parts of the body, like the feet. The loss of sensation makes it hard for older clients to feel pressure in specific areas of the body, which can result in complications, such as frostbites, burns, or even pressure ulcers. 

Next up is vision. If we zoom into the wall of the eye, there&amp;#39;s an outer fibrous layer made out of the cornea and sclera, which helps control and focus the entry of light. The light that passes through the cornea is directed to the lens, which in turn collects light arrays and focuses them into the retina at the back of the eye. Behind the lens is a gel-like structure call]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Urinary:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h7spJllPRhS3QMvCdDyzJZLHRlmaZIFg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Urinary: Nursing]]></video:title><video:description><![CDATA[Geriatrics is the branch of medicine that deals with the physiology and psychology of aging, as well as the diagnosis and treatment of diseases affecting older clients. Now, aging affects various organ systems, one of which is the urinary system. All right, let&amp;#39;s start by reviewing the physiology of the urinary system, which can be divided into the upper and lower urinary tracts. The upper urinary tract is made of the kidneys and the ureters, whereas the lower urinary tract includes the urinary bladder and the urethra. Each bean-shaped kidney sits just below and on each side of the diaphragm. They are about 12.5 centimeters long and weigh from 113 to 170 grams. They receive oxygenated blood through renal arteries, which arise from both sides of the abdominal aorta. 

Now, let’s take a closer look at the inside of the kidney, which consists of an outer cortex and an inner medulla, both of which house the functional units of the kidneys, called nephrons. These tiny nephrons consist of a tuft of capillaries, called the glomerulus, surrounded by a double-membrane called the Bowman capsule. From the nephron, there extends a group of tubules, called the proximal convoluted tubule, loop of Henle, and distal convoluted tubule, which eventually drain urine into collecting tubules and ducts. From there urine drains into the ureters, which have smooth muscles in their walls that contract to push the urine towards the bladder. Urine then passes from the bladder to the urethra, where it exits the body.

Now, the kidneys also regulate the volume and composition of body fluids by controlling water, electrolytes, and the excretion of waste products and medications. The amount of blood that gets filtered through the kidneys each minute is called glomerular filtration rate, or GFR. Additionally, the kidneys help control blood pressure, regulate acid-base balance, activate vitamin D, and produce erythropoietin, which is a hormone that stimulates red blood cell produ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_&amp;_development_-_Adolescent:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MCFtVicuSl6LuamhcA-IYkEQSZik7vxH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development - Adolescent: Nursing]]></video:title><video:description><![CDATA[Adolescence, also known as the teenage years, starts at the beginning of puberty and lasts approximately until 18 to 20 years of age. This period represents the transition from childhood to adulthood and, as such, it brings many important physical, mental and psychosocial changes. Developmental psychologists involved in studying development during the adolescent period include Jean Piaget, Erik Erikson, and Lawrence Kohlberg.

Alright, there are a couple terms that we need to review first, including growth and development. Growth refers to physical changes in height, weight, and the appearance of the body; whereas development refers to the acquisition of complex motor, cognitive, and social skills.

Alright, now the physical changes that occur during adolescence are related to the beginning of puberty, which is a period of rapid growth and sexual development. Puberty typically starts somewhere between 8 and 14 years of age, and tends to start earlier in those assigned female at birth than in those assigned male at birth. Puberty-related changes are driven by the increase in sex hormone level, which are mostly estrogen, progesterone and testosterone.

For those assigned female at birth, breast development is usually the first noticeable sign of puberty, and it is followed by the first menstrual cycle, or menarche, which typically occurs around 2 and a half years from the onset of puberty. Widening of the hips also occurs. 

In those assigned male at birth, puberty begins with an increase in testicular size, then the penis and pubic hair grow, the voice begins to deepen, and around 2 years later, sperm production begins. 

Other pubertal changes include the growth of pubic and underarm hair in both sexes, These hormone-driven changes are accompanied by growth spurts that transform children into physically mature teens as their bodies increase in height and weight.

Alright, now let’s switch gears and look at the motor, cognitive, psychosocial, and moral deve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_&amp;_development_-_Infant:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ikMQU7_RQ-iCKDuvVAjUsRoQRPSU7EhQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development - Infant: Nursing]]></video:title><video:description><![CDATA[Infancy is the period of life between birth and the age of 12 months. In this short period of time, infants undergo a series of rapid and dramatic changes involving both their physical growth and the development of motor, cognitive, and social skills that will set the basis for future development.  Now, developmental psychologists who were involved in studying infant development include Jean Piaget and Erik Erikson. 

Alright, now it’s important to note that growth and development are two different concepts. Growth refers to physical changes in height, weight, and the appearance of the body; whereas development refers to the acquisition of complex motor, cognitive, and social skills, such as walking, speaking, turning a page in a book, or smiling at familiar faces.  

Alright, now, let’s start by looking at the first month after birth, during which the infant is called a newborn. Newborns have a distinctive appearance, with a very large head and relatively short arms and legs in relationship to their body. Many newborns still have lanugo, or very thin, soft hair, on some areas of their body, but this usually disappears within a few weeks after birth. Head hair can vary from almost no hair to a full head of hair. Generally, the stub of the umbilical cord remains for a few weeks until it eventually dries up and falls off, giving rise to the navel or umbilicus. 

Now, in order to assess an infant&amp;#39;s growth, we can look at four parameters: length, weight, head circumference, and the time of closure of the skull’s fontanelles. Starting with length, most infants measure between 45.7 and 60 cm at the time of birth. From there, length is expected to increase by 2.5 cm every month during the first six months, and then slow down until an infant has doubled their height at birth, which is usually around 12 months of age.  

In terms of weight, the average birth weight is around 3.5 kg, but this can also vary between 2.5 kg and 4.5 kg for term infants. In the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_&amp;_development_-_Preschool-age:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q6-WEALCRhKq3sduWYPwyd-mSCqT-CcD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development - Preschool-age: Nursing]]></video:title><video:description><![CDATA[The preschool-age period lasts between 3 and 6 years of age, and is characterized by slow physical growth, but remarkable cognitive, language and psychosocial development compared to earlier stages.  Preschool-age children are naturally inquisitive and start to explore and interact with the world around them. This ensures that they continue to learn all the skills that will lead to later success in the school age. Now, developmental psychologists involved in studying development during the preschool period include Jean Piaget, Erik Erikson, and Lawrence Kohlberg. Now let’s quickly take a look at two important terms here, which are growth and development. Growth refers to physical changes in height, weight, and the appearance of the body; whereas development refers to the acquisition of complex motor, cognitive, psychosocial, and moral skills, such as walking, speaking, turning a page in a book, understanding the concept of time, or smiling at familiar faces.

All right, when it comes to growth, preschool-age children gain an average of 6.5 to 7.5 cm each year, with an expected increase of 2.25 kg per year in weight. So, an average 5-year-old is about 110 cm tall and weighs about 18 kg. However, it’s important to note that children of the same age are frequently at different points in their growth during childhood. Other growth features include a slight increase in the length of the skull, with the lower jaw becoming more pronounced. The upper jaw also widens to make space for the emergence of permanent teeth,  which usually start to appear at around 6 years of age. All right, let’s now take a quick look at the motor, cognitive, psychosocial, and moral development of preschoolers. Starting with motor development, this is a period where children improve their motor skills, and they become able to do certain things, like hold a good posture and tie their shoelaces.  During preschool-age years, coordination, balance, and rhythm improve as well, allowing childr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_&amp;_development_-_School-age:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cH1sFDIDQIKN2ulqOQ_yKkS9Rzi5UkfC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development - School-age: Nursing]]></video:title><video:description><![CDATA[The school-age period begins when children start elementary school, at 6 years old, and lasts until they have finished primary education at around 12 years of age. This stage is characterized by slow physical growth and accelerated social development, compared to earlier stages. As they become more independent, school-age children start to participate in various sports and social activities, and are now able to socialize with people other than family members, such as teachers, peers, and coaches. 

Now, developmental psychologists involved in studying development during the preschool period include Jean Piaget, Erik Erikson, and Lawrence Kohlberg.

Now let’s quickly take a look at two important terms here, which are growth and development. Growth refers to physical changes in height, weight, and the appearance of the body; whereas development refers to the acquisition of complex motor, cognitive, and social skills, such as walking, speaking, turning a page in a book, or smiling at familiar faces.

Alright, when it comes to growth, school-age children tend to get taller at a slower pace, growing about 6 to 7 centimeters each year, with an expected increase of 3 to 3.5 kg per year in weight. It’s important to note that children of the same age are frequently at different points in their growth during childhood. This is also a time where kids start to have feelings about how they look and how they’re growing, so it’s not uncommon that they become more interested in stepping on the scale or standing by a tape measure. 

Alright, now let’s switch gears and look at the motor, cognitive, psychosocial, moral, and spiritual development of a school-age child. Starting with motor development, this is a period where children refine fine motor skills, hand-eye coordination, and they become more skilled at things like writing, drawing, and playing a musical instrument. During school-age years, coordination, balance, and rhythm improve as well, allowing children to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_&amp;_development_-_Toddler:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7CS8UjyNSNam4S0iLziUrmwITQ2i-ihh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development - Toddler: Nursing]]></video:title><video:description><![CDATA[The toddler period spans years 1 to 3. During this time, toddlers become more independent, active, and curious; they begin to show defiant behavior; and start imitating the behavior of others, especially adults and older children. Although this period is a time of significant advancement in growth and development for the child, it can also be quite a challenging time for parents! 

Now, developmental psychologists who were involved in studying toddler development include Jean Piaget, Erik Erikson, and Lawrence Kohlberg.

It’s important to note that growth and development are two different concepts. Growth refers to physical changes in height, weight, and the appearance of the body; whereas development refers to the acquisition of complex motor, cognitive, and social skills, such as walking, speaking, turning a page in a book, or smiling at familiar faces.  

Alright, now compared to infancy, both physical growth and acquisition of new motor skills slows down, with the most dramatic changes occurring in bodily proportions. Infants have a relatively large head and short legs and arms. 

During toddlerhood, head growth slows down from 2 cm in the second year alone to 2 to 3 cm over the next ten years. At the same time, height and weight continue to increase steadily, though the increase occurs at a slower rate compared to infancy. In fact, toddler’s gains in height and weight tend to occur in spurts rather than in a linear fashion. On average, toddler weight gain is around 1.3 to 2.3 kg per year; and height increases by an average of 7.5 cm per year. 

Alright, let’s switch gears and look at toddler development. Typically, this is discussed in terms of developmental milestones that toddlers achieve at certain ages. By looking at these milestones, we can see how the toddler is developing and keep an eye out for any potential problems. There are several types of milestones that should be assessed: motor, cognitive, social, psychosocial, and moral and spiritual;]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bladder_exstrophy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tJ644bgOQyOAmcBSsZfZJIlaSZWE6QiU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bladder exstrophy: Nursing]]></video:title><video:description><![CDATA[Bladder exstrophy is a congenital malformation where the bladder protrudes outside of the abdomen due to an abdominal wall defect.

First, let’s quickly review  the embryological development of the bladder. The renal system, including the bladder, starts developing during week 4 of intrauterine life. At that point, the embryo is made up of three primitive germ layers: the ectoderm, the mesoderm and the endoderm. Towards the end of week 4 of development, the endoderm in the hindgut, which is the last portion of the primitive digestive tract, begins to expand forming the cloaca. The cloaca is a temporary structure connecting the urinary, digestive, and reproductive ducts. 

By week 7, a wall of tissue called the urorectal septum forms in the cloaca and splits it into a posterior anorectal canal for the digestive tract, and an anterior urogenital sinus for genital and urinary structures. And the top portion of the urogenital sinus stretches out to form the primitive bladder. Ultimately, the cloacal membrane opens to the outside of the body for these structures to have openings. Now, at around the same time in development, the muscles and connective tissue of the lower anterior abdominal wall also begin to form.

Alright now, bladder exstrophy occurs when there is a midline closure defect during fetal development. Although the exact cause remains unknown, several risk factors have been identified. These include having a family history of bladder exstrophy, being white, or being assigned male sex at birth. This condition is also more common in infants born through assisted reproductive technology, such as in vitro fertilization, or IVF.

Now, when it comes to pathology, the most widely accepted theory for how bladder exstrophy occurs is that the cloacal membrane grows too much, and pushes towards the front of the embryo like a wedge. This prevents the normal midline closure of the abdominal wall. Subsequently, the cloacal membrane ruptures, which renders lower ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemolytic_uremic_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MInDzcMVRhi2eC7OtMXi-KbNSb_ZO2vM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemolytic uremic syndrome: Nursing]]></video:title><video:description><![CDATA[Hemolytic uremic syndrome, or HUS for short, is a condition characterized by the triad of microangiopathic hemolytic anemia, or breakdown of red blood cells inside small blood vessels, thrombocytopenia, or low platelets, and acute kidney injury.

Alright, now first, let’s quickly review the physiology behind hemostasis or clotting. Hemostasis starts as a response to an injury of the endothelium, which is the inner lining of blood vessels, and it can be divided into primary and secondary hemostasis. In primary hemostasis, platelets form a “plug” at the site of the damaged blood vessel to stop the bleeding. In secondary hemostasis, proteins called coagulation factors start to activate each other eventually leading to formation of a fibrin mesh around the platelet plug to stabilize it.  

Now, the causes of HUS vary, so it can be classified as typical or atypical. Typical HUS is caused by bacterial toxins, including Shiga-like toxin which is produced by some strains of Escherichia coli, most commonly enterohemorrhagic E. coli or EHEC, serotype O157:H7, and Shiga toxin which is secreted by Shigella dysenteriae. These bacteria typically affect children, who become infected through contaminated food or drink, like contaminated beef, raw leafy vegetables, or unpasteurized milk from an infected cow; or by swimming in pools or lakes contaminated with feces. Rarely, typical HUS may also be caused by other bacteria, such as Streptococcus pneumoniae.

On the other hand, atypical HUS is typically non-infectious. It is caused by dysregulation of the complement system, which is part of the immune system, and can be genetic or acquired.  The main risk factors for atypical HUS are being above 65 years of age, or having a weakened immune system. 

Okay, now, pathology-wise, typical HUS begins when the bacteria enters the body and attaches itself to the intestinal wall and starts secreting toxins. These toxins get absorbed by the intestinal blood vessels and enter the bloods]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fever:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0cMaJu6mTGmDeyozhPTJ98mVTsCUTzw_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fever: Nursing]]></video:title><video:description><![CDATA[A fever is an abnormal increase in body temperature, and it’s part of a biologic response controlled by the central nervous system through thermoregulation. 

Normally, the average body temperature should be between 36.4 and 37.5°C, or 97.5 and 99.5°F, and it can vary due to numerous factors, including the time of day, activity, age, and the phase of the menstrual cycle. 

Now, let’s review the physiology of thermoregulation. The internal body temperature is maintained by the hypothalamus, which is a small part of the forebrain located just below the thalamus. 

So, when there is an increase in body temperature, the hypothalamus initiates heat dissipation mechanisms to reduce it, such as vasodilation of blood vessels near the skin, and increased sweat production by sweat glands. 

Meanwhile, heat production can occur as a result of metabolic processes that generate heat as a byproduct, even while at rest or during voluntary movement. Also, when the body needs to warm up, the hypothalamus initiates the cold stress response which includes involuntary shivering. 

Another contributing factor can be an increased release of the thyroid hormone, called thyroxine, which increases metabolism and in turn body temperature. In addition, neonates rely on nonshivering thermogenesis, which utilizes brown adipose tissue, a special type of fat that usually disappears after infancy.

Lastly, sympathetic stimulation helps avoid heat dissipation by triggering vasoconstriction of blood vessels on the skin, as well as piloerection, meaning erection of hairs due to contraction of the arrector pili muscles, creating an insulating layer. 

Most commonly, a fever is caused by an underlying infection. Fever can also occur because of inflammation in absence of an infection. This can also happen with hypersensitivity reactions in response to a medication like penicillin; malignant conditions like lymphoma; and chronic inflammatory conditions like inflammatory bowel disease, Kawasaki ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rocky_Mountain_spotted_fever_(RMSF):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mIDmBZOJTDS_N7pLLIhkUGaPTryQbLxR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rocky Mountain spotted fever (RMSF): Nursing]]></video:title><video:description><![CDATA[Rocky Mountain spotted fever is a tick-borne, infectious disease caused by the bacteria Rickettsia rickettsii, which are endemic in the Midwestern, Northeastern. and south Atlantic and south-central regions of the United States. The organism primarily attacks the endothelial cells lining the inside of small blood vessels causing small vessel vasculitis, or inflammation of small blood vessels. If not treated promptly, the disease can be fatal.

Alright, first let’s quickly review some physiology. The endothelium consists of a single layer of endothelial cells that line the inside of the entire circulatory system, from the heart to the smallest blood vessels supplying the various organ systems. In addition to being a protective barrier, the endothelium plays a major role in the regulation of the vascular tone by releasing vasoconstrictive and vasodilatory substances, while it is also an important regulator of inflammation. 

During an inflammatory response, the endothelial cells contribute to the release of small proteins, called cytokines, and other proinflammatory molecules that help modulate the activity of other immune cells, as well as promote the adhesion of immune cells, called leukocytes, to the endothelium, thereby facilitating their migration to the site of inflammation. Finally, the endothelium also helps to regulate blood flow, platelet aggregation, and blood clotting.

Okay, now Rocky Mountain spotted fever is caused by the obligate intracellular, Gram negative bacterium Rickettsia rickettsii. The infection is transmitted to humans through vectors primarily through the bite of an infected tick, like Dermacentor variabilis, or the American dog tick, which can be found in Eastern and South-central US; Dermacentor andersoni, or the Rocky Mountain wood tick, which can be found west of Mississippi River; and Rhipicephalus sanguineus, or the common brown dog tick, which can be found in Southwestern US.

Now, the infection is more common during the act]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Child_maltreatment:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/myc0gQnbTz63F6BbPRZT4gZnRq6ZiDls/_.jpg</video:thumbnail_loc><video:title><![CDATA[Child maltreatment: Nursing]]></video:title><video:description><![CDATA[Child maltreatment refers to physical, sexual, or psychological abuse or neglect committed by another individual such as a  parent or other caregiver. Abuse refers to any act that causes harm or significant risk of harm to a child; whereas neglect is the failure to provide the basic needs of a child.  

Now, risk factors for child maltreatment can be related to the child or the abuser. Factors related to the child include prematurity, and the presence of physical, psychological, or cognitive disabilities. Child maltreatment is also more common in children of younger age, if the child has behavioral problems, or if the child is unplanned or unwanted. 

Now, regarding the factors related to the caregiver, important risk factors include low self-esteem, poor impulse control, young age, low educational achievement, poor social support, mental illness, such as depression, anxiety and substance misuse, or and when there is a biologically unrelated adult male living in the household.

Social factors that increase the risk of child maltreatment include stressful situations such as poverty, unemployment, eviction, or involvement with law enforcement. In addition, parents or caregivers who have experienced child abuse or domestic violence are more likely to be abusive.

Alright, now, there are several types of child maltreatment, including physical, emotional or psychological, sexual, and medical maltreatment. 
First, physical refers to any intentional physical injury that can result in injuries such as fractures, burns, bites, internal bleeding, or even death. In infants, a particular manifestation of physical abuse is shaken baby syndrome, where violent shaking of a baby is so traumatic that it causes subdural hemorrhage; that can lead to cerebral edema and death. Physical neglect is the failure to provide a child with food, shelter, and supervision. Physical neglect can also be manifested in abandonment, where the child is left alone, and the location of the pare]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autism_spectrum_disorder_(ASD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_Q3TnM5iQ0WPmosUJt2him4mT1ODqVRh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autism spectrum disorder (ASD): Nursing]]></video:title><video:description><![CDATA[Autism spectrum disorder, or ASD, is a neurodevelopmental disorder that manifests during infancy or early childhood and is associated with social communication and interaction deficits, as well as restrictive or repetitive behavior, interests, and activities, which can interfere with how a client functions independently in society. Many previously separate disorders like Autistic disorder and Asperger disorder now fall under ASD. 

First, let’s look at childhood developmental milestones, which are skills or behaviors that most infants are able to perform at a specific age. These milestones can be divided into social, communication, cognitive, and movement.  

Social milestones include starting to smile at 2 months of age. By 4 months, they can copy facial expressions. At 6 months they can recognize familiar faces and enjoy playing with others.  At 1 year, they enjoy playing games like peekaboo and show fear with strangers.  By 2 years of age, they enjoy playing with other children, show more independence, and start being more defiant, the so-called terrible 2s.  

Communication-wise, at 2 months, infants can coo and say “ga” and will respond to sounds. By 4 months, they can babble and try to copy sounds they hear. By 6 months, they start stringing together vowels like ooh-ahh-ehh and respond to their own name. At 1 year, they can respond to simple requests like “come”, say simple words like mama and dada, and use simple gestures like waving bye bye. By 2 years of age, they can point to the correct object when named, and say sentences with 2 to 4 words. 

Next, regarding cognitive development, at 2 months they start following moving objects with their eyes, and pay more attention to faces.  By 4 months they’ll watch moving toys and reach for them, and by 6 months they’ll start showing curiosity about objects they can see. By 1 year, they can use simple objects correctly like brushing their hair with a comb, and they will experiment with different ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_psychosocial_needs_during_illness_&amp;_hospitalization:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iMMN9YspTFS5l5RuUYMK-rnBS5G6gcl4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric psychosocial needs during illness and hospitalization: Nursing]]></video:title><video:description><![CDATA[Psychosocial needs of pediatric clients during illness and hospitalization can be challenging for nurses and other caregivers to meet. There are three main psychosocial effects that children experience during hospitalization, including fear, separation anxiety, and loss of control.

First, fear may arise from an unexpected occurrence of illness, potential physical harm, injuries, and pain. Children typically have a harder time adjusting to changes in the environment which may include scary equipment, smells, noises, other children crying, strange words, needles, and strangers in weird outfits, such as surgical gowns, masks, and caps.

Next is separation anxiety, which refers to the anxiety or emotional distress that a child experiences when separated from their caregiver, or their family, home, and friends. It can be characterized by anger and rejection of those who try to help. Anger can be followed by despair, where they become quiet and withdrawn.

Also, the child’s loss of control over decisions, usual everyday routines, self-care, and play, can adversely affect their coping mechanisms and decrease their ability to deal with new stressful situations.

Now, a child’s reaction to illness and hospitalization can be affected by many things, including age, developmental and cognitive level, temperament, and coping skills. Other important factors include recent stressful situations, the nature and severity of the illness, and whether the hospitalization is planned, unplanned, or if it’s an emergency situation. Also, length of separation from parents, family members, and other familiar caregivers; their reaction to illness or hospitalization; as well as the child’s cultural, ethnic, and religious background, can all have an effect on a child’s reaction.

Okay, in terms of clinical manifestations, how a child expresses their emotions during illness or hospitalization varies depending on their age and stage of development. Starting with infants, children at thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clubfoot:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OmaRJ828QEW0EVfInQhIJ8XQT4GA_uTt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clubfoot: Nursing]]></video:title><video:description><![CDATA[Clubfoot, also called talipes equinovarus, is a complex congenital deformity that involves the ankle and foot. Let’s start by looking at the anatomy and physiology of the newborn’s foot. The foot is essential for stability, locomotion, balance and development of motor skills, so it’s important that the structures comprising the foot are well-developed. There are 3 regions of the newborn foot: hindfoot, also called rearfoot; midfoot; and forefoot. The hindfoot includes two bones: the talus and calcaneus. The midfoot includes the navicular bone, the cuboid bone and the cuneiform bones. Finally, the forefoot consists of metatarsals, which are the long foot bones; and the phalanges, which are the toe bones. Unlike the adult foot, the newborn arch is flat; has a greater range of motion and consists of more subcutaneous fat. The ankle is a synovial joint that results from interaction between the ends of the tibia and fibula, which are the bones of the lower leg, that allows the foot to move up and down. 

Now, the ultimate cause of clubfoot isn’t fully known, but causes can be classified as idiopathic, syndromic, or positional. If clubfoot is an isolated anomaly in an otherwise healthy neonate, it’s considered to be idiopathic. Sometimes, though, clubfoot can be syndromic, which means it’s associated with other genetic or anatomic abnormalities. Other times, the cause is positional, like with oligohydramnios, where there’s not enough amniotic fluid, or because of changes within the uterine environment that creates pressure on the fetal extremity during critical periods of development. All right, now, when it comes to pathology, clubfoot is associated with bone deformities and soft tissue contractures. There are four main components, which can be remembered by the acronym CAVE. The first one is an exaggerated arch, also known as Cavus. Second, there’s forefoot Adduction with supination, meaning that the forefoot is inverted and turned upwards.Third, inversio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_dysplasia_of_the_hip:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GNNWey51S6WV0fQlZxCmvqTMRVWuF_oP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developmental dysplasia of the hip: Nursing]]></video:title><video:description><![CDATA[Developmental dysplasia of the hip is a condition where the socket or acetabulum and the femoral head are misaligned, resulting in an unstable hip joint. Typically, the condition is present at birth, but sometimes it appears later as the bones develop over time.Now, let’s go over some anatomy and physiology. The hip joint is also called the acetabulofemoral joint. The main function of the hip joint is to support the weight of the body while providing mobility. It is a ball and socket synovial joint, where the ball-shaped head of the femur sits and rotates within the acetabulum of the pelvis, which is a cup-shaped socket. At the bottom of the acetabulum, known as the acetabular fossa, arises a ligament called the ligamentum teres, that attaches to the fovea capitis, which is a depression found on the tip of the femoral head. This ligament helps with joint stability, especially during hip flexion and abduction. 

Now, during embryonic development, the mesoderm is separated by a cleft to distinguish the acetabulum and the femoral head by the 7th week of pregnancy. The proper development of a hip joint requires that the femoral head stays fitted within the acetabulum, so that they both grow together keeping their sizes and shapes proportional. Finally, by the 11th week, the hip joint is fully recognizable. All right, now the exact causes of developmental dysplasia of the hip are unknown, but there are several risk factors. One of these is too much mechanical force being applied against a fetal thigh, which can cause the femoral head to slip out of the acetabulum. This can happen when a baby is lying in a breech position within the uterus. This sort of mechanical force can also occur with multiple gestations, macrosomic or large babies or with oligohydramnios, where there is not enough amniotic fluid to expand the uterine cavity. 

Additionally, having congenital musculoskeletal deformities increases the risk for developmental dysplasia of the hip. Other r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Phenylketonuria_(PKU):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CmaThLSVQrGzWI9MkoWfca_IRV_eZNIp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Phenylketonuria (PKU): Nursing]]></video:title><video:description><![CDATA[Phenylketonuria, or PKU for short,  is a rare genetic disorder that causes an amino acid called phenylalanine to build up in the body. If not treated, it can damage the central nervous system, resulting in developmental delays, intellectual disability, and seizures. All right, let’s review some physiology. Amino acids are the basic building blocks that make up proteins. Phenylalanine is one of the essential amino acids, meaning our bodies can&amp;#39;t make it so it must be acquired through protein in the diet. Since the body can’t store amino acids, any excess amino acids are converted into glucose or ketones to be used for energy. Normally, phenylalanine is converted into the amino acid tyrosine by the enzyme phenylalanine hydroxylase with the help of a cofactor called tetrahydrobiopterin, or BH4 for short. Tyrosine is then made into several other products, including dopamine and serotonin, which are neurotransmitters that neurons use to communicate; as well as norepinephrine and epinephrine, which are also neurotransmitters and hormones used by the sympathetic nervous system.

Now, PKU is an autosomal recessive genetic disorder caused by a mutation in the gene that codes for the hepatic enzyme phenylalanine hydroxylase, which helps break down phenylalanine. In autosomal recessive disorders, the client needs to inherit two copies of the mutated gene, one from each parent, to develop the condition. Because of that, PKU is more common in clients with a family history of this disorder, as well as in clients who originally come from the same region, since they frequently share versions of the same genes that have been passed down from generation to generation. Now, pathology-wise, clients with PKU have an impaired ability to use the amino acid phenylalanine due to low phenylalanine hydroxylase activity. Depending on the severity of the mutation, enzyme activity can vary from a complete absence of enzyme, resulting in very high levels of phenylalanine; to a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antepartum_assessment_-_Fetus:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cCdZpSzmQmiQ4iGJHMsZ6YCQTbuPdSA7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antepartum assessment - Fetus: Nursing]]></video:title><video:description><![CDATA[Antepartum fetal assessment refers to diagnostic procedures used to evaluate the fetal condition before birth.

Okay, let’s begin with assessment of fetal movement. Counting of fetal movements is a simple, cost-effective, and widely used method to monitor the well-being of a fetus. It’s based on the principle that if a fetus is compromised in some way, it will reduce its activity to conserve oxygen and energy. So, decreases in fetal movements or decreased activity in a previously active fetus might be due to a disturbance of placental function, and may precede an intrauterine fetal demise  Now, fetal movements start around the 7th to 8th week of gestation, and increase as gestation progresses. These movements can be felt by the client, typically starting around the 16th and 18th weeks of gestation. One of the most common methods is the “count to ten” method. The client is instructed to count fetal movements, including at the same time each day, ideally this will be a time when the client knows her fetus will be active, which is often during the evening hours. Although there is no well-established evidence of the number of fetal movements that are considered normal, generally, if less than 10 movements in a 2-3 hour period are felt, the client should contact her healthcare provider.  

Next up is ultrasound, which is a non-invasive test that uses high-frequency sound waves to visualize the fetus and monitor fetal growth; and can be done either transabdominally or transvaginally. Fetal growth can be assessed by measuring the biparietal diameter of the head and the fetal femur length, and birth weight can be estimated. Additionally, fetal anomalies such as open neural tube defects, including microcephaly or anencephaly, as well as ventral wall defects like omphalocele and gastroschisis can be detected. An ultrasound can also be used to measure nuchal translucency, which is a collection of fluid under the skin behind the fetal neck associated with trisomy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gestational_trophoblastic_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2CaDdPG_Q-6YHIcgFapXrW2lS-mLHbqX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gestational trophoblastic disease: Nursing]]></video:title><video:description><![CDATA[Gestational trophoblastic disease includes both benign and malignant proliferations of placental cells. At the benign end of the spectrum, there’s hydatidiform mole, also called molar pregnancy; while at the malignant end, there’s gestational trophoblastic neoplasia, which includes choriocarcinoma and trophoblastic tumors. Now, let’s quickly review the physiology of fertilization. Normally, at fertilization, a single female gamete, or the egg fuses with a single male gamete, called the sperm. Both the egg and the sperm normally have 23 chromosomes each, so half the set of human chromosomes. When combined, they give rise to a new organism, called the zygote, with 46 chromosomes. Now, the zygote undergoes repeated mitosis to produce more cells, which are grouped into the inner and the outer layer. The inner cells develop to become the embryo, whereas the outer cells, called the trophoblasts, form the embryonic part of the placenta, called the chorion, and its projections, known as chorionic villi. The chorion produces beta human chorionic gonadotropin, or beta-hCG for short, which is a hormone that helps in maintaining the pregnancy. Now, gestational trophoblastic disease is the result of genetic abnormalities that occur during fertilization, leading to abnormal proliferation of trophoblastic tissue.  

Risk factors include age extremes, like younger than 16, or older than 45; a personal history of gestational trophoblastic disease; and Asian race. All right let’s switch gears and talk about pathology. Hydatidiform mole develops when a chromosomally empty egg fuses with a normal sperm. The sperm&amp;#39;s genetic material duplicates to form 46 chromosomes. Because there are only paternal chromosomes, the mole develops into a mass of cells without any fetal parts or placenta. This is called a complete mole. An incomplete mole, on the other hand, appears when a normal egg is fertilized by two sperm, which develops 69 chromosomes.  In both cases there is a pro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis_B_virus_(HBV)_infection_in_pregnancy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6jUcAForQWOpsPxAulZPd1WlRwW7VPIw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis B virus (HBV) infection in pregnancy: Nursing]]></video:title><video:description><![CDATA[Hepatitis B virus, or HBV, is associated with hepatitis, or inflammation of the liver, which is often self-limiting, but in some cases, can result in extensive liver damage. During pregnancy the virus can be transmitted to the baby, potentially causing adverse health effects.

Now, let’s quickly review some anatomy and physiology. The liver is a large, solid organ located in the right upper quadrant of the abdomen, which has several functions, including the production of bile, cholesterol, and certain blood proteins like albumin and clotting factors. The liver is also involved in helping with glucose, fat, and bilirubin metabolism, as well as detoxification of certain toxins.

Now, HBV infection is caused by hepatitis B virus which is a DNA enveloped virus that belongs to the Hepadnavirus family. Hepatitis B virus is primarily transmitted through blood and other body fluids; so the main risk factors include blood transfusions, hemodialysis, IV drug use, working as a healthcare professional, as well as high-risk sexual behavior, such as having multiple partners or not using protection.

Now, hepatitis B virus can also be transmitted vertically from the mother to the baby. This can happen as the virus travels across the placenta; during invasive procedures like amniocentesis or chorionic villus sampling; if the amniotic membranes rupture prematurely; and during labor, as the newborn passes through the birth canal.

In terms of pathology, the virus causes progressive damage to the liver. Eventually, fibrosis and scarring occurs, which can progress to cirrhosis, as well as complications like hepatic encephalopathy, where toxins like ammonia build up in the blood. Chronic HBV also increases the risk of hepatocellular carcinoma. 

Now, in the case of vertical HBV transmission, the baby can be at risk for certain complications. Most neonates infected with HBV are asymptomatic at birth, but eventually will develop a chronic infection. Those born to clients with ch]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prenatal_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3HcICJjgTtuhvE7h25bafTn7QVOjW6iA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prenatal care: Nursing]]></video:title><video:description><![CDATA[The prenatal period refers to the time from before conception until the end of pregnancy. So, prenatal care refers to the care that is provided before and during pregnancy to evaluate maternal and fetal health, provide education to promote health, and to intervene when possible to ensure the birth of a healthy baby with minimal risk for the mother. For a successful pregnancy outcome, prenatal visits should continue every 4 weeks until week 28, every two weeks from week 28 to 36, and then weekly until delivery. 

All right, now the first step in prenatal care is preconception counseling, which seeks to identify any potential risks to the client’s fertility and pregnancy outcome. The first prenatal visit typically occurs when a client suspects they are pregnant or because they wish to conceive in the near future. No matter the case, the main focus of the first prenatal visit should be obtaining a thorough personal and obstetrical history, as well as family history, to identify any medical conditions that could pose a risk to the pregnancy. Now, in clients who suspect they are pregnant, pregnancy should be confirmed with a urine pregnancy test and an abdominal ultrasound. If pregnancy is confirmed, the estimated date of delivery, or EDD, should be calculated. It’s traditionally calculated using Naegele’s rule, which takes the first day of the last menstrual period, or LMP, subtracts 3 months, and then adds one year and seven days. So, if the LMP was September 10, 2021, counting back 3 months, adding 1 year and 7 days calculates the EDD as June 17, 2022.

The obstetrical history evaluates the gravidity, parity, and abortions. Gravidity, or G, refers to the number of times a client has been pregnant, including the current pregnancy. Parity, or P, refers to the number of times a client has carried the pregnancy to a viable gestational age, which is more than 20 weeks gestation. So, if a client is currently pregnant, has been pregnant once before, and has had one]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrapartum_assessment_-_Fetal_heart_rate_patterns:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/idl5boFiQ_SpnFlTCV3AZdHyQ7S5zvBt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intrapartum assessment - Fetal heart rate patterns: Nursing]]></video:title><video:description><![CDATA[Intrapartum assessment of the fetal heart rate, or FHR for short, refers to the assessment of the FHR and rhythm in response to uterine activity during the intrapartum period, which refers to the time of pregnancy from the onset of labor to delivery of the newborn and the placenta. Now, fetal monitoring can be external or internal. External fetal monitoring is a noninvasive method to monitor the FHR and uterine activity. An ultrasound transducer is placed on the maternal abdomen over the fetal back to record the FHR. A tocotransducer, sometimes called a tocodynamometer, or toco for short, is a pressure-sensitive button that is placed over the uterine fundus to track uterine activity. Both devices are held in place by belts or bands and then attached to the fetal monitor that can print out or display the FHR and uterine activity. 

Now, during the procedure, the client should avoid the supine position because the weight of the uterus and fetus can compress large blood vessels, such as inferior vena cava and aorta. This can decrease cardiac output and cause supine hypotension, which results in less blood pumping into the systemic circulation and the placenta, so less oxygen is delivered to the fetus. To alleviate the pressure on these vessels, the client should be turned to a lateral recumbent position, or a wedge should be placed under the right hip, displacing the uterus to the left and away from the vessels. On the flip side, internal fetal monitoring is an invasive procedure that requires cervical dilation of at least 2 to 3 centimeters and rupture of the fetal membranes. This way, a spiral electrode  can be placed through the cervix onto the presenting part of the fetus, most commonly the scalp, to track the FHR. 

If uterine contractions also need to be monitored more closely, an intrauterine pressure catheter can be placed inside the uterus.Now, let’s take a look at the fetal heart rate tracing, which is divided into two main parts. The upper part rec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain_management_during_labor:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YIiyUJv3RautBCXVQUihkkJTQzaRFBsj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pain management during labor: Nursing]]></video:title><video:description><![CDATA[Labor refers to a series of progressive contractions of the uterus that result in dilation and thinning of the cervix. This, in turn, allows the fetus to descend from the uterus, through the birth canal, and into the extrauterine environment. This process results in pain that can be managed in a variety of ways. Now, from a physiological standpoint, not only is labor pain normal, but it’s also easily anticipated, allowing time for preparation and acquisition of skills to help manage it. Secondly, although intense, labor pain is also time limited. It is usually intermittent and decreases rapidly after hitting its peak. Finally, it will end with the birth of a child, which is highly motivating for the mother, allowing for a higher pain threshold.

Pain during labor can be either visceral or somatic. Visceral pain mostly occurs during the first stage of labor due to uterine contractions that lead to hypoxia of the uterine muscles, dilation of the cervix, distension of the lower uterine segment, as well as pressure and pulling on pelvic structures such as the fallopian tubes, ovaries, and bladder. Then, somatic pain mostly occurs during the later part of the first stage and second stage of labor, as the uterine contractions become more intense. Also during this time, pain is increased as the fetus pushes directly on maternal tissues like the vagina, perineum, and the lumbosacral plexus during its descent.

Now, pain during labor can cause anxiety leading to a stress response that can have an adverse effect on the progression of labor and on the fetus. Excessive pain can heighten the individual’s fear and anxiety, causing the release of cortisol and catecholamines like epinephrine and norepinephrine. When these act on alpha receptors, the uterine blood vessels and muscles constrict, reducing uterine blood flow, reducing the fetal oxygen supply, and potentially leading to fetal hypoxia. Labor also increases the mother’s metabolic rate and demand for oxygen, maki]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Premature_rupture_of_membranes_(PROM):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K-JN8kaVQjmZH6slzscIsaorRBGfB_g4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Premature rupture of membranes (PROM): Nursing]]></video:title><video:description><![CDATA[Premature rupture of membranes, or PROM for short, is the rupture of the fetal membranes  before the onset of labor. In most cases, this occurs near term, but when membranes rupture before 37 weeks of gestation it is referred to as preterm premature rupture of membranes, or PPROM.            

Alright, let’s review some anatomy and physiology. The fetal membranes, also called the chorioamniotic membranes, include the chorion and the amnion. During fetal development, the two membranes fuse together forming the amniotic sac, which is filled with amniotic fluid in which the fetus is suspended. The chorion also forms the fetal part of the placenta, helping in the exchange of nutrients, waste products and gasses between the fetus and the mother. Now, when the amniotic sac ruptures, it releases the amniotic fluid, which is why a lot of people describe it as their “water breaking.” Normally, the rupture of membranes occurs right before the onset of labor and it’s associated with the beginning of uterine contractions.

Although there are several conditions associated with premature rupture of membranes, the exact cause isn’t always clear. Risk factors include a history of PROM or PPROM in a previous pregnancy; genital or urinary tract infections; cigarette smoking; acute abdominal trauma; and uterine overdistention, which can happen as a result of a multiple pregnancy or due to polyhydramnios, which is when there’s too much amniotic fluid inside the amniotic sac.

Now, the pathology of premature rupture of membranes results from a variety of factors that lead to accelerated membrane weakening, eventually causing its rupture. When membrane rupture occurs, a sudden release of amniotic fluid results in oligohydramnios, meaning there’s too little amniotic fluid surrounding the fetus. Premature rupture of membranes is associated with complications like umbilical cord prolapse, which is when the umbilical cord prolapses into the lower uterine segment. In addition,membra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brachial_plexus_injury:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Di6E8YWDRa2x-Vj-1SXV4CvPSoeG8IFw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brachial plexus injury: Nursing]]></video:title><video:description><![CDATA[Brachial plexus injury describes damage to the brachial plexus, which is a network of nerves that supply motor and sensory innervation to the upper limbs. 

First, let’s go over some anatomy and physiology. The brachial plexus is divided into roots, trunks, divisions, cords, and branches. The roots are the ventral rami coming from spinal nerves C5 to T1. These roots combine to form the next part of the brachial plexus, called the superior or upper, middle, and inferior or lower trunks. 

Then, these trunks give off divisions, which in turn recombine to form the lateral, posterior, and medial cords. Finally, these cords give off branches, which give rise to the musculocutaneous, axillary, radial, median, and ulnar nerves, which supply motor and sensory innervation to different areas of the upper limb. 

The musculocutaneous nerve gives motor innervation to the muscles of the anterior arm, as well as sensory innervation to the lateral side of the forearm. On the other hand, the axillary nerve carries motor information to the teres minor and deltoid muscles. It also carries sensory information from the shoulder joint, and the skin covering the inferior portion of the deltoid. 

The radial nerve gives sensory and motor innervation to the posterior arm and forearm. In the hand, it only supplies sensory innervation on the dorsal side. Here, it innervates the lateral hand, the thumb, and the proximal 2nd to 4th digits. 

Next, the median nerve provides motor innervation to most muscles of the anterior forearm. In the hand, it innervates the thenar muscles, which act on the thumb, and the lateral lumbrical muscles of the other digits. The median nerve also carries sensory information from the skin of the hand; on the palmar side, it innervates the lateral 3 ½ digits and the adjacent palm. On the dorsal side, it innervates the distal aspects of the lateral 3 ½ digits. 

Finally, the ulnar nerve carries motor information to the flexor carpi ulnaris, and the ulnar ha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Circumcision:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZW9ni9vZSC_t8nbZZYL6kIxfTY6eB-HO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Circumcision: Nursing]]></video:title><video:description><![CDATA[Circumcision is the surgical removal of the foreskin that covers the tip of the penis. It&amp;#39;s a common procedure for infants with a penis.

Let’s first review the anatomy of the male external genitalia, which consists of the scrotum and the penis. The scrotum is a skin and muscle pouch that hangs outside the body and contains the testes. The penis is composed of the body, or shaft, which ends with an enlarged tip, the glans penis, that has an opening called the external urethral orifice at its very tip, where semen or urine are released outside the body. Around the glans penis, a cuff of loose skin makes up the foreskin or prepuce. 

Now, there are various indications for circumcision, which can be religious, social, cultural, and personal. In fact, in some cultures, circumcision is a ceremony that is done outside the clinical setting, especially for those of the Jewish faith. On the other hand, other cultures have strong beliefs to keep the foreskin intact.

Other indications for circumcision include penile trauma and various deformities, such as phimosis, which is when the foreskin is too tight on the glans penis so that it can’t be pulled backward. A similar condition is paraphimosis, which is when the foreskin cannot be returned to its original position after retraction. Circumcision might also be indicated in clients with recurrent balanitis, which is inflammation of the glans penis, in addition to balanitis xerotica obliterans, which is a progressive inflammatory dermatosis of the foreskin and glans penis.

Finally, circumcision can also be done to prevent certain conditions, such as penile cancer, sexually transmitted diseases, including human immunodeficiency virus, or HIV, as well as to prevent urinary tract infections in infants with a type of congenital uropathy, where the flow of urine is obstructed.. 

The circumcision procedure starts under sterile conditions with the baby positioned on their back with arms and legs restrained. An anes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_diaphragmatic_hernia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YNE0FbcDQQ6h_Yi0Zt14_MqlRCOau_3T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital diaphragmatic hernia: Nursing]]></video:title><video:description><![CDATA[Congenital diaphragmatic hernia is a development defect of the diaphragm in which an opening in the diaphragm allows the abdominal organs to herniate into the thorax. Herniation can develop on any or both sides of the diaphragm but it typically occurs at the left side of the diaphragm.

Alright, let’s start by reviewing the anatomy and physiology of the diaphragm. During intrauterine life, the diaphragm develops  by the midline fusion of the paired retroperitoneal folds.

This results in the formation of a dome-shaped sheet of skeletal muscle that divides the thoracic cavity from the abdominal cavity. 

Now, the diaphragm is the chief muscle for inspiration. When it contracts, the diaphragm moves downwards, which increases the volume of the thoracic cavity, and with it,the volume in the lungs. This makes the intrapulmonary pressure fall below the atmospheric pressure, creating a partial vacuum that allows fresh air to be sucked in.  

Now, the exact cause of congenital diaphragmatic hernia is unknown, but it&amp;#39;s believed to be associated with certain genetic risk factors that can interfere with the development of the diaphragm,  including chromosomal abnormalities like the trisomy 13, 18, or 21.  

Alright, the pathology of congenital diaphragmatic hernia starts during the fetal period. If during development, retroperitoneal folds don’t fuse properly, the newly formed diaphragm will have a hole in it. This allows abdominal organs, like the stomach and intestines, to herniate into the thoracic cavity. 

The herniated organs push against the lung on the affected side, preventing the lungs from growing to normal size, a condition called pulmonary hypoplasia. 

Pulmonary hypertension develops along with a right-to-left shunting through the ductus arteriosus and foramen ovale, resulting in deoxygenated blood being pumped to the body, resulting in systemic hypoxemia. 

Long-term complications of congenital diaphragmatic hernia include chronic lung disease]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Craniosynostosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JCBWXhFDRk2SVTAJS_mdtULGTvKBTpJh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Craniosynostosis: Nursing]]></video:title><video:description><![CDATA[Craniosynostosis is a congenital disorder characterized by the premature closure of a cranial sutures that may lead to deformity of the skull shape and inhibition of brain growth.

Now, the skull consists of the paired frontal bones, the paired parietal bones, and the isolated occipital bone. The spaces between the skull bones are called cranial sutures and there are four major sutures: metopic, coronal, sagittal, and lambdoid. The sagittal, coronal, and metopic sutures meet at the anterior of the skull to form the anterior fontanelle, palpable just behind the forehead at the midline. The posterior fontanelle is formed by the intersection of the sagittal and lambdoid sutures. 

At birth, the cranial bones and sutures are not well developed and are not fused to accommodate momentary skull distortion at birth and allow brain growth and development after birth. At two months of age, the posterior fontanelle closes, followed by the closure of the anterior fontanelle at around 2 years old. The metopic cranial suture also closes at two years of age and all other sutures close in adulthood upon completion of the craniofacial growth.

Alright, now the exact causes of craniosynostosis are unknown, but it can be classified as non-syndromic, or isolated, which is the most common type, and syndromic, which is associated with other anomalies of the face, trunk, or extremities.

Risk factors for craniosynostosis include, maternal use of tobacco, alcohol, or other substances during pregnancy, advanced maternal age, and family history of craniosynostosis. Other causes include intrauterine constraint, where there’s pressure on the fetal skull during gestation, which can happen with maternal uterine malformations, multiple birth, or oligohydramnios, where there is not enough amniotic fluid to expand the uterine cavity.

Okay, moving on to pathology, craniosynostosis occurs when there’s a premature fusion of one or more cranial sutures, which restricts the growth of the skul]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meconium_aspiration_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OFR34_HxTeynCjtpc10vYG5SQWCeAZgz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meconium aspiration syndrome: Nursing]]></video:title><video:description><![CDATA[Meconium aspiration syndrome, or MAS for short, is a condition characterized by respiratory obstruction and distress caused by meconium entering the respiratory tract. Now, meconium is a thick, sticky, green-black substance that is the first stool of the newborn. It starts forming as early as the 12th week of gestation, and it’s made up of amniotic fluid, mucus, cells that have been shed from the skin or intestinal tract, and intestinal secretions, like bile. Normally, the meconium is passed by the newborn within the first 48 hours of life. All right, now the exact cause of meconium aspiration syndrome is unknown, but it’s believed to be initiated by a stressful intrauterine event that leads to the early passage of meconium. Risk factors for developing meconium aspiration syndrome include anything that can cause stress to the fetus, such as hypoxia, or low levels of oxygen in the fetal blood, caused by problems like  compression of the umbilical cord, insufficiency of the placenta, or prolonged labor. 

Meconium aspiration syndrome is also more common among post term infants, especially if they are small for gestational age. Other risk factors include babies who are Black or South Asian, as well as Pacific Islanders and indigenous Australians. The pathology of meconium aspiration syndrome starts with an intrauterine stressful event that leads to inadequate oxygen delivery to the fetus and subsequent hypoxia. Hypoxia causes increased intestinal motility and relaxation of the anal sphincter, which stimulates meconium excretion into the amniotic fluid, as well as fetal gasping, which can allow meconium to be aspirated into the respiratory tract. Meconium can also be aspirated spontaneously or when the baby takes the first breath after delivery. Now, aspiration of meconium can cause a number of complications. First, the bile salts and pancreatic enzymes contained in the meconium cause chemical pneumonitis. 

In addition, meconium occludes the airways with a ba]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neonatal_abstinence_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_jg2EGb2RySf9LBZxtK2mVCSS6_1ts9B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neonatal abstinence syndrome: Nursing]]></video:title><video:description><![CDATA[Neonatal abstinence syndrome or NAS for short, is a postnatal withdrawal syndrome that refers to signs and symptoms that a neonate experiences as they withdraw from prenatal exposure to certain substances, most commonly opioids. NAS is characterized by central nervous system hyperirritability, autonomic dysfunction, and gastrointestinal hyperactivity. NAS is also referred to as neonatal opioid withdrawal syndrome, or NOWS for short.  

Okay, first, let’s review the physiology of the placenta, which is an organ that’s co-created by the fetus and the mother during development. Zooming in, the placenta can be subdivided into two layers: the maternal layer called the decidua basalis and the fetal layer called the chorion. The decidua basalis looks like a flattened bag of blood with uterine arteries delivering blood in and uterine veins pulling blood out. Then, there’s the chorion, which consists of fingerlike projections called chorionic villi. These villi contain tiny fetal arterioles and venules, and push into decidua basalis, reaching into a warm pool of maternal blood.  

Gasses, nutrients, and other substances move back and forth between the decidua basalis and the fetal vessels, by diffusing through the intervillous spaces, which are the spaces between the chorionic villi. So, from there, oxygenated maternal blood, as well as nutrients, and substances can travel through the umbilical vein to the fetal circulation. Eventually, deoxygenated blood will head back towards the placenta through two umbilical arteries. That umbilical vein and the two umbilical arteries collectively form the vessels of the umbilical cord. 

The most common cause of NAS is maternal use of opioid substances, such as heroin, morphine, or methadone, and sedative medications, like benzodiazepines, barbiturates, and antidepressants.  

Now, the factors that increase the risk of NAS, are also the factors that increase the risk of maternal substance use. Individual risk factors can ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neonatal_sepsis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gilGHOBoTzOava0jGr_x3eJNQ8_w0zAf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neonatal sepsis: Nursing]]></video:title><video:description><![CDATA[Neonatal sepsis refers to the presence of bacteria in the blood or bacterial meningitis presenting in the first 30 days of life. It is classified as early-onset and late-onset sepsis. Early-onset sepsis occurs during the first three days of life, and is caused by exposure to a pathogen during the intrapartum period; while late-onset sepsis occurs after the first week of life, and is caused by pathogens that are acquired postnatally.

Now, let’s quickly review the immune system of newborns.  During the first six months of life, the immune system is immature, meaning that it reacts more slowly to an invasion when compared to older children. Because the infant’s immune system isn’t fully developed, they depend on the few antibodies acquired from the mother during the intrauterine life and from breast milk. These offer some protection but are too few to keep infections localized, so there’s a higher risk of infections spreading quickly throughout the body. Additionally, the newborn’s blood-brain barrier is underdeveloped, and that makes it easier for pathogens to enter the central nervous system and cause meningitis.

Now, neonatal sepsis is most commonly caused by bacteria from the mother’s genitourinary tract that infects the infant during delivery. The most common ones include group-B Streptococcus, Streptococcus pyogenes, Escherichia coli, Listeria monocytogenes, Haemophilus influenzae , Enterobacter spp. Less commonly, sepsis can be caused by fungi, such as Candida albicans. 

Risk factors for neonatal sepsis are grouped into fetal and maternal risk factors. Fetal risk factors include prematurity, low birth weight, and admission to the neonatal intensive care unit, or NICU for short. On the other hand, maternal risk factors include prolonged rupture of membranes that lasts 12 to 18 hours prior to delivery, in addition to chorioamnionitis, and vaginal colonization by group-B Streptococcus.

Alright, now the pathological process of neonatal sepsis starts wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neural_tube_defects:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IKJmsUcqSfqsbp1GN3ALTW25R-CrJdn8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neural tube defects: Nursing]]></video:title><video:description><![CDATA[Neural tube defects, or NTD for short, refer to developmental defects of the central nervous system secondary to failed closure of the neural tube during the fetus&amp;#39;s embryonic development. 

Now, let’s quickly look at the physiology of neural tube development. Let’s zoom in on a cross section of the early embryo.  

Here we can see it is made up of three main layers: the ectoderm, the mesoderm, and the endoderm. 

The ectoderm then goes on and differentiates into three populations of cells.  

The first one, located internally, gives rise to the neural tube;  the second one, located externally, gives rise to skin cells and the epidermis;  and the third population, called the neural crest cells, develop in between the neural tube and epidermis, and give rise to various structures throughout the body.  

The mesoderm, on the other hand, develops into a transient midline structure,  

called the notochord, which produces various signals that guide the development of other embryonic structures with respect to the midline.  

During the third and fourth weeks of development, the notochord signals for the formation of the neural tube, through a process called neurulation, which is highly dependent on adequate folic acid levels. Neurulation progresses in two stages.   

Primary neurulation begins when the ectoderm right above the notochord thickens and gives rise to the neural plate.  

At both ends of the neural plate, there are neural crest cells, and beyond them, the ectoderm that gives rise to the epidermis.  

Soon after, the edges of the neural plate thicken and tilt upward, forming the so-called neural folds.  

This allows for a u-shaped neural groove to form, which sets the limit between the right and left sides of the embryo.  

During secondary neurulation, the neural folds eventually fuse at the midline, forming the hollow neural tube, separate from the epidermis, above it.  

Now let&amp;#39;s look at a different view of the developing embr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Persistent_pulmonary_hypertension_of_the_newborn_(PPHN):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KjOQIpQjRkmQUXrx3M3L0eTIQ1CQicE4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Persistent pulmonary hypertension of the newborn (PPHN): Nursing]]></video:title><video:description><![CDATA[Persistent pulmonary hypertension of the newborn, or PPHN for short, is a condition in which the pulmonary arteries remain constricted after birth, resulting in increased pulmonary vascular resistance and right-to-left shunting of blood, ultimately leading to hypoxemia and acidosis. 

Alright, let’s quickly recap the physiology of pulmonary blood vessels. During intrauterine life, the fetal lungs are filled with fluid and the arteries are tightly constricted, so the pressure in the fetal lungs is high, and in the fetal heart, the pressure on the right side is higher than on the left side of the heart. This pressure difference between the right and left side of the heart allows the majority of the oxygenated blood coming from the placenta to the right atrium to bypass the lungs and pass directly through the foramen ovale, which is an opening between the two atria, into the left atrium. At the same time, the right ventricle pumps blood into the pulmonary trunk. Again, since the lungs are collapsed, most blood flows through the ductus arteriosus into the descending aorta and eventually to the umbilical arteries that lead to the placenta. 

Now, after birth, when the baby takes its first breath, their lungs expand and pulmonary blood flow increases. This makes pulmonary vessels expand, and decreases pulmonary blood pressure. In turn, this decreases the pressure in the right side of the heart, which causes the foramen ovale to close. As the baby continues to breathe, arterial oxygen levels increase, causing the ductus arteriosus to constrict. The process of closing these shunts is gradual and may take up to 48 hours to fully close. Deoxygenated blood can then flow into the lungs to get oxygenated, and the newborn circulation is established. 

Now, the exact cause of PPHN is unknown, but it&amp;#39;s believed to be associated with risk factors that can interfere with the development of the lungs. These include the maternal use of certain medications, such as no]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_-_Postpartum:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P5O0l3cJTaeJyDegalkejyWDTqeQveEp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment - Postpartum: Nursing]]></video:title><video:description><![CDATA[The postpartum period, also known as the puerperium, or “the fourth stage of labor”, starts after delivery of the fetus and the placenta, and it extends through the first six weeks after birth. During this period, the body gradually returns to its pre-pregnancy state. There are several complications that can arise during the postpartum period, and early diagnosis is essential for appropriate management of these conditions. 

Okay, let’s start with some physiology. So, after delivery, the uterus tends to regress back to its normal size and resume its pre-pregnancy position by the sixth week, a process known as involution. There are also some physiological changes that occur during pregnancy that begin to change back to pre-pregnancy levels in the postpartum period. For example, during pregnancy there is increased blood plasma volume in relation to red blood cell mass. As a consequence, maternal hemoglobin and hematocrit are usually relatively low during pregnancy, since the same amount of red blood cells are circulating in a higher volume of blood. 
After delivery, through increased diuresis or urine production, and increased diaphoresis or sweat production, blood volume returns to normal in about 6 to 12 weeks, and hemoglobin, and hematocrit levels normalize within 4 to 6 weeks. Likewise, during pregnancy, plasma fibrinogen and other pro-coagulant factors increase, and they stay elevated until 4 to 6 weeks following delivery. 

Now, there are some complications that can happen during the postpartum period, the main one being postpartum hemorrhage, meaning excessive blood loss following delivery. Other common complications include injuries to the genital tract, such as hematomas and lacerations. Hematomas are localized collections of blood that commonly affect the vulva, vagina, and perineum. They can cause significant pain and discomfort, and large hematomas can cause hemodynamic instability and even hypovolemic shock.

Lacerations, on the other hand, can ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_infections:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rhkko1VfTiGbwygUoga6ZPooRNej0RhY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postpartum infections: Nursing]]></video:title><video:description><![CDATA[Postpartum, or puerperal infections are infections of the genitourinary tract, surgical wounds, urinary tract, and breast that develop after the first 24 hours and on any two of the first 10 days postpartum.  First, let’s go over the physiology of the female reproductive system, which consists of the vulva, vagina, cervix, uterus, fallopian tubes and ovaries. The uterus is a hollow, pear-shaped organ that has an inner layer called endometrium and muscular layer called myometrium. During conception, the reproductive system undergoes changes that help support the fetus until birth, such as increased blood flow to the reproductive organs, increased uterine volume, weight, and fundal height, and increased activity of cervical mucus glands. After giving birth the uterus tends to regress back to its normal, pre-conception size and resume its pre-birth position, a process known as involution. 

The thick superficial layer of the endometrium also sloughs off, and there is a discharge of lochia from the endometrium, cervix, and vagina. Okay, so postpartum infections are typically caused by aerobic or anaerobic bacteria, such as Eschericia coli, Proteus spp, Enterobacter spp, Klebsiella spp, Clostridium spp, Staphylococcus aureus, and Streptococci spp. Other less frequent pathogens include Chlamydia trachomatis, Ureaplasma, Mycoplasma, and Gardnerella vaginalis. Risk factors for postpartum infections of the genitourinary tract include colonization of the vagina with group A and B Streptococcus, chorioamnionitis, prolonged rupture of membranes, prolonged labor, as well as retained placenta tissue. In addition, internal fetal monitoring, like fetal scalp electrodes or intrauterine pressure catheters, and repeated vaginal examinations, seem to also increase the risk for postpartum infections. 

Another important risk factor is trauma, which may involve abdominal wall trauma, as well as perineal tears, or lacerations to the endometrium, cervix, or vaginal mucosa. T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psychosocial_changes_-_Postpartum:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sqe4Ii3YSeGnXlcSP-P4_R9LS_aYtWM8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psychosocial changes - Postpartum: Nursing]]></video:title><video:description><![CDATA[Psychosocial changes during the postpartum period include various adjustments and changes that occur during the first 6 weeks after giving birth. The most important psychosocial changes include bonding, attachment, maternal touch and verbal behaviors, as well as adaptation and maternal role attainment. During this period, the nurse should provide support for the new family and intervene to promote a healthy outcome during the postpartum period. First, let’s start with the bonding. Simply said, bonding refers to the intense connection that parents develop for their baby. Important methods to promote maternal bonding include promoting skin-to-skin contact and breastfeeding. On the other hand, paternal bonding can be enhanced with methods including presence during labor and delivery, bathing the baby, changing diapers, and bottle feedings. 

Sometimes, the bonding process can be delayed due to neonatal complications that might require admission to the neonatal intensive care unit. When this happens, nursing care involves providing information, encouraging bedside visitation and involvement in their baby’s care, and coordinating resources to support the family. Now, bonding should not be confused with attachment, which refers to an enduring linkage between the parents and their child. It is a reciprocal relationship where the baby receives food, warmth, cuddling, and gentle interaction, and develops feelings of security and trust. In other words, babies can anticipate that their parents or caregivers will be available to support them in times of need. In turn, the baby demonstrates reciprocal attachment behaviors, including making eye contact, tracking their parent’s face or grasping their finger.

Okay, let’s switch gears and move on to maternal touch. Right after delivery, mothers usually use their fingertips to touch their baby. But, as time passes, they typically feel more comfortable and start to stroke their baby’s hair or chest with the palm of their ha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dependent_adult_abuse:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x4AATGavRdCZ-7hNS_50mb8FQdWkgY3G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dependent adult abuse: Nursing]]></video:title><video:description><![CDATA[Dependent adult abuse is the intentional mistreatment of dependent adults, which refers to anyone over the age of 18 who is unable to carry out daily activities or protect their rights due to physical or mental limitations. Most often, the abuse occurs at the hands of caregivers like their family members, partners, or institution workers, and can take place either at home or in long-term care facilities. 

Abuse can be classified into a few different types. First is physical abuse, which refers to inflicting pain or injury through physical force like slapping, kicking, or pushing. Next, emotional abuse refers to inflicting mental pain and inducing fear through threats, humiliation, or social isolation. Sexual abuse refers to non-consensual or forced sexual activities like molesting or touching. And financial abuse is the misuse of the client’s resources and property by concealing money, stealing, or forcing them to sign contracts.

In addition, a particular type of dependent adult abuse is neglect, where the caregiver fails to provide for basic needs, including food, water, clothing, shelter, and medical care, either intentionally or unintentionally. Neglect can also occur in the form of abandonment, where the dependent adult is intentionally left behind at a medical care facility. 

Now, important factors that can increase the risk of a dependent adult experiencing abuse or neglect include advanced age, as well as depending heavily on the caregiver due to physical limitations like mobility issues, or mental limitations like psychiatric conditions. 

There are also factors that increase the risk of a caregiver committing dependent adult abuse or neglect. These include stress and caregiver burnout, lack of bond with the dependent adult, psychiatric conditions, and substance use disorder. Other risk factors include low socioeconomic status and being financially dependent on the dependent adult, as well as prior history of domestic violence or abuse in the fa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Grief_&amp;_loss:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yEBd8yI0RfmeGQpcj0EiopOHSQWG9Hsn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Grief and loss: Nursing]]></video:title><video:description><![CDATA[Grief is the natural emotional response to loss that occurs when something or someone that is loved is taken away. Mourning is the process during which a person adapts to loss and experiences grief; and bereavement includes grief and mourning and involves the time period in which a person adjusts to their life after loss. All right, although grieving is typically associated with the loss of a loved one, grief can happen after other meaningful losses, such as the loss of a partner to divorce, the loss of their childhood home, or the loss of one’s health, a job, or a lifelong dream. While it is true that each person grieves in their own unique way, there are a series of stages that are experienced while coping with loss, and these include denial, anger, bargaining, depression, and acceptance. 

Right after experiencing a loss, clients may have a hard time accepting what has happened. Denial protects the client from feeling too many emotions at a time, and gives them a little time to adjust to the new reality. Once a client realizes the loss of a loved one, the reality of the situation begins to set in, bringing up more confusion, frustration, and pain. At this stage, clients might argue that what has happened is unfair, or try to place the blame on others. It’s also common to feel angry towards the one who has died for leaving too early, or angry at themselves for the things they did or didn’t do before their death. Next, bargaining occurs as an attempt to regain control. It’s common to go over and over the things that happened in the past and ask a lot of “what if” questions, wishing they could go back in time and change things in the hope they could have turned out differently.

After a while, the grieving client comes to terms with the certainty of death, and a sense of profound sadness and emptiness takes over. Often, the pain of loss can feel overwhelming, and depression may feel as if it will last forever. It is important to understand that this is not]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obsessive-compulsive_disorder_(OCD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qXzh68pnQoSWxhywFVzy8anJQUSRRysP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obsessive-compulsive disorder (OCD): Nursing]]></video:title><video:description><![CDATA[Obsessive-compulsive disorder or OCD for short, is a mental health condition characterized by the presence of obsessions, which are recurrent and intrusive thoughts that can often cause anxiety; and compulsions, which are actions that might be performed to try to reduce the anxiety associated with obsessions. 

Now, let’s go over some physiology. Within the brain, there are many different types of neurons that communicate with each other with small molecules called neurotransmitters. Neurotransmitters include serotonin, dopamine, and norepinephrine, which are released from one neuron and bind to receptors of another neuron to modulate its activity. 

Now, neurons that synthesize and release the neurotransmitter called serotonin are also known as serotonergic neurons and they are involved in the regulation of mood, sleep, appetite, and reproductive behavior. Serotonin is also important for the normal functioning of the corticostriatal-thalamocortical pathway or CSTC for short, which is an important brain pathway that connects the cortex with deeper structures of the brain, such as basal ganglia and thalamus. Moreover, the corticostriatal-thalamocortical pathway helps regulate habits, movement execution, and reward behavior.

Now, even though the exact cause of obsessive-compulsive disorder remains unknown, what is known is that risk factors include genetic predisposition; family history, and the presence of neurological conditions, like Huntington chorea, brain trauma, and epilepsy.

Now, the pathology of obsessive-compulsive disorder is also poorly understood, but there seems to be a dysfunction of serotonergic neurons, affecting the activity of the corticostriatal-thalamocortical pathway. As a result, normal communication between the cortex and deeper brain structures is impaired. Also, it’s thought that there’s also some kind of dysfunction in the orbitofrontal cortex, which is a part of the brain that’s responsible for switching from habitual to go]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Posttraumatic_stress_disorder_(PTSD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A1CVLOZORw2FpXYQU8RauDF3QrGvjQBt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Posttraumatic stress disorder (PTSD): Nursing]]></video:title><video:description><![CDATA[Posttraumatic stress disorder, or PTSD for short, is a mental health condition that occurs when a memory of a past traumatic event causes recurrent mental and physical distress. This condition usually occurs in clients who have either witnessed or directly experienced a traumatic event, like war or sexual assault.

Now, let’s focus on the physiology of the limbic system, which consists of a group of brain structures located under the cerebral cortex, including the amygdala, and hippocampus. Together these structures help regulate emotions, like anger and fear; as well as behavior, such as aggression and sexual activity. 

The limbic system also influences memory formation and recollection of memories, especially those that contain a fear element; and it can even affect the response of the autonomic nervous system, like cardiovascular or gastrointestinal functions. 

Additionally, the limbic system helps activate the fight or flight response, which occurs when a person is faced with a potential threat or stressful situation. The neurotransmitter involved in the regulation of the autonomic nervous system and fight or flight response is norepinephrine, which increases the heart rate, blood pressure, arousal, as well as startle response.

Now, the main cause of posttraumatic stress disorder is experiencing or witnessing a traumatic event, such as a life-threatening situation, physical injury, combat trauma, sexual assault, or child abuse. 

Even though most people don’t develop posttraumatic stress disorder in response to a stressful event, some factors that increase the risk of this condition include personal or family history of mental health conditions, such as anxiety or depression; being assigned female at birth; military experience; childhood trauma; and finally, lower level of education.

Now, the mechanisms underlying the pathology of posttraumatic stress disorder are poorly understood, but there seems to be abnormal neurotransmitter release. As a resu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Substance_use_disorder_-_Medications_&amp;_illicit_drugs:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d0LhY3yATPOjfZfr0rtj_oZkRCeKQWVa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Substance use disorder - Medications and illicit drugs: Nursing]]></video:title><video:description><![CDATA[Substance use disorder is a condition in which an individual is unable to control their use of legal or illegal substances. Some of the most commonly used substances include stimulants like cocaine and methamphetamine, inhalants like paint remover and airplane glue, hallucinogens like cannabis and ecstasy, and finally, depressants like barbiturates, benzodiazepines, and opioids such as heroin or morphine. There are three different stages of substance use disorder: tolerance where an increased amount of the substance is needed to have the same effect; dependence where the substance is repeatedly used to avoid symptoms of withdrawal; and addiction where the substance use is recurrent, uncontrolled, and continued despite its harmful effects.

Okay, let’s quickly review the physiology of the brain’s reward center. Inside the brain are small molecules called neurotransmitters that are produced and used by neurons to communicate with each other. This communication happens when one neuron releases a neurotransmitter which then binds to the receptors of another neuron causing the neuron to react.

Now, the reward system of the brain governs pleasure and motivation. The center is the nucleus accumbens, a cluster of cells located near the hypothalamus. The primary neurotransmitter used in this system is dopamine which is released by the nucleus accumbens, causing a feeling of pleasure. These neurotransmitters stay in the junction between neurons for a while until they’re all taken back into the neuron via dopamine reuptake transporters, and the feelings of pleasure stops.   

Now, there isn’t a single cause of substance use disorders, but rather it’s a multifactorial disease, meaning that there’s a combination of genetic predisposition and environmental risk factors and triggers. These include a family history of substance use disorder or having a mental health disorder like depression, ADHD, or PTSD. Certain experiences also put a client at high risk for developing]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Substance_use_disorder_-_Alcohol_&amp;_tobacco:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h4yQw_aIQJeB7av-yN8hrhuWQMy9ubMF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Substance use disorder - Alcohol and tobacco: Nursing]]></video:title><video:description><![CDATA[Substance use disorder is a condition in which an individual is unable to control their use of legal or illegal substances. Some of the most commonly used substances include alcohol and tobacco. There are three different stages of substance use: dependence where the substance is repeatedly used, tolerance where an increased amount of the substance is needed to have the same effect, and addiction where the substance use is recurrent and uncontrolled.

Okay, let’s quickly review the physiology of the brain’s reward center. Inside the brain are small molecules called neurotransmitters that are produced and used by neurons to communicate with each other. This communication happens when one neuron releases a neurotransmitter which then binds to the receptors of another neuron causing the neuron to react. 

Now, in the rewards system, dopamine is the primary neurotransmitter. And so, when a person experiences pleasure, a surge of dopamine is released from the nucleus accumbens, which is a cluster of nerves near the hypothalamus, more commonly known as the brain’s reward center.

Now, there isn’t a single cause of substance use disorders, but rather it’s a multifactorial disease, meaning that there’s a combination of genetic predisposition and environmental risk factors and triggers. These include a family history of substance use disorder or having a mental health disorder like depression, ADHD, or PTSD. Certain experiences also put a client at high risk for developing a substance use disorder like using the substance at an early age, or experiencing physical, sexual, or emotional abuse.

Okay, so the pathology of substance use disorder centers around the fact that alcohol contains ethanol, while tobacco contains nicotine. Both can trigger the release of dopamine and other neurotransmitters in the brain and create a pleasant and euphoric feeling when using the substance. This in turn motivates the client to repeatedly use the substance. 

It’s important to note ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integrative_&amp;_alternative_therapies:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AM_Qk1qXQWaKA41kti4VdNfQS82BFOGR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integrative and alternative therapies: Nursing]]></video:title><video:description><![CDATA[Nurse Ken works in an outpatient oncology office and is caring for a client named Naveen who recently underwent a partial colectomy to treat stage 3 colon cancer. Naveen tells Nurse Ken, “I’ve been taking my prescribed medications, but I’ve been using my own remedies too.” Nurse Ken responds, “Naveen, I want to gather some more information to ensure I understand the treatments you’re using.” 

Naveen goes on to explain that he’s been taking his antibiotics as prescribed; however, he’s using acupuncture and meditation to address his pain instead of taking his prescribed pain medication. He also mentions that he’s now taking a probiotic every day and he’s developed a special diet with his nutritionist which limits his intake of gluten and dairy. 

Nurse Ken says, “I’m glad to hear you’re taking such a proactive approach to your health. Let’s work together to safely incorporate these into your plan of care.” Nurse Ken will use what he knows about integrative and alternative therapies to provide support and empower Naveen in making health care decisions. 

Okay, so allopathic therapy, also called biomedicine, is what we know as conventional Western medicine, such as the use of medications, chemotherapy, and surgical procedures like Naveen’s partial colectomy procedure and prescribed antibiotics. 

Then there’s integrative therapy, also known as complementary therapy, which is when an allopathic treatment is combined with a non-conventional treatment, such as massage therapy, chiropractic medicine, or biofeedback. Naveen is using integrative therapy by taking his antibiotics while also using a probiotic supplement to complement his conventional treatment. 

Next is alternative therapy, which is where non-conventional therapies completely replace a conventional allopathic treatment. For example, Naveen is using acupuncture and meditation instead of his pain medication so this is considered alternative therapy. Now that we know more about integrative and alternat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Code_of_ethics:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hA2qi0ffQxiabITGvOltWSjETxWc9Wzs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Code of ethics: Nursing]]></video:title><video:description><![CDATA[Nurse Jocelyn works as a home health nurse. When at the market on one of her days off, she sees one of her friends, Sam, who says, “My aunt just told me that you are her home health  nurse! She says that you have been coming to her house ever since she got out of the hospital a few weeks ago. My aunt says that you take such great care of her. Has she been doing her physical therapy exercises like she’s supposed to? I know you are supposed to keep information confidential but my aunt wouldn’t mind you talking to me!” Nurse Jocelyn wants to answer her friend’s question but also wants to respect her client’s privacy. She is experiencing an ethical dilemma but she can use The Code of Ethics for Nurses to help determine how to respond.

To begin, ethics refers to moral principles that guide a person’s behavior and choices. Since ethics are determined by social standards, they are referred to as being externally driven, meaning they are not decided by a single person. Ethics help us to figure out what is “right” and what is “wrong.” Usually, ethical principles are not written down; they are considered common knowledge within a community. For example, stealing is considered “wrong” for most people. But professional groups, like doctors and nurses, often have a more formal, written summary of ethical guidelines. This is called a code of ethics and is used to inform the moral decision making of those in the group.

Now, a code of ethics provides a written statement of the ethical code of the profession. It also outlines a standard of care within the discipline, as well as identifies the purpose of the profession or why they do what they do.  

So the profession of nursing has its own code of ethics written by the American Nursing Association, or ANA. The Code of Ethics for Nurses was first published in the 1950s but it’s updated often to reflect changes in the nursing profession. Some of the most recent changes discuss the ethical responsibility of protecting clien]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Core_measures:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8gSLVg2sTcOVP45mpfbCibg-SLeNXshM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Core measures: Nursing]]></video:title><video:description><![CDATA[Nurse Selena works in the emergency department and is reviewing the discharge policy for clients diagnosed with heart failure with the Nurse Educator, Liam. Nurse Selena says to Nurse Liam, “I noticed that our facility’s discharge policy doesn’t align with the core measures for heart failure.” Nurse Liam notes that discharge paperwork for clients diagnosed with heart failure should include instructions for activity level, diet, discharge medications, follow-up appointments, weight monitoring, and what to do if symptoms worsen. However, information about follow-up appointments and weight monitoring is missing from the facility’s electronic discharge template. Nurse Liam says, “You’re right. Let’s work together to make our hospital compliant with these core measures.” Nurse Selena and Nurse Liam will use what they know about core measures to improve discharge care for clients diagnosed with heart failure. 

So, core measures are national standards of care for common conditions like diabetes and heart failure. Additional examples of core measures include instructions for tobacco screening and cessation, treatment of hypertension, and the scheduling of childhood immunizations. These standards are based on the best available evidence and are designed by The Joint Commission, or TJC, and the Centers for Medicare and Medicaid Services, or CMS. Although core measures differ depending on the condition, they usually include recommendations for prescribing and administering medications, assessment and treatment of disease, as well as client and family teaching. 

Okay, so now that you know what core measures are, let’s learn how they are assessed and monitored. All healthcare facilities in the United States must report their compliance with core measures to healthcare accreditation organizations like TJC and CMS. Healthcare facilities generally track their core measure performance by examining documentation in the electronic healthcare record. TJC and CMS compile thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genomics_-_DNA_mutations:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hfy1VLpqSBq1rOD5x_qRm1FRSuKSodV2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genomics - DNA mutations: Nursing]]></video:title><video:description><![CDATA[Nurse Andrea is working in the genetic counseling center at the local children’s hospital. Today she is meeting with George who was recently diagnosed with Duchenne muscular dystrophy and his mother Mrs. Hasan. Mrs. Hasan asks, “What could have caused this disease?” Nurse Andrea replies, “This condition can be the result of a DNA mutation known as deletion.” Mrs. Hasan asks, “What’s a DNA mutation?” Nurse Andrea says, “Well a DNA mutation is when there is an alteration to genetic material. Sometimes these alterations can result in diseases.” Let’s explore DNA mutations further to understand how they can lead to certain diseases.

Okay, so, there are several different types of DNA mutations, many of which happen during DNA replication. Mutations can affect the chromosomes in somatic cells, meaning any cell in our body other than the gametes, or sex cells, and they can occur in the gametes. If a mutation occurs in the gametes, these are called germline mutations, and this type of mutation can be passed on from one generation to the next. 
Some mutations may not cause any obvious changes to health and may never be detected. These are known as ‘silent’ mutations. Other mutations can alter function to the extent that it can be seen or felt with signs or symptoms. 

First, to better understand the major types of DNA mutations, let’s take a closer look at the structure of DNA. DNA has three basic components: deoxyribose, a five-carbon sugar molecule; a phosphate molecule; and a nitrogenous base also called a nucleobase or, simply, a “base.” Together, these make up a sub-unit, or piece of DNA, called a nucleotide. 

Now, there are four bases that make up DNA nucleotides: adenine and guanine, which are called purine bases; and  thymine and cytosine, which are called pyrimidine bases. Each of these bases are usually referred to by their first letters: A, G, T, and C. These bases form bonds according to the rule of “complementary base pairing” which states that in DN]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genomics_-_DNA_structure:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-LqIJ8kGTLaV-FmKPyyKeZ4wQ4CMNyeB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genomics - DNA structure: Nursing]]></video:title><video:description><![CDATA[Genetics is the study of biological inheritance, or what attributes you inherit from your parents. This can be things like eye color, hair color, or even a predisposition to different diseases. 

Genes are considered to be the most basic unit of inheritance that determine our traits. These genes can be found in the 23 pairs of chromosomes contained in the nucleus of our cells. There are hundreds to thousands of genes that make up each chromosome. When we take a closer look at a gene, we find that they are made up of precisely sequenced segments of deoxyribonucleic acid, called DNA.

Let’s take a closer look at the structure of DNA. DNA has three basic components that make up a sub-unit, or piece of DNA, called a nucleotide: deoxyribose, a five-carbon sugar molecule; a phosphate molecule; and a nitrogenous base also called a nucleobase - or, simply, a “base”. There are four nucleotide bases that make up and give DNA nucleotides their name - adenine, or A, thymine, or T, cytosine, or C, and guanine, or G. Bases form bonds according to the rule of “complementary base pairing” - which states that in DNA, A always pairs with T, by means of two hydrogen bonds, while C always pairs with G, through three hydrogen bonds.

Now, these DNA subunits come together in two strands that are spiraled around one another in what is known as a double helix. The helix has the appearance of a twisted ladder. When thinking about DNA as a ladder, the deoxyribose and phosphate molecules alternate in a linear pattern to make up each side rail of the ladder. The paired nucleotide bases span across the side rails to make the rungs. 

While we might think of DNA as being small, it’s actually incredibly long - over 2 meters long when fully stretched out. So how do 46 DNA molecules, one for each chromosome, fit into the tiny nucleus of a cell? Well, there are a few tricks.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genomics_-_Ethical,_legal,_&amp;_social_implications_(ELSI):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t2oNy87dScSY_MLiixQx6luWQYqwBjSz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genomics - Ethical, legal, and social implications (ELSI): Nursing]]></video:title><video:description><![CDATA[Nurse Mateo is meeting with Ms. Sullivan today at the women’s health clinic. “I’m very concerned about my risk of developing breast cancer,” says Ms. Sullivan. Nurse Mateo replies, “Can you tell me more about the reason for your concern?” Ms. Sullivan answers, “Well, my mother was diagnosed with breast cancer when she was 50 years old. Is there anything I can do aside from mammograms to assess my personal risk?” “There is a genetic screening, called BRCA screening that can help evaluate your risk. We can discuss some testing considerations,” replies Nurse Matteo. To better understand the impact of genetic screening, let’s take a look at the ethical, legal, and social implications of genetic testing.

Genomics is the branch of science that examines all of a person’s genes, including how the genes interact with one another and with the person’s environment. Genomics can help predict disease progression or the future development of disease, like how a BRCA screening can help predict Ms. Sullivan’s risk of developing breast cancer. This means that nurses have the opportunity to provide client education, and to reduce risk and improve outcomes with a more client-centered approach. While the introduction of genetic screening has had many positive impacts, it has also introduced new ethical, legal, and social implications.

Now, one of the most significant ethical implications of genomics is confidentiality and the right to privacy concerning a client’s unique genetic information. This means that the results about a genetic test cannot be shared without the client’s explicit permission. This can be an ethically complex issue if there are family members who may benefit from knowing the outcome of certain genetic screening tests, but the client chooses not to disclose the results. 

As the nurse, you should educate your client about the possible risks and benefits of their options, including the option to disclose their test results or to keep them confidentia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genomics_-_Pharmacogenomics:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Flo-KdzISAWRkzbAxsD4to1lSoCTRxgx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genomics - Pharmacogenomics: Nursing]]></video:title><video:description><![CDATA[Nurse Marta works in a primary care office and is caring for a client, Juan, who was recently diagnosed with HIV. Juan has come to the office for genetic counseling after testing positive for the HLA B*5701 allele. While Nurse Marta is documenting Juan’s admission information, Juan says, “So I know I can’t take certain HIV drugs because of my genes, but I don’t really know why.” Nurse Marta responds, “Some people with HIV can develop a serious reaction to the medication abacavir if they have a genetic variation called the HLA B∗5701 allele.” Juan nods his head but looks puzzled. He tells Nurse Marta, “I’m not following. Is there something wrong with me?” Nurse Marta assures Juan that they’ll work together to understand how his genes impact his response to this medication. Nurse Marta will use what she knows about pharmacogenomics to support, educate, and assess Juan during this process. 

Pharmacogenomics combines genomics and pharmacology to understand how a client’s genetic variations affect their response to medication. It examines the genetic factors that play a role in the effectiveness of medication therapy to provide individualized and safe care to clients.

Now, most medication metabolism depends on a family of CYP450 enzymes. And there are a number of genes that code for these enzymes. So, one way a variant in one of these genes can modify a client’s response to medications is by altering the medication’s metabolism. Depending on the genetic variant, when a client takes a certain medication, it can either cause an exaggerated response, leading to possible toxicity, or a muted response, leading to a reduction in the effect of the medication. 

For example, some clients have a form of the CYP450 enzyme CYP2D6, that is unable to convert codeine into morphine, which is the active form of codeine. So, when codeine is administered to a client with this altered enzyme, the medication is ineffective because it doesn&amp;#39;t reduce the client’s pain. Li]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_&amp;_illness_models:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hn5TH1QPTW2fki0QvKadC9K0SIebrtmj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health and illness models: Nursing]]></video:title><video:description><![CDATA[Nurse Bintou works on a surgical oncology floor where clients are admitted following surgical procedures related to cancer. Today, Nurse Bintou will be caring for a client named Helen who underwent a right total mastectomy yesterday for treatment of breast cancer. Before meeting the client, Nurse Bintou checks in the electronic health record, or EHR, to read Helen’s most recent progress note from the healthcare provider which states, “Client will require around the clock pain medication secondary to surgical trauma.” Nurse Bintou enters Helen’s room to introduce herself and finds Helen weeping quietly. Nurse Bintou says, “Helen, my name is Bintou and I’ll be your nurse today. It seems like you’re in pain?” Helen looks up, visibly shaken, and responds, “Yes, but the medicine isn’t going to help my pain; I keep telling everyone that!” Nurse Bintou moves to sit at the edge of the bed, gently touches Helen’s hand and asks her to clarify. Helen sighs and says, “Yes, my incision does hurt, but nothing compares to the pain in my heart.” Nurse Bintou nods as Helen continues, “How will people ever look at me the same when I’m not whole anymore?” Nurse Bintou realizes Helen’s priority need is psychosocial in nature instead of physiological. Nurse Bintou will use what she knows about health and illness models to support and care for Helen. 

Okay, so health is a state of complete physical, mental and social well-being which is different for each person based on their values and beliefs. Health is more than just a person being free from illness, which is the subjective experience of physical or mental symptoms which usually accompanies a disease diagnosis. So, now that you understand what health and illness are, it&amp;#39;s time to examine the models used to understand them. There are several health and illness models, but we will focus on three that are commonly used by nurses; The Health Belief Model, Maslow’s Hierarchy of Needs, and The Holistic Health Model. Fir]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_literacy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r69y-VbxRCmqZOgBSob2r7wQSHW8DJrG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health literacy: Nursing]]></video:title><video:description><![CDATA[Nurse Jerome works in an outpatient surgical center and is performing the intake assessment for a client named Julie who is scheduled for a colonoscopy. Nurse Jerome asks Julie, “When was the last time you ate?” Julie responds, “I just stopped to get a breakfast sandwich on the way here.” Nurse Jerome is confused since all clients scheduled for this procedure are instructed to ingest nothing but clear liquids after midnight the night before. He also notes that Julie has left several areas on her client forms blank and some spots have inappropriate information. 

Nurse Jerome says, “Julie, were you able to read through the colonoscopy preparation paperwork we sent you home with two weeks ago?” Julie bites her lip and looks around nervously, stating, “I did, but I guess I didn’t understand them too well, I’m sorry.” Nurse Jerome responds, “You don’t need to be sorry. Although you won’t be able to go for your colonoscopy today, let’s make sure you understand everything for next time.” Julie smiles and sighs a breath of relief. Nurse Jerome suspects Julie has low health literacy, so he’ll use what he knows about this topic to educate and support her.

Now, health literacy is the capacity to read, comprehend, and follow through on health-related information, so those who have low literacy skills are unlikely to properly understand the health-related information they need. Factors that can impact health literacy include the educational level of the client, as well as with the difficulty level of the reading material, since any client education material above the client’s reading comprehension level will lead to confusion and misunderstanding. Another factor is the native language of the client, so if educational materials aren’t written in the client’s native language, it can contribute to lower health literacy even if the client has overall high literacy in their primary language. 

It’s also important to keep in mind that even people with good literacy skills ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PVUPc9cYQ3uaO_lcii1ajeKrTwuvYE9K/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic disease: Nursing]]></video:title><video:description><![CDATA[Home health Nurse Svetlana is visiting a client named Betsy who was recently diagnosed with type 2 diabetes. Upon arrival, Nurse Svetlana notices that Betsy is sitting alone in her kitchen with her pajamas on even though it is 2 o&amp;#39;clock in the afternoon. 

Nurse Svetlana says, “Betsy, I’ve come to see how you’ve been managing your diabetes at home. How’s it been going?” Betsy responds, “I feel fine, but I didn’t realize how much this would change my life.” 

Nurse Svetlana sits down while Betsy describes the challenges she’s facing, including checking her own blood glucose and feeling isolated from her friends. Betsy continues, “My friends and I used to get pizza every week but now I can’t go because of my new diet.” Nurse Svetlana empathizes with Betsy, and reassures her that although there are many physical and emotional implications associated with a diabetes diagnosis, they’ll work together to address them.

Nurse Svetlana will use what she knows about the nature of chronic disease to support Betsy in managing her diabetes diagnosis. So, chronic disease is a biomedical condition lasting at least one year which requires consistent medical care. Examples of chronic diseases are hypertension, asthma, and diabetes. The rapidly growing population of older adults in the United States is resulting in more chronic illness. It’s estimated that 60 percent of all adults in the United States have at least one chronic disease and 40 percent have two or more chronic diseases. In fact, chronic disease is the leading cause of death and disability, adding up trillions of dollars in health care costs every year! 

On the other hand, chronic illness refers to the client’s personal experience of living with a chronic disease. For example, clients diagnosed with Alzheimer disease may experience fear or loss of independence. Therefore, nurses must consider the complex needs of clients with chronic disease as well as the numerous factors that play a role in chronic ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Quality_management:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XkQLb_dJRXyYxbTefDFn4vUqTFuMHwnP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Quality management: Nursing]]></video:title><video:description><![CDATA[Nurse Reggie works in a unit at a skilled nursing facility and has noticed that clients aren’t receiving consistent mouth care as prescribed and rates of nursing home-acquired pneumonia have risen. Nurse Reggie knows mouth care is important in preventing pneumonia so he asks Leyla, a Nursing Assistant, or NA, about the barriers to mouth care. NA Leyla says, “Honestly, mouth care isn’t listed on our daily task list, so I forget to do it.” Nurse Reggie thanks her and responds, “I want to begin a quality improvement project to address this issue. Would you help me?” NA Leyla agrees, so Nurse Reggie plans to create an updated NA task list which includes performing and documenting mouth care. Nurse Reggie and NA Leyla will measure the success of their project by tracking NA documentation of mouth care as well as the rate of hospital-acquired pneumonia six-months after implementation. Nurse Reggie and NA Leyla will work alongside the other members of the healthcare team at the facility to use quality management to improve this process. 

Healthcare facilities can achieve goals of improving the care delivered to clients through quality management and quality improvement. Quality management, or QM, is an overarching philosophy that focuses on optimizing patient care and outcomes. Healthcare institutions that adopt the QM philosophy use quality improvement, or QI, to implement these strategies by using specific processes to monitor and continually improve the quality of client care. Healthcare quality can be measured through identification of benchmarks, which are best practices for clinical care that can be compared between similar facilities to achieve outcomes such as client satisfaction and safety. QI consists of 6 steps,the first step is the identification of client needs, such as Nurse Reggie choosing mouth care as a clinical activity in need of improvement. 

The next step is assembling a team, which can be made up of interprofessional members inside and out]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Standards_&amp;_methods_of_documentation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rt5Zf4PnS0S-MeBfGTOagFOdT-O98iW6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Standards and methods of documentation: Nursing]]></video:title><video:description><![CDATA[Nurse Steve is a nurse working on a medical unit. He calls the healthcare provider to address a client’s pain, and the healthcare provider gives Nurse Steve an order over the phone, saying “You can put in a prescription for 30 mg codeine PO every 4 hours.” Nurse Steve reads the order back aloud and the healthcare provider confirms it. 

When Nurse Steve goes to enter the order into the computer system, he receives an alert from the pharmacy that the client has an allergy to codeine. 

Nurse Steve calls the healthcare provider back and informs them of the allergy alert. The healthcare provider tells Nurse Steve, “You can override that alert. They have taken this medication before and tolerated it fine.” 

After ending the call, Nurse Steve enters the client’s room to inquire about this documented allergy. The client reports that the first time she took codeine, she felt nauseous and vomited, so the nurse documented it as an allergy. But in reality, it was a side effect of taking the medication on an empty stomach. The client reports that she has taken codeine at home as prescribed without any allergic reactions. Nurse Steve will use what he knows about documentation to ensure there’s an accurate account of this clinical decision in the health record.

Documentation is a communication strategy that allows members of the healthcare team to provide a written account of client information, such as assessments, interventions and responses. Documentation can be handwritten or electronically stored within the health record, which provides a real-time account of medical and nursing care. 

Okay, accurate documentation in the health record is necessary to communicate with all members of the healthcare team regarding the client’s status, plan, and care. It is also crucial for several other reasons such as legal protection, facility reimbursement and quality improvement, or QI. 

First, documentation is one of the best defenses for litigation in healthcare, and b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Delegation_&amp;_supervision:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0Gdb7D7ETJGm2JhUvHE7TQXETkKxAcXl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Delegation and supervision: Nursing]]></video:title><video:description><![CDATA[Nurse Kai works at a long-term care facility and is assigned to care for 10 clients on the evening shift. There are two unlicensed assistive personnel, or UAPs, also working this shift: Nursing Assistant Sarah and Nursing Assistant Jamal. One client needs to be bathed, another needs help eating his dinner, a third client needs his blood glucose checked every hour, and a fourth who needs a respiratory assessment every four hours to see if the client needs a PRN nebulizer treatment. Nurse Kai knows that it will be impossible to meet the needs of all his clients without help and so, Nurse Kai will use delegation skills to make sure all the tasks are completed.

Client-centered care means meeting all of the physical, mental, and emotional needs for each client. This can be a lot of work when you are caring for multiple clients. To help make sure all your client’s needs are met in a safe and timely manner, you will need to use delegation skills. Delegation is when the nurse assigns tasks to another individual while maintaining accountability for the activity. Being accountable means that you are answerable to others as well as yourself for the actions you do and the judgments you make. In delegation, you will remain accountable for a task even if you are not the one performing the task. 

So, when Nurse Kai plans to delegate the task of blood glucose checks, he knows that even though he may not physically perform the task, he is responsible for making sure the task is completed safely. Delegation is an important tool for nurses because it helps maintain efficiency, enhances the care of clients, improves client safety, and even provides opportunities for staff training. Now, it is important to understand that different facilities will have their own guidelines for delegation, so it’s important to be familiar with your institutional practice guidelines before delegating care. 

Okay, so there are two primary roles in delegation, the delegator and the delegatee. T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Severe_chronic_neutropenia_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vb1xlaFuR7SUVn4Y5m_p1AtPQXCRbAOF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Severe chronic neutropenia (NORD)]]></video:title><video:description><![CDATA[Severe chronic neutropenia, or SCN, is a rare blood disorder characterized by decreased neutrophils in the blood lasting from several months to a lifetime and occurring in the absence of systemic disorders like blood cancers and autoimmune diseases or medication use. Neutrophils are the white blood cells that help fight bacterial infections by destroying the invading bacteria. Therefore, a lack of neutrophils results in increased susceptibility to bacterial infections throughout the body. Based on the underlying cause, SCN can be divided into three types - congenital, autoimmune, and idiopathic. 

Common signs and symptoms of SCN include recurring fevers; mouth ulcers or sores; gum inflammation which can lead to premature loss of teeth; and recurrent bacterial infections. These may include infections of the skin, referred to as cellulitis; and/or of the mouth, gums, and supportive tissue around the teeth, called stomatitis, gingivitis, and periodontitis, respectively. There may also be infections of the paranasal sinuses, called sinusitis; the throat called pharyngitis; and the lungs, called pneumonia. Sometimes, the infections may even progress to life-threatening complications like sepsis, which is when the body&amp;#39;s response to a bloodstream infection causes tissue damage and organ dysfunction.

Although the different SCN subtypes present with similar clinical features, they have varying causes. Congenital SCN, often the most severe subtype, typically presents in infancy or early childhood. It&amp;#39;s caused by mutations in the genes which result in the bone marrow producing inadequate or defective neutrophils. The most common mutation involves the ELANE gene, which is inherited in an autosomal dominant pattern. This means that a single defective copy of the gene inherited from either parent is enough to cause the disease. ELANE mutations are also responsible for a rare subtype of congenital neutropenia, called cyclic neutropenia, which is]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oxygenation_-_Oxygen_therapy:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HaM4M3lYRlOpEpL9gl8HF-zQS3K3LkGc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oxygenation - Oxygen therapy: Nursing skills]]></video:title><video:description><![CDATA[Oxygen therapy is the delivery of extra oxygen to those with conditions that cause hypoxemia, when oxygen levels in the blood are low; and hypoxia, which is when there is not enough oxygen at the tissue level to meet the needs of the body.  

This includes patients with diseases that interfere with the lungs’ ability to absorb oxygen, like pneumonia, chronic bronchitis, emphysema, and pulmonary fibrosis; blood problems, like anemia, where the blood doesn&amp;#39;t carry enough oxygen; and heart problems, like heart failure, where the heart has trouble pumping blood around the body.  

Now, oxygen is considered a medication, so an order is needed. 

An oxygen setup consists of an oxygen source and a delivery device. There are several sources for oxygen therapy. With a wall outlet, oxygen is delivered into each patient room from a central supply.  

In contrast, an oxygen tank contains oxygen gas under pressure and is typically portable, so it can be carried along as the patient moves. However, this should be moved very carefully; if the tank tips over and the valve breaks open, pressurized oxygen can burst out forcefully and result in severe trauma. Oxygen tanks have a gauge that shows how much oxygen is left. There are also liquid oxygen systems which store oxygen as a liquid at very cold temperatures and then convert it to a gas for use. They are used either for bulk storage of oxygen for a hospital system or can be portable for home use for patients with high oxygen needs, where having a compact way to storge large amounts of oxygen is helpful.  

Finally, oxygen concentrators pull in air from the atmosphere and selectively remove nitrogen to deliver air that is about 90 to 95% oxygen to the patient. These devices are easy to use and can deliver an unlimited amount of concentrated oxygen as long as they have a power supply. One caveat is that some units are designed to only deliver up to 5 liters of oxygen per minute, and so those aren’t a good fit for ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hygiene_-_Perineal_care:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6HoP5uEQTLWbp6MDnsBdZradQ3yZOHLI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hygiene - Perineal care: Nursing skills]]></video:title><video:description><![CDATA[The perineum is defined as the area between the anus and, either the vaginal opening or the root of the penis. The perineal area is close to the sites of fecal and urine excretion. Furthermore, it’s the ideal dim, damp, and warm sanctuary for germs to flourish, so keeping this region clean is essential for preventing infections, skin irritation, and getting rid of unpleasant body odors. As a nurse, perineal care is one of the tasks you will need to perform on a regular basis. It’s also a chance to closely observe the condition of their skin in the area. Now, before we talk about how to complete perineal care, here are some general considerations. Perineal care is typically done at least once every day during a bath. However, for specific clients, like those with diarrhea, fecal or urinary incontinence, or vaginal bleeding or discharge, perineal care might be needed more regularly. If they are able, let them perform perineal care on their own but stay close by in case they need help. Otherwise, encourage the client to participate as much as possible and don’t rush the procedure. 

Some clients may also find it comforting to have someone of their own gender present in the room. At all times, respect the client’s privacy and modesty by remembering to close the room’s door and bed curtains. Make sure the client is properly covered. Because bathing tends to trigger urination, remember to ask them if they need to use the bathroom, a bedpan, or urinal beforehand. At the same time, make sure to take the proper safety measures to protect yourself from possible exposure to the client’s body fluids or blood. Okay, so, when assisting with perineal care, first gather the supplies you’ll need including gloves, a bath blanket, paper towels, pre-moistened bath wipes or washcloths, a bed protector, towels, soap, a washbasin, clean clothing, and clean linens. Inform the client about the procedure before beginning and answer any questions related to the procedure. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vital_Signs_-_Temperature:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RuRtDZ58SN2mr59deBD88UnqRWGpbC1V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vital Signs - Temperature: Nursing skills]]></video:title><video:description><![CDATA[Now, as a nurse you will need to measure your client’s temperature. There are several areas of the body where you can do that, including the oral cavity; the rectum; the axilla, or armpit; the tympanic membrane, or eardrum; and the temporal artery on the forehead. Before we discuss how to measure your client’s temperature, we need to cover some definitions. Our body is always generating heat through metabolism, and a part of the brain, called the hypothalamus, tries to keep the core body temperature constant like a thermostat. When we are febrile, meaning we&amp;#39;ve got a fever, the thermostat is raised higher, and this can be due to an infection, inflammation, or cancer. However, body temperature could also be high in hyperthermia, where the thermostat is set at the right temperature, but the body simply can’t get rid of the heat. This can be due to an extremely hot environment, excessive exercise, and reduced sweat production. In contrast, hypothermia is when body temperature gets too low, and it might be due to exposure to cold for a prolonged period of time, either accidentally or in preparation for a medical procedure.

Starting with an oral temperature: This is an easy and relatively comfortable method. A normal oral temperature is between 97.6 to 99.6 degrees Fahrenheit, or 36.5 to 37.5 degrees Celsius, for adults, and 97 to 99 degrees Fahrenheit, or 36 to 37 degrees Celsius, for children. But because the mouth is a large space open to the outside environment, this is not a very accurate way to obtain a temperature because the temperature can change significantly. So, don’t take an oral temperature if the client has been eating, drinking, smoking, or chewing gum in the past 15 minutes. Oxygen therapy with a face mask can also interfere with the results. In addition, it&amp;#39;s important to hold the thermometer tightly in their mouth, so you should avoid this method for clients who are unable to do this, like those who have undergone]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutrition_-_Parenteral:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SqtZFsR8T_esEH-WeC--y987RK_Tb7rS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutrition - Parenteral: Nursing skills]]></video:title><video:description><![CDATA[There are many reasons why a client might encounter problems with eating or drinking. It could be due to difficulties with chewing, swallowing, or digestion as a result of trauma, surgery, or various medical conditions. Several alternative methods of providing them the nutrients and fluids they need are available. As the nurse, you will be responsible for the care of a client receiving these alternative delivery methods including parenteral nutrition.
Now, parenteral nutrition is a kind of liquid nutrition that is infused intravenously to prevent malnutrition. Each client’s parenteral nutrition is individualized based on their unique nutritional needs and is prepared in the pharmacy. There are two primary types of parenteral nutrition: total parenteral nutrition, or TPN, and peripheral parenteral nutrition, or PPN.  

TPN is delivered through a central line, which has a catheter that’s inserted into a large vein near the heart like the superior vena cava.  It is used for clients who cannot handle any food in their gastrointestinal tract. This could be due to gastrointestinal trauma; surgical procedures; or various disorders, like cancer or inflammation. In these cases, all nutrients are delivered, including carbohydrates, amino acids, lipids, vitamins, minerals, and water. 

PPN, on the other hand, is less calorie dense and can be administered through a peripheral intravenous line. It is used when a client does not have a central line or if they only need parenteral nutrition for less than 10 to 14 days. The length of time a client gets PPN should be limited because after 10 days, clients receiving PPN have a much higher risk of complications like infection or inflammation of the vein, called phlebitis. To help avoid this, you should rotate the PPN infusion site every 48 to 72 hours and check catheter patency regularly according to your facility’s protocol. 

So, when your client has an order for parenteral nutrition there are steps to take to keep your  c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutrition_-_Enteral:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/41VzvS_PSYGMO9YiPLaP1YI_S_CiDlEZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutrition - Enteral: Nursing skills]]></video:title><video:description><![CDATA[Enteral nutrition provides fluids and nutrients directly into the GI tract through a feeding tube. As a healthcare professional, you’ll be responsible for caring for patients receiving enteral nutrition. 

Now, enteral nutrition might be especially helpful for patients who have difficulty chewing or swallowing as a result of head or neck trauma; surgery; coma; dementia; nervous system disorders; or tumors of the head, neck, or esophagus. 

Now, there are various ways a feeding tube can go into the GI tract. The most common one is a nasogastric, or NG, tube that goes through the nose and then down into the stomach. A naso-intestinal, or NI tube, also goes through the nose, but it ends in the small intestines. 

Tubes can also be inserted through a surgical opening, or stoma, in the abdominal wall and into the stomach, known as a gastrostomy tube, or G-tube. A common type of gastrostomy tube is a percutaneous endoscopic gastrostomy tube, or PEG tube for short, that’s inserted directly into the stomach percutaneously with endoscopic guidance. Finally, tubes can also be inserted into a part of the small intestine called the jejunum, known as a jejunostomy tube, or J-tube.  

J-tubes, G-tubes, and PEG tubes are usually inserted if long-term tube feedings are anticipated and are typically used for more than six weeks; whereas NG and NI tubes are mostly preferred when tube feedings are needed for a short period of time, typically a few days or up to six weeks. 

Once the feeding tube is inserted, its placement is confirmed by X-ray. After that, your patient can start receiving enteral nutrition through the tube. There are different types of nutritional formulas that can be ordered depending on your patient’s needs. When you first start a feeding, you’ll usually begin feeding slowly while you watch for nausea, abdominal pain, or diarrhea that could indicate feeding intolerance. If the initial rate and amount of feeding is tolerated, the feedings can be increased t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genomics_-_Mendelian_genetics:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T-HmjhpFRemGj7-lCALTQ8y_RuySSVJK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genomics - Mendelian genetics: Nursing]]></video:title><video:description><![CDATA[Genetics is the science that studies inheritance patterns, or the different ways parents transmit certain traits to their descendants. And Mendelian genetics refers to the discoveries of Gregor Mendel, an Austrian monk, who studied inheritance by experimenting on pea plants. He cross-pollinated the flowers of different plants, took the seeds he developed from the pairing, planted those seeds, and took careful notes on the types of peas that resulted in the subsequent generations. Now, in addition to having lots and lots of peas in his garden, he rhelped to lay the foundation for understanding how traits are passed from one generation to another. 

So to start out, Mendel took plants with two different traits, purple flowers and white flowers. He called this original group of flowers the “P” generation, as in “parent.” Then, he crossbread the flowers, and called their offspring generation F1, or filial one. It turned out that F1 consisted of all purple flowers, so he called the purple trait dominant, while the white trait which appeared to be lost in the F1 generation, was called recessive.

Next, Mendel let the purple flowers in the F1 generation cross-pollinate amongst themselves, and he called the offspring generation from these plants F2 or filial two. It turned out that some of the plants in this F2 generation had white flowers, while most of the other plants had purple flowers! 

Mendel didn’t know this at the time, but the traits he was studying were genes, which are regions of DNA that carry information for specific features like flower color. For human traits, genes carry information for traits like eye color or blood type. Single gene traits have just one single pair of genes encode a trait, while polygenic traits have 2 or more genes influence a trait.

Now, our genes are scattered among 23 pairs of chromosomes, with one pair supplied by one parent and the other pair supplied by the other parent. The 22 of these pairs are somatic, or autosomic pa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vital_signs_-_Blood_pressure_(BP):_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sPFb8ynBRFO9ABtREgUKzxjnTTaMkkhp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vital signs - Blood pressure (BP): Nursing skills]]></video:title><video:description><![CDATA[As a healthcare professional, you will need to measure your patient’s blood pressure. Blood pressure refers to the force that the blood exerts on the walls of the arteries. Now, a blood pressure measurement has two values.  

The first and the highest is the systolic blood pressure, which is the force the blood exerts on the walls of the arteries during systole, or when the heart contracts to pump blood through the body. The second one is the diastolic blood pressure, which is the pressure on the walls of the arteries during diastole, or when the heart relaxes and refills with blood between heartbeats.  

Now, maintaining normal blood pressure is essential to ensure that tissues around the body are receiving an adequate amount of oxygen and nutrients from the blood.  

If blood pressure gets too low, the brain, heart, and other vital organs might stop functioning normally because they’re not getting enough blood.  

In contrast, blood pressure that’s too high can create a serious problem for the blood vessels and the organs they supply. Just like a garden hose that’s always under high pressure, in the long term, blood vessels may develop tiny cracks and tears. 

This can lead to serious problems like myocardial infarctions, or heart attacks; strokes, or brain attacks; and aneurysms, or bulges of a weakened blood vessel wall.  

Increased blood pressure can damage small blood vessels, like those seen in the kidney and eyes, leading to kidney failure and vision loss.  

Chronic increased blood pressure also makes it hard for the heart to pump blood out against the increased pressure. Over time, the heart gets overworked, and this can lead to heart failure.    

There are several factors that determine what a person’s blood pressure is at any given time. The first factor is the cardiac output, which is the total volume of blood the heart ejects in one minute. The cardiac output depends on the heart rate, or the number of times the heart beats per minute, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vital_signs_-_Pulse:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oopeEnQ1SLWs1m6xvu8t7eYdTHiY49ry/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vital signs - Pulse: Nursing skills]]></video:title><video:description><![CDATA[With every heartbeat, the heart creates a wave, or pulse, that’s sent to arteries all over the body in order to deliver oxygenated blood to our organs and tissues. As a healthcare professional, you need to be able to obtain a pulse and determine its characteristics, including the pulse rate, rhythm, and amplitude.  

You can calculate the pulse rate by counting the number of pulsations felt over an artery in one minute. This should be equal to the heart rate, or the number of times the heart beats per minute. The normal pulse rate varies among different age groups and individual patients.  

So, for adults and adolescents 12 years of age or older, the awake rate is typically between 60 and 100. For school-aged children between 6 and 12, it’s 75 to 118. For preschoolers from 3 to 5, it’s 80 to 120. Toddlers aged 1 and 2 years old have a normal pulse rate of 98 to 140. Finally, infants under one year of age normally have the fastest pulse rate, which ranges from 100 to 180 beats per minute.  

Besides age, the pulse rate can also be influenced by many factors, including sleep; physical activity; body temperature; emotions, like anger, fear, or stress; medications; or even the weather.  

So, tachycardia is when the pulse rate is faster than the normal range, or over 100 beats per minute for an adult. Tachycardia can occur in response to factors like strenuous exercise, fever, pain, anxiety, or certain medications. In contrast, bradycardia means that the pulse rate is too slow, or less than 60 beats per minute for an adult and can be due to heart problems or various medications.  

Another important characteristic is the pulse rhythm, which is normally regular, meaning that the intervals between the beats are equal. In an irregular rhythm, the beats don’t follow an even tempo and some of them might even be skipped. It’s also useful to note whether the irregularity happens in a predictable way or unpredictable way.  

A predictable, or “regularly irregular” pu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vital_signs_-_Oxygen_saturation_(SpO2):_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V8hHX-8nT82qjPnBBfIMUeMdQd6KHBBm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vital signs - Oxygen saturation (SpO2): Nursing skills]]></video:title><video:description><![CDATA[As a healthcare professional, you will help provide safe care to patients who have or are at risk for hypoxemia, or low levels of oxygen in the blood. These patients require pulse oximetry, or pulse-ox for short, which is a non-invasive, easy, and pain-free method of measuring the percentage of hemoglobin that’s saturated with oxygen. This is known as the saturation of peripheral oxygen or SpO2 for short. A normal SpO2 usually indicates that the amount of oxygen travelling through the bloodstream to the tissues is enough to meet the needs of the body. 

Now, a pulse oximeter consists of a probe, which is attached by a cable to a pulse oximeter. The probe has a light source on one side and a photodetector, or sensor, on the other side.  

So, when it gets clipped onto a body part, two different wavelengths of light shine through the tissues on one side, and on the other side, the sensor detects how much of each wavelength has been absorbed by the arterial blood in the tissues. The principle is that, when hemoglobin is bound to oxygen, it absorbs a different wavelength of light than when it is not bound to oxygen, so the percentage of hemoglobin bound to oxygen can be calculated by the device. LO1, LO2 

Now, there are several types of probes, depending on the site where they can be placed. The most commonly and easily used ones are digit probes, which can fit onto a finger or a toe. There are also earlobe probes, which attach to the patient’s ear. Less commonly, if the digits or earlobes are inaccessible, a pulse oximetry probe can be applied across the forehead and secured with a headband. Both earlobe and forehead probes tend to be more accurate than digit probes in cases when blood flow to the extremities is compromised or if the patient moves their hands or feet frequently, creating motion artifacts.  

There are also sensor pads that can be used on several different sites, including an adult&amp;#39;s nose bridge and a newborn&amp;#39;s palms or sole]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vital_signs_-_Respirations:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Oa2R5TsET6SjFUyR1lY8nxRHS8SyJFQv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vital signs - Respirations: Nursing skills]]></video:title><video:description><![CDATA[Breathing, also known as respiration, is how the air moves into and out of the lungs. It consists of repetitive cycles of inspiration, which is when air full of oxygen flows into the lungs, and expiration, when the air along with carbon dioxide leaves the lungs. In order for this cycle to happen, there are respiratory centers within the brain that control breathing. These centers receive information from a group of receptors, known as chemoreceptors, which detect any changes regarding the oxygen and carbon dioxide concentration in the body. Now, as a nurse, you need to be able to measure your client’s respirations and determine its characteristics, including the respiratory rate, rhythm, and depth of respiration and whether the respirations are quiet or noisy as well as easy or difficult. 

Okay, respiratory rate refers to the number of breaths a client takes in one minute. Normal respiratory rate varies among different age groups. So, for adults, it’s typically between 12 and 20. For adolescents between 12 and 20 years old, normal respiratory rate is 15 to 20. For school-aged children between 5 and 12 years old, it’s from 15 to 25. For preschoolers from 3 to 5, it’s 22 to 34, while toddlers from 1 to 3 have a normal respiratory rate of 24 to 40. Finally, infants under 1 year of age normally have the fastest respiratory rate, which ranges from 30 to 60 breaths per minute. 

Besides age, the respiratory rate can also be influenced by many factors, including physical activity; body temperature; emotions, like anger, fear, or stress; medications; smoking; certain diseases of the heart or lungs; or even the weather! A client can also voluntarily choose to increase their respiratory rate or hold their breath and, thus, decrease their respiratory rate. So, tachypnea is when the respiratory rate is faster than normal, and this can occur in response to strenuous exercise, fever, pain, anxiety, or specific medications. In contrast, bradypnea mea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infection_prevention_&amp;_control_-_Precautions_&amp;_personal_protective_equipment_(PPE):_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-4iEMMHMQTKYMIrYiO5ARmhhSyK0No5y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infection prevention and control - Precautions and personal protective equipment (PPE): Nursing skills]]></video:title><video:description><![CDATA[When providing client care, there are procedures you must follow to prevent the transmission of infection to and from the client. These include standard precautions, which are used for any client, at any time, in any situation; and transmission-based precautions for clients with a diagnosed or suspected infectious condition. Every time there’s a risk for exposure to blood; all types of body fluids, secretions, and excretions other than sweat; open skin lesions or rashes; mucosal surfaces; and possibly contaminated items or surfaces, make sure to utilize personal protective equipment, or PPE for short. This includes wearing gloves; a waterproof gown if there’s a possibility that your clothes get contaminated; and protective mask, face shield for procedures where splashes of body fluids are likely or goggles. 

When moving from a contaminated area, like a wound, to a clean body area, like the face, remember to change your gloves and wash your hands thoroughly. If there’s no access to water or soap and your hands aren’t visibly dirty, you can also use an alcohol-based sanitizer. Remember to still wash your hands afterwards as soon as you can. Do the same after touching any surfaces in or out of the care setting. Now, in the case of unexpected contact with blood or any body fluids, wipe up any spills, disinfect the area with a facility-approved cleaning product, and practice hand hygiene right away. In any case, before leaving the client’s room or moving on to another client, remove all your personal protective equipment and practice hand hygiene.

Next, to limit the potential transmission of respiratory infections, standard precautions include wearing a mask when caring for clients with suspicious signs or symptoms, like a cough. It’s also important to instruct these clients to keep at least a 1 meter, or 3 feet, distance between themselves and others or to otherwise wear a mask. You should encourage clients to cover their nose and mouth with a tissue wheneve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medical_asepsis:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TtEcjQwhRfecp7WiULdNIk8fRDyKB29f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medical asepsis: Nursing skills]]></video:title><video:description><![CDATA[Sepsis refers to infection, while the prefix “a&amp;#39;&amp;#39; means “the absence of.” In other words, asepsis is defined as the absence of pathogens. Now, there are two basic types of asepsis: medical asepsis and surgical asepsis. We will focus on medical asepsis, which is also known as “clean technique”. These  are practices that kill some microorganisms to prevent them from spreading.

Medical asepsis  includes sanitization, antisepsis, and disinfection. Sanitization refers to cleaning practices and techniques that physically remove microorganisms. These include hand washing and cleaning of clients’ personal equipment, clothing, and linens. Now, there are several things that you should know in order to maintain a sanitary environment. The most important one is hand hygiene which includes hand washing and use of hand sanitizer. Always wash your hands before meals, after using the bathroom, and before and after any contact with your clients. Don’t forget to wash your hands after touching your own or your client’s body fluids, such as urine, feces, blood, saliva, vomitus, or genital discharge. Next, when coughing or sneezing, always cover your nose and mouth with a tissue or your elbow. Teach your clients to do the same. 

Next up are personal items. Each client should have their own soap, cups, toothbrushes, and towels. Personal equipment should be regularly cleaned to prevent the growth of microorganisms. Also, when cleaning the room and objects, make sure to not stir up the dust. In other words, avoid shaking dirty linens, and use a moistened cloth or mop to wipe dust. When disposing dirty linens to laundry bins, keep them away from your uniform. This way, you will prevent the contamination of your uniform, and subsequently, you will prevent the spread of microorganisms. Also, regularly empty the garbage, because trash is a perfect environment for pathogens to grow. Finally, have good personal hygiene and assist your clients to achieve the same!

N]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Surgical_asepsis_&amp;_sterile_technique:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A2kH2G5kTyCIzIP7LR7NtEI9SJ2htdqU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Surgical asepsis and sterile technique: Nursing skills]]></video:title><video:description><![CDATA[Surgical asepsis, which is also known as “sterile technique,” includes practices that completely kill and eliminate microorganisms. Sterile technique refers to the practices that you may use as a nurse to reduce the chance of exposing your client to microorganisms and maintain sterility during certain procedures. 

For some procedures, like surgery, special precautions need to be taken to avoid exposing your client to microorganisms. This can be done with surgical asepsis. Examples of surgical asepsis include the use of disposable sterile supplies, such as syringes, needles, and surgical gloves and the use of reusable sterile equipment, such as surgical instruments.  

Most commonly, surgical asepsis is acquired through a process known as sterilization. You can think of sterilization as the highest level of asepsis because it kills both microorganisms and spores. Just like disinfection, sterilization is not used on people; instead, it is used on equipment and instruments that must be totally free of microorganisms. For example, a commonly used device to sterilize surgical instruments is the autoclave which uses high pressure and temperature to kill microorganisms and their spores. 

Finally, it’s important to note that before something can be disinfected or sterilized, organic materials, such as blood, feces, or urine, must be removed using sanitization practices and techniques.

As a nurse, some procedures will require you to use “sterile technique,” which is when you use sterilized supplies like gloves, gowns, and drapes to reduce the chance of exposing your client to organisms that might cause infection. Examples of procedures that use sterile technique include indwelling urinary catheter insertion and central line dressing changes.  

When preparing for a sterile procedure, you need to set up your sterile field which is a work space covered by a sterile drape where sterile items can be safely placed without contamination. Before setting up your sterile]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hygiene_-_Bathing:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u22LWch2SPukpdl5uPfiXhN5SiqiBTqP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hygiene - Bathing: Nursing skills]]></video:title><video:description><![CDATA[As a nurse, personal care, including assisting with bathing, is one of the most important, and sometimes challenging, tasks you will need to perform during your daily shifts. 
Now, before we talk about how to assist with bathing, here are some general considerations. Before beginning the procedure, explain to your client how you will assist them and why bathing is important. This can be especially helpful for confused clients or those with memory impairment. Be sure to answer any questions your client might have about the procedure. Then, start by closing the room’s door, all window covers, and ensuring the client is properly covered at all times to respect their privacy and modesty. Then, ask the client if they have special preferences for certain skin care products. Because bathing tends to trigger urination, remember to ask them if they need to use the bathroom, a bedpan, or urinal beforehand. Prepare the shower, tub room, or the bed if they’re doing a bed bath and make sure it’s clean. Watch out for a slippery bathtub or bathroom floor, place a non-slip mat and secure it to prevent a fall. 
Now, always check the water to make sure the temperature is safe and comfortable for the client. A water thermometer can be helpful to assess the temperature of the water before they enter. Before entering, ask your client to confirm the temperature is comfortable for them by dipping their finger in the water. Also, make sure that the ambient temperature is comfortable for them when they’re undressed. When bathing the client, encourage them to participate as much as possible. When providing a back massage, make sure to avoid reddened skin regions, sores, or bony parts because massaging these areas can damage the skin even more. 
Okay, so, when assisting a client with a shower, tub, or whirlpool bath, first gather the supplies you’ll need including gloves, soap, powder, lotion or cream, deodorant or antiperspirant, a bath blanket, washcloths, towels, and clean clothi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hygiene_-_Gastric_&amp;_intestinal_tube_care:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/meClL_FlQqC1ZZUFDEIu6Y2sS0y0IJOl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hygiene - Gastric and intestinal tube care: Nursing skills]]></video:title><video:description><![CDATA[There are many reasons why a client might encounter problems with eating or drinking. It could be due to difficulties with chewing, swallowing, or digestion as a result of trauma, surgery, or various medical conditions. Several alternative methods of providing nutrients and fluids are available. This might include delivery of fluid and nutrition through a surgically implanted tube like a gastrostomy or jejunostomy tube. As the nurse, you will be responsible for the care and maintenance of these tubes. 

There are several types of tubes that your clients may have. Some tubes are inserted through a surgical opening, or stoma, in the abdominal wall and into the stomach, known as a gastrostomy tube or G-tube. A common type of gastrostomy tube is the percutaneous endoscopic gastrostomy tube, or PEG tube for short. Here, an endoscope, or a tube with a light, camera, and guidewire, is inserted through the mouth and into the stomach. Then, a guide wire is used to place the PEG tube through an opening in the abdominal wall, creating a path directly into the stomach from the outside. Tubes can also be inserted into a part of the small intestine called the jejunum, which is known as a jejunostomy tube or J-tube.  

So, after a tube is surgically placed and while the incision site is healing, the dressing should be changed regularly using aseptic technique to prevent infection. During dressing changes, first remove the soiled dressing. Then, gently cleanse the stoma and surrounding skin with sterile water and pat the skin dry. Be sure to anchor the tube to the abdomen at an adjacent area. 

Finally, place a clean, dry dressing around the tube and secure it with tape as needed.    

Once the stoma has healed, clients no longer need the area to be dressed but skin care is still very important since drainage or leakage from the tube often contains gastric secretions, like stomach acid, which can be very harmful to the skin surrounding the stoma. To help keep skin healthy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hygiene_-_Ostomy_care:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KdYn6lRYQ9GqmkHlnRhBa7O4RzaCqGQw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hygiene - Ostomy care: Nursing skills]]></video:title><video:description><![CDATA[An ostomy is a surgically created connection between an internal organ and the outside of the body. When an ostomy is created within the abdominal wall, a piece of intestine is brought through the opening, and the part of the intestine that’s seen on the abdomen’s surface is called a stoma.  

The stoma is connected to a pouching system, also called an appliance, that’s composed of a skin barrier or adhesive wafer that attaches to the skin, and a pouch where stool and flatus collect. These ostomies can be permanent or temporary and can be necessary because of conditions like an intestinal tumor, bowel trauma, or inflammatory bowel disease; or to allow the bowel to rest and heal after surgery. 

Now, an ostomy can be either an ileostomy or a colostomy depending on its location within the intestines. An ileostomy involves part of the small intestine, called the ileum; whereas a colostomy involves the part of the large intestine, or colon.  

Keep in mind that normally, in the small intestine, the stool is mostly liquid because the majority of water is normally reabsorbed in the large intestine.  

So, with an ileostomy, the stool is usually semi-liquid, and it flows at a fairly constant rate.  

On the other hand, with a colostomy, the stool will have a different consistency depending on its location within the colon. So, if the colostomy is located near the beginning of the colon, like in the ascending colon, the stool is typically watery and loose; while if the colostomy is located near the end of the colon, like in the descending colon, the stool will be more solid. 

Okay, let’s move on and discuss the types of pouching systems. There are drainable, or open-ended pouches, which are sealed with a clip or Velcro-type system at the bottom so they can be drained and reused. Then there are closed-ended, or disposable pouches which can be removed and replaced when full. Additionally, some pouching systems have pre-cut skin barriers, so they come in different s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hygiene_-_Oral_care:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DRcedC-WT6C87CtR1R_eeYeYRHmHZoG9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hygiene - Oral care: Nursing skills]]></video:title><video:description><![CDATA[Now, oral hygiene is essential to prevent mouth infections and bad breath. Keeping the bacteria of the mouth under control is important to prevent certain health complications like soft tissue infections in the structures of the mouth, like abscess; tooth loss that can lead to problems with eating and nutrition; or even bacterial overgrowth that can lead to damage of the heart valves. To maintain proper oral hygiene, you have to remember three basic steps: brushing, flossing, and rinsing. The frequency of oral hygiene depends on the individual&amp;#39;s condition and comfort level, but it’s typically performed in the morning, after meals, and before bed. Clients who are unable to take food and fluids by mouth, like those who are unconscious, will require oral hygiene every 1 or 2 hours to keep their mouths fresh.

Before we continue, there are several important definitions that you should know. Halitosis refers to a chronic bad breath which can be the result of poor oral hygiene or an underlying health problem. Dental plaques are films of saliva and microbes that stick to the teeth and can lead to tartar which are crusty deposits. Dental caries, also known as tooth decay or cavities, is damage caused by acid-producing bacteria in the mouth. Stomatitis refers to any inflammation that affects mucous membranes of the mouth and lips. Next up is gingivitis which is non-destructive inflammation of the gingiva, or gums. If left untreated, gingivitis can lead to periodontitis which is a severe inflammation of the supporting structures of teeth, including soft tissue and bones. Moreover, in people over the age of 35, periodontitis is the main cause of tooth loss. If a person has lost a tooth, they can replace it with a prosthetic tooth which is also known as a dental implant. On the other hand, dentures are removable replacements of the missing teeth and surrounding tissue which allow people to chew food normally. When a person has no natural teeth left, it’s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hygiene_-_Urinary_catheter_care:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S9knRGpMQfCBhHUUlWyDdctyT0acqWfp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hygiene - Urinary catheter care: Nursing skills]]></video:title><video:description><![CDATA[A urinary catheter is a tube that goes into the bladder that drains urine. This is commonly used in a variety of situations, such as before, during, or after an operation, in order to keep the bladder empty. It’s also used to accurately measure the amount of urine produced by critically ill clients or clients receiving IV therapy, inclients with wounds or pressure ulcers that need to be protected from contact with urine, in clients with urinary obstruction or retention, or to collect sterile urine samples. Catheter care is essential for preventing catheter-associated urinary tract infections, called CAUTIs, because an indwelling catheter is a pathway for bacteria to move up from the perineum into the bladder. This is important because, during normal urination, the urine flow acts as a natural way to “flush” bacteria out of the urinary tract. 

Now, the most common types of urine catheters are straight, indwelling, and suprapubic catheters. Both straight and indwelling catheters are inserted into the bladder through the urethra, but the difference is that a straight catheter is removed once the urine is drained, while an indwelling urinary catheter, also called Foley catheter or retention catheter, remains in the bladder and lets the urine drain continuously into a drainage bag. With the suprapubic catheter, “supra-” means above and “pubic” refers to the pubic bone, so it is inserted into the bladder through a surgical incision made above the pubic bone. 

Let’s focus on the indwelling catheter. This consists of a soft balloon that is inflated inside the bladder to keep the catheter from slipping out and a length of tubing, which connects the catheter with a drainage bag for collecting urine. Indwelling catheters may have two or three lumens. In double-lumen indwelling catheters, one is for urine drainage and the other one is used to inflate the balloon. In triple-lumen indwelling catheters, the additional lumen is used to regularly deliver irrigation fluid]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immobility_-_Positioning_&amp;_alignment:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_C34D6p2Th2_gX8ItB5BBup7TVGtmSY7/_.png</video:thumbnail_loc><video:title><![CDATA[Immobility - Positioning and alignment: Nursing skills]]></video:title><video:description><![CDATA[A client’s position refers to how their body is situated. For a nurse, it’s important to know what position promotes comfort and recovery. Furthermore, a variety of special positions are needed for people with specific conditions, undergoing certain procedures, or doing certain activities. Nurses need to know these positions and when they’re used. In certain situations, you might need to position the client in a certain way to prepare for a procedure or to help them recover from one. You can also use positioning to help encourage client comfort or reduce pain.

Supine position, or the dorsal recumbent position, is where a person is lying on their back on a flat bed with a pillow under their head, and another pillow can be placed under the calves to prevent pressure injuries on the heels.Next is  Fowler’s position this is the same as the supine position, except the head of the bed is elevated. Fowler&amp;#39;s is 45-60 degrees; low Fowler’s, or semi Fowler’s, is 30-45 degrees; and high Fowler’s is 60-90 degrees. A pillow can be placed under the calves for support and comfort. The semi Fowler’s position is great if they want to watch TV or read. It’s also helpful if they have difficulty breathing in the supine position; if they have a feeding tube; or if they have gastroesophageal reflux disease, or GERD. The high Fowler’s is useful when the person is eating because it prevents choking. 

Let’s move on to the lateral position, where the client is lying on their side. The left lateral position is when the client’s lying on their left side, while right lateral is the opposite. A pillow can be placed behind the back and under the arm and leg that are on top. This position is great for people with back pains because the back isn’t pressed into the bed for long periods of time. It’s also preferred for people in body casts. So, a modified version of the lateral position is the Sims’ position, or lateral recumbent position. Here, they are on their side, but rotate]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mobility_-_Ambulation:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7fDlyuwxQDma8WX_9esX_27aSmGF9r-o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mobility - Ambulation: Nursing skills]]></video:title><video:description><![CDATA[Ambulation means “walking,” and your client might need to ambulate to get to places or may need to do it to prevent atrophy, which is when muscles waste away from prolonged bed rest.

Other health problems from long-term immobility include decreased cardiovascular and pulmonary functions, poor digestion, pressure injuries, contractures, urinary problems, and many others. So, even if they require assistance, clients are encouraged to ambulate frequently.

Before we talk about ambulation assistance, here are some general considerations. Start by checking the client’s chart for information on their most recent ambulation. This will let you know if the client tolerated the activity, if they had any difficulty, if an assistive device like a walker or cane was needed, or if they have a history of falls. 

It can also be helpful to review the client’s medication list to see if they are taking medications that might make them a higher risk for falls, like pain medications which can cause lethargy or blood pressure reducing medications which can cause dizziness. 

Next explain to the client how far you’ll be walking and how you will assist them.  If an ambulatory device is needed, check to see if it’s functional. Make sure the route is not slippery and that there are no obstacles. Make sure IV lines and poles are free from tangles and that the IV pump is unplugged from the wall and has enough battery to last during ambulation. Make sure they’re properly dressed and wearing non-skid footwear.

During ambulation, encourage them to walk normally without shuffling or sliding. You might need an additional assistant if the person’s unbalanced, weak, or not cooperative. Finally, and most importantly, be sure not to leave the client’s side at any time during the process.

Now, before getting a resting person to stand and walk, you need to get them into a sitting, or “dangling,” position, where they sit erect with their feet dangling off the side of the bed. The main reason]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mobility_-_Assistive_devices:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TSARItNlTvqZE14wVxHRqzBUTaCZUEPk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mobility - Assistive devices: Nursing skills]]></video:title><video:description><![CDATA[Assistive devices for ambulation, or just ambulation devices, are tools used to aid in walking.  The most common types include walkers, canes, and crutches. As the nurse, you need to know when each of these are appropriate and assess if the client is using them correctly. Remember that a client’s ambulation device is specially ordered and fits them specifically, kind of like glasses, so they should not be shared with other clients. Some devices like mechanical lift, are used by clients who aren’t able to ambulate independently and need assistance to move from one location to another. Nurses often use mechanical lifts to make sure the client is safe during transfer. Let’s start by looking at walkers. These are movable, lightweight devices that consist of a metal frame, 2 hand grips, and 4 legs. Walkers provide great stability due to their wide base, so they are great for people who can bear weight on their feet but have trouble walking due to weakness of the legs or balance issues. When assessing the proper fit of a client’s walker, make sure that the hand grips are at the client’s waist level. Check the legs because they should have non-slip tips like a rubber cover. 

To use a walker, the client should stand straight while holding the hand grips. When moving forward, they lift it up and move it another 6-10 inches in front of them and set it down. Because many clients have difficulty lifting a walker, many models now have wheels on the front legs. However, these are prone to rolling forward, so brakes are usually built in. So, when the client  is going to stand for a while, make sure the brakes are locked. Using the walker as support, they should move one leg forward and then the other. Once balance is reestablished, repeat the process. Next up, we have canes. These are also movable, lightweight devices made of a strong material like wood or metal. Canes consist of a handle, a shaft, and legs. There are single leg, triple leg or quad leg canes, and the on]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vital_signs_-_Pain:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UKfJSamYTomHiRgz9iQ2c8hPTNKlZzuj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vital signs - Pain: Nursing skills]]></video:title><video:description><![CDATA[Pain is a feeling of discomfort that ranges from mild to severe, usually caused by an underlying condition and is never normal. Acute pain is a sudden, usually severe pain that typically decreases over time once the underlying cause resolves. It can last from days to weeks and is often caused by some sort of tissue damage. This includes trauma, like burns, a sprained ankle, or broken bones; surgery; or diseases and conditions like appendicitis. Chronic pain lasts longer than a few months and is usually associated with headaches, back pain, arthritis, nerve pain, and many others. Pain can interfere with the client’s ability to function and their quality of life. Consequences of unresolved pain include depression, impaired sleep, concentration and memory problems, hypertension, sexual dysfunction, and many more. So it’s important that nurses  know how to recognize it. Many of your clients will feel pain, but it won’t be the same for everyone. Pain is an individualized sensation that depends on many factors. Each person has a different pain threshold, which is the point when they start noticing pain, and pain tolerance, which is the highest amount of pain they can handle. 

For example, if you pinch someone with a low pain threshold, they might immediately say it hurts, while someone with a high pain threshold will probably not report any pain at all. Now, the way someone handles pain is not just limited to pain threshold and tolerance. There are other factors to consider like anxiety, rest, energy level, hunger, culture, past experience with pain, and so on. Now, as a nurse, you might be the first to notice when a client is in pain. It is easy to notice when the client tells you they feel pain, but sometimes they won’t be able to tell you, or they might not want to. However, a client in pain will usually show some physical signs of pain that you should learn to recognize. These include irritability, restlessness, mood change, insomnia, clenching the jaw, fro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Healthcare_costs:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9sBLJSkbSmeDbpfeFZmM-PQoSV_lLVEp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Healthcare costs: Nursing]]></video:title><video:description><![CDATA[Nurse Irving is the charge nurse on a 24-hour observation unit where the majority of clients are admitted for chest pain. Then they go for a cardiac stress test, and are discharged if the test results are normal. During the unit huddle, Nurse Irving is informed that the hospital budget has become more limited due to price inflation, so every unit charge nurse is tasked with assessing ways to cut costs. After the huddle ends, Nurse Jade approaches Nurse Irving and says, “We waste so much money on broken equipment here.” Nurse Irving asks Nurse Jade what she means and she continues, “Just last week another portable heart monitor broke because it accidentally got sent down in the hospital laundry.” Nurse Irving realizes that these portable heart monitors cost thousands of dollars and says, “You’re right, we need to address this. Let&amp;#39;s create a plan to preserve these heart monitors.” Nurse Jade agrees to help Nurse Irving and speaks to the rest of the staff about possible solutions. Nurse Irving and Nurse Jade will use what they know about healthcare costs to provide quality client care in a cost-effective way.  

Healthcare costs in the United States are increasing every day; in fact, Americans spend over 3 trillion dollars on healthcare per year! But, increased spending of healthcare dollars hasn’t always translated into better health outcomes, such as average life expectancy. Healthcare facilities are tasked with improving health outcomes and delivering quality care in the most cost-effective way. Indicators of quality of care such as safety and client satisfaction scores directly influence how healthcare facilities are reimbursed. For example, increased rates of hospital acquired infections or hospital readmissions after discharge can decrease reimbursement.

 On the other hand, healthcare facilities that consistently demonstrate positive quality indicators are reimbursed accordingly. Now, within the healthcare environment there are healthcare con]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cognitive_load</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EaL2n9B2Sh2fZ9g7xhw_BOvdSkWMr3Dr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cognitive load]]></video:title><video:description><![CDATA[What is cognitive load theory? You probably know that learning takes effort, and this effort can feel like a load, cognitively. Sometimes the cognitive load isn’t very much at all and learning feels easy. Sometimes the task is too hard, and you have cognitive overload. Ideally there’s a perfect match between what you&amp;#39;re trying to learn and the cognitive load you can handle. Cognitive load theory starts with the idea that working memory is a bottleneck between new information processed by your sensory memory and knowledge that’s stored in your long term memory. Your senses are always taking in large amounts of information from the environment, like ambient sounds or the temperature, but you ignore most of it. The information you pay attention to gets filtered into your working memory. The working memory has limited capacity. Here, information can be manipulated and managed and then either lost and forgotten or stored in the long term memory which is more stable and has no known limits. Once information is in long term memory, it can be transferred to make decisions and solve problems in real life situations. 

Cognitive load theory is a living theory that is being adjusted based on new studies. 
Since the working memory has limited capacity, the amount of information it’s processing can be considered the “cognitive load.” Currently, there are two kinds of cognitive load: intrinsic and extraneous. 

Intrinsic load is the load related to the learning task, like the topic of a lecture, or the skill you’re supposed to practice. It’s the “good” load that’s intended and expected to be there. So, for example, if the task is to learn to identify arm muscles, the intrinsic load may involve the name and location of each muscle. 

Extraneous load is the load not related to the learning task. This can be irrelevant sounds and images from the environment like distracting buzzing from a mobile device or from the instructional content itself containing unnec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chest_X-ray_interpretation:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HBiZLEb8SaeEYoe7bAStKnwKQx2Ky3ul/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chest X-ray interpretation: Clinical sciences]]></video:title><video:description><![CDATA[Chest radiograph, or chest X-ray, is one of the most commonly performed imaging studies, and can provide a large amount of useful information. So understanding how to approach and interpret a chest X-ray is an incredibly important clinical skill.

So the most common indications for a chest X-ray include chest pain, shortness of breath, or cough. It is also often used as a part of trauma and preoperative evaluation, and after placement of monitoring and support devices. 

While there are no absolute contraindications for a chest X-ray, and the radiation dose is small, you do want to ensure it is truly necessary, especially if your patient is pregnant.

Now, let’s discuss a systematic approach to interpreting a chest X-ray. This is going to involve checking the patient and study details, then assessing the quality of the study. Next, you want to scan the chest X-ray systematically and completely. You are looking to identify any abnormalities. Finally, you want to get a radiologist’s review of the film. Let’s go through each of these steps in more detail.

The first step in interpreting a chest X-ray is to check the name and date of birth on the image to confirm it’s the right patient, and the date and time to confirm it’s the right study.

Once you’ve done that, you are going to assess the quality of the chest X-ray. You’ll look at six main factors: projection, orientation, rotation, angulation, penetration, and inspiration. Remember, a good quality image gives you a lot of information, and a bad quality image could cause you to misinterpret findings. 

Begin with projection. Look to see how the film was taken. Is it a PA, or posterior to anterior, AP, or anterior to posterior, or a lateral study? The standard chest x-ray is PA. However, AP films are often seen when the patient needs a portable machine, like when they’re bedbound. Lateral films can be obtained with both.

Next, look at the orientation of the chest X-ray. Check the left and right markings. Yo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_chest_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fWOJ27YhTZCjlyyIQeTv90ksTiOmd01v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to chest pain: Clinical sciences]]></video:title><video:description><![CDATA[Chest pain is a common chief complaint, with a broad differential diagnosis that includes some potentially life-threatening causes. So your workup needs to focus on ruling out these dangerous causes before considering more benign ones. 

Let’s take a look at this approach. 

Your first step in evaluating a patient presenting with chest pain is to systematically assess their ABCDEs, which stands for airway, breathing, circulation, then disability and exposure. This helps you judge if the patient is stable or unstable, so you can treat any issues at each step. Your patient may, for example, require endotracheal intubation.  
 In an unstable patient, your priority is to stabilize their airway, breathing, and circulation. Once they are stabilized, your next step is to evaluate for life-threatening causes of chest pain, such as ST-elevation myocardial infarction or STEMI for short, cardiac tamponade, aortic dissection, pulmonary embolism, or tension pneumothorax. And remember, even if your patient is stable, it does not rule out these life-threatening conditions. 
  So what do you do in the case of a stable patient presenting with chest pain?  

Your evaluation begins with a focused history and physical examination, or H&amp;amp;P, alongside an electrocardiogram, or ECG. That ECG needs to be performed and interpreted promptly! You’re going to use it to evaluate the patient for some life-threatening conditions.  

At the same time, if you suspect the patient has a critical illness or might become unstable, acute management will be required. First, place them on continuous cardiac monitoring with pulse oximetry and establish IV access. If they are hypoxemic, you should also provide supplemental oxygen. 

Okay, now that you’ve done the history and physical, the ECG, and acute management, it’s time to check for the acute coronary syndrome or ACS.  

The first condition to look for is an ST-elevation myocardial infarction, or STEMI.    In an ECG, look for localized]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_coronary_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3KKeNtEpSWaPX5ronzdW6EXuTFaQoY0F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute coronary syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Acute coronary syndrome, or ACS, is one of the can’t-miss-diagnoses that must be ruled out when a patient presents with acute chest pain. ACS is caused by sudden decreased coronary blood flow, also known as cardiac ischemia. The three types are ST-elevation myocardial infarction or STEMI, non-ST-elevation myocardial infarction or NSTEMI, and unstable angina, where the latter two are collectively referred to as non-ST-elevation or NSTE-ACS. STEMI results from complete acute blockage of a coronary artery, leading to transmural infarct of the myocardial wall supplied by that artery. NSTEMI results from a supply and demand mismatch, leading to non-transmural subendocardial infarct. Lastly, unstable angina also results from a supply and demand mismatch, leading to myocardial ischemia, but hasn’t yet caused infarction.

The first step in approaching a patient with chest pain is to do an initial assessment with a focused history and physical examination, or H&amp;amp;P, along with a 12-lead ECG. Prompt ECG should be obtained within 10 minutes of hospital arrival and shouldn’t be delayed by H&amp;amp;P. When chest pain is due to cardiac ischemia, it usually worsens with exertion, is not relieved with rest, and doesn’t change with body positioning. Some patients may complain of chest discomfort, pressure, tightness, or burning-like sensation, as well as palpitations, dyspnea, diaphoresis, nausea and vomiting, dizziness, and syncope. Ischemic chest pain often radiates to other parts of the body, including the epigastrium, left shoulder and arm, neck, and lower jaw. Relevant medical history in patients with chest pain includes hypertension, dyslipidemia, diabetes, tobacco use, and a family history of myocardial infarctions.

Physical examination findings in patients with ACS can be variable, since proximal blockages in large vessels result in more myocardial damage than distal blockages in smaller branches. If a large myocardial area is affected, it can lead t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutrition_-_Newborn:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aiO_f3MHT1C12jZeorcSblXuQKOU4e7C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutrition - Newborn: Nursing]]></video:title><video:description><![CDATA[The newborn’s diet must supply the calories and nutrients, including carbohydrates, proteins, fats, vitamins, and minerals needed to support the rapid growth and development that occurs in early life. During the first few months of life, newborn nutritional needs can be met by either breast milk or iron-fortified infant formula.

Alright, let&amp;#39;s look at the composition of breast milk, which differs with each of the three phases of milk production, also known as lactogenesis. Phase I of lactogenesis starts during pregnancy and continues throughout the first few days postpartum. During this phase, the breasts produce an early version of breast milk called colostrum which is a thick yellowish fluid that is high in protein, vitamins, minerals, immune cells, and immunoglobulins like IgA, which protects the infant’s gastrointestinal tract from infections and aids in establishing normal flora. Colostrum is low in fat and carbohydrates, so it has few calories. Colostrum also has a laxative effect, which promotes the passage of the infant’s first bowel movement called meconium, which helps prevent hyperbilirubinemia. Colostrum meets all the nutritional needs for the newborn during the first few days of life.

Now, Phase II of lactogenesis starts two to three days postpartum. The milk produced during this phase is called transitional milk. Compared to colostrum it contains less immunoglobulins and proteins, but has more vitamins, fats, and carbohydrates, so it’s higher in calories.

The last phase of lactogenesis is Phase III, during which mature milk is produced. Mature milk is present by 10 days to 2 weeks postpartum, and contains nutrients that are sufficient for appropriate infant growth. These include proteins, carbohydrates, and fats, as well as vitamins, minerals, and enzymes, like lysozyme, which has antibacterial properties.  

Now, the nutritional content of mature breast milk will vary during the course of the feeding session. So, foremilk, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_history:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lzGKdGVsSDizhzC27iuONX6-RFKOlYTr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health history: Nursing]]></video:title><video:description><![CDATA[Collecting a client’s health history provides the nurse with information about their perceived health and factors that can impact their health. It should be completed as part of a comprehensive client assessment, like upon admission to the hospital, during a medical office visit, or as part of a focused exam. Typically, the health history includes subjective data, or information the client is experiencing, such as when a client states, “I become nauseous after most meals.” This can guide the nurse to focus the physical assessment on the gastrointestinal system, as well as client education and the plan of care. Although the client is the preferred source of subjective data, if they’re unable to communicate a secondary data source can be used, such as a family member or caretaker. In addition, if the client doesn’t speak the same language as the nurse, an institutionally-approved medical interpreter should be used. Okay, let’s review how to conduct a health history. 

Now, you’ll want to collect your client’s health history in a private, quiet, and comfortable setting free from environmental distractions or interruptions. Also remember that as the nurse, you are responsible for collecting and documenting your client’s health history. And since it involves assessment and nursing judgment, the health history shouldn’t be delegated to another member of the healthcare team, like unlicensed assistive personnel. Begin by establishing rapport with your client. You can do this by introducing yourself, including your name and role, and asking them how they would like to be addressed or if they have a preferred nickname. If there is someone accompanying your client, ask their name and relationship to your client. As you collect data, remember to look at them, and avoid focusing your attention on the electronic health record, or EHR. This will help avoid the impression that you’re not listening to them or that you are rushed. With each question, allow them the time the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Overview:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4EIRGZgUQZCTs4ybyVWId2ETSfKA3nom/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Overview: Nursing]]></video:title><video:description><![CDATA[A physical assessment is an important nursing skill that is used to collect objective data about a client’s status by using the senses, like seeing a rash or hearing wheezes in the lungs. A physical assessment can also validate subjective information gathered from a health history, such as a client’s report of pain or dizziness. Additionally, assessment is the first step in the nursing process, which can be used to develop a plan of care or to evaluate the effectiveness of an intervention. Let’s review the process of completing a physical assessment.

Now, the two most common types of assessments you’ll do as a nurse are a comprehensive assessment and a focused assessment. A comprehensive assessment, sometimes referred to as a head-to-toe assessment, includes all body systems, and is usually performed during a general wellness visit or when a client is admitted to the hospital or other facility. This approach is most useful when you want to collect information about your client’s general health status. 

On the other hand, a focused assessment depends on the situation, and is often based on a client’s presenting symptoms. For example, if your client has abdominal pain, you’ll focus most of your assessment on their gastrointestinal system. Likewise, if your client is having difficulty breathing, a focused assessment would include their respiratory system as well as skin, vital signs, and level of consciousness. A focused assessment may also be needed if you are administering certain medications; for example, when you’re administering a cardiotonic medication, you’ll focus your assessment on your client’s heart rate and blood pressure. 

Okay, there are a few things to consider before performing a physical assessment. 
First, check to see if your client requires any precautions in addition to standard precautions such as transmission-based precautions, and don the appropriate personal protective equipment, or PPE. 
Then, explain the procedure to your client ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Comprehensive:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wo9-QbpqRLuoerew_h8kOUfrQEuhmwOm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Comprehensive: Nursing]]></video:title><video:description><![CDATA[A comprehensive assessment provides information on the overall status of a client’s health in addition to providing data about each individual body system. This type of assessment is useful when identifying priorities for client care or evaluating how an illness or condition is affecting the whole person. For example, chronic obstructive pulmonary disease, or COPD, commonly affects the lungs, but can also cause changes to the nails, extremities, and chest wall; so a comprehensive assessment will ensure you can avoid missing important assessment data from other body systems. Now, let’s review the process of completing a comprehensive assessment. 

Okay, the supplies you’ll need include a stethoscope, penlight, tongue depressor, an otoscope, drapes, and gloves. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands and stethoscope are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Methods of assessment for the comprehensive assessment include inspection, percussion,  palpation, and auscultation.

One of the most important things to remember when performing a comprehensive assessment is to use an organized approach so you don’t accidentally exclude a body system. One way you can organize your assessment is to perform what’s called a head to toe assessment, starting with the head and then systematically moving down the body all the way to the toes. Another technique is to prioritize the assessment of a body system that is potentially related to your client’s symptoms, like assessing the cardiovascular system first for a client with valvular disease, before]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Heart_&amp;_neck_vessels:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S20CcHWDTWSp2zMPAupYnLqiRzm0bMyx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Heart and neck vessels: Nursing]]></video:title><video:description><![CDATA[Assessment of the heart and neck vessels should be completed as part of a comprehensive client assessment or as part of a focused exam if the client is experiencing issues that might be related to the function of the heart, like chest pain or shortness of breath. Let’s review the process of completing an assessment of the heart and neck vessels.

Okay, the supplies you’ll need for your assessment include a stethoscope with a diaphragm and bell, gloves, and a good source of light. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands and stethoscope are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Before getting started, explain the procedure to the client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies. 

Now, locating the anatomical landmarks of the heart and neck vessels will guide placement of your hands and equipment. The neck is located between the clavicles and sternum and the base of the skull. It is supported by the cervical vertebrae, ligaments, as well as the sternocleidomastoid and trapezius muscles.

The carotid arteries are located on either side of the neck, behind the sternocleidomastoid muscle. The heart is positioned behind the sternum in the chest cavity, and is about the size of a clenched fist. When the client is upright, the top of the heart is called the base and the bottom of the heart is called the apex. The point where the apex reaches its farthest both laterally and inferiorly is called the point of maximal intensity, or PMI. The PMI usually rests at the midclavicular line at the 5th or 6th intercostal space.

Methods of assessment for the heart and neck vessels include inspection, palpation, and auscultation. Since this exam]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Peripheral_vascular_system:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OeUZR-5SSlu70yo8e75Ls71AQiSrExsV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Peripheral vascular system: Nursing]]></video:title><video:description><![CDATA[Assessment of the peripheral vascular system should be completed as part of a comprehensive client assessment, or as part of a focused exam if the client is experiencing issues that might be related to the function of the peripheral vascular system, like arterial or venous ulcers.  Let’s review the process of completing an assessment of the peripheral vascular system.

Okay, the supplies you’ll need for your assessment include a stethoscope with a diaphragm and bell, a skin marker, a doppler ultrasound device, drapes, and a good source of light. 

Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands and stethoscope are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Now, locating the anatomical landmarks of the peripheral vascular system will help guide your assessment.  Peripheral pulses that can be palpated include the carotid pulse, located on the neck behind the sternocleidomastoid muscle, or scm, just below the angle of the jaw; the brachial pulse, located in the center of the cubital fossa, medially to the biceps tendon; the radial pulse, found in the wrist along the lateral aspect of the forearm, just below the base of the thumb; the femoral pulse, located below the inguinal ligament, between the pubic and hip bones; the popliteal pulse, located behind the knees; the dorsalis pedis pulse, found on the dorsal aspect of the foot; and the posterior tibial pulse, located just behind the medial malleolus. 

Alright, methods of assessment for the peripheral vascular system include inspection, palpation, and auscultation. 

Let’s start with ins]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Thorax_&amp;_lungs:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eTmJxcPIQFqwWbx04CAf3CqQTTi9nRij/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Thorax and lungs: Nursing]]></video:title><video:description><![CDATA[Assessment of the thorax and lungs should be completed as part of a comprehensive assessment, like during a routine physical exam, or as part of a focused exam if a client is experiencing respiratory issues like shortness of breath, cough, or chest discomfort.  Examination of the thorax and lungs gives the nurse information about the movement of air and gas exchange. Let’s review the process of completing thorax and lung assessment.

Okay, the supplies you’ll need for your assessment include a stethoscope, a washable pen or marker, a centimeter ruler, tape, drapes, and a good source of light. 

Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands and stethoscope are warm,  and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Now, locating the anatomical landmarks of the thorax and chest will help guide the appropriate placement of your equipment and hands throughout your assessment. The thorax can be divided into the anterior chest and posterior chest. Commonly used anterior landmarks include the sternum, clavicles, manubrium, xiphoid process, the ribs and intercostal spaces, and trachea, as well as the costal angle, which is made up of the the costal margins just below the xiphoid process. The chest can be further divided into sections using the midsternal line, a vertical line that runs down the middle of the sternum; and the right and left midclavicular lines, which are parallel to the midsternal line and run from the middle of each clavicle to around the 6th intercostal space. Posteriorly, the landmarks include the scapulae and thoracic spine. Thes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Neurological_system:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NCB2u_uSQ1_QYhTIiFBRcLciSI6whJUI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Neurological system: Nursing]]></video:title><video:description><![CDATA[Assessment of the neurological system should be completed as part of a comprehensive client assessment, or as part of a focused exam if the client is experiencing issues that might be related to neurological function, like a facial droop or confusion. Now, let’s review the process of completing a neurological assessment. 

Okay, the supplies you’ll need include a cotton ball; a tuning fork; an object that can be easily recognized by touch like a paper clip, key, or coin; a reflex hammer; a tongue blade; drapes, and gloves. 

Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

While much of the neurological system assessment involves observation, you will need to locate the deep tendon reflexes to assess spinal cord intactness. Commonly tested deep tendon reflexes include the triceps, biceps, brachioradialis, patellar reflexes, and achilles reflexes. 

Alright, the methods of assessment for the neurological system include inspection and palpation. Your assessment will evaluate your client’s cerebellar function, which includes the client’s balance and coordination; sensory function, which includes their ability to feel and differentiate between light touch and pain; and motor function, which includes deep tendon reflexes. 

Okay, begin your assessment of cerebellar function by observing your client’s gait, or how they walk. You can take the opportunity to do this as they enter the examination room or, if they are seated or in a bed, you can ask them to stand and walk across the room. While they ambu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Mental_status:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xtdq_6QPRu6COOCFilOR_obFQauvXL-v/_.png</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Mental status: Nursing]]></video:title><video:description><![CDATA[Mental status should be completed as part of a comprehensive assessment, or as part of a focused exam if a client is experiencing issues like confusion or memory loss. The mental status assessment provides the nurse with information about cognitive and emotional functioning. Let’s review the process of completing a mental status assessment.

Okay, so generally, you’ll need paper, pencil, and a copy of the mental status test you plan to administer. Then, prepare for the exam by ensuring your client is in a comfortable position, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies. The method of assessment for a mental status exam is inspection.

First, let’s begin with appearance, which can be observed when your client moves into the exam room. When evaluating appearance, expect their posture to be erect and relaxed; and their movement should be smooth and purposeful. If your client appears restless or fidgety, this could be a sign of anxiety. Other unexpected findings include tics, which are sudden, repetitive movements like eye blinking or throat clearing; and tremors, which are rhythmic shaking movements. 

Then, observe your client’s grooming. Expected findings include good hygiene, appropriate dress for the client’s age, season, and weather; and there should be no obvious hygiene issues such as body or breath odor. Inappropriate dress or evidence of poor hygiene might indicate conditions like depression or cognitive disturbances like dementia.

Next, assess your client’s behavior, beginning with their level of consciousness. Your client should be awake, alert, oriented, and responsive to both internal to environmental stimuli. Unexpected findings include lethargy or drowsiness; or being obtunded, meaning y]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Cranial_nerves:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dEJFYRE4Rhuk8NuYAzubQeKLTMWs2hil/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Cranial nerves: Nursing]]></video:title><video:description><![CDATA[Assessment of the cranial nerves should be completed as part of a comprehensive assessment, like during a routine physical exam, or as part of a focused exam if a client is experiencing neurological issues like a drooping eyelid or trouble swallowing. Examination of the 12 pairs of cranial nerves provides information about the client’s sensory and motor function of the head, neck, and torso.  Let’s review the process of completing a cranial nerve assessment.

Okay, the supplies you’ll need for your assessment include a penlight; a sample of an odor that is easily identified like an alcohol pad, peppermint, or coffee; a cotton ball; a cotton swab;  sweet, sour, salty, and bitter taste solutions, a Snellen eye chart, a tongue blade, and gloves. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains.

 Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Methods of assessment for cranial nerve evaluation include inspection, mainly watching to see if the client is able to perform the requested tasks, and palpation.

Okay, let’s start  with cranial nerve I, the olfactory nerve. You can test the function of this nerve by asking your client to close their eyes, occluding one of the nares, and holding the sample about 6 inches from the open nare, and asking them to identify the odor. Repeat with the opposite nare. They should be able to correctly identify the odor. Clients who cannot identify the odor might have a partial or complete loss of smell, known as anosmia. 

Next is cranial nerve II, also known as the optic nerve, which is responsible for visual acuity, or how your client can see. If you are using a wall-mounted Snellen chart,  position your client 20 feet o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Abdomen:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A3vLEMsZS1GiGT2ao3_EDaksTwGki0nU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Abdomen: Nursing]]></video:title><video:description><![CDATA[An assessment of the abdomen should be completed as part of a comprehensive assessment, like during a routine physical exam, during an admission to the hospital, or as part of a focused exam if a client is experiencing abdominal issues like pain, nausea, or changes to bowel patterns. Let’s review the process of completing an abdominal assessment.

Supplies needed for the abdominal assessment include drapes, a stethoscope with a diaphragm and bell, gloves, a measuring tape, a washable skin marker, and a good source of light. 

Before beginning, ask your client to empty their bladder. 
Then prepare for the abdominal assessment by properly draping your client. Remember to keep your client covered and only expose areas of their body as needed to perform your assessment. 

Also, ensure privacy by closing any curtains or closing the door. 
Ensure your client is comfortable in the supine position, meaning they are lying flat on their back. You may also place a pillow under their knees to help relax their abdominal muscles.  Also warm your hands and stethoscope and ensure your client is comfortable with the temperature of the room, since cold temperatures can cause rigidity of the abdominal muscles, making it more difficult to perform some assessment techniques. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. 
Then, perform hand hygiene and collect your supplies. 

Locating the anatomical landmarks of the abdomen will help guide the appropriate placement of your equipment and hands throughout your assessment. Commonly used landmarks include the xiphoid process, costal margin, umbilicus, iliac crest, and the pubic crest. The abdomen can also be separated into four quadrants, to help you locate the abdominal organs. 

First is the right upper quadrant, called the RUQ for short, which contains the liver, gallbladder, and right colic flexure.Next, the left upper quadran]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Anus,_rectum,_&amp;_prostate:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pJs9KXt7T62r7XQaeMcCsLoYQzGwwwJp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Anus, rectum, and prostate: Nursing]]></video:title><video:description><![CDATA[Assessment of the anus and rectum should be completed as part of a comprehensive assessment like during a routine physical exam, or as part of a focused exam if a client is experiencing issues like rectal pain or changes to bowel patterns. For clients with a prostate, a prostate assessment provides the nurse with information about sexual health and genitourinary function. Let’s review the process of completing an assessment of the anus, rectum and prostate.

Okay, the supplies needed for this examination include a penlight, water soluble lubricant, drapes, gloves, a good source of light, and fecal occult blood testing material, as needed. 

Now, this exam can be uncomfortable, both physically and emotionally, or even embarrassing for some clients; 

which is why it’s important to explain every step in order to promote trust and relaxation. 

You should also let your client know that at any time the exam can be stopped or paused if they request. 

For clients with a known history of sexual abuse or trauma, remember not rush your examination, and use a gentle touch. 

You can assist your client into one of three positions for this examination: lying on their back with their knees to their chest, also known as lithotomy, 
lying on the left side with their hips and knees flexed, or standing and leaning over the examination table. 

In clients assigned male at birth, the last two positions work best for the anus, rectum, and prostate assessment, whereas with those assigned female at birth, anal and rectal examination is usually performed during a female reproductive exam while they’re already in the lithotomy position. 
It’s important to note that transgender clients should be examined in the position best suited for their preferance and identified gender. 

Prepare for the exam by ensuring your client is in a comfortable position. For all clients, it’s recommended to let them know you’re starting the examination by touching them in a neutral location, such as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Musculoskeletal_system:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O5uyADptR4eVKqIhVWYwyFOGRdOSA5qs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Musculoskeletal system: Nursing]]></video:title><video:description><![CDATA[Assessment of the musculoskeletal system should be completed as part of a comprehensive assessment, like during a routine physical exam, or as part of a focused exam if a client is experiencing musculoskeletal pain or has sustained an injury. Examination of the musculoskeletal system gives the nurse information about the mobility and stability necessary for physical movement. Let’s review the process of completing a musculoskeletal system assessment.

Okay, the supplies you’ll need for your assessment include a goniometer, scoliometer, a tape measure, and a good source of light. Prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination.

Remember to position your client to ensure they’re safe and stable, and adapt positioning to address any current injury or complaints. Assess for a history of unilateral weakness, stroke, or mobility issues, and plan to have an assistant in the room if your client has joint instability or is at risk for falling. Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Now, locating the anatomical landmarks of the musculoskeletal system will help guide the appropriate placement of your equipment and hands throughout your assessment. As you assess the various structures of the musculoskeletal system, you should move systematically, starting from the head and neck, and moving down to the feet and ankles, locating specific landmarks for each area. So, when you’re assessing the temporomandibular area, important landmarks include the tragus of each ear, whereas the landmarks of the hips are the iliac crests and greater trochanters. 

The me]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Lymphatic_system:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ERU3r-YLQXaL5zmHyBoqbuDRTh6_BTKX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Lymphatic system: Nursing]]></video:title><video:description><![CDATA[Assessment of the lymphatic system should be completed as part of a comprehensive assessment, like during a routine physical exam, or as part of a focused exam if a client is experiencing issues such as lymphadenopathy, or enlarged lymph nodes. The lymphatic system provides the nurse with information about the integrity of the immune system, as well as the body’s ability to regulate fluid and remove waste. Let’s review the process of completing a lymphatic system assessment. 

Okay, the supplies you’ll need to assess the lymphatic system include a tongue depressor, pen light, and washable marker or pen. 

Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Before getting started, explain the procedure to your client and be sure to answer any questions they have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies. 

Locating the anatomical landmarks of the lymphatic system will help guide the placement of your equipment and hands throughout your assessment. To find the  palpable lymph nodes in the head and neck region, start at the base of the skull to locate the occipital nodes. Then, move over the mastoid process to find the postauricular nodes, and then to the front of the ear to find the preauricular nodes. 

Next, the parotid and tonsillar nodes are accessible at the angles of the mandible; the submandibular nodes are halfway between the tip and angle of the mandible; and the submental nodes are just behind the tip of the mandible. 

Moving down the neck, locate the cervical nodes around the sternocleidomastoid muscle; the posterior cervical nodes along the anterior border of the trapezius muscle; and then move to the supraclavicular areas, which are in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Skin,_hair,_&amp;_nails:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/id-KyPkXSP24fh42yA0sXGI3SSC7xKzq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Skin, hair, and nails: Nursing]]></video:title><video:description><![CDATA[Assessment of the skin, hair, and nails should be completed as part of a comprehensive client assessment or as a part of a focused exam when a client is experiencing issues that affect the integumentary system, such as hair loss or skin irritation. Let’s review the process of completing an assessment of the skin, hair, and nails.

Okay, the supplies you’ll need for your assessment include a flexible ruler, penlight, a magnifying lens or dermatoscope, and a good source of light. 

Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands and stethoscope are warm,  and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

There are no specific landmarks for skin and hair, but the nails do have landmarks such as the nail plate or body, lunula, cuticles, the lateral folds and the proximal nail fold. Locating the anatomical landmarks of the nails will help guide your assessment. The methods of skin, hair and nails assessment include inspection and palpation.

Alright, first, you should start with a general inspection of the skin, which should be intact and have a uniformity of color without areas of discoloration or the presence of lesions. Be sure to also check any area that is not commonly visible, such as the axillae, perineum, and between the toes. 

During your inspection, note the thickness of the skin, which will vary depending on the body area. For example, calluses can appear on hands and feet due to frequent use, whereas the skin of the eyelids will be thin and delicate. 

Also note your client’s skin color, which normally ranges from various shades of black, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Nose,_mouth,_&amp;_throat:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ETQX8CCRRYqzlcrCqLkXsCC_R5WSBC0Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Nose, mouth, and throat: Nursing]]></video:title><video:description><![CDATA[Assessment of the nose, mouth, and throat should be completed as part of a comprehensive client assessment, or as part of a focused exam if the client is experiencing issues such as loss of smell, dental pain, or dysphagia. Examination of the nose, mouth, and throat provides the nurse with information about the integrity of these structures as well as the client’s ability to smell, taste, and swallow. Assessment of the nose, mouth, and throat can also help the nurse to identify any problems with the respiratory and digestive tracts. Let’s review the process of completing a nose, mouth, and throat assessment.

Okay, the supplies you’ll need for the nose, mouth, and throat assessment include a nasal speculum, tongue depressor, gauze, gloves, a penlight, and a good source of light. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the room is a comfortable temperature. Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Now, locating the anatomical landmarks of the nose, mouth, and throat will help guide your assessment. The landmarks of the external nose include the nasal bridge, nares, and the columella, which is the anterior tissue that covers the external part of the nasal septum. The landmarks of the nasal cavity include the nasal septum which divides the nose into two cavities called the vestibules, and the turbinates, which are bony structures that form the internal nasal walls. 

The maxillary sinuses are located on either side of the nose within the maxillary bone, while the frontal sinuses are within the frontal bone on the lower part of the forehead. 
The landmarks of the mouth include the lips, teeth, gingiva or gums, tongue, and the hard and soft palates; whereas the landmarks of the throat include the tonsillar pillars, posterior phar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Ears:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xwoKhAGBScuikdC7CUJNdC_JRjCFQM0B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Ears: Nursing]]></video:title><video:description><![CDATA[Assessment of the ears should be completed as part of a comprehensive client assessment, or as part of a focused exam if the client is experiencing issues such as ear pain or hearing loss. This assessment gives the nurse information about hearing and equilibrium while helping to identify ear problems, such as otitis media. Let’s review the process of completing an ear assessment.

Okay, the supplies you’ll need for the ear assessment include an otoscope, a penlight, gloves, and a good source of light. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Also remember to provide privacy by closing the door and curtains. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Now, locating the anatomical landmarks of the ears and surrounding tissue will help guide your assessment. The ear is divided into three sections: the external ear, middle ear, and the inner ear. Starting with the external ear, the landmarks include the auricle, also known as the pinna; the tragus; the lobule, or earlobe; the external auditory canal; and the mastoid process, which is the area directly behind the ear. Next, the middle ear contains the ossicles and the tympanic membrane which work together to transmit sound to the inner ear. 

Alright, the methods of ear assessment include inspection and palpation as well as special tests, including the whisper test and the Romberg test. 

First, you should inspect the external ear by viewing the auricles bilaterally, looking for size, shape, and symmetry. Also check that the skin on the auricles are the same color as their face. Be sure to inspect the position of the ears. Normally, the top of the auricle should align with the inner canthus of the eye. Clients with low-set ears may have a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Eyes:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CKze06VWTfiNf1KLQ-oApGUzSXmi1lKR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Eyes: Nursing]]></video:title><video:description><![CDATA[Assessment of the eyes should be completed as part of a comprehensive client assessment or as part of a focused exam when a client is experiencing ocular issues, such as eye pain or blurred vision. This assessment gives the nurse information about vision and general eye health while helping to identify ocular problems at an early stage, such as glaucoma or cataracts. Assessment of the eyes includes several tests which will examine the eye itself as well as screen for ocular diseases or systemic diseases that manifest through the eye, like diabetes or liver disease. Let’s review the process of completing an eye assessment.

Okay, the supplies you’ll need for the eye assessment include a Snellen or Sloan chart, a Rosenbaum or Jaeger near vision card, a penlight, and an eye cover. You should prepare for the eye exam by ensuring you have adequate light, and that your client is comfortable in either a standing or sitting position. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Now, locating the anatomical landmarks of the eyes and surrounding tissue will help guide your assessment. These landmarks include the upper eyelids and lower eyelids, eyebrows, the inner canthus and the outer canthus, pupil, lacrimal sac, conjunctival sac, and iris. 

Alright, the methods of ocular assessment include inspection and palpation as well as a series of visual tests.

First, you should inspect the external eyes and the surrounding structures, starting at the eyebrows and moving downward. Eyelashes and eyebrows should be evenly distributed. Eyelids should be able to close and open all the way, and upper eyelids should extend equally over both eyes. 

If an upper eyelid droops and partially covers the eye, ptosis is present, which may be due to neuromuscular weakness from conditions such as myasthenia gravis or damage to cran]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Female_reproductive_system:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3I0eZtjcQPmkewckapkJ3AeVTyWoXEix/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Female reproductive system: Nursing]]></video:title><video:description><![CDATA[Assessment of the female reproductive system should be completed as part of a comprehensive client assessment or as part of a focused exam if the client is experiencing issues, such as vaginal discharge or pain with intercourse. This assessment provides the nurse with information about the genitalia, as well as general sexual and reproductive health. This assessment applies to any client with female reproductive organs, regardless of their gender identity. 

Okay, the supplies needed for the female reproductive exam include drapes, gloves, and a good source of light. For certain parts of the exam, the nurse will assist the healthcare provider or act as a chaperone, which is often required by facilities to protect your client and clinician during female reproductive exams. 

Before getting started, ask your client to empty their bladder, because a full bladder can make the examination uncomfortable. Also, ensure the temperature in the room is comfortable, and warm your hands since cold temperatures can cause rigidity of the pelvic muscles. Remember to provide privacy by closing the door and curtains. 

Before getting started, be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies. Then, assist your client into the lithotomy position, meaning they are lying flat on their back with their feet in stirrups. You’ll help your client get into this position by sliding their buttocks to the end of the examination table and draping them in a way that minimizes unnecessary exposure. You should lay the drape above their knees, up to the symphysis pubis, and then let the drape hang low between the knees. 

During the examination, keep in mind that the female reproductive assessment can be uncomfortable, both physically and emotionally, so some special considerations should be made while completing this assessment. It’s crucial to explain exactly what will happen at every step. Furthermore, th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Male_reproductive_system:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qdue3L68TX2kfqXhKoFtFRNhRYC2LblD/_.png</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Male reproductive system: Nursing]]></video:title><video:description><![CDATA[Assessment of the male reproductive system should be completed as part of a comprehensive client assessment, like during a routine physical exam, or as part of a focused exam if the client is experiencing issues like testicular pain. This assessment provides the nurse with information about the client’s reproductive health. Now, let’s review the process of completing an assessment of the male reproductive system.

Okay, the supplies you’ll need include drapes, gloves, penlight, sterile swabs in the event a culture needs to be collected, and a good source of light. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Now, as the nurse, you may assist the healthcare provider or act as a chaperone, which is often required by facilities to protect clients and clinicians during exams of the reproductive system. During the examination, keep in mind that this process can be emotionally uncomfortable and anxiety-producing for some clients, particularly those who have experienced sexual trauma or who are transgender. Be sure to use the patient’s indicated pronouns and be aware of variations in the genitals for those who have had gender affirming surgeries. It’s also crucial to explain exactly what will happen at each step of the exam. Remember to avoid rushing your assessment, use a gentle touch, and to let your client know that at any time the exam can be stopped or paused if they request it.

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

During this assessment, you will locate the penis, which consists of the shaft, glans, and urethral meatus; s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutrition_-_Oral:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TTmZBTGOR8qDbFbNGMae0wOASF_Iz5vG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutrition - Oral: Nursing skills]]></video:title><video:description><![CDATA[As a nurse, you will need to prepare clients for their meals, serve them food, and depending on their needs, assist them in eating. Since clients can have different nutritional needs or might have issues with chewing or swallowing, the diet ordered for your client will be tailored to their specific needs. 

Now, before we talk about how to do these things, here are some general considerations. Always check that the name on the tray matches the identification card or bracelet of the client and that the meal served follows the nutritional guidelines for that particular client. Make sure to serve food as soon as it’s ready so that serving temperature is optimal. Try to create a friendly atmosphere, keep them company, and help them as much as they need, while encouraging them to participate as much as possible. 

Okay, so, when preparing a client for their meal, first gather the supplies you’ll need, including gloves, and paper towels. Next, assist the client with hand hygiene. Then, if they use eyeglasses, hearing aids, or dentures, check that those devices are properly positioned. Finally, check where they’ll be eating and make sure the room is free from disturbing sights, odors, or sounds. 

If available, the best location to eat for many clients is a community dining room, because it provides your clients with the opportunity to socialize. Whether in a dining room or a private room, position them in a chair or wheelchair so they’re upright; if they’re in bed, raise the head of the bed, so they’re as upright as possible. Clean and adjust the over-bed table to a suitable height. 

Some clients might also have dysphagia, meaning difficulty swallowing. This is often caused by nervous system conditions, like stroke or head trauma or tumors in the mouth or esophagus, blocking the passage of food. In these cases, the health care provider could order all liquids, like soup, to be thickened, making them less hard to swallow. 

To do that, start adding a thicke]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Care_of_an_intubated_client:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/a70rH1roRKa_fgKM0qPVtl0rTA6yx1Vk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Care of an intubated client: Nursing skills]]></video:title><video:description><![CDATA[Nurse Yasmine is receiving the nurse-to-nurse report on an elderly client named Earl who is being transferred from the emergency department to the intensive care unit, or ICU. The emergency department nurse explains, “Earl collapsed in his home following a cardiac arrest and was found unresponsive by a family member. After arriving at the emergency department, he was intubated and started on mechanical ventilation. He will be transferred to the ICU in about 10 minutes ” 

Nurse Yasmine notes that Earl is also receiving continuous IV sedation, and has a urinary catheter and a nasogastric tube. Nurse Yasmine will use what she knows about providing safe, effective, and quality care for an intubated client to promote positive client outcomes. 

Intubation is a procedure where an endotracheal tube, or ETT, is inserted through a client’s mouth and into their trachea, which is usually performed prior to surgery or during emergencies when the client’s airway is compromised, such as a cardiac arrest. The ETT keeps the airway patent in order for oxygen to reach the client’s lungs. 

After a client is intubated, the ETT tube can be attached to a mechanical ventilator to deliver oxygen and breaths to the client, which allows the client’s respiratory muscles to rest to promote healing and recovery. Mechanical ventilation can be used in the short-term, like during surgery, or more long-term, like with c respiratory failure or airway obstruction.   

Okay, so when a client undergoes intubation and is placed on mechanical ventilation, the client is at an increased risk of developing complications such as infection, airway trauma, pressure injury, deep vein thrombosis, and malnutrition. 

One of the main risks of mechanical ventilation is a particular type of infection called ventilator associated pneumonia, or VAP. This occurs when bacteria invade the lungs through the ETT.

Intubated clients can also develop barotrauma and ventilator-induced lung injuries, which occur wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arterial_blood_gas_(ABG)_-_Overview:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AvJ4IiAnQ_G_HqKMzlg9KJvsQ9_-WwRN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arterial blood gas (ABG) - Overview: Nursing]]></video:title><video:description><![CDATA[Arterial blood gas, or ABG for short, is a test used to measure the acid-base components and pressure of gasses in the arterial blood.  

Now, the components of an ABG are pH, bicarbonate, carbon dioxide, and oxygen. First, there’s pH which reflects the concentration of hydrogen ions, or H+, in the blood. 

There’s an inverse relationship between pH and H+, meaning that when there’s more H+, the pH decreases and becomes more acidic, and, when there’s less H+, the pH increases, and becomes less acidic. The normal pH ranges from 7.35 to 7.45. If the pH is less than 7.35, it&amp;#39;s considered acidosis; while a pH greater than 7.45 is alkalosis.

Then, there’s bicarbonate, HCO3-, which is a base: a substance that can combine with H+ and remove it from solution. When there’s more HCO3-, the pH increases and becomes more basic, and, when there’s less HCO3-, the pH decreases, and becomes more acidic. Normally, HCO3- ranges from 21 to 28 mEq/L.

Up next is the partial pressure of carbon dioxide, or PaCO2, which measures the amount of carbon dioxide dissolved in the arterial blood; and partial pressure of oxygen, or PaO2, which measures the amount of oxygen in the arterial blood. For these gasses, “P” stands for partial pressure and “a&amp;#39;&amp;#39; stands for arterial. The normal PaCO2 should range from 35 to 45mm Hg, and  PaO2 should range from 80 to 100mmHg.

Finally, there’s oxygen saturation or SaO2, which refers to the percentage of hemoglobin molecules in the blood that have oxygen attached to them. SaO2 should be 95% or more.

Now, when you think about it, acids are continually being produced by normal metabolic processes like cellular oxidation and the breakdown of nutrients, so the body needs a way to handle all these hydrogen ions to prevent major shifts in the overall pH. To accomplish this, the body has three lines of defense to help maintain an optimal pH: the cellular buffering system, the lungs, and the kidneys. 

The first line of defense]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arterial_blood_gas_(ABG)_-_Metabolic_acidosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jWtWETIMTF6bIk9-hTf19ZQ9RlWryyNj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arterial blood gas (ABG) - Metabolic acidosis: Nursing]]></video:title><video:description><![CDATA[A 55-year-old client with a history of type 1 diabetes mellitus is brought to the emergency department with a sudden onset of confusion. On assessment, her mucous membranes are dry; and she is tachycardic, hypotensive, and her respirations are deep and fast. The healthcare provider suspects metabolic acidosis secondary to diabetic ketoacidosis so, an arterial blood gas is ordered to assess for changes in acid-base balance.

So arterial blood gas, or ABG for short, is a test used to measure the acid-base components and pressure of gasses in the arterial blood. Normal ABG values for healthy adults are a pH ranging from 7.35 to 7.45, bicarbonate, or HCO3- ranging from 21 to 28 mEq/L; carbon dioxide or PaCO2 ranging from 35 to 45 mm Hg; PaO2 ranging from 80 to 100 mm Hg, and SaO2 should be more than 95%.

Okay, there are four major ways excess acid can accumulate in the body.  The first way is when there’s increased acid production, like with lactic acidosis, which is caused by decreased tissue perfusion and resulting anaerobic metabolism, or with diabetic ketoacidosis, which involves extreme hyperglycemia and an excessive breakdown of fatty acids in people with diabetes. It can also be caused by increased ingestion of acids, like methanol, salicylates, or ethylene or propylene glycol. 

Then there’s decreased elimination of acids, which can happen with renal failure; and finally increased elimination of base, like with excessive diarrhea, which eliminates too much HCO3- from the intestines.

You can easily remember causes of  metabolic acidosis by using the mnemonic MUDPILES, where M stands for methanol; U for uremia, which happens in renal failure; D for diabetic ketoacidosis, P for propylene glycol; I for iron tablets and isoniazid, which can cause acidosis with an overdose; L for lactic acidosis; E for ethylene glycol; and finally, S for salicylates. 

Now, as the pH continues to decrease and move out of the normal range, the body will attempt to corr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arterial_blood_gas_(ABG)_-_Respiratory_acidosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/igr_yX5VTKSp43E3SWRNppqOQkO_9t5m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arterial blood gas (ABG) - Respiratory acidosis: Nursing]]></video:title><video:description><![CDATA[A 75-year-old male client with a history of end-stage chronic obstructive pulmonary disease, or COPD, is brought to the emergency department with shortness of breath and disorientation. On assessment, he is tachypneic; cyanotic around his lips and earlobes; and respirations are rapid and shallow. The health care provider suspects respiratory acidosis secondary to end-stage COPD exacerbation, so an arterial blood gas is ordered to assess for changes in acid-base balance.

Alright, arterial blood gas, or ABG for short, is a test used to measure the acid-base components and pressure of gasses in the arterial blood. Normal ABG values for healthy adults  are a pH ranging from  7.35 to 7.45, bicarbonate, or HCO3- ranging from 21 to 28 mEq/L; carbon dioxide or PaCO2 ranging from 35 to 45 mm Hg; PaO2 ranging from 80 to 100 mm Hg, and SaO2 should be more than 95%.

Now, respiratory acidosis is a condition in which the normal mechanism of ventilation is disturbed, resulting in hypoventilation. During hypoventilation, the respiratory rate and depth  both decrease, the minute ventilation, which is the volume of air that moves in and out of the lungs in a minute, decreases, and the amount of CO2 eliminated from the body decreases. 

So, more CO2 is retained because there&amp;#39;s more CO2 produced by the body than can be eliminated.  In the blood,  increased CO2 binds to water, and forms carbonic acid, which then dissociates into hydrogen ions, and bicarbonate. Initially, the increase in bicarbonate helps buffer the hydrogen ions, slowing the drop in pH. Over time, the increased amount of hydrogen will eventually result in acidosis.

Now, there are some conditions that can alter ventilation, including those that can affect the respiratory center in the brain, as well as the lungs, the respiratory muscles, or gas exchange itself. For example, a stroke and medications like opiates and barbiturates depress the respiratory center in the brain, slowing respirations a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arterial_blood_gas_(ABG)_-_Respiratory_alkalosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wblrupCvTIey8jTBBAc73EanQc2YVAxF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arterial blood gas (ABG) - Respiratory alkalosis: Nursing]]></video:title><video:description><![CDATA[A 24-year-old female client arrives at the emergency department with a report of shortness of breath. She has a history of anxiety and was unable to pay for her medications this month. On assessment her lungs are clear, her heart rhythm is sinus tachycardia, and she is afebrile. Based on these findings, the health care provider suspects anxiety-induced hyperventilation so an arterial blood gas is ordered to assess for changes in the acid-base balance.

Alright, arterial blood gas, or ABG for short, is a test used to measure the acid-base components and pressure of gasses in the arterial blood. Normal ABG values for healthy adults  are a pH ranging from  7.35 to 7.45, bicarbonate, or HCO3- ranging from 21 to 28 mEq/L; carbon dioxide or PaCO2 ranging from 35 to 45 mm Hg; PaO2 ranging from 80 to 100 mm Hg, and SaO2 should be more than 95%.

Now,  respiratory alkalosis is a condition when increased pH is caused by hyperventilation due to central causes like head injury or by anxiety-induced hyperventilation; as well as pulmonary causes like pulmonary emboli; or iatrogenic causes like mechanical ventilation.

During hyperventilation, too much carbon dioxide, or CO2, is blown out by the lungs. Ultimately, more CO2 is removed from the body than what is created during normal cellular metabolism, leading to a hypocapnia, or low CO2. 

Now, as the pH continues to increase and move out of the normal range, the body will attempt to correct the imbalance, a process called compensation. With respiratory alkalosis, the renal system is the main mode of compensation. The process begins when the kidneys decrease reabsorption of HCO3-, which decreases the pH. However, compensation can’t completely correct the pH imbalance, and it won’t fix the underlying cause of the pH imbalance.

Okay, to interpret an ABG, the first thing you’ll do is look at the pH. If it’s less than 7.35 your client is acidotic; and if it’s greater than 7.45 your client is alkalotic. 

Once you know that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_cultures:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xnfcVa4nQNWrk63ExSkJhWhuT1yHweGR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood cultures: Nursing]]></video:title><video:description><![CDATA[A 70-year-old male client arrives at the emergency department after his wife noticed he developed a fever; fatigue; and a productive cough that have been worsening over the past few days. His medical history is significant for chronic obstructive pulmonary disease, or COPD; and on physical assessment, he has warm, flushed skin, tachypnea, and crackles in the lung bases. The healthcare provider suspects bacteremia secondary to pneumonia, so a blood culture is ordered. Okay, so normally blood is considered sterile, meaning in a healthy state, there are no pathogens floating around. Our bodies have various defenses in place to maintain this healthy state like the skin, which acts as a protective barrier; the mucociliary escalator in the bronchi, which moves mucus and pathogens up and away from the lungs; epithelial cells that line the urinary tract, which are highly impermeable to pathogens; and of course the immune system, which fights pathogens and removes them from the body.

Now, sometimes a pathogen is able to gain access to the blood if our defensive mechanisms are compromised, like with breaks in the skin, inefficient mucociliary clearance, or when urinary tract epithelial cells are outnumbered by pathogens. Pathogens can also enter the blood if a client is immunosuppressed, like in HIV or cancer. All right, so blood culture is obtained to detect the presence of pathogens, like bacteria or fungi, in the blood when there’s a history of conditions that can predispose a person to an infection; when there are signs and symptoms of infection like leukocytosis, fever, or chills; or if a client has a known infection, like pneumonia, cellulitis, or a urinary tract infection. The blood culture results are reported by the lab as the amount of growth after a specific number of days. A positive blood culture is an indication of bacteremia or septicemia. 

All right, let’s look at the nursing care you’ll provide for a client with suspected bacteremia. Priorities of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_biomarkers_-_Creatine_kinase_(CK):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e-5CkWwbRfu-t99GWb0zXf66TAmnxGDn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac biomarkers - Creatine kinase (CK): Nursing]]></video:title><video:description><![CDATA[A 71-year-old female arrives at the emergency department with reports of chest pressure and nausea. She has a history of high cholesterol and diabetes mellitus. Based on this assessment, the provider suspects acute coronary syndrome, and orders a creatine kinase level to be drawn. 

Okay, creatine kinase, or CK for short, also known as creatine phosphokinase or CPK, is an enzyme that helps create adenosine triphosphate, or ATP, which is an energy source, to supply to body tissues. Now, there are three types of CK: CK-MB, found mostly in heart muscle cells, or myocytes, with small amounts found in the skeletal muscle; CK-MM, found in skeletal muscle; and CK-BB, found in the brain. 

Alright, let’s focus on the cardiac biomarker, CK-MB. There are certain conditions that can cause an increased CK-MB level, most commonly any condition that causes damage to cardiac or skeletal muscle cells. 

Cardiac muscle cell damage can occur with acute coronary syndrome, which is any condition that decreases blood flow to the heart muscle, such as angina or myocardial infarctions, or MI for short. Decreased blood flow causes an imbalance between myocardial oxygen demand and supply from the coronary arteries, resulting in myocardial ischemia, a depletion of ATP, and a severe reduction in the ability of the heart to contract.

At the cellular level, damage to myocytes disrupts their membranes, causing the cellular contents, including CK-MB, to be released into the bloodstream. Now, when skeletal muscle cells are damaged, it can cause a condition called rhabdomyolysis, where the damaged muscle cells release their cellular contents into the bloodstream causing damage to the heart and kidneys.

Skeletal muscle can also be damaged by crushing trauma, which causes a traumatic form of rhabdomyolysis; and muscular dystrophy, a genetic condition causing progressive muscle weakness and loss of muscle mass.

Alright, so CK-MB is usually measured when there is a concern about cardiac ischemia or muscle damage. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_biomarkers_-_Troponin:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/33txvVqcSJKmcDFy6dML6N1GRwW6VlRQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac biomarkers - Troponin: Nursing]]></video:title><video:description><![CDATA[A 50-year-old client is brought to the emergency department by ambulance complaining of chest pain at rest and shortness of breath for the past 30 minutes. His medical history is significant for smoking and hypertension. An ECG reveals new T-wave inversions. The health care provider suspects acute coronary syndrome and orders a troponin level to be drawn.

Alright, troponin is a protein found in striated muscles, including skeletal muscles and the myocardium of the heart. There are three types: C, I, and T. Troponins I and T, are highly specific to myocardial tissue, and together, they are known as cardiac troponins, or cTn for short. 

Now, cardiac muscle cell, or myocyte, damage can occur with acute coronary syndrome, which is any condition that decreases blood flow to the heart muscle, such as angina or a myocardial infarction, or MI for short. Decreased blood flow causes an imbalance between myocardial oxygen demand and supply from the coronary arteries, resulting in myocardial ischemia and damage to cardiac muscle cells. As the cell membranes become damaged, cellular contents are released into the bloodstream, including proteins like cTn, and enzymes, like creatine kinase-MB, or CK-MB for short, which is found mostly in heart muscle cells.

Alright, so troponin levels will be measured when there is a concern about cardiac ischemia.

Troponin levels are usually drawn together with other cardiac biomarkers like CK-MB. Typically, a blood sample is drawn on admission and repeated to monitor for trends in the values, or if there are new signs and symptoms of ischemia, like new findings on ECG or evidence of new abnormalities on imaging tests.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coagulation_studies_-_Partial_thromboplastin_time_(PTT):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bk-1XT6xRwuupfxrwkvZGsCJQEOjOkON/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coagulation studies - Partial thromboplastin time (PTT): Nursing]]></video:title><video:description><![CDATA[A 2-year-old male is brought to the clinic by his mother because of a bloody nose that has continued to bleed for over an hour. The mother reports that her son has a history of easy bruising and is worried because one of her relatives has “some type of clotting disorder.” The child is holding a bloody cloth to his nose, with blood visible under his nose, mouth, chin, and T-shirt. On assessment, bright red blood is dripping from his nose. Based on these findings, the health care provider is concerned about a clotting disorder and orders a series of coagulation studies, including partial thromboplastin time. 

Now, normally, bleeding is stopped by the process of hemostasis. First, platelets stick together to form a plug. Then, the coagulation cascade is activated, which involves several clotting factors that interact within the intrinsic, extrinsic, and common pathways, ultimately creating a mesh that stabilizes the clot to help stop bleeding. 

Now, partial thromboplastin time, or PTT for short, assesses the intrinsic pathway by measuring, in seconds, the time it takes to form a clot. An activated partial thromboplastin time, or aPTT, is when an activator is added to the sample to speed up clotting time and produce a more narrow range. So, the normal range for PTT is 60 to 70 seconds, while the normal range for aPTT is 25 to 30 seconds, depending on the activator used. The critical level for PTT is 100 seconds and 70 seconds for aPTT.

Alright, PTT can be increased if there aren’t enough clotting factors, which can happen due to reduced production, inactivation, or if the clotting factors get used up. 

First up, inherited clotting disorders can cause a deficiency of a single factor, like with hemophilia A, when factor VIII is missing; and in hemophilia B, when factor IX is missing. Likewise, in von Willebrand disease, there’s no von Willebrand factor, which is a plasma protein that helps platelets stick to injured blood vessels, and acts as a carrier for c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_blood_count_(CBC)_-_Hemoglobin_&amp;_hematocrit_(H&amp;H):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kOwyvhGhSgOpXKp8YULXD8X9RQqZYJFR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete blood count (CBC) - Hemoglobin and hematocrit: Nursing]]></video:title><video:description><![CDATA[A client comes to the outpatient clinic and reports feeling fatigued, weak, and is experiencing frequent palpitations. On assessment, the client’s skin and mucous membranes look pale and their extremities feel cold. Based on these findings, a complete blood count, or CBC, is ordered to check their hemoglobin and hematocrit.

Now, hemoglobin, abbreviated as Hgb or Hb, and hematocrit abbreviated as Hct or sometimes Crit, are usually measured as part of a CBC, and they provide an indirect way to measure red blood cells or RBCs. Hemoglobin is an iron-containing protein found in RBCs, which allows them to carry oxygen from the lungs to peripheral tissues. The hematocrit represents the percentage of packed RBCs, also referred to as the Packed Cell Volume or PVC, in whole blood, that’s obtained after centrifuging part of the sample to allow for complete sedimentation of the RBCs.

The normal values of hemoglobin and hematocrit differ between the sexes. This is because in females, RBC production is stimulated by erythropoietin only, while in males, androgens provide additional stimulation for RBC production. So, in adult males, hemoglobin normally ranges from 14.0 to 18.0 g/dL, while in adult females it normally ranges from 12.0 to 15.0 g/dL. Hematocrit in males ranges from 41.0% to 51.0%, while in females it ranges from 36.0% to 45.0%.

Typically, the hematocrit will be about three times the value of hemoglobin. As an example, if a client’s hemoglobin is 14.0 g/dL, their expected hematocrit would be about 42%.

Alright, there are certain conditions that can alter a client’s hemoglobin and hematocrit.

When the number of RBCs increases, like in polycythemia vera, a condition where the bone marrow produces too many RBCs, hemoglobin also increases. These additional cells also increase the percentage of RBCs, which means that the hematocrit will go up as well.

Alternatively if the amount of fluid in the blood decreases, like with dehydration, the concentration of RB]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_blood_count_(CBC)_-_Platelets:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zg6StB87RPOmUZ1GGnuOA9OlQkO4tHm-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete blood count (CBC) - Platelets: Nursing]]></video:title><video:description><![CDATA[An older adult client is brought to the clinic because of a nosebleed that won’t stop. The client’s daughter states, “My dad has had frequent nosebleeds before, but it always stopped after a few hours.” On assessment, you notice pinpoint red spots on the client’s legs and trunk that don’t go away on pressure, and bruises on their arms and legs. Based on these findings, a complete blood count, or CBC, is ordered to check their platelet count. Now, platelets, also called thrombocytes, are cell fragments created in the bone marrow from cells called megakaryocytes. Plateletes are essential for beginning the process of coagulation. So, when a blood vessel is damaged, platelets stick to the inner surface of that blood vessel, aggregate together, and form a platelet plug to stop the bleeding. The lifespan of platelets is about 8 to 10 days. When they become old or damaged, they are removed by the spleen. 

All right, the platelet count measures the number of platelets in the blood, and is usually measured as part of a CBC.The normal range for platelet count is from 150,000 to 450,000/μL. Now, there are some conditions that can alter the platelet count. When the platelet level is too high, it is called thrombocytosis. Trauma, inflammation, or blood loss can cause reactive thrombocytosis, where the platelet count becomes temporarily elevated, and then goes back to normal once the condition resolves. The platelet count can also temporarily increase after a splenectomy, because the platelets are not removed as fast as they are created. In contrast, conditions that can cause a sustained increase in platelets include certain myeloproliferative neoplasms, which are malignancies that cause the bone marrow to make too many platelets. 

On the flipside, when the platelet level is too low, it is called thrombocytopenia. Now, sometimes the bone marrow doesn’t make enough platelets, which can happen in conditions like aplastic anemia, or with bone marrow depression from ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_blood_count_(CBC)_-_Red_blood_cells_(RBC):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9hRabHP2SOOpXLZtLip_tT8ISWSDNBXX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete blood count (CBC) - Red blood cells (RBC): Nursing]]></video:title><video:description><![CDATA[Ms. Poly is a 67-year-old client who arrives at the clinic for a scheduled appointment with her primary care physician. Ms. Poly reports experiencing fatigue, frequent headaches, and nosebleeds. She also mentions feeling itchy after taking a shower. Based on these findings, a complete blood count, or CBC, is ordered to check her red blood cell count. Red blood cell count, also known as an erythrocyte count, red cell count, or just RBC count, is a part of CBC that measures the number of red blood cells in one cubic millimeter of blood. Now, red blood cells, or RBCs for short, are created by the bone marrow, which is stimulated by erythropoietin from kidneys, or by a lack of oxygen in the tissue. RBCs carry oxygen from the lungs to peripheral tissues, collect the carbon dioxide there, and carry it back to the lungs, where it is exchanged for oxygen. 

The normal values of RBC count differ between sexes. This is because, in females, RBC production is stimulated by erythropoietin only, while in males, androgens provide additional stimulation for RBC production. So, in adult males, the RBC count ranges from 4.6 to 6.0 million/µL, while in adult females, it ranges from 4.0 to 5.4 million/µL. All right, there are some conditions that can alter the RBC count. An increased RBC count can result from a condition called polycythemia. Polycythemia vera is one type of polycythemia, when the bone marrow produces an excess amount of RBCs without being stimulated.  Another type is secondary polycythemia, which is when the bone marrow is stimulated by additional erythropoietin or a lack of oxygen to produce more RBCs. Alternatively if the amount of fluid in the blood decreases, like with dehydration, the concentration of RBCs increases, so the RBC count goes up. 

On the other hand, low RBC levels can be caused by a decreased RBC production, like in kidney disease, which decreases the synthesis of erythropoietin; bone marrow suppression, like in aplastic anemia; increased R]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_blood_count_(CBC)_-_White_blood_cells_(WBC)_&amp;_differential:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GQMX9oG0Qyi9ZRZ4Xh2OJPRdRlGg3Ob1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete blood count (CBC) - White blood cells (WBC) and differential: Nursing]]></video:title><video:description><![CDATA[A 16-year-old client is brought to the clinic by their mother, with a report of fever, malaise, nausea, and diarrhea. On assessment, you note a temporal artery temperature of 101.5 F or 38.6 C. Based on these findings, a complete blood count, or CBC, is ordered to check their white blood cell count and differential.

White blood cells, also called leukocytes or WBCs for short, are created by the bone marrow from precursor cells. White blood cells help to ward off pathogens like bacteria and viruses, destroy cancerous cells, and neutralize toxins.

There are five types of WBCs that circulate in the body. First, there are neutrophils, which are the most plentiful WBC. They are also called polymorphonuclear leukocytes or PMNs because of their distinct nuclei, which have 2 to 5 lobes. Immature neutrophils are called bands or stabs. Neutrophils are the first type of WBC to respond to an infection.

Next, there are eosinophils, which are involved in allergic reactions, and are responsible for fighting off parasitic infections.

Then there are basophils, which have granules that contain histamine, so they specialize in inflammation and allergic reactions.

Next, there are monocytes that serve as the clean-up crew by removing foreign particles and dead cells. Finally, there are lymphocytes, which respond to viral and bacterial infections. These include B cells that make antibodies and T cells which kill pathogens and help other immune cells.

Now, the WBC count, also known as leukocyte count, or just white count, measures the number of WBCs in the blood, as is a part of a CBC. A normal WBC count ranges from 4,500 to 11,000/µL. Additionally, a WBC differential can be used to measure the proportion of each type of WBC. Usually, neutrophils make up about 50% to 70%, with 0% to 5% bands. Eosinophils make up about 1% to 3%, while basophils range from 0% to 2%, monocytes make up 2% to 11%. Finally, lymphocytes normally make 18% to 42% of total WBCs.

Alright, there are ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Blood_urea_nitrogen_(BUN)_&amp;_creatinine_(Cr):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZjnAVszTSky3JCXI8_Qdd01-Rd_0cz5M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Blood urea nitrogen (BUN) and creatinine (Cr): Nursing]]></video:title><video:description><![CDATA[An elderly client is brought to the emergency department by ambulance, accompanied by his daughter, who reports her father has a history of systolic heart failure, that he’s been experiencing nausea, vomiting, and confusion. On assessment, there’s jugular vein distension, crackles on lung auscultation, and leg edema. Based on these findings, blood urea nitrogen or BUN, and creatinine are ordered to check the client’s renal function.

Alright, blood urea nitrogen, also known as urea nitrogen or just BUN, measures the blood level of urea nitrogen, which is a substance formed in the liver from protein metabolism. Most urea nitrogen is excreted in urine after filtration in kidneys, and only a small amount is reabsorbed. 

Serum creatinine, abbreviated Cr, is a by-product of muscle contraction, and it’s made at a relatively constant rate as part of regular, everyday activity. All of the creatinine produced by the body is eliminated by the kidneys, with no reabsorption. 

Because both urea and creatinine are eliminated by the kidneys, they are used to evaluate renal function. Also, to more closely determine the cause, the BUN to creatinine ratio is examined.

Now, BUN and creatinine can be drawn on their own, or as a part of the basic metabolic panel, or BMP, also known as the complete metabolic panel, or CMP. The normal value for BUN is 5 to 20 mg/dL. On the other hand, creatinine values tend to be higher in males, who tend to have a larger muscle mass. So, in healthy males, creatinine ranges from 0.7 to 1.3 mg/dL, while in females, it ranges from 0.6 to 1.1 mg/dL. Lastly, the BUN to creatinine ratio is somewhere between 10:1 and 20:1.

Alright, let’s switch gears and talk about conditions that can alter the client&amp;#39;s BUN, which can be non-renal or renal. So, for non-renal conditions, the amount of urea nitrogen in the blood level is related to how much urea is produced by the liver. It will rise when the liver metabolizes more protein, like with i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Chloride:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4l4FdZ06SiO56t9qRcsx2XLvRsyoWfTg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Chloride: Nursing]]></video:title><video:description><![CDATA[A client arrives at the emergency department by ambulance with a report of fatigue and weakness after recurrent episodes of vomiting over the past few days. Based on these findings, a basic metabolic panel, or BMP is ordered to check the client’s electrolytes, including their chloride level. 

Now, chloride, abbreviated as Cl-, is a negatively charged ion, or anion. Most of the body’s chloride is found in the extracellular fluid, and it is often found associated with positively charged ions, like sodium and potassium. Chloride helps to maintain fluid balance, serum osmolality, and acid-base balance. There’s a significant amount of chloride in the cerebrospinal fluid, and it’s  secreted by the gastric parietal cells in the form of hydrochloric acid to promote digestion. 

Chloride mostly comes from the diet where it can be found in a variety of foods that are also high in sodium, such as processed meat, canned fish and vegetables, as well as table salt. Once ingested, a small amount is eliminated through the gastrointestinal tract, while most of it is excreted through the kidneys in the urine. 

Now, plasma levels of chloride can be measured on its own, or as part of a CMP, or a complete metabolic panel; which is also called a basic metabolic panel, or BMP. In adults, normal chloride values range from 96 mEq/L to 106 mEq/L.  

Alright, there are certain conditions that can cause a high serum chloride level, or hyperchloremia. Hyperchloremia often happens along with hypernatremia, or a high sodium level; so, when the sodium level rises, so does the chloride level. On the other hand, chloride has an inverse relationship with bicarbonate, so a decrease in bicarbonate, like with acidosis, is associated with an increase in chloride. In fact, hyperchloremic acidosis can be the result of severe diarrhea, where excessive amounts of sodium bicarbonate is excreted in the stools. 

Hyperchloremia can also be caused by decreased excretion by the kidneys, like with rena]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Estimated_glomerular_filtration_rate_(eGFR):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Bu_F1RE5RRy-72ii7HpRZxRqQLiehiHn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Estimated glomerular filtration rate (eGFR): Nursing]]></video:title><video:description><![CDATA[An older adult client with a history of chronic kidney disease is seen by his primary care provider. The client’s kidney function and disease progression will be assessed by monitoring laboratory test results, including the estimated glomerular filtration rate, or eGFR.

So, the glomerular filtration rate, or GFR for short, measures the amount of fluid filtered by the kidneys in one minute. Now, because GFR is not always practical to perform, the estimated GFR, or eGFR, is measured using a formula, including the Cockcroft-Gault equation, which uses the blood creatinine level, weight, age, and sex;  

the Modification of Diet in Renal Disease formula, also called MDRD, which uses the blood creatinine level, age, and sex, along with an adjustment for Black people of African descent; and 

the Chronic Kidney Disease-Epidemiology Collaboration formula, or CKD-EPI, that  uses age, sex, and serum creatinine or cysteine C, or both to calculate the eGFR. In healthy adults, eGFR is about 120 mL/min/1.73m2 of body surface area.

Let’s switch gears and talk about the conditions that affect eGFR. Increased eGFR is often seen in conditions that cause osmotic diuresis, which is an increase in filtration and urination due to the presence of certain substances in the fluid filtered by the kidneys. 

So with uncontrolled diabetes and hyperglycemia, for example, the glucose pulls water with it as the kidneys work hard to eliminate the excess glucose. An increased eGFR is also expected when administering an osmotic diuretic like mannitol.

When it comes to decreased eGFR, this can be caused by impaired kidney function, which reduces the kidney’s filtering ability. An important cause of impaired kidney function is acute kidney injury, which can result from prerenal conditions like hypoperfusion due to shock or congestive heart failure; intrarenal conditions like acute tubular necrosis or acute glomerulonephritis; and postrenal conditions that impair the flow of urine such as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Glucose:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FR7Os5VJQHyqGCdomB5FAWtYSr2EUfFl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Glucose: Nursing]]></video:title><video:description><![CDATA[A 63-year-old female client comes to her primary care provider’s office with reports of excessive urination and thirst; and recent weight loss despite eating and drinking more than normal. Her medical history is significant for hypertension and a BMI of 32 kg/m2. Based on the client’s assessment and medical history, the provider suspects hyperglycemia due to diabetes mellitus, and thus orders a glucose level. 

Now, glucose, abbreviated as Glc, is a type of sugar that is typically obtained from consuming carbohydrates, such as bread or fruit. After a meal, glucose gets absorbed from the gut into the blood and from there it enters the cells where it is used as a source for energy. 

The body controls how much glucose is in the blood relative to how much gets into the cells with two hormones: insulin and glucagon. Insulin is used to reduce blood glucose levels, and glucagon is used to increase blood glucose levels. 

Both of these hormones are produced by clusters of cells in the pancreas called islets of Langerhans. Insulin is secreted by beta cells in the center of the islets, and glucagon is secreted by alpha cells in the periphery of the islets. 

Insulin reduces the amount of glucose in the blood by binding to insulin receptors embedded in the cell membrane of various insulin-responsive tissues like muscle cells and adipose tissue. When activated, the insulin receptors cause vesicles containing glucose transporters that are inside the cell to fuse with the cell membrane, allowing glucose to be transported into the cell. Glucagon does exactly the opposite, it raises the blood glucose levels by getting the liver to generate new molecules of glucose from other molecules and also break down glycogen into glucose so that it can all get dumped into the blood. 

Plasma glucose, also referred to as blood sugar, is usually measured as part of a complete metabolic panel, or CMP, or as part of a basic metabolic panel, or BMP. It can also be measured at the point o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Liver_function_tests_(LFT):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k_tJrLVTRPexCLjp44js0NDXSiKEITm5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Liver function tests (LFT): Nursing]]></video:title><video:description><![CDATA[A 24-year-old male client is seen in the emergency department, with a report of weakness, nausea, vomiting, and fever. On assessment, he has abdominal pain in the upper right quadrant of his abdomen, along with scleral icterus. When asked about recent travel, he states he returned from a trip to South America two weeks ago. Based on these findings, liver function tests are ordered. 

Now, liver function tests, or LFTs, are a set of tests that check the health of the liver by measuring the enzymes and other substances made by the liver. First up, is alkaline phosphatase, or ALP for short, which is an enzyme found mostly in liver cells, which are called hepatocytes, as well as in bone cells, and the placenta. Next, is alanine aminotransferase, also known as ALT; and aspartate aminotransferase, also known as AST. Both ALT and AST can be found in the liver, kidneys, heart, and skeletal muscle. 

Another enzyme is gamma-glutamyl transferase, or GGT, which is mostly present in the liver. Finally, there’s bilirubin, which is a product of the breakdown of hemoglobin found in red blood cells. This type of bilirubin is referred to as unconjugated or indirect bilirubin. Once it reaches the liver, bilirubin is converted into conjugated or direct bilirubin and eliminated through the bile. Total bilirubin is a measurement of both conjugated and unconjugated bilirubin. 

Now, LFTs can be drawn on their own as a liver panel, or as part of a complete metabolic panel. The normal value of ALP ranges from 30 to 120 units/L; ALT ranges from 4 to 36 units/L; AST ranges from 0 to 35 units/L; and GGT ranges from 8 to 38 units/L. These ranges can vary slightly between sexes, and could be higher for those with a higher body mass index. Lastly, total bilirubin values range from 0.3 to 1.0 mg/dL.  

Alright, there are some conditions, like hepatitis, liver cancer, and fatty liver disease, as well as certain medications like acetaminophen, that can damage the liver causing its enzymes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Potassium:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7_rTmngdScu26deKXPuOSBvGRNCpHmX-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Potassium: Nursing]]></video:title><video:description><![CDATA[A client with a history of chronic kidney disease arrives at the emergency department via ambulance and reports feeling weak and experiencing palpitations. The electrocardiogram, or ECG, reveals peaked T waves and a prolonged QRS interval. Based on these findings, a complete metabolic panel, or CMP, is ordered to check their serum potassium level.
Now, potassium, which has the symbol K+, is a positively charged ion, or cation. About 98 percent of the body’s total potassium is found in the intracellular fluid, while the remaining 2 percent is in the extracellular fluid. Potassium mostly comes from the diet, and once ingested,  a tiny amount is excreted through sweat and the gastrointestinal tract, while most of the excess potassium is excreted by the kidneys.

A normal potassium concentration is essential for maintaining the overall electrochemical gradient across the membrane of each cell, which supports nervous system function, and the contraction of skeletal, smooth, and cardiac muscles. So, the plasma level of potassium can be measured on its own or as part of a CMP or a complete metabolic panel; which is also called a basic metabolic panel, or BMP. This level represents the amount of potassium in the plasma. In adults, normal potassium levels range from 3.5 to 5.1 mEq/L. Critical values are 2.5 mEq/L or less and 6.0 mEq/L or more. All right, now there are certain conditions that can alter a client’s potassium level. The three primary causes of a high potassium, or hyperkalemia, are decreased potassium excretion, increased potassium intake, and a potassium shift from inside the cells to outside the cells. 

First, let’s look at decreased potassium excretion. This can occur from conditions like acute or chronic renal disease; or the use of certain medications, like potassium-sparing diuretics such as spironolactone; non-steroidal anti-inflammatory drugs, or NSAIDs, like ibuprofen; and angiotensin converting enzyme, or ACE, inhibitors, like captopril. Dec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Sodium:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0QsfrC_3SPyC2xiGKcUV6QMKS6G1EUun/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Sodium: Nursing]]></video:title><video:description><![CDATA[Ms. Blanco is an older adult client who has been lethargic for the past few hours and arrives at the emergency department via ambulance. During the previous three days, she had recurrent episodes of diarrhea due to gastroenteritis. Her family reports that during this time they encouraged Ms. Blanco to drink lots of water to keep hydrated. On physical assessment, Ms. Blanco has dry mucous membranes, sunken eyes, tachypnea, and tachycardia. Based on these findings, a complete metabolic panel, or CMP, is ordered to check her electrolyte levels, including sodium. Now, sodium is a positively charged ion, or cation, which is abbreviated as Na+. It is the major cation in the body, and most of it is located outside the cells in the extracellular fluid. It is the major factor in the fluid&amp;#39;s osmolality, which is the concentration of dissolved particles, including sodium and other electrolytes. Sodium is also a major determinant of how fluid is distributed around the body, and it helps maintain enough circulating volume for adequate tissue perfusion. 

In addition, sodium is essential for the conduction of nerve impulses and muscle contraction. Together with chloride and bicarbonate, sodium helps to maintain acid-base balance. Sodium is introduced into the body through a person’s diet, especially when foods high in sodium are consumed, such as canned soup, tomato juice, processed meats, canned tuna, salted crackers, and cheese. Once ingested, sodium is absorbed in the blood by the gastrointestinal tract, and travels through the bloodstream. Then, most of the sodium is excreted through the kidneys, but a lesser amount is excreted through sweat and feces. Now, maintaining a normal sodium concentration is essential to keep our bodies functioning normally. When there’s hypernatremia, or a high sodium level, the serum osmolality also increases. The increased osmolality is detected by the osmoreceptors in the thirst center of the hypothalamus. In response, it]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_&amp;_development_-_Early_&amp;_middle_adulthood:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/35MWKoi8RvGJK5Qiq4Yp0_ocRputtV4c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development - Early and middle adulthood: Nursing]]></video:title><video:description><![CDATA[Adulthood is the longest stage of life, spanning from 20 years of age until the end of life. Adulthood is further divided into three consecutive phases: early adulthood, between 20 and 40 years old; middle adulthood, between 40 and 65 years old; and late adulthood, from age 65 and onward.  

Now, developmental psychologists involved in studying development early and middle include Jean Piaget, Erik Erikson, and Lawrence Kohlberg. 

First, it’s important to note that growth and development are two different concepts. Growth refers to physical changes in height, weight, and the appearance of the body; whereas development refers to the acquisition of complex motor, cognitive, and social skills. 

Alright, now compared to other stages of life, adulthood is a time of minimal physical growth. By this point, physical maturation is complete, although height and weight can increase slightly. Young adults are at their peak in terms of physical abilities, including muscle strength, endurance, reaction time, and cardiac function; though poor lifestyle habits, such as smoking, as well as an unhealthy diet, or lack of exercise can increase the risk for future illnesses or trigger the onset of chronic conditions at an early age. 

The aging process actually begins during early adulthood, although very slowly, and continues through middle adulthood. Around the age of 30, the lens of the eye begins to stiffen and thicken, affecting the ability to focus on close objects, a condition known as presbyopia.   

Hearing can start to decrease as well, called presbycusis. Hair can start to thin out and become gray as early as the age of 35; the skin becomes drier and less elastic, wrinkles start to appear, and reproductive capacity starts to decline.  

Later, the basal metabolic rate decreases, so it’s more difficult to gain muscle mass, while at the same time, fat tends to accumulate, particularly on the abdomen and lower body.  

Now, cognitive development remains relatively st]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Contraception_-_Permanent_methods:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DS_v0F0CR5W61zQPdq1IWPerTaeGinDF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Contraception - Permanent methods: Nursing]]></video:title><video:description><![CDATA[Permanent methods of contraception are surgical procedures that permanently prevent future pregnancies. So, for individuals assigned females at birth, tubal ligation surgery is done to achieve permanent contraception, while in the case of individuals assigned males at birth, vasectomy is performed. Of note, even though they are widely accepted as “irreversible” methods, in some situations, these procedures can be reversed. 

Now, to understand the tubal ligation and vasectomy, let’s start by having a look at the anatomy and physiology of the fallopian tubes in assigned females and the vas deferens in assigned males at birth. 

The fallopian tubes, also known as oviducts or uterine tubes, are a pair of tube or pipe-like structures on each side of the uterus that connect it with the ovaries. This way, during the menstrual cycle, it helps in transporting the ova or oocyte from the ovary to the uterus. Each fallopian tube has four sections: the uterine section, which opens into the uterus; the isthmus, which is the tightest part of the tube; the ampulla, which is the widest part of the fallopian tube where fertilization usually occurs; and the infundibulum, which envelops the ovary with finger-like projections called fimbriae. 

Switching gears, let’s look at the anatomy of the vas deferens, which refers to a pair of thick long tubes that carry mature sperm from the epididymis to the ejaculatory ducts. The ductus deferens begins at the inferior pole of the testis, then ascends posterior to the testis to enter the spermatic cord, which connects the testes to the abdominal cavity. From there, the ductus deferens enters the pelvic cavity and goes over the bladder, and then descends medial to the seminal vesicle. 

The ductus deferens then terminates by joining the ducts of the seminal vesicle, forming the ejaculatory ducts which connect to the urethra. During transport from the vas deferens to the urethra, the sperm collects secretions from the male accessory sex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postmortem_care_&amp;_considerations:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OWKvTb6cQWOgLjTgzjJ8MpyXQpqUeu9c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postmortem care and considerations: Nursing]]></video:title><video:description><![CDATA[Nurse Molly works in a skilled nursing facility and is caring for a client, Santiago, at the end of his life. Santiago suffered a heart attack and subsequent stroke, and his extended family is at the bedside. Nurse Molly recognizes that Santiago is nearing the end of his life because his heart rate has slowed down, his skin is blotchy with a purplish tint, and his respirations have become noisy and irregular. Nurse Molly lets Santiago’s family know these clinical manifestations are expected and gives them some privacy during the last moments of his life. Later, Santiago’s daughter, Lucia, approaches the nurse’s station saying, “Please come, I think my dad’s soul has left his body.” Nurse Molly enters Santiago’s room to find his family openly weeping and praying at the bedside. She listens  to Santiago’s chest with her stethoscope and does not hear breathing or a heartbeat. Nurse Molly says, “Santiago has passed away. I’m going to let the doctor know. I’m so sorry for your loss.” Lucia grabs Nurse Molly’s hand and says, “I know my dad is no longer in his body but I can’t help but worry about what happens to the body now. He was always a rather private and proud person.” 

Nurse Molly looks into Lucia’s eyes and responds, “I’ll be here for you and your family and treat your father’s body with dignity and respect. Take as much time as you need and I will be in later to check on you.” Lucia smiles and thanks her. Nurse Molly will use what she knows about postmortem care to help bring comfort to Santiago’s family during this time. So, postmortem care is the care of a client’s body after death. It should be performed in a manner consistent with state law and facility policies as well as the client’s religious or cultural beliefs. The death of a family member can be stressful and confusing for the client’s loved ones, so after the death of a client, the nurse is responsible for providing the client’s family with education and support, completing appropriate docum]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cleft_lip_&amp;_palate:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9MuVA4McSlaW4u0316d98xwxSvyurEOs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cleft lip and palate: Nursing]]></video:title><video:description><![CDATA[Cleft lip is an opening or a split in the upper lip, whereas cleft palate describes an opening or a split in the roof of the mouth, called the hard palate. Cleft lip and palate are the most common congenital anomalies of the head and face.

Now, let’s quickly review the embryological development of the lips and palate. At the fourth week of pregnancy, multiple structures appear in the face of the embryo. These include the frontonasal prominence, which gives rise to the forehead and bridge of the nose; nasal placodes, which are two raised bumps on each side of the frontonasal prominence; as well as paired maxillary prominences; and paired mandibular prominences. Additionally, two small dimples develop at the center of each nasal placode, dividing these placodes into medial and lateral nasal prominences.

Now let’s look at a cross section of the embryo. As the embryo develops, the maxillary prominences grow medially to fuse with the medial nasal placodes, giving rise to the upper lip. In addition, the medial nasal placodes grow to the inside of the face, forming the intermaxillary segment, which later on forms the anterior one third of the hard palate, called the primary palate. Similarly, the maxillary prominences grow to the inside of the face, forming the palatal shelves. These shelves will then fuse above the tongue to form the remaining two thirds of the hard palate, called the secondary palate.

Alright, now the cause of cleft lip and palate is unknown, with some theories suggesting multifactorial genetic and environmental involvement. However, several risk factors for cleft lip and palate have been identified, including folate deficiency, as well as exposure to teratogens, such as maternal smoking and exposure to radiation, and using certain medications during pregnancy, such as anticonvulsants or steroids. Other risk factors include advanced maternal age, and certain infections during pregnancy, especially the rubella virus.

Moving on to pathology a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coagulation_studies_-_Prothrombin_time_(PT)_&amp;_international_normalized_ratio_(INR):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iAqtx6HxTMWzO5j2dMgHco_GTMmh6KfW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coagulation studies - Prothrombin time (PT) and international normalized ratio (INR): Nursing]]></video:title><video:description><![CDATA[A 48-year-old male is brought to the emergency department by his wife because of severe knee pain after falling while cleaning the garage. His medical history is positive for a mechanical mitral valve replacement with subsequent anticoagulation using warfarin. On assessment, the client’s knee is swollen and tender to palpation; he appears pale and there are multiple bruises on his arms and legs. Based on these findings, the health care provider suspects overcoagulation and orders a prothrombin time and international normalized ratio. 

Now, normally, bleeding is stopped by the process of hemostasis. First, platelets stick together to form a plug. Then, the coagulation cascade is activated, which involves several clotting factors that interact within the intrinsic, extrinsic, and common pathways, ultimately creating a mesh that stabilizes the clot to help stop bleeding.

Alright, prothrombin time, also known as pro time or just PT, measures the time, in seconds, it takes to form a clot. It is used to evaluate the extrinsic pathway.

Similarly, the international normalized ratio, or INR for short, is the time it takes to form a clot presented as a ratio of the client’s PT to a control, or standardized, PT. 

The normal values for PT range from 10 to 14 seconds, while INR ranges from 1.0 to 1.3. Now, there is a therapeutic value for INR, which is higher, for people that require some level of anticoagulation, like in the case of a mechanical heart valve. In this case, the INR range is 2.0 to 3.0. Typically, PT and INR are drawn together and referred to as PT/INR.

Alright, the PT and INR can be increased if there aren’t enough clotting factors, which can happen due to reduced production, or if the clotting factors get used up. 

Now, since clotting factors are created by the liver, severe liver disease like cirrhosis can reduce clotting factor synthesis. Now, the liver needs a supply of vitamin K to make clotting factors II, VII, IX, and X. So, another way PT ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Calcium:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xGutecAxRVK_7dQO6vx5nnNxStq-tIV9/_.png</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Calcium: Nursing]]></video:title><video:description><![CDATA[The nurse is caring for a 65-year-old client after a total thyroidectomy on the medical-surgical unit. While taking his blood pressure, the nurse notices involuntary contraction of the muscles in the hand and wrist. Based on these findings, a basic metabolic panel, or BMP is ordered to check the client’s electrolytes, including their calcium level. 

Calcium is a positively charged ion noted as Ca2+. About 99% of that calcium is in our bones in the form of calcium phosphate. The last 1% is split so that the majority, about 0.99% is extracellular, which means in the plasma and in the interstitial space between cells; and 0.01% is intracellular or inside cells. Most of the calcium in the plasma circulates in two forms; in a free, ionized form, or in a form bound to proteins, like albumin. 

The total of these two forms of calcium can be measured on its own or as part of a complete metabolic panel, or CMP, which is also called a basic metabolic panel, or BMP; and in adults, it normally ranges from 9 to 10.5 mg/dL. Calcium is essential for strong bones and teeth, muscle contraction, cell membrane stability, and blood coagulation. It also helps with regulating a normal heart rhythm, releasing neurotransmitters from neurons, as well as releasing hormones from the endocrine glands. 

Calcium comes from a variety of sources including dairy products like milk, cheese, and yogurt; as well as leafy green vegetables, and canned fish like salmon and sardines.  Once ingested, calcium is absorbed into the bloodstream. Most of it goes to the bone, and the rest of calcium circulates in the bloodstream, while some of it is excreted by the kidneys and in the stool. 

Now, calcium homeostasis is regulated by three molecules, parathyroid hormone, or PTH, a hormone made by the parathyroid glands located in the neck on top of the thyroid gland; calcitonin, which is produced by the parafollicular cells of the thyroid gland; and vitamin D, a fat-soluble vitamin synthesized in the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/PIK3CA-related_overgrowth_spectrum_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wB22VXzdTdelFBaAv6PZ5W4EQ7y1ju_l/_.jpg</video:thumbnail_loc><video:title><![CDATA[PIK3CA-related overgrowth spectrum (NORD)]]></video:title><video:description><![CDATA[PIK3CA-related overgrowth spectrum, or PROS, is a group of disorders caused by mutations in the PIK3CA gene, which plays a role in regulating cell growth and division. As a result, mutations can result in uncontrolled growth of affected tissues.

There are many subtypes of PROS, based on the areas and tissues affected. 

CLAPO syndrome involves Capillary malformation, also known as “port wine stain”, in the lower lip, Lymphatic malformation in the face and neck, Asymmetry of the face and limbs, and Partial or generalized Overgrowth of one or more body segments.

CLOVES syndrome involves Congenital Lipomatous Overgrowth resulting in fatty swellings on the trunk and/or overgrowth of arms and/or legs that leads to asymmetric enlargement; Vascular malformations including capillary, venous, and/or lymphatic malformations and/or combinations of all of those; Epidermal nevi, presenting as brown bumpy birthmarks on the skin; and Scoliosis, Skeletal, or Spinal anomalies.

Klippel-Trenaunay Syndrome, or KTS, includes capillary malformation, abnormal veins, and limb overgrowth. People with KTS often have lymphatic malformations as well, so depending on the distribution may have some overlap with CLOVES syndrome.

Diffuse Capillary Malformation with Overgrowth, or DCMO, involves capillary malformation over a large area of the body with accompanying overgrowth, often increased size of an involved limb due to increased muscle and bone, but does not include venous or lymphatic malformation.

Fibro-Adipose Vascular Anomaly, or FAVA, is characterized by the development of a mass of blood vessels and fatty tissue within muscles, which can be painful and reduce mobility. 

Fibroadipose Hyperplasia, or FAH, results from overgrowth of connective tissues. In a related disorder, Hemihyperplasia Multiple Lipomatosis Syndrome, or HHML, is characterized by multiple fatty growths, along with hemihyperplasia, which is abnormal enlargement of one limb or one side of the body. 

Macrod]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_athymia_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/de7pD8hmQWqBihb5mx6yKzBmRambdSGQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital athymia (NORD)]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Congenital athymia (NORD) through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Breast_exam:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FjmWH1y9RUSDn7jmuVnj3SX3Qs2zbp7R/_.png</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Breast exam: Nursing]]></video:title><video:description><![CDATA[Assessment of the breasts should be completed as part of a comprehensive client assessment or as part of a focused exam, if the client is experiencing issues, such as discovery of a breast lump or nipple discharge. This assessment provides the nurse with information about the breast tissue, lymphatic system, and general sexual and reproductive health. Let’s review the process of completing a breast exam. 

Okay, the supplies needed for the breast exam include drapes, gloves, and a good source of light. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. 

Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Now, as the nurse, you may assist the healthcare provider or act as a chaperone, which is often required by facilities to protect clients and clinicians during breast exams. During the examination, keep in mind that the breast assessment can be emotionally uncomfortable and anxiety-producing for some clients, particularly those who have experienced sexual trauma or who are transgender. Be sure to use preferred pronouns and be aware of variations in the breast for those who have had breast augmentation or gender affirming surgeries. 

It’s also crucial to explain exactly what will happen at each step of the exam. Remember to avoid rushing your assessment, use a gentle touch, and to let your client know that at any time the exam can be stopped or paused if they request.

 Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies. 

Alright, locating the anatomical landmarks of the breasts will help guide your assessment. The breasts are located on the anterior chest wall in front of the pectoralis major and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Psychosocial:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/37_OFskXSQi1OHK3QTAcF6VsR3a1X9mQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Psychosocial: Nursing]]></video:title><video:description><![CDATA[Geriatrics is the branch of medicine that deals with the physiology and psychology of aging, as well as the diagnosis and treatment of diseases affecting older clients. Now, as a person ages, they go through psychosocial development, which refers to how the client&amp;#39;s personal needs fit with the needs of the society. This occurs through a life-long series of events with multifactorial influences like personality, thinking, and behavior. Two psychiatrists and psychologists who were involved in studying psychosocial development are Carl Jung and Erik Erikson. 

Okay, now one particular theory of Carl Jung is called individualism, which describes the process by which a person develops into a unique individual by balancing their orientation between the external world and their own subjective, inner experiences. According to Jung, individuals age successfully when they accept the past, adapt to physical decline, and accept their life’s accomplishments as well as its limitations. 

Now, Erikson constructed a theory called the psychosocial theory of development, which describes development in eight life stages. Typically, an individual needs to fulfill a particular task in one stage to move to the next one. The eighth and final life stage in Erikson’s theory occurs in clients who are 65 years or older, and it is called integrity vs. despair. Integrity is when older clients review their lives with satisfaction, even in the presence of inevitable mistakes, whereas despair occurs when older clients regret missed opportunities in life. Finally, psychosocial development is closely related to decisions regarding the end of life. 

Now, psychosocial development can influence quality of life, or QOL for short, which can be health-related or environmental. Health-related QOL includes a client’s physical, mental, emotional, and social functioning, and their impact on quality of life. These can include mobility, independence in bathing and dressing, sensory acuity, i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Active_Learning_with_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CgqS6GVTTGy_2fJM_Hc6wRnBSmKuDypz/_.png</video:thumbnail_loc><video:title><![CDATA[Active Learning with Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Active Learning with Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_and_PA_Education:_Success_Stories_from_Partner_Programs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IxxFJ27vQ9y-Xxd3u0BVj3VxQNuN-1Dd/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis and PA Education: Success Stories from Partner Programs]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis and PA Education: Success Stories from Partner Programs through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cognitive_Load:_What_is_it_and_why_does_it_matter_in_health_professions_education</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4WDVg6X7TVaGVTeRjc_OyeVhRtCAQzm-/_.png</video:thumbnail_loc><video:title><![CDATA[Cognitive Load: What is it and why does it matter in health professions education]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Cognitive Load: What is it and why does it matter in health professions education through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Take_a_Peek_at_Osmosis!</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ISA8jScZS96iSy4efta4lkBMTdWO_FzJ/_.png</video:thumbnail_loc><video:title><![CDATA[Take a Peek at Osmosis!]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Take a Peek at Osmosis! through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Quick_Osmosis_Tutorial_for_Faculty</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qbkSDqD2TBGs4ruDXTgfoXYxT8_RvY5G/_.png</video:thumbnail_loc><video:title><![CDATA[Quick Osmosis Tutorial for Faculty]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Quick Osmosis Tutorial for Faculty through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Videos_in_education:_Quality_assessment_and_considerations_for_the_flipped_classroom</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hF60jCo6SEWeHzNqWW1m7WFhT1eS1KcB/_.png</video:thumbnail_loc><video:title><![CDATA[Videos in education: Quality assessment and considerations for the flipped classroom]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Videos in education: Quality assessment and considerations for the flipped classroom through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Title:_Osmosis_Nursing_supports_Teaching_and_Learning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fFGwnk4tRxqIj0zURr0DZ2kiSbinOXzp/_.png</video:thumbnail_loc><video:title><![CDATA[Title: Osmosis Nursing supports Teaching and Learning]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Title: Osmosis Nursing supports Teaching and Learning through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Get_to_know_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HUQaLxU8Q2K3TZGh3tDWWpE0RP2A2mWE/_.png</video:thumbnail_loc><video:title><![CDATA[Get to know Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Get to know Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticonvulsant_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-iYlrCrCT4C_4JoopV7kf28DQKCb05VR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticonvulsant Therapy]]></video:title><video:description><![CDATA[Anticonvulsants, also known as antiepileptics, are medications primarily used to treat seizures and, on rare occasions, are prescribed to treat mood disorders. The most commonly prescribed anticonvulsant to manage seizures is phenytoin. 

So seizures occur acutely due to abnormal, excessive, and synchronous firing of neurons in the brain, which manifests as a change in the patient&amp;#39;s level of consciousness, body movements, sensations, or autonomic functions. Seizures usually last for a few seconds or minutes. When a patient has two or more seizures separated by at least 24 hours without a known cause, it is considered epilepsy.  

Now, anticonvulsants are categorized by their mechanism of action in managing seizures, which include suppression of sodium influx, suppression of calcium influx, or enhancement of gamma-aminobutyric acid, or GABA. First let’s focus on medications like phenytoin and other hydantoins, that act by inhibiting sodium influx into neuronal cells, thereby stabilizing cell membranes and reducing repetitive neuronal firing.  

Next, succinimide medications like ethosuximide work by blocking the calcium influx, preventing the electrical current generated by the calcium ions into the T-type calcium channel, ultimately reducing neuronal cell discharge. Lastly, medications like phenobarbital and benzodiazepines increase the action of GABA, which inhibits neurotransmitters throughout the brain to reduce seizure activity. 

Alright, so common side effects of phenytoin include headaches, dizziness, and gingival hyperplasia. Some patients experience serious hypersensitivity reactions like Stevens-Johnson syndrome and toxic epidermal necrolysis. In addition, phenytoin can cause constipation and nausea, as well as impaired metabolism of vitamin D, which can result in osteomalacia. 

Moreover, phenytoin can impair the absorption of folic acid and vitamin B-12; which can lead to hematologic side effects, referred to as blood dyscrasias, such ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/CNS_Depressant_&amp;_Skeletal_Muscle_Relaxant_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O941bCKFRVa5jvsR_dxttnkqSDeNdA3C/_.jpg</video:thumbnail_loc><video:title><![CDATA[CNS Depressant &amp; Skeletal Muscle Relaxant Therapy]]></video:title><video:description><![CDATA[Central nervous system depressants, also called CNS depressants, are medications that slow brain activity, and are used to promote relaxation, relieve anxiety, and induce sleep. CNS depressants are also used for moderate sedation before and during invasive procedures such as colonoscopies. Commonly prescribed CNS depressants include benzodiazepines like diazepam, lorazepam, and midazolam.  

Next, muscle relaxants are medications that reduce muscle spasms and associated pain. They are used to relieve both acute spasms associated with injury or chronic muscle spasticity related to CNS disorders, like multiple sclerosis and stroke. Cyclobenzaprine is the most commonly prescribed muscle relaxant to treat spasms related to musculoskeletal injuries.   

Now, midazolam is a benzodiazepine that acts as a central nervous system depressant. It works by enhancing the inhibitory effects of the neurotransmitter gamma-aminobutyric acid, or GABA, which decreases neuronal excitability and promotes sedation.  

Okay, so when the CNS is depressed by medications like midazolam, side effects can include headache, slurred speech, weakness, and anterograde amnesia, meaning the patient can’t recall the events that occurred after receiving the medication. Other side effects include nausea and hypotension, as well as pain at the injection site. Importantly, midazolam has a Black Box warning for severe respiratory depression and respiratory arrest. It’s also considered a high-alert medication, meaning it has an increased risk of causing significant patient harm if administered in error. 

As far as contraindications go, midazolam should be avoided in patients with acute narrow-angle glaucoma, because it can increase intraocular pressure; and must not be combined with other CNS depressants, such as alcohol, opioids like morphine, or centrally acting muscle relaxants like cyclobenzaprine, because this can result in profound sedation.  

Additionally, midazolam shouldn’t be give]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antipsychotic_Drug_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ov3xSqf3Re2NnpJEJvi99fBVQmySp3dm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antipsychotic Drug Therapy]]></video:title><video:description><![CDATA[Antipsychotics are medications mainly used to treat symptoms of psychotic disorders, like schizophrenia and bipolar disorder. There are two main categories of antipsychotic medications, known as first generation, or typical antipsychotics, and second generation, or atypical antipsychotics.  

Typical antipsychotics, like haloperidol, are highly effective, but have an increased risk of adverse effects, so they’re prescribed less often. On the other hand, atypical antipsychotics, like aripiprazole, generally cause less side effects so they’re considered first-line therapy.  

Okay, so psychotic disorders can be broadly defined as mental disorders characterized by fragmented and abnormal patterns of thinking. These disorders cause patients to have a variety of symptoms that impair normal functioning, such as delusions, hallucinations, and disorganized speech and behavior. Two of the most common psychotic disorders are schizophrenia and bipolar disorder. 

Now, the mechanism of action of an antipsychotic medication depends on whether it’s a typical or an atypical antipsychotic. Typical antipsychotics work by antagonizing dopamine, or D2 receptors, as well as histamine, or H1, acetylcholine, or Ach, and alpha-1 receptors.  Atypical antipsychotics also antagonize H1, Ach, and alpha-1 receptors, but they are weaker D2 antagonists, and they are also serotonin, or 5-HT2 antagonists. It’s important to note that all atypical antipsychotics antagonize these receptors to varying degrees, except for aripiprazole, which is a partial agonist of D2 and 5-HT1 receptors, and a pure antagonist at 5-HT2 receptors.    

Alright, so common side effects of antipsychotics are called extrapyramidal symptoms, or EPS, which are associated with D2 blockade. These symptoms include acute dystonia, which refers to muscle spasms of the eyes, face, neck, and back; akathisia, which is categorized by restlessness and a constant urge to move the limbs; Parkinsonian symptoms, including muscle ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacokinetics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RuIEzWMZSdiO10LidPSwN-6DSfy9Owqx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharmacokinetics]]></video:title><video:description><![CDATA[Pharmacokinetics refers to the movement and modification of a medication inside the body, and involves absorption, distribution, metabolism, and excretion. Because nurses are licensed to administer medications, they must ensure patient safety by understanding pharmacokinetic principles of every medication they administer. 

The first step of pharmacokinetics is absorption, or the movement of a medication from the site of administration into the bloodstream. Now, the rate of absorption, or how quickly this process occurs, as well as the extent of the absorption, or how much of the medication reaches the bloodstream, can be affected by several factors.  

One factor is the pH of the environment where absorption takes place. Since most medications are either weak acids or weak bases, weakly acidic medications are better absorbed in an acidic environment, like the proximal duodenum, while weakly basic medications are better absorbed in an alkaline environment, like the distal ileum.  

Another factor is the route of administration. For instance, a medication given sublingually has a higher rate and extent of absorption than its oral form because the medication is easily absorbed through the thin epithelium into circulation without having to go through the gastrointestinal system. Lastly, food in the stomach can either slow down or promote absorption, depending on the medication. 

The second step is distribution, or movement of the medication from the bloodstream to the tissues and into the cells. One factor affecting distribution is blood supply to the tissues. Medications are more rapidly distributed to tissues receiving an ample blood supply, like the brain, liver, and kidneys; and less rapidly distributed to tissues with lower blood supply, like the skin, adipose tissue, and bones. 

Another factor affecting distribution is protein binding. Medications travel through the bloodstream partly bound to plasma proteins, like albumin, and partly unbound or free.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharmacodynamics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C-SSH-N-TGeenV4NtxC2C7ZBT8mf7cVv/_.png</video:thumbnail_loc><video:title><![CDATA[Pharmacodynamics]]></video:title><video:description><![CDATA[Pharmacodynamics refers to the mechanisms and effects of a medication within the body. Or more simply, it’s what medications do to the body and how they do it. 

Now, medications bind to receptors, which are specialized proteins found inside the cell or on its surface or, to cause a change in the cell’s activity that ultimately creates a physiological effect. 

When a medication binds a receptor and mimics the body’s own chemical messengers, like hormones and neurotransmitters, to produce a desired response, it&amp;#39;s called an agonist. So, an agonist is like a key that fits into a lock, causing it to open. There are also medications that are partial agonists. Like agonists, they fit into the lock, but not as well, so they produce a weaker response. Lastly, there are antagonists, which bind to a receptor and block it so it can’t be bound to and activated by other medications or the body’s own chemical messengers. So, it’s like a key that can’t turn the lock, and may even get stuck in the lock. 

Now, after a medication binds to a receptor, there are additional factors that determine how the body will respond, including the dose of the medication, its efficacy, and its potency. So, let’s draw a graph, to show the relationship between the dose, on the x axis, and the response on the y axis. What we get is an S-shaped curve, called the dose-response curve, which has three phases. At first, in phase 1, the curve is more or less flat; that’s because the dose of the medication is too low, so not enough receptors bind to the medication to cause a significant response. 

As the dose increases, in phase 2, more receptors are occupied by the medication until just enough is present in the body to produce an effect. This is called the minimum effective concentration, or MEC. As the dose continues to increase, so does the response; but eventually, in phase 3, we reach a point where all the receptors are occupied, and the curve starts to flatten out. This is where t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholinergic_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Drg3ZOniQ3WihUdDUhGWB-3PQZSCK-Y-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholinergic Therapy]]></video:title><video:description><![CDATA[Cholinergic therapy uses medications that affect the parasympathetic nervous system, which is often nicknamed the “rest and digest” or “feed and breed” system of the autonomic nervous system. When activated, the parasympathetic nervous system promotes activities such as digestion, elimination, and sexual arousal, and it helps the body calm down after periods of stress or danger. Commonly used cholinergic medications include bethanechol, a direct-acting cholinergic agonist, and atropine, a cholinergic antagonist. 

Now, bethanechol is referred to as a parasympathomimetic because it works by mimicking the parasympathetic neurotransmitter, acetylcholine. By stimulating the muscarinic receptors in the bladder, it stimulates the contraction of the bladder’s detrusor muscle and relaxes the external urinary sphincter, promoting urination in non-obstructive urinary retention. By stimulating muscarinic receptors in the gastrointestinal tract, it promotes bowel motility. 

In contrast, atropine is referred to as a parasympatholytic, because it binds to acetylcholine receptors, blocking its effects. This leads to inhibition of the parasympathetic nervous system which results in increased heart rate and cardiac output and other antimuscarinic effects. It’s used to treat conditions like overactive bladder and bradycardia. It can also be used to promote pupillary dilation during eye exams and can be given preoperatively to reduce excessive respiratory secretions.  

Alright, cholinergic medications have several side effects which are related to their actions on the parasympathetic nervous system. By promoting parasympathetic effects in the heart and lungs, bethanechol can cause hypotension, bradycardia, and bronchoconstriction. It also promotes exocrine gland activity, causing sweating and increased salivation.  In addition, increased gastrointestinal activity can cause cramping and diarrhea. Other effects include blurred vision due to miosis, or pupillary constriction,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenergic_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uUPiONY_Qg27FgxhU2ylrVEqRci09m4-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenergic Therapy]]></video:title><video:description><![CDATA[Adrenergic agonists are sometimes called sympathomimetics, because they work by mimicking the actions of the sympathetic nervous system. They can be classified as either catecholamines or noncatecholamines. Epinephrine is an example of a catecholamine used in emergency situations like anaphylaxis and cardiac arrest, while albuterol is a noncatecholamine used for the treatment and prevention of bronchospasm. 

Now, adrenergic agonists mimic the effect of endogenous catecholamines by stimulating adrenergic receptors, activating the sympathetic nervous system, and triggering the fight or flight response.  

There are four main adrenergic receptors, including alpha 1 receptors, which are primarily associated with vasoconstriction and increased blood pressure; alpha 2 receptors, which cause vasodilation, beta 1 receptors which cause effects like increased cardiac contractility and increased heart rate; and beta 2 receptors which are primarily associated with bronchodilation.  

Epinephrine’s therapeutic effects are due to activation of alpha 1, beta 1, and beta 2 adrenergic receptors, so it has multiple sympathomimetic effects on the heart, blood vessels, and lungs. Albuterol works by selectively activating beta 2 receptors in the lungs, causing bronchodilation.   

Okay, so most side effects of adrenergic agonists are the result of their action on the adrenergic receptors throughout the body. So, both albuterol and epinephrine affect the central nervous system, causing restlessness, anxiety, dizziness, and tremors.  Cardiac side effects like palpitations, chest pain, and tachycardia can also occur. In addition, gastrointestinal side effects such as nausea, vomiting, and anorexia are also common. Now, for both epinephrine and albuterol, there are specific life-threatening effects to be aware of. Epinephrine can cause pulmonary edema or ventricular fibrillation; and it’s considered a high alert medication, meaning that there’s an increased risk of patient harm i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antidepressant_and_Mood_Stabilizer_Drug_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jloHVYeDRLmMAYb8dLgKzfIUSDq0yZFk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antidepressant and Mood Stabilizer Drug Therapy]]></video:title><video:description><![CDATA[Antidepressants are medications primarily used to treat major depressive disorder, which is a condition associated with a persistent feeling of sadness and loss of interest in everyday activities. There are five classes of antidepressant medications, including tricyclic antidepressants, or TCAs, selective serotonin reuptake inhibitors, or SSRIs, serotonin and norepinephrine reuptake inhibitors, or SNRIs, monoamine oxidase inhibitors, or MAOIs, and atypical antidepressants.  

Mood stabilizers are used to treat bipolar disorder, which is manifested by alterations in mood and behavior, vacillating between mania and depression. Examples of mood stabilizers include lithium, carbamazepine, valproic acid, divalproex, and lamotrigine.  

First, let’s focus on the SSRI sertraline. Sertraline is taken orally, and is rapidly absorbed into the bloodstream. Once it travels to the brain it inhibits the reuptake of serotonin, increasing the level of serotonin within the synaptic cleft.  

Now, sertraline affects different types of receptors in the brain, such as those that regulate sleep, appetite, or sexual function, so sertraline can cause insomnia, loss of appetite or weight gain, and sexual dysfunction. Sertraline can also cause hyponatremia, possibly by increasing the secretion of antidiuretic hormone. Some other side effects are anxiety, nausea, diarrhea, constipation, and bruxism, or teeth clenching and grinding. 

Now, as far as contraindications and cautions go, SSRIs like sertraline can increase the risk of  bleeding, especially if given along with antiplatelet or anticoagulant medications.  

Additionally, sertraline can cause serotonin syndrome, which usually occurs when combined with other antidepressants that increase the level of serotonin in the brain, especially MAOIs. Patients that develop serotonin syndrome typically present with skin flushing, hyperthermia, agitation, muscle rigidity, seizures, altered mental status, or even coma.  

Sertraline shoul]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antianxiety_Drug_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/It7_3qAeQSGMCQDKxo1nC9THQk_DNAZr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antianxiety Drug Therapy]]></video:title><video:description><![CDATA[Antianxiety medications are used to treat anxiety disorders, usually in combination with psychotherapy. Three classes of medications commonly used to treat anxiety disorders include selective serotonin reuptake inhibitors, or SSRIs, which are also used to treat depression; benzodiazepines, which are also used for their sedative effects; and lastly, buspirone.   

Now, anxiety is a feeling of uneasiness, uncertainty, or dread, which can be caused by real or perceived threats. Generalized anxiety disorder, or GAD, is a condition that causes a person to worry excessively and lasts for 6 months or longer. It can also be accompanied by other symptoms like sweating, trembling, nausea, poor sleep, and impaired concentration.  

Although buspirone’s mechanism of action isn’t well understood, it’s thought it reduces anxiety by binding to serotonin receptors, and to a lesser extent dopamine receptors.  

Alright, now buspirone does not have the potential for abuse or CNS depression like some of the other antianxiety medications. It’s generally well-tolerated, but some common side effects are headaches, dizziness, changes in dreams, and nausea. Less commonly, it can cause tardive dyskinesia and, rarely, serotonin syndrome. 

Buspirone is contraindicated in patients who have been taking monoamine oxidase inhibitors, or MAOIs, within the previous 14 days, because it can increase the risk of serotonin syndrome.  It also should be taken cautiously in patients with existing hepatic or renal impairment. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Drugs_Impacting_the_Renin_Angiotensin_Aldosterone_System_(ACE_and_ARB)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xeaTnh1LRQm8rvil8AIG76A3QtWIAPQb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Drugs Impacting the Renin Angiotensin Aldosterone System (ACE and ARB)]]></video:title><video:description><![CDATA[The renin angiotensin aldosterone system, or RAAS for short, helps regulate blood pressure in the body through vasoconstriction and increased blood volume. Now, when blood pressure falls, the kidneys release the enzyme renin, which converts angiotensinogen into angiotensin I. Angiotensin I  is then converted into angiotensin II by angiotensin-converting enzyme, or ACE for short. Angiotensin II is a potent vasoconstrictor that causes the muscular walls of small arteries to constrict, increasing blood pressure. It also triggers the release of the hormone aldosterone from the adrenal cortex, as well as vasopressin, also known as antidiuretic hormone, from the pituitary gland, prompting the kidneys to retain sodium and excrete potassium. The increased sodium causes water to be retained, thereby increasing blood volume and blood pressure. 

Medications that impact RAAS include ACE inhibitors and angiotensin II receptor blockers, or ARBs for short. ACE inhibitors and ARBs are typically used to treat hypertension and heart failure, while ACE inhibitors are also used for patients who have had a myocardial infarction. Now, ACE inhibitors usually end in “-pril”, and include enalapril, lisinopril, ramipril, benazepril, and captopril. Whereas ARBs usually end in “-sartan,” like candesartan, valsartan, irbesartan and losartan. ACE inhibitors and ARBs are taken orally except one ACE inhibitor called enalaprilat that can be administered intravenously for hypertension when oral treatment isn’t practical. 

Alright, both ACE inhibitors and ARBs lower BP by inhibiting angiotensin II, but in different ways. ACE inhibitors prevent the conversion of angiotensin I to angiotensin II. In contrast, ARBs block the actions of angiotensin II. Both actions prevent the vasoconstricting effects of angiotensin II  as well as the volume expanding effects of aldosterone.  

Now, the most common side effects of ACE inhibitors and ARBs are mild and nonspecific, such as a headache, dizziness,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vasodilator_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BEjdJMcURR638bZaeXC7xddRQS6Zz6Lf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vasodilator Therapy]]></video:title><video:description><![CDATA[Vasodilators are medications that directly affect the smooth muscle of arteries and are used to treat hypertension. The most common direct-acting vasodilators are hydralazine and minoxidil. Alright, let’s focus on hydralazine. 

Hydralazine relaxes the smooth muscle of the arteries by inhibiting intracellular calcium release within the smooth muscle cells, which inhibits its ability to contract, leading to vasodilation, decreased peripheral vascular resistance, and decrease in blood pressure. 

Okay, so the side effects of hydralazine are mostly related to their vasodilatory effects, which cause hypotension; reflex tachycardia, where the sympathetic nervous system is stimulated to increase the heart rate in response to decreased peripheral vascular resistance and hypotension; flushing; headache; and dizziness.  Other more serious side effects of hydralazine are related to sodium and water retention and include peripheral edema, pulmonary edema, and dyspnea. Although the mechanism of action is unclear, hydralazine can also cause lupus-like symptoms, such as malaise, myalgia, and fever.   

Now, contraindications for use of hydralazine include certain cardiovascular diseases since a sudden drop in blood pressure and subsequent reflex tachycardia can lead to increased myocardial oxygen demand, angina, and myocardial infarction; and certain cerebrovascular diseases because vasodilation can increase cerebral blood flow, resulting in increased intracranial pressure. Hydralazine should also be avoided in patients with septic shock due to its vasodilatory effects. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Calcium_Channel_Blocker_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/65BiqwprQ_2XR0TMe0pWJG5hTC_84zVj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Calcium Channel Blocker Therapy]]></video:title><video:description><![CDATA[Calcium channel blockers are a class of medications used to treat cardiac conditions, such as hypertension, angina, and arrhythmias.  Calcium channel blockers are divided into two groups based on their chemical structure: nondihydropyridines, like verapamil and diltiazem; and dihydropyridines, like nifedipine and amlodipine.  

Now, calcium is essential for the normal function of vascular smooth muscle, as well as the contraction of heart muscle, and electrical conduction through the heart. Calcium channel blockers work by preventing calcium from entering cells and binding with receptors. This causes vasodilation of the coronary arteries, which increases the blood flow and oxygen supply to the heart.  

Vasodilation also occurs in arteries throughout the body, reducing peripheral vesicular resistance which decreases the heart’s workload and oxygen consumption. Blocking calcium also decreases the heart muscle’s force of contraction and it slows conduction through the atrioventricular node which slows the heart rate and helps treat cardiac arrhythmias.  

So, the side effects of calcium channel blockers are mostly due to vasodilation, and can include headache, flushing, dizziness, peripheral edema, and hypotension. Bradycardia is also a common side effect due to the decreased velocity of conduction through the heart.  There are also some medication specific side effects to be aware of. Verapamil and diltiazem can cause constipation and heart block; whereas amlodipine can lead to facial edema, and nifedipine is associated with reflex tachycardia, meaning the heart rate rises in response to vasodilation.  

As far as contraindications go, calcium channel blockers should not be used in patients with hypotension, acute myocardial infarction, second- and third-degree atrioventricular heart block, or sick sinus syndrome, unless the patient has a pacemaker. Also, verapamil and diltiazem should be used with caution in patients with liver impairment. Lastly, IV verap]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Centrally_Acting_Alpha2_Adrenergic_Agonist_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kcjXcCVvStGDYgmEwk3VIAhERQSe55_a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Centrally Acting Alpha2 Adrenergic Agonist Therapy]]></video:title><video:description><![CDATA[Centrally acting alpha2 adrenergic agonists are medications that are primarily used to treat hypertension. There are 3 centrally acting alpha2 adrenergic agonists: clonidine, methyldopa, and guanfacine.  

Okay, so normally, neurons in the brainstem carry signals to the spinal cord, where they release the neurotransmitter norepinephrine, which stimulates the sympathetic nervous system, or SNS. This triggers actions like an increase in heart rate and blood pressure, and vasoconstriction.  

Now, alpha2 adrenergic agonists, like clonidine, work by selectively stimulating alpha2 receptors in the brainstem which then activate inhibitory neurons that oppose the SNS. This results in reduced sympathetic outflow to the heart and blood vessels, promoting vasodilation, decreased heart rate, decreased blood pressure, as well as decreased cardiac output.    

Alright, common side effects of clonidine can include CNS depression, bradycardia, and hypotension.  Xerostomia, also known as dry mouth, is common but this usually decreases after 2 to 4 weeks of therapy. And rarely, nausea, taste changes, anorexia, loss of appetite, and even heart failure can occur.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bile-Acid_Sequestrant_and_Fibrate_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yMuDassYQBq5cqEHoDCpZlJLTO6jaLD2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bile-Acid Sequestrant and Fibrate Therapy]]></video:title><video:description><![CDATA[Bile-acid sequestrants and fibrates are medications used to treat hyperlipidemia, or abnormally high levels of fats or lipids in the blood. Bile-acid sequestrants, like colesevelam, are used to reduce low-density lipoproteins, or LDLs, in patients with primary hypercholesterolemia. On the other hand, fibrates, also known as fibric acid derivatives, like gemfibrozil, are primarily used to lower triglyceride levels, but they can also lower total cholesterol and LDL levels while increasing high-density lipoproteins, or HDLs.  

First, let’s focus on the bile-acid sequestrant, colesevelam, which is taken orally and isn’t absorbed by the GI tract. It works by binding with bile acid, preventing its reabsorption, and forming an insoluble complex that’s excreted in the stool. In response, the liver compensates by increasing bile salt production, which uses up a lot of cholesterol in its synthesis. Additionally, the liver increases uptake of LDLs, resulting in lowered LDL levels in both the liver and circulation. On the other hand, fibrates, like gemfibrozil, lower the triglyceride level by activating the peroxisome proliferator-activated receptor-alpha, or PPAR-α, receptor in the liver. This causes an increase in the production of lipoprotein lipase, an enzyme that increases lipolysis, reduces hepatic triglyceride production, and increases HDL formation. 

Okay, so common side effects of both bile acid sequestrants and fibrates include GI disturbances, such as constipation, nausea, vomiting, dyspepsia, bloating, and abdominal pain. However, as opposed to other bile acid sequestrants, colesevelam is associated with fewer of these side effects. Colesevelam can also decrease the absorption of fat-soluble vitamins, such as A, D, E, and K; which can increase the risk of bleeding due to decreased synthesis of vitamin K-dependent clotting factors. Side effects specific to gemfibrozil include increased risk of gallstone formation, liver injury, and myopathy.   

As far as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Class_I_Antidysrhythmic_Therapy_(Sodium_Channel_Blockers)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7UKf3z5CT3KDQO4IkIt7WN1bTJWWAP_5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Class I Antidysrhythmic Therapy (Sodium Channel Blockers)]]></video:title><video:description><![CDATA[Antidysrhythmic medications help correct irregular heart rhythms. Class I antidysrhythmic medications, also known as sodium channel blockers, are divided into three groups which differ by how they impact electrical conduction and repolarization.

Class IA antidysrhythmics like quinidine, are used for atrial and ventricular dysrhythmias, as well as supraventricular dysrhythmias; whereas class IB antidysrhythmics, such as lidocaine, are used for acute ventricular dysrhythmias; and class IC antidysrhythmics, like flecainide, are used to treat the most serious, life-threatening ventricular dysrhythmias that have not responded to other antidysrhythmic medications.

Alright, so class I antidysrhythmics work by blocking sodium channels and reducing the influx of sodium into cardiac cells. This slows the electrical impulses through the heart’s conduction system, ultimately resulting in a slower, more regular heart rhythm.

The three medication subgroups have minor differences in how they affect the electrical impulses. First, class IA antidysrhythmics slow conduction and prolong repolarization; class IB antidysrhythmics slow conduction and shorten repolarization; and class IC antidysrhythmics prolong conduction with little or no effect on repolarization. 

Now, even though antidysrhythmics are indicated to treat dysrhythmias, they tend to have pro-dysrhythmic properties, meaning they can make the dysrhythmia worse, or even cause new dysrhythmias. Other side effects of antidysrhythmic medications will vary depending on the subgroup.

So, quinidine can cause headaches, dizziness, bradycardia, and diarrhea. Some of the more severe effects include cardiotoxicity, including ventricular tachycardia, heart block, asystole, as well as arterial embolism. It can also cause cinchonism, which is an adverse effect of medications made from plant alkaloids from the cinchona bark, that causes symptoms like nausea, tinnitus, and visual disturbances. 

On the other hand, lidocaine ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Class_II_Antidysrhythmic_Therapy_(Beta_Blockers)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UX-41wSDTIaJTcJYbreRSmFcSc6OF3NX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Class II Antidysrhythmic Therapy (Beta Blockers)]]></video:title><video:description><![CDATA[Class II antidysrhythmic medications, also known as beta blockers, are a class of medications that help control dysrhythmias, or abnormal heart rhythms. Now, there are two types of beta blockers: nonselective beta blockers, like propranolol, and cardioselective beta blockers, like metoprolol.

Alright, beta1 and beta2 receptors are adrenergic receptors that bind with catecholamines like norepinephrine and epinephrine, which are neurohormones of the sympathetic nervous system, or SNS. Beta1 receptors are located in the heart and beta2 receptors are mostly in the lungs. You can remember this by thinking we have one heart and two lungs. In the heart, beta1 receptors stimulate cardiac activity, whereas in the lungs beta2 receptors cause smooth muscle and bronchial relaxation.

Nonselective beta blockers, like propranolol, block effects of both beta1 and beta2 receptors of the heart and lungs, while cardioselective beta blockers, like metoprolol, block only the beta1 receptors unless given at higher doses.

Now, by blocking adrenergic receptors, beta blockers decrease the effects of the SNS, and can be used to decrease dysrhythmias that are caused by an excessive amount of SNS stimulation.

For instance, the excessive catecholamine response after a myocardial infarction, or MI, makes the heart hyperirritable, which can lead to dysrhythmias. Beta blockers block the actions of catecholamines on the beta1 receptors, reducing the risk of post-MI ventricular dysrhythmias.

Specifically, beta blockers decrease the heart rate by delaying the conduction through the atrioventricular, or AV, node and decreasing automaticity of the sinoatrial, or SA, node. They also reduce myocardial contractility, which decreases the workload of the heart.

Now, even though antidysrhythmics are indicated to treat dysrhythmias, they tend to have prodysrhythmic properties, meaning they can make the dysrhythmia worse, or even cause new dysrhythmias.  Other effects include bradycardia and AV]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Class_III_Antidysrhythmic_Therapy_(Potassium_Channel_Blockers)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F3iXZg3_Try5nZThQ1Is8a4PRY6utrxp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Class III Antidysrhythmic Therapy (Potassium Channel Blockers)]]></video:title><video:description><![CDATA[Class III antidysrhythmic medications, also called potassium channel blockers, are a class of medications used to treat life-threatening dysrhythmias like ventricular tachycardia or ventricular fibrillation. They can also be used to treat certain atrial dysrhythmias when other medications have not been effective. Examples of potassium channel blockers include amiodarone and dronedarone.

Okay, amiodarone and dronedarone mostly work by blocking potassium channels, which prolongs repolarization and the refractory period of the heart.

They also block sodium channels, which slows conduction through the heart’s conduction system.

Finally, they also block calcium channels and beta-adrenergic receptors, which decreases sinoatrial, or SA, node automaticity, and delays the conduction through the atrioventricular, or AV, node.

Now, even though antidysrhythmics are indicated to treat dysrhythmias, antidysrhythmics do tend to have prodysrhythmic properties, meaning they can make the dysrhythmia worse, or even cause new dysrhythmias.

Potassium channel blockers also prolong the refractory period in the heart, which prolongs the QT interval, which is the length of time from the beginning of the QRS complex to the end of the T wave on an ECG. This represents the time it takes for the ventricles to depolarize, or contract; and repolarize, or relax.

Widening of the QT interval increases the risk of torsades de pointes, a dysrhythmia that can degenerate into ventricular fibrillation, which is a life-threatening dysrhythmia.

There&amp;#39;s also a high risk for organ toxicities, especially in patients taking the medication long-term or prescribed larger doses.

Both medications can cause pulmonary toxicity and hepatotoxicity. Amiodarone can cause cardiotoxicity, and thyroid toxicity.

Amiodarone can also cause other serious complications such as ophthalmic effects like optic neuropathy and neuritis. Amiodarone may also cause photosensitivity, and the skin can turn a bl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Class_IV_Antidysrhythmic_Therapy_(Calcium_Channel_Blockers)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/19WdH0ALRgSo17kjMM7wZNP8SCuOS6GL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Class IV Antidysrhythmic Therapy (Calcium Channel Blockers)]]></video:title><video:description><![CDATA[Antidysrhythmic medications help correct irregular heart rhythms. Class IV antidysrhythmic medications, also known as calcium channel blockers, are a class of medications that help control dysrhythmias. Verapamil and diltiazem are the two calcium channel blockers used to treat dysrhythmias and are classified as nondihydropyridines.

Alright, so calcium is essential for electrical conduction through the heart, the contraction of heart muscle, and the normal function of vascular smooth muscle. Calcium channel blockers work by preventing calcium from entering cells and binding with receptors. This slows sinoatrial, or SA, node automaticity, and delays conduction through the atrioventricular, or AV, node. It also reduces myocardial contractility, promotes decreased peripheral resistance, blood pressure, and cardiac workload.

Now, even though antidysrhythmics are indicated to treat dysrhythmias, they tend to have prodysrhythmic properties, meaning they can make the dysrhythmia worse, or even cause new dysrhythmias.  Other side effects of calcium channel blockers are mostly related to vasodilation and can include headache, flushing, dizziness, peripheral edema, and hypotension.

Bradycardia is also a common side effect due to the decreased velocity of conduction through the heart.  Calcium channel blockers can cause constipation and heart block, as well as acute renal failure, and Stevens-Johnson syndrome.

As far as contraindications go, calcium channel blockers should not be used in patients with hypotension, acute myocardial infarction, second- or third-degree heart block, or sick sinus syndrome, unless the patient has a pacemaker. They should also be used with caution in patients with liver impairment.

Lastly, IV verapamil is considered a high alert medication, meaning there’s an increased risk of patient harm when the medication is used in error.

As far as interactions go, verapamil should not be given to patients who are also taking digoxin, since this ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nitrate_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oUmvNsHsQcm9ezV2LHT22QMBRqOryS2o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nitrate Therapy]]></video:title><video:description><![CDATA[Nitrates are a group of medications that are called vasodilators, because they dilate the walls of blood vessels. Nitrates are primarily used to treat angina pectoris, which is pain caused by reduced blood flow to the heart muscle; as well as hypertension, and heart failure. The most commonly used nitrates include nitroglycerin, isosorbide dinitrate, and isosorbide mononitrate.   

Okay, let’s focus on nitroglycerin. Nitroglycerin is lipid soluble so it’s easily absorbed through cellular membranes, so it is typically given through rapidly absorbable routes like sublingual or oral spray to treat acute anginal pain or hypertension; or as transdermal patches or topical ointments for long-term prevention. Nitroglycerin can also be administered rectally for the treatment of anal fissures.  

Once absorbed into the blood, nitroglycerin is quickly converted into nitric oxide, which diffuses into the smooth muscle cells of both veins and arteries, causing vasodilation. The result of venous vasodilation is peripheral blood pooling, which decreases preload, or the pressure that stretches the heart as it fills with blood from venous return. At the same time, arterial vasodilation lowers the systemic vascular resistance, which will also reduce the afterload, or the pressure that the heart must work against to eject blood during ventricular contraction. Ultimately, by reducing preload and afterload, nitroglycerin reduces the amount of work the heart has to do, eventually decreasing the heart’s oxygen consumption. Nitroglycerin also dilates the coronary arteries, increasing the blood supply to cardiac muscle. 

Common side effects of nitroglycerin are related to its vasodilatory effects and include headache, dizziness, flushing, and peripheral edema. Another important side effect is orthostatic hypotension, when blood pressure falls significantly when the patient stands up too quickly. As a result, these patients could experience lightheadedness or syncope due to decrea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Oral_Anticoagulant_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/juBMSiTtTg2qC9WrwXCyxdHdTBWd57D7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Oral Anticoagulant Therapy]]></video:title><video:description><![CDATA[Oral anticoagulant medications impair the process of clot formation and are used to prevent thromboembolic conditions like pulmonary embolism or stroke. They can also reduce the risk of transient ischemic attacks and myocardial infarction. There are three types of oral anticoagulant medications: vitamin K antagonists, like warfarin; direct thrombin inhibitors, like dabigatran; and direct factor Xa inhibitors, like rivaroxaban.  

Okay, so, the main goal of coagulation is to form a stable blood clot to stop bleeding and allow time for the tissue to be repaired. Anticoagulants work by interfering with the normal function of clotting factors involved in the coagulation cascade. Now, the coagulation cascade consists of three pathways, the extrinsic, intrinsic, and common pathways, that interact together to form a stable blood clot.  

The extrinsic and intrinsic pathways both lead into the final common pathway by independently activating factor X. After factor X is activated, it becomes factor Xa, and the common pathway begins. Here, factor Xa converts prothrombin to thrombin, which then cleaves fibrinogen, into fibrin. Fibrin is a long, thin protein that ultimately creates fibrin crosslinks to form a mesh that stabilizes the clot and helps stop bleeding. 

Warfarin is a vitamin K antagonist. Vitamin K supports clotting by helping produce certain clotting factors in the coagulation cascade. So as a vitamin K antagonist, warfarin impairs the synthesis of these clotting factors, and prolongs clotting time, while also depleting the functional vitamin K reserves.  Dabigatran, a direct thrombin inhibitor, and rivaroxaban, a direct factor Xa inhibitor, both prevent the formation of fibrin. Fibrin provides strength to stabilize the clot, so without it, clot production is disrupted. 

Now, the most common side effect of anticoagulants is prolonged bleeding, ranging from minor hemorrhage and localized bruising to major hemorrhage. Hypersensitivity reactions like dermat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiplatelet_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ObR1kDEBT9SpL8SNpWPdqhDgS2u5z5dy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiplatelet Therapy]]></video:title><video:description><![CDATA[Antiplatelet medications inhibit platelet aggregation. They are used to prevent thrombosis in conditions like ischemic stroke or myocardial infarction in at risk patients.  There are 3 major classes of antiplatelet medications, including COX inhibitors, like aspirin; GP IIb/IIIa inhibitors, like tirofiban; and P2Y12 ADP receptor antagonists, like clopidogrel.Alright, let’s start with how platelet aggregation works. When there’s a vascular injury in the body, platelets aggregate, or stick to the damaged vessel wall. In addition, they release various activating substances, including thromboxane A2 and adenosine diphosphate or ADP, that cause platelets to express a surface receptor called glycoprotein IIb/IIIa or GPIIb/IIIa. These receptors help platelet-to-platelet adhesion and binding to fibrinogen, a protein that circulates in the blood, which helps link platelets together. This allows platelets to rapidly aggregate at the site of injury and form a platelet plug, as red blood cells become enmeshed in the fibrin. This forms a clot that can help stop the bleeding.Now, let’s focus on clopidogrel, a commonly used antiplatelet medication. Clopidogrel works by binding to a specific ADP receptor on the platelets called P2Y12, which prevents ADP from binding to it. Without ADP, the platelets can’t express GPIIb/IIIa on their surface, which inhibits clot formation. 
Okay, let’s look at the side effects of clopidogrel. While the medication is generally well-tolerated, clopidogrel increases bleeding risk which can lead to epistaxis, or bloody nose, and easy bruising. Other common side effects can include indigestion, diarrhea, abdominal pain, or rash.Rarely, thrombotic thrombocytopenic purpura, or TTP, can occur within the first 2 weeks of therapy. TTP causes clotting in small blood vessels throughout the body, resulting in thrombocytopenia, or a low platelet count, as well as fever, hemolytic anemia, renal and neurologic dysfunction. TPP is considered a medical emer]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antidiabetic_Therapy_-_Insulin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cIDCHAevRnOwoNAjG2G4BDmMSrGrKKzW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antidiabetic Therapy - Insulin]]></video:title><video:description><![CDATA[Insulin is a medication most often used to treat type 1 diabetes mellitus but can also be used to treat type 2 diabetes mellitus during periods of stress, illness, or hospitalization, or when measures, like lifestyle changes and oral antidiabetic medications, fail to provide adequate glycemic control.Now, there are 4 main types of insulin, which are classified based on their onset of action and duration of effect. These include rapid-acting; short-acting or regular; intermediate-acting; and long-acting insulins.Additionally, there are various combinations of insulin, like a short-acting insulin combined with an intermediate-acting insulin.Insulin can be administered as a basal dose to supply the insulin needed for basic metabolic functions, typically with an intermediate- or long-acting insulin.It can also be given as a bolus, like with a meal to cover the postprandial rise in glucose, usually with a rapid- or short-acting insulin.And it can be given as a correctional dose for acute episodes of hyperglycemia, typically with a rapid- or short-acting insulin.Insulin is usually administered either subcutaneously or intravenously, but it also comes in a powdered form that can be inhaled. 
Alright now, glucose is the body’s essential energy source and is controlled by insulin, a hormone which is released from the beta cells in the pancreas in response to a rise of glucose.Type 1 diabetes occurs when the beta cells in the pancreas are unable to produce insulin; whereas type 2 occurs when there’s insulin resistance, meaning cells have trouble responding to the insulin that is produced, so they aren’t able use the available glucose from the blood, leading to cell starvation, despite a high circulating glucose level.When administered, insulin binds to receptors on insulin-responsive tissues, mostly muscle and fat tissue, and facilitates the uptake of glucose from the blood. It also acts on the liver and muscles causing glycogenesis, or the storage of glucose as gly]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antidiabetic_Therapy_-_Non-insulin/Oral_Antidiabetic_Drugs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NphuiM69Rj6laN4ctqrvs10tQguG9o81/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antidiabetic Therapy - Non-insulin/Oral Antidiabetic Drugs]]></video:title><video:description><![CDATA[Non-insulin antidiabetic medications are used to treat type 2 diabetes mellitus. These medications work to overcome insulin resistance and lower blood glucose levels. One of the most used oral antidiabetic medications is metformin, which is classified as a biguanide. 
Now, type 2 diabetes mellitus is characterized by insulin resistance, which is when cells have difficulty responding to insulin in order to uptake glucose from the blood. As a result, cells starve because they don’t receive adequate energy, despite the blood having high blood glucose levels. 
Metformin lowers blood glucose by decreasing glucose production in the liver, reducing glucose absorption in the gut, and increasing insulin sensitivity of targeted cells, like those in fat and skeletal muscle. As an added benefit, metformin decreases triglyceride and cholesterol production in the liver, which helps to reduce plasma lipid levels, as well as weight and blood pressure. 
Okay, so, because metformin does not stimulate insulin release from pancreatic beta cells like other oral antidiabetic medications do, hypoglycemia is not one of its side effects. However, other side effects are common, including GI disturbances, such as anorexia, nausea, vomiting, and diarrhea. In addition, prolonged use of metformin decreases absorption of vitamin B12 which can lead to peripheral neuropathy.Metformin also can impair mitochondrial oxidation of lactic acid, so, as a Black Box warning, metformin can lead to lactic acidosis, which is a life-threatening condition characterized by hyperventilation, myalgia, malaise, and drowsiness, and can lead to kidney failure, and shock. 
So, as far as contraindications go, metformin is contraindicated in patients with hypoglycemia, diabetic ketoacidosis, metabolic acidosis, and severe renal dysfunction. Additionally, metformin should be used cautiously in patients with alcoholism, liver impairment, and heart failure; and it is not indicated for patients with type 1 diabetes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_and_Parathyroid_Drug_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Eefj6Ij8SXy7gMdajOGQ6gauTF666tL6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid and Parathyroid Drug Therapy]]></video:title><video:description><![CDATA[The thyroid and parathyroid glands produce hormones responsible for metabolism, growth, and development. The thyroid gland produces the thyroid hormones T3, or triiodothyronine, and T4, or thyroxine. Thyroid medications are primarily used to treat hypothyroidism which is a decrease in thyroid hormones; and hyperthyroidism, which is an increase in these thyroid hormones.The parathyroid glands, on the other hand, produce parathyroid hormone, or PTH for short. So parathyroid disorders include hypoparathyroidism, which is a decrease in PTH, and hyperparathyroidism, which is an increase in PTH. 
Let’s start with the treatment for hypothyroidism, which often presents with weight gain, weakness, fatigue, and cold intolerance. Treatment involves thyroid hormone replacement therapy with levothyroxine, which is a synthetic form of T4.In contrast, hyperthyroidism presents with weight loss, anxiety, an elevated heart rate and blood pressure, as well as bulging eyes, or  exophthalmos. Hyperthyroidism is treated with methimazole or propylthiouracil, which suppress the synthesis of thyroid hormones. 
Now, hypoparathyroidism, will often present with signs and symptoms of hypocalcemia, like numbness in the hands, feet, and mouth, as well as cardiac arrythmias and tetany, or involuntary muscle cramps. It’s treated with calcitriol, or vitamin D3, which increases blood calcium levels.In contrast, hyperparathyroidism presents with signs and symptoms of hypercalcemia, which can be remembered by ‘stones, bones, abdominal groans, and psychiatric overtones’ meaning kidney stones, osteoporosis, abdominal pain and constipation, and depression and fatigue. It can be treated with cinacalcet, which decreases blood calcium levels.As far as side effects go, levothyroxine can cause headaches, insomnia, nausea, and weight loss, as well as hyperthyroidism. Importantly, it has a Black Box warning that it should not be used for weight loss. Side effects of methimazole and propylthiouracil inc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Histamine2_Blocker_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/poWZ7cdIT2Kj1fx-iXMtpRcHQ16FZBzN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Histamine2 Blocker Therapy]]></video:title><video:description><![CDATA[Histamine H2-receptor blockers, also called H2-receptor antagonists or H2RAs, are medications that help reduce the production of gastric acid. They can be used to treat gastric and duodenal ulcers; gastroesophageal reflux disease, or GERD; heartburn; and Zollinger-Ellison syndrome, which is a rare condition caused by gastrin-secreting tumors. In addition, histamine H2-receptor blockers can be used to prevent stress-induced ulcers in critically ill patients.Histamine H2-receptor blockers include cimetidine, which can be administered orally, intravenously, and intramuscularly; famotidine, which is given orally or intravenously; and nizatidine, which is given orally. 
Now, in the stomach, on gastric parietal cells, histamine, stimulates H2 receptors, to secrete gastric acid to promote digestion.Histamine H2-receptor blockers obstruct these H2 receptors so histamine can’t bind to them. This results in decreased gastric acid secretion and reduces the acidity of the gastric acid.Alright, let’s focus on cimetidine. Some of the common side effects of cimetidine are due to its actions on H2 receptors located outside the gastrointestinal tract. So, in the brain, side effects can include headaches, dizziness, and confusion. In the skin, cimetidine may cause pruritus and rash. Cimetidine also binds to androgen receptors, which can lead to sexual side effects like decreased libido, impotence, and gynecomastia. Rarely, cimetidine can cause hematological side effects like agranulocytosis and thrombocytopenia.In addition, reduced production of gastric acid can favor bacterial growth in the stomach. This is associated with an increased risk of micro-aspiration and lung colonization, leading to pneumonia. Lastly, it’s important to note that prolonged use of histamine H2-receptor blockers for 2 years or more may lead to vitamin B12 malabsorption and subsequent deficiency. As far as contraindications go, cimetidine should be used with caution during pregnancy and breastfeedin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antiemetic_Drug_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PovSY4uZTfy8EgrkIBOvBijRTyyz4gVK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antiemetic Drug Therapy]]></video:title><video:description><![CDATA[Antiemetics are a class of medications used to treat nausea and vomiting. There are seven classes of antiemetics: antihistamines, like meclizine; anticholinergics, like scopolamine; dopamine antagonists, like promethazine; serotonin antagonists, like ondansetron; cannabinoids, like dronabinol; glucocorticoids, like dexamethasone; and substance P/Neurokinin 1 antagonists, like aprepitant.So, nausea is the uneasy feeling that often occurs before vomiting, or emesis. Emesis occurs when an area of the body, like the inner ear, the GI tract, or the cerebral cortex, sends a message to the chemoreceptor trigger zone in the brain, which then stimulates the vomiting center. 
Okay, let’s look closer at how some of these antiemetics work. Dopamine antagonists, like promethazine, block the dopamine 2 or D2 receptors in the chemoreceptor trigger zone, preventing nausea and vomiting. Promethazine also has anticholinergic and antihistamine effects. 
On the other hand, serotonin antagonists, like ondansetron, block type 3 serotonin or 5-HT3 receptors centrally in the chemoreceptor trigger zone and peripherally, on the vagal nerve in the upper GI tract, leading to suppression of nausea and vomiting. 
So, since promethazine blocks D2 receptors, it can cause extrapyramidal symptoms like muscle rigidity and a shuffling gait, restlessness, and facial grimacing; as well as neuroleptic malignant syndrome, an emergency condition which includes changes in mental status, hyperthermia, and muscle rigidity.In addition, anticholinergic side effects can include dry mouth, blurred vision, tachycardia, urinary retention, and constipation. Lastly, promethazine’s antihistamine effects can lead to dizziness and sedation. 
Common side effects of ondansetron include headache, dizziness, and constipation, and it can prolong the QT interval, leading to dysrhythmias. It can also cause a life-threatening side effect called serotonin syndrome, which is caused by an accumulation of serotonin t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Corticosteroid_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HJTJ67QrSzWG2EPv8Vm-bg8JS4W5xYW4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Corticosteroid Therapy]]></video:title><video:description><![CDATA[Corticosteroids are medications used for their anti-inflammatory and immunosuppressive effects to treat a broad range of conditions, including autoimmune diseases, asthma, rheumatoid arthritis, and inflammatory bowel disease; as well as preventing organ rejection in transplant recipients, and as a replacement in adrenal insufficiency. The two types of corticosteroids are glucocorticoids, like prednisone, and mineralocorticoids, like fludrocortisone. 
Okay, let’s start by reviewing the function of endogenous, or naturally occurring corticosteroids in the body, which come from the adrenal glands located on the top of each kidney. These glands secrete glucocorticoids such as cortisol, which is involved in the stress response, and metabolism of carbohydrates, fats, and proteins; and mineralocorticoids, like aldosterone, which play a role in fluid, sodium, and potassium balance, and blood pressure.Now, the level of these corticosteroids in the body is regulated by the hypothalamic-pituitary-adrenal, or HPA axis. So, for example, stimuli like stress, pain, trauma, or low cortisol levels prompt the hypothalamus to release corticotropin hormone, or CRH, which tells the anterior pituitary gland to release adrenocorticotropic hormone, or ACTH.ACTH will then travel to the adrenal cortex, stimulating it to release cortisol. Once cortisol reaches the needed level, this information is fed back to the hypothalamus, which stops secreting corticotropin, ultimately stopping the continued secretion of cortisol by the adrenals. This negative feedback mechanism keeps hormone activity within a normal range. 
Alright, prednisone impacts the inflammatory process by inhibiting the release of pro-inflammatory molecules such as prostaglandins, histamine, and interleukin-1, which results in a reduction of fever, swelling, warmth, redness, and pain.Prednisone also suppresses the activation and migration of immune cells, increases glucose levels, suppresses protein synthesis, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nonsteroidal_Antiinflammatory_Drugs_(NSAIDs)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3Uwk8mzLQ9a0JfZgytn3F1mrSXOEdy6A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nonsteroidal Antiinflammatory Drugs (NSAIDs)]]></video:title><video:description><![CDATA[Anti-inflammatory medications help to reduce inflammation, and restore function and mobility, all while decreasing pain.  

Nonsteroidal anti-inflammatory drugs, or NSAIDs for short, are one type of anti-inflammatory medication that are used for their anti-inflammatory, analgesic, and antipyretic properties. Commonly prescribed NSAIDs include aspirin and aspirin-like drugs, such as ibuprofen and celecoxib. 

NSAIDs treat a variety of symptoms related to inflammation such as headaches, fever, arthralgia, myalgia,  and pain associated with certain conditions like rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, and gout.  

So, inflammation is the body’s protective response to tissue injury, which can be caused by internal triggers, like cellular injury, and external triggers, such as infectious pathogens, physical trauma, and exposure to allergens or toxins.  

During the inflammatory response, the body releases proinflammatory mediators, like cytokines and prostaglandins, that send signals to cells to stop the cause of tissue injury, rid the body of dead cells, and begin tissue repair. The inflammatory process leads to the five cardinal clinical manifestations of erythema, edema, pain, heat, and loss of function.  

Now, NSAIDs treat the symptoms of inflammation by inhibiting proinflammatory mediators, which helps to limit the impact of the inflammatory response. Specifically, NSAIDs inhibit the enzyme cyclooxygenase, or COX, both in the central nervous system, and peripheral tissues. There are two forms of COX: COX-1 and COX-2.  

First, COX-1 is known as “good” COX since it’s involved in protective activities such as platelet aggregation, production of protective mucus in the stomach, and maintenance of renal function.  

On the other hand, COX-2, or “bad” COX, is only active in inflammatory cells and the vascular endothelium during inflammation and is involved in the production of small pro-inflammatory compounds like prostaglandins. When C]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diuretics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F11veXPOSK21JxA9gZ_glW2FRDan9np_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diuretics]]></video:title><video:description><![CDATA[Thiazide and thiazide-like diuretics, also called water pills, are medications that act on the kidneys’ basic unit, the nephron, to induce changes in electrolyte and water balance. They are generally used to treat mild to moderate hypertension, as well as peripheral edema. However, these medications can’t induce immediate or large volume diuresis. For this reason, they’re not typically used alone for fluid overload conditions, such as heart failure and pulmonary edema.

Okay, thiazide diuretics include chlorothiazide and hydrochlorothiazide, while examples of thiazide-like diuretics are chlorthalidone and indapamide. 

Thiazide and thiazide-like diuretics can be administered orally or intravenously. Once administered, they act on the distal convoluted tubule of the nephron, which has a sodium-chloride transporter that reabsorbs sodium and chloride ions from the tubule. Thiazide and thiazide-like diuretics block this transporter, which inhibits the reabsorption of sodium and chloride ions. And since water follows sodium, more urine is produced, which reduces the body’s total fluid volume. Thiazide and thiazide-like diuretics also cause vasodilation of the arterioles, decreasing blood pressure. 

Side effects of thiazide and thiazide-like diuretics mainly manifest as dehydration and electrolyte imbalance. First off, these diuretics can cause orthostatic hypotension, due to decreased circulating volume and vasodilation. They also tend to cause retention of calcium and uric acid, which can result in hypercalcemia and hyperuricemia. They can cause electrolyte imbalances like hypomagnesemia, hypochloremia, hyponatremia, as well as hypokalemia. Finally, they can alter the metabolism of glucose and fat, which may lead to hyperglycemia and hyperlipidemia.

As far as contraindications go, thiazide and thiazide-like diuretics should be avoided in patients with conditions like gout, diabetes mellitus, and hyperlipidemia. They are also contraindicated in patients who h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Beta-adrenergic_Blockers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EavqhvewSG2GR0KY7IYBm8CwTi2N_DjM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Beta-adrenergic Blockers]]></video:title><video:description><![CDATA[Beta-adrenergic blockers, or just beta blockers, are a group of medications that are mainly used to treat cardiovascular conditions like hypertension, coronary artery disease and its manifestations like angina pectoris and myocardial infarction, as well as heart failure and arrhythmias. Beta blockers can also be used to treat essential tremor, glaucoma, and as a prophylactic treatment of migraine attacks.

Now, beta blockers work by blocking beta receptors, of which there are three types, known as beta 1, which are mainly found in the heart and kidneys; beta 2, found in the lung bronchioles as well as the arteries of skeletal muscles; and beta 3, found in adipose tissue. So beta blockers are classified into two main groups; nonselective and selective. 

Nonselective beta blockers can block both beta 1 and beta 2 receptors, and include nadolol, propranolol, pindolol, and sotalol. On the other hand, selective beta blockers only block beta 1 receptors, and include atenolol, metoprolol, carvedilol, and nebivolol. So keep in mind that all beta blockers end in -lol (which is pretty funny), and they can be administered orally, intravenously, or even via the ophthalmic route. 

Once administered, beta blockers block beta receptors, thereby preventing the catecholamines norepinephrine and epinephrine from binding and activating them. As a result, beta blockers decrease the sympathetic nervous system response. 

Now, the main therapeutic effects of beta blockers come from the blockade of beta 1 receptors in the heart, which decreases heart contractility and slows the conduction through the atrioventricular or AV node. This helps decrease the heart rate, which ultimately decreases the cardiac output. In addition, the blockade of beta 1 receptors in the kidneys decreases the release of renin, which stimulates the adrenal glands to release aldosterone, which in turn acts on the kidneys to induce water and sodium reabsorption. So with beta blockers, there will be less r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_Glycosides</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v9AtTbOURaKL0Z_ZQ_ma6i1xTNaz5ND5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac Glycosides]]></video:title><video:description><![CDATA[Cardiac glycosides, also called digitalis glycosides, are medications derived from the foxglove plant, Digitalis purpurea. They are commonly used for the treatment of atrial arrhythmias, such as atrial flutter and atrial fibrillation, which are caused by rapid, uncoordinated contractions of the atria. In addition, cardiac glycosides can be prescribed for congestive heart failure when other medications fail. 

Now, the most commonly used cardiac glycoside is digoxin, which can be given orally, intravenously, and intramuscularly. Once administered, digoxin works by reversibly inhibiting the sodium-potassium ATPase located in the cell membrane of cardiomyocytes. Normally the sodium-potassium ATPase pumps three sodium ions out of the cell for every two potassium ions that it pumps in, and to do this, it consumes one ATP molecule for energy. When the sodium-potassium ATPase is inhibited by digoxin, sodium builds up inside the cell. This interrupts the sodium-calcium exchanger on the cell membrane, which normally pumps one calcium ion out in exchange for three sodium ions. As a result, digoxin causes calcium to build up within cardiomyocytes, allowing the cardiac muscle fibers to contract more efficiently, which leads to an increase in the force of the heart’s contractions and cardiac output. In turn, the increase in cardiac output increases the renal blood flow and urine output, which also helps reduce peripheral edema. 

Digoxin also stimulates the vagus nerve, which provides the parasympathetic supply to the heart, and reduces the conduction velocity through the AV node. These two effects combined result in a decreased heart rate. But because parasympathetic innervation is much richer in the atria, these effects mainly involve the atria. 

Now, a major drawback is that digoxin has a very narrow therapeutic window, which means that small variations in its blood concentration can easily cause toxicity. Some common side effects of digoxin that can indicate toxic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antihyperlipidemics_-_Statins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Dtctnz_UQmeGniGtKBM6jtTfSQiT2QdL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antihyperlipidemics - Statins]]></video:title><video:description><![CDATA[Antihyperlipidemics are medications used to treat clients with increased blood levels of lipids, like cholesterol, by decreasing the levels of low- density lipoproteins or LDLs, which is sometimes referred to as “bad” cholesterol; and to an extent, antihyperlipidemics can also decrease blood triglycerides. In addition, they’re indicated to treat clients with coronary artery disease and prevent myocardial infarction. 

Antihyperlipidemics include different classes of medications, among which some of the most commonly used are HMG-CoA reductase inhibitors, also called statins. Statins include simvastatin, rosuvastatin, atorvastatin, lovastatin, and pravastatin, which are administered orally. 

Once absorbed into the bloodstream, statins travel to the liver, where they inhibit the enzyme HMG-CoA reductase. As a result, there’s a decrease in cholesterol synthesis. This also causes hepatic cells to increase the number of LDL receptors on their surface. This facilitates the uptake of cholesterol-rich LDLs, and VLDLs to a smaller degree, which provides a moderate decrease in triglyceride level. So ultimately, statins help lower overall lipid levels.

Luckily, statins are very well tolerated. The most common side effects include gastrointestinal symptoms like abdominal cramps, diarrhea or constipation, flatulence, heartburn, and nausea. Especially with rosuvastatin, clients can develop a skin rash, and may experience headache and dizziness. 

Other side effects include blurred vision, cataracts, fatigue, and insomnia. Some of the more serious side effects of statins include myalgia, and rhabdomyolysis, or muscle breakdown. Next, although rare, statins can cause hepatotoxicity, especially in clients who already have a hepatic disease. Finally, simvastatin and atorvastatin can cause pancreatitis, while rosuvastatin can cause renal failure, and pancytopenia.

As far as contraindications go, statins are teratogenic, so they should be avoided during pregnancy. These me]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anticoagulants_-_Heparin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IM7YrUANSkaqylQZlVNTWecYTAKLmP7Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anticoagulants - Heparin]]></video:title><video:description><![CDATA[Anticoagulants are medications that work by interfering with the functional clotting factors in the coagulation cascade, and are used to prevent the formation of thrombi, or blood clots, and are used to prevent or treat thromboembolic events, such as deep vein thrombosis, pulmonary embolism, ischemic stroke, transient ischemic attack, coronary artery disease or myocardial infarction.  

They&amp;#39;re also used in clients with coagulation disorders, including antiphospholipid syndrome and disseminated intravascular coagulation; as well as in clients who underwent cardiac valve replacement or coronary angioplasty; and during surgical procedures like cardiopulmonary bypass, percutaneous coronary intervention, extracorporeal membrane oxygenation, and in clients undergoing dialysis. 

Among the most important anticoagulants are heparins. These include unfractionated heparin, which is derived from porcine sources, and can be administered intravenously or subcutaneously; as well as low molecular weight heparins or LMWHs, which are synthetic analogs of certain portions of the heparin molecule. These include enoxaparin, dalteparin, and tinzaparin, and are given subcutaneously. 

Once administered, heparins work by binding to and enhancing the activity of antithrombin III, which is an anticoagulant protein synthesized by the liver. Antithrombin III normally binds to and inhibits Factor Xa and Factor IIa, also known as thrombin, thus making them unavailable to participate in the coagulation cascade. Antithrombin III also inhibits factors VII, IX, XI, and XII, although with much less affinity. Ultimately, heparins stop the formation of the primary clot.  

Now, unfractionated heparin is usually used in immediate and short-term anticoagulation because it has a rapid onset of action, usually within seconds, and a short half-life. Additionally, unfractionated heparin doesn&amp;#39;t cross the placental barrier, making it the anticoagulant of choice during pregnancy. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Proton_pump_inhibitor_(PPIs)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kjQ0nL1YTKCQDm4kOfVLhUiwQOOpxT0o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Proton pump inhibitor (PPIs)]]></video:title><video:description><![CDATA[Proton pump inhibitors, or PPIs for short, are medications used to treat conditions like peptic ulcers, gastroesophageal reflux disorder or GERD, and Zollinger-Ellison syndrome, which is caused by a gastrin-secreting tumor that leads to excess gastric acid secretion which then results in peptic ulcers. Proton pump inhibitors are also included in the combination treatment against H. pylori, since they have a weak antibacterial effect.

Now, proton pump inhibitors usually end in “-prazole”, and include medications that are administered orally, like omeprazole, lansoprazole, dexlansoprazole, rabeprazole; as well as medications available intravenously, like pantoprazole and esomeprazole. 

Once administered, proton pump inhibitors act on the parietal cells in the stomach by binding to and inhibiting the H+/K+-ATPase or proton pumps. These pumps are involved in the secretion of gastric acid by exchanging potassium ions from the lumen with hydronium from the cells. As a result, proton pump inhibitors ultimately decrease gastric acid secretion. 

Side effects of proton pump inhibitors are uncommon, but can include headaches, dizziness, fatigue, and blurred vision, as well as dry mouth, increased thirst, and hiccups. In addition, some clients may experience gastrointestinal disturbances, such as increased or decreased appetite, nausea, abdominal pain, constipation, or diarrhea. Also, prolonged acid suppression can decrease the absorption of iron, calcium, magnesium, and vitamin B12, or cobalamin. 

When the gastric juices are less acidic, it also allows ingested pathogens, like Clostridioides difficile, to survive and invade the gastrointestinal tract. Therefore, clients treated with proton pump inhibitors are more susceptible to gastrointestinal infection; this is also associated with an increased risk of microaspiration and lung colonization, leading to pneumonia. Other side effects may include a skin rash, and osteoporosis.

Now, as far as contraindications go,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Analgesics</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1O4NCYFIT2m7rLeQEJpaGkQHSGygGFB4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Analgesics]]></video:title><video:description><![CDATA[Analgesics, also commonly known as painkillers, are medications primarily used to relieve pain, such as a headache, muscle and neuropathic pain, as well as pain related to trauma and fractures. Analgesics can be subdivided into two main groups: non-opioid analgesics, and opioid analgesics. Keep in mind though that there are a number of other medications that primarily serve other purposes, but can be used as analgesics. These medications include antidepressants like amitriptyline, anticonvulsants like gabapentin, and corticosteroids like dexamethasone, as well as local anesthetics like lidocaine. 

Now, let’s start with non-opioid analgesics, which include non-steroidal anti-inflammatory drugs or NSAIDs, and acetaminophen.

NSAIDs inhibit the enzyme cyclooxygenase or COX, both in the central nervous system and peripheral tissues. Now, there are two types of COX enzymes. The first one is called COX-1, which is indirectly involved in platelet aggregation, production of protective mucus in the stomach and vasodilation of the renal vasculature. On the flip side, COX-2 is only active in inflammatory cells and vascular endothelium during inflammation, and is involved in the production of small pro-inflammatory compounds like prostaglandins. 

Now, a very commonly used NSAID is acetylsalicylic acid, often referred to as aspirin, which is taken orally. On the other hand, non-aspirin NSAIDs can be further classified as non-selective COX inhibitors that act on both COX-1 and COX-2, like ibuprofen, naproxen and ketorolac; and selective COX-2 inhibitors, like celecoxib. Non-aspirin NSAIDs are most often administered orally, but some can also be given intramuscularly, intravenously, topically, or rectally.

Now the most important side effects of NSAIDs include gastrointestinal problems, such as gastritis, gastric ulcers, or even bleeding, and that’s a boxed warning! Additionally, chronic use of NSAIDs can impair normal blood flow in the kidneys and may increase the ris]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glucocorticoids_&amp;_Mineralocorticoids</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s6JJ2sTLTDi0W8vHwbQE-ekQSeafgcP9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glucocorticoids &amp; Mineralocorticoids]]></video:title><video:description><![CDATA[Glucocorticoids and mineralocorticoids are endogenous hormones normally produced by the adrenal glands. In clients with impaired adrenal function, these hormones can be administered as replacement therapy.

Synthetic glucocorticoids, also commonly known as corticosteroids, are medications that can be used in clients with decreased adrenal function, such as in adrenal insufficiency; this is also known as Addison disease, and specifically occurs when the adrenal glands don&amp;#39;t make enough endogenous glucocorticoids, so these clients need hormone replacement therapy with synthetic glucocorticoids. In addition, glucocorticoids are used in the treatment of numerous inflammatory conditions, such as asthma, rheumatoid arthritis, and inflammatory bowel disease, as well as  preventing organ rejection in transplant recipients.

Alright, now, based on the duration of action, synthetic glucocorticoids can be classified into three groups. The first group are short-acting glucocorticoids, such as cortisone and hydrocortisone. Cortisone needs to be converted into hydrocortisone in the liver in order to be active, so it can only be taken orally; while hydrocortisone can be given orally, intravenously, intramuscularly, and topically. 

The second group are intermediate-acting glucocorticoids, which include prednisone, prednisolone, and methylprednisolone. Prednisone can only be taken orally; while prednisolone can be administered orally, intravenously, or topically; and methylprednisolone can be given orally, intravenously, intramuscularly, or injected intra-articularly. 

The third and final group are long-acting glucocorticoids, which include betamethasone and dexamethasone. Both of these medications can be taken orally, intravenously, intramuscularly, or intra-articularly. In addition, betamethasone is also available for topical use.

Once administered, glucocorticoids act by binding to intracellular glucocorticoid receptors and then migrating into the nucleus to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchodilators</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FQxr_1WWRoWKwsAJ539NUCHoSiedu0RS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchodilators]]></video:title><video:description><![CDATA[Bronchodilators are a group of medications that help breathing by keeping the airways dilated. That being said, they are typically used in obstructive lung diseases, like asthma and chronic obstructive pulmonary disease, or COPD for short, where clients suffer from narrowing and obstruction of the airways. 

Asthma is characterized by chronic inflammation in the lungs, as well as asthma exacerbations or attacks, where certain triggers, such as viruses, allergens, stress, aspirin or other NSAIDs and exercise, lead to reversible bronchial smooth muscle spasms and mucus production, both of which make it hard to breathe. As a result, clients experience symptoms like dyspnea, wheezing, chest tightness, and coughing. 

On the other hand, in COPD, there’s chronic inflammation and fibrosis in the lungs, most commonly due to smoking. As a result, the airways become irreversibly obstructed and the lungs are not able to empty properly, which leaves air trapped inside the lungs. As a result, clients experience symptoms like dyspnea and a productive cough. 

Now, COPD generally refers to a group of progressive lung diseases that includes chronic bronchitis and emphysema. These two differ in that chronic bronchitis is defined by long-term inflammation of the bronchial tubes, whereas emphysema is defined by destruction and enlargement of the alveoli. Although the airway obstruction in COPD is irreversible, bronchodilators can often help prevent the complete closure of the airway during expiration, which provides mild symptomatic relief.  

Now, based on their mechanism of action, bronchodilators can be broadly divided into three main groups; β2-agonists; anticholinergics; and methylxanthines. The effect of all these medications is bronchial smooth muscle relaxation, which in turn results in dilation of the narrowed airways and improved air flow. 

In particular, β2-agonists, like albuterol and salmeterol, come in an aerosolized form, and can be taken via metered dose inh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inhaled_Corticosteroids</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x1zqomxFQEekz1xFkmI_r_NESemn_6DH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inhaled Corticosteroids]]></video:title><video:description><![CDATA[Inhaled corticosteroids are medications that improve breathing by decreasing lung inflammation. They are primarily used in clients with persistent asthma, meaning those who have asthmatic symptoms more than 2 days per week. Asthma is characterized by chronic inflammation in the lungs, as well as asthma exacerbations or attacks, where certain triggers, such as viruses, allergens, stress, aspirin or other NSAIDs and exercise, lead to reversible bronchial smooth muscle spasms and mucus production, both of which make it hard to breathe.

As a result, clients experience symptoms like dyspnea, wheezing, chest tightness, and coughing. Inhaled corticosteroids help decrease the frequency of symptoms and prevent exacerbations. Inhaled corticosteroids can also be used in clients with chronic obstructive lung disease, or COPD, to prevent exacerbation and slow the progression of the disease.

Now, commonly used inhaled corticosteroids include fluticasone, beclomethasone, budesonide, and mometasone. These medications are typically used as maintenance therapy to help control the underlying lung inflammation, and are often combined with inhaled bronchodilators, such as long acting beta-2 agonists like salmeterol, which provide immediate relief of symptoms by inducing airway smooth muscle relaxation. 

Now, once in the lungs, inhaled corticosteroids enter the respiratory epithelial cells and  suppress the expression of certain genes that code for inflammatory proteins. This leads to decreased movement of inflammatory and immune cells into the bronchi and lungs, as well as decreased production and release of inflammatory mediators like histamine and leukotrienes. As a result, there’s reduced airway inflammation and edema, as well as decreased mucus production, which ultimately leads to airway dilation and improved air flow. 

Because they work on the gene level, inhaled corticosteroids may need days or even weeks to demonstrate effectiveness. That&amp;#39;s why they are on]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Aminoglycosides</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rj1mc-HWRWyBQ65nAW9p-ndHSpCBp0ZN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Aminoglycosides]]></video:title><video:description><![CDATA[Aminoglycosides are a class of antibiotics used to treat severe systemic infections caused by aerobic, Gram negative bacteria, such as Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and the Enterobacter species. Additionally, aminoglycosides can be effective against certain Gram positive bacteria when used in combination with cell-wall inhibitors, like penicillins or cephalosporins. 

Now, aminoglycoside antibiotics used to treat bacterial infections include streptomycin, amikacin, gentamicin, tobramycin, and neomycin. These medications are poorly absorbed in the gastrointestinal tract, so they are primarily administered intramuscularly or intravenously. Streptomycin and amikacin can be used in the treatment of mycobacterial infections. Gentamicin can also be applied topically to treat eye or ear infections; while tobramycin can be given topically to treat eye infections, or in a nebulized form to treat Pseudomonas infections in clients with cystic fibrosis. Neomycin can be given orally to treat hepatic encephalopathy and before colorectal surgeries to act directly in the intestinal bacterial flora and reduce the risk of infection after surgery.

Aminoglycosides are powerful bactericidal antibiotics that work by binding to the 30S subunit of the bacterial ribosome. As a result, these medications disrupt bacterial protein synthesis and ultimately kill the bacteria. Since aminoglycosides need to enter the bacteria in order to be effective, they may be given alongside an antibiotic that inhibits bacterial cell wall synthesis, such as beta-lactams, to facilitate access of the aminoglycoside across the cell wall.

Regarding side effects, one thing to keep in mind is that aminoglycosides have a significant post-antibiotic effect, meaning that their bactericidal activity persists for a period of time even after the antibiotic is stopped. In addition, although aminoglycosides are very effective antibiotics, they also have a high risk of toxicity,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Cephalosporins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0cgCmkmCQEC-FBcwfiiFlTs0QyGauGbC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Cephalosporins]]></video:title><video:description><![CDATA[Cephalosporins are a large group of broad-spectrum antibiotics, which can be used to treat a wide variety of bacterial infections, including meningitis, pneumonia, urinary tract infections, and sepsis. These antibiotics get their name from Cephalosporium acremonium, a fungus from which they are derived.

Now, cephalosporins belong to beta-lactam antibiotics, which means they have a beta-lactam ring in their core, and they mainly work by disrupting the synthesis of the peptidoglycan layer, a major component of bacterial cell walls. This weakens the bacterial cell wall, ultimately killing the bacteria.

Now, cephalosporins are typically classified into five generations, each being used to treat certain types of bacterial infections. 

First-generation cephalosporins include cephalexin, which is administered orally; cefadroxil, which is administered orally and intravenously; and cefazolin, which is given intravenously and intramuscularly. In general, first-generation cephalosporins are effective against most gram-positive bacteria, such as Staphylococci and Streptococci spp; as well as some gram-negative bacteria like Escherichia coli, Proteus mirabilis, and Klebsiella pneumonia. 

So, first-generation cephalosporins are used to treat respiratory tract infections, urinary tract infections, some skin infections; and bone and joint infections. They can also be given as surgical antibiotic prophylaxis, to prevent infections from spreading to deeper tissues during surgical operations.

Next, second-generation cephalosporins include cefaclor and cefprozil which are administered orally; as well as cefotetan and cefoxitin, which are given intravenously and intramuscularly; and cefuroxime, which is given orally and intravenously. 

Compared to the first generation, second-generation cephalosporins are less effective against Staphylococcus spp. Instead, they are more effective against certain types of gram-negative bacteria, such as Haemophilus influenzae, which can c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Fluoroquinolones</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V5nWXWYaRwqDYPVM7H6Inz0KScaQfJl3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Fluoroquinolones]]></video:title><video:description><![CDATA[Fluoroquinolones are a group of broad spectrum antibiotics, which can be used to treat a wide variety of bacterial infections. These include eye infections like bacterial conjunctivitis; chest infections like Tuberculosis or pneumonia; gastrointestinal infections like shigellosis; urinary tract infections or UTIs; genital infections like gonorrhea; and in bone and joint infections. They are very effective against several gram negative organisms like Enterobacteriaceae spp., Haemophilus spp., Legionella spp., Neisseria spp., Moraxella spp., and even Pseudomonas spp. and gram positive bacteria like Streptococcus pneumoniae. 

Now, there are four generations of fluoroquinolones, but among all of them only few are commonly used. They are ciprofloxacin, levofloxacin, moxifloxacin, norfloxacin and ofloxacin. These medications can be administered both orally or intravenously, while ciprofloxacin and ofloxacin are also available in otic formulations, and ofloxacin and moxifloxacin are available as ophthalmic solutions.

Once administered, fluoroquinolones have a bactericidal effect by inhibiting a bacterial enzyme called DNA topoisomerase, also known as DNA gyrase, which is essential for bacteria to loosen up the tight coilings of DNA for the replication process. As a result, when DNA gyrase is inhibited by fluoroquinolones, bacterial DNA replication comes to a halt, ultimately killing the bacteria.

However, fluoroquinolones may cause side effects like central nervous system disturbances, including headache and restlessness, as well as dizziness, confusion, depression, nightmares, insomnia, and some may even present with seizures. Often, fluoroquinolones may also cause gastrointestinal disturbances like abdominal cramps, nausea, vomiting, diarrhea, and flatulence, as well as pancreatitis and hepatotoxicity.  In addition, fluoroquinolones may disrupt the normal intestinal flora, which can allow certain bacteria like Clostridioides difficile to survive and overgrow]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Macrolides</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4MjphducQjuoxXrE7nsP9uw8SoienPot/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Macrolides]]></video:title><video:description><![CDATA[Macrolides are a class of antibiotics used to treat a wide range of infections caused by gram-positive and gram-negative bacteria. These medications include erythromycin, azithromycin, and clarithromycin. All can be administered orally to treat mild to moderate bacterial infections of the respiratory, gastrointestinal, and genitourinary tracts; erythromycin can also be given intravenously, and azithromycin has an ophthalmic formulation to treat bacterial conjunctivitis.

Now, once administered, macrolides target the bacterial 50S ribosomal subunit in order to inhibit protein synthesis. As a result, these medications have a bacteriostatic effect, meaning they stop bacterial growth. They’re also considered broad spectrum antibiotics, as they’re active against most gram-positive bacteria and moderately active against some gram-negative bacteria.

Typically, macrolides are well tolerated, and rarely cause side effects. The most common ones can include headaches, a skin rash, and gastrointestinal disturbances like diarrhea, abdominal pain, nausea, and vomiting. 

In addition, macrolides may disrupt the normal intestinal flora, which can allow certain bacteria like Clostridioides difficile to survive and overgrow within the gastrointestinal tract, rarely but potentially leading to Clostridioides difficile infection or CDI for short. Some clients on macrolides may also develop vaginitis and candidiasis, and if they’re used for a prolonged time, they can also lead to ototoxicity and hearing loss. 

Now, more serious side effects include a prolonged QT interval, ventricular arrhythmias like torsade de pointes, and hepatotoxicity, potentially leading to hepatitis. They can also cause seizures, and rare but serious hypersensitivity reactions like angioedema, Stevens-Johnson syndrome, and toxic epidermal necrolysis. 

Finally, regarding specific side effects, erythromycin can cause esophagitis, while azithromycin can rarely cause thrombocytopenia; while clarithro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Tetracyclines_and_Glycylcyclines</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qV6ar2mVSPqGHv4MhXEH5YrjS2epgFyr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Tetracyclines and Glycylcyclines]]></video:title><video:description><![CDATA[Tetracyclines are a group of broad-spectrum antibiotics, which were originally derived from soil-dwelling Streptomyces bacteria. These medications can be used to treat a wide variety of bacterial infections, including central nervous system infections like meningitis, respiratory infections like community-acquired pneumonia, gastrointestinal infections like cholera, skin conditions like acne, and genitourinary infections like chlamydia and syphilis. In addition, tetracyclines can be used to treat rare infections like rocky mountain spotted fever, anthrax, lyme disease, and tularemia. 

Tetracyclines are very effective against gram-positive bacteria like Bacillus anthracis and Clostridium spp, as well as some gram-negative bacteria like Shigella spp, Escherichia coli, Rickettsia spp, Borrelia burgdorferi, Helicobacter pylori, and Neisseria meningitidis, and finally some atypical bacteria like Mycoplasma pneumoniae, Chlamydia trachomatis, Vibrio cholerae, and Francisella tularensis.  

However, some of these bacteria developed resistance against tetracyclines in time. So as a solution, tetracyclines were modified into a newer generation of antibiotics called glycylcyclines. These are commonly used in complicated skin infections and intra abdominal infections. 

Glycylcyclines are very effective against some gram-positive bacteria like Streptococcus pyogenes, Clostridium perfringens, both methicillin susceptible and methicillin resistant Staphylococcus aureus; and gram-negative bacteria like Klebsiella pneumoniae. 

Now, according to the duration of action and half-life, tetracyclines are divided into two groups. Short acting tetracyclines, like tetracycline itself, have a half-life of around 8 hours, while long acting ones like doxycycline and minocycline have a half-life of 16 to 22 hours. These medications can be administered both orally or intravenously. On the other hand, glycylcyclines are only administered intravenously. The main drug in this cate]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Lincosamides</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jcuR94KfRyW8y5jiPq7cCxVTQXSHW-dk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Lincosamides]]></video:title><video:description><![CDATA[Lincosamides are a class of antibiotics used to treat severe infections caused by gram positive and anaerobic bacteria. The lincosamide family of antibiotics includes both clindamycin and lincomycin, however, lincomycin has been widely replaced by clindamycin in almost all of its uses.

Now, clindamycin is most often used to treat skin and soft tissue infections caused by staphylococci and streptococci. It can be active against community-acquired strains of methicillin resistant Staphylococcus aureus, or MRSA for short, an increasingly common cause of cutaneous infections. Additionally, clindamycin is indicated for the treatment of anaerobic infections caused by Bacteroides species and other anaerobes that often participate in mixed flora infections. 

Consequently, it is often used in combination with cephalosporins or aminoglycosides to treat penetrating wounds of the abdomen and gut, infections originating in the female reproductive tract, and lung abscesses. 

Finally, clindamycin may be used for the prophylaxis of endocarditis in clients with underlying valvular heart disease, as well as to treat Pneumocystis jirovecii pneumonia in clients with HIV infection.

For the treatment of systemic infections, clindamycin can be administered orally or by intravenous or intramuscular injection. Additionally, clindamycin can be used topically for the treatment of acne and rosacea, as well as intravaginally for the treatment of bacterial vaginosis.

Alright now, once administered, clindamycin targets the 50S ribosomal subunit of the bacteria, thereby inhibiting protein synthesis and ultimately limiting the growth of bacteria. Although clindamycin has a primarily bacteriostatic effect, it can also act as a bactericidal antibiotic at higher concentrations. 

Since clindamycin tastes extremely bitter, it is not commonly prescribed to children. The most common side effects of clindamycin include gastrointestinal disturbances like nausea, vomiting, diarrhea, and abdom]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Glycopeptides</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TlO5jG9-SV2EYM4iHAueJMWLS3GQ76Xt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Glycopeptides]]></video:title><video:description><![CDATA[Glycopeptides are antibiotics primarily used to treat skin infections such as erysipelas, cellulitis, wound infections, and skin abscesses caused by gram-positive bacteria. Additionally, some glycopeptides can be used to treat staphylococcal enterocolitis, gastrointestinal Clostridioides difficile infection, joint or bone infections, and other serious infections like pneumonia, endocarditis, bacteriemia, and septicemia. 

Glycopeptides work well against Staphylococcus epidermidis, Staphylococcus agalactiae, Staphylococcus aureus, especially the methicillin-resistant type called MRSA, as well as Streptococcus pneumoniae, Streptococcus pyogenes, and vancomycin susceptible Enterococcus faecalis.

There are four medications in this group: vancomycin, telavancin, dalbavancin, and oritavancin. All glycopeptides are administered intravenously, while vancomycin can also be given orally. Once administered, glycopeptides inhibit bacterial cell wall synthesis by interfering with peptidoglycan polymerization and cross-linking, ultimately causing bacterial cell death. 

Common side effects of glycopeptides include ototoxicity, injection site reactions, and gastrointestinal disturbances like nausea, vomiting, and diarrhea. In some cases, glycopeptides can disrupt the healthy intestinal flora and allow resistant bacteria to overgrow, which may result in superinfection, such as Clostridioides difficile infection or CDI for short. For treatment, CDI and staphylococcal enterocolitis are the only indications for oral vancomycin. 

Some glycopeptides can also cause side effects like prolonged QT interval, arrhythmias, and peripheral edema. Clients taking glycopeptides can also develop anaphylactic reactions. Other serious side effects include nephrotoxicity, which is a boxed warning for telavancin! Some clients taking glycopeptides may also develop hematologic side effects like leukopenia and eosinophilia; while vancomycin can also cause immune thrombocytopenia and neutropeni]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Trimethoprim_and_Sulfonamides</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X_AKP1rRSc2aKANtRJ3MI-AgQDe7wqHC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Trimethoprim and Sulfonamides]]></video:title><video:description><![CDATA[Trimethoprim and sulfonamides are antibiotics that are typically administered in combination as trimethoprim-sulfamethoxazole, or TMP-SMX for short. TMP-SMX is most commonly used to treat acute and simple urinary tract infections or UTIs, acute otitis media, traveler&amp;#39;s diarrhea, and shigellosis. But it’s also effective in treating pneumonia and sinus infections caused by Streptococcus pneumoniae and Haemophilus influenzae. It’s the first line therapy for the treatment and prevention of Pneumocystis jirovecii infections, which are caused by a yeast-like fungus that can affect immunocompromised people. Finally, it’s effective against Methicillin-Resistant Staphylococcus aureus, or MRSA. Trimethoprim-sulfamethoxazole is most often given orally, and for serious infections and Pneumocystis jirovecii pneumonia, it can be administered intravenously. Now, sulfonamides can also be used alone as sulfadiazine orally to treat infection by Toxoplasma gondii, or as silver sulfadiazine, which is administered topically in clients with second and third-degree burns to help prevent and treat wound sepsis.

Now, once administered, these medications act to inhibit the synthesis of folate, also known as folic acid or vitamin B9, which is necessary for the synthesis of DNA and RNA. As a result, they interfere with bacterial DNA and RNA synthesis, which ultimately kills the bacteria.

Typically, topical silver sulfadiazine is very well tolerated and doesn’t cause many side effects. The most common is agranulocytosis. Others include skin necrosis, erythema multiforme, skin discoloration, burning sensation, rashes, and interstitial nephritis. 

On the flip side, the list of side effects for oral sulfadiazine, as well as trimethoprim-sulfamethoxazole, is larger. Luckily, the most common ones are mild and include gastrointestinal disturbances like nausea, vomiting, and abdominal pain. Now, in some cases, trimethoprim-sulfamethoxazole can disrupt the normal intestinal flora,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antibiotics_-_Penicillins</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QJzu3N4ZTQ2BxmWUL3KNzqwoQnyX8LkY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antibiotics - Penicillins]]></video:title><video:description><![CDATA[Penicillins are antibiotics that got their name from the Penicillium mold, from which they were originally extracted. They belong to the pharmacological group of beta-lactam antibiotics, because they have a beta-lactam ring in their structure. Penicillins are used to treat a wide range of infections, including streptococcal infections, like pharyngitis, tonsillitis, scarlet fever, and endocarditis; as well as pneumococcal infections; staphylococcal infections; diphtheria; anthrax; and syphilis. 

Now, to build their cell walls, bacteria need an enzyme called DD-transpeptidase, or penicillin binding protein, or PBP for short. Penicillins, like all beta lactam antibiotics, bind to this enzyme thanks to their beta-lactam ring, and prevent it from working.  

Now, some bacteria have developed resistance to beta lactam antibiotics. The most notable is Staphylococcus aureus, which has developed an enzyme called beta-lactamase or penicillinase, that breaks down the beta-lactam ring within the antibiotic, rendering it ineffective. 

So, penicillins are further classified into four groups: basic penicillins, broad-spectrum or aminopenicillins, penicillinase-resistant or antistaphylococcal penicillins, and extended-spectrum or antipseudomonal penicillins. 

Basic penicillins include penicillin V, which is given orally, and penicillin G, which is administered intramuscularly or intravenously. In addition, there’s a specific penicillin G called penicillin G benzathine, which is a long-acting penicillin that’s only administered intramuscularly. These are quite effective against common gram-positive bacteria, so they’re used to treat upper respiratory infections, otitis media, pneumonia, rheumatic fever, erysipelas, skin and soft-tissue infections, and STIs like syphilis. However, they don’t work well against most gram-negative bacteria. 

On the other hand, broad spectrum penicillins include amoxicillin, which is given orally, and ampicillin, which is administered oral]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antivirals_for_Hepatitis_B_and_C</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SOQhnAyuSlaAgxklEBeKkC_3RjWnfwuF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antivirals for Hepatitis B and C]]></video:title><video:description><![CDATA[Viral hepatitis is the inflammation of the liver caused by hepatitis viruses A, B, C, D, or E. Out of these, chronic hepatitis caused by hepatitis B virus, or HBV, and hepatitis C virus, or HCV, can be treated with antiviral medications. Now, chronic HBV infection can be treated with a class of antiviral medications called NRTIs, which include nucleotide reverse transcriptase inhibitors like adefovir and tenofovir, as well as nucleoside reverse transcriptase inhibitors like entecavir; these medications are administered orally. On the other hand, chronic HCV infection can be treated with antiviral medications that target different components of the virus, so they’re typically used in combination; these include nucleotide polymerase inhibitors like sofosbuvir, as well as nucleoside analogues like ribavirin, both of which are taken orally. Finally, there’s a third class of medications that can be used to treat both chronic HBV and HCV; these include interferons like peginterferon alfa-2a, which is administered by subcutaneous injection.

Now, once administered, all of these antivirals have a different mechanism of action. NRTIs used to treat hepatitis B act by inserting into the replicating viral DNA. As a result, viral DNA synthesis is halted, ultimately stopping viral replication. On the other hand, medications used to treat hepatitis C work in different ways, inhibiting different viral proteins or enzymes required for viral replication. Interferons, on the other hand, induce the innate antiviral immune response that helps kill off cells that are infected by the virus.

Now, clients taking NRTIs for hepatitis B infection can have side effects. All these medications come with a boxed warning for severe, acute hepatitis exacerbations on discontinuation of therapy. These medications also cause lactic acidosis, which is a boxed warning for adefovir and entecavir, as well as severe hepatomegaly with steatosis; and a risk for individuals with concurrent HIV infec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombolytic_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sAwKUt0aRbap8LYS2CuIFUTdRjyZN2vX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thrombolytic Therapy]]></video:title><video:description><![CDATA[Thrombolytics, also called clot busters, are medications that break up clots, and are used for the short-term emergency management of thrombotic conditions, such as myocardial infarction, pulmonary embolism, ischemic stroke, and thrombosis of prosthetic heart valves and stents. 

Now, thrombolytics are usually derived from enzymes involved in fibrinolysis, or the gradual degradation of the fibrin mesh. These include alteplase, reteplase, and tenecteplase, which are  derived from tissue plasminogen activator, or tPA, through recombinant DNA technology, and act locally at the clot site.

Thrombolytics are given intravenously. Once in the blood, they act on a protein produced by the liver called plasminogen, and convert it into its active form called plasmin. These medications directly bind to fibrin proteins in the clot and preferentially act on plasminogen trapped in the fibrin mesh, also called fibrin-bound plasminogen. The resulting plasmin then acts as a protease and cuts the fibrin into smaller pieces. This allows the trapped red blood cells and platelets to float away, dissolving the clot.

The main side effect of all thrombolytics is undue bleeding from other sites, including the injection site, gastrointestinal bleeds, and hemorrhagic stroke. In severe cases, thrombolytic-associated bleeding can be treated with medications like aminocaproic acid, which acts by binding to plasminogen and plasmin, ultimately inhibiting their action on fibrin. If aminocaproic acid fails, other transfusion products can be administered, such as platelets or coagulation factors in the form of fresh frozen plasma. 

In addition, thrombolytics, when given following a myocardial infarction, can precipitate an abnormal cardiac rhythm, or a reperfusion arrhythmia, which is usually benign. Other side effects include hypersensitivity reactions like anaphylaxis, nausea, vomiting, and fever.

Due to the risk of bleeding, thrombolytics are contraindicated in clients with active inte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Loss_and_Grief</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vbk4WX8DRM2gc85BH40In1iXTzuHhiV8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Loss and Grief]]></video:title><video:description><![CDATA[﻿Nurse Jamie works as a home health nurse, and is caring for Barbara, a 75-year-old female diagnosed with type 2 diabetes. This is her first home health care visit for a wound on her left lower extremity that developed from sitting in her recliner for long periods of time. Before performing a focused assessment and a dressing change, Nurse Jamie completes an assessment that includes questions about Barbara’s home life and support system.  

Nurse Jamie will go through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Barbara’s care by recognizing cues and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jamie recognizes important cues. She notes that Barbara has lived alone since her husband died a year ago; so, Nurse Jamie performs a grief assessment and discovers that Barbara’s adult children live out of state, and she has few visitors.  

Barbara shares she often dwells on missing her husband, feels sad most days, and lacks energy or motivation to do things she used to enjoy. Additionally, she reveals she is not paying attention to her blood glucose levels like she used to.  

Next, Nurse Jamie analyzes these cues. She recalls that after a loss of someone or something meaningful, a period of grief is normal and can present as sadness, anger, or regret, but varies for everyone. Nurse Jamie also understands dysfunctional grief can lead to suicidal thoughts, so she gathers additional information to rule out thoughts of self-harm.  

Okay, so using the information gathered from Barbara’s grief assessment and medical history, Nurse Jamie identifies a priority hypothesis of dysfunctional grief. Then, she generates solutions to address Barbara’s grief, including promoting coping strategies and coordinating care with a multidisciplinary team. Next, she establishes the desired outcome that within three weeks of intervening, Barbara will demonstrate posit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stress_and_Coping</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dpGJ9F6SS1CORgwHPiV75iuXTw_9--Gd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stress and Coping]]></video:title><video:description><![CDATA[﻿Stress is a normal human response to an internal or external threat to homeostasis, or the body’s stable equilibrium, and can be prompted by stressors. These stressors such as illness, high workload, or economic hardship, can induce the stress response, also known as an allostasis, in an attempt to reestablish homeostasis. In the short term, the body can adapt to the physiological changes to stress; however, when stress becomes chronic, it can have a negative impact on mental and physical health. 

Now, not all stress is harmful, in fact, it is essential for daily life. There are two types of stress; eustress and distress. Eustress is positive stress, which is necessary for normal development and motivation and can occur with beneficial life changes like having a baby or getting a new job; whereas distress is negative stress that occurs when a person is unable to adapt or cope effectively to the stressor. 

Okay, the body’s response to a stressful event can be explained by the General Adaptation Syndrome, or GAS, which has three stages. First, the alarm reaction stage occurs as the sympathetic nervous system is activated, triggering the fight-or-flight response, which involves the release of hormones and neurotransmitters to support the body’s reaction to stress. The posterior pituitary releases antidiuretic hormone, or ADH, and the adrenal cortex releases aldosterone, both of which increase circulating blood volume. The adrenal cortex also releases cortisol, which increases the body’s supply of glucose, while the adrenal medulla releases epinephrine and norepinephrine, which increases the heart rate, blood pressure, and blood flow to the skeletal muscles. Next, the resistance stage is when the body attempts to stabilize and return to homeostasis. If the stress has been dealt with effectively, the parasympathetic nervous system returns vital signs to normal and begins to repair tissue damage. However, if the stress continues, the sympathetic activation wi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Overview_of_Sleep</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/psdv5MLXRaKHIwwhx_BElHeSRXyUW-6c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Overview of Sleep]]></video:title><video:description><![CDATA[﻿Sleep is a basic human need that allows for the proper functioning of the body and mind. A lack of sleep can cause patients to develop chronic health conditions, like diabetes, obesity, and depression, and impair daily mental and physical functioning. Let’s review the rhythm,  cycles, and physiology of sleep. 

Now, the central nervous system integrates sleep using various parts of the brain, including the hypothalamus, which controls the circadian rhythm, the 24-hour sleep-wake cycle that includes a predictable pattern of physical, mental, and behavioral processes such as variations in body temperature, heart rate, blood pressure, hormone secretion, eating habits, and mood. 

The hypothalamus controls the circadian rhythm and can be impacted by the amount of environmental light and other factors, such as noise, pain, and illness. 

Now, there are two main phases of sleep: non-rapid eye movement, or NREM, and rapid eye movement, or REM. These phases typically occur in 90 minutes intervals, with a normal sleep pattern containing 3 to 5 cycles total. Now, we spend the most time in NREM, which has three stages, called NREM 1, 2, and 3, which progress from the lightest sleep to the deepest sleep, whereas REM only has one stage characterized by lucid dreams and rapid eye movements. 

Now, several physiological changes occur during sleep, including a decrease in heart rate, blood pressure, body temperature, respiration, and muscle tone. 

These changes occur because several central nervous system structures, hormones, and neurotransmitters work together to promote and regulate sleep. Starting with the hypothalamus, this structure controls the circadian rhythm and initiates sleep by secreting the neurotransmitter gamma-aminobutyric acid, or GABA. It also works with the brain stem to reduce activity in arousal centers and relax the body during sleep. Next, the pineal gland secures the hormone melatonin in response to decreased light to help regulate the sleep cyc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunizing_Agents</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BiSWJBwzSEqZv60P39qyWuXRTMKbA57U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunizing Agents]]></video:title><video:description><![CDATA[Vaccines are biological products designed to protect humans from potentially serious infections caused by various kinds of pathogens. Most vaccines are routinely administered to clients as part of a vaccination schedule; while other vaccines are only given to certain populations, such as chronically ill clients or those travelling to foreign countries. 

Now, there are five main types of vaccines: live attenuated, inactivated, subunit, toxoid vaccines, and mRNA vaccines. Live attenuated vaccines contain pathogens that have been weakened in the laboratory. As a result, these weakened pathogens are no longer able to cause infection, but are still able to trigger a protective immune response. These vaccines are used to protect against influenza with the live attenuated influenza vaccine or LAIV for short; as well as measles, mumps, and rubella, called the MMR vaccine, and can also include varicella zoster, also known as the MMRV vaccine; other live attenuated viruses include vaccines for rotavirus, smallpox, and yellow fever. 

On the other hand, inactivated vaccines use a pathogen that has been killed in the laboratory, so it is no longer able to replicate or cause infection, but is still able to trigger a protective immune response. These include vaccines against Hepatitis A, or HAV vaccine, as well as against polio, called the Salk vaccine or inactivated polio vaccine or IPV, and against rabies, or the rabies vaccine. Another important inactivated vaccine is again for influenza with the inactivated influenza vaccine or IIV for short. 

Next, subunit, recombinant, and polysaccharide vaccines contain just the portion of the pathogen that stimulates the immune response, such as a viral protein, DNA, or sugar. Some of these vaccines are combined with proteins to form conjugated vaccines, which elicit a much stronger and longer lasting immune response. These vaccines are used to protect clients against Haemophilus influenzae type B, or HiB vaccine; Hepatitis B,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antivirals_for_HSV</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xdo8Xxs6Specx1VwGluvBP9WQlC0JzGM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antivirals for HSV]]></video:title><video:description><![CDATA[Herpesviruses are a family of DNA viruses that include herpes simplex virus or HSV types 1 and 2, varicella-zoster virus or VZV, cytomegalovirus or CMV for short, Epstein-Barr virus or EBV, and human herpesvirus or HHV 6, 7, and 8. 

Certain herpesvirus infections can be treated with a class of antiviral medications called guanosine analogs, which include medications that end in the suffix -clovir. The main drugs used to treat herpes infections include valacyclovir, valganciclovir, and famciclovir, which are given orally, as well as acyclovir and ganciclovir, which can also be administered topically or intravenously in addition to orally.

Once administered, guanosine analogs act by inserting into the replicating viral DNA. As a result, viral DNA synthesis is halted, ultimately stopping viral replication.

Now, clients taking guanosine analogs may experience headache and nausea. These medications can also cause a skin rash, pruritus, nephrotoxicity, and hypersensitivity reactions like Stevens-Johnson syndrome and angioedema. 

Acyclovir and valacyclovir can cause neurological side effects, including agitation, tremors, confusion, and myoclonus; more rarely, clients can develop hallucinations, and even encephalopathy or seizures. Acyclovir and valacyclovir can also lead to  thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome. 

Acyclovir can also cause pain or phlebitis at the injection site when given intravenously. On the other hand, famciclovir can cause menstrual changes and hepatotoxicity. Finally, valganciclovir has boxed warnings for hematologic toxicity, carcinogenesis, impaired fertility, and fetal toxicity.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/NORD_-_WHIM_Syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rxlZYYQwQeqIf-uA9ScJAEBkTSSHYjFU/_.jpg</video:thumbnail_loc><video:title><![CDATA[NORD - WHIM Syndrome]]></video:title><video:description><![CDATA[WHIM syndrome is a rare primary immunodeficiency disorder, which means the body’s immune system doesn’t function properly, so individuals are more susceptible to infections caused by viruses and bacteria.

Components of the blood develop in the bone marrow, which is the spongy center of some bones. When they are mature, they move into the blood and circulate around the body.

Some of these cells, called white blood cells, are part of the immune system and fight against infections. And there are several types that have their own specialized functions. These include neutrophils and monocytes which are important in the initial infection response; T lymphocytes, called T cells which help regulate the immune response; and B lymphocytes, called B cells, which secrete antibodies. Antibodies are also called immunoglobulins and are abbreviated as Ig. They are proteins that coat viruses and bacteria, and either kill them or help white blood cells find them.

In WHIM syndrome, neutrophils and other immune cells don’t move out of the bone marrow efficiently. So, they are not present in high levels in the blood to fight infections.

Now, WHIM syndrome is an acronym for the common signs and symptoms of the disorder. But not all individuals will experience them or to the same severity. Warts are caused by a common virus called human papillomavirus, abbreviated HPV. Warts are most commonly found on the hands and feet, but occasionally also on the arms and legs as well as the face. They may also be found both externally and internally at the anus or genitals, where some can develop into cancer. Hypogammaglobulinemia means fewer antibodies are present in the blood caused by the low levels of B cells in the blood. But low levels of T cells, and especially neutrophils are seen. Bacterial infections can begin at an early age and may be chronic or recurring. These infections can happen anywhere in the body, but commonly involve the skin; ears, sinuses, mouth, lungs, joints and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Achalasia:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o1ZU4qmPQFaMjmu6Pdjg685NQA_7gP6O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Achalasia: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Achalasia: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_atresia_&amp;_tracheoesophageal_fistula:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Az80wz5PSrOeslKTjR7YqiuBQ6GAX6gg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal atresia and tracheoesophageal fistula: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Esophageal atresia and tracheoesophageal fistula: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Langerhans_cell_histiocytosis:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E2j8QYisQVGxTiilFmzHKNXNRdGyr_Ct/_.jpg</video:thumbnail_loc><video:title><![CDATA[Langerhans cell histiocytosis: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Langerhans cell histiocytosis: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Overview_of_Communication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xgMLhosATp_Isvbkv09Fct2MTSC3NUh7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Overview of Communication]]></video:title><video:description><![CDATA[Communication is the process of using words, symbols, and behaviors to transmit information between two individuals. As the nurse, you will use effective communication to form patient-centered relationships, and to collaborate with patients and the health care team to achieve patient goals and outcomes.  

Okay, let’s review the basic elements of communication. Communication involves six key elements: referent, sender, message, channel, receiver, and feedback. First, the referent is the event that initiates communication, like the patient feeling the sensation of pain. Next, the sender is the person who has a message to deliver, like when your patient tells you about their pain. Then, the channel is the way the message is conveyed and received through the five senses.  

For example, your patient may convey their message through the auditory channel by saying, “I have pain,” and through the visual channel by grimacing or wincing. Now, the receiver is the person who interprets the message from the sender, like when you hear and see the message about your patient’s pain. Lastly, the receiver provides feedback to the sender about the message and, if needed, asks for clarification about the message being sent. For example, you might say, “I understand you’re in pain. Could you describe how it feels?” 

So, there are two types of communication, verbal and nonverbal. Verbal communication uses words and can be transmitted by spoken, written, and electronic modes. On the other hand, nonverbal communication uses body language and cues, such as sighs, moans, and physical gestures. Another nonverbal technique involves altering voice inflection by changing the tone, volume, or cadence of speech to convey the significance of a statement, like when a patient increases the volume of their voice out of frustration. It’s important to note that nonverbal cues can enhance or inhibit communication. So, if your tone sounds condescending or rushed, your patient may fe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulse</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lpItmridRb_PQdEPzlbAjrf1SxmG5BF-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulse]]></video:title><video:description><![CDATA[Every time the heart beats, it creates a pulse that sends blood into the arteries throughout the body, delivering oxygen and nutrients to organs and tissues. When assessing your patient’s pulse, you are evaluating their general cardiovascular health, while following the steps of the Clinical Judgment Measurement Model or CJMM to make clinical decisions about patient care.  

Okay, let’s review the physiology of a pulse, which is a pressure wave that’s generated when the left ventricle contracts. This creates a palpable pulse as blood is pushed through the arterial system. You can assess your patient’s pulse centrally by auscultating the apical pulse over the apex of the heart at the point of maximal impulse and counting the beats for a full minute.  

Normally, the apical pulse has two sounds: S1, or lub, and S2, or dub. Both S1 and S2 are produced when certain heart valves close in response to heart muscle contraction. You can also assess a pulse distally, using your second and third fingers to lightly palpate over peripheral pulse sites, most commonly the radial artery.  

Now, the pulse is an indirect measure of cardiac output, which is the amount of blood the heart pumps in one minute. When you take your patient’s pulse, you’ll be assessing the rate, rhythm, and amplitude. When the pulse is faster than normal, it’s called tachycardia. With tachycardia the heart has less time to fill with blood, so there’s less blood pumped out with each heartbeat, reducing cardiac output. On the flipside, if the heart rate is too slow, it’s called bradycardia. With bradycardia, cardiac output is also reduced, since blood isn’t pumped out fast enough to meet the needs of the body.  

Your patient’s pulse should also be regular. An irregular pulse, or arrhythmia, can be caused by electrolyte imbalances or certain types of heart disease, and can affect cardiac output by decreasing cardiac filling time or impairing contraction of the ventricles. Likewise, an expected findi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Public_Health_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m9vVe8l8SxeO9g69jKXqSIM0RoSjkPLL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Public Health Nursing]]></video:title><video:description><![CDATA[Often when someone thinks of a nurse, they picture settings like hospitals and clinics. However, nursing care is just as important in other settings like with public health nursing, community-based nursing, and home health nursing.  

Each of these nursing specialties promote health by using primary prevention, which is aimed at minimizing the chance of developing an illness by reducing modifiable risk factors; secondary prevention, which involves screening for an illness in its early stages, before a patient develops signs and symptoms; and tertiary prevention, which is focused on slowing disease progression, preventing complications, and promoting optimal functioning.  

Now, the goal of public health nursing involves preventing disease and promoting health at three population levels: the individual and family level, directed at providing care for a patient and their support system; the community level, which encompasses a specific population, such as students living on a college campus or vulnerable populations like patients with developmental disabilities; and the system level, where care is directed at influencing the overarching systems that impact health, like healthcare policy.  

Okay, so public health nurses often work in interdisciplinary teams at local health departments or for state and federal health agencies. They collaborate with an interdisciplinary team to perform essential functions established by the American Nurses Association. These functions include coordinating services for patients to meet their health care needs, like when the nurse connects low-income families with affordable prescription programs; and maintain communication between patients and their health care providers.  

These functions help public health nurses focus care on primary prevention of illness within a population. Public health nursing also has roles in secondary prevention, such as providing screenings for tuberculosis, and tertiary prevention, like running a f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Temperature</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0CMqcrPERsufT0CtQWqWlryRR0KvMosj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Temperature]]></video:title><video:description><![CDATA[Temperature reflects the body’s ability to regulate body heat, a process called thermoregulation.  When measuring a patient’s temperature, the nurse should follow the steps of the Clinical Judgment Measurement Model or CJMM to make clinical decisions about patient care.  Before we cover how temperature relates to clinical judgment though, let’s review physiological regulation of body temperature.   

Now, the body works to maintain a consistent internal temperature through a part of the brain called the hypothalamus, which acts like the body’s own personal thermostat by controlling the body’s set point, or normal core temperature. When the hypothalamus senses that the temperature is increasing above the set point, it promotes heat loss by initiating sweating and vasodilation. Likewise, when the temperature goes below the set point, the hypothalamus initiates vasoconstriction, which reduces heat loss, and rhythmic muscle tremors, or shivering, to generate heat. So, if the hypothalamus is impacted by disease or trauma, the normal thermoregulatory process can become impaired.   

In addition, other biological processes can affect body temperature. For example, the body’s normal biological clock, called the circadian rhythm, affects temperature by causing it to peak in the late afternoon, and decrease at night as the body prepares for sleep. Then, just before waking up, body temperature begins to rise again.  

Okay so, the primary source of heat production in the body is through metabolism, which is the chemical process that produces energy for cellular functions. However, the body temperature can increase above normal in patients with a fever, which is where the thermostat’s set point is raised higher due to problems like infection, inflammation, or trauma. Body temperature can also increase with hyperthermia. This is where the thermostat set point remains normal, but the body’s thermoregulatory processes become overwhelmed and ineffective from prolonged exp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_Pressure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CoOM-_etSVWonTsEWvmlr4nLQP6dNRNm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood Pressure]]></video:title><video:description><![CDATA[Blood pressure is the force that blood exerts on vessel walls, as it circulates throughout the body to deliver nutrients and oxygen to tissues and organs. When measuring your patient’s blood pressure, you will follow the steps of the Clinical Judgment Measurement Model, or CJMM, to make clinical decisions about patient care.  

Okay, let’s review the physiological regulation of blood pressure. First, when the heart contracts and pumps blood through the body during systole, the blood pressure rises. On the other hand, when the heart relaxes and refills with blood during diastole, the blood pressure decreases.   

In addition to the heart, there are other internal factors that regulate blood pressure. The elastic arteries maintain blood pressure and help propel blood forward through the body by expanding and recoiling with each heartbeat. In addition, the autonomic nervous system can increase the blood pressure by increasing the heart rate and by causing vasoconstriction, where the arteries constrict, or it can decrease blood pressure by lowering the heart rate and by causing vasodilation, where the arteries relax.   

Blood pressure is also influenced by hormones, like the renin-angiotensin-aldosterone system, which increases blood pressure by causing vasoconstriction and increasing the circulating blood volume; and through antidiuretic hormone, which also increases blood volume.   

There are also some external factors that can increase blood pressure, too, like aging, which causes arteries to become stiffer and less compliant; and emotions, like anger and pain, which can stimulate the autonomic nervous system.     

Now, blood pressure is measured in millimeters of mercury, or mm Hg for short; and is written as a fraction, like 118 over 72. In this example, 118 represents the systolic, or peak pressure in the arteries during systole; whereas 72 represents the diastolic, or lowest pressure in the arteries during diastole. Blood pressure can be measured man]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiration_and_Oxygenation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5m7es57pS62W56-oafXOVQBTRF_fS3ij/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiration and Oxygenation]]></video:title><video:description><![CDATA[Respiration is the process of moving air in and out of the lungs, through inspiration and expiration. During inspiration, oxygen enters the lungs and crosses into the bloodstream, where it’s delivered to tissues, a process known as oxygenation. Then, during expiration, carbon dioxide is expelled from the lungs. When measuring your patient’s respiration and oxygenation, you’ll follow the steps of the Clinical Judgment Measurement Model to guide clinical decisions about patient care.  

First, let’s review physiological regulation of respiration and oxygenation. Now, respiration is generally an involuntary process controlled by the respiratory center in the brainstem. Here, chemoreceptors in the medulla assess changes in the level of carbon dioxide and pH in cerebrospinal fluid. When CO2 increases and pH decreases, the chemoreceptors signal the respiratory center to increase the respiratory drive, which increases the rate and depth of breathing to eliminate excess CO2. Now, these central chemoreceptors work in concert with peripheral chemoreceptors located in the aortic arch and carotid arteries to regulate respiration.  

Peripheral chemoreceptors are primarily sensitive to oxygen levels in the blood. When they detect low oxygen levels, they send a message to the respiratory center to increase the rate and depth of respirations, so more oxygen is inhaled. While respiration is predominantly passive, voluntary changes in respiration are controlled by the cerebral cortex like breaths during swimming or singing.   

Alright, let’s review how respiration delivers oxygen to the tissues of the body. During inspiration, oxygen enters the lungs and travels into the alveoli, where it diffuses into the pulmonary capillaries and binds to hemoglobin in red blood cells. From there, the red blood cells deliver oxygen to the body’s tissues. Meanwhile, carbon dioxide diffuses across the capillaries into the alveoli where it is exhaled from the body.    

Okay, so you’l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-dEiBSVGQA6mBM2AtNm5KRERQOS1MNnP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pain]]></video:title><video:description><![CDATA[Pain is a feeling of physical or emotional discomfort that’s different for every person and can range from mild to severe. When assessing your patient’s pain, follow the steps of the Clinical Judgment Measurement Model or CJMM to make clinical decisions about patient care.  

Now, to better assess and intervene for your patient’s pain, let’s review the physiology of pain. So, the pain process is called nociception which involves pain receptors, which are free nerve endings called nociceptors located throughout the body, that send pain signals to the central nervous system. There are four main processes involved in pain signaling: transduction, transmission, perception, and modulation.  

First, transduction is when a painful stimulus is converted into an electrical signal. This stimulus can be mechanical, like pinching someone; chemical, like a strong acid causing damage to the skin; or thermal, like spilling hot coffee on your lap.   

Next, the pain signal is transmitted from the site of injury by nerve fibers to the spinal cord. During this time, the body uses motor reflexes to protect itself by moving away from the stimuli that’s causing the pain; for example, pulling back from someone pinching you, or wiping the hot coffee off your leg.   

Then, perception occurs when the pain signal reaches the cerebral cortex. This is where an individual consciously perceives pain and its characteristics like location, intensity, and what makes the pain better or worse.   

And finally, modulation refers to how the brain regulates pain by sending inhibitory messages to the spinal cord to slow transmission of the pain signal and to release endogenous opioids, or the body’s natural pain killers. For example, if a runner sprains their ankle, they may not feel the pain fully until after the race due to the effects of endogenous opioids.  

Now, pain can be classified as acute or chronic. First, acute pain has a sudden onset and can be caused by trauma like cutting your]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Sexual_Health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RQwLVGfzQmOz-tQcibAlU511SCOQ2My9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Sexual Health]]></video:title><video:description><![CDATA[Nurse Sarah works in an urgent care clinic and is caring for Gia, a 24-year-old female who wants to be tested for sexually transmitted infections, or STIs, after her partner told her he tested positive for chlamydia.   

After settling Gia in the exam room, Nurse Sarah goes through the steps of the Clinical Judgment Measurement Model, or CJMM, to make clinical decisions about Gia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

To begin, Nurse Sarah recalls how sexual health encompasses a patient’s well-being related to their sexual orientation, gender identity, and intimacy with others. With this in mind, Nurse Sarah performs a sexual health assessment and recognizes important cues, including Gia’s report of increased vaginal discharge and dysuria over the past four days. She notes Gia has no previous history of STIs or pregnancies, has had three sexual partners in the last month, doesn’t use contraceptives, and reports feeling safe in her current relationship.   

Nurse Sarah ensures Gia’s privacy and stays in the room while the health care provider performs Gia’s pelvic exam and collects specimens for testing.   

Next, Nurse Sarah analyzes the cues. She notes the health care provider’s documentation of Gia’s exam, including the presence of copious vaginal discharge, with no signs of bruising or forced vaginal entry.  

So, using the information she’s gathered, along with Gia’s social and medical history, Nurse Sarah selects the priority hypothesis of acute STI. Then, she generates solutions to address Gia’s STI which will include treatment with the prescribed antibiotics and education on STI treatment and prevention; and she establishes the expected outcomes that Gia will accurately describe how to complete her antibiotic prescription and choose a reliable method to prevent future STIs by the end of today’s visit.   

Nurse Sarah then takes action to implement thes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Activity_and_Movement</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lzQV3EYKQqivpCY1H45Rwdy-RaSsXA2d/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Activity and Movement]]></video:title><video:description><![CDATA[Nurse Alex works on an intermediate care unit and is caring for Joan, a 45-year-old female who is being treated following a car crash two weeks ago. Since then, Joan has been experiencing significant weakness in the lower extremities, difficulty bearing weight, and difficulty changing position independently while in bed. Nurse Alex goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Joan&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.    

First, Nurse Alex recognizes important cues. He notices Joan is unable to bear weight, has adequate upper extremity strength and requires maximum assistance to transfer from bed to the chair and bedside commode.   

He reviews the electronic health record, or EHR, where he notes that a transfer board is recommended for Joan based on her initial evaluation by the physical therapist. Next, Nurse Alex analyzes these cues and determines Joan will need his support to reduce the impacts of immobility.   

Nurse Alex prioritizes the hypothesis of impaired mobility and generates solutions to address Joan’s impaired mobility that will include promoting safety and increasing her level of functioning. He establishes the expected outcome that after intervening, Joan will safely transfer from the bed to a chair using a transfer board with a one-person assist.  

Nurse Alex then takes action to implement the generated solutions. First, he institutes fall precautions to promote safety. Before proceeding, Nurse Alex ensures the bed and chair are locked and in proper position, that the chair is slightly lower than the height of the mattress, and that all obstacles are removed. He will also ensure Joan’s pain is controlled and her vital signs are stable prior to attempting to use the transfer board. He recalls that Joan has only used the transfer board once with physical therapy and plans to reorient Joa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Integumentary_System_and_Mucous_Membranes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LJc68HhATUS7y-L_06VJah67S6qzS_l2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Integumentary System and Mucous Membranes]]></video:title><video:description><![CDATA[Nurse Yoko works in a long-term care facility and is caring for Penny, a 79-year-old female, who was recently admitted with a history of a stroke with left-sided peripheral neuropathy and weakness. After introducing herself to the Penny, Nurse Yoko goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Penny&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Yoko recognizes important cues, including findings from her assessment of Penny’s skin, oral mucous membranes, and nails, as well as her functional ability. Nurse Yoko notes Penny has dry, cracked lips and a yellow-brown film on her teeth. On her lower extremities, Nurse Yoko notes dry, flaky skin, and after removing her socks, she sees that Penny has thick, discolored toenails and a pressure injury on her left heel.    

Nurse Yoko asks Penny about her activities of daily living, or ADLs.   

Nurse Yoko: Penny, can you tell me a little bit about how you’ve been doing with your daily routine?  

Penny: I’m used to being able to care for myself, but after the stroke, it’s been hard for me to do things I used to do.  

Nurse Yoko: I understand. Can you tell me what sort of things you used to do that you aren’t doing now?   

Penny: Well, I’m left-handed but now that my left arm is weak, it&amp;#39;s hard for me brush my teeth and clean myself up. I can’t even cook a meal for myself anymore.  

Nurse Yoko: That must be difficult. I also noticed you have a pressure injury on your left heel. How long has it been there?  

Penny: I have numbness and weakness in my left leg and it’s hard for me to move around. One day I bumped the back of my foot, and the sore hasn’t healed since. I didn’t even notice it was there until days later.   

Next, Nurse Yoko analyzes these cues. She reviews Penny’s electronic health record, or EHR, and notes that although she can w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Oxygenation_and_Perfusion</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e3aKjrTqSmeXukhmCM5qJ6tcTAWIJmv9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Oxygenation and Perfusion]]></video:title><video:description><![CDATA[Nurse Emily works in an emergency department and is caring for Carolyn, a 77-year-old female with a history of congestive heart failure, or CHF, who came to the emergency department after shortness of breath woke her up during the night. After settling Carolyn in her room, Nurse Emily goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Carolyn’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

Nurse Emily begins by recognizing important cues. During report, Nurse Emily learns Carolyn has gained 7 pounds in the last week and has been using extra pillows to prop her up at night since she&amp;#39;s short of breath when lying flat. Then, Nurse Emily assesses Carolyn’s vital signs, which are blood pressure 110/70 mmHg, heart rate 100 beats per minute, temperature 98.8 F or 37.1 C, respirations 24 breaths per minute and pain score of 0 out of 10. Pulse oximetry is 86 percent on room air. Nurse Emily notes Carolyn has bilateral lower extremitiy edema and upon auscultation she hears crackles bilaterally She also notices Carolyn’s increased work in breathing through cues like nasal flaring and intercostal retractions.  

Then, Nurse Emily analyzes these cues. She reviews Carolyn’s diagnostic test results and sees her CBC, basic metabolic panel, or BMP, and ECG are within normal limits; however, her arterial blood gas, or ABG, reveals a decreased partial pressure of oxygen, or PaO2. Nurse Emily remembers that since Carolyn has CHF, her heart is not pumping effectively, impairing oxygenation, which is the ability of the lungs to exchange oxygen and carbon dioxide. This also impairs perfusion, which is the ability of oxygen-rich blood to travel throughout the body. Nurse Emily also realizes Carolyn’s CHF is causing blood to pool in Carolyn’s pulmonary and systemic circulation, leading to her symptoms.  

So, using the information she’s gather]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Overview_of_Fluid_Balance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DDaLKOO0RqW1vn_XHFCuEJu-S0_BHi9Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Overview of Fluid Balance]]></video:title><video:description><![CDATA[Fluid balance is the regulation of the body’s fluid compartments to maintain a stable internal environment. Fluid affects essential functions like cellular metabolism, temperature regulation, and the delivery of oxygen and nutrients to the cells. Any change in the volume or concentration of fluid can negatively affect these vital life processes.  

Okay, so let’s start by reviewing some basics about fluid balance. First, fluid is found in two major compartments in the body: inside the cells, called intracellular fluid, and outside the cells, called extracellular fluid. The extracellular fluid compartment is further divided into the intravascular space, which is inside the blood vessels; the interstitial space, which is found between cells; and the transcellular space, where fluid, like pericardial, cerebrospinal, and synovial fluid, is contained in epithelial-lined spaces. 

Now, the fluid in these compartments is mostly made up of water. In fact, over half of an adult&amp;#39;s body weight and volume is water, which is called total body water. In addition, fluid is also made up of small and large solutes. Small solutes can easily cross cell membranes and are found in both intracellular and extracellular spaces. They include gases like oxygen and carbon dioxide, glucose, and electrolytes. On the other hand, large solutes can&amp;#39;t easily cross cell membranes and are typically found in the extracellular space. These solutes include plasma proteins and blood components like red blood cells, platelets, and white blood cells. 

Alright, fluid is in constant motion as it shifts in and out of cells and between fluid compartments through the processes of osmosis and filtration. First, osmosis is the diffusion of fluid across a semipermeable membrane from an area of low solute concentration, or osmolality, to an area of higher osmolality, until both sides are equalized. The force that pulls water from the area of low osmolality to high is called os]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Overview_of_Acid-Base_Regulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wQReDFKoTOy1CZAncTXkyPypTNScfxHs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Overview of Acid-Base Regulation]]></video:title><video:description><![CDATA[Acid-base balance refers to how the body maintains a balanced pH of body fluids within a narrow range. A balanced pH is essential for optimal cellular functioning; and any disruption in this balance can adversely affect important metabolic processes, such as the function of enzymes within cells, oxygen delivery to the tissues, and medication metabolism.  

Alright, so, pH, which means potential of hydrogen, reflects the concentration of hydrogen ions, or H+, in the blood. An acid is a substance that releases H+, and there’s an inverse relationship between pH and H+, meaning that when there’s more H+, the pH decreases and the blood becomes more acidic; and, when there’s less H+, the pH increases, and the blood becomes less acidic. Now, hydrogen ions are continually produced by normal metabolic processes like ketone production from fat metabolism; phosphoric acid from the breakdown of proteins; and lactic acid resulting from aerobic respiration, which can be due to excess exercise or hypoxia.  

On the flip side, a base is a substance that accepts hydrogen ions, which neutralizes acid. Bicarbonate or HCO3-, is a base found in plasma, and it plays a crucial role in acid-base balance. When there’s more HCO3- the pH increases, and the solution becomes more basic; and when there’s less HCO3-, the pH decreases, and the solution becomes less basic.   

Okay, so pH is measured on a scale that ranges from 0 to 14, with a pH of 7 being neutral, less than 7 being acidic, and more than 7 being more alkaline. Optimal metabolic functioning occurs when the pH is maintained between a range of 7.35 and 7.45. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Overview_of_Electrolyte_Balance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/erLBrdcWQKCnyjZulIf_vRy-TmiMzSFJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Overview of Electrolyte Balance]]></video:title><video:description><![CDATA[Electrolytes are charged molecules, or ions, that have many essential functions throughout the body, including transmission of nerve impulses, facilitating muscle contraction, and maintaining fluid osmolality. Because of their critical functions, maintaining electrolyte homeostasis is essential for normal functioning of the body. 

Okay, let’s review the major electrolytes and their functions. They can be categorized as either cations, which are positively charged, like sodium; or anions, which are negatively charged, like phosphate. Electrolytes can be measured in the urine, cerebrospinal fluid, and blood, and they’re usually expressed as milliequivalents per liter of fluid, mEq/L.  

So, first, there’s sodium, or Na+, which is the main cation in the extracellular fluid.  

It’s responsible for maintaining the extracellular fluid’s osmolality, or the concentration of the particles dissolved in the fluid, so it determines blood volume and blood pressure.  

Sodium also works closely with potassium, or K+, to maintain the cell’s resting membrane potential, which is the distribution of ions on either side of the cellular membrane. Sodium’s normal value is 135 to 145 mEq/L.  

Now, potassium is the main cation in the intracellular fluid, and it’s responsible for maintaining intracellular osmolality. Potassium is also essential for normal neuromuscular and cardiac function, and its normal range is between 3.5 and 5 mEq/L.  

Then there’s calcium, or Ca2+, which helps with releasing neurotransmitters from neurons, as well as releasing hormones from endocrine glands. It influences the excitability of nerve and muscle cells and is essential for muscle contraction. It’s also involved in blood clotting and maintaining strong bones and teeth. Calcium’s normal range is between 8.5 and 10.5 mg/dL.Now, magnesium, or Mg2+, influences the function of both cardiac and skeletal muscles through its actions in the neuromuscular junction, which is where muscles and nerves mee]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Pain_Management</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mRKYnIOJTguqo3pu3S3s5x3qQMCeHyZZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Pain Management]]></video:title><video:description><![CDATA[Nurse Nadia works on an orthopedic unit and is caring for Brian, a 51-year-old male with a history of degenerative joint disease, who was recently admitted for intractable back pain. After settling Brian in his room, Nurse Nadia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Brian’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Nadia recognizes important cues, including Brian’s vital signs, which are blood pressure 172/92 mmHg, heart rate 102 per minute, and respirations 22 per minute. She also notices Brian is gripping the side rails and clenching his jaw. When asked about his pain, he reports a current pain level of 9 out of 10, and that his tolerable level of pain is 5 out of 10.  

Next, Nurse Nadia analyzes these cues. She reviews the electronic health record, or EHR, and notes that Brian is prescribed 0.5 mg of IV hydromorphone every three hours PRN, and he received his last dose in the emergency department one hour ago. Nurse Nadia realizes Brian needs effective pain management.  

Prioritizing hypotheses, generating solutions, and taking action 
Now, using the information she has gathered, along with Brian’s medical history, Nurse Nadia chooses a priority hypothesis of acute pain.  

Then, she generates solutions to address Brian’s pain that will include pharmacologic and nonpharmacologic pain management interventions; and she establishes the expected outcome that after intervening, Brian will report a pain level of 5 or less out of 10 within two hours.  

Nurse Nadia then takes action to implement these solutions. She knows that since Brian’s most recent dose of pain medication was one hour ago, he can&amp;#39;t receive his next dose for two more hours. Since Brian is in severe pain, she verifies that Brian isn’t allergic to any medications and then calls the provider, reporting Brian’s current pain ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Urinary_Elimination</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1TTzt7wRTOywTy5hXgyLOHaWQLm4OOPw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Urinary Elimination]]></video:title><video:description><![CDATA[Nurse Michelle works at a pediatrician’s office and is caring for Emma, a fully toilet trained, 5-year-old female brought in by her father, Jim, for urinary frequency and crying when urinating. After settling Emma and her father in a room, Nurse Michelle goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Emma’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Michelle recognizes important cues, including vital signs, which are temporal temperature 98.8 F or 37 C, heart rate 84 beats per minute, and respirations 22 breaths per minute; as well as Jim’s description of Emma’s dark, amber-colored, and foul-smelling urine. Jim also reports Emma has been urinating more often than usual. Emma rates her pain during urination an 8 out of 10 on the Wong-Baker FACES pain scale. Then, Nurse Michelle obtains a clean catch urine sample from Emma for dipstick urinalysis and assesses for suprapubic and flank pain, which revealed mild discomfort with palpation over the suprapubic area. 

Next, Nurse Michelle analyzes these cues. She reviews the results of the urinalysis which shows positive for leukocytes, nitrites, and blood. Nurse Michelle recognizes that normal urinary elimination involves a controlled, painless release of urine that&amp;#39;s typically light to dark yellow in color, transparent, with a slight odor, with no evidence of bacteria or blood. Nurse Michelle realizes Emma is experiencing altered urinary elimination. She shares her assessments with the health care provider who diagnoses a urinary tract infection. 

Using information she&amp;#39;s gathered along with Emma’s medical history, Nurse Michelle chooses a priority hypothesis of urinary tract infection. 

Then, she generates solutions to address Emma’s infection that will include pharmacologic and nonpharmacologic interventions, and she establishes the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Bowel_Elimination</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k9CfvELcSvmjI4UjRjlhB4ewS3SG4QoQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Bowel Elimination]]></video:title><video:description><![CDATA[Nurse Thomas works at a primary care clinic and is caring for Donna, a 55-year-old female with a history of constipation, who’s being seen for abdominal discomfort. After settling Donna in her room, Nurse Thomas goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Donna’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

Nurse Thomas recognizes important cues such as Donna’s abdominal pain, which she describes as cramping with constant aching and rates as a 6 out of 10 on a pain scale. While gathering Donna’s health history, Nurse Thomas learns that although she typically has a bowel movement every two to three days, her last bowel movement was five days ago. She states it was hard, lumpy, difficult to pass, and there was a small amount of blood on the toilet paper after wiping.  

Donna reports she’s been managing occasional constipation for years, and it’s gotten worse since she started working from home. Nurse Thomas learns Donna usually drinks sodas throughout the day and typically eats a cheeseburger on a white bun for lunch. He performs an abdominal assessment by visually inspecting Donna’s abdomen, auscultating all four quadrants, and palpating her abdomen. His findings include mild abdominal distension, hypoactive bowel sounds, and a firm, elongated mass in her lower left quadrant. Results of a digital rectal exam by the health care provider reveals normal anal sphincter tone, and an absence of rectal pain, fissures, or hemorrhoids.  

Next, Nurse Thomas analyzes these cues. He knows bowel elimination should produce regular, soft, easy-to-pass bowel movements, and that other expected assessment findings include active bowel sounds in each quadrant, and a soft abdomen.  

Okay, so using Donna’s medical history and the information he’s gathered, Nurse Thomas chooses a priority hypothesis of constipation. Then, he generates]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Skin_Integrity_and_Wound_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TyHkjST5R9CNbrS610-iC6n3RuSeqLWh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Skin Integrity and Wound Care]]></video:title><video:description><![CDATA[Nurse Jess works at an urgent care clinic and is caring for Roger, a 56-year-old male, who arrived with a wound on his lower arm. After settling Roger in his room, Nurse Jess goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Roger’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jess recognizes important cues, including Roger’s vital signs, which are temperature 101 F, or 38.3 C, heart rate 98 per minute, respirations 14 per minute, and blood pressure 125/85 mmHg.  

She completes a skin assessment on Roger’s arm, and notes his wound is 1 centimeter across, open, and draining a small amount of purulent drainage. She also notices superficial erythema 2 centimeters around the wound. Extending from the wound towards his upper arm is a red streak, which Nurse Jess recognizes is a sign of lymphangitis, or inflammation of the lymph channels.  

When asked about the wound, Roger says he thinks it started with a bug bite he got while boating 3 days ago. 

Next, Nurse Jess analyzes cues. While reviewing the electronic health record, or EHR, she notes Roger was treated for a similar wound in the past. She also notes he’s been taking steroids prescribed for rheumatoid arthritis for the past 3 months, which can suppress the immune system. Nurse Jess realizes Roger needs treatment for his infected wound.  

Now, using the information she’s gathered, along with Roger’s medical history, Nurse Jess chooses a priority hypothesis of traumatic wound.  

Next, she generates solutions to address Roger’s wound that will include pharmacologic and nonpharmacologic interventions.  She establishes the expected outcome that after intervening, Roger will correctly demonstrate how to apply a dressing to his wound. 

Nurse Jess then takes action to implement these solutions. She begins by notifying the health care provider of Roger’s eleva]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Cognition_and_Sensation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ACbetZSzRl2kAzSkGxIPH1hqQRm7nb-S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Cognition and Sensation]]></video:title><video:description><![CDATA[Nurse Eric works on a medical-surgical unit and is caring for Maria, an 80-year-old female who was admitted for pneumonia. Maria’s husband, Leo, is at the bedside. Nurse Eric goes through the steps of the Clinical Judgment Measurement Model or CJMM to make clinical decisions about Maria&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Eric recognizes cues, by reviewing Maria’s electronic medical record, noting she has no personal or family history of dementia or mental illness. Then, he assesses her vital signs, which are blood pressure 118/72 mmHg, heart rate 90 per minute, temperature 101.4 F or 38.6 C, respirations 18 per minute, and oxygen saturation 97 percent on room air. He auscultates Maria’s lungs and notes rhonchi bilaterally, and he notices Maria is coughing up thick, green sputum.  

During his assessment, Maria is slow to respond and appears confused, so Nurse Eric asks some basic orientation questions.  

Nurse Eric: Maria, can you tell me what year it is? 

Maria: It’s 1983. Do you see those horses in my room? 

Leo: Maria, I told you there aren’t horses here. I don’t understand, she wasn’t confused until this morning. 

Nurse Eric continues his assessment by performing a neurological assessment to rule out life-threatening concerns. He performs a stroke assessment, which is negative for slurred speech, facial drooping, and asymmetrical weakness; and a Mini Mental State Examination reveals Maria has cognitive deficits in orientation, attention, calculation, and memory.  

Nurse Eric also reviews her most recent laboratory test results to check for other conditions associated with confusion in older adults, and notes Maria’s electrolytes and glucose are within normal limits, her urinalysis is negative for a urinary tract infection; but her white blood cell count is elevated 

Next, Nurse Eric analyzes these cues. After reviewing Maria’s tes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intraoperative_Phase_of_Surgery</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pOImtNVUR8CdP5irogJQqzlISTOjudOC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intraoperative Phase of Surgery]]></video:title><video:description><![CDATA[The intraoperative phase of surgery is when your patient undergoes a surgical procedure, beginning when they enter the operating room and ending when they leave the operating room. Your role during this period is to promote patient safety by performing frequent assessments, preventing infection, and advocating for them, since they cannot speak for themselves. When caring for your patients during the intraoperative phase, you will follow the steps of the Clinical Judgment Measurement Model, or CJMM, to make clinical decisions about patient care.  

Okay, let’s review the roles of the surgical team, which is typically separated into a sterile group and a nonsterile group. Sterile team members include the scrub nurse, surgeon, and registered nurse first assistant, or RNFA, and they work strictly within the sterile field. On the other hand, the nonsterile team members work outside the sterile field and include the circulating nurse, the anesthesiologist or certified registered nurse anesthetist, also known as the CRNA, and other assistive personnel. 

Now when it comes to the nursing team members, the scrub nurse is responsible for preparing and maintaining the sterile field, draping the patient, and assisting the surgeon by passing instruments and supplies. The circulating nurse advocates for the patient, coordinates communication between the nonsterile and sterile team members, and initiates the “time-out” procedure, when the team pauses before surgery to verify that they’re performing the right procedure on the right surgical site on the right patient. Additionally, the RNFA promotes optimal patient outcomes by fostering communication and collaboration with the team during surgery. It’s important to note that it’s the responsibility of every team member to practice surgical conscience through continual assessment and vigilance, to ensure adherence to sterile technique. 

Now, as the circulating nurse, you will ensure patient safety by using the Clinical Jud]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postoperative_Phase_of_Surgery</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZW5jE1l6QtqZDLvfF8v0k3fJRyuMPck1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postoperative Phase of Surgery]]></video:title><video:description><![CDATA[The postoperative phase starts when your patient is admitted to the post-anesthesia care unit, or PACU, immediately after surgery and ends when they’ve completely recovered from the surgical procedure. When caring for your patient during this phase, you’ll promote patient safety by following the steps of the Clinical Judgment Measurement Model to make clinical decisions about patient care.   

Okay, as a postoperative nurse, you’ll ensure patient safety by recognizing important cues. These cues can be gathered while receiving report from the operating room nurse and the anesthesia provider as well as during your initial assessment. Important cues may include indications of your patient’s response to anesthesia, like vital signs, ECG, and airway patency, as well as level of consciousness, IV status, estimated blood loss, and location of drains or dressings.  

Other important cues can include indicators of perfusion, such as capillary refill, skin color, and temperature; urine output; and laboratory results such as CBC. As you perform these assessments, you&amp;#39;ll document your patient’s condition using scoring systems like the Post-Anesthetic Discharge Scoring System, or PADSS, which helps the nurse to determine discharge readiness from the PACU.  

Next, you’ll analyze cues by determining the relationship between the cues and linking them to your patient’s history and clinical presentation. You’ll consider whether your patient’s current level of consciousness, quality of respirations, motor ability, and sensation correlate to the type of anesthesia received and the surgical procedure performed. You&amp;#39;ll also determine whether cues are associated with postoperative complications. For instance, you’ll consider whether a patient’s hypoactive bowel sounds are due to slowing of peristalsis secondary to general anesthesia or if it’s related to a paralytic ileus.     ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Issues_and_Changes_Affecting_Health_Care_Delivery</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9WcQ8opwToSiyaJmNj7Ihf3aTYCvSQEs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Issues and Changes Affecting Health Care Delivery]]></video:title><video:description><![CDATA[Nurse Irving is the charge nurse on a 24-hour observation unit where the majority of clients are admitted for chest pain. Then they go for a cardiac stress test, and are discharged if the test results are normal. During the unit huddle, Nurse Irving is informed that the hospital budget has become more limited due to price inflation, so every unit charge nurse is tasked with assessing ways to cut costs. After the huddle ends, Nurse Jade approaches Nurse Irving and says, “We waste so much money on broken equipment here.” Nurse Irving asks Nurse Jade what she means and she continues, “Just last week another portable heart monitor broke because it accidentally got sent down in the hospital laundry.” Nurse Irving realizes that these portable heart monitors cost thousands of dollars and says, “You’re right, we need to address this. Let&amp;#39;s create a plan to preserve these heart monitors.” Nurse Jade agrees to help Nurse Irving and speaks to the rest of the staff about possible solutions. Nurse Irving and Nurse Jade will use what they know about healthcare costs to provide quality client care in a cost-effective way.  

Healthcare costs in the United States are increasing every day; in fact, Americans spend over 3 trillion dollars on healthcare per year! But, increased spending of healthcare dollars hasn’t always translated into better health outcomes, such as average life expectancy. Healthcare facilities are tasked with improving health outcomes and delivering quality care in the most cost-effective way. Indicators of quality of care such as safety and client satisfaction scores directly influence how healthcare facilities are reimbursed. For example, increased rates of hospital acquired infections or hospital readmissions after discharge can decrease reimbursement. On the other hand, healthcare facilities that consistently demonstrate positive quality indicators are reimbursed accordingly. Now, within the healthcare environment there are healthcare consu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health,_Wellness,_and_Models_of_Health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WYlZq5nKSvOp3V6O_0uXG1kdSDKQ961u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health, Wellness, and Models of Health]]></video:title><video:description><![CDATA[Nurse Bintou works on a surgical oncology floor where clients are admitted following surgical procedures related to cancer. Today, Nurse Bintou will be caring for a client named Helen who underwent a right total mastectomy yesterday for treatment of breast cancer. Before meeting the client, Nurse Bintou checks in the electronic health record, or EHR, to read Helen’s most recent progress note from the healthcare provider which states, “Client will require around the clock pain medication secondary to surgical trauma.” 

Nurse Bintou enters Helen’s room to introduce herself and finds Helen weeping quietly. Nurse Bintou says, “Helen, my name is Bintou and I’ll be your nurse today. It seems like you’re in pain?” Helen looks up, visibly shaken, and responds, “Yes, but the medicine isn’t going to help my pain; I keep telling everyone that!” 

Nurse Bintou moves to sit at the edge of the bed, gently touches Helen’s hand and asks her to clarify. Helen sighs and says, “Yes, my incision does hurt, but nothing compares to the pain in my heart.” Nurse Bintou nods as Helen continues, “How will people ever look at me the same when I’m not whole anymore?” Nurse Bintou realizes Helen’s priority need is psychosocial in nature instead of physiological. Nurse Bintou will use what she knows about health and illness models to support and care for Helen. 

Okay, so health is a state of complete physical, mental and social well-being which is different for each person based on their values and beliefs. Health is more than just a person being free from illness, which is the subjective experience of physical or mental symptoms which usually accompanies a disease diagnosis. 

So, now that you understand what health and illness are, it&amp;#39;s time to examine the models used to understand them. There are several health and illness models, but we will focus on three that are commonly used by nurses; The Health Belief Model, Maslow’s Hierarchy of Needs, and The Holistic Health Mode]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion,_Illness_Prevention,_and_Levels_of_Preventive_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SzD26IZnRpuQ1cDACy5q2vE0QNKy1wrG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Promotion, Illness Prevention, and Levels of Preventive Care]]></video:title><video:description><![CDATA[Yousef is a community health nurse who’s volunteering at a free medical clinic. One of the clients who comes to the clinic is a 53-year-old construction worker, named Ben, who states, “I want to be tested for diabetes.” 

Nurse Yousef notes that Ben is moderately overweight, has a patch over his left eye, and is a current smoker. Nurse Yousef asks Ben to elaborate on why he wants to be tested for diabetes, and Ben responds, “I haven’t been going to the gym as much, so I’ve gained some weight. My dad has diabetes, so I want to make sure I don’t have it.” 

Nurse Yousef says, “Thank you for sharing, Ben. I’d be happy to get you screened for diabetes today. I think it would be a good idea for us to discuss some other aspects of your health too. 

I can’t help but notice you have a patch over your eye.” Ben nods in agreement and says, “Yeah, I went blind in my left eye about a year ago after a work accident. The doctor said there’s nothing they can do.” Nurse Yousef will use what he knows about health promotion and illness prevention to care for Ben.

Okay, so the concepts of health promotion and illness prevention are closely related since they both affect a client’s wellbeing and quality of life. Health promotion refers to activities that protect health and enhance an individual’s existing level of wellness, such as regular exercise and eating a balanced diet. On the other hand, illness prevention involves actions that can reduce an individual’s exposure to risk factors, which are things that increase the likelihood of developing an illness, disease, or trauma. Examples of illness prevention are high blood pressure screenings or wearing a helmet when riding a bike.

Although risk factors don’t cause an illness directly, they increase the chance of developing one and they can be categorized into modifiable and non-modifiable factors. Modifiable risk factors are ones that can be altered by lifestyle practices and behaviors, like drinking enough water or not te]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ethical_Considerations_in_Nursing_Practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s4mUFp-gQWe3lIC--C6z3ljpTn2CqiTo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ethical Considerations in Nursing Practice]]></video:title><video:description><![CDATA[Nurse Jocelyn works as a home health nurse. When at the market on one of her days off, she sees one of her friends, Sam, who says, “Jocelyn, my aunt just told me that you are her home health nurse! She says that you have been coming to her house ever since she got out of the hospital a few weeks ago. My aunt says that you take such great care of her. Has she been doing her physical therapy exercises like she’s supposed to? Oh I know you are supposed to keep information confidential but my aunt wouldn’t mind you talking to me!” 

Nurse Jocelyn wants to answer her friend’s question but also wants to respect her client’s privacy. She is experiencing an ethical dilemma but she can use The Code of Ethics for Nurses to help determine how to respond.

To begin, ethics refers to moral principles that guide a person’s behavior and choices. Since ethics are determined by social standards, they are referred to as being externally driven, meaning they are not decided by a single person. Ethics help us to figure out what is “right” and what is “wrong.” Usually, ethical principles are not written down; they are considered common knowledge within a community. For example, stealing is considered “wrong” for most people. But professional groups, like doctors and nurses, often have a more formal, written summary of ethical guidelines. This is called a code of ethics and is used to inform the moral decision making of those in the group.

Now, a code of ethics provides a written statement of the ethical code of the profession. It also outlines a standard of care within the discipline, as well as identifies the purpose of the profession or why they do what they do.  

So the profession of nursing has its own code of ethics written by the American Nursing Association, or ANA. The Code of Ethics for Nurses was first published in the 1950s but it’s updated often to reflect changes in the nursing profession. Some of the most recent changes discuss the ethical responsibility of pro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Patient_Education_in_Nursing_Practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pqjCGREwTnSnQBULwJqbDRHqS46XlPTq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Patient Education in Nursing Practice]]></video:title><video:description><![CDATA[Nurse Jerome works in an outpatient surgical center and is performing the intake assessment for a client named Julie who is scheduled for a colonoscopy. Nurse Jerome asks Julie, “When was the last time you ate?” Julie responds, “I just stopped to get a breakfast sandwich on the way here.” Nurse Jerome is confused since all clients scheduled for this procedure are instructed to ingest nothing but clear liquids after midnight the night before. He also notes that Julie has left several areas on her client forms blank and some spots have inappropriate information. 

Nurse Jerome says, “Julie, were you able to read through the colonoscopy preparation paperwork we sent you home with two weeks ago?” Julie bites her lip and looks around nervously, stating, “I did, but I guess I didn’t understand them too well, I’m sorry.” Nurse Jerome responds, “You don’t need to be sorry. Although you won’t be able to go for your colonoscopy today, let’s make sure you understand everything for next time.” Julie smiles and sighs a breath of relief. Nurse Jerome suspects Julie has low health literacy, so he’ll use what he knows about this topic to educate and support her.

Now, health literacy is the capacity to read, comprehend, and follow through on health-related information, so those who have low literacy skills are unlikely to properly understand the health-related information they need. Factors that can impact health literacy include the educational level of the client, as well as with the difficulty level of the reading material, since any client education material above the client’s reading comprehension level will lead to confusion and misunderstanding. Another factor is the native language of the client, so if educational materials aren’t written in the client’s native language, it can contribute to lower health literacy even if the client has overall high literacy in their primary language. 

It’s also important to keep in mind that even people with good literacy skills ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Documentation_in_the_Electronic_Health_Record</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8dksah3sTOehOectX6tKlGaASCWBVQ05/_.jpg</video:thumbnail_loc><video:title><![CDATA[Documentation in the Electronic Health Record]]></video:title><video:description><![CDATA[Nurse Steve is a nurse working on a medical unit. He calls the healthcare provider to address a client’s pain, and the healthcare provider gives Nurse Steve an order over the phone, saying “You can put in a prescription for 30 mg codeine PO every 4 hours.” Nurse Steve reads the order back aloud and the healthcare provider confirms it. 

When Nurse Steve goes to enter the order into the computer system, he receives an alert from the pharmacy that the client has an allergy to codeine. 

Nurse Steve calls the healthcare provider back and informs them of the allergy alert. The healthcare provider tells Nurse Steve, “You can override that alert. They have taken this medication before and tolerated it fine.” 

After ending the call, Nurse Steve enters the client’s room to inquire about this documented allergy. The client reports that the first time she took codeine, she felt nauseous and vomited, so the nurse documented it as an allergy. But in reality, it was a side effect of taking the medication on an empty stomach. The client reports that she has taken codeine at home as prescribed without any allergic reactions. Nurse Steve will use what he knows about documentation to ensure there’s an accurate account of this clinical decision in the health record.

Documentation is a communication strategy that allows members of the healthcare team to provide a written account of client information, such as assessments, interventions and responses. Documentation can be handwritten or electronically stored within the health record, which provides a real-time account of medical and nursing care. 

Okay, accurate documentation in the health record is necessary to communicate with all members of the healthcare team regarding the client’s status, plan, and care. It is also crucial for several other reasons such as legal protection, facility reimbursement and quality improvement, or QI. 

First, documentation is one of the best defenses for litigation in healthcare, and b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Safety_Promotion_and_Injury_Prevention</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZVBPNSh2TPqcEP7IWWdkRIFwTWG4A82T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Safety Promotion and Injury Prevention]]></video:title><video:description><![CDATA[Nurse Reggie works in a unit at a skilled nursing facility and has noticed that clients aren’t receiving consistent mouth care as prescribed and rates of nursing home-acquired pneumonia have risen. Nurse Reggie knows mouth care is important in preventing pneumonia so he asks Leyla, a Nursing Assistant, or NA, about the barriers to mouth care. NA Leyla says, “Honestly, mouth care isn’t listed on our daily task list, so I forget to do it.” Nurse Reggie thanks her and responds, “I want to begin a quality improvement project to address this issue. Would you help me?” 

NA Leyla agrees, so Nurse Reggie plans to create an updated NA task list which includes performing and documenting mouth care. Nurse Reggie and NA Leyla will measure the success of their project by tracking NA documentation of mouth care as well as the rate of hospital-acquired pneumonia six-months after implementation. Nurse Reggie and NA Leyla will work alongside the other members of the healthcare team at the facility to use quality management to improve this process. 

Healthcare facilities can achieve goals of improving the care delivered to clients through quality management and quality improvement. Quality management, or QM, is an overarching philosophy that focuses on optimizing patient care and outcomes. Healthcare institutions that adopt the QM philosophy use quality improvement, or QI, to implement these strategies by using specific processes to monitor and continually improve the quality of client care. Healthcare quality can be measured through identification of benchmarks, which are best practices for clinical care that can be compared between similar facilities to achieve outcomes such as client satisfaction and safety. 

QI consists of six steps. The first step is the identification of client needs, such as Nurse Reggie choosing mouth care as a clinical activity in need of improvement. The next step is assembling a team, which can be made up of interprofessional members inside an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infection_and_Infection_Control</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I2OHO7WuQeaiGTmrCgLSWNJYT4e3GQty/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infection and Infection Control]]></video:title><video:description><![CDATA[Sepsis refers to infection, while the prefix “a&amp;#39;&amp;#39; means “the absence of.” In other words, asepsis is defined as the absence of pathogens. Now, there are two basic types of asepsis: medical asepsis and surgical asepsis. We will focus on medical asepsis, which is also known as “clean technique”. These  are practices that kill some microorganisms to prevent them from spreading. Medical asepsis includes sanitization, antisepsis, and disinfection. 

Sanitization refers to cleaning practices and techniques that physically remove microorganisms. These include hand washing and cleaning of clients’ personal equipment, clothing, and linens. Now, there are several things that you should know in order to maintain a sanitary environment. The most important one is hand hygiene which includes hand washing and the use of hand sanitizer. Always wash your hands before meals, after using the bathroom, before and after any contact with your clients. Don’t forget to wash your hands after touching your own or your client’s body fluids, such as urine, feces, blood, saliva, vomitus, or genital discharge. Next, when coughing or sneezing, always cover your nose and mouth with a tissue or your elbow. Teach your clients to do the same. 

Next up are personal items. Each client should have their own soap, cups, toothbrushes, and towels. Personal equipment should be regularly cleaned to prevent the growth of microorganisms. Also, when cleaning the room and objects, make sure to not stir up the dust. In other words, avoid shaking dirty linens, and use a moistened cloth or mop to wipe dust. 

When disposing dirty linens to laundry bins, keep them away from your uniform. This way, you will prevent the contamination of your uniform, and subsequently, you will prevent the spread of microorganisms. Also, regularly empty the garbage, because trash is a perfect environment for pathogens to grow. Finally, have good personal hygiene and assist your clients to achieve the same! ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Overview_of_Oxygenation_and_Perfusion</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gPkhzILTR5iejR8cXQDr_2iZQWaD40J4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Overview of Oxygenation and Perfusion]]></video:title><video:description><![CDATA[Oxygen therapy is the delivery of extra oxygen to those with conditions that cause hypoxemia, when oxygen levels in the blood are low; and hypoxia, which is when there is not enough oxygen at the tissue level to meet the needs of the body.  

This includes patients with diseases that interfere with the lungs’ ability to absorb oxygen, like pneumonia, chronic bronchitis, emphysema, and pulmonary fibrosis; blood problems, like anemia, where the blood doesn&amp;#39;t carry enough oxygen; and heart problems, like heart failure, where the heart has trouble pumping blood around the body.  

Now, oxygen is considered a medication, so an order is needed. 

An oxygen setup consists of an oxygen source and a delivery device. There are several sources for oxygen therapy. With a wall outlet, oxygen is delivered into each patient room from a central supply.  

In contrast, an oxygen tank contains oxygen gas under pressure and is typically portable, so it can be carried along as the patient moves. However, this should be moved very carefully; if the tank tips over and the valve breaks open, pressurized oxygen can burst out forcefully and result in severe trauma. Oxygen tanks have a gauge that shows how much oxygen is left. There are also liquid oxygen systems which store oxygen as a liquid at very cold temperatures and then convert it to a gas for use. They are used either for bulk storage of oxygen for a hospital system or can be portable for home use for patients with high oxygen needs, where having a compact way to storge large amounts of oxygen is helpful.  

Finally, oxygen concentrators pull in air from the atmosphere and selectively remove nitrogen to deliver air that is about 90 to 95% oxygen to the patient. These devices are easy to use and can deliver an unlimited amount of concentrated oxygen as long as they have a power supply. One caveat is that some units are designed to only deliver up to 5 liters of oxygen per minute, and so those aren’t a good fit for ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutrition</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hTtVMTgvTt2Wl0SHdpFklik3R7_aDqPc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutrition]]></video:title><video:description><![CDATA[As a nurse, you will need to prepare clients for their meals, serve them food, and depending on their needs, assist them in eating. Since clients can have different nutritional needs or might have issues with chewing or swallowing, the diet ordered for your client will be tailored to their specific needs. 
Now, before we talk about how to do these things, here are some general considerations. Always check that the name on the tray matches the identification card or bracelet of the client and that the meal served follows the nutritional guidelines for that particular client. Make sure to serve food as soon as it’s ready so that serving temperature is optimal. 

Try to create a friendly atmosphere, keep them company, and help them as much as they need, while encouraging them to participate as much as possible. 
Okay, so, when preparing a client for their meal, first gather the supplies you’ll need, including gloves,  and paper towels. Next, assist the client with hand hygiene. Then,  if they use eyeglasses, hearing aids, or dentures, check that those devices are properly positioned. Finally, check where they’ll be eating and make sure the room is free from disturbing sights, odors, or sounds. 

The best location to eat for many clients is a community dining room, if available because it provides your clients the opportunity to socialize. Whether in a dining room or a private room, position them in a chair or wheelchair so they’re upright; if they’re in bed, raise the head of the bed, so they’re as upright as possible. Clean and adjust the over-bed table to a suitable height. 

Some clients might also have dysphagia, meaning difficulty swallowing. This is often caused by nervous system conditions, like stroke or head trauma or tumors in the mouth or esophagus, blocking the passage of food.  In these cases, the health care provider could order all liquids, like soup, to be thickened, making them less difficult to swallow. To do that, start adding a thicke]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EHDdzKExRRyg7xX29kMg_zlpRTaCOCWh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic Disease]]></video:title><video:description><![CDATA[Home health Nurse Svetlana is visiting a client named Betsy who was recently diagnosed with type 2 diabetes. Upon arrival, Nurse Svetlana notices that Betsy is sitting alone in her kitchen with her pajamas on even though it is 2 o&amp;#39;clock in the afternoon. 

Nurse Svetlana says, “Betsy, I’ve come to see how you’ve been managing your diabetes at home. How’s it been going?” Betsy responds, “I feel fine, but I didn’t realize how much this would change my life.” 

Nurse Svetlana sits down while Betsy describes the challenges she’s facing, including checking her own blood glucose and feeling isolated from her friends. Betsy continues, “My friends and I used to get pizza every week but now I can’t go because of my new diet.” Nurse Svetlana empathizes with Betsy, and reassures her that although there are many physical and emotional implications associated with a diabetes diagnosis, they’ll work together to address them. Nurse Svetlana will use what she knows about the nature of chronic disease to support Betsy in managing her diabetes diagnosis. 

So, chronic disease is a biomedical condition lasting at least one year which requires consistent medical care. Examples of chronic diseases are hypertension, asthma, and diabetes. The rapidly growing population of older adults in the United States is resulting in more chronic illness. It’s estimated that 60 percent of all adults in the United States have at least one chronic disease and 40 percent have two or more chronic diseases. In fact, chronic disease is the leading cause of death and disability, adding up trillions of dollars in health care costs every year! 

On the other hand, chronic illness refers to the client’s personal experience of living with a chronic disease. For example, clients diagnosed with Alzheimer disease may experience fear or loss of independence. Therefore, nurses must consider the complex needs of clients with chronic disease as well as the numerous factors that play a role in chronic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Integrative_&amp;_Alternative_Therapies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g3CHLltjSDinFPDaPXSvmILdQlK4bpi3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Integrative &amp; Alternative Therapies]]></video:title><video:description><![CDATA[Nurse Ken works in an outpatient oncology office and is caring for a client named Naveen who recently underwent a partial colectomy to treat stage 3 colon cancer. Naveen tells Nurse Ken, “I’ve been taking my prescribed medications, but I’ve been using my own remedies too.” Nurse Ken responds, “Naveen, I want to gather some more information to ensure I understand the treatments you’re using.” 

Naveen goes on to explain that he’s been taking his antibiotics as prescribed; however, he’s using acupuncture and meditation to address his pain instead of taking his prescribed pain medication. He also mentions that he’s now taking a probiotic every day and he’s developed a special diet with his nutritionist which limits his intake of gluten and dairy. 

Nurse Ken says, “I’m glad to hear you’re taking such a proactive approach to your health. Let’s work together to safely incorporate these into your plan of care.” Nurse Ken will use what he knows about integrative and alternative therapies to provide support and empower Naveen in making health care decisions. 

Okay, so allopathic therapy, also called biomedicine, is what we know as conventional Western medicine, such as the use of medications, chemotherapy, and surgical procedures like Naveen’s partial colectomy procedure and prescribed antibiotics. 

Then there’s integrative therapy, also known as complementary therapy, which is when an allopathic treatment is combined with a non-conventional treatment, such as massage therapy, chiropractic medicine, or biofeedback. Naveen is using integrative therapy by taking his antibiotics while also using a probiotic supplement to complement his conventional treatment. 

Next is alternative therapy, which is where non-conventional therapies completely replace a conventional allopathic treatment. For example, Naveen is using acupuncture and meditation instead of his pain medication so this is considered alternative therapy. Now that we know more about integrative and alternat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complications_of_Diabetes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xGFhah6mT76sKQ5m1m8WIuBcRRy5hrde/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complications of Diabetes]]></video:title><video:description><![CDATA[Diabetes mellitus is a chronic, multisystem disease characterized by high blood glucose, or hyperglycemia, which can lead to both acute and chronic complications.  

Okay, let’s review the pathophysiology of hyperglycemia. Normally, the beta cells in the pancreas release insulin, which is a hormone that helps glucose move from the bloodstream and into the tissue cells where it can be used for energy.  

In diabetes, though, either the pancreas doesn&amp;#39;t produce insulin, like with type 1 diabetes, or the body’s cells are resistant to insulin, like with type 2 diabetes.  

Either way, hyperglycemia results, causing symptoms like polyuria, or frequent urination; polydipsia, or increased thirst; and polyphagia, or increased appetite.  

Now, hyperglycemia can cause two serious acute complications: diabetes-related ketoacidosis, or DKA, and hyperosmolar hyperglycemia syndrome, or HHS.  

First, in DKA, glucose levels rise to 250 mg/dL or more, but since the cells are unable to use the glucose, they start breaking down adipose tissue, or fat, as a source of energy; a process called lipolysis. During lipolysis, ketone bodies are made as a byproduct, which increases the acidity of the blood, leading to metabolic acidosis.  

This manifests as deep and labored breathing, also called Kussmaul respirations, and fruity-smelling breath. As excess glucose is eliminated by the kidneys, large amounts of water is pulled along with it, a process called osmotic diuresis. Dehydration and electrolyte imbalances develop as fluids are depleted.  

On the other hand, in HHS, glucose levels rise to 600 mg/dL or more. This results in osmotic diuresis and dehydration that is much more severe than with DKA. But in contrast to DKA, there’s no breakdown of fat, so metabolic acidosis does not occur.  

If untreated, DKA and HHS can progress to cerebral edema, coma, and even death.   

Now, another acute complication is caused by hypoglycemia, or low glucose levels. Hypoglyce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_Older_Adults</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zaqWaldGRWeHXVNEQK6wx1-eSs6ss0H1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for Older Adults]]></video:title><video:description><![CDATA[Care of the older adult involves providing holistic care to meet the needs of patients as they mature through adulthood.  

Now, your goal when assessing your older patient is to identify common health issues of older adults, and to intervene to promote your patient’s health and safety.  

Begin by performing a mental status assessment. Observe their general appearance, posture, and facial expressions as indicators of mental function, and evaluate their level of consciousness and orientation to person, place, and time.  

As you talk with your patient, assess their speech patterns, organization of thoughts, and mood. Check for the presence of risk factors for depression, including situations like loss of a spouse, recent retirement, or isolation, as well as problems like pain or insomnia, which can be associated with depression. During your assessment, be sure to allow adequate time for them to respond to your questions. If your patient’s mental status is altered, adjust your approach accordingly. 

Next, assess their mobility and their ability to safely complete their activities of daily living, or ADLs, including bathing, dressing, toileting, and eating.  Be sure they have assistive devices, as needed, like a walker, cane, glasses, or hearing aids. Ask them if they have experienced a recent fall and talk to them about measures to increase safety in their home by removing throw rugs, ensuring adequate lighting, and installing handrails. Encourage physical activity according to their level of mobility to promote balance and maintain muscle mass.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_Administration:_Implement_and_Take_Action,_Evaluate</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u0HQc1dmTBCa9LZaqI-aRPKpRDC1m520/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication Administration: Implement and Take Action, Evaluate]]></video:title><video:description><![CDATA[Medication administration is a complex process which involves the application of a prescribed medication to a patient. As the nurse, you must identify medication safety risks, follow safe administration principles, and evaluate your patient’s condition after administration.  

Now, risks associated with medication administration include adverse medication reactions, cross-infection, or injury. Adverse reactions are unwanted effects that occur related to administration of a medication, which can be mild, like rash or nausea, or more severe, like kidney damage or GI bleeding.  

Next, cross-infection is when organisms, like bacteria or viruses, are transferred to your patient during administration. This can occur when administering a medication through your patient’s IV without thoroughly cleaning the hub or when touching the tip of an eye dropper to your patient’s eye during administration. Lastly, injury can occur to your patient when administering medications, like giving a hypertension medication to a patient who’s hypotensive or injecting a medication intramuscularly using incorrect technique, causing a hematoma or nerve injury. 

Alright, so there are several different routes for medication administration. The most common routes are oral, also known as per os or PO; parenteral, which includes IV, intramuscular, or IM, subcutaneous; and intradermal. Other routes for medication administration include inhalation, sublingual, rectal, topical, otic, and ophthalmic. 

Now, regardless of the route, prevent harm to your patient by following safe medication administration principles each time you administer a medication. The standard practice for safe medication administration involves adhering to the rights of medication administration, which include the: right patient, right medication, right dose, right time, right route, right indication, and right documentation. It’s important to note that there might be additional rights and you should follow the protocol outlined by your institution. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_and_Wellness</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tvq41bhIQB2llCUHR387eKmORXeNm2uR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health and Wellness]]></video:title><video:description><![CDATA[Health is more than just the absence of illness or disease and can be viewed as an objective state of functional stability, balance, and integrity. Illness is a subjective experience of poor health, and wellness can be thought of as a subjective experience of good health.  

Health, illness, and wellness are affected by multiple and interrelated dimensions of a person’s life, including physical, mental, social, environmental, and spiritual components.  

Now, the health of people and communities is influenced by social determinants of health, which are conditions where people live, work, play, worship, and age.  

Social determinants of health include genetic, social, and economic circumstances that promote health and wellness, such as having access to healthcare, healthy foods, education, and a safe place to live, as well as one’s genetic inheritance.  

Social determinants of health also include inequities like poverty, discrimination, and social inequities, and can limit access to the resources required to meet physical, mental, and emotional needs. This is especially true for specific groups, such as LGBTQ2, Black, and Indigenous peoples that have been disproportionately affected by health inequities.  

The Ottawa Charter for Health Promotion, created by the World Health Organization in 1986, identifies prerequisites for health, such as peace, shelter, a stable ecosystem, sustainable resources, and social justice.  

It developed strategies for health for people and their communities to work towards. There are 5 strategies.  Building healthy public policy shapes legislation, regulation and public policies that&amp;#39;ll determine how financial and material resources are allocated to people living in the community.  

By creating supportive environments, the community acknowledges the interrelationship between health and the natural and built environments; and it’s focused on creating and sustaining healthy and safe spaces through programs like provi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preoperative_Phase_of_Surgery</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V48uHKWPQnqsw1BUOE2hFG2iQU6fEiRB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preoperative Phase of Surgery]]></video:title><video:description><![CDATA[The preoperative phase of surgery starts when your patient’s time of surgery is confirmed and ends with the start of their surgery. When caring for your patient during this phase, you’ll promote patient safety by following the steps of the Clinical Judgment Measurement Model to make clinical decisions regarding patient care.  

Alright, as the preoperative nurse, you’ll ensure patient safety by recognizing important cues. These cues can be gathered from the patient or their family members during your assessment. Important cues may include your patient’s medical history such as medication allergies, previous response to anesthesia and pain medications, surgical history, prescription and over-the-counter medications; as well as underlying health conditions that could potentially lead to complications during the surgery and postoperative recovery like atherosclerosis, cardiac dysrhythmias, or diabetes mellitus. 

Other important cues can include results of preoperative tests, such as clotting factors or blood glucose. You’ll also ensure that consent for surgery has been signed. Also, evaluate your patient and their family members’ understanding of the surgical procedure and ensure their questions have been answered. Lastly, perform a psychosocial assessment to identify emotional support needs prior to surgery. 

Next, you&amp;#39;ll analyze these cues by determining the relationship between the cues and linking them to your patient’s history and clinical presentation. For example, you&amp;#39;ll determine if your patient’s elevated heart rate and respirations are related to anxiety about their upcoming procedure or if they’re related to an underlying cardiovascular condition.  

Next, you’ll determine a priority hypothesis related to the preoperative phase such as anxiety or risk for injury. You&amp;#39;ll rank the hypotheses according to urgency or likelihood, as well as considering whether they’re potentially life-threatening, like a new onset cardiac dy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infant_Feeding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1oF00zBvStCaDSz_IHYyR9l2R9KLpx3i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infant Feeding]]></video:title><video:description><![CDATA[The newborn’s diet must supply calories and nutrients, including carbohydrates, proteins, fats, vitamins, and minerals needed to support the rapid growth and development that occurs in early life. During the first few months of life, nutritional needs can be met by either breast milk or commercially prepared cow&amp;#39;s milk–based formula.  

Alright, let&amp;#39;s look at the composition of breast milk, which differs with each of the three phases of milk production, also known as lactogenesis.  

Phase I of lactogenesis starts during pregnancy and continues through the first few days of postpartum. During this phase, the breasts produce an early version of breast milk called colostrum which is a thick, yellowish fluid, high in protein, vitamins, minerals, and immunoglobulins like IgA, which protect the infant’s gastrointestinal tract from infections and aids in establishing normal flora in the infant’s digestive tract. Colostrum is low in fat and carbohydrates. It also has a laxative effect, which promotes the passage of the infant’s first bowel movement called meconium. 

Next, Phase II of lactogenesis starts two to three days postpartum. The milk produced during this phase is called transitional milk. Compared to colostrum it contains less immunoglobulins and proteins, but has more vitamins, fats, and lactose.  

The last phase of lactogenesis is Phase III, when mature milk is produced. Mature milk is the ideal food for infants, though it’s low in vitamin D, so a daily supplement of 400 international units, or IUs, is recommended until the baby starts eating solid foods. Mature milk is also low in iron, but since the iron found in breast milk is easily absorbed, supplementation is not needed. 

Now, the nutritional content of mature breast milk will vary during the course of the feeding session. So, foremilk, which is the first milk that flows from the breast, is rich in protein and carbohydrates, and low in fat and calories. It is also quite w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pernicious_anemia:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cx-O2yK8QWKc4Y7b2pvtG0mOStiJwAPf/_.png</video:thumbnail_loc><video:title><![CDATA[Pernicious anemia: Year of the Zebra]]></video:title><video:description><![CDATA[Pernicious anemia is an autoimmune disorder characterized by a decrease in the production of red blood cells due to lack of vitamin B12, an essential component for the development of red blood cells. 

In pernicious anemia, a protein found in the stomach, called intrinsic factor, or IF, or the stomach cells that produce IF, are attacked by the immune system. Intrinsic factor normally binds to vitamin B12 to allow the vitamin to be absorbed through the gastrointestinal tract. When there is insufficient intrinsic factor, vitamin B12 cannot be absorbed, ultimately leading to a decrease in red blood cell production. 

Now, the symptoms of pernicious anemia may include weakness, fatigue, abdominal discomfort after eating or drinking, palpitations, mouth ulcers, or even weight loss. Jaundice, or yellowing of the skin or sclera, can also occur. In more severe cases, symptoms can be due to damage to neurons and present as paresthesias, or ‘pins and needles’ sensations; spasticity, or abnormal muscle tone; and imbalance. 

The diagnosis of pernicious anemia is based on the individual’s detailed medical history, and thorough clinical evaluation, however, blood tests are required to confirm the diagnosis. Blood tests can include a complete blood count, or CBC; vitamin B12 levels; peripheral smear; and antibody testing.   ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Turner_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/82mXow_DS5qzCjs6D6SFqT5aQDGZb49W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Turner syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Turner syndrome: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tetralogy_of_Fallot:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wINvF8-9To_evqi5jsOJ1_5VS8CNCuKA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tetralogy of Fallot: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Tetralogy of Fallot: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tracheostomy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M4h4G0PBSXiO0ZITWhq7NiGeRFa9-kWA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tracheostomy]]></video:title><video:description><![CDATA[A tracheostomy is a type of artificial airway consisting of a small, plastic tube that’s inserted through a surgically created opening, or stoma, in the anterior neck, known as a tracheotomy.  

Typically, a tracheostomy is placed when a patient can’t keep their own airway open. It can be placed urgently when intubation by other means isn’t possible, or as a planned procedure, if the patient requires long-term airway assistance. 

Now, patients with a tracheostomy typically have a short tube that protrudes from the anterior of their neck, which is usually stabilized with a flange and ties that encircle the neck. Many tracheostomy tubes have an outer cannula, which keeps the airway patent, and an inner cannula, which can be disposable or non-disposable and is removed for cleaning.  

The tube may or may not be connected to a mechanical ventilator or another source of oxygen; and depending on the type of tracheostomy tube your patient has, they may or may not be able to talk. 

Okay, so tracheostomy tubes come in various sizes and configurations. First, tubes can be cuffed, meaning there is a balloon that can be inflated to provide a leak-proof connection; or uncuffed, where there is no balloon.  

Cuffed tubes are usually used short-term because they occlude the upper trachea and pharynx, and the pressure exerted can compress tracheal capillaries, limit blood flow, and predispose the patient to tracheal necrosis. On the other hand, uncuffed tubes are used for patients with long-term tracheostomies to decrease the risk to surrounding tissues. 

It’s also important to note that tracheostomy tubes can be fenestrated or non-fenestrated. A fenestrated tube has a hole on its dorsal surface, which helps promote spontaneous breathing.  

When patients have a cuffed, fenestrated tracheostomy tube, the cuff can be deflated and inner cannula removed. This allows air to pass from their lungs through the opening in the tube, enabling them to breathe spontaneously and sp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Child_with_Cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0OPaFACwQ4WKuVSr3IzPc_J4SbWgw3AA/_.jpg</video:thumbnail_loc><video:title><![CDATA[The Child with Cancer]]></video:title><video:description><![CDATA[Cancer is a group of conditions characterized by uncontrolled cell growth that goes unchecked by the immune system. Cancer can be broadly classified as hematologic or blood-borne cancers, and solid tumors. 

Hematologic cancers, such as acute lymphoblastic leukemia, acute myeloid leukemia, and Hodgkin lymphoma, arise from immature blood cells or lymphatic cells. In these cancers, the continued uncontrolled multiplication of immature cells interferes with the development and function of healthy blood and lymphatic cells. On the other hand, solid tumors develop from specific organs. These tumors can arise in the bones, like osteosarcoma; the kidneys, like nephroblastoma; or in the colon, like colon cancer.  

Regardless of the type, cancer is typically caused by genetic mutations altering cell division. Diagnosis involves a history; physical assessment; laboratory tests such as a CBC; diagnostic imaging, like MRI; and diagnostic procedures, like lumbar puncture or bone marrow biopsy. Treatment depends on the type and staging and can include surgery, chemotherapy, biotherapy, radiation therapy, and hematopoietic stem cell transplant. While treatment aims to destroy cancerous cells, it also destroys non-cancerous cells leading to undesired side effects in your patient. 

Now, when caring for a child with cancer, you’ll manage the side effects of cancer treatment. Chemotherapeutic agents and radiation therapy to the head or abdomen can cause GI side effects, like nausea and vomiting, which may cause your patient to eat or drink less. Given these side effects, you’ll monitor their nutritional status, weight, intake and output, and signs of dehydration.  

Also, remember to administer the prescribed antiemetic medications, and implement nonpharmacologic interventions for your patient, like distracting them through playing with toys or encouraging them to talk with their friends.  

To support their nutritional status, encourage your patient to drink fluids like P]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Perinatal_and_Postpartum_Mood_and_Anxiety_Disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6KtY3-iSThWgAa2i4Oj2C7JTTAackoYO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Perinatal and Postpartum Mood and Anxiety Disorders]]></video:title><video:description><![CDATA[Peripartum depression, also known as major depressive disorder with peripartum onset, and previously known as postpartum depression, is a type of depressive disorder that occurs during pregnancy or during the four weeks following delivery. 

First, let’s briefly review the physiology of some hormonal fluctuations that take place in the perinatal period. During pregnancy, the placenta releases hormones, including human placental lactogen, estrogen, and progesterone; while the pituitary gland releases prolactin, among others. These hormones travel through the bloodstream to their specific areas of action to regulate body functions during the pregnancy.  

Then, during labor, the pituitary gland secretes another hormone called oxytocin, which stimulates uterine muscle contractions to facilitate delivery. Once the baby’s delivered, most of these hormones start to decrease. 

Now, the exact cause of peripartum depression isn’t completely understood, but it’s likely multifactorial. It can be related to changes in hormone levels, as well as an imbalance of neurotransmitters like GABA, serotonin, dopamine, and glutamate that help regulate mood, reward-motivated behavior, appetite, and sleep.  

Some of the major risk factors include having a family or personal history of depression, as well as social factors like intimate partner violence, poor socioeconomic support, single marital status, undesired pregnancy, or age younger than 25 years. 

So, it’s thought that individuals who develop peripartum depression have an increased sensitivity to the hormonal fluctuations that occur during the perinatal period. This, alongside the psychological impacts of having a baby, such as anxiety, fatigue, and sleep deprivation, can all play a role in the pathology of peripartum depression. 

Clinical manifestations of peripartum depression typically include feelings of extreme sadness, fatigue, and anhedonia, which is a diminished interest in everyday activities that used to be p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community_Health_Nursing_Practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aCIO71XiStaqf28os9lcqaSPQAmvh-RF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community Health Nursing Practice]]></video:title><video:description><![CDATA[Community health nursing is a branch of nursing focused on preventative care and managing acute and chronic conditions within that community, which is a group of people who live in the same area or share certain values or characteristics. Community health nursing can include public health, home health, and primary care nursing. 

Now, as a community health nurse, you’ll first need to complete a community assessment to better understand the community’s environment, including physical locale, the social systems, and the people who live and work in the community.  

You can assess the physical locale by driving around the community and conducting a “windshield” survey, or by walking around the community and completing a walking survey. Your survey can determine a community’s access to resources such as recreation, shopping, and opportunities for socialization. During your survey, you may notice that there are several prominent houses of worship in the community, that the neighborhoods are composed of both single-family houses as well as multifamily dwellings, or the presence of well-maintained parks with open space where children can safely play. You may also notice if there are vacant lots, if there’s a direct bus route to the local grocery store, and the number of fast-food restaurants that are within walking distance of neighborhoods. 

Your assessment will also include the community&amp;#39;s social systems, which you can accomplish by visiting specific sites, like schools and health care facilities, and by interviewing community members. You can also review data from the local health department to gather health and demographic information and use this information to identify community strengths as well as potential problems. For example, you might notice that there’s been a decrease in local teen pregnancy, but also an increase in sexually transmitted infections, or STIs, in the last year. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heparin_Dosing_and_Administration_Protocols</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/321lp9oySMu9Y4Tjl-JwYLbBQoivy-l5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heparin Dosing and Administration Protocols]]></video:title><video:description><![CDATA[Anticoagulants are medications that work by interfering with the clotting factors in the coagulation cascade. These medications are used to prevent the formation of thrombi, or blood clots, and prevent or treat thromboembolic events, which are conditions that occur when a blood clot obstructs a blood vessel like in deep vein thrombosis, pulmonary embolism, ischemic stroke, transient ischemic attack, coronary artery disease, or myocardial infarction.  

They&amp;#39;re also used to treat patients with coagulation disorders, like disseminated intravascular coagulation, and patients who underwent cardiac valve replacement or coronary angioplasty; and they are used during procedures like cardiopulmonary bypass, percutaneous coronary intervention, extracorporeal membrane oxygenation, and hemodialysis.  

Now, heparin is a commonly used anticoagulant, and it’s a high-alert medication, meaning there’s an increased risk of patient harm if administered in error. This is because heparin can cause unwanted and potentially dangerous bleeding. 

Okay now, when administering a heparin IV infusion, you’ll likely follow a weight-based protocol, meaning the dose is based on the patient’s weight, which helps to ensure safe dosing for each patient. Then, the infusion is adjusted, or titrated, based on their activated partial thromboplastin time, or aPTT, results, which measures both the intrinsic and common pathways of the coagulation cascade.  

Alright, since heparin is a high-alert medication due to the risk for bleeding, you will always infuse it using an electronic IV infusion pump. It is delivered in milliliters per hour, but because heparin is dosed in units, you need to calculate the heparin infusion rate in units per hour and convert that dosage into milliliters per hour, which is what you program into the infusion pump.  

So, to calculate an IV heparin dose, you first need to understand how to calculate a weight-based calculation. Let’s look at the following scen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Externalizing_Disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EXnyUDE9SXmDeoDeNCeRJmyOS7iYhT0c/_.png</video:thumbnail_loc><video:title><![CDATA[Externalizing Disorders]]></video:title><video:description><![CDATA[Attention-deficit hyperactivity disorder, or ADHD, is classified as a neurodevelopmental disorder that develops before 12 years of age, and is characterized by developmentally inappropriate behaviors, including inattention, impulsiveness, and hyperactivity. 

The symptoms of ADHD are believed to be caused by decreased levels of certain neurotransmitters, specifically dopamine, which is involved in behaviors like risk taking, impulsiveness, and reward; norepinephrine, which is involved in alertness, attention, and focus; and serotonin, which plays a key role in regulating mood. There are also some structural abnormalities in parts of the brain, like the frontal lobe, cerebellum, and basal ganglia that are present in the brains of children with ADHD. 

Okay, so the exact causes of ADHD aren&amp;#39;t well understood, but it is likely due to a combination of genetic and environmental factors. ADHD has a strong genetic component, so a child with a parent or sibling diagnosed with ADHD is more likely to develop it themselves. ADHD is also associated with prenatal exposure to tobacco smoke, alcohol, or illicit drugs, as well as perinatal problems like prematurity or low birthweight. Other risk factors include exposure to lead; certain infections, like encephalitis; and adverse childhood experiences, such as neglect, abuse, or exposure to domestic violence. 

Now, children are often fidgety, talkative, and inattentive, but the behaviors of a child with ADHD are different because they’re considered developmentally inappropriate; they’re persistent, or always present; and they interfere with the child’s functioning and development.  

One of the major symptoms of ADHD is inattention, meaning the child may find it difficult to focus on tasks like conversations, games, or reading, and they&amp;#39;re easily distracted by extraneous stimuli like people talking, music, or other background noises. They often don’t appear to be listening when spoken to; they have diffi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Burn_Injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yoFOEYbpQ4aqEIPB3yIz8OtGRaOxRmUj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Burn Injury]]></video:title><video:description><![CDATA[Nurse Kamala works on an inpatient burn unit and is caring for Raul, a 42-year-old male who was recently admitted for a thermal burn following a house fire. After being stabilized in the emergency department through airway management and fluid therapy, Nurse Kamala settles Raul into his room on the inpatient burn unit. 

After introducing herself to Raul, Nurse Kamala goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Raul’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Kamala recognizes important cues, including Raul’s vital signs, which include blood pressure 128/88 mmHg, heart rate 105 beats per minute, and respirations 22 breaths per minute.  

From Nurse Kamala&amp;#39;s assessment of Raul’s skin, she notes Raul has partial- and full-thickness burns on his right lower extremity, extending up to his lower abdomen. The dressings over Raul’s burns are saturated with serosanguineous drainage and the surrounding skin is reddened and slightly swollen. She also notices that he appears uncomfortable and restless.  

Next, Nurse Kamala analyzes these cues.  She reviews Raul’s electronic health record, or EHR, and notes an order for sterile dressing changes with wound debridement and cleansing. She also sees that he’s prescribed medication for pain management and received his last dose in the emergency department 4 hours ago. She knows that dressing changes will facilitate healing and untreated pain can make dressing changes intolerable. Nurse Kamala realizes that Raul needs effective pain management so the prescribed wound care can be provided for his burns. 

Now, using the information she’s gathered, Nurse Kamala chooses a priority hypothesis of impaired skin integrity.  

Then, she generates solutions to address Raul’s impaired skin integrity using nonpharmacologic and pharmacologic interventions; and she establish]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Hypertension</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PE_rylKfTI2O_B5kMKD-ygWEQ4Gr-DDD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Hypertension]]></video:title><video:description><![CDATA[Nurse Tom works at a primary care clinic and is caring for Mahlik, a 62-year-old patient who is being seen for a wellness check. After settling Mahlik in the exam room, Nurse Tom goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Mahlik’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tom recognizes important cues, including temperature 99.4 F or 37.5 C, pulse 75 beats per minute; respirations 16 breaths per minute; blood pressure of 156/89 mmHg, and oxygen saturation 97% on room air.  

Next, Nurse Tom asks Mahlik about his history.  

Nurse Tom: Do you usually have high blood pressure? Do any of your family members have high blood pressure? 

Mahlik: My dad and older brother do. My job is stressful, so maybe that’s contributing. I’ve checked my blood pressure at the drug store, and it’s been high, but with work, I haven’t had time to come in and have it checked. 

Nurse Tom: Stress can contribute to high blood pressure, and family members with high blood pressure can increase your likelihood of having it too. What foods do you usually eat? 

Mahlik: I mostly eat fast food because I’m always on the go.  

Nurse Tom: Can you tell me about how often you smoke, drink alcohol, and exercise? 

Mahlik: I don’t smoke, never have. I drink maybe 1 to 2 beers a week on average, and honestly, I don’t exercise as much as I should. I’m just so busy with work.

Nurse Tom analyzes these cues. He reviews the electronic health record, or EHR, and notes Mahlik’s body mass index, or BMI, is 28 kg/m2. Nurse Tom alerts the health care provider to Mahlik’s blood pressure and history. They diagnose Mahlik with stage 1 primary hypertension and prescribe an oral antihypertensive medication. Nurse Tom realizes Mahlik needs effective blood pressure management.

Using the information gathered along with Mahlik’s history, Nurse Tom chooses a p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Atopic_Dermatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1uEX1CtRRj2tA5OVDrIOVA9hTnuM0pAj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Atopic Dermatitis]]></video:title><video:description><![CDATA[Nurse Lisa works in a primary care clinic and is caring for Jamie, a 2-and-a-half-year-old who was brought in for a rash, by her mother Claire. After settling Jamie in her room, Nurse Lisa goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Jamie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Lisa recognizes important cues, including Jamie’s skin assessment, which reveals several clusters of dry, red patches to her wrists and ankles. She also notes that Jamie is scratching her left wrist, which is eroded and excoriated. 

Nurse Lisa asks Claire about Jamie’s skin irritation. 

Nurse Lisa: I see that Jamie has some dry and reddened skin. When did these symptoms start? 

Claire: A few weeks ago, when the weather got colder. 

Nurse Lisa: Have you tried any treatments or therapies to help relieve the itching? 

Claire: Sometimes I put her in a hot bubble bath, but it doesn’t seem to help. I also put lotion on her every day, which helps a little. 

Next, Nurse Lisa analyzes these cues. Nurse Lisa understands that Jamie has an itchy inflammatory rash, and that Jamie’s scratching is causing excoriation. She also knows the breakdown of Jamie’s skin increases the risk for infection. Nurse Lisa recognizes that Jamie needs effective management of her rash.  

She reports her assessment findings to the health care provider, who diagnoses Jamie with eczema, or atopic dermatitis, and prescribes oral loratadine and a topical corticosteroid to reduce pruritis and inflammation.  

Now, using the information she’s gathered, Nurse Lisa develops a priority hypothesis of impaired skin integrity. 

Then, Nurse Lisa generates solutions to address Jamie’s impaired skin integrity that will include pharmacologic and nonpharmacologic interventions; and she establishes the expected outcome that after intervening, Jamie’s rash will show improvement in one month.   ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Pancreatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Gy58GcaxSb6YJXSXSTCL5VUwStGdtVPM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Pancreatitis]]></video:title><video:description><![CDATA[Nurse Gerdie works on a medical-surgical unit and is caring for Leo, a 47-year-old male who was recently admitted for acute pancreatitis secondary to alcohol use. After settling Leo in his room, Nurse Gerdie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Leo&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Gerdie recognizes important cues, including Leo’s vital signs, which include blood pressure 145/90 mmHg, heart rate 88 beats per minute, and respirations 18 breaths per minute. Nurse Gerdie notices Leo is diaphoretic, his gown is damp, and he’s lying in the fetal position clutching an empty emesis bag. She also sees that he has IV fluids infusing in his right forearm.  

Nurse Gerdie: Hi Leo, it looks like you&amp;#39;re not feeling well. What&amp;#39;s your pain level right now? 

Leo: It feels like I can’t lie down on my back or get comfortable at all. And I’m so nauseated.  

Nurse Gerdie: I understand, I’m going to help you feel more comfortable. 

Next, Nurse Gerdie analyzes these cues. She reviews the electronic health record, or EHR, and notes that Leo’s prescriptions include hydromorphone IV every 3 hours as needed, and his last dose was given two and a half hours ago in the emergency department; and ondansetron IV for nausea, but he hasn’t yet received a dose. She recognizes that Leo needs effective pain and nausea management to improve his comfort. 

Now, using the information she&amp;#39;s gathered, Nurse Gerdie chooses a priority hypothesis of impaired comfort.  

Then she generates solutions to address Leo’s pain and nausea that will include pharmacologic and nonpharmacologic interventions. Nurse Gerdie establishes the expected outcome that after intervening, Leo will report increased comfort within one hour. 

Nurse Gerdie then takes action to implement these solutions. She recognizes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Environmental_Emergencies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wiOIWnkTRoayAZ3dlXDt1crfRXqx1F2i/_.png</video:thumbnail_loc><video:title><![CDATA[Environmental Emergencies]]></video:title><video:description><![CDATA[An environmental emergency refers to an event or condition related to exposure to weather, which can include emergencies involving heat and cold. 

Alright, so heat-related emergencies happen when the body’s normal thermoregulatory mechanisms like sweating, vasodilation, and increased respirations, are less effective in situations where there’s prolonged exposure to heat, or if there’s brief exposure to intense heat.  

Heat exhaustion happens when heat exposure occurs over hours or days like during a hike on a hot day leading to a body temperature as high as 105.8° F or 41° C. Other assessment findings can include anxiety, fatigue, nausea, thirst, and pale skin. If left untreated, heat exhaustion can progress to heat stroke which is a medical emergency! With heat stroke, the body’s thermoregulatory mechanisms fail leading to a temperature above 105.8° F or 41° C. Other assessment findings can include weakness and hot, flushed, dry skin. 

Now, in both heat exhaustion and heat stroke, fluid and electrolytes are lost through perspiration, which can manifest as tachycardia, weak pulses, and decreased blood pressure. In heat stroke, an excessive loss of sodium can lead to cerebral edema, brain hemorrhage, and mental status changes ranging from confusion to coma.  

Alright, when caring for your patient with a heat-related emergency ensure they are in a cool environment. For heat exhaustion, provide fluid and electrolyte replacement orally, or intravenously, if needed. For heat stroke, provide high-flow oxygen and initiate continuous pulse oximetry; establish IV access to replace fluids and electrolytes; and initiate rapid cooling measures.  

These could include placing wet sheets over your patient and placing them in front of a fan to increase airflow over their body; placing ice packs on their groin and axillae; or immersing them in a tepid or cool water bath. Be sure to monitor their temperature closely to control shivering, which can lead to heat producti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Chronic_Obstructive_Pulmonary_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hzH6LWuoTsyfqswdfVYmVhbgQACh2SiJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Chronic Obstructive Pulmonary Disease]]></video:title><video:description><![CDATA[Nurse Seema works on a medical-surgical unit and is caring for Richard, a 75-year-old male with a history of smoking, who was admitted for an acute exacerbation of chronic obstructive pulmonary disease, or COPD. After settling Richard in his room, Nurse Seema goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Richard’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Seema recognizes important cues including Richard’s vital signs, which are temperature 99.6 F or 37.5 C, heart rate 98 beats per minute, respirations 28 breaths per minute, blood pressure 142/90 mmHg, and oxygen saturation 85 percent on room air. When asked about pain, Richard reports a current pain level of 0 out of 10. Upon assessment, Nurse Seema notes that Richard’s respirations are labored, he has expiratory wheezing, and he’s leaning over in a tripod position. 

Next, Nurse Seema analyzes these cues.  She reviews the electronic health record, or EHR, and notes Richard’s arterial blood gas, or ABG, shows a low PaO2, indicating hypoxemia. She also recognizes COPD causes airway inflammation, leading to obstructed airflow out of the lungs, causing CO2 retention, making gas exchange difficult. Nurse Seema knows that Richard’s hypoxemia, wheezing, and tripod positioning indicate he’s experiencing impaired respiratory function and needs effective respiratory management. 

Now, using the information she’s gathered, Nurse Seema chooses a priority hypothesis of impaired gas exchange. 

Then, she generates solutions to address Richard’s impaired gas exchange that will include pharmacologic and nonpharmacologic interventions. She establishes an expected outcome that after intervening, Richard will maintain an oxygenation saturation between 89 to 92 percent on 2 liters nasal cannula within one hour.   

Nurse Seema then takes action to implement these solutions.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Hypovolemic_Shock</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UCsD4teqQ2ic5Cye6RnqKlIAQ4iWCwYW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Hypovolemic Shock]]></video:title><video:description><![CDATA[Nurse Edwin works the night shift at the emergency department and is caring for José, a 67-year-old male with a history of liver cirrhosis and hepatic encephalopathy. After settling José in his room, Nurse Edwin goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about José’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Edwin recognizes important cues, including José’s vital signs, which are blood pressure 88/46 mmHg, mean arterial pressure, or MAP of 60 mmHg, heart rate of 110 beats per minute and regular, peripheral pulses are weak and thready, and respirations 22 breaths per minute. Pulse oximetry is 88 percent on room air. 

José is also confused and doesn’t know why he’s in the hospital. Nurse Edwin also notices that José appears pale, diaphoretic, and has a capillary refill of more than 3 seconds in his lower extremities. He also notes that José’s abdomen is round and distended. 

Next, Nurse Edwin analyzes these cues. He collaborates with the health care provider, who determines that José is in the early decompensated stage of hypovolemic shock, due to third spacing. Nurse Edwin realizes José needs effective tissue perfusion. 

Now, using the information he&amp;#39;s gathered, along with José’s medical history, Nurse Edwin chooses a priority hypothesis of fluid volume deficit. Then, he generates solutions to address José’s fluid and perfusion status with pharmacological and nonpharmacological interventions; and he establishes the expected outcome that after intervening, José’s MAP will be above 60 mmHg within one hour.  

Nurse Edwin then takes action to implement these solutions. He receives orders from the health care provider for IV fluids and albumin, oxygen at 10 liters per minute via non-rebreather mask, and insertion of an indwelling urinary catheter. Other orders include lactulose PO, and transfer to the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Pneumonia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wyS0VEwFR4S2oCc5DJCYgo71Ql__aqsN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Pneumonia]]></video:title><video:description><![CDATA[Nurse Jodie works on a Medical-Surgical unit and is caring for Ann, a 44-year-old female with a history of smoking who was recently admitted for community-acquired pneumonia. After settling Ann in her room, Nurse Jodie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ann’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jodie recognizes important cues including Ann’s vital signs, which are temperature 101.5 F or 38.6 C, heart rate 101 beats per minute, respirations 28 breaths per minute and regular, blood pressure 90/60 mmHg, and oxygen saturation 85 percent on room air. Upon auscultation, Nurse Jodie notes course crackles and slight wheezing. Nurse Jodie also observes that Ann can’t speak in full sentences without becoming short of breath.  

Next, Nurse Jodie analyzes these cues. Nurse Jodie reviews the electronic health record, or EHR, and notes Ann’s WBC count is elevated at 12,500 per mm3. Nurse Jodie knows that an infection is likely causing fluid to fill up Ann’s alveoli which is interfering with gas exchange; and that inflammation is causing her airways to narrow. Nurse Jodie recognizes that Ann needs effective respiratory management. 

Nurse Jodie chooses a priority hypothesis of ineffective gas exchange. 

Then, Nurse Jodie generates solutions to address Ann’s infection. She establishes the expected outcome that after intervening, Ann will maintain an oxygenation saturation above 92 percent during the shift.  

Nurse Jodie then takes action to implement these solutions.  

Nurse Jodie: I&amp;#39;m going to give you some oxygen to help you breathe a little easier. This plastic tubing will go around your ears and the prongs will go into your nose. It&amp;#39;s important that you breathe in through your nose so the oxygen will go into your lungs. 

Ann: Okay, I hope it helps. 

Nurse Jodie: Your health car]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Anaphylaxis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sBqhjJdiTn2lJu1iisUYHkZ8RZSK2U-3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Anaphylaxis]]></video:title><video:description><![CDATA[Nurse Milagros works on a Medical-Surgical unit and is caring for Jessica, a 32-year-old female with a history of intravenous drug use, who was recently admitted for endocarditis. After settling Jessica in her room, Nurse Milagros goes through the steps of the Clinical Judgement Measurement Model to make clinical decisions about Jessica’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Milagros recognizes important cues including Jessica’s vital signs, which are blood pressure 86/42 mmHg, heart rate 112 beats per minute, respirations 36 breaths per minute, and pulse oximetry 89 percent on room air.  

Upon auscultation, Nurse Milagros hears expiratory wheezes in all of Jessica’s lung fields and she also notes Jessica’s restless, fearful appearance. On closer inspection, Jessica appears flushed, and her lips are swollen.  

Next, Nurse Milagros analyzes these cues. She reviews the electronic health record, or EHR, and notes that Jessica has no known allergies to foods or medications. Also, Jessica hasn’t received any medications except the infusion of penicillin in the last four hours. Based on her assessment and recent infusion of penicillin, Nurse Milagros realizes Jessica is likely experiencing anaphylaxis.  

Now, using the information she&amp;#39;s gathered along with Jessica’s medical history, Nurse Milagros chooses a priority hypothesis of impaired gas exchange. 

Then, she generates solutions to address Jessica&amp;#39;s impaired gas exchange that will include pharmacologic and nonpharmacologic interventions; and she establishes the expected outcome that 30 minutes after intervening, Jessica’s respiratory status will stabilize.  

Nurse Milagros then takes action to implement these solutions. First, she stops the infusion of penicillin. Then, she calls the hospital operator and requests that a rapid response be called to Jessica’s room.  

Next, the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Atrial_Fibrillation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VWVn5A4FTPG8jG4gxtDm_Kh_TZO_TLh5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Atrial Fibrillation]]></video:title><video:description><![CDATA[Nurse Derek works on an inpatient cardiac unit and is caring for Mrs. Alvarez, a 76-year-old female with a history of hypertension, who was admitted with new-onset atrial fibrillation, or a-fib, with rapid ventricular rate, or RVR. She was given an IV bolus of diltiazem in the emergency department then started on a continuous diltiazem drip. After settling Mrs. Alvarez in the room, Nurse Derek goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about her care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Derek recognizes important cues, including Mrs. Alvarez’s vital signs, which are blood pressure 100/74 mmHg, heart rate 112 beats per minute, and respirations 22 breaths per minute. After placing Mrs. Alvarez on continuous cardiac monitoring, he evaluates her ECG, noting the QRS complexes are normal, but the rhythm is irregular and there are no P waves.  

She denies pain but reports mild shortness of breath, diaphoresis, and feeling dizzy and tired with movement. 

Next, Nurse Derek analyzes these cues. He determines that Mrs. Alvarez is still in a-fib. He then reviews the electronic health record, or EHR, and notes that her diltiazem drip is ordered to be titrated as needed to maintain a heart rate of less than 100 beats per minute; and the drip was last titrated in the emergency department one hour ago.  

Nurse Derek also realizes that rapid and irregular atrial contractions can lead to decreased cardiac output and tissue perfusion, causing Mrs. Alvarez’s symptoms, therefore, she needs more effective heart rate control.  

Now, using the information he&amp;#39;s gathered, Nurse Derek chooses a priority hypothesis of decreased cardiac output. 

Then, he generates solutions to promote heart rate control that will include pharmacologic interventions. He establishes the expected outcome that after intervening, Mrs. Alvarez w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Down_Syndrome,_Fragile_X,_and_Cystic_Fibrosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/io7O4KMeQxShxzmY3ZK5xcDMQVC2lPDS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Down Syndrome, Fragile X, and Cystic Fibrosis]]></video:title><video:description><![CDATA[Down syndrome is a chromosomal abnormality caused by a genetic mutation leading to an extra or partial copy of chromosome 21. 

Now, chromosomes are molecules that carry packaged DNA information for a person, like a storage bin. Every cell in our body has 46 chromosomes, organized into 23 pairs. During human fertilization, each parent donates half of their chromosomes to create a zygote with a total of 46 chromosomes. But in some cases, like in Down syndrome, one parent donates an extra chromosome, leaving the zygote with 47 chromosomes. People with Down syndrome receive an extra copy of chromosome 21, which is why Down syndrome is also referred to as Trisomy 21, or “three chromosome 21s.&amp;quot; 

The exact cause of Down syndrome is unknown. What we do know is that the likelihood of Down syndrome increases with the age of the mother. So, a 35-year-old mother is more likely to give birth to a baby with Down syndrome than a 25-year-old mother. Down syndrome also seems to arise more often from patients who have translocation of chromosomes 15, 21, or 22, where parts of one chromosome switch places with another chromosome, creating an atypical hybrid of the two original chromosomes. This is referred to as Robertsonian translocation. 

Down syndrome has a number of clinical manifestations. Several changes to the face occur. Skin folds covering the inner corner of the eyes develop, called inner epicanthal folds, along with an upward slant in the palpebral fissure. A depressed nasal bridge or flattening of the top part of the nose may also develop along with a protruding tongue. Speckling of the iris, known as Brushfield spots, might also appear. People with Down syndrome may also have small ears with narrow canals.  

Other clinical manifestations include a shortened rib cage, umbilical hernia, and protruding or loose abdominal muscles. People with Down syndrome typically have short stature, hyper-flexibility with muscle weakness, and atlantoaxial instabilit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Leukemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OPgsBn7yQzu4Ky2UZaAYwd5JTDadrZ7M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Leukemia]]></video:title><video:description><![CDATA[Nurse Tracy works on an inpatient oncology unit and is caring for Margie, a 60-year-old female with a history of chronic lymphocytic leukemia, or CLL. After settling Margie in her room, Nurse Tracy goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Margie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tracy recognizes cues, including Margie’s vital signs which are temperature 98.8 F or 37.1 C, heart rate 90 beats per minute, respirations 18 per minute, blood pressure 122/84 mmHg, and oxygen saturation of 98 percent.  

Nurse Tracy notes Margie has various small bruises on her back and legs and generalized lymphadenopathy, or swollen lymph nodes.  

She notices Margie grimacing with movement, and when asked about pain, Margie reports a pain level of 5 out of 10 in her legs and a pain tolerance level of 3 out of 10.  

Nurse Tracy sees a sign on Margie’s door requesting no visitors, so she asks Margie about how she’s feeling. 

Nurse Tracy: Margie, I see you don&amp;#39;t want visitors today.  

Margie: No, I’m very tired. Besides, I’ve been such a burden to them; they probably want a break from me.  

Nurse Tracy: You don’t have to have visitors if you aren’t feeling up for it. Have your family or friends mentioned not wanting to visit? 

Margie: No, they haven’t, but I’d rather be alone.  

There’s so much I can’t control right now with my leukemia,  

and I’m feeling overwhelmed. Also, my pain is bothering me.  

I have extra doses of pain medicine to take between scheduled doses,  

but I forget to ask until my pain is too bad.  

Next, Nurse Tracy analyzes these cues. She reviews the electronic health record, or EHR, and notes that Margie has scheduled pain medication as well as doses to take as needed, or PRN, for breakthrough pain. The medication administration record shows that Margie hasn’t received any PR]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Stroke</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SZJj34OUR_mHv7pYKAC2EitgSvCRRdB-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Stroke]]></video:title><video:description><![CDATA[Nurse Darius works on a neurology unit and is caring for Calvin, a 67-year-old male with a history of hyperlipidemia who was recently admitted following a stroke. After settling Calvin in his room, Nurse Darius goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Calvin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darius recognizes important cues including Calvin’s vital signs which are temperature 98.8 F, or 37.1 C, heart rate 98 beats per minute, respirations 16 breaths per minute, blood pressure 146/92 mmHg, and oxygen saturation 96 percent on room air.He rates his pain level is 0 out of 10.  

Nurse Darius also notes that the left side of Calvin’s face is drooping and sees that he favors his right hand. Nurse Darius also overhears Calvin mixing up his words while trying to talk to the dietary staff about his lunch tray.  

Next, Nurse Darius analyzes these cues. He reviews the electronic health record, or EHR, and sees Calvin has undergone an MRI of his head. The results show that Calvin had an ischemic stroke, where an occlusion in his artery caused inadequate blood flow to his brain.  

Nurse Darius knows Calvin’s hyperlipidemia was likely a contributing factor to his stroke, since it can lead to atherosclerosis and blockage of arteries.  

He also knows the loss of oxygenated blood flow to the brain can cause damage to areas that control language and motor functions and lead to muscle weakness and aphasia.  

Nurse Darius recognizes that he needs to effectively communicate with Calvin to properly care for him. 

Now, using the information he’s gathered, Nurse Darius chooses a priority hypothesis of impaired communication.   

Then, he generates solutions to address Calvin’s impaired communication that will include nonpharmacologic interventions; and he establishes the outcome that after intervening, Calvin ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_Patients_with_Vascular_Problems</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CZbrz-5MQz_ny4vRnrVW5urgS0aqJAAf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for Patients with Vascular Problems]]></video:title><video:description><![CDATA[Peripheral vascular disease includes disorders that change the natural flow of blood through the blood vessels of peripheral circulation, and includes peripheral artery disease, or PAD, and peripheral venous disease. 

PAD is characterized by a partial or total blockage of blood flow through arteries, which are high-pressure vessels that carry oxygen and nutrient-rich blood from the heart to the tissues.  

Blockage results in decreased perfusion and impaired delivery of oxygen,and nutrients to the tissues below the level of obstruction, causing tissue hypoxia and ischemia.  

The most common cause of PAD is atherosclerosis, or the build-up of plaque within the artery. Risk factors for atherosclerosis include smoking, uncontrolled hypertension, uncontrolled diabetes mellitus, and hyperlipidemia.   

On the other hand, peripheral venous disease is the result of prolonged pressure in the veins, which are low-pressure vessels that return deoxygenated and nutrient-depleted blood back to the heart.  

In the legs, the veins have to work against gravity to move blood up to the heart. To do this, they depend on the skeletal muscle pump, or the contraction of surrounding skeletal muscles, to compress the veins and propel blood upwards. These veins also have one-way valves that prevent blood from flowing backwards, away from the heart. If the valves fail to close properly, a condition called venous insufficiency, blood leaks backward and pools in the veins, causing venous hypertension, or high pressure within the veins. Over time, the veins become distended and twisted, as the pressure inside the veins increases. Venous hypertension can also occur when a blood clot, or thrombosis, obstructs blood flow.  

Common causes of peripheral venous disease include venous stasis, or slowing of blood through the vascular system; vascular injury; and hypercoagulable states.  

Also, people who have occupations that require prolonged standing, like nurses or teachers, or those ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Canadian_Health_Care_Delivery_System</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yeGjcZySSzOE9r7jub2uZAOOSWed1Oyw/_.jpg</video:thumbnail_loc><video:title><![CDATA[The Canadian Health Care Delivery System]]></video:title><video:description><![CDATA[A health care delivery system is a collection of institutions, organizations, and resources that help specific populations meet their health care needs.  

Now, in Canada, the Canada Health Act guides the health care delivery system to provide affordable and accessible care to all citizens through five principles.  

The first principle is public administration, where agencies and local authorities deliver health care services on a non-profit basis. The next principle is comprehensiveness, where all medically necessary treatments are covered by insurance without out-of-pocket charges. The third principle is universality which ensures that all residents receive treatment without discrimination due to their race, gender, income, ethnicity, or religion.  

The fourth principle is portability, meaning that residents can receive health care in any Canadian province or territory without additional costs. And lastly, the fifth principle is accessibility which guarantees availability of health care services based on medical need, rather than a person’s ability to pay.  

Using these principles, each territory or province administers its own separate health care system in institutional settings, such as hospitals or long-term care facilities, as well as community settings, like within a patient’s home or local health clinics.  

Now to improve health care delivery and patient outcomes, Canada’s federal, provincial, and territorial governments have adopted a model called Primary Health Care, or PHC.  

PHC is different from primary care, which is health care that prevents, diagnoses, and treats diseases. PHC, on the other hand, focuses on the continuum of care throughout the lifespan, across healthcare and non-healthcare settings with the goal of achieving better health for everyone. PHC incorporates a societal approach to address whole-system factors that affect peoples’ health, like housing, income, and education. PHC also takes a proactive approach to health care]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Retroperitoneal_fibrosis:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fPYlpxZaStuAe-7H1IW8ooviRDqv7kol/_.png</video:thumbnail_loc><video:title><![CDATA[Retroperitoneal fibrosis: Year of the Zebra]]></video:title><video:description><![CDATA[Retroperitoneal fibrosis is a chronic inflammatory disorder where fibrous, scar-like tissue develops in the retroperitoneal area. The peritoneum is the serous membrane that lines the abdominal cavity and covers the abdominal organs. The growth of fibrous tissue in the retroperitoneal space, or the space behind the peritoneum, leads to compression of the structures in that area, such as blood vessels like the inferior vena cava, and the ureters, which are the fibromuscular tubes that carry urine from the kidneys into the urinary bladder. 

Initially, retroperitoneal fibrosis may be asymptomatic or cause nonspecific symptoms, like lack of energy, loss of appetite, unexplained weight loss, and low-grade fever. 

As the disease progresses, the most common symptom is dull, low back or flank pain. In some cases, a palpable mass may be found in the abdomen or rectum. External compression of the ureters may obstruct the normal flow of urine, resulting in the back-up of urine into the kidneys, which can result in kidney damage over time. Compression of the inferior vena cava may result in swelling of the lower limbs and deep vein thrombosis, whereas compression of the retroperitoneal gonad vessels may lead to testicular pain and swelling. 

Often, retroperitoneal fibrosis is discovered incidentally on a CT scan or other imaging techniques, which reveal a fibrous mass in the retroperitoneal space. There are no specific laboratory tests for retroperitoneal fibrosis, but most individuals present elevated inflammatory markers and low blood cell counts, or anemia, due to chronic inflammation. In cases where the diagnosis is not clear, a tissue biopsy may be done to distinguish between retroperitoneal fibrosis and other underlying conditions, such as an infection or malignancy. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pierre_Robin_sequence:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2lLGpiGaQOCWVDNIoIXqZbKwTJej8G57/_.png</video:thumbnail_loc><video:title><![CDATA[Pierre Robin sequence: Year of the Zebra]]></video:title><video:description><![CDATA[Pierre Robin sequence describes a combination of congenital birth defects that occur during fetal development, specifically micrognathia, or underdevelopment of the lower jaw, and glossoptosis, or a backward positioned tongue, leading to airway obstruction. The cause of Pierre Robin sequence isn’t fully understood but often occurs as an isolated genetic mutation, or it can be part of a syndrome, like Stickler syndrome. 

Alright, now infants with Pierre Robin sequence have a high risk of airway obstruction due to the tendency of their tongue to slide backwards into the pharynx. In mild cases, obstruction only occurs when lying down, sleeping, or feeding, when the infant leans back into the caregiver’s arms. In severe cases, however, the obstruction can make normal breathing difficult and lead to stridor, a high-pitched whistling sound made by the collapsed airway.

Most infants with Pierre Robin sequence also have cleft palate, which is an opening in the roof of the mouth. This opening can make it difficult for the infant to suction milk from the breast or a bottle, causing poor weight gain, food aspiration, and frequent coughing and gagging. Cleft palate can also affect speech development later in life, and might contribute to frequent ear infections and even secondary hearing loss. 

Now, Pierre Robin sequence may be found on ultrasound prenatally, and if this is the case, these infants are more severely affected so further testing can be done. After birth, diagnosis is usually made based on history and physical examination. A nasolaryngoscopy, a technique where a small tube is inserted from the nose and into the throat, may be done to help locate the level and severity of airway obstruction. Further evaluation may involve radiologic imaging of the head and neck and a polysomnography, which records oxygen levels and brain activity during sleep.

Treatment of Pierre Robin sequence depends on the degree of airway obstruction. Mild cases may be treated with]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Wernicke-Korsakoff_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JYY2V2e8QM2WcRfmJfL3qvbnRuuURFNl/_.png</video:thumbnail_loc><video:title><![CDATA[Wernicke-Korsakoff syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Wernicke-Korsakoff syndrome is a rare neurological condition that causes degeneration of brain cells, or neuronal atrophy. It is caused by thiamine, or vitamin B1, deficiency. Thiamine is a vitamin absorbed in the intestines and used for energy metabolism to support growth, development, and cellular functioning, especially in the brain and nervous system. 

Thiamine deficiencies are commonly seen with conditions that lead to malnutrition, such as chronic alcohol use. The condition includes two stages: Wernicke encephalopathy, which is the acute and reversible stage; and Korsakoff syndrome, which is when the condition progresses to a chronic and irreversible stage.

Now, Wernicke-Korsakoff syndrome commonly presents with the triad of altered mental status, including confusion and memory deficits; nystagmus, or involuntary, rapid, and repetitive movement of the eyes; and ataxia, or impaired coordination of voluntary movements, balance, and speech. 

Other symptoms that may develop include agitation, hallucinations, and confabulation, which is when affected individuals create stories they believe to be true, to fill gaps in their memory. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epidermolysis_bullosa:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SveIwEsyQqSb4dqxCcUQdOfBSoGBxLrd/_.png</video:thumbnail_loc><video:title><![CDATA[Epidermolysis bullosa: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Epidermolysis bullosa: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia_of_chronic_disease:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n7hGkZzhTHiMNdMBhyy6jprZQaimvjJB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia of chronic disease: Year of the Zebra]]></video:title><video:description><![CDATA[Anemia of chronic disease refers to a low red blood cell, or RBC, count that may be associated with many chronic disease states like infections, malignancy, diabetes, or autoimmune disorders. The disease used to be called anemia of chronic inflammation because the underlying cause anemia is the continuous inflammation generated by chronic disease, which impairs iron metabolism and, in turn, RBC production. The anemia itself is usually mild and it’s the second most common type of iron deficiency anemia. 

RBCs are produced in the bone marrow, in response to erythropoietin - which is a molecule secreted by the kidneys in response to low levels of oxygen in the blood. Taking a closer look at our RBCs, we can see they’re loaded with millions of copies of the same exact protein called hemoglobin, which binds to oxygen and turns our RBCs into little oxygen transporters that move oxygen to all the tissues in our body. Zooming in even closer, each hemoglobin molecule is made up of four smaller heme molecules, which have iron right in the middle. Oxygen binds to the iron, so each hemoglobin molecule can bind four molecules of oxygen. In addition, iron is also an important part of proteins like myoglobin, which delivers and stores oxygen in muscles; and mitochondrial enzymes like cytochrome oxidase, which help generate ATP.

Now, we get the iron required for RBC production from our diet. Following breakdown of food in the stomach, iron is released, and then it’s absorbed in the small intestine - specifically, the duodenum. Inside the duodenal cells, iron molecules bind to a protein called ferritin, which temporarily stores the iron.  When iron is needed in the body, some iron molecules are released from ferritin and transported into the blood, where they bind to an iron transport protein called transferrin that carries iron to various target tissues and releases them there.

Now, the mechanisms that underlie anemia of chronic disease are complex and still under inve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_cancer:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cOX34l76QEiR658ywodMjOQKRIi-h_GS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal cancer: Year of the Zebra]]></video:title><video:description><![CDATA[Esophageal cancer is when malignant or cancerous cells arise in the esophagus. This cancer can appear in any segment of the esophagus and it’s further classified into squamous cell carcinoma and adenocarcinoma - depending on the type of cells it originates from. Squamous cell carcinoma, as you can tell by its name, arises from squamous epithelium. On the other hand, adeno- means gland. So, adenocarcinoma arises from columnar glandular epithelium. Esophageal cancer is generally considered a poor prognosis cancer, because it doesn&amp;#39;t cause symptoms until later stages. 

The esophagus is a long tube going from the pharynx to the stomach, and it’s connected to the pharynx through the upper esophageal sphincter, and to the stomach through the lower esophageal sphincter. Both relax during swallowing to allow the passage of food or liquids. Additionally, the lower esophageal sphincter is tightly closed between meals to prevent acid reflux. Now, the esophageal wall has four layers - from the outside in, these are the adventitia; the muscular layer; the submucosa and the mucosa. The mucosa comes into direct contact with food, and it protects the esophageal wall from friction. The mucosa also has three layers of its own: a layer made of stratified squamous epithelium; a layer of connective tissue, called the lamina propria; and a layer of muscle cells, called the muscularis mucosae. Finally, at the lower esophageal sphincter, the squamous epithelium joins the columnar gastric epithelium to form the gastroesophageal junction. 

Now, squamous cell carcinoma is the most common type of esophageal cancer worldwide, and it originates in the squamous epithelium of the esophagus, most often in the upper two thirds. When this epithelium is repeatedly exposed to risk factors like alcohol, cigarette smoke, or hot fluids, it gets damaged, so the squamous cells divide to replace the old damaged cells. With each division, there is a risk that a mutation can occur in ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leprosy:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6oNr1oofSSeZGdZ-I5-0GTMxTVy82N5d/_.png</video:thumbnail_loc><video:title><![CDATA[Leprosy: Year of the Zebra]]></video:title><video:description><![CDATA[Leprosy, also known as Hansen disease, is a chronic infectious disease caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis. Likely transmitted through respiratory droplets from the nose or mouth during close contact with an affected individual, the bacteria mainly attack the skin and peripheral nerves but can also damage the eyes and upper respiratory tract mucosa. 

Now, the symptoms of leprosy vary depending on each infected individual’s immune response to the bacteria. Skin symptoms typically include lesions that can vary in appearance. The most common skin lesion includes well-demarcated lesions with central hypopigmentation that may become erythematous, or reddened, and raised due to skin inflammation. In some cases, nodules may also form. Other skin lesions may have a ‘punched out’ appearance or a ‘target-like’ appearance. Lesions are typically distributed randomly across the body.

Peripheral nerve symptoms can include hypoesthesia, or loss of sensation, and paralysis, typically of the hands and feet. If the nerves of the eyelid muscles or cornea are affected, paralysis of the eyelid may occur and lead to incomplete eyelid closure, or lagophthalmos; or corneal abrasion, ulceration, and even blindness. 

If the nasal mucosa is affected, a saddle-nose deformity, or a collapsed nasal bridge, may occur. 

Alright, so the diagnosis of leprosy is based on history, physical examination, and laboratory tests. A skin or nerve biopsy may be performed on affected areas looking for foam cells, or immune cells that have engulfed the bacteria but are unable to digest them; or for acid-fast bacilli that can be seen after staining. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemophilia:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VoPAvlwYQ8eFXXE7Tgxp0DsfQrSlWS6V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemophilia: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Hemophilia: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nail-patella_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xKpctW9TTsGWPlOQZFOn9VfeSTSSjuH6/_.png</video:thumbnail_loc><video:title><![CDATA[Nail-patella syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Nail-patella syndrome: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fibromuscular_Dysplasia:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4Sy2iHgkS5O7tQY8XmoXyUvTSOSRmHlU/_.png</video:thumbnail_loc><video:title><![CDATA[Fibromuscular dysplasia: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Fibromuscular dysplasia: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ovarian_cancer:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fs2pc12XSDu49tTxZnBI_CX8RWi_trQD/_.png</video:thumbnail_loc><video:title><![CDATA[Ovarian cancer: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Ovarian cancer: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Huntington_disease:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-SDsfkzjSU2jQh1r2vsAZ9LKTwm8FJ_l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Huntington disease: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Huntington disease: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_insufficiency:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C3qRa0mvSl2gYnoA4YQUFGGmQLqTZiYn/_.png</video:thumbnail_loc><video:title><![CDATA[Adrenal insufficiency: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Adrenal insufficiency: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/PHACE_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/csoIqvgIRy_E31M7C0oyINNRTpKlR5JF/_.png</video:thumbnail_loc><video:title><![CDATA[PHACE syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of PHACE syndrome: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alkaptonuria:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MIQoLx9ERROWb8EvyC2SkbxUTQOi0NF5/_.png</video:thumbnail_loc><video:title><![CDATA[Alkaptonuria: Year of the Zebra]]></video:title><video:description><![CDATA[Alkaptonuria is a rare genetic metabolic disorder that causes a deficiency in the homogentisate 1,2 dioxygenase, or HGD, enzyme and is characterized by the accumulation of homogentisic acid, or HGA, in the body. Alkaptonuria is inherited in an autosomal recessive pattern, meaning that two copies of the defective gene are required to cause the disorder. Normally, HGA is converted, by the HGD enzyme, within the body and used for cellular processes. In alkaptonuria, the absence of the HGD enzyme leads to excess HGA being turned into hyperpigmented substances that accumulate in various tissues.

Now, alkaptonuria most commonly presents with manifestations in the urine, skin, and joints from HGA accumulation. The most common symptom is the presence of dark brown or black urine. Excess HGA that gets excreted in the urine is then exposed to the air, which can turn the urine black after time. In affected infants, this may appear as black stains in diapers.

In the skin, blue-black areas of hyperpigmentation appear, usually on ear cartilage or sclera of the eye. These hyperpigmented areas are called ochronosis.

Lastly, in the joints, arthritis occurs, most commonly the low back, hips, knees, and shoulders, and leads to pain and decreased joint mobility.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ehlers-Danlos_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rr6llb2FRIi7c7UImZpx8L0aR16d5XcL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ehlers-Danlos syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Ehlers-Danlos syndrome: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Buerger_disease:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xeL311ZkRF_gY-I8mGQqVYh9T6mzSUql/_.jpg</video:thumbnail_loc><video:title><![CDATA[Buerger disease: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Buerger disease: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hirschsprung_Disease:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rbiIegqiQ6S2I5hVK8mW2A65Q3yT-_X_/_.png</video:thumbnail_loc><video:title><![CDATA[Hirschsprung disease: Year of the Zebra]]></video:title><video:description><![CDATA[Hirschsprung disease is a congenital condition in which neural ganglia or clusters of nerves from segments of the colon are missing, which ultimately leads to a blocked colon, causing it to enlarge. This is why sometimes it’s also referred to as intestinal aganglionosis or just congenital megacolon.

Okay, so the intestines move the waste through the bowels in one direction only, via coordinated wave-like smooth muscle contractions called peristalsis. This is controlled by the autonomic nervous system, which is divided into two parts; the sympathetic, and the parasympathetic nervous systems. The sympathetic nervous system is our fight or flight response and increases heart rate, while slowing down digestion through reducing peristalsis. On the other hand, the parasympathetic nervous system is our rest and digest response and it slows down heart rate, and increases digestion by promoting peristalsis.

Now, if we look closely at the intestinal smooth muscle layer, it’s actually composed of a circular and a longitudinal muscle layer. Within these layers are two plexuses, or networks of nerves made up of ganglia, which are clusters of individual parasympathetic ganglion cells. First there’s the myenteric plexus, also known as Auerbach’s plexus, which when activated, primarily causes smooth muscle relaxation. The myenteric plexus connects with the submucous plexus, or also known as Meissner’s plexus, which is buried in the submucosa and is responsible for helping to control blood flow and epithelial cell absorption and secretion. 

Now, these two nerve plexuses are formed during early stages of fetal development when a group of fetal cells called neural crest cells start differentiating into neuroblasts. Around week 4 of development, these neuroblasts start migrating from the mouth towards the anus. Around week 8, they get to the proximal colon of the gut, and pass through the distal colon, and around week 12 they finally reach the rectum. Two specific genes th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/KIF1A-Associated_Neurological_Disorder:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ITFk_Im1QOmmoF39LjE95Id6SSK1mZL2/_.jpg</video:thumbnail_loc><video:title><![CDATA[KIF1A-associated neurological disorder: Year of the Zebra]]></video:title><video:description><![CDATA[KIF1A-associated neurological disorder, or KAND for short, is a group of rare genetic conditions that result in progressive neurological dysfunction due to alterations in the KIF1A gene. The KIF1A gene codes for a specialized protein called kinesin found in neurons. Kinesin helps transport nutrients and other important molecules along the neuron’s axon, like a minecart on a railway track. 

Alterations affecting the KIF1A gene lead to faulty kinesin that either stops or slows down axonal transport, resulting in neuronal dysfunction and even cell death. 

So far, researchers have identified over 100 alterations affecting the KIF1A gene. These alterations can be inherited in autosomal dominant or recessive patterns, however, the most common and most severe forms are caused by de novo alterations, meaning they arise spontaneously and are not inherited.

Now, KAND is a spectrum-type condition, meaning the symptoms and progression vary greatly from one individual to another depending on the underlying gene alteration and pattern of inheritance. 

One of the main features is spastic paraplegia, a condition where muscle weakness and stiffness in the legs causes the individual’s movements to jerk, affecting their ability to walk and move around. 

Some children may also have a delay in reaching childhood milestones, like walking and talking, and they may experience difficulty with coordination and balance; as well as seizures and visual disturbances. Additionally, because brain development can be affected, individuals may have microcephaly, which is when head size is smaller than expected for an individual’s age.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Castleman_disease:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_1UWsTDgSr6s5iWDFkQKhQ8rRKyyYh_W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Castleman disease: Year of the Zebra]]></video:title><video:description><![CDATA[Castleman disease describes a group of immune-related disorders characterized by lymph node enlargement resulting from the overactivation of the immune system. There are two main types of Castleman disease: unicentric, or localized, which only affects a single lymph node region; and multicentric, or generalized, where there is lymph node enlargement in multiple regions of the body along with a broad range of inflammatory symptoms. 

Castleman disease is linked to the overproduction of a protein called interleukin-6, or IL-6, which plays a key role in regulating immune responses. The exact reason for this abnormal IL-6 production is not entirely understood, but it may result from an exaggerated immune response to certain viral infections, such as human immunodeficiency virus, or HIV, the infection responsible for AIDS.

Individuals with unicentric Castleman disease are often asymptomatic. If they experience symptoms, they are usually mild and related to the compression of surrounding structures by enlarging lymph nodes. Common symptoms include feeling a lump under the skin in the neck, armpit or groin area; and a feeling of fullness or pressure in the chest that can make swallowing or breathing more difficult. 

On the other hand, multicentric Castleman disease is a potentially life-threatening condition, where individuals experience a wide range of systemic symptoms in addition to enlargement of the lymph nodes. These can include flu-like symptoms, such as fever, fatigue, night sweats, and unintentional weight loss; as well as enlargement of the liver and spleen. 

Although it is unclear why, some individuals with multicentric Castleman disease develop life-threatening organ dysfunction caused by a sudden and massive release of proinflammatory mediators, leading to significant tissue inflammation and organ damage. This may result in liver and kidney dysfunction and symptoms of fluid accumulation in the body, such as edema and ascites, or excess fluid in the abdomen. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Canavan_disease:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IIjGAoPJRxmYav7E05eUuloGRbyZdWyL/_.png</video:thumbnail_loc><video:title><![CDATA[Canavan disease: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Canavan disease: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Breast_Cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8nrN3Q4zRTKK7Jz_V2eog1j5RDyDZoW0/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Breast Cancer]]></video:title><video:description><![CDATA[Nurse Rebecca works at an oncology clinic and is caring for Patricia, a 53-year-old female who recently had a breast biopsy confirming the diagnosis of breast cancer. After settling Patricia in her room, Nurse Rebecca goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Patricia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Rebecca recognizes important cues, including Patricia’s vital signs, which include, temperature 98.6°F or 37°C, heart rate 105 beats per minute, respirations 21 breaths per minute, blood pressure 138/88 mmHg, and oxygen saturation 97% on room air. Nurse Rebecca also notes that Patricia is restless, crying, and shaking and states she just doesn’t know how to handle her diagnosis.  

Next, Nurse Rebecca analyzes these cues. She reviews the electronic health record, or EHR, and notes that Patricia has a family history of breast cancer. Nurse Rebecca also sees that previous nursing assessments document Patricia’s report of fatigue and difficulty sleeping. Nurse Rebecca recognizes that Patricia is experiencing emotional distress related to her breast cancer diagnosis.  

Now, using the information she&amp;#39;s gathered, along with Patricia&amp;#39;s medical history, Nurse Rebecca chooses a priority hypothesis of difficulty coping.  

Then, she generates solutions to address Patricia’s coping difficulties that will include nonpharmacologic interventions, and she establishes the expected outcome that Patricia will demonstrate effective coping skills regarding her breast cancer diagnosis by her next follow-up visit.  

Nurse Rebecca then takes action to implement these solutions. After the health care provider discusses the expected treatment plan with Patricia, Nurse Rebecca follows up to see how she’s feeling about the information she’s received.  

Nurse Rebecca: How are you feeling after talking ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Acute_Respiratory_Distress_Syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WTQ3rTCYSL6FCMHcXMBxvdWbRWGb33gr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Acute Respiratory Distress Syndrome]]></video:title><video:description><![CDATA[Nurse Claire works in the Emergency Department and is caring for Joseph, a 65-year-old male with a history of smoking who was diagnosed with acute respiratory distress syndrome, or ARDS, secondary to pneumonia. As Nurse Claire stabilizes Joseph and prepares him for transfer to the ICU, she goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Joseph’s care.  She does this by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Claire recognizes important cues including Joseph’s vital signs, which are temperature of 102 F, or 38.9 C, heart rate 120 beats per minute, respirations 24 breaths per minute and shallow, blood pressure of 100/60 mmHg, and oxygen saturation 85 percent on 6 liters high flow nasal cannula. Joseph reports a pain level of 2 on a 0 to 10 scale. She also notices Joseph has clammy, flushed skin, and he’s short of breath. Upon auscultation, she notes fine crackles at his lung bases, bilaterally.  

Next, Nurse Claire analyzes these cues. She reviews the electronic health record, or EHR, and notes that Joseph’s arterial blood gas, or ABG, results show a low partial pressure of oxygen, or PaO2, an elevated partial pressure of carbon dioxide, or PCO2, and a decreased SaO2, or oxygen saturation of arterial blood. 

Nurse Claire recognizes that ARDS can happen in patients with pneumonia and, when paired with Joseph’s history of smoking, his risk of developing ARDS increases. She also recalls that with ARDS, there’s inflammation, injury to the alveolar-capillary membrane, and decreased lung compliance, leading to hypoxemia and retention of carbon dioxide. Nurse Claire realizes Joseph needs effective respiratory management to prevent respiratory failure.  

Now, using the information she has gathered, Nurse Claire chooses a priority hypothesis of impaired gas exchange. 

Then, she generates solutions to address Joseph’]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Cirrhosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wwYNHKK4Rlqfw6QToH79cB1zTrW8zJBP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Cirrhosis]]></video:title><video:description><![CDATA[Nurse Abigail works on a Medical-Surgical unit and is caring for Thomas, a 72-year-old male with a history of hyperlipidemia and obesity, who was recently admitted for cirrhosis secondary to nonalcoholic fatty liver disease. After settling Thomas in his room, Nurse Abigail goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Thomas’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Abigail recognizes important cues, including Thomas’ vital signs, which are temperature 98.8°F or 37°C, heart rate 98 beats per minute, respirations 22 breaths per minute, blood pressure 106/68 mmHg, and oxygen saturation 97 percent on room air. His pain is 2 out of 10.  

Upon assessment, Nurse Abigail notes his sclera and skin are yellow-tinged, he has scattered petechiae, and his abdomen is round and distended. When asked to turn side-to-side during assessment, Thomas becomes fatigued and short of breath. 

Next, Nurse Abigail analyzes these cues. She reviews the electronic health record, or EHR, and notes that Thomas has gained 17 pounds since his last health care provider visit, which was approximately two weeks ago.  

Nurse Abigail recognizes that the fluid build-up in Thomas’ abdomen, also known as ascites, has contributed to his weight gain, and can make it difficult to perform physical activities because of increased pressure on his diaphragm, leading to dyspnea. She also knows that chronic illness in general can cause fatigue. Nurse Abigail realizes Thomas needs management of his fatigue in order to promote physical mobility. 

Now, using the information she&amp;#39;s gathered, along with Thomas’ medical history, Nurse Abigail chooses a priority hypothesis of activity intolerance. Then, she generates solutions to address Thomas’ activity level that will include pharmacologic and nonpharmacologic interventions; and she establi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemorrhagic_Conditions_of_Early_and_Late_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zKSE32uCS9ewcOSQsKHocc6NSe2jOQMQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemorrhagic Conditions of Early and Late Pregnancy]]></video:title><video:description><![CDATA[Hemorrhagic conditions during pregnancy are complications involving excessive blood loss that can jeopardize the health and well-being of the pregnant patient and fetus.  

In general, conditions that increase the risk of hemorrhage during pregnancy include multiparity, which refers to having two or more previous pregnancies; multiple gestation or being pregnant with more than one fetus at a time; and using assisted reproductive techniques, like in vitro fertilization or intrauterine device contraceptives. Other risk factors include a history of uterine surgery, sexually transmitted infections, or a hemorrhagic condition during a previous pregnancy; as well as alcohol use, excessive caffeine consumption, or cigarette smoking during pregnancy. 

First, let’s review early hemorrhagic conditions, which occur before 20 weeks of gestation, starting with spontaneous abortion. Spontaneous abortion, also known as miscarriage, is the involuntary loss of pregnancy during the first 20 weeks, or the loss of a fetus weighing 500 grams or less. Threatened abortion is when there’s only vaginal bleeding and the cervix remains closed. This can progress to cervical dilation, membrane rupture, and loss of the uterine contents, at which time it’s called a complete abortion. A missed abortion is when the fetus dies but remains in the uterus.   

Another early hemorrhagic condition is ectopic pregnancy, which is when the fertilized ovum doesn’t complete its journey to the uterus and implants elsewhere, like the abdominal cavity, ovaries, fallopian tube, or cervix. Depending on the implantation site, the embryo may receive enough blood supply to cause early pregnancy signs and symptoms, like a missed menstrual period. But eventually, the implantation site can no longer support the embryo.  

And if the ectopic pregnancy happens in the fallopian tube, the growing embryo eventually runs out of space and damages the walls of the tube, potentially causing it to rupture, leading to m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Videos_in_Pre-Clerkship_Medical_and_Health_Professions_Education</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0lggMYZXR7uSo0K5zqcxFObZRJac1o-X/_.png</video:thumbnail_loc><video:title><![CDATA[Videos in Pre-Clerkship Medical and Health Professions Education]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Videos in Pre-Clerkship Medical and Health Professions Education through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rehabilitative_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kSmtNk3fSF_p7GkfcQbt78H6SPGppR-v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rehabilitative Care]]></video:title><video:description><![CDATA[Rehabilitative care refers to the management of disabilities and chronic health conditions across the lifespan. It can take place in many settings like an acute care hospital, inpatient rehabilitation center, or at your patient’s home.  

As a nurse, you’ll collaborate with the interprofessional health care team, including nurses, social workers, case managers, physical therapists, dietitians, speech-language pathologists, and physicians, to support your patient’s functional abilities and prevent complications. 

When caring for your patient in rehabilitative care, your assessments will include physical, functional, psychosocial, vocational, and home safety assessments.  

Begin by completing a physical assessment of your patient’s major body systems with a focus on their current functional abilities. Assess their ability to complete activities of daily living, or ADLs, such as bathing, bowel and bladder elimination, and dressing.  

You’ll also assess their nutritional status, including the presence of chewing or swallowing problems, and their ability to prepare meals. Then, determine their level of mobility, their history of falls, and their need for any assistive devices, such as walkers or canes.  

Also be sure to assess their sensory function, and the use of glasses or hearing aids. During your assessment, note any signs or symptoms that may impact your patient’s ability to participate in rehabilitation, like shortness of breath or uncontrolled pain. 

Next, assess their psychosocial status by determining how they feel about their changes in health and loss of function, sources of stress, and their support system. Look for indications of anxiety or depression, such as loss of appetite or problems with sleep.  

Also, take note of any cultural, spiritual, or religious needs that may impact care. 

If your patient is employed, you’ll also perform a vocational assessment to examine the cognitive and physical demands of your patient’s job. Then, along wi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abdominal_Pain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dMDzMQfZQmeHkX7u-6WrP4JiT2uxwKc1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abdominal Pain]]></video:title><video:description><![CDATA[Abdominal pain is discomfort felt anywhere between the chest and groin that can occur because of tissue injury, which could be due to mechanical, inflammatory, and ischemic mechanisms. 

Mechanical mechanisms of tissue injury include processes that can cut, tear, or crush abdominal contents, like penetrating injuries seen with knife wounds or blunt injuries that occur during a car crash. Next, inflammatory mechanisms involve swelling, stretching, and distention. This can occur due to infectious processes like appendicitis, diverticulitis, or gastroenteritis. Lastly, ischemic mechanisms can be caused by any condition that obstructs blood flow to abdominal contents, like with mesenteric artery occlusion, which is when a blood clot blocks the artery that supplies oxygenated blood to the intestines.   

Abdominal pain can be acute, meaning it develops quickly and resolves over hours to days; or chronic, meaning it can come and go over months or even years. Pain can also be visceral, parietal, or referred. 

Visceral pain is typically dull, crampy, or burning in nature and difficult to localize. It can be felt with conditions like appendicitis.  Parietal pain tends to be sharp and easy to localize, like with the right upper quadrant pain felt in acute cholecystitis.  Referred pain can be dull or sharp, difficult or easy to localize, but is typically noted outside the abdominal region, like when biliary tract disease causes pain in the right shoulder.  

Other clinical manifestations that accompany acute abdominal pain may include fever, an elevated white blood cell count, nausea, and vomiting, as well as changes in bowel patterns, like constipation, diarrhea, or the presence of blood or mucus in stool.  

Okay, diagnosis of abdominal pain begins with a complete history and physical assessment. Laboratory testing depends on the suspected cause, but can include a CBC, to look for indications of infection, inflammation, and anemia; a comprehensive metabolic panel ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eating_Disorders_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KtsnhsPQQ8K3DylCQiau3I__RqGUiGkG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eating Disorders in the Pediatric Patient]]></video:title><video:description><![CDATA[Obesity is a nutritional problem that involves an increase in body weight and accumulation of excess fat, relative to lean body mass. On the other hand, eating disorders are mental health disorders characterized by abnormal eating patterns that can negatively impact physical and mental health. The two most common types are anorexia nervosa, which is a condition characterized by behaviors to prevent weight gain, like restricting the intake of food; and bulimia nervosa, which involves periods of binge eating followed by weight loss techniques like taking laxatives, diuretics, self-induced vomiting, or over-exercising. 

Now, the causes of obesity and eating disorders are likely multifactorial, involving genetic, neurochemical, and sociocultural factors. So, a family history of obesity or eating disorders increases the risk of developing these problems.  

As far as neurochemical factors go, obesity is associated with alterations in hypothalamic function and regulation of feelings of hunger and satiety, or the feeling of being full after eating. Likewise, eating disorders are thought to be related to changes in brain function that regulate motivation, self-control, and reward, which can impact food intake.  

Regarding sociocultural factors, pressure to lose weight, to have a socially defined body type, and partaking in activities that emphasize leanness, like modeling, ballet, gymnastics, and running, can increase the risk for eating disorders. Obesity risk is increased in those who are sedentary and have limited access to healthy food options, most often due to low socioeconomic status or other environmental factors, like communities located in food deserts, or areas with limited access to fresh, quality food.  

Now, obesity and eating disorders manifest as changes to the patient’s body mass index, or BMI, which is calculated based on their height and weight.  

Generally, pediatric patients who are obese will have a BMI greater than or equal to the 95th p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Conditions_with_Cerebral_Dysfunction_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NMOdzYX8SJaOsOfIs0VTjRRfQaG1DfFa/_.png</video:thumbnail_loc><video:title><![CDATA[Conditions with Cerebral Dysfunction in the Pediatric Patient]]></video:title><video:description><![CDATA[Head injuries involve trauma to the brain and its surrounding structures that are the result of an external force, and can include injuries like lacerations, skull fractures, and concussions. 

Alright, so, lacerations are tears of the scalp typically caused by blunt trauma or penetration with a foreign object. Skull fractures are breaks in the skull bone, and include linear fractures, which cause a crack in the skull bone that does not cross suture lines; comminuted fractures, which consist of multiple linear fractures; depressed fractures, where pieces of skull bone push inward, causing hematomas, which is a pooling of blood outside a blood vessel, or lacerations of the brain tissue; and basilar fractures, which occur at the base of the skull.  

Then, there are mild traumatic brain injuries, or concussions, which cause a transient disruption in normal neurologic function resulting in an alteration in mental status and sometimes a temporary loss of consciousness. 

Now, head injuries can be caused by several mechanisms, like contact head injuries, acceleration-deceleration injuries, and penetrating injuries. Contact head injuries occur when a child hits their head on a hard surface, like when falling down the stairs; or when they receive a violent blow or jolt to the head, like when a child is tackled during a football game.  

On the other hand, acceleration-deceleration injuries happen when the brain bounces around inside the skull, like in a car accident, or if a child is repeatedly shaken, like with shaken baby syndrome. The bouncing of the brain inside the skull causes a contusion, or bruising of the brain, at the site of impact, called coup injury.  

Then, the recoil force directs the brain the other way to strike the opposite side of the skull, resulting in a contusion on the other side of the brain, called contrecoup injury. Lastly, head injuries can also be caused by penetrating injuries, like knife or gunshot wounds.  

Risk factors for h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Heart_Failure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7E3rx2G9Tj_zMa0gXmT1xLP9TO6o08lP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Heart Failure]]></video:title><video:description><![CDATA[Nurse Pilar works on an inpatient cardiac unit and is caring for Esperanza, a 72-year-old female admitted for an exacerbation of heart failure with reduced ejection fraction. After settling Esperanza in her room, Nurse Pilar goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Esperanza’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Pilar recognizes important cues, including Esperanza’s vital signs, which are heart rate 104 beats per minute, respirations 28 breaths per minute, oxygen saturation 87 percent on room air, and pain 3 out of 10, located in her back.  

Nurse Pilar also notes that Esperanza’s breathing is labored and she’s using accessory muscles. Upon auscultation, Nurse Pilar notes fine inspiratory crackles in both lung bases. There’s also 2+ pitting edema in Esperanza’s ankles and feet.  

Next, Nurse Pilar asks Esperanza about her recent activities and medications. 

Nurse Pilar: I see your health care provider has prescribed two medicines for you. When was the last time you took them? 

Esperanza: Well, I ran out of my medicines a week ago, and I haven’t been to the pharmacy to get my refills yet. I haven’t gone out of the house much the last two weeks because my back’s been hurting, and I’ve been so tired.  

Nurse Pilar: I’m sorry you’ve been having back pain. Has anything helped with the pain? 

Esperanza: Yes, ibuprofen helps. I’ve been taking it two times each day.  

Nurse Pilar then analyzes these cues. She reviews Esperanza’s electronic health record, or EHR, and sees that she&amp;#39;s prescribed two medications to control her heart failure, an ACE inhibitor and a beta blocker. Because Esperanza has been without her medications for a week, she is now showing symptoms of heart failure.  

Additionally, Nurse Pilar knows taking non-steroidal anti-inflammatory drugs, or NSAIDs, like ibupro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Ears</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zWmPwsxUSVSf7KWYZ1FkdJ6bRf_MoLC1/_.png</video:thumbnail_loc><video:title><![CDATA[Assessment of Ears]]></video:title><video:description><![CDATA[Assessment of the ears should be completed during a comprehensive assessment or as part of a focused assessment if your patient is experiencing issues with their ears.Methods of ear assessment include inspection and palpation as well as special tests for hearing and balance.  

First, inspect the external ear by viewing the auricles bilaterally, looking for size, shape, and symmetry, and checking that the skin on the auricles is the same color as your patient’s face. Then, note the position of the ears. Normally, the upper part of the auricle should align with the inner canthus of the eye. Patients with low-set ears may have a congenital abnormality.  

The ears should also be free of lesions; however, a thickening of the upper helix of the auricle, called a Darwin tubercle, is an expected finding in some patients. Other ear abnormalities include cauliflower ear, tophi, or sebaceous cysts. Cauliflower ear appears as an enlarged and thickened auricle and occurs from repeated trauma to the ear. Tophi are small white deposits of uric acid that appear along the auricles and are associated with gout. Sebaceous cysts appear as elevations in the skin around the ear from blocked sebaceous glands.  

Okay, let’s move on to the external auditory canal. You may need a penlight to view the canal, especially if your patient has a build-up of cerumen. A foul smell or purulent drainage can be signs of otitis externa, or it may indicate the presence of a foreign body. Bloody drainage can be associated with trauma.  

Then, continue your inspection using an otoscope. The external auditory canal should be free from lesions, impacted cerumen, and foreign bodies. Normally there’s minimal cerumen and the tissue is often covered with fine hairs. You’ll also view the tympanic membrane, which separates the external ear from the middle ear. The tympanic membrane should appear flat, gray, and translucent. Possible abnormal findings include a perforated membrane, which can occur fro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Get_to_Know_Osmosis_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R03QOzj6SYmnpcy-7KbWl8UjQ2KI9-sU/_.png</video:thumbnail_loc><video:title><![CDATA[Get to Know Osmosis Nursing]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Get to Know Osmosis Nursing through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_biliary_colic:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0EKPhPLoQX_XNNbRtzset6kSSGmpuUS-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to biliary colic: Clinical sciences]]></video:title><video:description><![CDATA[Biliary colic refers to sudden onset of epigastric or right upper quadrant pain caused by a transient blockage within the biliary tree, most commonly  caused by gallstones in the gallbladder, cystic duct, or the common bile duct. Biliary colic is often a diagnosis of exclusion, meaning it comes after you rule out more severe can’t-miss diagnoses.  

When assessing a patient with signs and symptoms of biliary colic, you should first perform an ABCDE assessment to determine whether your patient is unstable or stable. 

If the patient is unstable, consider cholangitis or another etiology of pain, and start with acute management to stabilize them first. This means that you might need to intubate the patient, obtain IV access, or administer fluids before continuing with your assessment. At this step, you should look for signs of conditions that cause instability, like sepsis.

Alright, now that we’re done with the acute management of unstable patients, let’s talk about stable patients. 

Your first step for stable patients with suspected biliary colic is to start supportive care. This means that you need to obtain IV access for fluid resuscitation, initiate bowel rest, and administer pain medication, antispasmodics, and antiemetics if needed. 

Once these important steps are done, obtain a focused history and physical examination.

Now, history typically reveals colicky right upper quadrant pain, which is described as a cramp or sharp pain that’s often severe and tends to start and end suddenly in spasms. The pain can radiate to the shoulder or scapula, and is often associated with fatty food intake, or the patient might report associated nausea and vomiting. 

On a physical exam, patients with gallbladder inflammation have pain on palpation of the right upper quadrant and a positive Murphy sign. You can elicit Murphy sign by palpating the right upper quadrant while asking the patient to take a deep breath. If the pain suddenly interrupts the inspiration, the M]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_periumbilical_and_lower_abdominal_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pb3slv6nQMWWjcyCItlUUfjSQ2_YlDmL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to periumbilical and lower abdominal pain: Clinical sciences]]></video:title><video:description><![CDATA[Abdominal pain is a symptom of many conditions, which can range from benign to serious ones that require surgical intervention. Based on the affected region of the abdomen, abdominal pain can be classified into right upper quadrant, left upper quadrant, right lower quadrant, and left lower quadrant. It can also be epigastric or periumbilical. 

The first step in evaluating a patient with abdominal pain is to assess their ABCDE to determine if they are stable or unstable. If the patient is unstable, start acute management before doing any diagnostic workup. This means that you might need to stabilize their airway, provide supplemental oxygen, establish IV access, and continuously monitor hemodynamics.  

Here’s a high yield fact! If an unstable patient presents with abdominal pain, be sure to rule out life-threatening conditions like acute mesenteric ischemia and perforated viscus, as well as abdominal aortic aneurysm.

On the other hand, for stable patients, your first step is to obtain a focused history and physical exam, or H&amp;amp;P for short. On history, you should characterize the pain based on its location, severity, and chronicity, and determine aggravating and alleviating factors as well as other associated symptoms. 

Next, you should quickly assess for any signs of an acute abdomen. In this case, history may reveal recent abdominal or GI procedures such as EGD, colonoscopy, or surgery; as well as abdominal or GI cancer. In some cases, the patient will have a history of abdominal aortic aneurysm. On physical exam, you’ll usually find severe distension with rigidity, diffuse tenderness, rebound, and guarding.

Because an acute abdomen is a surgical emergency, you need to call the surgical team right away. You should also get bedside imaging, including an abdominal x-ray that may show free air or small or large bowel obstruction; and an abdominal ultrasound, which may show abnormality of the aorta and free fluid. Depending on your suspicion for u]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_pneumoperitoneum_and_peritonitis_(perforated_viscus):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2D5fdujfSWSIdgkhLbNeMiVKRMuKYYt0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to pneumoperitoneum and peritonitis (perforated viscus): Clinical sciences]]></video:title><video:description><![CDATA[Pneumoperitoneum, or the presence of air or gas within the peritoneal cavity, is considered a surgical emergency because it often indicates perforation of the gastrointestinal tract. On the other hand, peritonitis refers to the inflammation of the peritoneum. Depending on the etiology, peritonitis can be divided into primary, secondary, and tertiary. 

Here is a clinical pearl! Even a small amount of bacterial seeding within the peritoneal space can progress quickly and become life-threatening. Keep in mind that bacterial infections can be spontaneous if there are preexisting ascites from liver or kidney failure or come from the GI tract through transmural infection or perforation. 

When approaching a patient with signs and symptoms suggestive of peritonitis and pneumoperitoneum, first perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, stabilize their airway, breathing, and circulation by providing supplemental oxygen, obtaining IV access, and continuously monitoring their hemodynamics.  

Alright, now that unstable patients are taken care of, let’s talk about stable ones. Your first step here is to obtain a focused history and physical examination and assess for an acute abdomen. Patients with acute abdomen usually report severe abdominal pain, nausea, vomiting, and bowel changes, as well as fever, chills, and generalized malaise. On a physical exam, you’ll find abdominal distension, tenderness, rigidity, rebound, guarding, decreased/absent bowel sounds. Now, when your clinical exam indicates an acute abdomen, the first thing you want to do is to find and treat the underlying cause. 

Let&amp;#39;s first look at pneupoeritoneum. When your clinical exam indicates an acute abdomen, your next step is to assess for pneumoperitoneum by obtaining an upright chest or 3 view abdominal x-ray. When it comes to the x-ray, air under the diaphragm is pathognomonic of pneumoperitoneum. Because pneumoperitoneum o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_postoperative_abdominal_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/neNFslqgR2uA3mztd3bWLH-bQvmE8S9b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to postoperative abdominal pain: Clinical sciences]]></video:title><video:description><![CDATA[Postoperative abdominal pain is commonly reported by patients after surgery. There are many causes, some even life-threatening, but they can all be summed up into three categories: disruption of normal healing, infection, or other benign physiologic processes. Abdominal pain can be superficial, or limited to the abdominal wall; or it can be deep, involving organ space. 

The first step in evaluating a patient with signs and symptoms suggestive of postoperative abdominal pain is to perform the ABCDE assessment to determine if the patient is stable or unstable. If the patient is unstable, start acute management before doing any diagnostic workup. This means that you might need to stabilize their airway, provide supplemental oxygen, establish IV access, and consider starting IV fluids, while continuously monitoring their vitals. 

Some important examples that can cause a patient to be unstable in the postoperative period include acute abdomen, caused by free air or diffuse fluid spillage; as well as vascular rupture, such as a ruptured abdominal aortic aneurysm; and necrotizing fasciitis, which is a deep bacterial infection along the fascial plane, causing the patient to be critically ill, with severe pain and crepitus under the skin, and it’s a surgical emergency.

Alright, now that unstable patients are stabilized, let’s talk about the stable ones. Your first step here is to obtain a focused history and physical examination. You should find out what type of operation the patient had and when, and quickly assess for any signs of acute abdomen. Now, if you find a severely distended and rigid abdomen with diffuse tenderness, rebound pain, guarding, and sometimes tachycardia and tachypnea, the patient has an acute abdomen, which is a surgical emergency. 

So, call the surgical team immediately for consultation and a possible exploratory laparotomy. Surgery should not be delayed to get  additional diagnostic tests, as exploratory laparotomy is both therapeutic a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_upper_abdominal_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tY_KK8cMRy29XvClsmF1GwCZRVORv_a8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to upper abdominal pain: Clinical sciences]]></video:title><video:description><![CDATA[Abdominal pain is a symptom of many conditions, which can range from mild to serious ones that require surgical intervention. Based on the affected region of the abdomen, abdominal pain can be classified into a right upper quadrant, epigastric, left upper quadrant, periumbilical, right lower quadrant, and left lower quadrant pain.

The first step in evaluating a patient with abdominal pain is to assess their ABCDE to determine if they are stable or unstable. If the patient is unstable, start acute management before doing any diagnostic workup. This means that you might need to stabilize their airway, provide supplemental oxygen, establish IV access, and continuously monitor hemodynamics.

On the other hand, for stable patients, your first step is to obtain a focused history and physical exam, or H&amp;amp;P for short. On history, you should characterize the pain based on its location, severity, and chronicity, and determine aggravating and alleviating factors as well as other associated symptoms. Next, you should quickly assess for any signs of an acute abdomen. In this case, ask for history of recent abdominal or GI procedures such as EGD, colonoscopy, or surgery; as well abdominal aortic aneurysm.

On physical exam, acute abdomen presents with signs of diffuse peritoneal inflammation, including diffuse tenderness, rebound pain, rigidity, and guarding. Also, upright chest x-ray or abdominal x-ray series should be done to check for free air under the diaphragm, which suggests perforation of the viscera.

Now, acute abdomen is also known as a surgical abdomen, since emergency surgical intervention is required for most causes, such as perforated viscus, abdominal sepsis, or ruptured abdominal aortic aneurysm. In this case, exploratory laparotomy is considered both diagnostic and therapeutic, so call for an emergent surgical consult while you continue resuscitation and the diagnostic workup.

Now, once you have ruled out an acute abdomen, the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abdominal_aortic_aneurysm:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Lpj0tW5AQxuxCCqdIV4rO5CCThSz3aCQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abdominal aortic aneurysm: Clinical sciences]]></video:title><video:description><![CDATA[Abdominal aortic aneurysm, or AAA, is defined as aortic dilatation greater than 3 cm in diameter. Most AAAs are fusiform, which means they’re spindle shaped and involve the entire circumference of the aortic wall. Based on the symptoms, AAA can be symptomatic or asymptomatic. While most triple As are asymptomatic and found incidentally on imaging studies, all AAAs are at risk for expansion and rupture. 

When a patient presents with signs and symptoms suggestive of AAA, you should first perform an ABCDE assessment to determine if the patient is stable or unstable. If the patient is unstable, start with acute management to stabilize their airway, breathing and circulation. This means you might need to intubate the patient, establish IV access, initiate fluid resuscitation, and manage the heart rate and blood pressure before continuing your workup. 

Once you have initiated acute management, your next step is to obtain a focused history and physical. The important thing to determine here is whether they have a prior history of AAA. In an unstable patient with a known AAA, history might reveal sudden onset abdominal, back, or flank pain. Physical examination might show a pulsatile abdominal mass with generalized diffuse tenderness, as well as tachycardia and hypotension. If this is the case, suspect AAA rupture. Then get a surgical consult for emergent open repair. However, some patients with complex comorbidities might be poor surgical candidates, so you can consider endovascular repair. The exact diagnosis of rupture, dissection, or mass effect impinging upon other surrounding blood vessels will be made intraoperatively.

Alright, let’s go back to history and physical and talk about unstable patients without known AAA. They might also present with a history of sudden onset abdominal, back or flank pain, and have tachycardia, hypotension, as well as a pulsatile abdominal mass on exam. If so, you should perform a point-of-care ultrasound or POCUS to look for ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_mesenteric_ischemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FSVO7Q-PRWm4jCf_Da8nAGs_RpuPylrp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute mesenteric ischemia: Clinical sciences]]></video:title><video:description><![CDATA[Acute mesenteric ischemia, or AMI, occurs when there is a sudden decrease of blood flow within the mesenteric vasculature, which can lead to infarction or necrosis of the bowel wall. Depending on the blood vessels involved, mesenteric ischemia can affect either the small or large bowel. Mesenteric ischemia is divided into 3 types based on the type of vasculature involved: arterial occlusion, venous occlusion, and non-occlusive arterial vasospasm. While each type can be acute or chronic, acute presentations require timely diagnosis and treatment, as they can rapidly progress to bowel necrosis, perforation, sepsis, and even death. 

Now, here’s a high-yield fact to keep in mind! The superior mesenteric artery, or SMA, supplies the GI tract from the small intestine to the proximal transverse colon, while the inferior mesenteric artery, or IMA, supplies the distal one-third of the transverse colon to the rectum. The celiac artery, which mainly supplies the stomach and the proximal portion of the duodenum, can provide some collateral flow to the proximal small bowel and transverse colon via communications called confluences. The intestines can actually survive off of only one of these major vessels. Venous drainage of the gut is quite similar to the arterial supply. The superior mesenteric vein, or SMV, drains the midgut organs, while the inferior mesenteric vein, or IMV, drains the hindgut. 

When approaching a patient who presents with signs and symptoms suggestive of acute mesenteric ischemia, your first step is to do an ABCDE assessment to determine if the patient is stable or unstable. 

If the patient is unstable, you should initiate acute management to stabilize their airway, breathing, and circulation. This means you might need to obtain IV access, administer IV fluids, begin empiric broad-spectrum antibiotics, make sure the patient is NPO, and insert an NG tube if needed to decompress the bowel. These measures are important, as there&amp;#39;s a high ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_pancreatitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZWwkzpqrS3K9HLJ8abLRPHUZR-WayNGc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute pancreatitis: Clinical sciences]]></video:title><video:description><![CDATA[Acute pancreatitis is an inflammation of the pancreas, most commonly caused by biliary stones, followed by alcohol use and hypertriglyceridemia, but can also be idiopathic. There are many other causes of acute pancreatitis, including trauma, iatrogenic post-endoscopic retrograde  cholangiopancreatography or ERCP, autoimmune disorders, genetic diseases, infections, malignancies, toxic exposure, and medications like thiazides, antiretrovirals, and valproic acid. Depending on the severity of the disease, pancreatitis can range from mild to moderate or even severe, life-threatening pancreatitis.

The first step in assessing a patient with signs and symptoms suggestive of acute pancreatitis is to perform the ABCDE assessment to determine if the patient is stable or unstable. If the patient is unstable, start acute management and stabilize the airway, breathing, and circulation. Next, obtain IV access and initiate IV fluids for aggressive resuscitation. Make sure the patient is NPO, and provide supportive care including pain management and antiemetic medication. 

Alright, now let&amp;#39;s talk about stable patients. Start by taking a focused history and physical examination. Usually, patients with acute pancreatitis present with persistent, unremitting epigastric abdominal pain that radiates to the back, worsens after meals, and improves when leaning forward. The pain is often associated with nausea and vomiting, while some patients might report a fever as well. It is also possible for patients to present with jaundice as a sign of biliary obstruction. Additionally, some patients might develop tetany, or involuntary muscle spasms, as a result of hypocalcemia. Finally, don’t forget to ask about a history of similar previous episodes, cholelithiasis, or alcohol use. 

Physical exam typically reveals epigastric abdominal tenderness, distention, or guarding. Some patients&amp;#39; physical examinations may show ecchymosis due to associated intra-abdominal o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alcohol-induced_hepatitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zl0EdptmSgK6fBLvVfOTrT8PTUmpgf1C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alcohol-induced hepatitis: Clinical sciences]]></video:title><video:description><![CDATA[Alcohol-induced hepatitis, or simply alcoholic hepatitis, refers to acute liver inflammation caused by recent excessive alcohol intake, that presents with jaundice and elevated liver enzymes. Prolonged alcohol intake can result in lipid infiltration and increased production of free oxygen species. Over time, this can lead to inflammation and neutrophilic infiltration of hepatocytes that can eventually lead to fibrosis, cirrhosis, and liver failure. As hepatocytes degenerate, they release intracellular enzymes, such as alanine aminotransferase or ALT, aspartate aminotransferase or AST, and gamma glutamyl transferase or GGT.

Now, if you suspect alcohol-Induced hepatitis, first you should perform an ABCDE assessment to determine if the patient is unstable or stable. If your patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. 

Ok, now let’s go back to the ABCDE assessment and take a look at stable individuals. 

If the patient is stable, proceed with a focused history and physical exam. Ask your patient specifically about their recent alcohol consumption. Your patient may report heavy drinking, consuming 3 or more drinks per day, usually for a minimum of 6 months. If your patient is hesitant to discuss their alcohol use habits, you could use clinical tools, such as the AUDIT and CAGE questionnaires, which can help you identify harmful drinking patterns. Additionally, your patient might report right upper quadrant pain, nausea, and vomiting. In advanced cases, history might also reveal easy bruising and unintended weight loss. 

On the other hand, physical exam often reveals jaundice, right upper quadrant tenderness, hepatomegaly, and splenomegaly. In advanced cases you might see ascites, primarily due to portal hypertension, but also asterixis, agitation, and confusion.

At this point, you should susp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_ascites:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QKjO6N3mQLKdw_-UznzxpZwOTBSpBurR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to ascites: Clinical sciences]]></video:title><video:description><![CDATA[Ascites refers to an abnormal collection of fluid in the peritoneal cavity, which can be a sign of various underlying conditions. In some cases, ascites can arise in the absence of portal hypertension, which is typically seen in conditions such as peritoneal carcinomatosis; pancreatic ascites, protein-losing enteropathy, and nephrotic syndrome.

More commonly, ascites is associated with portal hypertension, which can occur due to prehepatic, hepatic, and posthepatic causes. The most common prehepatic cause is portal vein thrombosis; while common hepatic causes include cirrhosis, infiltrative liver disease, and acute liver failure. Finally, important posthepatic causes include right-sided heart failure, constrictive pericarditis, and pulmonary hypertension.

Now, when approaching a patient with new ascites, you should first obtain focused history and physical examination, as well as labs, including CBC, CMP, and coagulation profile. History typically includes progressive abdominal distension; while physical exam reveals bulging flanks, a palpable fluid wave, and shifting dullness to percussion.

Additionally, order an abdominal ultrasound, which can help you detect free fluid in the peritoneal cavity, which is commonly seen as an anechoic space.

Next, obtain a diagnostic paracentesis to remove a small amount of ascitic fluid for analysis. Initial tests on the ascitic fluid include albumin, total protein, and cell count with differential. With these values, calculate the serum ascites albumin gradient, or SAAG for short, by subtracting the ascites albumin from the serum albumin. The SAAG results will help you determine if portal hypertension is present or absent. Moreover, SAAG less than 1.1 means there’s no portal hypertension, so your next step is to assess the ascitic fluid WBC count and differential.

Elevated WBCs in ascitic fluid with predominant lymphocytes should make you think of peritoneal disease, so test ascitic fluid for TB cultures and order c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholecystitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SdKJmsbfTnSGLS5bkd9Gqd93SuStjCWI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholecystitis: Clinical sciences]]></video:title><video:description><![CDATA[Acute cholecystitis is a sudden inflammation of the gallbladder, usually caused by conditions that impair the outflow of bile. Think of the biliary tree as one of the many plumbing systems in the body! Disrupted bile outflow increases the pressure within the gallbladder, leading to bile stasis. This in turn can lead to complications such as inflammation, infection, gangrene, and perforation. Acute cholecystitis is most commonly related to a stone, which is called calculous cholecystitis. However, gallbladder inflammation can also occur without stones, which is known as acalculous cholecystitis.

When assessing a patient with suspected acute cholecystitis, first you should determine if your patient is stable or unstable by doing an ABCDE assessment. If the patient is unstable, you should stabilize them first, which means that you might need to intubate the patient, establish IV access, or administer fluids before continuing with your assessment.

After completing those important steps, you should obtain a history and physical exam, as well as labs such as CBC, ESR, CRP, and CMP, which includes ALP, GGT, ALT, AST, and total bilirubin; also obtain lactate, and blood cultures, as well as amylase and lipase to rule out pancreatic involvement. 
The history usually reveals symptoms like nausea, vomiting, and right upper quadrant or epigastric abdominal pain that might radiate to the shoulder or scapula; symptoms typically occur after eating a high fat meal. 

On a physical exam, you might find signs such as tenderness to palpation in the right upper quadrant, with a positive Murphy sign. You can elicit Murphy sign by palpating the right upper quadrant while asking the patient to take a deep breath. If the pain stops inspiration, Murphy sign is considered positive. Additional findings on physical exam include jaundice, fever, and signs of hemodynamic instability like tachycardia and hypotension. These systemic signs are more common in those with severe disease. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Choledocholithiasis_and_cholangitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3U4HrtfwTBGUbh5hNpDpHtQfTjCd0rkJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Choledocholithiasis and cholangitis: Clinical sciences]]></video:title><video:description><![CDATA[Choledocholithiasis occurs when one or more stones are present in the common bile duct. Stones are usually formed in the gallbladder, then pass through the cystic duct, get lodged in the common bile duct, and obstruct the bile outflow. Occasionally, stones can even form in the common bile duct, called de novo choledocholithiasis. Because of the obstructed bile outflow, bacteria from the small intestine can colonize the common bile duct, leading to infection and inflammation, which is known as acute or ascending cholangitis. 

When assessing a patient with suspected choledocholithiasis or cholangitis, you should first determine if your patient is stable or unstable by doing an ABCDE assessment. If the patient is unstable, stabilize the airway, breathing, and circulation first. This means that you might need to intubate the patient, obtain IV access, or administer fluids before continuing with your assessment. 

Alright, so let’s see what’s next once the patient has been stabilized. Now, when it comes to stable patients, you have a bit more time to obtain the history and physical examination, as well as to draw labs, which can include CBC, CMP, amylase or lipase, lactate, and blood cultures. 

Now, history usually reveals symptoms suggestive of cholangitis, like itchy skin from jaundice, as well as abdominal pain in the right upper quadrant, nausea, vomiting, and possible altered mental status. Additionally, the history might also reveal some important risk factors for choledocholithiasis and cholangitis like biologically female sex, obesity, age over 40, or prior gallstones. 

When it comes to the physical exam, it might reveal jaundice, and elevated temperature, as well as signs of biliary inflammation like tenderness to palpation in the right upper quadrant, possible guarding or rebound pain, and signs of hemodynamic instability, like tachycardia and hypotension. 

Here’s a high-yield fact to keep in mind! The most important signs and symptoms of severe c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_mesenteric_ischemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bTqgg1ULRRySxbrSAsdjwp68TyClcuxf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic mesenteric ischemia: Clinical sciences]]></video:title><video:description><![CDATA[Chronic mesenteric ischemia, or CMI, occurs when there is a decrease of blood flow within the mesenteric vasculature. Mesenteric ischemia can affect either the small or large bowel, depending on the blood vessels involved, and is characterized by narrowing of these blood vessels due to atherosclerotic plaques.  The mesenteric vasculature has an extensive network of collateral vessels, which usually helps maintain perfusion in patients with atherosclerotic disease.  However, if one of the larger vessels is occluded, particularly the celiac artery and the superior mesenteric artery, or SMA, then patients typically become symptomatic. Therefore, the diagnosis of CMI depends on first identifying the presence of stenosis with a duplex ultrasound, then assessing the severity of the occlusion with a CTA.

Now, if you suspect chronic mesenteric ischemia, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, you should initiate acute management to stabilize their airway, breathing, and circulation. This means you might need to obtain IV access, administer IV fluids, and begin empiric broad-spectrum antibiotics.

Here’s a clinical pearl to keep in mind! If you suspect CMI and your patient is unstable, be sure to evaluate for the possibility of bowel infarction due to acute-on-chronic mesenteric ischemia. These patients often have sudden, severe abdominal pain and may have abdominal distension with guarding and rebound on exam. An abdominal x-ray will show pneumatosis intestinalis, or gas within the intestinal wall, which indicates bowel infarction and necrosis; it may also show pneumoperitoneum, or gas in the abdominal cavity, which means that a perforation occurred. These patients need emergent surgical consultation for exploratory laparotomy, which will be both diagnostic and therapeutic. Remember, the only treatment for a necrotic bowel is surgical resection.

Okay, now that we covered how to a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_pancreatitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rYAtIGSrRBOKcG8IfHOWIpP0TrqNh8q0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic pancreatitis: Clinical sciences]]></video:title><video:description><![CDATA[Chronic pancreatitis refers to persistent, chronic inflammation of the pancreas, that’s associated with irreversible changes, such as fibrosis, calcifications, and atrophy. This eventually decreases the function of the exocrine pancreas, subsequently causing difficulties with digestion and absorption of nutrients, as well as abdominal pain that’s worse with eating, steatorrhea, and unintentional weight loss. Additionally, the destruction of the endocrine pancreas can lead to difficulties in producing hormones, such as insulin. Now, there’s a variety of conditions that can cause chronic pancreatitis, including toxins like chronic alcohol consumption and metabolic conditions; genetic and autoimmune conditions; as well as recurrent acute pancreatitis and ductal obstruction. An important thing to remember is that tobacco smoking may not be a direct cause, but it is a strong risk factor. 

Now, if you suspect chronic pancreatitis, first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize the patient’s airway, breathing, and circulation. Next, obtain IV access and, if needed, start IV fluids. Finally, put your patient on continuous vital sign monitoring. 

Ok, now let’s go back to the ABCDE assessment and take a look at stable individuals.  

If the patient is stable, obtain a focused history and physical examination. These patients typically report upper abdominal pain that can range from constant and dull, to acute and stabbing. Sometimes, the pain might radiate to the back and can be relieved by leaning forward. Other important history findings include nausea, vomiting, and diarrhea. Also, they might report fatty stools that are difficult to flush, abdominal bloating, and unexplained weight loss.  

Moreover, these findings typically occur due to progressive loss of acinar cells that eventually result in decreased production of digestive enzymes and subsequent malabsorption. This condition is called Pancreati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diverticulitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5acG5a-PRS2pyzknVQf0OSPdSIGkxDpW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diverticulitis: Clinical sciences]]></video:title><video:description><![CDATA[Diverticulitis is inflammation of a diverticulum, which is a small pouch protruding from the bowel wall. Be sure not to mix it up with diverticulosis, which is the presence of multiple diverticula that develop because of a high-fat and low-fiber diet. However, even though it is commonly believed, eating things like seeds, nuts, and popcorn does not increase the risk of developing diverticulosis or diverticulitis.

Now, diverticulitis occurs when increased bowel pressure, from things like food or stool, causes a tiny hole or micro perforation in the diverticulum wall. This allows bacteria from the lumen to seed the diverticulum, which results in infection and inflammation. Diverticulitis can be classified as uncomplicated or complicated diverticulitis. In uncomplicated diverticulitis, only the diverticulum is inflamed, while in complicated diverticulitis, perforation, abscess, or fistula might be present as well.

Alright, when a patient presents with signs and symptoms of diverticulitis, you should first perform an ABCDE assessment. The individual can be  unstable if septic shock develops, so you should stabilize their airway, breathing, and circulation. This means that you may need to intubate the patient, establish IV access, or administer fluids before continuing with your assessment.

However, if the patient is stable, the next step is to obtain a focused history and physical examination. History typically reveals abdominal pain, most often in the left lower quadrant, and sometimes symptoms like fever, nausea, vomiting, and recent changes in bowel habits, such as constipation or diarrhea.

Physical examination usually reveals abdominal distention and tenderness in the affected area, most commonly in the left lower quadrant. There can also be elevated temperature. The most dangerous signs to look for are guarding, rigidity, and rebound pain, which point to peritonitis.

A rectal examination may reveal a palpable mass within the distal sigmoid colon. The]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_gastroenteritis_and_enterocolitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-JOJkN4qQVusIRxJVCUuIj7kQAeVPThS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious gastroenteritis: Clinical sciences]]></video:title><video:description><![CDATA[Gastroenteritis refers to inflammation of the gastrointestinal tract, typically caused by infectious pathogens. These pathogens injure the intestinal lining, leading to fluid shifts and water loss through diarrhea and vomit. The diagnosis of what’s causing gastroenteritis is made by first evaluating whether the patient’s diarrhea is watery or bloody, as well as identifying common pathogens such as bacteria, viruses, or parasites.   

Now, if you suspect gastroenteritis, you should perform an ABCDE assessment to determine if your patient is unstable or stable. 

If the patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, start IV fluids, and begin continuous vital sign monitoring including blood pressure, heart rate, and oxygen saturation. Provide supplemental oxygen if needed, and start broad spectrum antibiotics. Okay, let’s go back to the ABCDE assessment and take a look at stable patients.  

First, start by taking a focused history and physical exam. Your patient may report diarrhea, nausea, vomiting, and abdominal pain. Other common symptoms include flatulence, fecal urgency, and possibly fever. 

On the other hand, physical exam findings will reveal abdominal tenderness, and may show signs of dehydration, such as dry skin and mucous membranes, decreased skin turgor, and decreased capillary refill time. At this point, you should suspect gastroenteritis. 

Here’s a clinical pearl! Be sure to always clarify stool frequency and consistency whenever taking a history. Diarrhea is defined as passing of three or more unformed stools in 24 hours. If your patient is passing formed stools, or has not had multiple episodes per day, they do not have diarrhea. 

Once you suspect gastroenteritis, determine if the diarrhea is watery or bloody. Let’s first talk about watery diarrhea. 

If your patient has watery diarrhea, first assess the patient’s level of dehydration. Signs of mild dehydration include mild tachycardia, dr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastroesophageal_reflux_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7aeXrszARoKNlG8titZh1fsTRM6j8ser/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastroesophageal reflux disease: Clinical sciences]]></video:title><video:description><![CDATA[Gastroesophageal reflux disease, or GERD for short, is a chronic condition in which the lower esophageal sphincter becomes weak or relaxes at the wrong time. This allows acidic content from the stomach to flow back up into the esophagus. Over time, exposure to gastric acid can irritate and damage the lining of the esophagus and cause a variety of symptoms, which are commonly grouped into typical, atypical, and alarm symptoms.  

Now, if your patient presents with signs and symptoms suggestive of GERD, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and administer IV fluids, and don’t forget to put your patient on continuous vital sign monitoring. Finally, if you identify signs of active gastrointestinal bleeding, such as melena or hematemesis, perform an emergent esophagogastroduodenoscopy, or EGD. 

Now, let’s go back and take a look at stable patients.  

In this case, start with a focused history and physical examination. Individuals with GERD might report classic symptoms, like heartburn, also known as pyrosis, acid regurgitation, or a sour or bitter taste in the back of the mouth.  

Some might also experience non-specific symptoms, such as chronic cough, hoarseness, or frequent throat clearing.  

On physical exam, findings are usually normal. However, in some cases, you might notice subtle signs of acid damage, such as dental erosion. If your patient reports any of these symptoms, suspect GERD. 

Next, assess the patient for alarm signs and symptoms that warrant urgent evaluation for GERD complications. These include anemia, dysphagia or odynophagia, gastrointestinal bleeding, frequent vomiting, or unintentional weight loss. 

If one or more alarm signs and symptoms are present, you should suspect a GERD complication and proceed with an urgent EGD with biopsies.  

If the biopsy reveals friable, erythematous epi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis_C:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NQujxms_QUu3bZcfXJz3i9oISWOnGwQh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis C: Clinical sciences]]></video:title><video:description><![CDATA[Hepatitis C virus, or HCV for short, is a bloodborne viral infection that’s typically transmitted through contaminated blood, or sexual contact. Once inside the body, hepatitis C virus circulates through the blood, eventually reaching the liver, where it infects hepatocytes. Acute hepatitis C infections are usually asymptomatic, but if the virus sticks around long enough in the body, acute infection can progress to chronic infection, which can lead to the development of cirrhosis, and even hepatocellular carcinoma. 

Now, if you suspect hepatitis C infection, first perform an ABCDE assessment to determine if your patient is unstable or stable.  

If unstable, your patient may present with alarming signs and symptoms, such as altered mental status, asterixis, upper GI hemorrhage, and ascites. In this case, immediately stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry.  

Here’s a clinical pearl to keep in mind! These findings can be seen in individuals with fulminant hepatitis, often referred to as acute liver failure, which is most often caused by viral hepatitis or acetaminophen overdose. Hepatic encephalopathy is a key feature, while lab findings suggestive of fulminant hepatitis include elevated transaminases like AST and ALT, as well as elevated PT/INR and serum bilirubin. It’s important to recognize these patients on time, and once stable, refer them to a liver transplant center for further management!  

Ok, let’s go back to the ABCDE assessment and take a look at stable individuals.  

If the patient is stable, obtain a focused history and physical examination. History typically reveals symptoms such as fatigue, anorexia, low-grade fever, as well as nausea and vomiting. Additionally, your patient might report right upper quadrant abdominal pain and difficulty sleeping.  

Finally, history might be positive for I]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ileus:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t9FDtlBySsKaoUKO0dsAVfJFQMuKMkwj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ileus: Clinical sciences]]></video:title><video:description><![CDATA[Ileus is a functional obstruction of the intestines caused by reduced or absent peristalsis without evidence of mechanical blockage. 

Both functional and mechanical obstructions present with similar signs and symptoms. So, before you diagnose ileus, you must first rule out a mechanical obstruction such as small bowel obstruction. Ileus most commonly occurs after abdominal operations, which is referred to as postoperative ileus. However, it can also be caused by a wide variety of underlying medical conditions like heart failure, systemic infection, or medications such as opiates. This is called a non-postoperative ileus.

Alright, when assessing a patient with signs and symptoms suggestive of ileus, you must first perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, start acute management immediately to stabilize their airway, breathing, and circulation. This means that you might need to intubate the patient, administer supplemental oxygen, obtain IV access, administer fluids, and monitor their vitals before continuing with your assessment. Also, if your patient is postoperative, don’t forget to examine their surgical wounds!

Now that we’re done with acute management of unstable patients, let’s get back to the ABCDE assessment and talk about stable patients. The first step here is to obtain a focused history and physical exam, as well as order labs like CBC, CMP, and lactate. In stable patients, the history typically reveals inability to tolerate oral intake, bloating, abdominal pain, and obstipation, with or without nausea and vomiting. 

Here is a high-yield fact! You can suspect some causes of ileus based on history. For example, remember to ask your patients about any recent abdominal operations or opioid usage. Both are common causes of reduced intestinal motility on their own; together they can lead to a prolonged state of intestinal paralysis. 

Ok, let’s get back to the physical examinatio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_bowel_disease_(Crohn_disease):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sDDDguxtRBGOA5SzaDu8qhxtTPe2qAM9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory bowel disease (Crohn disease): Clinical sciences]]></video:title><video:description><![CDATA[Inflammatory bowel disease, or IBD for short, is a condition characterized by chronic gastrointestinal tract inflammation that can be subdivided into Crohn Disease and Ulcerative Colitis. Crohn Disease, or CD, can affect any part of the GI tract, mouth to anus, and is characterized by transmural skip lesions, which can lead to abdominal pain, diarrhea, fatigue and fever.  Management is based on the severity of disease and it can be categorized as mild to moderate, moderate to severe, or severe.   

Now, when evaluating a person with suspected CD, you should first perform an ABCDE assessment to determine if they are stable or unstable. They might present with signs of shock like tachycardia and hypotension. Because of the high mortality-risk in these individuals, it is essential to hospitalize them, obtain intravenous access, and start them on IV fluids. Once they are stable, you should determine the cause of their instability, which can be small bowel obstruction, or SBO for short, or sepsis. 

Alright, individuals with SBO typically report severe nausea, vomiting, and the absence of flatus, while physical exam might reveal a distended abdomen and high pitched, tinkling, bowel sounds. An abdominal X-ray will show dilated loops of small bowel with air-fluid levels. 

Now, when it comes to individuals with sepsis, which often occurs from an abscess, they might report fever, fatigue, localized pain and sometimes a mass in the perianal area. On a physical exam, you might be able to palpate an abdominal or perianal mass, but sometimes you’ll need to use a CT or MRI of the abdomen and pelvis to detect the abscess. 

As for the treatment, all unstable individuals should be hospitalized, get IV antibiotics and a surgery consultation for laparoscopy or abscess drainage. Additionally, for an SBO, you should place a nasogastric tube for suction. 

Ok, let’s switch gears and talk about stable individuals. The first step is to obtain a focused history and physical]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_bowel_disease_(ulcerative_colitis):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zlHPXrdITzWnx3FkjWVnYNksTeuObPOY/_.png</video:thumbnail_loc><video:title><![CDATA[Inflammatory bowel disease (ulcerative colitis): Clinical sciences]]></video:title><video:description><![CDATA[Inflammatory bowel disease, or IBD, is a condition characterized by chronic gastrointestinal tract inflammation. It can be subdivided into Ulcerative Colitis and Crohn Disease. 

Ulcerative Colitis, or UC, primarily affects the colon and is characterized by continuous ulcerations of the mucosa and submucosa, which may lead to abdominal pain, bloody diarrhea, and tenesmus. Management is based on the severity of disease and they can be categorized as mild to moderate, moderate to severe, or acute severe.  

Now, when assessing an individual with suspected ulcerative colitis, you should first perform an ABCDE assessment to determine if they are stable or unstable. Unstable individuals might present with signs of shock, like tachycardia and hypotension, so you might have to secure their airway, breathing, and circulation before further workup. Unstable patients may also have signs of complications like toxic megacolon, perforated colon, or severe refractory hemorrhage. These patients should be hospitalized, and given intravenous fluids and antibiotics. 

Once they are stable, you should find out what caused the instability. If the patient presents with pallor and profuse rectal bleeding, consider anemia and hypovolemic shock due to severe refractory hemorrhage. In this situation, begin systemic corticosteroids and transfuse blood products. If the abdomen is distended or firm, consider toxic megacolon. An X-ray might reveal an enlarged colon and possibly signs of perforation, like pneumoperitoneum. 

These patients should also have stool studies to rule out C. difficile infection. A high yield fact to keep in mind about unstable patients is that you should avoid colonoscopy because there is a high risk of colon perforation. If an unstable patient has evidence of severe refractory hemorrhage, toxic megacolon, or perforated viscus, you can consult surgery for possible colectomy. 

Now, when it comes to stable individuals, the first step is to obtain a focuse]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intra-abdominal_abscess:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HvZN0UyDRfmzeIcc6dlXOBOuSpyr61ja/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intra-abdominal abscess: Clinical sciences]]></video:title><video:description><![CDATA[Intra-abdominal abscesses are a dangerous type of infection that, if left untreated, can progress to sepsis and death. They commonly arise from disruptions in the gastrointestinal or genitourinary tract, either from inflammation that causes microscopic leaks in the mucosal barrier or on a gross level from surgery or trauma. Disruption allows intra-luminal bacteria to leak into the abdominal cavity and cause infection. 

Now, the immune system may try to contain the infected fluid by forming a discrete, walled-off pocket, called an intra-abdominal abscess. If the infection doesn’t remain contained within the abscess, the free fluid containing the pathogen can lead to diffuse peritonitis. Based on the location, localization, and contents of the abscess, they can be grouped as abscesses with and without complicating features.

When a person presents with signs and symptoms suggestive of an intra-abdominal abscess, you should first perform an ABCDE assessment to determine whether they are stable or unstable. If the individual is unstable, you need to stabilize their airway, breathing, and circulation, which usually involves intubation, establishing an IV access, or administering fluids. 

Once you stabilize them, the next step is to obtain a focused history and physical examination, which might reveal signs and symptoms of diffuse peritonitis. These patients often report severe, diffuse abdominal pain that worsens with movement. Additionally, the physical exam might reveal distention, rigidity, guarding, and rebound tenderness. If this is the case, start empiric IV antibiotics and consult the surgical team immediately for further management, including imaging like CT scan, or bedside ultrasound if the patient is too unstable, followed by emergent laparotomy to explore and treat the infection. 

Alright, now let’s take a look at a stable patient that presents with signs and symptoms suggestive of intra-abdominal abscess. Start with a thorough history and physic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ischemic_colitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XUzMCLxkSOW-8PVtoBfVYahjRIm-UMFB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ischemic colitis: Clinical sciences]]></video:title><video:description><![CDATA[Ischemic colitis, or IC for short, is the most common form of intestinal ischemia. It is typically caused by reduced intestinal blood flow, usually due to small vessel occlusion or hypoperfusion of the colon. Hypoperfusion usually follows the blood supply pattern and is most common in the watershed areas, so the splenic flexure and rectosigmoid junction. This occurs because the arteries supplying the watershed areas are the most distal branches, so when blood flow to the intestine decreases, they’re the most likely to suffer from insufficient blood supply. Reduced intestinal perfusion causes injury to the colon mucosa. However, prolonged hypoperfusion can result in transmural ischemia, which can further lead to complications, such as fulminant gangrene, perforation, and peritonitis. 

Now, when assessing a patient with suspected IC, start with an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, you should prioritize acute management to stabilize their airway, breathing, and circulation. This means that you might need to intubate the patient, establish IV access, or administer fluids before continuing with your assessment.

Once the patient is stable, determine the cause of their instability, and proceed with a focused history and physical examination. History usually reveals severe abdominal pain, tenesmus, and bloody diarrhea; while a physical exam might reveal signs of shock, such as hypotension and tachycardia. Sometimes, you may also find signs of peritonitis, like rebound pain, rigidity, or guarding.

If you see these signs, start supportive care, which means continuing IV fluids, and administering empiric, broad-spectrum antibiotics. But, here’s the thing. These findings are not specific to ischemic colitis only, so you should order abdominal imaging such as X-ray or CT to look for bowel dilation and signs of complications such as perforation or peritonitis. 

Important findings to look for include pneu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Large_bowel_obstruction:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rxptn5IJSly77cV9HtrOrkU9QZ_KqSnR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Large bowel obstruction: Clinical sciences]]></video:title><video:description><![CDATA[Large bowel obstruction occurs when a blockage interferes with the passage of intraluminal contents like stool and gas through the colon. When this leads to infrequent or difficulty passing stool or flatus, it’s called constipation; while total inability to pass stool and flatus is known as obstipation. 

Blockages can be mechanical, which is when there is a physical obstruction, such as a tumor or volvulus; or pseudo-obstructions, also known as Ogilvie syndrome, which means that the obstruction is functional and the bowel isn&amp;#39;t working properly, so normal peristalsis is disrupted. Because the content of the bowel is unable to pass, large bowel obstruction can lead to bowel dilatation, ischemia, perforation, and finally sepsis.

When assessing a patient with signs and symptoms suggestive of large bowel obstruction, first perform an ABCDE assessment to determine if the patient is unstable. If the patient is unstable, start acute management immediately to stabilize their airway, breathing, and circulation. This means that you might need to intubate the patient, obtain IV access, administer fluids, and monitor their vitals before continuing with your assessment.

The next step is to obtain a focused history and physical exam, as well as labs like CBC, CMP, and lactate. Now, history might reveal abdominal bloating, abdominal pain ranging from crampy to diffuse in nature, obstipation, and sometimes nausea and vomiting. The onset of symptoms usually ranges from hours to days. Physical exam typically shows abdominal distension and signs of peritonitis, such as diffuse tenderness to palpation, rebound pain, and guarding. Finally, labs may show leukocytosis, as well as lactic acidosis from bowel ischemia. 

Alright, if you see these signs and symptoms, suspect large bowel obstruction. The next step is to start supportive care. Supportive care involves IV fluid resuscitation and vasopressor support, electrolyte replacement, broad-spectrum antibiotics, as we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lower_urinary_tract_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tMx_1IcRTtSVOEqM6w39ZkHwRUegiJxc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lower urinary tract infection: Clinical sciences]]></video:title><video:description><![CDATA[Lower urinary tract infections, or lower UTIs, primarily include infections of the urinary bladder and urethra, called cystitis and urethritis respectively. Most UTIs are caused by bacteria that typically compose the normal gastrointestinal flora, especially gram-negative rods, such as E. coli, followed by Klebsiella pneumoniae and Proteus mirabilis. Depending on the setting and patient’s risk factors, lower UTIs can be classified as uncomplicated, complicated, CAUTI, and UTI in pregnancy.

Alright, if a patient presents with signs and symptoms suggestive of a lower UTI, you should first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, first stabilize the airway, breathing, and circulation. This means you might have to intubate the patient, provide supplemental oxygen, obtain IV access, and monitor vital signs before doing further workup. 

Now that you know how to manage unstable patients, let’s go back to the ABCDE assessment and discuss stable ones. If your patient is stable, you should first perform a focused history and physical examination, and order labs like a urinalysis and urine culture. History might reveal symptoms like dysuria, urinary frequency and urgency, and sometimes even blood in urine.  On the other hand, physical exam could reveal suprapubic tenderness to palpation. As far as labs go, the urinalysis will be positive for nitrites and leukocyte esterase, and will reveal pyuria or WBCs and possibly hematuria or RBCs. 

Now here’s a clinical pearl to keep in mind! It’s important to note whether hematuria is painful or painless. Painful hematuria suggests diagnoses like infection or nephrolithiasis. On the other hand, painless hematuria can be a sign of underlying conditions such as renal malignancies, polycystic kidney disease, or autoimmune rheumatologic conditions, such as IgA nephropathy. At this point, you should suspect a lower UTI. 

Now, if your patient is a healthy, pre-menopausal biologically f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peptic_ulcer_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GCRupNDTQDiUYGN7i0PVYRx5SbC1Cv9s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peptic ulcer disease: Clinical sciences]]></video:title><video:description><![CDATA[Peptic Ulcer Disease, or PUD for short, is a condition characterized by ulcers in areas exposed to excess gastric acid and peptic juices. So, peptic ulcers can be located in the stomach, typically on the lesser curvature, which are referred to as gastric ulcers; or in the duodenum, usually in the duodenal bulb, which are referred to as duodenal ulcers. 

There are two main causes of PUD - Helicobacter Pylori, or H. Pylori infections, and Non-Steroidal Anti Inflammatory Drugs, or NSAIDs. PUD can result in complications, such as bleeding, perforation, and malignancy. 

Now, when assessing a patient with suspected PUD, the first thing you should do is an ABCDE assessment, to determine if your patient is unstable or stable. In unstable individuals, history might reveal alarm symptoms such as melena, severe hematochezia, or large-volume hematemesis, indicating a GI bleed. They may also report persistent severe epigastric pain. Additionally, physical exam findings can include orthostatic hypotension, tachycardia, pallor, and epigastric tenderness to palpation, suggesting a possible active GI bleed or even perforation. 

A high yield fact to remember is if your patient with suspected PUD also reports unintentional weight loss, be on the lookout for malignancies!

Now for unstable patients, the goal is to immediately stabilize them.  You might need to place two large bore IVs, initiate cardiac monitoring, start IV fluid resuscitation and transfuse blood products.

After you’ve stabilized the patient, you should determine the cause of the instability. The peptic ulcer itself can be causing a severe GI bleed or worse yet, it may have perforated. But, to confirm any of these diagnoses, first you need to order a diagnostic 
Esophagogastroduodenoscopy, or EGD with biopsies. Order iron studies and monitor the patient with serial CBCs. Consider a surgical consultation if there’s a perforation. 

Alright, moving on to treatment. If a bleeding ulcer is suspected, you shoul]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pyelonephritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V0NQTPwgRJSxyD1Rg96f4tMCSfOdYlUB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pyelonephritis: Clinical sciences]]></video:title><video:description><![CDATA[Acute pyelonephritis is an upper urinary tract infection that typically occurs when bacteria, most commonly E. Coli, make their way from the lower urinary tract, such as the urethra and bladder, up the ureters and kidneys. Now, based on the patient’s clinical features, acute pyelonephritis can be classified as complicated or uncomplicated. Complicated pyelonephritis occurs when the patient has functional or structural abnormalities, like neurogenic bladder, or like urinary obstruction due to nephrolithiasis. Complicated pyelonephritis also occurs when the patient has specific host risk factors, such as immunosuppression, advanced age, or male sex. On the other hand, a patient has uncomplicated pyelonephritis when there are no urinary tract abnormalities and no host specific risk factors. 

Now, if you suspect acute pyelonephritis, you should first perform an ABCDE assessment to determine if they are stable or unstable. Unstable individuals might present with signs of sepsis or shock, like tachycardia and hypotension, so don’t forget to stabilize their airway, breathing, and circulation. Additionally, obtain IV access, administer supplemental oxygen, and put your patient on continuous vital sign monitoring.

Ok, let’s return to the ABCDE assessment.  If the patient is stable or once you stabilize them, obtain a focused history and physical examination. Your patient will likely report fever, chills, malaise, flank pain, nausea and vomiting, and sometimes dysuria. On the other hand, physical exam may reveal elevated body temperature, hypotension, tachycardia, costovertebral angle and flank tenderness, and abdominal tenderness to palpation.

At this point you should suspect pyelonephritis, so your next step is to order labs, including CBC and CMP, as well as urinalysis and urine cultures. 

So, upon reviewing the labs, the CBC will reveal a leukocytosis with a left shift and the CMP might show an elevated BUN and creatinine, indicating renal insufficiency. The]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rectus_sheath_hematoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/adwZx6PHTK_4-VsDkQJlL9xQTj_QVS5q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rectus sheath hematoma: Clinical sciences]]></video:title><video:description><![CDATA[Rectus sheath hematoma refers to an accumulation of blood within the sheath of the rectus abdominis muscle. It typically occurs as a result of an injury to the epigastric artery or one of its branches, either due to abdominal trauma, or forceful contractions of the abdominal wall.  There are three types of rectus sheath hematoma. Type I is located within the rectus abdominis. Type II is when the blood builds up between the muscle and the fascia, while Type III extends into the peritoneum.

Alright, the first thing you should do if you suspect a rectus sheath hematoma is an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, you need to stabilize their airway, breathing, and circulation. This means that you may need to intubate the patient, establish IV access, and administer fluids before continuing with your assessment. If the patient doesn’t respond to these measures, consult the surgical team right away. 

On the flip side, if the patient is stable, your next step is to obtain a focused history and physical examination, and order labs such as CBC followed by serial hemoglobin and hematocrit levels every 4 to 6 hours, and coagulation studies, including PT, INR, and PTT. Now, patients with a rectus sheath hematoma usually report acute abdominal pain, which is often sharp, persistent, and non-radiating. 

History might also reveal some important risk factors like anticoagulation or antiplatelet therapy; recent abdominal surgery; pregnancy; biological female sex ; or chronic conditions such as renal disease, cirrhosis, arteriosclerosis, and hypertension. Additionally, patients with a history of asthma and COPD may also be at an increased risk due to repeated and forceful contractions of the rectus abdominis muscle during coughing spells. 

On the other hand, the physical exam usually reveals abdominal wall ecchymosis as well as tender, palpable, and non-pulsating abdominal mass in the area of the hematoma, which ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Retroperitoneal_hematoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6FbrZsy4S8isfCaDwwwUxICsQVak9q-Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Retroperitoneal hematoma: Clinical sciences]]></video:title><video:description><![CDATA[A retroperitoneal hematoma is a collection of blood within the retroperitoneal space. It can be caused by injury to parenchymal tissue or vascular structures secondary to blunt trauma, like motor vehicle accidents, or penetrating trauma, like stab or gunshot wounds. Retroperitoneal hematomas may also be a result of non-traumatic causes in patients who recently had percutaneous or endovascular interventions or patients on anticoagulation therapy.

When assessing a patient with signs and symptoms suggestive of a retroperitoneal hematoma, you should first perform an ABCDE assessment to determine if the patient is stable or unstable. Now, if the patient is unstable, first stabilize their airway, breathing, and circulation. This means that you may need to intubate the patient, establish IV access, and administer IV fluids before continuing with your assessment. In addition, perform blood typing and crossmatching, and prepare for massive blood transfusion.

Next, you should obtain a focused history and physical examination. If your patient is conscious, they might report abdominal, flank, or back pain, as well as dizziness or syncope. Additionally, they might have a history of blunt or penetrating trauma, or a recent endovascular procedure. On physical exam, you might find tachycardia or hypotension, and possibly pallor, visible traumatic injuries, or an unstable pelvis. 

Additional signs that may lead you to suspect a retroperitoneal hematoma include Grey-Turner, Fox, or Bryant signs. A Grey-Turner sign refers to flank ecchymosis. Fox sign refers to inguinal ecchymosis, and finally, the Bryant sign refers to scrotal ecchymosis. Although these signs may be suggestive of a retroperitoneal bleed, they are not always evident, especially since it often takes days for them to appear. 

Alright, if based on history and physical exam you suspect retroperitoneal hematoma, order a CT of the abdomen and pelvis with IV contrast. Imaging might sometimes show additional tra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Small_bowel_obstruction:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8oWgnmFdS6eLX4mMe-ZPTIJkSpmtRNft/_.jpg</video:thumbnail_loc><video:title><![CDATA[Small bowel obstruction: Clinical sciences]]></video:title><video:description><![CDATA[Small bowel obstruction, or SBO, occurs when intraluminal contents like chyme and gas are unable to pass through the small intestine due to a blockage. Blockages can be mechanical, which is a physical obstruction, such as adhesion, hernia, or tumor; or functional, which is caused by reduced or absent peristalsis, also called an ileus. Some SBOs resolve with conservative management, but others may require surgical intervention.

When approaching a patient with signs and symptoms suggestive of small bowel obstruction, first perform an ABCDE assessment to determine if the patient is stable or unstable. 

Let’s start with what to do if the patient is unstable. 

Start acute management immediately to stabilize their airway, breathing, and circulation. This means that you might need to intubate the patient, obtain IV access, administer fluids, and monitor their vitals before continuing with your assessment. Your next step is to obtain a focused history and physical exam, as well as labs.  Labs will include CBC, CMP, and lactate. 

Now, history might reveal bloating, abdominal pain, obstipation, and nausea and vomiting. 

Here’s a high-yield fact! You can suspect some causes of SBO based on history. For example, ask your patients about any prior abdominal surgeries or known hernias. Both are common causes of mechanical SBO. 

Okay, let’s move on to the physical examination. The exam may reveal tachycardia and hypotension, as well as abdominal distension and signs of peritonitis, like diffuse tenderness to palpation, rebound pain, and guarding. Remember to look for surgical scars and hernias during your exam! An incarcerated ventral or inguinal hernia often presents as a tender palpable mass, sometimes with overlying inflammatory skin changes. Finally, labs may show leukocytosis, as well as lactic acidosis from bowel ischemia. If you see these signs and symptoms, suspect SBO.

The next step is to start supportive care. You should initiate IV fluid resuscitation, e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_acid-base_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CH-5T0sxRA_7uLXzAyIgZJUGTDOmr98N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to acid-base disorders: Clinical sciences]]></video:title><video:description><![CDATA[An acid-base disorder is any process that causes the arterial pH to move outside its normal range of 7.35 to 7.45. When the arterial pH decreases below this range, the process is called acidosis. On the other hand, if the pH increases above this range, then it’s referred to as alkalosis. Now, depending on the cause, acid-base disorders can be classified as either respiratory or metabolic. Respiratory acid-base disorders are due to an increase or decrease in the removal of carbon dioxide from the body through the lungs. On the other hand, metabolic acid-base disorders result from the loss or accumulation of acids or bicarbonate. 

Now, if a patient presents with a chief concern suggesting an acid-base disorder, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If your patient is unstable, stabilize their airway, breathing, and circulation, which may require endotracheal intubation with mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen! 

Now, let’s go back to the ABCDE assessment and discuss stable patients. In this case, first, obtain a focused history and physical examination, and order labs, including a comprehensive metabolic panel or CMP, and an arterial blood gas or ABG. The history will vary greatly depending on the type of acid-base disorder and the underlying cause. Your patient might report fatigue, nausea, and vomiting, or recent medication changes, including diuretics or salicylates. The physical exam might reveal an abnormal respiratory rate, whereas the CMP might show electrolyte abnormalities depending on the type of the disorder, mainly involving bicarbonate, potassium, and chloride.

Next, assess the arterial pH from the ABG results. If the pH is under 7.35, you can diagnose acidosis. Your next step is to determine ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_metabolic_acidosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fqqAOUrrRoiUsgwruiI9BkR0SfWT4HH-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to metabolic acidosis: Clinical sciences]]></video:title><video:description><![CDATA[Metabolic acidosis refers to an increase in hydrogen ion concentration and a decrease in bicarbonate concentration in the blood. This can cause the pH to fall below 7.35 and serum bicarbonate level under 22 milliequivalents per liter. As a reference bicarbonates normally range from 22 to 27 miliequivalents per liter. Metabolic acidosis can be classified as either normal anion gap metabolic acidosis, which occurs in conditions like renal tubular acidosis, or elevated anion gap metabolic acidosis, which is seen in conditions like ketoacidosis. 

If a patient presents with a chief concern suggesting metabolic acidosis, first perform an ABCDE assessment to determine if they are unstable.  

If your patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, put your patient on continuous vital sign monitoring, and provide supplemental oxygen, if needed.  Here’s a clinical pearl! Severe cases might present with nausea, vomiting, lethargy, and tachypnea; and might need treatment with hemodialysis.  

Let’s move on to stable patients.  First, obtain a focused history and physical exam and order labs, including an arterial blood gas analysis or ABG, and CMP. 

Patients may report diarrhea and vomiting, or they may have a history of diabetes mellitus. The physical exam might reveal signs of dehydration, such as dry oral mucous membranes and decreased skin turgor, and there might be an increased respiratory rate as the body tries to compensate for the acidosis.  

If the ABG shows an arterial pH below 7.35 and the CMP shows decreased serum bicarbonate, typically below 22 milliequivalents per liter, that’s metabolic acidosis.  

Here’s a clinical pearl! In metabolic acidosis, the body tries to compensate by increasing the rate and depth of breathing, which eliminates CO2 and lowers the pCO2.  

To assess if the compensation is adequate, use the Winter formula: the range of expected pCO2 is equal to 1.5 times the bicarbon]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_metabolic_alkalosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/plQy2jdTTDeTRwy7G-gnDZ0-T5WKTPL1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to metabolic alkalosis: Clinical sciences]]></video:title><video:description><![CDATA[Metabolic alkalosis refers to an increase in serum bicarbonate concentration, either due to the loss of hydrogen ions from the body or the gain of bicarbonate itself. This can cause the arterial pH to rise above 7.45, and the serum bicarbonate above 27 milliequivalents per liter. As a reference bicarbonates normally range from 22 to 27 miliequivalents per liter. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. 

If a patient presents with a chief concern suggesting metabolic alkalosis, first perform an ABCDE assessment to determine if they are stable or unstable. If your patient is unstable, stabilize their airway, breathing, and circulation; obtain IV access and put them on continuous vital sign monitoring. Also, provide supplemental oxygen, if needed.  

Here’s a clinical pearl! Patients with severe metabolic alkalosis, meaning pH over 7.6 sometimes require urgent correction of blood pH with hemodialysis, especially if there is volume overload or renal dysfunction. 

Let’s move on to stable patients. After the ABCDE assessment, obtain a focused history and physical examination; and order labs, including an arterial blood gas analysis or ABG, and CMP. 
The history may reveal vomiting or use of loop or thiazide diuretics. Alkalosis increases the protein binding of ionized calcium, so you might find headaches, lethargy, neuromuscular excitability, delirium, tetany, and seizures. Additionally, alkalemia lowers the threshold for anginal symptoms and arrhythmias. Lastly, if there is hypokalemia, the patient might report weakness.  

The physical exam might show signs of dehydration, like dry mucous membranes, and decreased skin turgor. As for the labs, ABG typically shows an arterial pH above 7.45, while CMP reveals elevated serum bicarbonate, often above 27 milliequivalents per liter. If you see these findings in history, physical exams and labs, that’s metabolic alkalosis.  

Here’s a clinical pearl! Metabolic alkalosis c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_respiratory_acidosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9zL_fp65RUy7W5HnsoZmJ8b3QjO-rxMl/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to respiratory acidosis: Clinical sciences]]></video:title><video:description><![CDATA[Respiratory acidosis refers to an increase in partial pressure of carbon dioxide or pCO2, with or without a compensatory increase in bicarbonate resulting in increased hydrogen ion concentration in the blood. This is almost always caused by hypoventilation, usually from the central nervous system, pulmonary, or iatrogenic conditions.Generally, respiratory acidosis is characterized by an arterial pH below 7.35 and a pCO2 above 45 millimeters of mercury. As a reference, the normal pCO2 range is between 35 and 45 millimeters of mercury. 

If a patient presents with a chief concern suggesting respiratory acidosis, first perform an ABCDE assessment to determine if your patient is stable or unstable.  

If your patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring. Finally, provide supplemental oxygen, if needed. 

Here’s a clinical pearl! Respiratory acidosis can be acute or chronic.The chronic form is asymptomatic. However, if it worsens, or if the patient has an acute case, they might present with headache, confusion, and altered mental status. Their exam might show tremors, myoclonic jerks, and asterixis. These patients may require adequate ventilation by either endotracheal intubation or noninvasive positive pressure ventilation.  

Now that unstable patients are taken care of, let’s talk about stable ones.  Your next step here is to obtain a focused history and physical examination and order labs, including an arterial blood gas analysis or ABG, and BMP. 

History findings depend on the specific cause, but most patients have shortness of breath. The physical exam might show abnormal breathing patterns, such as a decreased respiratory rate, and signs of hypoxemia, like cyanosis. 

As for the labs, ABG typically reveals an arterial pH below 7.35, and a pCO2 above 45 millimeters of mercury. BMP usually reveals normal or increased serum bicarbonate depending]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_respiratory_alkalosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uDLbrUF7R764DWA2gUzWBoEdRnqYzxEg/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to respiratory alkalosis: Clinical sciences]]></video:title><video:description><![CDATA[Respiratory alkalosis refers to a decrease in the partial pressure of carbon dioxide or pCO2, resulting in a decrease in the concentration of hydrogen ions in the blood. This is almost always caused by hyperventilation, which increases carbon dioxide removal relative to carbon dioxide production.Hyperventilation typically occurs in response to triggers such as hypoxia, infection, metabolic acidosis, pain, anxiety, overdose of certain medications, or increased metabolic demand. Respiratory alkalosis is characterized by a pH above 7.45, and a pCO2 below 35 millimeters of mercury. As a reference, the normal pCO2 range is between 35 and 45 millimeters of mercury. 

If a patient presents with a chief concern suggesting respiratory alkalosis, perform an ABCDE assessment to determine if your patient is stable or unstable.  

If they are unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring. Lastly, provide supplemental oxygen, if needed.  

Let’s jump back to the ABCDE assessment and talk about stable patients.  Your next step here is to obtain a focused history and physical examination and order labs, including an arterial blood gas analysis, or ABG, and BMP. 

The history will vary depending on the specific cause, but your patient may report shortness of breath, while the physical exam might show an increased rate and depth of breathing.  

ABG typically shows an arterial pH above 7.45, and a pCO2  lower than 35 millimeters of mercury. Finally, BMP will show normal or decreased serum bicarbonate, depending on whether or not there is metabolic compensation; and might show electrolyte imbalances, such as hypokalemia. With these findings, you can diagnose respiratory alkalosis.  

Here are some clinical pearls! Once you’ve diagnosed respiratory alkalosis, remember to assess for metabolic compensation by checking the serum bicarbonate level. A compensated respiratory alkalosis is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_tachycardia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P9zA6Jk6QuKp43MdK7MRLpBtTtetiSuQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to tachycardia: Clinical sciences]]></video:title><video:description><![CDATA[Tachycardia refers to a heart rate above 100 beats per minute, or bpm for short. Once identified, a 12-lead ECG can be used to determine if the tachycardia has a regular or irregular rhythm, and if the QRS complex is narrow or wide. Further examination of the ECG can reveal details that help identify which type of tachycardia is present. 

Here’s a high-yield fact! The typical definition of a normal heart rate is between 60 and 100 bpm. However, although tachycardia is technically considered to be above 100 bpm, the SIRS criteria consider tachycardia to be above 90 bpm. 

Now, if a patient presents with signs or symptoms of tachycardia, first perform an ABCDE assessment to determine if they are unstable or stable. 

If they’re unstable and a pulse is present, then follow the ACLS guidelines for Tachycardia with a Pulse.

Next, stabilize their airway, breathing and circulation. Provide supplemental oxygen, if hypoxemic, to maintain oxygen saturation above 90%. Next, obtain IV access and put your patient on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry. 

Then assess for signs and symptoms of unstable tachycardia, including heart rate above 150 bpm, hypotension, altered mental status, signs of shock, ischemic chest pain, or acute heart failure. 

If your patient has unstable tachycardia, perform immediate synchronized cardioversion.

Now let&amp;#39;s go back to the ABCDE assessment and discuss stable patients. 

First, perform a focused history and physical examination. Individuals with tachycardia may report symptoms like palpitations, exercise intolerance, lightheadedness, or even syncope. Additionally, physical exam might reveal a rapid heart rate, and if it’s over 100 beats per minute, you can diagnose stable tachycardia. 

Next, obtain a 12-lead ECG and assess the heart rhythm by evaluating the consistency of the intervals from one R wave to the next, which is the R to R interval. If the R to R interval is t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aspiration_pneumonia_and_pneumonitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5mz5ZU_QS_aqPnSYij4JT3_oQM_IxOwm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aspiration pneumonia and pneumonitis: Clinical sciences]]></video:title><video:description><![CDATA[Aspiration pneumonia and pneumonitis refer to lung inflammation that typically occurs in individuals with impaired swallowing function or decreased level of consciousness. Aspiration pneumonia occurs when a person aspirates oropharyngeal content colonized by pathogenic bacteria, most commonly Streptococcus pneumoniae, Staphylococcus aureus, and Haemophilus influenzae. 

On the other hand, aspiration pneumonitis occurs when a patient aspirates a large volume of sterile acidic gastric content that causes lung inflammation. 

Now, if you suspect aspiration pneumonia or pneumonitis, you should first perform an ABCDE assessment to determine whether your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. 

This often requires bronchoscopy and suctioning of the aspirated content to prevent asphyxia. In some cases, you might need to consider intubation and mechanical ventilation. 

Next, obtain IV access and, if the patient is hypotensive, start IV fluids for volume resuscitation. Finally, put your patient on continuous vital sign monitoring, such as pulse oximetry, blood pressure, and heart rate.

Alright, now, let’s go back to the ABCDE assessment and talk about stable individuals. Start by obtaining focused history and physical, as well as chest X-ray, which can all help you differentiate aspiration pneumonia from pneumonitis. 

First, let’s start with aspiration pneumonia. 

In patients suspected with aspiration pneumonia, history reveals a gradual onset of symptoms that typically include pleuritic chest pain, shortness of breath, and fever. 

Most of the time, the aspiration is not witnessed, since pneumonia is usually associated with microaspirations due to impaired swallowing function, such as dysphagia. 

Additionally, history might reveal neurologic conditions that can also affect swallowing, such as stroke, seizures, or a period of decreased consciousness, like sedation or intoxication. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community-acquired_pneumonia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kvUmdREuR7OlZk1vyjNXFAniQlahQ5od/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community-acquired pneumonia: Clinical sciences]]></video:title><video:description><![CDATA[Pneumonia is a lung infection that results in inflammation of one or both lungs. Usually, it is caused by bacteria, like Streptococcus pneumoniae; and viruses, such as influenza, but rarely, pneumonia can be caused by fungi as well.  

Now, based on the setting in which pneumonia develops, we can subdivide it into two main types:  community-acquired pneumonia, or CAP for short; and hospital-acquired pneumonia, or HAP. When a person develops pneumonia outside of a hospital or within 48 hours after the admission to hospital, it’s considered CAP.  

On the other hand, HAP develops after 48 hours of the admission to hospital. Finally, there’s a special subtype of HAP called ventilator-acquired pneumonia, or VAP. VAP refers to pneumonia that occurs in individuals on mechanical ventilation, 48 hours after the endotracheal intubation.  

The first thing to do when approaching a patient with suspected CAP is to obtain a focused history and physical examination; send labs, such as ABG, CBC and BMP; monitor pulse oximetry; and get a chest x-ray.  

Let’s start with the history. Patients with CAP might report coughing, difficulty breathing, and chest pain during inspiration. Keep in mind that these symptoms develop either outside of the hospital or within 48 hours of admission. They may also have a history of risk factors like COPD, diabetes, smoking, or alcohol use.  

Here are some high-yield facts to keep in mind! A productive cough can occur with bacterial infections. However, if the sputum is blood-tinged, consider specific organisms like Streptococcus pneumoniae, Klebsiella pneumoniae, or Legionella pneumophila.  

Now, the physical examination often reveals an elevated temperature, tachypnea, and tachycardia. Pay close attention to lung auscultation, which might reveal rales over the affected area. Additionally, if there’s lobar consolidation, the physical exam might demonstrate bronchial breath sounds, egophony, and increased tactile fremitus in the affected ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coronary_artery_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qpMEMdcsSdqMPzMzr4z8MwbvSkSnHhBd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Coronary artery disease: Clinical sciences]]></video:title><video:description><![CDATA[Coronary artery disease, or CAD, is caused by atherosclerosis of the coronary arteries, which occurs when plaque builds up in the vessels, eventually narrowing the lumen, and causing a mismatch between oxygen supply and demand of the heart. Over time, reduced oxygen supply can lead to myocardial ischemia or even infarction. 

The diagnosis of CAD is based on atherosclerotic risk factors that categorize patients into low, intermediate, or high risk groups based on their probability for obstructive disease. 

Now, if you suspect CAD, first perform an ABCDE assessment. This is to determine if the patient is unstable or stable. 

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, provide supplemental oxygen, and put them on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry. 

At this point, you should suspect CAD with acute coronary syndrome, which includes unstable angina, non-ST elevated myocardial infarction, or NSTEMI, or ST-elevated myocardial infarction, or STEMI. 

Once you stabilize the patient, obtain a focused history and physical examination, and order serial troponin levels and an ECG.

Okay, let’s focus on unstable angina, your patient may report sudden chest discomfort that doesn’t improve with rest, and feelings of uneasiness or “impending doom”. 

Other common symptoms include dizziness, shortness of breath, sweating, as well as nausea. 

Physical exam typically reveals a distressed, anxious, and diaphoretic individual. 

Ok, next take a look at the serial troponins. If there’s no myocardial infarction, troponins will typically be normal.  

While ECG may or may not show signs of ischemia like ST segment depression or new T wave inversion. 

This combination of history, physical exam, labs, and ECG findings are characteristic of unstable angina, where chest pain is caused by an insufficient supply of oxygen to the cardiac tissue. 

In these individuals, treatment cons]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemothorax:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HFO6V4I2RXScQhSUE274wCwFQzqF09DB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemothorax: Clinical sciences]]></video:title><video:description><![CDATA[A hemothorax is the collection of blood within the chest cavity, or the pleural space to be more specific. This collection can be a result of direct trauma to the chest, or can occur spontaneously when patients have pre-existing clotting disorders. It’s important to address the hemothorax in a timely manner to acutely avoid a potentially life-threatening hemorrhage, as well as to avoid chronically the formation of a fibrothorax, which is an organized clot within the chest cavity surrounding and restricting the patient’s lung from expanding.

When approaching a patient who presents with signs and symptoms suggestive of a hemothorax, your first step is to do an ABCDE assessment in order to determine if the patient is stable or unstable. If the patient is unstable, you need to secure their airway, obtain IV access, and begin resuscitation, as well as monitor and manage their vital signs. Next, obtain a quick focused history and physical exam. Unstable patients with hemothorax typically present with dyspnea and chest pain. 

Additionally, they might have a history of an underlying cause, such as chest trauma or recent chest or cardiac procedures like thoracentesis or coronary angiography, as well as a history of cancer, potentially causing erosion into great vessels; thoracic aortic aneurysm; or prior clotting disorders or coagulopathy. On physical examination, you’ll find these patients to be hypotensive and tachycardic. Now, as one side of the chest is full of blood, that lung will be restricted, so you’ll typically find absent unilateral breath sounds. In addition, since that side has no airflow, you might also notice dullness to percussion and decreased tactile fremitus on the affected side.

Okay, because the patient is unstable, you need to act fast! Start by ordering a chest x-ray, which will reveal fluid within the pleural cavity, and can help you rule out several life-threatening conditions. Another quick and reliable way to get an idea of what’s goin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hospital-acquired_and_ventilator-associated_pneumonia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/haGUedD9RCiUUFgrW7GOM4kKTMG0xUMt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hospital-acquired and ventilator-associated pneumonia: Clinical sciences]]></video:title><video:description><![CDATA[Pneumonia is a lung infection that results in inflammation of one or both lungs. Most often, it is caused by bacteria like Streptococcus pneumoniae; or viruses, such as influenza; but rarely, pneumonia can be caused by fungi as well. 

Now, based on the setting in which pneumonia develops, we can subdivide it into two main types: community-acquired pneumonia, or CAP for short, which is when a person develops pneumonia outside of a hospital or within 48 hours after hospital admission; and hospital-acquired pneumonia, or HAP, which develops after 48 hours from hospital admission. Finally, there’s a special subtype of HAP called ventilator-acquired pneumonia, or VAP, which refers to pneumonia that occurs in patients on mechanical ventilation, 48 hours after endotracheal intubation. 

Now, when a patient presents with signs and symptoms suggestive of HAP or VAP, the first step is to obtain a focused history and physical examination and order labs such as CBC and procalcitonin. You should also use pulse oximetry to check oxygen saturation levels, and collect a blood sample for cultures. Finally, don’t forget to obtain imaging, such as chest x-ray or point-of-care lung ultrasound. 

Alright, first, let’s talk about the diagnosis and acute management of patients with HAP. Let&amp;#39;s start with History. These patients usually report a fever, productive cough, pleuritic chest pain, and shortness of breath. Keep in mind that these symptoms develop at least 48 hours after admission. Now, the physical examination typically reveals elevated temperature, tachypnea, and tachycardia, as well as rales, and decreased breath sounds. When it comes to labs, they are likely to show elevated WBC count and procalcitonin levels, while pulse oximetry can reveal a drop in oxygen saturation. Finally, a chest X-ray usually reveals a new lung infiltrate, consolidation, or effusion.

Now, if a patient presents with these findings, you can diagnose HAP and start acute management. Thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pericarditis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zpM28qq4T1a0f9Hh7YOh_hA4Rv_U0nJ6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pericarditis: Clinical sciences]]></video:title><video:description><![CDATA[Pericarditis is inflammation of pericardium, sometimes associated with the accumulation of fluid, known as a pericardial effusion. The underlying inflammation might be due to viral infection, uremia, autoimmune disease, or after trauma, but regardless of cause, is associated with severe chest pain due to the pericardium’s abundant nerve supply. 

Additionally, pericarditis may lead to the development of dangerous complications, such as pericardial effusion, which is characterized by accumulation of fluid around the heart; as well as cardiac tamponade, where the accumulated fluid compresses the heart. 

So, if you suspect pericarditis or one of its complications, first you should perform an ABCDE assessment, to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation, which typically requires obtaining IV access and intubating the patient if you need to secure the airway. 

Next, perform a focused history and physical examination. On physical exam be on the lookout for Beck triad, which includes hypotension, jugular venous distension, and muffled heart sounds. Additionally, a physical exam might reveal pulsus paradoxus, which is when the systolic blood pressure drops with inspiration, and no audible pericardial friction rub. 

All of these findings should lead you to suspect that a large pericardial effusion has resulted in cardiac tamponade, so your next step is to order an ECG and chest x-ray immediately to evaluate your suspicions. Alternatively, if available, perform point of care ultrasound, or POCUS for short. 

ECG typically shows sinus tachycardia with low QRS voltage and electrical alternans, defined as beat-to-beat variation in the QRS amplitude. This occurs as a result of swinging of the heart in the pericardial fluid, which can be seen with a large pericardial effusion. On the other hand, chest x-ray might show an enlarged cardiac silhouette with clear lung fields. Finally, you]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pneumothorax:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G6XDhcAhQIa-SvwafQpucehqQlGY5pCw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pneumothorax: Clinical sciences]]></video:title><video:description><![CDATA[Pneumothorax refers to an abnormal presence of air within the pleural space that can result in a deflated or collapsed lung. The pleural space has a parietal layer, which lines the chest wall, and a visceral layer, which lines the parenchyma of the lung. Disruption of either of the pleural layers can allow air to enter the pleural space. 

This can occur spontaneously, usually due to rupture of anatomic lung defects called blebs and bullae, or traumatic, which might occur after a penetrating chest injury or even a medical procedure. Based on the underlying cause, pneumothorax can be classified as spontaneous pneumothorax, which is further subdivided into primary- and secondary spontaneous pneumothorax; and non spontaneous pneumothorax.

Now, if you suspect pneumothorax, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. This means that you’ll need to assess the need for ventilatory support and might need to intubate the patient. Next, obtain IV access, provide supplemental O2 to maintain SaO2 &amp;gt;92% and put your patient on continuous vital sign monitoring, such as pulse oximetry, blood pressure, and heart rate. 

Next, perform a focused history and physical and get a chest x-ray as soon as possible. Your patient might report sudden chest pain and shortness of breath while your exam will reveal an asymmetric chest and tracheal deviation away from the affected side, as well as hypotension, respiratory distress, and decreased or absent breath sounds on the affected side. Keep in mind that tension pneumothorax is a clinical diagnosis and doesn’t need further testing. 

However, if you were to perform a chest x-ray, it would show a distinct visceral pleural edge with an absence of lung markings distally, often with a depressed hemidiaphragm ipsilateral to the collapsed lung, known as a deep sulcus sign. In severe cases, you’d see shi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_embolism:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m9mYhN8_RDK348FGWy2FA8sWThWK6oyw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary embolism: Clinical sciences]]></video:title><video:description><![CDATA[Pulmonary embolism, or PE, is a blockage of the pulmonary artery or one of its branches by an embolus, which is a traveling blood clot, tumor, fragment of fat, or air, that originates from somewhere else in the body. 

In most cases, the embolus originates from a thrombus in the iliac, femoral, or popliteal veins that broke loose. Once the embolus reaches the pulmonary circulation, it blocks alveolar blood flow and increases dead space ventilation. This causes ventilation perfusion mismatch, eventually reducing blood oxygenation and causing damage to lung tissue. In addition, there’s increased pulmonary vascular resistance and right ventricular afterload, which can lead to right ventricular heart failure. Because of this, patients who are unstable need immediate management, and those who are stable should be evaluated quickly with the Wells criteria.  

When assessing a patient with a suspected pulmonary embolism, first do an ABCDE assessment to determine if your patient is stable or unstable. An unstable presentation is commonly caused by a large embolus in the main pulmonary artery. Because of the high mortality-risk in these patients, it’s essential to stabilize their airway, breathing, and circulation first. You should establish intravenous access for fluids or vasopressors, and attach an automatic blood pressure cuff, chest leads, and digital pulse oximeter to monitor blood pressure, cardiac rhythm, and oxygen saturation. Additionally, provide supplemental oxygen to maintain the oxygen saturation above  90%. 

On examination, unstable patients typically present with severe hypotension, tachypnea, and tachycardia. They might also have dyspnea, pleuritic chest pain, hemoptysis, fatigue, and weakness. Additional physical findings found in physical examination might reveal rales, JVD, a loud P2, calf tenderness and swelling, and pedal edema. In severe cases, the patient can progress to bradycardia, which can be associated with right ventricular strain and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ventricular_tachycardia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-STMnhK7SuC1C6VeAYmWUtqwRE28AP-G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ventricular tachycardia: Clinical sciences]]></video:title><video:description><![CDATA[Ventricular tachycardia, also known as VT or V-tach, is a wide-complex tachycardia originating from an ectopic ventricular pacemaker, often in the setting of myocardial ischemia or structural heart disease. 

Ventricular tachycardia is a poorly perfusing rhythm, so patients may present with or without a pulse. It often presents with hemodynamic instability, which requires emergent intervention to restore a perfusing rhythm. 

Bear in mind that some patients with VT might be hemodynamically stable upon presentation, but they’re at risk of becoming unstable quickly and with no warning, potentially even deteriorating to ventricular fibrillation, so they’re still managed emergently. 

Now, based on duration, VT can be classified as non-sustained, which lasts less than 30 seconds, or sustained, which lasts more than 30 seconds. Additionally, based on the pattern of QRS complexes, VT can be described as monomorphic or polymorphic. 

Now, if an individual presents with signs or symptoms of VT, you should first perform an ABCDE assessment. These patients will generally be unstable, so begin acute management. Stabilize their airway, breathing, and circulation. Next, obtain IV access, attach a cardiac rhythm monitor, and provide supplemental oxygen if they’re hypoxemic. 

Here’s a high-yield fact! While providing acute management, it’s also important to look for reversible causes, which can be remembered as the 5 H&amp;#39;s and T&amp;#39;s. The H’s include Hypoxia, Hypothermia, Hypovolemia, Hydrogen ions for acidosis, and Hyper- or Hypokalemia; while the T’s include Toxins, cardiac Tamponade, Thrombosis for myocardial infarction, Thrombosis again for pulmonary embolism, and Tension pneumothorax. Next, assess for signs of VT on the cardiac rhythm monitor.    

Signs of VT include a heart rate above 150 beats per minute, QRS complex width of 140 milliseconds or greater, and the presence of AV dissociation, which means there’s no clear relationship between the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_dyspnea:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I4NY__rwSICLmhjjgaNJzsStQSi7-Zq2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to dyspnea: Clinical sciences]]></video:title><video:description><![CDATA[Acute dyspnea is the sensation of difficult or uncomfortable breathing that develops over hours to days. Dyspnea is a common symptom with a wide range of causes including respiratory, cardiovascular, metabolic, neuromuscular, and neurologic conditions. Many causes of acute dyspnea are life-threatening, so it is important to have a systematic approach to evaluating these patients.

When approaching a patient with dyspnea, first you should perform an ABCDE assessment, to determine if your patient is unstable or stable. If they are unstable, first check for alarm signs and symptoms! Check for upper airway obstruction by auscultating for stridor, a high-pitched breathing sound, and by directly examining the airway for oropharyngeal swelling or the presence of a foreign body.

If the airway is clear, evaluate the patient’s breathing by assessing respiratory rate and oxygen saturation. A respiratory rate less than 10 or greater than 20 breaths per minute, or oxygen saturation less than 90% requires acute management.

You should also look for red flag features that signal impending respiratory failure such as confusion, inability to speak in complete sentences, and the use of accessory respiratory muscles, such as the scalenes and intercostals.

In this case, stabilize the airway, breathing, and circulation, which may require removing any airway obstruction, endotracheal intubation and mechanical ventilation. Some patients might require supplemental oxygen only, but, in both cases, don’t forget to obtain IV access and put your patient on continuous vital sign monitoring.

Now, here’s a high-yield fact to keep in mind! Causes of acute airway obstruction, that might present with stridor, include anaphylaxis, epiglottitis, and the presence of a foreign body.

Suspect anaphylaxis if the patient reports exposure to a known allergen, such as an insect sting, and presents with urticaria, stridor, or wheezing.

On the other hand, epiglottitis most commonly presents ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_postoperative_respiratory_distress:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BqQ3IcbYQeiHDrozs8BsKJ_KT_qsrjiG/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to postoperative respiratory distress: Clinical sciences]]></video:title><video:description><![CDATA[Postoperative respiratory distress can occur after any operation due to issues with the airway and lung parenchyma itself, or from respiratory muscle dysfunction. It can be life-threatening if left untreated. Although there are many different causes, the life-threatening conditions you must first identify are tension pneumothorax, acute respiratory distress syndrome or ARDS, upper airway obstruction, and pulmonary embolism. Other urgent causes include atelectasis, pneumonia, pleural effusion, pulmonary edema, aspiration pneumonitis, and bronchospasm. Keep in mind that any cause of postoperative respiratory distress can become life-threatening if not managed appropriately, and any of these complications require immediate intervention.

Your first step in assessing a patient with postoperative respiratory distress is to evaluate their ABCDE. If you determine that the patient is unstable, initiate acute management immediately. First, stabilize the airway. Keep in mind that some patients might require intubation or even a surgical airway like a cricothyroidotomy. Next, provide supplemental oxygen and support with mechanical ventilation, obtain IV access, and monitor their vitals. Once these important steps are done, you should perform a focused history and physical exam to quickly assess for life-threatening conditions. 

Here’s a clinical pearl! Regardless of the cause, many patients will have similar signs and symptoms, such as dyspnea, tachypnea, increased work of breathing, and hypoxemia. So if you see any of these in a postoperative patient, make sure to act quickly!

Alright, let’s first talk about tension pneumothorax. If the patient required high airway pressure or a central line placement, or if they had a difficult airway, and on the exam you find absent lung sounds, unequal breath sounds, hyperresonance to percussion, and tracheal deviation, you can make your diagnosis of tension pneumothorax. Remember, tension pneumothorax is a clinical diagno]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_respiratory_distress_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CY7Egu15RDOGIQmsQ2MbzYM5QD2CsL77/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute respiratory distress syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Acute respiratory distress syndrome, or ARDS for short, is a life-threatening condition associated with acute lung injury that results in progressive respiratory dysfunction and hypoxia. ARDS is caused by inflammatory alveolar damage and capillary endothelial injury, which ultimately leads to decreased lung compliance and pulmonary arterial vasoconstriction. Based on arterial oxygenation, patients are grouped into mild, moderate, and severe ARDS.

Now, if you suspect ARDS, you should first perform an ABCDE assessment. Patients with ARDS are usually unstable, so begin acute management immediately! Stabilize the airway, breathing, and circulation, which means you will likely need to intubate the patient and place them on mechanical ventilation. Next, obtain IV access, put your patient on cardiac telemetry, and begin continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry.

Once you stabilize the patient, obtain a focused history and physical examination. Your patient will report progressive shortness of breath and may have a history of trauma, sepsis, pneumonia, pancreatitis or drug toxicity. Physical exam often reveals features of hypoxia like cyanosis, tachypnea, accessory respiratory muscle use, and diffuse pulmonary crackles. In addition, pulse oximetry will reveal low oxygen saturation level. At this point, you should suspect ARDS!

Next, order an arterial blood gas, or ABG, and chest x-ray. In addition, you should estimate the fraction of oxygen in the patient’s inspired air, or FiO2. FiO2 is typically 0.21 when breathing room air. For patients on supplemental oxygen, it varies depending on the mode of oxygen delivery, and the amount of oxygen being delivered.

Now, here’s a high-yield fact! To help rule out cardiac dysfunction as the cause of lung infiltrates, look for absence of jugular venous distension on examination, normal troponin or B-type natriuretic peptide levels, a normal ECG, and a normal echocardiogram.
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Airway_obstruction:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KyY_nNgsQ5CC6ylcx5p4CtPjRtGR8ds5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Airway obstruction: Clinical sciences]]></video:title><video:description><![CDATA[An airway obstruction is defined as the inability to move air, or ventilate, from a direct occlusion or anatomic narrowing. It requires an immediate assessment and swift intervention, since it can be fatal if left untreated. There are many causes that can lead to airway obstruction, including trauma, tracheal narrowing, foreign body aspiration, mucus plugging, malignancy, and deep neck infection. Keep in mind that all of these causes have the potential to cause hemodynamic instability due to respiratory failure, especially trauma and foreign body aspiration.

When assessing a patient with signs and symptoms suggestive of airway obstruction, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. Be sure to look for red flags of impending airway compromise like stridor, tachypnea, accessory muscle use like gasping or nostril flaring, as well as bleeding in the nasopharynx or the oropharynx, large or expanding neck hematoma, crepitus in the neck or upper chest, and tracheal deviation. 

If the patient is unstable with red flags, you must initiate acute management right away to stabilize their airway, breathing, and circulation. The goal here is to maintain oxygenation above 90% initially with a high-flow nasal cannula or non-rebreather. However, if the patient desaturates or cannot protect their airway, proceed with rapid sequence intubation. This involves administering an induction agent like etomidate; and a paralytic agent like succinylcholine or rocuronium. Once medications start working, you can intubate the patient. 

Here’s a clinical pearl! If airway obstruction is anticipated, make sure to have multiple sizes of small endotracheal tubes available. Keep in mind that, although securing the airway is the top priority, the workup will likely require laryngoscopy and bronchoscopy. 

Now, if intubation is unsuccessful after 3 attempts or you cannot maintain oxygenation above 90%, consider cricothyroidotomy to c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anaphylaxis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eSnjIRZLTbaoKLBKr4W9M7EXRiuKgsXk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anaphylaxis: Clinical sciences]]></video:title><video:description><![CDATA[Anaphylaxis refers to an acute, potentially life-threatening allergic reaction that occurs in response to antigens that don’t cause problems for most people. Common anaphylactic triggers include foods like nuts, milk, shellfish, and eggs, as well as certain medications like penicillin, IV contrast agents; and insect stings. 

The first exposure to a specific antigen is called sensitization and typically occurs with minimal or no signs or symptoms. But, on second exposure, IgE-mediated activation of basophils and mast cells leads to the release of pro-inflammatory mediators, such as histamine, prostaglandins, and cytokines. These mediators reach the bloodstream and spread throughout the body, causing an overwhelming systemic inflammatory reaction that can ultimately result in anaphylactic shock or even death.

Now, if you suspect anaphylaxis, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient. Do this as soon as possible, since airway edema can progress quite quickly and become more severe, making intubation very difficult. However, if you are unable to intubate, immediately call the surgery team to evaluate for possible surgical airway management, such as cricothyrotomy. 

Next, obtain IV access and, if your patient is hypotensive, start IV fluids for volume resuscitation. In severe cases, you may need to administer immediate intramuscular epinephrine, even before obtaining very focused history and physical examination. Finally, put your patient on continuous vital sign monitoring, such as pulse oximetry, blood pressure, and heart rate.

Let’s go back to the ABCDE assessment. Now, if the patient is instead stable, obtain IV access and put them on continuous vital sign monitoring. Now that you’ve initiated the acute management, in both, stable and unstable individuals, it’s im]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_bradycardia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dWTdAk06Rye1SpcVxIE7rMw9TvCecTN4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to bradycardia: Clinical sciences]]></video:title><video:description><![CDATA[Bradycardia is typically defined as a heart rate below 60 beats per minute, or bpm, although in some instances it can be considered below 50 bpm. Bradycardia may originate from physiologic changes in vagal tone, pathologic changes to the cardiac conduction system, infectious causes, or medication effects.

The severity might range from completely asymptomatic to life-threatening, and based on 12-lead ECG findings, you can determine if the bradycardia is physiologic, or if it’s due to sinus or sinoatrial or SA node dysfunction, or even atrioventricular or AV node dysfunction.

Now, if a patient presents with bradycardia, you should first perform an ABCDE assessment to determine if they are unstable or stable. If they’re unstable and there’s a detectable pulse, follow the ACLS guidelines for Bradycardia with a Pulse. 

First stabilize their airway, breathing, and circulation. Provide supplemental oxygen if they’re hypoxemic, to maintain oxygen saturation above 90%. Next, obtain IV access and put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry. 

Now let&amp;#39;s go back to the ABCDE assessment and discuss the approach to a stable patient. First, perform a focused history and physical examination. Your patient may report exercise intolerance, lightheadedness, or even syncope, and some patients may experience ischemic-type chest pain or nausea. 

Additionally, on a physical exam, cardiac auscultation and pulse palpation will reveal a slower than normal heart rate. Moreover, if the heart rate is below 60 beats per minute, you can diagnose bradycardia. 

Here’s a clinical pearl! The typical definition of a normal heart rate is between 60 and 100 bpm. However, although technically anything below 60 bpm should be considered bradycardia, you may find it defined as below 50 bpm, since most patients with a heart rate in the 50s are actually asymptomatic and require no treatment.

Next, obtain a 12-lead elect]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Asthma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/norsyQ8GQzaAacI0eixvubLyTVaF1Oru/_.jpg</video:thumbnail_loc><video:title><![CDATA[Asthma: Clinical sciences]]></video:title><video:description><![CDATA[Asthma is an episodic, chronic respiratory disorder characterized by airway obstruction caused by inflammation and hyperresponsiveness of the bronchial smooth muscle. Asthma is reversible, which means the obstruction can virtually disappear with medications like bronchodilators, and inducible, which means the obstruction can occur in response to a variety of stimuli; including allergens, irritants, and respiratory tract infections. 

Clinical manifestations are highly variable, ranging from infrequent and mild symptoms that have minimal functional limitations, to frequent acute asthma exacerbations causing significant impairment in functional capacity, and even life-threatening respiratory failure that’s often referred to as status asthmaticus.

Now, if you suspect asthma, you should first perform an ABCDE assessment to determine whether your patient is stable or unstable. If they’re unstable, stabilize their airway, breathing and circulation, obtain IV access, and begin continuous vital sign monitoring including heart rate and blood pressure. 

Next, obtain focused history and physical, order labs, including ABG, and perform spirometry to assess the patient’s peak expiratory flow, or PEF, for short. Finally, don’t forget to place your patient on pulse oximetry. History typically reveals shortness of breath, cough, and chest tightness. On the flip side, physical exam is likely to show tachypnea and use of accessory inspiratory muscles. In addition, auscultation can reveal bilateral wheezing due to inflamed and narrowed airways, and if the condition worsens, you may find decreased or even absent breath sounds, since less air is reaching alveoli. 

Next ABG might reveal arterial pH of 7.35 or less and pCO2 above 45 mmHg, indicating respiratory acidosis and hypercapnia; while spirometry usually shows PEF less than 40%. Finally, pulse oximetry might demonstrate saturation below 90%.

If this is the case, suspect acute asthma exacerbation, or even sta]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atelectasis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5uhr4FyOSvGEhXcP6kKy-3CQRoesOdbc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atelectasis: Clinical sciences]]></video:title><video:description><![CDATA[Atelectasis is a condition that results in the reversible partial or complete collapse of a lobe of the lung or the entire lung. Based on the cause, atelectasis can be divided into obstructive and non-obstructive atelectasis. The obstructive type occurs when there is a blockage of an airway, possibly due to a mass like intrathoracic tumors, aspirated foreign bodies, or mucous plugs. On the other hand, non-obstructive atelectasis can be caused by compression or the loss of surfactant.

Alright, when you encounter a patient who presents with signs and symptoms of atelectasis, you should first perform an ABCDE assessment to determine if the patient is stable or unstable. Now, if the patient is unstable, first stabilize their airway, breathing, and circulation. This means that you may need to intubate the patient, establish IV access, and administer IV fluids before continuing with your assessment. 

Once these important steps are done, obtain a focused history and physical exam. History might reveal recent major cardiac, thoracic, or abdominal surgery where general anesthesia was used. The patient may also report a cough with or without sputum production, dyspnea, and chest pain. 

On physical examination, you might notice altered mental status, tachypnea, and hypoxemia, as well as cyanosis if hypoxemia is severe. Additionally, the exam might reveal decreased chest expansion, decreased or absent breath sounds, or crackles on auscultation. With these symptoms suspect respiratory failure due to atelectasis.

After examining your patient, you should order an ABG and a chest X-ray. Now, ABG typically reveals a normal or low partial pressure of carbon dioxide. Sometimes, ABG may show respiratory alkalosis ​​if the patient is taking rapid, shallow breaths. When it comes to imaging, the X-ray might reveal increased opacification; narrowing of intercostal spaces; shifting of hilar or cardiomediastinal structures toward the affected side and elevation of the diaphragm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiac_tamponade:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t1K6f7UiSBSzCbr6QOFPVd78S_y1i15l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cardiac tamponade: Clinical sciences]]></video:title><video:description><![CDATA[Cardiac tamponade is a life-threatening condition characterized by excessive fluid accumulation in the pericardial sac. The excess fluid exerts pressure on the heart and decreases the filling of the cardiac chambers, eventually reducing cardiac output. Patients with cardiac tamponade are typically hemodynamically unstable and may quickly develop cardiovascular collapse and cardiac arrest, so they require prompt recognition and treatment with emergent drainage of the pericardial fluid to restore cardiac output. 

Cardiac tamponade can occur due to bleeding, which is also known as hemopericardium, which typically occurs as result of chest trauma, aortic dissection, left ventricular free wall rupture, or iatrogenic as a result of medical intervention. Cardiac tamponade can also occur due to effusive-constrictive pericarditis, often as a result of infection, uremia, or malignancy.

Now, if an individual presents with signs or symptoms of cardiac tamponade, you should first perform an ABCDE assessment. These individuals are typically unstable, so immediately stabilize their airway, breathing and circulation. Next, obtain IV access, put your patient on continuous cardiac and vital sign monitoring, and provide supplemental oxygen if needed.

Now, here’s a clinical pearl to keep in mind! Cardiac tamponade is associated with decreased cardiac filling that can result in obstructive shock. So, be careful with the administration of IV fluids, since an excess of fluid could increase cardiac preload. In the setting of cardiac tamponade, where the cardiac filling is already impaired, an increase in the preload can potentially precipitate cardiovascular collapse. Similarly, mechanical ventilation can increase intrathoracic pressure, causing further impairment to venous return and cardiac output. Therefore, it’s best to avoid or delay it whenever possible.

Next, you should obtain a focused history and physical exam. History usually includes chest pain and shortness of bre]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_obstructive_pulmonary_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QydCqMZBQQuycfOzLRi76qD5QhOWq3mD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic obstructive pulmonary disease: Clinical sciences]]></video:title><video:description><![CDATA[Chronic Obstructive Pulmonary Disease, or COPD, refers to a heterogeneous, usually progressive lung condition that results in airflow obstruction and breathing difficulties, often due to long-term exposure to irritants, such as tobacco smoke. Over time, COPD can lead to irreversible lung damage, making breathing difficult and limiting everyday activities, such as physical exercise.  

Some patients with COPD may first show up with chronic breathing difficulties and no prior history of COPD, while others might come in with COPD flare-ups, which are also known as COPD exacerbations. 

Now, if your patient presents with signs and symptoms suggestive of COPD, you should perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry.  

Most of the time, these individuals will present with severe respiratory distress that requires supplemental oxygen or even mechanical ventilation. 

Now, here’s a clinical pearl to keep in mind. When treating individuals with severe respiratory distress, always be on the lookout for signs of life-threatening respiratory failure. These include altered mental status, the use of accessory respiratory muscles, and a respiratory rate greater than 24 breaths per minute.  

It’s also important to recognize abnormal arterial blood gas analysis results that suggest impaired alveolar gas exchange, such as acidosis, hypercarbia, and hypoxemia. 

Now, let’s go back to the ABCDE assessment and take a look at stable individuals. Start by obtaining a focused history and physical exam as well as pulse oximetry. 

First, let&amp;#39;s focus on individuals with no previous diagnosis of COPD who are reporting persistent and slowly progressive shortness of breath, which worsens with exercise.  

In this case, history typically reveals]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congestive_heart_failure:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3FD4xARCS12jTVz27t7xxEnjRM2c0WAj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congestive heart failure: Clinical sciences]]></video:title><video:description><![CDATA[Congestive heart failure, CHF, or the newer term, advanced heart failure, is a condition that occurs when the heart cannot pump or fill properly, leading to fluid accumulation in the lungs and other body tissues. It is a leading cause of morbidity and mortality worldwide. Based on the side of the heart that is affected, CHF can be classified as right-sided or left-sided heart failure.

Alright, the first thing to do when assessing a patient with signs and symptoms suggestive of CHF is to perform an ABCDE assessment to determine if they are stable or unstable. If the patient is unstable, stabilize their airway, breathing, and circulation, which might require intubation. Additionally, obtain IV access, administer supplemental oxygen, and put your patient on continuous vital sign monitoring.

OK, now that you’re done with acute management, obtain a focused history and physical exam, and order imaging, like Chest X-ray. History typically reveals fatigue, shortness of breath, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. On the flip side, a physical exam commonly reveals conversational dyspnea, rales, S3 heart sound, bilateral lower extremity edema, and jugular venous distention. Finally, a chest X-ray might show an enlarged cardiac silhouette and evidence of pulmonary congestion, such as a “batwing” or “butterfly” appearance from alveolar edema and Kerley B lines from interstitial edema.

Now, these findings should make you think of acute decompensated heart failure with pulmonary edema, so order B-type natriuretic peptide, or BNP for short; ECG; and a transthoracic echocardiogram, or TTE. BNP greater than 400; ECG findings associated with arrhythmias or ischemia, as well as TTE findings of ventricular dysfunction and valve abnormalities support the diagnosis of acute decompensated heart failure with pulmonary edema.

Alright, let’s switch gears to treatment. First, treat the underlying cause whenever possible. For example, cardioversion fo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lung_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xINgrF58QZS9XMzsVa7hU8GmS6KqT7BM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lung cancer: Clinical sciences]]></video:title><video:description><![CDATA[Lung cancer, or bronchogenic carcinoma, is defined as a tumor originating in the lung parenchyma or within the bronchi. It typically arises from lung epithelial gene mutations due to long-term exposure to cancer-causing agents, mainly tobacco use, but also exposure to asbestos or radon. Based on histopathological findings, lung cancer is classified into two main groups, small cell lung cancer or SCLC, and non-small cell lung cancer or NSCLC, which includes adenocarcinoma, squamous cell carcinoma, large cell carcinoma, and bronchial carcinoid tumor.  

If a patient presents with a chief concern suggesting lung cancer, first, you should perform an ABCDE assessment to determine whether the patient is unstable or stable. If the patient is unstable, such as from severe respiratory distress or hypotension, then you must first stabilize the patient&amp;#39;s airway, breathing, and circulation. Provide supplemental oxygen to maintain oxygen saturation above 90%. In severe cases, you may even need to intubate the patient. Next, establish intravenous access for fluids and medications. Finally, don’t forget to put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry. 

Alright, now let’s go back to the ABCDE assessment and discuss stable patients.  

First, obtain a focused history and physical examination; order labs like a CBC and CMP, and finally, order imaging, primarily a chest X-ray and chest CT scan.  

Here’s a clinical pearl! Yearly lung cancer screening with CT scan is recommended for individuals who are 50 to 80 years of age who either currently smoke or have quit smoking within the past 15 years; AND have at least a 20 pack-year smoking history. 

History typically reveals cough, shortness of breath, pleuritic chest pain, as well as unintentional weight loss, and fatigue. If the lung cancer invades surrounding blood vessels, the patient could report hemoptysis, or coughing up blood. Some patients]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Opioid_intoxication_and_overdose:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DR2WqiP8QJyt6sIm0Uhoa3HmRvSKPIDS/_.png</video:thumbnail_loc><video:title><![CDATA[Opioid intoxication and overdose: Clinical sciences]]></video:title><video:description><![CDATA[Opioid intoxication and overdose are terms used to describe the physiological and psychological changes that result from an excessive dose of opioids. Now, opioids include heroin and powerful pain relievers like morphine, fentanyl, and oxycodone. Opioids can be taken through multiple routes, including ingestion, inhalation, intravenous injection, as well as by transdermal patch.  

Once in the body, they bind to major opioid receptors, which are found in organs such as the brain, heart, blood vessels, and gastrointestinal tract, causing effects such as euphoria or dysphoria; miosis, or constricted pupils; bradycardia and hypotension; and decreased bowel motility leading to constipation. Sometimes, opioid use can result in opioid overdose, which can lead to severe respiratory depression, significant sedation, coma, and even death.  

Now, if you suspect opioid intoxication or overdose, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. Often, you might need to intubate, since unstable patients typically present with respiratory depression or apnea and require mechanical ventilation. Next, provide supplemental oxygen, obtain IV access, and, if needed, administer fluids for volume resuscitation. Finally, don’t forget to put your patient on continuous vital sign monitoring, such as heart rate, blood pressure, and oxygen saturation. 

Next, obtain a focused history and physical examination, as well as point-of-care glucose at bedside. The history and physical are critical in these patients, so, if your patient is comatose or intubated, you should gather information from witnesses, friends, family members, or emergency personnel!  

History might reveal opioid use or a previous diagnosis of substance use disorder. On the other hand, the physical exam typically shows signs of respiratory depression, such as severely decreased respiratory rate, apne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pleural_effusion:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CXxJkioKRaqa7-ZePPyEcicmTSyUe8QW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pleural effusion: Clinical sciences]]></video:title><video:description><![CDATA[Pleural effusion refers to a fluid that accumulates between the parietal pleura and visceral pleura, known as the pleural space, and can be caused by conditions such as congestive heart failure, pneumonia, cancer, cirrhosis, and kidney disease, to name a few. 

Depending on the fluid characteristics and how it accumulates, pleural effusions are broadly classified as either transudates or exudates. Transudate occurs when too much fluid starts to leave the capillaries, either because of increased hydrostatic pressure or decreased oncotic pressure. On the other hand, exudate is typically associated with inflammation, which allows immune cells and large proteins to leak out of the capillaries. 

Based on the type of fluid and etiology, exudates can be further subdivided into parapneumonic effusions, malignant effusions, inflammatory effusions, and chylous effusions. 

Now, if you suspect a pleural effusion, first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and provide supplemental oxygen, if needed. Finally, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry. 

Alright, now let’s go back to the ABCDE assessment and take a look at stable individuals. If the patient is stable, you should start with acute management, like obtaining IV access, providing supplemental oxygen, and initiating continuous vital sign monitoring. Next, you should perform a focused history and physical, and order labs, including a CBC.

Individuals with pleural effusion typically report cough, shortness of breath, and pleuritic chest pain, which is typically described as a severe, sharp pain that worsens with breathing. Some patients may also report a fever. 

On the flip side, physical exam findings usually include dullness to chest percussion, as well as decreased tactile fremitus and absent basilar breath ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cirrhosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TEUcbyunRLS5VxaBPvljEDZjT9i06vrM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cirrhosis: Clinical sciences]]></video:title><video:description><![CDATA[Cirrhosis refers to chronic progressive fibrotic changes of the liver parenchyma that occur in response to chronic injury and inflammation. A variety of conditions can cause this injury, including viral hepatitis, chronic alcohol use, autoimmune disease, and hereditary conditions like hemochromatosis or alpha-1 antitrypsin deficiency, and the ensuing fibrotic changes eventually impair liver function. 

Early in the disease process, cirrhotic patients remain relatively asymptomatic and are considered to have compensated cirrhosis, while those who present with symptoms are considered to have decompensated cirrhosis. Complications due to cirrhosis include spontaneous bacterial peritonitis, ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome, which can be life-threatening, therefore it’s important to quickly identify these patients who may suddenly decompensate.

Now, if you suspect cirrhosis, first perform an ABCDE assessment to determine if your patient is unstable. Keep in mind that cirrhosis is never unstable unless it&amp;#39;s decompensated and the patient develops complications. If this is the case, you may need to secure the airway, breathing, and circulation, which might require intubating the patient, and starting mechanical ventilation. Next, obtain IV access and, if your patient is hypotensive, start IV fluids for volume resuscitation. If there are signs of blood loss, they might even need a transfusion of blood products, such as packed red blood cells, platelets, and even fresh frozen plasma. You should also continuously monitor vital signs. 

Additionally, if you suspect decompensated cirrhosis complications, it’s important to identify the underlying cause and complication. To do so, start by performing a focused history and physical examination, and depending on the suspected complication, you may want to order labs or ultrasound.

Alright, if your patient presents with abdominal distension and a palpable fluid wav]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_lower_limb_edema:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b_1NCpI_S7aoDImW-5fLu8jjR9KOUc4D/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to lower limb edema: Clinical sciences]]></video:title><video:description><![CDATA[Edema is an abnormal accumulation of interstitial fluid in the tissues. This occurs due to an imbalance between the hydrostatic and oncotic forces at the level of the capillaries. The lower limbs are especially prone to the development of edema because of gravity. 

Based on location and symmetry, lower limb edema can be classified as unilateral and bilateral. Unilateral lower limb edema is usually caused by a pathological process in the limb itself, such as DVT or compartment syndrome, while bilateral lower limb edema is usually due to systemic causes like heart, liver, and kidney failure. A more severe type of edema is anasarca, where the whole body develops generalized edema, and can be caused by things like malnutrition, as well as cirrhosis, nephrotic syndrome, or even burns.

When approaching a patient with lower limb edema, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If your patient is unstable, you should first stabilize their airway, breathing, and circulation before trying to identify the cause. This means that you might need to intubate the patient and establish IV access before continuing with your assessment.

On the other hand, if the patient is stable, the next step is to obtain a focused history and physical examination. Your history should explore if one or both lower limbs are affected, time span over which edema developed, associated symptoms such as pain or shortness of breath, known acute or chronic medical conditions, and a list of medications. Your physical exam should focus on describing the characteristics of the edema, like location, symmetry, and whether it’s pitting or non-pitting, as well as other features like skin discoloration and the quality of the pulse in the affected limbs. 

First, let’s start with conditions that cause unilateral edema. Unilateral edema generally affects a single limb and can be acute, that is developing over a period of 72 hours or less, or it might]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_kidney_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8jui_jtlQjmXQKP_gC6UHBf5RRCTIBHJ/_.png</video:thumbnail_loc><video:title><![CDATA[Chronic kidney disease: Clinical sciences]]></video:title><video:description><![CDATA[Chronic Kidney Disease, or CKD, refers to an impairment in renal function that persists for 3 or more months. This functional impairment occurs most commonly when comorbid conditions, like hypertension or diabetes mellitus, cause progressive sclerosis of the nephrons. Most commonly, CKD is classified by underlying cause, the degree of albuminuria, and the estimated glomerular filtration rate, or eGFR for short, which can help determine appropriate treatment and assess prognosis.

Now, if you suspect CKD, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. 

If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and provide supplemental oxygen to maintain adequate oxygenation. Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and if necessary, obtain dialysis access as well. 

Here’s a clinical pearl to keep in mind! Patients with CKD that present as unstable will often have end-stage renal disease and may have missed scheduled dialysis. In that case, they might present with hyperkalemia, metabolic acidosis, fluid overload, as well as uremia. Moreover, in uremia, your patient might develop uremic frost, which occurs when serum BUN is elevated to the extent that urea seeps through the skin in the sweat and crystallizes, giving a frosty appearance. Additionally, they might have pericardial friction rub, which suggests the development of uremic pericarditis; or they may develop confusion and asterixis, indicating uremic encephalopathy. Finally, keep in mind that after initial stabilization, these patients will require urgent dialysis as a definitive treatment.

Okay, now let’s go back to the ABCDE assessment and discuss stable patients. 

In stable individuals, you should first obtain a focused history and physical examination, and order labs, including CMP. History often reveals nonspecific symptoms,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Deep_vein_thrombosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D2yqneJKTpmh3WqEeEyUXElgQouTTW4X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Deep vein thrombosis: Clinical sciences]]></video:title><video:description><![CDATA[Deep vein thrombosis, or DVT, is a blood clot that develops in the deep veins, most commonly of the lower limbs. Less commonly, DVT can form in the deep veins of the arms or mesenteric veins of the bowel. 

The pathogenesis of DVT centers around the Virchow triad, which includes venous stasis, hypercoagulability, and endothelial injury. 

If untreated, the thrombus can lead to limb ischemia, hemodynamic instability, pulmonary embolism, and even death. 

Now, if your patient presents with signs and symptoms suggestive of DVT, first you should perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and start continuous vital sign monitoring, including pulse oximetry, blood pressure, and heart rate. If needed, provide supplemental oxygen to maintain the oxygen saturation above 92%.

Alright, now let’s go back to the ABCDE assessment and discuss how to manage stable individuals. First, obtain a focused history and physical examination. History usually reveals pain, swelling, and warmth in the affected limb as well as DVT risk factors, 

such as age above 65, recent surgery, prolonged immobilization, and active cancer, as well as smoking and obesity. 

Also keep in mind that estrogen increases the risk of venous thrombosis, so pregnancy and the use of oral contraceptives are also important risk factors. 

Finally, a family history of DVT can indicate a familial inheritance of genetic conditions predisposing to DVT, such as Factor V Leiden mutation.

On the other hand, the physical examination usually reveals edema, erythema, warmth, and tenderness of the affected area. 

In some individuals, you might even be able to palpate the thrombotic vein.  

Another important test is to see if you can elicit the Homan sign. 

To do this, lift the affected leg and slightly bend it in the knee. Next, abruptly and firmly perform dorsiflexion of the pa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hematochezia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i8c4pIKZShyfhuEoq_xV4QBKRne85B_s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hematochezia: Clinical sciences]]></video:title><video:description><![CDATA[Hematochezia refers to the passage of bright red blood or blood clots from the rectum. It is seen in patients with acute lower gastrointestinal bleeding that originates from a site distal to the Ligament of Treitz. Hematochezia might also occur in massive upper gastrointestinal bleeds. 

When bleeding comes from the right side of the colon patients usually pass dark or maroon-colored stool while those with bleeding from the left side pass bright red blood or stool.

The first thing to do when assessing a patient with hematochezia is the ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, begin acute management by stabilizing the airway, breathing, and circulation. Next, obtain IV access and initiate IV fluids for immediate resuscitation. If your patient is actively hemorrhaging, you may need to transfuse your patient with blood products as well. Finally, start continuous vital sign monitoring, including pulse oximetry, blood pressure, and heart rate.

Once acute management is initiated, the next step is to obtain a focused history and physical exam, and order labs, such as blood type and crossmatch, CBC to monitor hemoglobin and hematocrit, coagulation studies, and CMP. Your patient may present with massive hemorrhage or have brisk bleeding. You should be on the lookout for signs of hemodynamic instability including hypotension and tachycardia. At times, the bleeding may cease, but you should always monitor for rapid rebleeding. Initial labs may show low hemoglobin and a normal blood urea nitrogen-to-creatinine ratio for a lower gi bleed. However, if the ratio is elevated, consider upper gastrointestinal bleeding.

Alright, now that history, physical, and labs are obtained, let’s move on to nasogastric lavage. Nasogastric lavage is performed by placing a nasogastric tube and instilling water or normal saline into the stomach. The liquid is then aspirated. If blood returns you have confirmed an upper gastroi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anal_fissure:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qw5fIkX_Rr6E7cTl-a67r_kNTrKV3uPG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anal fissure: Clinical sciences]]></video:title><video:description><![CDATA[Anal fissures are longitudinal tears in the anal mucosa under the dentate line. Since this region is innervated by somatic nerves, anal fissures are often quite painful. Now, there are two types of anal fissures: typical or primary fissures, caused by local trauma, and atypical or secondary fissures, which are associated with some other condition, such as Crohn disease. 

Alright, the first step when approaching a patient with signs and symptoms suggestive of an anal fissure is to obtain a focused history and physical examination.

Patients with typical, or primary, anal fissures usually report severe anal pain that might be present at rest, but worsens during defecation and may persist for several hours. Additionally, they might report anal bleeding or hematochezia. History might reveal local trauma, such as constipation and passing large, hard stools. 

On physical exam, typical anal fissures usually present as superficial lacerations located in the posterior midline. Less commonly, they can be seen in the anterior midline, or in both the anterior and posterior midline.

Similarly, individuals with atypical or secondary anal fissures usually report anal bleeding and pain that’s present at rest but worsens during defecation. History typically reveals chronic, multiple, recurring, and non-healing fissures. On physical examination, you may see multiple wide, deep fissures that are healing poorly. 

In contrast to typical fissures, atypical fissures are found in locations other than the midline, often the lateral region. Additionally, a patient might have perianal skin tags, which are remnants from previous bouts of inflammation. In some cases, perianal skin tags can become edematous and painful.

Alright, now that you’ve obtained a history and physical examination, let’s move on to the management of typical anal fissure. Individuals with typical anal fissures are initially treated with supportive care, which includes stool softeners, sitz baths, and a fiber]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colorectal_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QDuKox70RUaIBjtyLXFDtB4IRxuw7QGE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colorectal cancer: Clinical sciences]]></video:title><video:description><![CDATA[Colorectal cancer most commonly refers to adenocarcinoma, and it’s usually located in the colon, but it can be found in the rectum as well. The presentation of colorectal cancer is not always clear, so early detection depends on screening. Staging is based on the TNM classification, meaning that tumor size, lymph node invasion, and the presence of metastasis are taken into account when making a treatment plan. 

When assessing a patient with signs and symptoms suggestive of colorectal cancer, you should first perform an ABCDE assessment to determine if your patient is stable or unstable. If the patient is unstable, start acute management and stabilize the airway, breathing, and circulation. Next, obtain IV access and initiate IV fluids for resuscitation. Finally, be sure to monitor their vital signs, including pulse oximetry, blood pressure, and heart rate.

Once these important steps are done, you should determine what caused their instability. Tumors located on the descending colon are generally infiltrating masses, meaning they tend to be ring-shaped and involve the whole circumference of the colonic wall. This causes luminal narrowing, referred to as napkin-ring constriction, or apple core lesions because of their appearance on imaging. What&amp;#39;s important is that these lesions can lead to an obstruction, which can result in bowel necrosis and perforation. 

These patients typically have a history of abdominal pain, nausea, and vomiting; and will also have changes in bowel habits, as well as small caliber or narrow stools described as pencil-thin. On a physical exam, you might find abdominal distention, and signs of peritonitis like rebound pain and guarding. Finally, labs might show leukocytosis. Based on these findings, you should suspect obstruction or perforation caused by the tumor. 

Okay, now that we have a diagnosis in mind let’s talk about confirming your suspicion. Your next step is to order an upright abdominal x-ray. You might se]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemorrhoids:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V_cfvQCAR_WbUCxBtgmfdEbqRSi6vGBM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemorrhoids: Clinical sciences]]></video:title><video:description><![CDATA[Hemorrhoids are a type of varicose veins in the anorectum that form when there is a persistently elevated venous pressure in the hemorrhoidal plexus.  Based on the location to the dentate line, hemorrhoids can be classified as external, which are located distal to the dentate line; internal, which are located proximal to it; and combined, which are found on both sides of the dentate line. 

Alright, the first step when approaching a patient with signs and symptoms suggestive of hemorrhoidal disease is to obtain a focused history and physical examination. Patients with external hemorrhoids typically present with a history of palpable external lump, anal pruritis, and perianal pain, usually without bleeding. In some individuals, they can become thrombosed and cause excruciating pain. Next, on examination of the anal verge and perianal area, uncomplicated external hemorrhoids may appear as tender, soft, swollen, red lumps. Additionally, patients may have non tender skin tags from previous episodes of inflammation and thrombosis. On the other hand,  an acutely thrombosed external hemorrhoid will be firm and extremely tender to palpation and may have a purplish hue. 

On the flip side, individuals with internal hemorrhoids typically present with painless bleeding with defecation, anal pruritis, and a prolapse. The prolapse might spontaneously reduce, require manual reduction, or even be unreducible, which is also known as incarceration. Now, incarceration can slow blood flow in the veins, leading to thrombosis. It can also cut off blood flow completely causing ischemia, and this is known as strangulation. Both of these complications can cause excruciating pain. On a digital rectal exam, internal hemorrhoids are generally not visible or palpable; however, they might be palpable if thrombosed, strangulated, or prolapsed. Finally, some individuals might have combined internal and external hemorrhoids and present with symptoms and signs of both types.

Alright, aft]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_melena_and_hematemesis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rsdh4GkCRXqvfZAYorRsB5MRQnePqdVo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to melena and hematemesis: Clinical sciences]]></video:title><video:description><![CDATA[Melena, or stool containing partly broken down blood, and hematemesis, or vomit containing blood, are most commonly seen in patients who present with acute upper gastrointestinal bleeding, which is typically defined as the gastrointestinal portion that’s proximal to the ligament of Treitz. It’s important to keep in mind that melena may sometimes be caused by slow bleeds from the lower gastrointestinal tract. Melena presents as black or tarry stools and can be seen in variable amounts of blood loss. 

On the other hand, hematemesis can present as frank, bright red bloody emesis suggesting a recent or ongoing bleed that might be moderate to severe; or coffee-ground emesis, which suggests that the bleeding is limited or the blood is older. The presentation of emesis can help you start localizing the bleed, since coffee-ground emesis usually develops when blood comes in contact with gastric acid, such as a peptic ulcer; while bright red blood can indicate either a brisk bleed or that the blood didn’t come in contact with gastric acid, such as an epistaxis draining posteriorly, oropharyngeal or esophageal bleeds.

When assessing a patient with melena or hematemesis, you should first perform an ABCDE assessment to determine whether your patient is unstable or stable. If the patient is unstable, first stabilize the airway, breathing, and circulation. You might need to intubate the patient to protect the airway. Next, obtain IV access and start IV fluids. Additionally, patients who are acutely hemorrhaging might require blood product transfusions. Finally, put your patient on continuous vital sign monitoring, including pulse oximetry, blood pressure, and heart rate.

Once these important steps are done, you can move on to obtaining a focused history and physical exam, as well as labs like CBC and CMP. History might reveal massive hemorrhage, or lesser but brisk bleeding. On the flip side, the physical exam might show signs of hemodynamic instab]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastroesophageal_varices:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/26ODIUtbQ7Gunj-9GGS2T700QumRWYet/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastroesophageal varices: Clinical sciences]]></video:title><video:description><![CDATA[Gastroesophageal varices are abnormally enlarged veins in the distal esophagus and stomach. They arise when the veins that connect the portal circulation with the systemic circulation become dilated due to portal hypertension. 

Now, when scar tissue in the liver or portal vein thrombosis cause portal vein hypertension, the blood starts flowing through smaller veins, like the ones in the distal esophagus or stomach, which are not designed to carry large volumes of blood. This can result in complications such as bleeding, which is considered an emergency. Depending on the cause, varices can result from cirrhotic or non-cirrhotic portal hypertension. 

When assessing a patient with signs and symptoms suspective of gastroesophageal varices, you should first perform an ABCDE assessment to determine whether your patient is stable or unstable. Now, if the patient is unstable, first initiate acute management to stabilize the airway, breathing, and circulation. This means that you might need to provide supplemental oxygen, or sometimes intubate the patient to protect the airway, establish IV access, and possibly perform gastric lavage to remove bloody stomach content. Additionally, give fluid resuscitation to prevent death from hemorrhagic shock; if the patient doesn&amp;#39;t stabilize with IV fluids, they may need an uncrossmatched blood transfusion. 

Once these important steps are done, obtain a focused history and physical exam, as well as labs like CBC to assess the severity of blood loss, and PT, PTT, and INR to check for a possible coagulopathy that might have contributed to bleeding, which is common in patients with liver disease. In addition, order blood typing and crossmatch in case the patient needs a blood transfusion. History usually reveals hematemesis, melena, or sometimes hematochezia. The patient might also report lightheadedness. When it comes to the physical exam, you might notice that the patient is vomiting large amounts of bright red blood ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stress_ulcers:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EXS28dozQquWz4m8hqCqU7mjTpWDMqH4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stress ulcers: Clinical sciences]]></video:title><video:description><![CDATA[Stress ulcers are erosions or ulcerations in the upper GI tract caused by the effects of stressors such as hypovolemia, shock, sepsis, and trauma, as well as excessive stimulation of parietal cells by gastrin. They are also known as stress-induced gastropathy, stress-induced gastritis, or stress-related mucosal damage. 

Stress ulcers usually develop in the stomach fundus and body within hours of major trauma or serious illness; or in the distal antrum and duodenum after several days in the hospital. Stress ulcers are more common in patients admitted to the ICU since they are more likely to experience stressors that injure the mucosal barrier. Based on their appearance, stress ulcers can be shallow or deep.

When assessing an ICU patient with signs and symptoms suggestive of stress ulcers, you should first determine if your patient is unstable or stable by doing an ABCDE assessment. If the patient is unstable, start acute management to stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient to establish or maintain the airway, provide supplemental oxygen, obtain IV access, administer fluids and electrolytes, and sometimes place a nasogastric tube for gastric lavage, or even transfuse blood products before continuing with your assessment. 

After you complete the acute management, obtain a focused history and physical, and order labs like CBC, and coagulation studies such as PT, PTT, and INR. The history might reveal hematemesis, as well as the presence of frank blood or coffee-ground emesis in the nasogastric aspirate. Additionally, some patients might have melena. On physical exam, you might find signs of hemodynamic instability like tachycardia and hypotension, as well as signs of bleeding like blood on rectal exam. 

When it comes to labs, they usually reveal signs of severe bleeding like low hemoglobin and hematocrit levels, or levels that have decreased since admission; as well as signs of coagulopathy ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_nosocomial_infections:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/joiulVZbRnyY7vlRvskQV4yuT8WVxmnJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to nosocomial infections: Clinical sciences]]></video:title><video:description><![CDATA[Nosocomial infections, also called healthcare-associated infections, or HAIs for short, are infections that patients acquire while receiving medical care for another condition. Anyone who is hospitalized, lives in long-term care, or receives care at an outpatient facility, such as a dialysis unit or rehabilitation center, can develop a nosocomial infection. 

Nosocomial infections are most commonly caused by multidrug-resistant bacteria, such as Methicillin-Resistant Staphylococcus Aureus or MRSA, Vancomycin-Resistant Enterococcus or VRE, and Carbapenem-Resistant Enterobacteriaceae or CRE. Less common causes include viruses and fungi. 

The most common nosocomial infections include catheter-associated urinary tract infections or CAUTI; central line-associated bloodstream infections or CLABSI; surgical site infections or SSI; hospital-acquired pneumonia or HAP; ventilator-associated pneumonia or VAP; and Clostridioides Difficile infection or CDI. 

If your patient presents with signs and symptoms suggestive of nosocomial infection, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, first stabilize the airway, breathing, and circulation, and start broad-spectrum antibiotics, before continuing with further workup. 

Now, let’s go back to the ABCDE assessment and take a look at stable patients. In this case, obtain a focused history and physical examination, and order labs including a complete blood count with a differential. History typically reveals current or recent treatment at an inpatient or outpatient healthcare facility, as well as systemic symptoms of infection, such as fever, chills, and fatigue. 

On exam, the patient might present with altered mental status, like confusion or lethargy, but also localized findings depending on the type of infection. Additionally, labs typically show leukocytosis. Alright, now if these features are present, you should suspect nosocomial inf]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Catheter-associated_urinary_tract_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3-lWV0nmTh6zdE34kvUXtHi-TrOWr2fo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Catheter-associated urinary tract infection: Clinical sciences]]></video:title><video:description><![CDATA[Catheter-associated urinary tract infection, or CAUTI for short, is a urinary tract infection in the presence of an indwelling urinary catheter or after the recent removal of the catheter, typically in the last 48 hours. So to decrease the chances of patients developing CAUTIs, you should try to avoid urinary catheters if possible, or remove them as soon as they are no longer needed. When they arise, CAUTIs are most commonly caused by Escherichia coli and Klebsiella pneumoniae, which can colonize the catheter and use it to gain access to the urinary tract. 

Now, CAUTIs can be symptomatic or asymptomatic. Symptomatic UTI, or SUTI, is the more commonly diagnosed type because the patient will have symptoms. On the other hand, asymptomatic UTIs are often discovered incidentally when blood and urine cultures are ordered during the workup for other conditions like sepsis. Asymptomatic bacteriuria, or ASB, is when pathogens are found in the urine but not the blood. Asymptomatic bacteremic urinary tract infection, or ABUTI, is when the pathogen is found in both the urine and blood.

Now, if you suspect CAUTI, first, you should obtain a focused history and physical examination, and order labs, such as CBC, CMP, and urinalysis. Based on the findings, we can either suspect ABUTI or CAUTI. 

First, let’s take a look at a patient who might have an ASB or catheter-associated ABUTI. The patient might have a history of a current or recently removed indwelling catheter, and although they have no history of UTI symptoms and no findings on physical exam, their labs reveal pyuria and bacteriuria, meaning that their urine cultures are positive. 

These findings are often consistent with ASB. However, if blood and urine cultures were ordered as workup of another condition, such as fever or sepsis, and both come back positive for the same pathogen, meaning that they match, this is catheter-associated ABUTI. In that case, you should start antibiotics, and if indicated, remove or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Central_line-associated_bloodstream_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hwsow3MNTO6lWhFWDhQluwRlQ46-2e45/_.jpg</video:thumbnail_loc><video:title><![CDATA[Central line-associated bloodstream infection: Clinical sciences]]></video:title><video:description><![CDATA[Central line-associated bloodstream infection, or CLABSI for short, is a primary bloodstream infection that develops at least 48 hours after central line placement when no other source of infection is identified. CLABSI also refers to a primary blood infection that occurs on the day of central line removal or the day after. Now, the most common causes of CLABSI include bacteria, such as coagulase-negative staphylococci, Staphylococcus aureus, and enterococci. Less commonly, CLABSI can be caused by fungi, such as Candida. These pathogens can colonize the central line and use its extraluminal or intraluminal surface to reach the bloodstream. 

Extraluminal migration is usually specific for organisms that represent a part of normal skin microflora, while intraluminal migration is associated with contamination of the central line, typically from the hands of health care providers. CLABSI can be defined as complicated when the patient has CLABSI with septic shock, septic thrombophlebitis, or metastatic infection; while uncomplicated is CLABSI without these associated complications.

Now, if you suspect CLABSI, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient. Next, obtain IV access, and, if your patient is hypotensive, start IV fluids for volume resuscitation. 

Once you are done with the acute management, obtain a focused history and physical examination, and order labs, including CBC and lactate. History typically reveals a central line that’s been in place for more than 2 days, and symptoms such as fever, chills, and fatigue. But, keep in mind that CLABSI can also occur once the central line is removed. In this case, the patient might report symptoms on the day of, or the day after, the catheter removal. Physical exam findings might reveal hypotension and altered mental statu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Clostridioides_difficile_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BvDDF9wpTNGoziGFVWZCYSHdSdGMduYg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Clostridioides difficile infection: Clinical sciences]]></video:title><video:description><![CDATA[Clostridioides difficile infection, or CDI, is an infection caused by the organism Clostridioides difficile, or C. difficile for short. Infection typically occurs through the fecal-oral route, by ingestion of spores found on contaminated surfaces, in soil, in water, or even on unwashed hands. Once the spores reach the intestines, the GI flora, or microbiota, protects the gut and doesn’t allow C. difficile to proliferate. But, if the diversity of GI flora is disrupted, often by recent antibiotic use, as well as proton pump inhibitors, or hospitalization, C. difficile can overgrow and infect the colon. 

As a result, it starts producing toxins A and B, which can damage the gastrointestinal mucosa and eventually cause an inflammatory condition called pseudomembranous colitis. The presentation can range from non-severe disease to severe or even fulminant infection.

Now, if you suspect CDI, the first thing you should do is an ABCDE assessment, to determine if your patient is unstable or stable. 

If the patient is unstable, stabilize the airway, breathing, and circulation, which typically requires obtaining IV access, resuscitating with IV fluids, and intubating the patient if you need to secure the airway. Once you stabilize the patient, obtain a focused history and physical examination, and order labs, including CBC, CMP, and lactic acid. 

History typically reveals watery diarrhea, usually more than 3 loose stools in 24 hours, which might be associated with mucus or blood, while some may present with ileus. Additionally, individuals may report lower abdominal pain, fever, lethargy, and confusion, as well as recent or current antibiotic use. 
Physical examination might reveal abdominal distention and tenderness, decreased bowel sounds, and hypotension. Some individuals can present with altered mental status or even shock. Finally, lab results may show an elevated WBC count, serum creatinine, and lactic acid. 

Now here’s a high-yield fact! If you suspect CDI]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_endocarditis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dBIAULNBR26TBGmG7lOVemrzRKSXdcYt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious endocarditis: Clinical sciences]]></video:title><video:description><![CDATA[Infective endocarditis, or IE for short, refers to the inflammation of the endocardium due to a pathogenic infection. As microorganisms spread through the blood, they can attach to the intracardiac surface, forming vegetations on the endocardium, most commonly on the heart valves. Vegetations can also form on the septa, mural endocardium, and even implantable electronic devices. To diagnose infective endocarditis, you need to identify the Modified Duke Criteria using blood cultures, echocardiogram, and history and physical exam findings. 

Now, here’s a high-yield fact to remember! There are several common pathogens involved in infective endocarditis. For example, the viridans group streptococci are most commonly associated with native valve infective endocarditis. Staphylococci are most commonly associated with intravenous substance use or patients with health care contact; they tend to affect the right sided heart valves, like the tricuspid valve. Next up is enterococcal endocarditis, which can be seen in both community- and hospital-acquired infective endocarditis.

You should also be aware of a group of gram-negative organisms commonly found in the human oropharynx known as the HACEK organisms, which include the species Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella. Finally, if you have a patient with recent cardiac valve surgery, prolonged use of an indwelling vascular catheter, or immunodeficiency, you should keep in mind fungal causes, like Aspergillus and Candida species. This is especially applicable if your patient is on empiric antibiotics and worsening. 

Now, if you have a patient presenting with signs and symptoms of infective endocarditis, first, you should perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, start IV fluids, and begin continuous vital sign monitoring including blood pres]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pressure-induced_skin_and_soft_tissue_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HkxsjU-YQASfKQ9XqcMMyNHcRR_NYO33/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pressure-induced skin and soft tissue injury: Clinical sciences]]></video:title><video:description><![CDATA[Pressure-induced skin and soft tissue injury, sometimes called pressure ulcer, or bed sores, refers to damage to the skin and underlying soft tissues caused by prolonged pressure. Pressure injuries most commonly develop over bony prominences, such as the sacrum, greater trochanter, lateral and medial malleoli, calcaneus, scapula, and occiput. Pressure decreases blood flow to the affected skin and soft tissues, leading to hypoxia, ischemia, and necrosis. Based on the depth of the tissue involved, pressure injuries can be subdivided into four main stages. In stage one, there’s intact skin with non-blanchable erythema; in stage two, there’s partial thickness loss of dermis; while in stage three, there’s a full thickness skin loss. Finally, stage four is associated with full thickness skin loss and exposure of underlying muscles, tendons, or even bones.

The first step in evaluating a patient with signs and symptoms of pressure injury is to obtain a focused history and physical examination. Patients often have a history of risk factors such as immobility, like using a wheelchair or being bed bound, in fact they can start developing pressure injuries after just 2 hours of immobility! Other risk factors include malnutrition; neurological diseases like stroke and neuropathy; diabetes; or perfusion disorders, like heart failure and peripheral vascular disease. Additionally, they typically have pain in the affected area, but keep in mind that individuals with sensory neuropathy, diabetes, or altered mental status may not report pain. 

Now, during the physical examination, you’ll need to assess the wound bed and depth, which are the most important factors as they determine the grade of the injury. The wound bed is the base of the wound, while the depth is how deep the wound bed is from the skin surface. While examining the wound, don’t forget to note the type and quality of tissue seen at the wound bed. You may find exudate, or a wet, fibrinous biofilm caused by ce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Surgical_site_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wF3ZKOXGReeZGFZU5t7xaSiqQKGlMcNZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Surgical site infection: Clinical sciences]]></video:title><video:description><![CDATA[Surgical site infection, or SSI for short, is a common postoperative complication. This is most commonly caused by gram-positive bacteria living on the skin, but can also be caused by other pathogens such as anaerobic gut bacteria encountered during bowel surgery. Depending on the depth of infection, SSI is subdivided into three types. Superficial incisional SSI is the least invasive type that’s limited to the skin and subcutaneous tissue; deep incisional SSI affects deeper tissues like muscle and fascia layers; and organ space SSI, which is deep within the organ or body cavity where the surgery occurred. 

The first step in approaching someone suspected to have SSI is to obtain a focused history and physical examination. The person’s history is especially important. Most cases of SSI develop between 4 and 30 days after surgery, but this does not include necrotizing infections like Group A strep or Clostridia, which would present within 48 hours and progress rapidly.  Individuals with SSI may report pain or tenderness at the surgical site. Importantly, the person’s surgical history will provide details to help determine their risk of infection. 

Next, you can use surgical wound classification to identify those at risk for SSI. Surgical wound classification is based on the degree of contamination and includes four main categories: Clean, Clean-contaminated, Contaminated, and Dirty. The likelihood of SSI increases drastically across these groups. Classification depends on infectious risk factors, such as location, trauma history, or breaks in sterile technique. For example, wounds in colonized areas like the mouth or urinary tract are at a much higher risk for developing SSI, as are open traumatic wounds.

Some high yield facts to keep in mind!  One major consideration when evaluating SSI is any history of surgical implant, such as joint replacement surgery or mesh hernia repair. Implants are a big risk factor for SSI, since bacteria can cling to the foreig]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_mellitus_(Type_2):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hEMKrFhEQ5Ow2RA5pAQ9mFwIS_yw0fj6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes mellitus (Type 2): Clinical sciences]]></video:title><video:description><![CDATA[Diabetes mellitus is a condition where glucose can’t be properly moved from the blood into the cells. Now, there are two types of diabetes mellitus, type 1 and type 2, and the main difference between them is the underlying mechanism. Type 2 diabetes mellitus is most commonly seen in patients with obesity, when peripheral tissue becomes resistant to insulin, which is also known as insulin resistance. 

Since tissues don’t respond as well to normal insulin levels, beta cells in the pancreas ramp up their insulin production. In order to have the same effect on peripheral tissue and therefore move glucose out of the blood, and into tissue cells. Over time, beta cells become dysfunctional and can no longer secrete sufficient insulin, which eventually results in impaired insulin secretion and high blood glucose levels. This can cause clinical manifestations ranging from prediabetes, diabetes mellitus, to severe life-threatening conditions, like hyperosmolar hyperglycemic state or HHS and diabetic ketoacidosis or DKA.

Now, if you suspect type 2 diabetes mellitus, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient. Next, obtain IV access and, if your patient is hypotensive, start IV fluids for volume resuscitation. Finally, put your patient on continuous vital sign monitoring, such as pulse oximetry, blood pressure, and heart rate.  

Next, you want to know if your unstable patient with type 2 diabetes has HHS or, less frequently, DKA. Obtain a focused history and physical exam, and order labs, such as random blood glucose, serum osmolality, BMP, urinalysis, hemoglobin A1c, as well as ABG or VBG. Your patient might be too obtunded or confused to speak, so be sure to review the chart thoroughly and speak with caretakers to get an accurate history. Some patients have a known history o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dyslipidemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TaQ0lKk4QH_Ch_5dkkitqsgNQXeHYWd1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dyslipidemia: Clinical sciences]]></video:title><video:description><![CDATA[Dyslipidemia, or high lipid levels in the blood, is a condition associated with an increased risk of atherosclerotic cardiovascular disease, or ASCVD for short, which includes myocardial infarction, stroke, and peripheral arterial disease. Because of this, the management of individuals with dyslipidemia is usually more aggressive if your patient has a history of ASCVD. 

Dyslipidemia is usually asymptomatic, but can be found on labs like a lipid panel. Next, consider whether they have severe dyslipidemia or diabetes.  If they do not have any of these conditions, management is based on their 10 year risk of developing ASCVD.   

The first step when evaluating a patient for dyslipidemia is performing a focused history and physical, and sending labs for a lipid panel. The history will help identify risk factors for ASCVD, like smoking, diabetes, or hypertension. ASCVD is also more common as you get older, and there’s an increased risk in biological males and people with previously diagnosed ASCVD. 

Now, the physical exam is usually unremarkable in patients with dyslipidemia. They may have elevated blood pressure, and if the cholesterol level is very high, you might see xanthomas, which are cholesterol deposits in the skin, classically around the eyes. 

Next, let’s discuss the lipid panel, which is the best screening test for dyslipidemia. It includes the total cholesterol, or TC for short, high-density lipoprotein cholesterol, or HDL, low-density lipoprotein cholesterol, or LDL-C, and triglycerides, or TG. The LDL-C value is important for determining which patients need medications for dyslipidemia. You’ll also use TC and HDL values to help predict the 10-year ASCVD risk, which impacts treatment decisions for dyslipidemia.

Alright, now that you have the history and lipid panel results, let’s move on to management. Treatment for dyslipidemia varies based on whether the patient has ASCVD. Patients with ASCVD and dyslipidemia should be started on a high-inten]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Essential_hypertension:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OOdDGiIiSm63_wDD99W9Yk_kT_aDpDXR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Essential hypertension: Clinical sciences]]></video:title><video:description><![CDATA[Essential hypertension is a chronic condition that occurs when an individual’s blood pressure is persistently elevated, without an identifiable cause. It’s a significant contributor to the development of atherosclerotic cardiovascular disease, or ASCVD. Diagnosis also includes assessing for the presence of other ASCVD risk factors; ruling out secondary causes with screening history, physical and labs; and classifying your patient’s blood pressure readings into one of the three groups: Elevated Blood Pressure, formerly known as pre-hypertension, with a systolic blood pressure between 120 and 129 and diastolic blood pressure less than 80 mmHg; Stage 1 hypertension with a systolic blood pressure between 130 and 139 or diastolic blood pressure between 80 to 89 mmHg; or Stage 2 hypertension with a systolic blood pressure greater than or equal to 140 or diastolic blood pressure greater than or equal to 90 mmHg. 

Now, if you suspect essential hypertension, perform an ABCDE assessment to determine if the patient is stable or unstable. If unstable, stabilize their airway, breathing, and circulation. Additionally, obtain IV access, provide supplemental oxygen, and put them on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry.  

Next, proceed with a focused history and physical examination and obtain CMP, troponin, and urinalysis. Also, don&amp;#39;t forget to order an ECG and chest X-ray. Together, these will help you identify target organ damage.  

Now, your patient might report vision changes, headache, shortness of breath, chest pain, or back pain. Their physical exam may reveal a systolic blood pressure of 180 or a diastolic blood pressure of 120 or greater. Additionally, the exam might reveal altered mental status, respiratory crackles, or decreased peripheral pulses.  

As for labs, you may see an elevated creatinine on CMP, an elevated troponin, and proteinuria on the urinalysis. The ECG might show ST segment change]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obesity_and_metabolic_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sUEsqcHBR42Hg-kNqOG315nXQ06uuD99/_.png</video:thumbnail_loc><video:title><![CDATA[Obesity and metabolic syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Obesity is a condition characterized by excessive fat accumulation in the body, and is strongly associated with the development of other conditions, such as type 2 diabetes mellitus, dyslipidemia, cardiovascular disease, and even malignancy. Multiple factors contribute to the development of obesity, including genetics, western diet, sedentary lifestyle, inadequate sleep, and certain medication side effects. 

Body fat, also known as adipose tissue, secretes adipokines, which can lead to widespread systemic inflammation and insulin resistance. Based on the body mass index, or BMI for short, individuals with obesity can be categorized into 4 main groups that include overweight, class I obesity, class II obesity, and class III obesity.

Now, if you suspect obesity, first you should obtain a focused history and physical. History may reveal symptoms like joint pain, snoring, fatigue, and dyspnea, as well as mood symptoms, such as depression. Additionally, the patient might present with obesity-related comorbidities, such as metabolic syndrome, diabetes mellitus, hypertension, and dyslipidemia. On the other hand, physical exam will reveal excess adipose tissue and larger waist circumference, and some patients may also have abdominal striae, acanthosis nigricans, and lower extremity edema.

Okay, the next step is to calculate the BMI using the patient’s weight in kilograms and height in meters. If the BMI is 25 to 29.9, the patient is overweight; if the BMI is between 30 and 34.9, the patient falls under class I obesity; between 35 and 39.9 is class II obesity; and finally, a BMI greater than or equal to 40 is class III obesity. 

Here’s a clinical pearl for you! Though the diagnosis of obesity hinges on BMI, keep in mind that it&amp;#39;s an imperfect individual measure. In fact, certain racial and ethnic groups, such as those with ancestry from some parts of Asia, may experience complications of obesity at lower BMIs, while others with higher BMIs but low adip]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tobacco_use:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/spLAhI2TQK2GeMqY8oLQX-PiTWSjeAXT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tobacco use: Clinical sciences]]></video:title><video:description><![CDATA[Tobacco use disorder, or TUD for short, is a condition that develops after continued tobacco use, and it’s associated with nicotine dependence. These individuals have an increased risk of developing conditions like COPD, atherosclerosis, myocardial infarction, and sudden cardiac death. Now, based on the status of tobacco use, you can classify your patients into three main groups, including patients who never used tobacco, those who currently use tobacco, and former tobacco users.   

Now, if a patient presents with a chief concern suggesting tobacco use disorder, your first step is to obtain a focused history and physical. Your patient will typically report a history of tobacco use, or they might report exposure to secondhand smoke. On physical exam, you will typically see signs, such as nicotine-stained fingertips or stained dentition.

At this point, you should suspect tobacco use disorder and assess the patient’s status of tobacco use. If your patient has never used tobacco, no further workup is needed, and your management should focus on prevention. This includes encouraging the patient to continue to abstain from smoking, and offering guidance on avoiding secondhand tobacco exposure. 

On the other hand, if your patient is currently using tobacco, assess the DSM-V criteria for tobacco use disorder. To diagnose tobacco use disorder, your patient must present with at least two of the following criteria over 12 months. 

First, your patient is consuming large amounts of tobacco over long periods. They have a persistent desire or effort to quit or cut down tobacco use. They are spending a considerable amount of time obtaining or using tobacco, and they have cravings and a strong desire to use tobacco. 

Additionally, their tobacco use interferes with their daily responsibilities, but also with their social and occupational activities. Next, the patient continues to use tobacco despite it causing problems. They use tobacco in risky situations and cont]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Appendicitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lw2u8ZKbSCiNW9hboBiWHuMrSlKDVKLz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Appendicitis: Clinical sciences]]></video:title><video:description><![CDATA[Appendicitis refers to inflammation of the appendix, which is usually caused by obstruction of the appendiceal lumen by tumors, fecaliths, or hard fecal masses, and lymphoid hyperplasia. When the appendix is obstructed, the pressure inside it increases. This causes local stasis of lymphatic flow, occlusion of small vessels, and bacterial overgrowth, which can eventually lead to ischemia and necrosis of the appendix. 

Now, appendicitis can be classified as uncomplicated or complicated. In uncomplicated appendicitis, the appendix is only inflamed; while in complicated appendicitis, it may develop perforation, phlegmon, or abscess.

If you suspect appendicitis the first thing you should do is an ABCDE assessment, to determine if your patient is unstable or stable. If the patient is unstable, which usually results from sepsis, you should first stabilize their airway, breathing, and circulation. This means that you may need to intubate the patient, establish IV access, or administer fluids before continuing with your assessment. 

However, if your patient is stable, your next step is to obtain a focused history and physical examination, as well as labs such as a CBC and CRP. Now, history typically reveals abdominal pain, which starts around the umbilicus and migrates to the right lower quadrant. Additionally, the patient might report fever, nausea, vomiting, and anorexia. 

On physical examination, individuals usually present with tenderness in the affected area, most commonly the right lower quadrant, especially at a region called McBurney point, located one-third of the distance from the anterior superior iliac spine to the umbilicus. Some additional physical exam findings that can help you recognize appendicitis include the Rovsing, psoas, and obturator signs. 

A Rovsing sign is positive when you palpate your patient’s left lower quadrant and your patient feels pain in the right lower quadrant. This indicates peritoneal irritation of the right side of the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_jaundice_(conjugated_hyperbilirubinemia):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jYFbS1OWTQ6vQMnKrmOP4-p5SBm4tqsJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to jaundice (conjugated hyperbilirubinemia): Clinical sciences]]></video:title><video:description><![CDATA[Jaundice is yellow discoloration of the skin and mucous membranes caused by high levels of bilirubin in the serum, called hyperbilirubinemia. 
More specifically, jaundice develops when total bilirubin exceeds 2 to 3 mg/dL. Bilirubin is produced as a result of red blood cell turn over. When heme is broken down, unconjugated or indirect bilirubin is released into the serum. It travels to the liver, where it is conjugated to glucuronic acid, and then the conjugated or direct bilirubin is released into the biliary tract. Conditions that cause elevations in either conjugated or unconjugated bilirubin can result in jaundice. 

When approaching a patient with jaundice, first you should perform an ABCDE assessment to determine if your patient’s unstable or stable. 

If your patient is unstable, stabilize their airway, breathing, and circulation before trying to identify the cause. Additionally, obtain IV access and put your patient on continuous vital sign monitoring. 

Now, let’s go back to the ABCDE assessment and take a look at stable individuals. 

In these patients, you should obtain a focused history and physical examination, and check labs, including CBC, AST, ALT, alkaline phosphatase or ALP, INR, and total and fractionated bilirubin. Fractionated bilirubin will distinguish between conjugated and unconjugated bilirubin and allow you to determine whether a conjugated or unconjugated hyperbilirubinemia is present. 

If elevation in conjugated bilirubin predominates, then the patient has a conjugated hyperbilirubinemia.

Conjugated hyperbilirubinemia can be the result of direct hepatocellular injury, which might occur in viral and alcohol-induced hepatitis; or from blockage of the biliary tract, also called cholestasis, which might occur in choledocholithiasis. 

Now, to determine which process is taking place, assess the liver transaminase and alkaline phosphatase levels. 

If AST and ALT elevations predominate, we call it a hepatocellular pattern. Many cond]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_jaundice_(unconjugated_hyperbilirubinemia):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/imxymQ1qQuCZGYbMjDoRMbjPTBS6B74r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to jaundice (unconjugated hyperbilirubinemia): Clinical sciences]]></video:title><video:description><![CDATA[Jaundice is yellow discoloration of the skin and mucous membranes caused by high levels of bilirubin in the serum, called hyperbilirubinemia. 

More specifically, jaundice develops when total bilirubin exceeds 2 to 3 mg/dL. Bilirubin is produced as a result of red blood cell turn over. When heme is broken down, unconjugated or indirect bilirubin is released into the serum. It travels to the liver, where it is conjugated to glucuronic acid, and then the conjugated or direct bilirubin is released into the biliary tract. Conditions that cause elevations in either conjugated or unconjugated bilirubin can result in jaundice. 

When approaching a patient with jaundice, first you should perform an ABCDE assessment to determine if your patient’s unstable or stable. 

If your patient is unstable, stabilize their airway, breathing, and circulation before trying to identify the cause. Additionally, obtain IV access and put your patient on continuous vital sign monitoring. 

Now, let’s go back to the ABCDE assessment and take a look at stable individuals. 

In these patients, you should obtain a focused history and physical examination, and check labs, including CBC, AST, ALT, alkaline phosphatase or ALP, INR, and total and fractionated bilirubin. Fractionated bilirubin will distinguish between conjugated and unconjugated bilirubin and allow you to determine whether a conjugated or unconjugated hyperbilirubinemia is present. 

If elevation in unconjugated bilirubin predominates, then the patient has unconjugated hyperbilirubinemia. 

Unconjugated hyperbilirubinemia can be the result of excessive erythrocyte destruction, or hemolysis, decreased uptake of bilirubin by the liver; or problems with bilirubin conjugation by the liver.

Now to determine, which process is taking place, order some additional lab tests to assess for hemolysis, like CBC, haptoglobin, LDH and reticulocyte count. 

If laboratory results show normocytic anemia and low haptoglobin, with high LD]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pancreatic_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eWfeGQuUQMCwP8202uCanjBuTUuftK5K/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pancreatic cancer: Clinical sciences]]></video:title><video:description><![CDATA[Pancreatic cancer is most commonly adenocarcinoma, though there are some other rare types such as neuroendocrine or lymphoma. Pancreatic adenocarcinomas are exocrine tumors and are most often located in the head of the pancreas. Unfortunately, pancreatic cancer has an insidious onset, making it difficult to detect. Staging is based on tumor size, invasion of lymph nodes or nearby structures like major blood vessels, and presence or absence of distant spread and metastasis. Staging ultimately determines if the tumor is resectable or not.

The first step in evaluating a patient with signs and symptoms suggestive of pancreatic cancer is to obtain a focused history and physical examination. Now, the tumor might grow large enough to compress or invade the biliary tree and cause biliary obstruction and cholangitis. Because of this, you should be on the lookout for any red flags, which are actually signs of biliary obstruction and cholangitis. These include fever, severe jaundice with pruritus, altered mental status, and signs of sepsis such as tachycardia and hypotension. If any of these signs are present, you must first stabilize the patient. This means that you might need to secure the airway, provide supplemental oxygen, establish IV access, and consider starting broad-spectrum IV antibiotics. 

In addition, order an ultrasound to rule out gallstones, as well as a CT scan to evaluate the site and cause of biliary obstruction. Next, because the mortality rate associated with biliary obstruction is high, you’ll have to relieve the obstruction before proceeding with further diagnostic workup. To do this, you should order an emergent ERCP with stenting to actually diagnose the obstruction and treat it immediately. However, if the patient can’t undergo ERCP with stenting, place a percutaneous cholecystostomy tube instead. 

Now, let’s switch gears and talk about patients without red flags. Because most pancreatic cancers are insidious, patients usually present wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_postoperative_fever:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vqp6dPSrSyauH4t2LefXxUgEQyCBQuEj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a postoperative fever: Clinical sciences]]></video:title><video:description><![CDATA[Postoperative fever is defined as a systemic body temperature at or above 38 degrees Celsius or 100.4 degrees Fahrenheit within the postoperative period. Causes of postoperative fever include drug or transfusion reaction, infection, and derangements of the normal healing process. Based on the time of onset, postoperative fever is divided into 4 phases: immediate, acute, subacute, and delayed. 

Now, the first step in evaluating a patient with postoperative fever is to perform an ABCDE assessment to determine if the patient is stable or unstable. For unstable patients, you must secure the airway, provide supplemental oxygen, establish IV access, start IV fluids if tachycardia and hypotension are present, monitor their vitals, and examine the surgical site. 

When it comes to stable patients, the first step is to obtain a history and physical examination, and labs like CBC. In history, you should find out the type of operation performed, date of the operation, and the time of fever onset. CBC is used to establish a baseline and help monitor the response to treatment. 

Let&amp;#39;s begin with the immediate postoperative period or fever that presents within 24 hours of the operation. While the most common cause of fever during this time is physiologic, it can also be caused by life-threatening causes like an acute transfusion reaction or adverse drug reaction. 

First up, physiologic fever frequently occurs after operations that involve high levels of tissue trauma, like burns or multi-trauma exploratory laparotomy. Often, fevers are transient and self-limited, but you should still order a CBC, chest x-ray, and urinalysis to rule out other causes. Because surgery induces a systemic inflammatory response, the patients may have a physiologic fever with mild leukocytosis. 

Next, let&amp;#39;s move on to dangerous causes of fever in the immediate postoperative period. You should suspect an acute transfusion or drug reaction if the patient has a personal or fa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_postoperative_acute_kidney_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S0f4j61qTyKWOOOzhRVBYL3SSV6mMQo0/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to postoperative acute kidney injury: Clinical sciences]]></video:title><video:description><![CDATA[Postoperative acute kidney injury, or AKI, is defined as a decrease in kidney function within 7 days after surgery. It is relatively common, as fluid shifts occur in the preoperative disease state, during surgery, and in the postoperative recovery period. 

The most common cause of postoperative AKI is inadequate fluid resuscitation. Similar to nonsurgical AKI, postoperative AKI is divided into three types: prerenal, intrinsic renal, and postrenal. Prerenal AKI occurs when there is a decrease in blood flow to the kidneys; while intrinsic renal AKI is caused by direct damage to the renal parenchyma; and postrenal AKI often reflects an obstruction of urinary outflow.  

Your first step in evaluating a patient presenting with signs and symptoms suggestive of postoperative AKI is to assess their ABCDE. Now, if the patient is unstable, start with acute management like ensuring adequate airway, providing supplemental oxygen, and obtaining IV access right away. Remember that AKI in an unstable patient can be a consequence of postoperative shock which would require immediate management.

Alright, now that the acute management for unstable patients has been started, let’s talk about stable patients. If the patient is stable, the next step is to obtain a focused history and physical exam. One of the first things you’ll notice is decreased urine output or oliguria. However, keep in mind that postoperative AKI can be asymptomatic and often presents with abnormal lab values, so keep an eye on serum creatinine during the postoperative observation. If you notice that it increased by 0.3 milligrams per deciliter or 1.5 times a patient’s baseline, that’s indicative of postoperative AKI. 

It is also important to identify all underlying risk factors in addition to the type of operation performed, any significant intraoperative events, and on what postoperative day the AKI developed. Remember to ask the anesthesiologist for the intraoperative intake and output to d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_postoperative_hypotension:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N0mKX2JyQG20rDgETboGrRtPRKyTba0o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to postoperative hypotension: Clinical sciences]]></video:title><video:description><![CDATA[Postoperative hypotension is one of the most common complications in the immediate period after any operation and is associated with an increased risk of morbidity and mortality. The most common causes of postoperative hypotension are general anesthesia and inadequate fluid resuscitation. Other causes include life-threatening conditions like respiratory failure, hemorrhage, and cardiovascular events.

When assessing a patient with postoperative hypotension, your first step is to perform an ABCDE assessment to determine if the patient is unstable or stable. Remember that all hypotensive patients are considered unstable so your priority is to stabilize their hemodynamic status as quickly as possible. To do this, initiate acute management like stabilizing the airway, providing supplemental oxygen, establishing IV access, continuously monitoring vitals, and consider starting IV fluid resuscitation and vasopressors right away. 

After that, obtain a focused history and physical exam. Be sure to get the information about the type of operation performed; when it was performed; the type of anesthesia and medications used; as well as preoperative disease and physiologic state of the patient; and allergies. 

Following the ABCDE, first assess for respiratory distress. In particular, you’ll want to look for causes of respiratory distress like tension pneumothorax, pulmonary embolism, or anaphylaxis. These conditions may lead to a decrease in left ventricular filling, which can in turn reduce the cardiac output, ultimately resulting in hypotension. 

Now, the patient might have a history of underlying lung disease, sustained thoracic trauma, a thoracic procedure, or prolonged ventilatory support, as well as a complication of central line placement. Additionally, the physical exam might reveal absent lung sounds, jugular venous distension with or without tracheal deviation in addition to tachypnea, hypoxia, tachycardia, and altered mental status. With these findings, y]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Delirium:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KIPZ-JkCQZWC0rLxT9ni8bf3TpOItXxM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Delirium: Clinical sciences]]></video:title><video:description><![CDATA[Delirium is a transient and reversible condition characterized by an acute change in consciousness and cognition, as well as a decreased ability to maintain or shift attention. 

Delirium is usually seen in older patients, and is always associated with some underlying condition or trigger. The mnemonic “PINCH ME” can help you remember the most common causes of delirium, which include Pain, INfection, Constipation and urinary retention, Hydration, Medications and substances, and finally, Environmental triggers. 

Now, if a patient presents with signs and symptoms suggestive of delirium, you should first perform an ABCDE assessment to determine if they are unstable or stable.

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, and, if needed, provide supplemental oxygen to maintain saturation above 90%. Finally, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and oxygen saturation.

Now let&amp;#39;s go back to the ABCDE assessment and discuss stable patients. 

First, perform a focused history and physical. Most often, patients are over 65 years old, and might have a history of neurologic conditions like dementia or Parkinson disease. They may present with acute hallucinations, while family members or caregivers often report that the patient has been exhibiting unusual behavior. 

Physical examination might reveal hyperactive delirium, with signs like agitation, restlessness, and combativeness. 

However, some patients might present with hypoactive delirium, with signs like drowsiness, apathy, withdrawal, or diminished speech. 

Finally, some patients can have mixed delirium, switching between hyperactive and hypoactive signs throughout the day. 

No matter what type of delirium your patient has, keep in mind that these findings must represent an acute change from baseline, with a fluctuating course described as waxing and waning. If that’s the case, you should suspect d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malignant_hyperthermia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gtK1dTsfSNOY2FkSzglSMMhiRamb6oSY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malignant hyperthermia: Clinical sciences]]></video:title><video:description><![CDATA[Malignant hyperthermia is a serious anesthetic complication that must be emergently recognized and treated. It can develop in susceptible individuals who have a genetic mutation in their dihydropyridine or ryanodine receptors, which normally regulate skeletal muscle contraction by controlling calcium release from the sarcoplasmic reticulum. When these individuals are exposed to a volatile anesthetic like isoflurane or sevoflurane, or less commonly, to the neuromuscular blocking agent succinylcholine, there is an unregulated calcium release in the muscle cells. As a result, intracellular calcium overload causes sustained muscle contraction and breakdown, leading to a hypermetabolic state called malignant hyperthermia.

Alright, malignant hyperthermia typically develops while a patient is getting anesthesia, or less commonly within one hour of stopping the anesthetic. The first step in approaching someone suspected to have malignant hyperthermia is to assess their ventilatory status and vitals. To assess the ventilatory status, check the respiratory rate and see if it matches the ventilator settings. Next, look for hypercarbia, which is the most common presenting sign of malignant hyperthermia. Hypercarbia is an unexplained increase in exhaled CO2 caused by widespread muscle contraction and hypermetabolism despite adequate ventilation. Additionally, be sure to rule out other causes of hypercarbia, such as hypoventilation, rebreathing, or gas absorption during laparoscopy. Finally, check the vital signs for tachypnea, tachycardia, and hyperthermia, which might occur later in the course of malignant hyperthermia.

After checking the vitals, you should obtain a brief physical examination. A physical exam might show signs of hyperthermia, such as warmth and sweating. Individuals might also exhibit generalized muscle rigidity due to widespread skeletal muscle contraction. Less often, this rigidity is confined to the masseter muscles, leading to jaw tightness and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication-induced_constipation:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KPbeMIXwTnyW_SyC0t8R90x7RGmXpRPO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication-induced constipation: Clinical sciences]]></video:title><video:description><![CDATA[Medication-induced constipation refers to a decreased stooling frequency or difficulty passing stool due to medication side effects, most commonly opioids.

Opioids are medications that can bind mu receptors in the central nervous system, and provide analgesic effects, but they can also affect the gastrointestinal tract, eventually decreasing gastrointestinal motility. In severe cases, this can result in constipation.

Other important non-opioid medications that may cause constipation include anticholinergics, antidepressants, antispasmodics, and calcium channel blockers.

DMT_1 Now, if a patient presents with signs and symptoms suggestive of medication-induced constipation, you should first perform a focused history and physical examination.

Your patient might report decreased stooling, such as two or fewer bowel movements per week; as well as difficulty passing stools; firm stool consistency; or a sense of incomplete stool evacuation after defecation.

Additionally, history might reveal the use of medications like opioids, or non-opioid medications like anticholinergics, antidepressants, antispasmodics, or calcium channel blockers.

On physical examination, you’ll typically find mild to moderate abdominal distension, while rectal exam may reveal fecal impaction, hemorrhoids, anal fissures, or even rectal prolapse. Based on these findings, you should suspect medication-induced constipation.

Now here’s a clinical pearl to keep in mind! Whenever a patient presents with signs and symptoms of constipation, you’ll first need to rule out medical causes, like dehydration or hypothyroidism. Look for red-flag symptoms, like a history of unintentional weight loss or blood in the stool, as well as physical exam findings like significant abdominal distension or tenderness.

If any of these are present, evaluate for other causes of constipation, such as colon cancer or bowel obstruction.

DMT_ 2 Now, once you suspect medication-induced constipation, review your pati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_shock:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t1XI1vyNRgKY3_ZVdRqhuVpVQueSPstW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to shock: Clinical sciences]]></video:title><video:description><![CDATA[Shock is a life-threatening condition that occurs when inadequate tissue perfusion and oxygen delivery leads to end organ damage and potentially death. 

Now, the four types of shock include distributive, hypovolemic, cardiogenic, and obstructive. Distributive shock occurs in the setting of excessive systemic vasodilation, leading to impaired blood flow distribution. Next up, hypovolemic shock occurs due to a critical loss of fluid volume. Cardiogenic shock results from a compromise of myocardial performance, leading to a severely decreased cardiac output. Finally, obstructive shock results from obstruction of blood flow from either filling the heart or ejecting into the great vessels, which also ultimately leads to a decreased cardiac output. 

Now, patients presenting with signs and symptoms of shock will be unstable, so immediately perform an ABCDE assessment and begin acute management.  Start by stabilizing their airway, breathing, and circulation.  This means that you might need to intubate the patient. Next, obtain IV access, and consider giving IV fluids, as well as placing a central venous catheter for administration of medications and hemodynamic monitoring. 

Additionally, you can insert an arterial catheter for continuous monitoring of the mean arterial pressure, or MAP. Occasionally, you may also place a pulmonary artery catheter, or PAC, to measure certain hemodynamic parameters. Finally, put the patient on continuous vital sign monitoring, including heart rate, pulse oximetry, and blood pressure. 

Ok, now that you’ve initiated acute management, it’s important to obtain a focused history and physical, as well as order lab tests. Patients may describe generalized weakness, fatigue, lethargy, and postural dizziness. 

Physical exam typically reveals hypotension and weak peripheral pulses, as well as tachycardia, and possibly altered mental status. At this point you can suspect shock, so your next step is to assess the patient’s skin temperature]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_organ_dysfunction_syndrome_(MODS):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Usm-AwTVTwGbQCgbCtD8ZbtYQYeqBjiH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple organ dysfunction syndrome (MODS): Clinical sciences]]></video:title><video:description><![CDATA[Multiple organ dysfunction syndrome or MODS is a life-threatening condition that occurs in the setting of shock. Now, a condition that precedes MODS is a systemic inflammatory response syndrome, or SIRS for short, which can be triggered by both infectious and non-infectious causes, including burns and trauma. 

Now, no matter what the initial trigger is, in SIRS, the immune system overproduces inflammatory cytokines and mediators, such as TNF-alpha, as well as IL-1, IL-6, and IL-8. This overproduction of inflammatory cytokines is often referred to as “cytokine storm”, and in combination with prolonged hypotension, it can lead to hypoperfusion of multiple organs, hypoxic damage, and progressive organ dysfunction. 

Now, if you suspect MODS, immediately perform an ABCDE assessment and begin acute management. 

Start by stabilizing their airway, breathing, and circulation, which means that you might need to intubate the patient. Next, obtain IV access, start IV fluids, and consider placing a central venous catheter for the administration of medications and hemodynamic monitoring. 

Additionally, you can insert an arterial catheter for continuous monitoring of the mean arterial pressure or MAP; or you may also place a pulmonary artery catheter or PAC to measure hemodynamic parameters and guide the administration of IV fluids and even vasopressors. Finally, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry. 

Now, once you stabilize the patient, perform a focused history and physical examination and obtain labs, including a CBC, CMP, lactate, ABG, as well as cardiac enzymes and BNP. 

Next, use physical exam findings and some of the lab values to perform the SIRS assessment, which is based on four main criteria. The first criterion is either leukopenia, defined as WBCs below 4,000, leukocytosis, defined as WBCs above 12,000, or bandemia, defined as bands greater than 10% bands. The second one is body ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sepsis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3m3JtSLFQWW1W7MCDkq5fpyRT7yNNtJL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sepsis: Clinical sciences]]></video:title><video:description><![CDATA[Sepsis is an exaggerated immune response to infection associated with organ dysfunction, shock, and death. The infection can be bacterial, viral, or fungal, and may originate from any tissue, initiating a complex interplay between infectious virulence factors and host defense mechanisms. The main goals of management are to identify and treat the infection while maintaining hemodynamic stability to prevent or minimize organ damage. Once you identify sepsis or septic shock, you should provide immediate supportive care and begin searching for the underlying source of infection. 

When you encounter a patient presenting with signs and symptoms of sepsis, first perform an assessment with a validated metric, such as the systemic inflammatory response syndrome, or SIRS criteria. There are numerous causes of SIRS like sepsis, dehydration, and adrenal insufficiency; so sepsis will cause SIRS, but SIRS is not always due to sepsis.  

To diagnose SIRS, at least two criteria must be met. These include WBCs either below 4,000, so leukopenia, or above 12,000, so leukocytosis; as well as a body temperature either below 36 degrees celsius, so hypothermia, or over 38 degrees celsius, so fever; heart rate above 90 beats per minute, so tachycardia; and respiratory rate over 20 breaths per minute, so tachypnea. Now, if the SIRS criteria are not met, you should consider an alternative diagnosis. On the other hand, the presence of known or suspected infection together with SIRS should raise suspicion for sepsis. In addition, if systolic blood pressure, or SBP, is below 90 mmHg or falls 40 mmHg below baseline, your patient has septic shock. 

While the SIRS criteria help you identify patients with sepsis, other metrics, such as the Sequential Organ Failure Assessment or SOFA score, may help identify those at greatest risk of poor outcomes. SOFA evaluates parameters including mental status, mean arterial pressure, or MAP, respiratory function, creatinine, bilirubin levels, a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypovolemic_shock:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/heTu_GLbTeCATHHnGzOw7AQZRPS9xgcv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypovolemic shock: Clinical sciences]]></video:title><video:description><![CDATA[Hypovolemic shock is a life-threatening condition associated with decreased intravascular volume, which in turn leads to decreased venous return to the heart, decreased cardiac output, and eventually shock. 

Now, hypovolemic shock can be defined as hemorrhagic or non-hemorrhagic. Hemorrhagic shock is associated with blood loss, which can be seen in traumatic conditions, such as a ruptured spleen; or non-traumatic conditions, like variceal bleeding. 

On the other hand, non-hemorrhagic shock is associated with fluid loss, most commonly from dehydration, like after prolonged vomiting or diarrhea, as well as severe widespread burns. 

Now, patients presenting with signs and symptoms of hypovolemic shock will generally present as unstable. Start by immediately performing an ABCDE assessment, then begin acute management. Stabilize their airway, breathing, and circulation. This means that you might need to intubate the patient. Next, obtain IV access with 2 large bore IVs and start IV fluids. Finally, put your patient on continuous vital sign monitoring, such as pulse oximetry, blood pressure, and heart rate.

Once you’ve stabilized the patient, obtain a focused history and physical examination. History often reveals the underlying cause or source of fluid or blood loss, as well as symptoms of organ hypoperfusion. For example, hypoperfusion of the brain can result in lethargy and confusion, while kidney hypoperfusion can lead to oliguria. 

Additionally, individuals might report postural dizziness. 

On the other hand, a physical exam primarily reveals signs of shock, such as hypotension, and tachycardia, as well as weak peripheral pulses and low jugular venous pressure. Additionally, patients can present with pale, clammy skin; decreased skin turgor; dry mucous membranes; and cold extremities.

If you suspect hypovolemic shock, the next step is to order labs, which can also help you determine the type of shock. These include CBC, lactate, and CMP, as well]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Burns:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1XjcX-fiRPatkakNxLidjYr_REO9QSIs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Burns: Clinical sciences]]></video:title><video:description><![CDATA[Burns are injuries caused by heat, cold, friction, radiation, electricity, or chemical exposure. When significant heat is applied to the skin, either in the form of a hot liquid, solid object, or flame, this thermal energy can result in irreversible tissue destruction. Extensive tissue destruction, especially in burns larger than 40% of the total body surface area, or TBSA; can cause fluid loss, and with it, hypovolemic shock! Burns are classified based on the depth of injury into first-, second-, third-, and fourth-degree burns, as well as burns accompanied by smoke inhalation.

When evaluating a patient with burns, your first step should be an ABCDE assessment to see if the patient is unstable or stable. If the patient is unstable, first stabilize their airway, breathing, and circulation. This means that you may need to intubate the patient, obtain IV access, and administer fluids before continuing with your assessment. 

Now let’s move on to the stable patients. If your patient is stable, start with a focused history and physical examination. History reveals thermal injury and can identify the mechanism of injury, such as hot liquids, flames, or grease. The physical exam will vary depending on the depth of the burn.

Some burns might be accompanied by smoke inhalation, so let’s talk about that. History might reveal delayed extrication from a fire in an enclosed space. On physical examination, your patient may have facial burns, singed facial hair, wheezing, or stridor. They may also cough up carbonaceous material, or soot. 

Once you suspect inhalation injury, you should obtain labs, including an ABG and carboxyhemoglobin level. Findings may include decreased paO2 and oxygen saturation. However, ABG might be completely normal initially. When it comes to carboxyhemoglobin, in non-smokers with inhalation injury it might increase over 3%; however, in smokers, those levels might be greater than 10%, since they are chronically exposed to carbon monoxide from]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Sickle_Cell_Anemia_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R2X7EoN8Q0SfspLWVNkN0iBtTqywqBom/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Sickle Cell Anemia in the Pediatric Patient]]></video:title><video:description><![CDATA[Nurse Maggie works in a pediatric hematology unit and is caring for Marcus, a 9-year-old with a history of sickle cell disease who was admitted for a vaso-occlusive crisis, or VOC. After settling Marcus in his room, Nurse Maggie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Marcus’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Maggie recognizes important cues, including Marcus’ vital signs which are temperature 99.0 F or 37.2 C, heart rate 104 beats per minute, respiratory rate 22 breaths per minute, blood pressure 122/72 mmHg, and oxygen saturation 97 percent on room air. She notices that Marcus’ hands and feet are edematous, and that he’s grimacing.  

Nurse Maggie: Marcus, you look uncomfortable. Can you rate your pain from zero to ten, zero being no pain and ten being the worst pain you’ve ever felt? 

Marcus: It’s about an eight in my hands and feet.  

Nurse Maggie: When did your pain start? 

Marcus: It started yesterday when I was playing in the snow, and it got worse this morning. 

Nurse Maggie then speaks with Marcus’ mother, who’s at the bedside. 

Nurse Maggie: Has Marcus taken any medications to help with the pain? 

Marcus’ mother: Not since we were in the emergency department a few hours ago.  

Nurse Maggie then analyzes these cues. She understands that VOC occurs when rigid, sickled red blood cells tangle together, adhere to blood vessel endothelium, and block vascular blood flow, causing inflammation, tissue ischemia, and necrosis, as well as pain and swelling in Marcus’ hands and feet. She understands that the cold temperature likely triggered the episode. Nurse Maggie recognizes that Marcus needs effective pain management. 

Now, using the information she&amp;#39;s gathered, Nurse Maggie develops a priority hypothesis of acute pain. Then, Nurse Maggie generates solutions to address Marc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Types_of_Infectious_Diseases_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Iw4ZNX3zSwafjCMZWLpQnWaCTD_OJORF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Types of Infectious Diseases in the Pediatric Patient]]></video:title><video:description><![CDATA[A communicable disease is an infection that spreads from person-to-person. These diseases can be transmitted through the air, respiratory droplets, or physical contact with a contaminated surface. Pediatric patients are more likely to contract communicable diseases because of their immature immune systems and lack of understanding of infection control.  

Now, some communicable diseases, like measles, influenza, rotavirus, and varicella have vaccines available to help prevent their spread; while other diseases, like scarlet fever and fifth disease, do not. Vaccines, along with infection control measures, like hand washing and personal protective equipment, or PPE, can help limit the spread of common communicable diseases.  

Okay, so, immunity can be acquired actively or passively. Active immunity happens when a person makes their own antibodies, like after recovering from a disease, like fifth disease, or is given a vaccination, like a flu shot for influenza. Now, vaccines use a weakened or inactivated version of a pathogen and the body’s natural defenses to strengthen the immune system against that pathogen. This can help prevent a disease, and may limit its spread, if a person encounters the pathogen in the future.  

On the other hand, passive immunity occurs when a person receives the antibodies needed to fight the disease, like when a fetus receives IgG antibodies through the placenta, or when a newborn exposed to the hepatitis B virus is given immune globulin.  

Alright, now along with vaccines, infection control measures also limit the spread of communicable diseases.  

Standard, or routine, precautions are broad protocols used to prevent infection when caring for all patients and involve hand hygiene by either washing with soap and water or alcohol-based disinfectants; and preventing contact with infectious agents using PPE, like gloves, gowns, masks, or face shields.  

On the other hand, transmission-based precautions are based on the specific]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Communication_and_Relational_Practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oPRj2c1LRPiJg0nWGh3AKEQ4QDCW4kGZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Communication and Relational Practice]]></video:title><video:description><![CDATA[Communication is the exchange of information, thoughts, and feelings between individuals, groups, or organizations. Nurses use effective communication to create a therapeutic patient-nurse relationship that supports a high level of patient care, encourages interprofessional collaboration, and promotes quality health outcomes. 

As a nurse, you can promote effective communication by using concepts of relational practice. This can involve skills like reaching out to your patients and listening to them to better understand their needs; being authentic in your communication by demonstrating respect for yourself and others; and creating a sense of mutuality by partnering with your patient to accomplish shared goals. 

Now, when your patient needs assistance with communication, you can use the five steps of the nursing process, assessment, diagnosis, planning, implementation, and evaluation, to guide your communication while providing care. 

Starting with assessment, you’ll gather data to determine all the contextual factors that can influence communication so you can understand your patient’s unique communication needs. During this step, you’ll assess the context in which the communication will occur between you and your patient. You can start by assessing physical and emotional factors, like visual or hearing impairments, as well as conditions like stroke, that can cause aphasia. Also be sure to look for emotional factors like anxiety, which can affect your patient’s ability to concentrate on what’s being said; or psychotic states which can cause distraction due to hallucinations.  

Also be sure to include developmental factors in your assessment so you can adapt your communication techniques to meet your patient’s unique age-related needs, like infants and young children.  

Next, you&amp;#39;ll establish a nursing diagnosis for your patient who needs assistance with communication, such as impaired verbal communication. You’ll also identify additional diag]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Social_Determinants_of_Health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z8eKvZF_THOsrq89u1laz7A7TO_yiORj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Social Determinants of Health]]></video:title><video:description><![CDATA[Social determinants of health, or SDOH for short, refers to the conditions where people live, work, play, worship, and age, that influence health.  

Now, there are five major categories of social determinants of health: Economic stability, neighborhood and built environment, education access and quality, social community and context and lastly, health care access and quality.  

First, there’s economic stability, which means that people have opportunities for employment and sufficient financial resources to afford basic needs like food, clothing, housing, and utilities. 

Then, there&amp;#39;s neighborhood and built environment, which includes characteristics like having access to a grocery store, availability of public transportation, the quality of housing, as well as factors like clean air and water and neighborhood crime rates.  Next, education access and quality addresses factors like the availability of early childhood education, high school graduation rates, and opportunities to enroll in college, as well as general literacy.  

Social community and context refers to the sense of community cohesion and connectiveness, like the interactions between family, friends, and coworkers and the degree of civic engagement.  Finally, health care access and quality includes the availability and coverage of health care services, the quality of care, and health literacy, which is the ability to locate, understand, and use health information to make well-informed decisions about health.  

Now, health equity means that every person has the opportunity to attain their full health potential, and that their socially determined situation does not place them at a disadvantage. However, health disparities can occur in socially disadvantaged populations, creating differences in the incidence and prevalence of disease, injury, and mortality. For example, individuals who have limited access to grocery stores with healthy foods are less likely to have proper nutrition, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_Illness</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EEgSmhwZT_iK4IDfFabapsk1QL_IOALG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic Illness]]></video:title><video:description><![CDATA[Illness refers to the personal experience of living with a biomedical disease that requires medical attention. Illness can be either acute, meaning the disease has a rapid onset and short duration, like influenza or gastroenteritis; or chronic, meaning the disease usually doesn’t resolve on its own, such as hypertension, diabetes mellitus, or asthma. Chronic illness can result in decreased physical functioning, productivity, and overall quality of life.  

Now, there are three levels of disease prevention: primary, secondary, and tertiary. Primary prevention looks at specific measures that can prevent a certain disease before it develops; and it includes health promotion efforts like encouraging healthy eating and exercise to prevent obesity, as well as protective measures like immunizations to prevent influenza, pneumonia, or COVID-19.  

Next, secondary prevention is aimed at preventing disability or death by screening patients to detect disease early, such as mammograms to test for breast cancer or colonoscopies to detect colon cancer; and it includes providing prompt treatment if a disease is detected.  

Then, tertiary prevention works to limit the impact of disease once a condition has already developed, such as cardiac rehabilitation for patients with heart disease or physical therapy for patients with spinal cord injuries. 

So, when caring for your patient with chronic disease, begin by assessing their current health status by performing a physical assessment, noting any indications of disease progression. Then, ask them if they’re having any difficulty performing activities of daily living, or ADLs; such as bathing, toileting, and eating; as well as instrumental activities of daily living, or IADLs, such as preparing food, taking medications, and keeping their living space clean.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_LGBTQ+_Patients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/26lkCIVZTAeFQVpgY_K1H-t3SIOvxKSX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for LGBTQ+ Patients]]></video:title><video:description><![CDATA[As a nurse, you’ll be providing care for patients who are lesbian, gay, bisexual, transgender, queer or questioning, and other orientations and identities, also known as LGBTQ+. Members of the LGBTQ+ community often experience health inequities that can be explained by the minority stress model. This model describes how disparities can be traced to cultural stressors like stigma, harassment, and discrimination. For example, people who identify as LGBTQ+ experience higher rates of substance and tobacco use as well as increased rates of mental health disorders, like depression and anxiety.  

Historically, people who identify as LGBTQ+ have experienced discrimination within the health care system. In fact, a significant majority of people who are gay, lesbian, bisexual and transgender report discrimination by a health care provider.  

Additionally, health care providers receive limited education on how to provide culturally appropriate care to people who identify as LGBTQ+. This lack of training can add to the health inequities, but by using correct terminology and creating an inclusive environment, nurses can provide culturally appropriate care to the patients who identify as LGBTQ+. 

First, let‘s focus on terminology, starting with the difference between biologic sex and gender identity. Someone’s biologic sex, or sex assigned at birth, is determined by their genitalia, reproductive organs, and chromosomes, and can be classified as male, female, or intersex. On the other hand, gender identity refers to someone&amp;#39;s self-perceived gender and may or may not align with their sex assigned at birth. 

So, a person who’s cisgender has a gender identity that’s the same as their sex assigned at birth, and a person who&amp;#39;s transgender is someone whose gender identity is different from their sex assigned at birth. For example, a transgender man is someone who was assigned female at birth but identifies as a male. Additionally, peop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Pressure_Injuries</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tO5Z0VpzSO6kMhrgchRtUoosTPmC7MWC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Pressure Injuries]]></video:title><video:description><![CDATA[Nurse Hailey works on an orthopedic unit and is caring for Margaret, a 91-year-old female with a recent fall at home requiring surgical repair of a fractured hip. After settling Margaret in her room, Nurse Hailey goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Margaret’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Hailey recognizes important cues, including Margaret’s vital signs, which are blood pressure 118/62 mmHg, heart rate 88 beats per minute, respirations 18 breaths per minute, and temperature of 100.4 F or 38 C. Nurse Hailey also notes that Margaret is incontinent; and a skin assessment reveals an area on her coccyx that’s pink and moist, without slough or eschar.  

Next, Nurse Hailey analyzes these cues. She reviews the electronic health record, or EHR, and notes that Margaret has declined working with physical therapy due to the pain in her hip and coccyx. Nurse Hailey recognizes that immobility and pain can contribute to pressure injuries and realizes that Margaret is experiencing impaired tissue integrity. She shares her assessments with the wound care nurse who classifies Margaret’s coccyx redness as a stage 2 pressure injury. 

Now, using the information she has gathered, along with Margaret’s medical history, Nurse Hailey chooses a priority hypothesis of impaired tissue integrity. Then, she generates solutions to address Margaret’s impaired tissue integrity that&amp;#39;ll include nonpharmacologic and pharmacologic interventions; and she establishes the expected outcome that after intervening, Margaret will demonstrate a healing pressure injury without further breakdown of skin or the development of infection by time of discharge. 

Nurse Hailey then takes action to implement these solutions. She knows that since Margaret has a stage 2 pressure injury, she needs to complete the wound care rec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Healthcare-Associated_Infection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kvqksChUR7WBxYFPiIaFo96vR5m6-B0O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Healthcare-Associated Infection]]></video:title><video:description><![CDATA[Nurse Monique begins her shift on a medical-surgical unit caring for Sam, a 78-year-old male who was admitted two days ago for chronic heart failure. After introducing herself, Nurse Monique begins her shift assessment and goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Sam&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Monique recognizes important cues. First, she notices Sam has an indwelling urinary catheter, which is draining cloudy urine. Then, she takes his vital signs and notes his temperature is 100.6 F, or 38.1 C. She palpates Sam’s abdomen, which elicits suprapubic pain that Sam rates as a 4 out of 10. He also reports that he didn’t have this type of pain until this morning. 

Next, Nurse Monique analyzes these cues. She reviews the electronic health record, or EHR, which shows Sam’s vital signs during the previous shift were within normal limits and his urine was clear. Nurse Monique knows that due to Sam’s increased age and presence of an indwelling catheter, he&amp;#39;s at high risk for a health care-associated infection, or HAI, which is an infection that develops from exposure to microorganisms in a health care setting.  

Nurse Monique considers these risk factors along with Sam’s new onset of fever, pain, and cloudy urine. She suspects that Sam is experiencing a type of HAI known as a catheter-associated urinary tract infection, or CAUTI. Now, using the information Nurse Monique has gathered, she chooses a priority hypothesis of impaired urinary elimination. 

Then, she generates solutions to address this hypothesis that will include pharmacologic and nonpharmacologic interventions. She also establishes the expected outcome, that after intervention, Sam’s temperature will be within normal range, and his symptoms of CAUTI will improve. 

Next, Nurse Monique takes action to implem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complications_of_Cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vgdURdpTT76ZOl-balhly-OGSmWt8quk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complications of Cancer]]></video:title><video:description><![CDATA[Cancer, or malignancy, refers to a group of diseases characterized by abnormal cell growth and differentiation, which changes cellular appearance and function. These changes are harmful to normal cells and can cause several complications, which can be directly related to cancerous tissue, a side effect of treatment, or a combination of both. 

Let’s look at some of the complications of cancer, starting with pain. Patients with cancer are at risk for acute and chronic pain, which can decrease quality of life. When caring for your patient with cancer, perform a comprehensive pain assessment on an ongoing basis. Discuss their pain management goals, and the use of pharmacologic interventions, including nonsteroidal antiinflammatory drugs, or NSAIDs; opioids; and adjuvant medications like corticosteroids; and nonpharmacologic interventions, such as guided imagery, relaxation breathing, distraction, massage, and acupuncture.  

Then, coordinate care with the interdisciplinary team to provide other interventions, such as radioactive medications for bone pain, nerve blocks, and epidural or intrathecal analgesia as indicated. You may also refer your patient to a pain management or palliative care specialist to help control their pain and improve quality of life. 

Alright, next let’s explore infection as a complication of cancer. Several factors can lead to an infection in your patient with cancer, including tissue damage from ulceration; necrosis caused by cancerous tissue; tumors compressing organs; and decreased immunity due to cancer or treatment-induced neutropenia, which is a low number of neutrophils, or the infection-fighting white blood cells.  

When providing care, be sure to monitor your patient for signs or symptoms of infection, such as a temperature of 100.4 F or 38 C or higher, cough, or diarrhea. However, keep in mind neutropenia can diminish signs of infection, so your patient may have an infection and be asymptomatic.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caring_for_the_Patient_in_the_Emergency_Department</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u1Qjr049Quyl058X049YV5NsRBOm8FDg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caring for the Patient in the Emergency Department]]></video:title><video:description><![CDATA[The role of a nurse in the emergency department, or ED, is to identify and respond to patients with potentially life-threatening conditions using a standardized triage process. Triage involves rapidly classifying patients based on the severity of their condition and then caring for the most critically ill first.  

The triage process includes a primary survey, to identify emergent conditions, like hemorrhage or skull fractures, and manage them as they are identified; followed by a secondary survey, to identify urgent and nonurgent conditions and injuries, like a broken arm or leg wound. 

Now the primary survey is the initial assessment of your trauma patient, that can be guided using the mnemonic ABCDE, which stands for Airway, Breathing, Circulation, Disability and Exposure.  Your primary survey begins when you see your first patient. If, during this time, you identify an obvious and significant external hemorrhage, your focus will shift from ABCDE to CABDE, meaning you should control the hemorrhage first before moving on with your assessment.  

If no external hemorrhage is noted, you&amp;#39;ll start your assessment with A, where you’ll assess alertness and airway patency. To determine alertness, assess your patient’s level of consciousness using the mnemonic AVPU. A is for alert, V is for responsiveness to voice, P is for responsiveness to pain, and U is for unresponsiveness.  

For airway patency, look for signs of a compromised airway, like gasping, or agonal breaths, dyspnea, and facial or neck trauma. Be sure to identify airway obstructions, like secretions, emesis, an enlarged tongue, or foreign objects, like loose teeth or dentures. For patients who are unable to keep their airway patent, prepare them for rapid sequence intubation. Also, if your patient is suspected of having a spinal cord injury, stabilize their cervical spine using a cervical collar or immobilization device. 

Next, for B, you’ll assess breathing. Even with a patent airway, o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Anemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GpXePwZ1RxWsUirDTrpymHd5SBCxWMzH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Anemia]]></video:title><video:description><![CDATA[Nurse Michael works on an inpatient Medical-Surgical unit and is caring for Hannah, a 26-year-old female with a history of Crohn disease who was admitted for iron deficiency anemia. After settling Hannah in her room, Nurse Michael goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Hannah’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Michael recognizes important cues, like Hannah&amp;#39;s laboratory results from the emergency department showing a hemoglobin of 6.5 g/dL and a hematocrit of 19 percent.  Further assessments reveal pallor and a heart rate of 110 per minute with a bounding pulse. Next, Nurse Michael asks Hannah about her prescribed medications. 

Nurse Michael: I see in your chart you’ve been taking infliximab for eight months. Has that helped your Crohn&amp;#39;s symptoms? 

Hannah: Well, I took it for a while, but I’ve had to skip my last two infusion appointments. I don&amp;#39;t have the money to keep going to the infusion clinic.   

Nurse Michael: I understand. How has that affected your symptoms? 

Hannah: The medicine really helped while I was getting it, especially since I didn’t feel as tired as I do now. I could also eat more foods that I like without pain.  

Nurse Michael: That makes sense. So, what types of food are you eating now? 

Hannah: Crackers and bananas, mostly. Sometimes an egg. That’s about it, because I feel like my symptoms are really flaring up. My belly really hurts after I eat. 

Nurse Michael: I&amp;#39;m sorry to hear that. I&amp;#39;m glad you are here so we can help you. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Acute_Coronary_Syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sriXxLNiQg6bYuCy7yvMwTBERUiabjp7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Acute Coronary Syndrome]]></video:title><video:description><![CDATA[Nurse Cameron works on a Cardiovascular Care Unit, or CCU, and is caring for Kevin, a 55-year-old male with a history of coronary artery disease for which he’s prescribed aspirin at home. He was recently admitted to the CCU after undergoing Percutaneous Coronary Intervention, or PCI, with placement of one stent to treat an ST-segment myocardial infarction, or STEMI for short. After settling Kevin in his room, Nurse Cameron goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Kevin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Cameron recognizes important cues including Kevin’s vital signs, which are blood pressure 101/82 mmHg, heart rate 99 beats per minute and regular, respirations 19 breaths per minute, oxygen saturation 96 percent on 2 liters per nasal cannula, and temperature 98.8 F, or 37.1 C. When asked about pain, Kevin reports a current pain level of 3 out of 10 in his groin incision. Upon assessment, Nurse Cameron notes that Kevin has a moderate amount of bright red blood on his groin dressing and the surrounding area is ecchymotic and tender to palpation. He is also receiving an infusion of heparin through his peripheral IV that was initiated during the procedure.  

Next, Nurse Cameron analyzes these cues.  He reviews the electronic health record, or EHR, and notes that Kevin’s activated partial thromboplastin time, or aPTT, is elevated over the therapeutic range ordered by the health care provider. Nurse Cameron realizes that although Kevin needs anticoagulation following stent placement, the combination of the heparin infusion and Kevin’s history of aspirin therapy places him at risk for bleeding. Now, using the information he&amp;#39;s gathered, along with Kevin’s medical history, Nurse Cameron chooses a priority hypothesis of risk for bleeding. Then, he generates solutions to address Kevin’s risk f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Valvular_Heart_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4Oy1xuchQbGpWNHfrs_eAwXiQ0q189Se/_.jpg</video:thumbnail_loc><video:title><![CDATA[Valvular Heart Disease]]></video:title><video:description><![CDATA[Valvular heart disease refers to damage or defects involving one or more heart valves, and can be either stenosis, or narrowing of the valvular opening; or regurgitation, also called insufficiency or incompetence, or failure of the valve to adequately close. 

Alright so, valvular heart disease is caused by damage or defects involving one or more heart valves. One cause of valvular heart disease is rheumatic fever, which is an inflammatory condition that typically occurs after a strep throat infection from Streptococcus pyogenes, also referred to as group A beta-hemolytic streptococcus. Other important causes include congenital defects, infective endocarditis, atherosclerosis, myocardial infarction, as well as autoimmune diseases like rheumatoid arthritis or systemic lupus erythematosus; or connective tissue disorders, like Marfan syndrome.  

Now, the heart valves control blood flow through the heart. The two atrioventricular, or AV, valves include the tricuspid valve that separates the right atrium from the right ventricle and the mitral valve, which separates the left atrium from the left ventricle. The two semilunar valves are the pulmonary valve that separates the right ventricle from the pulmonary artery and the aortic valve that separates the left ventricle from the aorta. The type of valvular heart disease depends on the affected valve and the type of defect.  

So, let’s start with mitral stenosis, which is where the valve leaflets either fuse together or stiffen, impairing the valve opening, making it harder for blood to flow from the left atrium to the left ventricle. As a result, the pressure in the left atrium increases, which compensates by undergoing hypertrophy and dilation to accommodate the extra blood. 

Then there&amp;#39;s mitral valve regurgitation, where the valve fails to close completely during systole; or sometimes, the leaflets bulge back, or prolapse, into the left atrium. Either way, blood flows back from the left ventricle in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malnutrition</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1hG_byidQE6hfNFs66CWQOw9SSe9mg4k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malnutrition]]></video:title><video:description><![CDATA[Nutrition is the process by which nutrients are taken in and used by the body to support overall health and essential functions, such as metabolism, growth, and maintaining and repairing body tissues. When nutrition is imbalanced, it&amp;#39;s called malnutrition. Now, malnutrition can be overnutrition, or the ingestion of more nutrients and energy than the body needs; or undernutrition, where nutrient and energy intake is insufficient to meet the body’s daily needs. 

Okay, let’s review the different types and causes of malnutrition. First, starvation-related malnutrition, also called primary protein-calorie malnutrition, occurs when nutritional needs aren’t met due to starvation, like with anorexia nervosa. Then, there’s chronic disease–related malnutrition, also known as secondary protein-calorie malnutrition, where dietary intake is insufficient to meet the increased metabolic demands related to chronic inflammatory conditions, like rheumatoid arthritis.  Lastly, there’s acute disease–related or injury-related malnutrition, where there is significant inflammation, like with major infections, burns, and trauma, and dietary intake is unable to supply enough calories for energy or protein for tissue repair. 

So, there are several risk factors for malnutrition, including socioeconomic factors, like food insecurity; health conditions, like prolonged physical illness, surgery, trauma, or prolonged immobility; incomplete diets, like with fad diets or poorly planned veganism; and malabsorption, like with vitamin B12 deficiency that occurs when intrinsic factor is lost after a gastrectomy.   

Now, as protein stores are depleted, synthesis of plasma proteins, like albumin, decreases.   This lowers oncotic pressure in the intravascular space, which causes a shift of fluids out into the interstitial tissues, leading to edema, as well as drying of the skin and mucous membranes. Protein deficits can also result in brittle nails and hair loss, as well as decreased]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obesity_and_Health_Risks</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kby_Gf61TJ6cI-38QNzOxvR0QIC41ufS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obesity and Health Risks]]></video:title><video:description><![CDATA[Obesity refers to an increased number and size of fat cells, which are referred to as adipocytes. It is often classified using body mass index, or BMI, and is calculated by dividing weight in kilograms by the square of height in meters. A person is considered obese if their BMI is 30 kg/m2 or higher, and a BMI above 40 kg/m2 signifies extreme obesity, also known as morbid obesity. Obesity can seriously impact a person’s health, leading to chronic medical conditions, increased mortality, and reduced quality of life. 

Now, most people have primary obesity, meaning it’s the result of consuming more calories than the body requires for their metabolic needs. Causes of primary obesity include lifestyle factors such as dietary choices, like eating foods high in calories, drinking sweetened beverages, and consuming large portion sizes; eating outside the home or in front of the television or computer; and being sedentary.  

Environmental factors also contribute to obesity, for example, patients with low income are at increased risk of obesity since inexpensive foods often have high calories and low nutritional value. Additionally, psychosocial factors can play a role in obesity, such as using food for comfort, reward, or eating more during times of stress, sadness, and anxiety. Lastly, certain genes can increase the risk of obesity by influencing appetite; satiety, or the feeling of fullness after eating; and how fat is stored or distributed in the body. 

On the other hand, secondary obesity is caused by medical conditions, such as certain congenital, endocrine, or central nervous system disorders. For instance, hypothyroidism slows metabolism, which can lead to excess weight gain. There are also certain medications that can contribute to obesity, including corticosteroids, estrogens, antipsychotics, antiepileptics, and oral antidiabetics.  

Okay, now let’s look at the health risks associated with obesity from head to toe. First, obesity can increase the risk ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Cholecystitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OYLOltqbSn_lNcPjls3PZO-fQZaYlkJ4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Cholecystitis]]></video:title><video:description><![CDATA[Nurse Sandy works in the emergency department and is caring for Natasha, a 40-year-old female with a history of obesity who&amp;#39;s been diagnosed with acute cholecystitis requiring surgical intervention. While Nurse Sandy prepares Natasha for surgery, she goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Natasha&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Sandy recognizes important cues, including Natasha’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 102 beats per minute, respirations 22 breaths per minute, blood pressure 159/97 mmHg, and pulse oximetry 99 percent on room air. Natasha rates her pain at 3 on a zero to 10 scale. She also notices that Natasha is holding an emesis bag, which contains a small amount of green emesis. 

Nurse Sandy performs a focused abdominal assessment, noting active bowel sounds in all quadrants. However, upon palpation, Natasha grimaces and puts her hand over her mouth. 

Natasha: Please don’t press down on my stomach, I feel like I’m going to throw up again. 

Nurse Sandy provides Natasha with a fresh emesis bag and rubs her back as she vomits.  

Afterwards, Nurse Sandy analyzes these cues. She reviews the electronic health record, or EHR, and notes that Natasha initially presented to the emergency department with right upper quadrant pain and vomiting that occurred hours after eating fried chicken for dinner. She also notes that Natasha is taking oral contraceptives, which Nurse Sandy recalls increases the risk for developing cholecystitis. Additionally, Nurse Sandy sees that, two hours ago, Natasha received 4 milligrams of ondansetron and 4 milligrams of morphine sulfate IV. 

Nurse Sandy then acknowledges the new preoperative orders for Nastasha, including NPO status, and a maintenance infusion of normal saline to run at 100 milliliters ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Chronic_Kidney_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/a0d_FFOEQ6iZ8ZmLU9dcFYuUR8q4yX9L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Chronic Kidney Disease]]></video:title><video:description><![CDATA[Nurse Marisol works in a family practice office and is caring for Robert, a 55-year-old male with a history of chronic kidney disease and type 2 diabetes, who&amp;#39;s arrived for a follow-up appointment. After settling Robert in the exam room, Nurse Marisol goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Robert’s care by recognizing cues, analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Marisol recognizes important cues including mild, pitting edema in Robert’s lower extremities, a blood glucose of 214 mg/dL, blood pressure of 145/85 mmHg, and a weight gain of 4.5 pounds since his last visit. 

Nurse Marisol asks about Robert’s insulin management at home. 

Nurse Marisol: I see that your blood sugar is higher than your last visit. Have you made any changes to your medications or the foods you eat? 

Robert: Yeah, my blood sugar’s been a little high. Sometimes I get tired and forget to take my insulin at night. 

Nurse Marisol: I also noticed that your ankles are swollen, too. Can you tell me how much water you’ve been drinking lately? 

Robert: Well, I’ve been really thirsty lately, so I’ve been drinking more than usual. Anyway, someone told me that drinking water helps to flush out my kidneys. 

Next, Nurse Marisol analyzes these cues. She reviews the electronic health record, or EHR, and notices that Robert is prescribed ten units of long-acting insulin nightly. She also notes that he’s recommended to follow a 1.5-liter fluid restriction daily. She knows that chronic kidney disease is a progressive and irreversible loss of kidney function, and that uncontrolled diabetes can worsen damage to nephrons over time. She also understands that nephron loss reduces the glomerular filtration rate, or GFR, leading to decreased fluid output, increased fluid retention, edema, and increased blood pressure.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Head_Injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xo3FmnTFRf6yWKZ1Rt6V1i_mTsiLopfD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Head Injury]]></video:title><video:description><![CDATA[Nurse Laquanna works on an oncology unit but was floated to the neurology unit earlier today. She&amp;#39;s caring for Molly, a 74-year-old female with a history of atrial fibrillation, or a-fib, who was recently admitted for a head injury. After settling Molly in her room, Nurse Laquanna goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Molly’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Laquanna recognizes important cues including a Glasgow Coma Scale, or GCS, score of 14, and vital signs which are temperature 98.2 F, or 36.8 C, heart rate 98 beats per minute, respirations 16 breaths per minute and regular, blood pressure 134/62 mmHg, and oxygen saturation 95 percent on room air. Nurse Laquanna also notices Molly seems slightly agitated.  

Next, Nurse Laquanna analyzes important cues. She reviews the electronic health record, or EHR, and sees Molly was involved in a head-on motor vehicle collision with airbag deployment, and she takes an anticoagulant daily to treat her a-fib. Nurse Laquanna recognizes that a head injury coupled with Molly’s history of anticoagulation places her at risk for intracranial bleeding. She also knows that subtle neurologic changes can be early indicators of complications. Nurse Laquanna knows Molly will require frequent neurological assessments, or neuro checks, to monitor for changes in her mental status.  

During Molly’s neuro check an hour later Nurse Laquanna notes Molly opens her eyes when her name is called; she’s disoriented; and does not respond when asked to move her fingers. Nurse Laquanna realizes her GCS is now 12, and that Molly needs intervention quickly. She&amp;#39;s unsure what to do next, so she enlists the help of a fellow staff nurse. 

Nurse Laquanna: Hi, Nurse Elijah. My patient has had a change in her neurologic status. I don’t have much experience in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Dementia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MPOWyZTpS6iG6PBN-fyUeDz5ROqQCRlN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Dementia]]></video:title><video:description><![CDATA[Nurse Darian works on an inpatient orthopedic floor and is caring for Rosemary, an 84-year-old female with a history of Alzheimer disease who was admitted for a hip fracture. After settling Rosemary in her room, Nurse Darian goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Rosemary’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darian recognizes important cues, including Rosemary’s inability to recall her daughter’s name, and disorientation to date and time. He also notices that Rosemary becomes agitated when asked several questions in a row; and as the evening progresses, she becomes more impulsive, and tries to get out of bed on her own. 

Next, Nurse Darian analyzes these cues. He recalls that Rosemary’s dementia can be exacerbated by illness, such as her hip fracture, and changes to her familiar environment, and he realizes Rosemary needs effective safety management. After reviewing her electronic health record, or EHR, he enters Rosemary’s room. 

Nurse Darian: Hi Rosemary, my name is Nurse Darian. I was your nurse yesterday and I&amp;#39;ll be your nurse again today.  

Rosemary: I&amp;#39;ve never met you. 

Nurse Darian: That’s okay, Rosemary. Are you having any pain right now? 

Rosemary: Why does everyone have so many questions all the time?  

Nurse Darian notes that Rosemary begins to sit up in bed and tries to swing her legs to the side of the bed to stand up. The two siderails by Rosemary’s head are up, as well as one siderail by her feet. She then moves towards the open space in the bed to exit, so Nurse Darian moves to prevent her from getting up on her own. 

Nurse Darian: Careful there. Let’s get you comfortable and back in bed safely Rosemary. We can put your favorite show on the television. 

Rosemary: Okay. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoarthritis_and_Rheumatoid_Arthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DjAGgwzeTLShLx0qNLo0H40ARSmh7grW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteoarthritis and Rheumatoid Arthritis]]></video:title><video:description><![CDATA[Arthritis refers to inflammation of a joint, it&amp;#39;s one of the most common causes of disability due to joint dysfunction and pain. Osteoarthritis, or OA, is a progressive disorder affecting the synovial joints. Another type of arthritis is rheumatoid arthritis, or RA, which is a chronic autoimmune disorder characterized by inflammation of connective tissue in the synovial joints. Unlike OA, RA is also a systemic disorder, impacting other organs, such as the lungs and blood vessels.  

Okay, so one of the main causes of OA are conditions or events that damage the synovial joints, such as repeated wear and tear over time. Having medical conditions, such as obesity and skeletal deformities like congenital hip dislocation can also increase the risk of OA. It’s also more common in people over the age of 50 and those assigned female at birth. On the other hand, RA is likely due to a combination of both environmental and genetic factors that trigger an autoimmune response. RA can occur at any age, though its onset is usually between age 30 to 50; and like OA, its more common in those assigned female at birth.  

Now, the main clinical manifestations for both OA and RA are joint pain and stiffness that limit mobility and impact quality of life. In OA, pain typically affects larger weight-bearing joints, such as the knees and hips, and it&amp;#39;s usually relieved by rest. Conversely, joint stiffness often develops after periods of rest, and it typically resolves within 30 minutes. Pain associated with RA is usually located in smaller joints, like the hands and feet, and it usually improves with movement.  

Patients with OA and RA can also develop joint nodules. In OA, nodules can form in the distal interphalangeal joints, called Heberden nodes, and on the proximal interphalangeal joints, called Bouchard nodes. In patients with RA, firm, subcutaneous rheumatoid nodules develop, usually in bony areas exposed to pressure, like the fingers and elbows; howeve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Problems_of_the_Prostate_Gland</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L7-zMAZwQJqWoVPFvnIhWTIvQhmIlcOO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Problems of the Prostate Gland]]></video:title><video:description><![CDATA[Nurse Suleena works on a Surgical Step-Down Unit and is caring for Pedro, a 55-year-old male with a history of benign prostatic hyperplasia, or BPH, who was admitted two days ago following a transurethral resection of the prostate, or TURP. After settling Pedro in his room, Nurse Suleena goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Pedro’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Suleena recognizes important cues, including vital signs, which are temperature 98.0 F or 36.7 C, blood pressure 140/ 90 mmHg, heart rate 88 beats per minute, respirations 20 breaths per minute, and oxygen saturation 95 percent on room air. She also notices Pedro grimacing and shifting uncomfortably in bed. When examining the collection bag for Pedro’s continuous bladder irrigation, or CBI, Nurse Suleena notices large blood clots and amber-colored drainage.  

Next, Nurse Suleena analyzes these cues. She knows that the CBI output should be light pink, and that blood clots and amber-colored urine in the CBI drainage bag can indicate that the irrigation rate likely needs to be increased. Also, Pedro’s non-verbal cues and vital signs indicate he’s experiencing discomfort, which is also likely due to his ineffective urinary drainage. She also recognizes that bladder spasms resulting from his TURP procedure can cause additional pain. Then, she reviews the electronic health record, or EHR, and notes that Pedro’s last dose of pain medication was four hours ago. 

Nurse Suleena: Pedro, how are you feeling after your procedure? 

Pedro: I’m fine. Isn’t there a male nurse on this floor?  

Nurse Suleena: I understand that having a female nurse care for you after your TURP procedure can be unfamiliar. There are no male nurses available today, but I’m going to do my best to take care of you and make you comfortable. Is there anything I can ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Fractures</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2vBRLafPTl2B1m5xpsM6XzDhRemZcJav/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Fractures]]></video:title><video:description><![CDATA[Nurse Kenji works on an orthopedic unit and is caring for Sharon, a 74-year-old female with a history of osteoporosis who was recently admitted for a left hip fracture requiring an open reduction and internal fixation, or ORIF. After settling Sharon in her room, Nurse Kenji goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Sharon’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Kenji recognizes important cues, including Sharon’s vital signs, which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 19 breaths per minute, and blood pressure 123/88 mmHg. During the bedside report, Nurse Kenji learned that Sharon declined repositioning during the night shift. Upon assessment, he notes that her hip appears mildly swollen and her surgical dressing is clean and dry. Nurse Kenji also notes that Sharon’s left foot is warm with intact sensation, 2+ palpable pulses, and she can wiggle her toes.  

Nurse Kenji asks Sharon about her comfort.  

Nurse Kenji: I see that you stayed in the same position throughout the night. Could you tell me your current pain level? 

Sharon: I don’t have any pain right now, but I don’t want to move because I know it&amp;#39;ll hurt my hip. 

Nurse Kenji: I understand. Have you considered taking the prescribed medications to manage your pain? 

Sharon: I really don’t like pain medicine because I’m worried about becoming addicted. 

Next, Nurse Kenji analyzes these cues. He reviews the electronic health record, or EHR, and notes that Sharon is scheduled to begin physical therapy today. He also notes that Sharon is prescribed ice packs to reduce hip swelling, as well as oxycodone and acetaminophen every four hours as needed for pain management but hasn’t taken any medication since early yesterday evening. Nurse Kenji realizes that Sharon’s fear of pain is limiting he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Gastroesophageal_Reflux_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hvy7ZlYfQ86oLWOOw5epnDTnSu68HGt_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Gastroesophageal Reflux Disease]]></video:title><video:description><![CDATA[Nurse Max works in a primary care office and is caring for Anuja, a 54-year-old woman with a history of gastroesophageal reflux disease, or GERD, who&amp;#39;s being seen for a three-month follow-up appointment. After settling Anuja in her room, Nurse Max goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Anuja’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Max recognizes important cues including vital signs which are temperature 98.2 F or 36.9 C, heart rate 76 beats per minute, respirations 14 breaths per minute and regular, blood pressure 128/84 mmHg, and oxygen saturation 98 percent on room air. Nurse Max asks Anuja if she’s having pain, and she reports a burning in her mid upper abdomen after eating, despite taking her prescribed medication.   

Next, Nurse Max analyzes these cues. They review the electronic health record, or EHR, and note Anuja has been on proton pump inhibitor, or PPI, therapy for three months to treat her GERD.  Nurse Max then talks to Anuja about her lifestyle modifications.  

Nurse Max: I’m glad you’ve been taking your PPI every day and I’m sorry it hasn’t been working for you. I want to figure out what might be happening. What time do you take your medication? 

Anuja: I take it every night after dinner. I set an alarm, so I don’t forget. 

Nurse Max: Setting an alarm is a great idea! What do you typically eat at home?  

Anuja: I’ve been making a noodle dish lately with lots of fresh jalapenos drizzled with sriracha, my family loves it! 

Now, using the information they’ve gathered, Nurse Max chooses a priority hypothesis of knowledge deficit.  

Then, they generate solutions to address this problem that will include pharmacologic and nonpharmacologic interventions, and they establish the outcome that after intervening, Anuja will verbalize an understanding of GERD management.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Seizure_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bAvhrgh8Ti2w-aDLzGjplq5rR3mWMMmQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Seizure Disorder]]></video:title><video:description><![CDATA[Nurse Karla works on an inpatient neurology unit and is caring for Nisha, a 24-year-old female with a history of generalized onset tonic-clonic seizures. After settling Nisha in her room, Nurse Karla goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Nisha’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Karla recognizes important cues. As she reviews the electronic health record, or EHR, Karla notes Nisha is on seizure precautions and has an order for lorazepam IV push for seizures, per protocol. As she enters Nisha’s room, she finds Nisha lying supine on her bed. 

Nisha: I don’t feel right. I feel like I’m going to have a seizure. 

Nurse Karla: Okay Nisha, I’ll stay with you. 

Then, Nisha’s body begins cycling through periods of intermittent jerking movements and muscle tightening. Her breathing is sporadic, and she alternates between rapid breathing and apnea. Her pupils are dilated, she&amp;#39;s intermittently biting her cheek, and doesn’t respond to verbal cues. 

Nurse Karla calls for help while noting the time the seizure activity began. Then, she protects Nisha from injury by ensuring there are no objects in Nisha’s bed that could hurt her during the seizure.  

Next, Nurse Karla analyzes these cues. Nurse Karla realizes that during tonic-clonic seizures, the airway can become obstructed, and she recognizes Nisha needs effective airway management. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Urinary_Tract_Infection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8EKMASPMQSCl1Pafzd3gHitnQs2B4jy-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Urinary Tract Infection]]></video:title><video:description><![CDATA[Nurse Alfred works on a Medical-Surgical unit and is caring for Alma, a 72-year-old Spanish-speaking female with a history of multiple sclerosis, or MS, who was recently admitted for pyelonephritis. After settling Alma in her room, Nurse Alfred goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Alma&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Alfred recognizes important cues, including Alma’s vital signs, which are temperature 101.3 F, or 38.5 C, heart rate 108 beats per minute, respirations 20 breaths per minute, blood pressure 136/78 mmHg, and oxygen saturation 98 percent on room air. Nurse Alfred knows that Alma’s primary language is Spanish, so he uses an interpreter to communicate with her over the phone. Alma&amp;#39;s lower abdomen is moderately distended, and she rates her abdominal pain at 9 out of 10.  

Nurse Alfred gathers that, at home, Alma usually empties her bladder via straight catheterization every four hours, but has been having difficulty due to increasing weakness from her MS. She reports that yesterday, she was too weak to catheterize herself.  

Next, Nurse Alfred analyzes these cues. He reviews the electronic health record, or EHR, and notes a straight catheterization was performed on Alma in the emergency department to obtain a urine sample, which revealed the presence of leukocytes and nitrites and drained 150 milliliters. Nurse Alfred realizes that, due to her inability to catheterize herself properly, Alma developed urinary retention which likely contributed to her pyelonephritis. Nurse Alfred realizes Alma needs effective urinary elimination and infection management. 

Now, using the information he&amp;#39;s gathered, along with Alma’s medical history, Nurse Alfred chooses a priority hypothesis of infection.  

Then, he generates solutions to address Alma’s infection that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Venous_Thromboembolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iKzmm8uCRw_UQYnC-yVzB3xiREuAbGyc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Venous Thromboembolism]]></video:title><video:description><![CDATA[Nurse Hakeem works on a Medical-Surgical unit and is caring for Lucille, a 72-year-old female who&amp;#39;s being admitted for a deep vein thrombosis, or DVT in her left iliofemoral vein. After settling Lucille in her room, Nurse Hakeem goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Lucille’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

Nurse Hakeem starts by recognizing important cues. He notes signs and symptoms consistent with Lucille&amp;#39;s diagnosis of DVT, including redness and swelling of the affected area. Upon light palpation, Nurse Hakeem notes Lucille’s leg is warm, the skin is taut and tender, and she rates her pain as 6 out of 10 and describes it as throbbing. 

Then, Nurse Hakeem analyzes these cues. He reviews the electronic health record, or EHR, and sees that Lucille recently had surgery to repair a fractured left hip, and that an ultrasound report identified the DVT.  

He knows that immobility after surgery increased Lucille’s risk for a DVT, and that the thrombus lodged in her vein is causing inflammation and decreasing venous return to her heart, causing swelling and pain in her leg.  

He also understands that Lucille is at risk of a venous thromboembolism, or VTE, if the thrombus breaks free and travels up through the inferior vena cava,  to the right side of the heart,  and then into her lungs,  causing a pulmonary embolism, or PE.  

Now, using the information he&amp;#39;s gathered, Nurse Hakeem chooses a priority hypothesis of impaired tissue integrity.  

Next, he generates solutions to address Lucille’s DVT that will include pharmacologic and nonpharmacologic interventions, and he establishes the expected outcome that after intervening, Lucille’s tissue integrity will show signs of improvement by the end of the shift.  

Nurse Hakeem then takes action to implement these solutions. He revie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postoperative_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/voG2hW4mRgamz2_GLonR8iExSJOXLCL3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postoperative Care]]></video:title><video:description><![CDATA[Postoperative care is the management of a patient’s health during the postoperative period. This typically begins when the patient is transferred from the operating suite to the post-anesthesia care unit, or PACU for short, and lasts until the patient is discharged from the health care facility.  

Now, the most common complications during the postoperative period include pain, hemorrhage, hypothermia, and infection at the site of the surgery, called surgical site infection, or SSI for short, as well as wound dehiscence and evisceration. There can also be respiratory complications, like airway obstruction, laryngospasm, pneumonia, atelectasis, and pulmonary embolism.  

Cardiovascular complications can also occur, such as hypotension, hypertension, and dysrhythmias. Patients can also develop nervous system complications, including delirium and delayed emergence from anesthesia.  On the other hand, gastrointestinal complications include postoperative nausea and vomiting, constipation, and postoperative ileus; while urinary complications can manifest as urinary retention and urinary tract infections. Finally, fluid and electrolyte imbalances can also occur. 

Okay, let’s look at the care you’ll provide to your patient during the postoperative period. Your priority goals of care are to promote your patient’s recovery by managing pain, supporting oxygenation and cardiovascular stability, maintaining fluid balance, providing wound care, monitoring bowel function, and preventing complications.  

First, obtain a handoff report from the PACU nurse. Then, perform an initial assessment of your patient’s incision site, dressings, and surgical drains, and perform dressing changes, wound care, and maintain patency and suction of surgical drains, as needed. Also check their IV site, as well as the IV solutions, and infusion rate.  

Then, begin a focused assessment by taking a full set of vital signs. Assess their pain, administer the prescribed analgesics, as needed, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dialysis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o30YlIuYQCS0--72ilJALG-URPSUB0C1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dialysis]]></video:title><video:description><![CDATA[Dialysis is a type of kidney replacement therapy that removes metabolic waste products, toxins, as well as excess fluid and electrolytes from the blood. Most often, dialysis is required due to end-stage renal disease, which means the kidneys have lost almost all their function. Dialysis can also be used to correct fluid, acid-base, and electrolyte imbalances, and to treat drug overdoses. The two types of dialysis are hemodialysis and peritoneal dialysis.  

Now, to perform dialysis, either vascular access for hemodialysis, or abdominal access for peritoneal dialysis will be needed. So, for hemodialysis in an acute setting, temporary venous access can be obtained through a catheter in the internal jugular or femoral vein. When permanent access is needed for long-term hemodialysis, an arteriovenous or AV fistula or graft is created surgically in the patient’s arm. This creates a connection between a small artery and a vein, which causes the vein to become “arterialized,” meaning it increases in size, develops thicker walls, and blood flow is increased.  

Peritoneal access can be obtained by inserting a catheter into the peritoneal cavity. 

Okay, let’s look at the principles of dialysis, which include diffusion, osmosis, and ultrafiltration. Diffusion is the movement of solutes from a greater concentration to a lesser concentration until the two solutions have the same concentration of solutes on either side of a semipermeable membrane. Osmosis is the health education platform that makes learning easy and fun, but in this case, it refers to the movement of fluid through a semipermeable membrane from an area of lesser solute concentration to an area of greater solute concentration. For example, glucose creates an osmotic gradient across a membrane and is able to pull fluid through that gradient. Finally, ultrafiltration is when a driving pressure moves fluid and solutes across a semipermeable membrane. 

Now, to understand how hemodialysis works, let’s ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spinal_Cord_Injury_and_Spinal_Cord_Tumors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k5efou_ZTw2hxyy6jIrVHCl2SnSLgfpU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spinal Cord Injury and Spinal Cord Tumors]]></video:title><video:description><![CDATA[A spinal cord injury refers to any damage to the spinal cord, which is a bundle of nerve fibers that serves as a highway that carries information between the brain and the body.  

Now, a spinal cord injury can involve primary and secondary injury. Primary injury typically involves a sudden, traumatic impact on the spine that fractures or dislocates the protective vertebrae, damages the spinal cord, or interrupts its blood supply.  

Then, after the primary injury, there’s usually additional damage, or secondary injury, that occurs due to the body’s natural response to trauma. Secondary injury begins immediately after the spinal injury, and includes bleeding, inflammation, and edema. This is followed by compression of the spinal cord, ischemia, and neuronal damage. As time goes by, additional neuronal cell death occurs. 

Eventually, specialized glial cells begin to form scar tissue at the site of injury, which creates a barrier across the injured tissue, impairing cellular regeneration, which can result in permanent nerve damage and subsequent neurologic deficit. 

Now, spinal cord injuries can have several different causes, including trauma, like with a motor vehicle crash or falls, such as falling from a ladder; penetrating trauma, like a stab wound in the back or a gunshot; or recreational injuries, like those caused by impact sports. They can also be caused by medical conditions, including spinal tumors, infections, or degenerative diseases of the spine, like a protruding intervertebral disk.  

Risk factors for developing a spinal cord injury include engaging in high-risk behaviors, such as not wearing safety equipment when playing sports or speeding while driving. Lastly, a history of bone or joint disorders increases the risk, since even minor trauma could damage already weakened bones and injure the spinal cord. 

Alright, now clinical manifestations of spinal cord injuries depend on the severity and location of the injury and may include partial ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intracranial_Regulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xsVUV8q_Qlaf3w0jGxoWkVCaRfuZMSoD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intracranial Regulation]]></video:title><video:description><![CDATA[Increased intracranial pressure, or ICP, is a life-threatening condition characterized by increased pressure within the skull.  

Now, increased ICP can occur if there’s an increase in the components of the brain, including brain tissue, cerebrospinal fluid, or CSF, or the blood supplying the brain. An increase in brain components might develop in the case of cerebral edema, which can be due to infections, trauma, or hypoxia; space-occupying lesions such as brain tumors, abscesses, or intracranial hemorrhage; or disruptions in CSF circulation, like with hydrocephalus.   

Alright, so, when it comes to regulating ICP, remember that the mature skull is a rigid structure that can’t expand. So, to maintain a normal ICP, there must be a balance between the volume of brain tissue, CSF, and blood. If there’s an increase in any one of these three, there should be a compensatory decrease in the other two, which is known as the Monro-Kellie hypothesis. Normally, the volume of the brain remains relatively stable, so ICP can be regulated by changes in CSF and blood volume. When needed, CSF production can be decreased, or reabsorption can be increased, to help normalize ICP. Similarly, cerebral blood volume can be decreased either by cerebral vasoconstriction or increasing venous blood drainage out of the skull. 

Now, the compensatory mechanisms that keep ICP within a normal range have limits and can be overwhelmed. When this happens, ICP starts to increase, which puts pressure on the ventricles and cerebral blood vessels. In turn, this decreases cerebral blood flow and cerebral perfusion. Decreased cerebral perfusion means that less oxygen is delivered to the brain tissue, which causes neurons to swell and die, further increasing ICP. At the same time, hypercarbia, or a build-up of carbon dioxide can occur, causing vasodilation, which also contributes to increased ICP.  

If not corrected, increased ICP can lead to complications like papilledema, or swelling of the o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Diabetes_Mellitus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2ONmk8iqR6q6hn6kfSzA7NL6RMWCg-q2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Diabetes Mellitus]]></video:title><video:description><![CDATA[Nurse Andrea works on a medical-surgical unit and is caring for Mario, a 32-year-old male with a history of type 1 diabetes mellitus, who was recently admitted from the emergency department for diabetic ketoacidosis, or DKA. After settling Mario in his room, Nurse Andrea goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Mario’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Andrea recognizes important cues, including Mario’s vital signs which are temperature 99.4 F, or 37.5 C, heart rate 115 beats per minute, respirations 24 breaths per minute, blood pressure 90/65 mmHg, and oxygen saturation 99 percent on room air. His pain rating is 2 out of 10. Upon assessment, Nurse Andrea notes Mario is alert and oriented, his mucous membranes are dry, and he reports nausea with two episodes of emesis. Nurse Andrea also notes that he has a continuous insulin drip and IV fluids infusing into a peripheral IV, and his current blood glucose level is 265 mg/dL. 

Next, Nurse Andrea analyzes these cues. She reviews the electronic health record, or EHR, and verifies Mario is on the correct rate of insulin and IV fluids. She understands that the elevated  glucose levels in DKA cause osmotic diuresis and significant fluid loss, and that the acidosis is causing Mario’s nausea and vomiting, resulting in additional loss of fluid and electrolytes. She also knows that fluid loss will continue until Mario’s blood glucose level is stabilized, and that tachycardia and hypotension are signs of dehydration. Nurse Andrea recognizes that Mario needs fluid management. 

Prioritizing Hypotheses, Generating Solutions, and Taking Action 
Now, using the information she&amp;#39;s gathered, Nurse Andrea chooses a priority hypothesis of fluid volume deficit. 

Then, she generates solutions to address Mario’s fluid volume deficit, including pharmacologi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Hypothyroidism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8kj8_4loSFmVul4rYt4zGsRYQXq52-yM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Hypothyroidism]]></video:title><video:description><![CDATA[Nurse Kyle works at a family practice clinic and is caring for Amara, a 54-year-old female who presents for a follow-up appointment after being prescribed levothyroxine 3 months ago for newly diagnosed hypothyroidism. After settling Amara in her room, Nurse Kyle goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Amara’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

Nurse Kyle recognizes important cues, including Amara’s report of fatigue and constipation. He also notes that Amara shivers and pulls her jacket around her shoulders.  

Nurse Kyle: Amara, tell me about what’s been going on since your last appointment. 

Amara: A lot of the same things, like I still feel tired and cold. But my main issue is that I’m really constipated and it&amp;#39;s making my stomach hurt.  

Next, Nurse Kyle analyzes these cues. He reviews the electronic health record, or EHR, and notes that Amara started levothyroxine 3 months ago. He also notes her labs today show an elevated thyroid stimulating hormone, or TSH, and low free T4. Nurse Kyle realizes that since Amara is not yet therapeutic on her medication, she is still experiencing symptoms of hypothyroidism.  

Now, using the information he’s gathered, along with Amara’s medical history, Nurse Kyle chooses a priority hypothesis of constipation. Then, he generates solutions to address Amara’s complaint of constipation that will include pharmacologic and nonpharmacologic interventions. Nurse Kyle establishes the expected outcome that after intervening, Amara will have one bowel movement each day by the time she has her next follow-up in 6 weeks.  

Nurse Kyle then takes action to implement these solutions. He knows that although Amara started on levothyroxine 3 months ago, it can take time for the medication to correct her thyroid hormone level, so she may still experience symptoms of hypothyro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Overview</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gY5tYClGTaiYIvdoWlLv7tyyRhGJj03-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Overview]]></video:title><video:description><![CDATA[A physical assessment is an important nursing skill that is used to collect objective data about a client’s status by using the senses, like seeing a rash or hearing wheezes in the lungs. A physical assessment can also validate subjective information gathered from a health history, such as a client’s report of pain or dizziness. Additionally, assessment is the first step in the nursing process, which can be used to develop a plan of care or to evaluate the effectiveness of an intervention. Let’s review the process of completing a physical assessment.

Now, the two most common types of assessments you’ll do as a nurse are a comprehensive assessment and a focused assessment. A comprehensive assessment, sometimes referred to as a head-to-toe assessment, includes all body systems, and is usually performed during a general wellness visit or when a client is admitted to the hospital or other facility. This approach is most useful when you want to collect information about your client’s general health status. 

On the other hand, a focused assessment depends on the situation, and is often based on a client’s presenting symptoms. For example, if your client has abdominal pain, you’ll focus most of your assessment on their gastrointestinal system. Likewise, if your client is having difficulty breathing, a focused assessment would include their respiratory system as well as skin, vital signs, and level of consciousness. A focused assessment may also be needed if you are administering certain medications; for example, when you’re administering a cardiotonic medication, you’ll focus your assessment on your client’s heart rate and blood pressure. 

Okay, there are a few things to consider before performing a physical assessment. First, check to see if your client requires any precautions in addition to standard precautions such as transmission-based precautions, and don the appropriate personal protective equipment, or PPE. Then, explain the procedure to your client an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Palliative_and_Hospice_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/p7ydjWRfTz_ZhIpkpXtdMY4LSwayR1sd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Palliative and Hospice Care]]></video:title><video:description><![CDATA[Nurse Sumara works in an oncology unit at a hospital. She has been caring for a client named Monique during her chemotherapy treatment for stage IV breast cancer. Monique has been experiencing pain, nausea, fatigue, and decreased appetite due to the treatment, so the oncologist initiates palliative care to better manage her symptoms. Over the next 30 days the palliative care provides symptom relief for Monique, however, the cancer isn’t responding to treatment and continues to progress. Monique’s oncologist plans a meeting with Monique, her family, and Nurse Sumara to discuss Monique’s options. The oncologist discusses Monique’s disease progress and then says, “Your options are to continue palliative care and cancer treatment or consider hospice. This decision is totally up to you and your healthcare team will support you no matter what you decide.” 

Palliative care is a type of specialized care that focuses on managing symptoms for those with serious illnesses to reduce suffering and maintain quality of life. This includes treatment for a wide range of symptoms like pain, depression, constipation, and insomnia. Palliative care is often provided together with curative treatment, like surgery or chemotherapy in Monqiue’s case. 

On the other hand, hospice care is also focused on supportive care and symptom management but without treating the actual disease. Hospice care is usually reserved for clients with six months or less to live who have no options for curative treatment or have chosen not to pursue treatment. 

Okay, so both palliative and hospice care are ways of providing holistic care for clients with a serious or life-threatening medical condition with the goal of helping them and their families to achieve the best quality of life. Palliative and hospice care teams are multidisciplinary, and can include physicians, social workers, case managers, nutritionists, spiritual advisors, and nurses.

Nurses who provide care for clients receiving palliativ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preoperative_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Laftg7PhSHCWMQ4YWmRFEZwpRDOdXbDX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preoperative Care]]></video:title><video:description><![CDATA[Preoperative care is the preparation and management of a client during the preoperative period, which is the time period between the decision to perform a surgery and the beginning of the surgical procedure. 

Alright, so the first step of preoperative care starts with the surgeon, with a registered nurse as witness, obtaining informed consent from the client. Then comes the client’s history, asking about current medications, especially the high risk ones like anticoagulants; as well as alcohol intake; cigarette smoking; illicit drug use; in addition to a personal or family history of complications from anesthesia; also allergies; or chronic illnesses, such as hypertension, diabetes, and anemia. 

Clients should also be assessed for risk factors of obstructive sleep apnea since this condition can interfere with breathing when the client is under general anesthesia. The risk factors are summarized with the STOP-BANG mnemonic that stands for snoring history, tiredness during the day, observed breathing cessation during sleep, high blood pressure, in addition to a body mass index of higher than 35 kg/m2, age over 50 years, as well as neck circumference larger than 40 centimeters, and gender assigned male at birth. 

This is typically followed by diagnostic studies as needed like electrocardiogram or ECG; as well as imaging studies. In addition, clients should obtain the indicated laboratory tests, such as a complete blood count or CBC, coagulation profile, blood typing, and pregnancy test as needed. 

Lastly, the preoperative care is wrapped up with the client&amp;#39;s education, in order to prepare them for the surgical procedure and let them know what to expect after the procedure.

Okay, let’s look at the nursing care you’ll provide to a client during the preoperative period. Your priority goals of care include preparing the client for surgery, establishing a baseline assessment, and providing psychosocial support.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Management:_Delirium</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w2xwMKgDQxang4l5vdX4DNDTRO6GWlT1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Management: Delirium]]></video:title><video:description><![CDATA[Delirium is an abrupt decline in mental function, including memory, orientation, perception, behavior, language, and personality, which can fluctuate from day-to-day and can last for hours, days, or weeks. In contrast, dementia has a gradual onset, lasts for months to years, and progressively worsens over time.  

Okay, now, delirium usually occurs as a consequence of an underlying condition. Health problems like heart failure, cognitive impairment, or visual and hearing impairment can make patients more vulnerable to the impact of stress, pain, sleep deprivation, immobility, dehydration, or malnutrition, which can lead to delirium.  Other risk factors include advanced age, infections, electrolyte imbalances, as well as being hospitalized, being in intensive care, the use of mechanical ventilation, and sensory deprivation. Some medications, such as benzodiazepines, opioids, and anticholinergics, can also contribute to delirium. Notably, dementia is a leading risk factor for delirium, and delirium increases the risk of developing dementia. 

Now, although the exact cause of delirium is unclear, it&amp;#39;s likely not due to a single factor. One theory is that impaired oxidative metabolism can lead to low oxygen levels in the brain. Another theory is that abnormal levels of neurotransmitters in the brain, like decreased acetylcholine, increased dopamine, and either increased or decreased serotonin, can promote the development of delirium. It is also thought that in delirium, neuronal membranes may not be able to depolarize properly, and therefore, the action potential cannot be efficiently transmitted from one neuron to another. Alternatively, delirium might be related to inflammatory cytokines that are released during infection or trauma, which interfere with neuronal function.  

Okay, so clinical manifestations include disorientation, meaning the patient doesn’t know where they are or what day it is; or they might have difficulty concentrating. Based on]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion_of_the_Newborn_and_Family</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bCXKhKE7QH2WPAihWhYqmBqaTXOHI0Oq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Promotion of the Newborn and Family]]></video:title><video:description><![CDATA[During the first 28 days of life, the infant is considered a newborn. This is a time when newborns undergo dramatic changes as they adjust to the extrauterine environment and are completely reliant on others for their care. To promote the health of the newborn and their caregivers, the nurse will focus on preventing infection, optimizing nutrition, and promoting attachment. 

As the nurse caring for a newborn, preventing infection is one of your most important considerations. This is because the newborn’s immune system is underdeveloped, making them highly susceptible to infections. So, the most important thing you can do to prevent infection is to perform diligent hand hygiene. You’ll also administer antibiotic eye ointment to prevent an eye infection called ophthalmia neonatorum, and most newborns will get their first hepatitis B vaccine before discharge.  

You’ll also teach the newborn’s caregivers how to prevent infection in their newborn once they’re discharged home. For example, since bacteria can easily grow on the umbilical stump while it’s healing, teach them to fold the diaper below the umbilical stump to prevent irritation, to gently cleanse it with warm water if it becomes wet or soiled, and to watch for signs of infection such as redness, swelling, and tenderness.   ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aspects_of_Safe_Medication_Administration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2STjSi7lRsKZD6clZhbWyIbPRaSyGO74/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aspects of Safe Medication Administration]]></video:title><video:description><![CDATA[Medication administration is a complex process which involves the application of a prescribed medication to a patient. As the nurse, you must identify medication safety risks, follow safe administration principles, and evaluate your patient’s condition after administration.  

Now, risks associated with medication administration include adverse medication reactions, cross-infection, or injury. Adverse reactions are unwanted effects that occur related to administration of a medication, which can be mild, like rash or nausea, or more severe, like kidney damage or GI bleeding.  

Next, cross-infection is when organisms, like bacteria or viruses, are transferred to your patient during administration. This can occur when administering a medication through your patient’s IV without thoroughly cleaning the hub or when touching the tip of an eye dropper to your patient’s eye during administration. Lastly, injury can occur to your patient when administering medications, like giving a hypertension medication to a patient who’s hypotensive or injecting a medication intramuscularly using incorrect technique, causing a hematoma or nerve injury. 

Alright, so there are several different routes for medication administration. The most common routes are oral, also known as per os or PO; parenteral, which includes IV, intramuscular, or IM, subcutaneous; and intradermal. Other routes for medication administration include inhalation, sublingual, rectal, topical, otic, and ophthalmic. 

Now, regardless of the route, prevent harm to your patient by following safe medication administration principles each time you administer a medication. The standard practice for safe medication administration involves adhering to the rights of medication administration, which include the: right patient, right medication, right dose, right time, right route, right indication, and right documentation. It’s important to note that there might be additional rights and you should follow the protocol outlined by your institution. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_Order_Interpretation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O7lgeoywTCObNbg9FJcUXpoeRfWyvWbh/_.png</video:thumbnail_loc><video:title><![CDATA[Medication Order Interpretation]]></video:title><video:description><![CDATA[Medication orders are used to communicate which medications to administer to patients and are obtained from the health care provider in the form of written, electronic, or verbal orders. Written and electronic orders are entered directly by the health care provider, whereas verbal orders can be taken in-person or over the phone in certain situations, transcribed by the nurse, and then signed by the health care provider within a certain timeframe. All medication orders will include the date and time the order was made; the name of the medication; its dosage strength, route, and frequency; as well as the signature of the provider.  

As the nurse, you’ll provide safe medication administration by correctly interpreting medication orders. Start by ensuring all the elements of the order are provided. If the order is unclear or if there’s missing information, you’ll clarify it with the health care provider. If the order is handwritten, ensure that it’s legible. Importantly, be sure the order only uses approved abbreviations, since unapproved abbreviations can lead to medication errors. For example, the unapproved abbreviation QD is intended to mean “daily” but could be mistaken for the approved abbreviation QID, meaning “four times a day.” Instead, “daily” should be written out. Finally, be sure you know which medications and dosages are safe for your patient, so you can identify and clarify any concerns with the health care provider. 

Okay, let’s interpret a handwritten medication order to ensure all the elements are provided. You see the date and time the order was written, followed by the medication name, ondansetron. The dosage strength is 4 mg, the route  is IV, and the frequency is every 8 hours. Finally, it’s signed by the prescribing health care provider. Since all the required elements are present and clearly communicated in the medication order, you can begin the medication administration process. 

Let&amp;#39;s look at another handwritten medicatio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Reading_Medication_Labels</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n5EbbafMQH26lZThamTK9-CtSHqHWou9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Reading Medication Labels]]></video:title><video:description><![CDATA[Medications come packaged with specific information about the medication on the label, which includes details such as the brand name, generic name, dosage strength, medication form, expiration date, lot number, manufacturer name, bar code, and additional information and directions for use. As a nurse, you’ll read the labels of all prescribed medications to ensure safe administration. 

Okay, so let’s identify the information on this label and what it means. Starting with the medication’s brand name, also known as the proprietary or trade name, which you’ll find in large, bold letters. This is the commercial name given to a medication by the manufacturer.   

The generic name is its nonproprietary name, which is an internationally recognized name based on the medication&amp;#39;s active ingredient or chemical structure. You’ll find the generic name in smaller, non-bolded letters, typically written below the brand name.  

Next, you&amp;#39;ll find the dosage strength and formulation. Dosage strength is the amount of medication contained in the medication form, like tablet, capsule, or suspension, and it’s indicated by a number with units of measurement.  

The formulation may follow the dosage strength  or be noted after the generic name.  

Then, you’ll find the medication’s expiration date, or the date after which the medication shouldn’t be used anymore, since it may have lost potency. The expiration date is usually abbreviated as “exp” followed by a month and year.  

The lot number, which refers to the batch the medication came from during the manufacturing process, is usually found near the expiration date and is a string of numbers, letters, or both. You’ll use the lot number to determine if the medication is safe for use in the event a certain lot of medications are recalled due to a manufacturing error. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Forms_and_Calculations_of_Oral_Medication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QRl6fnziTOuC-2pCtiUH37bDT5eYL5Yp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Forms and Calculations of Oral Medication]]></video:title><video:description><![CDATA[Enteral medications are administered through the GI tract, either orally, rectally, or by a nasogastric or gastrostomy tube.  

Oral medications are available in tablets, capsules, and liquids, which can be either solutions or suspensions, and are the most commonly prescribed form of enteral medications for patients who are able to swallow.

As the nurse, you’ll perform medication calculations to ensure the correct dose of an enteral medication is administered.  

To calculate a dosing using the Dimensional Analysis, or DA, method, the three components you need are D, for the Desired dose, or dose ordered by the health care provider; H, for Have, or the dosage you have available; and V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid.

First, you’ll read the order, which is: acetaminophen 1 gram PO every 6 hours. 

Then, look at the medication label.

Since the medication comes in 500 mg per tablet, you’ll calculate how many tablets you should administer to achieve the desired dose. To do this, first identify your components, Desired, Have, and Vehicle. 

In this case, D is 1 gram, which was obtained from the health care provider’s order. H is 500 mg, which was obtained from the medication label. And V, is 1 tablet, which was also obtained from the label.  

Next, you’ll determine if a conversion factor is required. To determine this, compare the units of D with the units of H, and see if they’re the same. Because D and H are in different units, a conversion factor is needed. In this case, you’ll use the following conversion factor from grams to milligrams: 1 gram equals 1000 mg.

Now, set up your equation, where X is the dose you&amp;#39;ll administer in tablets, written like this: X number of tablets equals Vehicle over Have multiplied by Desired multiplied by the conversion factor for grams to milligrams. 

Remember, you should put the units you’re trying to convert to as the denominator so you can cancel, or cr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dimensional_Analysis_Method_for_Dosage_Calculation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lYb89pGhT4WpSEGe4kTEy5PQSHqCBAQp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dimensional Analysis Method for Dosage Calculation]]></video:title><video:description><![CDATA[As the nurse, you’ll perform medication calculations to ensure the correct dose of a prescribed medication is administered. The three methods for drug calculations are the basic formula, also called Desired over Have; ratio and proportion; and dimensional analysis. Let’s take a deeper look into the dimensional analysis method.  

As with the other methods for drug calculation, the three components involved in dimensional analysis, or DA for short, are D, for the Desired dose, or dose ordered by the health care provider; H, for Have, or the dosage you have available; and V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid. 

The dimensional analysis method is set up like this: 

X = Vehicle   x   Desired 
    	Have 

Now, before the drug dosage can be calculated, all units of measurement must be converted into one system, so they’re all the same. For example, if the medication is ordered in grams and comes in mg, then grams are converted to mg or mg are converted to grams. So, to do this, you&amp;#39;ll use conversion factors, which are simply equivalents of measurements, like 1 gram equals 1000 mg or 1 L equals 1000  mL.  

Let’s look at some drug calculations using the DA method. First, you’ll read the order, which is: acetaminophen 1 gram PO one time. Now, let’s look at the following label. Since the medication comes in 500 mg per 1 tablet, you’ll calculate how many tablets to administer to achieve the desired dose. To do this, first identify your components, Desired, Have, and Vehicle.  In this case, D is 1 gram, which was obtained from the health care provider’s order.  H is 500 mg, which was obtained from the medication label. And V, is 1 tablet, which was also obtained from the label.  

Next, you’ll determine if a conversion factor is required. To do this, compare the units of D with the units of H; and if they&amp;#39;re the same, no conversion factor is needed.  Because D is in grams and H is in mg, a conv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ratio_and_Proportion_Method_for_Dosage_Calculation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JugtgiWMSUCEHvx4EIqylcubTaefJzht/_.png</video:thumbnail_loc><video:title><![CDATA[Ratio and Proportion Method for Dosage Calculation]]></video:title><video:description><![CDATA[As the nurse, you’ll perform medication calculations to ensure the correct dose of a prescribed medication is administered. The three methods for medication calculations are the basic formula method; dimensional analysis; and the ratio and proportion method, or R&amp;amp;P for short.  

R&amp;amp;P is a method of dosage calculation using a ratio, which shows the relationship between two quantities, like 1:2; and a proportion, which shows the relationship between two ratios. 

Ratios and proportions can be set up two ways: vertically with fractions, or horizontally with colons.   

To solve an R&amp;amp;P problem set up as fractions, you&amp;#39;ll cross-multiply the numerator of the first fraction by the denominator of the second fraction, and then cross-multiply the denominator of the first fraction by the numerator of the second fraction. After that, division is needed as the final step to solve for the dose. 

To solve an R&amp;amp;P problem when it’s set up horizontally, the inside numbers, which are called means, are multiplied and then the outside numbers, which are called extremes, are multiplied. Then division is used to solve for the dose. 

Now, as with the other methods for medication calculation, the three components involved in Ratio and Proportion are D, for the Desired dose, which is the dose ordered by the health care provider; H, for Have, or amount you have available; and V, for Vehicle or the form in which the medication comes, like tablets or liquid.  

Now, before the drug dosage can be calculated, all units of measurement must be converted into one system of measurement, so they’re all the same. For example, if the medication is ordered in grams and comes in milligrams, then grams are converted to milligrams or milligrams are converted to grams. To do this, you&amp;#39;ll use conversion factors, which are simply equivalents of measurements, like 1 gram equals 1000 mg or 1 liter equals 1000 mL.  

Let’s look at some med]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Formula_Method_for_Dosage_Calculation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YVUEnaCNQNyQrv8zVtjvng2uRiKmhIIL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Formula Method for Dosage Calculation]]></video:title><video:description><![CDATA[As the nurse, you’ll perform medication calculations to ensure the correct dose of a prescribed medication is administered. The three methods for drug calculations are basic formula, also called Desired over Have; ratio and proportion; and dimensional analysis.  Let’s take a deeper look into the basic formula method.  

As with the other methods for drug calculation, the three components involved in the basic formula method are D for the Desired dose, or dose ordered by the health care provider; H for Have, or the dosage you have available; and V, for Vehicle or the form in which the medication comes, like tablets or liquid.  

The basic formula method is set up like this:  

X = Desired    x   Vehicle 
      	Have 

Now, before the drug dosage can be calculated, all units of measurement must be converted into one system, so they’re all the same. For example, if the medication is ordered in grams and comes in milligrams, then grams are converted to milligrams or milligrams are converted to grams. To do this, you&amp;#39;ll use conversion factors, which are simply equivalents of measurements, like 1 gram equals 1000 mg or 1 liter equals 1000 mL.Let’s look at some drug calculations using the basic formula method. 

First, you’ll read the order, which is: diphenhydramine 25 mg IV one time.  

Now, let’s look at the medication label:  

Since the medication comes in 50 mg per 1 mL, you’ll calculate how many mL you should administer to achieve the desired dose. To do this, first identify your components, Desired, Have, and Vehicle. 

In this case, D is 25 mg, which was obtained from the health care provider’s order. H is 50 mg, which was obtained from the medication label. And V, is 1 mL, which was also obtained from the medication label.  

Next, you’ll determine if a conversion factor is required. To determine this, compare the units of D with the units of H, and see if they’re the same. Because both D and H are in milligrams, no conversion factor is ne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parenteral_Medication_Administration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1MTFp_PMTIGfogMtwMG_9Qa5Te2fwRky/_.png</video:thumbnail_loc><video:title><![CDATA[Parenteral Medication Administration]]></video:title><video:description><![CDATA[Parenteral medications bypass the gastrointestinal system and can be administered through injection or the intravenous route. Four types of parenteral routes are intradermal, or ID; subcutaneous, or SUBQ; intramuscular, or IM; and intravenous, or IV.

Now, parenteral medications come in vials, ampules, or premixed IV bags. Vials are single- or multi-dose containers that are sealed with a rubber top through which a dose is drawn up with a needle and syringe. Another type of vial is the mix-o-vial, where a powdered medication and solvent are stored in separate compartments of the same vial and are mixed by pushing a plunger and releasing the stopper that separates them. Then, ampules are single-dose glass containers designed to break open by snapping along a scored line on the narrowed portion of the ampule’s neck. Be sure to open ampules using an alcohol wipe or sterile gauze to protect your fingers and use a filter needle to draw up the dose to prevent the medication from becoming contaminated with glass shards.

As the nurse, you’ll choose an appropriate syringe and needle to administer medication, so let’s review the types and parts of a syringe first. The three syringe types are hypodermic, tuberculin, and insulin. Hypodermic syringes come in a variety of sizes, with the 3 mL and 5 mL syringes typically used for injectable medication volumes between 0.5 mL and 5 mL, whereas tuberculin syringes are 0.5 mL or 1 mL in size and used when the volume of medication administered is less than 1 mL, like tuberculin skin tests. Then, there are insulin syringes, which are marked in units instead of milliliters and should only be used to administer insulin. They typically can hold up to 100 units.

So, all syringes have three main parts. The barrel, which is the outer shell that holds the medication, and the tip, which is also called a hub, is the end where the needle attaches. Lastly, the plunger is the inner part that fits inside the barrel and can move to withdra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Insulin_Dosing_and_Administration_Protocols</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uhBWkQhfTZuXpc9XX78oGUZyQge15R1_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Insulin Dosing and Administration Protocols]]></video:title><video:description><![CDATA[Insulin is a hormone secreted by beta cells in the pancreas that helps glucose enter the body’s cells, so it can be used for energy. In diabetes mellitus, insulin is either not produced at all, like in type I diabetes; or cells are resistant to insulin, like in type II diabetes. In either case, glucose can&amp;#39;t be utilized by the body’s cells, so it builds up in the bloodstream.   

Exogenous insulin, or synthetic insulin, can be administered to help regulate glucose levels, and is most often administered by subcutaneous, or SUBQ injection. It’s a commonly used, high-alert medication, meaning there’s an increased risk of patient harm if administered in error. This is because insulin can cause potentially dangerous hypoglycemia, or low blood glucose levels. 

Alright, so insulin typically comes in either a vial or a pen. Most insulin vials contain a concentration of 100 units of insulin per milliliter. It’s important to note that insulin doses are prescribed and measured in units, not milliliters so you’ll always use an insulin syringe, which measures increments of insulin in units. Insulin vials can include rapid-, short-, intermediate-, or long-acting insulins as well as pre-mixed solutions like 70/30 preparations, which contain 70 percent intermediate-acting insulin and 30 percent rapid-acting insulin. Most insulins are clear, but a type of insulin called NPH, which is short for neutral protamine Hagedorn is cloudy because a protein called protamine is added to prolong its action in the body over an extended period. 

There are also pre-filled insulin pens, which contain either 150 units of insulin per 1.5 milliliters or 300 units of insulin per 3 milliliters. These devices can be used for multiple injections for one patient. Before administering the insulin, a small disposable needle is placed on the end of the pen and the indicator dial is turned to the correct insulin dose. Following administration, the dose indicator returns to zero and the nee]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Principles_for_Drug_Reconstitution</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K812x4YsRcKtVQVYknAzM9RARkaRbaM_/_.png</video:thumbnail_loc><video:title><![CDATA[Principles for Drug Reconstitution]]></video:title><video:description><![CDATA[Reconstitution is the process of adding a liquid diluent, or solvent, to a powdered medication, or solute, and then dissolving the medication to form a solution. In some cases, reconstitution is necessary because a medication doesn&amp;#39;t remain stable long enough to be distributed in solution form, so it comes from the manufacturer in a powdered form and must be reconstituted with a liquid prior to administration.  

Now, if your patient is prescribed a medication that requires reconstitution, you’ll follow the steps of drug reconstitution to perform safe medication administration. First, read the directions on the medication label or medication insert; or you can consult the pharmacist at your facility. This information will tell you the type and amount of solvent to add to the powdered medication. Commonly used solvents include sterile water, bacteriostatic water, or sterile normal saline.  

Next, you’ll use a syringe and needle to draw up the desired volume of solvent from its vial and inject the solvent into the vial of powdered medication. After disposing of the syringe and needle according to your facility’s policy, you’ll typically roll the vial between your hands to mix it, unless the label specifies that you can shake it, making sure the medication dissolves completely, forming a solution. 

Some reconstituted medications are packaged in single-dose vials, meaning the vial and its contents should be disposed of following administration. Other reconstituted medications are packaged in multi-dose vials, meaning the contents can be stored and used later for additional doses. For multi-dose vials, be sure to label the vial with the date and time it was reconstituted, the expiration date and time, the dosage strength, and your initials. 

Okay, let’s look at some drug reconstitution examples. 

Let’s take a look at this label for methylprednisolone. 

First, read the directions on the label, which instruct you to use 2 mL of bacteriostatic water ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_Intravenous_Administration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sOMjH65FSGyZws2VN4O85ofoTVCKx21r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical Care Intravenous Administration]]></video:title><video:description><![CDATA[Medications used in critical care settings have significant physiologic effects; are typically administered intravenously, or IV; and they are usually administered by titrating, or adjusting, the infusion rate according to the health care provider’s order until the desired therapeutic effect is reached. Many of these medications are high alert medications, meaning they may cause significant harm to the patient if administered incorrectly, so these medications are always delivered through an IV pump to ensure accuracy. As the nurse, you’ll calculate volumes per unit of time, and dosages based on body weight.

To calculate a dose using the Dimensional Analysis, or DA method, the three components you need are D, for the Desired dose, or dose ordered by the health care provider; H, for Have, or the dosage you have available; and V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid.

Now let’s calculate an infusion rate using Dimensional Analysis.

First, you’ll read the order, which is: heparin 1300 units/hr IV continuous infusion.

Then, check the medication label.

Since the available dose is 25,000 units per 500 mL, you will calculate how many milliliters per hour to administer to achieve the Desired dose. To do this, first identify your components, Desired, Have, and Vehicle. And since there’s a time component, we also have T, for Time. 

In this case, D is 1300 units, which was obtained from the health care provider’s order; H is 25000 units, which was obtained from the medication label; V is 500 mL, which was also obtained from the medication label; and T is 1 hour, which was also obtained from the health care provider’s order.

Next, you’ll determine if a conversion factor is required. To determine this, compare the units of D with the units of H. They’re the same, so no conversion factor is needed. Likewise, since T is in hours and the infusion rate you’re calculating is in mL/hr, no conversion factor is need]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_Medication_Administration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ApP2yZhmQaa0JiU30G1ehClTQFmQqNzJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric Medication Administration]]></video:title><video:description><![CDATA[Physiological differences between children and adults alter the way medications are absorbed, distributed, metabolized, and eliminated, which means children require different dosages of medications and special techniques for administration. Most pediatric medications are dosed according to the patient’s current weight using either a prescribed dosage per kilogram of body weight or body surface area, known as BSA.  

Now, oral medications for pediatric patients are often formulated in a liquid or suspension. When measuring the quantity of a medication, be sure to use the measuring device supplied with the medication, like a dropper, oral syringe, spoon, or cup as these are calibrated to allow accurate measurement of a specific medication. 

As the nurse, you’ll perform medication calculations to ensure the correct dose of medication is administered.  

To calculate a dose using the Dimensional Analysis, or DA method, the three components you need are D, for the Desired dose, or dose ordered by the health care provider; H, for Have, or the dosage you have available; and V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid.    

Let’s look at a pediatric oral dosage calculation where a weight-based calculation is required.  

First, you’ll read the order which is: amoxicillin 15mg/kg PO every 8 hours. 

Then, check the medication label: 

Since the medication comes in 125 mg per 5 mL, you’ll calculate how many mLs you should administer to achieve the Desired dose. To do this, first identify your components, Desired, Have, and Vehicle.  

In this case, D is 15mg/kg, which was obtained from the health care provider’s order. H is 125 mg, which was obtained from the medication label. And V is 5 mL, which was also obtained from the medication label. You also need to know the patient’s weight, which is 33 pounds. 

Next, you’ll determine if a conversion factor is required. Since the ordered dose is in milligrams per kilogram a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intravenous_Medication_for_Labor_and_Delivery</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_kisIthWRe_I7plfe4GDUaZ_QYqcYGaT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intravenous Medication for Labor and Delivery]]></video:title><video:description><![CDATA[The administration of IV medications used during labor and delivery requires the nurse to calculate medication concentrations, infusion rates, and titration factors, along with close monitoring of how both the pregnant patient and the fetus respond to the medication. Some medications used in this setting, like magnesium sulfate and oxytocin, are considered high-alert medications, meaning they can cause significant harm if administered incorrectly. These medications are always delivered through an IV pump to ensure accuracy. 

To calculate a dose using the Dimensional Analysis, or DA method, the three components you need are V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid, H, for Have, or the dosage you have available; and D, for the Desired dose, or dose ordered by the health care provider; and since there’s a time component, we also have T, for Time. 

Magnesium sulfate is a medication used as tocolytic to slow contractions in preterm labor or to reduce the risk of seizures in patients with preeclampsia. It&amp;#39;s typically administered starting with a loading dose, or a higher dose given over a shorter duration, so the desired therapeutic effect is achieved more quickly. After the loading dose is administered, a maintenance dose, or a slower rate of administration is administered to maintain a therapeutic level.  

Let’s look at how to calculate a loading dose of magnesium sulfate in mL/hr. First, you’ll read the order, which is: magnesium sulfate 6 g IV in Lactated Ringer’s solution over 30 minutes. Then, check the medication label: The medication is available in a concentration of 40 g in 1000 mL of Lactated Ringer’s solution. In this case, D is 6 g, which was obtained from the health care provider’s order; H is 40 g, which was obtained from the medication label; V is 1000 mL, which was also obtained from the label; and T is 30 minutes, which was obtained from the health care provider’s order. 

Next]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Basic_Intravenous_Administration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xY-ZxdahSA2a03vxenfhfjrTSYauKjVc/_.png</video:thumbnail_loc><video:title><![CDATA[Basic Intravenous Administration]]></video:title><video:description><![CDATA[The intravenous, or IV, route is a common route for the administration of medications and solutions. Some common ones are antibiotics, electrolytes, and fat emulsions. 

IV medications can be administered through a peripheral intravenous catheter, or PIV, or a central venous catheter, or CVC. PIV catheters are typically inserted into veins on the hand or lower arms and are used for less than 1 week.  

On the other hand, CVCs are used for patients who need long-term infusions. They can be inserted at sites such as the internal jugular vein, subclavian vein, or femoral vein; and terminate at the junction of the superior or inferior vena cava and right atrium. If a central line is inserted peripherally, like in the basilic or brachial vein, it&amp;#39;s called a peripherally inserted central catheter, or PICC.  

Now, medications can be administered in 3 different ways: direct injection, continuous infusion, or intermittent infusion. 

First, medications given by direct injection are often referred to as IV push. This route uses the patient’s intravenous line to administer a small volume of medication directly into the bloodstream.  

When administering medications via direct injection, first, ensure the patency and status of the IV site by flushing with saline before use and assessing for redness, swelling, or pain at the site. Be sure to note the medication’s push rate, or the time spent administering the medication through the IV, since some medications should be pushed slowly, like furosemide, while other medications should be pushed quickly, like adenosine. Finally, if your patient is receiving multiple medications through the IV, ensure the medications and any fluids are compatible.  

As the nurse, you’ll perform medication calculations to ensure the correct dose of an IV medication is administered.  

To calculate a dose using the Dimensional Analysis, or DA, method, the three components you need are D, for the Desired dose, or dose ordere]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Eczema_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7y6_T-uETj21tw-bCzfA7kZvSTyZBJ1n/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Eczema in the Pediatric Patient]]></video:title><video:description><![CDATA[Nurse Lisa works in a primary care clinic and is caring for Jamie, a 2-and-a-half-year-old who was brought in for a rash, by her mother Claire. After settling Jamie in her room, Nurse Lisa goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Jamie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Lisa recognizes important cues, including Jamie’s skin assessment, which reveals several clusters of dry, red patches to her wrists and ankles. She also notes that Jamie is scratching her left wrist, which is eroded and excoriated. Nurse Lisa asks Claire about Jamie’s skin irritation. 

Nurse Lisa: I see that Jamie has some dry and reddened skin. When did these symptoms start? 

Claire: A few weeks ago, when the weather got colder. 

Nurse Lisa: Have you tried any treatments or therapies to help relieve the itching? 

Claire: Sometimes I put her in a hot bubble bath, but it doesn’t seem to help. I also put lotion on her every day, which helps a little. 

Next, Nurse Lisa analyzes these cues. Nurse Lisa understands that Jamie has an itchy inflammatory rash, and that Jamie’s scratching is causing excoriation. She also knows the breakdown of Jamie’s skin increases the risk for infection. Nurse Lisa recognizes that Jamie needs effective management of her rash.  She reports her assessment findings to the health care provider, who diagnoses Jamie with eczema, or atopic dermatitis, and prescribes oral loratadine and a topical corticosteroid to reduce pruritis and inflammation.  

Now, using the information she’s gathered, Nurse Lisa develops a priority hypothesis of impaired skin integrity. Then, Nurse Lisa generates solutions to address Jamie’s impaired skin integrity that will include pharmacologic and nonpharmacologic interventions; and she establishes the expected outcome that after intervening, Jamie’s rash will show improvemen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Cerebral_Palsy_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1eJG9aWqQii3SZ5n-8unt5HyQMi9zblZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Cerebral Palsy in the Pediatric Patient]]></video:title><video:description><![CDATA[Nurse Jamie works as a nurse navigator at a pediatric neurology clinic and is caring for Lily, a 9-month-old with a history of cerebral palsy. Nurse Jamie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Lily&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jamie recognizes important cues including Lily’s vital signs, which are temperature of 99 F, or 37.2 C, heart rate 115 beats per minute, respirations 32 breaths per minute, and oxygen saturation 95% on room air. Lily’s weight is stable when compared to her last visit. Nurse Jamie also speaks with Lily’s caregiver, Linda, who reports that during feedings at home, Lily frequently gags and doesn&amp;#39;t swallow her food. When Nurse Jamie attempts to feed Lily a spoonful of baby food, he notices Lily produces a tongue thrust, which moves the food out of Lily’s mouth.   

Next, Nurse Jamie analyzes these cues. He reviews the electronic health record, or EHR, and sees that Lily has a history of delayed oral-motor skills and poor jaw control when feeding from a bottle. He remembers that children with cerebral palsy often have issues with oral-motor skills that can result in difficulty feeding, weight loss, and speech delays. He also notes that coughing and choking while eating can predispose children with cerebral palsy to aspiration and other respiratory problems.  

Nurse Jamie realizes that Lily needs effective management of care from a multidisciplinary team to support her activities of daily living, or ADLs, such as feeding. Now, using the information she&amp;#39;s gathered, along with Lily’s medical history, Nurse Jamie chooses a priority hypothesis of impaired oral intake. Then, he generates solutions to address Lily’s impaired oral intake that will include nonpharmacologic interventions; and he establishes the expected outcome that after interveni]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skeletal_Disorders_and_Immobilization_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ACPlDb7nTQW3UYfI9EPJTTWbTIiXHR8h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skeletal Disorders and Immobilization in the Pediatric Patient]]></video:title><video:description><![CDATA[Scoliosis refers to a 3-dimensional deformity of the spine, that includes a rotational and lateral curvature that resembles an “S” or “C” shape.  

Now, scoliosis can be idiopathic, congenital, or neuromuscular. Idiopathic scoliosis is the most common type, which has no identifiable cause. On the other hand, congenital scoliosis develops due to abnormal intrauterine development of the spine and is present at birth. Lastly, neuromuscular scoliosis is associated with neuromuscular conditions like cerebral palsy, muscular dystrophy or atrophy, as well as spinal cord tumors and myelomeningocele. 

Okay so, scoliosis typically becomes apparent during adolescence, during the physiological growth spurt. This is when the body grows at a faster rate, and sometimes the skeletal system doesn’t keep up, resulting in a skeletal deformity like scoliosis, where there’s an abnormal rotation of the vertebral bodies around their vertical axis. As a result, the affected vertebral bodies rotate to the side of the spine that is curved outward, eventually causing the spine to take the shape of a letter “S” or “C.” This curvature further causes chest deformation, rib displacement, and asymmetry of distant parts of the body. 

Important complications include spinal stenosis, which is the narrowing of the spinal canal; pinched nerves; and altered body image that can impact the patient’s self-image and mental health. Additionally, abnormal anatomy of the chest can decrease pulmonary capacity and compromise respiratory as well as cardiac function. 

Clinical manifestations of scoliosis primarily include asymmetry of the shoulder and hip height, as well as differences in leg lengths. Some patients might also have one prominent shoulder blade or a prominence on one side of the back when bending forward.  

Diagnosis of scoliosis begins with the patient’s history and physical assessment. An X-ray is often used to determine the Cobb angle, which measures the severity of spinal deformity]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Diabetes_Mellitus_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ikPJDcSGQbGGnN1UUnQdTUQeQq6Z88gU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Diabetes Mellitus in the Pediatric Patient]]></video:title><video:description><![CDATA[Nurse Camden works on a pediatric Medical-Surgical unit and is caring for Tate, an 11-year-old who was recently admitted for new onset type 1 diabetes mellitus. After settling Tate in his room, Nurse Camden goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Tate’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Camden recognizes important cues including temperature 97.3°F or 36.2°C, pulse 101 beats per minute, respirations 19 breaths per minute, oxygen saturation 98% on room air, and blood pressure 105/70 mmHg. Tate’s mother is at the bedside and reports that lately, Tate’s been irritable, unusually hungry and thirsty, and he’s urinating frequently.   

Next, Nurse Camden analyzes these cues. He reviews the electronic health record, or EHR, and notes that Tate’s blood glucose level is 240 mg/dl and his hemoglobin A1C level is 7.8 percent. Nurse Camden also sees that Tate has lost four pounds in the past two months and that Tate’s urine is positive for glucose.  

Nurse Camden realizes that the glucose from the food Tate eats can’t move from his blood into his cells, due to a lack of insulin. Because of this, Tate isn’t able to convert the food he eats to energy, causing him to experience fatigue and increased hunger. He also realizes that Tate’s kidneys can’t reabsorb the excess glucose, so it ends up in the urine, where it pulls water out along with it as it&amp;#39;s eliminated, causing his other symptoms of frequent urination and increased thirst. Nurse Camden recognizes that Tate needs effective management of his blood glucose.  

Now, using the information he’s gathered, along with Tate’s medical history, Nurse Camden chooses a priority hypothesis of unstable blood glucose. Then, he generates solutions to address Tate’s unstable blood glucose using pharmacologic and nonpharmacologic solutions. Nurse C]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Genitourinary_Defects,_Disorders,_and_Infections_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PRvGdnOhTXWoiPRFbdfQlk79TdeIk_0C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Genitourinary Defects, Disorders, and Infections in the Pediatric Patient]]></video:title><video:description><![CDATA[Enuresis, also known as bedwetting, refers to involuntary urination in children who have passed the age of toilet training, which is typically around five years of age. Enuresis can be primary, which is when involuntary urination occurs in individuals who have never developed bladder control; or secondary, which is when involuntary urination occurs in individuals who had previously developed bladder control. If the involuntary urination occurs mainly during the day, it is called diurnal enuresis; and if it mainly occurs at night, it is called nocturnal enuresis.   

Now, the exact pathological process of enuresis remains unclear, though there are several factors that contribute to its development, and the cause is likely multifactorial.  

So, enuresis can be associated overproduction of urine, like with polydipsia and polyuria due to diabetes mellitus; or central diabetes insipidus, where there’s a lack of antidiuretic hormone, or ADH, which helps regulate the amount of water released by the kidneys into the urine.  

Then, sleep disorders, like obstructive sleep apnea can interrupt normal sleep patterns and prevent the child from waking up in response to a full bladder.  

Enuresis can also occur due to delays in motor or social functioning which can be associated with delayed bladder maturation and reduced functional capacity.  

In addition, psychosocial stressors, like abuse and family disruptions, like divorce or birth of a sibling, can be associated with enuresis. Other factors include medications, like valproate; infections, like cystitis, which can cause bladder inflammation leading to uncoordinated contractions; and constipation, which can reduce bladder capacity.  

The most important clinical manifestation of enuresis is recurrent, involuntary urination in bed or on clothes.  

Diagnosis of enuresis is based on detailed history and physical assessment and is confirmed using the Diagnostic and Statistical Manual for Mental Disorders fifth editio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Anaphylaxis_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9l3YORbRQ7q_wqh5mRvVPZErTtuGfEyL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Anaphylaxis in the Pediatric Patient]]></video:title><video:description><![CDATA[Nurse Anya works in the emergency department and is caring for Pablo, a 10-year-old who’s having difficulty breathing following a bee sting. After settling Pablo in his room, Nurse Anya goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Pablo’s care, by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Anya recognizes important cues, including Pablo’s vital signs which are temperature 98.2 F or 36.8 C, heart rate 128 beats per minute, respiratory rate 30 breaths per minute and labored, blood pressure 94/56 mmHg, and oxygen saturation 89 percent on room air.  

She notes angioedema to Pablo’s eyelids, lips, and tongue. She also notices that Pablo appears anxious.  While auscultating Pablo’s lungs, Nurse Anya hears wheezing in the upper lobes. She asks Pablo’s father, Ramón, who’s at the bedside, about the onset of Pablo’s symptoms. 

Nurse Anya: Has Pablo had a reaction to a bee sting before? 

Ramon: Well, he’s been stung once before, but nothing like this happened. 

Nurse Anya: Did you give Pablo any medicine before coming to the hospital? 

Ramon: No, we came straight here. 

Nurse Anya then analyzes these cues. She understands that Pablo’s first exposure to a bee sting caused his body to produce antibodies against bee venom, sensitizing him. Then, on his second exposure, the antibodies triggered the release of chemical mediators, causing smooth muscle contraction and bronchoconstriction, leading to Pablo’s wheezing and difficulty breathing.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Ventricular_Septal_Defect</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WbO5Q2z4StizOqx2J_kdybhiSB62KlJj/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Ventricular Septal Defect]]></video:title><video:description><![CDATA[Nurse Antoinette works on a pediatric cardiac unit and is caring for Mabel, a 1-year-old female with a history of ventricular septal defect, or VSD, who was admitted for a surgical repair. After settling Mabel in her room, Nurse Antoinette goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Mabel’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Antoinette recognizes important cues, including Mabel&amp;#39;s vital signs, which are temperature 98.6 F or 37 C, heart rate 142 beats per minute, respirations 35 breaths per minute, and oxygen saturation 92 percent on room air. Upon assessment, Nurse Antoinette notes a systolic heart murmur and crackles in the bases of her lungs. She also notices that Mabel appears to be irritable.  

Next, Nurse Antoinette analyzes these cues. She reviews the electronic health record, or EHR, and sees that Mabel was diagnosed with a VSD as a newborn. The health care provider recommended close monitoring of the condition rather than immediate surgical correction because she was hemodynamically stable and asymptomatic.  

Nurse Antoinette knows that a VSD causes a left-to-right shunting of blood in the heart, causing a mixture of deoxygenated and oxygenated blood to go back to the right side of the heart and then into the lungs, creating fluid overload in the lungs and increased pulmonary vascular resistance.She also understands that the shunting of blood is causing Mabel’s systolic murmur, and that the pulmonary congestion is causing the crackles in her lungs. Additionally, Nurse Antoinette knows that less oxygen is being delivered to the tissues, so Mabel’s impaired perfusion is causing tachycardia and decreased oxygen saturation. Nurse Antoinette recognizes that Mabel needs effective perfusion management.  

Now, using the information she’s gathered, Nurse Antoinette chooses a priority hy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Appendicitis_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2gttG4W3Sr_qx3tQglNbgWzmTtiBm0Do/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Appendicitis in the Pediatric Patient]]></video:title><video:description><![CDATA[Nurse Cameron works in the emergency department and is caring for Trevor, a 14-year-old patient who was brought in by his father, Steve, because of abdominal pain and vomiting. After settling Trevor in his room, Nurse Cameron goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Trevor’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Cameron recognizes important cues such as Trevor’s vital signs, which are temperature 100.4 F, or 38 C, heart rate 112 beats per minute, blood pressure 140/90 mmHg, respiratory rate 22 breaths per minute, and pain 9 out of 10 in his abdomen. He also notices Cameron appears anxious, grimacing, and is holding on to his right lower abdomen.  

Nurse Cameron: Trevor, can you tell me more about your pain? 

Trevor: I don’t know, it just really hurts. 

Steve: He hasn’t been acting like himself all week. Yesterday, he missed soccer practice because he didn’t feel good and then he threw up and had diarrhea last night. He can’t really keep any food or liquids down. I thought it was a stomach bug, but his pain got much worse this morning, so I brought him here. 

Nurse Cameron: Did Trevor have any injuries to his abdomen?  

Steve: Not that I know of. 

Nurse Cameron then performs an abdominal assessment and notes tenderness in Trevor’s right lower quadrant. Then, in the area between Trevor’s navel and anterosuperior iliac spine, known as the McBurney point, he presses down and quickly releases, which reveals rebound tenderness.  

Next, Nurse Cameron analyzes these cues. He reviews the electronic health record, or EHR, and sees that Trevor’s blood work shows leukocytosis with a left shift, and an elevated C-reactive protein, or CRP. Nurse Cameron notifies the health care provider who comes to the bedside and performs abdominal ultrasound which is positive for appendicitis. Trevor will need to unde]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Asthma_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e5KSXnSsQqauL0snUttTNSJ-SLerosrn/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Asthma in the Pediatric Patient]]></video:title><video:description><![CDATA[Nurse Lin works at a primary care clinic and is caring for Joey, an 8-year-old who’s had a cough for two months and recently developed chest tightness over the last two days. After settling Joey in the examination room, Nurse Lin goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Joey’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Lin recognizes important cues, including Joey’s vital signs which are temperature 98 F or 36.6 C, heart rate 94 beats per minute, respirations 26 breaths per minute, and oxygen saturation 93 percent on room air. Nurse Lin then completes a respiratory assessment and finds that Joey has expiratory wheezes in all lobes.  

She gathers additional information from Joey and his aunt, Angel, who’s at the bedside. 

Nurse Lin: Joey, I notice you’re having a hard time taking deep breaths, can you tell me more about that? 

Joey: My chest feels so tight. It’s hard to breathe.  

Nurse Lin: That must be very uncomfortable. When did you start feeling like this?  

Joey: I don’t know, I don’t feel good.  

Angel: He’s had a nagging cough for a while now. At first, I thought it was just the change in the weather making his allergies flare up, but his allergies don’t normally affect his breathing. That’s why I made the appointment.  

Nurse Lin: I’m glad you brought Joey in.  

Next, Nurse Lin analyzes these cues. She reviews the electronic health record, or EHR, and notes that Joey has no relevant medical history, other than seasonal allergies. She performs the ordered spirometry testing by having Joey breathe into a mouthpiece that’s connected to a device to measure the amount of air he’s able to breathe in and out. Nurse Lin notes that Joey can&amp;#39;t expel all the air after taking a deep breath.Then, she consults with the health care provider, who diagnoses Joey with asthma. 

Nurse Lin ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Family-Centered_Nursing_Care_During_Hospitalization</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GdlwI1_0SCKYitTL-nOaoNVvS-ekmynz/_.png</video:thumbnail_loc><video:title><![CDATA[Family-Centered Nursing Care During Hospitalization]]></video:title><video:description><![CDATA[Psychosocial needs of pediatric clients during illness and hospitalization can be challenging for nurses and other caregivers to meet. There are three main psychosocial effects that children experience during hospitalization, including fear, separation anxiety, and loss of control.

First, fear may arise from an unexpected occurrence of illness, potential physical harm, injuries, and pain. Children typically have a harder time adjusting to changes in the environment which may include scary equipment, smells, noises, other children crying, strange words, needles, and strangers in weird outfits, such as surgical gowns, masks, and caps.

Next is separation anxiety, which refers to the anxiety or emotional distress that a child experiences when separated from their caregiver, or their family, home, and friends. It can be characterized by anger and rejection of those who try to help. Anger can be followed by despair, where they become quiet and withdrawn. Also, the child’s loss of control over decisions, usual everyday routines, self-care, and play, can adversely affect their coping mechanisms and decrease their ability to deal with new stressful situations.

Now, a child’s reaction to illness and hospitalization can be affected by many things, including age, developmental and cognitive level, temperament, and coping skills. Other important factors include recent stressful situations, the nature and severity of the illness, and whether the hospitalization is planned, unplanned, or if it’s an emergency situation. Also, length of separation from parents, family members, and other familiar caregivers; their reaction to illness or hospitalization; as well as the child’s cultural, ethnic, and religious background, can all have an effect on a child’s reaction.

Okay, in terms of clinical manifestations, how a child expresses their emotions during illness or hospitalization varies depending on their age and stage of development. Starting with infants, children at this]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Externalizing_Disorders_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F8mRh4pZSzmZpZCK-bDNaxXYRySvdU8u/_.png</video:thumbnail_loc><video:title><![CDATA[Externalizing Disorders in the Pediatric Patient]]></video:title><video:description><![CDATA[Attention-deficit hyperactivity disorder, or ADHD, is classified as a neurodevelopmental disorder that develops before 12 years of age, and is characterized by developmentally inappropriate behaviors, including inattention, impulsiveness, and hyperactivity. 

The symptoms of ADHD are believed to be caused by decreased levels of certain neurotransmitters, specifically dopamine, which is involved in behaviors like risk taking, impulsiveness, and reward; norepinephrine, which is involved in alertness, attention, and focus; and serotonin, which plays a key role in regulating mood. There are also some structural abnormalities in parts of the brain, like the frontal lobe, cerebellum, and basal ganglia that are present in the brains of children with ADHD. 

Okay, so the exact causes of ADHD aren&amp;#39;t well understood, but it is likely due to a combination of genetic and environmental factors. ADHD has a strong genetic component, so a child with a parent or sibling diagnosed with ADHD is more likely to develop it themselves. ADHD is also associated with prenatal exposure to tobacco smoke, alcohol, or illicit drugs, as well as perinatal problems like prematurity or low birthweight. Other risk factors include exposure to lead; certain infections, like encephalitis; and adverse childhood experiences, such as neglect, abuse, or exposure to domestic violence. 

Now, children are often fidgety, talkative, and inattentive, but the behaviors of a child with ADHD are different because they’re considered developmentally inappropriate; they’re persistent, or always present; and they interfere with the child’s functioning and development.  

One of the major symptoms of ADHD is inattention, meaning the child may find it difficult to focus on tasks like conversations, games, or reading, and they&amp;#39;re easily distracted by extraneous stimuli like people talking, music, or other background noises. They often don’t appear to be listening when spoken to; they have diffi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion_of_the_Adolescent_and_Family</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bYdQCy6OTx_HZxvUX4GqEDibRhG0Sd2a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Promotion of the Adolescent and Family]]></video:title><video:description><![CDATA[Adolescence starts at the beginning of puberty and lasts until around 18 to 20 years of age. This period represents the transition from childhood to adulthood and encompasses important physical and emotional changes. To promote the health of your adolescent patient, you’ll support them through puberty and psychosexual development. Puberty is a complex physical and emotional process that typically begins between the ages of ages eight and 14.  

Now, puberty is under the control of the hypothalamic-pituitary-gonadal axis, which is a system of hormone signaling between the hypothalamus, pituitary gland, and gonads, either the testes or ovaries. During puberty, the hypothalamus begins secreting gonadotropin-releasing hormone, or GnRH, which stimulates the secretion of follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH, from the pituitary. These hormones then travel to the gonads and stimulate ovulation and menarche, or the first menstrual cycle in those assigned female at birth; and the production of sperm in those assigned male at birth. They also stimulate the production of sex-specific hormones, which are estrogen and progesterone in those assigned female at birth and testosterone in those assigned male at birth.  

The increased production of these sex hormones drives the development of primary and secondary sex characteristics in both sexes. Primary sex characteristics refers to growth of the genitals, which are the organs directly involved in sexual reproduction. Secondary sex characteristics refers to sex-specific physical characteristics that are not directly involved or necessary in sexual reproduction, like the growth of pubic hair in both sexes, the deepening of the voice in those assigned male at birth, and the development of breasts in those assigned female at birth.  

When caring for your adolescent patient, be sure to maintain modesty as much as possible, and give them a choice to speak to you without their caregiver in the r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion_of_the_School-Age_Child_and_Family</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fz4isPqjSyu3yahILe4NpxpDSZqtg8kK/_.png</video:thumbnail_loc><video:title><![CDATA[Health Promotion of the School-Age Child and Family]]></video:title><video:description><![CDATA[The school-age period begins when children start elementary school, at about 6 years of age, and lasts until they finish elementary school, at around 12 years of age.  Compared to younger stages, physical growth is slower and steadier, whereas social development is accelerated. To promote the health of your school-age patient, you&amp;#39;ll support the child’s nutrition, exercise and activity, and social development. 

Now, despite slower growth and decreased caloric needs during this period, the quality of the school-aged child’s diet takes on increased significance since their bodies are in the process of preparing for the increased growth that takes place during adolescence. However, there are certain factors that can cause gaps in nutrition during this period, such as changes in food preferences and increased access to foods that are not nutrient-dense, like foods that are high in sugar and fat.  

In addition, the school-aged child may have limited knowledge of how to balance what tastes good with what’s healthy for them. To promote nutrition, ask your patient about their likes and dislikes and what kinds of foods they’re eating while at school. Also ask their caregivers about typical meals eaten at home and teach them about the importance of a balanced healthy diet, which should include around three meals and 2 snacks each day.  

Since school-aged children tend to mimic the eating patterns and habits of their family and those around them, be sure to talk to your patient’s caregivers about how to role-model healthy eating habits, and encourage them to serve a variety of vegetables, fruits, dairy products, proteins, and whole grains. Also, advise them to limit fruit juice, soft drinks, salty snacks, and fast foods. Lastly, instruct them to minimize distractions from television and smart phones during mealtimes. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Poison_Exposure_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GrOPHqZpTfaKP04N8A9bLhXHQnyDpRzu/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Poison Exposure in the Pediatric Patient]]></video:title><video:description><![CDATA[Nurse Olivia works in the emergency department and is caring for Daisy, a 2-year-old who was brought in by Ellen, Daisy’s caregiver, after accidentally ingesting acetaminophen. After settling Daisy in her room, Nurse Olivia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Daisy’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Olivia recognizes important cues including Daisy’s vital signs which are temperature 98.6 F, or 37 C, heart rate 118 beats per minute, respiratory rate 30 breaths per minute, and blood pressure 92/52 mmHg. Nurse Olivia notes Daisy is pale and sweating. She also notices Daily is restless, whimpers occasionally, and is easily consoled by Ellen, so she determines Daisy’s pain rating is 3 out of 10 according to the Face, Legs, Activity, Cry, and Consolability, or FLACC, scale. A gentle abdominal assessment reveals no tenderness.  

Nurse Olivia: Ellen, can you tell me about what happened before you brought Daisy here? 

Ellen: Well, I was at home making dinner, when I noticed Daisy chewing while holding an open bottle of our acetaminophen pills.   

Nurse Olivia: How long ago was that? 

Ellen: About two hours ago. I must’ve left the bottle open after I took some pills for my headache. Then the phone rang, and I completely forgot to put the lid back on.  

Nurse Olivia: Do you have any idea how many pills she ingested? 

Ellen: I think she had about 13; it was a new bottle and I had only taken a couple for myself. 

Nurse Olivia: Do you know how many milligrams are in each pill? 

Ellen: 160 milligrams. 

Nurse Olivia: Okay. Then, after you discovered Daisy had taken the medicine, what happened next? 

Ellen: I called Poison Control right away, and they asked me how many pills were in the bottle too. Then they told me to bring Daisy to the hospital immediately. 

Nurse Olivia: You did the ri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion_of_the_Preschooler_and_Family</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wAwx8TKUSWKXdebSN_kgEh1TSW_Ds8h5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Promotion of the Preschooler and Family]]></video:title><video:description><![CDATA[The preschool period begins at about three years of age and lasts until about six years of age. During this stage, physical growth is maintained at a slow and steady pace, whereas cognitive and psychosocial development begin to accelerate. To promote the health of your preschool-age patient, you’ll support the child’s nutrition and their language and psychosocial development. 

Nutrition during the preschool period should include a variety of nutrient-dense foods to support the child’s growth, development, and activity levels. At the beginning of the preschool period, the child will have all their deciduous, or primary teeth, which allows them to eat a variety of foods, so this is a good time for caregivers to offer a range of healthy foods for their preschoolers to try.  

You can promote good nutrition by teaching caregivers how to help their child develop good eating habits. Begin by reminding them that their child’s eating habits can change during their preschool years. For instance, let them know that although the typical 3- to 4-year-old will still have distinct food preferences, older preschoolers tend to be more willing to try new types of foods. Likewise, younger preschoolers may have difficulty sitting down for the entire duration of a meal, while older preschoolers can start learning table manners and how to sit for the duration of a meal.  

Also encourage caregivers to help their preschoolers learn the social aspects of mealtimes by offering food at regular times, minimizing distractions during mealtimes, and teaching their child that mealtimes are not only a time to enjoy good food, but a fun time to spend together. Be sure to teach them that the quality of their child’s food is more important than the quantity eaten, so remind them that they shouldn’t force their child to remain at the dinner table until all their food is eaten, as this can make mealtimes unpleasant and lead to overeating.  

Teach them to provide three meals and two snacks ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion_of_the_Toddler_and_Family</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cpm3cEJgReush0Ewz9wMpcQUQkqHTk7F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Promotion of the Toddler and Family]]></video:title><video:description><![CDATA[The toddler stage of development begins at twelve months of age and ends at thirty-six months. During this stage, toddlers begin to explore the world around them as they grow and develop their social and motor skills. As the nurse, you’ll promote health of the toddler by supporting nutrition, toileting, social development, and safety. 

Toddlerhood is marked by slower physical growth than infancy, yet height and weight continue to increase steadily. At the same time, their stomach increases in size allowing toddlers to eat around three meals and 2 snacks per day. To support the growth and the increased energy requirements during this period, toddlers require nutrient dense foods, including vegetables, dairy products, proteins, and whole grains.  

When assessing the toddler&amp;#39;s nutrition, keep in mind that toddlers tend to develop distinct likes and dislikes of foods, and can become fussy eaters, and this can make it challenging for caregivers to ensure they&amp;#39;re getting all the necessary nutrients they need. So, be sure to assess for any nutritional gaps by asking caregivers about their toddler’s eating habits. Then encourage them to introduce alternative sources of nutrients, like mixing vegetables into a fruit smoothie, and providing additional nutrients, like vitamin D- and C-fortified beverages and iron-fortified cereal. Lastly, instruct caregivers to limit empty calorie products, like fruit juices and candy. 

A key developmental milestone of toddlerhood is becoming toilet trained. Toilet training becomes possible as the toddler’s bladder and bowel grow to accommodate urine and stool for longer durations. During this time, toddlers can wake up dry from a nap and can stay dry for at least 2 hours during the day. In addition, they start to sense the need to void and can sit on the toilet long enough to allow bowel movements to pass.  

When teaching caregivers about toilet training, reassure them that every toddler will develop this skill]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Common_Health_Problems_of_Infants</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NfvT3QSDSLup2zpslAbqH6OQQGiWz-FV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Common Health Problems of Infants]]></video:title><video:description><![CDATA[Failure to thrive refers to impaired growth and development due to inadequate nutrients that are needed to carry out the body’s essential functions, like bone and muscle growth, brain development, and cellular processes. 

Alright, so healthy growth and development requires the right balance of nutrients, like iron, calcium, fat, protein, and essential vitamins. Most infants get the nutrition they need from breastmilk or vitamin-D fortified formula during the first six months of life, and then from nutritious foods once they start eating solids. Without the proper nutrients, growth parameters like weight, length, and head circumference can be delayed, as well as developmental milestones, like rolling over and crawling. 

Now, there are four main mechanisms that contribute to failure to thrive. First, inadequate caloric intake can cause growth failure because there’s insufficient energy to meet the infant’s growth needs. This can occur due to inappropriate feeding methods, such as over-dilution of formula or giving the infant nutrient-poor foods, like juice; or problems with breastfeeding.  

Next, dietary deficiencies or chronic diseases can cause inadequate absorption of essential nutrients. For instance, a lack of vitamin D impairs the absorption of calcium required for bone growth, while celiac disease impairs absorption of essential nutrients in the small intestine. Then, there are conditions that cause increased metabolism, such as hyperthyroidism and congenital heart disease that lead to increased energy expenditure.  

Lastly, underlying diseases or conditions can contribute to defective utilization of nutrients, which can happen with genetic anomalies like Trisomy 21. Additionally, societal factors that can increase the risk of failure to thrive include poverty, food insecurity, child abuse and neglect, and inadequate nutritional knowledge.  

In failure to thrive, infants typically appear shorter or smaller than other infants of the same age, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion_of_the_Infant_and_Family</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VwbGMZQ8QQuTc0ciQLRCS6tJQuWL1UpH/_.png</video:thumbnail_loc><video:title><![CDATA[Health Promotion of the Infant and Family]]></video:title><video:description><![CDATA[Infancy is the stage between birth and twelve months, where infants undergo a series of rapid and dramatic changes involving their growth and development. It’s important to note that growth and development are two different concepts. Growth refers to physical changes in height, weight, and the appearance of the body; whereas development refers to the acquisition of complex motor, cognitive, and social skills, such as walking, speaking, turning a page in a book, or smiling at familiar faces.  To promote the health of the infant, you’ll assess gross motor development, social development, and promote safety.  

Gross motor skills, which are required for large body movements, like head control, rolling over, crawling, or walking, can be thought of in terms of developmental milestones. Infants typically achieve certain developmental milestones at specific ages, so you can monitor these milestones to see how the infant is developing, while keeping an eye out for any potential problems. 
 So, by 2 months, infants should be able to keep their head steady when being held and bring their head up and look forward while on their stomach. By 4 months, infants can sit with support, grasp objects with their hands, and start to roll over to one side.  

By 6 months, infants should be able to roll both ways and sit in a highchair with their back straight. Then, by 7 months, they can sit alone while leaning forward on their hands for support and by 8 months they can sit unsupported.  

At 9 months, infants are able to crawl and hold objects between the pads of the thumb and the index finger, known as the crude pincer grasp.  

Finally, at 12 months, infants can throw objects and might be able to stand by themselves and walk while their hands are held.  

As far as education goes, you should teach caregivers what to expect as their baby grows. In addition, teach them ways to promote their infant’s gross motor skills by placing them in a safe place so they can move their legs]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Common_Health_Problems_of_the_Neonate</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n5QJ9n0BTRKsr3-qzl-UjRZcSNeQmK-N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Common Health Problems of the Neonate]]></video:title><video:description><![CDATA[Birth injuries are bodily injuries sustained by the newborn during the birthing process. They are more likely to occur if there’s uterine dysfunction, like with prolonged labor or precipitous labor, which is labor that lasts less than three hours, resulting in a rapid delivery.  

Common risk factors for birth injuries are when the baby is large for gestational age; when there’s cephalopelvic disproportion, meaning that the presenting part is too large to fit through the mother’s pelvis;  when the fetal body is misaligned, like with a breech or brow presentation; when there’s shoulder dystocia, which can happen when one of the baby’s shoulders get stuck during delivery; or during a forceps or a vacuum-assisted delivery. 

The most common kind of birth injuries are soft tissue injuries, which typically occur as a result of excessive pressure as the fetus is pressed against the maternal pelvis. With sustained pressure, petechiae and bruising can often be seen on the baby’s head, neck, and face. Also, small blood vessels in the sclera can break, causing subconjunctival hemorrhages which look like red spots on the whites of the eyes. Lastly, when instruments, like forceps, are used, bruises and abrasions may appear on the sides of the face in the same shape as the instrument. Similarly, when a vacuum extractor is used, a clearly marked circle of petechiae, bruises, or abrasions can be seen on the occiput. 

Injuries can also occur when there’s trauma to the nerves during the birth process. Injury to the brachial plexus, which is a network of nerves responsible for carrying sensory and motor signals to the upper limbs, is one of the most common types of birth-related nerve injuries. This can happen when the position of the baby’s arm, shoulder, or neck are altered, so that stretching, pulling, or tearing of the brachial plexus occurs.  

When the upper plexus is damaged, it&amp;#39;s known as Erb palsy, and the resulting paralysis causes the affected arm ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vital_Signs_and_Pain_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9-r-yYi0R8uG9RX5k6OSN8V0TJ2R7CUA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vital Signs and Pain in the Pediatric Patient]]></video:title><video:description><![CDATA[Pain is a feeling of discomfort and an emotional experience that is a common occurrence in children of all ages. To provide optimal pain management, the nurse must perform age-appropriate pain assessments and interventions. 

Now, pain starts with a stimulus that can be mechanical, chemical, or thermal, which causes damage to tissue, and triggers the release of molecules like prostaglandins, histamine, and bradykinin. Special pain receptors called nociceptors are activated by these molecules, and in response, they initiate an action potential that’s transmitted from the site of injury to the cortex of the brain. Once it reaches the cortex, the patient experiences the pain and its characteristics, like its location and intensity, and an emotional response to the pain occurs.  

The first step in assessing your patient’s pain is by understanding their previous experience with pain. Then, to assess the severity of their pain, use a pain assessment tool. The choice of a pain assessment tool depends on the child’s age, cognitive development, and ability to communicate.  Usually, older school-age children can report their pain numerically on a zero to ten scale, with zero meaning no pain, and ten meaning the worst pain they can imagine. 

There’s also a verbal scale which allows children to describe their pain using adjectives, like “mild,” “moderate,” and “severe.” In addition, the Wong-Baker FACES Pain Rating Scale uses faces, each representing a level of pain, where the child points to the face that depicts how they feel. 

During your assessment, remember that the most reliable indicator of pain is your patient’s own report of pain, but there may be times that you’ll need to base your pain assessment on observing your patient’s behaviors and nonverbal cues such as irritability, restlessness, grimacing, and moaning in situations where they are not able to verbalize their pain.  

For example, the Premature Infant Pain Profile, known as PIPP, is a scoring syst]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_Sequence_and_Techniques_in_the_Pediatric_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JGVI9KFdQQ61aCXiCXHPappIR-GoV4Jc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment Sequence and Techniques in the Pediatric Patient]]></video:title><video:description><![CDATA[A comprehensive physical assessment allows the nurse to assess a child’s growth, development, and health status. As the nurse, you’ll assess the child’s general appearance, growth and physiologic measurements, and each body system.  

Now, unlike assessing an adult where a head-to-toe sequence is generally followed, with children, the sequence can be individualized to their developmental level. For instance, when examining infants, you’ll often need to auscultate lungs and heart when they are quiet and examine their oral cavity when they’re crying.  

You’ll also consider the child’s developmental stage when choosing techniques to prepare them for the examination. For infants, you could examine the child on their caregiver’s lap. For toddlers, you could use a doll to demonstrate what to expect during the examination or tell a story like “I’m checking to see if your tummy is hungry.” Likewise, you can teach school-age children about body parts and their function as you examine them. 

As you begin your assessment, observe the child’s general appearance including facial expression, activity level, speech, posture, and interactions with you and their caregivers. Take note of certain observations that warrant further investigation, like if you notice the child is tilting their head to a specific side, it could mean they’re having trouble hearing or seeing; or if they have dirty clothes or an unusual body odor, this may indicate neglect or financial difficulties at home.  

Next, you’ll assess the child’s physical growth by measuring their length or height, weight, and head circumference. Until the child is around 2 years old, you’ll typically measure length using a length board with the child in a supine position. Once they’re older and can stand, height is measured in the upright position, usually against a wall chart. Once you’ve obtained the measurements, you’ll plot them on a growth curve, and compare them to the expected percentile for age and sex. S]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Patient_History</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e7e0u0u1T7i_QfY8Ryx7BrSkR_yKQ_wl/_.jpg</video:thumbnail_loc><video:title><![CDATA[The Patient History]]></video:title><video:description><![CDATA[Collecting a client’s health history provides the nurse with information about their perceived health and factors that can impact their health. It should be completed as part of a comprehensive client assessment, like upon admission to the hospital, during a medical office visit, or as a part of a focused exam. 

Typically, the health history includes subjective data, or information the client is experiencing, such as when a client states, “I become nauseous after most meals.” This can guide the nurse to focus the physical assessment on the gastrointestinal system, as well as client education and the plan of care. 

Although the client is the preferred source of subjective data, if they’re unable to communicate a secondary data source can be used, such as a family member or caretaker. In addition, if the client doesn’t speak the same language as the nurse, an institutionally-approved medical interpreter should be used. 

Okay, let’s review how to conduct a health history. Now, you’ll want to collect your client’s health history in a private, quiet, and comfortable setting free from environmental distractions or interruptions. Also remember that as the nurse, you are responsible for collecting and documenting your client’s health history. And since it involves assessment and nursing judgment, the health history shouldn’t be delegated to another member of the healthcare team, like unlicensed assistive personnel.

Begin by establishing rapport with your client. You can do this by introducing yourself, including your name and role, and asking them how they would like to be addressed or if they have a preferred nickname. If there is someone accompanying your client, ask their name and relationship to your client. 

As you collect data, remember to look at them, and avoid focusing your attention on the electronic health record, or EHR. This will help avoid the impression that you’re not listening to them or that you are rushed. With each question, allow them the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_status_Physical_and_Cognitive_Examination_and_Findings</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PNj4PcBcQ6S-hiiUecSk6GZqSYWfkPG7/_.png</video:thumbnail_loc><video:title><![CDATA[Mental status Physical and Cognitive Examination and Findings]]></video:title><video:description><![CDATA[Mental status should be completed as part of a comprehensive assessment, or as part of a focused exam if a client is experiencing issues like confusion or memory loss. The mental status assessment provides the nurse with information about cognitive and emotional functioning. Let’s review the process of completing a mental status assessment.

Okay, so generally, you’ll need paper, pencil, and a copy of the mental status test you plan to administer. Then, prepare for the exam by ensuring your client is in a comfortable position, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains. Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

The method of assessment for a mental status exam is inspection.

First, let’s begin with appearance, which can be observed when your client moves into the exam room. When evaluating appearance, expect their posture to be erect and relaxed; and their movement should be smooth and purposeful. If your client appears restless or fidgety, this could be a sign of anxiety. Other unexpected findings include tics, which are sudden, repetitive movements like eye blinking or throat clearing; and tremors, which are rhythmic shaking movements. 

Then, observe your client’s grooming. Expected findings include good hygiene, appropriate dress for the client’s age, season, and weather; and there should be no obvious hygiene issues such as body or breath odor. Inappropriate dress or evidence of poor hygiene might indicate conditions like depression or cognitive disturbances like dementia.

Next, assess your client’s behavior, beginning with their level of consciousness. Your client should be awake, alert, oriented, and responsive to both internal to environmental stimuli. Unexpected findings include lethargy or drowsiness; or being obtunded, meaning yo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Skin,_Hair,_and_Nails</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5n0UtFFCQLiiygpaPE3-ALCvRU_IfT6G/_.png</video:thumbnail_loc><video:title><![CDATA[Assessment of Skin, Hair, and Nails]]></video:title><video:description><![CDATA[Assessment of the skin, hair, and nails should be completed as part of a comprehensive assessment or as a focused assessment if your patient is experiencing issues that affect the integumentary system. The methods of skin, hair, and nails assessment include inspection and palpation. 

Alright, start with a general inspection of the skin, which should be intact and without discoloration or lesions. Remember to check areas that are not commonly visible, such as the axillae, perineum, and between the toes.  

Begin by noting the thickness of the skin, which will vary depending on the body area. For example, calluses can appear on hands and feet due to frequent use, whereas the skin of the eyelids will be thin and delicate.  

Also note your patient’s skin color, which will range from shades of black, brown, and tan, to shades of pink and white. These variations in pigmentation are often due to factors like genetics and sun exposure. Remember to consider these natural variations in skin color and tone when assessing your patient’s skin. For example, in patients with lighter skin, rashes may appear pinkish-red, but in patients with darker skin, rashes may appear hyperpigmented or purplish in color. Bruising can appear purple, blue, or green in lighter skin but deep blue or black in darker skin.  

Likewise, cyanosis in lighter skin appears blue or purple, while cyanosis in darker skin can appear gray or green, and is more easily seen in the mucous membranes, lips, conjunctiva, and nail beds. Likewise, the yellow discoloration in jaundice can be obvious in those with lighter skin but can be subtle in those with darker skin, so looking at the sclera and palms of the hands may more easily reveal the discoloration. 

Some of the lesions you may see during inspection include macules, papules, vesicles, bullae, pustules, and plaques. A macule is a flat lesion, usually less than 1 centimeter in diameter that’s a different pigmentation from the rest of the skin. Exampl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Eyes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D7ATrQ0sTT2LR9NPDeeLNDRzRs2IjQ-U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of Eyes]]></video:title><video:description><![CDATA[Assessment of the eyes should be completed as part of a comprehensive client assessment or as part of a focused exam when a client is experiencing ocular issues, such as eye pain or blurred vision. This assessment gives the nurse information about vision and general eye health while helping to identify ocular problems at an early stage, such as glaucoma or cataracts. Assessment of the eyes includes several tests which will examine the eye itself as well as screen for ocular diseases or systemic diseases that manifest through the eye, like diabetes or liver disease. Let’s review the process of completing an eye assessment.

Okay, the supplies you’ll need for the eye assessment include a Snellen or Sloan chart, a Rosenbaum or Jaeger near vision card, a penlight, and an eye cover. You should prepare for the eye exam by ensuring you have adequate light, and that your client is comfortable in either a standing or sitting position. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Now, locating the anatomical landmarks of the eyes and surrounding tissue will help guide your assessment. These landmarks include the upper eyelids and lower eyelids, eyebrows, the inner canthus and the outer canthus, pupil, lacrimal sac, conjunctival sac, and iris. 

Alright, the methods of ocular assessment include inspection and palpation as well as a series of visual tests.

First, you should inspect the external eyes and the surrounding structures, starting at the eyebrows and moving downward. Eyelashes and eyebrows should be evenly distributed. Eyelids should be able to close and open all the way, and upper eyelids should extend equally over both eyes. 

If an upper eyelid droops and partially covers the eye, ptosis is present, which may be due to neuromuscular weakness from conditions such as myasthenia gravis or damage to cran]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Nose,_Mouth,_and_Throat</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k9qoCVBGTE2KuyKNVCjDKLB8Rg2J7Fvi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of Nose, Mouth, and Throat]]></video:title><video:description><![CDATA[Assessment of the nose, mouth, and throat should be completed as part of a comprehensive assessment or as a focused assessment if your patient is experiencing issues with their nose, mouth, or throat. The methods of nose, mouth, and throat assessment include inspection and palpation. 

Alright, first, you’ll inspect the external nose. The skin should be smooth, and the color should match the rest of the face. The nares, or nostrils, should be positioned symmetrically and appear relaxed. Flaring could indicate respiratory distress, and narrowing can obstruct the airway. Nares should also be free from discharge. Thick or purulent discharge may occur with an infection; and bloody drainage is typically related to trauma or injury.  

Next, using a nasal speculum and a penlight, gently push the tip of the nose up so you can inspect the internal nasal cavity. The tissue is normally slightly red and covered with fine hairs. The nasal septum should be smooth, without perforation, and positioned at midline. A lateral displacement of the septum, called a deviated septum, is often the result of an injury.  

Next, inspect the lips, which should be symmetrical, slightly moist, and smooth, with a distinct vermillion border between the lips and the skin of the face. The overall color should be pink in patients who have lighter skin, and there’s often a bluish undertone in patients with darker skin, which can give a false impression of cyanosis.  

Pale lips might be seen with anemia and cracked, or dry lips are associated with dehydration or exposure to wind and cold. Angular cheilitis, or cracks and redness at the corners of the mouth, can occur with iron or a vitamin B deficiency. Lesions on or around the lips can be caused by herpes simplex virus, skin cancer, or trauma. Lip swelling can be related to an allergic reaction or an injury.  

Following inspection of the lips, inspect the teeth and gums. The teeth can range in color including white, yellow, or grayish; an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Thorax_and_Lungs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Xj5iA1DWS52zaEwKWvZxN93HS-S-W9uA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of Thorax and Lungs]]></video:title><video:description><![CDATA[Assessment of the thorax and lungs should be completed during a comprehensive assessment or as part of a focused assessment if your patient is experiencing issues with their chest or lungs. Methods of assessing the thorax and lungs include inspection, palpation, percussion, and auscultation.  

Okay, as you begin your assessment, observe your patient for indications of respiratory discomfort. These may include a distressed facial expression or other cues such as a fast respiratory rate. Then, visualize the symmetry and shape of the chest both anteriorly and posteriorly. The anterior-posterior diameter of the chest should be less than the lateral diameter. When these are equal, it’s referred to as barrel chest. With a barrel chest, you may also notice the slope of the ribs will be more parallel, rather than the normal slightly downward slope, and the costal angle will be more than 90 degrees. A barrel chest can indicate a chronic respiratory condition, such as chronic obstructive pulmonary disease, or COPD for short.  

You should also inspect the chest, spine, rib cage, sternum, and trachea for structural abnormalities, such as pectus carinatum, also known as pigeon chest, where the sternum bulges outward, and pectus excavatum, or funnel chest, where the sternum is depressed inward. Other structural abnormalities include scoliosis, where there’s an abnormal lateral curve of the thoracic and lumbar spine; and kyphosis, or an exaggerated outward curvature of the thoracic spine. 

Also observe your patient’s respirations, which should typically be around 20 breaths per minute for the average healthy adult.  A respiratory rate over 25 0 breaths per minute is generally considered tachypnea and may occur due to anxiety, pain, or infection, whereas a respiratory rate of less than 12 breaths per minute is generally considered bradypnea and may occur because of an electrolyte imbalance or the effects of sedative medications. Also remember, when you&amp;#]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heart:_Examination_and_Findings</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cUSH4tpKTwGi4aRMgj7Itn11SrKKrhdU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heart: Examination and Findings]]></video:title><video:description><![CDATA[Assessment of the heart and neck vessels should be completed as part of a comprehensive client assessment or as part of a focused exam if the client is experiencing issues that might be related to the function of the heart, like chest pain or shortness of breath. Let’s review the process of completing an assessment of the heart and neck vessels.

Okay, the supplies you’ll need for your assessment include a stethoscope with a diaphragm and bell, gloves, and a good source of light. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands and stethoscope are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Before getting started, explain the procedure to the client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies. 

Now, locating the anatomical landmarks of the heart and neck vessels will guide placement of your hands and equipment. The neck is located between the clavicles and sternum and the base of the skull. It is supported by the cervical vertebrae, ligaments, as well as the sternocleidomastoid and trapezius muscles.

The carotid arteries are located on either side of the neck, behind the sternocleidomastoid muscle. The heart is positioned behind the sternum in the chest cavity, and is about the size of a clenched fist. When the client is upright, the top of the heart is called the base and the bottom of the heart is called the apex. The point where the apex reaches its farthest both laterally and inferiorly is called the point of maximal intensity, or PMI. The PMI usually rests at the midclavicular line at the 5th or 6th intercostal space.

Methods of assessment for the heart and neck vessels include inspection, palpation, and auscultation. Since this exam]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Blood_Vessels_-_Examination_and_Findings</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SAbImiO6QM_O15M24A_D8rNfRQiWusZn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Blood Vessels - Examination and Findings]]></video:title><video:description><![CDATA[Assessment of the peripheral vascular system should be completed as part of a comprehensive client assessment, or as part of a focused exam if the client is experiencing issues that might be related to the function of the peripheral vascular system, like arterial or venous ulcers.  Let’s review the process of completing an assessment of the peripheral vascular system.

Okay, the supplies you’ll need for your assessment include a stethoscope with a diaphragm and bell, a skin marker, a doppler ultrasound device, drapes, and a good source of light. 

Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands and stethoscope are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

Now, locating the anatomical landmarks of the peripheral vascular system will help guide your assessment.  Peripheral pulses that can be palpated include the carotid pulse, located on the neck behind the sternocleidomastoid muscle, or scm, just below the angle of the jaw; the brachial pulse, located in the center of the cubital fossa, medially to the biceps tendon; the radial pulse, found in the wrist along the lateral aspect of the forearm, just below the base of the thumb; the femoral pulse, located below the inguinal ligament, between the pubic and hip bones; the popliteal pulse, located behind the knees; the dorsalis pedis pulse, found on the dorsal aspect of the foot; and the posterior tibial pulse, located just behind the medial malleolus. 

Alright, methods of assessment for the peripheral vascular system include inspection, palpation, and auscultation. 

Let’s start with ins]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Abdomen</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ETCsibH0TLODQztSHb3XwpBuQIWOgEM5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of Abdomen]]></video:title><video:description><![CDATA[An assessment of the abdomen should be completed during a comprehensive assessment or as part of a focused assessment if your patient is experiencing issues with their abdomen or GI system. Methods of abdominal assessment include inspection, auscultation, percussion, and palpation, as well as special tests. Unlike other body system assessments, you should always auscultate first when performing an abdominal assessment, so you can avoid stimulating bowel sounds or inflicting pain during percussion or palpation. 

Beginning with inspection, look between the costal margins and the symphysis pubis, and note the abdomen’s normal contour, which will be either flat; slightly convex, which is a curved outward appearance; or slightly concave, which is a curved inward appearance. An abdomen that’s profoundly concave could indicate malnourishment and a profoundly convex abdomen is associated with ascites, poor muscle tone, or an accumulation of subcutaneous fat.  

The skin of the abdomen should be free from lesions, including open wounds or ecchymosis. However, as a normal finding, you may note striae, or stretch marks, as well as hair, moles, or freckles. Also note any bodily modifications like tattoos, piercings, or surgical scars.  

Now, if you are inspecting the abdomen of a very thin patient, you might be able to see pulsations in the region of the abdominal aorta. This can be normal, however, if pulsations are prominent, it may represent an abdominal aortic aneurysm. Also, inspect for any obvious bulging or protrusions, which can represent herniation.   

Next up is auscultation. Start with the diaphragm of your stethoscope and begin in the lower right quadrant, moving in a clockwise fashion, listening for bowel sounds, which sound like high-pitched clicks and gurgles. It’s normal to hear bowel sounds in each quadrant at a frequency of 5 to 35 sounds per minute.  

If bowel sounds are not heard, you should auscultate up to a full 5 minutes in each quadrant. B]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lymphatic_System:_Examination_and_Findings</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZawEloNGT2uzLyetK3qW-VjGQi2fQxvi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lymphatic System: Examination and Findings]]></video:title><video:description><![CDATA[Assessment of the lymphatic system should be completed as part of a comprehensive assessment, like during a routine physical exam, or as part of a focused exam if a client is experiencing issues such as lymphadenopathy, or enlarged lymph nodes. The lymphatic system provides the nurse with information about the integrity of the immune system, as well as the body’s ability to regulate fluid and remove waste. Let’s review the process of completing a lymphatic system assessment. 

Okay, the supplies you’ll need to assess the lymphatic system include a tongue depressor, pen light, and washable marker or pen. 

Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Before getting started, explain the procedure to your client and be sure to answer any questions they have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies. 

Locating the anatomical landmarks of the lymphatic system will help guide the placement of your equipment and hands throughout your assessment. To find the  palpable lymph nodes in the head and neck region, start at the base of the skull to locate the occipital nodes. Then, move over the mastoid process to find the postauricular nodes, and then to the front of the ear to find the preauricular nodes. 

Next, the parotid and tonsillar nodes are accessible at the angles of the mandible; the submandibular nodes are halfway between the tip and angle of the mandible; and the submental nodes are just behind the tip of the mandible. 

Moving down the neck, locate the cervical nodes around the sternocleidomastoid muscle; the posterior cervical nodes along the anterior border of the trapezius muscle; and then move to the supraclavicular areas, which are in the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Male_Genitalia:_Examination_and_Finding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i-U23MwARm2gxdWOpo75-463SeiMWNiQ/_.png</video:thumbnail_loc><video:title><![CDATA[Male Genitalia: Examination and Finding]]></video:title><video:description><![CDATA[Assessment of the male reproductive system should be completed as part of a comprehensive client assessment, like during a routine physical exam, or as part of a focused exam if the client is experiencing issues like testicular pain. This assessment provides the nurse with information about the client’s reproductive health. Now, let’s review the process of completing an assessment of the male reproductive system.

Okay, the supplies you’ll need include drapes, gloves, penlight, sterile swabs in the event a culture needs to be collected, and a good source of light. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. 

Now, as the nurse, you may assist the healthcare provider or act as a chaperone, which is often required by facilities to protect clients and clinicians during exams of the reproductive system. During the examination, keep in mind that this process can be emotionally uncomfortable and anxiety-producing for some clients, particularly those who have experienced sexual trauma or who are transgender. Be sure to use the patient’s indicated pronouns and be aware of variations in the genitals for those who have had gender affirming surgeries. It’s also crucial to explain exactly what will happen at each step of the exam. Remember to avoid rushing your assessment, use a gentle touch, and to let your client know that at any time the exam can be stopped or paused if they request it.

Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

During this assessment, you will locate the penis, which consists of the shaft, glans, and urethral meatus; s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Female_Genitalia:_Examination_and_Findings</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Uc9exwchQZed7CkwOu7x7q4PRm_wr7XO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Female Genitalia: Examination and Findings]]></video:title><video:description><![CDATA[Assessment of the female reproductive system should be completed as part of a comprehensive client assessment or as part of a focused exam if the client is experiencing issues, such as vaginal discharge or pain with intercourse. This assessment provides the nurse with information about the genitalia, as well as general sexual and reproductive health. This assessment applies to any client with female reproductive organs, regardless of their gender identity. 

Okay, the supplies needed for the female reproductive exam include drapes, gloves, and a good source of light. For certain parts of the exam, the nurse will assist the healthcare provider or act as a chaperone, which is often required by facilities to protect your client and clinician during female reproductive exams. 

Before getting started, ask your client to empty their bladder, because a full bladder can make the examination uncomfortable. Also, ensure the temperature in the room is comfortable, and warm your hands since cold temperatures can cause rigidity of the pelvic muscles. Remember to provide privacy by closing the door and curtains. 

Before getting started, be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies. Then, assist your client into the lithotomy position, meaning they are lying flat on their back with their feet in stirrups. You’ll help your client get into this position by sliding their buttocks to the end of the examination table and draping them in a way that minimizes unnecessary exposure. You should lay the drape above their knees, up to the symphysis pubis, and then let the drape hang low between the knees. 

During the examination, keep in mind that the female reproductive assessment can be uncomfortable, both physically and emotionally, so some special considerations should be made while completing this assessment. It’s crucial to explain exactly what will happen at every step. Furthermore, th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Anus,_Rectum,_and_Prostate</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6TjD3vTvT1a0srydwOXI5x8xTWeKNNU4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of Anus, Rectum, and Prostate]]></video:title><video:description><![CDATA[Assessment of the anus, rectum, and prostate should be completed during a comprehensive assessment or as part of a focused assessment if your patient is experiencing issues with their anus, rectum, or prostate. Inspection and palpation are used to assess the anus; and the rectum and prostate are palpated through a digital rectal exam, or DRE, performed by the health care provider. As the nurse, you will act as a chaperone or assist with this part of the assessment. 

Begin your assessment by inspecting the pilonidal area, which is the area at the base of the tailbone at the cleft of the buttocks, just where the buttocks begin to divide. The skin should appear smooth without lumps, hair, warts, rashes, excoriation, or dimpling. If a pilonidal cyst, or sinus is present, this could be due to a congenital anomaly or related to excessive or repeated pressure on the sacrococcygeal area.  

Next, to inspect the perianal area and anus, spread apart the buttocks, and use a penlight for adequate visualization. The skin directly surrounding the anus is normally more coarse and darker in pigmentation than the rest of the surrounding skin. Unexpected findings include anal warts, which are related to infection with human papilloma virus, or HPV; and irritation, which may occur with fungal infections or pinworm. Other unexpected findings include lesions, polyps, fissures, and skin tags. You’ll also inspect for signs of constipation, such as a protrusion of a dry, hard stool, and the presence of external hemorrhoids, or swollen, inflamed veins. 

Now, palpation is typically performed by the health care provider with assistance from the nurse. Starting with the perianal area, this location should be free from tenderness or lumps. If your patient reports pain or tenderness upon palpation, this may indicate a perianal abscess, or an infection of the anal tissue; an anal fistula, where an inflammatory tract forms at the anus and runs through the perianal skin; or pruritus ani]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Musculoskeletal_System</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ESTjeOAkQDGFGHErQEWPpPNjRNCoCN-n/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of Musculoskeletal System]]></video:title><video:description><![CDATA[Assessment of the musculoskeletal system should be completed during a comprehensive assessment or as part of a focused exam if your patient is experiencing issues with their musculoskeletal system. Methods of musculoskeletal assessment include inspection, palpation, and special tests. 

Alright, so inspection begins when you first meet your patient, as you observe their posture, which should be upright, and movement should be even, smooth, and painless. While your patient is standing, inspect their general body shape and structure. Inspect the spine from the neck to the hips, and check for the normal curves of the spine, which include a concave curve of the cervical and lumbar spines, and a convex curve of the thoracic and sacral spines.  

Note any alterations in spinal curvature such as lordosis, or an exaggerated inward curvature of the lumbar spine, sometimes seen in pregnant patients; kyphosis, where the upper spine appears more rounded, which can occur in elderly patients; and scoliosis, or a lateral curvature of the spine, usually discovered in childhood.  

Next, inspect the posterior head and neck. The head should be positioned midline and aligned with the shoulders, spinal column, and gluteal cleft, which is the area just below the sacrum where the buttocks begin to separate. The shoulders should be symmetrically positioned on either side of the upper trunk, and the iliac crests of each hip should be even and symmetrical.  

Then, check the knees, which point forward and be aligned with the trunk. If they deviate outward, it&amp;#39;s called genu varum or bow leg; if they deviate inward, it’s called genu valgum, or knock knee. Move to the ankles, feet, and toes, which should face forward and align with the tibia bones. Each foot should have a longitudinal arch; however, over time, the feet can begin to flatten as a result of weight bearing. Other foot variations include pes planus, or a foot that stays flat even when not bearing weight, and pes ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neurologic_System_-_Examination_and_Findings</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I7vHNXz3TR_DkhmKEnCbcDR0SN_AKwVf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neurologic System - Examination and Findings]]></video:title><video:description><![CDATA[Assessment of the neurological system should be completed as part of a comprehensive client assessment, or as part of a focused exam if the client is experiencing issues that might be related to neurological function, like a facial droop or confusion. Now, let’s review the process of completing a neurological assessment. 

Okay, the supplies you’ll need include a cotton ball; a tuning fork; an object that can be easily recognized by touch like a paper clip, key, or coin; a reflex hammer; a tongue blade; drapes, and gloves. Then, prepare for the exam by ensuring your client is in a comfortable position, that your hands are warm, and that the temperature in the room is comfortable. Provide privacy by closing the door and curtains, properly draping your client, and only exposing areas of their body as needed to perform your examination. Before getting started, explain the procedure to your client and be sure to answer any questions they might have before obtaining verbal consent. Then, perform hand hygiene and collect your supplies.

While much of the neurological system assessment involves observation, you will need to locate the deep tendon reflexes to assess spinal cord intactness. Commonly tested deep tendon reflexes include the triceps, biceps, brachioradialis, patellar reflexes, and achilles reflexes. 

Alright, the methods of assessment for the neurological system include inspection and palpation. Your assessment will evaluate your client’s cerebellar function, which includes the client’s balance and coordination; sensory function, which includes their ability to feel and differentiate between light touch and pain; and motor function, which includes deep tendon reflexes. 

Okay, begin your assessment of cerebellar function by observing your client’s gait, or how they walk. You can take the opportunity to do this as they enter the examination room or, if they are seated or in a bed, you can ask them to stand and walk across the room. While they ambulate]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Comprehensive_Assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wwonvmAISc6MrSk1AoyP8SnpSuyv1pdN/_.png</video:thumbnail_loc><video:title><![CDATA[Comprehensive Assessment]]></video:title><video:description><![CDATA[A comprehensive assessment is a complete, head-to-toe physical examination, and should be done when first encountering your patient or when changes to their health status occur. Methods of comprehensive assessment include inspection, percussion, palpation, and auscultation. 

To begin, perform a general overview of your patient. Observe their mobility as they enter the room, which should be smooth and coordinated. While your patient is standing, measure their height, weight, and waist circumference. Next, with your patient in a seated position, assess their general appearance, including nutritional status, any obvious signs of distress, or physical deformities. Observe their level of alertness and orientation to person, place, time, and circumstance. You will also observe the qualities of their speech, including word selection, fluidity, and vocal clarity.  

As you move through your assessment, assess your patient’s hair, skin, and nails. Check for lesions, discoloration, and changes in skin and nail texture. To assess your patient’s head and face, inspect and palpate scalp, hair, and cranium, checking for any defects or lesions. Inspect their face for expression and symmetry, which represents an intact cranial nerve VII. You can also test cranial nerves V and VII by asking them to clench their teeth, squeeze their eyes tightly shut, and puff out their cheeks. Then, using the pads of your index and middle finger, palpate the temporomandibular joint as your patient opens and closes their mouth. Lastly, palpate the maxillary sinuses and the frontal sinuses by applying firm pressure over each sinus region. 

Next, move on to the eyes. Inspect the external eye structures and the conjunctiva, sclerae, and iris. Assess their near vision to test the function of cranial nerve II and assess the extraocular muscles of the eyes using the six cardinal positions of gaze, which will test cranial nerves III, IV, and VI. Lastly, use a penlight to test for PERRLA, meaning]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_During_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XgnsCbGlQaaYhxs-tDz1E_KMTR6LmHTp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment During Pregnancy]]></video:title><video:description><![CDATA[Assessment during pregnancy involves evaluating maternal and fetal health with the goal of a healthy pregnancy outcome. During the assessment, you’ll collect subjective data, or information your patient states, as well as objective data, or information you collect through observation. 

Begin by collecting information about your patient’s reproductive and sexual health. Ask about their history of gynecological surgeries, especially those involving the cervix, since this could increase the risk of cervical insufficiency and early pregnancy loss; or the uterus, since this can increase the risk of obstetric complications like fetal malpresentation or uterine rupture.  

Also, review your patient’s obstetric history using the GTPAL notation, to document Gravidity or how many times your patient has been pregnant; the number of Term pregnancies and Preterm births; if they’ve had either a spontaneous or elective Abortion; and the number of Living children.  

Lastly, determine if they have a history of sexually transmitted infections, or STIs, which are risk factors for premature rupture of membranes, preterm labor, as well neonatal infections and birth defects. 

Next, focus on their current pregnancy. Ask them about the first day of their last menstrual period and use this date to calculate the expected date of delivery, or EDD for short, using Naegele’s rule. Then, inquire about any new symptoms like pain, vaginal discharge, fatigue, or nausea and vomiting. Also be sure to ask them how they are feeling about their pregnancy, if the pregnancy was planned, and if they have any concerns that could adversely affect their pregnancy, such as intimate partner violence, lack of social support, or economic constraints. 

Finally, review their medical history. Inquire about conditions that could complicate the pregnancy, like diabetes, hypertension, or asthma; current medications; known allergies; and immunizations. Also ask about their daily routine, including diet, ph]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Examination_Techniques</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FSSln2P3QIOSh82rNDOREsO7Qj6CyALM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Examination Techniques]]></video:title><video:description><![CDATA[A physical assessment involves using examination techniques to collect data about a patient’s health, and includes inspection, palpation, percussion, and auscultation.  

Inspection involves visually assessing your patient. It begins when you first see your patient and continues throughout the examination. These initial observations can include their general demeanor, facial expression, gait, and how they answer your questions. Your findings during your initial inspection can affect how you approach the rest of your exam; for example, if you notice your patient is guarding their stomach, you’ll likely start with an abdominal assessment. In addition to your visual assessment, use your sense of smell to alert you to issues such as a strong body odor or a foul-smelling discharge from a wound. 

Palpation is where you’ll use touch to assess texture, temperature, moisture, pulsations, organ location and size, as well as the presence of swelling, lumps, and pain. You’ll use light palpation to detect superficial problems, like the presence of tenderness or changes in skin texture; followed by deeper palpation for determining the characteristics of organs and masses. Keep in mind that with deep palpation you should apply intermittent pressure and stop if your patient experiences pain. 

Now, depending on what aspect you’re assessing, you’ll use different parts of your hands during palpation. For example, the pads of your fingers are best suited to feel skin texture, swelling, pulsation, and masses; the dorsal, or back side of your hand, is most sensitive to temperature, so it can be used to feel heat and cold; and the ulnar surface, or side of the hand closest to the pinky fingers, can be used to detect vibrations.  

Percussion involves tapping on the surface of your patient’s skin with short, sharp strokes to produce sounds or vibrations, which can help determine the size, shape, and density of body tissue. Percussion can be direct, where you’ll percuss directly]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Examination_Equipment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WrESPSOrQEGNoerHczcw3VerQO_OshIv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Examination Equipment]]></video:title><video:description><![CDATA[As the nurse, you’ll use examination equipment as you perform a physical assessment to collect information about your patient’s health status. Several commonly used items include a stethoscope, otoscope, ophthalmoscope, penlight, and tape measure.  

A stethoscope is used to auscultate, or listen to sounds made by your patient&amp;#39;s body, like lung, heart and bowel sounds. Your stethoscope should have both a diaphragm and a bell. The diaphragm is used to detect high-frequency sounds like bowel or lung sounds, while the bell is used to detect low-frequency sounds, like heart sounds. When you’re using the diaphragm, you’ll place it firmly against your patient’s skin. But when you’re using the bell, you’ll place it lightly on your patient’s skin, since too much pressure causes the bell to act like the diaphragm, and it won’t effectively transmit low-frequency sounds.  

Also remember to eliminate potential artifacts, which are extra sounds that can affect what you hear through the stethoscope. These can be caused by noises in the room, the patient’s body hair or clothing, or touching the tubing on the stethoscope. To eliminate artifacts, perform auscultation in a quiet setting, avoid bumping the tubing, and be sure to place the diaphragm or bell directly on your patient’s skin instead of auscultating through clothing. Lastly, when putting the earpieces into your ears, remember to keep them pointed in the same direction as your ear canals, which means they should be pointing toward your nose.  

Next is the otoscope, which is a device that shines light into the ear to visualize the ear canal and eardrum, also known as the tympanic membrane. The base of the otoscope serves as the handle, which also contains the batteries for the light source and the on-off switch. The handle attaches to the head, which contains the magnifying lens and light source. You’ll attach an appropriately sized, disposable, plastic speculum to the head, which funnels the light into ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_Vital_Signs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y4koierKSGewwUbKN3Ug0-kiQNmVEG8T/_.png</video:thumbnail_loc><video:title><![CDATA[Assessment of Vital Signs]]></video:title><video:description><![CDATA[Vital signs are objective measurements of some of the body’s essential functions and include temperature, pulse, respiratory rate, blood pressure, and oxygen saturation.

Now, the body’s cells need a stable thermal environment in order to maintain basic metabolic processes, so the hypothalamus works like a thermostat to keep the body’s core temperature stable. This process, called thermoregulation, balances heat production with heat loss.

To assess your patient’s temperature, you’ll use a thermometer and measure from one of five sites: the oral cavity, tympanic membrane, temporal artery, axilla, or rectum. The rectum is the most accurate because it closely reflects the body’s core temperature but is typically only used when other routes are impractical, like with a very confused patient. In general, you should select a route based on your facility’s policies, available equipment, and your patient’s needs.  

A normal temperature is around 37.2 C or 99 F but can vary based on route. For infants and children, normal temperature range can be wider compared to adults because their thermoregulatory mechanisms are less effective.

Okay, moving on to pulse. As the heart pumps blood to the body, the blood causes a pressure wave against the arterial walls called a pulse, which correlates with the heart rate. It can be felt in arteries close to the skin, like the carotid artery, radial artery, or femoral artery; as well as the apex of the heart.

To assess the pulse, you’ll use two to three fingers to firmly palpate the artery, being sure not to obliterate it. If the rhythm is regular, count the pulsations for thirty seconds, and then multiply that number by two to calculate the beats per minute. If the rhythm is irregular, count for a full minute. At the same time, assess the amplitude of each pulsation, which is how strong the pulse feels against your fingers.

The pulse rate in adults is typically 60 to 100 beats per minute with a regular rhythm. In infants and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain_Assessment_and_Associated_Behaviors</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-yq6IBzoRPynp7ET2GZjfiTRQf2R22BM/_.png</video:thumbnail_loc><video:title><![CDATA[Pain Assessment and Associated Behaviors]]></video:title><video:description><![CDATA[Pain is a feeling of discomfort that ranges from mild to severe, usually caused by an underlying condition, and can be acute or chronic. Acute pain is typically short-term and resolves once the underlying cause is addressed, while chronic pain lasts for six months or more. To perform a pain assessment, you’ll collect subjective and objective data about your patient’s pain. 

Pain is a subjective experience, meaning that it’s based on a person’s perceptions and feelings, which can differ depending on their pain threshold, or the point when they start noticing pain; and pain tolerance, which is the amount of pain someone can endure. So, your patient’s report and description of pain is the most reliable source of information about their pain. 

To obtain subjective data about your patient’s pain, ask them a series of questions. Begin by asking them to rate their pain using a standard tool, like a numeric scale that uses zero to ten to indicate pain level, with zero meaning no pain and ten meaning the worst pain possible. Sometimes older adults might prefer a pain scale that uses words like no pain, mild pain, or severe pain. For pediatric patients, it’s common to use the Faces Pain Scale where each face represents a different level of pain.  

For a more detailed description of your patient&amp;#39;s pain, use the mnemonic OPQRST. First, O stands for onset, or when the pain started, which can be sudden, gradual, or progressive. Then, P stands for provocation and palliation, meaning whether certain factors make the pain worse, like pressure or movement; or better, like ice or medication. Q is for quality of pain, such as sharp, dull, burning, or achy; and if it&amp;#39;s intermittent or constant. R stands for region, which is the area of the body where the pain is felt; and radiation, or if the pain spreads to other areas of the body. 

Next, S is for severity, which your patient can quantify using a standardized pain scale. The severity can also determine w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessing_Nutrition_Status</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/REPInK2aRmu1mZRVB4kBtvfURQWhl9eD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessing Nutrition Status]]></video:title><video:description><![CDATA[Nutritional assessment involves the collection and analysis of subjective data, or the information your patient shares with you, and objective data, or the information you observe. As the nurse, you’ll use information about your patient’s nutritional status, which is the balance of nutrient requirements and intake, to provide insight into your patient’s overall health. 

Start your collection of subjective data by gathering information about your patient’s eating patterns and access to food. You can use tools such as a 24-hour diet recall, where your patient lists everything they have had to eat or drink in the past 24 hours; a food frequency questionnaire, that estimates how often they eat certain foods; or a food diary, where they keep track of everything consumed over a certain period. Then, ask about religious or cultural diet traditions or restrictions, as well as food allergies or intolerances that could influence their eating patterns. Lastly, be sure to gather information about their access to transportation to a grocery store, who shops for and prepares their food, and any difficulties obtaining or preparing food.   

Next, determine if there are any physiological factors that can impact their nutritional status. Ask about changes in appetite, taste, smell, chewing, or swallowing; gastrointestinal issues such as nausea, vomiting, diarrhea, or constipation; and psychological symptoms like depression or anxiety. Inquire about any chronic medical conditions such as diabetes or inflammatory bowel disease, as well as acute conditions such as recent trauma or surgery.  

Also gather information about any diet modifications, exercise regimens, medications, or surgery used to resolve weight-related problems; and ask them if they’ve recently experienced unintentional weight loss. Also, determine if they are taking any medications that can impact digestion, absorption, and metabolism of nutrients, including laxatives, steroids, or anticonvulsants; as well a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Concepts_of_Cultural_Assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eQsHWRHITcCa6yNH6UGz36mDQGW6myF_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Concepts of Cultural Assessment]]></video:title><video:description><![CDATA[Culture is a complex phenomenon that includes the ever-changing attitudes, beliefs, self-definitions, norms, roles, values, and communication styles a person develops throughout life.   

When performing a cultural assessment, you’ll use a relational approach that accounts for the socio-environmental, geographical, historical, and other individual factors involved in your patient’s response to health and illness. 

Completing a cultural self-assessment will support a relational approach by clarifying your own background and values, and by building self-awareness and accountability for any biases or prejudices you may have.  

To perform a cultural self-assessment, consider how your own social and cultural heritage could impact your beliefs about health and illness and how you relate to your patients. You can also think about how your decision to become a nurse and your professional experiences can influence the assumptions you make and the care you provide for your patients.    

When assessing your patient’s culture, you’ll use clinical practice guidelines that support a relational approach, which include building trust, engaging through listening, conveying respect, and paying attention to context. During your initial interview, work on building trust by asking questions in a nonjudgmental way. For example, when gathering information about your patient’s presenting health concerns, you could ask them “What do you think might be causing you to feel this way?”  

You can build trust by conveying interest in their life context. So, if your patient has recently moved to your city, ask them about where they moved from or what language they are most comfortable speaking. Once trust is established, your patient will often be more willing to share more sensitive information.  

As you ask questions, engage with your patient through listening to their responses about their background, identity, values, as well as their health beliefs and practices.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3qT6HqBzRJWZBj68vO78VvK6QG6mQyMZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of the Older Adult]]></video:title><video:description><![CDATA[The assessment of older adults is focused on identifying their self-care abilities and helping them achieve an optimal level of functioning. In addition to completing a comprehensive physical examination, you’ll assess their functional, cognitive, environmental, and social status. 

Alright, a functional assessment evaluates your patient’s physical mobility and functional independence. Now, before assessing mobility, make sure your patient is wearing appropriate footwear, has their necessary assistive devices, and that you’re standing nearby to prevent falls.  

Then, assess your patient’s physical mobility and gait by having them perform the “Timed Up and Go” test, or TUG for short, where you’ll ask them stand up from a seated position, walk ten feet, then return to the chair and sit down. During this time, note their ability to get up from the chair, their balance, gait, and speed, and balance.  

Then to assess their functional independence, use your facility&amp;#39;s approved tool to evaluate their ability to perform basic activities of daily living, or ADLs like bathing, dressing, feeding, and toileting.  

Next, ask them about how they perform more complex tasks, known as instrumental ADLs, or IADLs, like washing their clothes and shopping for groceries. You can also ask them to demonstrate how to use their phone and how they organize their medications.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_the_Infant,_Child,_and_Adolescent</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aTOsejkBTDKO_6pCKG3WXjcVQ_W-LB-2/_.png</video:thumbnail_loc><video:title><![CDATA[Assessment of the Infant, Child, and Adolescent]]></video:title><video:description><![CDATA[Assessment of the infant, child, and adolescent involves a variety of techniques depending on the patient’s age and development. As the nurse, you’ll collect subjective and objective data, while keeping in mind age-specific techniques and variations. 

During your assessment, keep in mind the techniques you’ll use based on your patient’s age and developmental stage. Infants are typically examined on their caregiver’s lap during the quiet parts of the exam like cardiac and respiratory auscultation; then, you’ll complete the rest of the exam with the infant on the examination table. Remember that stranger anxiety begins around six to nine months of age, so you’ll need to build trust before starting your assessment by taking time to let the infant adjust to their new surroundings and by speaking to them softly before touching them.  

When examining a toddler, you’ll want to keep them on their caregiver’s lap for the duration of the exam and encourage them to hold a security object like a stuffed toy or blanket during the exam. Also, remember that most toddlers and preschoolers are learning to gain independence, so offer them choices when possible, such as asking them which ear you should look at first. They also enjoy playing games and pretending, so you can use a doll to demonstrate what to expect during the exam.  

When examining school-aged patients and adolescents, promote relaxation by asking about school or hobbies, and explaining how the body works as you examine each system. Adolescents are often ready to receive health teaching regarding how they can stay safe and healthy, so you can teach as you examine them.Also, be sure to give your adolescent patient a choice to speak to you without their caregiver in the room to ensure confidentiality about specific problems like sexual activity, substance use, or mental health issues.  

Begin your examination by collecting subjective data, or information your patient or their caregiver shares. For patients u]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hereditary_and_Environmental_Influences_on_Childbearing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Dd2T_syGR6a4ZZ-NxxEjmgg8SaeLdajU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hereditary and Environmental Influences on Childbearing]]></video:title><video:description><![CDATA[Hereditary and environmental factors influence a person’s development, even before conception. Hereditary factors refer to the genetic determination of traits, like eye color or the inheritance of disorders, like cystic fibrosis. On the other hand, environmental factors refer to external influences found where people live, work, and play that can impact how genes are expressed. Often, the impact on a person’s development is multifactorial, meaning it results from a combination of hereditary and environmental factors.

The hereditary material that determines a person’s development is contained in their chromosomes. Tightly packed into each chromosome is DNA, which is organized into genes that carry a person’s unique genetic code.

During fertilization, each parent donates half their chromosomes to create a fertilized ovum, called a zygote, which contains a total of 46 chromosomes organized into 23 pairs. These chromosome pairs are numbered from 1 to 22, with the 23rd pair, the sex chromosomes, labeled as X or Y.

Now, if chromosomes are altered, the person’s development can be negatively affected. These chromosomal alterations can involve changes in the structure of a chromosome, and can involve deletions, duplications, translocations, and inversions.  

A deletion is when part of the DNA is missing, like with cri-du-chat syndrome, where the short arm of chromosome 5 is missing.  

If there’s extra genetic material in a chromosome, it’s called duplication, like when there’s an extra copy of some of the genes found in the long arm of chromosome 7, resulting in developmental delay, behavioral problems, and other anomalies.  

Another structural alteration is translocation, where part of a chromosome moves to another chromosome. An example is the Philadelphia chromosome, which is chromosome 22 with a bit of chromosome 9 on it, resulting in a type of leukemia.  

Lastly, an inversion, which is where part of a chromosome is rearranged in reverse order. Inversion]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Intervention_for_Nutritional_Health_During_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vFz0-0u7RvKwDP-m5RfayamUScOmNNUK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Intervention for Nutritional Health During Pregnancy]]></video:title><video:description><![CDATA[During pregnancy, the patient and growing fetus require a variety of macro- and micronutrients and increased caloric intake to support sufficient weight gain and development.

Extra calories are needed during pregnancy to supply the energy needed to fuel the increased maternal basal metabolic rate and to support the production and maintenance of maternal tissues, placenta, and fetus. These calories should primarily come from nutrient-dense foods, like vegetables, meats, dairy products, legumes, and nuts; instead of empty calories, like fast food, cookies, cakes, and sweetened beverages.

Macronutrients are needed by the body in large amounts, and include carbohydrates, fats, and proteins. Carbohydrates are the primary source of calories used for energy. Carbohydrates can be simple, like the sucrose found in fruits; or complex which are found in sources of starch, like legumes, pasta, sweet potatoes, and whole grains. In addition to providing calories, complex carbohydrates contain additional nutrients like vitamins, minerals, and fiber. Fiber is the non-digestible part of carbohydrates that provide bulk to stool to help prevent constipation, which commonly occurs during pregnancy due to hormonal changes that slow the motility of the intestines.

Next, fats provide calories and fat-soluble vitamins. Good sources of fats include nuts, seeds, oils, meats, and dairy products. Fats also supply fatty acids that help with fetal neurological and visual development, such as alpha-linolenic acid, found in flax seeds; linoleic acid, found in vegetable or canola oils; and docosahexaenoic acid, found in cold-water fish like salmon.

Lastly, proteins are needed for essential processes like building and repairing tissue, making enzymes used in metabolic processes, and maintaining fluid balance. Proteins can also be used for energy when other sources aren’t available. Some sources of protein include eggs, legumes, tofu, nuts, meats, and fish.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/General_Concepts_In_Prenatal_Screening_And_Diagnosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/msWgOpokSVexvXn3MJiC4galQ-a5u_0J/_.jpg</video:thumbnail_loc><video:title><![CDATA[General Concepts In Prenatal Screening And Diagnosis]]></video:title><video:description><![CDATA[Prenatal screening can be done to identify the likelihood that a certain fetal disorder or condition is present. Screening is typically completed during the first and second trimesters and can be followed by diagnostic testing to confirm if the fetus is affected.

Alright, so first trimester screenings are done between 11 to 14 weeks of gestation to look for evidence of chromosomal abnormalities, including aneuploidies, which means there’s an abnormal number of chromosomes. These tests include nuchal translucency, or NT, using ultrasound; as well as a measurement of maternal serum levels of pregnancy-associated plasma protein-A, or PAPP-A; human chorionic gonadotropin, or hCG; and cell-free fetal DNA, or cfDNA.

Nuchal translucency measures the fluid-filled space behind the fetus&amp;#39; neck. An increased amount of fluid is associated with chromosomal abnormalities, including Trisomy 21, also known as Down syndrome, where there’s an extra copy of chromosome 21.

Next, PAPP-A is a glycoprotein made by the placenta. Low levels of PAPP-A are also linked to Trisomy 21. Then, there’s hCG, which is a hormone made by the placenta. Increased levels of hCG are associated with Trisomy 21, whereas decreased levels are associated with both Trisomy 18, or Edward syndrome, where there’s an extra copy of chromosome 18; and Trisomy 13, known as Patau syndrome, where there’s an extra copy of chromosome 13.

Lastly, cfDNA refers to fragments of DNA from the breakdown of maternal and fetal cells. cfDNA can be used to screen for trisomies, sex chromosome aneuploidies, and other chromosomal microdeletions or duplications.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertensive_Disorders_of_Pregnancy_and_Nursing_Considerations</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j-fUfcyxQ36vNDYqjzPAYXFDTl2OOwI1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertensive Disorders of Pregnancy and Nursing Considerations]]></video:title><video:description><![CDATA[Preeclampsia is a multisystem disorder that occurs during pregnancy after 20 weeks of gestation or during the postpartum period. It’s characterized by new-onset hypertension, proteinuria, and end-organ dysfunction, or damage to major organs like the kidneys, liver, brain, and placenta. Eclampsia occurs when a patient with preeclampsia develops generalized seizures. 

When it comes to blood pressure regulation during pregnancy, there are three key factors to keep in mind: cardiac output, which is the amount of blood the heart pumps out to the systemic circulation in one minute; intravascular volume, which is the amount of blood in the circulation; and peripheral vascular resistance, which is the resistance of blood flow in peripheral arteries.  

During pregnancy, the cardiac output and intravascular volume increase but the peripheral vascular resistance decreases. That’s because there’s a relative decrease in the response to vasoconstrictor molecules, like angiotensin II, and there are also higher levels of vasodilator molecules, like prostacyclin PGI2. As a result, blood vessels dilate to accommodate the increased blood volume, and this keeps blood pressure in a normal range.  

Now, the exact cause of preeclampsia is not well understood, but it seems to begin with abnormal implantation and vascularization of the placenta, as early as the first trimester. During this time, the spiral arteries, which are usually highly dilated vessels that supply the placenta and fetus with a rich supply of blood, become constricted. This results in placental hypoxia, which is followed by a release of chemical mediators that cause systemic vascular endothelial dysfunction and vasospasm, thereby decreasing perfusion to target organs such as the kidneys, liver, and brain. 

In the placenta, decreased perfusion means low blood flow to the developing fetus, which can cause intrauterine growth restriction, low birth weight, preterm birth, or even fetal death. Additionally, pree]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_During_and_After_Childbirth</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bBhvRBiAQzWt01QgTm1e-a0vSeacv7K8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care During and After Childbirth]]></video:title><video:description><![CDATA[The postpartum period, also known as the fourth stage of labor, begins after delivery of the fetus and placenta, and it extends through the first six weeks after birth. During this time, you’ll provide care for the newborn, the postpartum patient, and their family. 

When caring for the newborn, you’ll focus on maintaining cardiopulmonary function, supporting thermoregulation, and accurately identifying the newborn.  

Immediately after birth, you’ll assess cardiopulmonary function by calculating an Apgar score, which is a scoring system that assesses how the newborn is adapting to extrauterine life. The newborn&amp;#39;s heart rate, respiratory effort, muscle tone, reflexes, and skin color are scored 0, 1, or 2 for a total of 10 possible points. You’ll calculate the Apgar score at one minute and five minutes and then every 5 minutes, as needed until the score reaches 7 or more. During this time, if the newborn shows signs of distress, such as bradycardia or a weak respiratory effort, immediate intervention should be provided. 

Next, you’ll take steps to support thermoregulation. Remember that immediately after birth the newborn is covered in bodily fluids, putting them at risk for evaporative heat loss. If their temperature drops, the newborn will need to work hard to maintain their temperature, which will increase their need for oxygen and increases the risk of problems like hypoxemia and hypoglycemia. To prevent this, be sure to immediately dry them off with warm towels and provide warmth by either placing them on their parent’s chest to initiate skin-to-skin contact or by placing them on a radiant warmer. Once their temperature has stabilized, swaddle them in warm blankets, place a cap on their head, and continue to monitor their temperature. 

Lastly, you’ll attach identification bands on the newborn that will match the parents’ identification bands. To ensure the newborn is always returned to their family after separation, these bands won’t be remo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrapartum_Complications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BRMyQ6KTSuaEZ0C-S61ggHauS9iozHqY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intrapartum Complications]]></video:title><video:description><![CDATA[The intrapartum period begins with the onset of labor and lasts until the delivery of the newborn and placenta. Complications during the intrapartum period can be related to premature rupture of membranes, or PROM, and preterm labor.

PROM is when the amniotic membranes spontaneously rupture before the beginning of true labor. PROM can lead to complications such as oligohydramnios, meaning there isn’t enough amniotic fluid left to surround the fetus; and umbilical cord prolapse, which is when the umbilical cord moves ahead of the fetus and becomes compressed, which cuts off circulation to the fetus. PROM also makes it easy for microorganisms in the vagina to travel into the uterus, causing chorioamnionitis, which is an infection of the remaining amniotic tissue and fluid.

PROM can present as either a gush of vaginal fluid or a slow leaking of fluid from the vagina.  Diagnosis of PROM is made by sterile speculum exam to look for a pool of fluid near the cervix. If fluid is present, PROM can be confirmed if pH testing shows alkalinity of the fluid. Other information can be gathered during the speculum exam, including an estimation of cervical dilation and effacement, as well as testing the fluid for the presence of phosphatidylglycerol, or PG, which is an indication of fetal pulmonary maturity.

Nursing management of PROM primarily depends on the gestational age and involves weighing the risks of preterm birth versus expectant management, which consists of observation for infection, labor onset, and testing for fetal well-being. In all cases, you’ll administer antibiotics prophylactically, as ordered, even if infection isn’t suspected. If your patient is at 37 weeks of gestation and labor doesn&amp;#39;t start soon, labor will typically be induced with oxytocin after cervical softening agents like prostaglandin E2 have been administered, as needed.

If gestation is between 34 to 36 weeks and there’s evidence of chorioamnionitis and fetal compromise, labor ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_Physiologic_Changes_and_Nursing_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KhlReatYQVWEfWIjGWCNvk2jRGaBC8eo/_.png</video:thumbnail_loc><video:title><![CDATA[Postpartum Physiologic Changes and Nursing Care]]></video:title><video:description><![CDATA[The postpartum period, also known as puerperium, is the first six weeks after delivery. Physiological and anatomical changes that occur during the postpartum period include the reversal of changes that occurred during pregnancy.

Now, immediately after delivery, patients usually lose 4.5 to 5.8 kilograms, or 10 to 13 pounds, which includes the weight of the fetus, amniotic fluid, blood, and placenta. Weight loss continues over the next several months due to normalization of blood volume and increased caloric expenditure from milk production.

Okay, let’s now focus on reproductive changes, starting with the uterus. After delivery, the uterus begins to return to its nonpregnant size and position, a process called uterine involution. As soon as the placenta is delivered, uterine muscle fibers constrict around uterine blood vessels to control bleeding. Then, intermittent uterine contractions, referred to as afterpains, continue to further aid uterine involution. The progress of involution can be monitored by palpating the top part of the uterus, called the fundus. At about 12 hours after delivery, the fundus can be palpated at 1 cm above the umbilicus. After that, it normally descends about 1 centimeter, or 1 fingerbreadth, per day, until it reaches the pelvic cavity by the 14th day.

Next, let’s look at the vaginal discharge that occurs after birth, called lochia. The three types of lochia include lochia rubra, lochia serosa, and lochia alba. Lochia rubra refers to the dark red vaginal discharge that’s present for the first 3 days. It consists of blood, small blood clots, decidua, and mucus. As the bleeding reduces, the volume of vaginal discharge reduces, and lochia rubra transforms into lochia serosa. Lochia serosa is a thin, pinkish-brown vaginal discharge that lasts until the 10th day after delivery. It consists of white blood cells, serous exudate, and cervical mucus. As time passes, lochia serosa transforms into lochia alba, which is a yellowish-white d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_Complications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y8Ryj2MQS5GjBPtSJDbxGGc6SkSYBymY/_.png</video:thumbnail_loc><video:title><![CDATA[Postpartum Complications]]></video:title><video:description><![CDATA[The postpartum period, also known as the fourth stage of labor, begins after delivery of the fetus and placenta, and it extends through the first six weeks after birth. Several complications can arise during the postpartum period, including postpartum hemorrhage, thromboembolic disorders, and infection. 

Now, postpartum hemorrhage is defined as cumulative blood loss of 1,000 mL or more, or blood loss that’s accompanied by signs or symptoms of hypovolemia within 24 hours after birth. Common causes can be remembered by the four Ts, including tone for uterine atony, or weak uterine muscle tone, which includes subinvolution, meaning the return of the uterus to its nonpregnant state is impaired; trauma to the birth canal, such as lacerations or hematomas; tissue, meaning retention of placental fragments; and thrombin, representing coagulation deficiencies, like von Willebrand disease. Other causes include placenta previa, or when the placenta is abnormally implanted over the cervix; and placenta accreta or abnormal placental adherence to the uterine wall.  

Signs and symptoms of hemorrhage may include a soft or displaced uterus and saturating one or more peri-pads per hour. If the hemorrhage is concealed within a hematoma, there could be severe perineal pain or rectal pain; a discolored bulging mass in the perineum; and abnormal vital signs like tachycardia.  

Treatment depends on the cause and may include fundal massage; bimanual compression of the uterus; uterotonic, antifibrinolytic, and analgesic medications; IV fluid and blood product administration; or surgery, like uterine artery ligation, hematoma repair, or hysterectomy.  

When caring for your patient with postpartum hemorrhage, closely monitor their vital signs, pain, skin color and temperature, and urine output. Assess their uterine tone and perform fundal massage to keep the uterus firmly contracted. Monitor the color and amount of lochia, or vaginal discharge, and weigh all blood-soaked pads an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_of_the_Newborn</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kNw5vIWqT5W7OtZVWouDfvT3T2CcZx91/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment of the Newborn]]></video:title><video:description><![CDATA[The newborn assessment is an ongoing process to monitor the newborn’s adaptation to extrauterine life, and to identify problems that need immediate intervention. A focused assessment occurs immediately after birth, followed by a more comprehensive admission assessment. Some of the assessments you will do include the cardiovascular and respiratory systems, thermoregulation, and measurements.  

To assess the newborn’s respiratory and cardiovascular systems, begin by observing their respirations. You’ll notice that their abdomen will rise and fall with each respiration; this is normal, because newborns primarily use their diaphragm to breathe, which tends to push their abdomen up with each breath. Be sure to count their respirations for a full minute, since they’re usually irregular, with occasional 5 to 10 second pauses. Normally, newborns have unlabored respirations of around 30 to 60 breaths per minute.  

Upon auscultation, soft, low pitched vesicular lung sounds should be noted throughout the lung fields, though fine crackles could be noted immediately after birth as fetal lung fluid is still being cleared. Some assessment findings associated with respiratory problems include apnea, or a pause in breathing lasting 20 seconds or longer, and tachypnea, or a respiratory rate more than 60 breaths per minute. Other concerning assessment findings include substernal or intercostal retractions and nasal flaring during inspiration, as the newborn works hard to bring in air during inspiration; and during expiration, grunting, which increases pressure within the alveoli to promote gas exchange.   

Next, auscultate the apical heart for a full minute, assessing for rate and rhythm. It’s a good idea to assess this when the newborn is in a quiet state. A newborn’s heart rate normally varies between 120 and 160 beats per minute, but it can rise to 180 beats per minute when the newborn is crying or drop as low as 80 to 90 beats per minute when in deep sleep. Also, keep]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/High-Risk_Newborn:_Complications_Associated_with_Gestational_Age_and_Development</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7dsJDgjATzauOVjgFRqXdfpHQFaeaJbT/_.jpg</video:thumbnail_loc><video:title><![CDATA[High-Risk Newborn: Complications Associated with Gestational Age and Development]]></video:title><video:description><![CDATA[A preterm infant is born before 37 completed weeks of gestation, which refers to the period between conception and birth, that typically lasts for 40 weeks.  

Now, the cause of preterm birth can be medically indicated, when there are maternal, fetal, and placental complications such as preeclampsia, fetal anomalies, or placenta previa.  

Preterm birth can also be spontaneous, in which case the cause is often unknown, but there are certain factors that can lead to premature birth.  

These include maternal factors such as extremes of age, like teenage pregnancy or age over 40 years; history of prior preterm birth; being underweight or having a poor nutritional status; use of assisted reproductive technology, like with in vitro fertilization; cervical insufficiency; substance use, including tobacco, alcohol, or illicit drugs; infections, like bacterial vaginosis or an intrauterine infection; as well as factors like late or no prenatal care; high levels of stress; long working hours, especially when there’s long periods of standing; lack of social support; and intimate partner violence. 

Regardless of the cause, preterm infants are more likely to develop severe or life-threatening complications. Respiratory complications are common and are mostly related to insufficient surfactant production. This prevents the alveoli from expanding completely, resulting in hypoxia and respiratory distress syndrome. Other respiratory complications include transient tachypnea of the newborn, because of decreased absorption of fetal lung fluid and subsequent decreased gas exchange;  pulmonary hemorrhage; apnea with accompanying bradycardia; as well as persistent pulmonary hypertension of the newborn, where pulmonary pressure remains high, resulting in continued shunting of blood away from the lungs through a patent ductus arteriosus.  

Given these complications, preterm infants may remain on prolonged mechanical ventilation. Unfortunately, mechanical ventilation can damage ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/High-Risk_Newborn:_Acquired_and_Congenital_Conditions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1xZNw7pST9_mNN7HDorezUhHRnKKi3Pf/_.jpg</video:thumbnail_loc><video:title><![CDATA[High-Risk Newborn: Acquired and Congenital Conditions]]></video:title><video:description><![CDATA[Congenital and acquired conditions are high-risk complications requiring prompt recognition and intervention. Congenital conditions refer to genetic disorders or physical anomalies that occur during fetal development, such as phenylketonuria, cleft palate, and cardiac defects.  

On the other hand, acquired conditions occur postnatally, meaning at or shortly after birth, and include pathologic jaundice, sepsis neonatorum, and meconium aspiration syndrome.

Okay, so jaundice, also known as hyperbilirubinemia, is a condition caused by the build-up of a yellow pigment called bilirubin, that’s produced in the liver by breaking down hemoglobin from red blood cells. Most newborns develop mild hyperbilirubinemia, called physiologic jaundice, which is a self-limiting condition that requires no treatment.

On the other hand, pathologic jaundice, sometimes called non-physiologic jaundice, is a more severe form of jaundice, that is most commonly caused by excessive hemolysis, or red blood cell destruction, leading to an excessive build-up of bilirubin in the blood.  

Risk factors for excessive hemolysis include incompatibility between the maternal and fetal ABO and Rh blood types; polycythemia, or an excessive amount of circulating red blood cells; or the presence of extravascular blood, like bruising or cephalohematoma from birth trauma. Other risk factors include sepsis and liver impairment.

Without proper treatment, pathologic jaundice can lead to acute bilirubin encephalopathy, where bilirubin crosses the blood-brain barrier, deposits in the brain, and causes impaired neurologic function. This can progress to kernicterus, or chronic bilirubin encephalopathy, which is irreversible neurological damage, resulting in long-term effects like cerebral palsy and hearing loss. 

Clinical manifestations of pathologic jaundice include a rapid rise in bilirubin within the first 24 hours of life that persists at an elevated level longer than expected. The newborn may have y]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Methods_of_Contraception</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/djftn-89RruQcwPiHejbQ5NESCCx-WQS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Methods of Contraception]]></video:title><video:description><![CDATA[Contraception refers to methods to prevent pregnancy which range from devices to medications to procedures and can be either temporary or permanent. Temporary contraception methods include barrier and hormonal methods.

Barrier methods can be mechanical, like devices such as male and female condoms and diaphragms; or chemical, like spermicides.

Now, male condoms are a thin stretchable sheath, commonly made of latex, that’s applied over the penis.

Female condoms are a small pouch made of synthetic rubber with flexible rings at both ends; the closed end is inserted into the vagina and secured around the cervix, and the open end covers the labia. Both male and female condoms are single use and applied immediately prior to intercourse.

Diaphragms are dome-shaped silicone devices that cover the cervix and are usually used with a spermicide. They can be inserted six hours before intercourse and should remain in place for at least six hours following intercourse, but no longer than 24 hours. If they’re left in place longer than 24 hours or if they’re used during menses, there’s a risk of toxic shock syndrome.

Next, spermicides are chemical-based formulations that destroy sperm cell membranes and reduce sperm motility, reducing their ability to reach the cervix, and are available as foams, tablets, suppositories, vaginal films, creams or gels.

Spermicides should be inserted deep into the vagina about 15 minutes before intercourse and must be reapplied before repeat intercourse since they&amp;#39;re only effective for about an hour. When used together with a mechanical barrier like a diaphragm, the contraceptive effectiveness is improved.

Now, with all barrier methods, there are some common advantages and disadvantages. The advantages are that they’re inexpensive, relatively easy to use, and effective when applied properly. Condoms and spermicides are readily available without a prescription, whereas diaphragms require a prescription and fitting by a he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Women's_Health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TdD1Ocw0TTOY-l4fJIScyN-0T2yQt9gJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Women&apos;s Health]]></video:title><video:description><![CDATA[Women’s health focuses on strategies to promote the health and well-being of patients assigned female at birth. Common problems addressed in women’s health are menstrual and breast disorders.  

Okay, so two common menstrual disorders are amenorrhea and abnormal uterine bleeding.Amenorrhea is the absence of menses, or a menstrual period, which can be primary or secondary. Primary amenorrhea is when the first menses doesn&amp;#39;t occur by age 15 or within 3 years after developing breasts. It’s often caused by disorders in the hypothalamic-pituitary-ovarian axis; chromosomal abnormalities; or structural abnormalities of the uterus, vagina, or hymen that obstruct flow.  

Secondary amenorrhea is when a regular menstrual cycle stops for at least 3 months, or when an irregular menstrual cycle stops for at least 6 months. Secondary amenorrhea can be caused by natural processes, like pregnancy, lactation, and menopause; or by underlying conditions, like polycystic ovarian syndrome, thyroid disease, or an eating disorder.      

Diagnosis begins with a history and physical examination. Then, laboratory tests will be performed to identify potential causes, like human chorionic gonadotropin, or hCG to confirm pregnancy; thyroid stimulating hormone, or TSH to check for a thyroid disorder; and reproductive hormone levels, such as serum follicle-stimulating hormone, luteinizing hormone, and androgens to identify endocrine problems.  

Treatment will address the underlying condition and can include hormone replacement therapy or contraceptives to restart regular menstruation and promote normal ovarian function.  

Now, abnormal uterine bleeding, or AUB, refers to bleeding that’s heavy, extended, frequent, or irregular. AUB can be caused by an underlying condition, like uterine fibroids or polyps; cancerous lesions; coagulation problems, from medications like anticoagulants or clotting disorders, like von Willibrand disease; or complications of pregnancy, such as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preventative_Health_Care_for_Women</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QZYdcqiuR8CcKMZ2PSoGgmiMS7_ucWyB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preventative Health Care for Women]]></video:title><video:description><![CDATA[Preventative health care refers to screenings that can identify diseases in the early stages, so they can be treated before they progress. Common preventative screenings for patients assigned female at birth include mammograms for breast cancer; Papanicolaou, or Pap, tests for cervical cancer; and bone density tests for osteopenia and osteoporosis.  

Mammograms screen for breast cancer and involve taking X-rays of the breasts. Patients typically start mammograms around age 45 but can be started earlier or later, depending on risk factors, like a positive family history of breast cancer or certain genetic mutations, like BRCA1 or BRCA2. 

When teaching your patient who&amp;#39;s having a mammogram, explain that the procedure involves the compression of the breast tissue between two plates while an X-ray is taken. Reassure them that the procedure uses a very low dose of radiation and that it causes brief discomfort. Be sure to recommend that they schedule their mammogram after their menstrual period when their breasts are less swollen and sensitive. Lastly, remind them to avoid wearing deodorant, lotions, or powder on the day of their mammogram, since these can cause white spots on the X-ray. 

Screening for cervical cancer involves the Papanicolaou, or Pap test, which screens for cervical cancer by swabbing the cervix during a pelvic examination and looking for abnormal cervical cells and testing for human papillomavirus, or HPV test, which detects strains of HPV, including the high-risk strains that may cause cervical cancer. When Pap and HPV tests are done together, it&amp;#39;s known as co-testing. Screening for cervical cancer should begin at age 21 and occur every three years until age 30. Then at age 30, testing can be done every five years.  

For patients with small-grade changes to cervical cells, testing should occur more frequently whereas those with high-grade cervical cell changes should have the cells removed through loop electrosurgical ex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endocrine_and_Metabolic_Disorders_Impacting_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gybftFgcRlq5QfWmy8S4px2FRZiXtXnU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endocrine and Metabolic Disorders Impacting Pregnancy]]></video:title><video:description><![CDATA[Gestational diabetes, also known as gestational diabetes mellitus, or GDM for short, is glucose intolerance that occurs during pregnancy, whereas pregestational diabetes is diabetes that is present prior to pregnancy.

Alright, so, hormones produced during pregnancy cause changes in maternal glucose metabolism to support the pregnancy and to allow the fetus to receive a steady supply of glucose necessary for fetal growth and development.

The early part of pregnancy can be described as an anabolic state, which increases fat stores, augments blood supply, and supports the growth of the fetus and maternal tissue like uterus, placenta, and breast tissue. During this time, insulin secretion increases, along with glucose utilization and storage in adipose and muscle cells.  

Later, as the pregnancy progresses, it begins to exert a diabetogenic effect on glucose metabolism, which means that there’s increasing maternal insulin resistance and decreased utilization of glucose. This results in higher levels of maternal blood glucose and increased transfer of glucose to the fetus. During this time GDM can develop when maternal insulin production is unable to compensate for the increased insulin resistance, resulting in hyperglycemia.

GDM is more likely to affect those who have risk factors for diabetes mellitus, including obesity, a family history of diabetes, and advanced maternal age.

Like all types of diabetes mellitus, clinical manifestations of GDM include polyuria, or increased urine production; polydipsia, or increased thirst; and polyphagia, or increased hunger.  
If left untreated, gestational diabetes can lead to complications. For example, excessive fetal nutrient intake can lead to macrosomia, or large birth weight, and result in the need for cesarean birth.

Screening for GDM occurs between 24 and 28 weeks of gestation by measuring fasting blood glucose levels during an oral glucose tolerance test, or OGTT. The patient is given an oral glucose drink, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anatomy_and_Physiology_of_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7Mt8bL1lRTi-y56uWaLcgULlQTS5LyBZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anatomy and Physiology of Pregnancy]]></video:title><video:description><![CDATA[Common discomforts of pregnancy refer to all temporary symptoms and changes that pregnant clients experience as their babies grow and develop within the uterus. The most common discomforts of pregnancy include nausea, vomiting, heartburn, backache, round ligament pain, urinary frequency, constipation, hemorrhoidal disease, varicose veins, and finally, leg cramps. 

First, let’s start with nausea and vomiting which is often attributed in part to pregnancy hormones. It typically occurs in the morning and as a result, is often referred to as morning sickness. Nausea and vomiting are some of the earliest discomforts of pregnancy and can be worsened by fatigue, cooking smells, and fried, greasy, or spicy food. 

Now, morning sickness should not be confused with hyperemesis gravidarum, which is a condition that also occurs during pregnancy that’s characterized by severe vomiting that interferes with the client’s daily life. It could also result in weight loss, dehydration, electrolyte imbalance and may require hospitalization, IV fluids and antiemetics. 

Management of nausea and vomiting includes eating small and frequent, high protein meals, maintaining hydration, eating slowly, and avoiding odors or other factors that can trigger nausea. Increasing intake of vitamin B6 can also be helpful, as well as consuming beverages containing ginger, like ginger ale or ginger tea.

Next up is heartburn or pyrosis. Now, the esophagus and the stomach are separated by a muscular valve called the lower esophageal sphincter, which prevents the reflux of stomach contents back into the esophagus. Early in pregnancy, hormonal changes lead to a decreased tone of the lower esophageal sphincter, thereby allowing the stomach contents to reach the esophagus and cause heartburn. Later in pregnancy, the growing fetus can directly exert pressure on the stomach, causing the stomach contents to move back into the esophagus. Management of heartburn includes eating small, frequent meals and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_of_the_Family_During_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3LMV82ULQ2SksteJZR1bN2t6RxCZTGay/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care of the Family During Pregnancy]]></video:title><video:description><![CDATA[The prenatal period refers to the time from before conception until the end of pregnancy. So, prenatal care refers to the care that is provided before and during pregnancy to evaluate maternal and fetal health, provide education to promote health, and to intervene when possible to ensure the birth of a healthy baby with minimal risk for the mother. For a successful pregnancy outcome, prenatal visits should continue every 4 weeks until week 28, every two weeks from week 28 to 36, and then weekly until delivery. 

Alright, now the first step in prenatal care is preconception counseling, which seeks to identify any potential risks to the client’s fertility and pregnancy outcome. The first prenatal visit typically occurs when a client suspects they are pregnant or because they wish to conceive in the near future. No matter the case, the main focus of the first prenatal visit should be obtaining a thorough personal and obstetrical history, as well as family history, to identify any medical conditions that could pose a risk to the pregnancy.

Now, in clients who suspect they are pregnant, pregnancy should be confirmed with a urine pregnancy test and an abdominal ultrasound. If pregnancy is confirmed, the estimated date of delivery, or EDD, should be calculated. It’s traditionally calculated using Naegele’s rule, which takes the first day of the last menstrual period, or LMP, subtracts 3 months, and then adds one year and seven days. So, if the LMP was September 10, 2021, counting back 3 months, adding 1 year and 7 days calculates the EDD as June 17, 2022.

The obstetrical history evaluates the gravidity, parity, and abortions. Gravidity, or G, refers to the number of times a client has been pregnant, including the current pregnancy. Parity, or P, refers to the number of times a client has carried the pregnancy to a viable gestational age, which is more than 20 weeks gestation. So, if a client is currently pregnant, has been pregnant once before, and has had one ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Labor_and_Birth_Processes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-8Pk6BMrR96nVMD_BW7rM2xFQPWM7VzV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Labor and Birth Processes]]></video:title><video:description><![CDATA[The main components of the birth process refer to the factors that interact with each other during childbirth. These components are grouped into 4Ps: power, which refers to uterine contractions and maternal pushing efforts; passage, which refers to the maternal pelvis that the baby passes through during labor; passenger, which refers to the fetus and placenta; and psyche, which refers to the client’s psychological status during labor. 

Now, let’s look at each of these components, starting with power. Involuntary uterine contractions are the primary force of labor that dilate and efface the uterine cervix, after which maternal pushing efforts kick in. The descending fetus puts pressure on the vaginal wall and the rectum, which triggers the urge to push. These pushing efforts aid uterine contractions to push the fetus through the maternal pelvis. 

The next P stands for passage, namely the maternal soft tissues, like the cervix, as well as the pelvis.  Now, during labor, the cervix dilates and effaces, meaning it gets wider and thinner, to allow for an easier passage of the fetal head. The pelvis is divided by an imaginary line called the pelvic brim into the upper or false pelvis, and the lower or true pelvis. The true pelvis is divided into the pelvic inlet above; the pelvic cavity in the middle; and the pelvic outlet below. Now, the right and left sides of the maternal pelvis are connected by cartilage called the symphysis pubis. During pregnancy, a hormone called relaxin increases, which softens joints, including, the symphysis pubis, which helps it to widen somewhat during childbirth to help accommodate the fetal head. 

Overall, the shape of the pelvis can be classified into 4 types: the wider, more open gynecoid pelvis; the narrower android pelvis; the narrow and elongated anthropoid pelvis; and the wide but shallow platypelloid pelvis. The pelvic shape, as well as the diameters of the pelvic inlet and outlet, can influence how easily the fetus can p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maximizing_Comfort_for_the_Laboring_Woman_-_Nursing_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hQuHJTphSBOzETy9SVJ-tLBjQgC72B9L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Maximizing Comfort for the Laboring Woman - Nursing Care]]></video:title><video:description><![CDATA[Labor refers to a series of progressive contractions of the uterus that result in dilation and thinning of the cervix. This, in turn, allows the fetus to descend from the uterus, through the birth canal, and into the extrauterine environment. This process results in pain that can be managed in a variety of ways.

Now, from a physiological standpoint, not only is labor pain normal, but it’s also easily anticipated, allowing time for preparation and acquisition of skills to help manage it. Secondly, although intense, labor pain is also time limited. It is usually intermittent and decreases rapidly after hitting its peak. Finally, it will end with the birth of a child, which is highly motivating for the mother, allowing for a higher pain threshold.

Pain during labor can be either visceral or somatic. Visceral pain mostly occurs during the first stage of labor due to uterine contractions that lead to hypoxia of the uterine muscles, dilation of the cervix, distension of the lower uterine segment, as well as pressure and pulling on pelvic structures such as the fallopian tubes, ovaries, and bladder. Then, somatic pain mostly occurs during the later part of the first stage and second stage of labor, as the uterine contractions become more intense. Also during this time, pain is increased as the fetus pushes directly on maternal tissues like the vagina, perineum, and the lumbosacral plexus during its descent.

Now, pain during labor can cause anxiety leading to a stress response that can have an adverse effect on the progression of labor and on the fetus. Excessive pain can heighten the individual’s fear and anxiety, causing the release of cortisol and catecholamines like epinephrine and norepinephrine. When these act on alpha receptors, the uterine blood vessels and muscles constrict, reducing uterine blood flow, reducing the fetal oxygen supply, and potentially leading to fetal hypoxia. Labor also increases the mother’s metabolic rate and demand for oxygen, mak]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fetal_Assessment_During_Labor</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rEhXwS0kRLqJoPfE637TCvpuSJGbcZmV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fetal Assessment During Labor]]></video:title><video:description><![CDATA[The intrapartum period refers to the time of pregnancy from the onset of labor to delivery of the newborn and the placenta. During this period, the uterus contracts to provide the main force necessary for delivery. So intrapartum assessment of uterine activity refers to assessing the frequency, duration, and intensity of these contractions. Of note, the assessment of the fetus during labor is always interpreted relative to uterine activity.  

First, let’s go over the physiology of the uterus, which is a pear-shaped, hollow, muscular organ that protects and nurtures the fetus, but also promotes its delivery during labor. The superior part of the uterus is called the fundus, the middle part is the body and the bottom, cylindrical portion is the cervix. Zooming in, the uterus has three layers: the outer serosal layer, or perimetrium; the middle muscular layer, or myometrium; and the inner mucosal layer, or endometrium. 

The myometrium consists of smooth muscle fibers, which can tighten to produce uterine contractions in response to certain hormones, like oxytocin. Now, the number of oxytocin receptors in the myometrium are low during most of the pregnancy, but they increase dramatically during the third trimester, reaching the greatest concentration during active labor. The oxytocin receptors, especially those in the fundus, respond to oxytocin by promoting rhythmic synchronized endometrial contractions from the fundus towards the cervix, causing  dilation and effacement, or thinning of the cervix, as well as pushing the fetus through the birth canal. Normal uterine activity during labor involves 5 contractions or fewer in a 10 minute period, averaged over 30 minutes. Between contractions, the uterus relaxes to allow adequate blood flow to the placenta and fetus. 

Now, let’s switch gears and go through some types of dysfunctional labor. First up, is tachysystole, which is defined as more than 5 contractions in a 10 minute period, averaged over 30 minutes.T]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_of_the_Family_During_Labor_and_Birth</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UjIBvU4mRomSp-VM1EoBTadWTaehTJs4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care of the Family During Labor and Birth]]></video:title><video:description><![CDATA[Labor is the process at the end of pregnancy during which the baby passes through the birth canal. It occurs spontaneously, usually between 37 and 42 weeks of pregnancy. Labor involves a series of continuous and progressive contractions of the uterus, as well as dilation and thinning of the cervix. 

Now, let’s look at the physiology of labor, which is made up of the first, second, third, and fourth stage. The first stage of labor begins with the onset of true labor and ends when the cervix is 100% effaced, or thinned and shortened, and fully dilated at 10 centimeters. Now, the first stage can further be subdivided into a latent phase, an active phase, and a transitional phase. 

The latent phase starts with the beginning of regular contractions, which usually start out as mild, and then increase in frequency, duration, and intensity. Cervical dilation progresses from 0 to 3 cm and effacement progresses from 0% to 40%. Also during this phase, the fetal membranes usually rupture spontaneously, if they haven’t ruptured already. The length of the latent phase is typically much longer in nulliparous individuals, meaning those who have never previously given birth, then for multiparous individuals, who have previously given birth.

Next, during the active phase, the frequency, duration, and intensity of contractions continues to increase, and the rate of cervical dilation and effacement accelerates, expanding from 4 to 7 cm, along with an effacement of 40% to 80%.The fetus starts to descend, and is usually between stations − 2 to 0. Remember that the fetal stations represent the number of centimeters that the fetal presenting part is above or below the ischial spines of the maternal pelvis; so essentially, they measure fetal descent through the birth canal. 

Finally, during the transition phase, the frequency, duration, and intensity of contractions continues to increase, cervical dilation progresses from 8 to 10 cm, effacement progresses from 80% to 100%, and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_Physiologic_Changes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3ZUAaj2vTvSl9TqWIdfYvN-bSFSoj7P1/_.png</video:thumbnail_loc><video:title><![CDATA[Postpartum Physiologic Changes]]></video:title><video:description><![CDATA[The postpartum period, also known as puerperium, is defined as the first six weeks after delivery. Physiologic changes during the postpartum period include the reversal of changes that occurred during pregnancy. Moreover, these changes are primarily caused by a rapid drop in estrogen and progesterone.

Now, after delivery, a client usually loses 4500 to 5800 grams or 10 to 13 lb, which covers the weight of the fetus, amniotic fluid, and the placenta. The weight loss starts immediately after delivery and continues over the next several months due to normalization of blood volume and  increased caloric expenditure from milk production. 

Okay, let’s focus on reproductive changes, starting with the uterus. After delivery, the uterus begins to return to its nonpregnant state of size and position, a process called uterine involution. As soon as the placenta is delivered, uterine muscle fibers constrict uterine blood vessels, preventing a life-threatening condition called postpartum hemorrhage. Uterine contractions, often referred to as afterpains because they cause sharp pain in the lower abdomen, continue during the postpartum period to further aid uterine involution. Now, clinicians can track the progress of involution by palpating the top part of the uterus, called the fundus. At about 12 hours after delivery, the fundus can be palpated at 1 cm above the umbilicus. After that, it normally descends by about 1 centimeter, or 1 fingerbreadth, per day, until it reaches the pelvic cavity by the 14th day. 

Now, let’s take a look at vaginal discharge after birth, called lochia. There are three types; lochia rubra, lochia serosa, and lochia alba. Lochia rubra refers to the dark red vaginal discharge that is present for the first 3 days. It consists of blood, small blood clots, decidua, and mucus. As the bleeding reduces, the volume of vaginal discharge reduces, and lochia rubra transforms into lochia serosa. Lochia serosa refers to the thin, red to brown vaginal di]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physiologic_and_Behavioral_Adaptations_of_the_Newborn</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LGffO4b-Qry1iBqN83AcKNxJTkigV-jB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physiologic and Behavioral Adaptations of the Newborn]]></video:title><video:description><![CDATA[During intrauterine life, the placenta supplies the fetus with oxygen and nutrients essential for its growth and development. After birth, this supply ceases, the infant has to adapt to the extrauterine environment. The main changes during this adaptation period include those of the respiratory and cardiovascular system. 

Now, in order to understand the changes that take place during transition to extrauterine life, let’s review some key differences between fetal and newborn circulation. Remember that during intrauterine life, the fetal lungs are not functional in terms of gas exchange. Instead, they are filled with fluid, and the arteries in the lung are constricted, resulting in high vascular resistance in the lungs. Because of this high pressure, relatively little blood reaches the lungs. Because no gas exchange occurs in the lungs, the fetus needs to get oxygen from the placenta. 

Now, there are three fetal shunts to help divert most of the blood away from the lungs, while maximizing the delivery of oxygenated blood to key organs like the brain and heart.  First is the ductus venosus that connects the umbilical vein to the inferior vena cava, thus allowing most of the oxygenated blood to bypass the liver and travel up to the heart. Next is the foramen ovale in the atrial septum, that allows blood from the right atrium to flow directly into the left atrium. This allows oxygenated blood to bypass the non-functional lungs and get pumped to the rest of the body instead by the left ventricle. The last shunt is the ductus arteriosus which connects the pulmonary artery to the aorta and also helps bypass the lungs. The liver and lungs still receive enough blood to keep their tissue healthy and growing, but the three shunts allow large quantities of blood to bypass them and help the fetus optimize its limited oxygen and nutrient supply. 

Now, toward the end of gestation, the fetal lungs start to prepare for extrauterine life. First, there’s increased product]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_of_the_Newborn_and_Family</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W8uIj4bDTUOTN43H4-9-sCiIRcuYIiLO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care of the Newborn and Family]]></video:title><video:description><![CDATA[Psychosocial changes during the postpartum period include various adjustments and changes that occur during the first 6 weeks after giving birth. The most important psychosocial changes include bonding, attachment, maternal touch and verbal behaviors, as well as adaptation and maternal role attainment. During this period, the nurse should provide support for the new family and intervene to promote a healthy outcome during the postpartum period. 

First, let’s start with bonding. Simply said, bonding refers to the intense connection that parents develop for their baby. Important methods to promote maternal bonding include promoting skin-to-skin contact and breastfeeding. On the other hand, paternal bonding can be enhanced with methods including presence during labor and delivery, bathing the baby, changing diapers, and bottle feedings. Sometimes, the bonding process can be delayed due to neonatal complications that might require admission to the neonatal intensive care unit. When this happens, nursing care involves providing information, encouraging bedside visitation and involvement in their baby’s care, and coordinating resources to support the family.

Now, bonding should not be confused with attachment, which refers to an enduring linkage between the parents and their child. It is a reciprocal relationship where the baby receives food, warmth, cuddling, and gentle interaction, and develops feelings of security and trust. In other words, babies can anticipate that their parents or caregivers will be available to support them in times of need. In turn, the baby demonstrates reciprocal attachment behaviors, including making eye contact, tracking their parent’s face or grasping their finger.

Okay, let’s switch gears and move on to maternal touch. Right after delivery, mothers usually use their fingertips to touch their baby. But, as time passes, they typically feel more comfortable and start to stroke their baby’s hair or chest with the palm of their hands]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medical-Surgical_Disorders_Impacting_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EgdN5sxhTH2tAZ1DDpPQtHCaSqS8Wr4d/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medical-Surgical Disorders Impacting Pregnancy]]></video:title><video:description><![CDATA[Pregestational conditions are chronic medical problems that are present from before pregnancy and can pose a risk to the mother or the fetus during pregnancy. They include diabetes mellitus, thyroid problems, and certain cardiac conditions, as well as asthma.

Alright, now let’s quickly go over each of these conditions, starting with diabetes mellitus, which  is when the body has trouble moving glucose from the blood into the cells, so blood glucose levels are constantly high. There are two main types of diabetes: type 1 diabetes, which is when the body doesn’t make enough insulin; and type 2 diabetes, which is when the body makes enough insulin, but the cells are insulin resistant, meaning they don’t respond to insulin by taking glucose in. 

Next, there are thyroid problems, which can be split into hyper- and hypothyroidism. Hyperthyroidism occurs where there’s excess thyroid hormones, and this is generally caused by overproduction from the thyroid gland. Conversely, hypothyroidism is typically caused by an immune attack targeting the thyroid gland, causing destruction and inflammation, which results in low circulating thyroid hormones. Thyroid hormones are important because they increase the rate of metabolism in all cells, so they make us think, move, and talk faster, and they also increase heat generation. They also activate the sympathetic nervous system, the part of the nervous system responsible for the ‘fight-or-flight’ response, increasing cardiac output. 

Third, there are cardiac conditions, which can be either congenital or acquired. Common congenital heart defects include atrial septal defect, or ASD; ventricular septal defect, or VSD; and patent ductus arteriosus, or PDA. On the other hand, acquired conditions that can complicate pregnancy include rheumatic heart disease; valvulopathies, which are caused by a defect in one or more of the four valves of the heart; and cardiomyopathies, which are disorders affecting the heart muscle, called th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Substance_Abuse_and_Mental_Health_Disorders_Impacting_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gN51OUS4Q86Q0NDqhbou08-tR6mj4NZK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Substance Abuse and Mental Health Disorders Impacting Pregnancy]]></video:title><video:description><![CDATA[Perinatal depression, also known as major depressive disorder with peripartum onset, and previously known as postpartum depression, is a type of depressive disorder that most often occurs during pregnancy or during the four weeks following delivery.

Now, let’s quickly review the physiology of some hormonal fluctuations that take place in the perinatal period. During pregnancy, the placenta releases a couple of hormones, including human placental lactogen, estrogen, and progesterone; while the pituitary gland releases prolactin, among others. All these hormones travel through the bloodstream to their specific areas of action to regulate specific body functions. During labor, the pituitary gland secretes another hormone called oxytocin, which stimulates uterine muscle contractions to facilitate delivery. Once the baby’s delivered, these hormones start rapidly decreasing. 

Now, the exact cause of perinatal depression isn’t understood, but it’s likely related to changes in hormone levels, as well as an imbalance of GABA, serotonin, dopamine, and glutamate. All of these are neurotransmitters that help regulate mood, reward-motivated behavior, appetite, and sleep. These changes come along with the emotional and physical stress that can accompany the birth of a child. Now, the main risk factors for perinatal depression seem to include having a family or personal history of trauma, such as sexual abuse, as well as a history of depression, premenstrual syndrome, or premenstrual dysphoric disorder. Clients who are younger than 25; single; or who have an unwanted pregnancy; as well as those who struggle with stressful life events before or after delivery; have inadequate social or financial support;  those who smoke, or have difficulty breastfeeding, also seem to be at an increased risk.

So, pathology-wise, the exact mechanism that leads to perinatal depression is not clear. It is thought that clients who develop perinatal depression have an increased sensitivity ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Learning_to_Communicate_Professionally</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/drCMehmQTHOLBvxom9EinlSiQmuFvv_a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Learning to Communicate Professionally]]></video:title><video:description><![CDATA[Nurse Rose works in an outpatient mental health clinic and has noticed that one of the clients, Gabriella, is visibly upset and sitting by herself away from the other clients. Nurse Rose says, “Gabriella, what’s wrong? Is something bothering you?” Gabriella rolls her eyes and shakes her head stating, “I just want to be left alone.” Nurse Rose is formulating a response when Gabriella stands up and yells, “Why don’t you go and talk to one of the other patients? You like them better anyway!” Nurse Rose is surprised by the increase in intensity of Gabriella’s emotions and does not understand what she is referring to. Nurse Rose will use what she has learned about therapeutic communication to determine how best to handle this situation. 

Communication is the process of sending and receiving information between two or more people. One type of communication that is used by many disciplines, including nurses, is therapeutic communication. Therapeutic communication is a type of communication where information between clinicians and clients is exchanged in order to collaborate effectively and promote the physical and psychological well-being of clients. Therapeutic communication is crucial to the formation of client-centered relationships, which can foster trust and respect, especially for clients experiencing emotional distress, like Gabriella.

Another use of therapeutic communication is de-escalation, which is a goal of communication when escalation occurs. Escalation refers to an increase, or rise in intensity, during an interpersonal interaction. This is what is occurring between Nurse Rose and Gabriella. Nurse Rose can recognize Gabriella’s emotions are escalating when she stands up and yells. When faced with an escalating interaction, it is important for the nurse to de-escalate the situation. De-escalation occurs when a person reduces the intensity of a conflict. One way to do this is through therapeutic communication.

There are two main types of communica]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psychological_Needs_of_Patients_with_Medical_Conditions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rmsdDnAsQ6C5-iKACdv7C9foRNizxCij/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psychological Needs of Patients with Medical Conditions]]></video:title><video:description><![CDATA[Medical conditions can sometimes be accompanied by psychological symptoms that can cause negative health outcomes. Common psychological responses to medical conditions include stress, anxiety, depression, grief, and denial. 

Stress is a common physical and psychological response to a challenging experience. When diagnosed with a medical condition, patients may think about the amount of pain they could experience due to their illness; they may wonder if the condition will affect their quality of life and relationships with others; or they might worry about being able to continue to work. How the patient responds to questions like these will shape their perception of their illness, which will then impact the amount of stress they experience.  

Next is anxiety, which is apprehension about a stressful situation that causes feelings of fear, worry, and nervousness, as well as physical symptoms like breathlessness and palpitations. 

When a medical condition is diagnosed, it’s often accompanied by experiences like waiting for test results or surgical procedures, which can increase anxiety due to loss of control and feelings of helplessness. Overwhelming anxiety can negatively influence a patient’s ability to cope and adapt to their medical condition and can lead to the use of unhealthy defense mechanisms or compulsive behaviors.  

Now, depression is a persistent sadness or loss of interest in daily life. Depression can impact a patient’s course of illness by impairing their motivation or ability to adhere to the prescribed treatment regimen, and it can lead to unhealthy lifestyle choices, like not exercising, continuing to smoke, or indulging in an unhealthy diet. 

Grief is a psychological response to a medical condition that occurs when a patient deals with the loss of their physical well-being. When experiencing grief, patients may feel confused, frustrated, sad, and vulnerable as they work toward reaching a sense of acceptance and peace. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_Health_Care_for_Older_Adults</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hoj3_y8cSzizaAUA8QnOyFNwQcuEw3tR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mental Health Care for Older Adults]]></video:title><video:description><![CDATA[Geriatrics is the branch of medicine that deals with the physiology and psychology of aging, as well as the diagnosis and treatment of diseases affecting older clients. Now, as a person ages, they go through psychosocial development, which refers to how the client&amp;#39;s personal needs fit with the needs of the society. This occurs through a life-long series of events with multifactorial influences like personality, thinking, and behavior. Two psychiatrists and psychologists who were involved in studying psychosocial development are Carl Jung and Erik Erikson. 

Okay, now one particular theory of Carl Jung is called individualism, which describes the process by which a person develops into a unique individual by balancing their orientation between the external world and their own subjective, inner experiences. According to Jung, individuals age successfully when they accept the past, adapt to physical decline, and accept their life’s accomplishments as well as its limitations. 

Now, Erikson constructed a theory called the psychosocial theory of development, which describes development in eight life stages. Typically, an individual needs to fulfill a particular task in one stage to move to the next one. The eighth and final life stage in Erikson’s theory occurs in clients who are 65 years or older, and it is called integrity vs. despair. Integrity is when older clients review their lives with satisfaction, even in the presence of inevitable mistakes, whereas despair occurs when older clients regret missed opportunities in life. Finally, psychosocial development is closely related to decisions regarding the end of life. 

Now, psychosocial development can influence quality of life, or QOL for short, which can be health-related or environmental. Health-related QOL includes a client’s physical, mental, emotional, and social functioning, and their impact on quality of life. These can include mobility, independence in bathing and dressing, sensory acuity, i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Therapeutic_Settings_in_Mental_Health_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9UQoKlL8Sp6LJBIn8aS6VG7_RkuQK4ZN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Therapeutic Settings in Mental Health Care]]></video:title><video:description><![CDATA[Patients with mental health disorders require treatment in settings specific to their condition and unique needs. These settings include outpatient settings, where treatment is conducted in the community; or inpatient settings, where treatment occurs in a hospital-like facility. 

Therapeutic activities provided in these settings include individual and group therapy; psychoeducation, which combines cognitive-behavior therapy, group therapy, and education; and nursing care for medication management and monitoring of existing medical conditions. 

Depending on the setting, patients may also partake in activities like rehabilitation services, such as occupational and physical therapy; gardening; yoga; or dance therapy. These services are provided by a multidisciplinary health care team, including providers, nurses, therapists, social workers, and case managers.

Outpatient settings include group homes, partial hospitalization, and day treatment centers.  
Group homes are a structured, home-like living situation that provides 24-hour support for patients who are unable to function independently, such as adults with mental health conditions like schizophrenia or pediatric patients with behavioral or conduct disorders. In the group home setting, patients develop necessary life skills, like learning to adhere to house rules, including nighttime curfews and abstaining from illegal substances. Group homes can also serve as residential treatment centers for patients with substance use disorders.  

Next, partial hospitalization centers are short-term programs that provide ongoing treatment for patients who are transitioning from an inpatient facility. Patients typically spend four to six hours each day, five days per week in therapy, with the goal of decreasing the likelihood of being readmitted to inpatient treatment. After completing a partial hospitalization program, patients are often transferred to a lower level of care in a day treatment center, which are comm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Therapeutic_Modalities_in_Mental_Health_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HUrCFfseT-O109d9pxQJ86dKTGWOCyBQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Therapeutic Modalities in Mental Health Care]]></video:title><video:description><![CDATA[Therapeutic modalities refer to the different types of care provided by psychiatric nurses to individual patients, groups, and families.  

Now, individual modalities are centered on the therapeutic relationship between the patient and nurse. Trust, respect, empathy, and clear boundaries are the pillars of an effective therapeutic relationship that supports your patient in reaching their goals. With a therapeutic relationship as the foundation, other specific modalities like medication therapy and cognitive behavioral therapy can be more successful.  

Okay, so your role as the nurse is to focus on your patient’s needs, feelings, and goals while helping them grow and realize their strengths.  First, you’ll assess their needs and collaborate with them about their desired goals. Then, provide them with a safe place to express their emotions while being empathetic and providing them with emotional support. You’ll also guide them on how to work through their thoughts, feelings, and behaviors.  

For instance, for your patient who experiences anxiety during their workday you might discuss healthy stress or anxiety management techniques, like deep breathing exercises and mindfulness.  

Before your patient is discharged, you’ll discuss their progress towards their goals, and refer them to additional resources for future help, if needed.  

Now, group modalities involve two or more patients meeting to discuss their shared goals or interests. Group modalities allow patients to learn about their behaviors and thoughts, as well as to discover new interpersonal skills or coping strategies. For instance, learning to use “I” statements to promote accountability by saying, “I feel angry when you interrupt me” to express their feelings with others.  

Group modalities can provide patients with a sense of belonging, a setting to practice new skills, and peers who can provide feedback or reassurance. On the other hand, group modalities can be affected by time constraints, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stress_Management</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bBptOzBTQwSuwTQygl_AvqI3TNyCSDCf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stress Management]]></video:title><video:description><![CDATA[Stress is a normal human response to an internal or external threat to homeostasis, or the body’s stable equilibrium, and can be prompted by stressors. These stressors such as illness, high workload, or economic hardship, can induce the stress response, also known as an allostasis, in an attempt to reestablish homeostasis. In the short term, the body can adapt to the physiological changes to stress; however, when stress becomes chronic, it can have a negative impact on mental and physical health. 

Now, not all stress is harmful, in fact, it is essential for daily life. There are two types of stress; eustress and distress. Eustress is positive stress, which is necessary for normal development and motivation and can occur with beneficial life changes like having a baby or getting a new job; whereas distress is negative stress that occurs when a person is unable to adapt or cope effectively to the stressor. 

Okay, the body’s response to a stressful event can be explained by the General Adaptation Syndrome, or GAS, which has three stages. First, the alarm reaction stage occurs as the sympathetic nervous system is activated, triggering the fight-or-flight response, which involves the release of hormones and neurotransmitters to support the body’s reaction to stress. The posterior pituitary releases antidiuretic hormone, or ADH, and the adrenal cortex releases aldosterone, both of which increase circulating blood volume. The adrenal cortex also releases cortisol, which increases the body’s supply of glucose, while the adrenal medulla releases epinephrine and norepinephrine, which increases the heart rate, blood pressure, and blood flow to the skeletal muscles. 

Next, the resistance stage is when the body attempts to stabilize and return to homeostasis. If the stress has been dealt with effectively, the parasympathetic nervous system returns vital signs to normal and begins to repair tissue damage. However, if the stress continues, the sympathetic activation w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Crisis_Intervention</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pi33ABimQh6Y0Hs7NDlCIICWSFGpahm9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Crisis Intervention]]></video:title><video:description><![CDATA[A crisis is a sudden, temporary, overwhelming emotional reaction caused by a stressful event perceived as a threat. Crisis intervention is a short-term management method used by health professionals in clients who are experiencing a crisis.

Now, there are three main types of crises: developmental, situational, and existential crises. Developmental crises are predictable and expected occurrences during life. Common examples of developmental crises include graduation, new job, marriage, the birth of a child, and retirement. Situational crises are unpredictable random and unexpected events. Common examples of situational crises include severe illness, job loss, unwanted pregnancy, divorce, and the death of a loved one. Finally, existential crises are usually related to one’s life&amp;#39;s meaning, purpose, and freedom. One common example of existential crisis occurs when an older person reflects on their life and accomplishments only to feel unfulfilled and dissatisfied.

Now, regardless of the type of crisis, there are typically four main phases. During the first phase, the client encounters a stressful situation or a precipitating event that disrupts their psychological balance and causes discomfort and anxiety. As a result, the client activates problem-solving and coping mechanisms to resolve the crisis. 

If the client fails to resolve the crisis, they enter the second phase. During the second phase, discomfort and anxiety continue to rise, and the client starts perceiving this stressful situation as a threat, resulting in it affecting their daily function and quality of life. Since problem-solving and coping mechanisms have failed, the client switches to a trial and error method, which uses various mechanisms in an attempt to resolve the crisis. 

But, if the trial and error method fails, the client enters the third phase, which is associated with further negative impact on their daily function, severe panic, and even physical symptoms, such as sweati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Schizophrenia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/u_FEWag_QcqlqR1ytE11rWdYQEKBuTdE/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Schizophrenia]]></video:title><video:description><![CDATA[Nurse Kit works on an inpatient psychiatric unit and is caring for Albert, a 31-year-old with a history of schizophrenia, paranoid type, who was recently admitted for psychotic symptoms. After settling Albert in his room, Nurse Kit goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Albert’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Kit recognizes important cues, including Albert’s vital signs, which are temperature of 37 C, or 98.6 F, heart rate 98 beats per minute, respirations 22 breaths per minute, and blood pressure 136/82 mmHg. Nurse Kit notices that Albert appears disheveled, restless, and is looking back and forth suspiciously across the room.

Nurse Kit: Hi Albert, how are you doing today? 

Albert: There’s a man coming after me, I’ve seen him watching me from inside the closet. 

Nurse Kit turns to look inside the closet, which is empty.  

Nurse Kit: That sounds scary. Although I don’t see anyone else here with us, I’m here to support you and keep you safe.

Next, Nurse Kit analyzes these cues. They review the electronic health record, or EHR, and read that Albert has visited the emergency department three times in the past month for symptoms associated with his schizophrenia. Nurse Kit knows the development of schizophrenia is related to both genetic and environmental factors that disturb the brain’s structure and balance of neurotransmitters like dopamine and glutamate, leading to disabling alterations in behavior, emotions, thinking, and perception, like delusions and hallucinations. Nurse Kit realizes that Albert needs management of his acute episode of schizophrenia.

Now, using the information they’ve gathered, along with Albert’s medical history, Nurse Kit chooses a priority hypothesis of altered perception.  

Then, Nurse Kit generates solutions to address Albert’s altered perception that will ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Bipolar_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rSjtDBtaQuypIowRpTPZZiUcSCeLAHU7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Bipolar Disorder]]></video:title><video:description><![CDATA[Nurse Nikil works on an inpatient psychiatric unit and is caring for Octavia, a 28-year-old with a history of bipolar I disorder, who was recently admitted for a manic episode. After settling Octavia in her room, Nurse Nikil goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Octavia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Nikil recognizes important cues, including Octavia’s vital signs, which are temperature 98.4 F or 36.9 C, heart rate 75 beats per minute, respirations 16 breaths per minute, and blood pressure 117/72 mmHg.  

Upon entering her room, Nurse Nikil notes Octavia is pacing back and forth, stopping intermittently to rearrange the items on her bedside table.  

Nurse Nikil: Hi Octavia, I see you’re cleaning your room. Could you pause for a moment and speak with me? 

Octavia: Oh sure, I totally have time for you. Don’t you see I’m doing something important? I really need to get my room cleaned so I can start writing. I have an amazing idea for a best-selling book about a forest like the one I grew up next to. My mom would know the name. I should call her. Do you have her number? Oh, look, what’s that on the floor? I’ll fix it!   

Next, Nurse Nikil analyzes these cues. They review the electronic health record, or EHR, and note Octavia is prescribed lithium but reports that she stopped taking it about two weeks ago. They note Octavia&amp;#39;s blood level of lithium is 0.5 mEq/L, but Nurse Nikil knows that the therapeutic index should be between 0.6 and 1.0 mEq/L.  

The nursing report from the night shift also stated that Octavia did not sleep.  

Nurse Nikil recognizes patients with bipolar I disorder experience extremes in emotions, moving from manic to depressive moods.  

Those in a manic state experience a persistent period of extreme emotions and may have symptoms, like racing thought]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Generalized_Anxiety_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R-j93oG_RcCBAT4q9E5rLmz7RJ_35eeI/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Generalized Anxiety Disorder]]></video:title><video:description><![CDATA[Nurse Becca works in a family practice clinic and is caring for Holly, a 32-year-old who presents with anxiety. After settling Holly in the room, Nurse Becca goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Holly’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Becca recognizes important cues, including Holly’s vital signs which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respiratory rate 19 breaths per minute, and blood pressure 136/75 mmHg. Nurse Becca notes that Holly appears restless and is biting her nails. She gathers more information about Holly’s symptoms. 

Nurse Becca: Hi Holly, tell me how you’re feeling. 

Holly: Well, I’m feeling really overwhelmed lately. I’m worried about so many things. And I’m having trouble concentrating at work.  

Nurse Becca: That sounds difficult. How are you sleeping? 

Holly: I only sleep a few hours each night, I can’t stop thinking about things.  

Nurse Becca: When did your symptoms start? 

Holly: Around seven months ago right after I moved and started my new job. 

Next, Nurse Becca administers the Generalized Anxiety Disorder 7-item screening tool, or GAD-7, and notes Holly has a score of 12 out of 21, which is consistent with moderate anxiety. 

Nurse Becca then analyzes these cues. She reviews the electronic health record, or EHR, and notes that Holly has no previous history of mental health disorders. She reports her assessment findings to the health care provider who diagnoses Holly with generalized anxiety disorder, or GAD.  

Nurse Becca remembers that one of the main features of GAD is excessive worry; and although the exact cause of GAD isn’t known, but it’s thought to be caused by an imbalance of the neurotransmitters, where serotonin system activity is low and noradrenergic system activity is elevated. This leads to symptoms of rest]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Somatic_Symptom_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-h1qW7GkQza3uA20jKTgAGKMR6Ozq9UK/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Somatic Symptom Disorder]]></video:title><video:description><![CDATA[Nurse Heidi works in a primary care office and is caring for Katya, a 43-year-old with a history somatic symptom disorder. After introducing herself, Nurse Heidi goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Katya’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Heidi recognizes important cues. She obtains Katya’s vital signs, which are temperature 98.6 F, or 37 C, heart rate 75 beats per minute, respirations 16 breaths per minute, and blood pressure 110/70 mmHg. Katya also states she&amp;#39;s having dull lower back pain, which comes and goes, that she rates at 4 out of 10 on a numeric pain scale. Nurse Heidi then gathers additional information from Katya.

Nurse Heidi: Katya, tell me about what brought you to the office today. 

Katya: Well, same thing as in the past. I keep having back pain that comes and goes even though my health care provider ran several tests and told me nothing is wrong. It never goes away, and I don’t know what to do. 

Nurse Heidi: Tell me about how this pain affects your daily life. 

Katya: I’m not able to do things I used to love doing, like hanging out with my friends, because I’m always worried my pain will return. So, I end up staying home alone all day instead. 

Nurse Heidi: That sounds difficult and isolating.

Next, Nurse Heidi analyzes the cues. She reviews the electronic health record, or EHR, and notes that Katya is diagnosed with somatic symptom disorder. She also sees that the health care provider recommended counseling, but Katya declined.

Nurse Heidi knows that patients with somatic symptom disorder experience physical symptoms that aren’t explained by any known physical or psychiatric conditions. She also understands that patients with this disorder are unable to cope with their unpleasant emotions and instead, displace them into physical symptoms, like pain and wea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Personality_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4hKtVJRbR6u8L6DveGS-Qa4lRu23KmcY/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Personality Disorder]]></video:title><video:description><![CDATA[Nurse Amirah works on an inpatient psychiatric unit and is caring for Yang, a 42-year-old with a history of borderline personality disorder, who was recently admitted for a self-harm ideation following a breakup with his partner. After settling Yang in his room, Nurse Amirah goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Yang’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Amirah recognizes important cues, including Yang’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 70 beats per minute, respirations 16 breaths per minute, and blood pressure 132/82 mmHg. She notes Yang is pacing back and forth and that his breakfast tray is untouched on the bedside table.  

Nurse Amirah: Hi Yang, I noticed you haven’t eaten your breakfast.  

Yang: This is the most disgusting food I’ve ever seen. Where is my boyfriend? I’m serious, I’ll hurt myself if he really decides to leave me. 

Nurse Amirah: I understand you’re upset. Do you have a plan to injure yourself? 

Yang: No, but I’ll do it. I just don’t get what happened. I thought I’d found my soulmate. 

Next, Nurse Amirah analyzes these cues. She reviews electronic health record, or EHR, and notes Yang was diagnosed with borderline personality disorder, or BPD, five years ago, and has been hospitalized for self-harm ideation in the past.  

Nuse Amirah recognizes that BPD is a condition where individuals have unstable moods and relationships. Those with BPD may also experience fear of abandonment, leading to threats of self-harm to keep someone from leaving them. Nurse Amirah recognizes that Yang needs mood stabilization to prevent self-harm. 

Now, using the information she&amp;#39;s gathered, along with Yang’s medical history, Nurse Amirah chooses a priority hypothesis of risk for violence against self. 

Then, she generates solutions to address Ya]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Delirium</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m5XuxIbhQg20tygEstGEXynIT2SMbAie/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Delirium]]></video:title><video:description><![CDATA[Nurse Melinda works on a medical surgical unit and is caring for Kadija, a 72-year-old with a history of heart failure who was admitted for pyelonephritis. After settling Kadija in her room, Nurse Melinda goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Kadija’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Melinda recognizes important cues, including Kadija’s vital signs, which are temperature of 102.2 F or 39 C, heart rate 102 beats per minute, respirations 19 breaths per minute, and blood pressure 140/80 mmHg.  

Nurse Melinda notices Kadija appears anxious, and her eyes are moving back and forth across the room. She gathers additional information from Kadija. 

Nurse Melinda: Hi Kadija, how are you feeling today? 

Kadija: Don’t you see that? There are a bunch of spiders on the wall behind you. 

Nurse Melinda turns around and notes there is nothing on the wall. 

Nurse Melinda: I don’t see any spiders, but I understand that must be very scary for you. You&amp;#39;re safe here with me. 

Nurse Melinda conducts a brief cognitive screening and determines that Kadija is oriented to self, but not time, place, or situation.  

Next, Nurse Melinda analyzes these cues. She reviews the electronic health record, or EHR, and notes that Kadija has no history of psychiatric illness.  

Nurse Melinda recognizes that underlying factors, such as infection, fever, pain, sleep deprivation, fluid and electrolyte imbalance, as well as certain medications, can lead to alterations in a patient’s mental status, causing problems like delirium, especially in patients with advanced age and preexisting medical conditions. 

She also recalls that delirium can develop over several hours or days and can result in a waxing and waning of mental function, including memory, thinking, language, behavior, mood, and personality. Hallucinations]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Substance_Misuse_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yltmA-zhRpOrEw__BW34qF-eRDW06mQi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Substance Misuse Disorder]]></video:title><video:description><![CDATA[Nurse Jacob works on a medical-surgical unit and is caring for Dallas, a 62-year-old patient with a history of substance use disorder, who was admitted three days ago for alcohol detoxification. After settling Dallas in his room, Nurse Jacob goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Dallas’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Jacob recognizes important cues, including Dallas’ vital signs, which are temperature 98.6 F or 37 C, heart rate 105 beats per minute, respirations 20 breaths per minute, and blood pressure 140/90 mmHg. He also notices Dallas&amp;#39; hands are trembling, he’s sweating, and he has IV fluids infusing in his left antecubital peripheral IV.

Nurse Jacob: Hi Dallas, how are you feeling?

Dallas: I have a pounding headache, I can’t concentrate, and I just can’t relax.

Nurse Jacob: I understand. Are you hearing or seeing anything that isn’t normally there?

Dallas: No, I’m not hallucinating, I just feel super nervous, I can’t explain it.

Next, Nurse Jacob analyzes these cues. He reviews the electronic health record, or EHR, and notes that, prior to admission, Dallas was drinking about ten shots of vodka per day.

Nurse Jacob completes the Clinical Institute Withdrawal Scale-Alcohol Revised, or CIWA-Ar, and tallies Dallas’ CIWA score as 15, indicating moderate withdrawal symptoms.

Nurse Jacob knows that the maximum CIWA score is 67, and as withdrawal symptoms become more severe, the score increases.

Nurse Jacob recognizes that when patients with alcohol use disorder stop drinking abruptly, they can develop symptoms like anxiety, irritability, tachycardia, diaphoresis, and auditory and visual hallucinations, and they can develop delirium tremens, a severe complication that can lead to seizures and death.

Nurse Jacob realizes Dallas needs effective management of his alcohol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Eating_Disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l4Be9pv8St_FH3pza7pzmrG6S9WUatmg/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Eating Disorders]]></video:title><video:description><![CDATA[Nurse Pat works in a medical psychiatric unit and is caring for Lily, a 22-year-old who was recently admitted for malnourishment secondary to anorexia nervosa. After settling Lily in her room, Nurse Pat goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Lily’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Pat recognizes important cues, including Lily’s vital signs, which are temperature 97.7 F or 36.5 C, heart rate 44 beats per minute, respirations 14 breaths per minute, and blood pressure 92/58 mmHg. Nurse Pat notices that Lily is very thin, and her skin is dry, pale, and has poor turgor. When asked how she’s feeling, Lily is tearful and reports that she’s very anxious about going out in public because she’s concerned that she’s gained weight. She also states she&amp;#39;s been restricting her food intake and hasn’t eaten anything in two days.  

Next, Nurse Pat analyzes these cues. They review the electronic health record, or EHR, and note that Lily&amp;#39;s ECG shows sinus bradycardia, her basic metabolic panel indicates hypokalemia, or low potassium level, at 3.4 mEq/L, and her most recent body mass index, or BMI, is 16, which is below normal. Nurse Pat knows that patients with anorexia nervosa restrict the amount of food they eat, and prolonged food restriction causes malnourishment which can lead to complications like dehydration and electrolyte depletion, causing hypotension and bradycardia. Additionally, prolonged anorexia can affect the brain, causing symptoms like confusion, irritability, or restlessness, as well as mental health problems like depression or anxiety. Nurse Pat realizes Lily needs nutritional management and emotional support. 

Now, using the information they’ve gathered, along with Lily’s medical history, Nurse Pat chooses a priority hypothesis of imbalanced nutrition. Then, they genera]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Autism_Spectrum_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2zne4E6mQe2lRnraf3oW3jubQ_CL18qw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Autism Spectrum Disorder]]></video:title><video:description><![CDATA[Nurse Abisola works at a primary care clinic and is caring for Nico, a three-year-old child recently diagnosed with moderate autism spectrum disorder, or ASD. After settling Nico and his caregiver, Anne, in a room, Nurse Abisola goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Nico’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Abisola recognizes important cues, including Nico’s vital signs, which are temperature 97.7 F or 36.5 C, heart rate 96 beats per minute, respirations 24 breaths per minute , and blood pressure 100/62 mmHg. She also notices that Nico appears withdrawn, isn’t making eye contact, and when addressed, he doesn’t respond.

Next, Nurse Abisola analyzes these cues. She reviews the electronic health record, or EHR, and notes that other than ASD, Nico has no medical or surgical history. Nurse Abisola reviews previous notes from the pediatrician, who states that Nico has missed some communication milestones for his age; for example, he&amp;#39;s unable to participate the normal back and forth of a conversation, he rarely initiates social interactions, and he often repeats unusual phrases over and over.  

Nurse Abisola understands that although the exact pathophysiology of ASD is not well understood, it seems to be caused by a combination of genetic and environmental causes, some of which are responsible for regulating social and communication behaviors. Nurse Abisola realizes Nico needs effective management of ASD to support his communication.

Now, using the information she&amp;#39;s gathered, along with Nico’s medical history, Nurse Abisola chooses a priority hypothesis of impaired communication.  

Then, she generates solutions to address Nico’s impaired communication, and she establishes the expected outcome that Nico will communicate his needs effectively after meeting with a speech language ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Attention-Deficit/Hyperactivity_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KJ5JhDVGQ2u9mNMZKgqkbvcMQQWKwssC/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Attention-Deficit/Hyperactivity Disorder]]></video:title><video:description><![CDATA[Nurse Sienna works in a family practice clinic and is caring for Paul, an 11-year-old who was brought in by his caregiver, Erin, for poor school performance over the past year. After settling Paul in his room, Nurse Sienna goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Paul’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Sienna recognizes important cues, including Paul’s vital signs which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respiratory rate 14 breaths per minute, and blood pressure 105/66 mmHg. She notices that Paul is restless and regularly stands up to look at and touch objects in the examination room.  

Nurse Sienna gathers more information from Erin and Paul.  

Nurse Sienna: Hi Paul, how are you doing today? 

Paul: Okay, I guess. I don’t know why I have to be here.  

Erin: Paul’s been having trouble in school. His grades have been getting worse over the past few months. He&amp;#39;s also been turning in his assignments late or not at all, and when he does turn them in, they’re incomplete.  

Paul: (shrugs) It&amp;#39;s hard to pay attention. 

Erin also reports that Paul’s teachers say he often disrupts class by standing up and blurting out answers to questions instead of raising his hand; and that he has difficulty following rules and waiting for his turn during group activities. When asked about the home environment, Erin reports that when Paul is asked to perform a household chore, he either forgets to do the chore or doesn&amp;#39;t finish it once he starts it.  

Nurse Sienna then analyzes these cues. She reviews Paul’s electronic health record, or EHR, and notes that he’s been to the clinic twice in the past year for similar behavioral difficulties and tested negative for underlying vision, hearing, or cognitive disorders. Nurse Sienna confers with the health care ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Child_Maltreatment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/USXZ5ch2QMWi_hdi-wYzwD6pTnim0lYP/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Child Maltreatment]]></video:title><video:description><![CDATA[Nurse Angelo works in a family practice clinic and is caring for Maya, a 2-and-a-half-year-old who&amp;#39;s brought in for a required wellness check before entering preschool. After settling Maya in the room, Nurse Angelo goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Maya’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Angelo recognizes cues, including Maya’s vital signs which are temperature 98.6 F or 37 C, heart rate 105 beats per minute, and respiratory rate 23 breaths per minute. Nurse Angelo notes that Maya has multiple circular bruises ranging in color from pale yellow to deep purple on her upper arms, as well as a rounded, punctate burn to the back of her left shoulder about one centimeter in diameter.  

Nurse Angelo also notes Maya grimaces occasionally and appears tense, so he determines Maya’s pain rating is two out of 10 according to the Face, Legs, Activity, Cry, and Consolability, or FLACC scale. Nurse Angelo also notes that when he asks Maya questions, she doesn’t respond or make eye contact with him.  

He gathers additional information from Maya’s mother, Josie, about her injuries. 

Nurse Angelo: I see that Maya has some bruising on her arms. Can you tell me what happened? 

Josie: Oh, those? She’s just clumsy. She’s always bruised easily. She probably fell down while she was playing or something. 

Nurse Angelo: I also noticed an injury to her left shoulder that looks like a burn. Do you know what happened there? 

Josie: That doesn’t look like a burn to me. Like I said, I think she probably scraped herself when she was playing. 

Nurse Angelo then analyzes these cues. He reviews Maya’s electronic health record, or EHR, and notes that she has a history of a humerus fracture at age one year. When asked about the fracture, Josie says it was caused by a fall when Maya was learning to walk.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Dependent_Adult_Abuse_and_Neglect</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Tvr12aaBSXuryIZvsbBt2D4wRrmvUMhx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Dependent Adult Abuse and Neglect]]></video:title><video:description><![CDATA[Nurse Madison works night shift in a long-term care facility, and is caring for Edward, a 71-year-old patient with a history of dementia. Nurse Madison goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Edward’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Madison recognizes important cues. As she approaches Edward’s room, she notices a chair has been placed in front of the door, preventing it from opening all the way. When Nurse Madison asks the unlicensed assistive personnel, or UAP, about it, the UAP admits they placed the chair there to prevent Edward from wandering off the unit.  

Then, upon entering the room, Nurse Madison notes Edward&amp;#39;s hair is unkempt, and his shirt is stained with dried food. She also sees that Edward’s bed sheets are soaked with urine and he’s visibly upset. 

Next, Nurse Madison analyzes these cues. She recalls that the electronic health record, or EHR, documents that Edward is at high risk for elopement, and that he’s attempted to leave the unit several times before being stopped by security. She also notes that Edward is normally continent of urine. Nurse Madison recognizes that preventing Edward from leaving his room by forcing him into physical confinement is considered restraints abuse. It also appears that Edward has been neglected, meaning that his basic needs, such as hygiene, haven’t been met.  

Now, using the information she’s gathered, Nurse Madison chooses a priority hypothesis of powerlessness.  

Then, she generates solutions to address Edward’s powerlessness, and she establishes the expected outcome that after intervening, Edward will have his basic needs met while remaining safe in his environment.  

Nurse Madison then takes action to implement these solutions. She makes sure Edward is safe by ensuring he&amp;#39;s free from injuries and confirming his room]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Management_of_the_Suicidal_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3ONgXhiQRJKPh6eCTFO0A5JTStmpjDIE/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Management of the Suicidal Patient]]></video:title><video:description><![CDATA[Nurse Iris works on an inpatient psychiatric unit and is caring for Dee, a 30-year-old patient with a history of depression and previous suicide attempts, who was recently admitted for suicidal ideation. After settling Dee in his room, Nurse Iris goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Dee’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Iris recognizes important cues, including Dee’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 65 beats per minute, respirations 16 breaths per minute, and blood pressure 116/70 mmHg. She also notices Dee looks straight ahead during the assessment and has a flat affect. 

Nurse Iris: Hi Dee, I’ll be your nurse today. How are you feeling? 

Dee: I’m upset. I wanted to take all my pills at home, but my friend brought me to the hospital before I could. I don’t want to be here anymore. I wish I was dead. 

Nurse Iris: I’m sorry to hear that. I want you to know that I and the rest of your medical team care about you. We&amp;#39;re here to support you and keep you safe.  

Next, Nurse Iris analyzes these cues. She reviews the electronic health record, or EHR, and notes that Dee is prescribed fluoxetine for depression and has been hospitalized in the past year for suicidal ideation. She also notes that Dee scored a 19 out of 27 on his PHQ-9 assessment, which is a nine-question, self-reporting depression survey, indicating a moderately severe level of depression. Nurse Iris recognizes that Dee needs a safe environment while he receives treatment for his depression and suicidal ideation. 

Now, using the information she’s gathered, along with Dee’s medical history, Nurse Iris chooses a priority hypothesis of risk for suicide.  

Then, she generates solutions to address Dee’s suicidal ideation that will include pharmacologic and nonpharmacologic interventions; and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_of_the_Family_During_Pregnancy_-_Psychosocial_Changes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T__lBVXTQ-mUEqdM1b8eJUm6TBme3bC8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care of the Family During Pregnancy - Psychosocial Changes]]></video:title><video:description><![CDATA[Psychosocial changes during pregnancy include the rollercoaster of emotions that parents experience from the moment they find out about the pregnancy to the moment they accept that they are going to be parents all the way up to birth. During this period, the nurse should support the client and the client’s partner and help promote a healthy outcome. 

Now, during the first trimester, clients typically feel uncertainty because they are not sure if they are actually pregnant. Some may respond to uncertainty by talking to friends or family and looking for signs and symptoms of pregnancy. Others might use over-the-counter pregnancy tests, while others might seek professional help from a healthcare provider. Once the pregnancy is confirmed, they may experience a feeling of ambivalence or internal conflict. Particularly if it&amp;#39;s their first pregnancy, they may begin to worry about the added responsibility and life changes that come with having a child. But, with time, ambivalence usually gives way to acceptance of their new reality. 

Next comes self-focus, meaning they start focusing on themselves and the effects of the pregnancy symptoms. At this point, pregnancy symptoms, such as nausea and fatigue begin to present. At the same time, hormonal changes in the body can trigger mood swings that can range from being extremely happy to irritability and even to sadness. Finally, they might experience changes in their sexuality, which can vary based on their individual cultural or religious beliefs. So, some clients might notice a rise in their sexual interest or a fall due to the pregnancy symptoms, particularly nausea and breast tenderness. During the first trimester, nurses can assist their clients by reassuring them about these normal changes and by suggesting ways they can cope with the discomforts of pregnancy, as well as any psychological stress they are experiencing.

Once the client enters their second trimester, they have more physical evidence of p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maximizing_Comfort_for_the_Laboring_Woman_-_Pharmacologic_Management</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f1B4yH6VTXOZk2PgC7jFlKfsTuqLb7Rw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Maximizing Comfort for the Laboring Woman - Pharmacologic Management]]></video:title><video:description><![CDATA[Analgesics are medications used to relieve pain, and can be used for various reasons in obstetrics, such as during pregnancy to manage headaches, back, or pelvic pain during delivery to help reduce pain from uterine contractions, cervical stretching, and vaginal distension; as well as following vaginal delivery for perineal lacerations, and following cesarean delivery for pain at the incisional site.

Commonly used analgesics in obstetric settings include acetaminophen, which is mainly used during pregnancy; as well as systemic analgesics like opioids and regional analgesics like local anesthetics, which are typically used once the client goes into labor. However, other analgesics like NSAIDs, such as ibuprofen, should be avoided during pregnancy, since they can cause fetal harm, including fetal renal impairment, oligohydramnios, and premature closure of the fetal ductus arteriosus.

Now, opioids can be full opioid agonists like fentanyl and remifentanil; and partial opioid agonists like butorphanol and nalbuphine; whereas regional anesthetics include bupivacaine and ropivacaine.

Now, in general, analgesics act by blocking neurons that transmit pain sensations. Opioids act on opioid receptors called the mu, kappa, and delta receptors. These receptors are typically  located on the pre- and post-synaptic membranes of the pain-conducting neurons in the spinal cord and brain. Now, opioids are primarily given orally, intramuscularly, and intravenously. When opioids bind to their receptors, they result in a decreased sensitivity to pain by increasing the pain threshold and altering pain transmission. 

On the other hand, regional anesthetic medications act by reversibly blocking sodium channels on the neurons and prevent the transmission of pain. Regional anesthetics can either be injected locally into the pudendal nerve area, called a pudendal anesthesia or nerve block, to numb the lower vagina, vulva, and perineum, which is often used in the repair of episiot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Empathy,_Psychological_Safety,_and_Confidence_in_Returns_to_Classroom-Based_Learning_Webinar</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A0rDAS1rQjy7yo_MlpvG8PEeSp_UlBkb/_.png</video:thumbnail_loc><video:title><![CDATA[Empathy, Psychological Safety, and Confidence in Returns to Classroom-Based Learning Webinar]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Empathy, Psychological Safety, and Confidence in Returns to Classroom-Based Learning Webinar through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gorlin_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_GsUHmtsTcyzQD1R_53r4XGLRp2M6kNU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gorlin syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Gorlin syndrome is a rare genetic disorder that affects approximately 1 in  31,000 people worldwide. At the most basic level, people with Gorlin syndrome have an increased lifetime risk of tumors, both cancerous and non-cancerous, in nearly any organ of their body. The most common tumor experienced is a skin cancer  called basal cell carcinoma, so  the disease is also known as basal cell carcinoma nevus syndrome. 

Because of the rarity of the disease, your doctors might not recognize or know much about Gorlin syndrome. Medical care may be delayed or compromised if it is not identified, so it is important for people with Gorlin syndrome and their family members to learn about the syndrome and be able to effectively manage care. 

Gorlin syndrome is caused by a defect in a gene that suppresses tumors in a person’s body. Genes are like instructions for cells. Every cell has two copies of each gene. We inherit one gene from each parent. Sometimes, we inherit a mutated gene from one parent, and sometimes a gene mutates on its own. If one gene is mutated then the other gene can suppress tumor growth on its own to a degree. This means that if a person with Gorlin syndrome has only one broken copy of a tumor suppressing gene in each cell, they may have some features of the disease. If any cell in their body develops a second mutation that affects the working copy of  the tumor suppressing gene, then the cell has no way to prevent itself from replicating out of control.The cells will begin to pile up into a mass, and a tumor will form. People with Gorlin syndrome usually have tumor growth at some point in their lives, but how many develop, at what age and which organs are affected is variable. 

There are three genes known to cause Gorlin syndrome: PTCH1, PTCH2 and SUFU. Genetic testing may identify which defect you have. The specific gene that is altered can affect which manifestations and symptoms you experience. A genetic counsellor can explain the risks associ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Get_to_Know_Osmosis_RTL_Faculty_Award_Event</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MxKM65dxQfihmdrZCErxTAXNQI_5gYug/_.png</video:thumbnail_loc><video:title><![CDATA[Get to Know Osmosis RTL Faculty Award Event]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Get to Know Osmosis RTL Faculty Award Event through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Get_to_Know_Osmosis_Nursing_April_20th,_2023</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mXyda5Y4RP2XoOpxd-sL3uSMRvahrXfD/_.png</video:thumbnail_loc><video:title><![CDATA[Get to Know Osmosis Nursing April 20th, 2023]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Get to Know Osmosis Nursing April 20th, 2023 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_supporting_Wikipedia_editors_is_helping_improve_trust_in_science</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fJcadjizRnOvepUAVteCUIbsQtq9TI12/_.png</video:thumbnail_loc><video:title><![CDATA[How supporting Wikipedia editors is helping improve trust in science]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How supporting Wikipedia editors is helping improve trust in science through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Care_of_the_Patient_with_Hypertension</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qqyKQDErRXaBbWQTlm269GeUSeGX7m4Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Care of the Patient with Hypertension]]></video:title><video:description><![CDATA[Nurse Kendra works in a family practice office and is caring for Peter, a 60-year-old male who presents for a follow-up appointment for elevated blood pressure readings and mild fatigue. After settling Peter in his room, Nurse Kendra goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Peter’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Kendra recognizes important cues, including Peter’s vital signs, which are temperature 99.0 F or 37.2 C, heart rate 90 beats per minute, respirations 16 breaths per minute, and blood pressure 156/96 mmHg taken manually five minutes apart and averaged over two readings. Peter’s oxygen saturation is 98 percent on room air, and his pain rating is zero out of 10. Next, Nurse Kendra measures Peter’s height and weight and calculates his body mass index, or BMI, at 32 kg/m2.

Nurse Kendra asks Peter about his health history. She learns that he doesn’t take any medications, but says his father has high blood pressure and is taking medication for it. He reports smoking a few cigarettes after work daily and denies drinking alcohol. He also tells Nurse Kendra that his job requires him to sit at a desk most of the day.

Then, Nurse Kendra analyzes these cues. She reviews the electronic health record, or EHR, and notes Peter’s blood pressure at his last two appointments was above 140/90 mmHg, and his ECG and cardiac labs were normal. Nurse Kendra reports her assessment findings to the health care provider who diagnoses Peter with primary hypertension, and prescribes the oral antihypertensive medication, lisinopril, along with lifestyle modifications. Nurse Kendra realizes Peter needs effective health maintenance.

Now, using the information she’s gathered along with Peter’s history, Nurse Kendra chooses a priority hypothesis of inadequate health maintenance.  

Then, she generates solutions ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Care_of_the_Patient_with_Breast_Cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tsdho_mQQX2RYotqUp4ZVRSWSP_EZeRR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Care of the Patient with Breast Cancer]]></video:title><video:description><![CDATA[Nurse Jacques works at an outpatient oncology clinic and is caring for Elisapie, a 55-year-old female with a history of breast cancer who presents with severe left arm swelling. After settling Elisapie in her room, Nurse Jacques goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Elisapie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Jacques recognizes important cues, including Elisapie’s vital signs, which include temperature 98.6 F or 37 C, heart rate 92 beats per minute, respirations 18 breaths per minute, blood pressure 128/82 mmHg, and oxygen saturation 98 percent on room air. Elisapie reports a pain level of 6 out of 10 in the left chest wall and upper arm and mild tingling in her fingers and a feeling of heaviness in her arm. Nurse Jacques’ assessment reveals a healing surgical wound to the left chest. He also sees that Elisapie’s left arm is edematous, has limited range of motion, and that the skin is shiny and red.

Next, Nurse Jacques analyzes these cues. He reviews the electronic health record, or EHR, and notes that Elisapie is recovering from a left mastectomy with axillary lymph node dissection, or ALND for short, and has undergone radiation therapy. Nurse Jacques knows that having ALND, plus radiation therapy, can cause obstruction of lymph fluid flow, causing it to accumulate in the soft tissue of the arm. This puts pressure on the veins, preventing venous return and adding to the edema. He understands that the extra fluid causes a feeling of heaviness in Elisapie’s arm and the tingling in her fingers. Nurse Jacques recognizes that Elisapie needs management of her lymphedema.

Now, using the information he’s gathered, Nurse Jacques chooses a priority hypothesis of impaired tissue integrity. 

Then, he generates solutions to address Elisapie’s impaired tissue integrity that will include nonpharmacolo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Announcing_Year_of_the_Zebra_in_2023:_Educating_millions_about_rare_disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xB2FsCi2S82olQs9ZrkMDp4zQ6SkYDNA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Announcing Year of the Zebra in 2023: Educating millions about rare disorders]]></video:title><video:description><![CDATA[In medical school, we’re taught “When you hear hoofbeats, think of horses, not zebras.” Put another way, think of the most common condition, not the rare one. The  advice is meant to avoid over-testing, though it didn’t sit well with our founder for two reasons. First, it was dismissive of hundreds of millions of patients and their families who suffer from these rare diseases and have not had access to an equitable and inclusive healthcare system. Second, he was born in Sub-Saharan Africa, where zebras are far more common than in the US where the phrase was coined. 

So what exactly is a “zebra” in the context of medicine? It’s a rare disorder, which is defined as affecting fewer than 200,000 people in the US or less than 1 in 2,000 people in Europe. However there are over 7,000 “zebra” disorders with new ones being discovered all the time, and they collectively affect more than 300 million people around the world, half of whom are children. These conditions range from Adrenoleukodystrophy to Zellweger Spectrum Disorders, and given how little we know and teach about them it can take 4-9 years for patients to receive the correct diagnosis, during which time their condition can deteriorate. 

Zebras matter for a few very important reasons. 

First and foremost, as per our core pillars at Elsevier Health, if we truly want to build an inclusive and equitable healthcare system we need to take care of our entire society, including patients who for centuries were dismissed by the medical establishment as anomalies. As Mahatma Gandhi once said, “The true measure of any society can be found in how it treats its most vulnerable members.” 

Second, these patients and their families are incredibly tenacious, dedicated, and resourceful, and serve as models for highly engaged patients. For example, Dr. David Fajgenbaum helped find an effective drug for his own battle with Castleman Disease, and John Crowley led the development of a therapy for Pompe Disease after t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Year_of_the_Zebra_music_video</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PxiHn4uyQ_O3dBld2Aixz-WSS3qUGNjf/_.jpg</video:thumbnail_loc><video:title><![CDATA[The Year of the Zebra music video]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of The Year of the Zebra music video through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alagille_syndrome_(NORD):_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7iEHxSapS4ui4xHEGD8jfhCNRLq8Ing1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alagille syndrome (NORD): Year of the Zebra]]></video:title><video:description><![CDATA[Alagille syndrome, or ALGS, is a genetic disorder that can affect multiple organs in the body and cause a variety of abnormalities. Alagille syndrome typically affects the liver but it can also cause problems in the heart, kidney, eyes, and bones. 

One of the main liver features of Alagille syndrome is the disruption of bile flow from the liver to the gallbladder. Affected individuals have a reduced number of bile ducts in the liver. As a result, there is a decrease in bile flow, also known as cholestasis. The symptoms and signs of cholestasis include jaundice, or the yellowing of skin and eyes, severe itching, pale colored stools, and dark urine. Some patients may also have an enlarged spleen or liver. 

Because many necessary vitamins and nutrients need bile to be properly absorbed, people with Alagille syndrome may also experience select vitamin deficiencies, or poor weight gain and growth. Deficiencies in specific vitamins may result in vision problems from a lack of Vitamin A, bone weakness from a lack of vitamin D, developmental delays from a lack of Vitamin E, and blood clotting problems from a lack of Vitamin K. 

The heart can also be impacted by Alagille syndrome. The most common finding in ALGS patients is peripheral pulmonary arterial stenosis. This means that the blood vessels carrying blood to the lungs are narrowed. The stenosis typically manifests as a heart murmur, or an extra sound in the heartbeat. Symptoms are based on the degree of narrowing of the blood vessel and some people may have no symptoms while others may have dizziness, shortness of breath, increased sweating, chest pains, and cyanosis, or bluish colored skin. 

Children with Alagille syndrome may also have congenital heart defects, or heart problems that one is born with. The most common congenital heart defect in ALGS patients is tetralogy of Fallot. Other possible defects include atrial septal defects, patent ductus arteriosus, and coarctation of the aorta. Congenital hea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gaucher_disease_(NORD):_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ov7lI_2ZQJuePSpAdVoG4-CBS4OsWbb8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gaucher disease (NORD): Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Gaucher disease (NORD): Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/PIK3CA-related_overgrowth_spectrum_(NORD):_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UyBsZ9-_SfGs5v8WJ25feWE3TlyEa9_B/_.jpg</video:thumbnail_loc><video:title><![CDATA[PIK3CA-related overgrowth spectrum (NORD): Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of PIK3CA-related overgrowth spectrum (NORD): Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_Nursing_Interventions_and_Skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JSUjdwQLR3SXJGSFkXX7GjcUSXWNNtew/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric Nursing Interventions and Skills]]></video:title><video:description><![CDATA[Pediatric patients who are hospitalized require individualized care based on their developmental level. As the nurse caring for a hospitalized child, you’ll prepare them and their caregivers for procedures while promoting their comfort and safety.    

When providing care, begin by establishing rapport and trust with the child and their caregivers. You can do this by using therapeutic communication skills, like speaking in a calm tone, listening actively, and practicing therapeutic body language, like sitting down and leaning forward toward your patient.  

When explaining the plan of care, remember to avoid words that can cause confusion or fear. So, instead of using medical jargon like “edema,” you can describe a swollen body part as being “puffy.” Likewise, instead of “shot” when talking about an injection, you can use less threatening language like “medicine under the skin.”  

You can also ensure your patient and caregivers are familiar with other members of the health care team and their role in the child’s care. Lastly, be sure to collaborate with the child life specialist, who can provide therapeutic play activities that can decrease fear and anxiety in children and their families.   

Now, before your patient undergoes a procedure, you’ll need to ensure that informed consent is obtained from their caregiver, by verifying that the health care provider has explained the condition, proposed treatment plan, treatment alternatives, as well as potential risks and benefits of the procedure. As the nurse, you’ll witness the signatures on the consent form and reinforce the information provided by the health care provider. Also be sure to include the child in the discussion, and obtain their assent, as appropriate.  

During teaching, you may use a doll or stuffed animal to show a younger child where electrodes are placed or where their surgical dressing will be; whereas, with an adolescent, you can provide them with detailed information, since they’re typically eager to receive health teaching. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Early_Care_of_the_Newborn</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4XojP6rHRyGGZ2JcUoaTDgafTfues5il/_.jpg</video:thumbnail_loc><video:title><![CDATA[Early Care of the Newborn]]></video:title><video:description><![CDATA[Early care of newborns after birth involves supporting cardiorespiratory function and thermoregulation, monitoring for problems that need immediate intervention, and administering prophylactic medications. 

Okay so, you can quickly assess the newborn immediately after delivery by using the APGAR score to determine when cardiorespiratory support interventions are needed. The APGAR score is calculated 1- and 5-minutes following birth, and consists of these five parameters: Appearance, or skin color; Pulse; Grimace, or the newborn’s reaction to stimulation; Activity, or the amount of flexion and movement; and Respiration, or the strength of their respiratory effort. Each parameter is scored 0, 1, or 2 for a total of 10 possible points. Scores 7 and above are normal and require no special intervention. A score below 7 requires interventions  

Interventions such as tactile stimulation, oxygen administration, and other resuscitation efforts, as well as repeat scoring every 5 minutes. If the newborn is having difficulty clearing secretions from their airway, you should position them on their back, with their head in a neutral position, and use a bulb syringe to suction their mouth first, and then their nose. 

You’ll also support the newborn’s thermoregulation, which is the ability to maintain a steady core temperature by balancing heat loss with heat production. You can help prevent heat loss by establishing a neutral thermal environment, or NTE. Be sure the delivery room is warm and free of drafts; and immediately after birth, dry the newborn with warm linens to remove amniotic fluid. You’ll also perform your initial assessments under a radiant warmer; and then, you can either wrap them in a warm blanket and place a warm hat on their head, or initiate skin-to-skin contact with the mother.  

Now, a common problem in the newborn period is jaundice, also known as hyperbilirubinemia, which can cause yellowish pigmentation of the skin, sclera, and mucous membrane]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Femoral_hernias:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t1PYWD4OTuyKnQJG_8_GKAUrTFyaxzQG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Femoral hernias: Clinical sciences]]></video:title><video:description><![CDATA[A femoral hernia is the protrusion of abdominal contents, such as preperitoneal fat, omentum, or bowel, through a defect in the lower abdominal wall, which passes through the femoral canal and eventually exits through the femoral ring. 

Anatomically, the boundaries of the femoral ring include the lacunar ligament medially, the femoral vein laterally, the pectineal ligament posteriorly, and the inguinal ligament anteriorly. A femoral hernia usually occurs just inferior to the inguinal ligament and lateral to the pubic tubercle. 

Some risk factors can increase the chance of developing a femoral hernia. For example, biological females are more likely to develop femoral hernias due to a larger distance between the pubic tubercle and internal ring, as well as a wider rectus abdominis muscle. Other risk factors in both males and females include age-related atrophy of the pectineus muscle, as well as widening of the femoral ring either due to injury or age. 

Femoral hernias can present in four ways: asymptomatic, symptomatic, incarcerated, or strangulated. Keep in mind that femoral hernias are more likely to incarcerate and strangulate than other types of hernias, such as inguinal hernias, so they might need immediate attention. 

Alright, you should first perform an ABCDE assessment to determine if the patient is stable or unstable. If the patient is unstable, stabilize their airway, breathing, and circulation. This means that you might need to intubate the patient, establish IV access, and administer fluids before continuing with your assessment. 

Now that unstable patients are stabilized, let’s go back to the ABCDE assessment and talk about stable patients. If the patient is stable, your first step will be to obtain a focused history and physical examination. There are a few findings you might see here. First, some patients will present with asymptomatic hernias. In this case, they don’t have any symptoms. However, physical examination reveals a small bulg]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_postoperative_wound_complications:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i4Re3ajRT-CAbhFHLuSRIJY0Qie9712L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to postoperative wound complications: Clinical sciences]]></video:title><video:description><![CDATA[Postoperative wound complications involve the disruption of anatomical layers that were manipulated or closed during surgery, and include wound disruptions such as evisceration, dehiscence, seroma, or hematoma; abnormal communications known as fistula; and wound infections, which can be superficial or deep. 

There are some risk factors that can predispose the patient to postoperative wound complications. These include factors that contribute to poor healing, like smoking, malnutrition, and chronic steroid use, as well as conditions like diabetes or anemia, and ascites. Other risk factors don’t affect the healing but increase the risk of bleeding, such as coagulopathy or receiving anticoagulation. 

When assessing a patient with signs and symptoms suggestive of postoperative wound complication, you should first perform an ABCDE assessment to determine whether your patient is unstable or stable. If the patient is unstable, start with acute management to stabilize them. This means that you might need to intubate the patient, obtain IV access, or administer fluids before continuing with your assessment. At this step, you should look for signs of conditions that cause instability, such as abdominal compartment syndrome, sepsis, or severe blood loss.

Alright, now that unstable patients are taken care of, let’s talk about stable patients. For a stable patient, your first step is to start supportive care. This means that you need to obtain IV access for fluid resuscitation, administer pain medication, wound care, and in some cases, NPO status for bowel rest with nutritional support if needed. Keep in mind though that oral or enteral nutrition is preferred in most cases, and should be instituted as soon as possible. Once these important steps are done, obtain a focused history and physical examination.

Let’s start with wound disruptions, which occur when the integrity of the surgical closure has been compromised. Wound disruptions include evisceration, dehiscenc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Narcolepsy_(NORD):_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZI-N7qyURBuN7xzRNAqd9Fr3SFCa_nSB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Narcolepsy (NORD): Year of the Zebra]]></video:title><video:description><![CDATA[At one time or another you’ve probably had to force yourself to stay awake, maybe while driving or when you’re in a looong lecture. In these situations, you were exerting control over your sleep-wake cycles. Narcolepsy is a disorder in which the ability to regulate sleep-wake cycles is impaired, so the normal boundaries between sleeping and being awake are weak leading to frequent lapses into sleep and the occurrence of elements of sleep while a person is awake. 

In a deep part of the brain called the hypothalamus, there is a special group of neurons that help stabilize wakefulness and sleep. These neurons produce the neurotransmitters orexin A and B, also called hypocretin 1 and hypocretin 2, which connect to key sites in the brainstem and elsewhere that regulate wake and sleep states. Specifically, orexins have an excitatory effect, which helps stabilize wakefulness across the day, and sleep throughout the night. 

In individuals with the classic form of narcolepsy, an autoimmune process kills off nearly all the orexin-producing neurons during adolescence, resulting in five key symptoms: daily sleepiness despite adequate sleep at night; episodes of muscle weakness known as cataplexy; an inability to move at the start or end of sleep; vivid hallucinations at the start or end of sleep; and fragmented sleep.  

Sleepiness is usually the most challenging symptom.People with narcolepsy can doze off with little warning, usually when sitting down, like in a class or while working at a computer, but they generally don’t sleep more than healthy people in a given 24 hour period. Most individuals with narcolepsy find that a short, 15-minute nap substantially improves their alertness for a few hours, which suggests that the sleepiness of narcolepsy is caused by a problem with the brain circuits that normally promote full alertness, rather than poor quality or insufficient sleep. Normally when a healthy person goes to bed, they go through a sleep cycle lasting an ho]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Phenylketonuria_(NORD):_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6sltALnRRm_-yhFR9Fz8J7OOTWiCAClO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Phenylketonuria (NORD): Year of the Zebra]]></video:title><video:description><![CDATA[Phenylketonuria or PKU is a rare metabolic disease that can lead to severe brain disorders caused by the accumulation of the amino acid phenylalanine to toxic levels in the blood and brain.

Amino acids are the basic building blocks that make up proteins. Phenylalanine, or Phe, is one of the essential amino acids.  It is necessary for life, but our bodies can&amp;#39;t make it; therefore, Phe must be acquired through foods that contain protein. Normally, once Phe enters the body, most of it is converted to tyrosine by the enzyme phenylalanine hydroxylase. Tyrosine is then turned into neurotransmitters important for normal brain development and function.

PKU is an autosomal recessive genetic disorder that affects function of the phenylalanine hydroxylase enzyme. The phenylalanine hydroxylase gene is located on chromosome 12 and over 600 mutations have been described. The degree of enzyme function can vary. When untreated, people with PKU develop symptoms such as severe intellectual disability, psychiatric disorders, and seizures. A pregnant woman with PKU must pay special attention to her Phe levels to reduce the risk of Maternal PKU Syndrome that can result in heart defects, microcephaly, and developmental disability in her baby.

In PKU, elevated Phe levels and reduced tyrosine levels can change the way the brain functions. This is because Phe uses the same transporters to get across the blood-brain barrier as other amino acids including- tyrosine and tryptophan. Tyrosine is needed to synthesize dopamine and norepinephrine, and tryptophan is needed to synthesize the neurotransmitter serotonin. As Phe levels rise, it occupies all the transporters, making it hard for tyrosine and tryptophan to get across the blood-brain barrier. As a result, dopamine, norepinephrine, and serotonin levels in the brain begin to fall, leading to abnormal brain development and intellectual disability.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arterial_blood_gas_(ABG)_-_Metabolic_alkalosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zY7W9eZKQIiCdRVJZS-uq2sJTm_cAnEm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Arterial blood gas (ABG) - Metabolic alkalosis: Nursing]]></video:title><video:description><![CDATA[An elderly client is brought to the emergency department from a nursing home. The nurse from the nursing home reported that the client has been experiencing nausea, vomiting, and diarrhea for the past few days. On assessment, the client is confused and has a slow and shallow respiratory rate. Based on these findings, the health care provider suspects metabolic alkalosis secondary to dehydration, so an arterial blood gas is ordered to assess for changes in the acid-base balance.

Alright, arterial blood gas, or ABG for short, is a test used to measure the acid-base components and pressure of gasses in the arterial blood. Normal ABG values for healthy adults  are a pH ranging from  7.35 to 7.45, bicarbonate, or HCO3- ranging from 21 to 28 mEq/L; carbon dioxide or PaCO2 ranging from 35 to 45 mm Hg; PaO2 ranging from 80 to 100 mm Hg, and SaO2 should be more than 95%.

Now, metabolic alkalosis is a condition where the pH is increased, which can occur due to an excessive loss of acid, or hydrogen ions; or a gain of base, or bicarbonate ions. A common way for this to occur is through the gastrointestinal system. First, too much acid can be lost from excessive vomiting or prolonged gastric suctioning. In this situation, the amount of base remains the same, but the amount of acid is reduced, resulting in a relative base excess. Metabolic alkalosis can also be caused by an increased intake of base, like an excessive oral intake of bicarbonate-containing antacids. When this happens, the amount of acid remains the same, but the amount of base increases, resulting in an absolute base excess. 

Another way metabolic alkalosis can happen is through the renal system. One common cause is when there’s too much of the hormone aldosterone. Now, excess aldosterone can be the result of an adrenal tumor that secretes excess aldosterone. It can also happen when the renin-angiotensin-aldosterone mechanism is triggered by volume depletion from loop or thiazide diuretic use, or from]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complete_metabolic_panel_(CMP)_-_Total_protein:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ma_V4iXbS4yHkcv7p1aDsvcWS86GZl8o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complete metabolic panel (CMP) - Total protein: Nursing]]></video:title><video:description><![CDATA[A 78-year-old male is brought to the clinic by his daughter, who says she noticed her father has been losing weight and has recently become lethargic and confused. Based on these findings, the health care provider is concerned about undernutrition and orders a complete metabolic panel, or CMP, to evaluate his nutritional status.

Alright, total serum protein measures two proteins found in the serum: albumin and globulins. Albumin is produced by the liver, and is the body’s most abundant protein. It keeps fluids from leaking out into the tissues by helping to maintain oncotic pressure within the intravascular space. Albumin also functions as a transport for lipids, bilirubin, and many other compounds like medications; and provides a protein reserve for creating and repairing tissue. 

Next, globulins include alpha, beta, and gamma globulins. These proteins also serve as carrier proteins, as well as enzymes, immunoglobulins, and clotting factors. The albumin value can be divided by the globulin value, to get the albumin:globulin ratio, also known as the A/G ratio. Now, total serum proteins can be drawn on their own, or as a part of a complete metabolic panel. In healthy adults, total protein ranges from 6.4 to 8.3 g/dL; albumin ranges from 3.1 to 4.3 g/dL; globulin ranges from 2.6 to 4.1 g/dL, the A/G ratio is usually slightly higher than 1.

Alright, there are some conditions that can increase a client’s total serum protein. Chronic inflammatory diseases, such as systemic lupus erythematosus and multiple myeloma can increase the production of some types of protein. Alternatively, if the amount of fluid in the blood decreases, like with dehydration, the blood becomes more concentrated, and the protein value can increase. 

On the other hand, decreased total serum protein can be caused by a long-term decrease in protein intake, like in undernutrition; or decreased absorption of nutrients. Low total serum protein can also be caused by decreased production, lik]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Facioscapulohumeral_muscular_dystrophy:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j66sXI59SWe1NGMsC-eXidiqQKmhB0QG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Facioscapulohumeral muscular dystrophy: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Facioscapulohumeral muscular dystrophy: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Medical_Platform_Walkthrough</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hjsW5n1NT8GtogzowLpGCW9YQuibFy6R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osmosis Medical Platform Walkthrough]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis Medical Platform Walkthrough through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fecal_impaction:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D9o-Ri_SS3WPtTT5pFxR9oPHQsqjzx23/_.png</video:thumbnail_loc><video:title><![CDATA[Fecal impaction: Clinical sciences]]></video:title><video:description><![CDATA[Fecal impaction occurs when a hard mass of compacted stool in the colon cannot be voluntarily evacuated. It usually results from chronic constipation and is highly associated with elderly, immobile, and institutionalized patients because of their reduced ability to sense and respond to the increasing burden of stool. If left untreated, fecal impaction can lead to complications like bowel ulceration and perforation. 

When assessing a patient with signs and symptoms suggestive of fecal impaction, first perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, start acute management immediately to stabilize their airway, breathing, and circulation. This means that you might need to intubate the patient, obtain IV access, administer fluids, and monitor their vitals before continuing with your assessment. 

Next, obtain a focused history and physical exam, as well as labs such as CBC, CMP, and lactate. History might reveal chronic constipation, bloating, abdominal pain, and possibly opioid usage. Physical exam typically shows abdominal distension and signs of peritonitis, such as diffuse tenderness to palpation, guarding, and rebound pain. 

On digital rectal examination, you’ll usually notice a large, hardened mass of stool in the rectum and possibly rectal bleeding. Finally, labs may show leukocytosis, lactic acidosis, or anemia. In some patients, you might also notice electrolyte abnormalities like hypercalcemia, hyperkalemia, or hypermagnesemia which might actually be the cause of their constipation; or hypernatremia due to dehydration from excessive vomiting. Alright, if you see these signs and symptoms, suspect fecal impaction. 

Okay, your next step is to start supportive care. Initiate IV fluid resuscitation, electrolyte replacement, broad-spectrum antibiotics, and bowel rest. Additionally, if the patient has nausea and vomiting, place a nasogastric tube to decompress the bowel. However, if the patient h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_Alveolar_Proteinosis,_PAP_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Cj2wClMESAa49mGNOht855GwQAuIhaB3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary Alveolar Proteinosis, PAP (NORD)]]></video:title><video:description><![CDATA[Pulmonary alveolar proteinosis, also called PAP, is a rare syndrome characterized by progressive accumulation of surfactant in the alveoli. Alveoli are the tiny air sacs in the lungs where gas exchange occurs. Surfactant is a substance produced by alveolar cells that reduces the surface tension in the alveoli and prevents them from collapsing. In PAP, there’s so much surfactant that it blocks air from entering the alveoli, making breathing more difficult and causing other respiratory issues.

Disorders of surfactant production can be divided into primary, secondary, and congenital PAP. 

Primary PAP is characterized by reduced function of the granulocyte-macrophage colony-stimulating factor, also called GM-CSF. GM-CSF stimulates alveolar macrophages to remove excess surfactant from alveoli. When less GM-CSF is present, surfactant builds up in the alveoli. 

Primary PAP can be categorized further as autoimmune or hereditary. In autoimmune PAP, the body creates a protein that attacks GM-CSF and blocks the stimulation of alveolar macrophages. In hereditary PAP, individuals are born with genetic changes that destroy alveolar macrophage proteins, preventing GM-CSF from stimulating the macrophages. 

Secondary PAP can be caused by any underlying condition, such as myelodysplastic syndrome, that reduces the number of working alveolar macrophages, or by breathing in high levels of environmental toxins such as silica and talc. 

Congenital PAP occurs in individuals with inherited changes in genes  that cause the production of abnormal surfactant.  These genes include ABCA3, NKX2.1, SFTPB, and SFTPC, but there are likely other genes yet to be discovered.  The abnormal surfactant not only leads to excess surfactant in the alveoli, but other effects that cause reduced lung function or respiratory failure.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fibroadenoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yVA_r7-GSnKMb9x6N4yuXolPQauVexAT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fibroadenoma: Clinical sciences]]></video:title><video:description><![CDATA[A fibroadenoma is one of the most common benign tumors of the breast and occurs frequently in patients between the ages of 15 and 35 years. Fibroadenomas arise from stromal and epithelial connective tissue cells, which contain receptors for both estrogen and progesterone, which makes these tumors sensitive to hormonal changes. Although the exact etiology of fibroadenomas is unknown, reproductive hormones play a role in their development as they appear during the reproductive years, enlarge during pregnancy, and eventually regress after menopause. Fibroadenomas can be classified as simple, complex, or giant.

Alright, when a patient presents with signs and symptoms of a fibroadenoma, the first step is to obtain a focused history and physical examination. Patients typically present with a breast lump that’s usually painless. In addition, your patient may report changes in size throughout their menstrual cycle, as well as increase in size during pregnancy, or a decrease in size after menopause. On physical examination, you can expect to find a solitary, palpable, unilateral breast mass. The lesion is usually solid, firm, and rubbery in nature with regular borders. In addition, the mass is mobile and non-tender. Although the lesion can be located anywhere in the breast, it is most commonly found in the upper outer quadrant. 

Based on your history and physical exam findings, you should suspect a fibroadenoma. Next, order some imaging to get a better idea of what’s going on. If your patient is younger than 35 years, you can order a breast ultrasound; but, if your patient is 35 years of age or older, you should obtain both a breast ultrasound and a mammogram. 

Here’s a clinical pearl! Breast findings on imaging can be categorized with a standardized system called BI-RADS, which stands for Breast Imaging-Reporting and Data System. The imaging findings are assigned into categories labeled as 0 to 6. First, 0 means incomplete, which needs additional imaging or com]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Venous_insufficiency_and_ulcers:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e730E7joQdWpHYLP-T4O49rxS9Snxzhf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Venous insufficiency and ulcers: Clinical sciences]]></video:title><video:description><![CDATA[Venous insufficiency occurs when the veins in the legs are not able to effectively return blood to the heart due to defective valves, obstruction, or insufficient muscle pump function. These can cause blood to reflux and pool in the veins, leading to venous congestion, hypertension, and dilation. Venous insufficiency can occur in superficial veins, which include greater and lesser saphenous, and in deep veins, like femoral and popliteal. 

Over time, fluid and other substances leak out into the surrounding tissues, causing increased hydrostatic pressure within the capillary bed. This reduces oxygen transport and promotes accumulation of metabolic waste, causing skin changes, and eventually can lead to the development of an ulcer. 

Your first step in evaluating a patient presenting with signs and symptoms suggestive of venous insufficiency with or without an ulcer is to obtain a focused history and physical examination. An important thing to keep in mind about venous insufficiency is that abnormal blood flow can increase risk of infection especially if there is a break in the skin that can introduce bacteria into the area. Because of this, you should be on the lookout for any red flag signs of superimposed infection such as fever, rapidly progressive erythema with a possible crepitus, and septic shock. 

If you see any of these red flags, obtain a wound culture, start IV broad-spectrum antibiotics, and obtain an emergent surgical evaluation for debridement of the infected ulcer. Timely diagnosis and treatment is very important because these infections can quickly progress into necrotizing soft tissue infection, which can be life-threatening.

Now that we’ve treated the superimposed infection, let’s turn to chronic venous insufficiency and venous insufficiency ulcers without infection. History often reveals lower extremity heaviness , pain, and swelling. Sometimes, patients report pruritus, tingling, and numbness of their lower extremities as well. Some of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Compartment_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YUhDHh7wT0SiJ9AryWKfuvkNSbuoUBc4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Compartment syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Acute compartment syndrome is a surgical emergency that occurs when muscle compartments, which are bounded by noncompliant fascial membranes, have an increase in pressure, causing tissue ischemia. Although it’s usually associated with extremity trauma, any condition that increases intracompartmental pressure can lead to compartment syndrome. 

Acute compartment syndrome is typically a clinical diagnosis, but you can confirm the diagnosis of unclear cases with a direct measurement of compartment pressures. Compartment syndrome can lead to irreversible tissue damage requiring amputation, without rapid diagnosis and surgical decompression by fasciotomy.

When assessing a patient with signs and symptoms suggestive of acute compartment syndrome, first perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, start acute management immediately to stabilize their airway, breathing, and circulation. This means that you might need to intubate the patient, obtain IV access, begin fluid resuscitation, and monitor their vitals before continuing with your assessment. Once this important step is complete, obtain a focused history and physical exam, as well as labs like CBC, CMP, CPK and lactate. 

Now, let&amp;#39;s first look at history. The patient might present with ongoing severe extremity pain, swelling, and rapid progression of symptoms over a few hours. You can also suspect some causes of acute compartment syndrome based on history. The patient may have a known history of extremity trauma, such as a fracture, burn, or crush injury. They might have a history of prolonged ischemia with reperfusion, such as a recent surgical revascularization procedure. Other causes include extended immobility or extreme exercise, which can lead to rhabdomyolysis, and even massive DVT, like phlegmasia cerulea dolens. 

Okay, the exam may reveal tachycardia and hypotension, as well as a tense “wood-like” muscle compartment on palpatio]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pilonidal_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f78kb83sTTi28v7_Uavjlt0lQ2_H3UUN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pilonidal disease: Clinical sciences]]></video:title><video:description><![CDATA[Pilonidal disease refers to an acute or chronic infectious process within the natal cleft of the intergluteal or sacrococcygeal region. To review some embryology, the natal cleft or sulcus forms as a result of the anchoring of the deep layers of the skin to the anococcygeal raphe and the dorsum of the coccyx up to the tip of the sacrum.

Pilonidal disease is related to mechanical forces causing damage on the skin around the area, as well as disruption and breakage of hair follicles, and ultimately leading to the formation of natal cleft pores, where broken hairs and skin debris can accumulate. This is most commonly seen in young biologically male patients. 

Pilonidal disease can present acutely as an infection such as folliculitis or cellulitis or the infectious process can further develop into an abscess. On the other hand, in chronic pilonidal disease, there are pilonidal cysts, sinuses, or tracts that contain inspissated debris such as hair and skin debris. That&amp;#39;s right, we’re talking about a crack attack!

When a patient presents with a chief concern suggesting pilonidal disease, your first step is to obtain a focused history and physical examination, which will help determine if they have an acute or chronic disease.

Alright, some patients might report mild to moderate pain at the location of the intergluteal or sacrococcygeal region. The pain is usually associated with movement that causes the skin area to stretch. They might also report intermittent swelling along with purulent, mucoid, or bloody drainage from the location, as well as a fever, which means that an abscess might have formed. 

Now, on a physical exam, you’ll typically find primary or midline natal cleft pores that may be acutely infected with signs of cellulitis like erythema and swelling; or folliculitis such as papules or pustules on an erythematous base. If your patient presents with this clinical picture, you can diagnose your patient with acute pilonidal disease. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inguinal_hernias:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ipMTQtMXTvySfsvAhmC368S-Q3CUWyLL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inguinal hernias: Clinical sciences]]></video:title><video:description><![CDATA[An inguinal hernia is a defect or weakness in the abdominal wall that allows the passage of abdominal contents through the lower abdominal wall into the inguinal region, or groin. Some common risk factors for the development of an inguinal hernia include male sex, age younger than 5 years or older than 75 years, family history of inguinal hernia in first-degree relatives, impaired collagen metabolism, and previous history of benign prostatic hyperplasia or prostatectomy.

Inguinal hernias can be classified by etiology, meaning they can be either congenital or acquired. Congenital inguinal hernias occur when the processus vaginalis fails to close during gestation. On the other hand, acquired hernias can be due to patent processus vaginalis or a weakness in the abdominal wall, allowing intra-abdominal contents to protrude through the defect. Common causes of tissue weakness include abdominal wall injury or connective tissue abnormalities. 

Inguinal hernias can also be classified anatomically as either direct or indirect. A direct inguinal hernia protrudes medially to the inferior epigastric vessels within Hesselbach’s triangle, which is formed inferiorly by the inguinal ligament, laterally by the inferior epigastric vessels, and medially by the rectus abdominis muscle. Direct hernias are usually a result of a weakened inguinal canal floor.

On the other hand, indirect inguinal hernias occur in the internal inguinal ring, lateral to the inferior epigastric vessels. In males, this is the site where the spermatic cord exits, while in females it’s the site where the round ligament exits the abdomen. Indirect inguinal hernias are the most common type of hernia, and they occur more frequently on the right side. Both direct and indirect hernias can present as either asymptomatic, symptomatic, incarcerated, or strangulated.

When you encounter a patient with signs and symptoms suggestive of an inguinal hernia, you should first perform an ABCDE assessment to determi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Fractures</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YrwfmJpTRVuPIQEpJEMoDn9PRHusdvi6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Fractures]]></video:title><video:description><![CDATA[Nurse Kenji works on a rehabilitation unit and is caring for Sharon, a 74-year-old female with a history of osteoporosis who was admitted post-surgery for a left hip fracture requiring an open reduction and internal fixation, or ORIF. In collaboration with the registered nurse, RN Betty, Nurse Kenji goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Sharon’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Kenji recognizes important cues, including Sharon’s vital signs, which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 19 breaths per minute, and blood pressure 123/88 mmHg. During the bedside report, Nurse Kenji learned that Sharon declined repositioning during the night shift. Upon inspection, he notes that her hip appears mildly swollen and her surgical dressing is clean and dry. Nurse Kenji also notices that Sharon’s left foot is warm with intact sensation, 2+ palpable pulses, and she can wiggle her toes, which is consistent with RN Betty’s earlier assessment.  

Nurse Kenji asks Sharon about her comfort.  

Nurse Kenji: I see that you stayed in the same position throughout the night. Would you tell me your current pain level? 

Sharon: I don’t have pain right now, but I don’t want to move because I know it&amp;#39;ll hurt my hip. 

Nurse Kenji: I understand. Have you considered taking the prescribed medications to manage your pain? 

Sharon: I really don’t like pain medicine because I’m worried about becoming addicted. 

Next, Nurse Kenji analyzes these cues. He reviews the electronic health record, or EHR, and notes that Sharon is scheduled for physical therapy today. He also notes that Sharon is prescribed ice packs to reduce hip swelling, as well as oxycodone and acetaminophen every four hours as needed for pain management but hasn’t taken any medication since early yester]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Head_Injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jobFVXi2QrWBUmpjuPfKzm0wTWChYHCT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Head Injury]]></video:title><video:description><![CDATA[Nurse Kristin works at a university health clinic and is caring for Jay, a 20-year-old who is being seen after a mild concussion that occurred while playing football last week. In collaboration with the registered nurse, RN Sarika, Nurse Kristin goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Jay’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Kristin recognizes important cues, including Jay’s vital signs, which are temperature 98.0 F or 36.7 C, heart rate 66 beats per minute, respirations 14 breaths per minute, and blood pressure 110/60 mmHg. Jay reports that he has a headache, which he rates as a 2 out of 10 on the pain scale, and states he hasn’t needed medication to manage his pain. He also tells Nurse Kristin that he continues to be fatigued. 

Nurse Kristin then gathers additional information about Jay’s prescribed activity restrictions. 

Nurse Kristin: I know your health care provider explained that you’ll need to limit your activities for one more week. How has that been going so far?  

Jay: It’s been hard. Football is such a big part of my life. Without it, I don’t know what to do. And not being able to drive doesn’t help either. I’m getting stir crazy in my dorm. It got so bad that I drove to a friend’s house the other day even though I know I’m not supposed to yet.  

Then, Nurse Kristin analyzes these cues. She reviews the electronic health record, or EHR, and notes Jay’s concussion occurred following helmet-to-helmet contact during a football game. She notes his score on the Glasgow Coma Scale, or GCS was 13 at the time of the injury, and today RN Sarika scored the GCS at 15. Nurse Kristin knows a concussion is a type of traumatic brain injury that occurs when an event, like the head striking a hard object, causes the brain to hit the skull. This leads to a temporary disruption of neural acti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Safety_in_Medication_Administration</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KuB5cpWNT1iLimS-7MhNBpIeQDKc_ZJ5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Safety in Medication Administration]]></video:title><video:description><![CDATA[Medication administration is a multifaceted process which involves the application of a prescribed medication to a patient. As the licensed practical nurse, or LPN, or licensed vocational nurse, or LVN, you are responsible for administering certain medications, which requires the use of critical thinking and clinical judgment to promote patient safety and avoid medication errors, or preventable events that lead to inappropriate medication use or patient harm. Although numerous protocols exist to promote safe medication administration, as the nurse, you are the patient’s last line of defense against medication errors. 

To safely administer medications, you must be familiar with measurement systems, approved medical abbreviations, and methods of dosage calculation. First, measurement systems used to prescribe medications include the metric system, which uses grams, liters, and meters to calculate doses, and is preferred for medication prescription. The household system uses drops, teaspoons, tablespoons, and cups to measure doses, and although it’s familiar to patients, it tends to be inaccurate.  

Okay, so most facilities have a list of medical abbreviations that shouldn’t be used in order to decrease the risk of medication errors. For example, some facilities state that health care providers shouldn’t use the letter “u” to denote units since it can be mistaken for the number 0. 

Next, nurses must be competent in dosage calculation. Although there are various methods of dosage calculation, dimensional analysis is the preferred method. 

Now, the standard practice for medication administration is to use the rights of safe medication administration because they are shown to reduce medication errors. These principles include: the right medication, right dose, right time, right route, right patient, and right documentation.  These rights must be confirmed at least three times prior to administering a medication to a patient. The first check happens when coll]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Cerebral_Vascular_Accidents</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/emEBSFrPSTSPWc_t8vEbr2-NT7OLmaaq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Cerebral Vascular Accidents]]></video:title><video:description><![CDATA[Nurse Darius works in a rehabilitation unit and is caring for Calvin, a 67-year-old with a history of hyperlipidemia who was admitted following a stroke. In collaboration with the registered nurse, RN Alli, Nurse Darius goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Calvin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darius recognizes important cues including Calvin’s vital signs which are temperature 98.8 F, or 37.1 C, heart rate 98 beats per minute, respirations 16 breaths per minute, blood pressure 146/92 mmHg, and oxygen saturation 96 percent on room air.  Nurse Darius also notes that the left side of Calvin’s face is drooping and sees that he favors his right hand. Nurse Darius also overhears Calvin mixing up his words while trying to talk to the dietary staff about his lunch tray.  

Next, Nurse Darius analyzes these cues. He reviews the electronic health record, or EHR, and sees Calvin has undergone an MRI of his head. The results show that Calvin had an ischemic stroke, where an occlusion in an artery caused inadequate blood flow to his brain.  

Nurse Darius knows Calvin’s hyperlipidemia was likely a contributing factor to his stroke, since it can lead to atherosclerosis and blockage of arteries.  He also knows the loss of oxygenated blood flow to the brain can cause damage to areas that control language and motor functions and lead to muscle weakness and aphasia. Nurse Darius recognizes that he needs to effectively communicate with Calvin to properly care for him. 

Now, using the information he’s gathered, Nurse Darius discusses his findings with RN Alli, and they choose a priority hypothesis of impaired communication.   

Then, they generate solutions to address Calvin’s impaired communication; and they establish the outcome that after intervening, Calvin will effectively communicate his needs by]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Delirium</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K9aSVbZATOaEQqK6I_-uWBIRQXitu5VA/_.png</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Delirium]]></video:title><video:description><![CDATA[Delirium is an acute condition characterized by an abrupt decline in mental function, including memory, orientation, judgment, and reasoning. It is reversible and can fluctuate from day-to-day, and can last for hours, days, or weeks.  

Okay, now, delirium is usually related to an underlying condition, such as fluid and electrolyte imbalance, glucose dysregulation, malnutrition, or systemic infections. Certain medications, like benzodiazepines, opioids, and anticholinergics, can also contribute to delirium.  

Other risk factors include advanced age, untreated pain, sleep deprivation, immobility, and sensory deprivation or sensory overload; as well as being hospitalized and being in intensive care. Dementia is another risk factor for delirium; and likewise, delirium can increase the risk of developing dementia. Now, although the exact cause of delirium is unclear, it likely involves an interaction between one or more risk factors and a vulnerable patient that ultimately results in alterations in neuronal function in the brain.   

Clinical manifestations include disorientation, meaning the patient doesn’t know where they are or what day it is; difficulty concentrating; and altered speech, that might be rambling and difficult to understand. Their emotional state can range from being irritable and agitated to being withdrawn and depressed. Also, they may experience hallucinations, which means they see, hear, or even smell things that are not actually real but feel very real to them; as well as illusions, or misinterpretations of reality; and delusions, or beliefs that are objectively false. 

Alright, now the diagnosis of delirium is typically based on the patient’s history as well as a physical and psychological assessment. In addition, certain tools, like the Confusion Assessment Method, or CAM, can be used to gather information. After the diagnosis is confirmed, laboratory tests, as well as imaging tests, like CT or MRI scans are performed to identify the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Nursing_Care_for_Urinary_Retention</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sGuqfawEStid8wnvaTIUiv25SzCjBr7e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Nursing Care for Urinary Retention]]></video:title><video:description><![CDATA[Nurse Tabitha works on an inpatient medical-surgical unit and is caring for Richard, a 61-year-old with a history of benign prostatic hyperplasia, or BPH, who underwent a cholecystectomy three days ago. In collaboration with the registered nurse, RN Jesse, Nurse Tabitha goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Richard’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Tabitha recognizes important cues, including Richard’s vital signs, which are temperature 98.6 F or 37 C, heart rate 100 beats per minute, respirations 20 breaths per minute, and blood pressure 130/80 mmHg. He also reports his pain as 4 out of 10 in his suprapubic region. Nurse Tabitha notices Richard appears restless, and he states that he has an urge to urinate but can’t.  

Next, Nurse Tabitha analyzes these cues. She reviews the electronic health record, or EHR, and sees that Richard received general anesthesia during his surgical procedure. She realizes that this can lead to urinary retention, due to disruption of the normal neuromuscular processes that control urination.  

Nurse Tabitha also realizes that Richard’s enlarged prostate is likely contributing to his urinary retention since it can block the outflow of urine from the lower part of the bladder and urethra. Nurse Tabitha realizes Richard is likely retaining urine due to a combination of the anesthesia from his surgery and history of BPH, and that he needs effective urinary elimination. 

Next, she notes that Richard has a PRN order for bladder scans. Nurse Tabitha then performs a bladder scan, which reveals 900 milliliters of urine in Richard’s bladder. 

Now, using the information she has gathered, along with Richard’s medical history, Nurse Tabitha reports her findings to RN Jesse, and they choose a priority hypothesis of altered urinary elimination.  

Then, they generate s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Spinal_Cord_Injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qK6KBEHITOmjgG3QPQhWJuw5Sp2Z8ZNw/_.png</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Spinal Cord Injury]]></video:title><video:description><![CDATA[A spinal cord injury refers to any damage to the spinal cord, or the bundle of nerves, called cauda equina, that protrude from the bottom of the spinal cord. 

Now, spinal cord injuries can have different causes. In younger patients, most spinal cord injuries are caused by motor vehicle crashes; or recreational injuries, like those caused by impact sports. In older patients, though, spinal cord injuries are often caused by falls, as well as medical conditions, like degenerative diseases of the spine. 

Risk factors for developing a spinal cord injury include engaging in high-risk behaviors, such as speeding when driving or not wearing safety equipment when playing sports. Lastly, patients with a history of bone or joint disorders are also at a higher risk, since even minor trauma could damage the weakened bones and injure the spinal cord. 

Okay, so the pathology of a spinal cord injury involves primary and secondary injury. Primary injury typically involves a sudden, traumatic impact on the spine that fractures or dislocates vertebrae, causing compression on the spinal cord.  

Following the primary injury, secondary injury causes additional damage. The acute phase of the secondary injury begins immediately after the spinal injury, and includes bleeding, ischemia, and swelling at the site of the injury. As time passes, additional neuronal cell death can be caused by oxidative stress, neurotransmitter accumulation, and demyelination of surviving axons. Eventually, specialized glial cells begin to form a scar at the site of injury, which creates a barrier across the injured tissue that prevents the spread of neuronal damage. Unfortunately, since neurons have limited regenerative capacity, these injuries tend to yield permanent damage to the spinal cord. 

Alright, now clinical manifestations of spinal cord injuries depend on the severity and location of the injury and may include partial or complete loss of sensation and motor function below the level of in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Influenza:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fAaFRHjiQISLTu2Rl2foEGx7Riq7ph2I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Influenza: Clinical sciences]]></video:title><video:description><![CDATA[Influenza is a highly transmissible viral infection that can primarily affect the upper and lower respiratory tract. It spreads via aerosols and directly infects the respiratory epithelium, causing inflammation. If you suspect influenza, you should determine whether your patient has a high risk of complications, and perform viral testing to confirm the diagnosis and guide treatment decisions.

Now, if a patient presents with signs and symptoms of influenza, you should first perform an ABCDE assessment to determine if they are unstable or stable. If they’re unstable, begin acute management. First stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry. Provide supplemental oxygen if they’re hypoxic, to maintain oxygen saturation above 90%.

Now let&amp;#39;s go back to the ABCDE assessment and discuss the approach to stable patients. First, perform a focused history and physical examination. Your patient may report a sudden onset of fever, chills, myalgia, malaise, and headache. Additionally, local inflammation can result in dry cough, sore throat, and rhinorrhea. Your patient might also report exposure to a possible influenza contact within the previous 1 to 4 days, especially if there’s high transmission of influenza in the community. 

Physical exam may reveal nonpurulent conjunctivitis, diaphoresis, and pharyngeal erythema, as well as abnormal lung sounds, such as crackles, rhonchi or wheezing. 

At this point you can suspect influenza, so your next step is to assess whether your patient presents with high-risk features. Individuals are considered to be at high risk if they have chronic medical conditions, like diabetes, obesity, or heart disease, or if they are immunocompromised, like those with HIV or an organ transplant. In addition, certain populations are at higher risk, such as patients who are pregnant or less than]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperosmolar_hyperglycemic_state:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/onJPQNmBTmOjC1TrlHUYabDSS7SGjOGv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperosmolar hyperglycemic state: Clinical sciences]]></video:title><video:description><![CDATA[Hyperosmolar hyperglycemic state, or HHS for short,  is a life-threatening complication of type 2 diabetes mellitus. It is usually triggered by a precipitating factor, such as illness or infection, that eventually leads to relative insulin deficiency, hyperglycemia, and elevated serum osmolality. 

Keep in mind that there’s a higher risk of HHS in older individuals, especially those with impaired cognitive function or thirst perception, as well as those who do not adhere to their treatment regimen for diabetes. The diagnosis of HHS requires lab workup that demonstrates an elevated blood glucose and serum osmolality, as well as the absence of metabolic acidosis and ketonuria.

Now, if you suspect HHS, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. HHS generally presents as unstable, so stabilize the airway, breathing, and circulation. Next, obtain IV access and give 1-liter bolus of isotonic IV fluid. Next, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, and provide supplemental oxygen, if needed.

Once you stabilize the patient, obtain a focused history and physical exam. Your patient typically reports polyuria, polydipsia, weakness, lethargy, or even seizures. These are commonly associated with a recent precipitating illness or infection. Additionally, there might be a known history of diabetes with inadequate glycemic control or recent disruption in therapy. 

On the other hand, a physical exam might reveal signs of severe dehydration, such as dry mucous membranes, tachycardia, and hypotension. In severe cases, you might even notice somnolence and focal neurologic deficits, such as visual disturbance. 

Based on these findings, suspect HHS and order labs, including an ABG or VBG, a serum osmolality, a CMP, and a urinalysis. Next, review the lab results and assess diagnostic criteria for HHS, which include blood glucose above 600 mg/dL; s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_mellitus_(Type_1):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Tj3oW7MBRqWAvMoplblBuB6bTWuKJUc2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes mellitus (Type 1): Clinical sciences]]></video:title><video:description><![CDATA[Diabetes mellitus is a chronic condition where tissue cells can’t properly absorb and use glucose, so it stays and builds up in the blood. Normally, pancreatic islet beta cells produce insulin, which acts on insulin receptors on tissue cells to promote uptake and storage of glucose, amino acids, and triglycerides, as well as stimulate glycolysis, protein synthesis, and lipogenesis. 

Now, there are two types of diabetes, type 1 and type 2. In type 1 diabetes, there’s autoimmune destruction of the pancreatic islet beta cells, resulting in severe insulin deficiency and, ultimately, hyperglycemia. This is in contrast to type 2 diabetes mellitus, where the pancreatic islet beta cells stop properly responding to stimulation to produce insulin, combined with insulin resistance, meaning that the tissue cells aren’t able to appropriately respond to the little insulin that’s still being produced. 

In either disease type, the resulting hyperglycemia can cause clinical manifestations ranging from prediabetes and diabetes mellitus, to severe life-threatening conditions, like diabetic ketoacidosis, or DKA, most commonly seen in patients with type 1 diabetes, and, hyperosmolar hyperglycemic state, or HHS, most commonly in type 2 diabetes.

Now, if you suspect type 1 diabetes mellitus, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.  If the patient is unstable, stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient. Next, obtain IV access and, if your patient is hypotensive, start IV fluids for volume resuscitation. Finally, put your patient on continuous vital sign monitoring, such as pulse oximetry, blood pressure, and heart rate.  

Next, you want to assess for DKA or, less frequently, HHS. Obtain a focused history and physical exam, and order labs, such as point-of-care blood glucose, serum osmolality, BMP, urinalysis, hemoglobin A1c, as well as ABG or VBG. 

Pati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Get_to_know_Osmosis:_Demonstration_and_Q-A_July_12,_2023</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c7Wy76ZQRxmnvBGsdCy23dvxT0iilctM/_.png</video:thumbnail_loc><video:title><![CDATA[Get to know Osmosis: Demonstration and Q&amp;A July 12, 2023]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Get to know Osmosis: Demonstration and Q&amp;A July 12, 2023 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypoglycemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k8yUvvUTQCeaudsviTmzhd-ORrmc3wPr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypoglycemia: Clinical sciences]]></video:title><video:description><![CDATA[Hypoglycemia is defined as a blood sugar below 55 milligrams per deciliter that occurs in the presence of symptoms, but some individuals can become symptomatic at levels like 70. Some important causes of hypoglycemia include medication-induced and alcohol-induced hypoglycemia, as well as endogenous hyperinsulinism and non-insulin-mediated hypoglycemia.

Now, if you suspect hypoglycemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain a fingerstick glucose level, while obtaining IV access to give IV glucose immediately. In addition, begin continuous vital sign monitoring, such as blood pressure, heart rate, and pulse oximetry; and if needed, provide supplemental oxygen.

Here’s a high-yield fact to keep in mind! Most individuals don’t develop symptoms until their blood glucose level falls below 55 milligrams per deciliter. However, some patients may become symptomatic when their blood glucose falls below 70 milligrams per deciliter; while other patients with diabetes may experience impaired hypoglycemia awareness and experience symptoms only when their glucose falls severely low, which puts them at higher risk for life-threatening consequences. Because this range is highly variable, there’s no glucose value that defines hypoglycemia, so always correlate your patient’s symptoms with lab results. 

Hypoglycemia is often observed in the setting of critical conditions, such as renal failure, liver failure, and sepsis. Renal failure leads to reduced clearance of insulin, while liver failure decreases gluconeogenesis, both causing hypoglycemia. Sepsis triggers cytokine release, which increases glucose utilization and also inhibits gluconeogenesis. So, it’s important to treat the underlying condition to normalize your patient’s blood glucose. Lastly, keep in mind that nocturnal hypoglycemia warrants assessment of the basa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gout:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M12tcZvfS6eJnL4Qajk4yAQrRnewTFXB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gout: Clinical sciences]]></video:title><video:description><![CDATA[Gout is an acute inflammatory arthritis that occurs when monosodium urate crystals deposit in joints, soft tissue, and bones. This is typically associated with hyperuricemia due to either underexcretion or overproduction of uric acid. 

Risk factors include male sex, obesity, drinking too much alcohol, consuming certain foods like red meat and seafood, as well as dehydration, taking diuretics like thiazides, and increased cell turnover like in hemolysis or tumor lysis syndrome. 

The diagnosis of gout is made clinically and relies on the presence of classic symptoms, known risk factors, and lab findings. However, in some cases when the diagnosis is not clear, joint aspiration may be needed.  

Alright, if a patient presents with signs and symptoms suggestive of gout, you should first perform a focused history and physical examination. As well order labs like a serum urate, CBC, ESR, and CRP. 

Your patient may report rapid onset of redness, pain, and swelling in a joint, most commonly involving the big toe, but can involve other joints, such as the knee.  

This is especially common after drinking alcohol, or consuming purine-rich foods like red meat or seafood. Other risk factors include high fructose intake, diuretic use, obesity, history of diabetes, hypertension, and chronic kidney disease.  

Physical exam usually reveals redness, tenderness, and swelling in the involved joints, most often in the first metatarsophalangeal joint.  You may also see subcutaneous nodules, or tophi, on the joints and pads of the digits. 

As far as labs go, the serum urate will often be elevated, greater than 6.8 milligrams per deciliter, but keep in mind that urate levels can be difficult to interpret during a gout flare. 

CBC typically reveals an elevated leukocyte count and inflammatory markers, such as ESR and CRP.  If you see this constellation of signs, symptoms, and lab findings, you can diagnose acute gout. 

Now lets look at patient with a different but similar f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lobular_carcinoma_in_situ:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VumGuW4HQ3GvRR3RCoAHFQ7pSiaor8qc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Lobular carcinoma in situ: Clinical sciences]]></video:title><video:description><![CDATA[Lobular carcinoma in situ, or LCIS, refers to the non-invasive proliferation of epithelial cells in the terminal ductal lobular unit of the breast. LCIS typically presents as an incidental finding on a breast biopsy done for a separate reason. Further management depends on its histologic type, which includes classic LCIS or other more aggressive variants. Classic LCIS is not considered a malignant finding requiring treatment, but rather a risk indicator for the later development of invasive carcinoma in either breast. On the other hand, more aggressive variants include pleomorphic or florid LCIS, which are more likely to progress into invasive lobular carcinoma.

When assessing a patient that presents with LCIS, first obtain a focused history and physical exam. Patients often discover LCIS from getting a core needle biopsy after an abnormal screening mammogram for a different concern. Your next step is to ask about risk factors, such as age over 40, a personal or family history of breast cancer or genetic mutations, and any usage of hormone replacement therapy, especially for more than five years. On physical exam, LCIS does not usually have any significant findings, but in rare cases, you might be able to palpate a breast lump. 

Ok, now that we’ve performed our history and physical exam, let’s take a closer look at the results of the biopsy specimen that showed LCIS in the first place. It’s important to know that LCIS can be broadly classified as classic LCIS and more aggressive variants. While they have a few things in common, they vary by the amount of cellular atypia and proliferation, and therefore the degree of risk for malignancy they carry. So, as you can imagine, each type has a different management. 

Alright, let’s start with classic LCIS. So, core needle biopsy might show small, round, uniform, discohesive cells that fill and expand greater than half of the acini of the breast lobule. Although the acini are distended, the overall architecture ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Perianal_abscess_and_fistula:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pCcvuIemTxyW0R8eKI8CysbrRRSdcAHr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Perianal abscess and fistula: Clinical sciences]]></video:title><video:description><![CDATA[Perianal abscesses and fistulas are anorectal diseases that result from obstructed glandular crypts of the rectum or anus. A perianal abscess is a collection of pus that can form in a number of spaces within the anus or rectum. On the other hand, perianal fistulas can form after an abscess is drained and typically result from chronic changes of the same infectious process. Now, the first step is to obtain a focused history and physical examination. You should also obtain basic labs, such as a CBC to look for any clues of spreading infection.

Now, a patient might report intermittent pain that’s typically associated with sitting, activity, and possibly with defecation. The patient may also report intermittent malodorous drainage with or without pruritus. On a physical exam, you’ll typically find a non-healing abscess or chronic purulent drainage. As you’re performing the exam, see if you can visualize the external opening of the fistula, which might be found with excoriation, inflammation, or induration, as well as drainage of purulent fluid. On a digital rectal exam, you may be able to palpate the internal opening or an abscess, if present. Lastly, labs may reveal leukocytosis. If the patient presents with this clinical picture, you can suspect a perianal fistula.

Now that we have a potential diagnosis in mind, let’s talk about imaging. The next step is to proceed with anoscopy or sigmoidoscopy, which can help confirm the diagnosis of a perianal fistula. If you don’t see any findings suggestive of a fistula on anoscopy or colonoscopy, consider an alternative diagnosis. However, if you find an internal opening of the fistula in the anus or rectum, this supports your suspected diagnosis of a perianal fistula. The next step is to proceed with diagnostic imaging, such as pelvic MRI or endosonography, which helps you get a better picture of the fistula and determine if it’s a simple or a complex fistula. 

Some high-yield facts to keep in mind! Crohn dise]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Urinary_Tract_Infection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oD9fKNNqRSGGvw1jfw8C-k3kTkKrkl1Q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Urinary Tract Infection]]></video:title><video:description><![CDATA[Nurse Steven is working in a long-term care facility and is caring for Louisa, a 79-year-old female with a history of diabetes mellitus. In collaboration with the registered nurse, RN Gene, Nurse Steven goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Louisa’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Steven recognizes important cues, including Louisa’s vital signs, which are temperature 99.0 F or 37.2 C, heart rate 86 beats per minute, respirations 16 breaths per minute, and blood pressure 108/52 mmHg. He also notices Louisa has asked to use the bedside commode to urinate four times in the past hour. Louisa also reports burning with urination and suprapubic discomfort that she rates as 6 out of 10 on the pain scale.  

Next, Nurse Steven analyzes these cues. He reviews the electronic health record, or EHR, and notes that Louisa&amp;#39;s biological sex, age, and medical history can increase the risk for developing urinary tract infections, or UTIs. He knows that patients assigned female at birth have shorter urethras, making it easier for bacteria to travel to the bladder; and that decreased estrogen following menopause results in atrophy of the urinary tract which can lead to decreased bladder emptying, urinary stasis, and more time for bacteria to grow in the urinary tract.  Urinary stasis can also occur in some patients with diabetes mellitus, where impaired smooth muscle contractility of the urinary tract leads to urinary retention.  

Nurse Steven also knows that as bacteria multiply within the urinary tract, they cause inflammation, which leads to suprapubic pain, feelings of bladder fullness, as well as urinary frequency and urgency. Nurse Steven realizes Louisa needs effective urinary elimination. 

Now, using the information he has gathered, along with Louisa’s medical history, Nurse Steven reports]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Generalized_Anxiety_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kmrI-o_6Rre27U_wQIS-OOzcRGWJ-w5P/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Generalized Anxiety Disorder]]></video:title><video:description><![CDATA[Nurse Aziza works in a primary care office and is caring for Clarence, a 25-year-old who presents with anxiety. Nurse Aziza, in collaboration with the registered nurse, RN Michael, go through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Clarence’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, nurse Aziza recognizes important cues, including Clarence’s vital signs which are temperature 98 F or 36.6 C, heart rate 88 beats per minute, respirations 18 breaths per minute, blood pressure 115/70 mmHg, and oxygen saturation 96 percent on room air. She notes that Clarence is biting his nails and appears restless. Nurse Aziza gathers more information from Clarence about his symptoms.

Nurse Aziz: Hi Clarence, tell me how you’re feeling.

Clarence: I&amp;#39;m having trouble sleeping lately. I’m worrying about everything, and I can’t seem to relax.

Nurse Aziza: That sounds stressful. Have you had any major changes in your life recently?

Clarence: Yeah, I lost my job two weeks ago.

Nurse Aziz: I’m sorry to hear that, but you’re in the right place and we’re here to support you.

Next Nurse Aziza analyzes these clues. She reviews the electronic health record, or EHR, and notes that RN Michael administered the Generalized Anxiety Disorder 7-item screening tool, known as GAD-7, and Clarence had a score of ten out of 21, indicating moderate anxiety.

Nurse Aziza knows that one of the major findings associated with GAD is excessive worry. Although the exact cause of GAD isn’t known, it’s thought to be caused by an imbalance of the neurotransmitters, where serotonin system activity is low and noradrenergic system activity is elevated. This imbalance can cause symptoms of restlessness, difficulty concentrating, and impaired sleep. She also knows GAD can be brought on by stressful events or life changes, like losing a job. Nurse Aziza recognizes that Clarence needs help managing his anxiety.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Care-Acquired_or_Associated_Infection</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aKy1FV9kRn2NZ0UecjA5hsRFQFqxWo_M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Care-Acquired or Associated Infection]]></video:title><video:description><![CDATA[A health care-associated infection, or HAI, is when a pathogen is transmitted to a patient who’s been hospitalized for at least 48 hours.
As the nurse, you can prevent health care-associated infections by breaking the chain of infection.

The process of transmitting infection is known as the chain of infection and occurs in six continuous links: the causative agent, reservoir, portal of exit, mode of transfer, portal of entry and susceptible host.

The first link is the presence of a causative agent, or pathogen, which is any disease-causing microorganism, like viruses, bacteria, yeast, fungi, or protozoa. Examples of common pathogens include the bacteria E. coli and the COVID-19 virus.

The second link is the reservoir, or environment where the pathogen normally lives, multiplies, and grows. Reservoirs can be living, like humans, animals, or insects; waste products, like stool; food; water; or wounds. Common reservoirs in health care settings are unwashed hands, soiled linens, or medical equipment, like stethoscopes.

Now, as the nurse you can reduce pathogens and reservoirs through asepsis, which is when pathogens are removed from the environment. There are two types of asepsis: medical asepsis and surgical asepsis. Medical asepsis, also known as clean technique, is when the number of pathogens or the risk of transmitting the pathogen, is reduced. This can be done through hand washing, wiping down equipment with a disinfectant, and preoperative skin cleansing. On the other hand, surgical asepsis, also known as sterile technique, is when equipment is sterilized eliminating all pathogens by using high heat or chemicals like when using surgical equipment that has been sterilized in an autoclave.

Then, there’s the third link, portal of exit, where the pathogen leaves the reservoir. Common portals of exit in health care settings include the GI tract, where pathogens exit via feces or emesis; and the respiratory tract, where pathogens leave via aerosolized dr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Measuring_Heart_Rate</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EsCpBVtcS2u5RRQL8fbLuJfoRueS-UZi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Measuring Heart Rate]]></video:title><video:description><![CDATA[As the heart pumps blood to the body, the blood causes a pressure wave against the arterial walls called a pulse, which correlates with the heart rate, or the number of heart beats per minute. As the nurse, you’ll measure your patient’s pulse and evaluate its characteristics including rate, rhythm, and amplitude.

Pulse Measurement The pulse can be felt in the superficial arteries close to the skin, including the radial, carotid, brachial, femoral, popliteal, posterior tibial, and dorsalis pedis. The radial artery is the most common site because it’s easy to access. To locate the radial pulse, place the flat part of your middle two or three fingers on the anterior of the patient’s wrist, just under the thumb. Then, to feel the pulse, you’ll use your fingers to firmly palpate the artery, being careful not to obliterate it.

Now, if your patient’s pulse is abnormal, or if they have heart disease or are taking medications that affect their pulse, count an apical pulse, or the pulse that’s heard right over the heart using your stethoscope. To measure the apical pulse, place your stethoscope at the apex, or lowest portion, of the heart on the left side of the chest between the 5th and 6th ribs. You should hear something that sounds like ‘lub-dub’ which repeats over and over again. Each ‘lub-dub’ is one heartbeat and should be counted for one full minute.

Now, when measuring a pulse, you also need to determine its characteristics, including the rhythm, rate, and amplitude. The rhythm is the measurement of the intervals between heart beats. If these intervals are equal, the rhythm is considered regular. On the other hand, if the intervals are unequal, the rhythm is considered irregular, and is known as an arrhythmia. To determine the rate when the rhythm is regular, count the pulsations for thirty seconds, and then multiply that number by two to calculate the beats per minute. If the rhythm is irregular, you’ll count for a full minute.

Amplitude refers to how s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Anaphylaxis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7tek9_lYSe_w1qUM0ure6l0KTUy4ueBk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Anaphylaxis]]></video:title><video:description><![CDATA[Nurse McKenzie works on an inpatient medical-surgical unit, and is caring for Demetrius, a 56-year-old, who was admitted for pyelonephritis. In collaboration with the registered nurse, RN Anita, Nurse McKenzie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Demetrius’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse McKenzie recognizes important cues, including Demetrius’ vital signs, which include temperature 100.4 F or 39 C, heart rate 110 beats per minute, respirations 23 breaths per minute, blood pressure 100/58 mmHg, and oxygen saturation of 91 percent on room air.  

She notices that Demetrius’ face is flushed, he has a has a worried expression, and that he’s short of breath. Nurse McKenzie auscultates his lung sounds and notes expiratory wheezes bilaterally. She also sees that ceftriaxone is currently infusing through Demetrius’ intravenous line along with normal saline.  

Next, Nurse McKenzie analyzes these cues. She reviews the electronic health record, or EHR, and notes that the infusion of ceftriaxone was started 10 minutes ago by RN Anita. She also sees that Demetrius has no documented allergy to ceftriaxone but understands that if Demetrius received the antibiotic in the past, that this first exposure may have caused his body to produce antibodies against it, sensitizing him, a process where certain immune cells, called T lymphocytes are activated and stimulate B lymphocytes to secrete IgE antibodies into the bloodstream.  

These IgE antibodies then bind to the surface of other cells, called mast cells and basophils, which are full of granules that contain proinflammatory molecules like histamine. Then, on his second exposure, the mast cells and basophils, which already have IgE antibodies on their surface, release their proinflammatory molecules, triggering an allergic reaction.  

Nurse McKenzie al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Arthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Pur-pa9gQgSppyrszA4SlpT9Qy2Ywi37/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Arthritis]]></video:title><video:description><![CDATA[Arthritis refers to inflammation of a joint, and it&amp;#39;s one of the most common causes of disability due to joint dysfunction and pain. Osteoarthritis, or OA, is a progressive disorder affecting the synovial joints. Another type of arthritis is rheumatoid arthritis, or RA, which is a chronic autoimmune disorder characterized by inflammation of connective tissue in the synovial joints. Unlike OA, RA is also a systemic disorder, impacting other organs, such as the lungs and blood vessels.  

Okay, so one of the main causes of OA are conditions or events that damage the synovial joints, such as repeated wear and tear over time. Having medical conditions, such as obesity and skeletal deformities like congenital hip dislocation, can also increase the risk of OA. It’s also more common in people over the age of 50 and those assigned female at birth. On the other hand, RA is likely due to a combination of both environmental and genetic factors that trigger an autoimmune response. RA can occur at any age, though its onset is usually between age 30 to 50; and like OA, it’s more common in those assigned female at birth.  

Now, the main clinical manifestations for both OA and RA are joint pain and stiffness that limit mobility and impact quality of life. In OA, pain typically affects larger weight-bearing joints, such as the knees and hips, and it&amp;#39;s usually relieved by rest. Conversely, joint stiffness often develops after periods of rest, and it typically resolves within 30 minutes. Pain associated with RA is usually located in smaller joints, like the hands and feet, and it usually improves with movement.  

Patients with OA and RA can also develop joint nodules. In OA, nodules can form in the distal interphalangeal joints, called Heberden nodes, and on the proximal interphalangeal joints, called Bouchard nodes. In patients with RA, firm, subcutaneous rheumatoid nodules develop, usually in bony areas exposed to pressure, like the fingers and elbows; ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Nursing_Care_for_Acute_Pain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VuXAcX-cTvmjrHlVZjlpj6GNTd_SoRLJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Nursing Care for Acute Pain]]></video:title><video:description><![CDATA[Nurse Nadia works on an orthopedic unit and is caring for Brian, a 51-year-old with a history of degenerative joint disease, who was admitted for intractable back pain. In collaboration with
the registered nurse, RN Katie, Nurse Nadia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Brian’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Nadia recognizes important cues, including Brian’s vital signs, which are temperature 98.8 F or 38.9 C, heart rate 99 beats per minute, respirations 21 breaths per minute, and blood pressure 152/82 mmHg. She also notices Brian is slightly diaphoretic and grimacing. When asked about his pain, he reports a current pain level of 6 out of 10, and that his tolerable level of pain is 3 out of 10.

Next, Nurse Nadia analyzes these cues. She reviews the electronic health record, or EHR, and notes that Brian is prescribed IV ketorolac every six hours PRN, and he received his last dose two hours ago. Nurse Nadia compares her findings to Brian’s assessment conducted by RN Katie and realizes Brian needs effective pain management.

Now, using the information she has gathered, along with Brian’s medical history, Nurse Nadia reports her findings to RN Katie who chooses a priority hypothesis of acute pain.

Then, Nurse Nadia collaborates with RN Katie to generate solutions to address Brian’s pain that will include pharmacologic and nonpharmacologic interventions; and they establish the expected outcome that after intervening, Brian will report a pain level of 3 or less out of 10 within one hour. 

Nurse Nadia then takes action to implement these solutions. She knows that since Brian’s most recent dose of ketorolac was two hours ago, he can&amp;#39;t receive his next dose for four more hours. Since Brian is in moderate pain, she verifies that Brian isn’t allergic to any medications and then calls t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Use_of_Mobility_Aids</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NZluyypdS9amyF2rNg_gS-5aSsC3bOBi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Use of Mobility Aids]]></video:title><video:description><![CDATA[Assistive devices are tools to promote patient movement, including ambulation devices and mechanical lifts that move a patient from one location to another. Before using an assistive device, the registered nurse or physical therapist will assess the patient, determine which device is best for the patient, and provide them with initial teaching on the selected device. However, as the licensed practice nurse, or LPN, also known as a licensed vocational nurse, or LVN, you should know when these devices are appropriate and determine if they’re being correctly used by the patient, while reinforcing any previous teaching. 

Common ambulation devices include walkers, canes, and crutches. Let’s start by looking at walkers. These are lightweight devices that consist of a metal frame, two hand grips, and four legs.  

They provide stability due to their wide base, so they&amp;#39;re used for patients who can bear weight on their feet but have trouble walking due to weakness or balance issues. Before using a walker, make sure the hand grips are positioned at your patient’s waist level and that the ends of the legs have non-slip covers. 

To use a walker, assist your patient to stand straight while holding the hand grips. If the walker doesn’t have wheels, they’ll move it forward by lifting their walker and moving it six to ten inches in front of them, and then setting it down on the ground. Then, using the walker for support, they’ll move one leg forward, followed by the other. If the walker has 2 wheels on the front legs, your patient can push it to move forward. There are also walkers with 4 wheels, called rollator walkers. These walkers tend to roll forward, so brakes are built into the device.  

Next up, canes are lightweight devices typically made of wood or metal that consist of a handle, a shaft, and legs. There are single leg, triple leg, or quad leg canes. Canes with multiple legs typically provide more stability but can be heavy or inconvenient to transpo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Emotions,_Anxiety,_and_the_Stress_Response</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LvoKAAFDQoaY4WiRxZKNHZ_CTd2LFHij/_.jpg</video:thumbnail_loc><video:title><![CDATA[Emotions, Anxiety, and the Stress Response]]></video:title><video:description><![CDATA[Stress is a normal human response to an internal or external threat to homeostasis, or the body’s stable equilibrium, and can be prompted by stressors. These stressors such as illness, high workload, or economic hardship, can induce the stress response, also known as allostasis, in an attempt to reestablish homeostasis. In the short term, the body can adapt to the physiological changes to stress; however, when stress becomes chronic, it can have a negative impact on mental and physical health.  

Now, not all stress is harmful, in fact, it is essential for daily life. There are two types of stress; eustress and distress.  is positive stress, which is necessary for normal development and motivation and can occur with beneficial life changes like buying a home or getting a new job; whereas distress is negative stress that occurs when a person is unable to adapt or cope effectively to the stressor. 

Okay, the body’s response to a stressful event can be explained by the General Adaptation Syndrome, or GAS, which has three stages. First, the alarm stage occurs as the sympathetic nervous system is activated, triggering the fight-or-flight reaction, which involves the release of hormones and neurotransmitters to support the body’s reaction to stress. The posterior pituitary releases antidiuretic hormone, or ADH, and the adrenal cortex releases aldosterone, both of which increase circulating blood volume. The adrenal cortex also releases cortisol, which increases the body’s supply of glucose, while the adrenal medulla releases epinephrine and norepinephrine, which increases the heart rate, blood pressure, and blood flow to the skeletal muscles. 

Next, the resistance stage is when the body attempts to stabilize and return to homeostasis. If the stress has been dealt with effectively, vital signs return to normal, and the body begins to repair tissue damage. However, if the stress continues, the sympathetic activation will continue, and the person moves to the exh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fluid_and_Electrolyte_Balance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/st_ilo07RJ2Gw-a3vPQtVkPkRyiwjDMb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fluid and Electrolyte Balance]]></video:title><video:description><![CDATA[Fluid and electrolyte balance is the regulation of fluids and electrolytes, or charged molecules known as ions,  to maintain a stable internal environment, known as homeostasis.  Maintaining fluid and electrolyte homeostasis is essential for normal functioning of the body. 

Now, fluid is needed for essential functions like cellular metabolism and the delivery of oxygen and nutrients to the cells.  It’s distributed in two major compartments: inside the cells, called intracellular fluid, and outside the cells, called extracellular fluid. The extracellular fluid compartment is further divided into the intravascular space, which is inside the blood vessels; the interstitial space, which is found between cells; and the transcellular space, where fluids, like pericardial, cerebrospinal, and synovial fluid, are contained in spaces lined with epithelial cells. 

Okay, so the fluid in these compartments is made up of water, as well as dissolved substances, called solutes. There are large solutes that can&amp;#39;t easily cross cell membranes, such as plasma proteins, like albumin; and small solutes that can easily cross cell membranes, such oxygen, glucose, and electrolytes. 

Now, electrolytes can be categorized as either cations, which are positively charged, like sodium; or anions, which are negatively charged, like phosphate. Electrolytes can be measured in the urine, cerebrospinal fluid, and blood, and they’re usually expressed as milliequivalents per liter of fluid, or mEq/L.  

Okay, so sodium, or Na+, is the most abundant cation in the extracellular fluid. Its major functions are maintaining fluid volume and  fluid osmolality, which is the concentration of particles dissolved in the fluid. Sodium’s normal range is between 135 to 145 mEq/L.  

Potassium, or K+, is the main cation in the intracellular fluid, and it’s responsible for maintaining the osmolality of the fluid within the cells. Potassium works closely with sodium to maintain the cell’s resting m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Communication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zdlioR_qSPeSb4uzSVaAKN3YRFuUJSMO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Communication]]></video:title><video:description><![CDATA[Communication is the process of sending and receiving information between two or more people, through verbal or nonverbal communication. Verbal communication uses spoken or written words, whereas nonverbal communication uses body language to convey information, like gestures and facial expressions. Nurses use communication to collaborate with members of the health care team and to foster trusting relationships with patients and their families. 

Alright, now there are a variety of factors that can affect communication. When there are differences in language between you and your patient, you can promote communication by following your facility’s policy for providing an interpreter. You’ll also need to be mindful of cultural influences that may affect how information is exchanged. For example, in some cultures direct eye contact is considered confrontational and rude, while in others, family members prefer to receive information as a group so they can participate in shared decision-making. Also keep in mind that when your patient is stressed, tired, or in pain, these emotions can make it difficult for them to effectively receive information; likewise, a depressed patient might be reluctant to communicate with their caregivers.  

Other factors that can affect communication include individual factors like age, developmental level, and underlying medical conditions. For instance, a patient with hearing impairment may require nonverbal or written cues; or a pediatric patient may receive information best when toys, play, and simple language are used. Lastly, environmental factors, such as an uncomfortable temperature or a noisy room can negatively impact communication, whereas a comfortable, quiet, and private setting can enhance it.  

Now, to promote patient-centered care, you’ll use therapeutic communication techniques, including active listening, silence, restating, and clarification. Starting with active listening, this is when you attend to what your ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetic_ketoacidosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ms-mLAhSTUiSMZOroFhF_Y5wQyy-eGsV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetic ketoacidosis: Clinical sciences]]></video:title><video:description><![CDATA[Diabetic ketoacidosis, or DKA for short, is a life-threatening complication of diabetes mellitus characterized by a severe insulin deficiency and glucagon excess. It typically but not exclusively occurs in the setting of type 1 diabetes, with common triggers that include illness or infection, as well as known diabetes with suboptimal glycemic control or interruption in therapy. 

The diagnosis of DKA relies primarily on blood work showing metabolic acidosis and hyperglycemia, as well as ketones in the urine.

Now, if you suspect DKA, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. 

DKA generally presents as unstable, so stabilize the airway, breathing, and circulation. Next, obtain IV access, and give a 1-liter bolus of isotonic IV fluid. 

Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and provide supplemental oxygen, if needed.

Once you stabilize the patient, obtain a focused history and physical exam. History often reveals polyuria, polydipsia, and unintentional weight loss, as well as nausea, vomiting, and diffuse abdominal pain. These are commonly associated with a recent precipitating factor like illness or infection. Additionally, there might be a known history of diabetes with inadequate glycemic control or recent disruption in therapy.

On the other hand, physical exam might reveal a confused, somnolent patient with tachycardia, hypotension, and dry mucous membranes. Also, you might see a pattern of deep, rapid breathing known as Kussmaul respirations, and a fruity odor to the breath.

Based on these findings, suspect DKA. Next, order labs, including an ABG or VBG, CMP, and serum and urine ketones like beta-hydroxybutyrate. 

Next, review the lab results and assess diagnostic criteria for DKA, which include a blood glucose above 250 milligrams per deciliter, a pH below 7.3, and a serum bicarbonate level less than 15 mil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Septic_arthritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NAxmvtp8RbekIyZjLtdP46fPTsy4dxjP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Septic arthritis: Clinical sciences]]></video:title><video:description><![CDATA[Septic arthritis refers to joint inflammation that occurs when a pathogen invades the joint space. Once within the synovial cavity, pathogens trigger the immune system and stimulate the production of cytokines that can eventually result in joint damage. 

Now, there are various ways for bacteria to get into a joint. For example, it can spread directly from an infection in the adjacent bone, such as osteomyelitis. It can also reach the joint through hematogenous spread from a distant infectious site in the body; or by direct inoculation, which can occur as a complication of orthopedic surgery. Septic arthritis is usually monoarticular, affecting one large joint, and the diagnosis typically relies on synovial fluid aspiration and analysis.

Now, if you have a patient presenting with signs and symptoms of septic arthritis, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, start IV fluids, and begin continuous vital sign monitoring including blood pressure, heart rate, and oxygen saturation. Provide supplemental oxygen, if needed, and don’t forget to start broad-spectrum IV antibiotics.

Okay, now let’s go back to the ABCDE assessment and look at stable patients. First, let’s start by taking a focused history and physical exam. Your patient will typically report monoarticular joint pain and swelling, commonly of the hips, knees, shoulders, or ankles. These joints are the most vulnerable to infection because they have a richer blood supply than small joints, and that enables pathogens to more easily reach the larger joints. Your patient might also report systemic symptoms, such as fever, malaise, and decreased appetite. They may also have a history of risk factors, including overlying skin infection or ulceration, history of a prosthetic joint or recent joint surgery, immunosuppression, IV drug use, and smoking.
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoarthritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lu__UGARQ9e1XexHq05FEdHvSFigPPFx/_.png</video:thumbnail_loc><video:title><![CDATA[Osteoarthritis: Clinical sciences]]></video:title><video:description><![CDATA[Osteoarthritis is a degenerative disease of the joints, characterized by mechanical wear and tear injury to articular cartilage, resulting in bony and synovial damage. This chronic inflammatory process is mediated by cytokines, such as interleukin-1 and tumor necrosis factor-ɑ, and can affect any joint, but it most commonly affects the knees, hips, hands, and feet! Important risk factors for osteoarthritis include age, being biologically female, obesity, and joint injury. Now, in most cases, osteoarthritis is a clinical diagnosis, but sometimes, imaging with X-ray might be needed if the diagnosis is not clear.  

Now, if your patient presents with signs and symptoms suggestive of osteoarthritis, first you should perform a focused history and physical examination. The patient will typically have a history of joint pain that began in an isolated joint, such as the knee; hand, like the interphalangeal joints; wrist; or feet, like the metatarsophalangeal joints. Also, your patient may describe joint pain that is worse with activity and have limited joint range of motion. They may also have minimal morning stiffness that typically lasts less than 30 minutes before improving. 

Now, here’s a clinical pearl to keep in mind! If your patient has morning stiffness that lasts longer than 30 minutes, then consider inflammatory arthritis, such as rheumatoid arthritis instead. Another way to distinguish between the two is by the pattern of affected joints.  Rheumatoid arthritis tends to be symmetric, meaning that joints on both sides of the body are equally affected, whereas patients with osteoarthritis are more likely to have asymmetric joint involvement. 

On the other hand, the physical exam may reveal tenderness along the joint line, and crepitus, which is a grating sound or sensation when the joint moves. Your patient may also have pain with range of motion testing of the joint, a limited range of motion, as well as bony enlargement of the interphalangeal joints. B]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rheumatoid_arthritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K54MaNcnTyaBI5z1pMEWVqxKRRez1Yux/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rheumatoid arthritis: Clinical sciences]]></video:title><video:description><![CDATA[Rheumatoid arthritis is a chronic, autoimmune disorder that involves symmetric inflammation of the synovial joints, leading to joint effusion with eventual destruction of cartilage and bones. This results in joint pain and severe functional impairment of the affected joints. 
Since there are no pathognomonic laboratory or imaging findings associated with rheumatoid arthritis, the diagnosis is clinical, meaning it is based on historical and physical exam findings.

Now, if your patient presents with signs and symptoms suggestive of rheumatoid arthritis, first you should obtain a focused history and physical exam. Your patient may report joint stiffness in the morning, or with prolonged inactivity, that lasts 30 minutes or longer, as well as joint swelling. Additionally, there might be nonspecific systemic symptoms such as fatigue, malaise, and depressed mood, as well as poor appetite. Patients usually report that these symptoms have been ongoing for more than 6 weeks.

Physical exam findings typically include symmetrical swelling and joint tenderness to palpation of the smaller joints. The most commonly affected joints are the proximal interphalangeal or PIP joints, and metacarpophalangeal or MCP joints. Typically, if one hand is involved, it is likely the other hand is also involved. You may also find swelling and tenderness of the wrists and metatarsophalangeal, or MTP, joints. Keep in mind that sometimes larger joints can also be involved. When a larger joint is affected, you might also notice a joint effusion. 

Now, here’s a clinical pearl to keep in mind! If your patient has less than 30 minutes of morning stiffness, then consider mechanical wear and tear, like osteoarthritis instead of rheumatoid arthritis, where the stiffness can last more than 30 minutes. Another way to distinguish between the two is by the pattern of affected joints.  Rheumatoid arthritis tends to be symmetric, meaning that joints on both sides of the body are equally affected, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Upper_respiratory_tract_infections:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5NDvPVX4S8mgjFcwByiqKbW8RluweILT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Upper respiratory tract infections: Clinical sciences]]></video:title><video:description><![CDATA[Upper respiratory tract infections, or URIs, are a common cause of acute illness. They occur when a pathogen causes inflammation in the nasal cavity, sinuses, and throat. Based on their clinical presentation, URIs can be classified as; pharyngitis; acute rhinosinusitis, also known as acute sinusitis; and unspecified URI.

Now, if you suspect a URI, you first should perform an ABCDE assessment to determine if the patient is unstable or stable. If they are unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, provide supplemental oxygen, and put them on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, don’t forget to start IV empiric broad-spectrum antibiotics.

Now, here’s a high-yield fact! If your patient presents with drooling, tender neck swelling, and inspiratory stridor, along with painful and difficult swallowing, you should suspect epiglottitis or retropharyngeal abscess. These conditions can be caused by Streptococcus pneumoniae or pyogenes, as well as Staphylococcus aureus, and can quickly lead to airway compromise. Also consider Lemierre syndrome, which is septic thrombophlebitis of the internal jugular vein and is caused by the anaerobe Fusobacterium necrophorum. 

Okay, now that we’ve dealt with unstable patients, let’s return to the ABCDE assessment and focus on stable patients. If your patient is stable, proceed with obtaining a focused history and physical exam. The history will commonly reveal symptoms of fatigue, runny nose, and fever. Additionally, the patient might report a sore throat, as well as cough. The general physical exam will reveal an ill-appearing person.

At this point, you should suspect a URI, so your next step is to classify it clinically as pharyngitis, acute rhinosinusitis, or unspecified URI.

Here’s a clinical pearl! Don’t forget to inquire about a history of allergies, lung disorders, immunosuppression, tobacco use, recent sick contact]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuronal_ceroid_lipofuscinoses_(Batten_disease):_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IiT2Su1CQ0m2oJAWaO_ipYMrQRGT60vH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neuronal ceroid lipofuscinoses (Batten disease): Year of the Zebra]]></video:title><video:description><![CDATA[Neuronal ceroid lipofuscinoses, or NCLs, also sometimes referred to as Batten disease, are a group of rare inherited neurodegenerative disorders that mainly affect children and adolescents and are one of the main causes of childhood dementia.

They belong to a larger group of diseases known as lysosomal storage disorders, a group of metabolic conditions that result in the inability of a cell to break down certain substances, causing them to build up, ultimately leading to cell damage and death. With NCLs, there is a buildup of ceroid lipofuscin and other toxic waste products within neurons due to defects in lysosomal proteases or related enzymes.

There are 14 different known subtypes of NCLs, named CLN1 to CLN14 each resulting from a specific gene mutation. Most of these mutations are inherited in an autosomal recessive pattern, meaning that an individual needs to inherit two copies of the mutated gene, one from each parent, to develop the disorder.

Alright, now NCLs predominantly affect the retina of the eye and brain. The most common symptoms include progressive visual impairment that eventually leads to blindness; and seizures, respectively.

With early infantile onset, there is usually muscle weakness, as well as a delay in development of motor milestones, like lifting the head or crawling. Later on, children may experience poor coordination, unsteady walking, and progressive loss of acquired motor abilities.

Infantile and juvenile onset are also characterized by learning difficulties and developmental regression, meaning that a child may lose certain developmental skills that they had previously acquired.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cellulitis_and_erysipelas:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fBFJRIbHTc6hCdHV0W9HM9mpRcq5p40w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cellulitis and erysipelas: Clinical sciences]]></video:title><video:description><![CDATA[Cellulitis and erysipelas are acute infections of the skin and subcutaneous tissues. Erysipelas is an infection of the upper layer of the dermis with the superficial lymphatics and vessels, while cellulitis affects the deeper layers of the dermis and the subdermal tissues. These infections usually occur when bacteria enter through breaks in the skin barrier, such as a laceration and puncture wound. The vast majority of infections are caused by beta-hemolytic Streptococci, such as Group A Streptococcus or Streptococcus pyogenes; as well as Staphylococcus aureus including methicillin-resistant or MRSA. While erysipelas is usually limited to the skin, cellulitis can sometimes present with or without systemic symptoms.

When approaching an individual with signs and symptoms suggestive of cellulitis and erysipelas, first obtain a focused history and physical examination. Alright, let’s start with erysipelas. On history, the patient might report an acute onset of skin redness, swelling, and pain usually around the face or the extremities. Notably, there won’t be systemic symptoms like fever and chills, and this is one of the main factors distinguishing erysipelas from cellulitis. A physical exam typically reveals a well-demarcated area of erythema with superficial induration that is warm and tender to touch. 

Because erysipelas is a local infection, you can start the patient on oral antibiotics such as a penicillin or first-generation cephalosporin. Then, assess the response at 24 to 48 hours. If the patient shows adequate response, in other words, erythema, induration, and pain have improved, they can continue the current treatment and complete the course of antibiotics. However, if the patient has an inadequate response, assess for signs of spreading infection or abscess and consider switching the antibiotics to broaden the coverage.

Alright, now that patients with erysipelas are treated, let’s go back to history and physical and talk about patients wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Invasive_lobular_carcinoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LMkyAz1hQB2zfrZ5sJJsp6UzTwGopUmZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Invasive lobular carcinoma: Clinical sciences]]></video:title><video:description><![CDATA[Invasive lobular carcinoma is the second most common subtype of invasive breast cancer and occurs when malignant epithelial cells from lobular tissue infiltrate through their basement membrane. It’s more common in older patients and more likely to be at an advanced stage on initial diagnosis. This cancer can be classified as early-stage, locally-advanced, or metastatic disease, and treatment is based on the stage. 

As a clinical pearl, shared multi-disciplinary decision making is a central standard to breast cancer care, which is managed by a breast team that consists of a breast surgeon, oncologist, radiation oncologist, pathologist, radiologist, and reconstructive surgeon.

When assessing a patient presenting with a new breast lump or abnormal finding, consider an invasive lobular carcinoma. The first step is to obtain a focused history and physical exam, as well as labs like CBC, CMP, LFTs, and alkaline phosphatase.

Typically, patients present with an abnormal screening mammogram or a new breast finding like a lump or asymmetric area of firmness. The history might also include changes in breast or nipple appearance, nipple discharge, or axillary lymphadenopathy. Make sure to ask your patient about risk factors, such as the personal or family history of breast or ovarian cancer, early menarche, late menopause, nulliparity, or first pregnancy after 30 years of age. 

Other important risk factors include age over 40, and alcohol use. Finally, look out for a known history of dense breast tissue, exogenous hormone use, as well as family or personal history of deleterious cancer gene mutations like BRCA.

Physical exam might reveal a palpable breast mass and skin or nipple changes. Now, lobular carcinomas are less likely to form a discrete mass, which makes them more difficult to detect on physical exam. So, pay close attention to any areas that feel asymmetric or firm. Another important finding is lymphadenopathy. When assessing lymph nodes, make sure]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skin_cancer_screening:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/En-nPuLiTxmvK9Ma19M7ntiBQWqHXaD6/_.png</video:thumbnail_loc><video:title><![CDATA[Skin cancer screening: Clinical sciences]]></video:title><video:description><![CDATA[Skin cancer is one of the most common cancers in the United States. It is estimated one in five individuals will develop some form of skin cancer within their lifetime. So, prevention is the most important way to limit the risk of developing skin cancer. Some of the most effective preventative methods include decreasing exposure to UV rays from sunlight by wearing sun-protective clothing and using broad spectrum waterproof sunscreen with an SPF of 30 or higher, as well as avoiding artificial UV rays like tanning beds. Because complete avoidance of UV rays is are not feasible, regular skin cancer screenings, which include risk factors assessments and skin exams, are used to identify individuals more susceptible for developing skin cancer. 

Alright, when a patient presents for a skin cancer screening, the initial step is to assess their risk factors for future skin cancer. Individuals at an increased risk for developing skin cancer include those who are older than 50 years; as well as sun-sensitive individuals with red or blonde hair, light eye color, light skin pigmentation, or freckling. 

Other important risk factors include a nevi count that is greater than 50 with or without large, atypical nevi; as well as personal or family history of skin cancer; and immunosuppression or chronic immunosuppressive therapy. Lastly, there’s an increased risk for skin cancer in patients with certain syndromes and genetic disorders, such as xeroderma pigmentosum or albinism. 

Now, if your patient does not have any of the risk factors mentioned above, then they are considered to be at low risk of developing skin cancer and no routine screening examination is recommended. Keep in mind, however, any suspicious skin lesions on these patients should be checked regularly by their primary care physicians or evaluated by a dermatologist.

On the other hand, if your patient has any of the risk factors mentioned previously, they are considered to be at a high risk for developing ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ductal_carcinoma_in_situ:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lJPc3Kc1Qz_6ndluhco6C1ccQwuldXnC/_.png</video:thumbnail_loc><video:title><![CDATA[Ductal carcinoma in situ: Clinical sciences]]></video:title><video:description><![CDATA[Ductal carcinoma in situ, or DCIS, previously known as intraductal, noninvasive, or non-infiltrating carcinoma, refers to a neoplastic lesion within the mammary ductal system that hasn’t yet invaded through its basement membrane into the surrounding tissues. If there’s evidence of basement membrane invasion, then the lesion is upstaged to invasive carcinoma.  

When assessing a patient with signs and symptoms consistent with DCIS, the first step is to obtain a focused history and physical exam. Sometimes, a patient may present after noticing a breast lump or even nipple discharge. However, the majority of patients will not have historical or physical exam findings, and they’ll be discovered on routine mammogram screening, which shows a lesion that may or may not have microcalcifications. 

Be sure to ask about risk factors, such as a personal or family history of breast cancer, prior diagnosis of atypical ductal hyperplasia, early menarche or late menopause, and nulliparity or first birth after the age of 30. Additional risk factors include age greater than 40, a known history of dense breast tissue, and more than five years of hormone replacement therapy. On the flip side, physical exam findings might include a palpable breast mass or changes in the appearance of the nipple or skin. Keep in mind that most patients won’t present with any physical exam findings.

Here’s a clinical pearl! Biologically male patients and those who identify as transgender or non-binary are also at risk for breast cancers, so it’s important to screen them, especially as these populations frequently go underdiagnosed. 

Okay, now that we have our history and physical exam, let’s move on to some imaging. The next step is to obtain a diagnostic mammogram. Unlike a screening mammogram, which is used on asymptomatic patients, diagnostic mammograms are performed in patients with evidence of disease, either in the history and physical, or with a prior abnormal screening mammogram, and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Iron_deficiency_anemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v-U2qLAHSRe78yRwMmE-SQENT06WVCt6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Iron deficiency anemia: Clinical sciences]]></video:title><video:description><![CDATA[Iron deficiency anemia is a condition that occurs when the body lacks sufficient iron to produce enough healthy red blood cells. 

Iron plays a vital role in the production of hemoglobin, which is the protein responsible for carrying oxygen in red blood cells. So, when iron levels are low, the body is unable to produce an adequate amount of hemoglobin, leading to a decrease in red blood cell production, and subsequent anemia. While history and physical examination findings can provide hints to iron deficiency anemia, confirming the diagnosis requires laboratory tests, primarily iron studies and a peripheral blood smear.

Now, if your patient presents with a chief concern suggestive of iron deficiency anemia, first, you should start with a focused history and physical examination. 

History typically reveals vague symptoms like fatigue and dizziness, as well as palpitations and dyspnea on exertion, which manifest as compensatory responses to inadequate tissue oxygen supply. 

Other symptoms may include pica, which is the compulsive consumption of non-nutritive substances like dirt or ice. Some patients may also develop Plummer-Vinson syndrome, which is characterized by the triad of iron deficiency anemia, esophageal webs, and dysphagia. 

Additionally, some patients with iron deficiency may experience restless leg syndrome. Be sure to assess your patient’s nutritional history, since they might have a diet deficient in iron-rich foods. For example, the patient might report that they seldom eat red meat, leafy greens, and fortified grains, which are all rich in iron! 

Next, your patient may have a history of gastrointestinal absorption problems that would prevent them from absorbing adequate dietary iron. These include inflammatory bowel disease, Helicobacter pylori infection, celiac disease, or a history of gastrointestinal surgery, such as bariatric surgery. 

There may also be a history of chronic blood loss, which could be caused by gastrointestinal blee]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aortic_dissection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F5fPWrQPQ1yUfiq12xocUfFWRMOov0-N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aortic dissection: Clinical sciences]]></video:title><video:description><![CDATA[Aortic dissection occurs often due to long-standing untreated high blood pressure, when blood tears through the intimal layer of the aortic wall and bleeds into the muscular layer, creating an intraluminal flap and a double lumen, which means that there is a true and a false lumen of the aorta. 

Acutely, blood will flow into the false lumen because there’s less resistance, which can lead to obstruction of the true lumen, resulting in malperfusion of end-organs, such as the brain, bowel, or kidneys. In addition, as blood accumulates in the false lumen with no way out, it may clot leading to the formation of thrombi. 

Lastly, as blood keeps flowing into the false lumen, the shear stress on the aortic wall can cause the tear to expand, or in the worst cases even lead to aortic rupture, causing mortality from cardiac tamponade or internal hemorrhage.

According to the Stanford classification, aortic dissection is either classified as Type A, which always involves the ascending aorta with or without involving the descending aorta; and Type B, which only involves the descending aorta. 

Let’s first look at an unstable case.  When approaching a patient who presents with signs and symptoms suggestive of an acute aortic dissection, your first step is to do an ABCDE assessment in order to determine if the patient is unstable or stable. If the patient is unstable, you need to stabilize their airway, breathing, and circulation first. This means that you should secure their airway, obtain IV access, and begin fluid resuscitation while continuously monitoring their vital signs, especially their blood pressure and heart rate. 

Next, take a focused history and physical exam. Patients with unstable aortic dissections typically report an acute and severe “tearing” or “ripping” chest pain, and since the aorta is mostly a retroperitoneal organ, the pain can radiate to the back. In fact, the location of the pain depends on which area of the aorta is affected, and sometimes ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hyperkalemia:_Clinical_Sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8BtpRarWQp2gQNBdsOcVuyluRoe2QJ6Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hyperkalemia: Clinical sciences]]></video:title><video:description><![CDATA[Hyperkalemia refers to an elevated serum potassium level, usually above 5.5 milliequivalents per liter. Mild hyperkalemia can be asymptomatic, while severe hyperkalemia can cause life-threatening symptoms like paralysis and cardiac arrhythmias. 

Some common causes of hyperkalemia include increased potassium intake and conditions associated with transcellular potassium shifts, like medication-induced hyperkalemia, metabolic acidosis, tumor lysis, rhabdomyolysis, or due to decreased effective arterial blood volume. Another very important cause is reduced renal function, or renal failure. Lastly, other causes include tubular resistance to aldosterone, hyporeninemic hypoaldosteronism, and adrenal insufficiency.

Now, if you suspect hyperkalemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on cardiac telemetry. This is important because extreme elevations in serum potassium can lead to myocardial instability and dangerous cardiac arrhythmias, such as ventricular fibrillation. You should also monitor vital signs and provide supplemental oxygen, if needed. 

Now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. If your patient is stable, first obtain a focused history and physical examination. Next, obtain labs, including a comprehensive metabolic panel or CMP, and an arterial or venous blood gas, as well as a 12-lead ECG. History typically reveals palpitations, paresthesias, muscle weakness, or even ascending paralysis in extreme cases. Additionally, there might be a known history of acute or chronic kidney disease. On the flip side, physical examination usually reveals generalized weakness or a strength deficit, but you could also see fasciculations, or involuntary muscle twitching, as well as flaccid paralysis. 
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Febrile_neutropenia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GvBXGqhKQd_FX-UkiY2ADxVJTmCUU12N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Febrile neutropenia: Clinical sciences]]></video:title><video:description><![CDATA[Febrile neutropenia is defined as either a single oral temperature of 101 degrees Fahrenheit or 100.4 degrees lasting an hour or more, both in the setting of an absolute neutrophil count or ANC lower than 1500 cells per microliter, while severe neutropenia is defined as an ANC lower than 500. 

Neutropenia is commonly caused by chemotherapy, but it can also result from other medications, autoimmune diseases, or infections. 
So, whether or not you confirm the source of infection, you can further classify as febrile neutropenia with confirmed infection or fever of unknown origin, or FUO for short. 

Now, if you suspect febrile neutropenia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. 

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and consider starting IV fluids. Keep in mind that septic patients with febrile neutropenia may have profound hemodynamic instability requiring urgent volume resuscitation. 

In addition, put your patient on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry, and provide supplemental oxygen if needed. Finally, don’t forget to start empiric broad-spectrum antibiotics.

Alright, now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. 

If your patient is stable, first obtain a focused history and physical examination. Your patient typically reports fever and malaise, as well as symptoms of infection, like a new onset cough, dysuria, diarrhea, or erythema of the skin. These symptoms usually occur while undergoing chemotherapy, or after starting a medication associated with neutropenia, like carbamazepine or an aminosalicylate. 

They may also report a history of a chronic viral infection, like HIV and hepatitis; or an autoimmune disease, such as rheumatoid arthritis or Sjogren syndrome. 

On the other hand, physical examination primarily revea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adrenal_insufficiency:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4gd_d5ZPTeGLD3h-ZgXnH-62REyXWsbR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adrenal insufficiency: Clinical sciences]]></video:title><video:description><![CDATA[Adrenal insufficiency is an uncommon, but potentially life-threatening condition, that occurs when hormones from the adrenal gland, like glucocorticoids and mineralocorticoids, are insufficient to meet the body’s demands. Common causes of adrenal insufficiency include autoimmunity, infections, malignancy, or exogenous use of glucocorticoids. And based on the location of the underlying cause, adrenal insufficiency can be classified as primary, which is when the adrenal gland cannot produce hormones; secondary, or when there are abnormalities in the hypothalamic-pituitary-adrenal axis or HPA axis for short; and tertiary, which is often due to exogenous glucocorticoid steroid use.  

Now, if you suspect adrenal insufficiency, first, you should perform an ABCDE assessment to determine if the patient is unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Additionally, obtain IV access, provide supplemental oxygen, if needed, and put them on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. 

Next, proceed with a focused history and physical examination, and obtain labs like a BMP Typically, your patient will report fatigue, nausea and vomiting, and abdominal pain; as well as headaches, muscle pain, and cramping. Additionally, they will likely have a history of some sort of exacerbated stress on the body. This could come from a recent acute illness, a recent medical procedure, or being under significant psychological stress. Or the stressor may be recent abrupt withdrawal of glucocorticoid therapy. 

On the other hand, physical exam findings usually include an acutely ill-appearing individual with hypotension or even shock, as well as altered mental status, and significant abdominal tenderness.  

Finally, labs can reveal hypoglycemia, as well as hyponatremia and hyperkalemia. Additionally, you might notice elevated BUN and creatinine from significant dehydration. 

At this point, you ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Graves_disease:_Clinical_Sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LXZ5H4JqS4_56Pf9aOi_WkpMSiWLInJU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Graves disease: Clinical Sciences]]></video:title><video:description><![CDATA[Graves disease is an autoimmune condition characterized by the production of TSH-receptor antibodies, or TRAb, for short. These antibodies mimic thyroid-stimulating hormone, or TSH, so they bind to TSH receptors on thyroid cells and stimulate them to produce thyroid hormone, causing hyperthyroidism. In fact, Graves disease is the most common cause of hyperthyroidism. 

Now, if your patient presents with a chief concern suggesting Graves disease, you should first perform an ABCDE assessment to determine if they are unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry; as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen.

Now, here’s a high-yield fact to keep in mind! If your patient presents with fever, tachycardia, delirium, or coma, you should suspect thyrotoxic crisis, also called thyroid storm. This is a severe, life-threatening presentation of Graves disease that typically occurs in patients with untreated or undertreated hyperthyroidism, and it’s triggered by an inciting event, such as major illness or surgery. 

Treatment includes the four Ps: Propranolol or other beta-blockers, Propylthiouracil, Prednisolone or other glucocorticoids, and Potassium iodide. These patients need close monitoring, and may require intensive measures such as volume resuscitation and whole-body cooling.

Okay, now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. First, obtain a focused history and physical examination. Your patient may report palpitations, heat intolerance, anxiety, and insomnia, as well as digestive issues, such as increased appetite associated with unintentional weight loss, and diarrhea. 

On the other hand, physical exam findings typically include the classic triad of Graves disease]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Herpes_zoster_infection_(shingles):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4g6Sd9Y0Q5W-T-ND7jzc-6S9T5ej5rQv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Herpes zoster infection (shingles): Clinical sciences]]></video:title><video:description><![CDATA[Herpes Zoster infection, also known as shingles, occurs in individuals who have had a primary infection called varicella, or chickenpox, which is caused by the Varicella Zoster Virus. Following the primary infection, the virus remains dormant in the dorsal root ganglia of spinal nerves or the trigeminal ganglion. In times of stress or immunosuppression, the virus can reactivate and travel down the sensory neurons, causing herpes zoster. 

Now, if your patient presents with a chief concern suggesting herpes zoster infection,  first you should perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry. Finally, If needed, provide supplemental oxygen. 

Now, here’s a high-yield fact to keep in mind! If your patient is unstable, they may have disseminated herpes zoster, which can present with associated hepatitis, encephalitis, or meningitis. This can happen because of compromised cell-mediated immunity, or following hematopoietic stem cell transplant, in which case high viremia causes an atypical presentation. These patients can also be unstable on presentation because of the high viral load. 

Okay, now let’s go back to the ABCDE assessment and take a look at stable patients.  If your patient is stable, obtain a focused history and physical exam. History typically reveals a prior history of varicella infection, as well as a painful, itchy, or tingly rash that may have been preceded by a prodromal illness of malaise, headache, fatigue, and a low-grade fever. 

Physical exam typically reveals a maculopapular or vesicular rash in the distribution of 1 to 2 adjacent dermatomes, which are areas of skin innervated by a single nerve. Typically, the rash appears on the trunk or the face, and it doesn’t cross the midline! At this poi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Acute_Coronary_Syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5o0oGSYxT2KRdgLRnKwsfUYQR3SAkyKK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Acute Coronary Syndrome]]></video:title><video:description><![CDATA[Nurse Cameron works on a cardiovascular inpatient unit, and is caring for Kevin, a 55-year-old with a history of coronary artery disease for which he’s prescribed aspirin at home. He was admitted the previous day after undergoing percutaneous coronary intervention, or PCI, with placement of one stent to treat an ST-segment elevation myocardial infarction, or STEMI for short. In collaboration with the registered nurse, RN Rachael, Nurse Cameron goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Kevin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Cameron recognizes important cues including Kevin’s vital signs, which are blood pressure 101/80 mmHg, heart rate 99 beats per minute and regular, respirations 17 breaths per minute, oxygen saturation 96 percent on 2 liters per nasal cannula, and temperature 98.2 F or 36.8 C 

When asked about pain, Kevin reports a current pain level of 3 out of 10 in his groin incision. Nurse Cameron notes that Kevin has a small amount of dried blood on his groin dressing and the surrounding area is ecchymotic and tender to palpation. Nurse Cameron also notes Kevin is prescribed the antiplatelet medication clopidogrel.  

Next, Nurse Cameron analyzes these cues. He understands that PCI is a minimally invasive procedure that involves inserting a catheter through the radial or femoral artery to locate blockages in the coronary arteries. After the blockage is located, a tiny balloon is inserted in the obstructed coronary artery to compress plaque against the artery wall. If needed, a stent can be placed during PCI to keep the artery patent. After the procedure, patients are typically given antiplatelet medications, like clopidogrel, to prevent additional clot formation, especially around the new stent. Nurse Cameron realizes that Kevin’s history of aspirin therapy, combined with c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Burn_Injuries</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WxS62iKoSQmemDmOi7Lq1vUwRGONroYh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Burn Injuries]]></video:title><video:description><![CDATA[Nurse Kamala works in a rehabilitation center and is caring for Raul, a 42-year-old who was admitted following a thermal burn in a house fire. In collaboration with the registered nurse, RN Amy, Nurse Kamala goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Raul’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Kamala recognizes important cues, including Raul’s vital signs, which include temperature 98.4 F or 36.9 C, heart rate 100 beats per minute, respirations 21 breaths per minute, and blood pressure 128/88 mmHg.  

Nurse Kamala notes that Raul has partial- and full-thickness burns on his right lower extremity, extending up to his lower abdomen. The dressings over Raul’s burns have a small amount of serosanguineous drainage and the surrounding skin is reddened. She also notices that he appears uncomfortable and restless.  

Next, Nurse Kamala analyzes these cues. She reviews Raul’s electronic health record, or EHR, and notes an order for sterile dressing changes. She also sees that he’s prescribed medication for pain management, and he received his last dose 4 hours ago. She knows that dressing changes will facilitate healing and untreated pain can make dressing changes difficult to tolerate. Nurse Kamala realizes that Raul needs effective pain management so the prescribed wound care can be performed for his burns. 

Now, using the information she’s gathered, along with Raul’s medical history, Nurse Kamala reports her findings to RN Amy, and they choose a priority hypothesis of impaired skin integrity.  

Then, they generate solutions to address Raul’s impaired skin integrity using nonpharmacologic and pharmacologic interventions; and they establish the expected outcome that Raul’s pain will be at a tolerable level to undergo all scheduled dressing changes. 

Nurse Kamala then takes action to implement these solu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Bacterial_Pneumonia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/46YjMSh6RCKGJud0sBI13N1HSX2Iof08/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Bacterial Pneumonia]]></video:title><video:description><![CDATA[Nurse Jodie works on a medical-surgical unit and is caring for Ann, a 44-year-old with a history of smoking who was recently admitted for community-acquired pneumonia. In collaboration with the registered nurse, RN Seth, Nurse Jodie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ann’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jodie recognizes important cues including Ann’s vital signs, which are temperature 101.5 F or 38.6 C, heart rate 100 beats per minute, respirations 21 breaths per minute and regular, blood pressure 105/68 mmHg, and oxygen saturation 90 percent on room air. Upon auscultation, Nurse Jodie notes coarse crackles and slight wheezing. Nurse Jodie also observes that Ann can’t speak in full sentences without becoming short of breath.  

Next, Nurse Jodie analyzes these cues. Nurse Jodie reviews the electronic health record, or EHR, and notes Ann’s WBC count is elevated at 12,500 cells per mm3. Nurse Jodie knows that an infection is likely causing inflammation in Ann’s lungs. This can result in fluid entering Ann’s alveoli, which can impair gas exchange; as well as narrowing of her airways, which can interfere with her breathing. Nurse Jodie recognizes that Ann needs effective respiratory management.  

Next, using the information she has gathered along with Ann’s medical history, Nurse Jodie discusses her findings with RN Seth, and they choose a priority hypothesis of ineffective gas exchange. 

Then, they generate solutions to address Ann’s infection that will include pharmacologic and nonpharmacologic interventions. They establish the expected outcome that after intervening, Ann will maintain an oxygenation saturation above 92 percent during the shift.  

Nurse Jodie then takes action to implement these solutions.  

Nurse Jodie: I&amp;#39;m going to give you some oxygen to help you br]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psychotherapeutic_Drug_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wNstQZ90RlW2gKAlElljo3T7SLSzqdcw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psychotherapeutic Drug Therapy]]></video:title><video:description><![CDATA[Psychotherapeutic medications produce their effects on the mind, emotions, and body by   changing the chemical balance of the CNS. Most psychotherapeutic medications work by altering the activity of neurotransmitters, which are the chemical messengers carrying information between neurons, or nerve cells. The four major classes of psychotherapeutic medications are anxiolytics, antidepressants, mood stabilizers, and antipsychotics. As the nurse, you’ll administer psychotherapeutic medications and monitor their effects on your patients.  

Anxiolytics are medications that reduce symptoms of anxiety such as uneasiness, fear, or panic, and are primarily used to treat anxiety disorders such as generalized anxiety disorder, or GAD; panic disorders; and trauma disorders, such as post-traumatic stress disorder, or PTSD.  

Examples of anxiolytics include benzodiazepines, like alprazolam; and azapirones, like buspirone. Benzodiazepines work by increasing the activity of gamma-aminobutyric acid, which is the main inhibitory neurotransmitter in the CNS. Their effects can be felt relatively quickly, so they’re useful for episodes of acute anxiety. Common side effects include sedation and dizziness, and they have a potential for dependency with long-term use.  

On the other hand, azapirones primarily bind with receptors for the neurotransmitter serotonin and can take up to 6 weeks of regular use for patients to experience symptom relief. Common side effects include dizziness, headache, and GI symptoms like nausea. 

Next, there are several categories of antidepressants used to treat mood disorders such as depression and bipolar disorder. These medications mostly work by increasing the availability of certain neurotransmitters like serotonin, norepinephrine, or dopamine. Typically, antidepressants take up to 4 weeks of regular use for patients to experience symptom relief.  

Now, as depressive symptoms start to improve early in therapy, antidepressants can actually inc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Nursing_Care_for_Constipation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YtVhnpFvSqK8pXPfejpdZhjPR-mEsUcE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Nursing Care for Constipation]]></video:title><video:description><![CDATA[Nurse Kelly works at a primary care office and is caring for Francesca, an 83-year-old who is experiencing constipation. In collaboration with the registered nurse, RN Evan, Nurse Kelly goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Francesca’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Kelly recognizes important cues, including Francesca’s vital signs, which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 18 breaths per minute, and blood pressure 116/64 mmHg. Francesca denies pain, but states her abdomen feels full and distended. 

When asked about her last bowel movement, Francesca replies that she hasn’t had a bowel movement in 3 days, and normally has 2 to 3 hard, lumpy bowel movements each week. Nurse Kelly listens to Francesca’s bowel sounds, which are hypoactive in all four quadrants.  

Next, Nurse Kelly analyzes these cues. She reviews the electronic health record, or EHR, and sees that Francesca takes a diuretic which can increase her risk for constipation due to the elimination of excess body fluids.  

Then, she gathers information from Francesca about other risk factors for constipation.  

Nurse Kelly: Francesca, how would you describe your activity level?  

Francesca: I walk around my house, but that’s it. Sometimes, my knees bother me, and I can’t get around that well. So, I guess I sit around a lot.  

Nurse Kelly: Okay, and how would you describe your fluid intake and diet?  

Francesca: I try not to drink too much water because then I have to go to the bathroom all the time, especially with my water pill. As for my diet, I mostly have my meals delivered. I really like the frozen dinners they send me.  

Nurse Kelly realizes that Francesca has several risk factors for constipation. She has a mostly sedentary lifestyle, and because of Francesca’s age, her gast]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Measuring_Temperature</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WrIDKYT0TuaHadUQMsG_DeHDS8miIlEN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Measuring Temperature]]></video:title><video:description><![CDATA[Temperature reflects the body’s ability to regulate body heat, a process called thermoregulation. As the nurse you’ll consider factors that affect your patient’s temperature and measure their temperature using the most appropriate route and thermometer type based on their developmental level and condition. 

Now, factors that affect body temperature include age, biological processes, and illness.  

A normal adult temperature varies between 97.5 to 99.5 F, or 36.4 to 37.5 C, whereas in infants and children, the range can be wider because their thermoregulatory mechanisms are less effective. In older adults, baseline temperature is often slightly lower due to decreased amounts of subcutaneous fat and slower metabolic rate.  

Illness can also be reflected in temperature readings. For instance, body temperature typically increases above normal in patients with an infection or inflammation, which can cause a fever; or it can decrease in patients experiencing excessive heat loss related to conditions like frostbite or hypothermia.  

Keep in mind that changes in your patient’s temperature should always be compared with their baseline readings, and any abnormalities should be reported to the registered nurse. 

You can measure your patient’s temperature from a variety of routes, including the temporal artery; tympanic membrane or eardrum; oral cavity; axilla or armpit; or rectum. The most accurate route is the rectum due to its proximity to core body temperature, and it’s typically about 1 degree F or 0.5 degree C higher than oral readings.  

The least accurate site is the axilla due to its distance from the core, and its typically about 1 degree F or 0.5 degree C lower than oral readings. For most stable and cooperative patients, you can use the tympanic membrane, temporal artery, or oral cavity; whereas, if your patient is clinically unstable, the rectal route is often used. For patients who are confused, uncooperative, or unable to follow commands, like inf]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Chronic_Kidney_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xothR6eXTIOSRXGUqLyGpRMASo_mZs1k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Chronic Kidney Disease]]></video:title><video:description><![CDATA[Nurse Marisol works in a family practice office and is caring for Robert, a 55-year-old with a history of chronic kidney disease and type 2 diabetes, who&amp;#39;s arrived for a follow-up appointment. In collaboration with the registered nurse, RN Rae, Nurse Marisol goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Robert’s care by recognizing cues, analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Marisol recognizes important cues including mild, pitting edema in Robert’s lower extremities, a blood glucose of 214 mg/dL, blood pressure of 145/85 mmHg, and a weight gain of 4.5 pounds since his last visit. 

Nurse Marisol asks about Robert’s insulin management at home. 

Nurse Marisol: I see that your blood sugar is higher than your last visit. Have you made any changes to your medications or the foods you eat? 

Robert: Yeah, my blood sugar’s been a little high. Sometimes I get tired and forget to take my insulin at night. 

Nurse Marisol: I also noticed that your ankles are swollen, too. Can you tell me how much water you’ve been drinking lately? 

Robert: Well, I’ve been really thirsty lately, so I’ve been drinking more than usual. Anyway, someone told me that drinking water helps to flush out my kidneys. 

Next, Nurse Marisol analyzes these cues. She reviews the electronic health record, or EHR, and notices that Robert is prescribed ten units of long-acting insulin nightly. She also notes that he’s recommended to follow a 1.5-liter fluid restriction daily. She knows that chronic kidney disease is a progressive and irreversible loss of kidney function, and that uncontrolled diabetes can worsen damage to nephrons over time. She also understands that nephron loss reduces the glomerular filtration rate, or GFR, leading to decreased fluid output, increased fluid retention, edema, and increased blood pressure.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Intrapartum_Complications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vnZV5So8RaqSpbOgUHJPvA3FQdyKTOBt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Intrapartum Complications]]></video:title><video:description><![CDATA[The intrapartum period begins with the onset of labor and lasts until the delivery of the newborn and placenta. Complications during the intrapartum period can be related to premature rupture of membranes, or PROM, and preterm labor. As the nurse, you’ll collaborate with the registered nurse, or RN, to care for patients with intrapartum complications.  

PROM is when the amniotic membranes spontaneously rupture before the beginning of true labor. PROM can lead to complications such as oligohydramnios, meaning there isn’t enough amniotic fluid left to surround the fetus; and umbilical cord prolapse, which is when the umbilical cord moves ahead of the fetus and becomes compressed, which cuts off circulation to the fetus. PROM also makes it easy for microorganisms in the vagina to travel into the uterus, causing chorioamnionitis, which is an infection of the remaining amniotic tissue and fluid. 

PROM can present as either a gush of vaginal fluid or a slow leaking of fluid from the vagina.  Diagnosis of PROM is made by sterile speculum exam to look for a pool of fluid near the cervix. If fluid is present, PROM can be confirmed if pH testing shows alkalinity of the fluid. Other information can be gathered during the speculum exam, including an estimation of cervical dilation and effacement, as well as testing the fluid for the presence of phosphatidylglycerol, or PG, which is an indication of fetal pulmonary maturity. 

Nursing management of PROM primarily depends on the gestational age and involves weighing the risks of preterm birth versus expectant management, which consists of observation for infection, labor onset, and testing for fetal well-being. In all cases, you’ll administer antibiotics prophylactically, as ordered, even if infection isn’t suspected. If your patient is at 37 weeks of gestation and labor doesn&amp;#39;t start soon, labor will typically be induced with oxytocin after cervical softening agents like prostaglandin E2 have been administer]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Attention-Deficit/Hyperactivity_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YAY3JImeQ66VSDRRtK36lZLwQ_SJo112/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Attention-Deficit/Hyperactivity Disorder]]></video:title><video:description><![CDATA[Nurse Sienna works in a family practice clinic and is caring for Paul, a 10-year-old who was brought in by his caregiver, Erin, for poor school performance over the past year.  In collaboration with the registered nurse, RN Joy, Nurse Sienna goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Paul’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Sienna recognizes important cues, including Paul’s vital signs which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respiratory rate 14 breaths per minute, and blood pressure 105/66 mmHg. She notices that Paul is restless and regularly stands up to look at and touch objects in the examination room.  

Nurse Sienna gathers more information from Erin and Paul.  

Nurse Sienna: Hi Paul, how are you doing today? 

Paul: Okay, I guess. I don’t know why I have to be here.  

Erin: Paul’s been having trouble in school. His grades have been getting worse over the past few months. He&amp;#39;s also been turning in his assignments late or not at all, and when he does turn them in, they’re incomplete.  

Paul: (shrugs) It&amp;#39;s hard to pay attention. 

Erin also reports that Paul’s teachers say he often disrupts class by standing up and blurting out answers to questions instead of raising his hand; and that he has difficulty following rules and waiting for his turn during group activities. When asked about the home environment, Erin reports that when Paul is asked to perform a household chore, he either forgets to do the chore or doesn&amp;#39;t finish it once he starts it.  

Nurse Sienna then analyzes these cues. She reviews Paul’s electronic health record, or EHR, and notes that he’s been to the clinic twice in the past year for similar behavioral difficulties and tested negative for underlying vision, hearing, or cognitive disorders. Nurse Sienna confers wi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Necrotizing_soft_tissue_infections:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VOscAEsnT-qaK3bDGNmrYaNTSSufniha/_.jpg</video:thumbnail_loc><video:title><![CDATA[Necrotizing soft tissue infections: Clinical sciences]]></video:title><video:description><![CDATA[Necrotizing soft tissue infections, or NSTIs, are rapidly progressing infections causing extensive destruction of soft tissues, including the epidermis, dermis, subcutaneous tissues, fascia, and muscle. Because the depth of the infection can vary, NSTIs can present as necrotizing forms of cellulitis, fasciitis, and myositis. 

These infections can occur anywhere in the body and rapidly lead to limb loss, severe systemic toxicity, and even death if left untreated. Of the various types, necrotizing fasciitis is associated with the highest mortality rate because of how quickly it can spread within the body. While the vast majority of NSTIs can be diagnosed clinically, additional tools like a CT scan and LRINEC score can be used to differentiate between NSTI, possible NSTI, and non-necrotizing infections.  

When a patient presents with chief concern suggesting NSTI, your first step is to perform an ABCDE assessment to determine whether the patient is stable or unstable. If the patient is unstable, you must stabilize the airway, breathing, and circulation first. This includes obtaining IV access, initiating IV fluid resuscitation, and continuously monitoring vital signs.

Once you have initiated your acute management, your next step is to perform a focused history and physical exam. History may include severe pain, fever, chills, and foul-smelling discharge. In addition, don’t forget to ask about risk factors for NSTI, such as recent trauma, recent surgery, injection drug use, immunosuppression, or diabetes mellitus. For patients with diabetes, also ask which medications they take, because some types are associated with Fournier’s gangrene, which is necrotizing fasciitis of the perineum. 

On exam, you might see signs of systemic instability such as altered mental status, tachycardia, or hypotension, which can all be attributed to sepsis or septic shock. The exam will also reveal signs of local infection like erythema, edema, and indurated skin or soft ti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lipoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qFtA_-YrRsivQ2fB7J-K8fBWQVuPQT2d/_.png</video:thumbnail_loc><video:title><![CDATA[Lipoma: Clinical sciences]]></video:title><video:description><![CDATA[Lipomas are benign fatty neoplasms that can occur anywhere in the body. While most are solitary, superficial, and limited to the subcutaneous space, some can arise within the deeper soft tissue like the muscle. Sometimes, systemic conditions like lipomatosis can lead to multiple, diffuse or recurrent lipomas. Usually, small and painless lipomas do not require any medical treatment. However, when the mass causes functional or cosmetic dysfunction or is suspicious for malignancy, treatment for removal should be considered. 

Alright, when assessing a patient with a chief concern suggestive of lipoma, your first step is to obtain a focused history and physical examination.  

Most subcutaneous lipomas are asymptomatic, and are noticed incidentally by the patient on inspection or palpation. History will usually reveal a painless, slow-growing, small, soft, and solitary mass found on the trunk or proximal extremities. 

Now, upon a physical exam, you can expect to find a superficial subcutaneous mass that is soft, round, mobile, and well-localized. The mass typically feels doughy with smooth, slippery edges. If these findings are present, you can make your diagnosis of a subcutaneous lipoma. 

Superficial lipomas can be diagnosed clinically, so additional work up is not necessary. Your treatment for superficial lipomas depends on the size. For example, small lipomas often can be managed with observation without any intervention; however, if the mass is large, like greater than 5 cm, or if it causes cosmetic concerns, it can be surgically excised.

Here&amp;#39;s a clinical pearl! Lipomas can occur anywhere in adipose tissue, including the subcutaneous, intramuscular, gastrointestinal tract, and retroperitoneum. For subcutaneous masses, slippage sign is characteristic for lipoma. It can be elicited by gently sliding fingers off the tumor feeling for its slippery edge, or capsule. Keep in mind that lipomas located deeper within the soft tissue might not elicit t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skin_abscess:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h5f1VworQry0Oj0M0zHO4f7TQQ2huIMF/_.png</video:thumbnail_loc><video:title><![CDATA[Skin abscess: Clinical sciences]]></video:title><video:description><![CDATA[A skin abscess is a common skin and soft tissue infection that occurs when a collection of pus accumulates, usually in the dermis or subcutaneous space. An abscess can result from a disruption in the skin barrier or prior skin infection, which allows the bacteria to get into the subcutaneous space. The most common cause of a skin abscess is bacteria, especially Staphylococcus aureus, either methicillin-susceptible or methicillin-resistant. When it comes to presentation, a skin abscess can present with or without systemic symptoms.

Alright, when assessing a patient who presents with signs and symptoms suggestive of a skin abscess, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation first. Next, obtain IV access and initiate IV fluids for resuscitation. 

Here’s a clinical pearl! Keep in mind that most patients with skin abscesses wouldn&amp;#39;t be unstable, and if they are unstable, then they’ve likely developed sepsis or even septic shock. So be sure to evaluate these patients for systemic signs and symptoms like hypotension, fever, and chills.

Now that acute management for unstable patients is initiated, let’s talk about stable patients. If the patient is stable, your first step is to obtain a focused history and physical examination, evaluating the affected area while also looking for associated systemic signs and symptoms  like fevers or chills; along with labs like CBC.

Let’s first look at a patient without systemic signs and symptoms. Your patient might report a small painful, erythematous nodule, with or without spontaneous drainage. On a physical exam, you might see a fluctuant nodule with or without erythema and tenderness. Finally, labs might be normal or show mild leukocytosis. In this case, you can diagnose a skin abscess. Now, since the patient doesn’t have any systemic signs or symptoms, we can refer to it as an absce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Activated_Phosphoinositide_3-Kinase_Delta_Syndrome,_APDS_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vuE1iOHhTTGT25W5vr1MYkZ2THOtqBa_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Activated Phosphoinositide 3-Kinase Delta Syndrome, APDS (NORD)]]></video:title><video:description><![CDATA[Activated Phosphoinositide 3-Kinase Delta Syndrome, also called APDS, is a rare syndrome characterized by the impaired growth, development, and function of lymphocytes. Lymphocytes are immune cells that protect the body from pathogens, like bacteria and viruses. B lymphocytes produce antibodies to fight infections, while T lymphocytes help to attack and destroy infected cells. In APDS, a genetic mutation, also called a pathogenic variant, causes both B and T lymphocytes to malfunction, which may lead to frequent infections, chronic lung disease, enlargement of lymphoid structures, like the lymph nodes, liver, and spleen, and autoimmune disorders. Individuals with APDS are also at an increased risk of malignant lymphoid disorders, like lymphomas.

APDS is caused by a gain-of-function mutation, also called an activating mutation, in the genes that encode phosphoinositide 3-kinase delta, also called PI3Kδ. PI3Kδ is a protein that plays an important role in lymphocyte  proliferation, survival, and activation.  APDS can be divided into two types. Type 1 is caused by a mutation in the PIK3CD gene, while Type 2 is caused by a mutation in the PIK3R1 gene. Both are inherited in an autosomal dominant manner, which means that patients need only one copy of the mutated gene for the disease to develop. The mutated gene can be inherited or occur for the first time in the affected individual.

Signs and symptoms of APDS typically present in early childhood. Although the clinical manifestations vary in range and severity, individuals typically present with frequent ear, sinus upper respiratory, and lung infections.

Individuals with APDS may also have swollen lymph nodes and an oversized liver or spleen. Other clinical findings may include hearing loss, permanent lung disease, chronic diarrhea, fatigue due to autoimmune anemia, easy bruising due to autoimmune thrombocytopenia, and lymphoma or other blood cancers.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Pediatric_Patients_With_Asthma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/caDCxwP3TnGX-n3ogB4ViRAPQgSzycu1/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Pediatric Patients With Asthma]]></video:title><video:description><![CDATA[Nurse Lin works at a primary care clinic and is caring for Joey, an 8-year-old who’s had a cough for two months and mild chest tightness over the last week. In collaboration with the registered nurse, RN Marge, Nurse Lin goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Joey’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

Recognizing and Analyzing Cues First, Nurse Lin recognizes important cues, including Joey’s vital signs which are temperature 98 F or 36.6 C, heart rate 94 beats per minute, respirations 20 breaths per minute, and oxygen saturation 95 percent on room air. Nurse Lin auscultates Joey’s lungs and hears mild wheezes in all lobes upon expiration, which is consistent with RN Marge’s previous assessment.

She gathers additional information from Joey and his aunt, Angel, who’s at the bedside.
Nurse Lin: Hi Joey, could you tell me about how your breathing has been?
Joey: Sometimes my chest feels a little tight and it&amp;#39;s hard to take a deep breath.
Nurse Lin: That must be uncomfortable. When did you start feeling like this?
Joey: I don’t know.

Angel: He’s had a nagging cough for a while now. At first, I thought it was just the change in the weather making his allergies flare up, but his allergies don’t normally affect his breathing. That’s why I made the appointment.
Nurse Lin: It’s good you brought Joey in.

Next, Nurse Lin analyzes these cues. She reviews the electronic health record, or EHR, and notes that Joey has no relevant medical history other than seasonal allergies. She assists Joey to a sitting position while RN Marge performs the ordered spirometry testing by having Joey breathe into a mouthpiece connected to a device that measures how much air he’s able to breathe in and out. They note that Joey can&amp;#39;t expel all the air after taking a deep breath. RN Marge then speaks to the healthcare provider, who diagnoses Joey with asthma.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cornelia_de_Lange_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0gceUX6jTt6r9IxGmEsWMqbIQhiOJJ4W/_.png</video:thumbnail_loc><video:title><![CDATA[Cornelia de Lange syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Cornelia de Lange syndrome: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Pre-existing_Conditions_Impacting_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N-BBz61lRgWbMvxxgapmrT3DRAWHQzOI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Pre-existing Conditions Impacting Pregnancy]]></video:title><video:description><![CDATA[Pre-existing medical conditions are chronic medical problems that are present before pregnancy that can pose a risk to the patient and fetus during pregnancy. These can include diabetes mellitus and heart failure, both of which require special monitoring and treatments to support the health of the patient and developing fetus throughout pregnancy.

Diabetes mellitus is a condition where there&amp;#39;s an excess amount of glucose in the blood, called hyperglycemia. Type 1 diabetes is caused by autoimmune destruction of beta cells in the pancreas that are responsible for producing insulin, a hormone that helps glucose to move into cells. On the other hand, type 2 diabetes is a result of genetic, environmental, and lifestyle factors, that primarily results in insulin resistance, where the body’s cells don’t respond normally to insulin, which impairs their ability to take up glucose from the blood.

Now, during pregnancy, all the nutrients the fetus receives come directly from the mother&amp;#39;s blood through the placenta, and glucose is the primary source of energy needed for growth and development. To ensure there’s a steady supply of glucose for the fetus, hormones released by the placenta increase maternal resistance to insulin, resulting in higher levels of maternal glucose. In patients with pre-existing diabetes, this increases the risk for hyperglycemia.

Complications of hyperglycemia in the mother include an increased risk of an operative delivery, due to a large fetus; preeclampsia; and premature labor; as well as worsening of chronic complications of diabetes like retinopathy, kidney disease, and cardiac disease. In the fetus, excessively high levels of glucose can lead to macrosomia, or a birth weight more than 4000 grams; congenital anomalies; intrauterine growth restriction; delayed lung maturity; birth injuries; and even death.
During pregnancy, treatment of diabetes begins with diet and exercise to control glucose levels, as well as close ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postoperative_Nursing_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PUE026jkRuOz-bE6VeJ_0VulTD20FSvC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postoperative Nursing Care]]></video:title><video:description><![CDATA[Postoperative care involves the management of a patient’s health during the postoperative period, which begins after the surgical procedure is complete and lasts until the patient is discharged from the health care facility. As a nurse, you’ll closely monitor your patient for postoperative complications and intervene as needed.
Now, some of the most common postoperative complications include respiratory complications, hemorrhage, pain, and emotional distress.
Starting with respiratory complications, these can include problems with airway obstruction and gas exchange. First, airway obstruction can result from laryngospasm, or a spasm of the vocal cords, caused by laryngeal irritation from intubation. This can narrow your patient’s airway and obstruct the flow of air into the lungs.
Then, gas exchange can be impaired due to the effects of anesthesia, because it reduces surfactant production in the lungs, which is needed to keep the air sacs, called alveoli, open and full of air. When there’s less surfactant, the walls of the alveoli tend to collapse, leading to atelectasis, where portions of the lungs are not fully expanded. Likewise, anesthesia tends to depress respirations, causing hypoventilation, resulting in the buildup of carbon dioxide, a decrease in oxygen, and hypoxemia, or low blood oxygen levels.

Next, hemorrhage can occur when blood is lost at or around the surgical site either internally or externally due to incomplete hemostasis, or clotting. Now, although some blood loss is expected during surgery, hemorrhagic blood loss typically means that at least 15 percent, or 750 milliliters of total blood volume is lost. Excessive blood loss can lead to hypotension, impaired perfusion, and hypovolemic shock.
Then there’s postoperative pain, which is typically related to the disruption of tissue integrity caused by the surgical procedure or by improper body alignment during the surgical procedure. Now, pain is an expected finding after surgery but uncon]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sanfilippo_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IkR9eo6GRgqNDWK6p41vBr4RQ7i3uETk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sanfilippo syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Sanfilippo syndrome: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypertension:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h7UPThW0RIeya65PlHpy27s1RzmD1wmM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypertension: Clinical sciences]]></video:title><video:description><![CDATA[Hypertension is defined as a systolic blood pressure greater than or equal to 130 millimeters of mercury, or a diastolic blood pressure greater than or equal to 80 millimeters of mercury, that’s measured on two separate occasions. Most cases of hypertension are primary or essential, meaning there’s no identifiable underlying cause. However, in some cases, hypertension can be secondary to an underlying cause, such as certain medications, renal, endocrine, or cardiovascular conditions, and sleep-disordered breathing.

Now, if you suspect hypertension, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen.

Now here’s a high-yield fact to keep in mind!  A hypertensive crisis occurs when the systolic pressure is above 180, or the diastolic pressure is above 120 millimeters of mercury. Now, the term hypertensive crisis includes both hypertensive emergency and hypertensive urgency. The difference between the two is that hypertensive emergency is associated with symptoms of imminent end-organ damage, such as stroke, retinal hemorrhage, papilledema, myocardial infarction, or acute kidney injury To prevent end-organ damage, you must immediately treat your patient with an IV antihypertensive, such as nitroprusside, to lower the blood pressure, but making sure it doesn’t exceed a 10 to 20% decrease over the first hour, and then gradually over 24 hours, in order to avoid cerebral and myocardial hypoperfusion. 

On the other hand, hypertensive urgency may present with symptoms like headache or chest pain, but is not associated with end-organ damage yet, although it also poses serious risk! For treatment here, you can give an oral antihypertensive, such as a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_anemia_(underproduction):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cgJAYSJsSqStS5qv4No8Lun9TJ_xizDa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to anemia (underproduction): Clinical sciences]]></video:title><video:description><![CDATA[Anemia is a condition characterized by a decrease in healthy red blood cells, indicated by low levels of hemoglobin and hematocrit or red blood cell count. Anemia can be caused by red blood cell sequestration, destruction, or underproduction of red blood cells. 

Now, if you suspect anemia, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. 

If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, give IV fluids, and if necessary, consider blood products, such as packed red blood cells. If needed, provide supplemental oxygen, and don’t forget to put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry.

Now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and look at the stable ones. 

In this case, obtain a focused history and physical examination, and order labs, including CBC with indices, and a reticulocyte count. 

The history could reveal fatigue, malaise, palpitations, and dyspnea; while physical exam might show tachycardia and conjunctival pallor. 

However, these findings are non-specific, so you need to check labs. If the labs reveal low hemoglobin and hematocrit, only then can you diagnose anemia. 

Here’s a clinical pearl! After confirming that your patient has anemia, you need to find what’s causing it by looking at additional clues in the lab results. Here, our approach is based on assessing reticulocyte count first, followed by the MCV; some people instead start from the MCV. Both approaches are valid! The important thing is to use a reliable approach that will make sure you consider all the appropriate causes and help you narrow your differential. 

So let’s assess the reticulocyte count. Reticulocytes are young red blood cells, and if their count is above the reference range, it suggests that the body is actively producing new red]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Uremic_encephalopathy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hN4xLV4iSvKNevZD8xFqm177Q8mp7cxU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Uremic encephalopathy: Clinical sciences]]></video:title><video:description><![CDATA[Uremic encephalopathy is a metabolic disorder characterized by progressive neurological dysfunction. Now, this typically occurs in the setting of acute kidney injury or AKI, progression of chronic kidney disease or CKD, or under dialysis.

Normally, the kidneys are in charge of cleaning our bodies by excreting toxins like urea into the urine. If our kidneys don’t function properly, these toxins can accumulate in the blood and eventually in the central nervous system, leading to progressive dysfunction, which can present with a wide range of neurologic symptoms, ranging from mild confusion and altered mental status to even coma.

Now, if your patient presents with a chief concern suggesting uremic encephalopathy, you should first perform an ABCDE assessment to determine if they are unstable or stable. Patients with uremic encephalopathy generally present as unstable, so immediately begin acute management! Stabilize the airway, breathing, and circulation. This means you might need to intubate the patient. Next, obtain IV access, and if your patient does not already have dialysis access, you’ll need to emergently place a dialysis catheter as well. Also, don’t forget to put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen.

Okay, now that you’ve stabilized your patient, let’s look at your next step. 

Start with obtaining a focused history and physical examination. You should also order labs like CMP and ABG, as well as a 12-lead ECG, and a chest X-ray. 

The history will typically reveal mental status changes like confusion and lethargy, as well as other symptoms of uremia, such as muscle cramps and itching. Additionally, the physical exam may reveal disorientation, impaired attention, and even hallucinations, but also tremor and asterixis. In extreme cases, your patient might experience seizures or even a coma.

On the flip ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_cough_(acute):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V2g4x3YuQt24K0uQapWj9AmNSLOecW_9/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to a cough (acute): Clinical sciences]]></video:title><video:description><![CDATA[Coughing is a protective physiologic response that facilitates the clearing of excessive secretions and debris from the airways. The distinction between acute, subacute, and chronic cough is based on duration. An acute cough lasts less than three weeks, while a chronic cough lasts for more than eight weeks, and a subacute cough lies in between.  

Most commonly, acute cough is due to an upper respiratory infection. If not, an abnormal chest X-ray is usually seen in pneumonia, bronchiectasis exacerbation, and congestive heart failure, whereas a normal chest X-ray is typically seen in acute bronchitis, pulmonary embolism, asthma exacerbation, and COPD exacerbation.  

Okay, if your patient presents with an acute cough, you should first perform an ABCDE assessment to determine whether your patient is unstable or stable. 

If they’re unstable, stabilize their airway, breathing, and circulation, which might require intubation and mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen!   

Now, here’s a clinical pearl! Even in stable patients, always evaluate patients with an acute cough for features like abnormal vital signs, symptoms of serious diseases like pulmonary embolism or pneumonia, and risk factors for serious diseases like lung cancer, which will require a different approach than patients without these features.  

Alright, now that we’ve addressed unstable patients, let’s go back to the ABCDE assessment and discuss stable ones.  

If your patient is stable, perform a focused history and physical examination. Your patient will report a cough lasting less than three weeks, which might be accompanied by sputum production, chest pain, and shortness of breath. They can also have a history of tobacco use, as well as known pulmonary conditions like asthma or COPD. 

Additionally, the phy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_cough_(subacute_and_chronic):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1IXKI5bqQQ6GsDDjphptYeBzRDyNww92/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to a cough (subacute and chronic): Clinical sciences]]></video:title><video:description><![CDATA[Coughing is a protective physiologic response that facilitates the clearing of secretions and debris from the airways of the lungs. The distinction between acute, subacute, and chronic cough is based on duration. An acute cough lasts less than three weeks, while a subacute cough lasts for three to eight weeks, and a chronic cough lasts more than eight weeks.  

For subacute or chronic coughs, an abnormal chest X-ray is usually seen in atypical pneumonia, bronchiectasis, lung cancer, and interstitial lung disease. On the flip side, a normal chest X-ray is typically seen in gastroesophageal reflux disease, non-asthmatic eosinophilic bronchitis, upper airway cough syndrome, asthma, and chronic obstructive pulmonary disease.   

Now, if your patient presents with a subacute or chronic cough, first perform a focused history and physical examination. Your patient will report a cough lasting at least three weeks and perhaps eight weeks or more, which might be accompanied by shortness of breath. They may also have a history of tobacco use, as well as known pulmonary conditions, like asthma or COPD. Additionally, the physical exam might reveal labored breathing and adventitious breath sounds such as wheezing or rales. With these clinical findings, diagnose subacute or chronic cough! 

Here’s a high yield fact! One of the most common non-disease related causes of cough is ACE inhibitor-induced cough. Individuals who are taking ACE inhibitors for hypertension or heart disease can develop a dry and hacking cough that typically occurs in 1 to 2 weeks after starting the medication; but in some cases, it might occur after 6 months! This is likely due to the accumulation of bradykinin and it typically resolves within a few days of stopping the medication. 

Alright, once you diagnose subacute or chronic cough, your next step is to obtain a chest X-ray! If your patient’s chest X-ray is abnormal, meaning there’s radiographic evidence of airway or lung involvement, your]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Carotid_artery_stenosis_screening:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ROOIZbJLQ7_aD_aw23WQPZVbRoG82yvr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Carotid artery stenosis screening: Clinical sciences]]></video:title><video:description><![CDATA[Carotid artery stenosis is defined as the narrowing of one or both of the internal carotid arteries most commonly due to atherosclerotic build-up in the vessels. Because this build-up takes years, the prevalence of carotid artery stenosis increases with age. Patients can be asymptomatic for years before the stenosis becomes so severe that it leads to symptoms and complications. The most significant complication of carotid artery stenosis is ischemic stroke. That is why patients who have carotid artery stenosis need to undergo aggressive medical or surgical therapy in order to prevent the progression of the disease and complications.

Alright, when your patient presents for carotid artery stenosis screening, the initial step will be to assess any risk factors. The big ones would be a personal history of atherosclerotic disease, such as peripheral arterial disease or coronary artery disease. If your patient has any of these risk factors, then they are considered at high risk for developing carotid artery stenosis. Other risk factors also include hypertension, hyperlipidemia, tobacco use, a family history of atherosclerosis diagnosed before age 60, as well as a family history of ischemic stroke. If two or more of these risk factors are present, then your patient is also considered at high risk for developing carotid artery stenosis. 

If your patient does not have any of the risk factors mentioned previously, then they are considered to be at low risk for developing carotid artery stenosis, and no routine screening is recommended. One thing to keep in mind is that even though these patients may not need to have any routine screening for carotid artery stenosis, they should still be re-evaluated for any new diagnoses such as hypertension or hyperlipidemia during their regular check-ups with their primary care provider as they might become high-risk over time.

Let’s look at what to do depending on what risk factors are present. (On the other hand,) So, if]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peripheral_arterial_disease_and_ulcers:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tUJNW3F5Rpq40yXDBrMV2QycRmuQmiZ9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Peripheral arterial disease and ulcers: Clinical sciences]]></video:title><video:description><![CDATA[Peripheral arterial disease, also known as PAD, is when an extremity, typically the lower limb, does not receive enough blood supply to meet the needs of its tissues. It’s often caused by chronic narrowing of the artery’s luminal diameter, simply known as stenosis, due to atherosclerosis, inflammation, or trauma. Over time, the stenosis decreases the blood supply to the tissue, which can lead to the formation of ischemic ulcers at distal zones of the affected arteries, like the toes. 

A more severe form of PAD is called chronic limb-threatening ischemia, or CLTI for short. Keep in mind that CLTI is sometimes called critical limb ischemia, so if you hear that name, don’t be confused. 

Alright, your first step in assessing a patient with a chief concern suggesting PAD or an ulcer is to perform a focused history and physical exam. On history, patients typically report intermittent claudication, which is a crampy pain in the calves when walking, and sometimes even pain at rest if the patient progresses to CTLI. You can expect patients to have some underlying comorbidities or risk factors, such as a history of smoking, hypertension, diabetes mellitus, hyperlipidemia, or chronic kidney disease. 

Common physical exam findings include cool lower extremities with trophic changes like hair loss, as well as absent or reduced distal pulses, and abnormal capillary refill. 

An important part of performing a vascular physical exam is to thoroughly assess for pulses. If you’re unable to palpate a pulse, use a handheld Doppler to listen for a signal. Sometimes you might hear Doppler signals for a pulse that’s not palpable. Make sure to examine proximal vessels like the femoral or popliteal arteries, as well as distal vessels, such as the anterior or posterior tibial arteries. When examining vessels, don’t forget to compare them bilaterally. Next, if you auscultate the femoral artery, you might hear a bruit, which is a sign of a turbulent blood flow in the vessel due to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypothyroidism:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6mqZOjpoRpqkQGYyYE4E5_gKS6C4Q0K2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypothyroidism: Clinical sciences]]></video:title><video:description><![CDATA[Hypothyroidism refers to low thyroid hormone levels, which leads to a reduction of the basal metabolic rate. Patients with hypothyroidism present with a wide spectrum of signs and symptoms which can range from subclinical disease to a life-threatening condition called myxedema coma.  

The diagnostic workup for hypothyroidism mainly involves checking thyroid-stimulating hormone, or TSH level, and free thyroxine, or free T4 level, to determine the cause of hypothyroidism.  

Now, if your patient presents with chief concerns suggesting hypothyroidism, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen. 

Now, here’s a clinical pearl to keep in mind! If your patient presents with hypothermia, bradycardia, hypoventilation, and lethargy, you should suspect myxedema coma, which is a severe, life-threatening form of hypothyroidism.  

Myxedema coma typically occurs later in patients with long-standing hypothyroidism. Treatment consists of supportive care, which in some patients means ventilatory or circulatory support, as well as corticosteroids, and thyroid hormone and electrolyte replacement. Any underlying precipitant such as an infection or heart failure should be identified and treated as well.  

Alright, now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones.  

First, obtain a focused history and physical examination. Your patient will likely report symptoms suggesting a low basal metabolic rate and sympathetic activity, including atigue, weight gain, and cold intolerance. In addition, constipation is common, and patients may develop depression,  hair loss, an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PWqqMPFoTHOQkBW19c79wTpxS3GiK_Up/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal cancer: Clinical sciences]]></video:title><video:description><![CDATA[Esophageal cancer is a malignant tumor of the esophagus or esophagogastric junction. Two main pathologic types of esophageal cancer include squamous cell carcinoma and adenocarcinoma. Esophageal cancer is associated with high morbidity and mortality as more than 50% of patients present with advanced disease. However, even with early diagnosis and treatment, esophageal cancers have very poor long-term outcomes. 

When a patient presents with chief concern suggestive of esophageal cancer, the first step is to obtain a focused history and physical, and labs including CBC and CMP. Although most patients are asymptomatic, some might report dysphagia, odynophagia, epigastric or retrosternal pain, regurgitation of food or saliva, cough, and hoarseness. They might also have associated anemia or weight loss. 

Additionally, history might reveal risk factors, such as tobacco or alcohol use, high BMI, gastroesophageal reflux disease or Barrett&amp;#39;s esophagus, as well as a family history of esophageal cancer, or genetic conditions like Fanconi Anemia or Bloom Syndrome. 

The physical exam is typically unremarkable, but might reveal cachexia, and sometimes lymphadenopathy and hepatomegaly if the disease has metastasized. Finally, labs typically show anemia, electrolyte abnormalities, or elevated liver enzymes. So, if you see these findings, suspect esophageal cancer.

Your next step is to obtain imaging. The first choice is an upper endoscopy with biopsy and an endoscopic ultrasound with fine-needle aspiration if there are any suspicious lymph nodes. However, bronchoscopy can be performed if you suspect a tumor above the carina. 

Endoscopy allows us to see macroscopic features, such as strictures, ulcerations, or an exophytic, fungating, or circumferential mass. Biopsy of these suspicious features will likely show invasive adenocarcinoma or squamous cell carcinoma, also known as SCC.

Here’s a clinical pearl! Imaging can be done, where upper GI fluoroscopy can s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hyperthyroidism_and_thyrotoxicosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/39Ddp5pmSRiCYgd-MgynEc6pQgyEBifr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hyperthyroidism and thyrotoxicosis: Clinical sciences]]></video:title><video:description><![CDATA[Hyperthyroidism refers to any condition in which thyroid hormone levels are inappropriately high, which increases the basal metabolic rate and potential thyroid hormone toxicity. Patients with hyperthyroidism present with a wide spectrum of signs and symptoms, which can range from subclinical disease to severe life-threatening conditions, like thyrotoxicosis. The diagnostic workup for hyperthyroidism mainly involves checking a thyroid-stimulating hormone, or TSH level, and a free thyroxine, or free T4 level, to determine whether your patient has primary, secondary, or subclinical hyperthyroidism.

Now, if your patient presents with chief concerns suggesting hyperthyroidism or thyrotoxicosis, you should first perform an ABCDE assessment to determine if your patient is unstable. If  unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Additionally, provide supplemental oxygen if the saturation is below 90%.

If your patient presents with fever, tachycardia, delirium, or coma, you should suspect thyrotoxic crisis, also called thyroid storm. This is a severe, life-threatening presentation that typically occurs in patients with untreated or undertreated hyperthyroidism, and it’s triggered by an inciting event, such as major illness or surgery. 

Treatment includes the four Ps: Propranolol or other beta-blockers, Propylthiouracil, Prednisolone or other glucocorticoids, and Potassium iodide. These patients need close monitoring, and may require intensive measures such as volume resuscitation and whole-body cooling.

Alright, now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. First, obtain a focused history and physical examination. Your patient will likely report symptoms suggesting a high basal metabolic rate and sympathe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_endocrine_neoplasia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6MDdJ4QFQjW96wzvrywJxPjATlG-YFAo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple endocrine neoplasia: Clinical sciences]]></video:title><video:description><![CDATA[Multiple endocrine neoplasia, or MEN, is a group of rare inherited conditions where tumors develop in multiple endocrine glands. These conditions can be associated with serious complications caused by excess hormone production. Based on the affected endocrine glands, MEN can be further subdivided into MEN1, MEN2A, and MEN2B.

Now, if your patient presents with chief concerns suggesting MEN, you should first perform an ABCDE assessment to determine if they are unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen.

Now, let’s go back to the ABCDE assessment and discuss stable patients. In this case, you should first perform a focused history and physical exam.

Alright, let’s start with MEN1! These individuals typically report a personal or family history of parathyroid, pituitary and gastro-entero-pancreatic tumors. Parathyroid tumors can cause hypercalcemia, so your patient might report symptoms, such as bone or abdominal pain, as well as a history of kidney stones or low-impact fractures. On the other hand, pituitary tumors can cause vision changes and headaches, while gastroenteropancreatic tumors can cause gastric ulcers, diarrhea, as well as hyper- or hypoglycemia. 

Here’s a clinical pearl! Gastro-entero-pancreatic tumors arise from neuroendocrine cells of the pancreas and small intestine, and can cause various manifestations, depending on the hormone secreted. 

For example, gastrinomas can arise either in the small intestine or the pancreas, and they secrete excess gastrin, which stimulates gastric acid production. This causes Zollinger-Ellison syndrome, a condition characterized by recurrent peptic ulcers. 

On the other hand, insulinomas secrete insulin, which can lead to hypoglycemia; while glucagonomas secrete glucago]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pheochromocytoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e8lM428PTNyrYXYNWkk3BeL-Q9KDgOWV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pheochromocytoma: Clinical sciences]]></video:title><video:description><![CDATA[A pheochromocytoma is a neuroendocrine tumor that develops from chromaffin cells. These cells are part of the sympathetic nervous system, so they secrete excessive catecholamines, such as norepinephrine and epinephrine, which causes severe hypertension.  

The majority of pheochromocytomas develop in the adrenal gland; however, extra-adrenal pheochromocytomas, also called paragangliomas, can develop in other locations, such as the thorax, abdomen and pelvis.  

Pheochromocytomas are commonly linked to genetic conditions like multiple endocrine neoplasia type 2, neurofibromatosis type 1, and Von Hippel-Lindau disease; but they can also occur sporadically in patients without a genetic condition. 

Now, if your patient presents with chief concerns suggesting pheochromocytoma, you should first perform an ABCDE assessment to determine if they are unstable or stable.  

If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen. 

Now here’s a high-yield fact! Patients with pheochromocytoma classically present with paroxysmal hypertension. When systolic blood pressure is above 180, or diastolic blood pressure is above 120 millimeters of mercury, that’s called a hypertensive crisis, which can lead to end-organ damage like heart failure, pulmonary edema, and intracranial hemorrhage.  

So urgent treatment with an intravenous anti-hypertensive, such as nitroprusside, is essential. Keep in mind that blood pressure should be lowered gradually, over a 24-hour period, to avoid cerebral and myocardial hypoperfusion.   

Alright, now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones.  

First, obtain a focused history and physical examination. Classically, patients with pheochromocytomas report ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Primary_aldosteronism_(hyperaldosteronism):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JDJOk7mrRbKf57k9bT6729XCT6G8FjCO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Primary aldosteronism (hyperaldosteronism): Clinical sciences]]></video:title><video:description><![CDATA[Primary aldosteronism, also known as primary hyperaldosteronism or Conn syndrome, is a condition in which the adrenal glands produce an excessive amount of aldosterone. These individuals typically present with hypertension that is refractory to medical management. Now, the most common causes of primary aldosteronism include adrenal adenomas, idiopathic hyperaldosteronism, as well as a genetic condition called familial hyperaldosteronism.

Now, if your patient presents with a chief concern suggesting primary aldosteronism, first, you should perform an ABCDE assessment to determine if your patient is unstable or stable. 

If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen.

Now here’s a high-yield fact to keep in mind! A patient with primary aldosteronism can present with a hypertensive crisis, which occurs when the systolic pressure is above 180 or the diastolic pressure is above 120. 

Blood pressure this high puts patients at risk for organ damage, such as acute myocardial infarction, acute renal failure, and intracranial hemorrhage. 

Moreover, if there’s evidence of end-organ damage, the hypertensive crisis is often referred to as a hypertensive emergency. On the flip side, the hypertensive crisis in the absence of end-organ damage is sometimes referred to as hypertensive urgency. 

In both cases, your patient requires immediate treatment with an IV antihypertensive, such as nitroprusside, with the goal of gradually lowering blood pressure over 24 hours. This way you are minimizing the risk of rapid drops in perfusion to vital organs and subsequent ischemic injuries.

Now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. First, obtain a focused history and physic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_nodules:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lvrwtYu1TBOwV0V0mmQQOwDxR2_CbKfu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid nodules: Clinical sciences]]></video:title><video:description><![CDATA[Thyroid nodules are discrete, solid, or fluid-filled lumps in the thyroid gland, often found incidentally on exam or imaging. Thyroid nodules are common and usually benign, though some can be malignant. When evaluating a thyroid nodule, you will want to determine if the patient has thyroid dysfunction and obtain a thyroid ultrasound. Patients who are hypothyroid or euthyroid require further work up based on concerning features on ultrasonography, while patients who are hyperthyroid will require a radioactive iodine uptake or RAIU test. 

Alright, when a patient presents with chief concern suggesting thyroid nodule, you should first perform a focused history and physical examination. Most patients with thyroid nodules are asymptomatic and the nodule is found on a routine exam or incidentally on imaging. If the patient does have symptoms, they may have signs of hyperthyroidism, such as tachycardia, weight loss, muscle weakness, heat intolerance, anxiety, or irritability; or signs of hypothyroidism like dry skin, depression, cold intolerance, fatigue, and constipation. Very rarely, if the nodule is large enough, it can put pressure on surrounding structures and cause symptoms, like a feeling of fullness in the throat or difficulty swallowing.

You should also assess for personal or family history of syndromes that increase the risk of developing cancer. This includes Cowden disease; familial adenomatous polyposis or FAP; multiple endocrine neoplasia or MEN II; Carney complex; or Werner syndrome, also called progeria. 

Meanwhile, on physical examination, you may feel the nodule as a palpable mass at the front of the neck, over the thyroid. Remember, the thyroid moves upward when the patient swallows, so if the nodule you feel also moves upward, you know it is part of the thyroid. If the nodule doesn’t move upward with swallowing, then it’s another type of neck mass. Now, in some cases, you may feel more than one nodule, what’s known as a multinodular thyroid,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_fatigue:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/a-S67bf4RXKbgF9SpgLthNC8Qf600Xq8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to fatigue: Clinical sciences]]></video:title><video:description><![CDATA[Fatigue is the feeling of being mentally or physically exhausted. People experiencing fatigue may describe feeling tired, lacking energy, or being unable to carry out their usual daily tasks. 

Fatigue can be caused by various conditions, which can be classified into four main groups. The first group covers conditions associated with fatigue and muscle weakness, such as hypercalcemia, hypokalemia, and neuromuscular conditions. The second one includes exertion-related fatigue, like cardiovascular and pulmonary disease. The third group covers conditions characterized by fatigue and excessive daytime sleepiness, like obstructive sleep apnea. Finally, the fourth group includes conditions characterized by generalized tiredness, like hypothyroidism, infections, depression, and myalgic encephalomyelitis.

When approaching a patient that presents with fatigue, start with a focused history and physical examination. Next, assess if your patient presents with muscle weakness. If there’s muscle weakness, your next step is to order labs, including BMP and calcium. 

Let’s get started! If your patient has a history of constipation, anorexia, nausea, nephrolithiasis, bone pain, and confusion or lethargy, it&amp;#39;s a classic presentation of hypercalcemia. This symptom combination is often summarized as  &amp;#39;groans, stones, bones, thrones, and psychiatric overtones&amp;#39;. In such cases, labs reveal a serum calcium level higher than 10.5, confirming the diagnosis.

On the other hand, your patients may report muscle cramps and palpitations. Additionally, there might be a history of chronic diarrhea or use of diuretics or laxatives. If labs reveal a serum potassium lower than 3.5, you can make a diagnosis of hypokalemia.

Here’s a clinical pearl! Mild hypokalemia is often asymptomatic, and can be easily corrected by giving oral potassium. However, severe hypokalemia, which occurs when potassium levels drop below 2.5, can lead to neuromuscular weakness and cardia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoporosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qryobXEYR8yjoBn8ZffS-S6bRL2_Zfxt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteoporosis: Clinical sciences]]></video:title><video:description><![CDATA[Osteoporosis is a metabolic bone disease characterized by low bone density, decreased bone mass, and increased risk of fracture. 

Osteoporosis can be either primary or secondary. Primary osteoporosis is more common in postmenopausal patients, and it refers to bone loss that occurs with aging due to low levels of sex hormones, namely estrogen. Low estrogen levels cause increased osteoclastic activity, and since osteoclasts break down bone, this means increased bone resorption and, as a consequence, low bone density. 

Secondary osteoporosis, on the other hand, occurs because of an underlying cause, typically a medical condition, like rheumatoid arthritis, or a side effect of medications like glucocorticoids, especially when used for long periods of time. Osteoporosis is typically diagnosed using a dual-energy X-ray absorptiometry or DXA scan, and sometimes a FRAX score.

Now, most patients with osteoporosis are asymptomatic, so perform a focused history and physical exam. When obtaining history, important risk factors include being postmenopausal, fracture history without major trauma, low BMI less than 20 kg/m2, osteopenia on imaging, a family history of osteoporosis or parental hip fracture, a history of smoking or  excessive alcohol use, as well as medical conditions like rheumatoid arthritis, or the use of medications like long-term glucocorticoids. 

Finally, regardless of risk factors, you should screen all biological females over 65, biological males over 70, and individuals who are 5 years postmenopause for osteoporosis. Additionally, physical exam findings might reveal skeletal deformities, such as kyphosis or loss of height. 

Ok, now, if you suspect osteoporosis based on the patient’s risk factors and physical exam, the next step is ordering a DXA scan, which tests a patient’s bone mineral density. A DXA scan is typically performed at the hip and lumbar spine level. In patients with either known or suspected hyperparathyroidism a DXA scan o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hashimoto_thyroiditis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1JS87MdpSauOVd3FeGnS-kHvQheTBuyA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hashimoto thyroiditis: Clinical sciences]]></video:title><video:description><![CDATA[Hashimoto thyroiditis, also known as chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis, is the most common cause of primary hypothyroidism in countries that fortify food with iodine.  

In Hashimoto thyroiditis, the immune system produces antithyroid antibodies, such as anti-thyroid peroxidase and anti-thyroglobulin, that destroy thyroid cells, eventually reducing thyroid hormone production and causing hypothyroidism.  

In fact, the presence of either of these autoantibodies confirms the diagnosis of Hashimoto thyroiditis!  

Now, if your patient presents with a chief concern suggesting Hashimoto thyroiditis, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.  

If the patient is unstable, stabilize the airway, breathing, and circulation. Some patients might even require intubation and mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, pulse oximetry, as well as cardiac telemetry. Finally, if needed, don’t forget to provide supplemental oxygen. 

Now, here are some high-yield facts to keep in mind! If your patient presents with hypothermia, bradycardia, hypoventilation, and lethargy, you should suspect myxedema coma, which is a severe, life-threatening form of hypothyroidism.  

Myxedema coma typically occurs later in the disease course of Hashimoto thyroiditis, when long-term thyroid damage results in profound hypothyroidism.  

Treatment consists of supportive care, which in some patients means ventilatory or circulatory support, as well as corticosteroids, and thyroid hormone and electrolyte replacement. Any underlying precipitant such as an infection should be identified and treated as well.  

On the flip side, some patients with Hashimoto can initially present with tachycardia, heat intolerance, sweating, increased appetite and weight loss. In this case, you should suspect Hashitoxicosis, whic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thyroid_carcinoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xCzItoIrR2_KgQS8cubaPZquSve_6aP7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Thyroid carcinoma: Clinical sciences]]></video:title><video:description><![CDATA[Thyroid carcinoma is a malignant degeneration of either follicular or C-cells of the thyroid. The vast majority of thyroid cancers are differentiated tumors, including papillary, follicular, and oncocytic carcinoma, formerly known as Hurthle cell carcinoma. These differentiated tumors carry a good prognosis. Medullary carcinoma of the C-cells, which produce calcitonin, is more aggressive, while undifferentiated tumors called anaplastic carcinoma have the worst prognosis.

Let’s talk about the first steps to assessing a patient. When assessing a patient with chief concern suggesting thyroid carcinoma, your first step is to obtain a focused history and physical exam. Your patient could be asymptomatic, and in fact might be presenting because a thyroid mass was found incidentally on a physical exam or on imaging done for another reason. 

If your patient is symptomatic, symptoms may include hoarseness or difficulty swallowing, especially if there&amp;#39;s a mass effect from the tumor compressing the recurrent laryngeal nerve or the esophagus. In some cases, the tumor can even compress on the trachea, leading to stridor. 

You should also ask your patient about risk factors that increase the likelihood of thyroid carcinoma. These include biological sex, as it’s more likely to occur in women, but aggressive tumors are more likely to occur in men. Thyroid carcinoma also presents in a bimodal age distribution, often in patients who are younger than 20 or older than 60 years. Finally, papillary thyroid cancer is associated with childhood neck irradiation.

Physical exam typically demonstrates a painless neck mass that might be firm, fixed, and asymmetric in shape. You should also examine the neck for lymph nodes, as they help later with cancer staging. 

Alright, your next step is to assess thyroid function with a TSH. If the TSH is below reference range, the patient has hyperthyroidism, and you should consider an alternative diagnosis. If the TSH is normal or a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypercalcemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QR353GUIRAyqmDa88m9bhrcsQK6-tiec/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypercalcemia: Clinical sciences]]></video:title><video:description><![CDATA[Hypercalcemia refers to a serum calcium level above the upper limit of normal, which varies among different labs but is often considered greater than 10.5 mg/dL. Calcium plays a vital role in various body functions, such as myocardial contractility and nerve signaling. So, calcium imbalances, such as hypercalcemia, can result in cardiac and neurologic dysfunction. Some important causes of hypercalcemia that you should keep in mind include medications, malignancy, as well as different endocrine conditions like hyperparathyroidism or hyperthyroidism.

Now, if your patient presents with a chief concern suggesting hypercalcemia, you should first perform an ABCDE assessment to determine if your patient is unstable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen.

Now, here’s a high-yield fact to keep in mind! Patients with severe or rapidly progressing hypercalcemia can present with lethargy, stupor, or even coma. Additionally, an ECG may reveal bradycardia, atrioventricular block, or a shortened QT interval. In this case, you should normalize calcium levels by starting intravenous hydration, as well as diuretics like furosemide or bisphosphonates like zoledronic acid.

Now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. First, obtain a focused history and physical examination, and obtain labs to check their serum calcium levels. Your patient may report personality and mood changes, as well as trouble concentrating, and even altered mental status. They might also experience gastrointestinal issues, such as abdominal pain, nausea, anorexia, and constipation. Additionally, history might reveal musculoskeletal pain; renal symptoms like pol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Empyema:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XAdqkZu8TVWJaGz1QvcOaXeERhyQa8AS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Empyema: Clinical sciences]]></video:title><video:description><![CDATA[Empyema is a collection of purulent fluid within the pleural cavity but outside of the lung. This occurs when there is inoculation of bacteria or other microorganisms within the pleural space leading to the development of frank pus. Pneumonia is the most common cause of empyema, but it can result from blunt or penetrating chest trauma, esophageal rupture, hematogenous seeding of infection, or mediastinitis. 

Empyema goes through three stages: exudative, fibrinopurulent, and organizing. In the exudative stage, fluid accumulates in the pleural space. Next, in the fibrinopurulent stage, invasion of bacteria activates the immune response that leads to septations. After a few weeks, the organizing stage occurs. In this stage, there is a formation of a thick connective tissue on both pleural surfaces that prevents the lung from fully expanding. This is known as pleural rind or peel. Empyema can quickly progress to a systemic infection so it should be diagnosed and treated promptly.

When a patient presents with a chief concern suggesting empyema, your first step is to perform an ABCDE assessment to determine whether the patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Consider intubation for patients with signs of impending acute respiratory failure. Then, obtain IV access and initiate IV fluids for resuscitation, while continuously monitoring vital signs like pulse oximetry, blood pressure, and heart rate.

Once you have initiated the acute management, your next step is to obtain a focused physical examination and order labs including CBC, CMP, CRP, and albumin. On history, patients typically report symptoms of severe infection, such as fever, chills, malaise, loss of appetite, and weight loss. Be sure to ask about any symptoms they had prior, since empyema takes time to develop. They might report respiratory symptoms in the previous weeks or even months like cough, pleuritic chest pain, and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tuberculosis_(pulmonary):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2MhwQY-sS4SpTEyNOmsBr6iVQ-SuSXmG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tuberculosis (pulmonary): Clinical sciences]]></video:title><video:description><![CDATA[Pulmonary tuberculosis, or pulmonary TB, is an infectious disease of the lungs caused by Mycobacterium tuberculosis. Primary infection with M. tuberculosis in adults is usually asymptomatic and followed by a latent phase, which, in some cases, can progress to active pulmonary tuberculosis, also called reactivation or post-primary tuberculosis.  

The gold standard for diagnosing pulmonary tuberculosis is mycobacterial culture, but preliminary diagnosis can be made with acid-fast bacilli smear and rapid nucleic acid amplification testing. 

Diagnostic testing should also include drug susceptibility testing, to identify cases of multi- and extensively-drug resistant tuberculosis. 

Now, if you suspect pulmonary TB, first, you should perform an ABCDE assessment to determine if your patient is unstable or stable.  If the patient is unstable, stabilize their airway, breathing, and circulation, which might require intubation. Additionally, obtain IV access, administer supplemental oxygen, and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry.

Now, let’s go back to the ABCDE assessment and take a look at the stable patients. In this case, perform a focused history and physical examination and get a chest x-ray. 

History typically reveals respiratory involvement, such as chronic cough and hemoptysis, but also systemic symptoms, like unintentional weight loss, anorexia, fever, and night sweats. 

Additionally, the individual might present with risk factors for exposure to tuberculosis, such as living in a facility like a nursing home, homeless shelter, or correctional facility; having a family member or close contact with tuberculosis; or spending time in a country with a high prevalence of TB. 

Also, the patient could report risk factors for developing active tuberculosis, like being immunocompromised due to HIV, malignancy, or immunosuppressive therapy. 

Now, here’s one clinical pearl to keep in min]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alcohol_withdrawal:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rt3QBHGeR1im6HZey7w5gTf9Rz6iE274/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alcohol withdrawal: Clinical sciences]]></video:title><video:description><![CDATA[Alcohol withdrawal refers to symptoms that develop when a person with a history of heavy alcohol use either significantly reduces their alcohol intake or stops drinking entirely. Now, remember that alcohol depresses the central nervous system, meaning that it has an inhibitory effect that slows down brain activity. Thus, if alcohol intake drops after long term use, that inhibitory effect is removed. As a result, the patient will experience hyperexcitability and hyperactivity of the central nervous system.  

If your patient presents with a chief concern suggesting alcohol withdrawal, you should first perform an ABCDE assessment to determine if they are unstable.  

If they are unstable, stabilize their airway, breathing, and circulation. This means you might need to intubate the patient. Next, obtain IV access, and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry. Finally, don’t forget to start pharmacologic therapy with benzodiazepines to prevent severe complications of alcohol withdrawal, such as delirium tremens, seizures, and even death.  

Now that we are done with unstable patients, let’s go back to the ABCDE assessment and take a look at stable individuals.  

If the patient is stable, obtain a focused history and physical examination, and don’t forget to order labs including a CMP, serum phosphorus, and serum magnesium.  

History often reveals a recent reduction or cessation of heavy alcohol use, which is typically defined as 8 or more drinks per week in biological females and 15 or more drinks per week in biological males. The first withdrawal symptoms can occur anywhere from several hours to over a day after the last drink, and based on severity, they can be mild, moderate and severe.  

Mild and moderate symptoms include sweating, nausea, vomiting, and tremors, as well as anxiety, palpitations, and insomnia.  

In severe cases, your patient could present with altered mental status, r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Opioid_withdrawal_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KMkXjmd5RHO-dYD3hX9tb3iTQ4_xxFPj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Opioid withdrawal syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Opioid withdrawal syndrome refers to signs and symptoms that occur after abrupt cessation or dose reduction in individuals who are physically dependent on opioids. The terms opiates and opioids are sometimes used interchangeably, but they actually refer to different entities. Opiates refer to only naturally occurring compounds derived from the poppy plant like heroin, morphine, and codeine, all of which have agonistic effects on the opioid receptor. On the flip side, opioids include synthetic and semisynthetic compounds that resemble opiates in structure and their effects on the opioid receptor.  

While opioid withdrawal syndrome is not usually life-threatening per se, it can cause significant distress and discomfort, has the potential to cause complications in individuals with chronic conditions, and can significantly interfere with patients receiving care for a medical illness, potentially causing fatalities that way. Now, based on the severity, opioid withdrawal syndrome can be classified as mild, moderate, or severe. 

Of note, it’s a common misconception that patients experiencing opioid withdrawal must have an opioid use disorder. In fact, opioid withdrawal can occur in anyone who develops physical dependence on opioids, which occurs at the cellular level and can happen even after one or two weeks of opioid use. This means that patients who are taking appropriate doses of opioids as prescribed for medical indications could also experience physical dependence and opioid withdrawal syndrome! Finally, you should anticipate opioid withdrawal syndrome in an opioid-dependent individual who receives an opioid antagonist, like naloxone or naltrexone.  

Now, if your patient presents with chief concerns suggesting opioid withdrawal syndrome, first, you should perform an ABCDE assessment to determine whether they’re unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation, which might require endotracheal intubation and mechanical ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_dysuria:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TeSSYF2sRIG9IZZDlZS85wafTIijK4-o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to dysuria: Clinical sciences]]></video:title><video:description><![CDATA[Dysuria is the sensation of painful or uncomfortable urination. Patients typically describe their discomfort as a burning, tingling, or stinging sensation that occurs when urine passes through an inflamed or irritated urethra. Bladder contractions can also worsen this pain.  

The main causes of dysuria are categorized as infectious and non-infectious. A good approach is to first assess for genital tract infections like cervicitis and epididymitis; next, look for lower urinary tract infections or pyelonephritis; and finally look for non-infectious causes like benign prostatic hyperplasia, nephrolithiasis, urologic malignancy, and interstitial cystitis. 

When approaching a patient with dysuria, first you should perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry.  

Here’s a clinical pearl! If a patient with dysuria is exhibiting signs of instability, there’s a concern that they may have developed sepsis. It&amp;#39;s crucial to quickly obtain blood and urine cultures, begin IV fluids and broad-spectrum antibiotics, and closely monitor their condition. 

Now, let’s go back to the ABCDE assessment and take a look at stable patients.  

If your patient is stable, you should perform a focused history and physical examination. Next, assess the history for symptoms of a genital tract infection, like vaginal irritation or discharge, urethral discharge, and scrotal pain.  

Additionally, the patient might report risk factors for sexually transmitted infections, such as unprotected sexual intercourse or having multiple sexual partners. In this case, you should consider a genital tract infection. 

Your next step is to proceed with a genital exam to diagnose.  

If your patient has a history of vulvar itching and vaginal discharge, and the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acetaminophen_(Paracetamol)_toxicity:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nc3RthAXTsGW8HDMa3JHdIkEQjW1dD0R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acetaminophen (Paracetamol) toxicity: Clinical sciences]]></video:title><video:description><![CDATA[Acetaminophen toxicity is the most common cause of acute liver failure in the United States. Acetaminophen, also known as paracetamol or N-acetyl-para-aminophenol or APAP for short, is a medication commonly used to treat pain and fever in children and adults.

Normally, acetaminophen is metabolized in the liver, but if consumed in large amounts, the toxic byproduct of acetaminophen metabolism called NAPQI can lead to hepatotoxicity, which can eventually result in liver failure. 

The management of acetaminophen toxicity is based on the amount of time that has passed since the drug was ingested, either within 4 hours, 5 to 24 hours, or longer than 24 hours ago.

If a patient presents with signs and symptoms suggestive of acetaminophen toxicity, the first step is to perform an ABCDE assessment to determine if the patient is stable or unstable. If the patient is unstable, stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient. Next, obtain IV access and put the patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen.

Alright, now let’s go back to the ABCDE assessment and discuss how to manage stable patients. If the patient is stable, first perform a focused history and physical exam. The patient will typically report acetaminophen ingestion, as well as loss of appetite, fatigue, and malaise. Additionally, they might report abdominal pain, nausea, vomiting, and confusion. The physical exam might reveal tachycardia, right upper quadrant abdominal tenderness, and altered mental status.

Now, here’s a high-yield fact! In adults, acute ingestion of 12 grams of acetaminophen or 150 milligrams per kilogram is considered a toxic dose. But, keep in mind that patients might be asymptomatic for hours after ingesting acetaminophen, so a lack of symptoms doesn’t mean the patient won’t ha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Irritable_bowel_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RDWo8UQrSqquzYfcR62tK6e9SHaQHt95/_.jpg</video:thumbnail_loc><video:title><![CDATA[Irritable bowel syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Irritable bowel syndrome, or IBS for short, is a chronic bowel condition characterized by recurrent abdominal pain associated with abnormal bowel movements. The cause is unknown but could be related to changes in the normal gut microbiota, autonomic dysfunction, altered motility of the gastrointestinal tract, and psychological factors. Now, based on the clinical manifestations, IBS can be diarrhea-predominant, constipation-predominant, or mixed.

Generally, individuals with irritable bowel syndrome are stable, so first, you should obtain a focused history and physical examination. History findings typically include bowel habit changes for at least 6 months, which are usually related to diarrhea or constipation. Your patient will also report abdominal pain or discomfort that’s typically relieved with defecation. In some cases, the patient could report abdominal bloating, or they might have a history of depression, anxiety, fibromyalgia, trauma, or recent infectious gastroenteritis. On the physical exam, you might notice abdominal tenderness during palpation, or find hemorrhoids or anal fissures on the rectal exam. 

Now, here’s a clinical pearl! Describing stools can be challenging for some patients. To make it easier, you can use a tool called the Bristol Stool Scale, which ranks stool from 1, solid lumps or balls to 7,  watery diarrhea.

Now, based on these history and physical exam findings, you should suspect a chronic bowel condition. But, before you diagnose irritable bowel syndrome, first, you need to assess your patient for red flag features, which could indicate serious underlying conditions, like colorectal cancer. These include hematochezia, unintentional weight loss, a family history of colon cancer, acute onset of constipation in an older adult, change in stool caliber, anemia, and the presence of a rectal mass. 

Next, order labs to rule out other non-malignant gastrointestinal conditions with similar clinical manifestations. Order CBC to asse]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nephrolithiasis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1Hm6bfPbSsSK-e_9WVyVJAIFQH6CnMAf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nephrolithiasis: Clinical sciences]]></video:title><video:description><![CDATA[Nephrolithiasis, also known as renal calculi or renal stones, is a painful condition where crystals form in the kidney, potentially causing urinary tract obstruction.  Renal stones usually form when urine becomes oversaturated with minerals and salts, including calcium, oxalate, and uric acid. Common renal stone types include calcium oxalate-, calcium phosphate-, uric acid-, cystine-, and struvite stones. 

Now, if your patient presents with a chief concern suggesting nephrolithiasis, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen.

Now, here’s a clinical pearl to keep in mind! Nephrolithiasis associated with a urinary tract infection is a medical emergency that requires immediate decompression and drainage. Left untreated, it can cause complications such as pyelonephritis, renal abscess, or even sepsis. Nephrolithiasis is also an emergency when it occurs alongside renal failure, anuria, bilateral ureteral obstruction, or a single-functioning kidney. In these cases, consult the urology team immediately.

Now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. In these individuals, first, obtain a focused history and physical examination and order a urinalysis. Patients with nephrolithiasis typically present with an acute onset of excruciating flank pain, along with hematuria. They may also experience dysuria, nausea, or vomiting. The physical examination usually reveals unilateral flank tenderness, and urinalysis can show red blood cells, white blood cells, and crystals in the urine. 

If your patient presents with these findings, you should suspect nephrolithiasis. Next, order a non-contrast h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prerenal_acute_kidney_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QPdzGWVnS3eBV69JLVZj1skFRLa7dUsK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prerenal acute kidney injury: Clinical sciences]]></video:title><video:description><![CDATA[Acute kidney injury, or AKI for short, is a sudden, potentially reversible decline in kidney function, resulting in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste such as ammonia and uric acid.  

You can split AKI into three causes depending on the location of the injury. Prerenal AKI is when the cause of the injury occurs before the kidneys, intrinsic AKI means the injury is within the kidneys, and postrenal AKI refers to injury after the kidneys.  

Focusing on prerenal AKI, its causes can be grouped into four main categories, which include medication-induced renal autoregulation impairment, hypovolemia, systemic vasodilation, and interstitial volume overload. 

Now, if your patient presents with a chief concern suggesting AKI, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, which might include dialysis access. Finally, put your patient on continuous vital sign monitoring and cardiac telemetry, and if needed, provide supplemental oxygen!  

Here’s a clinical pearl to keep in mind! Look out for life-threatening complications of AKI such as hyperkalemia, volume overload, or metabolic acidosis, and start emergent hemodialysis right away if needed!  

Okay, now let’s go back to the ABCDE assessment and take a look at stable patients. First, obtain a focused history and physical exam. Patients with AKI may report nonspecific symptoms, like fatigue and malaise, or urinary symptoms, such as reduced urine output or hematuria. They may have just started a new medication or have a known chronic medical condition, such as congestive heart failure, multiple myeloma, or systemic lupus erythematosus.  

Physical exam might reveal blood pressure abnormalities, a rash, or periorbital or peripheral edema. With these findings, suspect AKI, and then order a basic metabolic panel, and measure their urine out]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_cancer_screening:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HhvgnTrNT7mqyb3chPSJg6m2ScOn5G9-/_.png</video:thumbnail_loc><video:title><![CDATA[Breast cancer screening: Clinical sciences]]></video:title><video:description><![CDATA[Breast cancer is one of the most common cancers among biological females globally.  Although mortality rates have decreased over time, the incidence of breast cancer continues to increase every year.  

Because most patients remain symptom free until the late stages, breast cancer screening plays a major role in early detection and treatment of the disease, thereby increasing survival rates. 

Breast cancer screening focuses on identifying high-risk patients and utilizing imaging like screening mammography or breast ultrasound to evaluate for a mass. The screening schedule and modality can differ based on the patient’s risk classification. 

When a patient presents for breast cancer screening, your first step is to assess for risk factors that can contribute to the patient’s future development of breast cancer. The first screening should occur between the ages of 25 and 30 as a part of their primary care visit. The majority of risk factors can be obtained through a detailed health history.  

Then, you can use a validated risk-prediction model to calculate the patient’s risk of developing breast cancer, like the Breast Cancer Risk Assessment Tool, also known as the Gail model; and the Tyrer-Cuzick model.  

The Gail model calculates the estimated risk a patient has for developing breast cancer within the next 5 years, as well as their lifetime risk. It incorporates factors such as age; race and ethnicity; age at menarche; age at first live birth; age at menopause; history of breast cancer in a first-degree relative; and history of breast biopsies.  

Similarly, the Tyrer-Cuzick model calculates a 10-year risk and incorporates factors like the patient’s age; body mass index, or BMI; age at menarche; parity; age at first live birth; age at menopause; history of hormone replacement therapy; breast density; BRCA mutation status; history of personal breast disease; Ashkenazi ethnicity; history of breast disease in a first-degree or second-degree relative; as we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cervical_cancer_screening:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eeAsaSmWQRu8uRxXLGiQOg0aSkmUKsy8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cervical cancer screening: Clinical sciences]]></video:title><video:description><![CDATA[Cervical cancer screening is a preventive procedure that evaluates asymptomatic patients for cervical abnormalities, especially high-grade precancerous cells, or dysplasia, and invasive cervical cancer. Screening decreases cervical cancer incidence and mortality rates and is associated with higher cure rates for invasive cervical cancer due to timely diagnosis. 

Risk factors for cervical cancer include previous treatment of a high-grade precancerous lesion, HIV infection, and a compromised immune system. Additionally, high-risk HPV, or human papillomavirus, is associated with nearly all cases of cervical cancer. Guidelines for screening combine a patient’s current test results with their screening history to direct clinical decision-making, with consideration for the patient’s immunocompetence, presence of a cervix, and age.

Your first step in assessing a patient who presents for cervical cancer screening is to obtain a focused history and physical exam. Knowing which screening test to perform and how often to perform it depends on a number of factors, including patient age, previous screening interval, results of past screening and treatment if available, whether the patient has had a hysterectomy, and their immune status, specifically whether they are HIV positive or currently take immunosuppressive medications.Because cervical cancer screening is only appropriate for asymptomatic patients, the history should be negative for any abnormal uterine or vaginal bleeding. On the other hand, the physical exam includes a speculum examination to visualize the cervix, which should appear normal. If the patient has had a hysterectomy with removal of the cervix, inspect the vaginal cuff, which should appear normal as well. 

Here’s a clinical pearl! Any grossly visible abnormal lesions on the cervix should have a targeted biopsy for assessment.

Your next step is to assess the patient’s immunocompetence. Most patients who undergo cervical cancer screening have a n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colorectal_cancer_screening:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5BdfzzgWQaC7cP3XPYtlPBUzS8SnYpPS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colorectal cancer screening: Clinical sciences]]></video:title><video:description><![CDATA[Colorectal cancer screening is an important and effective tool aimed to identify populations who are at risk for developing colorectal cancer and to detect precancerous lesions early. Over the last few decades, early screening has become even more critical as the incidence of colorectal cancer has increased for patients between the ages of 40 and 54 years. The risk of developing colorectal cancer during one’s lifetime depends on both genetic and environmental factors. So, the initial portion of screening involves identifying these risk factors in order to help us determine which patients need to be screened earlier.

Alright, screening a patient for colorectal cancer starts with assessing for any risk factors that are associated with future development of the cancer. The top five risk factors that puts your patient at high risk include personal or family history of colorectal cancer; hereditary colon cancer syndromes such as familial adenomatous polyposis or FAP, and Lynch syndrome, also known as hereditary non-polyposis colorectal cancer; as well as inflammatory bowel disease or IBD for short, like ulcerative colitis and Crohn disease; abdominopelvic radiation treatments; and cystic fibrosis. If your patient has any of these risk factors, they are considered high risk and will need to be screened for colorectal cancer earlier than the average risk patient, depending on their specific risk factors. 

In addition, there are other less significant risk factors that put your patient at average risk for colorectal cancer. These include male sex; race such as Black, Native American, and Alaskan Native; history of transplantation or immunosuppression; obesity; tobacco and alcohol use; a diet high in red or processed meats; and long-term androgen deprivation therapy used for instance in prostate cancer treatment. Although these characteristics can be associated with increased incidence of colorectal cancer, patients with these factors are still considered average]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophageal_perforation:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/yNFKN6Y_TcevXI_Yq2mXwhqpSNi4Ry9X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophageal perforation: Clinical sciences]]></video:title><video:description><![CDATA[Esophageal perforation is a serious condition in which a hole in the esophagus exposes the surrounding tissues to the contents of the gastrointestinal tract.  Esophageal perforation typically results from iatrogenic trauma, for example in patients who recently underwent upper endoscopy or placement of a feeding tube. The second most common cause is Boerhaave syndrome due to forceful vomiting, and perforations can also result from swallowing foreign objects. Now, some individuals have anatomic etiologies that put them at higher risk for perforation such as Zenker diverticulum or esophageal stricture. 

When it comes to the site of the perforation, it most commonly occurs in the left posterolateral aspect of the distal intrathoracic esophagus.  Esophageal perforation can lead to severe and fatal complications like mediastinitis and sepsis. 

Your first step in assessing a patient with a chief concern suggestive of esophageal perforation is to perform an ABCDE assessment to determine if the patient is stable or unstable. If the patient is unstable, start acute management immediately to stabilize the airway, breathing, and circulation. Next, obtain IV access, start fluid resuscitation, keep the patient NPO, administer antibiotics, and give IV proton pump inhibitors as soon as possible. Once you have initiated the acute management, your next step is to obtain a focused history, physical exam, and order labs like CBC, ABG, blood cultures, and lactate.

Alright, let&amp;#39;s talk about history and physical examination. Symptoms may include fever, chills, and altered mental status. A patient will often have neck, chest, interscapular, and/or abdominal pain. Additionally, they might report dysphagia, odynophagia, or dyspnea. Lastly, some clues in history can point to the cause of the perforation. If a patient reports forceful vomiting, you should think about Boerhaave syndrome, which is when straining due to forceful vomiting causes esophageal perforation. Other ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_constipation:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_0WVeoNXTWCs3V1Q7BdDrWR0TtWMZulr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to constipation: Clinical sciences]]></video:title><video:description><![CDATA[Constipation is a common gastrointestinal condition characterized by infrequent bowel movements and difficulty passing stool. It happens when the intestines don&amp;#39;t move waste to the rectum properly, and pelvic muscles and anal sphincter don&amp;#39;t coordinate well to expel stool. Now, based on the cause, constipation can be classified as primary, also known as idiopathic or functional constipation; and secondary, which occurs as a side effect of some medications or due to another medical condition, such as malignancy.

Now, if your patient presents with constipation, first, you should obtain a focused history and physical exam. Always perform a digital rectal exam, including inspection, palpation at rest, and palpation during a simulated evacuation, which is performed by asking the patient to bear down on your finger as if they were having a bowel movement. Your patient will typically report a history of infrequent bowel movements, usually fewer than three stools per week, as well as straining, hard stools, and a feeling of incomplete evacuation. Additionally, history might reveal abdominal discomfort or bloating, and sometimes the patient might report the use of manual maneuvers to defecate. 

Now, here’s a clinical pearl to keep in mind! Many patients find it embarrassing to discuss bowel habits, so they might not describe their symptoms in detail. So, be sure to ask direct questions about things like digital manipulation to defecate, and ask them to describe the appearance of their stools. 

You can use tools like the Bristol stool chart, which lists seven categories of stool based on shape and texture, to help patients describe their stool. 

Next, in patients with acute onset constipation, always ask about the ability to pass gas, as failure to pass gas can signal bowel obstruction. Other symptoms that point to obstruction include obstipation, which refers to severe or complete constipation with practically no stool passage and absence]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anal_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cvAdu6XrRgSfBunPSmtQtnnhRzevgy3x/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anal cancer: Clinical sciences]]></video:title><video:description><![CDATA[Anal cancer is a malignancy of the anal canal or perianal area. The two main subtypes of anal cancer include squamous cell carcinoma or SCC, which is the most common, and adenocarcinoma. Although rare, the incidence of anal cancer has been increasing over the last decades likely due to the spread of human papillomavirus, or HPV, which is the number one cause of anal SCC. Treatment depends on the histopathologic subtype as well as the stage of the cancer at the time of diagnosis. 

Alright, when a patient presents with a chief complaint suggestive of anal cancer, the first step is to obtain a focused history and physical. Typically, patients report rectal bleeding, anorectal pain, and the sensation of a mass within or around the anus. On further history, patients might have risk factors like previous or current HPV infection, HIV infection, immunosuppression, a high lifetime number of sexual partners, receptive anal intercourse, genital warts, or smoking. 

Your examination should include a focused anorectal evaluation, including a digital rectal examination, or a DRE, and evaluation of the inguinofemoral lymph nodes.  DRE can reveal a hard, fixed, ulcerated mass in the perianal region or within the anal canal. Additionally, you might also find inguinal or femoral lymphadenopathy. If you see these findings, you should suspect anal cancer. On exam, you might see anogenital warts, perianal skin irritation, or mucus or bloody discharge at the anal verge.

Okay, now let’s talk about the initial work up when you suspect anal cancer. Your next step is to perform an anoscopy with biopsy of the lesion, and a fine needle aspiration or FNA of any clinically suspicious lymph nodes. The anoscopy with biopsy can help you gain better visualization of the mass including its size and location, and provide pathologic confirmation of your diagnosis. FNA can also confirm malignant nodal spread. 

Let&amp;#39;s break this down further starting with squamous cell carcinom]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Colonic_volvulus:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cSq47QcYTwCm7Iz4XgkpcS0fRCarLAXG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Colonic volvulus: Clinical sciences]]></video:title><video:description><![CDATA[Colonic volvulus occurs when a redundant segment of the colon twists on its mesentery, causing a closed loop obstruction where the blood supply to the colon can become compromised. Now, in this closed loop, gas and secretions continue to build up with nowhere to go. This worsens the distension of the segment, and can lead to ischemia, necrosis, and ultimately perforation. 

Colonic volvulus accounts for about 10% of large bowel obstructions and is more common in the elderly or in patients with chronic constipation. There are two major types of colonic volvulus depending on its anatomic location, which can involve the cecum or the sigmoid colon. Regardless of the type, timely diagnosis and treatment is very important to prevent necrosis and perforation of the involved bowel segment. 

When assessing patients with a chief concern suggesting colonic volvulus, your first step is to perform an ABCDE assessment to determine if the patient is stable or unstable. If the patient is unstable, begin acute management immediately to stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient, obtain IV access, administer fluids, and monitor vital signs. Additionally, keep the patient NPO and place a nasogastric tube for small bowel decompression. Next, quickly obtain a focused history and physical examination, and order labs such as CBC, CMP, and lactate, as well as an abdominal x-ray.

Okay, let’s discuss what you might find on history and physical examination. The history will typically reveal an acute onset of crampy abdominal pain, obstipation or constipation, and bloating. As the passage through the colon is blocked, the content of the intestine will start backing up. So over time, patients might develop nausea and vomiting as well. Be sure to ask about any previous episodes of colonic volvulus and what treatment they received at that time. 

On physical exam, you might find altered mental status, tachycardia,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/COVID-19:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OsmzhQEUSnuWyn7KS4b2RKruTTmP--f-/_.jpg</video:thumbnail_loc><video:title><![CDATA[COVID-19: Clinical sciences]]></video:title><video:description><![CDATA[COVID-19 is a respiratory infection caused by SARS-CoV-2, a highly contagious virus that primarily spreads via respiratory droplets. Once in the respiratory tract, the virus replicates and causes symptoms similar to the common cold, while in some cases, the virus causes a robust inflammatory response that can produce life-threatening illness. Based on clinical manifestations, COVID-19 can be mild, moderate, severe, or critical. 

Now, if your patient presents with chief concerns suggesting COVID-19, you should first perform an ABCDE assessment to determine if your patient is unstable. If the patient is unstable, stabilize their airway, breathing, and circulation. This might require you to intubate the patient and provide mechanical ventilation. Also, don’t forget to obtain IV access and place your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry. 

Once you stabilize the patient, obtain a focused history and physical exam; but also labs, such as a SARS-CoV-2 test; an arterial blood gas, or ABG; a CMP; inflammatory markers, including CRP and ESR; as well as D-dimer, BNP, troponin, and lactate. You should also obtain a chest X-ray and ECG. 

Typically, patients report respiratory symptoms, such as cough, rhinorrhea, nasal congestion, as well as shortness of breath, and difficulty breathing. They may also report new loss of taste or smell. Often, systemic symptoms like headache, fatigue, myalgia and fever, are associated. Some patients may also experience gastrointestinal symptoms like nausea, vomiting, or diarrhea.  Additionally, patient history can reveal a known SARS-CoV-2 exposure.

On physical exam, you can find evidence of respiratory distress, such as hypoxemia, as well as rales or rhonchi on auscultation, and accessory muscle use and retractions. In severe cases, your patient can be hypotensive as well! 

As for labs, these will reveal a positive SARS-CoV-2 test. The ABG and CMP can show respiratory ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atrioventricular_block:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qL0DrzQAQkyGGp_AQEBXCxBbR-yb_Cp_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atrioventricular block: Clinical sciences]]></video:title><video:description><![CDATA[Atrioventricular block, or AV block for short, is a conduction disturbance that occurs when an atrial impulse gets delayed or completely blocked at some point along the electrical conduction system of the heart. This conduction disturbance can occur within the AV node, the bundle of His, or bundle branches; and can be caused by either reversible causes, such as increased vagal tone; or irreversible causes, like fibrosis of the heart. AV block presents with bradycardia, which can range from asymptomatic and benign, to severe and life-threatening. Now, based on the severity of the AV block, we can classify it as either first-, second-, or third-degree.

If your patient presents with a chief concern suggesting an atrioventricular block, perform an ABCDE assessment to determine if the patient is unstable or stable. If they’re unstable and there’s a detectable pulse, follow the ACLS guidelines for Bradycardia with a Pulse. You should stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen to maintain oxygen saturation.

Now, here’s a high-yield fact! A first step in the acute management of an unstable patient with bradycardia and a pulse includes the administration of atropine, and if the bradycardia and hemodynamic instability persist, begin transcutaneous pacing and consider an infusion of epinephrine or dopamine.

Now, let’s go back to the ABCDE assessment and look at stable patients. In this case, obtain a focused history and physical examination. Your patient may report lightheadedness or fatigue, as well as shortness of breath with exertion or even angina or syncope. Additionally, the physical exam will reveal a heart rate below 60 beats per minute. 

At this point, you can diagnose bradycardia, so order a 12-lead electrocardiogram, or ECG fo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Protein-calorie_malnutrition:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4Wu5cvbkR_S364dODrJgmodhRXybPU5F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Protein-calorie malnutrition: Clinical sciences]]></video:title><video:description><![CDATA[Protein-calorie malnutrition occurs when someone loses weight, due to inadequate protein and calorie intake. Diagnosis and management of protein-calorie malnutrition are crucial, particularly in the elderly, as it is associated with poor outcomes. 

The most common causes of protein-calorie malnutrition are chronic conditions, oropharyngeal conditions, gastrointestinal malabsorption, anorexia nervosa, as well as social functional barriers.

When a patient presents with chief concerns suggesting protein-calorie malnutrition, the first step is to perform a focused history and physical exam. The most important history findings typically include reduced food intake, weight loss, weakness, and fatigue. 

Your patient may also have a background of chronic diseases, such as chronic kidney disease, COPD, congestive heart failure, or malignancy. 

Their physical examination will show thin, dry skin; hair thinning or loss; temporal wasting; muscle atrophy, and generalized muscle weakness. 

Additionally, there might be peripheral edema due to a decrease in serum albumin and a subsequent drop in oncotic pressure. 
If your patient presents with these symptoms and signs, you should suspect protein-calorie malnutrition. 

Your next step is to obtain the patient’s weight to calculate their Body Mass Index or BMI. If the patient’s unable to stand on the scale, such as patients using a wheelchair, you should estimate the patient’s muscle mass by measuring the circumference of your patient’s upper arm.

Now, here’s a high-yield fact to keep in mind! Mean upper arm circumference, or MUAC for short, is measured at the patient’s left upper arm. You can use it to track the patient’s muscle mass loss or gain, just as you can use their weight to follow their weight loss or gain. An upper arm circumference of less than 22 cm for women and less than 23 cm for men suggests malnutrition.

Okay, your next step is to assess if your patient meets the diagnostic criteria for protein]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypokalemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JYyMSwryTPOrMAGAbXU4ItDlSVqCHEYa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypokalemia: Clinical sciences]]></video:title><video:description><![CDATA[Hypokalemia is defined as a low serum potassium level, usually below 3.5 milliequivalents per liter. Mild hypokalemia can be asymptomatic, but more severe hypokalemia can cause life-threatening symptoms like paralysis and cardiac arrhythmias. Some common causes of hypokalemia include hypomagnesemia, low potassium intake, conditions associated with transcellular shift of potassium, as well as extrarenal potassium wasting, and increased mineralocorticoid activity. Finally, keep in mind that hypokalemia can also occur due to acid base disorders.

Now, if you suspect hypokalemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on cardiac telemetry. This is important  because extreme drops in serum potassium can lead to dangerous cardiac arrhythmias, such as Torsades de Pointes and ventricular fibrillation. You should also monitor vital signs and provide supplemental oxygen, if needed. 

Now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. If your patient is stable, first obtain a focused history and physical examination. Also obtain labs, including a comprehensive metabolic panel, and check a 12 lead ECG. History typically reveals weakness, muscle cramps, or in extreme cases, even ascending paralysis. Also, there might be a history of diuretic or laxative use, while others may report severe diarrhea. On the other hand, physical examination typically reveals an irregular pulse and decreased deep tendon reflexes; while lab results show a serum potassium level below 3.5 milliequivalents per liter. 

Here’s a clinical pearl to keep in mind! Pseudohypokalemia refers to the falsely low potassium level, often caused by a blood sample being left in a warm environment several hours before processing. This causes the potassium in t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastric_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8FOLahCIRe_6P_8P461uOsjKQruHAjAe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gastric cancer: Clinical sciences]]></video:title><video:description><![CDATA[Gastric cancer is a malignant tumor of the stomach that is typically diagnosed in advanced stages due to the lack of symptoms. Even with early diagnosis and treatment, the rates of morbidity and mortality remain high for these patients. Unfortunately, about half of patients present with distant metastasis, making curative treatment very difficult. The majority of gastric cancers are adenocarcinomas, as the tumor often starts in the mucosal lining of the stomach. The treatment of gastric cancer is based on the staging of the disease. 

Alright, when a patient presents with chief concern suggesting gastric cancer, the first step is to obtain a focused history and physical exam, as well as labs including CBC, CMP, and H. Pylori testing. Patients with gastric cancer are often asymptomatic, but some may report symptoms like dyspepsia, dysphagia, epigastric pain, nausea, or anorexia. 

They might also report a recent history of associated anemia or weight loss, which should get you to think about malignancy. There are several risk factors you should look for, including a history of H. pylori and Epstein-Barr virus infections, pernicious anemia, chronic gastritis, smoking,diet of  smoked or pickled foods, high-salt diet, or a family history of gastric cancer. The patient’s race might also be a risk factor, especially if they are of Eastern Asian, Eastern European, and South American descent.

When it comes to the physical exam, it’s usually unremarkable. However, in some cases, you might find a palpable epigastric mass or a distended stomach. Other findings may include hepatomegaly, or a Sister Mary Joseph nodule, which represents periumbilical metastatic disease. 

Make sure to examine other lymph nodes to check for lymphadenopathy, such as Virchow Nodes, located in the left supraclavicular region, and Irish Nodes around the anterior axillary area. Keep in mind that these physical exam findings usually indicate advanced disease. Finally, labs typically show anem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_breast_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h07YF_nGTgemVof3JXoUpnfpTGKhhvE-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory breast cancer: Clinical sciences]]></video:title><video:description><![CDATA[Inflammatory breast cancer is a highly aggressive form of locally advanced breast cancer. Due to similarities in physical appearance, inflammatory breast cancer can sometimes be mistaken for benign diseases such as acute mastitis. Therefore, careful consideration must be given to rule out underlying malignancy if the benign disease doesn’t respond or quickly resolve with treatment. 

When assessing a patient with a chief concern suggestive of inflammatory breast cancer, the first step is to obtain a focused history and physical exam, as well as labs such as CBC, CMP, LFTs, and Alkaline Phosphatase. Now, history might reveal breast pain, and a firm or enlarged breast, with rapid onset of symptoms, usually within 6 months. Some patients may report breast pruritus, swollen lymph nodes in the axilla or above the clavicle, fever, or even a recent history of suspected acute mastitis that hasn’t responded to antibiotics. 

On the other hand, a physical exam typically shows a warm, tender breast, with extensive erythema that involves at least one-third of the breast, and thickened skin. A very common skin finding is called peau d’Orange. This occurs when tumor microemboli block dermal lymphatics, leaving portions of the breast with an edematous and dimpled orange-peel appearance. While peau d’Orange is highly associated with inflammatory breast cancer, it is important to remember that it might not always be present! 

Other possible findings on physical exam include nipple changes, such as flattening or retraction, a palpable underlying breast mass, and regional lymphadenopathy, most commonly in the axilla. Finally, labs can show leukocytosis, and possibly elevated transaminases or alkaline phosphatase, which is concerning for metastatic disease to the liver or bones, respectively. 

Here’s a clinical pearl for you! Significant fever, leukocytosis, and acute onset within a few days are rare in inflammatory breast cancer but common in acute mastitis. While these fi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Invasive_ductal_carcinoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3eS4WmxHTMipkJlZSs6Jr70JSM_e_aUr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Invasive ductal carcinoma: Clinical sciences]]></video:title><video:description><![CDATA[Invasive ductal carcinoma is the most common form of breast cancer, and occurs when malignant epithelial cells from ductal tissue infiltrate through their basement membrane. Treatment of invasive breast cancer is based on the stage of cancer. Patients are roughly classified as early-stage, locally advanced, or metastatic disease. 

When a patient presents with a new breast lump or abnormal screening mammogram, you should consider an invasive ductal carcinoma. The first step is to obtain a focused history and physical exam. History may include changes in the breast or nipple appearance, nipple discharge, and the presence of swollen lymph nodes. 

You should also ask about common risk factors, such as a personal or family history of breast or ovarian cancer; early menarche or late menopause; nulliparity; first birth after 30 years of age; being older than 40; dense breast tissue; chest radiation; exogenous hormone use; and family or personal history of deleterious cancer gene mutations like BRCA.

On the flip side, a physical exam might reveal a palpable breast lump, which could be fixed and is more concerning for malignancy. There may also be skin changes; or nipple changes, like flattening or inversion. Some patients even have lymphadenopathy, which can be above and below the clavicle, and in the axilla.

Your next step will be to obtain some labs, including baseline CBC and CMP. Labs might show elevated transaminases or alkaline phosphatase.

Alright, these findings should prompt you to get imaging with a diagnostic mammogram and an ultrasound. 

Here’s a clinical pearl! Breast findings on imaging can be categorized with a standardized system called BI-RADS, which stands for Breast Imaging-Reporting and Data System. The imaging findings are assigned into categories labeled as 0 to 6. First, 0 means incomplete, which needs additional imaging or comparison with previous images if available. Next, 1 is negative, meaning that mammography is normal, with no fi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Systemic_lupus_erythematosus:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3-rTZPoaSiC6M98EZJnvVp4KQPG92puR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Systemic lupus erythematosus: Clinical sciences]]></video:title><video:description><![CDATA[Systemic lupus erythematosus or SLE for short, or simply lupus, is a chronic autoimmune condition that can affect pretty much any organ system! Affected individuals produce autoantibodies and immune complexes that mediate tissue damage, which commonly results in dermatologic, hematologic, renal, joint, and nervous system manifestations. 

Now, if a patient presents with a chief concern suggesting systemic lupus erythematosus, you should first perform a focused history and physical examination. Your patient will likely describe nonspecific systemic symptoms like fatigue, fever, malaise, or weight loss. They may also report photosensitivity of the skin, joint pain, pleuritic chest pain, as well as neurologic or psychiatric symptoms, such as cognitive dysfunction or even seizures. 

On the flip side, the physical exam usually reveals a classic malar rash, also known as a butterfly rash, since erythema specifically affects the nose and cheeks, sparing the nasolabial folds. Another skin finding is a discoid rash, which is a chronic erythematous rash in sun-exposed areas like the arms and legs that are plaque-like or patchy redness and can scar. Other important findings include painless oral and nasal ulcers, as well as symmetric tenderness and swelling of the small joints, most commonly in the hands and wrists. Finally, auscultation may reveal decreased breath sounds or a pericardial friction rub.Based on these findings, you should suspect SLE.

Now that we suspect SLE, based on our history and physical findings, your next step is to order labs. These include CBC and CMP, an antinuclear antibody; anti-double-stranded DNA and anti-Smith antibodies; as well as antiphospholipid antibodies. Also, don’t forget to check complement C3 and C4 levels. Finally, you should  send urine for a urinalysis, and order the urine spot protein-to-creatinine ratio to assess for proteinuria. 

Now let’s take a look at our lab results. The CBC could reveal low hemoglobin, WBCs, and p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hyponatremia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kE10i_rmTaefnpzploImOd9oREa1lKif/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hyponatremia: Clinical sciences]]></video:title><video:description><![CDATA[Hyponatremia is a common electrolyte disturbance in which the serum sodium concentration is less than 135 milliequivalents per liter. Several mechanisms can contribute to hyponatremia, including increased serum levels of antidiuretic hormone, or ADH, increased renal sensitivity to ADH, excessive free water intake, and low solute intake. Now, based on the underlying cause, hyponatremia can be categorized as hypovolemic, euvolemic, and hypervolemic.

Now, if your patient presents with hyponatremia, you should first perform an ABCDE assessment to determine if they are unstable or stable.

If unstable, stabilize the airway, breathing, and circulation; obtain IV access and consider giving your patient IV fluids. You can also consider central venous access. Next, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and don’t forget to monitor your patient’s urine output! Finally, if needed, provide supplemental oxygen.

Now, here’s a high-yield fact to keep in mind! Unstable individuals with hyponatremia often have a sodium level below 125 milliequivalents per liter, which can result in cerebral edema and severe clinical manifestations, like seizures or even respiratory arrest!

Now, let’s go back to the ABCDE assessment and look at stable patients. In this case, obtain a focused history and physical examination and order a basic metabolic panel or BMP. Your patient may report symptoms like headache, nausea, vomiting, or confusion; with lab results revealing a sodium level lower than 135 milliequivalents per liter. If these findings are present, your first step is to assess for true hyponatremia, so order a plasma osmolality.

Let’s first look at a plasma osmolality that’s greater than 280 milliosmoles per kilogram. This could be either normal if it’s between 280 and 295, or hypertonic when it’s higher than 295. If the plasma osmolality is between 280 and 295,  consider pseudohyponatremia.      

Ne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Syndrome_of_inappropriate_antidiuretic_hormone_secretion:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/akCiGXGnQdC6d_bBG9gS5aaQQ7GsehNs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Syndrome of inappropriate antidiuretic hormone secretion: Clinical sciences]]></video:title><video:description><![CDATA[Syndrome of inappropriate antidiuretic hormone secretion, or SIADH for short, is when too much antidiuretic hormone, also called ADH, or arginine vasopressin, is secreted. 

Normally, ADH is secreted when there’s too little water and too much sodium in the body, and it works by increasing water reabsorption in the renal tubule, restoring the water-sodium balance. 

However, with SIADH, there’s increased ADH secretion in the absence of fluid depletion, and this causes excessive water reabsorption, diluting the blood to the point of euvolemic hyponatremia. 

SIADH most often occurs as a secondary response to another condition, and is commonly seen in patients with pulmonary disease like pneumonia or lung cancer, as well as central nervous system disorders, like meningitis and head trauma. 

Now, if your patient presents with chief concerns suggesting SIADH, you should first perform an ABCDE assessment to determine if they are unstable or stable. 

If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Don’t forget to monitor the patient’s urine output closely! Finally, if needed, provide supplemental oxygen.

Now, here’s a high-yield fact! Unstable patients often have severe symptoms like seizures or even respiratory arrest! In severe hyponatremia, sodium levels can fall below 125 milliequivalents per liter, and the hyponatremia is frequently acute, meaning it developed within a 24- to 48-hour period. 

Symptomatic hyponatremia indicates the presence of cerebral edema, so if your patient presents with severe symptoms, obtain a serum sodium level to confirm hyponatremia, and administer intravenous 3% hypertonic saline to treat the cerebral edema and correct serum sodium. Make sure not to give 0.9% isotonic saline, because this can dilute the serum sodium even more! 

Also, keep in mind that, in patie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_knee_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5PPKkTwQSgCYagu45NVamD16RwSmsA7A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to knee pain: Clinical sciences]]></video:title><video:description><![CDATA[Knee pain is a common musculoskeletal symptom that can be caused by damage to any of the ligamentous, muscular, or bony structures comprising the joint. Most often, knee pain is associated with trauma and conditions such as fractures and ligament or meniscus injuries. 

On the other hand, non-traumatic causes can be classified based on the presence of joint effusion. No joint effusion is common in conditions, such as patellofemoral pain syndrome, prepatellar bursitis, and osteoarthritis; while joint effusion is typically seen in septic arthritis, crystal-induced arthropathy, and non-infectious inflammatory arthritis.

If a patient presents with knee pain, the first step is to perform a focused history and physical examination. Start by assessing the patient’s history of trauma preceding the onset of knee pain.

If the patient reports trauma to the knee, consider traumatic causes of knee pain and assess their risk for fracture using the Ottawa knee rules. 

Ottawa knee rules include the age of 55 or older, point tenderness at the fibular head, isolated point tenderness of the patella, inability to flex the knee to 90 degrees, or inability to bear weight on the affected knee. 

If the patient does not have any of these characteristics, your patient has a low risk for fracture, so no further evaluation is needed. 

On the flip side, if the patient meets any of the criteria, then they have a high risk of fracture, so you should order x-rays. If an x-ray is performed, it may reveal a fracture, for example a fracture of the tibia, patella, or other surrounding bones. 

Let’s take a look when x-ray findings are normal. If the x-ray findings show no fracture, consider ligamentous or meniscal injury. The mechanism of injury and physical exam can help distinguish between injuries of the anterior cruciate, posterior cruciate, and collateral ligaments. 

First, let’s start with the anterior cruciate ligament injury or ACL injury for short. Let’s say the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Melanoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TKloc3JrR_KGmPRCU3CE-QbxRhaHmqHV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Melanoma: Clinical sciences]]></video:title><video:description><![CDATA[Melanoma is a very serious type of skin cancer arising from pigment-producing cells called melanocytes. It’s the fifth most common cancer in the United States and is associated with high rates of mortality. Melanoma can develop anywhere on the body and has a high rate of spread, so early diagnosis and treatment are key to improve overall outcomes. 

Alright, when a patient presents with a chief concern suggesting melanoma, the first step is to obtain a focused history and physical. Typically, patients will report noticing a skin lesion with recent changes in size, color, or developing associated symptoms like pruritus. Sometimes they might even notice bleeding from the lesion. 

A patient may also experience systemic symptoms that are alarming for malignancy, including fevers, chills, fatigue, bone pain, or weight loss. History might reveal risk factors like a personal or family history of cutaneous malignancy or immunosuppression, as well as fair skin, a tendency to sunburn, chronic sun exposure, or previous sunburns. 

On a physical exam, you’ll typically find a pigmented skin lesion like a macule, plaque, or nodule with an irregular border. Make sure to do a full body exam checking for other similar lesions or nevi. 

Important findings can be summarized by the mnemonic ABCDE, which stands for Asymmetry; Border irregularities; Color variations, such as brown or black spots with other colors like red, blue, gray, or white; Diameter, often larger than 6 mm; and Evolution, like changes in size, shape, or color, depigmentation, development of streaks, pseudopods or irregular vascularity. 

Some of the suspicious characteristics you should look for include bleeding, crusting, or ulceration. If you see a lesion that differs from other nevi, it is called the &amp;quot;ugly duckling sign&amp;quot;. Last but not least, remember to check regional lymph nodes for lymphadenopathy, which is concerning for possible metastasis. If you see these findings, be very sus]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Umbilical_hernias:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uzvmhCh1TvW3LTv40FuQ0boYRmS_GOuV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Umbilical hernias: Clinical sciences]]></video:title><video:description><![CDATA[An umbilical hernia is a defect in the abdominal wall located at the umbilicus. This type of hernia usually occurs through the weakened umbilical fascia or through a defect formed at the site of involuted umbilical vessels. Small hernias often contain an empty sac, while larger ones can encase preperitoneal fat, omentum, or even a loop of bowel. 

Most umbilical hernias are acquired in adulthood in individuals with elevated intra-abdominal pressure due to conditions such as pregnancy, ascites, or obesity. Umbilical hernias can present in four different ways: asymptomatic, symptomatic, incarcerated, or strangulated. Keep in mind that incarcerated or strangulated hernias might require urgent surgical intervention.

Alright, when you encounter a patient with signs and symptoms suggestive of an umbilical hernia, your first step is to perform an ABCDE assessment to determine whether the patient is stable or unstable. If the patient is unstable, you should stabilize their airway, breathing, and circulation. This means that you may need to intubate the patient, obtain IV access, and administer fluids before continuing with your assessment.  

Now that unstable patients are taken care of, let’s talk about stable patients. 

If the patient is stable, your first step is to obtain a focused history and physical examination.

First, you might encounter a patient with no symptoms. However, the physical exam might reveal a soft, protruding mass protruding from the umbilicus with some mild tenderness on palpation, but no overlying skin changes. The mass will be easily reducible. This is a classic case of an asymptomatic umbilical hernia. 

In terms of treatment, these hernias can often be managed with watchful waiting. However, elective repairs can be considered for defects with high potential for becoming larger, which may increase the risk of incarceration and strangulation. If your patient wishes to wait, advise them to seek medical attention for any new-onset or wors]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ventral_and_incisional_hernias:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A0L96OVmQgCVkmenO3e8dMB3RtSzI5sN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ventral and incisional hernias: Clinical sciences]]></video:title><video:description><![CDATA[A ventral hernia is a defect in the fascia of the anterior abdominal wall. The majority of ventral hernias are acquired commonly from trauma to the abdominal wall and weakening of the fascia from repeated weight loss and subsequent weight gain, as well as straining, and coughing due to respiratory disease. Rarely, ventral hernia can be congenital like in omphalocele and gastroschisis. 

Incisional hernias, on the other hand, are defects of the anterior abdominal wall resulting from improper healing of previous abdominal surgeries. Large midline incisions, from an exploratory laparotomy for example, have the highest risk for incisional hernias. 

Risk factors for developing incisional hernias include obesity, smoking, malnutrition, and immunosuppressive therapies as they impede normal wound healing. 

Both ventral and incisional hernias can present as either asymptomatic, symptomatic, incarcerated, or strangulated. 

Alright, when you encounter a patient with signs and symptoms suggestive of a ventral or incisional hernia, you should first perform an ABCDE assessment to determine whether the patient is unstable. 

If the patient is unstable, you should stabilize their airway, breathing, and circulation. This means that you may need to intubate the patient, obtain IV access, and administer fluids before continuing with your assessment.  

Let’s take a look at  the different findings for stable patients. When it comes to stable patients,  your first step is to obtain a focused history and physical examination. There are a few findings you may notice here.   

Alright, first, the patient might be asymptomatic, with a possible history of prior abdominal surgery. On physical exam, you might find a small abdominal wall bulge that increases in size when the patient bears down or performs a Valsalva maneuver. To do this, tell your patient to breathe in and forcefully breathe out against closed glottis or closed mouth and pinched nose. The idea behind the Valsalva m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_cyst:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i2W7NeM5RtW62Y4H_UrwOoPOTJCLjU9f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breast cyst: Clinical sciences]]></video:title><video:description><![CDATA[Breast cysts are fluid filled masses that develop within the glandular tissue of the breast, usually in the upper outer quadrant; but they can appear anywhere in the breast. Overall, breast cysts are the most common cause of breast symptoms, and they typically arise in patients assigned female at birth between the ages of 35 and 50 years, usually because of an overproduction of estrogen and suppression of progesterone. Fortunately, most breast cysts are benign; but new cysts in older postmenopausal patients pose a higher risk of underlying malignancy, and this risk increases if they are currently on hormone replacement therapy.

Alright, now, when a patient presents with a chief concern suggesting a breast cyst, the first step is to obtain a focused history and perform a physical examination. The most commonly reported symptom is a breast lump and possibly localized pain that worsens just prior to menstruation each month. However, some patients can be asymptomatic, and a breast lump can be discovered as part of a physical examination performed for another reason.

Speaking of which, physical examination findings that suggest a breast cyst include a palpable, solitary, smooth and firm breast mass that is freely mobile. Occasionally, the mass can also be tender on palpation. With these findings, you can suspect a breast cyst. 

The next step is to order a breast ultrasound to confirm your diagnosis. If there are no findings on the ultrasound that would indicate a breast cyst, then you should consider an alternative diagnosis. On the other hand, if a breast cyst is identified, ultrasound findings can help classify it as either a simple, complicated or a complex cyst. 

Here’s a clinical pearl! Breast findings on imaging can be categorized with a standardized system called BI-RADS, which stands for Breast Imaging-Reporting and Data System. BI-RADS is typically used for mammography findings, but it can be applied for ultrasound as well. So, with BI-RADS, the im]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fibrocystic_breast_changes:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TeiKP-6_SamzZ-5Gvxr8ZJWjRxW43qSc/_.png</video:thumbnail_loc><video:title><![CDATA[Fibrocystic breast changes: Clinical sciences]]></video:title><video:description><![CDATA[Fibrocystic breast changes include a spectrum of benign breast changes characterized by multiple bilateral nodules within the breast tissue. This condition is most commonly found in females between the ages of 30 and 50 years. Although the exact etiology is not fully understood, a hormonal component, such as overproduction of estrogen and underproduction of progesterone is likely, especially since symptoms like breast pain, also known as mastalgia, tend to worsen in a cyclical pattern towards the end of the menstrual cycle.

Alright, now, when a patient presents with a chief concern suggesting fibrocystic breast changes, the first step is to obtain a focused history and perform a physical examination. The patient might report bilateral breast nodularity, pain, swelling, and possible straw-colored nipple discharge. These symptoms may worsen just prior to menstruation each month. On physical examination, you might find multiple nodular areas, a ropey and lumpy texture, and tenderness on palpation. At this point, you should suspect fibrocystic breast changes. 

The next step is to order a breast imaging to confirm your diagnosis. Now, if your patient is younger than 35 years, order a breast ultrasound; but, if your patient is 35 years of age or older, you should obtain both a breast ultrasound and a mammogram.

Okay, let’s talk about the results. If there are no findings on imaging that would indicate fibrocystic breast changes, then you should consider an alternative diagnosis. On the other hand, ultrasound findings consistent with fibrocystic breast changes include fibroglandular tissue, clustered microcysts, distorted breast parenchyma, and an absence of  discrete masses. As for the mammogram, it might show heterogeneous and dense breast parenchyma, partially circumscribed cysts, as well as crescent-shaped calcifications in multiple lobes. If you see these findings on imaging, then you are dealing with fibrocystic breast changes.

Alright, now that we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_abscess:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ez40OcC1TEuPJtV9fRaYpouhT6eKDVTf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breast abscess: Clinical sciences]]></video:title><video:description><![CDATA[A breast abscess occurs when a bacterial infection forms a collection of purulent fluid, or pus, which leads to the development of a painful mass in the breast tissue. It is most often a complication of mastitis, which involves inflammation and infection of the breast. 

Most cases of mastitis are lactational or puerperal, resulting from prolonged milk stasis, engorgement, and the entry of bacteria through breaks in the nipple. 

Rarely, mastitis can be non-lactational or non-puerperal, which can be idiopathic, related to malignancy, or due to infection from recent surgery, nipple piercings, tattoos, or other trauma. 

A breast abscess is more likely to occur in patients who smoke, have diabetes, or can even be a sign of a more serious pathology like inflammatory breast cancer. 

Most cases are usually caused by methicillin-sensitive Staphylococcus aureus, while other bacteria like Streptococci sp., Staphylococcus epidermidis, and methicillin-resistant Staphylococcus aureus or MRSA may also be implicated. 

Alright, when assessing a patient who presents with a chief concern suggesting a skin abscess, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway and breathing first. Next, address circulation by obtaining IV access and initiating IV fluids for resuscitation. 

Here’s a clinical pearl! Keep in mind that it’s very rare for breast abscess to be the sole cause of hemodynamic instability. Thus, if the patient is unstable, then they’ve likely developed sepsis or even septic shock. 

Okay, now that you have taken care of your unstable patients, let’s talk about stable patients. Your first step is to obtain a focused history and physical examination. 

Your patient will usually report breast pain, swelling, and purulent discharge from the nipple or from a lesion on the skin. 

Make sure to ask about risk factors like a history of smoking, diabetes, recent childbirth,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mastitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nH9xUJqYST__uAMbaIkl8zxtSRW1fA1C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mastitis: Clinical sciences]]></video:title><video:description><![CDATA[Mastitis is a benign breast condition that involves ductal or periductal inflammation, which can lead to secondary infection of the breast tissue. Mastitis is frequently associated with lactation, but can affect both lactating and non-lactating patients. During lactation, reduced milk drainage can lead to bacterial overgrowth and secondary infection. On the flip side, the exact causes of non-lactational mastitis are not well understood. Non-lactating patients with recurrent mastitis should be evaluated for a rare form of the disease called granulomatous mastitis. 

Alright, so when assessing a patient with a chief concern suggestive of mastitis, the first step is to obtain a focused history and physical exam, and labs such as a CBC. 

Let’s say a patient presents who is currently lactating. They might report a history of incomplete emptying of breast milk, either from difficult or infrequent breastfeeding or perhaps from a blocked duct and engorgement. They may also report mastalgia and malaise. 

On physical exam, you might discover breast fullness, erythema, induration, and tenderness. Additionally, you may see nipple fissures or skin breaks, and the patient might even have a fever. Finally on labs, the CBC may even show a leukocytosis. If this is the case, go ahead and diagnose puerperal mastitis. 

Here’s a clinical pearl! Remember that the puerperium is a period of about 6 weeks, right after childbirth, during which the patient’s body undergoes changes to return to their original state before the pregnancy, such as uterine involution with the uterus shrinking back to its normal size.

Now that we have made a diagnosis, let’s talk about management. Start with antibiotics. Here, you want to cover common skin flora, especially Staphylococcus aureus. Since the patient is breastfeeding, be sure to use antibiotics that are safe for the baby as they might get released in the milk. Now, you also need to consider covering for MRSA, which depends on the severit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_nipple_discharge:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LbOd1yHUS2iKMYduIY5Y0LRrRmelTEg2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to nipple discharge: Clinical sciences]]></video:title><video:description><![CDATA[Nipple discharge is the expression of fluid from the breast, and can be caused by both physiologic and pathologic conditions, ranging from normal lactation to cancer. Because nipple discharge can have so many different causes - some more worrisome than others - it’s crucial to perform a detailed diagnostic workup to differentiate between them. 

When assessing a patient with nipple discharge, the first step is to obtain a focused history and physical exam. When taking history, you want to find out if the discharge is one sided or bilateral; if it’s spontaneous or has any provoking factors; if it’s associated with other symptoms; and what the discharge fluid looks like. 

On physical exam, first look for lumps, asymmetries, or changes to the breast skin or nipple and areola, as well as regional lymph nodes. 

Then, try to elicit nipple discharge by carefully applying manual pressure in a clockwise fashion around the areola. If you are unable to elicit any nipple discharge, apply a warm compress to the breast and wait a few minutes before trying again. Make sure to apply pressure at the base of the areola and not the nipple itself. It can also be helpful to palpate from the periphery of the areola toward the nipple. Finally, make sure to note the quality of any expressed discharge.

Let’s start with physiologic nipple discharge. Patients typically report bilateral nipple discharge associated with breast or nipple stimulation. On physical exam you’ll find bilateral, multiductal nipple discharge that is white, clear, or milky. If this is the case, consider physiologic discharge, and order labs including hCG, prolactin, CBC, CMP, and TSH to help you find the cause. Also, don’t forget to check if the patients’ screening mammograms are up-to-date according to their age. 

Alright, our first cause of physiologic nipple discharge is pregnancy or lactation. This is common among patients who are or were pregnant, recently gave birth, or breastfed within the past year]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_papilloma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DQID8b2FSlWCJ49JIwyYaGzUQ_qxGLvy/_.png</video:thumbnail_loc><video:title><![CDATA[Breast papilloma: Clinical sciences]]></video:title><video:description><![CDATA[Breast papillomas result from the abnormal growth of epithelial cells into the ductal lumen. Papillomas can be solitary and centrally located, arising in the main lactiferous ducts, or they can be multiple and peripheral, involving the terminal ductal lobular unit. Papillomas are generally benign but can be associated with other high-risk lesions, and rarely, malignant pathologies. 

When assessing a patient with a chief concern suggestive of breast papilloma, first obtain a focused history and physical exam. Patients might report spontaneous unilateral nipple discharge, ranging in consistency from clear to bloody. They may have noticed a breast lump or had an abnormal screening mammogram. 

On physical exam, you might palpate a breast mass, but this is less common. An important thing to do is to attempt and elicit nipple discharge. Apply gentle pressure around the areola in a clockwise fashion, and if nipple discharge occurs note the location of the duct and the exact site of your applied pressure when it was expressed. Also take note if the discharge appears to be serous to serosanguinous, or frankly bloody.

Here’s a clinical pearl! If the nipple discharge does not appear to be bloody, it can be tested with a Guaiac test kit to assess for the presence of any occult blood. 

Now, if you see these findings in history and physical, you should suspect breast papilloma and order some imaging. The first step is to obtain a breast ultrasound and a diagnostic mammogram. On ultrasound, you might see a solid nodule or mass within a dilated breast duct, as well as its associated fibrovascular pedicle. On a diagnostic mammogram, findings are oftentimes normal or unremarkable. However, a round or   mass may be seen, and occasionally even a cluster of central or peripheral microcalcifications. If you see any of these findings, you’ll want to proceed to a core needle biopsy for further investigation. 

Here’s a clinical pearl! If your patient with unilateral spontaneo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypocalcemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/piJtfIE8T12Bbq5_28-Y3e6pSBCwZNqO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypocalcemia: Clinical sciences]]></video:title><video:description><![CDATA[Hypocalcemia refers to a serum calcium level that is below the lower limit of normal, which varies among different labs but is often considered below 8.5 mg/dL. Calcium plays a vital role in various body functions, such as cardiac muscle function and nerve signaling. So, calcium imbalances such as hypocalcemia often result in abnormal cardiac rhythm and neurologic dysfunction. Some important causes of hypocalcemia that you should keep in mind include hypomagnesemia, impaired vitamin D conversion, hypoparathyroidism, and secondary hyperparathyroidism.

Now, if your patient presents with a chief concern suggesting hypocalcemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen.

Now, here’s a high-yield fact to keep in mind! If a patient has hypocalcemia, they may experience laryngospasm, seizures, or a prolonged QT interval on an ECG. This is especially true when the hypocalcemia is severe or develops rapidly. In such cases, administer intravenous calcium gluconate to increase blood calcium levels. Also, don’t forget that hypomagnesemia often occurs along with hypocalcemia, so consider giving IV magnesium in this situation as well.

Now that we&amp;#39;re done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones. 

If your patient is stable, first obtain a focused history and physical examination, and order labs, including serum calcium and magnesium levels. 

Your patient may report numbness around the mouth, paresthesias of the fingers and toes, and even emotional lability. On the other hand, physical exam can reveal positive Chvostek or Trousseau signs. The Chvostek ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_retention:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b9VgVDARSOW3xVR1E_gami4eTkiRc-2J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary retention: Clinical sciences]]></video:title><video:description><![CDATA[Urinary retention refers to a condition characterized by the inability to voluntarily empty the urinary bladder. It can be acute or chronic, ranging from partial to complete urinary retention. Based on the underlying cause, urinary retention can occur due to spinal cord compression or injury; or as a result of medication side effects; urethral obstruction; or urinary tract infection.

Now, if your patient presents with urinary retention, your first step is to obtain a focused history and physical examination. Alright, let’s start with individuals that present with acute urinary retention. These patients typically report sudden inability to voluntarily void in combination with a sudden lower abdominal pain. On your physical exam, you will typically notice suprapubic tenderness and palpable bladder. These findings are highly suggestive of acute urinary retention. 

Now, let’s go back and take a look at patients with chronic urinary retention. These individuals typically report a gradual inability to voluntarily void and lower abdominal discomfort or pain. Some patients might report symptoms of urinary tract infection, such as fever and dysuria, while others might report use of medications associated with urinary retention. Finally, history might reveal benign prostate hyperplasia or diabetes mellitus. On the physical exam, again, you will notice suprapubic tenderness and palpable bladder. These history and physical exam findings are highly suggestive of chronic urinary retention! 

Now, here’s a clinical pearl to keep in mind! In biologically female individuals, assess for potential pelvic masses or organ prolapse, which can also result in urinary retention! Additionally, in all patients, you can order an ultrasound to check whether or not the bladder is full, and you can also assess for hydronephrosis.

Now, once you diagnose urinary retention, you should always consider bladder decompression using a urethral or suprapubic catheter. This way you will elimin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neurogenic_shock:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TO7SmXDFTWCLdEpIgHhbCWP1RKm2GFSI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neurogenic shock: Clinical sciences]]></video:title><video:description><![CDATA[Neurogenic shock is a serious condition associated with the loss of vascular sympathetic tone and a subsequent unopposed parasympathetic response usually from an injury to the spinal cord. 

When blood vessels lose sympathetic stimulation, they vasodilate leading to a sudden drop in blood pressure from a sharp decrease in peripheral vascular resistance.  

Classically, patients present with hypotension, bradycardia, and temperature dysregulation. Bradycardia in neurogenic shock is the result of the unopposed parasympathetic nervous system in the absence of the sympathetic stimulation. This is a unique characteristic of neurogenic shock that differentiates it from other types of shock. 

The most common cause of neurogenic shock is blunt traumatic injury to the spinal cord above the level of T6. Other less common causes include Guillain-Barré syndrome, spinal anesthesia, and transverse myelitis. One important thing you should keep in mind is that neurogenic shock is not the same as spinal shock. Spinal shock refers to flaccidity of muscles and a loss of reflexes after a spinal cord injury.  

Alright, let’s dive into how we can diagnose and treat a patient with neurogenic shock! When you encounter a patient with signs and symptoms suggestive of neurogenic shock, you should first perform an ABCDE assessment then immediately begin acute management. 

Start by stabilizing the patient’s airway, breathing, and circulation. This means that you may need to intubate the patient, obtain IV access, and administer fluids before continuing with your assessment. In addition, spinal cord stabilization is crucial in cases of neurogenic shock with suspected spinal cord injury to prevent further damage.

Make sure to continuously monitor the patient’s vital signs and hemodynamic status. You can consider placing an arterial line, which will allow for more accurate monitoring of the patient’s blood pressure and mean arterial pressure, or MAP.

Now that you have stabilized you]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bladder_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Lm8IQ3fqQ62H7-ySdipeEYjHSUqh7es5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bladder injury: Clinical sciences]]></video:title><video:description><![CDATA[Traumatic bladder injuries are rare injuries most often caused by blunt trauma to the genitourinary tract, but it can also be caused by penetrating or iatrogenic trauma. According to the anatomic location involved, these injuries are classified as intraperitoneal, extraperitoneal, or urethral injury. 

As with any trauma patient, the first step in assessing a patient with signs and symptoms suggestive of bladder injury is to perform the primary survey, including the ABCDE assessment. Acute management should be started immediately to stabilize the patient&amp;#39;s airway, breathing, and circulation. 

First, intubate or insert a surgical airway if needed. Next, ensure adequate ventilation. Then, obtain a large-bore IV or IO access, and monitor vitals continuously. Additionally, you’ll need to calculate the Glasgow Coma Scale. As well, position the patient supine in a flat position, and stabilize the cervical spine with a C-collar. It is essential to ensure that the patient&amp;#39;s entire skin is exposed, meaning back and front, to ensure there’s no other obvious injuries. 

Finally, you need to assess for pelvic injury, which can lead to severe bleeding. Keep in mind that a bladder injury, per se, wouldn’t typically cause your patient to be hemodynamically unstable; so, if your patient who has a bladder injury is unstable, you should suspect that they have an associated pelvic fracture, and manage accordingly. If the pelvis is unstable, stabilize it with a mechanical pelvic binder. This will hold the pelvis in place, and maintain internal pressure, which helps control the bleeding. Finally, place an indwelling urinary catheter, also known as Foley, to maintain a patent urinary outflow tract.

Here&amp;#39;s a clinical pearl! If you saw blood at the meatus, and therefore suspect urethral injury, avoid urethral catheterization, because it can cause further damage to the urethra and create a false passage with the catheter. Instead, consider placing]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypothermia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jBTkEkRuQrS6nFthOkteEr9KTwWoSer1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypothermia: Clinical sciences]]></video:title><video:description><![CDATA[Hypothermia is defined as a core body temperature of less than 95 degrees Fahrenheit or 35 degrees Celsius. It occurs when your body expends more heat than it creates  typically due to prolonged exposure to cold, like getting stuck in a snowstorm or losing heat in homes during the winter. Based on the core temperature, hypothermia is divided into mild, moderate, and severe hypothermia. Regardless of the severity, hypothermia puts the individual at a very high risk of becoming hemodynamically unstable and is life-threatening, so it must be managed promptly.

you should first perform an ABCDE assessment. Acute management should be started immediately to stabilize the patient&amp;#39;s airway, breathing, and circulation. Next, obtain IV access and consider starting warmed IV fluids. Next, put your patient on continuous vital sign monitoring, including body temperature, blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry! Finally, if your patient is in cardiac arrest, manage according to ACLS guidelines.

obtain a focused history and physical examination, as well as a 12-Lead ECG. Your patient will have a history of prolonged cold exposure. History could also reveal risk factors like a history of alcohol use, older age, or that your patient is experiencing homelessness; they may also have severe manifestations of psychiatric conditions, like mania or psychosis.

Physical examination will reveal a core temperature lower than 95 ºF or 35ºC, as well as hyperventilation initially, and may progress to hypoventilation as core temperature continues to decrease. In addition, you may notice shivering, but keep in mind that shivering will eventually stop if exposure to cold continues, and your patient may also develop confusion, lethargy, and reduced responsiveness.

The ECG may reveal sinus tachycardia initially, or progress to sinus bradycardia or a junctional rhythm. Keep in mind that junctional rhythm can be distinguished from a sinus brady]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pelvic_fractures:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/q4bbhEc6TeiCHZmqaHHPaabqQk6edpRc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pelvic fractures: Clinical sciences]]></video:title><video:description><![CDATA[Pelvic fractures occur in the bones that form the pelvic ring. They can be caused by low-energy trauma, like a fall, or a high-energy trauma, like a car crash. 

Pelvic fractures can be associated with damage to nearby structures, like venous plexus shear or arterial injuries, resulting in extensive blood loss, which can be life-threatening and is a surgical emergency; as well as rectal, vaginal, and bladder lacerations. Pelvic fractures can also be associated with neurological injuries that may cause bowel or bladder incontinence and dysfunctional sexual activity. 

Now, pelvic fractures can be stable or unstable. Stable fractures occur in one spot, so the pelvis remains stable. On the other hand, unstable fractures involve multiple fractures at different spots that can cause the bones of the pelvic ring to become displaced, and the entire pelvic ring to become unstable. A type of unstable pelvic fracture are &amp;quot;open-book&amp;quot; fractures, which involve disruption of the sacroiliac joints; and are associated with retroperitoneal hemorrhage.

As with any trauma patient, the first step in assessing a patient with a chief concern suggesting pelvic trauma is to perform the primary survey including the ABCDE assessment. Acute management should be started immediately to stabilize the patient&amp;#39;s airway, breathing, and circulation. 

First, secure the airway and ensure adequate ventilation. Then, place multiple large-bore peripheral IVs or IOs, immediately start fluid resuscitation, and monitor vital signs continuously. Next, you’ll calculate the Glasgow Coma Scale, position the patient supine in a flat position, and assess for spinal cord injury. Finally, it’s essential to ensure that the patient&amp;#39;s entire skin is exposed, meaning back and front, to be certain there are no other obvious injuries. 

Bear in mind that severe bleeding is commonly associated with pelvic fractures, so be on the lookout for it, and in addition to givin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sickle_cell_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tSKkKgvISbaeFLrQgh13HzkKRsO06Jcf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sickle cell disease: Clinical sciences]]></video:title><video:description><![CDATA[Sickle cell disease, or SCD for short, is a genetic disorder affecting hemoglobin that causes red blood cells to become deformed and sickle-shaped. Sickled cells can obstruct small blood vessels and disrupt the supply of oxygen to tissues, resulting in severe pain and tissue damage within any organ system. Once the diagnosis of SCD is confirmed, patients should be monitored for related complications.

Now, if your patient presents with a chief concern suggesting SCD, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, start IV fluids, and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen.

Now, here’s a clinical pearl! Severe complications of SCD include acute chest syndrome and acute episodes of vaso-occlusion and hemolysis that present with life-threatening ischemia or infarction of the central nervous system or pulmonary vasculature. Be on the lookout for the sudden development of red-flag signs such as new-onset weakness, altered mental status, chest pain, or respiratory distress. 

Now, let’s go back to the ABCDE assessment and take a look at stable patients.

 First, obtain a focused history and physical examination. Your patient might report weakness and fatigue, as well as a history of chronic anemia and recurrent infections. Additionally, the family history may be significant for other relatives with SCD. Patients often experience acute or chronic pain, especially in the long bones, pelvis, or back. 

On the other hand, a physical exam typically reveals an ill-appearing patient with tachycardia and an audible heart murmur on cardiac auscultation. Skin exam commonly reveals jaundice and pallor, and you might also notice scleral icterus. Finally, you might find bone and joint tenderness, warmth, or swelling.

At]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Pediatric_Musculoskeletal_Trauma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MledurL4QZ_rmdP8JkzgCOJPQoW7lAhn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Pediatric Musculoskeletal Trauma]]></video:title><video:description><![CDATA[Falls and minor accidents are common in childhood and sometimes result in musculoskeletal trauma, like fractures. Since a child’s musculoskeletal system isn&amp;#39;t yet fully developed, fractures can lead to permanent disability or premature death, if left untreated. As the nurse, you&amp;#39;ll provide care for your pediatric patients with fractures by monitoring for complications, providing supportive measures, and reinforcing education.   

Now, a fracture is defined as a complete or partial break in a bone, which occurs when the physical force applied to the bone is stronger than the bone itself. The most common type of fracture is a closed, or simple, fracture, which occurs when the bone breaks, but the overlying skin remains intact. Other types of fractures include comminuted fractures where the bone breaks into multiple fragments and open, or compound, fractures, which occur when the fractured ends of bone pierce through the overlying skin. 

Most often, fractures are caused by trauma, associated with a fall, sports injuries, or not wearing proper safety equipment, like a helmet or seatbelt.  However, in some cases, fractures result from child abuse. Usually these become apparent when a child presents with injuries that have implausible or inconsistent explanations, like femoral and humeral fractures in patients who can&amp;#39;t walk yet, or repeated injuries, shown on imaging as multiple fractures at different stages of healing. 

Okay, so, patients with fractures typically experience pain, swelling, and tenderness to the area of injury. You may also notice discoloration or bruising to the area, decreased range of motion, and numbness or tingling distal to the site of injury. Since clinical manifestations of fractures can look similar to other musculoskeletal injuries, diagnosis is confirmed using imaging, such as an X-ray, CT scan, or MRI.  

Most fractures are treated with rest and immobilization to promote proper healing and alignment, typ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Clinical_Sciences_Medical_Platform_Tour</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sEu-fRgETCWN7APnBlCM-EIaTiuZcOA2/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis Clinical Sciences Medical Platform Tour]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis Clinical Sciences Medical Platform Tour through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Clinical_Sciences_Osteopathic_Medicine_Platform_Tour</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c69dbK9rSECUxRGq8ux11bB-TAK62W2h/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis Clinical Sciences Osteopathic Medicine Platform Tour]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis Clinical Sciences Osteopathic Medicine Platform Tour through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Clinical_Sciences_Physician_Assistant_Platform_Tour</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7M1f0yh1ScG0XT1fnIhdxIITQrClAk9P/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis Clinical Sciences Physician Assistant Platform Tour]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis Clinical Sciences Physician Assistant Platform Tour through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Clinical_Sciences_Health_Professions_Platform_Tour</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Oz1O_ERwRQO_K7Z_apwiPTi5RTC8IVzI/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis Clinical Sciences Health Professions Platform Tour]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis Clinical Sciences Health Professions Platform Tour through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Syringomyelia:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d5JlHkejRpWdIWlI_BLUNjEMSyah9t_A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Syringomyelia: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Syringomyelia: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/PGAP3-congenital_disorder_of_glycosylation:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6YuuIt3NQSGE9Kid7K3a3evxSb2_h-kS/_.jpg</video:thumbnail_loc><video:title><![CDATA[PGAP3-congenital disorder of glycosylation: Year of the Zebra]]></video:title><video:description><![CDATA[PGAP3-congenital disorder of glycosylation, or PGAP3-CDG for short, also known as Mabry syndrome and previously known as hyperphosphatasia with impaired intellectual development syndrome 4, is a rare inherited neurological disorder caused by defects in one of the pathways of glycosylation.

Glycosylation is a biological process where a series of enzymes work sequentially to attach sugar chains, called glycans, to proteins and fatty molecules, forming glycoproteins and glycolipids, respectively. When there is a defect in glycosylation, one of the steps leading to the attachment of glycans does not take place correctly, which affects the final structure of multiple glycoproteins. 

In PGAP3-CDG, there is a defect in the enzyme involved in stabilizing and anchoring these glycoproteins to a cell’s surface, which can have effects on multiple biological processes, such as helping cells recognize, adhere, or communicate with one another. Alkaline phosphatase, or ALP, is an example of a glycoprotein that is normally bound to the cell membrane but when the anchor is defective, ALP is unable to bind properly and is instead released into the bloodstream.

Like most other disorders of glycosylation, PGAP3-CDG is an autosomal recessive disorder, meaning an individual must inherit two copies of the mutated PGAP3 gene, one from each parent, to develop the disorder.

Affected individuals can have distinctive facial features that include a broad and short nose, wide-set eyes, a thin upper lip, large ears, and full cheeks; though these features may not be apparent in infancy. In addition, some individuals are born with a small head circumference and cleft palate, which is when the roof of the mouth doesn’t fuse completely. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Clinical_Sciences_Nurse_Practitioner_Platform_Tour</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MVAxMPWBRRyy817mtEhYQlKtQ7uAkDJn/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis Clinical Sciences Nurse Practitioner Platform Tour]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis Clinical Sciences Nurse Practitioner Platform Tour through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_of_Cancer_Complications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kDuiA3pQTM_PKlKWVJmA5uNQR2uEqYJE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care of Cancer Complications for the LPN]]></video:title><video:description><![CDATA[Cancer, or malignancy, refers to a group of diseases characterized by abnormal cell growth and differentiation, which changes cellular appearance and function. These changes are harmful to normal cells and can cause several complications, which can be directly related to cancerous tissue, a side effect of treatment, or a combination of both. 

Let’s look at some of the complications of cancer, starting with pain. Patients with cancer are at risk for acute and chronic pain, which can decrease quality of life. When caring for your patient with cancer, ask about their pain and encourage open discussion about their pain on an ongoing basis. Be sure to report any uncontrolled pain to the registered nurse, or RN.  

Reinforce teaching about the use of pharmacologic interventions, including nonsteroidal anti-inflammatory drugs, or NSAIDs; opioids; and adjuvant medications like corticosteroids; and nonpharmacologic interventions, such as guided imagery, relaxation techniques, distraction, massage, and acupuncture.  

Reassure your patient that combinations of treatments can be tried to find pain management that is effective. Then, coordinate care with the RN and interdisciplinary team to provide interventions as indicated to carry out the plan of care.  

Alright, next let’s explore infection as a complication of cancer. Several factors can lead to an infection in your patient with cancer, including tissue damage from ulceration; necrosis caused by cancerous tissue; tumors compressing organs; and decreased immunity due to the cancer or treatment-induced neutropenia, which is a low number of neutrophils, or the infection-fighting white blood cells. 

When providing care, be sure to monitor your patient for signs or symptoms of infection, such as a temperature of 100.4 F or 38 C or higher, cough, or diarrhea. Keep in mind, though, that neutropenia can diminish signs of infection, so your patient may have an infection and be asymptomatic.  

Now, to help prevent infe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Pressure_Injury_Prevention</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ddv7Sk99QT_FixeOAOPMMNN2TnC0qSXl/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Pressure Injury Prevention]]></video:title><video:description><![CDATA[Nurse Nathan works at a rehabilitation hospital and is caring for Larry, a 72-year-old with a left below-the-knee amputation related to complications from diabetes mellitus. In collaboration with the registered nurse, RN Ashmeet, Nurse Nathan goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Larry’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Nathan recognizes important cues, including Larry’s vital signs, which are  temperature of 98.6 F or 37 C, heart rate 90 beats per minute, respirations 18 breaths per minute, blood pressure 130/80 mmHg, and oxygen saturation 95 percent on room air. Nurse Nathan notes that Larry has been incontinent of urine and is struggling to effectively reposition himself in bed. Nurse Nathan also notices that Larry has clinical signs of malnourishment such as dry, thin skin and brittle nails and hair.  

Next, Nurse Nathan analyzes these cues.  He reviews the electronic health record, or EHR, and notes that Larry developed a pressure injury on his sacrum during a past hospitalization that has since healed. He also sees that RN Ashmeet calculated Larry’s pressure injury risk using the Braden Scale which indicated that Larry is at high risk for developing another pressure injury.  

Nurse Nathan understands that pressure injuries involve damage to the skin or underlying tissue because of prolonged pressure, which causes reduced blood flow. This results in tissue hypoxia and ischemia, which ultimately leads to necrosis and ulceration. Nurse Nathan knows that most often, pressure injuries develop in patients who have difficulty moving around or are totally immobile. He also knows other factors increase the risk for pressure injury, like thinning of skin and subcutaneous tissue due to age and impaired nutrition and hydration; exposure to skin irritants, like urine; as well as diabetes mellit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preventative_Screenings_for_Women_and_Related_Nursing_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X3e_OSKcSIy2iuVGscP8DlmUTR2SRyHq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preventative Screenings for Women and Related Nursing Care]]></video:title><video:description><![CDATA[Preventative health care refers to screenings that can identify diseases in the early stages, so they can be treated promptly. Common preventative screenings for patients assigned female at birth include mammograms for breast cancer and Papanicolaou, or Pap, tests for cervical cancer.  

Mammograms screen for breast cancer and involve taking X-rays of the breasts. Patients typically start mammograms around age 45 to 50 but can be started earlier or later, depending on risk factors, like a positive family history of breast cancer or certain genetic mutations, like BRCA1 or BRCA2. 

When taking care of your patient who&amp;#39;s having a mammogram, reinforce teaching about the procedure. Explain how it involves compressing the breast tissue between two plates while an X-ray is taken. Reassure them that the procedure uses a very low dose of radiation and that it causes brief discomfort. Also let them know that they can schedule their mammogram after their menstrual period when their breasts are less swollen and sensitive. Lastly, remind them to avoid wearing deodorant, lotions, or powder on the day of their mammogram, since these can cause white spots on the X-ray. 

Screening for cervical cancer involves the Pap test, which screens for cervical cancer by swabbing the cervix during a pelvic examination and looking for abnormal cervical cells. Testing for human papillomavirus, or HPV, can also be done to detect strains of HPV, including the high-risk strains that may cause cervical cancer. When Pap and HPV tests are done together, it&amp;#39;s known as co-testing. The recommended age for cervical cancer screening can vary but typically begins around age 21 and is done every three to five years, depending on history, risk factors, and results of previous screenings.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Leukemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M4Fk2CBQS9Sjj2tgSFsx6JN5R4yl02bl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Leukemia]]></video:title><video:description><![CDATA[Nurse Tracy works on an inpatient oncology unit and is caring for Margie, a 60-year-old with a history of chronic lymphocytic leukemia, or CLL. In collaboration with the registered nurse, RN Lisa, Nurse Tracy goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Margie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tracy recognizes important cues, including Margie’s vital signs which are temperature 98.8 F or 37.1 C, heart rate 90 beats per minute, respirations 18 per minute, blood pressure 122/84 mmHg, and oxygen saturation of 98 percent.  

Nurse Tracy notes Margie has various small bruises on her back and legs and generalized lymphadenopathy, or swollen lymph nodes.  

She notices Margie grimacing with movement, and when asked about pain, Margie reports a pain level of 5 out of 10 in her legs and a pain tolerance level of 3 out of 10.  

Nurse Tracy sees a sign on Margie’s door requesting no visitors, so she asks Margie about how she’s feeling. 

Nurse Tracy: Margie, I see you don&amp;#39;t want visitors today.  

Margie: No, I’m very tired. Besides, I’ve been such a burden to them; they probably want a break from me.  

Nurse Tracy: You don’t have to have visitors if you aren’t feeling up for it. Have your family or friends mentioned not wanting to visit? 

Margie: No, they haven’t, but I’d rather be alone. There’s so much I can’t control right now with my leukemia, and I’m feeling overwhelmed. Also, my pain is bothering me. I have extra doses of pain medicine to take between scheduled doses, but I forget to ask until my pain is too bad.  

Next, Nurse Tracy analyzes these cues. She reviews the electronic health record, or EHR, and notes that Margie has scheduled pain medication as well as doses to take as needed, or PRN, for breakthrough pain. The medication administration record shows that Margie hasn’t receiv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preventing_Complications_of_Immobility</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MwPXv7reRouDER74Cn5rXXzxSbeyN7FD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preventing Complications of Immobility]]></video:title><video:description><![CDATA[Immobility is when a patient’s movement is restricted. Immobility can be purposeful and temporary like when a patient is immobilized to promote healing due to a broken bone; the result of a pathologic condition, like a stroke; or secondary to pain, which causes patients to be reluctant to move. As the nurse you are responsible for preventing complications of immobility. 

Now, immobility can affect multiple body systems and cause a number of complications. In the respiratory system, immobility can cause weakening of chest wall muscles, decreasing the ability to cough, and pooling of pulmonary secretions. This can result in respiratory complications, like atelectasis, which happens when the alveoli in the lungs collapse, leading to pneumonia, as well as hypoventilation and decreased gas exchange.  

In the cardiovascular system, a decreased autonomic response to position changes can lead to orthostatic hypotension; and decreased return of venous blood to the heart, along with slowed blood flow, promotes clot formation, increasing the risk of venous thromboembolism.  

Next, in the GI system, peristalsis is decreased, which can cause constipation. Anorexia is also common, which can result in a negative nitrogen balance and weight loss.  

Effects on the urinary system include urinary stasis and an increased risk of urinary tract infections.  

There are also musculoskeletal effects, like muscle atrophy and weakness. When immobility is prolonged, the skeletal muscle tissue attached to the bone becomes fibrotic, causing the muscle fibers to become short and stiff, resulting in a fixed joint that’s difficult and painful to move. Immobility also causes loss of calcium from the bones, causing decreased bone density and osteoporosis.  

Other complications of immobility affect the integumentary system, where prolonged pressure on the skin and underlying tissues can lead to tissue hypoxia and ischemia, and eventually pressure injuries.  

Lastly, psychosocial compl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Theories_and_Therapies_in_Mental_Health_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OqBPVm4dQpOEJodvNdcezUm3RXiO5ZuH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Theories and Therapies in Mental Health Nursing]]></video:title><video:description><![CDATA[Healthcare professionals can use theories to understand human development and behavior. Theories can also provide a framework for planning individualized care for patients and to guide the application of therapies to treat individuals with mental health disorders. 

Now, an early developmental theory about human behavior was developed by Sigmund Freud, called psychoanalytic theory. This theory is based on the idea that a person’s behaviors are influenced by their unconscious thoughts. Freud also developed the theory of psychosexual development, comprised of 5 stages from infancy to adulthood that explains how emotional disturbances are rooted in failure to progress through each stage.  

For example, a child aged 0 to 1 year is in the oral stage. During this stage, an infant finds pleasure and satisfaction through feeding and sucking. The child also begins to recognize their parent or caregiver as separate from themselves, and any disruption in the availability of the parent or caregiver could impair the child’s development, resulting in maladaptive behaviors later in life.  

Other developmental theories propose alternate ways to explain human development. Jean Piaget proposed a theory of cognitive development, which looks at how children develop their thinking and make sense of their world. According to Piaget, children&amp;#39;s development occurs in four distinct stages from birth to age 15. For example, during the concrete operations stage from age 8 to 11, children develop an understanding of the world in terms of words, numbers, and time. They also begin to use logic to understand principles like cause and effect, as well as size and difference; which allows the development of skills like arranging their toys according to their common or different characteristics, like color or shape. A learning disability or mental health disorder may be present if a child does not progress through the stages of cognitive development as expected.  

Another d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Nursing_Care_of_Suicidal_Patients</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Mz_dN-2aQuCTNsuVV-0Pq29pQ6qPf0yh/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Nursing Care of Suicidal Patients]]></video:title><video:description><![CDATA[Nurse Iris works on an inpatient psychiatric unit and is caring for Dee, a 30-year-old patient with a history of depression and previous suicide attempts, who was admitted for suicidal ideation. In collaboration with the registered nurse, RN Amrita, Nurse Iris goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Dee’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Iris recognizes important cues, including Dee’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 65 beats per minute, respirations 16 breaths per minute, and blood pressure 116/70 mmHg. She also notices Dee does not make eye contact and has a flat affect. 

Nurse Iris: Hi Dee, I’ll be your nurse today. How are you feeling? 

Dee: I’m upset.  My friend brought me to the hospital because I told him I wish I was dead.  I don’t want to be here anymore.  

Nurse Iris: I’m sorry to hear that. I want you to know that I and the rest of your medical team care about you. We&amp;#39;re here to support you and keep you safe.  

Next, Nurse Iris analyzes these cues. She reviews the electronic health record, or EHR, and notes that Dee is prescribed fluoxetine for depression and has been hospitalized in the past year for suicidal ideation. She also notes that Dee scored a 19 out of 27 on his PHQ-9 assessment, which is a nine-question, self-reporting depression survey, indicating a moderately severe level of depression. Nurse Iris recognizes that Dee needs a safe environment while he receives treatment for his depression and suicidal ideation. 

Now, using the information she’s gathered, along with Dee’s medical history, Nurse Iris reports her findings to RN Amrita, and together they choose a priority hypothesis of risk for suicide.  

Then, they generate solutions to address Dee’s suicidal ideation that will include pharmacologic and nonpharmacologic interv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutritional_Needs_During_Pregnancy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fdc58DirQBmhHG3NM98mZyrESo_xVR1k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutritional Needs During Pregnancy]]></video:title><video:description><![CDATA[During pregnancy, the patient and growing fetus have specific nutritional needs to support sufficient weight gain and development. These include increased calories; a variety of macronutrients such as carbohydrates, fats, and protein; as well as vitamins and minerals, like folic acid, iron, and calcium.  

Extra calories are needed during pregnancy to provide the energy to fuel the increased maternal basal metabolic rate; to support the production and maintenance of maternal and fetal tissues, amniotic fluid, and placenta; as well as develop fat stores used for energy during delivery and breastfeeding. By the second trimester, caloric intake should increase by about 340 calories per day, and by about 450 calories per day in the third trimester.  

Weight gain during pregnancy is gradual, and patients who are not under- or overweight should gain about 1 pound per week and up to 35 pounds by term delivery. Additional calories should come from nutrient-dense foods, like low fat dairy products, lean meats, legumes, whole grain breads and cereals, and fruits and vegetables; instead of fast food and sweets that have a lower nutritional value. 

Now let’s move on to some of the specific macronutrients including carbohydrates, fats, and proteins which are needed in large amounts. Carbohydrates are the primary source of calories used for energy. Good sources of carbohydrates are complex carbohydrates such as starchy vegetables and whole grains. In addition to providing calories, complex carbohydrates contain additional nutrients like vitamins, minerals, and fiber. Fiber is the non-digestible part of carbohydrates that provides bulk to stool to help prevent constipation, which commonly occurs during pregnancy due to hormonal changes that slow the motility of the intestines.  

Next, fats provide fat-soluble vitamins along with calories; and they supply fatty acids that help with fetal neurological and visual development. Sources of healthy fats include nuts, seeds, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Pediatric_Patients_With_Accidental_Poisoning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AtANJ_L-TLGXhbrLLUOeGCe1Q7GD22Av/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Pediatric Patients With Accidental Poisoning]]></video:title><video:description><![CDATA[Nurse Olivia works on a pediatric inpatient unit and is caring for Daisy, a 2-year-old who was admitted yesterday for observation after accidentally ingesting acetaminophen. In collaboration with the registered nurse, RN Tamika, Nurse Olivia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Daisy’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.
First, Nurse Olivia recognizes important cues including Daisy’s vital signs which are temperature 98.6 F, or 37 C, heart rate 118 beats per minute, respiratory rate 27 breaths per minute, and blood pressure 92/52 mmHg. Nurse Olivia notes Daisy is pale and is restless at times, but easily consoled by Ellen, her caregiver. Nurse Olivia determines Daisy’s pain rating is 3 out of 10 according to the Face, Legs, Activity, Cry, and Consolability, or FLACC, scale. Gentle abdominal palpation reveals no tenderness, which is consistent with RN Tamika’s previous assessment.

Next, Nurse Olivia analyzes these cues. She reviews the electronic health record, or EHR, and learns that prior to admission, Daisy consumed an unknown quantity of acetaminophen pills while Ellen was busy preparing dinner. After counting the remaining pills in the bottle, Ellen realized Daisy ingested about 13 pills and immediately contacted Poison Control, who told her to bring Daisy to the emergency department.
Nurse Olivia notes that Daisy’s weight is 12.7 kilograms, or 28 pounds. She also knows that the toxic dose of acetaminophen is 150 milligrams per kilogram in children, and since Daisy ingested 13, 160 milligram pills, she exceeded the toxicity level for her age and weight. Nurse Olivia recognizes that an overdose of acetaminophen can cause hepatotoxicity, and the clinical course progresses over time.
Based on Daisy’s presentation and history of acetaminophen ingestion, Nurse Olivia determines that Daisy needs effect]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fetal_Development_and_Related_Nursing_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LIBwy2soR6_Bv90tHeDtN21ATXCLSXkG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fetal Development and Related Nursing Care]]></video:title><video:description><![CDATA[Fetal development refers to the formation and growth of an infant that occurs over 39 to 40 weeks to prepare for extrauterine life.
Fetal development can be divided into three main stages: zygote, embryonic, and fetal.

The first stage, called the zygote stage, begins with conception, when a sperm fertilizes an egg forming a zygote. As the zygote undergoes cell division and develops, it travels through the fallopian tube until it implants in the inner lining of the uterus, or endometrium. This entire process takes about two weeks. 
Next is the second stage, called the embryonic stage, which takes place from weeks 3 through 8 of gestation. This is when the embryo begins to develop three primary germ layers called the ectoderm, mesoderm, and endoderm, which will eventually give rise to all the organs and tissues of the embryo. For instance, the ectoderm develops into the nervous system along with skin, and the bones that form the skull; the mesoderm develops into structures like skeletal muscles, bone, and the circulatory system; and the endoderm develops into the pulmonary, gastrointestinal, and endocrine systems. Since all major organ systems form during this time, the embryo is especially vulnerable to teratogens, or substances that can damage cells and cause abnormalities in development.
Finally, the third stage, called the fetal stage, takes place from the ninth week until birth and is characterized by rapid growth and development. During weeks 9 through 12, the central nervous system, GI system, and heart are fully developed. This is also when the heartbeat can be detected via doppler ultrasound, and spontaneous fetal movements occur. Other developmental milestones include differentiation of genitals as male or female; production and secretion of urine by the kidneys; and production of blood cells within the liver, spleen, and lymphatic tissue.

Between weeks 13 and 16, lanugo, or soft, fine hairs, cover the fetal body, The fetus also begins to swallow]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Cholecystitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l5_pElXzSVuaxyckrmAfjFamT-CzabxM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Cholecystitis]]></video:title><video:description><![CDATA[Nurse Sandy works on a medical-surgical unit and is caring for Natasha, a 40-year-old female with a history of obesity who&amp;#39;s been diagnosed with acute cholecystitis and is awaiting surgical intervention. In collaboration with the registered nurse, RN Mark, Nurse Sandy goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Natasha&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Sandy recognizes important cues, including Natasha’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 95 beats per minute, respirations 20 breaths per minute, blood pressure 109/83 mmHg, and pulse oximetry 99 percent on room air. Natasha rates her pain at 3 on the pain scale. She sees that Natasha is holding an emesis bag, which contains a small amount of emesis. Nurse Sandy also notices that Nastasha has IV fluids infusing into her peripheral IV.
Nurse Sandy auscultates Natasha’s abdomen and notes active bowel sounds in all quadrants, which is consistent with RN Mark’s assessment. However, upon palpation, Natasha grimaces and puts her hand over her mouth.

Natasha: Please don’t press down on my stomach, I feel like I’m going to throw up again.
Nurse Sandy provides Natasha with a fresh emesis bag and rubs her back as she vomits.
Afterwards, Nurse Sandy analyzes these cues. She understands that cholecystitis refers to inflammation of the gallbladder, which is a small, pear-shaped organ located beneath the liver. In patients with acute cholecystitis, bile or gallstones, which are made of bile that has hardened, build up inside the gallbladder, causing irritation of the mucosa lining its walls. This also causes pressure in the gallbladder to increase, leading to wall distension and inflammation.

Nurse Sandy then reviews the electronic health record, or EHR, and notes that Natasha initially presented to the emergency ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Pancreatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xi3JsHggQnizlIE5g6nOd6WBTlqRMaeG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Pancreatitis]]></video:title><video:description><![CDATA[Nurse Gerdie works on a medical-surgical unit and is caring for Leo, a 47-year-old who was admitted for acute pancreatitis secondary to chronic alcohol use. In collaboration with
the registered nurse, RN Don, Nurse Gerdie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Leo&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.
First, Nurse Gerdie recognizes important cues, including Leo’s vital signs, which include blood pressure 145/90 mmHg, heart rate 88 beats per minute, temperature 99.2 °F, and respirations 18 breaths per minute. Nurse Gerdie notices Leo is diaphoretic, his gown is damp, and he’s holding an empty emesis bag. She also sees that he has IV fluids infusing in his right forearm.

Nurse Gerdie: Hi Leo, it looks like you&amp;#39;re not feeling well. What&amp;#39;s your pain level right now on the 0 to 10 pain scale?
Leo: My pain is a six. It feels like I can’t lie down on my back or get comfortable at all. And I’m nauseated.
Nurse Gerdie: I understand, I’m going to help you feel more comfortable.
Next, Nurse Gerdie analyzes these cues. She reviews the electronic health record, or EHR, and notes that Leo’s prescriptions include hydromorphone IV every 3 hours as needed, and his last dose was given two and a half hours ago; and she sees sublingual ondansetron is ordered PRN for nausea, but he hasn’t yet received a dose today.

Nurse Gerdie understands that acute pancreatitis refers to the sudden inflammation and destruction of the pancreas, which is a long gland located in the upper abdomen, or the epigastric region, behind the stomach.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sanofi_Osmosis_Platform_Overview</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wP2br5SZTS6EBxZcZL2_fkdfRoWix7Y_/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis + Sanofi: Osmosis Platform Overview]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis + Sanofi: Osmosis Platform Overview through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autoimmune_polyglandular_syndrome_type_I_(NORD):_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L0eXBdWuQlyVZb9W8c6fUIE0T4KrLUgR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autoimmune polyglandular syndrome type I (NORD): Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Autoimmune polyglandular syndrome type I (NORD): Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vulvovaginal_candidiasis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vpAVJXMWRm2rWy-iF2FyJCm1TOqpjwdv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vulvovaginal candidiasis: Clinical sciences]]></video:title><video:description><![CDATA[Vulvovaginal candidiasis, or VVC, is the second most common form of vaginitis, after bacterial vaginosis. It is the result of inflammation of the vagina and vulva due to infection with yeast, most commonly by Candida albicans. Now, asymptomatic colonization of the vagina with Candida species is common. However, when these species overgrow and invade the epithelial cells of the vagina, inflammation occurs. 

Your first step in evaluating a patient who presents with a chief concern suggesting vulvovaginal candidiasis is a focused history and physical exam. Patients typically report an abnormal vaginal discharge, as well as vaginal itching. They may also describe vulvar symptoms, such as itching, pain, redness or swelling. Other symptoms might include dysuria; or dyspareunia, which is pain during sex. 

When taking history, be sure to ask about any risk factors. First up, there’s the recent use of medications like broad spectrum antibiotics, which can alter the vaginal flora and allow Candida to overgrow. Next, ask if they have recently treated their symptoms with over the counter medications. Many patients successfully treat VVC with over the counter antifungals. However, when patients present with incomplete or partial treatment, it can be more difficult to make a clinical diagnosis. Finally, the medical history should also include questions about underlying medical risk factors for VVC, such as a history of diabetes or immunosuppression, which may include conditions like HIV, or patients on systemic corticosteroids.    

Here is a clinical pearl! VVC is uncommon, before puberty, and in postmenopausal patients who are not using hormone replacement therapy, because Candida species are unlikely to proliferate in the vagina in the absence of estrogen.

Now for a focused physical exam. You’ll notice that the vaginal discharge is often thick, white and curd-like. The vulva may appear erythematous with edema and excoriations from scratching, and may develop ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Venous_Thromboembolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hrD5_Yz0SpiTFmbf8MBSBGTYR9_EIT1J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Venous Thromboembolism]]></video:title><video:description><![CDATA[Nurse Hakeem works on a medical-surgical unit and is caring for Lucille, a 72-year-old who was admitted for a deep vein thrombosis, or DVT in her left iliofemoral vein and is currently awaiting discharge. In collaboration with the registered nurse, RN Owen, Nurse Hakeem goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Lucille’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Hakeem recognizes important cues. He notes slight redness and swelling of Lucille’s left leg. Upon light palpation, Nurse Hakeem notes Lucille’s leg is tender, and she rates her pain as 2 out of 10 and describes it as aching, but tolerable. 

Next, Nurse Hakeem analyzes these cues. He reviews the electronic health record, or EHR, and sees that Lucille recently had surgery, and that an ultrasound identified the DVT. He also notes that Lucille has been receiving continuous IV heparin, which was discontinued yesterday, that she will be transitioned to oral anticoagulation therapy, and then discharged with a prescription for oral dabigatran.   

Nurse Hakeem recognizes that immobility after surgery increased Lucille’s risk for a DVT, and that the thrombus lodged in her vein caused inflammation and decreased venous return to her heart, resulting in swelling and pain in her leg. He understands that anticoagulants like heparin are often used initially to keep the clot from getting larger, to prevent the formation of new clots, and to decrease the risk of a venous thromboembolism, or VTE, which happens when the clot breaks free and travels to the heart and into the lungs.  

Nurse Hakeem also knows that oral anticoagulants, like dabigatran, can be used after a heparin infusion is discontinued to decrease the body’s ability to make clots, and that these treatments can also increase Lucille’s chances of bleeding.  

Now, using the information he&amp;#39]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Pediatric_Patients_With_Closed_Head_Injuries</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6OLNBRGPTS6jcKH63PpsrY8iTmq4eiEs/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Pediatric Patients With Closed Head Injuries]]></video:title><video:description><![CDATA[Nurse Tyisha works in a pediatric primary care clinic and is caring for Justin, a 10-year-old who is being evaluated following a concussion that occurred during a soccer game one week ago. In collaboration with the registered nurse, RN Christine, Nurse Tyisha goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Justin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tyisha recognizes important cues, including Justin’s vital signs which are temperature 98.9 F or 37.1 C, heart rate 100 beats per minute, respirations 16 breaths per minute and blood pressure 104/70 mmHg. Justin reports a mild headache and rates it as a 2 out of 10 on a numeric pain scale. Justin is alert and oriented to person, place, and time.  There’s also a small, healing bruise above his left eyebrow.  

Nurse Tyisha gathers additional information from Justin and his caregiver, Mary, who’s at the bedside. 

Nurse Tyisha: Hi Justin. How are you feeling? 

Justin: Uhm, okay, my head feels kind of…  

Mary: (Interrupting Justin) He just hasn’t been acting like himself since the injury. He’s been irritable and forgetful, especially with his chores, which just isn’t like him. He’s especially tired after school, and I noticed he gets frustrated when working on his computer or even when he’s playing video games or watching television. 

Justin: I can answer for myself, Mom. I just feel tired. It’s making me grumpy, and my head is kind of fuzzy.  

Next, Nurse Tyisha analyzes these cues. She reviews the electronic health record, or EHR and notes that Justin’s concussion occurred following head-to-head contact during a soccer game one week ago. Although he didn’t lose consciousness, he had poor coordination following the event.  

Nurse Tyisha knows a concussion is a type of closed head injury that occurs when an event, like the head striking a hard objec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Cirrhosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BjH_0-YcQyW_D0pkb0Ojs03FRuaqVA_C/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Cirrhosis]]></video:title><video:description><![CDATA[Nurse Abigail works at a long-term care facility and is caring for Thomas, a 72-year-old male with a history of hyperlipidemia and obesity who was diagnosed with cirrhosis secondary to nonalcoholic fatty liver disease. In collaboration with the registered nurse, RN Raashida, Nurse Abigail goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Thomas’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Abigail recognizes important cues, including Thomas’ vital signs, which are temperature 98.8 F or 37 C, heart rate 98 beats per minute, respirations 20 breaths per minute, blood pressure 106/68 mmHg, and oxygen saturation 97 percent on room air.  

Nurse Abigail notes his sclera and skin are jaundiced, or yellow-tinged; he has scattered petechiae, which are small, reddish-purple spots that occur because of bleeding from tiny blood vessels underneath the skin; and his abdomen is round and distended with fluid from a condition called ascites. When asked to turn during his bed bath, Thomas becomes fatigued and short of breath. 

Next, Nurse Abigail analyzes these cues. She reviews the electronic health record, or EHR, and notes that Thomas has gained 9 pounds since his weight was last taken, approximately one week ago. She also sees that Thomas was seen by the physical therapist last week but refused treatment.  

Nurse Abigail knows that cirrhosis is a condition where chronic inflammation causes the liver to become irreversibly scarred. Over time, bands of scar tissue compress the network of blood supply in the liver, leading to increased venous pressure and portal hypertension, which occurs as blood backs up into the portal vein. Higher portal vein pressure means that fluid in blood vessels gets pushed out of the veins and into the peritoneal cavity, causing ascites. And she understands that, as pressure in the portal syst]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Safety_and_Comfort</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zF27KfMQReW6vnW_1vZdGS-qS3W19C78/_.jpg</video:thumbnail_loc><video:title><![CDATA[Safety and Comfort]]></video:title><video:description><![CDATA[Ensuring patients&amp;#39; safety by protecting them from harm is one of the main goals of nursing care. As the nurse, you’ll take measures to promote your patient’s safety while ensuring their comfort. 

Now, there are several ways you can promote safety and comfort when providing patient care. To ensure you’re providing the right care to the right patient, you should always use at least two patient identifiers, such as their name and date of birth. You’ll also take steps to decrease medication errors by being familiar with the medications you administer, and always using safe medication administration principles, such as properly labeling medications and having another nurse double check high alert medications, like insulin.  

Another way you can promote safety is to keep your patient safe from infections by performing hand hygiene, and using clean or sterile techniques, as indicated. And you’ll also implement transmission-based precautions, as needed, to protect other patients, their families, and members of the health care team. For instance, when contact precautions are needed, you’ll place your patient in a private room or cohort them together with other patients who are either infected or colonized with the same infectious agent. 

Now, another goal of nursing care is promoting your patient’s comfort. You can do this by adjusting their room temperature, ventilation, and humidity to meet their preferences and medical needs. You’ll also provide adequate lighting so your patient can navigate their room without injury, but not too bright as to cause discomfort.  

Also remember that there are some odors common in the health care setting that can cause your patient to feel nauseated. You can control these odors by promptly emptying bedpans and bedside commodes; removing used food trays; changing soiled linens as soon as possible; throwing away foul-smelling items in the dirty utility room; and avoiding use of scented products, like wearing perfume. Las]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nausea_and_vomiting_of_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tWgaZIQ6S5etL53dpbJUuHE_Qvq0d834/_.png</video:thumbnail_loc><video:title><![CDATA[Nausea and vomiting of pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Nausea and vomiting of pregnancy is a common condition occurring in the majority of pregnancies. It’s generally referred to as “morning sickness” but can actually occur at any time of the day. The exact cause is unknown, though it is thought to be due to increased human chorionic gonadotropin, or HCG for short, associated with early pregnancy, as well as the effects of estrogen and progesterone, which relax the lower esophageal sphincter and slow gastric motility. Nausea and vomiting of pregnancy has a wide spectrum of presentations, from mild symptoms to severe disease and hyperemesis gravidarum, which may even require hospitalization.

When assessing a pregnant patient who presents with a chief concern suggesting nausea and vomiting, your first step is to obtain a focused history and physical. Patients typically report nausea, vomiting, malaise, and an inability to tolerate their diet. 

While obtaining history, pay attention to certain risk factors for nausea and vomiting of pregnancy, such as a history of nausea and vomiting in a prior pregnancy and a family history of nausea and vomiting during pregnancy. Additionally, you might find other risk factors like a history of migraine headaches, or motion sickness. Nausea and vomiting in pregnancy is also more likely to occur in multiple gestation like twins or triplets, and in a molar pregnancy. On a physical exam, you may find signs of dehydration, such as decreased skin turgor and dry mucous membranes.

Here’s a clinical pearl! The majority of patients with nausea and vomiting of pregnancy will have symptoms before 9 weeks of gestation. However, if your patient presents with nausea and vomiting for the first time after 9 weeks, or if they have additional signs and symptoms like fever, headache, abnormal neurologic examination, palpable goiter, or severe abdominal pain, then you should look for a more serious underlying condition.

Now, back to your patient! Based on these history and physical exam f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Diabetes_Mellitus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gc7ug7SyT7qXAh6wVByew6AVS2u-Qd00/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Diabetes Mellitus]]></video:title><video:description><![CDATA[Nurse Charlotte works on a medical-surgical floor and is caring for José, a 53-year-old with a history of type 1 diabetes mellitus who was admitted for diverticulitis and just returned to the unit after a CT scan. In collaboration with the registered nurse, RN Luke, Nurse Charlotte goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about José’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking actions, and evaluating outcomes.  

First, Nurse Charlotte recognizes important cues, including José’s vital signs which are temperature 98 F or 36.6 C, heart rate 87 beats per minute, respirations 18 breaths per minute, and oxygen saturation 95 percent on room air. She also notices that José’s hands are trembling slightly, and he’s diaphoretic.  

Nurse Charlotte gathers more information from José. 

Nurse Charlotte: Hi José, welcome back from your scan. How are you feeling this morning? 

José: I’m okay I guess; I just feel a little weak and shaky. It started about ten minutes ago. 

Nurse Charlotte: Have you had anything to eat today?  

José: No, I haven’t eaten since last night because of that test I had this morning. 

Next, Nurse Charlotte analyzes these cues. She reviews the electronic health record, or EHR, and notes that José received five units of insulin, for a blood glucose level of 121 mg/dL last evening. She also sees that José was ordered to be NPO after midnight for an abdominal CT scan that he underwent this morning. 

Nurse Charlotte understands that type 1 diabetes mellitus is a condition caused by autoimmune destruction of the pancreatic beta cells, so they can’t produce and secrete insulin, and that treatment typically requires subcutaneous insulin administration. She also knows that hypoglycemia, or blood glucose below 70 mg/dL, is likely to occur if insulin is taken when a patient isn’t eating, like when a patient is NPO, leading to clinical findings such as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Nursing_Care_at_the_End_of_Life</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/38hG6gonQqGcUfYPGVrzc4bWTUWJkKzk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Nursing Care at the End of Life]]></video:title><video:description><![CDATA[Nurse Leslie works in a hospice house and is caring for Esther, an 89-year-old with a history of end-stage chronic obstructive pulmonary disease, or COPD. In collaboration with the registered nurse, RN Zach, Nurse Leslie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Esther’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Leslie recognizes important cues, including Esther’s vital signs which are temperature 99 F or 37.2 C, heart rate 98 beats per minute, and blood pressure 88/42 mmHg. Her radial pulse is weak and thready. Esther’s breathing pattern is shallow, and there’s an audible gurgling sound as she breathes in and out. Nurse Leslie notices that Esther’s skin looks mottled and pale, and that it feels cool to the touch. She also notes that Esther appears restless and uncomfortable.  

Next, Nurse Leslie analyzes these cues. She reviews the electronic health record, or EHR, and sees that Esther has a current Do Not Resuscitate, or DNR, order and is on comfort care. She also notes that Esther’s urine output was 90 milliliters over the past 12 hours.  

Nurse Leslie knows that as death approaches, body functions begin to slow. Blood pressure and heart rate decrease, and pulses become weak. Then, as circulation slows, there’s less urine output due to decreased renal perfusion, and extremities can become edematous, mottled, dusky, and cool, since there’s less circulation to the periphery. Respirations become slow and irregular; and as death nears, a build-up of saliva and mucus in the throat and upper airways cause breathing to sound wet and gurgling. Episodes of apnea and hyperventilation, called Cheyne-Stokes respirations, may also occur. Nurse Leslie realizes that Esther needs supportive care at the end of her life. 

Now, using the information she has gathered, along with Esther’s medical history, Nurse Lesli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complementary,_Integrative,_and_Alternative_Therapies</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CpWyRg3qT4_SCg9xon5uWhpcSiuH19sz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complementary, Integrative, and Alternative Therapies]]></video:title><video:description><![CDATA[Complementary health approaches, or CHAs, are non-medical therapies that can be used alone or together with traditional medical care. When CHAs and traditional medical care are combined, it’s called integrative medicine. Most CHAs can be categorized as either mind and body therapies or natural products.  

Okay, so, mind and body therapies are practices where patients use their mind to impact body functions, with the goal of lessening undesirable physical and emotional symptoms, like pain or anxiety.  

Meditation is a type of therapy where patients decrease their attention on extraneous stimuli and focus on a sensation, like their breathing, or repeating a word, sound, or positive phrase. The goal is to bring about a restful state, promote a mind-body connection, and improve emotional and physical wellness.  

Next, guided imagery involves assisting patients to create a positive image in their mind, like thinking of a peaceful scenario such as sitting on the beach or walking in a forest.  

With biofeedback, patients receive specialized training to enhance awareness of their mind-body connection while learning to control certain physiological functions that typically occur involuntarily like pain, anxiety, and headaches. For instance, a patient’s respiratory rate and depth is monitored by placing electrodes on the skin to observe their physical responses. With practice, patients can use physical and mental techniques to bring about the desired physical changes    

Now, acupuncture, which is a component Chinese medicine, uses fine needles inserted into certain parts of the body to balance the flow of energy to help with problems like pain, nausea, anxiety, and depression.  

There’s also chiropractic therapy, where a patient’s spine is manipulated to bring it into proper alignment and relieve pain. It is often used in conjunction with other therapies like application of ice or heat, as well as massage, which involves soft tissue manipulation, including kn]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Using_Supplemental_Oxygen</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nA2joDEPSKC6fxzsW6_eooKsSrafUc7R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Using Supplemental Oxygen]]></video:title><video:description><![CDATA[Nurse Ahmad works on an inpatient medical-surgical unit and is caring for Marietta, a 72-year-old, who underwent a surgical procedure 3 days ago. In collaboration with the registered nurse, RN Laura, Nurse Ahmad goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Marietta’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Ahmad recognizes cues, including Marietta’s vital signs which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 24 breaths per minute, blood pressure 133/66 mmHg, and oxygen saturation 87 percent on room air. Nurse Ahmed notes that Marietta is taking short, shallow breaths and appears anxious. He also sees that Marietta is lying on her side, with the head of the bed flat.  

Nurse Ahmad raises the head of her bed and assists Marietta to reposition herself. 

Nurse Ahmad: Hi Marietta, it looks like you’re having trouble breathing. 

Marietta: It’s hard to take a deep breath. 

Nurse Ahmad: I’ve repositioned you, which should help your lungs expand. Focus on taking deep breaths in through your nose and out through your mouth.  

Then, Nurse Ahmad applies oxygen to Marietta via nasal cannula at two liters per minute, according to his unit’s protocol. 

Nurse Ahmad then analyzes these cues. He reviews the electronic health record, or EHR, and notes that despite seeing documentation that Marietta was taught how to use her incentive spirometer to help keep her lungs expanded, the device isn’t in her room. He also knows that anesthesia during surgery can reduce surfactant production in the lungs, which is needed to keep the little air sacs, called alveoli, open and full of air. He understands that when there’s less surfactant, the walls of the alveoli tend to collapse, leading to atelectasis, where portions of the lungs are not fully expanded.  

Nurse Ahmad realizes that thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Substance-Related_Disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_Lat4DkgRU_IqJ_LSdKXejNBREeqlJNr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Substance-Related Disorders]]></video:title><video:description><![CDATA[A substance use disorder, also sometimes referred to as a substance-related disorder, is when a patient is unable to control their use of a legal or illegal substance which interferes with the activities of their daily life. Commonly abused substances include CNS depressants, like alcohol and opioids; CNS stimulants, like cocaine; and combined CNS depressants and stimulants, like tobacco.   

Now, there isn’t a single cause of substance use disorders, but rather it’s a multifactorial condition, meaning that there’s a combination of genetic and environmental risk factors and triggers. These include a family history of a substance use disorder or having a mental health disorder like depression or anxiety. Certain experiences also put a patient at risk for developing a substance use disorder like using the substance at an early age, or experiencing physical, sexual, or emotional abuse.  

Okay, so, in general, clinical manifestations of a substance use disorder occur when long-term use of a substance leads to severe physical, psychological, or social impairment. This can include behavioral changes, like needing the substance daily, intense urges to use the substance, and using the substance despite disruption of the person’s life.  

Other clinical manifestations depend on the type of substance used. For example, CNS depressants, like alcohol, can cause neurological symptoms like slurred speech, weakness, and impaired mobility; and opioids can cause sleepiness and decreased respiratory rate. On the other hand, CNS stimulants, like cocaine, cause hyperactivity, tremors, and elevated heart rate; and combination CNS depressants and stimulants, like tobacco, initially cause stimulatory effects like sweating, tachycardia, and elevated blood pressure, followed by depressor effects like difficulty breathing, slurred speech, and muscle weakness.  

Diagnosis of a substance use disorder begins with the patient’s history and physical examination. The diagnosis is confi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_Health_Care_of_Older_Adults</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ORojEvXjRduRakQ0yMXk4InvTYOBCu0j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mental Health Care of Older Adults]]></video:title><video:description><![CDATA[Mental health care during older adulthood, or the time from 65 years of age until death, is focused on helping patients adapt to age-related changes. As the nurse, you’ll monitor your older adult patient’s mental health and collaborate with the registered nurse to intervene as needed.  

One of the most common experiences that impacts the mental health of the aging population is loss, which can take on various forms at this stage of life. One of the most significant ways losses can occur is through the death of lifelong partners or friends.  Also, retirement can mean there are fewer opportunities to socialize with colleagues and often leads to a loss of income.  

Other forms of loss include changes in physical function, such as decreased stamina and impaired mobility, vision, or hearing, which can impact their ability to function independently. Some individuals can adapt to the changes that come with loss, while others who are not able to cope effectively can become withdrawn and socially isolated.  

Another problem that impacts the mental health of older adults is elder abuse. This is when an older adult is taken advantage of in various ways, including physical harm, sexual abuse, neglect, and financial exploitation. Older adults are more vulnerable to abuse when they’re lonely, lack social support, or have impaired physical or mental health where they depend on others for their daily care.  

Abusers can be caregivers, like health care workers, friends, or even family members.  

An older adult experiencing elder abuse may be fearful or have depressive symptoms. Poor personal hygiene, unexplained injuries, or sexually transmitted infections may also be present.   

Now, depression is not a normal part of aging, but it’s the most common health disorder in older adults. Depression can occur late in life, or it could be a continuation of a preexisting problem that developed earlier in life. In older adults, depression is more likely to occur if they are l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sleep_apnea:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eHF47JXCShWAqj_SDh19IRJBTMe4ic_x/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sleep apnea: Clinical sciences]]></video:title><video:description><![CDATA[Sleep apnea is a condition characterized by episodes of either the reduction or cessation of inspiratory airflow during sleep, commonly resulting in recurrent nighttime hypoxemia. Untreated sleep apnea over time may lead to the development of complications, such as hypertension, heart disease, atrial fibrillation, stroke, diabetes, and sudden death.

Sleep apnea can be classified as obstructive sleep apnea or OSA, and central sleep apnea or CSA.

In OSA, respiratory effort is present but apnea occurs due to collapse of the patient’s upper airway, which is especially common in obesity, conditions associated with oropharyngeal crowding, and nasal allergies. 

On the other hand, in CSA, apneic episodes occur due to a lack of spontaneous respiratory effort, associated with alterations in central respiratory drive. This is typically seen in patients with heart failure, neurologic diseases, and sedating medications. 

Finally, if no underlying condition is associated with central sleep apnea, we are talking about primary, or idiopathic central sleep apnea. 

If your patient presents with a chief concern suggesting sleep apnea, the first step is to obtain a focused history and physical exam. Your patient may report either excessive daytime sleepiness or fatigue. 

They may also report loud snoring and morning headaches, as well as nighttime breathing disturbances, such as frequent awakenings, pauses in breathing, choking, or gasping. Also, history findings might include some underlying chronic conditions, like hypertension, or heart failure. 

On the flip side, physical examination typically reveals a neck circumference of greater than 16 inches in biologically female individuals and 17 inches in biologically male individuals. Other important physical exam findings include central obesity and enlarged oropharyngeal structures, such as the tonsils, uvula, or tongue.

If your patient presents with these signs and symptoms, you should suspect sleep apnea, so your ne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glioblastoma:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PiTrCs-IRkeNyqrz8fPE76k2TOaDHPNr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glioblastoma: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Glioblastoma: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Personal_Care_and_Hygiene_in_a_Hospitalized_Patient</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BGOwhdWzRrS5upnwkCXmygtRT6iWR3ut/_.png</video:thumbnail_loc><video:title><![CDATA[Personal Care and Hygiene in a Hospitalized Patient]]></video:title><video:description><![CDATA[Nurse Melinda works on a medical-surgical floor and is caring for Beatrice, an 80-year-old with a history of iron-deficiency anemia. In collaboration with the registered nurse, RN Elijah, Nurse Melinda goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Beatrice’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Melinda recognizes important cues including Beatrice’s vital signs, which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 19 breaths per minute, and blood pressure 123/88 mmHg. During bedside report, Nurse Melinda learns that Beatrice tires easily, becomes short of breath with activity, and needs assistance to get up to the bathroom.  

Nurse Melinda then gathers information from Beatrice. 

Nurse Melinda: Hi Beatrice, how are you this morning? 

Beatrice: I’m tired. I want to get cleaned up, but it takes so much energy. 

Nurse Melinda: I can help you get cleaned up. How about you do as much as you can, and when you feel tired, I can take over? 

Beatrice: Okay. 

Nurse Melinda analyzes these cues.  She reviews the electronic health record, or EHR, and notes that prior to admission, Beatrice lived independently, but began having trouble performing activities of daily living, or ADLs, due to fatigue.  

Nurse Melinda understands that iron is essential to produce hemoglobin in red blood cells, or RBCs, which deliver oxygen to the tissues, and that iron-deficiency anemia develops when there’s not sufficient iron to sustain normal hemoglobin production. As a result, there’s not enough hemoglobin to fill a normal-sized RBC, so the bone marrow starts producing microcytic, or smaller, cells that contain less hemoglobin. She also knows that a lack of hemoglobin can cause decreased oxygenation, leading to symptoms like weakness, fatigue, and reduced exercise tolerance, making it difficult t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chlamydia_trachomatis_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vBVoEoYyR2uGBoFpSZcxWRY_RBOkL1mG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chlamydia trachomatis infection: Clinical sciences]]></video:title><video:description><![CDATA[Chlamydia trachomatis is the most common bacterial sexually transmitted infection, and it’s a mandatory reportable infection as a public health measure. It can affect multiple anatomic sites, most commonly the urethra and cervix, but also the eyes, oropharynx, and rectum. Chlamydia is often asymptomatic, resulting in a large reservoir of untreated infections. 

These infections can lead to pelvic inflammatory disease and increase the risk of infertility, ectopic pregnancy, and chronic pelvic pain. Additionally, chlamydia during pregnancy also increases the risk of prelabor rupture of membranes, preterm labor, and low birth weight infants, and transmission to the neonate may cause conjunctivitis, called ophthalmia neonatorum, and pneumonia. 

Your first step in evaluating a patient who presents with a chief concern suggesting Chlamydia trachomatis infection is a focused history and physical exam. Let’s start with biologically male patients. Since chlamydia is a sexually transmitted infection, or STI, a complete sexual history is important including questions about new partners and both oral and anal intercourse. 

A private, confidential discussion is important for all patients, including young patients like adolescents. Although it can be difficult, you should ask caregivers of young patients to step out of the room for this discussion. Additionally, whenever a young patient has a positive sexual activity history, always consider sexual assault or abuse, especially if the patient is a child. If there is abuse going on, you will need to follow up with allegations of abuse in accordance with your State’s law.

Once sexual history is complete, you can move on to signs and symptoms. Patients may report symptoms at various anatomic sites. They may have a sore, itchy throat or difficulty swallowing. Or they may report genitourinary symptoms such as lower abdominal pain, dysuria, pyuria, and testicular pain or swelling. Lastly, anal and rectal symptoms include pa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neisseria_gonorrhoeae_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AP7mpGB_Q6iz5V7Il2i1uTzJTLSLtt_7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Neisseria gonorrhoeae infection: Clinical sciences]]></video:title><video:description><![CDATA[Neisseria gonorrhoeae is the second most common sexually transmitted bacterial infection in the United States, and it’s a mandatory reportable infection as a public health measure. It can affect multiple anatomic sites, most commonly the urethra and cervix, but also the eyes, oropharynx, and rectum. Many infections are asymptomatic. 

Now, untreated infections can result in pelvic inflammatory disease, which increases the patient’s risk for ectopic pregnancy, infertility, and chronic pelvic pain. Transmission of gonorrhea to the neonate can occur during vaginal delivery. Gonorrhea in neonates can lead to infections such as ophthalmia neonatorum, also called gonococcal conjunctivitis, which may lead to blindness. 

Your first step in evaluating a patient who presents with a chief concern suggesting Neisseria gonorrhoeae infection is a focused history and physical exam. 

Let’s begin with biologically male patients. First, obtain a complete sexual history including questions about new partners and both oral and anal intercourse. Be sure to discuss sexual activity, particularly recent sexual activity or new partners. Provide a private, confidential discussion. Although it may be difficult, you should ask caregivers of young patients to step out of the room for this discussion. Additionally, always consider sexual assault or abuse whenever a young patient has a positive sexual activity history, especially if the patient is a child. If there is abuse going on, you will need to follow up with allegations of abuse in accordance with your State’s law.

Now patients may report a variety of symptoms, corresponding to the site of infection. They may describe a sore, itchy throat and difficulty swallowing or pelvic symptoms such as pelvic pain, dysuria, thick greenish or yellow urethral discharge, or testicular pain or swelling. Lastly, they might report rectal symptoms including painful bowel movements or rectal spotting. 

On a physical exam, your findings will refl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bacterial_vaginosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-TRPSAAtQou_PpLux17SlADRRzWgWbck/_.png</video:thumbnail_loc><video:title><![CDATA[Bacterial vaginosis: Clinical sciences]]></video:title><video:description><![CDATA[Bacterial vaginosis, or BV, is the most common cause of abnormal vaginal discharge. Keep in mind this is not a true infection but a dysbiosis, meaning an imbalance of the normal microorganisms in the vagina. This happens when the hydrogen peroxide and lactic acid producing Lactobacillus species are replaced by an overgrowth of anaerobes such as Gardnerella vaginalis and Prevotella species. The presence of BV can increase the risk of pelvic inflammatory disease and postprocedural gynecologic infections, as well as increase one’s susceptibility to sexually transmitted infections such as HIV, chlamydia and herpes simplex virus type-2, or HSV-2. In pregnancy, it is associated with prelabor rupture of membranes, preterm birth, intra-amniotic infections, and postpartum endometritis. 

Your first step in evaluating a patient with a chief concern suggesting bacterial vaginosis is a focused history and physical exam. BV is often asymptomatic. However, patients might report a thin, watery, grayish-white discharge, and an unpleasant “fishy” vaginal odor. Many patients report increased symptoms during menses or after intercourse. 

Be sure to ask about risk factors for BV, starting with a sexual history. BV is not sexually transmitted, but it’s associated with certain sexual behaviors, such as having a new partner, having multiple partners, having HSV-2 seropositivity, and not using a condom. On the other hand, BV rarely occurs in patients who have never been sexually active. Additionally, BV is more prevalent in those using a copper intrauterine device. Using other contraceptives won’t increase one’s risk, but hormonal contraception might even be protective against it. Finally, another important risk factor for BV involves certain hygiene practices such as vaginal douching and vulvar shaving. 

Now, when performing a physical exam, you will find a thin grayish-white homogeneous vaginal discharge and an unpleasant “fishy” odor that results from volatile amines produce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Enteral_Nutrition</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/32wJIjxQSkqR2As5q0JVve5sT6KOyivM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Enteral Nutrition]]></video:title><video:description><![CDATA[Enteral nutrition provides fluids and nutrients directly into the GI tract through a feeding tube. As a healthcare professional, you’ll be responsible for caring for patients receiving enteral nutrition. 

Now, enteral nutrition might be especially helpful for patients who have difficulty chewing or swallowing as a result of head or neck trauma; surgery; coma; dementia; nervous system disorders; or tumors of the head, neck, or esophagus. 

Now, there are various ways a feeding tube can go into the GI tract. The most common one is a nasogastric, or NG, tube that goes through the nose and then down into the stomach. A naso-intestinal, or NI tube, also goes through the nose, but it ends in the small intestines. 

Tubes can also be inserted through a surgical opening, or stoma, in the abdominal wall and into the stomach, known as a gastrostomy tube, or G-tube. A common type of gastrostomy tube is a percutaneous endoscopic gastrostomy tube, or PEG tube for short, that’s inserted directly into the stomach percutaneously with endoscopic guidance. Finally, tubes can also be inserted into a part of the small intestine called the jejunum, known as a jejunostomy tube, or J-tube.  

J-tubes, G-tubes, and PEG tubes are usually inserted if long-term tube feedings are anticipated and are typically used for more than six weeks; whereas NG and NI tubes are mostly preferred when tube feedings are needed for a short period of time, typically a few days or up to six weeks. 

Once the feeding tube is inserted, its placement is confirmed by X-ray. After that, your patient can start receiving enteral nutrition through the tube. There are different types of nutritional formulas that can be ordered depending on your patient’s needs. When you first start a feeding, you’ll usually begin feeding slowly while you watch for nausea, abdominal pain, or diarrhea that could indicate feeding intolerance. If the initial rate and amount of feeding is tolerated, the feedings can be increased t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Chronic_Obstructive_Pulmonary_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1WNKr8RqQKiLTu1QNW6mNZzERXCWFeK2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Chronic Obstructive Pulmonary Disease]]></video:title><video:description><![CDATA[Nurse Seema works on a medical-surgical unit and is caring for Richard, a 75-year-old male with a history of smoking, who was admitted for an acute exacerbation of chronic obstructive pulmonary disease, or COPD. Nurse Seema goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Richard’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Seema recognizes important cues including Richard’s vital signs, which are temperature of 99.6 F or 37.5 C, heart rate 98 beats per minute, respirations 28 breaths per minute, blood pressure 142/90 mmHg, and oxygen saturation 85 percent on room air. When asked about pain, Richard reports a current pain level of 0 out of 10. Nurse Seema notes that Richard’s respirations are labored, he has expiratory wheezing, and he’s leaning over in a tripod position. 

Next, Nurse Seema analyzes these cues.  She reviews the electronic health record, or EHR, and notes Richard’s arterial blood gas, or ABG, shows a low PaO2, indicating hypoxemia. She also recognizes COPD causes airway inflammation, leading to obstructed airflow out of the lungs, causing CO2 retention, making gas exchange difficult. Nurse Seema knows that Richard’s hypoxemia, wheezing, and tripod positioning indicate he’s experiencing impaired respiratory function and needs effective respiratory management. 

Now, using the information she’s gathered, Nurse Seema chooses a priority hypothesis of impaired gas exchange. 

Then, she generates solutions to address Richard’s impaired gas exchange that will include pharmacologic and nonpharmacologic interventions. She establishes an expected outcome that after intervening, Richard will maintain an oxygenation saturation between 89 to 92 percent on 2 liters nasal cannula within one hour.   

Nurse Seema then takes action to implement these solutions. She places Richard on continuous pulse oximetry m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Anemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zkygdmw5TBunAWieJqPki_SaQtKdyZnh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Anemia]]></video:title><video:description><![CDATA[Nurse Lucia works on a medical-surgical unit and is caring for Ahmed, a 61-year-old with a history of peptic ulcer disease, who was admitted several days ago for gastrointestinal bleeding. In collaboration with the registered nurse, RN Jumei, Nurse Lucia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ahmed’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Lucia recognizes important cues, including Ahmed’s vital signs, which are temperature 98.6 F or 37 C, heart rate 102 beats per minute, respirations 22 breaths per minute, blood pressure 105/70 mmHg, and oxygen saturation 93 percent on room air. Ahmed appears pale and states that he has no energy. He also reports mild headache pain, which he rates as 3 out of 10.  

Next, Nurse Lucia analyzes these cues. She reviews the electronic health record, or EHR, and notes that Ahmed’s latest hemoglobin is 7.1 g/dL and his hematocrit is 21 percent. Nurse Lucia recognizes that Ahmed is exhibiting clinical manifestations of anemia, that can occur when a bleeding peptic ulcer causes gastrointestinal blood loss.  

She also knows that blood loss can result in loss of iron, which is needed to sustain normal hemoglobin production. This impairs the oxygen-carrying capacity of the blood, resulting in impaired tissue perfusion, and symptoms like weakness, fatigue, headaches, as well as signs like pallor and tachycardia. Nurse Lucia realizes that Ahmed needs management of his anemia to promote effective tissue perfusion and oxygenation. 

Now, using the information she has gathered, along with Ahmed’s medical history, Nurse Lucia works in collaboration with RN Jumei to choose a priority hypothesis of impaired peripheral tissue perfusion.  

Then, along with RN Jumei, she generates solutions to address Ahmed’s impaired perfusion that will include pharmacologic and nonpharmacologic me]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Hypertension</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h4ue960EQpSjHxkK3G8VVkp4TKm_U6iv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Hypertension]]></video:title><video:description><![CDATA[Nurse Tom works at a primary care clinic and is caring for Mahlik, a 62-year-old who is being seen for a wellness check. In collaboration with the registered nurse, RN Jenny, Nurse Tom goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Mahlik’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tom recognizes important cues, including temperature 99.4 F or 37.5 C, pulse 75 beats per minute, respirations 16 breaths per minute, blood pressure of 156/89 mmHg, and oxygen saturation 97% on room air.  

Next, Nurse Tom asks Mahlik about his history.  

Nurse Tom: Do you usually have high blood pressure? Do any of your family members have high blood pressure? 

Mahlik: My dad and older brother do. My job is stressful, so maybe that’s contributing to it. I’ve checked my blood pressure at the drug store, and it’s been around 150/90, but with work, I haven’t had time to come in and have it checked. 

Nurse Tom: Stress can contribute to high blood pressure, and having family members with high blood pressure can increase your likelihood of having it too. What foods do you usually eat? 

Mahlik: I mostly eat fast food because I’m always on the go.  

Nurse Tom: Can you tell me about how often you smoke, drink alcohol, and exercise? 

Mahlik: I don’t smoke, never have. I drink maybe 1 to 2 beers a week on average, and honestly, I don’t exercise as much as I should. I’m just so busy with work.  

Nurse Tom analyzes these cues. He reviews the electronic health record, or EHR, and notes Mahlik’s body mass index, or BMI, is 28 kg/m2. Nurse Tom knows that blood pressure is determined by factors like peripheral vascular resistance, or the force the heart needs to overcome to pump blood into circulation, and the total volume of blood circulating in the body; and he knows if these increase, blood pressure can also increase. Nurse Tom also un]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Left-sided_Heart_Failure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JJmHjH-ERIOdcqvgE1R2ivg4RviuH3Y_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Left-sided Heart Failure]]></video:title><video:description><![CDATA[Nurse Alex works on an inpatient cardiac unit and is caring for Manny, a 65-year-old with a history of hypertension, who was admitted for left-sided heart failure. In collaboration with the registered nurse, RN Donna, Nurse Alex goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Manny’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Alex recognizes important cues, including Manny’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 100 beats per minute, respirations 22 breaths per minute, blood pressure 100/60 mmHg, and pulse oximetry 89 percent on 2 liters nasal cannula. Upon auscultation, they note extra heart sounds, S3 and S4, as well as crackles throughout Manny’s lungs, which is consistent with RN Donna’s assessment. They also notice that Manny’s breathing is labored, and he reports increasing fatigue over the last week.  

Next, Nurse Alex analyzes these cues. They review the electronic health record, or EHR, and see that Manny’s most recent brain natriuretic peptide, or BNP, was 600 pg/mL and ejection fraction was 40 percent. Nurse Alex also notes that Manny is prescribed the loop diuretic, furosemide, and received his last PO dose yesterday. 

Nurse Alex understands that heart failure is a condition where the heart is unable to pump effectively enough to maintain cardiac output to meet the demands of the body. With left-sided heart failure, the left ventricle isn’t able to pump with enough force to push blood into the aorta and the rest of the body. When this happens, the blood remaining in the left side of the heart can back up into the lungs, causing pulmonary problems such as dyspnea, tachypnea, crackles, decreased oxygen saturation, and fatigue. Nurse Alex also knows that the heart’s extra workload and inability to pump out the excess fluid can cause extra heart sounds.  

Nurse Alex realiz]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Atrial_Fibrillation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2okmB1K7SSeuv78nCJ0sCH3nQYufjOq-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Atrial Fibrillation]]></video:title><video:description><![CDATA[Nurse Jamaal works on an inpatient cardiac unit and is caring for Laurie-Ann, a 64-year-old, with a history of hypertension. She was admitted two days ago after stabilization in the emergency department, or ED, for atrial fibrillation, commonly referred to as Afib, with rapid ventricular rate, or RVR. In collaboration with the registered nurse, RN Eden, Nurse Jamaal goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Laurie-Ann’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Jamaal recognizes important cues, including Laurie-Ann’s vital signs, which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respirations 16 breaths per minute, blood pressure 126/84 mmHg, and oxygen saturation of 95 percent on room air. Laurie-Ann is awake, alert, and appears comfortable. Nurse Jamaal also notes that the bedside cardiac monitor shows that she&amp;#39;s currently in an irregularly irregular heart rhythm.  

Next, Nurse Jamaal analyzes these cues. He reviews the electronic health record, or EHR, and notes that Laurie-Ann came to the ED for dizziness and shortness of breath and was diagnosed with Afib, which is a cardiac arrhythmia that occurs when the regular electrical impulses generated from the heart’s natural pacemaker, known as the SA node, are overridden by disorganized impulses from other areas of the heart. These areas have often been damaged from the effects of conditions like hypertension or coronary artery disease, and the impulses they generate result in many rapid mini contractions, usually between 350 and 600 per minute. 

So, instead of one efficient atrial contraction, the atria have a quivering, twitching movement, or fibrillation. The fibrillation causes inefficient emptying from the atria into the ventricles, which means that blood tends to stay in the atria for longer than usual, increasing th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Gastroesophageal_Reflux_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wo6ivAAnTEesRkKwjb4-VzJyTjWOhWrQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Gastroesophageal Reflux Disease]]></video:title><video:description><![CDATA[Nurse Max works in a primary care office and is caring for Anuja, a 54-year-old with a history of gastroesophageal reflux disease, or GERD, who&amp;#39;s being seen for a three month follow-up appointment. In collaboration with registered nurse, RN Steve, Nurse Max goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Anuja’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Max recognizes important cues including vital signs which are temperature 98.2 F or 36.9 C, heart rate 76 beats per minute, respirations 14 breaths per minute and regular, blood pressure 128/84 mmHg, and oxygen saturation 98 percent on room air. Nurse Max asks Anuja if she’s having any pain, and she reports burning in her mid-upper abdomen after eating, despite taking her prescribed medication.   

Next, Nurse Max analyzes these cues. Nurse Max understands that a band of smooth muscle located between the esophagus and the stomach, called the lower esophageal sphincter, or LES, opens during swallowing to allow food to move from the esophagus into the stomach, and then closes, to keep food from backing up into esophagus. Nurse Max also knows that in patients with GERD, the LES may not close properly, or it may relax when it shouldn’t, so the acidic gastric contents can flow back, or reflux, into the esophagus. They recognize that when the esophageal lining is exposed to gastric contents, it causes symptoms like heartburn and pain in the chest and upper abdomen.  

Nurse Max then reviews the electronic health record, or EHR, and notes that Anuja has been on proton pump inhibitor, or PPI, therapy for three months to treat her GERD and should be experiencing symptom relief by now; so, they talk with Anuja about what she knows about GERD and her prescribed medication.  

Nurse Max: Anuja, I’m glad you’ve been taking your PPI every day and I’m sorry it hasn]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Digestive_Tract_Disorders</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fz12UySJSR2GY-Amq_sseUxnQSiZUVaJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Digestive Tract Disorders]]></video:title><video:description><![CDATA[Abdominal pain is discomfort felt anywhere between the chest and groin that can occur because of tissue injury, which could be due to mechanical, inflammatory, and ischemic mechanisms. 

Mechanical mechanisms of tissue injury include processes that can cut, tear, or crush abdominal contents, like penetrating injuries seen with knife wounds or blunt injuries that occur during a car crash. Next, inflammatory mechanisms involve swelling, stretching, and distention. This can occur due to infectious processes like appendicitis, diverticulitis, or gastroenteritis. Lastly, ischemic mechanisms can be caused by any condition that obstructs blood flow to abdominal contents, like with mesenteric artery occlusion, which is when a blood clot blocks the artery that supplies oxygenated blood to the intestines.   

Abdominal pain can be acute, meaning it develops quickly and resolves over hours to days; or chronic, meaning it can come and go over months or even years. Pain can also be visceral, parietal, or referred. 

Visceral pain is typically dull, crampy, or burning in nature and difficult to localize. It can be felt with conditions like appendicitis.  

Parietal pain tends to be sharp and easy to localize, like with the right upper quadrant pain felt in acute cholecystitis.  

Referred pain can be dull or sharp, difficult or easy to localize, but is typically noted outside the abdominal region, like when biliary tract disease causes pain in the right shoulder.  

Other clinical manifestations that accompany acute abdominal pain may include fever, an elevated white blood cell count, nausea, and vomiting, as well as changes in bowel patterns, like constipation, diarrhea, or the presence of blood or mucus in stool.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Breast_Cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UW_1iyCuRPGAgs2RG6XAxieNQxKEeYhM/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Breast Cancer]]></video:title><video:description><![CDATA[Nurse Rebecca works at an oncology clinic and is caring for Patricia, a 53-year-old female who had a breast biopsy confirming the diagnosis of breast cancer. Nurse Rebecca goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Patricia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Rebecca recognizes important cues, including Patricia’s vital signs, which include, temperature 98.6 F or 37 C, heart rate 105 beats per minute, respirations 21 breaths per minute, blood pressure 138/88 mmHg, and oxygen saturation 97% on room air. Nurse Rebecca also notes that Patricia is restless, crying, and shaking and states she just doesn’t know how to handle her diagnosis.  

Next, Nurse Rebecca analyzes these cues. She reviews the electronic health record, or EHR, and notes that Patricia has a family history of breast cancer. Nurse Rebecca also sees that previous nursing assessments document Patricia’s report of fatigue and difficulty sleeping. Nurse Rebecca recognizes that Patricia is experiencing emotional distress related to her breast cancer diagnosis.  

Now, using the information she&amp;#39;s gathered, along with Patricia&amp;#39;s medical history, Nurse Rebecca chooses a priority hypothesis of difficulty coping.  

Then, she generates solutions to address Patricia’s coping difficulties that will include nonpharmacologic interventions, and she establishes the expected outcome that Patricia will demonstrate effective coping skills regarding her breast cancer diagnosis by her next follow-up visit.  

Nurse Rebecca then takes action to implement these solutions. After the health care provider discusses the expected treatment plan with Patricia, the registered nurse provides Patricia with education on coping strategies. Later, Nurse Rebecca follows up to see how she’s feeling about the information she’s received and to reinforce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Benign_Prostatic_Hyperplasia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ji95XvFYRJqvJhXmZ41-UaBpRSSbq3Ty/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Benign Prostatic Hyperplasia]]></video:title><video:description><![CDATA[Nurse Suleena works on a Surgical Step-Down Unit and is caring for Pedro, a 55-year-old male with a history of benign prostatic hyperplasia, or BPH, who was admitted two days ago following a transurethral resection of the prostate, or TURP. Nurse Suleena goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Pedro’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Suleena recognizes important cues, including vital signs, which are temperature 98.0 F or 36.7 C, blood pressure 140/ 90 mmHg, heart rate 88 beats per minute, respirations 20 breaths per minute, and oxygen saturation 95 percent on room air. She also notices Pedro grimacing and shifting uncomfortably in bed. When examining the collection bag for Pedro’s continuous bladder irrigation, or CBI, Nurse Suleena notices large blood clots and amber-colored drainage.  

Next, Nurse Suleena analyzes these cues. She knows that the CBI output should be light pink, and that blood clots and amber-colored urine in the CBI drainage bag can indicate that the irrigation rate likely needs to be increased. Also, Pedro’s non-verbal cues and vital signs indicate he’s experiencing discomfort, which is also likely due to his ineffective urinary drainage. She also recognizes that bladder spasms resulting from his TURP procedure can cause additional pain. Then, she reviews the electronic health record, or EHR, and notes that Pedro’s last dose of pain medication was four hours ago. 

Nurse Suleena: Pedro, how are you feeling after your procedure? 

Pedro: I’m fine. Isn’t there a male nurse on this floor?  

Nurse Suleena: I understand that having a female nurse care for you after your TURP procedure can be unfamiliar. There are no male nurses available today, but I’m going to do my best to take care of you and make you comfortable. Is there anything I can do to help you? 

Pedro: I feel li]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Seizure_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ClabM6uwSSaIWAT8oXpeAoxFQC6DbnzU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Seizure Disorder]]></video:title><video:description><![CDATA[Nurse Cody works in a long-term care facility and is caring for Estelle, a 78-year-old with a history of epilepsy. In collaboration with the registered nurse, RN William, Nurse Cody goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Estelle’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Cody recognizes important cues, including Estelle’s vital signs, which are temperature 98.2 F or 36.8 C, heart rate 78 beats per minute, respirations 16 breaths per minute, and blood pressure 118/72 mmHg. They review the electronic health record, or EHR, and note that Estelle takes lamotrigine twice daily for epilepsy and hasn’t had any seizures or associated auras recently. Nurse Cody also sees Estelle had a routine blood draw yesterday to monitor her lamotrigine serum level, and that Estelle’s lamotrigine level is below therapeutic level, meaning it’s too low to achieve the medication’s desired effect. 

Next, Nurse Cody analyzes these cues. They know that epilepsy is a chronic seizure disorder caused by abnormal, excessive, and synchronous firing from neurons in the brain. They also recognize that Estelle’s risk of having a seizure is greater when her antiepileptic medication is at a subtherapeutic level. Nurse Cody realizes that, until Estelle’s lamotrigine levels stabilize, she will need additional safety precautions to prevent injury related to a seizure.  

Now, using the information they’ve gathered, along with Estelle’s medical history, Nurse Cody reports their findings to RN William, and together they choose a priority hypothesis of risk for injury.   

Then, Nurse Cody collaborates with RN William to generate solutions to address Estelle’s increased risk for injury that include pharmacologic and nonpharmacologic interventions. Together, they establish the expected outcome that after intervening, Estelle will not sustain ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Alzheimer_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MjLt9iPAR4ST1i52foH02ucYRzSmVZQe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Alzheimer Disease]]></video:title><video:description><![CDATA[Nurse Darian works in a long-term care facility and is caring for Rosemary, an 84-year-old female with a history of Alzheimer disease who was admitted following an open reduction and internal fixation, or ORIF, for a hip fracture a few weeks ago. In collaboration with the registered nurse, RN Piper, Nurse Darian goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Rosemary’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darian recognizes important cues, including Rosemary’s inability to recall her daughter’s name, her disorientation to date and time, and that she becomes agitated when asked several questions in a row. Nurse Darian also notes that as the evening progresses, Rosemary becomes more impulsive, and tries to get out of bed on her own. 

Next, Nurse Darian analyzes these cues. He understands that dementia is a neurological condition, caused by structural changes in the brain, and is characterized by a progressive decline in mental functions, including memory, thinking, language, behavior, mood, and personality. He knows that Rosemary’s dementia can be exacerbated by illness, such as the surgery for her hip fracture, and changes to her familiar environment.  

Nurse Darian re-enters Rosemary’s room to gather additional information.  

Nurse Darian: Hi Rosemary. How are you feeling? 

Rosemary: I&amp;#39;ve never met you. 

Nurse Darian: That’s okay, Rosemary. I’m your nurse, Darian. I met you earlier today. Are you having any pain right now? 

Rosemary: Why does everyone have so many questions all the time?  

Nurse Darian notes that Rosemary begins to sit up in bed and tries to swing her legs to the side of the bed to stand up. The two siderails by Rosemary’s head are up, as well as one siderail by her feet. She then moves towards the open space in the bed to exit, so Nurse Darian moves to prevent her from ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Therapeutic_Communication</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fd4g-Ws1R12MXG4Po5pfOI4nRPeNTHLM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Therapeutic Communication]]></video:title><video:description><![CDATA[Nurse Rose works in an outpatient mental health clinic and has noticed that one of the clients, Gabriella, is visibly upset and sitting by herself away from the other clients. Nurse Rose says, “Gabriella, what’s wrong? Is something bothering you?” Gabriella rolls her eyes and shakes her head stating, “I just want to be left alone.” Nurse Rose is formulating a response when Gabriella stands up and yells, “Why don’t you go and talk to one of the other patients? You like them better anyway!” Nurse Rose is surprised by the increase in intensity of Gabriella’s emotions and does not understand what she is referring to. Nurse Rose will use what she has learned about therapeutic communication to determine how best to handle this situation. 

Communication is the process of sending and receiving information between two or more people. One type of communication that is used by many disciplines, including nurses, is therapeutic communication. Therapeutic communication is a type of communication where information between clinicians and clients is exchanged in order to collaborate effectively and promote the physical and psychological well-being of clients. Therapeutic communication is crucial to the formation of client-centered relationships, which can foster trust and respect, especially for clients experiencing emotional distress, like Gabriella.

Another use of therapeutic communication is de-escalation, which is a goal of communication when escalation occurs. Escalation refers to an increase, or rise in intensity, during an interpersonal interaction. This is what is occurring between Nurse Rose and Gabriella. Nurse Rose can recognize Gabriella’s emotions are escalating when she stands up and yells. When faced with an escalating interaction, it is important for the nurse to de-escalate the situation.

De-escalation occurs when a person reduces the intensity of a conflict. One way to do this is through therapeutic communication.

There are two main types of communic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Crisis_Intervention_Nursing_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LhycMYQoQeiEa88h4EBngJu0R86MCwwp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Crisis Intervention Nursing Care]]></video:title><video:description><![CDATA[A crisis is a self-limiting and stressful event that upsets a person’s homeostasis and isn’t resolved by the person’s usual coping mechanisms. Crisis intervention can be used by healthcare professionals as a short-term management method for patients experiencing a crisis.  

Now, when a person experiences a crisis, they typically progress through six stages. Let&amp;#39;s take a closer look at each stage with your patient, Jimmy, who just went through a breakup with his romantic partner.  

The first stage of crisis is perception, which occurs when the event is perceived as a crisis. In Jimmy’s case, he experiences this when his partner ends their relationship, which is seen as a threat to his emotional well-being.  

The next stage is denial, where the person is unwilling to believe the situation is happening. For Jimmy, denying that the relationship has ended is a protective coping mechanism to shield himself from the overwhelming stress and reality of the breakup. 

Then, as denial and other attempts to cope with the crisis fail to resolve the problem, the person enters the third stage, known as crisis. During this stage, anxiety and discomfort continue to rise as Jimmy understands the reality of his situation and begins to exhibit maladaptive behaviors, like projecting his frustrations onto those around him. 

The fourth stage, disorganization, is where preoccupation with the crisis impacts the person’s activities of daily living, or ADLs, and quality of life. During this stage, continuing anxiety can result in unpleasant physical symptoms, such as sweating, shaking, and increased heart rate, and even thoughts of self-harm. At this point, Jimmy could either continue with maladaptive behaviors, or he might reach out for help.  

This is when Jimmy can receive effective crisis intervention and move to the fifth stage: recovery. During recovery, Jimmy uses successful coping mechanisms like physical activity, meditation, or support systems, such as family]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Schizophrenia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HdLpfd_qQReIqIBMgRIA3puXTg_aC0GL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Schizophrenia]]></video:title><video:description><![CDATA[Nurse George works on an inpatient psychiatric unit and is caring for Kit, a 31-year-old with a history of schizophrenia, paranoid type, who was recently admitted for psychotic symptoms. In collaboration with the registered nurse, RN Juanita, Nurse George goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Kit’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse George recognizes important cues, including Kit’s vital signs, which are temperature of 37 C, or 98.6 F, heart rate 98 beats per minute, respirations 20 breaths per minute, and blood pressure 136/82 mmHg. Nurse George notices that Kit appears disheveled, restless, and is looking back and forth suspiciously across the room. 

Nurse George: Hi Kit, how are you doing today? 

Kit: There’s a man coming after me, I’ve seen him watching me from inside the closet.  

Nurse George turns to look inside the closet, which is empty.  

Nurse George: That sounds scary. Although I don’t see anyone else here with us, I’m here to support you and keep you safe.   

Next, Nurse George analyzes these cues. They review the electronic health record, or EHR, and note that Kit has visited the emergency department three times in the past month for symptoms associated with her schizophrenia.  

Nurse George knows the development of schizophrenia is related to both genetic and environmental factors that disturb the brain’s structure and balance of neurotransmitters, like dopamine and glutamate.  

This leads to disabling alterations in behavior, emotions, thinking, and perception, like delusions and hallucinations. Nurse George realizes that Kit needs management of her acute episode of schizophrenia. 

Now, using the information they’ve gathered, along with Kit’s medical history, Nurse George reports their findings to RN Juanita, and together they choose a priority hypothesis of altered p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Biploar_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1PePpJEGS3eVAn_pUtBEcYIiTIaOTky2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Biploar Disorder]]></video:title><video:description><![CDATA[Nurse Nikil works on an inpatient psychiatric unit and is caring for Octavia, a 28-year-old with a history of bipolar I disorder, who was recently admitted for a manic episode. In collaboration with the registered nurse, RN Andre, Nurse Nikil goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Octavia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Nikil recognizes important cues, including Octavia’s vital signs, which are temperature 98.4 F or 36.9 C, heart rate 75 beats per minute, respirations 16 breaths per minute, and blood pressure 117/72 mmHg.  

Upon entering her room, Nurse Nikil notes Octavia is pacing back and forth, stopping intermittently to rearrange the items on her bedside table.  

Nurse Nikil: Hi Octavia, I see you’re cleaning your room. Could you pause for a moment and speak with me? 

Octavia: Oh sure, I totally have time for you. Don’t you see I’m doing something important? I really need to get my room cleaned so I can start writing. I have an amazing idea for a best-selling book about a forest like the one I grew up next to. My mom would know the name. I should call her. Do you have her number?   

Next, Nurse Nikil analyzes these cues. They review the electronic health record, or EHR, and note that prior to her hospitalization, Octavia had not been taking her lithium as prescribed. The nursing report from the night shift also indicated that Octavia hasn&amp;#39;t slept for the past two nights.  

Nurse Nikil recognizes patients with bipolar I disorder experience extremes in emotions, moving from manic to depressive moods.   

The patient may have symptoms, like racing thoughts, hyperactivity, distractibility, insomnia, and feeling an inflated sense of self.   

They understand that in patients experiencing mania, sleep disturbances can lead to exhaustion which can perpetuate manic or hyp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Personality_Disorder</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wI1LK8HQTEmNO-ZANnPubJrXQaO_V9iE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Personality Disorder]]></video:title><video:description><![CDATA[Nurse Amirah works on an inpatient psychiatric unit and is caring for Yang, a 42-year-old with a history of borderline personality disorder, who was admitted a week ago for self-harm ideation following a breakup with his partner. In collaboration with the registered nurse, RN Francie, Nurse Amirah goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Yang’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Amirah recognizes important cues, including Yang’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 70 beats per minute, respirations 16 breaths per minute, and blood pressure 132/82 mmHg. She notes that Yang’s breakfast tray is untouched on the bedside table.  

Nurse Amirah: Hi Yang, I noticed you haven’t eaten your breakfast. How are you doing today? 

Yang: Sorry, no offense, but that food is disgusting. I’m good, actually, and I’m happy I don’t have a sitter anymore. I’m ready to pack up my stuff and go home.  

Nurse Amirah: I’m glad you feel ready for discharge. To make sure you’re safe to leave, Nurse Francie and I need to gather some information and give you your medicine. 

Yang:  I know, I know. I’m still sad my boyfriend broke up with me, but I’m able to talk about it now. I have other people in my life that care about me, so I feel less alone. 

Nurse Amirah: That’s good to hear. 

Next, Nurse Amirah analyzes these cues. She reviews the electronic health record, or EHR, and notes Yang was diagnosed with borderline personality disorder, or BPD, five years ago, and has been hospitalized for self-harm ideation in the past.  

Nurse Amirah reviews the progress notes and sees that following the breakup between Yang and his partner, Yang called his sister and told her he wanted to commit suicide. His sister then called the emergency services, and he was taken to the hospital.  

Nuse Amirah re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Patients_With_Alzheimer_Dementia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cTRacHmnRQWMHG7W7oRzL2BNSWOjPR-6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Patients With Alzheimer Dementia]]></video:title><video:description><![CDATA[Nurse Darian works in a long-term care facility and is caring for Rosemary, an 84-year-old female with a history of Alzheimer disease who was admitted following an open reduction and internal fixation, or ORIF, for a hip fracture a few weeks ago. In collaboration with the registered nurse, RN Piper, Nurse Darian goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Rosemary’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darian recognizes important cues, including Rosemary’s inability to recall her daughter’s name, her disorientation to date and time, and that she becomes agitated when asked several questions in a row. Nurse Darian also notes that as the evening progresses, Rosemary becomes more impulsive, and tries to get out of bed on her own. 
  Next, Nurse Darian analyzes these cues. He understands that dementia is a neurological condition, caused by structural changes in the brain, and is characterized by a progressive decline in mental functions, including memory, thinking, language, behavior, mood, and personality. He knows that Rosemary’s dementia can be exacerbated by illness, such as the surgery for her hip fracture, and changes to her familiar environment.  

Nurse Darian re-enters Rosemary’s room to gather additional information.  
  Nurse Darian: Hi Rosemary. How are you feeling? 

Rosemary: I&amp;#39;ve never met you. 

Nurse Darian: That’s okay, Rosemary. I’m your nurse, Darian. I met you earlier today. Are you having any pain right now? 

Rosemary: Why does everyone have so many questions all the time?  

Nurse Darian notes that Rosemary begins to sit up in bed and tries to swing her legs to the side of the bed to stand up. The two siderails by Rosemary’s head are up, as well as one siderail by her feet. She then moves towards the open space in the bed to exit, so Nurse Darian moves to prevent her fro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Nursing_Care_in_Cases_of_Child_Maltreatment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E-9CCA4XQde-US9yZb2sLgwhRgWujfdT/_.png</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Nursing Care in Cases of Child Maltreatment]]></video:title><video:description><![CDATA[Nurse Angelo works in a family practice clinic and is caring for Maya, a 2-and-a-half-year-old who&amp;#39;s brought in for a required wellness check before entering preschool. In collaboration with the registered nurse, RN Rose, Nurse Angelo goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Maya’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Angelo recognizes important cues, including Maya’s vital signs which are temperature 98.6 F or 37 C, heart rate 105 beats per minute, and respiratory rate 23 breaths per minute. Nurse Angelo notes that Maya has multiple circular bruises ranging in color from pale yellow to deep purple on her upper arms, as well as a rounded, punctate burn to the back of her left shoulder about one centimeter in diameter.  

Nurse Angelo also notes Maya grimaces occasionally and appears tense, so he determines Maya’s pain rating is 2 out of 10 according to the Face, Legs, Activity, Cry, and Consolability, or FLACC scale. Nurse Angelo also notes that when he asks Maya questions, she doesn’t respond or make eye contact with him.  

Then, he gathers additional information from Maya’s mother, Josie, about her injuries. 

Nurse Angelo: I see that Maya has some bruising on her arms. Can you tell me what happened? 

Josie: Oh, those? She’s just clumsy. She’s always bruised easily. She probably fell down while she was playing or something. 

Nurse Angelo: I also noticed an injury to her left shoulder that looks like a burn. Do you know what happened there? 

Josie: That doesn’t look like a burn to me. Like I said, I think she probably scraped herself when she was playing. 

Nurse Angelo then analyzes these cues. He reviews Maya’s electronic health record, or EHR, and notes that she has a history of a humerus fracture at age one year. When asked about the fracture, Josie says it was caused by a fall]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Family_Planning_and_Related_Nursing_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E_Sr49W8T0S_INPNSwfAuIURQ5m5x1_4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Family Planning and Related Nursing Care]]></video:title><video:description><![CDATA[Family planning refers to methods used to plan when pregnancy occurs, and includes natural family planning methods, contraceptive devices and medications, and surgical procedures.  

Natural family planning involves fertility awareness methods to predict fertile and infertile days to either avoid pregnancy or to conceive when pregnancy is desired. One method involves using a basal thermometer to monitor basal temperature, which is the body’s temperature first thing in the morning before getting out of bed. During ovulation, the temperature will rise around 0.4 degrees F, or 0.2 degrees C, and stay elevated until menstruation. The temperature is tracked for several months until a pattern is established, which helps predict when ovulation is likely to occur.  

Next, the Billings method involves monitoring changes in cervical mucus. A few days before ovulation, the amount of mucus increases, and it changes from thick and sticky to thin and slippery.  

Lastly, the calendar method, sometimes called the rhythm method, is used for those with regular menstrual cycles. It involves charting monthly cycles on a calendar for up to 12 months to estimate when ovulation is likely to occur, which is usually around the 14th day before the next menstrual cycle. 

Contraceptive devices are reversible methods of contraception.  First, there are barrier methods, like male condoms, cervical caps, and contraceptive sponges that prevent sperm from entering the uterus.  

Male condoms are a thin stretchable sheath, commonly made of latex, that’s applied over the erect penis. They are single use and applied immediately prior to intercourse. The effectiveness of condoms is enhanced when used together with spermicides, which are chemical-based formulations that destroy sperm cell membranes and reduce sperm motility, reducing their ability to reach the cervix.  

Spermicides can come pre-applied to condoms and are also available as foams, tablets, suppositories, vaginal films, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prenatal_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3VBU2dcmTj_VtXeZoqra7eIlRv6tcN7g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prenatal Care]]></video:title><video:description><![CDATA[The prenatal period refers to the time from before conception until the end of pregnancy. So, prenatal care refers to the care that is provided before and during pregnancy to evaluate maternal and fetal health, provide education to promote health, and to intervene when possible to ensure the birth of a healthy baby with minimal risk for the mother. For a successful pregnancy outcome, prenatal visits should continue every 4 weeks until week 28, every two weeks from week 28 to 36, and then weekly until delivery. 

Alright, now the first step in prenatal care is preconception counseling, which seeks to identify any potential risks to the client’s fertility and pregnancy outcome. The first prenatal visit typically occurs when a client suspects they are pregnant or because they wish to conceive in the near future. No matter the case, the main focus of the first prenatal visit should be obtaining a thorough personal and obstetrical history, as well as family history, to identify any medical conditions that could pose a risk to the pregnancy.

Now, in clients who suspect they are pregnant, pregnancy should be confirmed with a urine pregnancy test and an abdominal ultrasound. If pregnancy is confirmed, the estimated date of delivery, or EDD, should be calculated. It’s traditionally calculated using Naegele’s rule, which takes the first day of the last menstrual period, or LMP, subtracts 3 months, and then adds one year and seven days. So, if the LMP was September 10, 2021, counting back 3 months, adding 1 year and 7 days calculates the EDD as June 17, 2022.

The obstetrical history evaluates the gravidity, parity, and abortions. Gravidity, or G, refers to the number of times a client has been pregnant, including the current pregnancy. 

Parity, or P, refers to the number of times a client has carried the pregnancy to a viable gestational age, which is more than 20 weeks gestation. So, if a client is currently pregnant, has been pregnant once before, and has had on]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adaptations_to_Pregnancy_and_Related_Nursing_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/982_sviCSR2YdACuScyArHriSw62ajus/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adaptations to Pregnancy and Related Nursing Care]]></video:title><video:description><![CDATA[Adaptations to pregnancy include physiologic and psychosocial changes that occur in a pregnant patient in response to a developing fetus.  

Physiologic changes during pregnancy affect the body from head-to-toe, including the cardiovascular, respiratory, and reproductive systems.  

Starting with the cardiovascular system, pregnancy is considered a high-volume state, meaning that blood volume gradually increases during the pregnancy to provide circulation to expanding maternal tissues; exchange nutrients, oxygen, and waste in the placenta; and create a reserve for blood loss during delivery.  

The composition of blood changes too. Both plasma and red blood cells increase; although there’s a larger increase in plasma, which leads to dilutional anemia, sometimes referred to as a physiologic anemia of pregnancy, where hemoglobin and hematocrit levels are decreased. 

White blood cells, primarily neutrophils, increase along with clotting factors, like VII, VIII, X, and fibrinogen. Increased clotting factors minimize bleeding after delivery but also increase the risk of venous thromboembolism. 

Now, in order to pump the extra blood and increase cardiac output, the heart rate increases by 10 to 15 beats per minute; the stroke volume, or the amount of blood pumped with each heartbeat, increases as well; and the heart enlarges from this extra workload.  

In fact, the uterus also enlarges and pushes on the diaphragm, causing the heart to be slightly displaced up and to the left.  Blood pressure decreases despite increased blood volume, due to elevated progesterone and estrogen, which cause vasodilation and decreased vascular resistance, increasing the risk of orthostatic hypotension.  

Moreover, when lying flat, the weight of the uterus can compress the inferior vena cava, reducing blood return to the heart. As a result, cardiac output decreases and supine hypotension occurs, causing dizziness and lightheadedness.  

Also, as less blood circulates to the placen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Pregnancy-related_Complications</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E0j6Gp9pTNCh8QTfix8cb4vQRiO3iCCi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Pregnancy-related Complications]]></video:title><video:description><![CDATA[Pregnancy-related complications can cause harm to both the mother and fetus, and include preeclampsia, placental abruption, and placenta previa. As the nurse, you’ll collaborate with the registered nurse, or RN, to provide care for your patient experiencing pregnancy-related complications. 

Preeclampsia is a pregnancy-specific, multisystem condition characterized by new onset hypertension, which is defined as a systolic blood pressure greater than or equal to 140 mmHg, a diastolic blood pressure greater than or equal to 90 mmHg, or both, in a previously normotensive patient. It also includes proteinuria, or protein in the urine, or other evidence of organ damage. It typically occurs after 20 weeks of gestation, but it can also first occur during the postpartum period.  

If left untreated, it can progress to eclampsia, which is when a patient with preeclampsia develops seizures. The ultimate treatment is to deliver the fetus and placenta; however, the decision to induce delivery depends on both the gestational age of the fetus and the severity of the condition.   

Now, when caring for a patient with preeclampsia, collaborate with the RN to administer the prescribed IV fluids to maintain hydration, antihypertensives to control their blood pressure, and magnesium sulfate to help prevent seizures. Also be sure to have calcium gluconate, which is the antidote for magnesium sulfate toxicity, readily available. Then, apply an external fetal monitor, insert an indwelling urinary catheter, and institute seizure precautions. 

Work with the RN to closely monitor the patient’s condition, while keeping a close eye on the fetal heart rate. Immediately notify the RN if you observe signs or symptoms that the patient could be progressing to eclampsia, such as altered level of consciousness, severe headache, epigastric pain, or visual changes, as well as the presence of clonus, which is a repetitive muscle contraction.  

Then, assist the patient into a left, lateral po]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_of_Mother_and_Infant_During_Labor_and_Birth</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/57XxBS-6SV_LpbxXg4BNf9lhT0uCQ_EC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care of Mother and Infant During Labor and Birth]]></video:title><video:description><![CDATA[Labor is the process when uterine contractions cause the cervix to thin and dilate, allowing the fetus to pass through the birth canal. As the nurse, you’ll collaborate with the registered nurse, or RN, to provide care during labor and after delivery.  

During labor, you’ll assist with monitoring the mother and fetus. Begin by taking vital signs at regular intervals. Be sure to notify the RN if you note a temperature above 100.4 F or 38 C, which can indicate an infection; or a blood pressure above 140/90 mmHg or systolic blood pressures below 90 mmHg, both of which can cause a decrease in blood flow to the fetus. 

You’ll also assist with monitoring your patient’s uterine contractions and the fetal heart rate, or FHR, patterns that occur in response to each contraction. Uterine contractions can be monitored by palpating your patient’s uterus, or by using a tocotransducer, sometimes called a tocodynamometer, or toco for short, which is a pressure-sensitive button that’s placed over the uterine fundus to track uterine activity.  

Now, uterine contractions are described by their frequency, duration, and intensity. Frequency is the time in minutes between the start of one contraction to the start of the next contraction. Normally there should be no more than 5 contractions present in a 10-minute period, averaged over 30 minutes. Duration is the length of the contraction in seconds, measured from the beginning to the end of the contraction, and is typically between 30 to 60 seconds. Intensity is the relative strength of the contraction, and is assessed as mild, moderate, or firm by palpation. 

Keep in mind that during a contraction, the flow of blood to the placenta decreases, which means the fetus is receiving less oxygen. So, you should immediately report to the RN if you observe abnormal uterine activity, like tachysystole, meaning there are more than 5 consecutive contractions in a 10-minute period; or tetany, which means contractions last longer than 90]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Labor_Pain</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WRboutnURxKnGYgj5065Q3DsTdyGSHZt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Labor Pain]]></video:title><video:description><![CDATA[Labor refers to a series of progressive contractions of the uterus that result in dilation and thinning of the cervix. This allows the fetus to descend from the uterus, through the birth canal, and into the extrauterine environment. As the nurse, you’ll collaborate with the registered nurse, or RN, to manage your patient’s pain during the labor process. 

Now, pain during labor is expected and time-limited but can still cause anxiety, leading to a stress response that can have an adverse effect on the progression of labor and on the fetus. Excessive pain can heighten the mother’s fear and anxiety, causing the release of cortisol and catecholamines like epinephrine and norepinephrine. When these act on alpha receptors, the uterine blood vessels and muscles constrict, reducing uterine blood flow, reducing the fetal oxygen supply, and potentially leading to fetal hypoxia. Labor also increases the mother’s metabolic rate and demand for oxygen, making the hypoxia worse.  

Finally, after labor, poorly managed pain can make it difficult for the mother to interact with the newborn due to post-labor fatigue and exhaustion. 

Now, management of labor pain can include nonpharmacologic and pharmacologic methods. Non-pharmacologic methods begin with prenatal education, like offering realistic information on pain and expectations. This can reduce anxiety and allow the mother and partner o rehearse for labor and develop the necessary skills to cope with labor pain.  

Other specific nonpharmacologic methods include cognitive processes and cutaneous techniques. Cognitive processes include continuous labor support, where the presence of a support person provides emotional and physical support during labor; music therapy, which can increase pain tolerance and serve as a distraction from pain guided imagery where the patient focuses on a pleasant mental scene or experience; and breathing techniques that can be done either during or between contractions and include taking a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_the_Postpartum_Woman</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9rHl2CerSEOGqHTLWasSvqkbRXyzfx8w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for the Postpartum Woman]]></video:title><video:description><![CDATA[The postpartum period, also known as the puerperium, or the fourth trimester of pregnancy, occurs during the first six weeks after delivery. During this period, physiological adaptations occur to return the patient’s body to its pre-pregnancy state, including changes to the uterus, perineum, and cardiovascular system. 

Following delivery, the uterus begins the process of involution, meaning it returns to pre-pregnancy size and position. As soon as the placenta is delivered, uterine muscle fibers constrict around blood vessels at the placental attachment site and intermittent uterine contractions occur to control bleeding and promote involution. The fundus, or top of the uterus, is located midway between the umbilicus and the symphysis pubis immediately after the delivery of the placenta.  

Then, about 12 hours after delivery, it will rise to the level of the umbilicus. After that, the fundal height continues to descend by about one centimeter, or one fingerbreadth, per day, until it reaches the pelvic cavity by around day ten.  

Along with uterine involution, the quantity and characteristics of the lochia, or vaginal discharge after delivery, is monitored. Lochia should decrease in amount and lighten in color over time. 

When caring for your postpartum patient, monitor closely for signs of inadequate uterine involution, which can increase the risk of hemorrhage. Signs to watch for include a soft, or boggy uterus; a fundus that’s above the expected level or deviated away from midline; increasing amounts of lochia, return of a bright red color, or large clots. If the uterus is boggy, gently massage it until it’s firm; and if it’s not at midline, assist your patient to empty their bladder, since a full bladder can interfere with uterine involution. If you suspect postpartum hemorrhage, contact the registered nurse immediately.  

Following a vaginal delivery, the perineum can be swollen and tender, and may have stitches present from repaired lacerations o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_the_Postpartum_Woman_and_Family</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N2d-SNdTS42DORF4GH5IcCdETlaQZgYq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for the Postpartum Woman and Family]]></video:title><video:description><![CDATA[During the postpartum period, psychological changes influence how the mother adapts to their newborn and role as a caregiver. These changes tend to follow a pattern of three phases, which include the taking-in phase, the taking-hold phase, and the letting-go phase. As the nurse, you’ll provide care and support as your patient adapts to the psychological changes that occur during the postpartum period.  

So, during the taking-in phase, the mother is focused on taking care of their own basic needs like eating and sleeping. They typically let others take on duties to care for the newborn, like letting others change diapers or burp the baby after feeding. They may also seem preoccupied with their own thoughts and may spend their time reminiscing and speaking about their birth experience.  

As you care for your patient during this phase, assist with tasks like bathing the newborn to allow time for your patient to recover and regain their strength following childbirth. This is also a good time to promote attachment-forming activities, like skin-to-skin contact. Use active listening as your patient shares their thoughts and feelings with you; and remember that they may have difficulty retaining new information, so reviewing information about self-care and newborn care will be most effective when they begin to show signs of physical recovery and interest in providing care. 

Next, the taking-hold phase is when the mother becomes more active and engaged, and begins to take more responsibility for self-care and the care of their newborn. You can assist them to build confidence in their new role by involving them in activities like feeding and diaper changes, talking about their newborn’s behaviors, and reviewing typical newborn sleep-wake cycles.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_of_Women_With_Complications_After_Birth</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sBzR0UpIS5WayOxEFFPO4KiMSACJXIzy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care of Women With Complications After Birth]]></video:title><video:description><![CDATA[The postpartum period, also known as the puerperium, starts after delivery of the fetus and the placenta, and it extends through the first six weeks after birth. Complications can arise during this period, including hemorrhage, venous thromboembolism, and infection. As the nurse, you’ll collaborate with the registered nurse, or RN, to provide care for your patient experiencing postpartum complications.  

Postpartum hemorrhage is a significant loss of blood after giving birth and is an obstetric emergency. It’s generally defined as losing more than 500 milliliters of blood after a vaginal delivery or more than 1000 milliliters after a cesarean birth.  

It can also be defined as blood loss accompanied by clinical manifestations of hypovolemia within 24 hours of delivery, which may include tachycardia, tachypnea, hypotension, or palpitations. If left untreated, postpartum hemorrhage can result in hypovolemic shock and even death. 

Common causes of postpartum hemorrhage include uterine atony, or lack of uterine muscle tone; lacerations, or tears in the perineum; hematomas, which are a collection of blood in the tissues resulting from birth trauma; and retained placental fragments, or pieces of the placenta left inside the uterus after delivery of the fetus. 

Now, when caring for your patient during the postpartum period, you’ll monitor closely for clinical manifestations of postpartum hemorrhage. If you note heavy bleeding, numerous large clots or consistent blood flow that saturates a perineal pad within 15 minutes, especially if you note changes in vital signs that are consistent with loss of circulating volume, notify the RN immediately.  

Next, palpate your patient’s uterus, and if it’s boggy, massage it until it becomes firm. Also, replace lost volume by infusing the ordered IV crystalloid solution; place a urinary catheter to track urine output; and draw blood to monitor your patient’s CBC. You’ll also assist the RN by gathering medications, such as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_the_Term_Infant</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I9yZms_dRSKUM1qyzopCWovxSYiesRod/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for the Term Infant]]></video:title><video:description><![CDATA[A newborn, also called a neonate, is an infant that&amp;#39;s less than 28 days old; and is considered a term newborn once they reach 37 weeks of gestation. As the nurse, you’ll collaborate with the registered nurse, or RN, to support the newborn’s adaptation to extrauterine life, by monitoring their temperature as well as the adaptations of their cardiovascular and respiratory systems. 

Now, one of the major adaptations a newborn infant must make is establishing thermoregulation, which is the ability to balance heat loss and heat production with the goal of maintaining a steady core temperature. Keep in mind that newborns don’t have a lot of subcutaneous fat to help keep them warm, so be sure to keep them wrapped in a warm blanket. And because their heads provide a relatively large surface area for heat loss, put a cap on their head.  

Other steps you can take to prevent heat loss include keeping their diaper area dry to prevent heat loss by evaporation; avoid placing them on cold surfaces to prevent heat loss by conduction; ensuring they are not exposed to drafts to prevent heat loss by convection; and ensuring they are not placed next to a window to prevent heat loss by radiation. Also, be sure to measure the newborn’s temperature regularly, which should be between 97.1 F, or 36.2 C, and 99.8 F, or 37.7°C, and notify the RN if the infant is not able to maintain their temperature within the expected range.  

Next, auscultate the newborn’s apical pulse and remember to listen for a full minute. It’s a good idea to check this first when the infant is in a quiet state. Note their heart rate and rhythm, and keep in mind that it’s not uncommon for newborns to have a murmur during the first 48 hours of life, as the ductus arteriosus shunt closes. A term newborn’s heart rate normally varies between 110 and 160 beats per minute, but it can rise to 180 beats per minute when they’re crying or drop as low as 80 beats per minute during deep sleep. A consistently ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutritional_Needs_of_Growing_Children</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TCMOPg4iR8yEamWiK_tPGMQqQDeWeHMr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutritional Needs of Growing Children]]></video:title><video:description><![CDATA[Optimal nutrition, which is essential to support the growth and development of children, will vary depending on the child’s age and developmental stage. As the nurse, you’ll collaborate with the registered nurse, or RN, to support individualized nutritional needs of your pediatric patients. 

Now, due to the rapid growth during infancy, which is the period between birth and 12 months, infants require more nutrients in proportion to their weight than adults. Until six months of age, breastmilk supplemented with vitamin D or iron-fortified formula will meet the infant’s nutritional needs. Then, between four and six months of age, infants will start to show signs of being ready for solid foods. Their deciduous, or baby teeth, start to erupt; the extrusion reflex begins to disappear, which means they’re no longer pushing food out of their mouth as they protrude their tongue; and they are able to sit with good head control. They also start to watch others eat and reach for food. A variety of soft, easy-to-swallow solid foods should be introduced at this time, like pureed fruit and vegetables or cereals. 

Lastly, if their baby doesn’t have a history of eczema, foods that are potentially allergenic, such as peanut products or eggs, can typically be introduced after four months of age to help prevent development of food allergies as their child ages.  

Okay, the dietary needs of toddlers, aged one to three years, and preschoolers, aged three to six years, have a lot in common. During this time, growth begins to slow, and energy requirements decrease. Their stomach capacity increases so it can start to accommodate up to three meals a day, along with at least two healthy snacks. By the end of their second year, they begin to develop a sense of independence. They start feeding themselves and prefer finger foods like sliced banana and soft cheese. They also begin to regulate their own food intake and start to develop strong food preferences.  

Feeding difficulties ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_the_Preterm_Infant</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_AofSCMKQu2r-51_RHQXVhKHSJSf0gmy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for the Preterm Infant]]></video:title><video:description><![CDATA[Infants born prematurely, or before 37 completed weeks of gestation, miss beneficial time of intrauterine development, which places them at risk for complications. As the nurse, you’ll collaborate with the registered nurse, or RN, to manage complications that can arise, including respiratory and thermoregulation issues, hypoglycemia, and hyperbilirubinemia. 

Most respiratory complications that occur in preterm infants are due to insufficient production of surfactant, which is a lipoprotein produced by cells in the alveoli that helps keep the lungs expanded. Insufficient surfactant can impair gas exchange, leading to respiratory distress syndrome and hypoxia. Other characteristics of preterm infants that impair effective respirations include underdeveloped chest wall muscles; an immature respiratory center in the brain; and weak gag and cough reflexes.  

When caring for a preterm infant, you’ll monitor their respiratory status by checking their oxygen saturation, respiratory rate and effort, skin color, and arterial blood gas as indicated. You’ll also support oxygenation by administering warmed, humidified supplemental oxygen, and promote lung expansion by elevating the head of their mattress, or positioning them on their side. You can also help them conserve energy and oxygen consumption by keeping them warm, clustering care to allow time for uninterrupted rest, and handling them minimally and gently. If apnea occurs, rub their feet, ankles, or back to stimulate breathing. If the apnea continues, or if you notice signs of respiratory distress, like decreased oxygen saturation, dyspnea, grunting, nasal flaring, intercostal retractions, or cyanosis, immediately notify the RN.  

Now, preterm birth also affects an infant’s thermoregulation. They lack subcutaneous fat, which provides insulation, as well as brown fat, which is used to produce heat. Their large surface area-to-weight ratio creates a large area from which heat can be lost through radiation, and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion_and_Prevention_for_Infants</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0OX_VpwVRXan1W3AxXLtW3VDQMqzdjRj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Promotion and Prevention for Infants]]></video:title><video:description><![CDATA[Health promotion focuses on improving health and wellbeing; whereas illness prevention involves reducing risk factors for illness, disease, or trauma. As the nurse caring for infants, you’ll collaborate with the registered nurse, or RN, to provide guidance for caregivers on health promotion and illness prevention. 

One aspect of health promotion is encouraging bonding, or the emotional ties directed from the caregiver to the infant, that are built by meeting their infant’s needs and through activities like skin-to-skin contact and eye contact.  

You can assist caregivers to develop a strong bond with their infant by helping them recognize cues when their infant is cold, hungry, tired, or needs a clean diaper; reviewing ways to respond to their infant using calming techniques like rocking, swaddling, or feeding; offering nonnutritive sucking; or reducing environmental stimuli, like noise or bright lights.  

If their infant has colic, which is where their otherwise healthy infant has unexplained irritability and is difficult to soothe, remember to offer empathy and encourage them to use strategies to help soothe their infant, like carrying them face down while supporting their head and abdomen and providing a gentle rocking motion. You can also suggest taking turns with another trusted person to care for their infant to prevent caregiver fatigue, and discussing other options with their health care provider, like trying a modified formula to reduce gastric upset. 

Next, reinforce teaching about the role of nutrition in providing sufficient calories and nutrients to promote their infant&amp;#39;s rapid growth and development. Be sure to talk about how to recognize their infant’s hunger cues, such as crying; clenched fists; rooting, or moving their head and mouth in search of the nipple; and fullness cues, like falling asleep, relaxing their body, and ejecting the nipple.Provide them with support to breastfeed or bottle feed, as needed, and help them ident]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Promotion_and_Prevention_for_Toddlers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1cmUz5_pQPmfg87k9FbWy7k9Tb_asbH5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Promotion and Prevention for Toddlers]]></video:title><video:description><![CDATA[The toddler period of development spans ages one to three. During this time, toddlers become more independent, active, and curious. As the nurse caring for toddlers, you’ll collaborate with the registered nurse to assist caregivers to consider childcare options, encourage safe play, prevent injury, and provide adequate nutrition.    

Child care is an arrangement where the caregivers place their toddler in the supervision of others while they tend to personal and professional obligations. When choosing to place their toddler in child care, available options include leaving the child with a known and trusted family member or friend, enrolling them in a private licensed day care center, or using employer-supported child care.  

Regardless of the type of child care, caregivers may experience a sense of guilt or worry when placing their toddler in the care of others. As the nurse, you’ll assist families in choosing a care facility that meets their personal and cultural preferences, as well as their financial needs, and provide emotional support for any associated psychological symptoms they experience.  

Now, through the act of play, toddlers explore and learn about their environment. Toddlers tend to engage in egocentric thinking, meaning they relate everything back to themselves, which can manifest as difficulty sharing toys, or having a temper tantrum when they don’t get their way. By 18 months, they typically start playing with dolls or stuffed animals and engaging in parallel play, which is when children play next to each other but don’t interact. As they continue to grow, they start to prefer cooperative play, where they play and interact with others. 

As the nurse, encourage caregivers to provide a safe place for their toddlers to engage in unstructured, self-directed play, and review how to choose suitable toys and activities for their toddler by reading the safety labels and being aware of recalls. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_Milestones_in_Preschoolers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/94f2Ew51RReRHPws5r-KhTVETGefwUXM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developmental Milestones in Preschoolers]]></video:title><video:description><![CDATA[The preschool period lasts between three and five years of age. As the nurse, you’ll collaborate with the registered nurse, or RN, to support the preschool child’s physical growth, as well as their mental and social development.   

Physical development of the preschool child involves a slow and steady increase in their height and weight, and an acceleration of their motor skills. During this time, the preschool child loses some of the chubby appearance that’s characteristic of the toddler period. At the same time, they begin to hone their fine motor skills, like using scissors, dressing themselves, and tying their shoelaces.  

They also begin developing left- or right-handed dominance, showing a preference during certain activities like coloring or throwing a ball. Their gross motor skills also improve as balance and coordination increases. They begin to walk and run with a steadier gait which helps them participate in more coordinated activities like playing independently on swings and jumping rope.  

Mental development also accelerates during this period. They begin to use language to better express themselves and start to use words to express how they feel. By the end of this period, the preschool child typically has a vocabulary of more than 2000 words and can easily create six-word sentences. They also start to understand and follow directions when playing games and they can complete a task with more than one step. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nursing_Care_for_Pediatric_Patients_With_Congenital_Heart_Defects</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jh9pzdj0QnCCr3LGLzVVaczLTLiUdCct/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nursing Care for Pediatric Patients With Congenital Heart Defects]]></video:title><video:description><![CDATA[Congenital heart defects are cardiac anomalies present at birth that affect normal blood flow within the heart. They’re divided into two categories, acyanotic and cyanotic, based on the presence of cyanosis, or a bluish discoloration of the skin. Acyanotic heart defects don’t cause cyanosis, whereas cyanotic heart defects do. As the nurse, you’ll collaborate with the registered nurse, or RN, to provide care for children with congenital heart defects. 

Congenital heart defects are associated with risk factors that interfere with fetal cardiovascular development, causing cardiac structures to form improperly. Risk factors include fetal chromosomal abnormalities as well as exposure to infections like rubella, or teratogens, which are substances that cause developmental abnormalities, such as certain medications, alcohol, recreational drugs, tobacco smoke, and heavy metals like mercury. 

Now, with acyanotic heart defects, there’s an abnormal communication between the left- and right-sided circulation of the heart. Examples of acyanotic heart defects include ventricular septal defect, where there’s an opening in the interventricular septum that separates the left and right ventricles; atrial septal defect, where there’s an opening in the interatrial septum between the left and right atria; and patent ductus arteriosus, which is caused by continued circulation through the fetal shunt, which is a blood vessel that normally closes after birth. 

For example, with a ventricular septal defect, blood takes the path of least resistance going from the left ventricle, where the pressure is higher, through the defect to the right ventricle, where the pressure is lower, and then back into the pulmonary circulation. This is called left-to-right shunting. Now, this blood is already oxygenated so there&amp;#39;s no cyanosis, but the recirculation of blood increases pulmonary flow and leads to pulmonary hypertension, which may eventually progress to heart failure.   

Chil]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Adolescents_With_Type_1_Diabetes_Mellitus</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9N0x06cWS2iP78IxJsJAkqHSTG_Ny66p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Adolescents With Type 1 Diabetes Mellitus]]></video:title><video:description><![CDATA[Nurse Camden works on a pediatric medical-surgical unit and is caring for Tate, an 11-year-old who was admitted several days ago for new onset type 1 diabetes mellitus. In collaboration with the registered nurse, RN Kande, Nurse Camden goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Tate’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Camden recognizes important cues including temperature 97.3 F or 36.2 C, pulse 96 beats per minute, respirations 18 breaths per minute, oxygen saturation 98 percent on room air, and blood pressure 105/70 mmHg. Tate’s mother is at the bedside and reports that over the last month, Tate’s been irritable, unusually hungry and thirsty, and he’s urinating frequently.   

Next, Nurse Camden analyzes these cues. He reviews the electronic health record, or EHR, and notes that Tate’s last blood glucose level was 135 mg/dL and his hemoglobin A1C level is 7.8 percent. Nurse Camden also sees that Tate has lost four pounds in the past two months and that Tate’s urine was positive for glucose upon admission. Nurse Camden also sees that Tate’s regular IV insulin infusion has been discontinued by RN Marge to transition him to subcutaneous insulin, per the healthcare provider’s order.  

Nurse Camden realizes that the glucose from the food Tate eats can’t move from his blood into his cells, due to a lack of insulin. Because of this, Tate isn’t able to convert the food he eats to energy, causing him to experience fatigue and hunger. He also realizes that Tate’s kidneys can’t reabsorb the excess glucose, so it ends up in the urine, where it pulls water out along with it as it&amp;#39;s eliminated, causing his other symptoms of frequent urination and increased thirst. Nurse Camden recognizes that Tate needs effective management of his blood glucose.  

Now, using the information he’s gathered, along w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Caring_for_Pediatric_Patients_With_Burn_Injuries</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/a9x_OzV5Ro6TahXa-12btIRFSIq75yHH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Caring for Pediatric Patients With Burn Injuries]]></video:title><video:description><![CDATA[Nurse Lawrence works in a pediatric rehabilitation facility and is caring for Abigail, a 2-year-old who was admitted to the facility from a burn unit after being treated for an accidental scalding injury that resulted in partial- and full-thickness burns. In collaboration with the registered nurse, RN Miley, Nurse Lawrence goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Abigail’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Lawrence recognizes important cues, including Abigail’s vital signs, which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respirations 18 breaths per minute, blood pressure 96/52 mmHg, and oxygen saturation 100 percent on room air. Next, Nurse Lawrence uses the Face, Legs, Activity, Cry, and Consolability, or FLACC scale, and determines Abigail’s pain rating is 5 out of 10 according to her behavioral cues.  

Next, Nurse Lawrence analyzes these cues. He reviews the electronic health record, or EHR, with RN Miley, and they note an order for sterile dressing changes, and that Abigail is prescribed a topical antimicrobial to be applied to her burns. They also see that she’s been prescribed medication for pain management and that she received her last dose four hours ago.   

Nurse Lawrence recalls that a scald is a type of thermal burn caused by hot liquids or steam, and he knows that toddlers, like Abigail, are at high risk for these types of burns as they start to become more mobile and explore their environment.  He recalls that partial-thickness burns involve the epidermis and part of the dermis layers of the skin, and that full-thickness burns involve both the epidermis and the entire dermis.  

This destroys the network of immune cells that reside in the epidermis and the physical barrier the skin provides against microorganisms. He further understands that the risk ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vaginal_trichomoniasis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kJUQwP7DSQKli95Nmx16c6UkTNCkTgwM/_.png</video:thumbnail_loc><video:title><![CDATA[Vaginal trichomoniasis: Clinical sciences]]></video:title><video:description><![CDATA[Vaginal trichomoniasis is among the most prevalent sexually transmitted infections, or STIs, worldwide. It is caused by the protozoan parasite, Trichomonas vaginalis. Most patients infected with trichomonas have minimal or no symptoms, and untreated infections can last for months to years. Trichomonas infection is associated with an increased risk of both HIV acquisition and HIV shedding, and it increases the risk of pelvic inflammatory disease among HIV-positive patients. Additionally, it has been associated with an increased risk of cervical cancer. In pregnancy, trichomonas infection increases the risk of preterm birth, prelabor rupture of membranes and small for gestational age infants.

Your first step in evaluating a patient who presents with a chief concern suggesting vaginal trichomoniasis is obtaining a focused history and physical exam. This should include a sexual history, such as recent sexual activity or new partners, so be sure to have a private and confidential discussion. Although it might be difficult, you should ask caregivers of young patients to step out of the room for this discussion. Additionally, always consider sexual assault or abuse whenever a young patient has a positive sexual activity history, especially if the patient is a child. If there is abuse going on, you will need to follow up with allegations of abuse in accordance with your State’s law. 

Now, keep in mind that trichomoniasis can be spread through vaginal fluids So some practices like sharing of sex toys can cause infection. In addition to sexual history, ask about hygiene practices, such as douching, which can remove some of the bacteria that make up the normal vaginal flora, increasing the risk of overgrowth of infectious pathogens. Although most patients are usually asymptomatic, some may report a malodorous vaginal discharge, vulvar pruritus or irritation, and dysuria. 

Physical exam findings include a yellow frothy vaginal discharge; as well as vaginal or cervi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fb7aV9eEQp_WFDSaPWWwHbU9QYmx0Xkt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Anemia in pregnancy is characterized by a decrease in the hemoglobin in a pregnant patient. Now, a normal physiologic anemia of pregnancy occurs when both the red blood cell mass and plasma volume expand throughout gestation. However, the increase of red blood cells is disproportionately less than the increase in plasma volume, resulting in a dilutional anemia, or physiologic anemia of pregnancy. 

Other causes of anemia during pregnancy typically include nutritional deficiencies resulting in impaired red blood cell production. In addition, inherited mutations of hemoglobin structure, known as hemoglobinopathies, or conditions resulting in increased destruction of red blood cells can also be a cause of anemia during pregnancy. 

Given the potential for blood loss at delivery, which will worsen a preexisting anemia, it is important to identify and treat anemia during pregnancy to prevent adverse maternal and fetal outcomes. Consequently, universal screening of all pregnant patients for anemia should be done during the first and second trimesters.

Your first step is to perform a universal screening of your pregnant patient for anemia at their first prenatal visit.

Keep in mind that some patients may not have received their prenatal care, so they may present with a chief concern suggesting anemia in pregnancy. Start by obtaining a focused history and physical exam. And since anemia is diagnosed based on hemoglobin values, a CBC is essential. Additionally, as part of universal screening, all patients should be screened for hemoglobinopathies using hemoglobin electrophoresis at the start of their pregnancy, unless they have had prior testing. A positive family history of hemoglobinopathy increases their risk of having one too. This is important because any patient with a hemoglobinopathy is at risk for anemia due to the abnormal hemoglobin structure resulting in defective hemoglobin molecules. 

Other important risk factors ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Clinical_Sciences_platform_tour</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/p0GOu9EFSO6uO71siUsyiVYYQfWMeNDI/_.png</video:thumbnail_loc><video:title><![CDATA[Help your students think clinically | Osmosis Clinical Sciences platform tour]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Help your students think clinically | Osmosis Clinical Sciences platform tour through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Beta-thalassemia:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PYcrq_IcQ9uWJCPAmuk9cr-pThCjaf4D/_.jpg</video:thumbnail_loc><video:title><![CDATA[Beta-thalassemia: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Beta-thalassemia: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Lyme_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mhE90Iy9RPSg9vlH4dp9uXSoQKi_ORRO/_.png</video:thumbnail_loc><video:title><![CDATA[Lyme disease: Clinical sciences]]></video:title><video:description><![CDATA[Lyme disease is an infectious disease caused by the spirochete Borrelia Burgdorferi. It’s most commonly transmitted via the Ixodes Scapularis deer tick in Lyme-endemic areas like the Northeastern and Midwestern United States. After a tick bite, spirochetes replicate at the site of infection, causing symptoms ranging from an isolated rash to neurological, cardiac, and musculoskeletal involvement. Depending on the timing of infection and clinical presentation, Lyme disease is classified into early localized, early disseminated, and late Lyme disease. 

If your patient presents with chief concerns suggesting Lyme disease, your first step is to perform a focused history and physical. Let’s start with early localized Lyme disease! Your patient will report a known tick bite or exposure to a Lyme-endemic area in the last 4 weeks. Other symptoms may include fever, a non-painful rash, and non-specific symptoms, such as headache, myalgias, and fatigue. On physical exam, you’ll see a single skin lesion called erythema migrans, which looks like a red, warm, and swollen rash with central clearing that may resemble a bullseye! With these findings, diagnose early Lyme disease, and treat empirically with oral doxycycline for 10 days. 

Here’s a high-yield fact! Erythema migrans is found in 80% Lyme disease cases, most commonly appearing in the groin, axilla, and thighs. If a patient’s rash does not have typical characteristics of erythema migrans, you can delay treatment until laboratory testing confirms the presence of Borrelia antibodies. Early in the course of infection, initial testing can be negative, so if clinical suspicion remains high, consider retesting in 2 to 3 weeks, which is the time required for the immune system to produce antibodies.

And now a clinical pearl! Prophylactic treatment with a single 200-milligram dose of doxycycline orally is recommended after a tick bite within 72 hours of tick removal. However, you should give prophylactic treatment only i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemoglobinopathies_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/m-j0frD5QV6XIfdv_EGQGO4hSZu_clOy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemoglobinopathies in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Hemoglobinopathies are genetic disorders that cause abnormal hemoglobin production, most commonly affecting hemoglobin A, which is composed of two alpha and two beta chains.  Using electrophoresis or genetic testing, we can detect abnormalities that indicate a deletion in genes coding for the alpha chain, called alpha thalassemias; or beta chain, called beta thalassemias; as well as a mutation in genes coding for the beta chain, called sickle cell disease. 

Hemoglobinopathies have variable clinical presentations. Some cause mild anemia, while others lead to severe anemia requiring transfusions. Depending on the type and severity of hemoglobinopathy in pregnancy, complications range from anemia to increased risk of venous thromboembolism and even fetal demise.

Your first step is to screen your pregnant patient at their first prenatal visit; however keep in mind that some patients may not have received their prenatal care, so they may present with a chief concern suggesting hemoglobinopathies in pregnancy. Start by obtaining a focused history and physical exam. Now, most patients with hemoglobinopathies in pregnancy are asymptomatic, but in some cases, history might reveal a positive family history of hemoglobinopathy or mild anemia on an antepartum screening CBC. Additionally, patients may report fatigue or weakness, but keep in mind that both of these symptoms are very nonspecific in pregnancy! 

Physical exam could reveal pallor, as well as jaundice, or hepatosplenomegaly due to extramedullary hematopoiesis. 

Alright, since these patients are usually asymptomatic, universal screening is really important to make a diagnosis. Universal screening involves either hemoglobin electrophoresis or molecular genetic tests, both of which will give you a better idea than CBC alone. As your next step, you should obtain hemoglobin electrophoresis unless they’ve had one completed before, in which case you can use those results.

Let’s first look at normal hemoglobin ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_myeloma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7_ijJGQXTmWzouIWLbdMws11RZ6zblRA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple myeloma: Clinical sciences]]></video:title><video:description><![CDATA[Multiple myeloma is a type of bone marrow cancer that originates in plasma cells, which are cells that develop from B lymphocytes to produce antibodies to fight infections. In multiple myeloma, plasma cells grow uncontrollably, crowding out the healthy cells in the bone marrow. As a result, the overgrowth of plasma cells can lead to a reduction in the production of other types of blood cells by the bone marrow. This can lead to anemia due to low red blood cell count, problems with blood clotting due to decreased platelets, and even a weakened immune system due to a decrease in functioning white blood cells. 

Plasma cells also produce excessive monoclonal antibodies that are dysfunctional and, over time, can accumulate in tissues, such as the kidneys, causing renal failure. Additionally, these antibodies increase serum viscosity, which impairs normal blood flow. This is known as hyperviscosity syndrome. 

Now, if your patient presents with a chief concern suggesting multiple myeloma, you should first obtain a focused history and physical examination. Most patients will be over the age of 65, and will likely report vague and nonspecific symptoms, such as weight loss, fever, and symptoms of anemia, including fatigue, weakness, shortness of breath, and dizziness. Some patients might also experience gastrointestinal symptoms, including nausea, constipation, or diarrhea. Others might report bone pain or a history of fractures or kidney disease. Finally, a person might experience symptoms of hyperviscosity syndrome, including blurred vision and headache. 

On the physical exam, your patient will present with elevated temperature, tachycardia, pallor, and signs of fluid retention, like edema. They might also have bone tenderness or deformity, which are signs of pathologic fractures. Finally, the neurological exam can reveal findings like numbness, paresthesias, and weakness. 

At this point, you can suspect multiple myeloma, so your next step is to order some tes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_vaginal_discharge:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jrr4XTfpRKih7NOf-zvQOettQNWhDdCc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to vaginal discharge: Clinical sciences]]></video:title><video:description><![CDATA[Vaginal discharge is one of the most common reasons for patients to present for gynecologic care. Normal physiologic discharge is generally asymptomatic, but abnormal vaginal discharge can cause significant discomfort and pain, can adversely affect daily activities, and has a considerable impact on sexual functioning and self-image. Normal vaginal discharge is the result of a combination of endocervical and vaginal secretions, sloughing of vaginal epithelial cells, and the presence of normal vaginal flora. 

A disruption of these components results in abnormal vaginal discharge, which is associated with vaginal or vulvar irritation, pain, or pruritus. Common causes of abnormal vaginal discharge include a foreign body in the vagina; vaginal inflammation; and vaginal or cervical infection.

Your first step in evaluating a patient who presents with vaginal discharge is a focused history and physical examination. Let&amp;#39;s start with an assessment for a foreign body. During history taking, the patient may describe an increase in vaginal discharge and possibly recent sexual activity or tampon use. Patients may express concerns about a retained foreign body such as a tampon or condom. However, they may be unaware of the presence of a foreign object or unwilling to disclose the information. 

Physical examination will reveal an abnormal, often purulent or even bloody, vaginal discharge and, if a foreign body is present on speculum examination, you have made your diagnosis.

Here’s a clinical pearl. Malodorous purulent vaginal discharge is often caused by retained hygiene products such as tampons, and in prepubertal female patients, fragments of toilet paper are a common culprit. However, if the foreign body is an item that is unusual or unexpected, make sure to consider and screen for sexual abuse. 

If there is no evidence of a foreign body, the next step is to assess for the presence of vaginal inflammation or infection, known as vaginitis, starting with t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Uterine_atony:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H3qUhksHR3eUKAt7hsbkwWyNTlODC6QS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Uterine atony: Clinical sciences]]></video:title><video:description><![CDATA[Uterine atony is the failure of the uterus to contract adequately after childbirth. This occurs due to a poor response to oxytocin resulting in failure of myometrial contraction. Uterine atony can occur after either vaginal delivery or cesarean section and is the number one cause of postpartum hemorrhage. Some methods can be used to prevent uterine atony, including active management during the third stage of labor, such as prophylactic uterotonics, uterine massage, and placental delivery. 

Your first step in evaluating a postpartum patient who presents with a chief concern suggesting uterine atony is to perform CABCDE assessment. If the patient is unstable, you should stabilize their airway, breathing, and circulation right away. This means you may need to intubate the patient and obtain IV access. Ideally, two large bore IVs will already be present to allow for adequate resuscitation. Finally, you should continuously monitor their vitals. 

Once these important steps are done, you can move on to focused history and physical exam. Also, obtain labs like CBC, PT, INR, PTT, and fibrinogen. Now, patients may report feeling dizzy or anxious and may experience tunnel vision after giving birth. When taking history, be sure to see if the patient has any risk factors for uterine atony. These include high parity, multiple gestation such as twins or triplets, fetal macrosomia, chorioamnionitis, polyhydramnios, as well as general anesthesia, and prolonged oxytocin use. 

When it comes to a physical exam, it typically reveals hypotension and tachycardia, as well as an altered mental status to the point of being unconscious. Patients may look pale and their skin may feel cold or clammy due to the acute blood loss. On abdominal exam, the uterus will be soft, boggy, and poorly contracted, which will result in continuous bleeding from the uterus. Okay, let’s move on to labs. They typically reveal anemia and may also show thrombocytopenia, elevated coagulation s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Idiopathic_intracranial_hypertension:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jnOMyFCFTOyFQKdTs5dPospLQT2YCiPX/_.png</video:thumbnail_loc><video:title><![CDATA[Idiopathic intracranial hypertension: Year of the Zebra]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Idiopathic intracranial hypertension: Year of the Zebra through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_abdominal_wall_and_groin_masses:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MWf0-YCIRWSloIitQPoR1-g-RQuHz39L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to abdominal wall and groin masses: Clinical sciences]]></video:title><video:description><![CDATA[Abdominal wall or groin masses are common surgical symptoms that arise due to hernias, traumatic injuries, neoplasms, or infections. Each of these typically presents with a unique set of clinical features that can help you differentiate one from another. For example, some masses are reducible, while others are hard like a solid mass, or soft like a cystic mass. So, getting a good history and a thorough physical exam is very important in narrowing down your differential.

The first step in assessing a patient presenting with an abdominal wall or groin mass is to perform the ABCDE assessment to determine if they are stable or unstable. 

If the patient is unstable, start acute management right away by stabilizing the airway, breathing, and circulation. Make sure to obtain IV access, initiate IV fluid  resuscitation, and keep the patient NPO.

Alright, now that unstable patients are taken care of, let’s talk about stable ones. 

Your first step here is to obtain a focused history and physical exam. Start by assessing for an acute abdomen, which is always a surgical emergency. These patients typically report severe abdominal or groin pain around the mass, as well as nausea, vomiting, constipation, or obstipation, which are signs of bowel obstruction. 

Physical exam often reveals a distended abdomen with signs of peritonitis, such as diffuse tenderness with rebound pain and guarding, along with an irreducible mass. 

These are classic findings of incarcerated or strangulated hernias with acute abdomen. Since we are talking about a surgical emergency, these patients need operative intervention right away to relieve the obstruction and prevent the progression of abdominal sepsis from bowel ischemia and necrosis. Once abdominal sepsis occurs, patients can quickly deteriorate and become unstable. 

Alright, once acute abdomen has been ruled out, assess for other causes of abdominal wall or groin masses starting with abdominal wall or groin hernias. 

Usually, pati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_in_pregnancy_(GDM,_T1DM,_and_T2DM):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rwIS67p9SkKTi5xi_HQweA-hRRGhtiNY/_.png</video:thumbnail_loc><video:title><![CDATA[Diabetes in pregnancy (GDM, T1DM, and T2DM): Clinical sciences]]></video:title><video:description><![CDATA[Diabetes in pregnancy is characterized by hyperglycemia during gestation. Diabetes that initially arises during pregnancy is called gestational diabetes mellitus, or GDM. GDM develops in at-risk patients due to worsening insulin resistance that occurs in the second and third trimesters. Individuals might also present to obstetric care with type 1 or type 2 diabetes, which is referred to as pregestational diabetes. All types of diabetes in pregnancy increase the risk of complications, including fetal macrosomia, shoulder dystocia, preeclampsia, and cesarean birth. Pregestational diabetes has additional risks of congenital malformations, spontaneous abortion, and stillbirth. 

Your first step in evaluating a patient with a chief concern suggesting diabetes in pregnancy is to obtain a focused history. Start by determining if the patient has GDM or pregestational diabetes, and then review recent blood glucose measurements. Patients with diabetes in pregnancy usually check a fingerstick glucose four to five times daily, including fasting; postprandial, or after each meal; and sometimes at bedtime. Most patients keep a glucose log, or you can scroll through glucose readings on their glucometer. Target glucose levels include a fasting glucose of less than 95 and either a one-hour postprandial glucose of less than 140 or a two-hour postprandial glucose that’s less than 120.

Individuals with GDM who consistently achieve target glucose levels with diet and exercise have A1GDM. A1GDM is also called diet-controlled GDM because blood glucose levels are adequately controlled without medication. 

During the antepartum period, a patient with A1GDM should continue previously prescribed lifestyle modifications, including a carbohydrate-controlled diet and 30 minutes of moderate-intensity aerobic exercise at least 5 days per week, such as walking 10 to 15 minutes after each meal. Advise the patient to continue self-monitoring of fasting and postprandial glucose levels to a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis_B:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zjRnrGoQRxSFuodwwJUpAr6BS3O77cKi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatitis B: Clinical sciences]]></video:title><video:description><![CDATA[Hepatitis B virus, or HBV for short, is a bloodborne DNA virus transmitted through blood or sexual contact. Once inside the body, hepatitis B virus circulates through the blood, eventually reaching the liver, where it infects hepatocytes. After the acute phase of the infection, many patients fully recover as their immune system clears the virus. But, if the virus sticks around long enough in the body, acute infection can progress to chronic infection, which can lead to the development of cirrhosis, and even hepatocellular carcinoma.

Now, if your patient presents with a chief concern suggesting hepatitis B infection, perform an ABCDE assessment to determine if they are unstable or stable. Unstable patients may have signs like altered mental status, asterixis, upper GI hemorrhage, and ascites. In this case, immediately stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. 

Here’s a clinical pearl! In some individuals, acute hepatitis B infection can lead to fulminant hepatic failure, which is a life-threatening condition that&amp;#39;s often associated with hepatic encephalopathy! Labs usually reveal coagulopathy, with INR equal to or greater than 1.5, as well as elevated AST, ALT, and bilirubin. In this situation, stabilize your patient and consider consulting both your hepatology and surgery teams for further management, including a liver transplant.

Okay, let’s go back and discuss stable patients. First, obtain a focused history and physical examination. Patients will usually report systemic symptoms, such as fatigue, anorexia, and low-grade fever; and gastrointestinal symptoms, like nausea, vomiting, and right upper quadrant pain. Additionally, your patient might report a history of needlestick injury, intravenous substance use, unprotected sexual intercourse, or receiving a non-sterile tattoo. 

The physical exam t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Group_B_streptococcus_(GBS)_colonization_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DZ-35NvcTTqlOxVfgJ86SL8vRP_a_PmC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Group B streptococcus (GBS) colonization in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Group B streptococcus, or GBS, is a normal flora commensal found in gastrointestinal and vaginal microbiomes. Pregnant patients who are colonized with GBS can transmit the bacteria to their newborns during labor or after the rupture of membranes, so it is a significant cause of neonatal infection including pneumonia, meningitis, and sepsis. For that reason, universal GBS screening for vaginal-rectal colonization in pregnancy is recommended to prevent neonatal GBS early-onset disease, or EOD.  

Screening a patient for GBS colonization will vary depending on the time of presentation, so let&amp;#39;s start with antepartum patients. Assessment begins with obtaining a focused history to see if they have any risk factors that increase the chance of neonatal GBS EOD. The most significant risk factor is a history of a previous GBS-infected newborn. These patients are presumed to be colonized with GBS and will require IV intrapartum antibiotics. The preferred antibiotic is penicillin, though ampicillin is an acceptable alternative. However, if a patient has an allergy to penicillin, you should use alternative antibiotics. When the allergy is low-risk for anaphylaxis, use a first-generation cephalosporin like cefazolin. On the other hand, if the allergy is high-risk for anaphylaxis, you’ll need to have the lab assess the GBS isolate for clindamycin resistance. If the GBS is sensitive to clindamycin, you can use that, but if it’s resistant, then vancomycin is used instead. 

Here’s a clinical pearl. Many patients are unsure of their allergic reactions, especially when it comes to penicillin. In pregnant patients who report a history of penicillin allergy but are not sure of the severity of their reaction, penicillin allergy testing can be beneficial. 

Next, let’s talk about screening for patients without a history of a GBS-infected newborn. Typically, at the first prenatal appointment, a urine culture is obtained to check for asymptomatic bacteriuria. This is bec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pelvic_inflammatory_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xzMPBklgRum6qW7aztvTjByDTXKz30L7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pelvic inflammatory disease: Clinical sciences]]></video:title><video:description><![CDATA[Pelvic inflammatory disease, or PID for short, is an inflammatory condition that can affect the uterus, fallopian tubes, ovaries, and peritoneum. PID is often caused by infection with sexually transmitted organisms such as gonorrhea and chlamydia. However, it may also be caused by microorganisms normally found in the vaginal flora. 

Inflammation of the fallopian tubes, also known as salpingitis, increases the risk of infertility and ectopic pregnancy, while peritonitis can lead to pelvic adhesions and chronic pelvic pain. Even very mild cases of PID can lead to these sequelae. Finally, based on the severity, the clinical presentation of PID can range from asymptomatic or only mild symptoms to severe pelvic pain or even sepsis. 

Your first step in evaluating a patient presenting with a chief concern suggesting PID is to perform a CABCDE assessment in order to determine if they are stable or unstable, which in most cases would indicate they’ve developed sepsis.

If the patient is unstable, stabilize their airway, breathing, and circulation right away. This means that you might have to intubate the patient, obtain IV access and continuously monitor their vital signs. In addition, you should immediately obtain an HCG pregnancy test! 

Once you have initiated acute management, your next step is to take a focused history and physical exam. Patients typically report fever, nausea and vomiting, lower abdominal and pelvic pain, abnormal vaginal discharge, and intermenstrual or post-coital spotting. 

Here’s a high-yield fact! If this patient reports upper abdominal pain, you should consider perihepatitis, also known as Fitz-Hugh-Curtis syndrome. Perihepatitis develops when the pathogenic microorganisms causing PID spill from the fimbriae and settle in the space surrounding the liver and diaphragm. This leads to inflammation of the liver capsule, without involvement of the liver parenchyma, as well as to the formation of the so-called “violin string” adhesion]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malaria:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jurSntJ_RcGw_VAWTW8nzcdZQ5mlkk3e/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malaria: Clinical sciences]]></video:title><video:description><![CDATA[Malaria is a systemic, febrile illness caused by the protozoan parasite Plasmodium. It’s typically seen in recent travelers of endemic regions such as Africa, South Asia, and parts of Central and South America. 

Once transmitted via an infected female Anopheles mosquito, the parasites invade hepatic cells where they reproduce. Next, the parasites invade red blood cells, eventually causing their rupture and causing symptoms like fever, malaise, and chills. Based on the presence and degree of parasitemia, you can diagnose your patient with uncomplicated malaria or severe malaria.

Now, if your patient presents with chief concerns suggesting malaria, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and start IV fluids. Then put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen to maintain oxygen saturation greater than 90%. 

Once you stabilize your patient, proceed with a focused history and physical and order labs, primarily CMP, CBC, and coagulation studies, such as a PT and PTT. The history typically reveals fever, seizures, and recent travel to a malaria-endemic area. Physical examination will likely reveal an elevated temperature, hypotension, tachypnea, and altered level of consciousness. Some patients may even present with recurrent seizures and coma!

Here’s a clinical pearl to keep in mind! Cerebral malaria is a diffuse symmetric encephalopathy caused by parasites adhering to the cerebrovascular endothelium, and puts the patient at risk of permanent neurologic damage or death! If you suspect cerebral malaria, immediately treat with intravenous artesunate to reduce the patient’s risk of permanent neurologic damage or death!

Next, lab results are non-specific and could reveal hypoglycemia, low bicar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shwachman-Diamond_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jw8cowjXSG6pgZsKt1fRMq_KSxW-HwfW/_.png</video:thumbnail_loc><video:title><![CDATA[Shwachman-Diamond syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Shwachman-Diamond syndrome, or SDS, is a rare genetic condition that primarily affects the bones, pancreas, and bone marrow. Most cases result from alterations in the SBDS gene, which affects the assembly of cell organelles called ribosomes. Ribosomes are essential to maintain cell function, and in SDS, ribosomal function is altered, causing changes in multiple body systems. SDS is inherited in an autosomal recessive pattern, meaning an individual with SDS inherits two altered genes, one from each parent. 

Now, signs and symptoms of SDS are variable. If the bones are involved, individuals may have a short stature and skeletal changes like a short, flared rib cage or slowed ossification, or the formation of new bones. 

SDS can also cause a decrease in pancreatic function, leading to a decrease in digestive enzymes that break down fat and protein, causing malabsorption. If left untreated, this can lead to decreased weight gain, failure to thrive, and steatorrhea, or fat-containing stools. However, decreased pancreatic function may improve as individuals age.

Decreased bone marrow function ranges from mild to severe. It can result in low blood cell counts particularly involving neutrophils, red blood cells, and platelets. The most common is low levels of neutrophils, also known as neutropenia. Neutropenia increases susceptibility to bacterial infections, leading to an increased risk of infections. 

Low red blood cell counts, or anemia, can cause fatigue, pallor, and shortness of breath; and low platelet counts, or thrombocytopenia, can increase the risk of bleeding from minor injuries. Rarely, individuals with SDS may develop acute leukemia, or cancer of the blood; or other blood-related disorders, like myelodysplastic syndrome. 

Diagnosis of SDS is suspected in individuals with symptoms of decreased pancreatic and bone marrow function. Laboratory tests involve a complete blood count, pancreatic enzyme levels, and a blood smear. Additionally, a bone marr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Toxic_shock_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/35M00fKjSFyehCWG-lswQ7FwQ5qzYP3m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Toxic shock syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Toxic shock syndrome, or TSS for short, is a rare form of septic shock caused by bacteria like Streptococcus pyogenes or Staphylococcus aureus. Based on the causative agent, TSS is subdivided into two main types called streptococcal TSS and non-streptococcal TSS. 

TSS typically results from a skin and soft tissue infection, or a contaminated foreign body, such as retained surgical packing. 

At these points, bacteria produce toxins that can reach the bloodstream and spread throughout the body, eventually activating T lymphocytes. This triggers the release of inflammatory cytokines, causing fever, hypotension, and multiple organ failure. 

Now, when a patient presents with a chief concern suggesting toxic shock syndrome, the first step is to perform an ABCDE assessment. Patients with toxic shock syndrome are generally unstable, so initiate acute medical management to stabilize the airway, breathing, and circulation. 

Admit your patient to the ICU, and initiate continuous vital sign monitoring. Next, obtain IV access and consider placing catheters for invasive hemodynamic monitoring, including an arterial line and a central venous catheter, or CVC. 

Patients with toxic shock syndrome often have profound hypotension, so begin IV fluid resuscitation. 

In some cases,  to maintain hemodynamic stability, you may need to add vasopressors, targeting a mean arterial pressure or MAP of 65 millimeters of mercury or above. 

Lastly, obtain blood cultures and begin broad-spectrum IV antibiotics. 

Keep in mind that achieving hemodynamic stability, obtaining blood cultures and starting broad spectrum antibiotics is known as the “1-hour sepsis bundle”, and it should be performed within the first hour of patient presentation. 

Now, here’s a clinical pearl! You should obtain a blood lactate level in the first hour to check for organ hypoperfusion. These levels are then monitored serially to guide hemodynamic resuscitation efforts. If lactate levels are high initia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brown-Séquard_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h-iJMuWQQKSFcix7E7b9ivI-QEu1fnnA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brown-Séquard syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Brown-Séquard syndrome, first described by the physiologist Charles-Édouard Brown-Séquard, is a condition associated with hemisection or damage to one half of the spinal cord. The hemisection damages neural tracts in the spinal cord that carry information to and from the brain. This results in a loss of sensations like pain, temperature, touch, as well as paralysis or loss of muscle function in some parts of the body.

Now, if you look at the cross-section of the spinal cord, the white matter is on the outside and the gray matter is on the inside, and overall it looks like a butterfly. If we draw a horizontal line through the spinal cord, the front half is the anterior or ventral half, and the back half is the posterior or dorsal half. And the butterfly wings are sometimes referred to as horns; so we have two dorsal horns that contain cell bodies of sensory neurons and two ventral horns that contain cell bodies of motor neurons.  The white matter consists of myelinated axons which are separated into tracts that carry information to and from the brain. Think of them like highways for neural signals, where some highways carry sensory information to the brain and some carry motor information from the brain to the muscles.

There are a few main tracts to remember. First, there’s the spinothalamic tract which is an ascending pathway and it’s divided into two parts. The lateral tract carries sensory information for pain and temperature, while the anterior tract carries information for pressure and crude touch--or the sense one has been touched, without being able to localize where they were touched. Second, there are two ascending dorsal column tracts- the fasciculus gracilis which carries sensory information from the lower trunk and legs, and the fasciculus cuneatus which carries sensory information from the upper trunk and arms. These tracts both carry sensations like vibration; fine touch, which is where you can localize where you were touched; and propriocep]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Emergency_contraception:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W5sR_ayCSNaDBbQhSBExmFLuRB_e2f21/_.jpg</video:thumbnail_loc><video:title><![CDATA[Emergency contraception: Clinical sciences]]></video:title><video:description><![CDATA[Emergency contraception is used to prevent unintended pregnancy after unprotected or inadequately protected sexual intercourse. Many patients don’t fully understand what emergency contraception is or how it differs from medical abortion, which is why some of them don’t use it when needed. While medical abortion is used to end a confirmed pregnancy, emergency contraception works by preventing pregnancy after sexual intercourse and is ineffective after implantation. Different types of emergency contraception are available, including levonorgestrel, ulipristal acetate, combined oral contraceptives, and intrauterine devices.  Okay, let’s talk about what to do when a patient presents after unprotected or inadequately protected sexual intercourse and does not desire pregnancy.

The good news is that there are no exams or testing necessary! In fact, emergency contraception should be utilized as soon as possible after unprotected or inadequately protected intercourse. So, there’s no need to wait for any test results, not even a pregnancy test! First, ask how long it’s been in days or hours since intercourse and go from there. 

Here’s a clinical pearl! Always counsel patients on emergency contraception. Unfortunately, you may not know if your patient is experiencing intimate partner violence or if they’ve been or ever become a victim of sexual assault; so routinely discussing and prescribing emergency contraception can make a big difference. The oral levonorgestrel product is available over the counter without age restriction.   

Okay, if it’s been up to 5 days, or 120 hours, since intercourse the patient can receive emergency contraception. 

The first and most commonly used option is oral levonorgestrel, commonly known as Plan B. This method is most effective the sooner it’s taken from the act of unprotected sexual intercourse, ideally when taken within 72 hours, but continues to reduce the risk of pregnancy up to 120 hours. Unlike every other form of emergency]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vitamin_B12_deficiency:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/klcAQmSKTompn9slfUUwpCE7SOC6aA_F/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vitamin B12 deficiency: Clinical sciences]]></video:title><video:description><![CDATA[Vitamin B12 deficiency occurs when the body lacks sufficient vitamin B12, which is crucial for adequate DNA synthesis, nerve myelination, and fatty acid oxidation. Vitamin B12, also known as cobalamin, is found in animal products like meat, eggs, dairy, and fortified cereals. So, inadequate intake of these foods, malabsorptive conditions, and some medications, can lead to vitamin B12 deficiency. The diagnosis is primarily made based on vitamin B12 levels, complete blood count, and peripheral blood smear.

Now, when a patient presents with a chief concern suggesting vitamin B12 deficiency, the first step is to perform a focused history and physical examination. The patient may report fatigue, palpitations, numbness, and tingling in their extremities. In severe cases, they may also report impaired gait or falls; as well as neuropsychiatric symptoms, such as cognitive impairment or mood changes. Additionally, your patient might present with risk factors for vitamin B12 deficiency. These include inadequate dietary intake, seen in strict vegetarians or vegan diets, and conditions that decrease B12 absorption, like gastric bypass surgery or inflammatory bowel disease; as well as medications that interfere with B12 metabolism, such as metformin, or medications that interfere with B12 absorption, like proton pump inhibitors.

Additionally, the physical exam may reveal glossitis, often described as berry red patches on the lingual surface. In severe cases, vitamin B12 deficiency can lead to subacute combined degeneration, an advanced form of central nervous system neuropathy associated with demyelination of the dorsal and lateral columns of the spinal cord. Important findings in these individuals include sensory ataxia, as well as loss of proprioception, impaired vibratory sensation, and in some cases, progressive muscle weakness. At this point, you should suspect vitamin B12 deficiency.

Now, here’s a clinical pearl! Nitrous oxide, used either as an anestheti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Transforming_your_classroom_experience:_Using_Osmosis_to_support_teaching_and_learning</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uS0jtlcNTXSEriMrYGpk2FIoQZq3mIfF/_.png</video:thumbnail_loc><video:title><![CDATA[Transforming your classroom experience: Using Osmosis to support teaching and learning]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Transforming your classroom experience: Using Osmosis to support teaching and learning through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Desmoid_Tumor_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5okOlimyTJqT5rD_MTL2lGeZTFCM9K3z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Desmoid Tumor (NORD)]]></video:title><video:description><![CDATA[Desmoid tumors, also called aggressive fibromatosis, occur when connective tissue cells called myofibroblasts begin to multiply out of control, creating a tumor-like mass. The condition is similar to fibrosarcoma, a type of malignant cancer; however, desmoid tumors do not metastasize to other parts of the body. Given their cell of origin, they are part of a larger group of tumors called sarcomas.

Desmoid tumors are rare. The condition primarily affects young people, usually between 10 to 40 years of age, and is more common in females than males.

The pathology of desmoid tumors is currently not well known. In most patients, the disease occurs spontaneously, with no known specific trigger or cause. While estrogen or past surgeries in the same location as the tumor have been suggested as possible risk factors, more research needs to be done to confirm this.

That said, 3.5-32% of patients with familial adenomatous polyposis, an inherited syndrome where polyps develop in the intestine and skin, will develop desmoid tumors as part of this condition. These patients have a variant in their adenomatous polyposis coli, or APC gene, which is a tumor suppressor gene. The APC gene variant can cause uncontrolled cell division and, as a result, polyps develop within the patient’s body. Over time, if left untreated, these polyps can develop into tumors. Any patient who develops a desmoid tumor, particularly intra-abdominal, should be evaluated for this syndrome.

Symptoms vary from person to person, depending on the person’s age, where the tumor arises in the body, and the size of the tumor. The most common symptom is the development of a mass or swelling that is often painless to the touch. As the tumor gets bigger, the mass begins compressing the nerves and muscles around it, causing soreness or pain. This can lead to restricted movement or chronic limping if the tumor develops in the patient’s arms or legs. Tumors that arise in the bowels can cause abdomin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_breast_mass_and_asymmetry:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0XWuw6wVTxSuLvuRxN8lea63TM_KNYw3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a breast mass and asymmetry: Clinical sciences]]></video:title><video:description><![CDATA[Breast mass or asymmetry can occur at any age and can be benign or malignant. Because there’s a wide range of causes for a breast mass or asymmetry, one helpful way to narrow down your differential is to categorize its onset in relation to pregnancy or lactation. It’s important to keep in mind that a new mass or asymmetry can carry a risk of malignancy, so timely diagnosis of the underlying cause is very important.

Your first step in assessing a patient with a new breast mass or asymmetry is to obtain a focused history and physical. On history, make sure to obtain information about the onset of the mass or asymmetry, associated pain, growth or changes in shape, as well as other symptoms, like skin changes or nipple discharge. Patients might report recent breast trauma, as well as fluctuation in size of the mass or associated symptoms with their menstrual cycle. In patients of child bearing age, make sure to ask if they’re currently pregnant or lactating. Additionally, patients might have certain risk factors such as early menarche or late menopause, history of breast cancer, ovarian cancer or other high risk lesions, genetic mutations like BRCA1 or BRCA2, or hormone replacement therapy . 

Next, let’s move on to the physical exam. Your exam should include a complete clinical breast examination. On visual inspection you might see noticeable abnormalities or differences between the two breasts, including shape, size, dimpling, and skin or nipple changes. On palpation, you might feel a distinct mass, hardness of the breast or even elicit nipple discharge. Additionally, you might even find palpable lymphadenopathy of the cervical, clavicular, and axillary nodes.

The next step in our diagnostic work up is imaging. You may choose to order an ultrasound or mammogram. The modality of choice will depend on one factor: is the patient currently pregnant or lactating?

Alright, let’s start with patients who are pregnant or lactating. In this case, breast ultras]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_diabetes_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jvObAQSTSnOkDeK2K3DaD-1cSkujKb-R/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to diabetes in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Diabetes is one of the most common medical complications in pregnancy. Patients with diabetes in pregnancy are more likely to develop preeclampsia and undergo cesarean delivery. Additionally, higher glucose levels cross the placenta, resulting in an increased glucose supply to the fetus. The fetal pancreas responds by producing more insulin to handle the excess glucose. Fetal hyperinsulinemia promotes increased fat accumulation, particularly in the shoulders and chest, that can cause macrosomia; shoulder dystocia; and birth trauma. 

Moreover, once the umbilical cord is clamped after delivery, the maternal glucose supply is interrupted, which can lead to neonatal hypoglycemia. Most cases of diabetes in pregnancy are gestational diabetes mellitus, or GDM, which is hyperglycemia that develops during pregnancy. However, many patients don’t receive diabetes screening before pregnancy, so it can be challenging to differentiate between GDM and previously existing, or pregestational, type 1 or type 2 diabetes. 

The first step in evaluating a patient who presents for diabetes screening in pregnancy is to obtain a focused history and physical exam, ideally at the initiation of prenatal care. First, you want to assess whether a patient has a previous diagnosis of either type 1 or type 2 diabetes. If they do, that’s pregestational diabetes mellitus. This is an important distinction to make, because patients with pregestational diabetes are more likely to have significant maternal and fetal complications during pregnancy, and usually require additional monitoring. 

On the flip side, if your patient has no previous diagnosis of type 1 or type 2 diabetes, your next step is to assess whether they’re at high risk for GDM. A patient who is at high risk will have an elevated BMI of at least 25, or at least 23 in patients of Asian descent; plus one or more additional risk factors. These additional risk factors in history include GDM in a previous pregnancy; a first-degree ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypernatremia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3MTHh48dQiiSTygSitSjg8_2SfedfB6u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypernatremia: Clinical sciences]]></video:title><video:description><![CDATA[Hypernatremia is an electrolyte imbalance that occurs when the serum sodium concentration exceeds 145 milliequivalents per liter. It typically results from increased water loss or decreased water intake, but in rare cases, it can be caused by an excess salt load. Now, based on the volume status, hypernatremia can be classified as hypovolemic, euvolemic, and hypervolemic hypernatremia!  

Okay, if a patient presents with chief concerns suggesting hypernatremia, first, perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and consider giving your patient IV fluids. Next, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, be sure to monitor the patient’s urine output. 

Now, here’s a clinical pearl to keep in mind! Acute hypernatremia develops in less than 48 hours, with symptoms ranging from mild, such as nausea, to severe neurologic impairment, such as seizures and coma.  

On the other hand, chronic hypernatremia presents with no symptoms or only mild ones. This is because, in chronic hypernatremia, there&amp;#39;s enough time for the body to adjust to electrolyte changes, which makes neurological symptoms less likely.  

Finally, be cautious when treating hypernatremia since aggressive correction of serum sodium levels and aggressive fluid resuscitation can lead to rapid fluctuations in serum osmolality and subsequent cerebral edema. 

Alright, now let’s go back to the ABCDE assessment and look at stable patients.  

In this case, obtain a focused history and physical examination and order a basic metabolic panel. History might reveal symptoms like muscle weakness, increased thirst, polyuria, and polydipsia.  

In extreme cases, the patient might even report a history of seizures.  

Next, the physical exam might reveal blood pressure changes. Moreover, if the patient is hypervolemic,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_hypertension:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5F4aaYfPQA225avjL8OD5eFiTuel512a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pulmonary hypertension: Clinical sciences]]></video:title><video:description><![CDATA[Pulmonary hypertension, or PH for short, refers to an abnormally high pressure in the pulmonary circulation, which is divided into five main groups based on etiology. Group I refers to pulmonary arterial hypertension; Group II is PH due to left heart disease; Group III PH is associated with chronic lung disease or hypoxia; Group IV PH is due to pulmonary artery obstruction; and finally, Group V is PH with unclear or multifactorial mechanisms. 

Now, if your patient presents with a chief concern suggesting PH, perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation, which might require endotracheal intubation and mechanical ventilation. Next, obtain IV access and put them on continuous vital sign monitoring, as well as cardiac telemetry; and if needed, don’t forget to provide supplemental oxygen. Finally, in some cases, you might need to place an indwelling pulmonary artery catheter, also known as a Swan-Ganz catheter.  

Next, obtain a focused H&amp;amp;P. Your patient will typically report shortness of breath and chest discomfort, while their physical exam will usually reveal hypotension and tachycardia. You might also notice signs of right-sided heart failure, such as a right ventricular heave; jugular venous distention, with hepatojugular reflux; lower extremity edema; and cool extremities. On auscultation you might notice a loud P2 or a holosystolic murmur from tricuspid regurgitation. 

At this point, suspect cardiogenic shock.  Then order labs, including BNP; as well as a 12-lead ECG, chest X-ray, and echocardiogram. Labs will show an elevated BNP.  ECG will likely reveal right axis deviation; peaked P-waves on lead v2, indicating right atrial enlargement; and R-waves greater than 7mm in lead v1, consistent with right ventricular hypertrophy. The chest X-ray often reveals cardiomegaly. Finally, echocardiogram usually shows elevated estimated pulmonary artery pressure an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemochromatosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DxCSgMM9RCmP2BjculZiuMcFQIe7JrsE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemochromatosis: Clinical sciences]]></video:title><video:description><![CDATA[Hemochromatosis, or simply iron overload, is a condition associated with excess iron deposition throughout the body. 

In the early stage, hemochromatosis is usually asymptomatic, but over time, accumulated iron leads to long-term oxidative stress and eventual tissue fibrosis and organ dysfunction. The most commonly affected organs include the liver, heart, joints, endocrine organs, and the skin. 

Now, based on the underlying cause, hemochromatosis can be classified as primary and secondary. Primary hemochromatosis, also known as hereditary hemochromatosis, is an autosomal recessive disorder caused by mutations in genes that control iron absorption; while secondary hemochromatosis is associated with underlying causes of iron overload, such as chronic liver disease, anemia, or excessive iron supplementation.

If your patient presents with a chief concern suggesting hemochromatosis, your first step is to perform a focused history and physical examination. Typically, your patient will report fatigue in combination with symptoms based on the organ that’s affected. In most cases, your patient will also report skin changes like bronzing! 

As iron accumulates in the skin, it stimulates melanocytes to produce melanin, which eventually results in slate gray pigmentation that primarily affects the face, neck, genital region, and extensor surfaces of forearms and lower legs. 

Next, iron deposition in joints can result in joint pain, especially in the digits at the second and third metacarpophalangeal joints and in the knees. Additionally, it can affect the heart, causing cardiomyopathy and symptoms such as chest pain, shortness of breath, and dyspnea on exertion.

Additionally, there might be a history of alcohol use, liver disease, diabetes mellitus, or a family history of hemochromatosis. The physical examination could reveal bronze skin discoloration, joint swelling, as well as signs of cardiomegaly and hepatomegaly! 

Now, here’s our first clinical pearl!]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatic_encephalopathy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HbQ3UPrSQp6z-xfMFeIAcL7kRPiQcQWG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatic encephalopathy: Clinical sciences]]></video:title><video:description><![CDATA[Hepatic encephalopathy refers to a potentially reversible neuropsychiatric complication of advanced liver disease, most commonly cirrhosis. In cirrhosis, impaired liver function results in the accumulation of toxic substances, like ammonia, which can eventually reach the brain and cause neurological dysfunction. Symptoms can vary from mild confusion to severe brain dysfunction with features like stupor or coma. Mild cases are referred to as covert hepatic encephalopathy, while severe cases are called overt hepatic encephalopathy. 

If your patient presents with a chief concern suggesting hepatic encephalopathy, first perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen to maintain oxygen saturation above 90 percent.  

Okay, now let’s go back to the ABCDE assessment and focus on stable patients.  

If your patient is stable, your first step is to obtain a focused history and physical examination. History will typically reveal impaired mental status, which can range from mild confusion, changes in behavior, to coma. Family or caregivers may report deficits in memory, attention, and behavioral changes, as well as disturbances in the sleep-wake cycle.  

Additionally, the physical exam will usually reveal signs of underlying liver disease, like jaundice, ascites, palmar erythema, and telangiectasias. You might also notice hypertonia, hyperreflexia, and asterixis, which is characterized by a flapping tremor of the wrists that occurs when the arms are extended. With these findings, you should suspect hepatic encephalopathy! 

Now, here’s a clinical pearl to keep in mind! Hepatic encephalopathy typically doesn&amp;#39;t cause focal neurological deficits, such as unilateral body weakness or a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Portal_vein_thrombosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t73UN4Y8RrW5FIIv3EnkLFPVSu6EEybo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Portal vein thrombosis: Clinical sciences]]></video:title><video:description><![CDATA[Portal vein thrombosis, or PVT for short, refers to the formation of blood clots within the portal vein that can result in partial or complete obstruction of the blood vessel. This condition is commonly associated with cirrhosis and hepatocellular carcinoma, and can result in various complications, such as esophageal and gastric varices, as well as cavernous transformation, pylephlebitis, and mesenteric ischemia. 

Now, if your patient presents with a chief concern suggesting portal vein thrombosis, your first step is to perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, first stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen and ensure the patient is nil per os or NPO, meaning nothing by mouth. 

Now, here’s a clinical pearl! If your patient is unstable, be sure to assess for severe complications of portal vein thrombosis, like variceal bleeding or mesenteric infarction. For variceal bleeding, consider variceal banding or sclerotherapy. In case of mesenteric infarction, immediately obtain a surgical consultation!

Now, let’s go back to the ABCDE assessment and look at stable patients. In this case, obtain a focused history and physical examination. Your patient may complain of abdominal pain, which comes and goes abruptly, and could be generalized or localized in the right upper quadrant. Other symptoms may include bloody vomit or dark, tarry stools. 

The physical exam may reveal signs of portal hypertension, such as splenomegaly; or signs of cirrhosis, such as jaundice or ascites. Now, with these findings, you should suspect portal vein thrombosis.

Your next step is to order a Doppler ultrasound to assess the blood flow in the portal vein. If the Doppler ultrasound reveals normal portal vein blood flow, you shou]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spontaneous_bacterial_peritonitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/36PrEC1PQ_akSp9-vYfRtJRdSzGV8qHA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spontaneous bacterial peritonitis: Clinical sciences]]></video:title><video:description><![CDATA[Spontaneous bacterial peritonitis refers to a bacterial infection of ascitic fluid without an identifiable source. It typically affects individuals with liver cirrhosis, and it’s thought to be due to a bacterial migration from the gut. Based on ascitic fluid culture results, you can differentiate spontaneous bacterial peritonitis from secondary bacterial peritonitis, which is associated with an identifiable source of infection!

When a patient presents with a chief concern suggesting spontaneous bacterial peritonitis, first you should perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation, which means you may have to intubate the patient. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen!

Now, here’s a clinical pearl! Like any other infection, patients with spontaneous bacterial peritonitis can progress to septic shock. In that case, broad spectrum antibiotics with carbapenems are essential, and remember to also look for other potential sources of infection. In otherwise stable patients, a third generation cephalosporin is adequate.

Okay, now let’s go back to the ABCDE assessment and focus on stable patients. In this case, obtain a focused history and physical examination. Also, order labs including CBC, CMP, and serum albumin. Finally, don&amp;#39;t forget to order an abdominal ultrasound. Your patient will likely report systemic symptoms, such as fever and chills, as well as abdominal pain and progressive abdominal distention, as well as rigidity. 

There might also be a history of cirrhosis, with or without prior episodes of ascites. The physical examination will reveal mild abdominal tenderness and signs of ascites, like bulging flanks, a palpable fluid wave, and shifting dullness. In some cases, you might notice g]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Paraesophageal_and_hiatal_hernia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fUN28i6ZSz6Yp8PxrSmsR0UZSiit8Nm7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Paraesophageal and hiatal hernia: Clinical sciences]]></video:title><video:description><![CDATA[Paraesophageal and hiatal hernias are a condition where a part of the stomach or other abdominal organ moves upward through the diaphragmatic hiatus and into the chest cavity. This occurs when the phrenoesophageal membrane weakens and the diaphragmatic esophageal hiatus widens, allowing upward movement of intra-abdominal organs.  

These hernias are categorized into 4 types depending on the organs displaced into the chest. A Type I is  where the gastroesophageal junction, or GEJ for short,  migrates above the diaphragm.  This is also known as a sliding hernia because sometimes the GEJ can slide above and below the diaphragm.  

Type II occurs when part of the gastric fundus has herniated through the hiatus and lies next to the esophagus. The GEJ is usually in its normal location below the diaphragm. Type III is a combination of Types I and II, where both the GEJ and a part of the stomach are above the hiatus.  Finally, Type IV occurs when an intra-abdominal organ such as the colon, spleen, pancreas, or small intestine herniates through the hiatus. 

Now, when assessing patients with a chief concern suggesting a paraesophageal or hiatal hernia, your first step is to perform an ABCDE assessment to determine if the patient is stable or unstable.  

If the patient is unstable, begin acute management immediately to stabilize the airway, breathing, and circulation. This means you might need to intubate the patient to secure the airway, while obtaining IV access, beginning IV fluid resuscitation, and continuously monitor vital signs. Additionally, make the patient NPO and place a nasogastric tube for bowel decompression.  

Once acute management has been initiated, your next step is to obtain a focused history and physical examination; order labs such as CBC, CMP, and lactate; and order  imaging, including chest and abdominal X-rays.  

On history, patients might report acute chest or abdominal pain and retching.  On physical examination, you might find sign]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatitis_A_and_E:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v6rOnv0oRAW-Fj4iO7HoXDhsSTGmUHHO/_.png</video:thumbnail_loc><video:title><![CDATA[Hepatitis A and E: Clinical sciences]]></video:title><video:description><![CDATA[Hepatitis A and E viruses are RNA viruses typically transmitted by the fecal-oral route that infect hepatocytes, causing inflammation of the liver. Acute infection with both viruses usually causes a mild, self-limiting illness, although manifestations can range from asymptomatic infection to severe, life-threatening disease. Hepatitis E can also persist in the body and progress into a chronic infection. 

Now, if your patient presents with a chief concern suggesting Hepatitis A or E infection, perform an ABCDE assessment to determine if they are unstable or stable. If the patient is unstable, first stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen!

Now here’s a clinical pearl to keep in mind! In rare cases, acute Hepatitis A or E infection can lead to fulminant hepatic failure, causing an unstable presentation that requires acute management. Patients may present with manifestations of hepatic encephalopathy, like impaired mental status and asterixis; coagulopathy, with INR greater than or equal to 1.5; and elevated AST, ALT, and bilirubin. In addition to stabilization efforts, you should consult the surgical team, since these patients need rapid transfer to a liver transplant center!

Okay, now let’s go back to the ABCDE assessment and focus on stable patients. If your patient is stable, first obtain a focused history and physical examination, and order labs, including CMP, CBC, and INR. History typically reveals symptoms, such as malaise, loss of appetite, nausea, vomiting, and right upper quadrant pain. Your patient will also likely report a risk factor for fecal-oral transmission, such as exposure to contaminated food or water; travel to areas with poor hygiene and sanitation; and direct contact with an infected person. 

Next, the physical exam will ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_anemia_(destruction_and_sequestration):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/erjx4WBERPyG7o4iDsUiZLHjSTyBu5hk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to anemia (destruction and sequestration): Clinical sciences]]></video:title><video:description><![CDATA[Anemia is a condition characterized by a decrease in red blood cells, indicated by low levels of hemoglobin and hematocrit or red blood cell count. Anemia can be caused by red blood cell sequestration, destruction, or underproduction, as well as blood loss. 

Now, if you suspect anemia, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. 

If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, give IV fluids, and consider blood products, such as packed red blood cells. Usually, you want to transfuse patients with hemoglobin below 7 g/dL; unless the patient has cardiac history, in which case you’d transfuse if hemoglobin goes below 8; and lastly, if the anemia is causing severe symptoms like unresponsive tachycardia, or dyspnea at rest, you can transfuse regardless of the hemoglobin level! 

Additionally, provide supplemental oxygen if needed, and don’t forget to put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry.

Here’s a clinical pearl! A very important thing to consider in unstable patients with anemia is if they’re actively bleeding. Be sure to look for evidence of blood loss, such as visible trauma, hematochezia, melena, or hematuria. Additionally, you can search for the active bleed with a CT angiogram.

Now that we&amp;#39;re done with unstable patients, let’s look at the stable ones. 

Start with a focused history and physical examination, and order labs, including CBC with indices, and a reticulocyte count. 

The history could reveal fatigue, malaise, palpitations, and dyspnea; while the physical exam might show tachycardia and conjunctival pallor. However, these findings are non-specific, so you need to check labs. In biological females, normal hemoglobin lies between 12 and 16 g/dL, and normal hematocrit lies between 36 to 46%; while for biological males, normal hemoglobin lies between 13.5 and 1]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ankylosing_spondylitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rOnVNkN9SgmdKAFbshDR1z5oQfWHEgrV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ankylosing spondylitis: Clinical sciences]]></video:title><video:description><![CDATA[Ankylosing spondylitis, or AS for short, is a chronic inflammatory condition characterized by arthritis that primarily affects the spine. This chronic inflammation gradually erodes the lower spine, especially the sacroiliac joints, resulting in ankylosis or joint fusion, stiffness, and back pain. Ankylosing spondylitis is a type of spondyloarthropathy, which is a series of related conditions characterized by inflammation affecting the spine, entheses, and joints.

Now, if your patient presents with a chief concern suggesting ankylosing spondylitis, the first step is to perform a focused history and physical examination.

Your patients will usually be biological males less than 45 years old. They will typically report progressive low back pain and stiffness that has lasted three months or more. The pain and stiffness are worse in the morning and improve with activity, not rest. 

Next, family history might be positive for spondyloarthropathies, like ankylosing spondylitis, psoriatic arthritis, or reactive arthritis. 

The autoimmune process underlying ankylosing spondylitis can lead to several other extra-articular manifestations. These include anterior uveitis, which involves the inflammation of the front eye chamber with the iris and ciliary body. Other important manifestations include inflammatory bowel disease, pulmonary fibrosis, acute leukemia, cardiac conduction disturbances, and aortitis, which can potentially lead to aortic aneurysm and dissection. 

Additionally, the physical examination will reveal tenderness to palpation over the sacroiliac joints. Some individuals might also have a limited range of motion of the lumbar spine; as well as findings like tenderness consistent with enthesitis.

If your patient presents with these findings, you should suspect ankylosing spondylitis!

Next, order labs, including inflammatory markers, like ESR and CRP, as well as rheumatoid factor and antinuclear antibodies. Next, don’t forget to check whether or not y]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteomyelitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LzEdKvt-RkKcaYcF_onpD1QBQ2iZyDLj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteomyelitis: Clinical sciences]]></video:title><video:description><![CDATA[Osteomyelitis refers to an infection of the bone, which is typically caused by bacteria, such as Staphylococcus aureus. 

Osteomyelitis develops by one of three routes; direct inoculation of the bone, like from an open fracture; contiguous infection, like from an infected foot ulcer overlying the bone; or hematogenous spread, like from bacteremia due to endocarditis. Moreover, acute osteomyelitis develops within days to weeks of infection, whereas chronic osteomyelitis is characterized by long standing infection over months or even years. 

If your patient presents with chief concerns suggesting osteomyelitis, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and start IV fluids. Next, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Finally, if needed, provide supplemental oxygen, and don’t forget to start broad-spectrum antibiotics.

Okay, now let’s go back to the ABCDE assessment and take a look at stable individuals. In this case, first, obtain a focused history and physical examination. Next, order labs, including CBC, CRP, and ESR. 

Patients typically report fever, as well as pain, redness, and swelling at the site of the infection. Additionally, the physical exam usually reveals erythema, warmth, and purulent drainage, as well as tenderness to palpation over the affected bone area. Finally, labs usually show leukocytosis and elevated CRP and ESR. With these findings, you should suspect osteomyelitis.

Your next step is to order imaging, such as an X-ray or MRI. An MRI is the best imaging study to diagnose osteomyelitis, so make sure to order one if the X-ray results are normal but there&amp;#39;s high clinical suspicion. Additionally, a bone biopsy can help you reveal the histopathologic changes specific to osteomyelitis, and bone cultures, or deep tissue cu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spinal_infection_and_abscess:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/axiPxyMBSfev5L4Qzo_xaE2-SZ_OHSbS/_.png</video:thumbnail_loc><video:title><![CDATA[Spinal infection and abscess: Clinical sciences]]></video:title><video:description><![CDATA[A spinal infection and abscess occurs from an inoculation of bacteria, fungus, or parasites in the vertebrae, intervertebral disc, or adjacent paraspinal tissues. 

Spinal infections can progress into an epidural abscess, a walled-off collection of pus in the epidural space, which can compress and damage the spinal cord. If the infection is within the disc space, spondylodiscitis can occur, while infection of the vertebral bone itself is referred to as vertebral osteomyelitis. 

Although these infections are rare, they&amp;#39;re serious conditions that can lead to severe complications, such as paralysis or death, so timely diagnosis and appropriate treatments are very important.

Alright, when a patient presents with chief concern suggestive of spinal infection or abscess, your first step is to perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and initiate IV fluids for resuscitation. Then, continuously monitor vital signs including pulse oximetry, blood pressure, and heart rate. Once acute management has been initiated, your next step is to obtain a focused history and physical exam, in addition to labs including a CBC, CRP, ESR, and two sets of blood cultures. 

On history, your patient might report fevers, back pain, shooting nerve pain down the extremities, motor weakness, sensory changes, or bowel and bladder dysfunction. Additionally, history might reveal risk factors, such as diabetes, intravenous drug use, a chronic indwelling venous catheter, a concurrent infection elsewhere in the body such as tuberculosis, a recent spinal procedure, or immunocompromised state. 

Physical exam will reveal hypotension and tachycardia, both concerning signs of sepsis. On palpation, you’ll also notice spinal tenderness; and sometimes a focal area of fluctuance; as well as neurological deficits like motor weakness, radiculopathy, or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Tuberculosis_(extrapulmonary_and_latent):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J2ySAo0KTfiJqxmoBPtjqNuxRGCB2pic/_.jpg</video:thumbnail_loc><video:title><![CDATA[Tuberculosis (extrapulmonary and latent): Clinical sciences]]></video:title><video:description><![CDATA[Latent tuberculosis or TB refers to an asymptomatic condition where Mycobacterium tuberculosis is present in the body but held in check by the immune system. 

On the other hand, extrapulmonary TB occurs when Mycobacterium tuberculosis affects organs other than the lungs. Depending on the affected organs, extrapulmonary TB can be subdivided into tuberculous lymphadenitis, pleural TB, spinal TB, tuberculosis peritonitis, as well as tuberculosis meningitis, and genitourinary TB.

Okay, so if a patient presents with risk factors for tuberculosis, first perform a focused history and physical exam. History may reveal risk factors for TB exposure, like living in densely populated areas, like residents of a homeless shelter, correctional facility, or nursing home. Your patient might also be a healthcare worker with exposure to a patient with TB; a family member or close contact of a person with TB; or a traveler to a country with a high prevalence of TB. 

Additionally, the patient may have risk factors for developing TB disease, such as being immunocompromised due to HIV, malignancy, or treatment with immunosuppressive therapy. They could also have a history of latent TB. 

Okay, once you identify risk factors for tuberculosis, your next step is to assess for signs and symptoms of tuberculosis disease. These signs and symptoms typically include fever, night sweats, and chronic cough, which can be associated with purulent sputum or hemoptysis. They might also have unintentional weight loss, and general body weakness.

If these signs and symptoms are absent, suspect latent tuberculosis infection. Your next step here is to check an interferon-gamma release assay or IGRA, also known as QuantiFERON-TB Gold, or a tuberculin skin test.

Now, here’s a high-yield fact! The tuberculin skin test can produce false positives in individuals exposed to non-tuberculous mycobacteria, or those vaccinated with the BCG vaccine. For this reason, serum assays like the interferon-gamm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Esophagitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Yew5SwtDRTOHdFnHkslRMth2RDWg5_xZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Esophagitis: Clinical sciences]]></video:title><video:description><![CDATA[Esophagitis refers to the inflammation of the esophageal mucosa, which can be due to a wide range of underlying causes. This includes certain medications, pre-existing conditions like gastroesophageal reflux diseases, eosinophilic infiltration of the esophageal mucosa, infections, or even radiation exposure.

If a patient presents with a chief concern suggesting esophagitis, the first step is to obtain a focused history and physical examination. Your patient will likely report chest pain or upper abdominal discomfort, as well as symptoms like dysphagia and odynophagia. Additionally, some patients may report nausea, vomiting, and unintentional weight loss. The physical exam might reveal abnormalities in the oropharyngeal cavity, such as dental erosions, halitosis, oral thrush, or ulcers. If your patient presents with these signs and symptoms, you should suspect esophagitis and assess for an underlying cause. 

Let’s start with pill esophagitis! In this case, your patient will report that these symptoms started after taking certain oral medications, especially tetracyclines, NSAIDs, and bisphosphonates. Most of these patients usually report taking their medications right before sleep, or with little or no fluids. 

These findings are highly suggestive of pill esophagitis, so your next step is to discontinue the suspected medication. If your patient’s symptoms improve within 7 days, this confirms the diagnosis of pill esophagitis. 

In this case, management focuses on patient education, which includes instructing your patient to take medications sitting upright and with plenty of fluid. You should also encourage your patient to remain upright for at least 30 minutes after taking the medications.

Now, here’s a clinical pearl to keep in mind! Sometimes your patient’s symptoms will not resolve after discontinuing the medication. In this case, order esophagogastroduodenoscopy, or EGD for short, which might reveal a discrete erosion or ulceration of esophageal mu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Supraventricular_tachycardia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1MYbWMvcR52GZt5WYmUBkkSdQxSC6Fev/_.png</video:thumbnail_loc><video:title><![CDATA[Supraventricular tachycardia: Clinical sciences]]></video:title><video:description><![CDATA[Supraventricular tachycardia, or SVT, refers to tachyarrhythmia that originates from or above the atrioventricular node.  

An SVT can be physiologic due to physical exercise or emotional stress, or pathologic, which results from abnormal electrical activity outside the sinoatrial node.  

Based on 12-lead ECG findings, pathologic SVTs can be subdivided into  

SVTs with regular cardiac rhythm, like sinus tachycardia, focal atrial tachycardia, typical AVNRT, orthodromic AVRT, and atrial flutter; and  

SVTs with irregular cardiac rhythm, such as atrial fibrillation and multifocal atrial tachycardia.  

Now, if a patient presents with a chief concern suggesting SVT, perform an ABCDE assessment to determine if they’re unstable or stable.  

If unstable and have a pulse, follow the ACLS guidelines for Tachycardia with a Pulse. Stabilize their airway, breathing, and circulation, and obtain IV access. Put your patient on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry, as well as cardiac rhythm monitoring. Finally, if needed, provide supplemental oxygen!  

Next, assess for signs and symptoms of unstable tachycardia, which include signs of shock, hypotension, altered mental status, ischemic chest pain, and acute heart failure.  

If your patient has these features, diagnose unstable tachycardia and proceed with immediate synchronized cardioversion! 

Now, let&amp;#39;s go back and discuss stable patients. Start with a focused history and physical examination.  

Patients typically report palpitations, exercise intolerance, lightheadedness, and sometimes syncope.  

Additionally, if the physical exam reveals a heart rate of over 100 beats per minute, diagnose stable tachycardia.  

Next, obtain a 12-lead ECG and assess the heart rhythm. Start by evaluating the consistency of the R to R interval.  

If the R to R interval is the same from beat to beat, the rhythm is regular your next step is to assess the width or durati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_pneumoconiosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/E3HECbGoTuequaIFfReHCEU_StC56kJx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to pneumoconiosis: Clinical sciences]]></video:title><video:description><![CDATA[Pneumoconioses refer to a group of occupational lung diseases caused by prolonged exposure to inhaled mineral dust. Over time, inhaling these dust particles can lead to lung tissue inflammation, and eventually scarring and fibrosis. Common types of pneumoconiosis include asbestosis, silicosis, coal worker&amp;#39;s pneumoconiosis, berylliosis, and hard metal pneumoconiosis.

When a patient presents with a chief concern suggesting pneumoconiosis, the first step is to perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation, which means you may have to intubate the patient. Next, provide supplemental oxygen, and obtain IV access. Finally, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry.

Now, let’s go back to the ABCDE assessment and take a look at the stable patients. In this case, perform a focused history and physical examination. History typically reveals progressive dyspnea on exertion and a chronic dry cough. There’s also prior exposure to inhaled inorganic material, such as asbestos, silica, coal dust, beryllium, or hard metals. 

Here’s a clinical pearl to keep in mind! In most cases of pneumoconiosis, there is a long latent period between exposure and the onset of symptoms. For example, patients with pneumoconiosis due to asbestos may often present 20 to 40 years after exposure. 

Then, the physical exam will often reveal diffuse inspiratory crackles or wheezing. Patients with advanced disease may even have finger clubbing, which is the swelling of fingertips due to chronic hypoxia. With these findings, you should consider pneumoconiosis! 

Next, order pulmonary function testing and a chest X-ray. If pulmonary function tests reveal a normal or obstructive pattern, or  if chest X-ray reveals lung hyperinflation and flattening of the diaphragm, you should consider alternative diagnoses, such as chronic obs]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Human_immunodeficiency_virus_(HIV)_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EVl8MvD2T2eNjMbScQjGhDmxS0e3Icsy/_.png</video:thumbnail_loc><video:title><![CDATA[Human immunodeficiency virus (HIV) infection: Clinical sciences]]></video:title><video:description><![CDATA[Human immunodeficiency virus, or HIV for short, is a single-stranded RNA retrovirus that targets the body’s immune system. HIV is transmitted by contact with infected body fluids, such as blood, semen, and vaginal fluids. There are two types of HIV: HIV-1 and HIV-2; but generally, when we talk about HIV infection, we usually mean HIV-1 because it&amp;#39;s the most widespread.  

Now, HIV causes immunosuppression by targeting and infecting CD4 T cells, which are a type of white blood cell that helps coordinate the immune response to infection. The acute phase of HIV infection is called acute retroviral syndrome, after which the individual can be asymptomatic for as long as a couple of years. However, without appropriate medical management, HIV infection can progress to acquired immunodeficiency syndrome, or AIDS.  

Now, if your patient presents with chief concerns suggesting an HIV infection, first perform a focused history and physical examination.  These patients typically have nonspecific symptoms, such as fever, fatigue, night sweats and unintentional weight loss. Additionally, your patient might report myalgias, arthralgias, or gastrointestinal manifestations, like nausea, vomiting, and diarrhea. Your patient could also report a sore throat.  

Other historical findings may include high-risk sexual behavior such as unprotected sexual activities or multiple sexual partners; intravenous substance use; or occupational risk factors such as accidental needlestick injury.  

Physical examination might reveal a rash, lymphadenopathy, or signs of sexually transmitted infections, such as purulent urethral discharge or painful fluid-filled blisters around the genitals. You might also find needle marks on the skin overlying veins in individuals who have used intravenous drugs. Finally, distinctive but rare manifestations of HIV infection include mucocutaneous ulcers, which typically affect oral and genital regions. 

Here’s a clinical pearl! In some cases, pat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_myopathies:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6y5BOlr0T7OFIUittu61fEvcTEW5Wb3E/_.png</video:thumbnail_loc><video:title><![CDATA[Inflammatory myopathies: Clinical sciences]]></video:title><video:description><![CDATA[Inflammatory myopathies are a group of autoimmune conditions associated with muscle inflammation and subsequent progressive muscle wasting and weakness. These conditions occur when immune cells like lymphocytes and macrophages infiltrate skeletal muscle fibers, causing widespread inflammation. Inflammatory myopathies include five conditions: dermatomyositis, antisynthetase syndrome, immune-mediated necrotizing myositis, inclusion body myositis, and polymyositis. 

Now, if your patient presents with chief concerns suggesting inflammatory myopathy, your first step is to perform a focused history and physical. Patients usually report symptoms of proximal muscle weakness, commonly affecting the shoulder and pelvic girdle muscles. So, they might find it difficult to do activities like combing their hair, standing up from a sitting position, or climbing stairs. To remember this, think hair, chairs, and stairs! They might also report difficulty swallowing or a skin rash. Additionally, some individuals have a positive personal or family history of autoimmune or inflammatory diseases, like lupus, scleroderma, or Sjogren syndrome. 

Finally, the physical examination can reveal symmetric proximal muscle weakness, with or without skin abnormalities like a rash.

At this point, you should suspect inflammatory myopathy, so be sure to order serum creatine kinase and electromyography, or EMG. Now, If your patient’s creatine kinase levels are normal and EMG reveals normal findings or evidence of neuropathy, consider an alternative diagnosis, like motor neuron disease, peripheral polyneuropathy, or myasthenia gravis. On the other hand, if labs reveal elevated creatine kinase, usually ten times the upper limit of normal or more, and the EMG shows a myopathic process, such as fibrillations and early recruitment of muscle fibers, diagnose inflammatory myopathy!

Here’s a clinical pearl to keep in mind! Non-inflammatory conditions, such as electrolyte imbalances, hypothyro]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Temporal_arteritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l64o5YsPQ9_M3uc3yLJJd31jRgKtAKm3/_.png</video:thumbnail_loc><video:title><![CDATA[Temporal arteritis: Clinical sciences]]></video:title><video:description><![CDATA[Temporal arteritis, also known as giant cell arteritis, is an inflammatory vasculitis of medium and large arteries. In temporal arteritis, there’s inflammation and thickening of the vessel wall, which eventually can result in ischemia and complications, such as vision loss. Now, as the same suggests, the temporal artery is the most common vessel involved. But don’t let the name fool you! Other intracranial and extracranial vessels can be affected as well, especially the vertebrobasilar arterial system. More remote sites of vascular involvement include the aorta and its proximal branches, like the carotid, subclavian, axillary, and brachial arteries. 

Okay, if a patient presents with a chief concern suggesting temporal arteritis, first perform a focused history and physical exam, and order labs, including an erythrocyte sedimentation rate, or ESR, C-reactive protein or CRP, and complete blood cell count, or CBC.

Your patient will generally be older than 50, and likely report a new onset of localized headache, typically described as unilateral pain in the temporal region that worsens over time. These symptoms are often associated with scalp pain; as well as systemic symptoms like fatigue, malaise, fever, and unintentional weight loss. In more severe cases, you might notice symptoms suggestive of ischemia, including sudden vision changes ranging from diplopia to complete vision loss. There might also be pain with chewing, known as jaw claudication. 

Here’s a high-yield fact! Temporal arteritis is closely associated with polymyalgia rheumatica, another inflammatory disorder that primarily affects the shoulders and hips. These patients typically report morning pain and stiffness in the muscles of the neck, shoulders, and hips. So, if you have clinical suspicion of polymyalgia rheumatica, be sure to evaluate your patient for temporal arteritis too!

Moving on physical exam findings, these may reveal an abnormal temporal artery exam, such as tenderness to palp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_fever:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3RkZIjYPSuKV7L4mIruX0W1-T7W9bbqH/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to a fever: Clinical sciences]]></video:title><video:description><![CDATA[Fever is generally defined as a temperature of 100.4 degrees Fahrenheit or 38 Celsius, or higher. It occurs when chemical  triggers, called pyrogens, stimulate the thermoregulatory center in the hypothalamus, which in turn elevates the body temperature. Pyrogens can be either endogenous, like cytokines from various inflammatory processes or tumors; or exogenous, like antigens from various pathogens. Now, some important causes of fever to keep in mind include infection, venous thromboembolism, malignancy, autoimmune disease, and certain medications, as well as fever of unknown origin. 

Now, if your patient presents with a fever, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and start fluid resuscitation as well as broad-spectrum intravenous antibiotics. Place your patient on continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Finally, if needed, provide supplemental oxygen!

Okay, let’s jump right back to the ABCDE assessment and take a look at stable patients. In this case, start by obtaining a focused history and physical examination. A body temperature of 100.4 degrees Fahrenheit or 38 degrees Celsius or higher confirms a fever, which could be accompanied by tachycardia.  Once you confirm the presence of fever, your next step is to determine the underlying cause by taking a deeper look at history and physical examination for additional clues. 

Okay, the first cause of fever to consider is infection! Your patient’s history may include close contact with a sick individual, recent travel, IV substance use, or high-risk sexual activity. They may report symptoms like cough, malaise, chills, muscle or joint pain, painful urination, or decreased appetite, as well as additional symptoms based on the organ system involved. 

Additionally, physical exam findings might reveal tachycar]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Folliculitis,_furuncles,_and_carbuncles:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vETAjXLXQJyceMyhv_XyHYveQw2wmA1v/_.png</video:thumbnail_loc><video:title><![CDATA[Folliculitis, furuncles, and carbuncles: Clinical sciences]]></video:title><video:description><![CDATA[Folliculitis is a common skin condition where a hair follicle becomes infected and forms a papule or pustule over the hair-bearing skin. The infection is most commonly bacterial, but in rare cases, it can be fungal, viral, or parasitic. As the infection brews, it can form a furuncle which is an abscess involving the hair follicle and its surrounding tissue. When there are multiple furuncles, they can grow and connect subcutaneously forming a carbuncle. The diagnosis of folliculitis, furuncle, or carbuncle is clinical, so performing a thorough history and physical examination is very important. 

When a patient presents with chief concern suggesting folliculitis, a furuncle, or a carbuncle, the first step is to obtain a focused history and physical in addition to labs such as a CBC. Patients typically report skin redness, pain, pruritus over a skin bump, and sometimes even fever. They might also report recent or frequent waxing or hair removal over the affected area, or that they had a pimple they tried to pop. Finally, patients might have a history of uncontrolled diabetes. 

When it comes to the physical exam, it typically reveals erythema, swelling, tenderness, and possibly induration surrounding a folliculocentric papule, pustule, or nodule within the hair-bearing skin. You might also see a focal area of fluctuance with or without purulent drainage. Lastly, CBC is often normal or may show mild leukocytosis. If your patient presents with these clinical findings, suspect folliculitis, furuncle, or carbuncle.

Alright, let’s start with folliculitis, which is usually limited to the superficial dermis. On further examination, you can expect to find superficially inflamed papule around a hair follicle without any areas of fluctuance. This is very characteristic of folliculitis, so that’s your diagnosis. Once you have made the diagnosis, your next step is to treat with topical antibiotics and advise cessation of hair removal. Then, assess the response between ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mallory-Weiss_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O4MIimsnRyKWxCrjvwmaKUU1Si_NgMtw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mallory-Weiss syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Mallory-Weiss syndrome, also known as a Mallory-Weiss tear, is a superficial longitudinal mucosal tear at or near the gastroesophageal junction, often presenting as acute upper gastrointestinal bleeding. These mucosal tears occur after repetitive and forceful retching and vomiting, most frequently from alcohol use disorder. The tear can cause severe bleeding if there are other comorbidities, such as portal hypertension or esophageal varices. 

Alright, when assessing a patient with a chief concern suggestive of Mallory-Weiss syndrome, your first step is to perform an ABCDE assessment to determine if they are stable or unstable. If the patient is unstable, stabilize the airway, breathing, and circulation. First, check the airway for any compromise. You might need to intubate if the patient is at risk for aspiration. 

Next, obtain IV access and initiate IV fluids for resuscitation. Consider transfusion of blood products for patients with significant blood loss. Additionally, insert a nasogastric tube and keep the patient NPO. Then, continuously monitor vital signs including pulse oximetry, blood pressure, and heart rate. Finally, be sure to admit these patients to the ICU for close monitoring, as they might deteriorate further.

Once you’ve initiated acute management, your next step is to obtain a focused history and physical exam, as well as labs including CBC and CMP. Patients often report a history of hematemesis, sometimes with epigastric or back pain, and non-bloody emesis and retching. They might have risk factors, such as alcohol use disorder or ingestion of acetylsalicylic acid. 

On physical exam, you may find evidence of massive hematemesis, such as a large pool of bloody vomitus, in addition to hypotension and tachycardia. Finally, CBC might show decreased hemoglobin, while CMP might show electrolyte abnormalities suggestive of acute blood loss anemia and dehydration. If this is the clinical presentation, you should suspect an acute upper GI blee]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Calcium_pyrophosphate_deposition_disease_(pseudogout):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uNeqQtrUS4S9l_kLX_ZSZo6sS8SL4bIg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Calcium pyrophosphate deposition disease (pseudogout): Clinical sciences]]></video:title><video:description><![CDATA[Calcium pyrophosphate deposition or CPPD disease, also known as pseudogout, is a type of arthritis associated with the precipitation of calcium pyrophosphate crystals in the synovial and periarticular tissues. CPPD disease can be asymptomatic, so in some individuals, it can be diagnosed incidentally with X-ray imaging. However, some patients can develop an acute or chronic type of CPPD disease.

Now, if your patient presents with a chief concern suggesting CPPD disease, you should first perform a focused history and physical examination. Next, order labs, including CBC, inflammatory markers, such as erythrocyte sedimentation rate and C-reactive protein, and serum urate.

Now, first, let’s focus on acute CPPD disease! Your patient will usually be over 60 and report a rapid onset of monoarticular or oligoarticular joint pain, redness, and swelling. These changes most commonly involve the knee, wrist, and metacarpophalangeal joints. 

Additionally, history might reveal systemic symptoms, like fever and fatigue, and in some cases, conditions, such as hypomagnesemia, hyperparathyroidism, and hemochromatosis. 

Now, here’s a clinical pearl to keep in mind! Hypomagnesemia, hyperparathyroidism, and hemochromatosis are conditions commonly associated with CPPD disease. Other important risk factors that you should keep in mind include trauma or surgery to the joint, as well as bisphosphonate use.

Additionally, the physical exam typically reveals signs of joint inflammation, such as joint redness, warmth, swelling, and tenderness to palpation. You might also notice a limited range of motion. Finally, lab results may reveal normal CBC or leukocytosis, elevated inflammatory markers, and in some cases, normal serum urate. 

With these findings, you should suspect acute inflammatory arthritis. Your next step is to perform synovial fluid aspiration of the affected joint and send the fluid for microscopic analysis, gram stain, and culture.

Now, here’s a high-yield fa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psoriatic_arthritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MWjMI-1PT-ex49Vtg-3wBLvjTEiRcmDe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psoriatic arthritis: Clinical sciences]]></video:title><video:description><![CDATA[Psoriatic arthritis, or PsA for short, is a type of autoimmune arthritis that’s associated with a chronic inflammatory skin disorder known as psoriasis. In psoriatic arthritis, inflammation leads to joint erosion and destruction, causing joint pain, swelling, and stiffness. 

The assessment of patients with psoriatic arthritis involves Classification criteria for Psoriatic Arthritis, or CASPAR, which is a validated clinical tool used for diagnosis. 

Okay, let’s look at a patient presenting with a chief concern suggesting psoriatic arthritis. The first step is to perform a focused history and physical examination. You should also order labs including rheumatoid factor, or RF, antinuclear antibodies, or ANA, C-reactive protein, or CRP, and erythrocyte sedimentation rate, or ESR for short. Additionally, you should obtain X-rays of any affected joints. 

Your patient will typically report joint pain, stiffness, and swelling most commonly in the fingers and toes. Psoriatic arthritis often targets the small joints of fingers and toes, but it can affect any joint. So don’t forget to ask about pain, stiffness, and swelling in larger peripheral joints like knees and elbows, and even in axial joints like spinal intervertebral and sacroiliac joints. 

They may also have a personal or family history of psoriatic skin lesions. These present with dry, thick, and silvery-white scales, as well as a positive Auspitz&amp;#39;s sign, which is the appearance of punctate bleeding spots when psoriasis scales are scraped off.

Moving on, physical exam findings typically reveal joint tenderness and effusion, as well as dactylitis, sometimes described as sausage fingers. 

You might also notice scaly erythematous plaques on the scalp, extensor surfaces of the limbs, and perineum. Other findings may include pitting of the nails. 

Lab results will reveal a negative rheumatoid factor and ANA, and may show elevated CRP and ESR. Additionally, you will see positive HLA-B27 in around ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Reactive_arthritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mljsqIcLTqmZL5wccceZRUPmTpyaiDJ7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Reactive arthritis: Clinical sciences]]></video:title><video:description><![CDATA[Reactive arthritis, formally known as Reiter syndrome, belongs to a group of conditions called seronegative spondyloarthropathies. Seronegative means that the autoantibody called rheumatoid factor or RF is absent. Reactive arthritis is associated with autoimmune inflammation of joints that usually develops after genitourinary infections, most commonly chlamydia and gonorrhea; or intestinal infections, usually salmonella or shigella. Keep in mind that in most cases, this inciting infection is asymptomatic! 

Okay, if your patient presents with chief concerns suggesting reactive arthritis, first, you should perform a focused history and physical. 

Reactive arthritis doesn&amp;#39;t just affect the joints, so don’t let the name fool you! Your patient will typically report pain in the large joints of the lower extremities, including knees, ankles, and feet. Keep in mind that the pain is usually asymmetric! Additionally, they will report systemic symptoms like fatigue, malaise, and low-grade fever; with possible ocular symptoms, such as burning of the eyes. 

Additionally, this condition can affect almost any genitourinary structure, including the urethra, bladder, cervix, and prostate. They might also report recent genitourinary symptoms, like dysuria and urethral discharge; or gastrointestinal symptoms, such as diarrhea. Typically, symptoms of reactive arthritis occur several days to weeks after the inciting infection. 

Additionally, the physical examination may reveal a tender lower extremity joint with effusion; and tenderness in the sacroiliac joint. You may also observe several extra-articular manifestations, such as enthesitis, or inflammation of the attachment sites of tendons to bones; as well as dactylitis, also known as sausage fingers. 

Look out for common dermatologic findings, like nail pitting and onycholysis, where the nail separates from the nail bed. You may also notice keratoderma blennorrhagicum, which causes psoriatic nodules on the pal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Basal_cell_carcinoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uTomEXq1RUeXZIYnaUqC7JG5QYm4hF45/_.jpg</video:thumbnail_loc><video:title><![CDATA[Basal cell carcinoma: Clinical sciences]]></video:title><video:description><![CDATA[Basal cell carcinoma, or BCC for short, is the most common type of skin cancer. It develops on parts of the skin exposed to high levels of sunlight or ultraviolet radiation, such as the head, neck and the upper extremities. 

BCC arises from basal cells, which are stem cells responsible for producing new skin cells. They are located in the deepest layer of the epidermis. 

Most BCCs are slow growing, so they can go unnoticed for a long period of time, and they rarely metastasize. Treatment is based on risk of recurrence rate, and can be surgical or medical. 

Alright, when a patient presents with a chief concern suggesting a BCC, the first step is to obtain a focused history and physical. Typically, patients notice a skin lesion that has been changing gradually in size or color, or one that won’t heal. Additionally, they might have risk factors like fair skin complexion and prolonged sun exposure.  Patients may have a  family history of cancers, or personal history of genetic disorders or immunosuppression. 

Here’s a high yield fact! Xeroderma Pigmentosum is a rare autosomal recessive genetic condition characterized by impaired DNA repair mechanisms. When the UV rays from the sunlight cause damage to the skin cell DNA, the body is not able to repair the damage. As a result, these patients are at increased risk of developing skin cancers like BCC.

Now, on physical exam, you can expect to see a skin lesion that looks like a small raised bump or non-healing sore. The nodule can be translucent, shiny, waxy, or “pearly” in appearance, or it can appear as an ulcer with central depression and raised, rolled or elevated edges. 

Occasionally, you might see surrounding telangiectasia, which is evidence of abnormal angiogenesis associated with skin malignancies.

In the late stages, BCCs can become quite large, with a fungating appearance indicating local invasion. These findings should lead you to suspect BCC.  

The best way to confirm your diagnosis is to biops]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_syncope:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cCA8-Xf6SZSs9RGhVujmiGG6QeO5Yn1p/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to syncope: Clinical sciences]]></video:title><video:description><![CDATA[Syncope is a sudden, transient loss of consciousness triggered by a temporary decrease in cerebral perfusion. Based on the underlying cause, syncope can be categorized into several types. These include cardiogenic syncope caused by heart-related issues, reflex-mediated syncope triggered by various stimuli like neck pressure, syncope due to orthostatic hypotension, and neurologic syncope, which is associated with neurological conditions.

Now, if your patient presents with a chief concern suggesting syncope, perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and consider giving IV fluids. Next, put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen.

Okay, now that we’re done with unstable patients, let’s go back to the ABCDE assessment and take a look at stable ones. In this case, obtain a focused history and physical examination, as well as an ECG. Your patient, and ideally any witnesses present, will likely report a brief loss of consciousness and postural tone, typically lasting less than a minute. You might also be able to uncover a clear trigger, like a sudden change in position, dehydration, exertion, strong emotional reaction, defecation, urination, or even coughing. Additionally, your patient might report prodromal symptoms, typically lightheadedness, feeling warm or clammy, nausea, and visual changes. During the physical exam, you might notice myoclonic jerks, which are non-rhythmic muscle twitches that may happen during a witnessed syncopal event, lasting less than 15 seconds. With these findings, you can diagnose syncope!

Now, here’s a clinical pearl to keep in mind! There are other causes of transient loss of consciousness that can mimic syncope. One of these is hypoglycemia. So, remember to check a finger]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hyperparathyroidism:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TyTc9kXCSqyFh4hGmgmBp-MTQoqfOjVS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hyperparathyroidism: Clinical sciences]]></video:title><video:description><![CDATA[Hyperparathyroidism is when excess parathyroid hormone, or PTH for short, is produced. PTH is produced by the parathyroid glands, which lie behind the thyroid, and it controls calcium balance in the body. 

Now, primary hyperparathyroidism occurs  when the parathyroid glands autonomously make too much PTH. 

In contrast, secondary hyperparathyroidism is caused by an appropriate rise in PTH levels, as the parathyroid glands attempt to correct hypocalcemia caused by other conditions, such as vitamin D deficiency, or chronic kidney disease. 

Finally, there’s tertiary hyperparathyroidism, which is usually caused by long-standing secondary hyperparathyroidism that eventually results in parathyroid hyperplasia and unregulated, autonomous PTH overproduction.

Now, if your patient presents with a chief concern suggesting hyperparathyroidism, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. 

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry. Finally, if needed, provide supplemental oxygen.

Here’s a high-yield fact to keep in mind! Patients with hyperparathyroidism can develop severe or rapidly progressing hypercalcemia, which can cause lethargy, stupor, or even coma. Additionally, an ECG may reveal bradycardia, atrioventricular block, or a shortened QT interval. To normalize serum calcium, you should start intravenous hydration; and diuretics, like furosemide; or bisphosphonates, like zoledronic acid can also be used.

Now, let’s go back to the ABCDE assessment and discuss the stable patients. First, obtain a focused history and physical examination. Many patients with hyperparathyroidism are asymptomatic, but some may report personality and mood changes, trouble concentrating, and even altered mental status. They might also experience g]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_pancreatic_masses:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sDNveTSkS_iEldGYth65J4mERimKYgiX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to pancreatic masses: Clinical sciences]]></video:title><video:description><![CDATA[Pancreatic masses are either cystic or solid lesions, and can be benign or malignant. Often, these masses are found incidentally during abdominal imaging performed for an unrelated reason. 

Cystic pancreatic lesions are more commonly found, and fall into three categories: non-neoplastic pancreatic cysts, pancreatic cystic neoplasms, and inflammatory fluid collections. Solid masses are less common and include tumors of the exocrine pancreas, such as adenocarcinoma and benign adenomas; as well as pancreatic neuroendocrine tumors.

When a patient presents with a chief complaint suggesting a pancreatic mass, your first step is to obtain a focused history and physical examination. Patients often report vague symptoms like abdominal pain that radiates to the back. In some cases, they might have a history of chronic pancreatitis. The physical exam is typically unremarkable, but depending on the size and location of the mass, you might find tenderness in the upper abdomen. 

If you suspect a pancreatic mass, your next step is to order a CT scan of the abdomen and pelvis. A CT scan can help you determine if the mass is cystic, solid, or indistinct. Understanding these key features will help you narrow down your differential further.

Let&amp;#39;s start our discussion with pancreatic cysts. For these patients, your next step is to order labs like liver function tests and a basic metabolic panel, as well as a more detailed CT scan of the pancreas, known as the triphasic pancreatic protocol. You may also consider an MRI. 

Alright, first up we have non-neoplastic pancreatic cysts or NNPCs for short. Most patients are asymptomatic. In some cases, history might reveal associated risk factors, such as cystic fibrosis or polycystic kidney disease. The physical exam is usually unremarkable with a soft, non-tender abdomen; and labs are often normal, although LFTs might be elevated in some cases. 

On CT scan with pancreatic protocol, you can expect to find a single,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_non-healing_wounds:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vloOMjjMSFCK5BMPWKz7GH28QGupqEsD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to non-healing wounds: Clinical sciences]]></video:title><video:description><![CDATA[A non-healing wound refers to a chronic skin and soft tissue wound that fails to heal within the normal healing time frame, which is 4 to 6 weeks. In the majority of cases, there is an underlying condition or an infection that prevents normal healing. These factors often lead to the loss of normal skin and soft tissue anatomy and function. 

In general, non-healing wounds are divided into two main categories: ulcers, which include pressure, neuropathic, venous, and arterial ones; and other non-ulcer related chronic wounds like postoperative wound complications, neoplastic or radiation-induced skin lesions, and infectious or inflammatory wounds. 

Alright, when a patient presents with a non-healing wound, your first step is to obtain a focused history and physical exam. On history, patients typically have underlying chronic medical conditions such as diabetes or peripheral arterial disease known to prevent proper wound healing by causing inadequate nutritional status or poor blood supply. They might report first noticing a small wound that progressed to a larger or deeper one over the course of weeks to months. In this case, consider ulcers.

Okay, let’s start with pressure ulcers. These ulcers form when prolonged pressure decreases the blood flow to an area of skin and its underlying soft tissue. Typically, patients have a history of immobility, like being bed- or wheelchair-bound, and poor nutrition. Additionally, they might have multiple comorbidities such as stroke or paralysis. Patients who are hospitalized or reside in nursing homes are at a greater risk of developing pressure ulcers. 

On exam, you might see partial or complete skin loss with areas of dark ischemic discoloration or necrosis over bony prominences like the sacrum. Sometimes you might even see the underlying fat, muscle, or bone exposed. With these findings, you can diagnose pressure ulcers. 

Here’s a clinical pearl! Although imaging is not needed to make a diagnosis, an MRI is of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_limb_ischemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g5EqNHiWQRapN1KXc3WBdBFxRPGQ_cHi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute limb ischemia: Clinical sciences]]></video:title><video:description><![CDATA[Limb ischemia is the acute reduction of blood flow to an extremity, resulting in decreased oxygen delivery. The acute reduction of blood flow most commonly occurs from a thromboembolism, which is when a clot travels from a different area of the body and occludes the blood flow in the limb. It can also occur when a diseased vessel is narrowed by atherosclerotic plaque, resulting in slower blood flow, stasis, and clot development. Regardless of the cause, ischemia can quickly lead to tissue necrosis if it’s left untreated, and can become a medical emergency, as skeletal muscle can only tolerate ischemia for 4 to 6 hours before dying. Depending on the patency of the blood flow, ischemia can range from mild to severe.  

Now, limb ischemia is categorized by the Rutherford classification system. A Rutherford class I limb is viable and not immediately threatened, whereas a Rutherford class IIa limb is marginally threatened but salvageable if promptly treated. A Rutherford class IIb limb is immediately threatened but salvageable with immediate revascularization. Finally, a Rutherford class III limb is where major tissue loss or permanent nerve damage is inevitable, and the limb is irreversibly damaged.  

Alright, when a patient presents with a chief concern suggesting limb ischemia, your first step is to perform an ABCDE assessment to determine if the patient is unstable or stable.  

If the patient is unstable, stabilize their airway, breathing and circulation. Obtain two large bore intravenous lines and start IV fluid resuscitation. Continuously monitor their vital signs including blood pressure and heart rate; and, if needed, don’t forget to provide supplemental oxygen. 

Next, assess for red flag symptoms like profound sensory loss and paralysis, which indicate severe ischemic injury of the affected limb, along with sensory and motor nerve damage. Typically, most patients experience a progression of symptoms starting with worsening pain followed by pulseless]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_perianal_problems:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rx8t7DJ2Qgae82eXNuVYukDdRxeGUYw_/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to perianal problems: Clinical sciences]]></video:title><video:description><![CDATA[Perianal diseases are conditions that affect the anus and the surrounding skin. They are common and usually benign, but sometimes they might be malignant. For the majority of perianal diseases, there are 4 main clinical features that can help you narrow down your differential diagnoses. They include pain, palpable mass, bleeding, and drainage. For example, painless or minimally painful conditions include fistulas, carcinomas, warts, prolapses, and hemorrhoids. On the other hand, painful perianal diseases include thrombosed hemorrhoids, abscesses, anal fissures, and pruritus ani.

When assessing a patient with a chief concern suggesting perianal disease, your first step is to obtain a focused history and physical examination, including a digital rectal exam. Start by evaluating for perianal pain. If the patient reports no pain, your next step is to assess for a mass. 
If there is no palpable mass too, you should be thinking about a fistula. 

Now, even though the patient might deny pain at the time of evaluation, they might report a history of mild cyclical discomfort and swelling around the perianal region in addition to noticing some foul-smelling or bloody drainage. Sometimes they might have risk factors like Crohn disease or previous episodes of a perianal abscess. 

On physical exam, you’ll usually see an external skin opening that looks like a large pore. Additionally, there might be erythema and inflammation around the opening. Keep in mind that some patients might have multiple external openings, especially those with Crohn disease. On palpation, you might even feel a superficial cord-like structure under the skin. If you see these findings, consider perianal fistula. 
Next, perform an anoscopy to look for an internal opening of the fistula tract. If anoscopy is not able to provide adequate visualization or the patient is unable to tolerate the exam, you can perform an exam under anesthesia, or EUA. Once you see the internal opening of the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_skin_and_soft_tissue_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HgjpZ_i2QKyzQqdY_t0ppOmkTe_FxaVr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to skin and soft tissue injury: Clinical sciences]]></video:title><video:description><![CDATA[Skin and soft tissue injury refers to damage to the skin and its underlying structures such as fat, fascia, muscles, tendons, and ligaments. The majority of these injuries are caused by blunt or penetrating trauma, but they can also result from burns or infections. 

Generally, skin and soft tissue injuries are categorized as either open or closed, ranging from superficial minor injuries to severe polytrauma involving the bone. In severe cases, these injuries can even be limb or life-threatening, so timely diagnosis is very important.

Alright, your first step in evaluating a patient presenting with skin and soft tissue injury is to perform the ABCDE assessment to determine if they are stable or unstable. If the patient is unstable, start acute management by stabilizing the airway, breathing, and circulation. Next, establish IV access and start IV fluid resuscitation. Additionally, continuously monitor the patient&amp;#39;s vital signs. 

Here’s an important clinical pearl to keep in mind! Make sure to avoid the injured extremity when obtaining IV access and placing a blood pressure cuff or arterial line.

Now that these important steps are done, you can move on to obtaining a focused history and physical exam as well as labs including CBC, CMP, arterial blood gas, and a urinalysis. Your initial assessment should be focused on identifying any life-threatening injuries and signs of impending hemodynamic collapse. Unstable patients typically present with a history of severe traumatic injury, burns or rapidly progressing infection. 

On the physical exam, you might find altered mental status, tachycardia, and hypotension which are all signs of instability. Additionally, you might see obvious skin or soft tissue injury with surrounding edema, erythema, and even an eschar. 

For open injuries, subcutaneous fat, muscle, or bone might be exposed. On the flip side, with closed injuries like crush injuries, you can expect to see tense skin and soft tissue wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_blunt_chest_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-bUTkWT3RtigEl_1cImNgtdeQJ2bpFSL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to blunt chest injury: Clinical sciences]]></video:title><video:description><![CDATA[Blunt chest injury commonly occurs from motor vehicle accidents, falls, and assault, and can range in severity from mild to life-threatening. Most of the blunt chest injuries are mild and can be managed non-surgically. However, severe injuries can become rapidly fatal, so timely diagnosis and immediate surgical intervention is key. These life-threatening injuries include tension pneumothorax, massive hemothorax, and aortic rupture, as well as cardiac tamponade and thoracic vertebral fracture. Other urgent but less serious injuries include rib fractures, flail chest, sternal fracture, thoracic vertebral fractures, and tracheobronchial and esophageal injuries, in addition to parenchymal lung injuries, hemopneumothorax, blunt aortic injury, and diaphragmatic injury. 

Alright, your first step in evaluating a patient presenting with blunt chest injury is to perform the primary survey using the ABCDE assessment. First, secure the Airway while stabilizing the cervical spine. Have a low threshold for endotracheal intubation or a surgical airway, especially if the patient cannot protect or maintain their own airway. Once you’ve secured the airway, ensure adequate Breathing or ventilation by providing supplemental oxygen.  

Next, assess Circulation and obtain 2 large bore IVs or IO access while continuously monitoring vitals, such as heart rate and blood pressure. Then, assess Disability and neurologic status by calculating their GCS and examining the pupils and spine, as well as for sensory and motor deficits. Make sure to ensure spine immobilization until spinal injury has been ruled out. Finally, Expose the patient and remove all clothing to assess for any other associated injuries, and cover the patient with warm blankets to prevent hypothermia. 

Once you’ve determined your patient is unstable, your next step is to quickly perform the secondary survey, which is a head-to-toe exam, and adjunctive tests like an e-FAST exam to look for any life-threatening injur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_penetrating_chest_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/w5tlZy0bSN2b9LMqL2lHSpxQRqesAHLG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to penetrating chest injury: Clinical sciences]]></video:title><video:description><![CDATA[Penetrating chest injury is a dangerous type of trauma that commonly occurs from gunshot wounds, stabbings, and impalement. For any patient presenting with penetrating injury to the chest, you must have a high clinical suspicion for life-threatening injuries to heart, lungs, and the great vessels. Timely diagnosis and immediate intervention is key to reducing morbidity and mortality. In clinical practice, the majority of penetrating chest injuries can be managed nonoperatively, but if left untreated, even a minor wound can become fatal in a short span of time.

Alright, your first step in evaluating a patient presenting with a penetrating chest injury is to perform a primary survey by assessing their ABCDE, which will help you determine if the patient is stable or unstable. Start by evaluating and securing the airway. Stabilize the C-spine with a C-collar to immobilize the spine, keeping in mind that the spinal cord could be injured from the penetrating trauma. If needed, intubate or create a surgical airway like a cricothyroidotomy. Then, check for breathing, ensure adequate ventilation, provide supplemental oxygen, and auscultate the lungs for bilateral breath sounds. 

Next, obtain two large bore IVs or an intraosseous line and start fluid resuscitation including transfusion of blood products if massive hemorrhage is suspected. At the same time, continuously monitoring vital signs including heart rate, blood pressure, and oxygen saturation. Then, assess disability, or neurologic status, by calculating the patient’s GCS, and perform a pupillary exam and a neurologic exam. Lastly, expose the patient by removing all clothing and bandages to ensure no injuries are missed. After examining the patient, place a warm blanket over them to avoid hypothermia.

Okay, let’s first discuss unstable patients. Once you have completed the primary survey and initiated the acute management, your next step is to perform the secondary survey, which is a head to toe physical ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_traumatic_brain_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZRRWJZilSgydcEwJy0TwQYg1QuaUnAtB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to traumatic brain injury: Clinical sciences]]></video:title><video:description><![CDATA[Traumatic brain injury, or TBI for short, is caused by a penetrating or blunt force to the head resulting in temporary or permanent impairment of brain function. Common mechanisms of injury include direct head trauma from falls or being struck by an object, acceleration-deceleration or whiplash from motor vehicle crashes, or foreign body penetration like gunshot wounds. 

The degree of injury ranges from mild to severe as classified by the Glasgow coma scale, or GCS. This scale measures eye-opening, verbal, and motor responses to stimuli on a scale from 3 to 15, with 3 representing a comatose state, and 15 being normal. Traditionally, a GCS score of 13 to 15 represents mild TBI, 9 to 12 indicates moderate injury, and a score of 8 or below is considered to be severe. 

Your first step in evaluating a patient presenting with TBI is to perform the primary survey by assessing their ABCDE. First, secure the Airway and consider endotracheal intubation or a surgical airway if the patient cannot protect or maintain their own airway. Be sure to immobilize the cervical spine and maintain immobilization during endotracheal intubation until cervical spine fracture has been ruled out. Next, ensure adequate Breathing or ventilation. Then, assess Circulation and obtain 2 large bore IVs or IO access while continuously monitoring vitals. Next, assess the patient’s Disability and neurologic status by calculating their GCS and assessing pupillary reflex. Keep in mind that the patient’s GCS can change rapidly. Also, remember that a GCS of 8 means intubate if you haven’t already! Finally, Expose the patient and remove all clothing to assess for any other associated injuries, and then cover the patient with warm blankets to prevent hypothermia.

Once these important steps are done, you can move on to a secondary survey, which includes history and physical exam. 

Here are some important clinical pearls! First, if the patient is not lucid, family members, bystanders, or EMTs who]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hepatic_masses:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4IMO0qdTSISeXiLTEKqo9Et7RVeHeYsN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hepatic masses: Clinical sciences]]></video:title><video:description><![CDATA[Hepatic masses are liver lesions that are often found incidentally on imaging performed for unrelated reasons. They can be solid or cystic, and arise from benign, malignant, or infectious etiologies. Most lesions have distinct characteristics on CT or MRI, so understanding these features can help you narrow down your differential diagnoses. 

Alright, when a patient presents with a chief concern suggesting a hepatic mass, your first step is to obtain a focused history and physical examination. Most patients with an incidental finding of a liver mass are asymptomatic, but some can have symptoms such as fever, chills, and right upper quadrant abdominal pain. Additionally, patients might report recent travel to foreign countries, or a history of prior malignancy or cirrhosis. 

Physical exam is usually unremarkable, but in some cases you might see abdominal distension, right upper quadrant tenderness, a palpable liver edge below the costal margin indicating hepatomegaly, as well as scleral icterus and jaundice. 

These clinical features are concerning for a hepatic mass, so your next step is to order a triple-phase abdominal CT with a liver protocol. This type of CT scan uses three phases, arterial, portal venous, and delayed washout phase to better characterize the hepatic lesion. Based on the imaging, hepatic masses are broadly divided into two categories: solid and cystic lesions.

Here’s a clinical pearl! Abdominal duplex ultrasound is an acceptable alternative imaging modality to avoid radiation exposure, particularly in pediatric and pregnant patients. Ultrasound can show whether the mass is solid or cystic, and if there’s vascularity within the lesion.

Okay, let’s talk about solid masses first. Solid liver masses can be benign, but they carry a higher malignant potential than cystic ones. So your work-up should focus on ruling out malignant lesions first. To do that, order a serum alpha fetoprotein, or AFP, which is a marker for liver cancer, and live]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_blunt_traumatic_cervical_spine_injuries:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jxp-18ojSQOHExSBHIFRyncUQvSEj0af/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to blunt traumatic cervical spine injuries: Clinical sciences]]></video:title><video:description><![CDATA[Blunt traumatic cervical spine injury is an injury to the bone, discs, muscle, ligaments or spinal cord of the c-spine. It commonly occurs from flexion-extension injuries from motor vehicle collisions, and compression injuries from falls or contact sports. The cervical spine is particularly vulnerable to these mechanisms of injury because of its mobility and exposure.  

Anatomically, the c-spine is made of 7 vertebrae starting from C1, or atlas, which attaches to the base of the skull to C7, also known as the vertebra prominens, located at the base of the neck connecting to the thoracic spine. C1 and C2 are often referred to as cranio-cervical spine, while C3 to C7 are known as the subaxial c-spine. Any injury to the cervical spine can result in deficits below the level of injury.  

Alright, your first step when evaluating a patient with a blunt cervical spine injury is to perform a primary survey by assessing their ABCDE.  First, stabilize their spine with a rigid c-collar and lay the patient on a flat board for spine immobilization. If a c-collar is not available, manually stabilize the neck to prevent movement of the spine and potentially to prevent further damage of the spinal cord.  

Then you can move on to the rest of the ABCDEs. Evaluate and secure the airway as soon as possible. The big concern here is the injury of the phrenic nerve, which originates at C3 through C5 spinal nerve roots. Any injury at this level or above prevents breathing due to diaphragm paralysis.  

Now, when intubating these patients, you need to be very careful. When the cervical spine is injured, you cannot tilt the head and lift the chin to intubate. Use a jaw thrust instead! Keep in mind that patients with phrenic nerve injury might need a surgical airway like tracheostomy and mechanical ventilation.  

Next, check for breathing and ensure adequate ventilation by providing supplemental oxygen. Then, obtain two large bore IVs or an intraosseous line and start fluid resus]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preconception_care:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/18czh49-RbWtAtziulH_cVnuS1yQMeIB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preconception care: Clinical sciences]]></video:title><video:description><![CDATA[Preconception care involves optimizing health, addressing modifiable risk factors, and providing education prior to pregnancy. The goal of preconception care is to ensure that your patient&amp;#39;s health is optimized to allow for a safe pregnancy. A simple question like, “Do you have a desire to become pregnant in the next year?” opens the door for preconception counseling if the answer is “yes;” it also helps facilitate a contraceptive counseling discussion if the answer is “no.” Preconception counseling can be completed during a specific scheduled visit or during any encounter with a patient who expresses interest in becoming pregnant. 

Okay, when a patient presents for preconception care, you should start with screening and assessing for key components of preconception care. First, you’ll review any major medical conditions that can affect pregnancy. These include diabetes mellitus or DM; thyroid dysfunction; hypertension; thrombophilias; history of bariatric surgery; HIV; mood disorders; and previous pregnancy complications.

Now let’s go into details a bit. Counsel your patients with DM that the goal for pre-pregnancy hemoglobin A1c is less than 6.5%. This is to reduce the risk of congenital anomalies and pregnancy complications. Recommend vision screening for vasculopathy, urine protein testing for renal disease, and an electrocardiogram for cardiac disease screening. In addition, thyroid function screening is appropriate for patients with pregestational type 1 diabetes, a personal or family history of thyroid disease, age greater than 30, obesity, and history of pregnancy loss, preterm delivery, or infertility.

If your patient has long-standing or uncontrolled hypertension recommend similar testing as for diabetic patients including vision screening, urine protein evaluation, and an electrocardiogram. Also assess your patient’s current blood pressure medications as some are teratogenic, such as ACE inhibitors and angiotensin receptor blockers. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antepartum_care_(first_trimester):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zt99eA-zSYiNfnEjsvvZea3MQtOMaJ71/_.png</video:thumbnail_loc><video:title><![CDATA[Antepartum care (first trimester): Clinical sciences]]></video:title><video:description><![CDATA[First trimester antepartum care refers to pregnancy care prior to 14 weeks of gestation. It’s important for patients to receive early prenatal care to prevent complications and optimize pregnancy outcomes. This is also the optimal time to confirm both viability and gestational age of the pregnancy. During this time, all pregnant patients in the first trimester warrant a complete history and physical exam; screening for high-risk conditions; baseline lab tests; genetic counseling and screening; diet and exercise counseling; and overall education in regard to pregnancy. 

When assessing a patient presenting for an initial first trimester antepartum care visit, meaning an initial visit through 13 and 6/7 weeks gestation, your first step is to obtain a focused history and physical exam. History may reveal common first trimester symptoms, such as nausea, vomiting, breast pain, fatigue, cramping, and bleeding. The physical may demonstrate the Hegar sign as early as 6 weeks, which is when the cervix feels softened and enlarged. This is the earliest exam finding of pregnancy. After 12 weeks of gestation, the uterus may appear above the pubic symphysis on a bimanual exam. 

Speculum exam may show a Chadwick sign, which is a blue discoloration of the cervix secondary to venous congestion. Keep in mind that patients usually present for this initial visit suspecting pregnancy because of a positive home pregnancy test or missing a menstrual period, but it’s important to confirm the pregnancy with a human chorionic gonadotropin, or hCG, test. If the hCG is negative, consider an alternative diagnosis. However, if the hCG is positive, go ahead and initiate first trimester antepartum care.

Here’s a clinical pearl! If hCG is positive, be sure to note the first day of their last menstrual period, which will provide a clue about the gestational age; and use the Naegale rule by subtracting 3 months and adding 7 days from their last menstrual period, which will give you a prel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antepartum_care_(second_trimester):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/COHeB2TbQWeTysFe6K9kazE7T52vm-py/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antepartum care (second trimester): Clinical sciences]]></video:title><video:description><![CDATA[Second trimester antepartum care refers to pregnancy care from 14 weeks of gestation through 27 weeks and 6 days of gestation. It is critical that patients receive appropriate care during this time of rapid fetal growth and development to prevent complications and optimize pregnancy outcomes. 

During this time, all patients in the second trimester warrant an obstetrical ultrasound; genetic counseling; screening for abdominal wall and open neural tube defects; gestational diabetes screening; consideration of repeat antibody screening; and trimester-specific pregnancy education.

When assessing a patient presenting for a second trimester antepartum visit, your first step is to obtain a focused history and physical. The history may reveal common symptoms, such as nausea, vomiting, heartburn, and round ligament pain. Patients may report feeling fetal movement once around 20 weeks, but it may be as early as 16 weeks; this is called quickening. It’s also important to review aspects of the first trimester history, like rescreening for depression, anxiety, and intimate partner violence at least once per trimester.

Your focused physical should include reviewing weight, as both insufficient and excess weight gain can result in complications. Trend blood pressure as well, as two or more elevations prior to 20 weeks suggest chronic hypertension, and after 20 weeks it could indicate gestational hypertension. Perform fetal heart rate Doppler assessment at each visit. Starting at 20 weeks of gestation, include a fundal height to track uterine growth, as well to screen for macrosomia and growth restriction.

With the history and physical complete, it’s time to initiate second trimester antepartum care. Perform an obstetric ultrasound between 18 and 22 weeks of gestation. During this ultrasound, assess the cervical length, placental location, and fetal anatomy. A short cervical length of less than 25 mm may indicate an increased risk of preterm birth. Vaginal proges]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antepartum_care_(third_trimester):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BkbYqshHTna0VK1nc5iJrem7Rb2YxqqB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antepartum care (third trimester): Clinical sciences]]></video:title><video:description><![CDATA[Third trimester antepartum care refers to pregnancy care from 28 weeks of gestation through the end of pregnancy. Care during this time is critical to monitor for high-risk conditions and prepare for delivery. All patients in the third trimester warrant consideration of additional ultrasounds; screening tests; assessment of fetal well-being; counseling on birth plans; trimester-specific pregnancy education; and counseling on postpartum contraception.

When assessing a patient presenting for a third trimester antepartum visit, your first step is to obtain a focused history and physical. The history should include asking whether they’re experiencing contractions, possible leakage of fluid, vaginal bleeding, and appropriate fetal movements. 

Additionally, patients may report common benign pregnancy symptoms, such as Braxton Hicks contractions, back aches, round ligament pain, edema, acid reflux, and mild shortness of breath

Here&amp;#39;s a clinical pearl! Braxton Hicks contractions, often referred to as “false labor,” present with infrequent and minimally painful tightening of the abdomen. On the flip side, contractions representing “true labor” are painful, regular, and increase in frequency over time. Typically, false labor is felt only in the front of the abdomen, while true labor is felt in the lower back as well as the abdomen. 

Your physical exam should include a review of weight, since both insufficient and excessive weight gain can lead to complications. Also, pay attention to blood pressure, as new elevations could indicate gestational hypertension or preeclampsia. Perform fetal Doppler assessment at each visit and follow up on any abnormality with prolonged monitoring. 

With the focused history and physical complete, it’s time to initiate third trimester antepartum care. 

For patients with abnormal fundal heights or those with conditions that raise the risk of macrosomia or growth restriction, growth ultrasounds are done every 3 to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Antepartum_fetal_surveillance:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QoLR0ZPvRqCNX2Q7IBPvYFajSGejO3vp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Antepartum fetal surveillance: Clinical sciences]]></video:title><video:description><![CDATA[Antepartum fetal surveillance is the evaluation of fetal well-being, which is performed after 32 weeks of gestation to reduce the risk of stillbirth. In the third trimester, the fetal heart rate pattern, fetal activity, and the amniotic fluid volume are sensitive to fetal oxygen levels and acid-base status. Surveillance techniques, such as fetal heart rate tracing and real-time ultrasound, can identify a compromised fetus and provide an opportunity to intervene before worsening hypoxemia and metabolic acidosis result in fetal demise. However, these tests don’t reflect the severity or duration of  oxygenation and acid-base impairment, and don’t predict stillbirths related to acute events, such as placental abruption or an umbilical cord prolapse. 

The first step in evaluating a patient who presents for antepartum fetal surveillance is to obtain a focused history. You’ll start by identifying the indication for testing, which will help you determine the preferred surveillance method and testing intervals. A number of maternal, fetal, and placental factors are associated with an increased risk of stillbirth, and multiple risk factors can add up. Monitoring fundal height measurements during prenatal care visits is one of the first steps in determining fetal well-being. 

After 20 weeks of gestation, the fundal height should correlate to estimated gestational age. A discrepancy in fundal height should prompt you to obtain a growth scan. Certain maternal conditions typically prompt serial growth ultrasounds starting in the second trimester, including hypertension or preeclampsia; pre-existing diabetes; obesity; a history of previous pregnancy with growth restriction; and multifetal gestation. Fetal growth is an important factor to test, because fetal growth restriction is strongly associated with an increased risk of stillbirth, as well as other perinatal complications, including perinatal asphyxia, neurodevelopmental impairment, and complications related t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fetal_aneuploidy_screening:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LtsDx48GQEyOHtn_6ny6Yh2xSkqa5QX7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fetal aneuploidy screening: Clinical sciences]]></video:title><video:description><![CDATA[Fetal aneuploidy screening refers to non-invasive testing that assesses the risk of chromosomal abnormalities present in a fetus. Many gestations affected by aneuploidy result in nonviable pregnancies and subsequent miscarriages. 

However, for pregnancies that result in live-born neonates, aneuploidy may lead to congenital birth defects, intellectual disability, failure to thrive, infertility, and a shortened lifespan. Fetal aneuploidy screening should be offered to all patients during their pregnancy. Also keep in mind that aneuploidy screening is not required and some patients may decline screening, even after thorough counseling. 

When your patient presents for fetal aneuploidy screening, start by obtaining a focused history and ultrasound.

Starting with the history, assess your patient&amp;#39;s age, particularly noting if they are over 35 years old, which is considered advanced maternal age, as the risk of chromosomal abnormalities increases in this group. Also, confirm your patient&amp;#39;s estimated delivery date, or EDD, as screening tests must be performed during specific gestational times. Some patients may report a history of early pregnancy loss or a prior pregnancy affected by a chromosomal abnormality, both of which can increase the risk of aneuploidy. Additionally, assess if your patient has a personal history of a chromosomal abnormality. 

Next, obtain an ultrasound and confirm the presence of a viable intrauterine pregnancy, or IUP. If a viable IUP is not confirmed, you may choose to hold off on aneuploidy counseling until early pregnancy loss is ruled out. 

Here&amp;#39;s a clinical pearl: The most common autosomal chromosomal aneuploidies in live-born infants are Down syndrome or trisomy 21; Edward syndrome, also known as trisomy 18; and Patau syndrome, or trisomy 13. Klinefelter syndrome, or 46XXY, is the most common sex chromosome aneuploidy, while Turner syndrome, or 45 X, is the only viable monosomy. 

No]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Induction_of_labor:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/58knzwlaRdu0l7YgpIv9vyuZQl_reamM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Induction of labor: Clinical sciences]]></video:title><video:description><![CDATA[Induction of labor is the initiation of parturition through the use of medications and other processes that mimic normal labor. This procedure can be done when the benefits of delivery outweigh the risks of continuing a pregnancy. Depending on the patient’s initial cervical exam, you may need to ripen the cervix or stimulate contractions with a variety of methods. Ultimately the goal of labor induction is to have a spontaneous vaginal delivery. 

Okay, when a pregnant patient presents for induction of labor, you should assess if there are any contraindications present before doing anything. 

Contraindications are conditions that prevent a safe vaginal delivery, such as transverse fetal lie, non-reassuring fetal status, or umbilical cord prolapse.

Here’s a clinical pearl! An umbilical cord prolapse occurs when the umbilical cord falls below the presenting part of the fetus, usually through a dilated cervix into the vagina. This is an obstetric emergency that needs immediate C-section delivery!

Additional contraindications include patients with previous disruption of the myometrium, including a prior classical c-section with a uterine incision, a prior myomectomy entering the uterine cavity, or a prior uterine rupture. These patients are at a high risk of uterine rupture during labor, which makes induction inadvisable. 

Additionally, some patients may have abnormal placentation, such as a placenta previa, where the placenta covers the cervical os and bleeds profusely if cervical dilation occurs; as well as abnormal vascular presentation like vasa previa, where the umbilical vessels are unprotected and found in the membranes that cover the cervical os. Others may have conditions such as invasive cervical cancer, which can block the cervical os and obstruct the ability of a fetus to pass through the birth canal, while also increasing the risk of severe maternal hemorrhage. 

Another contraindication is an active viral disease that can be passed to the fetu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain_management_during_labor:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/omswANK6QdWMhFn-W05csRpNS5SV9gf1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pain management during labor: Clinical sciences]]></video:title><video:description><![CDATA[Labor is defined as the onset of regular uterine contractions that cause the cervix to efface and dilate. Pain is a natural component of labor and each person experiences it differently. Supporting your patients’ desires on how to manage their pain in labor is an important part of obstetric care, and all available options should be discussed with each patient, including non-pharmacological or pharmacological options; a combination of both; or they may choose to have no pain interventions.

Alright, let’s first talk about when your patient presents with pain during labor, and assessment of their desire for pain management intervention. Often, the options for pain management are discussed during prenatal care visits or birthing classes. Some of your patients will have specific desires and plans, while others will take a “let’s see how labor goes” approach and are open to suggestions. Remember that your patient&amp;#39;s desires may change throughout their labor course. It’s completely okay if your patient starts out wishing to avoid all medications and then later in their labor course requests an epidural or another pharmacological option!

Okay, let’s review what can be offered when your patient desires non-pharmacological pain management. There are lots of different options to help labor pain that are non-pharmacological pain management. These include massage, movement, immersion in water during the first stage of labor, acupuncture, relaxation, aromatherapy, and hypnotherapy. These can be performed in any order and one isn’t necessarily better than another. 

Some patients choose to hire a birth doula, or professional labor coach, to provide one-on-one support during labor. This can be very helpful, especially in patients who want to avoid pharmacological interventions. 

Next, let’s discuss what can be offered when your patient desires pharmacological pain management. Keep in mind the difference between analgesia and anesthesia. Analgesia is when pain i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_acute_pelvic_pain_(GYN):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XkpLGVs5Ruumrkq5nmFiYWTWScOnfQyr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to acute pelvic pain (GYN): Clinical sciences]]></video:title><video:description><![CDATA[Acute pelvic pain is defined as pain that arises from the pelvic organs and structures and has been present for less than 3 months. It’s a common gynecologic problem that may require urgent evaluation and treatment, as in cases of ruptured ectopic pregnancy or adnexal torsion. Other, usually less urgent, gynecologic causes of acute pelvic pain include early pregnancy loss, primary dysmenorrhea, endometriosis, adnexal masses, and pelvic inflammatory disease. 

Acute pelvic pain also can be secondary to intimate partner violence or assault. Finally, it may arise from non-gynecologic sources, such as the gastrointestinal tract, urinary tract, or musculoskeletal system.

When assessing a patient with acute pelvic pain, the first step is to assess their CABCDE to determine if they’re stable or unstable. If the patient is unstable, control hemorrhage; stabilize airway, breathing, and circulation; obtain IV access; and monitor vital signs. Then, perform a focused history and physical exam, obtain an hCG to assess for pregnancy, and get a pelvic ultrasound. A rapid bedside ultrasound might be necessary to avoid a delay in treatment.

Now, if the hCG test is positive, consider an ectopic pregnancy. The history may reveal syncope and vaginal bleeding, and physical exam might be positive for hypotension and tachycardia, as well as abdominal tenderness with rebound pain or guarding. If the ultrasound indicates an absence of an intrauterine pregnancy and possible free fluid or adnexal mass, consider a ruptured ectopic pregnancy. Proceed with an operative laparoscopy to confirm your diagnosis and stabilize the patient.

Alright, if the hCG test is negative, consider another gynecologic emergency, adnexal torsion, although keep in mind this may also occur during pregnancy. This is most commonly due to the presence of an ovarian cyst, and occurs when an enlarged adnexa, consisting of the ovary, fallopian tube, and supporting ligaments, twists upon itself and stops blood f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_first_trimester_bleeding:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aTLv40CWQty0jKpiii1GrGPLSX_46tay/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to first trimester bleeding: Clinical sciences]]></video:title><video:description><![CDATA[First trimester bleeding includes is any vaginal or uterine bleeding that occurs from the first day of a patient’s last menstrual period through 13 weeks and 6 days gestation. Pregnant patients who present with vaginal bleeding in the first trimester require a timely evaluation to rule out any life-threatening conditions. The most concerning cause is an ectopic pregnancy because it can progress to tubal rupture and intraperitoneal hemorrhage. Other common etiologies include genital tract pathology, implantation bleeding, spontaneous abortion, pregnancy of unknown location, and molar pregnancy 

Your first step in evaluating a patient with first trimester bleeding is to perform a CABCDE assessment to determine if they are stable or unstable. If your patient is unstable, think about ruptured ectopic pregnancy and incomplete abortion. Regardless of the cause, your next step is to start acute management. Stabilize airway, breathing, and circulation; consider intubation as clinically indicated; obtain IV access and a type and cross for possible packed red blood cell transfusion; and continuously monitor vital signs.

Alright, now that unstable patients are covered, let’s talk about stable ones. First, obtain a focused history and physical examination. On history, determine the first day of your patient&amp;#39;s last menstrual period, whether an intrauterine pregnancy, or IUP, has already been documented by ultrasound, and any previously assigned estimated due date. Next, assess if the patient has any risk factors for ectopic pregnancy or pregnancy loss, such as a history of either one of these. Also, characterize their vaginal bleeding, taking note of onset, frequency, quantity, and associated abdominal or pelvic pain. Additionally, ask if they have passed any large blood clots or tissue prior to your evaluation. 

On physical exam, evaluate for any abdominal tenderness to palpation or peritoneal signs, like rebound pain and guarding. Next, perform a speculum]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ectopic_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QLIeBZe4TPim2yQM8Hqd2C00S3Ws-MV9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ectopic pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[An ectopic pregnancy is a pregnancy that develops outside of the uterine cavity. Now, in an intrauterine pregnancy, embryonic tissue implants within the decidualized endometrium at or near the top of the uterus. However, in ectopic pregnancy, the embryonic tissue typically implants in the fallopian tube, most commonly in the ampulla, but it can also occur in the isthmus or interstitial areas of the tube. Other sites of abnormal implantation include the abdomen, cervix, or c-section scar. Rarely, an ectopic pregnancy can be present along with an intrauterine pregnancy, which is called a heterotopic pregnancy.

Your first step in evaluating a patient presenting with a chief concern suggesting an ectopic pregnancy is to assess their CABCDE to determine if they are unstable. An ectopic pregnancy can rupture at any time leading to extensive intraperitoneal hemorrhage. Because of this, start your management with type and cross for possible packed red blood cell transfusion. Then, stabilize their airway, breathing, and circulation. Also, consider intubation as clinically indicated, obtain IV access, and continuously monitor vital signs.

Next, obtain a focused history and physical exam, and check labs, including CBC, CMP, and hCG, or human chorionic gonadotropin. Additionally, perform an ultrasound to assess pregnancy location and evaluate for the presence of free fluid in the abdomen or cul-de-sac of the pelvis. 

Alright, the patient might report delayed or missed menses, syncope, abdominal or pelvic pain, and vaginal bleeding. On physical exam, you’ll find signs of hemodynamic instability like hypotension and tachycardia, altered mental status, and pale and clammy skin. Next, you’ll usually see signs of acute abdomen like abdominal tenderness, guarding, and rebound pain indicating intraperitoneal bleeding is present. Lastly, on pelvic exam, you may observe bleeding from the cervical os. As for the labs, they usually reveal a positive hCG and probably anemia. F]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Early_pregnancy_loss:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bvmhkCwzShiYAEXjjfpWQ2IIS5CCMCkx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Early pregnancy loss: Clinical sciences]]></video:title><video:description><![CDATA[Pregnancy loss, also known as miscarriage or abortion, is the loss of an intrauterine pregnancy  up to 19 weeks 6 days, and when it occurs in the first trimester, it’s called early pregnancy loss. Early pregnancy loss is common and approximately half are caused by fetal chromosomal abnormalities. 

There are several different types of early pregnancy loss defined by patient symptoms, open versus closed cervical os, and if there has been passage of products of conception, or POC. Incomplete abortion with hemorrhage and septic abortions can cause patients to be unstable, while missed, threatened, inevitable, and complete abortions typically occur in stable patients. 

Your first step in evaluating a patient presenting with a chief concern suggesting early pregnancy loss is to perform a CABCDE assessment to determine if they are stable or unstable. If your patient is unstable, start with acute management. Control the hemorrhage if present and stabilize the airway, breathing, and circulation. You may need to intubate the patient. Then, obtain IV access and continuously monitor their vital signs. 

Next, obtain a focused history, physical exam, and labs including hCG, CBC, and blood type with crossmatch in case a transfusion is needed. Also, get a bedside pelvic ultrasound focusing on the uterine contents, which will help with the diagnosis. However, don’t delay treatment while waiting for the diagnosis, since hypovolemic or septic shock can be life-threatening!

Alright, history might reveal heavy vaginal bleeding, painful uterine cramping, and possible syncope. Vital signs will likely show hypotension and tachycardia. On pelvic exam, you may observe profuse bleeding coming from the cervical os. On closer inspection, the cervical os will be open, and you might see POC protruding from the os. 

When it comes to labs, you’ll usually find a positive hCG, and possibly anemia. Keep in mind that the CBC may not accurately reflect the degree of blood l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Asthma_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6E-yCnTiQbq3m0RLOeBTUWJuTMy5N7fi/_.png</video:thumbnail_loc><video:title><![CDATA[Asthma in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Asthma is an obstructive airway disease characterized by increased airway responsiveness to stimuli, reversible airway obstruction, and chronic airway inflammation. Asthma has a variable course in pregnancy with about a third of patients experiencing improvement in their symptoms, a third having worsening of their symptoms, and a third whose symptoms remain the same. It’s classified as mild, intermittent, or severe and requires close surveillance to ensure adequate oxygenation of the fetus by preventing hypoxic episodes in the patient. Those with mild and well-controlled moderate asthma tend to do well and have excellent pregnancy outcomes. 

However, those with severe and poorly controlled asthma may have an increased risk of perinatal complications like preeclampsia, fetal growth restriction, and premature birth. Additionally, severe asthma exacerbations may cause life-threatening respiratory failure. When counseling patients on treatment options it’s important to use a stepwise approach to medical intervention based on their asthma classification and emphasize that a healthy fetus first requires a healthy patient!  

If a patient presents with a chief concern suggesting asthma in pregnancy you should first perform an ABCDE assessment to determine if the patient is stable or unstable. In unstable patients, the first step involves acute management to stabilize the airway, breathing, and circulation. Then, obtain IV access and monitor maternal vital signs. Also, be sure to assess fetal well-being, depending on the gestational age. If the pregnancy is previable, obtain fetal heart tones via Doppler. In pregnancies past 22 weeks, perform continuous electronic fetal monitoring and consider a biophysical profile. Finally, if a patient has severe asthma symptoms, including drowsiness, confusion, or an elevated partial pressure of carbon dioxide or PCO2, consider hospitalization with admission to the intensive care unit. 

Now that unstable patients are tak]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_hypertension_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HwcjcVcCQpaxFsY6NaBZHzPTSRKsv8Nb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Chronic hypertension in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Chronic hypertension in pregnancy is defined as an elevated blood pressure that’s present prior to conception or first identified before 20 weeks of gestation. This condition requires increased surveillance because of the significant risks to the patient, including stroke, renal insufficiency, superimposed preeclampsia with or without severe features, placental abruption, and postpartum hemorrhage; as well as the risks to a fetus like congenital anomalies, growth restriction, and preterm birth. 

Your first step is to perform a CABCDE assessment and conduct a primary obstetric survey. 

If the patient is unstable, first check for uncontrolled bleeding and control any hemorrhage, as severely elevated blood pressures may cause a placental abruption. 

Next, stabilize their airway, breathing, and circulation, and consider intubation when appropriate. Obtain IV access and continuously monitor maternal vital signs, especially blood pressure. 

Perform your primary obstetric survey, which includes monitoring the fetal heart rate as well as possibly testing for rupture of amniotic membranes and checking cervical dilation.

Alright, let’s talk about stable patients. Start by obtaining a focused history and physical exam, and measure their blood pressure. History might reveal pre-existing hypertension, and your patient may already be taking antihypertensive medications. As for their blood pressure, measure it on two separate occasions at least 4 hours apart. If both measurements show a systolic blood pressure of 140 mmHg or more, a diastolic blood pressure of 90 mmHg or more, or both, that’s hypertension. 

So, if your patient has pre-existing hypertension, or develops newly elevated blood pressures before 20 weeks of gestation, you can diagnose chronic hypertension in pregnancy. 

Here’s a clinical pearl! The normal physiologic changes of pregnancy generally cause a patient&amp;#39;s blood pressure to decrease in the first half of pregnancy and then rise to preco]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypertensive_disorders_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fea-CNtMRTSukIaxl0qYZ44KRf2saqDj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypertensive disorders in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Hypertension in pregnancy is a spectrum of disorders, all characterized by elevated blood pressure. These include chronic hypertension, gestational hypertension, preeclampsia without or with severe features, HELLP, and eclampsia.

Your first step in evaluating a patient who presents with a hypertensive disorder of pregnancy is to perform a CABCDE assessment along with a primary obstetric survey to determine if they’re stable or unstable. 

If the patient is unstable, check for uncontrolled bleeding and control any hemorrhage, as severely elevated blood pressure may cause a placental abruption. Next, stabilize their airway, breathing, and circulation and consider intubation when appropriate. 

Obtain IV access and continuously monitor maternal vital signs. As for the primary obstetric survey, monitor the fetal heart rate and contraction pattern; possibly test for rupture of amniotic membranes; and consider checking cervical dilation if indicated.

Here’s a clinical pearl! Urgent hypertension is defined as 160/110 or higher that persists after retake in 15 to 20 minutes; this requires antihypertensive medication to reduce the risk of maternal stroke. 

Let’s take a look at stable patients. Alright, now that unstable patients are taken care of, let’s talk about stable patients. First, obtain a focused history and physical examination. This should include an accurate blood pressure measurement. A systolic blood pressure greater than or equal to 140, a diastolic blood pressure greater than or equal to 90, or both is considered abnormal during pregnancy. Once you have recognized the patient has elevated blood pressure, it’s time to investigate further; the first step is to assess the patient’s gestational age.

Let’s take a look when the patient is less than 20 weeks gestation.

If the patient is less than 20 weeks gestation, assess whether they have a history of hypertension prior to pregnancy. If the patient does report a history of hypertension, your diagnosi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gestational_hypertension,_preeclampsia,_eclampsia,_and_HELLP:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JY_6Z_cYRVivwA5evXNmg18yRnCS4uXi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gestational hypertension, preeclampsia, eclampsia, and HELLP: Clinical sciences]]></video:title><video:description><![CDATA[Hypertension in pregnancy is not one disorder, but actually a spectrum. This spectrum begins with gestational hypertension, where a patient only has elevated blood pressure.If you add proteinuria to hypertension, then we’re talking about preeclampsia without severe features. Now, progression to preeclampsia with severe features occurs if any of the following are observed; severely elevated blood pressures; labs indicating end-organ damage like thrombocytopenia, elevated liver enzymes, or renal insufficiency; or worrisome symptoms like new onset headache, visual changes, right upper quadrant pain, or epigastric pain. 

Next, HELLP syndrome occurs when a patient presents with Hemolysis, Elevated Liver enzymes, and Low Platelets. These conditions have significant maternal and fetal risks, such as stroke, pulmonary edema, renal failure, and placental abruption. Finally, if the patient had a seizure, that’s eclampsia. Most hypertensive disorders resolve by 12 weeks postpartum, and they all increase a patient&amp;#39;s risk of developing chronic hypertension in the future. 

Your first step in evaluating a pregnant patient who presents with a chief concern suggesting a hypertensive disorder in pregnancy is to perform a CABCDE assessment and conduct a primary obstetric survey. 

If the patient is unstable, check for uncontrolled bleeding and control any hemorrhage, as severely elevated blood pressure may cause a placental abruption. Next, stabilize their airway, breathing, and circulation and consider intubation when appropriate. Obtain IV access and continuously monitor maternal vital signs. Perform your primary obstetric survey, which includes monitoring the fetal heart rate; possibly testing for rupture of amniotic membranes; and consider checking cervical dilation.

Alright, let’s talk about stable patients. Your first step is to obtain a focused history and physical exam. Ask about any history of hypertension, which is a big risk factor. Additional risk fac]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Protraction_and_arrest_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wms-cGmfRcOPhAMBEEKU8CnWR1OpZ8_O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Protraction and arrest disorders: Clinical sciences]]></video:title><video:description><![CDATA[Protraction refers to labor progressing at a slower rate than expected, while arrest refers to the complete cessation of labor progress. Given the increased morbidity with prolonged labor and the need for C-section with labor arrests, it’s important to promptly recognize these disorders.

Your first step in evaluating patients for protracted or arrested labor is a focused history and physical. This includes evaluation of the 4 Ps: passage, meaning pelvis; passenger, meaning fetal size and position; power, meaning strength of contractions and maternal pushing efforts; and psyche, referring to the patient’s mental state and social support. 

Risk factors for abnormal labor will influence these 4 Ps in a number of ways. Nulliparity can affect ‘passage’, since having a previous birth can open the pelvis for subsequent deliveries. Nulliparity may also affect the patient’s ‘psyche’ if they have insufficient support. Post-term pregnancy or gestational diabetes may result in a larger than average ‘passenger’, while intraamniotic infection and epidural analgesia can affect the ‘power’ of contractions and pushing efforts. 

Physical exam findings may reveal risk factors like obesity, which increases the risk of a macrosomic ‘passenger’; or short stature, which is associated with a smaller pelvis. You may also note that the ‘passage’ space feels narrow, possibly from a prior pelvic fracture or simply because of genetic variation. 

Additionally, the ‘passenger’ can impact labor if the fetus is macrosomic or in a non-occiput anterior position. A non-reassuring fetal heart rate pattern also raises the risk of protracted or arrested labor, because it limits your ability to target ‘power’ with labor augmentation using a uterotonic agent like oxytocin.

Once your history and physical are complete, assess the phase and stage of labor. Patients in the first stage, from the onset of labor until 10 centimeters dilation, can be further separated by labor phase. Patients are in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Shoulder_dystocia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kqDzzELyQDCI1WOeH13ZGif1RZig4lAc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Shoulder dystocia: Clinical sciences]]></video:title><video:description><![CDATA[Shoulder dystocia is an unpredictable obstetric emergency! It most often occurs during a vaginal delivery when the anterior fetal shoulder becomes impacted behind the maternal symphysis pubis, thereby preventing spontaneous delivery of the fetal body after delivery of the head. 

Less frequently, it may occur if the posterior shoulder becomes impacted by the sacral promontory. Once diagnosed, time is of the essence, as the longer a fetus remains impacted, the higher the risk of maternal and fetal morbidity. 

Okay, when a patient presents with a chief concern suggesting shoulder dystocia, you should first obtain a focused history and physical exam. The patient may have a history of prior shoulder dystocia, a pregnancy complicated by suspected fetal macrosomia, or they may have gestational or pregestational diabetes. While these findings are associated with an increased risk of shoulder dystocia, it most often occurs in non-diabetic patients with normal-sized infants. 

Additional risk factors that may increase the risk of shoulder dystocia include maternal obesity, as this is associated with maternal diabetes and fetal macrosomia; post term pregnancies, or those lasting beyond 42 weeks; an abnormal pelvic structure; or a short maternal stature. Also, a prolonged second stage of labor should raise suspicion, although this alone is not a good predictor for shoulder dystocia.

When it comes to the physical exam, you might see the delivered fetal head retracting against the perineum, which is called the “turtle sign.” Additionally, the fetal shoulders will not easily deliver despite gentle downward traction of the fetal head. Basically, if you see a fetal head that delivers without spontaneous delivery of the body, you can diagnose shoulder dystocia. 

Here’s a high-yield fact! Be sure to avoid forceful traction on the fetal head, as it may cause a brachial plexus injury! Erb’s palsy, or injury to C5 through C7 causes the classic “waiter&amp;#39;s tip” postur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_third_trimester_bleeding:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HAqUybMDQfCoToLUE8eYjDPhSf2p684q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to third trimester bleeding: Clinical sciences]]></video:title><video:description><![CDATA[Third trimester bleeding is defined as bleeding from 28 weeks of gestation through delivery, and is considered an obstetric emergency if severe or accompanied by maternal or fetal instability. Bleeding at this stage of pregnancy can be classified based on the presence or absence of abdominal pain. Painless causes include cervical or vaginal lesions, placenta previa, and ruptured vasa previa; while painful causes include placental abruption, uterine rupture, or normal labor. Severe third trimester bleeding requires rapid assessment and stabilization, along with timely management in order to prevent maternal and fetal morbidity and mortality.

Your first step in evaluating a patient presenting with third trimester bleeding is to perform a CABCDE assessment along with a primary obstetric survey to determine if they are stable or unstable. If the patient is unstable, control any life-threatening hemorrhage. Then stabilize the airway, breathing, and circulation. Obtain IV access if not already present, and monitor maternal vital signs closely. Once the patient is stabilized, be certain to assess the fetal status by monitoring the fetal heart rate. A labor evaluation may then be performed by testing for rupture of membranes and checking cervical dilation.

Here’s a clinical pearl! A digital cervical exam should never be performed prior to confirming placental location, either through a review of the patient’s prenatal records or on a bedside ultrasound if not previously documented. Palpation of a placenta previa through a partially dilated cervix can result in life-threatening hemorrhage and should be avoided. 

Alright, now let’s talk about stable patients. First, obtain a focused history and physical examination. During history, characterize the bleeding and take notes of the quantity, the presence or absence of abdominal pain, and any associated precipitating events. Specifically, question the patient regarding any recent history of trauma, and if reported, w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Placental_abruption:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7wD8991aQ8OGCDYSYUsSSFLoTxut8Xpn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Placental abruption: Clinical sciences]]></video:title><video:description><![CDATA[Placental abruption is the partial or complete separation of the placenta from the uterine wall prior to delivery. This is due to rupture of maternal vessels within the basal layer of the endometrium. Blood accumulates and splits the placental attachment, which can cause leakage of blood into the myometrium, painful uterine contractions, as well as maternal blood loss through the vagina, which results in decreased blood flow and oxygenation to the fetus. 

Some patients may present acutely requiring immediate delivery, while others may stabilize and be candidates for expectant management of the pregnancy with close surveillance.

When evaluating a patient presenting with a chief concern suggesting placental abruption, your first step is to perform a CABCDE assessment as well as a primary obstetric survey to determine if they are stable or unstable. If the patient is unstable, immediately attempt to control the hemorrhage and stabilize their airway, breathing, and circulation. You may need to intubate the patient, obtain IV access, and continuously monitor their vitals. Remember that you have two patients here, so you must assess the fetus as well! First, check the fetal heart rate to ensure well-being, and if at a viable gestational age, perform continuous fetal monitoring and assess for fetal movement. Bleeding from a placental abruption can stimulate uterine contractions, so you should also assess for labor. 

Once you have initiated the acute management, your next step is a focused history and physical exam. Labs are important because of the potential for life-threatening hemorrhage, so order a CBC as well as PT, INR, PTT, and fibrinogen. Finally, order a Kleihauer-Betke test, also called a “KB” for short, to look for the presence of fetal blood in maternal circulation. This test is highly specific for abruption and lets you know how much Rh immune globulin is needed to prevent alloimmunization.

In the history, patients may report feeling dizzy or anxi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Placenta_previa_and_vasa_previa:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ku9ezbA-T3_8n67iN4UtseCfS0_Feo3l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Placenta previa and vasa previa: Clinical sciences]]></video:title><video:description><![CDATA[Placenta previa is when placental tissue partially or completely covers the internal cervical os. When the placental edge is within 20 millimeters of the internal cervical os but isn’t actually covering it, it’s called a low-lying placenta. In contrast, in vasa previa, the fetal vessels either cross the internal os or are within 20 millimeters of it. The etiologies are unknown, though each condition has independent risk factors. These entities are important because they can cause bleeding, especially in labor or when membranes rupture. In placenta previa, the source of bleeding is maternal, whereas bleeding in vasa previa comes from the fetus.

Your first step in evaluating a patient presenting with a chief concern suggesting placenta previa or vasa previa is to do a CABCDE assessment to determine if they unstable. Unstable patients may have heavy vaginal bleeding, so prepare for urgent surgical management. Stabilize the airway, breathing, and circulation, and intubate the patient if necessary. Obtain IV access, and continuously monitor their vital signs. Initiate continuous fetal heart rate monitoring, and check for any signs of labor. Perform a sterile speculum exam to assess the volume of bleeding and check visually if the cervix is dilated. 

Keep in mind that you should never perform a digital cervical exam on a patient with placenta previa or vasa previa, as it can disrupt the placenta and vessels and worsen the situation.

After the primary assessment, obtain a focused history, physical exam, and labs including CBC, PT, INR, PTT, fibrinogen, and a type and crossmatch. You may also need to perform an ultrasound to help with diagnosis, but don’t delay treatment while waiting for imaging. 

Let’s talk about the history of those with placenta previa. Your patient may report dizziness, tunnel vision, and anxiety due to the acute blood loss, which occurs when shearing forces from uterine contractions and cervical changes disrupt the placental attachment s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prelabor_rupture_of_membranes:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hxpfs78_R6SsPz8bh9nffKkESZ_ddyEz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prelabor rupture of membranes: Clinical sciences]]></video:title><video:description><![CDATA[Prelabor rupture of membranes or PROM is the spontaneous rupture of membranes that occurs before the onset of labor. Term PROM occurs when membranes rupture at 37 weeks of gestation or later whereas preterm PROM or PPROM occurs before 37 weeks. Membrane rupture prior to labor at term may be due to a normal physiologic weakening of membranes, whereas preterm PROM may have a variety of pathologic causes, such as intraamniotic infections. The management of PROM is based on gestational age as well as maternal and fetal status. 

Your first step in evaluating a patient presenting with a chief concern suggesting PROM is to assess their CABCDE and conduct a primary obstetric survey to determine if they are stable or unstable. If the patient is unstable, you should immediately control any hemorrhage. Always keep in mind that patients with PROM are at an increased risk of placental abruption, which can lead to hemorrhage. Then, stabilize their airway, breathing, and circulation. Additionally, obtain IV access; type and cross if packed RBCs are needed; continuously monitor maternal vital signs; and consider intubation when appropriate. 

Next, monitor the fetal heart rate and perform your primary obstetric survey. Perform a sterile speculum examination to visually check cervical dilation and assess for rupture of membranes or ROM. Evidence of membrane rupture includes visualizing amniotic fluid from the cervix; pooling of amniotic fluid in the vagina; or ferning of the fluid on microscopic examination. 

Another quick test you can do is a pH test. Amniotic fluid is more alkaline than the vaginal environment. If PROM has occurred, the fluid sampled from the vagina will turn nitrazine paper, or pH strips, a blue color that indicates a basic pH between 7.1 to 7.3. That being said, the pH test isn’t perfect, and false positive results from the presence of blood, semen, alkaline antiseptics, or bacterial vaginosis may occur. A false negative result may also occur if ther]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preterm_labor:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oOnthZhpQrOQcNrrtTFwGuGUSH_lxikO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preterm labor: Clinical sciences]]></video:title><video:description><![CDATA[Preterm labor is defined as regular uterine contractions accompanied by a change in cervical dilation, effacement, or both, that occurs between 20 and 0/7 weeks of gestation and 36 and 6/7 weeks of gestation. It’s diagnosed when a patient presents with regular uterine contractions and a cervical dilation of at least 3 cm. Preterm labor can be either spontaneous or preceded by premature rupture of membranes; or it can be iatrogenic due to maternal or fetal causes necessitating early delivery. The majority of patients who initially present with evidence of preterm labor do not deliver prematurely; however, when labor progresses to preterm birth, there’s an increased risk of neonatal morbidity and mortality. 

When a patient presents with a chief concern suggesting preterm labor, your first step is to perform a focused history and physical exam. To meet criteria for preterm labor your patient’s pregnancy must be at least 20 weeks and less than 37 weeks of gestation. They may report uterine contractions, abdominal cramps, low back pain, pelvic pressure, spotting, or vaginal bleeding. 

Additionally, history might reveal some important risk factors for preterm birth, including a prior preterm birth; short interval pregnancy, defined as less than 18 months between deliveries; a known short cervix, meaning less than 25 mm in the current pregnancy; past procedures on the cervix; infections during the current pregnancy, such as urinary or genital tract infections; maternal prepregnancy body mass index less than 18.5; extremes of maternal age, specifically those younger than 17 or older than 35 years; and tobacco or substance use during pregnancy. Also, certain social determinants of health are associated with preterm birth, specifically lower levels of education, living in an disadvantaged area, and lack of access to prenatal care. An additional important consideration is that preterm birth is higher for Non-Hispanic Black and Indigenous individuals.

Here’s a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_postpartum_hemorrhage:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ouJ6L3nNSgq7NgSr4hmClqzmSKKR6eFQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to postpartum hemorrhage: Clinical sciences]]></video:title><video:description><![CDATA[Postpartum hemorrhage is bleeding after delivery that results in either a cumulative blood loss of at least 1000 mL or blood loss associated with signs and symptoms of hypovolemia, no matter the route of delivery. 
Immediate, or primary postpartum hemorrhage occurs in the first 24 hours following delivery, while delayed, or secondary postpartum hemorrhage occurs more than 24 hours to 12 weeks following delivery. 
All postpartum hemorrhages are obstetric emergencies and require timely recognition and management.

All patients presenting with postpartum hemorrhage are considered unstable and need acute management. First, you’ll need to stabilize their airway, breathing, and circulation. Next, monitor their vital signs and obtain IV access, if not already present. 
Begin a crystalloid infusion or increase the rate if already administered. 
Then, obtain a blood type and crossmatch to prepare blood products in case a transfusion is necessary. 
Also, activate the obstetric hemorrhage team or personnel you’ll need to assist you. 
Lastly, take a moment to review the patient’s clinical course for the most likely cause of their hemorrhage.

Once these steps are done, it’s important to assess time from delivery. If 24 hours or less has passed since delivery, we are talking about immediate postpartum hemorrhage. The first step is to obtain a focused history and physical examination; as well as labs, including a CBC, PT, PTT, INR, and fibrinogen to evaluate for anemia and coagulopathy.

Patients with immediate hemorrhage will have profuse bleeding, sometimes continuous in nature and other times in the form of large intermittent clots.
History might also reveal potential risk factors for postpartum hemorrhage, such as high parity, prolonged use of oxytocin, intraamniotic infection, multifetal gestation, or precipitous delivery. 

Here’s a clinical pearl! Although the definition of postpartum hemorrhage as 1000 mL of blood loss applies to both vaginal and c-sections, a b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Placenta_accreta_spectrum:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Pk_QZFklTK_qsn_nVGktKEHIR__vpG6W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Placenta accreta spectrum: Clinical sciences]]></video:title><video:description><![CDATA[The placenta accreta spectrum, known as PAS, refers to a range of abnormal placental invasion and adherence into the myometrial tissue of the uterus. It occurs when there is an abnormal interface between the uterine endometrium and myometrium. 

This often occurs over a uterine scar, which is why placental trophoblasts anchor deeper than normal into the uterine wall. The spectrum ranges from placenta accreta, where the placenta attaches to the myometrium; then, placenta increta, where invasion into the myometrium occurs; and placenta percreta, where the placenta penetrates through the myometrium and attaches to the uterine serosa; sometimes adjacent organs are also invaded, like the bladder. 

PAS can be suspected antenatally, but sometimes isn’t discovered until after delivery, where life-threatening hemorrhage is often encountered when placental separation is attempted, due to this abnormally deep attachment.

Your first step in evaluating a patient presenting with a chief concern suggesting PAS is to do a CABCDE assessment to determine if they are stable or unstable. 

Unstable patients typically present right after delivery of the baby, when attempting to deliver the placenta. This should already make you suspect PAS. In this case, first, control the hemorrhage and stabilize the airway, breathing, and circulation. You may need to intubate the patient. Then, obtain IV access, and continuously monitor their vital signs. 

To confirm the diagnosis of PAS, you will need to obtain a focused history, physical exam, and labs including CBC, PT, INR, PTT, and fibrinogen. Additionally, a uterine ultrasound performed at the bedside will help with diagnosis. However, don’t delay treatment while waiting for the diagnosis, since the hemorrhage can be life-threatening! 

Okay, so your patient may have a history of procedures that lead to uterine scarring. The big one to look out for is a prior c-section birth. Others include myomectomy or dilation and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Well-patient_care_(GYN):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M4uHgoOOQn6TfG9SojQUDl1lRp2wWp-M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Well-patient care (GYN): Clinical sciences]]></video:title><video:description><![CDATA[Well-patient gynecologic care focuses on screening and prevention of disease in otherwise healthy individuals. All patients benefit from basic preventative care, which is focused on counseling on a variety of topics including substance use, mental health, contraception, interpersonal and domestic violence, obesity, urinary incontinence, sexually transmitted infections or STIs, and age-appropriate immunizations and cancer screenings. Additional recommendations are based on the patient’s age and health risks. 

When a patient presents for well-patient care, begin with a complete history and physical exam.This includes your patient&amp;#39;s obstetrical, gynecological, menstrual, and contraceptive history, along with their family and social history. Key factors that will guide your screening include age, past and current sexual activity, smoking status, and review of medical conditions like hypertension, dyslipidemia, diabetes mellitus, and cancers like cervical, breast, colorectal, and skin cancer. Next, complete an age-appropriate physical exam including height, weight, and vital signs. 

Now let’s talk about the recommended screening and counseling that applies to all patients.  Screening for alcohol, tobacco, and substance abuse can be completed either through a direct conversation with your patient or by using a validated questionnaire. Regarding alcohol use, the recommended limits for alcohol are one drink or less per day or seven drinks per week. Additional alcohol use beyond this is a common cause of preventable diseases such as alcoholic liver disease, injuries from events like motor vehicle crashes, and overall premature mortality. 

Likewise, tobacco use and substance abuse are significant preventable causes of disease, disability, and death. As needed, provide counseling for patients and connect them to resources and referrals for further intervention and support. 

Next, screen for anxiety and depression - both of which are common conditions - u]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexually_transmitted_infection_screening_(GYN):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M2jtvHS7Qo_-qVWbqP5Wis9BSRm1cG1V/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sexually transmitted infection screening (GYN): Clinical sciences]]></video:title><video:description><![CDATA[Sexually transmitted infections, or STIs, are infections that are transmitted through sexual contact. The goal of screening for STIs is to diagnose and treat infections, and provide education, which then prevents further transmission. While some STIs cause symptoms such as lesions or cervical discharge, many are asymptomatic. STI screening is encouraged for all patients, and specifically in special populations such as pregnant patients, where some STIs, like syphilis, can cause congenital disease.

When a patient presents for STI screening, begin with a focused history and physical exam. Start by reviewing your patient’s age, pregnancy status, and HIV status. Ask your patient if they have had a known exposure to an STI. If yes, inquire about the timing of sexual exposure,  review previous screenings or treatment results, and ask if they’re experiencing symptoms. 

On a physical exam, look for cervical discharge or genital lesions which may prompt additional screening. Also keep in mind that STI screening can be completed at a specific STI screening visit or as part of a preventative visit, like a well-patient care exam. STI screening can also be completed without a physical exam by patient-collected swabs, and lab tests such as blood and urine tests; however, this is only appropriate for asymptomatic patients.

Okay, let’s start by talking about which infections are screened for and how that screening is completed. Chlamydia, caused by Chlamydia trachomatis, is the most frequently reported bacterial STI with the highest prevalence in patients who are under 25 years of age. Gonorrhea, caused by Neisseria gonorrhoeae is the second most frequently reported bacterial STI. Testing for both is completed through a nucleic acid amplification test or NAAT. If a provider obtains a sample for testing, a specimen collection swab is used to obtain the sample from the patient’s cervix. If the patient collects their own sample, either a vaginal swab or first catch urine ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_postmenopausal_bleeding:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QW_0jWiWSpCb1PbwKWNA3CvJTUGzyxx3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to postmenopausal bleeding: Clinical sciences]]></video:title><video:description><![CDATA[Postmenopausal bleeding is any vaginal bleeding that occurs after menopause. Menopause is defined as an absence of menstrual bleeding for twelve months in patients 40 years and older, with an average age of 51, who don&amp;#39;t have another reason for amenorrhea, such as a hysterectomy. Vaginal bleeding after menopause is the presenting symptom in the majority of cases of postmenopausal endometrial carcinoma, as well as in other genital tract cancers. Benign causes of postmenopausal bleeding can arise from any site along the genital tract and can come from structural problems, such as fibroids, polyps, and urogenital atrophy. 

Your first step in evaluating a patient who presents with postmenopausal bleeding is to perform a CABCDE assessment to determine if they are stable or unstable. If the patient is unstable, control any life-threatening hemorrhage by using IV hormone therapy, with or without surgical intervention. Also stabilize the airway, breathing, and circulation; obtain IV access; and monitor vital signs. 

Here’s a clinical pearl! It’s unusual for a patient to present with uncontrolled postmenopausal bleeding. In this situation, strongly consider underlying comorbidities like coagulopathy, anticoagulation therapy, or malignancy. 

Alright, now that unstable patients are taken care of, let’s talk about stable patients. The first step is to obtain a focused history and physical examination. Always determine menopausal status by obtaining an accurate menstrual history, and if the patient’s menopausal status is uncertain, obtain an hCG test to rule out pregnancy. 

Here’s a high-yield fact! Menopausal patients with significant vasomotor symptoms can be treated with systemic hormone therapy like oral or transdermal options, as long as there’s no personal history of breast cancer or undiagnosed abnormal uterine bleeding. It’s common for patients to have irregular light vaginal bleeding during the first six months of hormone replacement therapy. Howe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/1p36_deletion_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JbZh7GtVQAWKFrOIhEYETvsaSpmBfg09/_.png</video:thumbnail_loc><video:title><![CDATA[1p36 deletion syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[1p36 deletion syndrome is a rare genetic disorder where a small portion of the short arm of chromosome 1 is deleted.  

Now, our DNA is packaged into 23 pairs of chromosomes, one from each parent, for a total of 46 chromosomes. Each chromosome contains thousands of genes which are essentially the recipes for making every protein found in the body. Chromosomes are divided into two sections, or arms, hooked together in the middle by a centromere. The shorter arm is called “p”, from the French “petit” that means small; and the long arm is called “q”. In 1p36 deletion syndrome, the final portion of the short, or “p,” arm of chromosome 1 is deleted, resulting in a loss of genetic material that is essential for development. 

In most cases, 1p36 deletions are a result of a de novo mutation, which means they occur on their own without being inherited. However, in a small number of cases, the deletion can be inherited from one of the parents. 

Alright, now signs and symptoms of 1p36 deletion syndrome vary depending on the amount of missing genetic material. Typically, individuals with 1p36 deletion syndrome will have a short stature and unique facial features like a small head with a large, rounded forehead and small, pointed chin; deeply set eyes; straight eyebrows; and epicanthal folds, which are skin folds of the upper eyelids that cover the inner eye. The nose is usually flat with a wide nasal bridge, and there can be orofacial defects like cleft palate, which is an opening in the roof of the mouth. 

Common symptoms include moderate to severe intellectual disability; slower motor development; dysphagia, or difficulty swallowing; and hypotonia, or weak muscle tone, which usually improves with age. Individuals may also exhibit seizures; vision and hearing problems; dysarthria, or difficulty speaking; and self-harm or other behavioral problems; as well as delayed closure of the fontanelles, or soft spots in the skull. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/FOXG1_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J11lTdPkTZyGTMkB1UogTLewTYmkdPw7/_.png</video:thumbnail_loc><video:title><![CDATA[FOXG1 syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[FOXG1 syndrome is a rare neurologic condition caused by alterations in the FOXG1 gene. The FOXG1 gene codes for a protein that plays an essential role in early brain development and is particularly important for the formation of the cerebral cortex. It also helps to establish connections between the right and left hemispheres through a large nerve tract called the corpus callosum, and is important for regulating the proliferation and survival of cells in the brain. Alterations in the FOXG1 gene usually occur sporadically, meaning they are typically not inherited from a parent and do not run in families. 

Symptoms of FOXG1 syndrome are generally present since early childhood. Most children have severe developmental delays affecting speech and motor skills. They can also have autism-like traits, such as difficulty with social interactions and communication. As they grow older, some children develop acquired microcephaly, which is when there is a deceleration in head growth despite having an average head circumference at birth. 

A classic feature of FOXG1 syndrome is the presence of a hyperkinetic movement disorder  characterized by involuntary muscle twitching or jerky contractions, as well as choreoathetosis, which is a combination of chorea, or involuntary and irregular spasmodic movements, and athetosis, or involuntary twisting movements. Individuals may also exhibit stereotypies, which are repetitive sounds or movements, like body rocking or finger tapping.

Additionally, the majority of children develop seizures that are often resistant to medication and can evolve into epilepsy syndromes. In addition to neurologic symptoms, FOXG1 syndrome is associated with feeding difficulties and gastrointestinal problems like reflux and constipation; as well as sleeping problems like difficulty falling or staying asleep and unexplained episodes of crying. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Long-chain_3-hydroxyacyl-CoA_dehydrogenase_deficiency:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TxHfDUn3Rkyb8TH5H9oCa_zTQUWg0QAg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: Year of the Zebra]]></video:title><video:description><![CDATA[Long-chain 3-hydroxyacyl-CoA dehydrogenase, or LCHAD, deficiency is a rare disorder of fatty acid metabolism that prevents the body from metabolizing certain types of fat. 

Normally, the primary source of energy in the body is glucose. However, when glucose levels are running low, like with prolonged fasting or exercise, the body is able to obtain energy from stored fats. 

The simplest form of fats are fatty acids, which are grouped by length into short-, medium-, and long-chain fatty acids based on their size and length. When the body needs extra energy, fatty acids are mobilized from fat stores and broken down, or oxidized, in the mitochondria of cells. 

Fatty acid oxidation results in the formation of acetyl-CoA, which can be further metabolized to obtain more energy; or sent to the liver to get converted into ketone bodies. Ketone bodies are important because they are the brain’s alternate source of energy when there’s no glucose available.

Now, in LCHAD deficiency, a genetic mutation in the HADHA gene results in a deficiency in an enzyme called long-chain 3-hydroxyacyl-CoA dehydrogenase, which is one of the enzymes involved in the oxidation of long-chain fatty acids. This deficiency leads to long-chain fatty acids that cannot be broken down, so they end up accumulating in cells.  

LCHAD deficiency is an autosomal recessive disorder, meaning an individual must inherit two copies of the mutated gene to develop the disorder.

Alright, now LCHAD deficiency usually first manifests in infants or young children as hypoketotic hypoglycemia, which is an episode of low blood sugar that can’t be compensated for by producing ketone bodies to obtain energy. 

Symptoms of hypoketotic hypoglycemia are often precipitated by fasting, strenuous exercise, or viral infections like gastroenteritis or influenza; and can include lack of energy, nausea and vomiting, seizures, altered mental status, and even coma. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thoracic_outlet_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uocAKbaNQo69MR5UaMw3GH8eQZmaaNdG/_.png</video:thumbnail_loc><video:title><![CDATA[Thoracic outlet syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Thoracic outlet syndrome refers to a group of neurovascular symptoms that arise from compression of the nerves and blood vessels passing through the narrow space between the collarbone and first rib, called the thoracic outlet. This condition can be caused by a variety of factors that can compress the thoracic outlet and its structures. Factors can include neck injuries; certain cancers that invade the thoracic outlet or surrounding area; anatomical variants that predispose to neurovascular compression, such as the presence of an extra cervical rib; and certain activities or sports involving repetitive movements of the arm and shoulder, like swimming or baseball. 

Regardless of the cause, thoracic outlet syndrome can present with a variety of symptoms which vary depending on the specific structures that are affected; and symptoms are usually unilateral, occuring on only one side of the body. The most common symptoms result from compression of the nerves that innervate the upper limb, which can cause muscle weakness, numbness, and tingling in the arm and hand on the affected side, especially when performing overhead activities or carrying heavy objects.  

On the other hand, compression of the veins that drain the upper limb decreases blood drainage from the affected arm and hand, leading to swelling of the upper limb and dilation of the veins of the neck and chest.  

Finally, arterial compression decreases blood supply to the affected arm and hand muscles, resulting in a cold and pale extremity, numbness, and cramping pain that occurs during activity and is relieved with rest. Individuals with arterial compression may also have weak pulses and a lower blood pressure in the affected arm. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Reiter_syndrome:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9FEi08HhSYO0F-Wi6WyZ917DSSuItu2d/_.jpg</video:thumbnail_loc><video:title><![CDATA[Reiter syndrome: Year of the Zebra]]></video:title><video:description><![CDATA[Reactive arthritis, formerly known as Reiter syndrome, is a rare autoimmune condition primarily affecting the joints, which develops in response to an infection in another part of the body. Typically, the infection affects the genitourinary or gastrointestinal tract, although it can often go unnoticed by the individual. 

The immune system reacts to the infection’s causative agent, usually a bacteria, and due to structural similarities between the bacteria and the body’s tissues, the immune system mistakenly attacks the body’s tissues. 

Reactive arthritis is more common in individuals who are positive for the HLA-B27 gene, a genetic marker that increases susceptibility to certain inflammatory conditions like psoriasis and ankylosing spondylitis.

Symptoms of reactive arthritis often start several days to three weeks following a genitourinary or gastrointestinal infection. The main symptom is usually pain and swelling of a single, large joint like the knee. Less often, it involves other joints like the ankles, hips, and smaller joints in the feet; or affect multiple joints. There can also be inflammation of tendons where they connect to bone, called enthesitis; as well as inflammation of the fingers, called dactylitis, also known as “sausage fingers.”

In addition to joint pain, individuals often develop symptoms in other parts of the body, notably the urethra and conjunctiva of the eyes. When the urethra is involved, it can lead to burning pain with urination; and when the conjunctiva is affected it causes inflammation, or conjunctivitis, which leads to redness of the eyes. Rarely, reactive arthritis can cause skin lesions affecting the palms and soles of the feet, as well as ulcers in the glans of the penis. 

Reactive arthritis is often self-limiting and usually fades over the course of a year without causing any permanent joint damage or immobility. However, in a small percentage of individuals the condition may become chronic, with symptoms persisting]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infantile_neuroaxonal_dystrophy:_Year_of_the_Zebra</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6sRwIJzMQ5GxMqyJynSvIbHpR-OSnHur/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infantile neuroaxonal dystrophy: Year of the Zebra]]></video:title><video:description><![CDATA[Infantile neuroaxonal dystrophy, or INAD for short, is a rare and rapidly progressive neurodegenerative disorder that begins in early childhood. 

It is caused by mutations affecting the PLA2G6 gene, which provides instructions for making an enzyme called phospholipase A2. This enzyme is important for breaking down fatty molecules called phospholipids, which are one of the main components of the cell membrane. Impaired function of phospholipase A2 is thought to disrupt the structure of the cell membrane, resulting in the degeneration of nerve cells. 

INAD is typically inherited in an autosomal recessive pattern, meaning two copies of the mutated gene must be present for individuals to develop the disorder. 

Alright, now clinical manifestations of INAD typically begin between six  months and three years of age. 

Initially, children with INAD can meet their developmental milestones but then begin to experience delays in reaching milestones like crawling or talking. As the disorder progresses, children experience a regression in motor, verbal, and cognitive skills. For example, a child who could initially speak a few words or grasp objects with their hand will gradually lose these skills. Of note, individuals with INAD commonly experience progressive dementia by three years of age.

Individuals with INAD may also have visual problems like strabismus, where the eyes do not align with each other; nystagmus, which is the presence of involuntary, rapid eye movements; and some may even develop vision loss.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholestasis_of_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oyJ6-c9TS7GxBg7pjBaajiI3QVS8GkXi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholestasis of pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Intrahepatic cholestasis of pregnancy, or ICP, is a rare pregnancy-specific liver disease that is characterized by pruritus and elevated serum bile acid levels. Typically, it presents in the third trimester with itching on the palms of the hands and soles of the feet, without a rash. It is a relatively uncommon disease but is associated with poor fetal outcomes, including preterm delivery, meconium-stained amniotic fluid, and stillbirth, due to an accumulation of bile acids in the fetus, as well as the amniotic fluid. 

Let’s talk about the first steps to assessing a patient… When assessing patients who present with a chief concern suggesting ICP, start with a focused history and physical exam as well as labs, including total bile acids and liver transaminases, such as ALT and AST. 

The hallmark symptom of ICP is pruritus, most often on the palms of the hands and soles of the feet which is worse at night. In general, symptoms start in the third trimester with the majority of cases diagnosed after 30 weeks gestation. 

Risk factors include a personal or family history of ICP or preexisting hepatobiliary diseases, such as hepatitis C, nonalcoholic cirrhosis, and nonalcoholic pancreatitis, as well as gallstones and cholecystitis. ICP is also associated with advanced maternal age, multiple gestations, and in vitro fertilization. 

On physical exam, there should be no rash present. If you visualize a rash, consider an alternative diagnosis, such as a dermatoses of pregnancy like atopic eruption of pregnancy, polymorphic eruption of pregnancy, or pemphigoid gestationis. That being said, you may note excoriations, since the pruritus can be quite intense.

When it comes to labs, the key finding in ICP is total bile acids greater than 10. Your patient’s liver transaminases may also be elevated. If the total bile acids are greater than 10 along with pruritus of the palms and soles without a rash, you can make the diagnosis of ICP. Also be sure to rule out]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Primary_dysmenorrhea:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BTV1DP7DQx22K7xy-lLwqvmVSXu6yHt9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Primary dysmenorrhea: Clinical sciences]]></video:title><video:description><![CDATA[Primary dysmenorrhea refers to painful menstruation in the absence of pelvic pathology. It often starts in adolescence, usually within the first 6 to 12 months of menarche. In fact, dysmenorrhea is the most common menstrual-related symptom in young women. The pathophysiology is likely related to the increased release of inflammatory mediators like prostaglandins and leukotrienes during menses. 

When assessing a patient who presents with a chief concern suggesting primary dysmenorrhea, start with a focused history. Patients typically report painful menstruation without a history of underlying pelvic pathology. Their pain usually starts 6 to 12 months of menarche, which is when ovulatory cycles are most often achieved. Now, some patients might also experience a range of associated symptoms, such as pain localized in the lower back, pelvis, or upper thighs as well as possible nausea, vomiting, diarrhea, headaches, muscle cramps, and poor sleep. If you see these history findings, you can diagnose primary dysmenorrhea. 

Here’s a clinical pearl! Some individuals do not achieve ovulatory cycles until 1 to 3 years after menarche. In these patients, suspect primary dysmenorrhea if pain began during this time frame and if there is no history of symptoms that suggest associated pelvic pathology. Pelvic examination, including pelvic ultrasound, is not needed, but it could be considered if symptoms progress or fail to improve with medical treatments.

Now that you’ve diagnosed primary dysmenorrhea, let’s talk about treatment. First-line treatment involves nonsteroidal anti-inflammatory drugs, or NSAIDs, for pain relief. Common NSAIDs include ibuprofen, naproxen, and celecoxib. These work by inhibiting the enzyme cyclooxygenase, which converts arachidonic acid into prostaglandins, thus decreasing the production of  prostaglandins, which cause the muscles and blood vessels of the uterus to contract. 

Be sure to tell your patient that NSAIDs should be taken a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Otitis_media_and_externa_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oE6a8aGHTJWE8pvhf8FVREuITkS79Iw0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Otitis media and externa (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Otitis, or inflammation of the ear, is commonly caused by bacterial infection. It is most often seen in children, but it can occur at any age! Pediatric patients typically present with either acute otitis media, which is an infection of the middle ear most commonly caused by Moraxella catarrhalis, Streptococcus pneumoniae, or Haemophilus influenzae; or acute otitis externa, which is an infection of the outer ear, and is usually caused by Pseudomonas aeruginosa or Staphylococcus aureus. 

If your patient presents with a chief concern suggesting acute otitis media or acute otitis externa, you should first perform a focused history and physical exam. Let’s start with acute otitis media. The history is usually significant for symptoms of discomfort; for instance, a nonverbal infant or child may be fussy, have changes in appetite or trouble sleeping, and they may tug, rub, or hold the affected ear. On the other hand, a verbal child will commonly describe new-onset ear pain. In addition, patients may or may not report ear drainage, fever, or concurrent symptoms of an upper respiratory infection, such as rhinorrhea, nasal congestion, and cough. 

The physical exam using an otoscope will reveal a red, bulging tympanic membrane, as well as impaired mobility with pneumatic otoscopy. Keep in mind that redness is a non-specific sign of inflammation, so a sole finding of redness without bulging does not necessarily indicate acute otitis media. You may even see purulent drainage within the ear canal, which suggests that the tympanic membrane has ruptured. 

Here’s a clinical pearl! A trick to systematically approach the otoscopic exam is to divide the tympanic membrane into four quadrants, and each quadrant should be assessed for its position, color, translucency, and mobility.

At this point, you can diagnose acute otitis media! Your next step is to assess the severity of otitis media by checking the patient’s temperature, as well as the degree and duration of ota]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Education_in_the_Clinical_Years:_Challenges_and_Opportunities</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NFDxSt7BQFGV1qTdJY5w7PG_Rhq9HJiI/_.png</video:thumbnail_loc><video:title><![CDATA[Education in the Clinical Years: Challenges and Opportunities]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Education in the Clinical Years: Challenges and Opportunities through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adnexal_torsion:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/25d-u0_sQNuJSKotJ0Oqp5stQwS9mOhb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adnexal torsion: Clinical sciences]]></video:title><video:description><![CDATA[Adnexal torsion occurs when the ovary and fallopian tube twist, either completely or partially, on their ligamentous support, causing obstruction of their blood supply. You may also see this process referred to as ovarian torsion, which occurs when the ovary twists on its supporting ligaments without involvement of the fallopian tube. On the other hand, the tube itself rarely rotates alone and instead often twists alongside the ovary.

As a little reminder, the ovary is suspended to the pelvic sidewall by the infundibulopelvic, or IP, ligament and to the uterus by the utero-ovarian ligament. Blood is supplied to the ovary from both the ovarian and uterine arteries. Now, if the ovary is enlarged, such as in the presence of a cyst, it may rotate on the axis of the two ligaments. Often, this occurs in ovaries measuring between 5 to 10 centimeters and occurs more frequently in the right adnexa, as the left adnexa has less space due to the presence of the sigmoid colon. 

Adnexal torsion can cause edema, venous congestion, and compression of blood vessels. The venous supply is compromised first, and with time, the arterial supply might be affected too. Adnexal torsion is a surgical emergency and requires urgent reversal of the torsion to prevent necrosis and loss of the ovary. 

When assessing a patient with a chief concern suggesting adnexal torsion, your first step is to perform a focused history and physical examination and obtain an hCG. The patient may report fever, nausea, and vomiting, as well as abdominal or pelvic pain. If pain is present, it is usually sudden, non-radiating, and intermittent in nature. On physical exam, you may note abdominal or pelvic tenderness, rebound pain or guarding, and possibly the presence of a pelvic mass. Lastly, hCG is typically negative.

Here’s a clinical pearl! While extremely rare, adnexal torsion can occur in a pregnant patient. The enlargement of the ovary due to the presence of the corpus luteum cyst and increased l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_dysplasia_of_the_hip:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YMs1ireSTaKx69wsu_idMilpQ7i_kx6Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developmental dysplasia of the hip: Clinical sciences]]></video:title><video:description><![CDATA[Developmental dysplasia of the hip, or DDH for short, is a condition associated with misalignment of the femoral head and acetabulum, which results in an unstable joint. 

Normally, the femoral head sits within the acetabulum, allowing both to grow together over the first few years of life to create a ball and socket joint. But, when the acetabulum is too shallow, the femoral head is unable to stay in place, and both of these bony structures grow independently. If this persists, eventually they will no longer fit together. 

It’s critical to screen all infants for DDH for early identification and treatment, as early treatment ensures better functional outcomes and reduces the risk of hip joint osteoarthritis. Screening for DDH is often done during well-child visits via the hip exam, which differs based on whether the child is younger or older than 6 months.

For infants under 6 months old, you should perform a thorough physical exam and check for any abnormalities on the hip exam using the Ortolani and Barlow maneuvers. Both maneuvers begin with the infant on their back with their hips flexed. The Ortolani maneuver involves slowly abducting the hip and then gently pressing upwards on the lateral thigh. 

If the femoral head is dislocated, the Ortolani maneuver will push the femoral head up and into the acetabulum, making a “clunk.” This is also known as the Ortolani clunk. On the other hand, the Barlow maneuver involves slowly adducting the hip and then gently pressing down on the knee. If there’s hip joint instability, the femoral head will be pushed down and out of the acetabulum, making a “click.” This is also called the Barlow click. 

If the infant’s hip exam is normal, meaning the Ortolani and Barlow maneuvers are negative, you should assess for DDH risk factors. These include a family history of DDH, as well as breech orientation during pregnancy but after 34 weeks of gestation, regardless if an external cephalic version was successful. 

If the inf]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Permanent_contraception_(sterilization):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z40upDtlSV2oeTAy0inVJi3wQyCKwROo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Permanent contraception (sterilization): Clinical sciences]]></video:title><video:description><![CDATA[Permanent contraception, or sterilization, refers to surgery that closes off or removes the fallopian tubes to prevent fertilization of an egg by sperm, thereby preventing pregnancy. Female sterilization can be achieved by occluding the fallopian tubes, removing a portion of the fallopian tubes, or removing the tubes entirely. It is a good option for patients who have contraindications or barriers to using other forms of contraception as well as those who do not wish to use other forms of contraception. 

When a patient presents for permanent contraception, your first step is to obtain a focused history. Assess the patient’s age, gravidity, and parity. Keep in mind that there is no minimum necessary age, number of pregnancies, or number of children required for a patient to undergo sterilization. 

Next, assess their medical and surgical history. Specifically ask about conditions such as endometriosis or a history of extensive surgery resulting in adhesions, which may distort the normal anatomy making a procedure technically more difficult. Finally, assess the patient’s preference for contraception. There are many reversible contraceptive options available, including long-acting reversible contraceptives or LARCs. Patients should never feel pressured or coerced into a permanent procedure such as sterilization. 

If the patient no longer desires permanent contraception, or remains unsure, do not proceed with permanent sterilization and instead counsel them on all available contraceptive options. On the flip side, if the patient continues to desire permanent contraception, your next step is comprehensive counseling.

You can begin by counseling on all contraceptive options available. Many patients are not aware of options beyond condoms and birth control pills. LARCs are just as effective as sterilization and provide patients with a good alternative to surgery. Some patients may also choose for their partner to undergo sterilization, which can be achieved vi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_primary_amenorrhea:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c51sgR0XSj_vVpYoaxq8B6sVRFWGmck4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to primary amenorrhea: Clinical sciences]]></video:title><video:description><![CDATA[Primary amenorrhea is defined as the absence of menses by age fifteen in a patient with normal growth and secondary sexual characteristics. However, the absence of menses by age thirteen in a patient without secondary sexual characteristics also requires evaluation. The most common causes of primary amenorrhea are genetic or anatomic, but it is also caused by pituitary or hypothalamic dysfunction. 

Once a diagnosis is established, psychosocial and emotional support are an essential part of patient care, as the treatment may be complex and lifelong, particularly if the underlying condition can not be corrected. 

When assessing a patient who presents with primary amenorrhea, your first step is to obtain a focused history and physical exam, as well as an hCG to asses for pregnancy. If the hCG is positive, the patient is pregnant, so that’s your diagnosis.

On the other hand, if the patient isn’t pregnant, your next step is to assess secondary sexual characteristics. Let’s say your patient is 13 years old but has not developed secondary sexual characteristics like breast development, defined as breast Tanner Stage 1, and pubic hair Tanner Stage 2 to 3. In this case, you can continue your evaluation with FSH level. 

Here’s a high-yield fact! Lack of breast development implies lack of estrogen, since estrogen is needed for thelarche, meaning breast development. So, estrogen is not being made either because the pituitary is not instructing the ovary to do so, or the ovary is not responding to it.

If the FSH is greater than twenty, the problem is likely gonadal. So, consider hypergonadotropic hypogonadism and order a chromosome analysis. 

If the genotype is 46,XX, think about ovarian dysfunction and obtain prolactin and estradiol levels. With normal prolactin and low estradiol, the diagnosis is primary ovarian insufficiency. 

Here is a clinical pearl! The etiology of primary ovarian insufficiency is often unknown but it is associated with other endocrinopath]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Building_Practice-ready_Confidence_with_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oQNOVHSXSFC_mlshL46VGzuMQ0KG72cE/_.png</video:thumbnail_loc><video:title><![CDATA[Building Practice-ready Confidence with Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Building Practice-ready Confidence with Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_suspected_bone_tumor_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RWnikDKpQDGfo8t8fDgKBfKwSzGCdXY2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a suspected bone tumor (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[A bone tumor is a growth or lesion of bone that can be malignant or benign. It’s important to recognize a bone tumor early to provide prompt life- and limb-saving treatment. 

History, physical exam, and imaging findings can be used to categorize bone tumors as high risk or low risk. High-risk bone tumors are likely to be aggressive and malignant and these include osteosarcoma, Ewing sarcoma, and aneurysmal bone cyst. 

On the flip side, low-risk tumors are more likely to be benign and these include osteoid osteoma, osteochondroma, and non-ossifying fibroma, as well as simple bone cyst and Langerhans cell histiocytosis.

Okay, if your patient is presenting with chief concerns suggesting a bone tumor, your first step is to obtain a focused history and physical. Your patient will typically be between 10 and 20 years old and report symptoms like localized bone pain, swelling, or even a mass. Sometimes, your patient might have a history of a pathologic fracture. 

On physical exam, you could notice a localized tenderness or a palpable mass, with or without a limited range of motion in the adjacent joint. With this spectrum of findings, you should consider a bone tumor, and order an X-ray.

Now here’s a clinical pearl to keep in mind! When evaluating a bone lesion on X-ray, you should consider its border, if it’s lytic or sclerotic, and the presence or absence of a periosteal reaction. 

Borders can be well-defined, suggesting a slow, localized process, or poorly defined, suggesting a more rapid, destructive process. The bone lesion itself can either be described as lytic, meaning it is bone-destroying and appears radiolucent on X-ray; or sclerotic, meaning it is bone-producing and appears radiodense on X-ray. 

Finally, the presence of a periosteal reaction, which refers to new bone production in the periosteum caused by irritation, suggests a more aggressive bone lesion. Periosteal reactions can range from mild, appearing as “onion skinning”, to a “sunburst” ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_fever_(0-60_days):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-Vfqqd3GR6GQ3bVP-wCKpJ6lR1qlB8Sc/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to a fever (0-60 days): Clinical sciences]]></video:title><video:description><![CDATA[Fever in infants 60 days of age and younger is defined as a body temperature of 38 degrees Celsius, or 100.4 degrees Fahrenheit, or higher. Infants in this age group have a higher risk of invasive bacterial infection, when compared with older infants, so it’s important to promptly identify and treat the source of a fever. Young infants can be stratified by age and initial lab findings in order to guide the subsequent diagnostic workup and determine the need for treatment.

If a patient 60 days of age or younger presents with a fever, you should first perform an ABCDE assessment. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, and consider starting IV fluids. Begin continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation, and provide supplemental oxygen  if needed. 

Okay, now let’s go back to the ABCDE assessment and look at stable patients. First, obtain a focused history and physical exam, and make sure to ask about exposure to sick individuals. Febrile infants often have vague symptoms, like fussiness, lethargy, and poor oral intake. Occasionally, caregivers might report symptoms that suggest a focus of infection, such as diarrhea, vomiting, cough, nasal congestion, or rash. Be sure to ask about perinatal and birth history. 

The physical exam will confirm a temperature of 38 degrees Celsius or higher, frequently with an elevated heart rate. Next, you might notice signs of respiratory distress, like nasal flaring, grunting, or retractions, as well as abnormal lung sounds, like crackles and wheezing. Finally, the abdomen exam might reveal distention or tenderness. The presence of a fever, with or without other findings, in an infant 60 days or younger, should make you suspect infection.

To search for a focus of infection, order basic labs, including a CBC, inflammatory markers such as CRP and procalcitonin, and a blood culture. In addition, send urine ob]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_tract_infection_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_8QW2a8qSHqxGpGZcD9ANQRSS6aGKyBD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary tract infection (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Urinary tract infection, or UTI for short, is a common bacterial infection in children that can involve any part of the urinary tract. In children, UTIs are usually caused by gastrointestinal flora, such as Escherichia coli, that ascend into the bladder or kidneys, causing cystitis, pyelonephritis, or even urosepsis. If not treated promptly, UTIs can result in long-term complications, such as renal scarring, hypertension, and chronic renal disease. The management of UTIs depends on the patient’s age; more specifically, whether they are less or more than 2 months old.

If a child presents with a chief concern suggesting a UTI, you should first perform an ABCDE assessment to determine whether the child is stable or unstable. If your patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, administer IV fluids, and start broad-spectrum antibiotics. Finally, begin continuous vital sign monitoring, including blood pressure, heart rate, respiratory rate, and oxygen saturation. If needed, don’t forget to provide supplemental oxygen. 

Okay, now let’s go back to the ABCDE assessment and take a look at stable patients. In this case, start by obtaining a focused history and physical exam. Next, assess the patient&amp;#39;s age, which will guide the treatment!

First, let’s take a look at term infants of 2 months of age and younger. These patients typically present with vague systemic symptoms, like fever, fussiness, and lethargy. Additionally, caretakers may report poor oral intake or vomiting, and they may describe the baby’s urine as foul-smelling. Next, the physical exam typically reveals an ill-appearing, uncomfortable infant with a body temperature of 38 degrees Celsius or higher. The physical exam could also reveal tachycardia and suprapubic tenderness. 

Based on these findings, you should suspect a UTI, so your next step is to order labs, which include CBC, CRP, procalcitonin, and urinalysis, as well as urine and blood ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intraamniotic_infection:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DBwLGa2_TFGZfvQAJv-nXGOfS3KqVALx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intraamniotic infection: Clinical sciences]]></video:title><video:description><![CDATA[Intraamniotic infection, commonly called chorioamnionitis, is an infection that causes inflammation of the amniotic fluid, placenta, decidua, fetus, fetal membranes, or any combination of these. 

It is usually caused by an ascending infection of polymicrobial bacteria, including both aerobic and anaerobic species, that are present in the vaginal flora. While both preterm and term pregnancies can be affected, it most commonly affects full term pregnancies and usually presents while patients are in labor. 

Intraamniotic infection is associated with an increased risk of both maternal and neonatal complications. Maternal complications include dysfunctional labor, postpartum uterine atony leading to hemorrhage, endometritis, peritonitis, sepsis, acute respiratory distress syndrome and, in some instances, death. In neonates, acute complications include pneumonia, meningitis, sepsis, and possibly death; as well as long-term complications such as bronchopulmonary dysplasia and cerebral palsy.

When assessing a patient who presents with a chief concern suggesting an intraamniotic infection, start with a focused history and physical exam. Patients may have one or more risk factors, including low parity, exposure to multiple digital examinations, use of internal monitors like an intrauterine pressure catheter or fetal scalp electrode, meconium-stained amniotic fluid, genital tract pathogens such as group B Streptococcus or a sexually transmitted infection, prolonged rupture of membranes, defined as greater than 18 hours, and prolonged labor. 

Next, evaluate your patient for intraamniotic infection.  This is done by checking your patient&amp;#39;s temperature, reviewing the fetal heart tracing, obtaining or reviewing a CBC, and performing a sterile speculum exam. 

A suspected intraamniotic infection is diagnosed clinically when a patient has either a one-time fever, with a temperature of at least 39.0 degrees Celsius; or an elevated temperature between 38.0 ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adenomyosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/URB67_oMRoSr0gMi0ZZcsbfNQs676pzR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adenomyosis: Clinical sciences]]></video:title><video:description><![CDATA[Adenomyosis is a condition characterized by abnormal growth of endometrial glands and stroma into the myometrium, often resulting in an enlarged and globular uterus. Although adenomyosis can occur at any age, it’s most commonly diagnosed in multiparous patients in their 30s and 40s. Diagnosis can be challenging as the symptoms often mimic those of other gynecological conditions, like endometriosis or uterine leiomyomas. Treatment options vary depending on the severity of symptoms and the reproductive goals of the patient. 

When a patient presents with a chief concern suggesting adenomyosis, start by obtaining a focused history and physical exam. Commonly reported symptoms include heavy menstrual bleeding, dysmenorrhea, or pain during menstruation, chronic pelvic pain, and possibly dyspareunia, which is pain during intercourse. On physical exam, you may note an enlarged or globular uterus and possibly uterine tenderness. Based on these findings, you can suspect adenomyosis. 

The next logical step is to confirm your diagnosis by obtaining some imaging studies. A pelvic ultrasound, incorporating both transvaginal and transabdominal views, is the first choice for identifying adenomyosis. In some situations, like when you need a more detailed look or an ultrasound can’t make the diagnosis, you can consider an MRI. 

Alright, characteristic findings on ultrasound include a heterogeneous myometrium with streaky shadowing, asymmetric myometrial thickness, and often you can see myometrial cysts. Sometimes, you will see only some but not all of these findings. In this situation, adenomyosis should be high on your differential, so proceed with this clinical diagnosis.  

Here’s a clinical pearl! The gold standard for diagnosis is histological examination of the uterus after hysterectomy. Obviously, this requires loss of the organ, so usually adenomyosis is clinically diagnosed unless hysterectomy is indicated.

Alright, now that we’ve confirmed the diagnosis o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_urinary_incontinence_(GYN):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6OXECyLaSbm8BxguBaw_mD74RcW_sbic/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to urinary incontinence (GYN): Clinical sciences]]></video:title><video:description><![CDATA[Urinary incontinence refers to the involuntary leakage of urine. This is a common problem that impacts both physical and psychological well-being. Often, patients do not disclose symptoms of urinary incontinence due to feelings of embarrassment, but these symptoms can adversely impact daily activities and diminish quality of life. Underlying causes of incontinence include pregnancy, childbirth, urinary tract infections, changes to the pelvic floor, or bladder dysfunction. It’s also associated with medical conditions such as diabetes or certain neurologic disorders, as well as physical immobility, or cognitive impairment. There are several categories of urinary incontinence including stress, urgency, mixed, overflow, and functional urinary incontinence.

When a patient presents with a chief concern suggesting urinary incontinence, the first step is to perform a focused history and physical examination and obtain an hCG to assess for pregnancy. If the hCG is positive you have a diagnosis. Urinary incontinence is common in pregnancy, mostly during the second and third trimesters due to increased pressure on the bladder and pelvic floor. Also, pregnant patients are at increased risk for asymptomatic bacteriuria and urinary tract infections, which can cause urinary leakage. 

After assessing for pregnancy, the next step is to assess for a urinary tract infection by obtaining a urinalysis. Now, it might come back positive for nitrites and leukocyte esterase, and possibly heme or blood. In this case, the patient will likely report an acute onset of incontinence. They may also report associated symptoms of dysuria, urinary frequency or urgency, and gross hematuria. The physical examination might reveal suprapubic tenderness. So, consider a lower urinary tract infection and send the urine for culture. If the culture is positive, you have made your diagnosis of a lower urinary tract infection.

Here is a clinical pearl! If urinary leakage persists after successful t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Well-child_visit_(newborn_and_infant):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S-gg0oR8Tx_VsG3i1Dgw0u4dTxa43JCc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Well-child visit (newborn and infant): Clinical sciences]]></video:title><video:description><![CDATA[Well-child visits promote the health and well-being of children from birth through adolescence. In the first year of life, each well-child visit starts with a comprehensive history and physical exam, followed by age-specific interventions and recommendations. 

Your goal at each well-infant visit is to provide age-appropriate screenings and immunizations; assess development; counsel on nutrition and oral health as indicated; and provide anticipatory guidance. 

When a newborn or infant presents for a well-child visit, your first step is to obtain a comprehensive history and physical examination. Be sure to review birth history, including gestational age, birth weight, and any pregnancy, delivery, or postpartum complications. You should also take an interval history, noting any health changes that may have occurred since the last office visit. 

Then, remember to ask caregivers if they have any concerns, as they are often the first to notice when something isn’t quite right. Finally, be sure to ask about social determinants of health, like tobacco exposure, intimate partner violence, or food insecurity; as well as protective factors such as social support and a positive caregiver-infant relationship.

Next, perform a physical exam, starting with an assessment of the infant’s general appearance. Then, perform a full body exam, paying close attention to fontanels, head shape, and muscle tone; and look for symmetric movement of all extremities. Also, don’t forget to check the red reflex, to assess for congenital cataract or tumor. Finally, review the patient’s growth chart, and track the infant’s length, weight, weight-for-length, and head circumference, over time.

Now, your next steps are determined by assessing your patient’s age. Let’s start with the first well-child visit, which occurs during the first week of life, often within 48 to 72 hours after discharge from the hospital. First, check the results of the bilirubin screening, and follow-up as needed. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Uterine_leiomyoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4DiLQVZZRJGTTQHpz2SqUKWmTvmYg2v_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Uterine leiomyoma: Clinical sciences]]></video:title><video:description><![CDATA[Uterine leiomyomas, also known as fibroids, are benign, solid neoplasms made up of smooth muscle cells and fibroblasts. They can vary in size and location in the uterus, including intramural that are found within the width of the myometrium; submucosal that grow towards the mucosa of the uterus; subserosal that are found near the outer layer or serosa of the uterus; and pedunculated fibroids that grow on a stalk out of the uterine walls, either inside and outside the uterus. 

Uterine leiomyomas are very common, and the majority of women have at least one by menopause. They are often asymptomatic, but symptomatic leiomyomas can cause a variety of issues, such as heavy bleeding and pelvic pressure or pain. In fact, leiomyoma is one of the important causes of abnormal uterine bleeding or heavy menstrual bleeding, which can be easily remembered with the mnemonic PALM COEIN. This stands for Polyps, Adenomyosis, Leiomyoma, Malignancy, Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, and Not yet classified. Additionally, leiomyomas can cause infertility in some patients, and depending on their location in the uterus, they can even be associated with recurrent pregnancy loss. 

When assessing a patient who presents with a chief concern suggesting they have a uterine leiomyoma, your first step is to obtain a focused history and physical. Patients may report prolonged or heavy menstrual bleeding; anemia; or symptoms of uterine enlargement such as pelvic pressure or pain, urinary frequency, and constipation. While obtaining a history, pay attention to certain risk factors for uterine leiomyomas, such as premenopausal status, a family history of leiomyomas, increasing interval since last birth, hypertension, and obesity. On a physical exam you may note an enlarged uterus or an irregular uterine contour.

Here’s a clinical pearl! Black individuals have a 2 to 3 times higher rate of having uterine leiomyomas compared to white individual]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endometriosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3s2wc7cuQBipFc1bxA7i9ltrRNW6Pacg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Endometriosis: Clinical sciences]]></video:title><video:description><![CDATA[Endometriosis is when endometrial stroma or glands are found outside of the endometrium. Normally, endometrial cells are only present within the endometrial lining of the uterine cavity, which thickens and sheds during each menstrual cycle. The exact cause of endometriosis is complex but there are three theories. 

First, it’s believed to be due in part to retrograde menstruation leading to attachment of endometrial glands and stroma to the peritoneum. Second, distant lesions might be established by the hematogenous or lymphogenous route. And third, the theory of coelomic metaplasia says that cells of the visceral and parietal peritoneum undergo metaplastic change into endometriotic lesions. Endometriosis is commonly diagnosed in reproductive-age biological women, specifically those with a history of chronic pain and infertility. 

Let’s dive into the steps to take when a patient presents with a chief concern suggesting endometriosis. The initial approach involves obtaining a focused history and physical exam as well as a pelvic ultrasound. Patients might report chronic pelvic pain; dysmenorrhea, meaning painful periods; menorrhagia, or heavy menstrual bleeding; as well as deep dyspareunia, or painful intercourse; low back pain during periods, and bowel and bladder symptoms like diarrhea and dysuria. An easy way to remember common symptoms of endometriosis is to think of the 4 Ds: dysmenorrhea, dyspareunia, dyschezia, and dysuria. 

Other common historical findings include infertility and a family history of endometriosis. In fact, patients with an affected first-degree relative have nearly a 7 to 10 times increased risk of developing endometriosis themselves! Additionally, risk factors for developing endometriosis include early menarche specifically occurring before age 11; shorter cycles, commonly less than 27 days; and heavy, prolonged periods. 

Here’s a clinical pearl! Be sure to rule out sexually transmitted infections like gonorrhea or chlamydia, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aortic_stenosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qrUjhc2YSg29F4B37x65cw0eTmqk02tO/_.png</video:thumbnail_loc><video:title><![CDATA[Aortic stenosis: Clinical sciences]]></video:title><video:description><![CDATA[Aortic stenosis is a type of valvular heart disease that occurs when the aortic valve narrows and prevents blood from flowing normally. Because the heart has to pump harder through a narrowed aortic opening there is a chronic pressure overload, which leads to left ventricular hypertrophy, reduced stroke volume, and left ventricular dysfunction. Symptoms involve the classic triad of chest pain, syncope, and heart failure. 

Alright, if a patient presents with a chief concern suggestive of aortic stenosis, you should first perform an ABCDE assessment to determine if they are stable or unstable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and start IV fluids for resuscitation. Finally, initiate continuous vital sign monitoring, including pulse oximetry, blood pressure, and heart rate. Your next step is to obtain a focused history and physical exam.  

When dealing with unstable patients with aortic stenosis, always think of cardiogenic shock. The patient might report a history of angina, shortness of breath, orthopnea, decreased exercise tolerance, and edema.  In addition, patients may have a history of heart failure or atrial fibrillation. On the other hand, the physical exam might reveal hypotension, tachycardia, and possible arrhythmia. The skin might appear cold, clammy, and pale due to heart failure.  

Your most important clue will come from auscultation. Here, you will notice a loud mid-late peaking systolic murmur in the second right intercostal space. Also, you might find an S4 heart sound due to pressure overload, or lung crackles, indicating edema. With these findings, suspect aortic stenosis.  

Okay, the next step is to order an ECG and transthoracic echocardiogram, which is vital in the management of aortic stenosis. ECG may show an arrhythmia like atrial fibrillation, or left ventricular hypertrophy.  On echo, you may find thickened aortic leaflets with or without calcification, redu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_interstitial_lung_disease_(diffuse_parenchymal_lung_disease):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RAo-TPbST_mYpZ2xJAg55ql4Tc_4Ro6S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to interstitial lung disease (diffuse parenchymal lung disease): Clinical sciences]]></video:title><video:description><![CDATA[Interstitial lung disease, or ILD, is a group of lung disorders that cause inflammation and scarring of the lung parenchyma.  

Based on the underlying cause, ILDs can be subdivided into four main categories: exposure-related ILDs, caused by inhaling harmful substances like asbestos;  

iatrogenic ILDs, which occur as a result of side effects from certain medications or radiation therapy;  

ILDs related to systemic diseases, seen in conditions like sarcoidosis;  and finally, idiopathic ILDs, where the causes are unknown, like idiopathic pulmonary fibrosis. 

Okay let&amp;#39;s begin our assessment of a  patient presenting with a chief concern suggesting ILD. First obtain a focused history and physical examination, as well as pulmonary function tests, or PFTs, and chest X-ray.  

Patients typically report shortness of breath on exertion, and chronic, dry cough.  

The physical exam might reveal wheezing, and diffuse inspiratory crackles.  There can also possibly be finger clubbing, cyanosis, and low oxygen saturation.  

You might also see signs of extrapulmonary systemic disease like polyarthritis or thickened skin, but that will depend on the cause of ILD. 

Here’s a clinical pearl! In ILD, patients often present with a normal oxygen saturation when they are at rest, which is about 95-100%, but it drops during physical activity as their body&amp;#39;s oxygen demand rises. So, if a patient initially shows normal oxygen saturation, test for exercise-induced hypoxemia by checking pulse oximetry while they ambulate. 

Next, PFTs typically reveal reduced diffusing capacity of the lungs for carbon monoxide and might show a restrictive pattern on spirometry.  

Finally, a chest X-ray might reveal diffuse bilateral reticular opacities, which appear net-like in texture,often in the lower and lateral lung zones. With these findings, consider ILD and order a high-resolution chest CT to confirm your diagnosis. 

On a chest CT, the main findings typically]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Disseminated_intravascular_coagulation:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F-h86F71RTWVmf00jS6SMp7WQHapcCHS/_.png</video:thumbnail_loc><video:title><![CDATA[Disseminated intravascular coagulation: Clinical sciences]]></video:title><video:description><![CDATA[Disseminated intravascular coagulation, or DIC for short, occurs when a trigger over-activates the coagulation and fibrinolytic cascades, leading to widespread thrombosis and organ ischemia. As DIC progresses, excessive bleeding occurs due to the consumption of platelets and coagulation factors. Based on the timing of onset, clinical presentation, and lab findings, DIC can be classified as acute and chronic. 

Now, if your patient presents with chief concerns suggesting DIC, you should first perform an ABCDE assessment to determine if the patient is unstable or stable.  

If the patient is unstable, stabilize the airway, breathing, and circulation, obtain IV access, and give IV fluids. Next, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if your patient is hypotensive, add vasopressors and if their saturation is low, don’t forget to provide supplemental oxygen to keep saturation above 90 percent.  

Now, once you stabilize your patient, obtain a focused history and physical examination.  Your patient is likely to report an acute onset of bleeding; and in some cases, they might report symptoms of thrombosis, such as sudden-onset dyspnea or limb pain. The sudden onset of dyspnea should make you suspect pulmonary embolism, while limb pain could be associated with limb ischemia due to thrombosis.  

Next, history will typically reveal a trigger like sepsis, trauma, malignancy, or obstetric complications, such as placental abruption and amniotic fluid embolism.  

The physical exam will reveal petechiae, purpura, and ecchymosis; and possibly evidence of thrombosis, such as limb swelling and redness. Additionally, you might find signs of underlying illness like fever, hypotension, and tachycardia; or findings consistent with organ dysfunction, like respiratory distress, jaundice, and decreased urine output.  

With these findings, you should suspect acute DIC, so your next step is to order]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Polycystic_ovary_syndrome_(PCOS):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZEOTlqWFS0mgIOE-dlFThmS3QXS7Rxwc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Polycystic ovary syndrome (PCOS): Clinical sciences]]></video:title><video:description><![CDATA[Polycystic ovary syndrome, or PCOS, is the most common endocrine disorder in reproductive-aged biological females and is characterized by a combination of anovulation, clinical or biochemical hyperandrogenism, and multiple small cysts in the ovaries. Additionally, a lot of patients with PCOS have some degree of metabolic abnormalities, such as insulin resistance. The anovulation and hyperandrogenism often result in additional symptoms in patients, ranging from amenorrhea to abnormal uterine bleeding, as well as infertility. So overall, management of PCOS focuses on addressing the key findings in each patient, whether that’s infertility, hyperandrogenism, or insulin resistance.  

Your first step in evaluating a patient who presents with a chief concern suggesting polycystic ovary syndrome is to obtain a focused history and physical exam. Individuals with PCOS typically report menstrual abnormalities. Be sure to ask about their menstrual history, including the length of their cycles from the first day of one period to the first day of the next, in the absence of hormonal contraception use. Typically, patients with PCOS will report signs of ovulatory dysfunction, meaning irregular menstrual cycles, which are either shorter than 21 days or longer than 35 days. 

Another common presentation is secondary amenorrhea, meaning the absence of menses for 3 or more consecutive months after menarche. Ovulatory dysfunction in PCOS can lead to female factor infertility, which might be the patient’s primary concern. Patients may also report the gradual onset of coarse dark hair growth in androgen-sensitive locations, such as the face, chest, back, and abdomen. This is characteristic of hirsutism related to PCOS. 

On physical exam, you may notice evidence of hyperandrogenism, including hirsutism, acne, and possibly androgenic alopecia. Your patient may also show signs of insulin resistance, such as elevated body mass index, or BMI, above 25, and centripetal fat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Right_heart_failure_(cor_pulmonale):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N0G_AVxiSv6W5mUCWgT9rrkRQaOAYtH5/_.png</video:thumbnail_loc><video:title><![CDATA[Right heart failure: Clinical sciences]]></video:title><video:description><![CDATA[Right heart failure occurs when the right side of the heart cannot function properly, resulting in elevated central venous pressure and impaired pulmonary circulation. Assessing for right heart failure involves reviewing your patient&amp;#39;s history and physical, lab results, performing an echocardiogram, and evaluating right and left heart catheterization findings. This helps to categorize it as right heart failure due to valvular disease, myocardial disease, or pulmonary hypertension. Keep in mind that right-sided heart failure secondary to pulmonary hypertension is also called cor pulmonale. 

Now, if your patient presents with a chief concern suggesting right heart failure, perform an ABCDE assessment to determine if they’re unstable or stable. If unstable, stabilize their airway, breathing, and circulation, which might require endotracheal intubation and mechanical ventilation.  

Next, obtain IV access and put them on continuous vital sign monitoring. Provide supplemental oxygen to maintain saturation above 90% and put your patient on cardiac monitoring. Finally, in some cases you might consider placing an indwelling pulmonary artery catheter, also known as a Swan-Ganz catheter, in order to obtain right sided filling pressures.  

Next, obtain a focused history and physical examination. Your patient may report shortness of breath and chest pain, while physical exam might reveal hypotension, tachycardia, diaphoresis, and cold extremities. You might also notice jugular venous distention with hepatojugular reflux and lower extremity edema. Cardiac exam typically reveals a right ventricular heave, loud P2, and right-sided S3. At this point, you should suspect cardiogenic or obstructive shock due to right heart failure!  

Here’s a clinical pearl! Cardiogenic shock could be due to an acute right ventricular myocardial infarction, acute right-sided valvular dysfunction, severe myocarditis, or cardiomyopathy. On the other hand, obstructive shock could re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Consumptive_coagulopathy_from_massive_transfusion:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lIcb3P4GSsymDzod23Tar-pSTWiiogSn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Consumptive coagulopathy from massive transfusion: Clinical sciences]]></video:title><video:description><![CDATA[Massive transfusion refers to the rapid administration of blood products to patients suffering from life threatening hemorrhagic shock or severe coagulopathy caused by trauma, major high risk operations, obstetric complications, or disseminated intravascular coagulopathy or DIC.  

Massive transfusion protocol, or MTP for short, is a systematic approach in providing a balance of blood products, such as packed red blood cells or PRBC, fresh frozen plasma or FFP, and platelets in a 1 to 1 to 1 ratio.  

Remember, platelets and fibrinogen play an important role in primary hemostasis by forming a platelet plug. Then, the clotting factors through the coagulation cascade help to form a blood clot to stop the bleeding. In the setting of massive hemorrhage, the body consumes as much of these factors as it can in an attempt to stop the bleeding. Without proper replacement, coagulopathy can worsen and become fatal very quickly.  

So, it’s very important to determine which factors are deficient so that proper balance of blood products can be given. Balanced transfusion decreases the risk of serious transfusion-related complications, such as consumptive coagulopathy; this occurs when one type of blood product is given in excess, causing dilution and consumptive depletion of platelets and clotting factors, and ultimately leading to worsening coagulopathy and bleeding.  

Now, when a patient presents with chief concerns suggestive of consumptive coagulopathy from massive transfusion, the first step is to perform a focused history and physical. Keep in mind that patients who are unstable, intubated, or have altered mental status might not be able to provide history. So, make sure to check their medical chart to determine the injury, estimated loss of blood, as well as the type and amount of blood products transfused.  

Typically, the history will include a recent massive transfusion, which may have been given following trauma, high-risk surgery like cardiac or aortic p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_adnexal_masses:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/atem81R7SveINIkuNCtruzC6Tuet_xrJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to adnexal masses: Clinical sciences]]></video:title><video:description><![CDATA[Adnexal masses arise from the ovary, fallopian tube, or surrounding tissues. They may be cystic or solid, simple or complex, unilateral or bilateral. Most of these masses are benign, but an important diagnostic goal is to rule out malignancy. There are many types of adnexal masses, ranging from simple functional ovarian cysts to ovarian malignancy. 

When a patient presents with an adnexal mass, the first step is to perform a CABCDE assessment. If the patient is unstable, control hemorrhage; stabilize airway, breathing, and circulation; obtain IV access; and monitor vital signs. Next, perform a focused history and physical examination, order an hCG to assess for pregnancy, and quickly obtain a pelvic ultrasound. 

If the hCG test is positive, think about a ruptured ectopic pregnancy. In this case, the history will reveal unilateral pelvic pain, and possibly vaginal bleeding. The patient may report a history of fallopian tube injury, such as prior pelvic inflammatory disease or tubal surgery, and may report a delayed or missed last menstrual cycle. The physical examination may include abdominal or pelvic tenderness with possible rebound pain and guarding, and possibly an adnexal mass. 

The ultrasound will demonstrate the absence of an intrauterine pregnancy and possibly an adnexal mass. In this case, consider an ectopic pregnancy and perform an operative laparoscopy. If on laparoscopy, you find an extrauterine pregnancy with bleeding or a ruptured fallopian tube, as well as intraperitoneal blood and clot, the diagnosis is a ruptured ectopic pregnancy. 

As a clinical pearl: remember that methotrexate is contraindicated in unstable patients!

Okay, if the hCG is negative in unstable patients, they might have an adnexal torsion or a ruptured hemorrhagic cyst. The patient may report fever, nausea, and vomiting. The physical exam will reveal abdominal tenderness with possible rebound pain or guarding, and possibly a pelvic mass. 

The ultrasound will show]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ovarian_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZZONBUDURgyvIk02UHKgTa3tTE_fmgXt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Ovarian cancer: Clinical sciences]]></video:title><video:description><![CDATA[Ovarian cancer is the second most common gynecologic cancer after endometrial cancer, and the leading cause of gynecologic cancer death. The three main types of ovarian cancer are germ cell tumors which arise from primordial germ cells; sex cord or stromal cell tumors that arise from supporting tissues of the ovary; and epithelial cell tumors, which come from the mesothelium that covers the ovary. 

The majority of ovarian malignancies are epithelial cell tumors, which primarily occur in older patients. Due to their vague symptoms, they are usually diagnosed at a later stage. Germ cell and sex cord or stromal cell tumors commonly occur among younger patients. They might produce hormones that cause symptoms of pregnancy, precocious puberty, abnormal bleeding, or virilization; and are therefore diagnosed at an earlier stage. 

When a patient presents with a chief concern suggesting ovarian cancer, the first step is to perform a focused history and physical examination. Patients often report a history of abdominal or pelvic pain or bloating, and possibly a decrease in appetite, early satiety, or a change in bowel habits. The physical examination reveals an abdominal, pelvic, or adnexal mass and sometimes abdominal or pelvic tenderness, or abdominal distension. With these findings, suspect an adnexal mass and obtain a pelvic ultrasound. 

Here’s a clinical pearl! When reproductive-age patients present with abdominal or pelvic symptoms, be sure to assess for pregnancy with an hCG. Keep in mind that some germ cell tumors produce hCG which may result in a false positive pregnancy test. Also, a diagnosis of pregnancy does not exclude malignancy.

Okay, if the ultrasound reveals a thin, anechoic, smooth walled cyst that is less than 10 centimeters without septations, internal blood flow, or solid components, the probable diagnosis is a benign adnexal mass. In this case, manage the patient expectantly with serial ultrasounds. However, if the patient has severe or pe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_anemia_in_the_newborn_and_infant_(destruction_and_blood_loss):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mIcmlMQdRwCc4xpMlT0PMu4VQ_miO1Ck/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to anemia in the newborn and infant (destruction and blood loss): Clinical sciences]]></video:title><video:description><![CDATA[Anemia is a condition characterized by a decrease in healthy red blood cells, as indicated by low hemoglobin and hematocrit, or a low red blood cell count. Based on the underlying cause, anemia can be classified as anemia due to red blood cell underproduction, or due to red blood cell destruction or loss. 

Now, if a pediatric patient presents with a chief concern suggesting anemia, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, give IV fluids, and if necessary, consider blood products, such as packed red blood cells. Don’t forget to put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and provide supplemental oxygen if needed.

Here’s a clinical pearl! When a patient with anemia is unstable, be sure to look for active bleeding due to trauma, as well as signs of internal bleeding such as hematochezia, melena, or hematuria.

Now, let’s go back to the ABCDE and look at stable patients. First, obtain a focused history and physical examination and order labs, including CBC with indices, and a reticulocyte count. History might reveal symptoms like fatigue, malaise, or dyspnea; while the physical exam might demonstrate tachycardia, pallor, jaundice, or scleral icterus. Hepatosplenomegaly may also be present. 

Next, check the CBC, and if results reveal a low hemoglobin and hematocrit for gestational and postnatal age, you can diagnose anemia. 

Now, once you diagnose anemia, your next step is to assess the reticulocyte count. Reticulocytes are immature red blood cells produced by the bone marrow. If the reticulocyte count is below the reference range, then the bone marrow isn’t producing enough red blood cells to meet the body’s demand. In such cases, you can diagnose anemia due to red blood cell underproduction.

On the other hand, a reticulocyte count above the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_anemia_in_the_newborn_and_infant_(underproduction):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gHQU5s9aTjSAEP26G_UVuYuXQsaybjaR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to anemia in the newborn and infant (underproduction): Clinical sciences]]></video:title><video:description><![CDATA[Anemia is a condition characterized by a decrease in healthy red blood cells, or RBCs, indicated by low hemoglobin and hematocrit or a low RBC count. Based on the mean corpuscular volume, or MCV for short, anemia can be classified as microcytic, normocytic, or macrocytic.

When a pediatric patient presents with a chief concern suggesting anemia, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and give IV fluids. Next, place  your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry; and, if indicated, consider transfusion of blood products, such as packed RBCs. If needed, provide supplemental oxygen to maintain oxygen saturation above 90%.

Here’s a clinical pearl! When a patient with anemia is unstable, be sure to look for active bleeding due to trauma, as well as signs of internal bleeding such as hematochezia, melena, or hematuria.

Now, let’s go back to the ABCDE and look at stable patients. First, obtain a focused history and physical examination and order labs, including CBC with indices, and a reticulocyte count. History could reveal symptoms like fatigue, malaise, palpitations, or dyspnea; while the physical exam might demonstrate tachycardia or pallor. Next, check the CBC, and if results reveal a low hemoglobin and hematocrit for gestational and postnatal age, you can diagnose anemia.

Alright, your next step is to assess the reticulocyte count. A reticulocyte count above the reference range indicates the body is actively producing new RBCs, which is suggestive of anemia due to RBC destruction, like hemolysis; or blood loss, like hemorrhage.

On the other hand, a reticulocyte count within or below the reference range is suggestive of anemia due to RBC underproduction. In this case, your next step is to classify the anemia based on the size of the RBCs, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Iron_deficiency_and_iron_deficiency_anemia_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y5tQmkQtThGk3gGaJQJ2DckxQ9aIRKSz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Iron deficiency and iron deficiency anemia (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Iron deficiency is a condition that occurs when the body lacks sufficient iron for normal growth, development, and production of enough healthy red blood cells. Iron plays a vital role in the production of hemoglobin, which is the protein responsible for carrying oxygen in red blood cells. Consequently, when iron levels are low, the body is unable to produce an adequate amount of hemoglobin, leading to impaired red blood cell production. You can differentiate between iron deficiency without anemia and iron-deficiency anemia by examining your patient’s laboratory results.

Now, if a pediatric patient presents with a chief concern suggestive of iron deficiency or iron-deficiency anemia, first, you should obtain a focused history and physical examination. The history typically reveals vague symptoms like fatigue, lightheadedness, low muscular endurance, and palpitations, which manifest as a compensatory response to inadequate tissue oxygen supply. 

Caregivers may also report behavior changes, such as poor concentration or irritability, as well as pica, which is the compulsive consumption of non-nutritive substances like dirt or ice. Finally, keep in mind iron deficiency risk factors, like heavy menstrual bleeding, exposure to lead, certain chronic conditions, low dietary iron intake, and active participation in athletics. Additionally, the physical exam might reveal tachycardia and tachypnea. You may also notice pallor, which is most often visible in the conjunctivae, lips, and nail beds. Other common findings include brittle nails and koilonychia, characterized by nails that are concave or spoon-shaped. Finally, you might notice glossitis, which is a smooth and glossy tongue, as well as angular stomatitis, which refers to inflammation and cracking at the corners of the mouth. 

Now, here’s a clinical pearl to keep in mind! Certain medications can potentially result in iron deficiency, such as nonsteroidal anti-inflammatory drugs or NSAIDs, which can increas]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_skin_and_soft_tissue_lesions:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X6jWNfHuSH_Xyf3Zkxp5K84ZQq_NkNGf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to skin and soft tissue lesions: Clinical sciences]]></video:title><video:description><![CDATA[Skin and soft tissue lesions are dermatological abnormalities that look different from the surrounding skin in terms of color, size, or texture. 

Most skin and soft tissue lesions are benign. However, some can be malignant or premalignant, so it&amp;#39;s important to have a high clinical suspicion for any patient presenting with a new lesion. 

Alright, your first step in evaluating a patient who presents with a skin or soft tissue lesion is to obtain a focused history and physical exam to help differentiate between a benign or a malignant lesion. If, on history, the patient reports a slow growing asymptomatic lesion with minimal changes over time that doesn’t bleed easily, and a physical exam reveals that it’s symmetrical in color, shape, and structure, consider benign lesions.

Now, let&amp;#39;s dive into our first diagnosis, a benign vascular lesion. Patients often report a mass or a lump that had an early onset in the first few months of life. They might have associated congenital syndromes like Sturge-Weber Syndrome. 

On examination, you might find a salmon-colored patch, port-wine stain, strawberry or bright cherry red dome-shaped papules or macules that are blanchable when you press on them. These lesions are usually located on the trunk, face, or upper extremities. 

If these are your findings, you are dealing with a benign vascular lesion.  Examples of benign vascular lesions include hemangioma, arteriovenous malformations, or pyogenic granuloma. 

Most vascular lesions tend to decrease in size as the patient gets older, so they usually don’t need any treatment. If there are aesthetic concerns, you can offer topical agents like timolol, silver nitrate, or in some cases laser ablation or surgical excision.

Alright, let&amp;#39;s talk about another group of benign lesions: cysts and lipomas. History will reveal solitary, or multiple, slow growing lesions. Moving on to the physical exam.

Skin cysts are divided into two types: epide]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_vulvar_skin_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iGhMiZWiQWOM7iAHO7P-DN8YTraV8Rmf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to vulvar skin disorders: Clinical sciences]]></video:title><video:description><![CDATA[Many vulvar skin disorders are chronic and may adversely affect sexual function and the patient’s overall sense of well-being. There are a wide variety of skin conditions associated with vulvar skin disorders that can be related to infectious, inflammatory, or neoplastic processes. 

When a patient presents with a vulvar skin disorder, the first step is to perform a focused history and physical examination. Let’s start with contact dermatitis. The patient will present with the acute onset of vulvar itching, burning, and irritation. They will also report exposure to a vulvar irritant or allergen such as scented soaps or body wash, laundry detergent, condoms, topical medications, or vaginal hygiene products. 

The physical examination will reveal varying degrees of erythema, and might show excoriations of the vulva or vaginal discharge. In this case, consider contact dermatitis. Then perform potassium hydroxide and saline wet mount microscopy of the vaginal discharge. 

If the microscopy demonstrates mature squamous cells and lactobacilli and is negative for motile trichomonads or pseudohyphae, you have ruled out vulvovaginal candidiasis or vaginal trichomoniasis and have made a diagnosis of contact dermatitis. 

Next up is lichen simplex chronicus. Patients typically report symptoms of intense pruritus with scratching and rubbing that may even cause sleep disturbance. They might also have a history of an allergic condition such as seasonal allergies, asthma, or childhood eczema. In addition, they may reveal an exposure to a vulvar irritant or allergen. 

The physical exam will show erythematous, lichenified plaques; possibly scaling and excoriation; thickened, leathery skin; erosions; ulcers; and vaginal discharge. With these findings, consider lichen simplex chronicus. 

Perform potassium hydroxide microscopy and perhaps a vulvar biopsy. The microscopy may reveal pseudohyphae, indicating underlying vulvovaginal candidiasis, and if the vulvar biopsy demonst]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_rash_in_the_well_newborn_and_infant:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/owg1qbZdRrC9Z7zo0b51QZETTq2KhQi-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a rash in the well newborn and infant: Clinical sciences]]></video:title><video:description><![CDATA[Rashes in well-appearing newborns and infants are usually benign and self-limited. These rashes can be associated with factors like hormonal shifts, immature circulation, and environmental exposures; but occasionally rashes have no apparent cause. Newborn and infant rashes can be categorized by age of onset and by rash appearance and distribution.

Now, if a well-appearing newborn or infant presents with a rash, first, you should obtain a focused history and physical exam and assess your patient’s age at the onset of the rash.

Let’s start with rashes that appear before 1 week of age. In this case, your next step is to assess the rash’s appearance. 

First, let’s take a look at newborns with skin peeling. In this case, you should consider physiologic desquamation. 

While most newborns experience mild skin peeling, more extensive skin peeling is seen in post-term neonates. Physical exam reveals desquamation primarily on the hands and feet, and it may extend to the limbs or trunk, especially if your patient is post-term. With these findings, you can diagnose physiologic desquamation. This benign and self-limited skin condition represents the natural shedding of the outer skin layer and requires no treatment.

Alright, let’s move on to rashes that present with transient color changes. In this case, you should assess the rash’s pattern of distribution. 

First, if the color change is unilateral, you should consider a harlequin color change. 

Caregivers may report a sudden onset of redness occurring exclusively on one side of the body, which resolves within 20 minutes. During the physical examination, place the infant on their side, and you may observe unilateral erythema of the dependent side, with a clear demarcation along the midline. Based on these findings, you can diagnose harlequin color change. Although the color change appears dramatic, this phenomenon is benign, self-limited, and does not require intervention.

Here’s a clinical pearl to keep in min]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_diarrhea_(chronic):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oFHhicanTvSG4bd0HTLYfxq_QSSAEQkV/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to diarrhea (chronic): Clinical sciences]]></video:title><video:description><![CDATA[Chronic diarrhea is defined as more than three loose stools per day for at least four weeks. Now, based on the underlying cause, chronic diarrhea can be divided into several types, including steatorrhea, secretory, osmotic, inflammatory, dysmotile, and iatrogenic diarrhea. 

Now, if your patient presents with chronic diarrhea, first, obtain a focused history and physical examination.  Your patient will typically report having more than 3 loose stools per day, or a significant change in stooling habits for at least 4 weeks. In some cases, your patient might report abdominal pain. Physical examination may reveal abdominal tenderness and hyperactive bowel sounds. 

With these findings, you should suspect chronic diarrhea, so your next step is to assess the type of chronic diarrhea. To do so, order labs, which could include CBC with differential, CMP,  vitamins including A, D, B12, and K, along with iron and calcium levels. You could also order inflammatory markers, such as ESR and CRP, as well as TSH and a tissue transglutaminase IgA test. Lastly, other helpful stool studies include stool electrolytes, fecal fat content, occult blood, and tests for fecal calprotectin or lactoferrin.  

Now, here’s a clinical pearl! Keep in mind that the labs you choose to order in a particular situation will depend on the history and physical examination. For example, if your assessment findings suggest inflammatory diarrhea, you’ll need to order fecal calprotectin or lactoferrin. These are proteins found in neutrophils, which are released during cell lysis, and their detection in stool samples indicates an inflammatory process in the gastrointestinal tract. 

First, let’s focus on individuals with steatorrhea! In this case, your patient will often describe their stool as greasy, foul-smelling, and difficult to flush. They might also report increased flatus and weight loss. Labs typically reveal low levels of albumin, vitamins A, D, B12, and K, along with low iron and calcium]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_group_A_streptococcal_infections_and_sequelae_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TTHm88MpRu_atgSCDilRU4vUTnGYgFsa/_.png</video:thumbnail_loc><video:title><![CDATA[Acute group A streptococcal infections and sequelae (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Streptococcus pyogenes, also called group A Strep or GAS for short, is a toxin-producing bacterium that can cause various upper respiratory, skin, and soft tissue infections, as well as associated sequelae. These include life-threatening conditions like streptococcal toxic shock syndrome, or STSS; as well as less severe conditions, like impetigo, erysipelas, cellulitis, pharyngitis, or scarlet fever. GAS is also known to cause clinical sequelae such as poststreptococcal glomerulonephritis and acute rheumatic fever.

Now, if your patient presents with a chief concern suggesting a GAS infection or its sequela, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation; obtain IV access, and consider starting IV fluids. Next, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, and if needed, provide supplemental oxygen! Finally, if your patient’s condition permits, don’t forget to obtain a blood culture, as well as a wound culture if a wound is present. Then, start broad-spectrum intravenous antibiotics right away! 

Now, here’s a high yield fact! Patients with GAS infections may present as unstable for a number of reasons. One you should especially consider is toxic shock syndrome due to GAS. This is often associated with some sort of strep infection, such as cellulitis or a recent strep pharyngitis, as well as vital sign instability, skin desquamation, and possibly necrosis. 

If you suspect toxic shock syndrome, provide supportive care, consult surgery to debride any necrotic tissue, and treat with antibiotics that have activity against GAS. These antibiotics should include clindamycin or linezolid because they have an antitoxin effect. Also keep in mind that some patients are so sick that you may even consider additional treatment with intravenous immunoglobulins.

Okay, now let’s go back to the ABCDE assessment a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meningitis_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZGXSQnrTQ9OMcMsWQYX-YQFySTqTwudC/_.png</video:thumbnail_loc><video:title><![CDATA[Meningitis (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Meningitis refers to the inflammation of the meninges, which are protective membranes that surround the brain and spinal cord. Meningitis commonly occurs as a result of bacterial infection. In newborns, the most frequent causative pathogens include Group B streptococci, Escherichia coli, and Listeria monocytogenes; while in children and teens, more common causes include Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis. Finally, if there are no bacteria, consider aseptic forms of meningitis, such as viral meningitis!

Now, if your patient presents with a chief concern suggesting meningitis, perform an ABCDE assessment to determine whether the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, start IV fluids, and put the patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen.

Now, let’s go back and take a look at stable patients. First, assess your patient’s age, since the diagnostic evaluation and management are age-dependent. The main cut-off is at age 60 days.

Let’s start with patients 60 days of age and younger. Start by obtaining a focused history and physical exam. History typically reveals non-specific symptoms, such as fussiness, inconsolability, sleepiness, weakness, or even apnea. Additionally, caretakers might report vomiting, poor feeding, and, in some cases, even seizures. The physical exam typically reveals temperature instability, poor tone, irritability when moved, and lethargy. In some cases, you might notice increased head circumference, as well as full or bulging anterior fontanelle. 

At this point, you should suspect meningitis! Begin your diagnostic workup by ordering labs, including blood cultures, a CBC, and inflammatory markers, including CRP and procalcitonin. Additionally, perform lumbar puncture to obtain CSF for analysis,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pharyngitis,_peritonsillar_abscess,_and_retropharyngeal_abscess_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tk75GKBHR32rXPZLSZqh7ESVTRaN0S8T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pharyngitis, peritonsillar abscess, and retropharyngeal abscess (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Pharyngitis, or simply inflammation of the pharynx, can be caused by non-infectious conditions, like allergic rhinitis, as well as viral and bacterial infections. Pharyngitis is a common pediatric condition that’s easy to treat, but, in rare cases, it can progress to complications, such as peritonsillar or retropharyngeal abscess.

Now, if your patient presents with chief concerns suggesting pharyngitis, peritonsillar abscess, or retropharyngeal abscess, first perform an ABCDE assessment. If the patient is unstable, stabilize their airway, breathing, and circulation; obtain IV access; and consider starting IV fluids. Next, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen.

Now here’s a clinical pearl to keep in mind! Audible stridor and stertor are highly suggestive of airway obstruction, so, in this case, be sure to examine your patient in the operating room in case you need to establish an artificial airway emergently!

Okay, now let’s go back and take a look at stable patients. In this case, you should first obtain a focused history and physical examination. These individuals usually report a sore throat that may or may not be associated with odynophagia and fever. On the exam, you will find pharyngeal erythema, and you may also detect tonsillar exudates as well as cervical lymphadenopathy. With this combination of findings, you can diagnose pharyngitis.

Your next step is to assess the underlying cause. Patients with noninfectious causes of pharyngitis may report rhinorrhea, nasal congestion, sneezing, and coughing, but they don’t have fever, and they don’t feel acutely ill. On exam, the posterior pharynx may have a cobblestone appearance, and the nasal mucosa may appear boggy and pale. These findings are highly suggestive of noninfectious pharyngitis, which is most commonly due to allergic rhinitis or gastroesophageal reflux i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pneumonia_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gywdL7iYQpa6CnbTUFf-ING4RhiE7uvE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pneumonia (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Pneumonia is an infection of the lower respiratory tract that involves the airways and surrounding lung tissue. In all age groups, one of the most common causes of pneumonia is Streptococcus pneumoniae. Other common causes include viruses in young infants, and atypical organisms such as Mycoplasma pneumoniae and Chlamydophila pneumoniae in children ages 5 and older. 

When a pediatric patient presents with a chief concern suggesting pneumonia, first, perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation, and you may even need to intubate your patient. Next, obtain IV access, and consider starting IV fluids. Begin continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring, and administer supplemental oxygen as needed. Finally, administer empiric antibiotics early on.

Now, let’s go back to the ABCDE assessment and take a look at stable patients. In this case, first, obtain a focused history and physical exam, and measure your patient’s oxygen saturation using pulse oximetry. 

Infants and children with pneumonia commonly present with fever and a cough. The physical exam usually reveals an elevated respiratory rate and an increased work of breathing, with nasal flaring or grunting commonly seen in young infants, as well as intercostal or subcostal retractions in all age groups. Meanwhile, auscultatory findings may include crackles, rhonchi, or decreased breath sounds, and pulse oximetry might show an oxygen saturation below 90%. A combination of these findings should make you suspect pneumonia. 

The next step is to assess the criteria for hospitalization, which include an age less than 6 months, oxygen saturation below 90%, respiratory distress or signs of dehydration, an ill or toxic appearance, if the patient is unable to maintain oral hydration, if they’ve already received and failed outpatient treatment, or social facto]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_joint_pain_and_swelling:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nwZ9KHvAQqmx9vXXAcR2TlvHRlSdwivg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to joint pain and swelling: Clinical sciences]]></video:title><video:description><![CDATA[Joint pain and swelling are common patient concerns that stem from a range of conditions affecting ligamentous, cartilaginous, or bony structures. Based on the underlying cause, joint pain and swelling can occur in combination or separately, and can be associated with traumatic and non-traumatic causes. Moreover, based on the duration of symptoms, non-traumatic conditions can be further subdivided into acute and chronic.  

Now, if your patient presents with joint pain and swelling, perform a focused history and physical examination.  

Your patient will report joint pain and their physical exam will usually reveal edema, erythema, and warmth over the affected joints, as well as joint line tenderness. Additionally, they might have an effusion, limited range of motion, or associated crepitus. These findings are suggestive of arthralgia or arthritis. 

Your next step is to assess for trauma.  If your patient presents shortly after an obvious mechanism of injury, such as a motor vehicle collision or sports accident, and has exam signs that suggest trauma, like ligamentous laxity or  joint deformity, consider traumatic joint injury, order imaging, primarily an X-ray of the affected joint! Additionally, if you suspect internal derangement of soft tissue, order an MRI! If imaging confirms the presence of a fracture, dislocation, or soft-tissue derangement, diagnose a traumatic joint injury!  

On the other hand, if there’s no evidence of joint trauma, assess the duration of symptoms.  

If your patient is presenting with acute joint pain, meaning less than 6 weeks, assess the underlying cause!  

Here’s a clinical pearl! When approaching a patient with painful joints, consider ordering inflammatory markers, such as ESR and CRP because elevated levels support the diagnosis of underlying infectious and inflammatory causes.  

First up is septic arthritis!  In this case, history typically reveals fever and malaise, with a possible history of immunosuppression ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Septic_arthritis_and_transient_synovitis_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XOckM0znSeyncIHrnNndXkfNRjihF4x3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Septic arthritis and transient synovitis (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Septic arthritis is a bacterial infection of the synovium and joint space, while transient synovitis, also called toxic synovitis, refers to a non-infectious synovial inflammation. While transient synovitis is a benign and self-limited illness, it’s crucial to identify and treat septic arthritis promptly to prevent permanent bone and joint damage. 

When a pediatric patient presents with a chief concern suggesting septic arthritis or transient synovitis, first perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, consider starting IV fluids, and put your patient on continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring. Finally, if needed, don’t forget to provide supplemental oxygen and administer broad-spectrum intravenous antibiotics.

Now, let’s go back to the ABCDE assessment and take a look at stable patients. In this case, obtain a focused history and physical exam; and order labs, including CBC, CRP, and ESR. 

First, let’s focus on septic arthritis! Affected children typically experience a rapid onset of monoarticular joint pain and swelling that most commonly involves a large joint in a lower extremity, such as the knee or hip. Caregivers also often report systemic symptoms, like fever, malaise, or decreased appetite. 
Some ambulatory children may develop a limp, but most will refuse to bear weight on the affected limb. Finally, infants and non-ambulatory children may display “pseudoparalysis,” which is an inability to move the affected joint due to pain. 

On physical exam, patients are usually ill-appearing, with signs of inflammation, including erythema, warmth of the skin overlying the affected joint, and joint effusion. Patients classically display limited range of motion in the affected joint, and those with hip involvement typically prefer to keep their hips flexed, abducted, and ext]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_lower_airway_obstruction_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y8sINV2IRXOIjol2cAaUSYXeS0yBwLoS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to lower airway obstruction (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Lower airway obstruction occurs when any part of the airway below the thoracic inlet is blocked or narrowed, resulting in flow limitation and expiratory prolongation. Clinically, this typically presents with symptoms related to lung overinflation and air trapping, such as wheezing and a prolonged expiratory phase. Underlying causes of lower airway obstruction can be differentiated by the symptom onset as well as an assessment of triggers. 

Now, if your patient presents with a chief concern suggesting lower airway obstruction, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. You might even need to intubate your patient. Additionally, obtain IV access, and begin continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring. Finally, if needed, don’t forget to provide supplemental oxygen. Once you stabilize the patient, obtain a focused history and physical examination.

Unstable presentation is typically associated with anaphylaxis. In this case, history usually reveals a rapid onset of facial swelling and dyspnea, without a fever. They may also have a known allergy with exposure to a specific food like peanuts or another allergen like insect venom. Physical exam may reveal hypotension with audible stridor and wheezing. Additionally, you may notice facial edema and a diffuse urticarial rash. These findings are highly suggestive of anaphylaxis. 

Now, let’s return to the ABCDE assessment and go over stable patients. Again, obtain a focused history and physical exam and check the patient’s pulse oximetry. Patients often report difficulty breathing and may have a cough. 

Physical exam findings might include tachypnea and signs of labored breathing, like suprasternal, intercostal, and subcostal retractions, while lung auscultation commonly reveals wheezing. Finally, in some cases, oxygen saturation might be below 90%. With these]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_upper_airway_obstruction_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M_ji75ybQDKfTEkCP5hdGtnsSiinFMWm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to upper airway obstruction (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Upper airway obstruction occurs when any part of the airway above the thoracic inlet is blocked. 

Based on the site of obstruction, upper airway obstruction can be subdivided into nasopharyngeal, supraglottic, glottic, subglottic, and tracheal.

If your patient presents with a chief concern suggesting upper airway obstruction, first perform an ABCDE assessment to determine if your patient is unstable or stable.

If unstable, stabilize their airway, breathing, and circulation. In some cases, you might need to intubate your patient or even place a surgical airway emergently. Next, obtain IV access and put your patient on continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring. Finally, if needed, don’t forget to provide supplemental oxygen.

Once you stabilize the patient, obtain a focused history and physical exam to determine the underlying cause.

First, let’s start with epiglottitis. In this case, your patient’s caregiver will usually report a rapid onset of high fever, as well as difficulty breathing and swallowing, with drooling and the absence of a cough. The physical exam typically reveals an anxious-appearing child sitting upright with their neck extended in a tripod position, with the chin pushed forward. Additionally, your patient may have a muffled voice, audible stridor with labored breathing, and a cherry-red epiglottis! These findings are highly suggestive of epiglottitis.

Here’s a clinical pearl! If the findings don’t clearly point to epiglottitis, you can order a lateral neck X-ray. If imaging reveals a “thumb sign” and swelling of the aryepiglottic folds, you can confirm the diagnosis of epiglottitis.

Next up is bacterial tracheitis.

These patients might have a recent history of a viral upper respiratory infection, with rapid onset of high fever, hoarseness, progressive stridor, and respiratory distress that’s not responsive to nebulized racemic epinephrine. 

Additionally, physical exam reve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bronchiolitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ToUHWpiaR_uajEnRQFH9rDj8RKmLFuU-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Bronchiolitis: Clinical sciences]]></video:title><video:description><![CDATA[Bronchiolitis refers to a viral infection of the lower respiratory tract that primarily affects the bronchioles, and causes airway inflammation and obstruction. This is most often caused by respiratory syncytial virus, or RSV for short, but can also be caused by other viruses, including human metapneumovirus and parainfluenza. Bronchiolitis primarily affects children under 2 years of age, most often during fall and winter months, and it’s typically mild and self-limited, but infants with certain risk factors can develop severe respiratory distress. As far as the treatment goes, bronchiolitis can be managed in the outpatient or hospital setting.

If your patient presents with a chief concern suggesting bronchiolitis, first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Additionally, obtain IV access and  put your patient on continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring. Finally, if needed, don’t forget to provide supplemental oxygen.

Now, let’s go back to the ABCDE assessment and take a look at stable patients. In this case, you should first obtain a focused history and physical exam. Your patient is likely to be under 2 years of age; with a history of illness that started with milder symptoms, such as fever and rhinorrhea for the first three days, followed by worsening of symptoms like respiratory distress. It’s important to note that a young infant under 2 months of age could present with apnea as their first sign, in the absence of any other symptoms! 

Physical exam typically reveals labored breathing, tachypnea, and hypoxia. You may detect nasal flaring or grunting, as well as abdominal breathing or suprasternal, intercostal, and subcostal retractions; while auscultatory findings may include wheezing, crackles, and a prolonged expiratory phase. Infants with poor oral intake may have signs of dehydrati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_vomiting_(newborn_and_infant):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7bvMcKgYQ92ievo8ba_krkBtS9iWSvFn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to vomiting (newborn and infant): Clinical sciences]]></video:title><video:description><![CDATA[Vomiting, also known as emesis, is defined as the forceful expulsion of gastrointestinal contents, and is a common symptom caused by a wide variety of underlying conditions. Based on the vomitus characteristics, vomiting can be described as bilious or non-bilious. 

Now, if a newborn or infant presents with vomiting, perform an ABCDE assessment to determine if the patient is unstable or stable.  If unstable, stabilize their airway, breathing, and circulation; obtain IV access, and if needed, provide IV fluids. Next, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, and if needed, provide supplemental oxygen.  

You may also need to make your patient NPO and insert a nasogastric tube to decompress the stomach and prevent further vomiting. Finally, if you suspect an underlying infection, don’t forget to start broad-spectrum antibiotics. 

Now, here’s a clinical pearl! Infants who are unstable and present with vomiting may have peritonitis, intestinal perforation, or shock, especially if there’s also abdominal distension or tenderness. In addition to acute management, consult your surgical team for consideration of an emergent laparotomy, and consider starting broad spectrum IV antibiotics.  

Now, let’s go back to the ABCDE assessment and take a look at stable patients presenting with vomiting. Start by obtaining a focused history and physical examination. Next, assess for bilious emesis, which caregivers may describe as green or bright yellow. It’s critical to identify bilious emesis quickly, as it suggests an intestinal obstruction that requires emergency surgical intervention!  

Okay, first, let’s focus on nonbilious emesis. In this case, your next step is to assess for projectile vomiting. If your patient has non-projectile vomiting, assess the onset of vomiting, which could be either sudden or gradual. In this context, a sudden onset means that vomiting developed quickly over the course of 2]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Well-child_visit_(toddler_and_child):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FLFBvGYYQcWiCPoF4ODZ9l30QmKzc3iD/_.png</video:thumbnail_loc><video:title><![CDATA[Well-child visit (toddler and child): Clinical sciences]]></video:title><video:description><![CDATA[Well-child visits promote the health and well-being of children, from birth through adolescence. For toddlers and children, each well child visit starts with a comprehensive history and physical exam, followed by anticipatory guidance and age-specific developmental assessments, interventions, and recommendations.

Now, when a pediatric patient presents for a well child visit, you should start by obtaining a comprehensive history and physical exam. Review the birth and interval histories, including any health changes since their last visit; and ask the caregiver if they have questions or concerns about the child. As far as the physical exam goes, first consider the patient’s general appearance, and then perform a full body exam, including a chaperoned genitourinary exam starting around age 7 or 8.

Your next step is to review the patient’s growth chart, which includes trends in the height, weight, and calculated body mass index, or BMI. Remember to also review blood pressure measurements starting at 3 years of age, and the results of vision screenings or hearing screenings. 

For vision screening, you can begin instrument-based testing at 1 year of age, until chart-based acuity testing can be started from 3 years on; while hearing screening begins at 4 years of age.

Finally, you should assess puberty-related changes, using the sexual maturity rating, or SMR, which is also called Tanner staging. SMR is used to track the development of secondary sex characteristics, starting with Stage 1, which is prepubertal, and ending at Stage 5, which is complete sexual maturity. The Tanner scale consists of two independent criteria, including the appearance of pubic hair in both sexes; and either the increase in testicular volume and penis size and length in biological males; or the breast development in biological females.

Okay, once you complete your comprehensive history and physical exam, your next step is to provide anticipatory guidance. 

Start by recommending b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Well-child_visit_(adolescent):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_gvsDNXNTQqxmDhEQP4iiAPgTTiI6RaN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Well-child visit (adolescent): Clinical sciences]]></video:title><video:description><![CDATA[The well-child visits for an adolescent between 11 and 21 years of age is a yearly check-up that promotes physical, mental, and social health while building trust between caregivers, adolescents, and the healthcare provider. Each visit includes a comprehensive history and physical exam, followed by an interview about general self-care, administration of immunizations; and finally, a one-on-one interview with the adolescent, using the “HEADSSS” assessment.

When a pediatric patient presents for an adolescent well child visit, begin with a comprehensive history and physical exam. First, review the interval history, taking note of any changes in health since the last office visit; and ask the family or caregiver to share any questions or concerns they might have. During the physical exam, first, consider the patient’s general appearance and then perform a full body exam, including chaperoned genitourinary and breast exams, if applicable. 

Next, review the patient’s growth chart, which trends the height, weight, and calculated body mass index, or BMI; and don’t forget to measure the blood pressure to screen for hypertension. Adolescents also receive routine hearing screens once between 11 to 14 years, once between 15 to 17 years, and once between 18 to 21 years of age , and vision screens at 12 and 15 years of age.

Finally, you should assess puberty-related changes using the sexual maturity rating, or SMR, which is also called Tanner staging. SMR is used to track the development of secondary sex characteristics in biologically male and female patients.

Now, here’s a high yield fact! SMR starts with Stage 1, which is prepubertal, and ends at Stage 5, which is complete sexual maturity. This scale consists of two independent criteria, including the appearance of pubic hair in both sexes; and either the increase in testicular volume and penis size and length in biological males; or the breast development in biological females.

Okay, your next step is to talk t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_milestones_(newborn_and_infant):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RV-CJgX6SViBEktCMIVv7au7Siy-aBSm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developmental milestones (newborn and infant): Clinical sciences]]></video:title><video:description><![CDATA[Developmental milestones during the first years of life are crucial for lifelong development and learning. These milestones are functional skills that follow a predictable sequence by specific ages, and are divided into five major categories: gross motor development, which relates to the movement of large muscles; fine motor development, which relates to the movement of small muscles; cognitive development, which covers reasoning, memory, and problem-solving; social-emotional development, which describes attachment to and interactions with others; and finally, language development, which covers both receptive and expressive communication. 

Understanding normal developmental milestones will help you recognize when a child could be at risk for a developmental delay. Early intervention services can then be implemented to improve developmental outcomes.

When an infant presents for assessment of their developmental milestones, you should begin your examination with a focused history and physical exam. During the history portion, be sure to review birth history, including gestational age and birth weight; and remember to ask about family history of developmental delays. You should also take an interval history by asking the family what new skills their baby has learned since the last clinic visit. Additionally, ask the caregiver if they have any concerns about their baby’s development; since they spend the most time with their baby, they are often the first to notice when something isn’t quite right. 

Now, here’s a clinical pearl to keep in mind! If the caregiver has a concern about their baby’s development, that’s a red flag; so, during your assessment, pay special attention to the caregiver’s concern!

The examination is also an opportune time for you to see first-hand what the baby can do. During your exam, take some time to play with the baby. A playful and interactive exam is entertaining for the infant and gives you a snap-shot of the baby’s development]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_milestones_(toddler):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tkzLEKKlQ5ulMAHRYDTMgg28QaSr5urK/_.png</video:thumbnail_loc><video:title><![CDATA[Developmental milestones (toddler): Clinical sciences]]></video:title><video:description><![CDATA[Developmental milestones are behaviors and functional skills that children are expected to acquire by a specific age. These milestones are typically achieved in a predictable sequence and are divided into five major categories: gross motor development, which relates to the movement of large muscles; fine motor development, which relates to the movement of small muscles; cognitive development, which includes reasoning, memory, and problem-solving; social-emotional development, which describes attachment to and interactions with others; and finally, language development, which consists of receptive and expressive communication. 

Understanding normal developmental milestones will help you recognize when a child is at risk for a developmental delay that would benefit from a more detailed evaluation and early intervention services, such as physical, occupational, or speech-language therapy. 

Now, when a toddler presents for assessment of their developmental milestones, first, you should obtain a focused history and physical exam. During the history, be sure to review birth history, including gestational age and weight at birth, since prematurity and low birth weight are associated with developmental delays. Also, ask whether there is a family history of developmental delays, as some developmental disorders have  a genetic component. You should also take an interval history to determine what new skills the toddler has learned since the last clinic visit. 

Now, here’s a clinical pearl to keep in mind! Caregivers spend the most time with their toddler and are often the first to notice when something isn’t quite right. Whenever a caregiver is concerned about their child’s development, that is a red flag, so be sure to investigate further!

When it comes to the physical exam, you should check reflexes, assess muscle tone, and test their balance. You should also observe how the child interacts with their caregiver, the world, and with you, as this can help you gau]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Developmental_milestones_(childhood):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DkDKzB_LSrOiUC1_7yafchGKS6mYnSBY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Developmental milestones (childhood): Clinical sciences]]></video:title><video:description><![CDATA[Developmental milestones are behaviors and functional skills that children are expected to acquire by a specific age. These milestones are typically achieved in a predictable sequence and are divided into five major categories: gross motor development, which relates to the movement of large muscles; fine motor development, which relates to the movement of small muscles; cognitive development, which includes reasoning, memory, and problem-solving; social-emotional development, which describes attachment to and interactions with others; and finally, language development, which consists of receptive and expressive communication.

Your overall goal is to assess the child’s developmental milestones according to their age, using the caregiver’s report as well as direct observation. Understanding normal developmental milestones will help you recognize when a child is at risk for a developmental delay that would benefit from a more detailed evaluation and early intervention services. 

Now, when a pediatric patient presents for assessment of their developmental milestones, first, obtain a focused history and physical exam. During the history, be sure to review birth history, including gestational age and birth weight, as both prematurity and low birth weight are associated with developmental delays. 

Also ask about family history of developmental delays, as some developmental disorders such as autism spectrum disorder have a genetic component. You should also take an interval history to determine what new skills the child has learned since the last clinic visit. 

Additionally, observe the interactions between the child and their caregiver, and ask the caregiver if they have any concerns about their child’s development.

Now, here’s a clinical pearl to keep in mind! Caregivers spend the most time with their child and are often the first to notice when something isn’t quite right. Whenever a caregiver is concerned about their child’s development, be sure to invest]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Reversible_contraception:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4i_Jj_ZVTkqejOd00ImM5rC-RvO2ZPrx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Reversible contraception: Clinical sciences]]></video:title><video:description><![CDATA[Reversible contraception refers to any method of pregnancy prevention that doesn’t impact future fertility. Options for reversible contraception include hormonal birth control pills, patches, vaginal rings, and injections; long-acting-reversible-contraceptives, or LARC’s, such as implants and IUDs; and non-hormonal, non-LARC options like spermicides, fertility awareness, withdrawal and barrier methods. All individuals who desire contraception should be offered comprehensive counseling, with a focus on their values, preferences, and lived experiences. Shared decision-making is recommended when providing care to help individuals achieve their reproductive goals. 

When a patient presents for reversible contraception, start with a focused history and physical exam. First, assess your patient’s preference and provide patient-centered contraceptive counseling. Be sure to incorporate a reproductive justice framework, which is focused on the understanding that all people have a fundamental right to bodily autonomy, to have or not have children, and to parent their children in safe and sustainable communities. Part of acknowledging this framework is awareness of the systemic and structural barriers that people of different descent, low incomes, mental illness, and incarceration have been subject to throughout history. Specifically, marginalized groups have undergone contraceptive experimentation without informed consent, government-sponsored forced sterilization, and other mistreatment. 

As such, counseling should be viewed as an opportunity to review your patient&amp;#39;s individual values, preferences, and lived experiences, in an open and safe environment. Additionally, take time to reflect and recognize any of your own unconscious or explicit biases that may influence the efficacy of your counseling. Finally, be sure to incorporate shared decision-making into your practice.

Next, assess your patient&amp;#39;s medical eligibility criteria, or MEC, for]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunizations_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D69Hi9yWSVuUn3FEhrNYwdCwQnCB1NZm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunizations (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Immunizations promote immunity by activating the adaptive immune system to produce microbe-specific antibodies. These circulating antibodies protect against infection by binding to invading microbes and disabling them. 

Based on standardized schedules, routine vaccinations are performed during well-child visits at specific ages. You should keep in mind some special considerations that may arise, such as international travel or an immunocompromised status, that may alter the usual sequence of immunization. Families will often have questions or concerns about vaccines, and you play an important role in providing education about vaccine safety and benefits!

Now, in order to determine which vaccine to give, first you need to assess your patient’s age. At birth, infants should receive their first dose of the hepatitis  B vaccine within 24 hours of life, to prevent vertical transmission from mother to baby. 

Hepatitis B immunization also protects against acute and chronic hepatitis B infection, which is a known cause of liver disease; hepatocellular carcinoma; and liver failure. 

Here’s a clinical pearl! For infants weighing less than 2 kilograms at birth, delay their first dose of the hepatitis B vaccine until 1 month of age, or until discharged from the hospital, as long as the maternal status for hepatitis B surface antigen, or HBsAg for short, is negative. 

On the other hand, in cases where the maternal HBsAg status is positive or unknown, administer hepatitis B immune globulin, or HBIG, plus a dose of the hepatitis B vaccine within 12 hours of birth. Remember, though, this dose shouldn’t count as part of their vaccine series. In other words, this patient will receive three additional doses of the hepatitis B vaccine, for a total of four doses!

Next up are vaccines given at 2 months of age. First, all infants should receive their second dose of the Hepatitis B vaccine. 

Next, they should receive their first dose of the rotavirus vaccine. This vaccine ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cardiovascular_disease_screening:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IVjTbklvSZ_1A8fNHTgTyy9JRvWcK0N1/_.png</video:thumbnail_loc><video:title><![CDATA[Cardiovascular disease screening: Clinical sciences]]></video:title><video:description><![CDATA[Cardiovascular disease screening plays a significant role in preventive healthcare and early intervention for patients with atherosclerotic cardiovascular disease, or ASCVD for short. ASCVD is associated with plaque build-up within arterial walls that can eventually rupture and result in blood clot formation. These blood clots can partially or completely obstruct the blood flow to downstream tissues, eventually causing tissue ischemia or infarction. Because the plaque develops over time, there is an opportunity to intervene before symptoms appear or a major adverse event occurs, such as myocardial infarction or stroke. The ASCVD screening helps determine the risk in adult individuals with no symptoms or history of ASCVD to determine their risk of future cardiovascular events.

Alright, when your patient presents for cardiovascular disease screening, first, assess your patient’s risk factors. The first risk factor to consider is age. While there is no specific age cutoff that defines an increase in ASCVD risk, it is accepted that the older the patient, the higher the risk. Race also has a significant impact on ASCVD risk. For example, Black individuals carry more than double the risk of death from cardiovascular events compared to white individuals. Next, biologically male individuals have a higher risk than biologically female individuals due to the protective effects of estrogen. This protection lasts until biologically female individuals reach menopause, at which point, their risk is higher than males. Individuals with a history of tobacco use or who are currently using tobacco are also at greater risk of ASCVD due to the chemicals in cigarettes that damage arterial vessel lining. 

Other conditions that carry an increased risk for ASCVD include hypertension, diabetes mellitus, and dyslipidemia. 

Now, here’s a clinical pearl! Don’t forget other risk factors like family history of premature cardiovascular disease, obesity, and a sedentary lifestyle. Non-]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Primary_biliary_cholangitis_and_primary_sclerosing_cholangitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ntevaMKrQQWcpJmnWSPqbYx5QVigmlbW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Primary biliary cholangitis and primary sclerosing cholangitis: Clinical sciences]]></video:title><video:description><![CDATA[Primary biliary cholangitis, or PBC, and primary sclerosing cholangitis, or PSC, are immune-mediated cholestatic liver diseases associated with inflammation and destruction of bile ducts. 

Although these disorders present with common clinical features, PBC affects biological females more and targets small intrahepatic bile ducts; whereas PSC occurs more frequently in biological males and is characterized by damage of medium to large extrahepatic and intrahepatic bile ducts. 

Ultimately, both conditions can lead to subsequent bile leakage into the liver parenchyma. Over time, this can result in liver complications, such as liver fibrosis and cirrhosis. Now, primary biliary cholangitis and primary sclerosing cholangitis can be differentiated based on right upper quadrant imaging findings.

Okay, if a patient presents with chief concerns suggesting primary biliary cholangitis or primary sclerosing cholangitis, your first step is to perform a focused history and physical exam. History typically reveals symptoms such as severe fatigue and pruritus, but some individuals might also report right upper quadrant pain. Additionally, there might be a history of autoimmune conditions like inflammatory bowel disease or Sjögren syndrome. 

The physical examination might reveal jaundice and skin excoriations due to severe pruritus; as well as yellowish skin deposits of cholesterol called xanthomas, which, when present around the eyelids, are called xanthelasmas. In advanced cases, you might find hepatomegaly, splenomegaly, and, if the synthetic function of the liver is severely compromised, you might notice ascites and peripheral edema! 

With these findings, you should suspect liver disease, so your next step is to order labs to differentiate hepatocellular disease and cholestatic liver disease. However, it’s important to note that it’s not all black and white, and some liver diseases can have mixed features of both hepatocellular and cholestatic disease.

Okay, s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Systemic_sclerosis_(scleroderma):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wqVwdiPsRs_LZZJD3_0O0IP9Rb6HxrFA/_.png</video:thumbnail_loc><video:title><![CDATA[Systemic sclerosis (scleroderma): Clinical sciences]]></video:title><video:description><![CDATA[Systemic sclerosis, also known as scleroderma, is a chronic connective tissue disorder characterized by microvascular damage and fibrosis in various organs and tissues, including the skin. When damage is limited to the skin, that’s simply called scleroderma, which is the hallmark feature of the disease. Based on the pattern of skin fibrosis, systemic sclerosis can be categorized as limited cutaneous, which is the more common type, and diffuse cutaneous systemic sclerosis. However, when the disease affects the skin and the internal organs, it’s called systemic sclerosis, and it can affect any organ system.

When a patient presents with a chief concern suggesting systemic sclerosis, the first step is to obtain a focused history and physical exam. Most patients with systemic sclerosis are biological females. They usually report hand swelling and pain. Patients often experience Raynaud phenomenon, which is a condition that affects blood flow, usually in the fingers and toes. When exposed to  cold temperature or emotional stress, the blood vessels narrow, leading to reduced blood supply to certain areas, causing them to turn white or blue and feel cold and numb. Once the circulation improves, the affected areas might turn red and tingle, before going back to normal. Additionally, patients might have gastrointestinal symptoms related to acid reflux, like heartburn and voice hoarseness.

Physical examination reveals skin thickening, also known as scleroderma. There might also be sclerodactyly, which refers to the hardening of the skin of the hands, causing the fingers to flex inward. Some patients might also have digital ulcerations, and telangiectasia, which refers to dilated blood vessels visible under the skin.

With these findings, you should suspect systemic sclerosis. To confirm the diagnosis, you need to order labs, including an antinuclear antibody, or ANA for short, as well as anticentromere, anti-topoisomerase, and anti-RNA polymerase III antibodie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cushing_syndrome_and_Cushing_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FFsq9HV0TjWlipHtxJnkepMUSt2j2P4A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cushing syndrome and Cushing disease: Clinical sciences]]></video:title><video:description><![CDATA[Cushing syndrome refers to a combination of clinical features and symptoms that arise as a result of long-term exposure to high glucocorticoid levels in the blood. Based on the underlying cause, Cushing syndrome can be iatrogenic, which occurs from exogenous administration of glucocorticoids; ACTH-independent, which is specific to adrenal cortisol hypersecretion; and ACTH-dependent, which can be due to either ectopic ACTH secretion by non-pituitary tumors or excessive pituitary ACTH secretion.  

Moreover, Cushing syndrome caused by excessive secretion of ACTH by pituitary adenoma is called Cushing disease! 

Now, if your patient presents with a chief concern suggesting Cushing syndrome, the first step is to obtain a focused history and physical examination as well as labs, including a basic metabolic panel or BMP.  

High glucocorticoid levels in the blood affect almost every system in the body, so your patient will have various clinical manifestations. For example, history will often reveal central nervous system symptoms, such as irritability and depressed mood; as well as metabolic conditions, like glucose intolerance or diabetes mellitus. Next, high glucocorticoid levels can suppress gonadotropin secretion, so your patients might report symptoms involving the reproductive system, like decreased libido and amenorrhea.  

The physical exam reveals the glucocorticoid effects on fat redistribution and findings like central obesity, moon facies or round face, and “buffalo hump”, which refers to fat accumulation on the back of the neck. Additionally, you might notice skin changes, such as thin skin, acne, hirsutism, and purple and broad abdominal striae!  

Next, let’s take a look at cardiovascular findings! Normally, the kidneys inactivate cortisol by converting it into cortisone, which cannot bind mineralocorticoid receptors and exert cardiovascular effects.  

But, in Cushing syndrome, there’s too much cortisol, so the kidneys are unable to inactivate ev]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_leukemia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GVB3le7OTOekXLsR3QQsrr4QTrCqMYya/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to leukemia: Clinical sciences]]></video:title><video:description><![CDATA[Leukemia is a blood malignancy characterized by an abnormal proliferation or differentiation of hematopoietic cells. These malignant cells build up and gradually replace healthy blood cells, causing a decline in normal white and red blood cells, and platelets.  

Leukemia can be categorized as either acute or chronic and is further differentiated based on whether it originates from myeloid or lymphoid cells. Thus, there’s four main types: acute myeloid leukemia or AML, acute lymphoblastic leukemia or ALL, chronic myeloid leukemia or CML, and chronic lymphocytic leukemia or CLL. 

Here’s your first clinical pearl! The most common types of leukemia in children are ALL and AML, but CML and CLL are rare in this age group.  

Now, if your patient presents with a chief concern suggesting leukemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and start IV fluids. Next, put your patient on continuous vital sign monitoring, including pulse oximetry, blood pressure, and heart rate. Finally, if needed, don’t forget to provide supplemental oxygen and start broad-spectrum intravenous antibiotics. 

Once you stabilize the patient, your next step is to rule out common oncologic emergencies, including tumor lysis syndrome, febrile neutropenia, leukostasis, and disseminated intravascular coagulation or DIC!  

Tumor lysis syndrome occurs when a large number of tumor cells break down over a short period of time and release intracellular contents into the bloodstream.  

This can occur spontaneously or in the setting of chemotherapy and other interventions.  

Patients will report a rapid onset of symptoms, within hours to days; including fever, bone pain, easy bruising or bleeding, or night sweats.  

Physical exam will usually reveal tachycardia, low blood pressure, pallor, and generalized weakness.  

Other findings may include severe mucosa]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immune_thrombocytopenia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Hj0z9vjwRuCQf8FHPTO1jryQQiKcL47G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immune thrombocytopenia: Clinical sciences]]></video:title><video:description><![CDATA[Immune thrombocytopenia, or ITP for short, is an autoimmune condition characterized by a dysregulated immune system that produces autoantibodies against platelets. As a result, platelets are coated by these antibodies and marked to get destroyed by macrophages in the spleen and liver. Additionally, these autoantibodies damage megakaryocytes, preventing the bone marrow from pumping out more thrombocytes and compensating for the loss. 

Now, based on the underlying cause, ITP can be classified as primary ITP, which has no identifiable trigger, or secondary ITP, which can occur as a result of medication side effects and infections, as well as immunodeficiency  or autoimmune conditions. Regardless of the type, this is a diagnosis of exclusion, meaning you should first rule out other potential causes of thrombocytopenia to diagnose ITP!

Now, if your patient presents with a chief concern suggesting ITP, first, perform an ABCDE assessment to determine if they are unstable or stable. 

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and start IV fluids. Once other conditions are ruled out and diagnosis of ITP is confirmed, start immediate treatment with glucocorticoids, such as prednisone, which inhibit the production of anti-platelet autoantibodies. 

Next, you should always give intravenous immunoglobulins, or IVIG IVIGs, which bind and inactivate antibodies already present in the circulation, thereby preventing the coating of platelets and subsequent platelet destruction by macrophages. Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and if needed, don’t forget to transfuse blood products, such as packed red blood cells and platelets.

Now here’s a clinical pearl! Unstable patients with ITP might present with hypotension from hemorrhagic shock, so you must quickly locate the source of bleeding in order to stabilize the patient! Some clues to look]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pulmonary_transfusion_reactions:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6LbIMEFmTLmEnyjVLoAd7o9bTRak17EQ/_.png</video:thumbnail_loc><video:title><![CDATA[Pulmonary transfusion reactions: Clinical sciences]]></video:title><video:description><![CDATA[A pulmonary transfusion reaction refers to an acute lung injury within 6 hours of a blood product transfusion that results in pulmonary edema and respiratory distress. Now, based on the underlying mechanism, there are two main types of pulmonary transfusion reactions! The first one is a nonimmunologic reaction called transfusion-associated circulatory overload, or TACO for short. TACO occurs due to volume overload and subsequent increase in hydrostatic pressure that eventually leads to cardiogenic pulmonary edema. 

The second type refers to an immune-mediated reaction called transfusion-related acute lung injury, or TRALI for short. In TRALI, the donor’s blood products usually contain anti-leukocyte antibodies that bind the recipient leukocytes and cause an inflammatory reaction. This ultimately results in endothelial damage, capillary leakage, and eventually noncardiogenic pulmonary edema, often also associated with fever and hypotension.

Okay, if a patient presents with a chief concern suggesting a pulmonary transfusion reaction, first, you should perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation and stop transfusion! If your patient is hypotensive, start intravenous fluids for volume resuscitation and consider vasopressors. Next, provide supplemental oxygen to maintain oxygen saturation. In severe cases, you might need to intubate the patient and put them on mechanical ventilation. Finally, put your patient on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry. 

Here’s a clinical pearl to keep in mind! Unstable patients with rapidly progressive dyspnea and bilateral pulmonary edema have a wide differential diagnosis. While a recent blood product transfusion may point you in the direction of a pulmonary transfusion reaction, be sure to consider similar clinical presentations, such as acute respirator]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_insipidus:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2Jf74ZZhSeO5rgJvbssAIRNTSVOdU0aR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes insipidus: Clinical sciences]]></video:title><video:description><![CDATA[Diabetes insipidus, or DI for short, is a type of polyuria-polydipsia syndrome, meaning increased fluid intake and urination, specifically resulting in more than 3 liters per day of dilute urine. The most common cause of polyuria-polydipsia syndrome is diabetes mellitus; but three other causes include diabetes insipidus, which can be central or nephrogenic; and primary polydipsia. In central DI, the pituitary doesn’t make enough vasopressin, also called antidiuretic hormone or ADH for short, which normally increases water reabsorption in the kidneys;  while with nephrogenic DI, the kidneys don’t respond to vasopressin.  

Finally, in primary polydipsia, there’s increased fluid intake, which naturally suppresses vasopressin secretion.  

Now, if your patient presents with a chief concern suggesting diabetes insipidus, first, perform an ABCDE assessment to determine if they’re unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen. 

Now, here’s a clinical pearl! In most cases, patients with diabetes insipidus can compensate for the fluid loss through increased fluid intake. However, individuals who aren’t able to drink fluids, like those with impaired regulatory thirst mechanisms or impaired consciousness, can develop severe dehydration and hyperosmolality! Severe dehydration can cause hypotension, renal hypoperfusion, subsequent tubular necrosis, and even shock.  

On the flip side, hyperosmolality leads to an osmotic shift of intracellular fluid toward the extracellular space, causing neurons in the brain to become dehydrated. Eventually, this causes various neurologic manifestations, including irritability, seizures, and even coma. Now, let’s go back to the ABCDE assessment and take a look at stable patients.  

In this case, obtain a foc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stevens-Johnson_syndrome_and_toxic_epidermal_necrolysis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HFklTkMeTkC7xRYHyYw8rfSaRUikMg3P/_.png</video:thumbnail_loc><video:title><![CDATA[Stevens-Johnson syndrome and toxic epidermal necrolysis: Clinical sciences]]></video:title><video:description><![CDATA[Stevens-Johnson syndrome, or SJS, and toxic epidermal necrolysis, or TEN for short, are rare immune-mediated mucocutaneous conditions characterized by widespread blistering and sloughing. The exact cause of these conditions is still not fully understood, but it is thought to involve type 4 hypersensitivity against certain antigens, including different medications and pathogens. Now, Stevens-Johnson syndrome is associated with less than 10% of epidermal detachment, while in TEN, there&amp;#39;s more than 30% of the skin affected. Finally, the Stevens-Johnson syndrome-TEN overlap describes epidermal detachment of more than 10% but less than 30%.

Now, if your patient presents with a chief concern suggesting Stevens-Johnson syndrome or TEN, first, perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation; obtain IV access, and start IV fluids. Next, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, provide supplemental oxygen to maintain oxygen saturation greater than 90%, and don’t forget to discontinue suspected triggering medications. 

Here’s a clinical pearl! In severe cases, Stevens-Johnson syndrome and TEN can cause extensive skin damage, which can leave your patient vulnerable to severe dehydration, electrolyte imbalances, severe pain, infections, and hypothermia. Because of that, these severe cases are often managed in a burn intensive care unit. It’s important to make sure that your patient is properly hydrated and provide them with pain relief medications, like acetaminophen and opioids. Additionally, encourage sterile handling of the patient to prevent secondary infection and ensure that they’re in a warm area to prevent hypothermia.

Now, let’s return to the ABCDE assessment and take a look at stable patients. In this case, obtain a focused history and physical exam. Your patient will typically repor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_peripheral_lymphadenopathy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j7CFYHJYTF6sZjJfUTmRfoe9R02MtoPQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to peripheral lymphadenopathy: Clinical sciences]]></video:title><video:description><![CDATA[Peripheral lymphadenopathy refers to enlarged peripheral lymph nodes that may have an abnormal consistency. Enlarged lymph nodes are generally defined as 1 cm or larger; however, some lymph nodes are considered abnormal if they’re larger than 5 mm, like those in the supraclavicular, epitrochlear, or popliteal regions. The timing of symptom onset and the characteristics of the lymphadenopathy are helpful in distinguishing peripheral lymphadenopathy due to infection or malignancy, as well as immunologic or inflammatory conditions. 

If your patient presents with peripheral lymphadenopathy, first perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and begin continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry. Provide supplemental oxygen, if needed. 

Okay, let’s go back to the ABCDE assessment.  If your patient is stable, first obtain a focused history and physical exam. Patients may report feeling a mass or a lump, and they might have a fever.  Physical exam typically reveals enlarged, palpable lymph nodes, usually in the region of the neck, axilla, or groin. These lymph nodes might also be painless or tender to palpation;  mobile or fixed to surrounding tissue; or soft or hard in consistency. Lymph nodes may also become matted, meaning that they’re joined together so they feel connected when palpated. If you encounter enlarged lymph nodes with an abnormal consistency, diagnose peripheral lymphadenopathy! 

Here’s a clinical pearl! Localized or regional lymphadenopathy is limited to one area of the body, whereas generalized lymphadenopathy occurs in two or more non-contiguous lymph node groups. Look for other areas of enlarged lymph nodes if you encounter localized lymphadenopathy; and if otherwise asymptomatic, reexamine in 3 to 4 weeks. On the other hand, generalized lymphadenopathy should always prompt ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrapartum_care_(1st,_2nd,_3rd,_and_4th_stages):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mjqxTTOhRfi6DxAt5X_FFPJ8QZyA2ZWf/_.png</video:thumbnail_loc><video:title><![CDATA[Intrapartum care (1st, 2nd, 3rd, and 4th stages): Clinical sciences]]></video:title><video:description><![CDATA[Intrapartum care of a pregnant patient encompasses all things related to labor, delivery, and the immediate postpartum period. This period spans the first stage of labor, which begins with the onset of labor and ends with complete cervical dilation; the second stage, which starts with complete cervical dilation and ends with delivery of the neonate; the third stage, which begins with the delivery of the neonate and lasts until delivery of the placenta; and the fourth stage, which is the immediate postpartum period. While it’s important to recognize when interventions are needed during the normal, physiologic processes of labor and delivery, it’s equally important to be aware that for the majority of patients, interventions are not essential and therefore, the focus should be on patient-centered care.

Your first step when a laboring patient presents for intrapartum care includes a focused history and physical exam, assessment of fetal presentation, and monitoring of fetal heart rate and uterine contractions. Here, you should identify risk factors relevant to labor and the postpartum period. Next, assess the fetal presentation, either by ultrasound or, if cervical dilation is adequate, by digital palpation of the presenting part, and assess the fetal response to uterine contractions by monitoring the fetal heart rate patterns. 

Because each contraction decreases blood flow to the placenta, it temporarily interrupts oxygen delivery to the fetus. So, if the placenta isn’t delivering adequate oxygen to the fetus and nonreassuring fetal status occurs, you should attempt intrauterine resuscitation with position changes, providing an intravenous fluid bolus and supplemental oxygen, discontinuing any uterotonic medications, and maybe administering a tocolytic.
You may even need to proceed with an emergent C-section if there’s no improvement with these conservative interventions. 

That being said, if initial monitoring is reassuring, low-risk patients may only ne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cytomegalovirus_(CMV),_parvovirus_B19,_varicella_zoster,_and_toxoplasmosis_infection_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4avXjluvRqe44rfKzCp20V5OSWySsyJp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cytomegalovirus (CMV), parvovirus B19, varicella zoster, and toxoplasmosis infection in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Cytomegalovirus, or CMV, parvovirus B19, varicella zoster, and toxoplasma are infectious organisms that can cause congenital infection in pregnancy. These conditions often have nonspecific maternal symptoms; however, they can lead to congenital anomalies or even fetal demise depending on the timing and severity of infection. 

Let’s first take a look at when a patient presents a chief concern of CMV, you should first obtain a focused history and physical exam, as well as an obstetric ultrasound. 

Patients are usually asymptomatic but might report headaches, fatigue, and muscle or joint pains. You may find risk factors like childcare or healthcare workers that are exposed to body fluids, including urine, saliva, nasopharyngeal secretions, and tears. 

Physical exam could show a low-grade fever, runny nose, pharyngitis, or hepatomegaly. Lastly, obstetric ultrasound may reveal periventricular calcifications, ventriculomegaly, hepatic calcifications, echogenic bowel, growth restriction, microcephaly, and hepatosplenomegaly. 

Based on these findings, suspect that vertical transmission of CMV has resulted in infection and order CMV IgM and IgG antibody testing. If both IgM and IgG antibodies are negative, repeat testing in 2 to 4 weeks to ensure no seroconversion. If antibodies remain negative, consider an alternate diagnosis. Now, if IgM is negative but IgG is positive, that suggests remote CMV infection. These carry a low risk of fetal transmission from viral reactivation or infection with a new strain. Counsel the patient and offer fetal diagnostic testing via amniocentesis and PCR of the amniotic fluid if ultrasound is suspicious for fetal infection. 

If both IgM and IgG antibodies are positive, then check CMV IgG avidity to determine if the infection is recent. 

If there’s high avidity, IgG has been present for a significant amount of time, meaning the infection is remote. Inform your patient that there’s a lower risk of fetal transmission, but offer di]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abdominal_trauma_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IIlP8cAaTkeXij9oq9MrB0WFTROsNdZf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abdominal trauma in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Abdominal trauma in pregnancy is any abdominal injury ranging from minor bumps to the abdomen to significant blunt trauma or penetrating injury. Penetrating abdominal trauma can lead to rupture of the uterus, and blunt trauma can cause shearing forces resulting in placental abruption. Trauma is the number one cause of nonobstetric maternal death with even seemingly minor traumas risking fetal injury.  

Your first step in evaluating a patient presenting with abdominal trauma is to perform a CABCDE assessment to determine if they are unstable. If your patient is unstable, control hemorrhage and stabilize their airway, breathing, and circulation right away. This means you may need to intubate your patient. Obtain IV access, ideally by placing two large bore IVs to allow for adequate fluid resuscitation. Continuously monitor maternal vital signs, and remember…

You have two patients; so you must assess the fetus as well!   Check the fetal heart rate, and if at a viable gestational age, perform continuous fetal monitoring; also assess for fetal movement. And since bleeding in the uterus can stimulate uterine contractions, you should assess for labor. 

Then, assess the mechanism of injury to the maternal abdomen and fetus to determine your next steps. If the mechanism of injury is penetrating abdominal trauma, perform a focused history and physical exam; obtain labs including a CBC, PT, INR, PTT, and fibrinogen; obtain type and screen, which is important in case your patient requires transfusion; and perform a focused assessment with sonography in trauma, or FAST exam. 

Your patient may report dizziness, anxiety, or tunnel vision due to significant blood loss; and they’re likely to have abdominal pain and contractions. A history of intimate partner violence is a risk factor for injury, especially if there’s access to weapons; so your patient may also report a gunshot or knife wound. 

When it comes to the physical exam, expect hypotension and tachycardia, as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maternal_D_alloimmunization_(prevention):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-gacrGpEQTOBnWaJxOFRFLW0STa9YMVB/_.png</video:thumbnail_loc><video:title><![CDATA[Maternal D alloimmunization (prevention): Clinical sciences]]></video:title><video:description><![CDATA[Maternal D alloimmunization, sometimes called isoimmunization, occurs when a pregnant patient with Rh-negative blood type is exposed to Rh-positive blood and develops antibodies against the Rh-factor antigen. Maternal sensitization can occur when the fetus is Rh-positive, either during pregnancy, or during delivery, which is when fetal-maternal hemorrhage is most likely to occur. Then, in subsequent pregnancies with an Rh-positive fetus, maternal anti-D antibodies can cross the placenta and attack the fetus’ red blood cells, causing fetal anemia. Severe cases can result in fetal hydrops and death. 

Your first step when evaluating a pregnant patient who is Rh negative is to obtain a focused history. The initial prenatal visit is an ideal opportunity to evaluate a patient’s risk and provide education about sensitization. Additionally, the 28-week visit is the recommended time to administer anti-D immune globulin for routine prophylaxis. Keep in mind that maternal D alloimmunization can occur in asymptomatic patients who don’t receive immune globulin prophylaxis at 28 weeks, because some antenatal mixing of fetal and maternal blood occurs despite the separate circulations.  

Alright, other important findings include vaginal bleeding, or other sensitizing events in pregnancy that could have caused maternal exposure to fetal red blood cells, such as abdominal trauma, chorionic villus sampling, amniocentesis, cordocentesis, and external cephalic version. Additionally, spontaneous abortion, ectopic pregnancy, and pregnancy-related uterine curettage can also cause maternal exposure. 

Ask patients who are known to be Rh-negative if they have received immune globulin in the past 12 weeks, because this could result in a positive antibody screen. Knowing the paternal blood type can also be helpful because Rh-negative patients are not at risk of Rh D alloimmunization when paternity is certain and paternal blood type is Rh-negative. Finally, gestational age is import]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maternal_D_alloimmunization_(management):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zTDT9RH5SAmSVnNxAz1ts9K2Q9Ky_QJY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Maternal D alloimmunization (management): Clinical sciences]]></video:title><video:description><![CDATA[Maternal D alloimmunization management

Maternal D alloimmunization, also called isoimmunization, occurs when an Rh-negative pregnant patient produces antibodies against the Rh-D antigen on the surface of Rh-positive, fetal red blood cells. Maternal sensitization can develop following antepartum or intrapartum fetal-maternal bleeding if the fetus is Rh-positive, or after a blood transfusion with mismatched blood. In subsequent pregnancies with an Rh-positive fetus, maternal IgG anti-D antibodies can cross the placenta and attack the fetal red blood cells, causing hemolytic disease of the fetus and newborn characterized by anemia, jaundice, hydrops, and possibly fetal demise. 

Your first step in evaluating a pregnant patient with a chief concern suggesting maternal D alloimmunization is to obtain a focused history. All pregnant patients are tested at the first prenatal visit for their ABO blood group, Rh-D type, and the presence of erythrocyte antibodies. Rh-negative individuals are rescreened at 28 weeks, and after delivery, before receiving anti-D immune globulin for prophylaxis. Patients with maternal D alloimmunization have an Rh-negative blood type and a positive anti-D antibody screen without having received anti-D immune globulin within the past 12 weeks.

Knowing the gestational age is helpful to guide the timing of fetal assessment and treatment when moderate to severe fetal anemia occurs. Finally, be sure to ask the patient at the initial prenatal visit if they had a previous pregnancy affected by alloimmunization and hemolytic disease. 

If you suspect maternal D alloimmunization, your next step is to confirm the paternal Rh-D antigen status, whenever possible. If paternity is certain and paternal Rh status is negative, there’s no risk of Rh D-associated hemolytic disease and the patient can resume routine prenatal care. 

However, in most cases, the paternal Rh status is either positive or unknown. In this situation, you should assess the pater]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Late-term_and_postterm_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-mh85i6ES8ykIOl4E_l5Du8GTay8FgXN/_.png</video:thumbnail_loc><video:title><![CDATA[Late-term and postterm pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Late-term and postterm pregnancies occur when a pregnancy continues beyond the standardized 40 weeks of gestation. More specifically, late-term refers to those pregnancies at or beyond 41 weeks of gestation and postterm refers to pregnancies at or beyond 42 weeks of gestation. Both are associated with increased risks of maternal and fetal morbidity and mortality. Intrapartum risks are related to an increased incidence of oligohydramnios, which is a decreased amniotic fluid that’s associated with umbilical cord compression, fetal heart rate abnormalities, and meconium-stained fluid. 

When it comes to delivery risks, there is an increased risk of operative-assisted vaginal deliveries or c-section deliveries, shoulder dystocia, severe perineal lacerations, and postpartum hemorrhage. Now, there are also some neonatal risks as well, such as meconium aspiration syndrome, neonatal convulsions, 5-minute Apgar scores of less than 4, and increased rates of NICU admissions. 

Finally, while the absolute risk is low, the risk of stillbirth increases with each subsequent week of gestation after week 40. Thus, it is important to accurately identify late-term and postterm pregnancies, categorize pregnancies into high and low-risk states, and initiate appropriate antenatal testing once a patient enters this stage of gestation. 

When a patient presents with a late-term or postterm pregnancy, you should start with a focused history and physical exam. History might reveal some associated risk factors for late-term and postterm pregnancy including nulliparity, a history of a prior late-term or postterm pregnancy, carrying a male fetus, and certain fetal disorders in the current pregnancy, such as anencephaly. On physical exam, you may note a BMI of 30 or more, as obesity is a risk factor for prolonged pregnancy. Additionally, the dating of the pregnancy will be confirmed to be at least 39 and 0/7 weeks of gestation.

Now that you have obtained some helpful information, your]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fetal_growth_restriction:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-SDdUvkFQu_mKH0UgdNxmeLRRWC7opKH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fetal growth restriction: Clinical sciences]]></video:title><video:description><![CDATA[Fetal growth restriction, or FGR, is also known as intrauterine growth restriction, or IUGR; and is defined as a fetal weight or abdominal circumference below the 10th percentile for gestational age, as determined by ultrasound measurements. In contrast, small for gestational age, or SGA, refers to a term newborn with a birth weight less than the 10th percentile for gestational age. FGR can result from a variety of maternal, placental and fetal conditions. It requires increased antenatal surveillance, possibly early delivery, and it contributes to poor perinatal outcomes and negative long-term health impacts for the child.

When a patient presents with a chief concern suggesting fetal growth restriction, your first step is to perform a focused history and physical examination. Key findings on history include prior delivery of an SGA infant, multiple gestation in the current pregnancy, and inadequate maternal weight gain with or without a maternal malabsorptive syndrome. Other risk factors include an intrauterine infection like cytomegalovirus, toxoplasmosis, rubella, or varicella zoster; maternal chronic disorders with a vascular component such as chronic hypertension, long-standing, poorly controlled diabetes, or chronic kidney disease; or a history of antiphospholipid syndrome, also known as APS 

Here’s a clinical pearl! Acquired thrombophilias such as APS can contribute to FGR, but inherited thrombophilias do not. 

Finally, be sure to ask about any substance use during pregnancy, like tobacco or alcohol, as well as teratogen exposure, including medications like valproic acid, cyclophosphamide, and warfarin.

On physical examination, note your patient’s weight and ensure adequate weight gain. Beginning at 24 weeks, measure the fundal height and note whether it is appropriate for the gestational age, by measuring from the top of the pubic symphysis to the fundus of the uterus using a flexible measuring tape. 

The measurement should approximate the gest]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vaginal_birth_after_cesarean_(VBAC):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PLJbezAGRryZ_vaQOhvR8WRfS4u2SUNC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vaginal birth after cesarean (VBAC): Clinical sciences]]></video:title><video:description><![CDATA[.Vaginal birth after cesarean, also known as VBAC, refers to a successful vaginal delivery in a patient with a prior C-section. While many patients may choose to undergo a trial of labor after cesarean, also known as TOLAC, to avoid the risks of major abdominal surgery, others may elect for a repeat C-section due to the increased operative risks with an intrapartum C-section compared to a planned one. 

Ultimately the decision must be individualized but it is important to know the risks, benefits, and contraindications, so you can provide your patient with the best information to make their decision.

The first step when a patient presents desiring a TOLAC is to perform a focused history and physical examination, …

with particular attention to their obstetric history. This means obtaining the past operative note to know what kind of C-section they had. The most common type of C-section is one where a low transverse incision is made in the lower uterine segment of the uterus to deliver the infant. 

However, sometimes a classical C-section is performed where a vertical incision is made in the contractile portion of the uterus. This is important because TOLAC is not recommended for a patient with a prior classical C-section, due to a higher risk of the uterus rupturing during labor. 

Patients with a history of an extreme preterm delivery, a history of significantly large fibroids, or a history of a difficult extraction of the infant may have had a classical C-section. 

Here are a couple of clinical pearls! You can’t determine the type of uterine scar by looking at the direction of the skin incision. Sometimes vertical skin incisions are made while the uterine incision is low transverse; alternatively, a patient may have a low transverse skin incision but their uterine incision is vertical, meaning it’s classical. Additionally, some types of uterine surgery should be treated as if the patient had a classical C-section. This happens when incisions are made ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_chronic_pelvic_pain_(GYN):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-y8SfGHgRfWxXYcf2YoC2u6iSr6L1oSD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to chronic pelvic pain (GYN): Clinical sciences]]></video:title><video:description><![CDATA[Chronic pelvic pain arises from pelvic and other structures in non-pregnant patients, and lasts more than 6 months. It can affect quality of life and negatively impact the ability to participate in other daily activities, such as school or work. In addition to physical pain, many patients have associated symptoms of anxiety, distress, or even depression. 

The diagnosis of chronic pelvic pain is often difficult because there can be more than one condition causing it, and sometimes there’s overlap between several coexisting causes of pain. So be sure to complete the evaluation and don’t stop just because one possible etiology is found. Gynecologic causes include endometriosis, adenomyosis, leiomyomas, adnexal masses, and pelvic organ prolapse. On the other hand, non-gynecologic causes can be urinary, musculoskeletal, psychosocial, or gastrointestinal. 

When a patient presents with chronic pelvic pain, the first step is to perform a focused history and physical examination, and obtain an hCG to assess for pregnancy. If hCG is positive, your patient is pregnant. Thus, consider diagnoses associated with pregnancy, such as ectopic pregnancy or musculoskeletal pain. On the other hand, if the hCG is negative, assess for causes of chronic pelvic pain.

Let’s start with gynecologic causes, and the first one is endometriosis. This is characterized by endometrium-like tissue outside of the endometrial cavity. A focused history may reveal the 4 “Ds” of endometriosis: dysmenorrhea, dyspareunia, dyschezia, or dysuria. These symptoms, as well as generalized pelvic pain, are often exacerbated by menses and can be cyclic in nature. On physical exam, you might find lower abdominal or pelvic tenderness, a pelvic mass, reduced uterine mobility, a tender posterior vaginal fornix, and rectovaginal nodularity. If this is the case, consider endometriosis. Next, obtain a pelvic ultrasound, and consider performing a diagnostic laparoscopy to confirm your diagnosis. 

Her]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_secondary_amenorrhea:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3zAMSIzYQTeBG9tK8wWzTXMJQnyMFaYJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to secondary amenorrhea: Clinical sciences]]></video:title><video:description><![CDATA[Secondary amenorrhea is defined as the absence of menses for more than 3 months in a patient who has a history of regular menstrual cycles; or greater than 6 months in a patient with a history of irregular menstrual cycles. Secondary amenorrhea can be caused by dysfunction of the hypothalamus, pituitary, ovaries, thyroid, or uterus. Secondary amenorrhea is important because it can be a sign of systemic illness; it is associated with infertility; and, in some cases, can lead to an increased risk of endometrial cancer, osteoporosis, or cardiovascular disease. 

The first step in evaluating a patient who presents with secondary amenorrhea is to  perform a focused history and physical examination. You should also obtain some labs, including hCG, FSH, estradiol, prolactin, and TSH. The first test you should always look at when evaluating menstrual abnormalities is the hCG because if it’s positive, you have a diagnosis of pregnancy, which is a common cause of secondary amenorrhea.

Here’s a clinical pearl! Many hormonal contraceptives, such as continuous oral contraceptives or progestin-containing intrauterine devices, have the desired side effect of amenorrhea. This effect can persist for several months after discontinuation of these medications, and can also affect the assessment of hormone levels. Be sure to keep this in mind when evaluating a patient for amenorrhea. 

Once you have ruled out pregnancy, consider and assess for other causes of secondary amenorrhea. The FSH level is a useful tool to triage patients as it helps to determine where the dysfunction lies along the hypothalamic-pituitary-ovarian axis. Remember that an elevated FSH indicates that the ovaries are not producing enough estradiol, while a low FSH indicates that there might be dysfunction at the level of the hypothalamus or pituitary gland. 

Let’s start with ovarian dysfunction. In this case, the FSH is greater than twenty and history reveals a patient under the age of forty, with vasomot]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Perimenopause,_menopause,_and_primary_ovarian_insufficiency:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IjpzcY6KT8u6xPLKbryOywk_TxmvB3GZ/_.png</video:thumbnail_loc><video:title><![CDATA[Perimenopause, menopause, and primary ovarian insufficiency: Clinical sciences]]></video:title><video:description><![CDATA[Menopause is defined as the cessation of menses due to loss of ovarian function. The diagnosis is made once menses have been absent for twelve months and, on average, occurs around age fifty-one. However, it can occur as early as between 40 and 45 years, in which case it’s called early menopause.  Moreover, if menopausal symptoms and cessation of menses occur prior to the age of 40, that’s called premature ovarian insufficiency. Finally, perimenopause, or the menopause transition, defines the period of time between the onset of menopausal symptoms and one year after cessation of menses, regardless of age. 

When a patient presents with a chief concern suggesting perimenopause menopause, or primary ovarian insufficiency… your first step should be a focused history and physical examination. The history might include abnormal uterine bleeding, amenorrhea, vasomotor symptoms such as hot flashes or night sweats, vaginal or vulvar dryness and itching and dyspareunia; as well as sleep disturbances. 

Other reported symptoms might include changes in mood, weight gain, headaches, decreased libido, and cognitive changes. Of note, there’s high individual variability as to how long these symptoms last, for some women lasting up to 12 years! 

Now, on the physical exam, you might find evidence of vaginal and vulvar atrophy. If you see these findings, your next step is to assess the patient’s menstrual status. 

Here’s a high-yield fact! Genitourinary syndrome of menopause, or GSM, refers to a group of symptoms that are related to decreased estrogen levels at the genital epithelium. These symptoms include vaginal and vulvar dryness, burning, and irritation; dyspareunia; urinary urgency and frequency; and frequent urinary tract infections. 

Let’s begin with patients who have had menstrual bleeding within the past twelve months. They might report fluctuations in bleeding patterns such as shortened cycle length, oligomenorrhea, or heavy bleeding. Bear in mind that bleedin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infertility:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XQACzXEfSDeQRgXjtRq3o_8AQiyH8DTE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infertility: Clinical sciences]]></video:title><video:description><![CDATA[Infertility is defined as the inability to become pregnant after 12 months of timed, unprotected intercourse or donor insemination when the biologically female partner is under 35 years of age; or after 6 months when they’re older than 35. 

When evaluating a patient with a chief concern suggesting infertility your first step is to obtain a focused history and physical. 

Key history findings include intercourse for 6 to 12 months that is regular, timed, and unprotected  without pregnancy; history of previous infertility treatment; irregular menses; history of STIs, such as cervical infections with gonorrhea or chlamydia; pelvic infection such as pelvic inflammatory disease, or PID; galactorrhea; and hirsutism. 

Additionally, when taking a history you should consider their prior pregnancies and birth control, presence of sexual dysfunction, family history of birth defects, developmental delay or early menopause, substance use including tobacco and alcohol; and occupational exposure to environmental hazards. 

You should also ask about important information like surgical history, focusing on prior surgeries involving the pelvis, previous serious illness or hospitalization, and current medications including supplements. 

Here’s a clinical pearl! Timed intercourse means having unprotected intercourse during the most fertile time of the menstrual cycle or “fertile window”. This is during the 3 to 5 days leading up to ovulation. So if your patient has a 28-day cycle, you can predict they ovulate on day 14 and thus calculate their fertile window as days 10 through 14, with day 1 of their cycle being the first day of their period.

Alright, if you found any of the key findings in history, you should suspect infertility and see if your patient meets the criteria for infertility. Now, if your patient is less than 35 years old and has not become pregnant after 12 months of regular, timed, unprotected intercourse or donor insemination, or if they are at least 35 ye]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gestational_trophoblastic_disease_(GTD)_and_neoplasia_(GTN):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/M-f0i8f5SqKz2rcLb7S47QqcQvOoCuR7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gestational trophoblastic disease (GTD) and neoplasia (GTN): Clinical sciences]]></video:title><video:description><![CDATA[Gestational trophoblastic disease, or GTD, is a group of conditions where trophoblastic cells of pregnancy grow improperly. The most common type of GTD is benign hydatidiform mole, which includes complete molar pregnancies and partial molar pregnancies that arise from abnormal fertilization. 

Diagnosis and treatment of GTD is important because early recognition and proper management reduces the risk of gestational trophoblastic neoplasia, or GTN, which is a malignant type of GTD. While GTN can arise from pregnancies that aren’t GTD, such as miscarriages or viable pregnancies, GTN is most common after a molar pregnancy and therefore, close surveillance is warranted in all cases of GTD. 

When a patient presents with a chief concern suggesting gestational trophoblastic disease, perform a focused history and physical exam, order a quantitative human chorionic gonadotropin, or hCG, test, and obtain a pelvic ultrasound. Your patient will usually report amenorrhea and present for care thinking they are pregnant. But unlike a normal pregnancy, the patient might report pelvic pain or pressure from early uterine enlargement, or vaginal bleeding with possible passage of “grape-like” vesicles. The patient may also report symptoms specific to high hCG levels often seen with GTD, such as tremors or heat intolerance which are due to hCG stimulation of the thyroid. Or the patient might experience hyperemesis and weight loss. Risk factors for GTD include a prior molar pregnancy; extremes of maternal age including those older than 40 years and those younger than 20 years; and individuals of Asian ancestry. 

On examination, you might see signs of preeclampsia like new blood pressure elevations and protein in the urine. You may also find that the uterus is larger or smaller than you would expect for the estimated gestational age. You might also feel an adnexal mass on a bimanual exam because high hCG levels can stimulate the formation of large]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Henoch-Schonlein_purpura:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GX7ZCCoaQ3_5fbhJy3BhhSGhR6_ucWmj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Henoch-Schonlein purpura: Clinical sciences]]></video:title><video:description><![CDATA[Henoch-Schönlein purpura, or HSP for short, is the most common systemic vasculitis of childhood and typically affects the skin, intestines, and kidneys. HSP is also known as IgA vasculitis, since it’s associated with vasculitis of small blood vessels due to immunoglobulin A deposition. While HSP is a self-limited condition that often improves after a few weeks of supportive care in the outpatient setting, some children may develop HSP nephritis, which can result in kidney injury and, in rare cases, lead to kidney failure. 

Now, when a patient presents with a chief concern suggesting HSP, you should start by obtaining a focused history and physical examination. Most children with HSP are between 3 and 15 years old, and often present with a reddish-purple rash. Some patients may also complain of migratory joint pain that mainly affects the knees and ankles. Some patients may also present with colicky abdominal pain. HSP is associated with various infectious organisms, such as group A streptococcus or other upper respiratory infections, so be sure to ask whether they have recently recovered from an infection.

The physical exam typically reveals palpable purpura, which is a reddish-purple rash consisting of elevated, firm, and hemorrhagic papules and plaques that can be detected by touch. These skin changes typically appear in clusters on the legs and buttocks. You may also notice edema of the hands or feet, or in other gravity-dependent areas, such as the periorbital area or the scrotum. Additionally, you might detect swelling of the soft tissues around the joints, tenderness of the joints, or even joint effusion, especially in the knees or ankles, but overlying joint erythema does not usually occur.. 

With these clinical findings, you should suspect HSP. Once you suspect HSP, your next step is to order labs. These should include a CBC, PT and PTT, and serum creatinine. In addition, send urine for urinalysis and a urine protein level, and send stool f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_abnormal_uterine_bleeding_in_reproductive-aged_patients:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0SxB7EmmQJOTSCIjJbAlW0s0RfiuIdeg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to abnormal uterine bleeding in reproductive-aged patients: Clinical sciences]]></video:title><video:description><![CDATA[Abnormal uterine bleeding, or AUB, is a common problem for reproductive-aged patients. In general, normal menses has a duration of 5 days with a cycle length between 21 and 35 days, with no bleeding in between cycles, while the volume differs between individuals. AUB is defined as menstrual bleeding that deviates from normal duration, regularity, frequency, or volume. The International Federation of Gynecology and Obstetrics has established a classification system for AUB that defines it by bleeding pattern and etiology, and has replaced historical terms for abnormal bleeding, such as menorrhagia, metrorrhagia, and polymenorrhea. The two bleeding patterns include Heavy Menstrual Bleeding and Intermenstrual Bleeding. 

The etiologies can be remembered with the mnemonic PALM-COEIN. PALM includes structural causes of AUB: Polyp, Adenomyosis, Leiomyoma, and Malignancy. COEIN includes nonstructural causes: Coagulopathy, Ovulatory Dysfunction, Endometrial, Iatrogenic, and Not yet classified. Keep in mind that PALM-COEIN refers only to gynecological causes of AUB, not pregnancy-related ones. 

The first step in evaluating a reproductive-aged patient who presents with AUB is to perform a CABCDE assessment to determine if they are stable or unstable. If the patient is unstable, control life-threatening hemorrhage, which may include IV hormonal therapy or surgical intervention. Also, stabilize the airway, breathing, and circulation; obtain IV access and monitor vitals.

On the flip side, if the patient is stable, the first step is to obtain a focused history and physical exam, as well as an hCG to assess for pregnancy.

If the hCG test is positive, the patient is pregnant. Any vaginal bleeding during pregnancy is abnormal and potentially dangerous, so be sure to evaluate immediately for life-threatening conditions, such as an ectopic pregnancy. 

On the other hand, if hCG is negative, assess for non-pregnancy related causes of AUB. For this, you’ll need to obta]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Croup_and_epiglottitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/70r0iYaFSa6F7UvLRjuV4zi_ST2VJBdR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Croup and epiglottitis: Clinical sciences]]></video:title><video:description><![CDATA[Croup and epiglottitis are causes of acute upper airway obstruction in children. Croup, also known as laryngotracheitis, is a common viral infection, mostly caused by the parainfluenza virus or other respiratory viruses, that results in subglottic inflammation and narrowing. 

On the other hand, epiglottitis is typically a bacterial infection, most often caused by Haemophilus influenzae or Streptococcus pneumoniae, that can cause rapid and life-threatening swelling of the epiglottis and supraglottic structures. 

Signs and symptoms on a focused history and physical examination can help distinguish croup from epiglottitis.

When a patient presents with a chief concern suggesting croup or epiglottitis, first perform an ABCDE assessment to determine if your patient is unstable or stable.

If unstable, stabilize their airway, breathing, and circulation. In some cases, you might need to intubate your patient. Next, obtain IV access, put your patient on continuous vital sign monitoring, including pulse oximetry, respiratory rate, and cardiac monitoring, and don’t forget to provide supplemental oxygen if needed.

Here’s a clinical pearl to keep in mind! Whenever possible, ensure the child’s airway is secured before any anxiety-producing procedures like obtaining IV access. That’s because discomfort and agitation can exacerbate symptoms, increase narrowing of the airway, and ultimately cause an acute airway obstruction.

Once you stabilize the patient, obtain a focused history and physical exam.

If your patient’s caregiver reports a rapid onset of high fever as well as difficulty breathing and swallowing, with drooling and the absence of a cough, you should immediately think of epiglottitis! Physical exam will usually reveal an anxious-appearing child sitting upright with their neck extended in a tripod position, with the chin pushed forward. Additionally, your patient may have a muffled voice and audible stridor with labored breathing.

If you’re able to visuali]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cystic_fibrosis_and_primary_ciliary_dyskinesia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IRuBWa3lQ3ac8FnVKPqeB8S8TWCRFVmr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cystic fibrosis and primary ciliary dyskinesia: Clinical sciences]]></video:title><video:description><![CDATA[Cystic fibrosis and primary ciliary dyskinesia are distinct autosomal recessive disorders, both of which are associated with recurrent respiratory infections and chronic bronchiectasis. 

Cystic fibrosis, or CF for short, is associated with a mutation of the cystic fibrosis transmembrane conductance regulator, or CFTR, gene coding for the CFTR protein. Normally, the CFTR protein acts as a channel that controls the flow of chloride and water in and out of tissues as needed to regulate viscosity of secretions. In CF, these channels are dysfunctional, resulting in abnormally viscous secretions that are thick and sticky. This primarily impairs airway clearance and increases the risk of respiratory infection.  

On the flip side, primary ciliary dyskinesia, or PCD for short, is associated with abnormal ciliary movement, which can also lead to poor airway clearance and chronic respiratory infections. 

Now, if your patient presents with a chief concern suggesting cystic fibrosis or primary ciliary dyskinesia, first perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, and begin continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring. Finally, if needed, don’t forget to provide supplemental oxygen. 

Now, let’s go back to the ABCDE assessment and take a look at stable patients. In this case, first obtain a focused history and physical exam, which will help you differentiate between CF and PCD. 

First, let’s start with cystic fibrosis! CF primarily affects organs with secretory functions, like the lungs, gastrointestinal tract, and pancreas. Normally, these secretions are thin, but a defect in a chloride channel leads to thick mucus secretions that can congest the airways and GI ducts. 

Newborns with CF commonly present with meconium ileus or prolonged jaundice. Additionally, you may identify a positive ne]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_rheumatic_fever_and_rheumatic_heart_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DAN93vDITyyV8-q0SoSzC1pZT8a53eZx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute rheumatic fever and rheumatic heart disease: Clinical sciences]]></video:title><video:description><![CDATA[Acute rheumatic fever, or ARF for short, is a systemic inflammatory condition that develops after an infection with Group A Streptococcus, or GAS for short. Acute rheumatic fever, which is thought to be an immune-mediated condition, affects the joints, skin, nervous system, and heart. Moreover, if not recognized and treated on time, it can cause damage and scarring of the heart valves and structures. This condition is also known as rheumatic heart disease or RHD. 

Now, if a pediatric patient is presenting with a chief concern suggesting ARF or RHD, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, consider starting IV fluids, and begin continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, start broad-spectrum intravenous antibiotics, and, if needed, don’t forget to provide supplemental oxygen.

Okay, now let’s go back to the ABCDE assessment and take a look at stable patients. Start by obtaining a focused history and physical exam. First, let’s discuss patients with ARF. Your patient will likely report a history of fever and joint pain, as well as a recent history of infection characterized by a sore throat, with or without tonsillar exudates. On the other hand, physical exam findings typically include joint tenderness, with or without effusion; a serpiginous rash; painless nodules on the shin; and even abnormal, uncontrolled movements. In some patients, you might detect a heart murmur as well!

These history and exam findings should make you suspect a recent GAS infection. Your next step is to obtain a rapid strep antigen test or a throat culture. Additionally, you should check strep antibodies, including antistreptolysin O; or anti-DNase B antibodies. Finally, don’t forget to check the patient’s inflammatory markers, like ESR and CRP; and obtain an ECG and echocardiogram.

Now, here’s a clin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypocalcemia_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/W-FVLFVCRN_QVgbBFOMqnOQ5R8uf2Kzg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypocalcemia (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Hypocalcemia refers to a serum calcium level that is below the lower limit of normal, which is often considered below 8.5 mg/dL. Calcium plays a vital role in various body functions, such as cardiac muscle function and nerve signaling, so hypocalcemia can result in abnormal cardiac rhythm and neurologic dysfunction. The evaluation of hypocalcemia depends on whether a patient is a newborn or an older infant or child.

Now, if a pediatric patient presents with a chief complaint suggesting hypocalcemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. 

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen.

Now, here’s a clinical pearl to keep in mind! Hypocalcemia can occur in the setting of critical illness. In cases where hypocalcemia is severe or develops rapidly, your patient might have stridor secondary to laryngospasm, as well as seizures or a prolonged QT interval on an ECG. 

In such cases, you should administer intravenous calcium gluconate to restore blood calcium levels. Also, don’t forget that hypomagnesemia often occurs along with hypocalcemia, so consider giving IV magnesium as well. 

Okay, let’s go back to the ABCDE assessment and discuss the stable patients. 

If your patient is stable, first obtain a focused history and physical examination, and order a serum calcium level. 

Your patient may report weakness, paresthesias of the fingers and toes, and muscle cramps. Additionally, the physical exam might reveal positive Chvostek or Trousseau signs. The Chvostek sign is positive if tapping over the muscles overlying the facial nerve causes facial muscle spasms. On the other hand, the Trousseau sign occurs when inflating a blood pressure cuff over a patient’s arm causes a spasm of their hand. Y]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hyponatremia_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zJx0QLTkQ-iEPtV7ams4YB_PTxOl4BeB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hyponatremia (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Hyponatremia is a common electrolyte disturbance in which the serum sodium concentration is less than 135 milliequivalents per liter. Several mechanisms can contribute to hyponatremia, including increased serum levels of antidiuretic hormone, or ADH; increased renal sensitivity to ADH; excessive free water intake; and low solute intake. Now, based on the underlying cause, hyponatremia can be categorized as hypovolemic, euvolemic, and hypervolemic.

Okay, if a pediatric patient presents with a chief concern suggestive of hyponatremia, you should first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation; obtain IV access and consider giving your patient IV fluids. Next, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and don’t forget to monitor your patient’s urine output! Finally, if needed, provide supplemental oxygen.

Now, here’s a high-yield fact to keep in mind! Unstable individuals with hyponatremia often have a sodium level below 125 milliequivalents per liter, which can result in cerebral edema and severe clinical manifestations, like seizures or even respiratory arrest! If these findings are present, emergent administration of hypertonic saline might be necessary. 

Now, let’s go back to the ABCDE assessment and look at stable patients. In this case, obtain a focused history and physical examination and order a basic metabolic panel, or BMP. Your patient may report symptoms like headache, nausea, vomiting, or confusion. Lab results will reveal a sodium level lower than 135 milliequivalents per liter. With these findings, consider hyponatremia and order a plasma osmolality to help you determine the underlying cause.

Let’s take a look when the plasma osmolality is above 295 milliosmoles per kilogram. In this case, the plasma is considered hypertonic and indicates the presence of other osmotically active s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_limp_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kx_y8eWgTdOBQCi56wSochKkQGi9d2bv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a limp (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[A limp is a gait abnormality that’s usually caused by pain, weakness, or deformity, and if it goes unrecognized, it can lead to permanent disfigurement and loss of function. 

Based on history, exam, and imaging findings, you can differentiate between a painful limp, which is typically associated with infectious, traumatic, inflammatory, or mechanical causes; and a painless limp, which can occur due to mechanical or developmental causes. 

When a child presents with a limp, begin by obtaining a focused history and physical exam, including a thorough musculoskeletal and neurologic exam. Keep in mind that young children may not be able to describe their pain well, so in non-verbal children, look for indicators of pain, such as irritability, crying, or refusal to stand or walk. 

Okay, now your first step when evaluating a limp is to assess for pain. If the patient is presenting with a painful limp, your next step is to assess the onset of the limp, which could be either sudden or gradual. Any painful limp with a sudden onset, should make you consider infection, so assess for the presence of fever. If fever is present, the main causes to consider include septic arthritis, meaning an infection of the joint, and osteomyelitis, which is an infection of the bone. 

First, let’s discuss septic arthritis. These individuals may report joint swelling and pain, with refusal to bear weight on the affected extremity. The physical exam might reveal joint tenderness, effusion, and warmth, as well as a limited range of motion. In addition, you may observe that the child &amp;quot;guards&amp;quot; the joint. At this point, consider septic arthritis and order labs, including a CBC, CRP, ESR, and a blood culture. Additionally, perform a joint aspiration to collect synovial fluid for analysis and culture. 

The labs will typically show elevated WBCs, CRP, and ESR, and sometimes, blood cultures might reveal a causative pathogen. The synovial fluid will likely appear puru]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Juvenile_idiopathic_arthritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MvQNAXUcRZWXbwxUrGNhBPanTs2QNcpZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Juvenile idiopathic arthritis: Clinical sciences]]></video:title><video:description><![CDATA[Juvenile idiopathic arthritis, or JIA for short, describes a broad group of autoimmune conditions associated with inflammatory synovitis and arthritis, which can potentially result in bony erosion and joint destruction. It’s important to diagnose and treat JIA early in order to limit joint damage, preserve joint functionality, and avoid chronic pain. Based on the history, physical exam, and lab findings, you can classify subtypes of JIA as oligoarticular, polyarticular, systemic, enthesitis-related, and psoriatic JIA.

When a patient presents with a chief concern suggesting JIA, you should first obtain a focused history and physical exam. Your patient will be younger than 16 years old, with 6 or more weeks of joint swelling. Affected joints might also be warm or painful. Patients will also describe stiffness lasting greater than 30 minutes, either in the morning after waking up, or after periods of inactivity. In either case, the stiffness improves with movement. On exam, you may notice a joint effusion, which can be accompanied by tenderness to palpation or limited range of motion. 

With these clinical findings, you can diagnose JIA. Keep in mind that JIA is a clinical diagnosis, meaning it’s typically based on the history and physical exam findings. However, JIA is also a diagnosis of exclusion, meaning you might need labs and imaging to rule out other conditions, such as infections like septic arthritis, or malignancies like leukemia. 

Once you diagnose JIA, be sure to order a CBC, CRP, ESR, and serum ferritin; as well as a rheumatoid factor, or RF; anti-cyclic citrullinated peptide or anti-CCP antibodies; and an antinuclear antibody or ANA. Finally, don’t forget to check whether or not your patient is HLA-B27 positive.

Next, assess for a quotidian fever. This is a high fever that spikes and then quickly remits in a daily pattern, such as once in the morning and once in the evening. Assessing for a quotidian fever will help you determine which s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Legg-Calve-Perthes_disease_and_slipped_capital_femoral_epiphysis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d63TeKDIRGSUKUl7BuvbnqSKRlK3r0ZY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Legg-Calve-Perthes disease and slipped capital femoral epiphysis: Clinical sciences]]></video:title><video:description><![CDATA[Legg-Calvé-Perthes disease, or LCPD, and slipped capital femoral epiphysis, or SCFE for short, are distinct hip conditions that commonly cause limp in children. In LCPD, a disrupted blood supply causes deformation of the femoral head and subsequently leads to osteonecrosis. On the other hand, in SCFE, a weakness of the growth plate causes displacement of the femoral head from the femoral neck. It’s important to identify and treat both of these conditions quickly to ensure better functional outcomes and reduce the risk of hip osteoarthritis. Based on history, exam, and imaging findings, you can differentiate between LCPD and SCFE.

If your patient presents with a chief concern suggesting either LCPD or SCFE, you should first perform a focused history and physical exam. Children with LCPD are usually less than 8 years old and classically present with a painless limp, which is usually unilateral. However, patients with more severe disease may develop a painful limp and could report pain in the hip, as well as the groin, thigh, or knee. LCPD is more common in biologically male children, and there could be a family history of LCPD.

Now here’s a clinical pearl to keep in mind! Whenever a child reports pain in a specific joint, always be sure to examine the joints directly above and below, since pain can refer to adjacent joints. For instance, if a child reports knee pain, you should examine the knee, as well as the hip and ankle.

The physical exam of a child with LCPD will often reveal limited internal rotation and abduction of the affected hip. While your patient is standing or walking, you might notice the Trendelenburg sign, which is a pelvic tilt caused by hip muscle weakness. The hip could also be tender to palpation, and in more severe cases, the affected leg could even be noticeably shorter than the unaffected leg. Finally, you might notice a smaller circumference due to atrophy of the anterior thigh muscle.

These findings should make you suspect LCPD.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_murmur_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IX8DeDQ_SYOXhqRk7DB5TblJT1u_rL29/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a murmur (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[A heart murmur is a sound produced by blood flowing through the heart and large vessels. While innocent murmurs are common in healthy infants and children, clues from the history and physical exam can identify pathological murmurs that require additional investigation. Now, there are three main types of murmurs: systolic, diastolic, and continuous.

If a child presents with a murmur, you should first perform an ABCDE assessment. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, consider IV fluids, and begin continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Finally, if needed, provide supplemental oxygen. 

Okay, now let’s go back to the ABCDE assessment and look at stable patients. Your first step is to perform a focused history and physical exam. Physical examination will reveal a heart murmur, which you can characterize based on its location, timing and duration, quality, and intensity. 

You can assign a grade to the murmur, according to its intensity, which can vary from I, which is barely audible, to grade VI, which can be heard with the stethoscope barely touching the chest wall. In addition, be sure to note any positional changes in the murmur, and determine whether the murmur radiates to other locations. Once you identify a heart murmur, assess for characteristics of an innocent murmur. These include a musical or vibratory quality, murmurs that are systolic, grade I to II out of VI, low-intensity and soft, and the absence of abnormal cardiac signs and symptoms. 

If these characteristics are present, consider innocent murmurs. These include adolescent Ejection murmur, Carotid bruit, Still’s murmur, Peripheral pulmonic stenosis, and Venous hum. To easily remember these innocent murmurs, think of the mnemonic Every Child Should Play Vigorously!

A short crescendo-decrescendo murmur best heard at the right or left upper sternal border that typically d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Febrile_seizure_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/48rTY3FES8Cl5rowFulr6vdXSb2o3yO2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Febrile seizure (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Febrile seizures occur in children 6 months to 5 years of age, with a temperature of at least 38 degrees Celsius, and without concurrent central nervous system infection, metabolic disturbance, or history of prior afebrile seizures. Based on the child’s manifestations, febrile seizures can be classified as simple or complex.

Now, if a pediatric patient presents with a chief concern suggesting febrile seizure, you should first perform an ABCDE assessment to determine whether they are unstable or stable. If the patient is unstable, first stabilize the airway, breathing, and circulation, obtain IV access, and consider starting IV fluids. Next, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and oxygen saturation. Finally, if needed, don’t forget to provide supplemental oxygen to maintain saturation, and consider administering an anti-seizure medication.

Now here’s a clinical pearl to keep in mind! If your patient experiences a seizure in front of you, and the seizure activity persists for 5 minutes or more, place them on their side, on a flat surface, and administer a short-acting benzodiazepine such as IV lorazepam or IM midazolam as first choices, or rectal diazepam as second choice. 

If the seizure doesn’t resolve after two doses of a benzodiazepine or after 20 minutes of seizure activity, administer a different anti-seizure medication, such as IV phenobarbital if your patient is an infant, or IV fosphenytoin if they are an older child. 

A febrile seizure lasting longer than 30 minutes is considered febrile status epilepticus, which is a neurologic emergency requiring the prompt administration of additional anti-seizure medication and further diagnostic evaluation.

Now, let&amp;#39;s go back and take a look at stable patients. In this case, your first step is to obtain a focused history and physical exam. History typically reveals a high or rapidly rising fever before the onset of a seizure. Ask the caregiv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_respiratory_distress_(newborn):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cSVJOKjcQ6OoQP5w-c4HssN4T5S6wqBB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to respiratory distress (newborn): Clinical sciences]]></video:title><video:description><![CDATA[Newborn respiratory distress refers to an increased work of breathing beginning in the first days of life. If not recognized and treated promptly, respiratory distress can lead to respiratory failure. 

Some important risk factors that can lead to respiratory distress in newborns include prematurity; conditions such as congenital diaphragmatic hernia and congenital heart disease; meconium aspiration syndrome; infections such as pneumonia and sepsis; pneumothorax; and transitory tachypnea of the newborn.

When a newborn presents with respiratory distress, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. In severe cases, you might need to intubate your patient and start mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including respiratory rate and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen.

Now, let’s return to the ABCDE assessment and take a look at stable patients. In this case, obtain a focused history and physical exam and check pulse oximetry. History reveals the beginning of respiratory distress in the newborn period. The physical exam reveals signs of respiratory distress, such as grunting, nasal flaring, and suprasternal, intercostal, or subcostal retractions. 

Tachypnea, or a respiratory rate above 60 per minute, will also be present. Depending on the underlying cause, you may also hear wheezing or crackles on auscultation.  Finally, pulse oximetry might show oxygen saturation below 90 percent.

These findings are suggestive of respiratory distress, so your next step is to look for an underlying cause. Start by assessing prenatal ultrasound findings. If you detect an abnormal prenatal ultrasound finding that increases the risk of respiratory distress, you should consider congenital defects.  Then order a chest X-ray, as well as an echocardiogram, if needed.

Fir]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Necrotizing_enterocolitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V3xEwCygTIeHzndF5vnWK3hNTKqdTWsR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Necrotizing enterocolitis: Clinical sciences]]></video:title><video:description><![CDATA[Necrotizing enterocolitis, or NEC for short, is a life-threatening condition most often seen in premature infants that can lead to intestinal necrosis and perforation. NEC commonly presents with feeding intolerance, bloody stools, and abdominal distension soon after enteral feeds are initiated. 

Infants who survive NEC face many long-term sequelae, including short-gut syndrome, intestinal strictures, and neurodevelopmental delays. On the basis of history and physical exam findings, you can make a clinical diagnosis of NEC, and imaging can be used to support the diagnosis.

Now, here’s a clinical pearl! Breast milk contains macronutrients, micronutrients, natural prebiotics, and antibodies that offer protection against NEC in premature and low birth weight infants! For this reason, donor breast milk is often given to premature neonates whose caregiver is absent or cannot produce sufficient breast milk. 

When a pediatric patient presents with a chief concern suggesting NEC, you should first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation; and you may even need to intubate the patient. Next, obtain IV access and start broad-spectrum IV antibiotics. Put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and begin supplemental oxygen, if needed.

Once you stabilize the patient, obtain a focused history and physical exam, and order abdominal X-rays in the anteroposterior and lateral views. When obtaining the history, be sure to note any risk factors for NEC, which include prematurity or low birth weight. The infant may have developed a sudden change in feeding tolerance, or you may note vomiting, diarrhea, or bloody stools. Additionally, some infants with NEC might have apneic episodes lasting 20 seconds or more. 

On the physical exam, the infant may show signs of hemodynamic instability, like hypotension; and signs o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pyloric_stenosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/d3It8MNmQYCbQd3Qm-MBp7JbQEOWVSYS/_.png</video:thumbnail_loc><video:title><![CDATA[Pyloric stenosis: Clinical sciences]]></video:title><video:description><![CDATA[Pyloric stenosis occurs from hypertrophy of the circular and longitudinal muscle fibers of the pylorus, which acts as a muscular valve between the stomach and the duodenum. This most commonly presents between 2 and 6 weeks of age. Pyloric stenosis often leads to complete or near complete gastric outlet obstruction, which can present as forceful vomiting. Excessive vomiting can in turn cause further complications, such as dehydration and metabolic abnormalities like hypokalemic, hypochloremic metabolic alkalosis with paradoxical aciduria. Management of pyloric stenosis includes fluid resuscitation and correction of metabolic derangements, as well as surgical pyloromyotomy, which is considered curative.

Alright, if a patient presents with a chief concern suggesting pyloric stenosis, you should first perform an ABCDE assessment to determine whether your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and initiate IV fluids for resuscitation. Most infants will show signs of severe dehydration and severe electrolyte abnormalities that need to be corrected during resuscitation. Finally, make sure to continuously monitor vital signs and keep the patient NPO.

Okay, once you’ve done acute management, your next step is to obtain a focused history and physical exam, along with labs like a CBC and CMP. The history is typically obtained from your patient’s caregivers, who may report episodes of immediate, post-prandial, nonbilious, projectile vomiting, as well as fewer wet diapers, which suggests dehydration.

Here’s a clinical pearl for you! “Projectile” vomiting refers to vomiting so forcefully that stomach contents are launched across a long distance. Be sure to ask caregivers for details when taking the history, because they might describe vomiting as “projectile” when their infant is simply spitting up!

Now, on physical exam, you might find signs of severe dehydration, such as h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_short_stature:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O0kAJUchTeyooXLxTBaUcuS-QLybE-LE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to short stature: Clinical sciences]]></video:title><video:description><![CDATA[Short stature in children refers to a height more than two standard deviations below the average of other children of the same age and biological sex. Short stature is often a variant of normal growth, but can also be caused by underlying conditions. Now, important types of non-pathologic short stature include constitutional delay of growth and puberty and familial short stature. 

On the flip side, important causes of pathologic short stature include skeletal conditions, malnutrition, chronic conditions, as well as endocrine or genetic disorders. 

Your first step to evaluate a child with short stature is to perform a history and physical exam, including measuring height and weight. 

History may reveal family members who were “late bloomers”, and one or both parents may also have short stature. In some cases, caregivers could report a history of chronic conditions, like recurrent infections or known congenital heart disease; as well as symptoms that could indicate systemic illness, like fever, vomiting, diarrhea, or fatigue. Be sure to obtain dietary and birth history as well. Then, physical exam could reveal findings suggestive of an underlying condition, such as dysmorphic features, pallor, heart murmurs, skin lesions, or lymphadenopathy. 

Next, be sure to measure their weight, in case nutritional causes are being considered; as well as their height, since the suspected growth failure may actually be due to an inaccurate measurement. If your patient is under 2 years of age, measure their length in a supine position; and if your patient is over 2, measure their height in a standing position. Next, plot your patient’s height on a standardized growth chart that’s appropriate for the child&amp;#39;s age and sex, and assess their height-for-age by comparing their growth against previous growth measurements. If the height is more than 2 standard deviations below the mean, or if the height has crossed 2 major percentile lines, diagnose short stature.

Once ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stress,_urge,_overflow,_and_mixed_urinary_incontinence_(GYN):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qo4o4tiSSL64TbvFxhMf93U2QEST0Vqv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stress, urge, overflow, and mixed urinary incontinence (GYN): Clinical sciences]]></video:title><video:description><![CDATA[Urinary incontinence, or the involuntary leakage of urine, is a common and often underreported problem that impacts both physical and psychological well-being. It can adversely impact activities of daily living and diminish quality of life. 

Urinary incontinence is associated with the effects of childbirth, urinary tract infections, changes to the pelvic floor, and bladder dysfunction. In addition, it can be secondary to neurologic conditions, diabetes, and medications such as diuretics. The most common types of urinary incontinence are stress, urgency, overflow, and mixed incontinence. 

When a patient presents with a chief concern suggesting urinary incontinence, the first step is to obtain a urinalysis and urine culture. If the urinalysis is positive for nitrites, leukocyte esterase, and possibly heme; and if the urine culture is positive, the diagnosis is a lower urinary tract infection. Treat the patient with appropriate antibiotic therapy. 

Here is a clinical pearl! If urinary leakage persists after successful treatment of a urinary tract infection, evaluate the patient for other causes of urinary incontinence! 

On the other hand, if the urinalysis is negative for nitrites, leukocyte esterase, and heme; and the urine culture is negative, then your patient does not have a urinary tract infection. Proceed with your next step, which is to perform a focused history and physical examination, as well as a simple office evaluation consisting of a urinary cough stress test and a post-void residual, or PVR. A cough stress test is the observation of urine leaking from the urethra when the patient coughs. This can be performed while the patient is supine or standing and may require a full bladder. A PVR involves the measurement of residual urine in the bladder after the patient voids. This can be done with the aid of bladder ultrasonography or catheterization. A normal PVR is generally considered to be less than 150 milliliters. 

Here’s another clinical pea]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Identifying_and_supporting_student_success_with_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2-mtU6_8TN_mYUfwFIDARtBJS2yn2zYX/_.png</video:thumbnail_loc><video:title><![CDATA[Identifying and supporting student success with Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Identifying and supporting student success with Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intussusception:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wkrgYVFmRyeS_w0m_dLeFENqQpevLGSi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intussusception: Clinical sciences]]></video:title><video:description><![CDATA[Intussusception is a type of intestinal obstruction that occurs when one segment of the intestine telescopes inside of another segment of the intestine. This telescoping often occurs around the ileocecal junction, which is where the ileum of the small intestine and cecum of the large intestine meet. Typically, the distal ileum folds into the cecum. If left untreated, it can result in intestinal edema due to venous and lymphatic congestion, and can ultimately lead to ischemia, necrosis, and intestinal perforation. Intussusception is a true emergency and must be treated promptly, either through reduction with an enema, or if unsuccessful, by surgical intervention.

Alright, if a pediatric patient presents with a chief concern suggesting intussusception, your first step is to perform an ABCDE assessment to determine if your patient is unstable or stable. If they’re unstable, initiate acute management by stabilizing the airway, breathing, and circulation. Next, obtain IV access and initiate IV fluids for resuscitation. Make sure to continuously monitor vital signs, including pulse oximetry, blood pressure, and heart rate. Finally, make your patient NPO and consider placing an NG tube for gastric decompression. 

Okay, once you’ve acutely managed your patient, your next step is to obtain a focused history and physical exam. Symptoms typically occur in patients who are 4 to 36 months old, consisting of sudden, severe, paroxysmal abdominal pain and cramping; and the child will often draw their knees up toward the chest. The pain is characterized by intermittent severe pain with pain-free periods in between. Additionally, caregivers typically note the child has had bloody stools that are often intermixed with mucus, called “currant jelly” stools; as well as vomiting, which can start out as nonbilious but may become bilious. Additional symptoms may include lethargy and fever. 

You will also want to ask about potential risk factors in your patient’s histo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chopra-Amiel-Gordon_syndrome:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SKUu5B6FRAKUEvQzIe_xbY9pRYmVZ0-a/_.png</video:thumbnail_loc><video:title><![CDATA[Chopra-Amiel-Gordon syndrome: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Chopra-Amiel-Gordon syndrome, or CAGS for short, also known as ANKRD17-related neurodevelopmental syndrome, is a rare genetic condition that primarily affects the development of the brain, eyes, face, and limbs. 

CAGS is caused by mutations in the ankyrin-repeat domain-containing protein 17, or ANKRD17, which is a type of protein structure involved in many cellular functions. Ankyrin repeat proteins have a unique shape that allows them to act like hooks, connecting them with other proteins to help in the formation of more complex structures. It is thought that ANKRD17 is involved in the development of blood vessels, yet, how the mutation in this protein leads to the clinical manifestations of CAGS is currently unknown. 

Most cases of CAGS come from de novo mutations, meaning they arise on their own and are not inherited. However, several cases of familial inheritance have also been reported. 

Typically, individuals with CAGS have unique facial features, which include a triangular face shape, high anterior hairline, low-set ears, a thin upper lip, and deep-set or almond-shaped eyes. Less common features include scoliosis and cleft lip or palate, which are openings in the upper lip or roof of the mouth, respectively. 

Individuals with CAGS also typically have varying degrees of learning disabilities and delays in reaching developmental milestones, such as sitting, crawling, and speaking. Additionally, they may have difficulties with tasks that require coordination and balance, like walking. Some individuals may experience epilepsy and have eye abnormalities; and there may also be neurobehavioral symptoms, like repetitive behaviors and difficulty with social interactions. 

Finally, children with CAGS tend to have feeding problems and frequent respiratory infections, which, if left untreated, can result in failure to thrive and decreased weight gain. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypoplastic_left_heart_syndrome:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/shP8TCT5RX2FM09YH0eivO9AQYy7jtIx/_.png</video:thumbnail_loc><video:title><![CDATA[Hypoplastic left heart syndrome: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Hypoplastic left heart syndrome, or HLHS for short, is a congenital heart defect that affects the left side of the heart, most notably the left ventricle and the aorta.The exact mechanism that causes HLHS is unknown, but one theory is that another primary heart defect reduces blood flow through or out of the left ventricle during fetal development, so that part of the heart does not grow and develop as expected.HLHS is often associated with other heart defects, particularly an atrial septal defect, which is an opening between the left and right atria.Normally, the left ventricle receives oxygenated blood and pumps that blood out to the body.  

In babies with HLHS, oxygenated blood, has a difficult time getting into the underdeveloped left ventricle,  so instead, most of the blood flows from the left atrium to the right atrium through the atrial septal defect,  where it mixes with deoxygenated blood.This mixture of blood then goes to the right ventricle,  where most of it is sent to recirculate through the lungs.However, some of this blood can exit the right ventricle and be sent to the body, through the ductus arteriosus, a duct connecting the pulmonary artery and aorta.This duct is present in all babies at birth, fully closes within several days following birth, and, in babies with HLHS, provides an essential pathway for some oxygenated blood to get to the body.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Exocrine_pancreatic_insufficiency:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WfHE2kIjSGO2ChmN7dvcrdiQS-CywAhU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Exocrine pancreatic insufficiency: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Exocrine pancreatic insufficiency: Year of the Zebra 2024 through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Necrotizing_enterocolitis:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BVW-BcBNTTyt2GPWUd6XFSHbTdCBQhqb/_.png</video:thumbnail_loc><video:title><![CDATA[Necrotizing enterocolitis: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Necrotizing enterocolitis, or NEC for short, is a rare life-threatening condition that involves inflammation and necrosis, or tissue death, of the intestines. This can lead to perforation of the intestinal wall and severe infection.  

NEC usually occurs within the first 2 weeks of life and mostly affects premature babies, especially those with very low birth weights, though it can occur in full-term infants too. This is because their immune system and gut barrier are not fully mature, making it easier for harmful bacteria to invade the intestinal wall.  

Among premature babies, those fed with formula rather than breast milk seem to be at higher risk. This is likely due to the protective effect of breast milk in the intestines, as it contains a more natural balance of sugars that promote the growth of beneficial bacteria in the baby’s gut, as well as antibodies and other anti-inflammatory compounds that prevent harmful microbes from adhering to the intestinal lining.   

Early symptoms of NEC include feeding intolerance, where the baby has difficulty digesting formula or breast milk, and abdominal bloating or swelling. Infants may also present vomiting, sometimes containing bile, along with diarrhea and bloody stools. As the condition progresses, the baby&amp;#39;s abdomen may become tender, red, or shiny. In cases of intestinal perforation, crepitus—or a crackling sound—may be heard when lightly pushing on the abdomen due to free air in the abdomen. Infants may also show signs of infection, such as fever, breathing problems, low blood pressure, and poor circulation.  

Despite advancements in care, NEC continues to have a high mortality rate, especially in extremely premature infants, meaning those born before 28 weeks’ gestation. Infants who survive usually face many long-term complications including short bowel syndrome, intestinal strictures, and neurodevelopmental delays.   ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sphincter_of_Oddi_dysfunction:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Fqm6kAF4Sk65pu7kkPT33kJ6QEeDkLU9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sphincter of Oddi dysfunction: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Sphincter of Oddi dysfunction, or SOD for short, is a group of rare conditions that occur when the sphincter of Oddi spasms, narrows, or relaxes inappropriately. The sphincter of Oddi is a muscular valve located between the biliary tree and small intestine. It’s responsible for regulating the flow of bile and pancreatic juices into the small intestine, and preventing reflux of intestinal content into the biliary tree.

With SOD, normal flow of bile and pancreatic juices is disrupted leading to biliary pain, which is pain typically located in the upper right abdominal quadrant.

There are three types of SOD. Type I consists of biliary pain, elevated liver enzymes, and a dilated common bile duct; type II includes biliary pain and either elevated liver enzymes or a dilated common bile duct; and type III includes biliary pain only.

The cause of SOD is unclear; though risk factors include being assigned female at birth; age 20 to 50 years; and a history of gallbladder removal.

The classic manifestation of SOD includes intermittent attacks of biliary pain, which is a type of colicky, abdominal pain that is typically located in the upper right quadrant, and can radiate to the back and shoulder. The pain can be mild to severe; lasts greater than 30 minutes; and can resolve spontaneously. These attacks feel and look similar to gallbladder attacks, though some individuals with SOD may not have a gallbladder. Other associated signs and symptoms may include nausea, vomiting, and pancreatitis, which is inflammation of the pancreas.

Diagnosis of SOD begins with a thorough history and physical examination. Typically, other more common causes of biliary pain are ruled out first, including gallstones. If SOD is suspected, blood tests and imaging may be done to aid in diagnosis. Blood tests may show elevated liver and pancreatic enzymes in those with types I or II. Imaging of the abdomen, including ultrasound, CT, or MRI may be done, as well as a HIDA scan, which can ass]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Coats_disease:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9ILgjl2NQS2G2nM32pw5oIWcSsaRiOnX/_.png</video:thumbnail_loc><video:title><![CDATA[Coats disease: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Coats disease is a rare eye disorder that causes abnormal development of the blood vessels in the retina. The retina is a layer of tissue at the back of the eye that contains specialized cells called photoreceptors. These photoreceptor cells are sensitive to light and convert it into electrical signals, which are then sent to the brain for visual processing.

In Coats disease, the blood vessels that supply the retina become dilated or enlarged, leading to the formation of retinal telangiectasias, which are the key manifestation of the disorder. These blood vessels are more fragile and prone to leakage, which can result in the accumulation of fluid beneath the retina.

Usually, Coats disease affects young individuals, more commonly those assigned male at birth, and it typically only affects one eye. The exact cause is unknown, but it may be related to mutations in the NDP gene, which codes for a protein involved in the vascular development of the retina.

Alright, now symptoms of Coats disease generally begin in childhood or adolescence and can include blurry vision, loss of visual acuity, and strabismus, or misalignment of the eyes. Most often, vision problems are related to retinal detachment, which is when the retina peels away from its underlying layer of support tissue, resulting in degeneration of the photoreceptors and, eventually, vision loss. Retinal detachment is generally painless, and is often accompanied by flashes or “floaters” in the affected individual’s vision.

When the retina detaches, it can also disrupt the normal structure of the eye, causing the pupil to appear white or yellow instead of black. This occurs because the detached retina reflects light differently, leading to leukocoria or a “white pupil”.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acoustic_neuroma:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tnjeU1c3SGefKrRPYUSJazdqQ7ynwvFb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acoustic neuroma: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Acoustic neuroma, also known as vestibular schwannoma, is a benign tumor arising from Schwann cells—the cells responsible for producing the myelin sheath that insulates nerve fibers. Schwannomas can develop along any nerve in the body, but they have a predisposition for the 8th cranial nerve, also called the vestibulocochlear nerve, which sends sensory information about hearing and balance from the inner ear to the brain. 

The cause of acoustic neuroma isn’t clear; however, a small number are related to a condition called neurofibromatosis type 2, which causes a mutation that allows Schwann cells to start dividing uncontrollably.  

The most common symptoms of acoustic neuromas are tinnitus, or a ringing sound in the ears, and gradual hearing loss on one side. For individuals with neurofibromatosis type 2, acoustic neuromas typically occur bilaterally, so individuals tend to have hearing problems in both ears. 

Peripheral vertigo, often described as a sense of imbalance or unsteadiness, can also occur; and it typically has a mild, gradual onset. This is because acoustic neuromas grow slowly, so the central nervous system has time to compensate for the loss of balance function, making the symptoms very subtle. As a result, individuals are more likely to notice symptoms like hearing loss and tinnitus earlier than vertigo.  

Acoustic neuromas don’t typically spread to other tissues, but if they grow large enough, they can compress nearby structures, particularly the facial nerve, causing facial weakness and paralysis.  

Diagnosis of acoustic neuroma is suspected in individuals with tinnitus, one-sided sensorineural hearing loss, and peripheral vertigo. Follow-up evaluation may include assessment by an ENT specialist, who may order hearing tests and other specific exams to assess the integrity of the vestibulocochlear nerve.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alpha-1_antitrypsin_deficiency:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fG8CKPrgTRaLPmoozJWOeGxUTmOhtzGR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alpha-1 antitrypsin deficiency: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Alpha-1 antitrypsin, or AAT, deficiency is a genetic disorder in which a protein called alpha-1 antitrypsin is absent or defective. The main function of AAT is to protect the lungs from damage caused by enzymes called proteases. These proteases can help fight off infections by breaking down proteins in bacteria, but they can also damage healthy tissues if their activity goes unchecked. Without AAT, the lung’s proteases break down the elastic fibers in the air sac walls, resulting in destruction of healthy lung tissue.  

The severity of the disorder varies depending on the amount of AAT in the blood. While some mutations result in little to no AAT being made, others, like the most common mutation, called Pi*Z, result in a misfolded AAT protein that gets trapped in the liver where they are normally produced, causing damage and ultimately death of liver cells.  

People with PiZ mutations are at risk of both lung disease and liver damage, whereas those with non-PiZ mutations only have an increased risk of lung disease.Symptoms of alpha-1 antitrypsin deficiency typically involve the lungs and liver. Damage to the lungs can result in shortness of breath, as well as wheezing, increased mucus production, and a chronic cough due to inflammation of the airways.  

Ultimately, the death of liver cells can lead to cirrhosis, a process in which healthy liver tissue is replaced with scar tissue. Long-term cirrhosis can lead to a number of complications, including easy bruising due to decreased production of clotting factors by the liver; jaundice, characterized by yellowing of the skin and eyes; and swelling in the abdomen and legs. In some cases, chronic cirrhosis can predispose individuals to hepatocellular carcinoma, which is the most common primary liver cancer. 
Aside from lung and liver manifestations, some individuals experience skin manifestations, including red nodules, bumps, or plaques in areas of the body with accumulation of subcutaneous fat like the buttocks, thighs, and abdomen. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Von_Hippel_Lindau_disease:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jZWId_JFSyeL9S-fOkwlgej-QB_LME0Q/_.png</video:thumbnail_loc><video:title><![CDATA[Von Hippel-Lindau disease: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Von Hippel-Lindau, or VHL, disease is a genetic disorder characterized by tumor development in many different organs, like the central nervous system, including the eyes; kidneys; adrenal glands; and pancreas.  

It’s caused by a mutation in a tumor suppressor gene found in chromosome 3. Tumor suppressor genes code for proteins that regulate the cell cycle, preventing cells from growing out of control.  

When a tumor suppressor gene gets turned off, like in VHL disease, cell growth goes unchecked, allowing cells to keep dividing uncontrollably, increasing the risk of tumor formation.  

The VHL mutation is inherited in an autosomal dominant pattern, meaning only one copy of the mutation causes disease, and individuals have a 50% chance of passing the mutation to their offspring with each pregnancy. However, some people have what’s called a new, or de novo, mutation, where the mutation occurs randomly and is not inherited.  

The most common and characteristic type of tumor in VHL disease is hemangioblastoma, a benign blood vessel tumor that typically develops in the brain, spinal cord, and retina in the eye. Even though they are benign, hemangioblastomas can cause symptoms if they push against surrounding tissues. For example, if the tumor is in the cerebellum, it can cause loss of balance; whereas in the eyes, it can cause blindness. 

Another benign tumor is pheochromocytoma, a tumor of the adrenal glands that can cause symptoms like headaches, sweating, palpitations and increases in blood pressure due to the release of adrenal hormones.  

Some people also develop cyst-like tumors in the liver, lungs, kidneys and pancreas, as well as near the uterus or testicles. 

Finally, some tumors associated with VHL disease are cancerous, such as renal cell carcinoma, a malignant tumor that can affect both kidneys and metastasize quickly. 

Not every person with VHL disease will have every type of tumor, but they will almost always develop at least one. On averag]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Ankylosing_spondylitis:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/he7PxTAyRr2pfBxXSwHPCc-WQDefypnX/_.png</video:thumbnail_loc><video:title><![CDATA[Ankylosing spondylitis: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Ankylosing spondylitis, or AS for short, is a chronic inflammatory condition that primarily affects the spine and sacroiliac joints, which connect the pelvis to the lower spine. In AS, inflammation primarily affects the vertebral joints in the spine, specifically the points where ligaments, tendons, and joint capsules attach to bone.  

Chronic inflammation causes new bone to form along the outer edges of the spine. Now the affected part of the spine becomes more rigid, limiting its range of motion. As the condition progresses, the bony outgrowths grow bigger until they form bridges among adjacent vertebrae, causing ankylosis—or fusion—of the entire spine. 

The exact cause of inflammation in AS is unclear, but it’s thought to be due to an autoimmune process, which is when the immune system attacks its own tissue; in this case, the collagen found in the joints. While no autoantibody has been specifically linked to the disease, most individuals with AS carry the gene HLA-B27, which plays a key role in helping the body distinguish between its own cells and foreign substances. 

The most common symptom of AS is chronic back pain and stiffness, especially in the lower back and buttocks.  

The pain and stiffness are usually worse in the morning and improve with activity, not rest. Over time, pain can extend up the spine and cause neck or upper back pain and immobility.  

Because the ribs and vertebrae are involved in breathing, stiffness in the thoracic, or chest, region of the spine can result in shortness of breath.  

The autoimmune process underlying AS can lead to pain in tendons and peripheral joints such as the hips, knees, and ankles. It can also lead to several other extra-articular manifestations, such as anterior uveitis, causing painful, red eyes with increased sensitivity to light.  

Other important manifestations include inflammatory bowel disease, pulmonary fibrosis, psoriasis, heart blocks, and aortic inflammation, which can potentially lead to aortic aneurysm and dissection.   ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myasthenia_gravis:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rZP-zWtLTwCVSr6XO9V8p9v8SoeFqeUT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myasthenia gravis: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Myasthenia gravis is an autoimmune disorder that causes weakness in skeletal muscles. It occurs when the body mistakenly produces antibodies that attack the neuromuscular junction, which is the meeting point between nerve endings and muscle fibers.  

Typically, when the brain sends a signal to move a muscle, it travels down motor nerves until it reaches the neuromuscular junction. At this junction, nerve cells release a chemical messenger called acetylcholine, a neurotransmitter which crosses a small gap and binds to receptors on the surface of muscle cells, triggering muscle contraction.  

With myasthenia gravis, antibodies bind to these receptors, blocking their interaction with acetylcholine and weakening muscle contraction. Over time, these antibodies can damage and reduce the amount of receptors on the muscle cell surface, further leading to weak and easily fatigued muscles.  

Although it is unclear why, myasthenia gravis tends to affect young females in their twenties and thirties and older males in their sixties and seventies. It is also more common in people who have a thymoma, which is a type of tumor that develops in the thymus gland.  

The hallmark symptom of myasthenia gravis is muscle weakness that worsens after activity and improves with rest. Initially, myasthenia gravis may only affect the muscles that control movement of the eye and eyelids, causing symptoms like double vision or drooping eyelids. When the arm and leg muscles are involved, people might experience severe fatigue and difficulties with walking or climbing stairs. Weakness in the muscles responsible for swallowing and speech production can cause symptoms like a change in voice and slurred speech, as well as difficulty swallowing.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neuroblastoma:_Year_of_the_Zebra_2024</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SWUpBBT8Tj2P-ytfEVttgDWcQZ2pBE1I/_.png</video:thumbnail_loc><video:title><![CDATA[Neuroblastoma: Year of the Zebra 2024]]></video:title><video:description><![CDATA[Neuroblastoma is a type of cancer that arises from neural crest cells, which are cells involved in the development of the nervous system. 

Normally, neural crest cells migrate throughout the body to form a range of structures including the sympathetic chain ganglia, nerve cells that lie on either side of the spinal cord, and the adrenal medulla, the innermost part of the adrenal gland.

With neuroblastomas, some of these neural crest cells do not mature properly during fetal development, and instead continue to divide in their immature state until they form a tumor. 

Most commonly, neuroblastomas form in the adrenal medulla, but they can also develop in other areas of the sympathetic chain, including the neck, chest, abdomen, or near the spine. 

These tumors typically affect infants and are rarely seen in children over five years old.

While no one knows the exact cause, this abnormal cell development has been associated with mutations in growth-regulating genes, such as the MYC, ALK, and PHOX2B genes.

Clinical manifestations of a neuroblastoma depend on the location and size of the tumor.

For example, a tumor in the adrenal glands can present with a large, painful abdominal mass that causes abdominal swelling; whereas a tumor in the chest can grow into the lungs, causing breathing difficulties and abnormal breath sounds.

Tumors near the spine may compress one or more spinal nerves causing neurologic symptoms, like muscle weakness and bowel or bladder dysfunction.

Similarly, tumors in the neck can press on the nerves originating from that region, resulting in a collection of symptoms known as Horner syndrome.

Horner syndrome may result in a drooping eyelid, small pupil in one eye, and decreased sweating on one side of the face.

About half of all neuroblastomas spread to the bones, causing bone pain and an increased risk of fractures.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cholinergic_therapy_-_Overview:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qh7LEvCSTqWmGTuO8Xdw0EHLTlqYbPJq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cholinergic therapy - Overview: Nursing pharmacology]]></video:title><video:description><![CDATA[Cholinergic therapy uses medications that affect the parasympathetic nervous system, which is often nicknamed the “rest and digest” or “feed and breed” system of the autonomic nervous system. When activated, the parasympathetic nervous system promotes activities such as digestion, elimination, and sexual arousal, and it helps the body calm down after periods of stress or danger. Commonly used cholinergic medications include bethanechol, a direct-acting cholinergic agonist, and atropine, a cholinergic antagonist.

Now, bethanechol is referred to as a parasympathomimetic because it works by mimicking the parasympathetic neurotransmitter, acetylcholine. By stimulating the muscarinic receptors in the bladder, it stimulates the contraction of the bladder’s detrusor muscle and relaxes the external urinary sphincter, promoting urination in non-obstructive urinary retention. By stimulating muscarinic receptors in the gastrointestinal tract, it promotes bowel motility.

In contrast, atropine is referred to as a parasympatholytic, because it binds to acetylcholine receptors, blocking its effects. This leads to inhibition of the parasympathetic nervous system which results in increased heart rate and cardiac output and other antimuscarinic effects.  It’s used to treat conditions like overactive bladder and bradycardia. It can also be used to promote pupillary dilation during eye exams and can be given preoperatively to reduce excessive respiratory secretions.

Alright, cholinergic medications have several side effects which are related to their actions on the parasympathetic nervous system. By promoting parasympathetic effects in the heart and lungs, bethanechol can cause hypotension, bradycardia, and bronchoconstriction. It also promotes exocrine gland activity, causing sweating and increased salivation.

In addition, increased gastrointestinal activity can cause cramping and diarrhea. Other effects include blurred vision due to miosis, or pupillary constriction, as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Public_health_nursing:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JlHlijw3RqihIVIDiatPHDhkQWa3VSEo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Public health nursing: Nursing]]></video:title><video:description><![CDATA[Often when someone thinks of a nurse, they picture settings like hospitals and clinics. However, nursing care is just as important in other settings like with public health nursing, community-based nursing, and home health nursing.  

Each of these nursing specialties promote health by using primary prevention, which is aimed at minimizing the chance of developing an illness by reducing modifiable risk factors; secondary prevention, which involves screening for an illness in its early stages, before a patient develops signs and symptoms; and tertiary prevention, which is focused on slowing disease progression, preventing complications, and promoting optimal functioning.

Now, the goal of public health nursing involves preventing disease and promoting health at three population levels: the individual and family level, directed at providing care for a patient and their support system; the community level, which encompasses a specific population, such as students living on a college campus or vulnerable populations like patients with developmental disabilities; and the system level, where care is directed at influencing the overarching systems that impact health, like healthcare policy.

Now, the goal of public health nursing involves preventing disease and promoting health at three population levels: the individual and family level, directed at providing care for a patient and their support system; the community level, which encompasses a specific population, such as students living on a college campus or vulnerable populations like patients with developmental disabilities; and the system level, where care is directed at influencing the overarching systems that impact health, like healthcare policy.

These functions help public health nurses focus care on primary prevention of illness within a population. Public health nursing also has roles in secondary prevention, such as providing screenings for tuberculosis, and tertiary prevention, like running a foot c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vulvar_skin_disorders_(benign):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I21DotzKRfu0QiWpt9rgf2nqQl_WTw9S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vulvar skin disorders (benign): Clinical sciences]]></video:title><video:description><![CDATA[There are several benign skin disorders of the vulva, including contact dermatitis, lichen simplex chronicus, lichen sclerosus, and lichen planus. These skin disorders are often chronic and can cause significant discomfort, decreased sense of well-being, and adversely affect sexual function. 

When evaluating a patient with a chief concern suggesting a benign vulvar skin disorder your first step is to obtain a focused history and physical. The first thing you should ask about is symptom…onset, duration, location, and nature. 

Other factors that will aid in your diagnosis include the timing of symptoms in relation to the patient’s menstrual cycle and a review of any possible precipitating or known risk factors. The vulva is particularly sensitive to irritants including cleansers, fragrances, lubricants, and other topical products such as antibiotics and local anesthetics, bathing, shaving, and the use of incontinence pads, or menstrual products.

Now, for patients with acute concerns of vulvar pruritus, especially for those with concomitant vaginal discharge, first consider possible alternative diagnoses, such as vulvovaginal infections and conditions like bacterial vaginosis, candidiasis, trichomoniasis, or molluscum contagiosum. On the other hand, for those whose symptoms are more chronic, consider a benign vulvar skin disorder.  

Here’s a clinical pearl! History and physical examination are typically enough to make your diagnosis. However, when the diagnosis is not clear or treatment does not improve your patient’s symptoms, be sure to obtain additional labs. These may include wet mount microscopy, yeast culture, screening for sexually transmitted infections, and vulvar biopsy. 

A vulvar biopsy is a powerful diagnostic test for vulvar skin disorders as it can definitively confirm your diagnosis. 
A biopsy is indicated if you are unsure about the diagnosis or if on physical exam you see any of the following; an atypical lesion such as one with new pigm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Generalized_anxiety_disorder:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D36ltnXsRoWQfJPX5QcGZwDcQhqVihwE/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Generalized anxiety disorder: Nursing]]></video:title><video:description><![CDATA[Nurse Becca works in a family practice clinic and is caring for Holly, a 32-year-old who presents with anxiety. After settling Holly in the room, Nurse Becca goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Holly’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Becca recognizes important cues, including Holly’s vital signs which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respiratory rate 19 breaths per minute, and blood pressure 136/75 mmHg. Nurse Becca notes that Holly appears restless and is biting her nails. She gathers more information about Holly’s symptoms.   

Nurse Becca: Hi Holly, tell me how you’re feeling. 

Holly: Well, I’m feeling really overwhelmed lately. I’m worried about so many things. And I’m having trouble concentrating at work.    
Nurse Becca: That sounds difficult. How are you sleeping? 

Holly: I only sleep a few hours each night, I can’t stop thinking about things.    
Nurse Becca: When did your symptoms start?   
Holly: Around seven months ago right after I moved and started my new job. 

Next, Nurse Becca administers the Generalized Anxiety Disorder 7-item screening tool, or GAD-7, and notes Holly has a score of 12 out of 21, which is consistent with moderate anxiety. 

Nurse Becca then analyzes these cues. She reviews the electronic health record, or EHR, and notes that Holly has no previous history of mental health disorders. She reports her assessment findings to the health care provider who diagnoses Holly with generalized anxiety disorder, or GAD.  

Nurse Becca remembers that one of the main features of GAD is excessive worry; and although the exact cause of GAD isn’t known, but it’s thought to be caused by an imbalance of the neurotransmitters, where serotonin system activity is low and noradrenergic system activity is elevated. This leads to symptoms of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Somatic_symptom_disorder:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r0kJ7EdgSlWJ5h2oewF4LywNTiqwSyTX/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Somatic symptom disorder: Nursing]]></video:title><video:description><![CDATA[Nurse Heidi works in a primary care office and is caring for Katya, a 43-year-old with a history somatic symptom disorder. After introducing herself, Nurse Heidi goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Katya’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Heidi recognizes important cues. She obtains Katya’s vital signs, which are temperature 98.6 F, or 37 C, heart rate 75 beats per minute, respirations 16 breaths per minute, and blood pressure 110/70 mmHg. Katya also states she&amp;#39;s having dull lower back pain, which comes and goes, that she rates at 4 out of 10 on a numeric pain scale. Nurse Heidi then gathers additional information from Katya. 

Nurse Heidi: Katya, tell me about what brought you to the office today. 

Katya: Well, same thing as in the past. I keep having back pain that comes and goes even though my health care provider ran several tests and told me nothing is wrong. It never goes away, and I don’t know what to do. 

Nurse Heidi: Tell me about how this pain affects your daily life. 

Katya: I’m not able to do things I used to love doing, like hanging out with my friends, because I’m always worried my pain will return. So, I end up staying home alone all day instead. 

Nurse Heidi: That sounds difficult and isolating. 

Next, Nurse Heidi analyzes the cues. She reviews the electronic health record, or EHR, and notes that Katya is diagnosed with somatic symptom disorder. She also sees that the health care provider recommended counseling, but Katya declined.  

Nurse Heidi knows that patients with somatic symptom disorder experience physical symptoms that aren’t explained by any known physical or psychiatric conditions. She also understands that patients with this disorder are unable to cope with their unpleasant emotions and instead, displace them into physical symptoms, like pain an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Safety_principles:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8aiEkke-RLW92QO3mCcYHLchSyWxbDO1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication administration - Safety principles: Nursing pharmacology]]></video:title><video:description><![CDATA[Medication administration is a complex process which involves the application of a prescribed medication to a patient. As the nurse, you must identify medication safety risks, follow safe administration principles, and evaluate your patient’s condition after administration.  

Now, risks associated with medication administration include adverse medication reactions, cross-infection, or injury. Adverse reactions are unwanted effects that occur related to administration of a medication, which can be mild, like rash or nausea, or more severe, like kidney damage or GI bleeding.

Next, cross-infection is when organisms, like bacteria or viruses, are transferred to your patient during administration. This can occur when administering a medication through your patient’s IV without thoroughly cleaning the hub or when touching the tip of an eye dropper to your patient’s eye during administration.

Lastly, injury can occur to your patient when administering medications, like giving a hypertension medication to a patient who’s hypotensive or injecting a medication intramuscularly using incorrect technique, causing a hematoma or nerve injury.

Alright, so there are several different routes for medication administration. The most common routes are oral, also known as per os or PO; parenteral, which includes IV, intramuscular, or IM, subcutaneous; and intradermal. Other routes for medication administration include inhalation, sublingual, rectal, topical, otic, and ophthalmic.

Now, regardless of the route, prevent harm to your patient by following safe medication administration principles each time you administer a medication. The standard practice for safe medication administration involves adhering to the rights of medication administration, which include the: right patient, right medication, right dose, right time, right route, right indication, and right documentation. It’s important to note that there might be additional rights and you should follow the protoc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Sexually_transmitted_infection_(STI):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pbPafzuXS8GyYQFLWNc-TQqUTSSo-Jg7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Sexually transmitted infection (STI): Nursing]]></video:title><video:description><![CDATA[Nurse Sarah works in an urgent care clinic and is caring for Gia, a 24-year-old female who wants to be tested for sexually transmitted infections, or STIs, after her partner told her he tested positive for chlamydia.  

After settling Gia in the exam room, Nurse Sarah goes through the steps of the Clinical Judgment Measurement Model, or CJMM, to make clinical decisions about Gia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

To begin, Nurse Sarah recalls how sexual health encompasses a patient’s well-being related to their sexual orientation, gender identity, and intimacy with others. With this in mind, Nurse Sarah performs a sexual health assessment and recognizes important cues, including Gia’s report of increased vaginal discharge and dysuria over the past four days. She notes Gia has no previous history of STIs or pregnancies, has had three sexual partners in the last month, doesn’t use contraceptives, and reports feeling safe in her current relationship.  

Nurse Sarah ensures Gia’s privacy and stays in the room while the health care provider performs Gia’s pelvic exam and collects specimens for testing.  

Next, Nurse Sarah analyzes the cues. She notes the health care provider’s documentation of Gia’s exam, including the presence of copious vaginal discharge, with no signs of bruising or forced vaginal entry.

So, using the information she’s gathered, along with Gia’s social and medical history, Nurse Sarah selects the priority hypothesis of acute STI.  Then, she generates solutions to address Gia’s STI which will include treatment with the prescribed antibiotics and education on STI treatment and prevention; and she establishes the expected outcomes that Gia will accurately describe how to complete her antibiotic prescription and choose a reliable method to prevent future STIs by the end of today’s visit.  

Nurse Sarah then takes action to implement these soluti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fostering_Interprofessional_Partnerships_for_Optimal_Care_and_Positive_Patient_Outcomes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bYgL1MmjQm2etYtuJO7K9FXmRtORBtlV/_.png</video:thumbnail_loc><video:title><![CDATA[Fostering Interprofessional Partnerships for Optimal Care and Positive Patient Outcomes]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Fostering Interprofessional Partnerships for Optimal Care and Positive Patient Outcomes through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Acute_pain:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fJytZWxrTmeoj-dkWz9zm4IzSn21jSIv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Acute pain: Nursing]]></video:title><video:description><![CDATA[Nurse Nadia works on an orthopedic unit and is caring for Brian, a 51-year-old male with a history of degenerative joint disease, who was recently admitted for intractable back pain. After settling Brian in his room, Nurse Nadia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Brian’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Nadia recognizes important cues, including Brian’s vital signs, which are blood pressure 172/92 mmHg, heart rate 102 per minute, and respirations 22 per minute. She also notices Brian is gripping the side rails and clenching his jaw. When asked about his pain, he reports a current pain level of 9 out of 10, and that his tolerable level of pain is 5 out of 10.  

Next, Nurse Nadia analyzes these cues. She reviews the electronic health record, or EHR, and notes that Brian is prescribed 0.5 mg of IV hydromorphone every three hours PRN, and he received his last dose in the emergency department one hour ago. Nurse Nadia realizes Brian needs effective pain management.  

Now, using the information she has gathered, along with Brian’s medical history, Nurse Nadia chooses a priority hypothesis of acute pain.  

Then, she generates solutions to address Brian’s pain that will include pharmacologic and nonpharmacologic pain management interventions; and she establishes the expected outcome that after intervening, Brian will report a pain level of 5 or less out of 10 within two hours.  

Nurse Nadia then takes action to implement these solutions. She knows that since Brian’s most recent dose of pain medication was one hour ago, he can&amp;#39;t receive his next dose for two more hours. Since Brian is in severe pain, she verifies that Brian isn’t allergic to any medications and then calls the provider, reporting Brian’s current pain assessment and vital signs. The provider prescribes a one-time dos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pediatric_urinary_tract_infection:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/B3s-7pEHRMOWrtMDS89BzoxZQY6Pbt8w/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pediatric urinary tract infection: Nursing]]></video:title><video:description><![CDATA[Nurse Michelle works at a pediatrician’s office and is caring for Emma, a fully toilet trained, 5-year-old female brought in by her father, Jim, for urinary frequency and crying when urinating. After settling Emma and her father in a room, Nurse Michelle goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Emma’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Michelle recognizes important cues, including vital signs, which are temporal temperature 98.8 F or 37 C, heart rate 84 beats per minute, and respirations 22 breaths per minute; as well as Jim’s description of Emma’s dark, amber-colored, and foul-smelling urine. Jim also reports Emma has been urinating more often than usual. Emma rates her pain during urination an 8 out of 10 on the Wong-Baker FACES pain scale. Then, Nurse Michelle obtains a clean catch urine sample from Emma for dipstick urinalysis and assesses for suprapubic and flank pain, which revealed mild discomfort with palpation over the suprapubic area. 

Next, Nurse Michelle analyzes these cues. She reviews the results of the urinalysis which shows positive for leukocytes, nitrites, and blood. Nurse Michelle recognizes that normal urinary elimination involves a controlled, painless release of urine that&amp;#39;s typically light to dark yellow in color, transparent, with a slight odor, with no evidence of bacteria or blood. Nurse Michelle realizes Emma is experiencing altered urinary elimination. She shares her assessments with the health care provider who diagnoses a urinary tract infection. 

Using information she&amp;#39;s gathered along with Emma’s medical history, Nurse Michelle chooses a priority hypothesis of urinary tract infection. 

Then, she generates solutions to address Emma’s infection that will include pharmacologic and nonpharmacologic interventions, and she establishes the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Constipation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-ZdU7xLdT56wKzfSdWvRFOZVTseOGqQ5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Constipation: Nursing]]></video:title><video:description><![CDATA[Nurse Thomas works at a primary care clinic and is caring for Donna, a 55-year-old female with a history of constipation, who’s being seen for abdominal discomfort. After settling Donna in her room, Nurse Thomas goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Donna’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

Nurse Thomas recognizes important cues such as Donna’s abdominal pain, which she describes as cramping with constant aching and rates as a 6 out of 10 on a pain scale. While gathering Donna’s health history, Nurse Thomas learns that although she typically has a bowel movement every two to three days, her last bowel movement was five days ago. She states it was hard, lumpy, difficult to pass, and there was a small amount of blood on the toilet paper after wiping.  

Donna reports she’s been managing occasional constipation for years, and it’s gotten worse since she started working from home. Nurse Thomas learns Donna usually drinks sodas throughout the day and typically eats a cheeseburger on a white bun for lunch. He performs an abdominal assessment by visually inspecting Donna’s abdomen, auscultating all four quadrants, and palpating her abdomen. His findings include mild abdominal distension, hypoactive bowel sounds, and a firm, elongated mass in her lower left quadrant. Results of a digital rectal exam by the health care provider reveals normal anal sphincter tone, and an absence of rectal pain, fissures, or hemorrhoids.  

Next, Nurse Thomas analyzes these cues. He knows bowel elimination should produce regular, soft, easy-to-pass bowel movements, and that other expected assessment findings include active bowel sounds in each quadrant, and a soft abdomen.  

Okay, so using Donna’s medical history and the information he’s gathered, Nurse Thomas chooses a priority hypothesis of constipation. Then, he generates]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Wound_infection:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vcx9eLpWRAOun4DtOjQ3XRqTRMuJCPNz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Wound infection: Nursing]]></video:title><video:description><![CDATA[Nurse Jess works at an urgent care clinic and is caring for Roger, a 56-year-old male, who arrived with a wound on his lower arm. After settling Roger in his room, Nurse Jess goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Roger’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jess recognizes important cues, including Roger’s vital signs, which are temperature 101 F, or 38.3 C, heart rate 98 per minute, respirations 14 per minute, and blood pressure 125/85 mmHg.  

She completes a skin assessment on Roger’s arm, and notes his wound is 1 centimeter across, open, and draining a small amount of purulent drainage. She also notices superficial erythema 2 centimeters around the wound. Extending from the wound towards his upper arm is a red streak, which Nurse Jess recognizes is a sign of lymphangitis, or inflammation of the lymph channels.  

When asked about the wound, Roger says he thinks it started with a bug bite he got while boating 3 days ago. 

Next, Nurse Jess analyzes cues. While reviewing the electronic health record, or EHR, she notes Roger was treated for a similar wound in the past. She also notes he’s been taking steroids prescribed for rheumatoid arthritis for the past 3 months, which can suppress the immune system. Nurse Jess realizes Roger needs treatment for his infected wound.  

Now, using the information she’s gathered, along with Roger’s medical history, Nurse Jess chooses a priority hypothesis of traumatic wound.  

Next, she generates solutions to address Roger’s wound that will include pharmacologic and nonpharmacologic interventions.  She establishes the expected outcome that after intervening, Roger will correctly demonstrate how to apply a dressing to his wound. 

Nurse Jess then takes action to implement these solutions. She begins by notifying the health care provider of Roger’s eleva]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intraoperative_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X58Gm5MpRZ2-7gINpztfuXZiQjOGfuWc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intraoperative care: Nursing]]></video:title><video:description><![CDATA[The intraoperative phase of surgery is when your patient undergoes a surgical procedure, beginning when they enter the operating room and ending when they leave the operating room. Your role during this period is to promote patient safety by performing frequent assessments, preventing infection, and advocating for them, since they cannot speak for themselves. When caring for your patients during the intraoperative phase, you will follow the steps of the Clinical Judgment Measurement Model, or CJMM, to make clinical decisions about patient care.  

Okay, let’s review the roles of the surgical team, which is typically separated into a sterile group and a nonsterile group. Sterile team members include the scrub nurse, surgeon, and registered nurse first assistant, or RNFA, and they work strictly within the sterile field. On the other hand, the nonsterile team members work outside the sterile field and include the circulating nurse, the anesthesiologist or certified registered nurse anesthetist, also known as the CRNA, and other assistive personnel. 

Now when it comes to the nursing team members, the scrub nurse is responsible for preparing and maintaining the sterile field, draping the patient, and assisting the surgeon by passing instruments and supplies. The circulating nurse advocates for the patient, coordinates communication between the nonsterile and sterile team members, and initiates the “time-out” procedure, when the team pauses before surgery to verify that they’re performing the right procedure on the right surgical site on the right patient. Additionally, the RNFA promotes optimal patient outcomes by fostering communication and collaboration with the team during surgery. It’s important to note that it’s the responsibility of every team member to practice surgical conscience through continual assessment and vigilance, to ensure adherence to sterile technique. 

Now, as the circulating nurse, you will ensure patient safety by using the Clinical Jud]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Social_determinants_of_health_(SDOH):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Kq1arg9tTZOksgbTeGRiYbvaSeGb9MGf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Social determinants of health (SDOH): Nursing]]></video:title><video:description><![CDATA[Social determinants of health, or SDOH for short, refers to the conditions where people live, work, play, worship, and age, that influence health.  

Now, there are five major categories of social determinants of health: Economic stability, neighborhood and built environment, education access and quality, social community and context and lastly, health care access and quality.  

First, there’s economic stability, which means that people have opportunities for employment and sufficient financial resources to afford basic needs like food, clothing, housing, and utilities. 

Then there’s neighborhood and built environment, which includes characteristics like having access to a grocery store, availability of public transportation, the quality of housing, as well as factors like clean air and water and neighborhood crime rates.  

Next, education access and quality addresses factors like the availability of early childhood education, high school graduation rates, and opportunities to enroll in college, as well as general literacy.  

Social community and context refers to the sense of community cohesion and connectiveness, like the interactions between family, friends, and coworkers and the degree of civic engagement.  

Finally, health care access and quality includes the availability and coverage of health care services, the quality of care, and health literacy, which is the ability to locate, understand, and use health information to make well-informed decisions about health.  

Now, health equity means that every person has the opportunity to attain their full health potential, and that their socially determined situation does not place them at a disadvantage.   

However, health disparities can occur in socially disadvantaged populations, creating differences in the incidence and prevalence of disease, injury, and mortality. For example, individuals who have limited access to grocery stores with healthy foods are less likely to have proper nutrition, whic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Care_of_an_older_adult_client:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hi8OU8VkTyGMcWVlMdBvlfD8T-CYj-8r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Care of an older adult client: Nursing]]></video:title><video:description><![CDATA[Care of the older adult involves providing holistic care to meet the needs of patients as they mature through adulthood.  

Now, your goal when assessing your older patient is to identify common health issues of older adults, and to intervene to promote your patient’s health and safety.  

Begin by performing a mental status assessment. Observe their general appearance, posture, and facial expressions as indicators of mental function, and evaluate their level of consciousness and orientation to person, place, and time.  

As you talk with your patient, assess their speech patterns, organization of thoughts, and mood. Check for the presence of risk factors for depression, including situations like loss of a spouse, recent retirement, or isolation, as well as problems like pain or insomnia, which can be associated with depression.  

During your assessment, be sure to allow adequate time for them to respond to your questions. If your patient’s mental status is altered, adjust your approach accordingly. Next, assess their mobility and their ability to safely complete their activities of daily living, or ADLs, including bathing, dressing, toileting, and eating.  

Be sure they have assistive devices, as needed, like a walker, cane, glasses, or hearing aids.  Ask them if they have experienced a recent fall and talk to them about measures to increase safety in their home by removing throw rugs, ensuring adequate lighting, and installing handrails. Encourage physical activity according to their level of mobility to promote balance and maintain muscle mass.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pressure_injury:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z-Ua4hCsQcmtN8lkdfudtkfiTSC-6sTC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pressure injury: Nursing]]></video:title><video:description><![CDATA[Nurse Hailey works on an orthopedic unit and is caring for Margaret, a 91-year-old female with a recent fall at home requiring surgical repair of a fractured hip. After settling Margaret in her room, Nurse Hailey goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Margaret’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Hailey recognizes important cues, including Margaret’s vital signs, which are blood pressure 118/62 mmHg, heart rate 88 beats per minute, respirations 18 breaths per minute, and temperature of 100.4 F or 38 C. Nurse Hailey also notes that Margaret is incontinent; and a skin assessment reveals an area on her coccyx that’s pink and moist, without slough or eschar.  

Next, Nurse Hailey analyzes these cues. She reviews the electronic health record, or EHR, and notes that Margaret has declined working with physical therapy due to the pain in her hip and coccyx. Nurse Hailey recognizes that immobility and pain can contribute to pressure injuries and realizes that Margaret is experiencing impaired tissue integrity. She shares her assessments with the wound care nurse who classifies Margaret’s coccyx redness as a stage 2 pressure injury. 

Now, using the information she has gathered, along with Margaret’s medical history, Nurse Hailey chooses a priority hypothesis of impaired tissue integrity.  

Then, she generates solutions to address Margaret’s impaired tissue integrity that&amp;#39;ll include nonpharmacologic and pharmacologic interventions; and she establishes the expected outcome that after intervening, Margaret will demonstrate a healing pressure injury without further breakdown of skin or the development of infection by time of discharge. 

Nurse Hailey then takes action to implement these solutions. She knows that since Margaret has a stage 2 pressure injury, she needs to complete the wound care ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Healthcare-associated_infection_(HAI):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0pZL2L7WQlumvI_p2ovs_OqVRuOgjwGF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Healthcare-associated infection (HAI): Nursing]]></video:title><video:description><![CDATA[Nurse Monique begins her shift on a medical-surgical unit caring for Sam, a 78-year-old male who was admitted two days ago for chronic heart failure. After introducing herself, Nurse Monique begins her shift assessment and goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Sam&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Monique recognizes important cues. First, she notices Sam has an indwelling urinary catheter, which is draining cloudy urine. Then, she takes his vital signs and notes his temperature is 100.6 F, or 38.1 C. She palpates Sam’s abdomen, which elicits suprapubic pain that Sam rates as a 4 out of 10. He also reports that he didn’t have this type of pain until this morning. 

Next, Nurse Monique analyzes these cues. She reviews the electronic health record, or EHR, which shows Sam’s vital signs during the previous shift were within normal limits and his urine was clear. Nurse Monique knows that due to Sam’s increased age and presence of an indwelling catheter, he&amp;#39;s at high risk for a health care-associated infection, or HAI, which is an infection that develops from exposure to microorganisms in a health care setting.  

Nurse Monique considers these risk factors along with Sam’s new onset of fever, pain, and cloudy urine. She suspects that Sam is experiencing a type of HAI known as a catheter-associated urinary tract infection, or CAUTI.  

Now, using the information Nurse Monique has gathered, she chooses a priority hypothesis of impaired urinary elimination. 

Then, she generates solutions to address this hypothesis that will include pharmacologic and nonpharmacologic interventions. She also establishes the expected outcome, that after intervention, Sam’s temperature will be within normal range, and his symptoms of CAUTI will improve. 

Next, Nurse Monique takes action to imp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Complications_of_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6rc_XliJQWejSyAfeJtDCmkERGGpVgE3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Complications of cancer: Nursing]]></video:title><video:description><![CDATA[Cancer, or malignancy, refers to a group of diseases characterized by abnormal cell growth and differentiation, which changes cellular appearance and function. These changes are harmful to normal cells and can cause several complications, which can be directly related to cancerous tissue, a side effect of treatment, or a combination of both. 

Let’s look at some of the complications of cancer, starting with pain. Patients with cancer are at risk for acute and chronic pain, which can decrease quality of life. When caring for your patient with cancer, perform a comprehensive pain assessment on an ongoing basis. Discuss their pain management goals, and the use of pharmacologic interventions, including nonsteroidal antiinflammatory drugs, or NSAIDs; opioids; and adjuvant medications like corticosteroids; and nonpharmacologic interventions, such as guided imagery, relaxation breathing, distraction, massage, and acupuncture.  

Then, coordinate care with the interdisciplinary team to provide other interventions, such as radioactive medications for bone pain, nerve blocks, and epidural or intrathecal analgesia as indicated. You may also refer your patient to a pain management or palliative care specialist to help control their pain and improve quality of life. 

Alright, next let’s explore infection as a complication of cancer. Several factors can lead to an infection in your patient with cancer, including tissue damage from ulceration; necrosis caused by cancerous tissue; tumors compressing organs; and decreased immunity due to cancer or treatment-induced neutropenia, which is a low number of neutrophils, or the infection-fighting white blood cells.  

When providing care, be sure to monitor your patient for signs or symptoms of infection, such as a temperature of 100.4 F or 38 C or higher, cough, or diarrhea. However, keep in mind neutropenia can diminish signs of infection, so your patient may have an infection and be asymptomatic.  

Now, to help prevent infe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Care_of_a_client_in_the_emergency_department:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/c8zHwaUNSWS2n2soiy9F7gZ1StCjv_dc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Care of a client in the emergency department: Nursing]]></video:title><video:description><![CDATA[The role of a nurse in the emergency department, or ED, is to identify and respond to patients with potentially life-threatening conditions using a standardized triage process. Triage involves rapidly classifying patients based on the severity of their condition and then caring for the most critically ill first.  

The triage process includes a primary survey, to identify emergent conditions, like hemorrhage or skull fractures, and manage them as they are identified; followed by a secondary survey, to identify urgent and nonurgent conditions and injuries, like a broken arm or leg wound. 

Now the primary survey is the initial assessment of your trauma patient, that can be guided using the mnemonic ABCDE, which stands for Airway, Breathing, Circulation, Disability and Exposure.  Your primary survey begins when you first see your patient.  

If, during this time, you identify an obvious and significant external hemorrhage, your focus will shift from ABCDE to CABDE, meaning you should control the hemorrhage first before moving on with your assessment.  

If no external hemorrhage is noted, you&amp;#39;ll start your assessment with A, where you’ll assess alertness and airway patency. To determine alertness, assess your patient’s level of consciousness using the mnemonic AVPU. A is for alert, V is for responsiveness to voice, P is for responsiveness to pain, and U is for unresponsiveness.  

For airway patency, look for signs of a compromised airway, like gasping, or agonal breaths, dyspnea, and facial or neck trauma. Be sure to identify airway obstructions, like secretions, emesis, an enlarged tongue, or foreign objects, like loose teeth or dentures.  

For patients who are unable to keep their airway patent, prepare them for rapid sequence intubation. Also, if your patient is suspected of having a spinal cord injury, stabilize their cervical spine using a cervical collar or immobilization device. 

Next, for B, you’ll assess breathing. Even with a patent air]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Borderline_personality_disorder:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wtTWLqvXTPqyf6niKr7iUx3cQJWu3YNQ/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Borderline personality disorder: Nursing]]></video:title><video:description><![CDATA[Nurse Amirah works on an inpatient psychiatric unit and is caring for Yang, a 42-year-old with a history of borderline personality disorder, who was recently admitted for a self-harm ideation following a breakup with his partner. After settling Yang in his room, Nurse Amirah goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Yang’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Amirah recognizes important cues, including Yang’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 70 beats per minute, respirations 16 breaths per minute, and blood pressure 132/82 mmHg. She notes Yang is pacing back and forth and that his breakfast tray is untouched on the bedside table.  

Nurse Amirah: Hi Yang, I noticed you haven’t eaten your breakfast.  

Yang: This is the most disgusting food I’ve ever seen. Where is my boyfriend? I’m serious, I’ll hurt myself if he really decides to leave me. 

Nurse Amirah: I understand you’re upset. Do you have a plan to injure yourself? 

Yang: No, but I’ll do it. I just don’t get what happened. I thought I’d found my soulmate. 

Next, Nurse Amirah analyzes these cues. She reviews electronic health record, or EHR, and notes Yang was diagnosed with borderline personality disorder, or BPD, five years ago, and has been hospitalized for self-harm ideation in the past.  

Nuse Amirah recognizes that BPD is a condition where individuals have unstable moods and relationships. Those with BPD may also experience fear of abandonment, leading to threats of self-harm to keep someone from leaving them. Nurse Amirah recognizes that Yang needs mood stabilization to prevent self-harm. 

Now, using the information she&amp;#39;s gathered, along with Yang’s medical history, Nurse Amirah chooses a priority hypothesis of risk for violence against self. 

Then, she generates solutions to address Ya]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Substance_use_disorder_(SUD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GFrPgvTdQfuu7XU5hkd9vyrkQTOb-hU9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Substance use disorder (SUD): Nursing]]></video:title><video:description><![CDATA[Nurse Jacob works on a medical-surgical unit and is caring for Dallas, a 62-year-old patient with a history of substance use disorder, who was admitted three days ago for alcohol detoxification. After settling Dallas in his room, Nurse Jacob goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Dallas’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jacob recognizes important cues, including Dallas’ vital signs, which are temperature 98.6 F or 37 C, heart rate 105 beats per minute, respirations 20 breaths per minute, and blood pressure 140/90 mmHg. He also notices Dallas&amp;#39; hands are trembling, he’s sweating, and he has IV fluids infusing in his left antecubital peripheral IV.  

Nurse Jabob: Hi Dallas, how are you feeling? 

Dallas: I have a pounding headache, I can’t concentrate, and I just can’t relax.  

Nurse Jacob: I understand. Are you hearing or seeing anything that isn’t normally there?  

Dallas: No, I’m not hallucinating, I just feel super nervous, I can’t explain it.    
Next, Nurse Jacob analyzes these cues. He reviews the electronic health record, or EHR, and notes that, prior to admission, Dallas was drinking about ten shots of vodka per day.  

Nurse Jacob completes the Clinical Institute Withdrawal Scale-Alcohol Revised, or CIWA-Ar, and tallies Dallas’ CIWA score as 15, indicating moderate withdrawal symptoms.  

Nurse Jacob knows that the maximum CIWA score is 67, and as withdrawal symptoms become more severe, the score increases. 

Nurse Jacob recognizes that when patients with alcohol use disorder stop drinking abruptly, they can develop symptoms like anxiety, irritability, tachycardia, diaphoresis, and auditory and visual hallucinations, and they can develop delirium tremens, a severe complication that can lead to seizures and death.  

Nurse Jacob realizes Dallas needs effective managem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Head_injury:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HLzi6YHcSR6e0beslOhw4tP5T6eM6Uud/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Head injury: Nursing]]></video:title><video:description><![CDATA[Nurse Laquanna works on an oncology unit but was floated to the neurology unit earlier today. She&amp;#39;s caring for Molly, a 74-year-old female with a history of atrial fibrillation, or a-fib, who was recently admitted for a head injury. After settling Molly in her room, Nurse Laquanna goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Molly’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Laquanna recognizes important cues including a Glasgow Coma Scale, or GCS, score of 14, and vital signs which are temperature 98.2 F, or 36.8 C, heart rate 98 beats per minute, respirations 16 breaths per minute and regular, blood pressure 134/62 mmHg, and oxygen saturation 95 percent on room air. Nurse Laquanna also notices Molly seems slightly agitated.  

Next, Nurse Laquanna analyzes important cues. She reviews the electronic health record, or EHR, and sees Molly was involved in a head-on motor vehicle collision with airbag deployment, and she takes an anticoagulant daily to treat her a-fib. Nurse Laquanna recognizes that a head injury coupled with Molly’s history of anticoagulation places her at risk for intracranial bleeding. She also knows that subtle neurologic changes can be early indicators of complications. Nurse Laquanna knows Molly will require frequent neurological assessments, or neuro checks, to monitor for changes in her mental status.  

During Molly’s neuro check an hour later Nurse Laquanna notes Molly opens her eyes when her name is called; she’s disoriented; and does not respond when asked to move her fingers. Nurse Laquanna realizes her GCS is now 12, and that Molly needs intervention quickly. She&amp;#39;s unsure what to do next, so she enlists the help of a fellow staff nurse. 

Nurse Laquanna: Hi, Nurse Elijah. My patient has had a change in her neurologic status. I don’t have much experience in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Dementia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s_7seYagSFSBQldxxbt3io90RK_lq-C9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Dementia: Nursing]]></video:title><video:description><![CDATA[Nurse Darian works on an inpatient orthopedic floor and is caring for Rosemary, an 84-year-old female with a history of Alzheimer disease who was admitted for a hip fracture. After settling Rosemary in her room, Nurse Darian goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Rosemary’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darian recognizes important cues, including Rosemary’s inability to recall her daughter’s name, and disorientation to date and time. He also notices that Rosemary becomes agitated when asked several questions in a row; and as the evening progresses, she becomes more impulsive, and tries to get out of bed on her own. 

Next, Nurse Darian analyzes these cues. He recalls that Rosemary’s dementia can be exacerbated by illness, such as her hip fracture, and changes to her familiar environment, and he realizes Rosemary needs effective safety management. After reviewing her electronic health record, or EHR, he enters Rosemary’s room. 

Nurse Darian: Hi Rosemary, my name is Nurse Darian. I was your nurse yesterday and I&amp;#39;ll be your nurse again today.  

Rosemary: I&amp;#39;ve never met you. 

Nurse Darian: That’s okay, Rosemary. Are you having any pain right now? 

Rosemary: Why does everyone have so many questions all the time?  

Nurse Darian notes that Rosemary begins to sit up in bed and tries to swing her legs to the side of the bed to stand up. The two siderails by Rosemary’s head are up, as well as one siderail by her feet. She then moves towards the open space in the bed to exit, so Nurse Darian moves to prevent her from getting up on her own. 

Nurse Darian: Careful there. Let’s get you comfortable and back in bed safely Rosemary. We can put your favorite show on the television. 

Rosemary: Okay. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Anaphylaxis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tYRKyuCPQhe6rnnhIoP3dtyGToyf_KFY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Anaphylaxis: Nursing]]></video:title><video:description><![CDATA[Nurse Milagros works on a Medical-Surgical unit and is caring for Jessica, a 32-year-old female with a history of intravenous drug use, who was recently admitted for endocarditis. After settling Jessica in her room, Nurse Milagros goes through the steps of the Clinical Judgement Measurement Model to make clinical decisions about Jessica’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Milagros recognizes important cues including Jessica’s vital signs, which are blood pressure 86/42 mmHg, heart rate 112 beats per minute, respirations 36 breaths per minute, and pulse oximetry 89 percent on room air.  

Upon auscultation, Nurse Milagros hears expiratory wheezes in all of Jessica’s lung fields and she also notes Jessica’s restless, fearful appearance. On closer inspection, Jessica appears flushed, and her lips are swollen.  

Next, Nurse Milagros analyzes these cues. She reviews the electronic health record, or EHR, and notes that Jessica has no known allergies to foods or medications. Also, Jessica hasn’t received any medications except the infusion of penicillin in the last four hours. Based on her assessment and recent infusion of penicillin, Nurse Milagros realizes Jessica is likely experiencing anaphylaxis.  

Now, using the information she&amp;#39;s gathered along with Jessica’s medical history, Nurse Milagros chooses a priority hypothesis of impaired gas exchange. 

Then, she generates solutions to address Jessica&amp;#39;s impaired gas exchange that will include pharmacologic and nonpharmacologic interventions; and she establishes the expected outcome that 30 minutes after intervening, Jessica’s respiratory status will stabilize.  

Nurse Milagros then takes action to implement these solutions. First, she stops the infusion of penicillin. Then, she calls the hospital operator and requests that a rapid response be called to Jessica’s room.  

Next, the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Benign_prostatic_hyperplasia_(BPH):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N1WptEgyTV_f7rx1N3m0jG86RnWKW0_G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Benign prostatic hyperplasia (BPH): Nursing]]></video:title><video:description><![CDATA[Nurse Suleena works on a Surgical Step-Down Unit and is caring for Pedro, a 55-year-old male with a history of benign prostatic hyperplasia, or BPH, who was admitted two days ago following a transurethral resection of the prostate, or TURP. After settling Pedro in his room, Nurse Suleena goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Pedro’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Suleena recognizes important cues, including vital signs, which are temperature 98.0 F or 36.7 C, blood pressure 140/ 90 mmHg, heart rate 88 beats per minute, respirations 20 breaths per minute, and oxygen saturation 95 percent on room air. She also notices Pedro grimacing and shifting uncomfortably in bed. When examining the collection bag for Pedro’s continuous bladder irrigation, or CBI, Nurse Suleena notices large blood clots and amber-colored drainage.  

Next, Nurse Suleena analyzes these cues. She knows that the CBI output should be light pink, and that blood clots and amber-colored urine in the CBI drainage bag can indicate that the irrigation rate likely needs to be increased. Also, Pedro’s non-verbal cues and vital signs indicate he’s experiencing discomfort, which is also likely due to his ineffective urinary drainage. She also recognizes that bladder spasms resulting from his TURP procedure can cause additional pain. Then, she reviews the electronic health record, or EHR, and notes that Pedro’s last dose of pain medication was four hours ago. 

Nurse Suleena: Pedro, how are you feeling after your procedure? 

Pedro: I’m fine. Isn’t there a male nurse on this floor?  

Nurse Suleena: I understand that having a female nurse care for you after your TURP procedure can be unfamiliar. There are no male nurses available today, but I’m going to do my best to take care of you and make you comfortable. Is there anything I can ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Breast_cancer:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JikC5z2fScGrOBTvf6JMpASCRj211EMY/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Breast cancer: Nursing]]></video:title><video:description><![CDATA[Nurse Rebecca works at an oncology clinic and is caring for Patricia, a 53-year-old female who recently had a breast biopsy confirming the diagnosis of breast cancer. After settling Patricia in her room, Nurse Rebecca goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Patricia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Rebecca recognizes important cues, including Patricia’s vital signs, which include, temperature 98.6 F or 37 C, heart rate 105 beats per minute, respirations 21 breaths per minute, blood pressure 138/88 mmHg, and oxygen saturation 97% on room air. Nurse Rebecca also notes that Patricia is restless, crying, and shaking and states she just doesn’t know how to handle her diagnosis.  

Next, Nurse Rebecca analyzes these cues. She reviews the electronic health record, or EHR, and notes that Patricia has a family history of breast cancer. Nurse Rebecca also sees that previous nursing assessments document Patricia’s report of fatigue and difficulty sleeping. Nurse Rebecca recognizes that Patricia is experiencing emotional distress related to her breast cancer diagnosis.  

Now, using the information she&amp;#39;s gathered, along with Patricia&amp;#39;s medical history, Nurse Rebecca chooses a priority hypothesis of difficulty coping.  

Then, she generates solutions to address Patricia’s coping difficulties that will include nonpharmacologic interventions, and she establishes the expected outcome that Patricia will demonstrate effective coping skills regarding her breast cancer diagnosis by her next follow-up visit.  

Nurse Rebecca then takes action to implement these solutions. After the health care provider discusses the expected treatment plan with Patricia, Nurse Rebecca follows up to see how she’s feeling about the information she’s received.  

Nurse Rebecca: How are you feeling after talking ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Grief_and_loss:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H9pKZjOZRMiNTKpcu0GAmJJCRVWzDjxh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Grief and loss: Nursing]]></video:title><video:description><![CDATA[Nurse Jamie works as a home health nurse, and is caring for Barbara, a 75-year-old female diagnosed with type 2 diabetes. This is her first home health care visit for a wound on her left lower extremity that developed from sitting in her recliner for long periods of time. Before performing a focused assessment and a dressing change, Nurse Jamie completes an assessment that includes questions about Barbara’s home life and support system.

Nurse Jamie will go through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Barbara’s care by recognizing cues and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Jamie recognizes important cues. She notes that Barbara has lived alone since her husband died a year ago; so, Nurse Jamie performs a grief assessment and discovers that Barbara’s adult children live out of state, and she has few visitors.  

Barbara shares she often dwells on missing her husband, feels sad most days, and lacks energy or motivation to do things she used to enjoy. Additionally, she reveals she is not paying attention to her blood glucose levels like she used to.

Next, Nurse Jamie analyzes these cues. She recalls that after a loss of someone or something meaningful, a period of grief is normal and can present as sadness, anger, or regret, but varies for everyone. Nurse Jamie also understands dysfunctional grief can lead to suicidal thoughts, so she gathers additional information to rule out thoughts of self-harm.

Okay, so using the information gathered from Barbara’s grief assessment and medical history, Nurse Jamie identifies a priority hypothesis of dysfunctional grief. Then, she generates solutions to address Barbara’s grief, including promoting coping strategies and coordinating care with a multidisciplinary team. Next, she establishes the desired outcome that within three weeks of intervening, Barbara will demonstrate positive copi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Care_of_a_client_identifying_as_LGBTQ+:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n17frC01Tw6NntHclltn-QbqRiOV33A8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Care of a client identifying as LGBTQ+: Nursing]]></video:title><video:description><![CDATA[As a nurse, you’ll be providing care for patients who are lesbian, gay, bisexual, transgender, queer or questioning, and other orientations and identities, also known as LGBTQ+. Members of the LGBTQ+ community often experience health inequities that can be explained by the minority stress model. This model describes how disparities can be traced to cultural stressors like stigma, harassment, and discrimination. For example, people who identify as LGBTQ+ experience higher rates of substance and tobacco use as well as increased rates of mental health disorders, like depression and anxiety.  

Historically, people who identify as LGBTQ+ have experienced discrimination within the health care system. In fact, a significant majority of people who are gay, lesbian, bisexual and transgender report discrimination by a health care provider.  

Additionally, health care providers receive limited education on how to provide culturally appropriate care to people who identify as LGBTQ+. This lack of training can add to the health inequities, but by using correct terminology and creating an inclusive environment, nurses can provide culturally appropriate care to the patients who identify as LGBTQ+. 

First, let‘s focus on terminology, starting with the difference between biologic sex and gender identity. Someone’s biologic sex, or sex assigned at birth, is determined by their genitalia, reproductive organs, and chromosomes, and can be classified as male, female, or intersex. On the other hand, gender identity refers to someone&amp;#39;s self-perceived gender and may or may not align with their sex assigned at birth. 

So, a person who’s cisgender has a gender identity that’s the same as their sex assigned at birth, and a person who&amp;#39;s transgender is someone whose gender identity is different from their sex assigned at birth. For example, a transgender man is someone who was assigned female at birth but identifies as a male. Additionally, peop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Hip_fracture:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XO-HfG3xQ0SveTeh_lEkvLvUTSW8Waw2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Hip fracture: Nursing]]></video:title><video:description><![CDATA[Nurse Kenji works on an orthopedic unit and is caring for Sharon, a 74-year-old female with a history of osteoporosis who was recently admitted for a left hip fracture requiring an open reduction and internal fixation, or ORIF. After settling Sharon in her room, Nurse Kenji goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Sharon’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Kenji recognizes important cues, including Sharon’s vital signs, which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 19 breaths per minute, and blood pressure 123/88 mmHg. During the bedside report, Nurse Kenji learned that Sharon declined repositioning during the night shift. Upon assessment, he notes that her hip appears mildly swollen and her surgical dressing is clean and dry. Nurse Kenji also notes that Sharon’s left foot is warm with intact sensation, 2+ palpable pulses, and she can wiggle her toes.  

Nurse Kenji asks Sharon about her comfort.  

Nurse Kenji: I see that you stayed in the same position throughout the night. Could you tell me your current pain level? 

Sharon: I don’t have any pain right now, but I don’t want to move because I know it&amp;#39;ll hurt my hip. 

Nurse Kenji: I understand. Have you considered taking the prescribed medications to manage your pain? 

Sharon: I really don’t like pain medicine because I’m worried about becoming addicted. 

Next, Nurse Kenji analyzes these cues. He reviews the electronic health record, or EHR, and notes that Sharon is scheduled to begin physical therapy today. He also notes that Sharon is prescribed ice packs to reduce hip swelling, as well as oxycodone and acetaminophen every four hours as needed for pain management but hasn’t taken any medication since early yesterday evening. Nurse Kenji realizes that Sharon’s fear of pain is limiting he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Gastroesophageal_reflux_disease_(GERD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jC8oRUMsREKiVPcQwu3vb3-VQIeXkUzb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Gastroesophageal reflux disease (GERD): Nursing]]></video:title><video:description><![CDATA[Nurse Max works in a primary care office and is caring for Anuja, a 54-year-old woman with a history of gastroesophageal reflux disease, or GERD, who&amp;#39;s being seen for a three-month follow-up appointment. After settling Anuja in her room, Nurse Max goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Anuja’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Max recognizes important cues including vital signs which are temperature 98.2 F or 36.9 C, heart rate 76 beats per minute, respirations 14 breaths per minute and regular, blood pressure 128/84 mmHg, and oxygen saturation 98 percent on room air. Nurse Max asks Anuja if she’s having pain, and she reports a burning in her mid upper abdomen after eating, despite taking her prescribed medication.   

Next, Nurse Max analyzes these cues. They review the electronic health record, or EHR, and note Anuja has been on proton pump inhibitor, or PPI, therapy for three months to treat her GERD.  Nurse Max then talks to Anuja about her lifestyle modifications.  

Nurse Max: I’m glad you’ve been taking your PPI every day and I’m sorry it hasn’t been working for you. I want to figure out what might be happening. What time do you take your medication? 

Anuja: I take it every night after dinner. I set an alarm, so I don’t forget. 

Nurse Max: Setting an alarm is a great idea! What do you typically eat at home?  

Anuja: I’ve been making a noodle dish lately with lots of fresh jalapenos drizzled with sriracha, my family loves it! 

Now, using the information they’ve gathered, Nurse Max chooses a priority hypothesis of knowledge deficit.  

Then, they generate solutions to address this problem that will include pharmacologic and nonpharmacologic interventions, and they establish the outcome that after intervening, Anuja will verbalize an understanding of GERD management.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Hypertension:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0G81XyAfTCWTgUVooN4CYNEeQdyTOSej/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Hypertension: Nursing]]></video:title><video:description><![CDATA[Nurse Tom works at a primary care clinic and is caring for Mahlik, a 62-year-old patient who is being seen for a wellness check. After settling Mahlik in the exam room, Nurse Tom goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Mahlik’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tom recognizes important cues, including temperature 99.4 F or 37.5 C, pulse 75 beats per minute; respirations 16 breaths per minute; blood pressure of 156/89 mmHg, and oxygen saturation 97% on room air.  

Next, Nurse Tom asks Mahlik about his history.  

Nurse Tom: Do you usually have high blood pressure? Do any of your family members have high blood pressure? 

Mahlik: My dad and older brother do. My job is stressful, so maybe that’s contributing. I’ve checked my blood pressure at the drug store, and it’s been high, but with work, I haven’t had time to come in and have it checked. 

Nurse Tom: Stress can contribute to high blood pressure, and family members with high blood pressure can increase your likelihood of having it too. What foods do you usually eat? 

Mahlik: I mostly eat fast food because I’m always on the go.  

Nurse Tom: Can you tell me about how often you smoke, drink alcohol, and exercise? 

Mahlik: I don’t smoke, never have. I drink maybe 1 to 2 beers a week on average, and honestly, I don’t exercise as much as I should. I’m just so busy with work.  

Nurse Tom analyzes these cues. He reviews the electronic health record, or EHR, and notes Mahlik’s body mass index, or BMI, is 28 kg/m2. Nurse Tom alerts the health care provider to Mahlik’s blood pressure and history. They diagnose Mahlik with stage 1 primary hypertension and prescribe an oral antihypertensive medication. Nurse Tom realizes Mahlik needs effective blood pressure management. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stress_and_coping:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2FUY4d1BScuyQcyK5UZmbBesRqSjJY94/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stress and coping: Nursing]]></video:title><video:description><![CDATA[Stress is a normal human response to an internal or external threat to homeostasis, or the body’s stable equilibrium, and can be prompted by stressors. These stressors such as illness, high workload, or economic hardship, can induce the stress response, also known as an allostasis, in an attempt to reestablish homeostasis. In the short term, the body can adapt to the physiological changes to stress; however, when stress becomes chronic, it can have a negative impact on mental and physical health.

Now, not all stress is harmful, in fact, it is essential for daily life. There are two types of stress; eustress and distress. Eustress is positive stress, which is necessary for normal development and motivation and can occur with beneficial life changes like having a baby or getting a new job; whereas distress is negative stress that occurs when a person is unable to adapt or cope effectively to the stressor.

Okay, the body’s response to a stressful event can be explained by the General Adaptation Syndrome, or GAS, which has three stages. First, the alarm reaction stage occurs as the sympathetic nervous system is activated, triggering the fight-or-flight response, which involves the release of hormones and neurotransmitters to support the body’s reaction to stress. The posterior pituitary releases antidiuretic hormone, or ADH, and the adrenal cortex releases aldosterone, both of which increase circulating blood volume. The adrenal cortex also releases cortisol, which increases the body’s supply of glucose, while the adrenal medulla releases epinephrine and norepinephrine, which increases the heart rate, blood pressure, and blood flow to the skeletal muscles. Next, the resistance stage is when the body attempts to stabilize and return to homeostasis. If the stress has been dealt with effectively, the parasympathetic nervous system returns vital signs to normal and begins to repair tissue damage. However, if the stress continues, the sympathetic activation will ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Immobility:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1Uc5QO3WSbq9z2GDug1H1z3mTgmJy1DJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Immobility: Nursing]]></video:title><video:description><![CDATA[Nurse Alex works on an intermediate care unit and is caring for Joan, a 45-year-old female who is being treated following a car crash two weeks ago. Since then, Joan has been experiencing significant weakness in the lower extremities, difficulty bearing weight, and changing position independently while in bed. Nurse Alex goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Joan&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Alex recognizes important cues. He notices Joan is unable to bear weight, has adequate upper extremity strength and requires maximum assistance to transfer from bed to the chair and bedside commode.  

He reviews the electronic health record, or EHR, where he notes that a transfer board is recommended for Joan based on her initial evaluation by the physical therapist.  

Next, Nurse Alex analyzes these cues and determines Joan will need his support to reduce the impacts of immobility.

Nurse Alex prioritizes the hypothesis of impaired mobility and generates solutions to address Joan’s impaired mobility that will include promoting safety and increasing her level of functioning. He establishes the expected outcome that after intervening, Joan will safely transfer from the bed to a chair using a transfer board with a one-person assist.

Nurse Alex then takes action to implement the generated solutions. First, he institutes fall precautions to promote safety.  

Before proceeding, Nurse Alex ensures the bed and chair are locked and in proper position, that the chair is slightly lower than the height of the mattress, and that all obstacles are removed.  

He will also ensure Joan’s pain is controlled and her vital signs are stable prior to attempting to use the transfer board.

He recalls that Joan has only used the transfer board once with physical therapy and plans to reorient Joan to the pr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Self-care_deficit:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9qPGRGzbRR2pcZNxdYAmwjM4S6GBsCZo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Self-care deficit: Nursing]]></video:title><video:description><![CDATA[Nurse Yoko works in a long-term care facility and is caring for Penny, a 79-year-old female, who was recently admitted with a history of a stroke with left-sided peripheral neuropathy and weakness. After introducing herself to Penny, Nurse Yoko goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Penny&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

First, Nurse Yoko recognizes important cues, including findings from her assessment of Penny’s skin, oral mucous membranes, and nails, as well as her functional ability. Nurse Yoko notes Penny has dry, cracked lips and a yellow-brown film on her teeth. On her lower extremities, Nurse Yoko notes dry, flaky skin, and after removing her socks, she sees that Penny has thick, discolored toenails and a pressure injury on her left heel.

Nurse Yoko asks Penny about her activities of daily living, or ADLs.  

Nurse Yoko: Penny, can you tell me a little bit about how you’ve been doing with your daily routine? 

Penny: I’m used to being able to care for myself, but after the stroke, it’s been hard for me to do things I used to do. 

Nurse Yoko: I understand. Can you tell me what sort of things you used to do that you aren’t doing now?  

Penny: Well, I’m left-handed but now that my left arm is weak, it&amp;#39;s hard for me brush my teeth and clean myself up. I can’t even cook a meal for myself anymore. 

Nurse Yoko: That must be difficult. I also noticed you have a pressure injury on your left heel. How long has it been there?

Penny: I have numbness and weakness in my left leg and it’s hard for me to move around. One day I bumped the back of my foot, and the sore hasn’t healed since. I didn’t even notice it was there until days later.

Next, Nurse Yoko analyzes these cues. She reviews Penny’s electronic health record, or EHR, and notes that although she can walk short distances,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Heart_failure_with_reduced_ejection_fraction_(HFrEF):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OGtysGxqTfSUKGoF6btOLHbrTQiX6xbz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Heart failure with reduced ejection fraction (HFrEF): Nursing]]></video:title><video:description><![CDATA[Nurse Pilar works on an inpatient cardiac unit and is caring for Esperanza, a 72-year-old female admitted for an exacerbation of heart failure with reduced ejection fraction.  After settling Esperanza in her room, Nurse Pilar goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Esperanza’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Pilar recognizes important cues, including Esperanza’s vital signs, which are heart rate 104 beats per minute, respirations 28 breaths per minute, oxygen saturation 87 percent on room air, and pain 3 out of 10, located in her back.  

Nurse Pilar also notes that Esperanza’s breathing is labored and she’s using accessory muscles. Upon auscultation, Nurse Pilar notes fine inspiratory crackles in both lung bases. There’s also 2+ pitting edema in Esperanza’s ankles and feet.  

Next, Nurse Pilar asks Esperanza about her recent activities and medications. 

Nurse Pilar: I see your health care provider has prescribed two medicines for you. When was the last time you took them? 

Esperanza: Well, I ran out of my medicines a week ago, and I haven’t been to the pharmacy to get my refills yet. I haven’t gone out of the house much the last two weeks because my back’s been hurting, and I’ve been so tired.  

Nurse Pilar: I’m sorry you’ve been having back pain. Has anything helped with the pain? 

Esperanza: Yes, ibuprofen helps. I’ve been taking it two times each day.  

Nurse Pilar then analyzes these cues. She reviews Esperanza’s electronic health record, or EHR, and sees that she&amp;#39;s prescribed two medications to control her heart failure, an ACE inhibitor and a beta blocker. Because Esperanza has been without her medications for a week, she is now showing symptoms of heart failure.  

Additionally, Nurse Pilar knows taking non-steroidal anti-inflammatory drugs, or NSAIDs, like ibupr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Leukemia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tftct0riRka1q119GOypZFnRSfq3dXM9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Leukemia: Nursing]]></video:title><video:description><![CDATA[Nurse Tracy works on an inpatient oncology unit and is caring for Margie, a 60-year-old female with a history of chronic lymphocytic leukemia, or CLL. After settling Margie in her room, Nurse Tracy goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Margie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tracy recognizes cues, including Margie’s vital signs which are temperature 98.8 F or 37.1 C, heart rate 90 beats per minute, respirations 18 per minute, blood pressure 122/84 mmHg, and oxygen saturation of 98 percent.  

Nurse Tracy notes Margie has various small bruises on her back and legs and generalized lymphadenopathy, or swollen lymph nodes.  

She notices Margie grimacing with movement, and when asked about pain, Margie reports a pain level of 5 out of 10 in her legs and a pain tolerance level of 3 out of 10.  

Nurse Tracy sees a sign on Margie’s door requesting no visitors, so she asks Margie about how she’s feeling. 

Nurse Tracy: Margie, I see you don&amp;#39;t want visitors today.  

Margie: No, I’m very tired. Besides, I’ve been such a burden to them; they probably want a break from me.  

Nurse Tracy: You don’t have to have visitors if you aren’t feeling up for it. Have your family or friends mentioned not wanting to visit? 

Margie: No, they haven’t, but I’d rather be alone. There’s so much I can’t control right now with my leukemia, and I’m feeling overwhelmed. Also, my pain is bothering me. I have extra doses of pain medicine to take between scheduled doses, but I forget to ask until my pain is too bad.  

Next, Nurse Tracy analyzes these cues. She reviews the electronic health record, or EHR, and notes that Margie has scheduled pain medication as well as doses to take as needed, or PRN, for breakthrough pain. The medication administration record shows that Margie hasn’t received any PRN pain medic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Acute_pancreatitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/646HDlDoQSqKXlPv6Um4A6BcRyCFJwiI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Acute pancreatitis: Nursing]]></video:title><video:description><![CDATA[Nurse Gerdie works on a medical-surgical unit and is caring for Leo a 47-year-old male who was recently admitted for acute pancreatitis secondary to alcohol use. After settling Leo in his room, Nurse Gerdie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Leo&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Gerdie recognizes important cues, including Leo’s vital signs, which include blood pressure 145/90 mmHg, heart rate 88 beats per minute, and respirations 18 breaths per minute. Nurse Gerdie notices Leo is diaphoretic, his gown is damp, and he’s lying in the fetal position clutching an empty emesis bag. She also sees that he has IV fluids infusing in his right forearm.  

Nurse Gerdie: Hi Leo, it looks like you&amp;#39;re not feeling well. What&amp;#39;s your pain level right now? 

Leo: It feels like I can’t lie down on my back or get comfortable at all. And I’m so nauseated.  

Nurse Gerdie: I understand, I’m going to help you feel more comfortable. 
 Next, Nurse Gerdie analyzes these cues. She reviews the electronic health record, or EHR, and notes that Leo’s prescriptions include hydromorphone IV every 3 hours as needed, and his last dose was given two and a half hours ago in the emergency department; and ondansetron IV for nausea, but he hasn’t yet received a dose. She recognizes that Leo needs effective pain and nausea management to improve his comfort. 

Now, using the information she&amp;#39;s gathered, Nurse Gerdie chooses a priority hypothesis of impaired comfort.  

Then she generates solutions to address Leo’s pain and nausea that will include pharmacologic and nonpharmacologic interventions. Nurse Gerdie establishes the expected outcome that after intervening, Leo will report increased comfort within one hour. 

Nurse Gerdie then takes action to implement these solutions. She recognizes ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Epilepsy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fWHPNCFiSSysoENqA9FtwC0CTKKbbTXT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Epilepsy: Nursing]]></video:title><video:description><![CDATA[Nurse Karla works on an inpatient neurology unit and is caring for Nisha, a 24-year-old female with a history of generalized onset tonic-clonic seizures. After settling Nisha in her room, Nurse Karla goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Nisha’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Karla recognizes important cues. As she reviews the electronic health record, or EHR, Karla notes Nisha is on seizure precautions and has an order for lorazepam IV push for seizures, per protocol. As she enters Nisha’s room, she finds Nisha lying supine on her bed. 

Nisha: I don’t feel right. I feel like I’m going to have a seizure. 

Nurse Karla: Okay Nisha, I’ll stay with you. 

Then, Nisha’s body begins cycling through periods of intermittent jerking movements and muscle tightening. Her breathing is sporadic, and she alternates between rapid breathing and apnea. Her pupils are dilated, she&amp;#39;s intermittently biting her cheek, and doesn’t respond to verbal cues. 

Nurse Karla calls for help while noting the time the seizure activity began. Then, she protects Nisha from injury by ensuring there are no objects in Nisha’s bed that could hurt her during the seizure.  

Next, Nurse Karla analyzes these cues. Nurse Karla realizes that during tonic-clonic seizures, the airway can become obstructed, and she recognizes Nisha needs effective airway management. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Stroke:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FEGEaDEET3KLsqsAptwTboA_QZGOkt0k/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Stroke: Nursing]]></video:title><video:description><![CDATA[Nurse Darius works on a neurology unit and is caring for Calvin, a 67-year-old male with a history of hyperlipidemia who was recently admitted following a stroke. After settling Calvin in his room, Nurse Darius goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Calvin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darius recognizes important cues including Calvin’s vital signs which are temperature 98.8 F, or 37.1 C, heart rate 98 beats per minute, respirations 16 breaths per minute, blood pressure 146/92 mmHg, and oxygen saturation 96 percent on room air.  
He rates his pain level is 0 out of 10.  

Nurse Darius also notes that the left side of Calvin’s face is drooping and sees that he favors his right hand. Nurse Darius also overhears Calvin mixing up his words while trying to talk to the dietary staff about his lunch tray.  

Next, Nurse Darius analyzes these cues. He reviews the electronic health record, or EHR, and sees Calvin has undergone an MRI of his head. The results show that Calvin had an ischemic stroke, where an occlusion in his artery caused inadequate blood flow to his brain.  

Nurse Darius knows Calvin’s hyperlipidemia was likely a contributing factor to his stroke, since it can lead to atherosclerosis and blockage of arteries.  

He also knows the loss of oxygenated blood flow to the brain can cause damage to areas that control language and motor functions and lead to muscle weakness and aphasia.  

Nurse Darius recognizes that he needs to effectively communicate with Calvin to properly care for him. 

Now, using the information he’s gathered, Nurse Darius chooses a priority hypothesis of impaired communication.   

Then, he generates solutions to address Calvin’s impaired communication that will include nonpharmacologic interventions; and he establishes the outcome that after intervening, Calv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pyelonephritis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RmmCFeh7SmO5qO8RtVUePu9sRLCZ7i-l/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pyelonephritis: Nursing]]></video:title><video:description><![CDATA[Nurse Alfred works on a Medical-Surgical unit and is caring for Alma, a 72-year-old Spanish-speaking female with a history of multiple sclerosis, or MS, who was recently admitted for pyelonephritis. After settling Alma in her room, Nurse Alfred goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Alma&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Alfred recognizes important cues, including Alma’s vital signs, which are temperature 101.3 F, or 38.5 C, heart rate 108 beats per minute, respirations 20 breaths per minute, blood pressure 136/78 mmHg, and oxygen saturation 98 percent on room air. Nurse Alfred knows that Alma’s primary language is Spanish, so he uses an interpreter to communicate with her over the phone. Alma&amp;#39;s lower abdomen is moderately distended, and she rates her abdominal pain at 9 out of 10.  

Nurse Alfred gathers that, at home, Alma usually empties her bladder via straight catheterization every four hours, but has been having difficulty due to increasing weakness from her MS. She reports that yesterday, she was too weak to catheterize herself.  

Next, Nurse Alfred analyzes these cues. He reviews the electronic health record, or EHR, and notes a straight catheterization was performed on Alma in the emergency department to obtain a urine sample, which revealed the presence of leukocytes and nitrites and drained 150 milliliters. Nurse Alfred realizes that, due to her inability to catheterize herself properly, Alma developed urinary retention which likely contributed to her pyelonephritis. Nurse Alfred realizes Alma needs effective urinary elimination and infection management. 

Now, using the information he&amp;#39;s gathered, along with Alma’s medical history, Nurse Alfred chooses a priority hypothesis of infection.  

Then, he generates solutions to address Alma’s infection that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Deep_vein_thrombosis_(DVT):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wIPyBelvTbqdnanI8vMlTxvZSsuRLhQQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Deep vein thrombosis (DVT): Nursing]]></video:title><video:description><![CDATA[Nurse Hakeem works on a Medical-Surgical unit and is caring for Lucille, a 72-year-old female who&amp;#39;s being admitted for a deep vein thrombosis, or DVT in her left iliofemoral vein. After settling Lucille in her room, Nurse Hakeem goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Lucille’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

Nurse Hakeem starts by recognizing important cues. He notes signs and symptoms consistent with Lucille&amp;#39;s diagnosis of DVT, including redness and swelling of the affected area. Upon light palpation, Nurse Hakeem notes Lucille’s leg is warm, the skin is taut and tender, and she rates her pain as 6 out of 10 and describes it as throbbing. 

Then, Nurse Hakeem analyzes these cues. He reviews the electronic health record, or EHR, and sees that Lucille recently had surgery to repair a fractured left hip, and that an ultrasound report identified the DVT.  

He knows that immobility after surgery increased Lucille’s risk for a DVT, and that the thrombus lodged in her vein is causing inflammation and decreasing venous return to her heart, causing swelling and pain in her leg.  

He also understands that Lucille is at risk of a venous thromboembolism, or VTE, if the thrombus breaks free and travels up through the inferior vena cava, to the right side of the heart, and then into her lungs, causing a pulmonary embolism, or PE.  

Now, using the information he&amp;#39;s gathered, Nurse Hakeem chooses a priority hypothesis of impaired tissue integrity.  

Next, he generates solutions to address Lucille’s DVT that will include pharmacologic and nonpharmacologic interventions, and he establishes the expected outcome that after intervening, Lucille’s tissue integrity will show signs of improvement by the end of the shift.   

Nurse Hakeem then takes action to implement these solutions. He reviews]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pneumonia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MJVBmr4QTqGA-1BqiYyLp8ODRB69Nz95/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pneumonia: Nursing]]></video:title><video:description><![CDATA[Nurse Jodie works on a Medical-Surgical unit and is caring for Ann, a 44-year-old female with a history of smoking who was recently admitted for community-acquired pneumonia. After settling Ann in her room, Nurse Jodie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ann’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jodie recognizes important cues including Ann’s vital signs, which are temperature 101.5 F or 38.6 C, heart rate 101 beats per minute, respirations 28 breaths per minute and regular, blood pressure 90/60 mmHg, and oxygen saturation 85 percent on room air. Upon auscultation, Nurse Jodie notes course crackles and slight wheezing.  Nurse Jodie also observes that Ann can’t speak in full sentences without becoming short of breath.    

Next, Nurse Jodie analyzes these cues. Nurse Jodie reviews the electronic health record, or EHR, and notes Ann’s WBC count is elevated at 12,500 per mm3. Nurse Jodie knows that an infection is likely causing fluid to fill up Ann’s alveoli which is interfering with gas exchange; and that inflammation is causing her airways to narrow. Nurse Jodie recognizes that Ann needs effective respiratory management. 

Nurse Jodie chooses a priority hypothesis of ineffective gas exchange. 

Then, Nurse Jodie generates solutions to address Ann’s infection. She establishes the expected outcome that after intervening, Ann will maintain an oxygenation saturation above 92 percent during the shift.  

Nurse Jodie then takes action to implement these solutions.  

Nurse Jodie: I&amp;#39;m going to give you some oxygen to help you breathe a little easier. This plastic tubing will go around your ears and the prongs will go into your nose. It&amp;#39;s important that you breathe in through your nose so the oxygen will go into your lungs. 

Ann: Okay, I hope it helps. 

Nurse Jodie: Your health ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Chronic_obstructive_pulmonary_disease_(COPD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9Hs0xFH_RUCNPq1g6OurnLP8Tc_j4Vd2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Chronic obstructive pulmonary disease (COPD): Nursing]]></video:title><video:description><![CDATA[Nurse Seema works on a medical-surgical unit and is caring for Richard, a 75-year-old male with a history of smoking, who was admitted for an acute exacerbation of chronic obstructive pulmonary disease, or COPD. After settling Richard in his room, Nurse Seema goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Richard’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Seema recognizes important cues including Richard’s vital signs, which are temperature 99.6 F or 37.5 C, heart rate 98 beats per minute, respirations 28 breaths per minute, blood pressure 142/90 mmHg, and oxygen saturation 85 percent on room air. When asked about pain, Richard reports a current pain level of 0 out of 10. Upon assessment, Nurse Seema notes that Richard’s respirations are labored, he has expiratory wheezing, and he’s leaning over in a tripod position. 

Next, Nurse Seema analyzes these cues.  She reviews the electronic health record, or EHR, and notes Richard’s arterial blood gas, or ABG, shows a low PaO2, indicating hypoxemia. She also recognizes COPD causes airway inflammation, leading to obstructed airflow out of the lungs, causing CO2 retention, making gas exchange difficult. Nurse Seema knows that Richard’s hypoxemia, wheezing, and tripod positioning indicate he’s experiencing impaired respiratory function and needs effective respiratory management. 

Now, using the information she’s gathered, Nurse Seema chooses a priority hypothesis of impaired gas exchange. 

Then, she generates solutions to address Richard’s impaired gas exchange that will include pharmacologic and nonpharmacologic interventions. She establishes an expected outcome that after intervening, Richard will maintain an oxygenation saturation between 89 to 92 percent on 2 liters nasal cannula within one hour.   

Nurse Seema then takes action to implement these solutions.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Cirrhosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/j7R8KfsyTAivmoYKjuyiUo8bTG6fLqw3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Cirrhosis: Nursing]]></video:title><video:description><![CDATA[Nurse Abigail works on a Medical-Surgical unit and is caring for Thomas, a 72-year-old male with a history of hyperlipidemia and obesity, who was recently admitted for cirrhosis secondary to nonalcoholic fatty liver disease. After settling Thomas in his room, Nurse Abigail goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Thomas’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Abigail recognizes important cues, including Thomas’ vital signs, which are temperature 98.8 F or 37 C, heart rate 98 beats per minute, respirations 22 breaths per minute, blood pressure 106/68 mmHg, and oxygen saturation 97 percent on room air. His pain is 2 out of 10.  

Upon assessment, Nurse Abigail notes his sclera and skin are yellow-tinged, he has scattered petechiae, and his abdomen is round and distended.  

When asked to turn side-to-side during assessment, Thomas becomes fatigued and short of breath. 

Next, Nurse Abigail analyzes these cues. She reviews the electronic health record, or EHR, and notes that Thomas has gained 17 pounds since his last health care provider visit, which was approximately two weeks ago.  

Nurse Abigail recognizes that the fluid build-up in Thomas’ abdomen, also known as ascites, has contributed to his weight gain, and can make it difficult to perform physical activities because of increased pressure on his diaphragm, leading to dyspnea.  

She also knows that chronic illness in general can cause fatigue. Nurse Abigail realizes Thomas needs management of his fatigue in order to promote physical mobility. 

Now, using the information she&amp;#39;s gathered, along with Thomas’ medical history, Nurse Abigail chooses a priority hypothesis of activity intolerance.  

Then, she generates solutions to address Thomas’ activity level that will include pharmacologic and nonpharmacologic interventions; and she est]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Diabetic_ketoacidosis_(DKA):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vfg076vFTUqfbf1SBjr2iVOGSdyu6X1q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Diabetic ketoacidosis (DKA): Nursing]]></video:title><video:description><![CDATA[Nurse Andrea works on a medical-surgical unit and is caring for Mario, a 32-year-old male with a history of type 1 diabetes mellitus, who was recently admitted from the emergency department for diabetic ketoacidosis, or DKA. After settling Mario in his room, Nurse Andrea goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Mario’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Andrea recognizes important cues, including Mario’s vital signs which are temperature 99.4 F, or 37.5 C, heart rate 115 beats per minute, respirations 24 breaths per minute, blood pressure 90/65 mmHg, and oxygen saturation 99 percent on room air. His pain rating is 2 out of 10. Upon assessment, Nurse Andrea notes Mario is alert and oriented, his mucous membranes are dry, and he reports nausea with two episodes of emesis. Nurse Andrea also notes that he has a continuous insulin drip and IV fluids infusing into a peripheral IV, and his current blood glucose level is 265 mg/dL. 

Next, Nurse Andrea analyzes these cues. She reviews the electronic health record, or EHR, and verifies Mario is on the correct rate of insulin and IV fluids. She understands that the elevated  glucose levels in DKA cause osmotic diuresis and significant fluid loss, and that the acidosis is causing Mario’s nausea and vomiting, resulting in additional loss of fluid and electrolytes. She also knows that fluid loss will continue until Mario’s blood glucose level is stabilized, and that tachycardia and hypotension are signs of dehydration. Nurse Andrea recognizes that Mario needs fluid management. 

Now, using the information she&amp;#39;s gathered, Nurse Andrea chooses a priority hypothesis of fluid volume deficit. 

Then, she generates solutions to address Mario’s fluid volume deficit, including pharmacologic and nonpharmacologic interventions; and she establishes the expe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Impaired_gas_exchange:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6lPMSXFFS6CzVH88ecclOeQLSzyuxByH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Impaired gas exchange: Nursing]]></video:title><video:description><![CDATA[Nurse Emily works in an emergency department and is caring for Carolyn, a 77-year-old female with a history of congestive heart failure, or CHF, who came to the emergency department after shortness of breath woke her up during the night. After settling Carolyn in her room, Nurse Emily goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Carolyn’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.

Nurse Emily begins by recognizing important cues. During report, Nurse Emily learns Carolyn has gained 7 pounds in the last week and has been using extra pillows to prop her up at night since she&amp;#39;s short of breath when lying flat. Then, Nurse Emily assesses Carolyn’s vital signs, which are blood pressure 110/70 mmHg, heart rate 100 beats per minute, temperature 98.8 F or 37.1 C, respirations 24 breaths per minute and pain score of 0 out of 10. Pulse oximetry is 86 percent on room air. Nurse Emily notes Carolyn has bilateral lower extremity edema and upon auscultation she hears crackles bilaterally. She also notices Carolyn’s increased work in breathing through cues like nasal flaring and intercostal retractions. 

Then, Nurse Emily analyzes these cues. She reviews Carolyn’s diagnostic test results and sees her CBC, basic metabolic panel, or BMP, and ECG are within normal limits; however, her arterial blood gas, or ABG, reveals a decreased partial pressure of oxygen, or PaO2. Nurse Emily remembers that since Carolyn has CHF, her heart is not pumping effectively, impairing oxygenation, which is the ability of the lungs to exchange oxygen and carbon dioxide. This also impairs perfusion, which is the ability of oxygen-rich blood to travel throughout the body. Nurse Emily also realizes Carolyn’s CHF is causing blood to pool in Carolyn’s pulmonary and systemic circulation, leading to her symptoms.

So, using the information she’s gathered, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Electrolyte_balance_-_Overview:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V9hfd191QbWfJtD0IxLo3O2lTUSC9EAJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Electrolyte balance - Overview: Nursing]]></video:title><video:description><![CDATA[Electrolytes are charged molecules, or ions, that have many essential functions throughout the body, including transmission of nerve impulses, facilitating muscle contraction, and maintaining fluid osmolality. Because of their critical functions, maintaining electrolyte homeostasis is essential for normal functioning of the body. 

Okay, let’s review the major electrolytes and their functions. They can be categorized as either cations, which are positively charged, like sodium; or anions, which are negatively charged, like phosphate. Electrolytes can be measured in the urine, cerebrospinal fluid, and blood, and they’re usually expressed as milliequivalents per liter of fluid, mEq/L.  

So, first, there’s sodium, or Na+, which is the main cation in the extracellular fluid.  

It’s responsible for maintaining the extracellular fluid’s osmolality, or the concentration of the particles dissolved in the fluid, so it determines blood volume and blood pressure.  

Sodium also works closely with potassium, or K+, to maintain the cell’s resting membrane potential, which is the distribution of ions on either side of the cellular membrane. Sodium’s normal value is 135 to 145 mEq/L.  

Now, potassium is the main cation in the intracellular fluid, and it’s responsible for maintaining intracellular osmolality. Potassium is also essential for normal neuromuscular and cardiac function, and its normal range is between 3.5 and 5 mEq/L.  

Then there’s calcium, or Ca2+, which helps with releasing neurotransmitters from neurons, as well as releasing hormones from endocrine glands. It influences the excitability of nerve and muscle cells and is essential for muscle contraction. It’s also involved in blood clotting and maintaining strong bones and teeth. Calcium’s normal range is between 8.5 and 10.5 mg/dL.Now, magnesium, or Mg2+, influences the function of both cardiac and skeletal muscles through its actions in the neuromuscular junction, which is where muscles and nerves mee]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sleep_-_Overview:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/k3Vhs3BPRiid4BaWtBd3HbstQ8y-DM9j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sleep - Overview: Nursing]]></video:title><video:description><![CDATA[Sleep is a basic human need that allows for the proper functioning of the body and mind. A lack of sleep can cause patients to develop chronic health conditions, like diabetes, obesity, and depression, and impair daily mental and physical functioning. Let’s review the rhythm,  cycles, and physiology of sleep.

Now, the central nervous system integrates sleep using various parts of the brain, including the hypothalamus, which controls the circadian rhythm, the 24-hour sleep-wake cycle that includes a predictable pattern of physical, mental, and behavioral processes such as variations in body temperature, heart rate, blood pressure, hormone secretion, eating habits, and mood.

The hypothalamus controls the circadian rhythm and can be impacted by the amount of environmental light and other factors, such as noise, pain, and illness. 

Now, there are two main phases of sleep: non-rapid eye movement, or NREM, and rapid eye movement, or REM. These phases typically occur in 90 minutes intervals, with a normal sleep pattern containing 3 to 5 cycles total. Now, we spend the most time in NREM, which has three stages, called NREM 1, 2, and 3, which progress from the lightest sleep to the deepest sleep, whereas REM only has one stage characterized by lucid dreams and rapid eye movements.

Now, several physiological changes occur during sleep, including a decrease in heart rate, blood pressure, body temperature, respiration, and muscle tone. 

These changes occur because several central nervous system structures, hormones, and neurotransmitters work together to promote and regulate sleep. Starting with the hypothalamus, this structure controls the circadian rhythm and initiates sleep by secreting the neurotransmitter gamma-aminobutyric acid, or GABA. It also works with the brain stem to reduce activity in arousal centers and relax the body during sleep. Next, the pineal gland secures the hormone melatonin in response to decreased light to help regulate the sleep cycle. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Anorexia_nervosa:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eE-yYPtuTwa6ytflFTGA-oKJQY2jA49x/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Anorexia nervosa: Nursing]]></video:title><video:description><![CDATA[Nurse Pat works in a medical psychiatric unit and is caring for Lily, a 22-year-old who was recently admitted for malnourishment secondary to anorexia nervosa. After settling Lily in her room, Nurse Pat goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Lily’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Pat recognizes important cues, including Lily’s vital signs, which are temperature 97.7 F or 36.5 C, heart rate 44 beats per minute, respirations 14 breaths per minute, and blood pressure 92/58 mmHg. Nurse Pat notices that Lily is very thin, and her skin is dry, pale, and has poor turgor. When asked how she’s feeling, Lily is tearful and reports that she’s very anxious about going out in public because she’s concerned that she’s gained weight. She also states she&amp;#39;s been restricting her food intake and hasn’t eaten anything in two days.  

Next, Nurse Pat analyzes these cues. They review the electronic health record, or EHR, and note that Lily&amp;#39;s ECG shows sinus bradycardia, her basic metabolic panel indicates hypokalemia, or low potassium level, at 3.4 mEq/L, and her most recent body mass index, or BMI, is 16, which is below normal. Nurse Pat knows that patients with anorexia nervosa restrict the amount of food they eat, and prolonged food restriction causes malnourishment which can lead to complications like dehydration and electrolyte depletion, causing hypotension and bradycardia. Additionally, prolonged anorexia can affect the brain, causing symptoms like confusion, irritability, or restlessness, as well as mental health problems like depression or anxiety. Nurse Pat realizes Lily needs nutritional management and emotional support. 

Now, using the information they’ve gathered, along with Lily’s medical history, Nurse Pat chooses a priority hypothesis of imbalanced nutrition.  

Then, they gen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Autism_spectrum_disorder:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s6KDIdilTKuH5BKaJZ8fs56HT6iAIjqF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Autism spectrum disorder: Nursing]]></video:title><video:description><![CDATA[Nurse Abisola works at a primary care clinic and is caring for Nico, a three-year-old child recently diagnosed with moderate autism spectrum disorder, or ASD. After settling Nico and his caregiver, Anne, in a room, Nurse Abisola goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Nico’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Abisola recognizes important cues, including Nico’s vital signs, which are temperature 97.7 F or 36.5 C, heart rate 96 beats per minute, respirations 24 breaths per minute , and blood pressure 100/62 mmHg. She also notices that Nico appears withdrawn, isn’t making eye contact, and when addressed, he doesn’t respond.  

Next, Nurse Abisola analyzes these cues. She reviews the electronic health record, or EHR, and notes that other than ASD, Nico has no medical or surgical history. Nurse Abisola reviews previous notes from the pediatrician, who states that Nico has missed some communication milestones for his age; for example, he&amp;#39;s unable to participate the normal back and forth of a conversation, he rarely initiates social interactions, and he often repeats unusual phrases over and over.  

Nurse Abisola understands that although the exact pathophysiology of ASD is not well understood, it seems to be caused by a combination of genetic and environmental causes, some of which are responsible for regulating social and communication behaviors. Nurse Abisola realizes Nico needs effective management of ASD to support his communication.  

Now, using the information she&amp;#39;s gathered, along with Nico’s medical history, Nurse Abisola chooses a priority hypothesis of impaired communication.  

Then, she generates solutions to address Nico’s impaired communication, and she establishes the expected outcome that Nico will communicate his needs effectively after meeting with a speech lan]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Accidental_ingestion:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Oj1m2BHBT9KJt67LlTBkn9OaQsiSGM_j/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Accidental ingestion: Nursing]]></video:title><video:description><![CDATA[Nurse Olivia works in the emergency department and is caring for Daisy, a 2-year-old who was brought in by Ellen, Daisy’s caregiver, after accidentally ingesting acetaminophen. After settling Daisy in her room, Nurse Olivia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Daisy’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Olivia recognizes important cues including Daisy’s vital signs which are temperature 98.6 F, or 37 C, heart rate 118 beats per minute, respiratory rate 30 breaths per minute, and blood pressure 92/52 mmHg. Nurse Olivia notes Daisy is pale and sweating. She also notices Daily is restless, whimpers occasionally, and is easily consoled by Ellen, so she determines Daisy’s pain rating is 3 out of 10 according to the Face, Legs, Activity, Cry, and Consolability, or FLACC, scale. A gentle abdominal assessment reveals no tenderness.  

Nurse Olivia: Ellen, can you tell me about what happened before you brought Daisy here? 

Ellen: Well, I was at home making dinner, when I noticed Daisy chewing while holding an open bottle of our acetaminophen pills.   

Nurse Olivia: How long ago was that? 

Ellen: About two hours ago. I must’ve left the bottle open after I took some pills for my headache. Then the phone rang, and I completely forgot to put the lid back on.  

Nurse Olivia: Do you have any idea how many pills she ingested? 

Ellen: I think she had about 13; it was a new bottle and I had only taken a couple for myself. 

Nurse Olivia: Do you know how many miligrams are in each pill? 

Ellen: 160 milligrams. 

Nurse Olivia: Okay. Then, after you discovered Daisy had taken the medicine, what happened next? 

Ellen: I called Poison Control right away, and they asked me how many pills were in the bottle too. Then they told me to bring Daisy to the hospital immediately. 

Nurse Olivia: You did the right th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Dependent_adult_abuse_and_neglect:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WFoXeHxnT_u4btz3DWxnVEEXRR6cpkg2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Dependent adult abuse and neglect: Nursing]]></video:title><video:description><![CDATA[Nurse Madison works night shift in a long-term care facility, and is caring for Edward, a 71-year-old patient with a history of dementia. Nurse Madison goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Edward’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Madison recognizes important cues. As she approaches Edward’s room, she notices a chair has been placed in front of the door, preventing it from opening all the way. When Nurse Madison asks the unlicensed assistive personnel, or UAP, about it, the UAP admits they placed the chair there to prevent Edward from wandering off the unit.  

Then, upon entering the room, Nurse Madison notes Edward&amp;#39;s hair is unkempt, and his shirt is stained with dried food. She also sees that Edward’s bed sheets are soaked with urine and he’s visibly upset. 

Next, Nurse Madison analyzes these cues. She recalls that the electronic health record, or EHR, documents that Edward is at high risk for elopement, and that he’s attempted to leave the unit several times before being stopped by security. She also notes that Edward is normally continent of urine.  Nurse Madison recognizes that preventing Edward from leaving his room by forcing him into physical confinement is considered restraints abuse. It also appears that Edward has been neglected, meaning that his basic needs, such as hygiene, haven’t been met.  

Now, using the information she’s gathered, Nurse Madison chooses a priority hypothesis of powerlessness.  

Then, she generates solutions to address Edward’s powerlessness, and she establishes the expected outcome that after intervening, Edward will have his basic needs met while remaining safe in his environment.  

Nurse Madison then takes action to implement these solutions. She makes sure Edward is safe by ensuring he&amp;#39;s free from injuries and confirming his roo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Hypothyroidism:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P7oRtb6VQIWM0CqokbtW8VrFSwmYgY8J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Hypothyroidism: Nursing]]></video:title><video:description><![CDATA[Nurse Kyle works at a family practice clinic and is caring for Amara, a 54-year-old female who presents for a follow-up appointment after being prescribed levothyroxine 3 months ago for newly diagnosed hypothyroidism. After settling Amara in her room, Nurse Kyle goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Amara’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

Nurse Kyle recognizes important cues, including Amara’s report of fatigue and constipation. He also notes that Amara shivers and pulls her jacket around her shoulders.  

Nurse Kyle: Amara, tell me about what’s been going on since your last appointment. 

Amara: A lot of the same things, like I still feel tired and cold. But my main issue is that I’m really constipated and it&amp;#39;s making my stomach hurt.  

Next, Nurse Kyle analyzes these cues. He reviews the electronic health record, or EHR, and notes that Amara started levothyroxine 3 months ago. He also notes her labs today show an elevated thyroid stimulating hormone, or TSH, and low free T4. Nurse Kyle realizes that since Amara is not yet therapeutic on her medication, she is still experiencing symptoms of hypothyroidism.  

Now, using the information he’s gathered, along with Amara’s medical history, Nurse Kyle chooses a priority hypothesis of constipation.  

Then, he generates solutions to address Amara’s complaint of constipation that will include pharmacologic and nonpharmacologic interventions. Nurse Kyle establishes the expected outcome that after intervening, Amara will have one bowel movement each day by the time she has her next follow-up in 6 weeks.  

Nurse Kyle then takes action to implement these solutions. He knows that although Amara started on levothyroxine 3 months ago, it can take time for the medication to correct her thyroid hormone level, so she may still experience symptoms of hypoth]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vital_signs_-_Pediatric_pain:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KSuvEHTOR9KPdRKJWHhVntzCSyqDxoar/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vital signs - Pediatric pain: Nursing skills]]></video:title><video:description><![CDATA[Pain is a feeling of discomfort and an emotional experience that is a common occurrence in children of all ages. To provide optimal pain management, the nurse must perform age-appropriate pain assessments and interventions. 

Now, pain starts with a stimulus that can be mechanical, chemical, or thermal, which causes damage to tissue, and triggers the release of molecules like prostaglandins, histamine, and bradykinin. Special pain receptors called nociceptors are activated by these molecules, and in response, they initiate an action potential that’s transmitted from the site of injury to the cortex of the brain. Once it reaches the cortex, the patient experiences the pain and its characteristics, like its location and intensity, and an emotional response to the pain occurs.   

The first step in assessing your patient’s pain is by understanding their previous experience with pain. Then, to assess the severity of their pain, use a pain assessment tool. The choice of a pain assessment tool depends on the child’s age, cognitive development, and ability to communicate.  Usually, older school-age children can report their pain numerically on a zero to ten scale, with zero meaning no pain, and ten meaning the worst pain they can imagine. 

There’s also a verbal scale which allows children to describe their pain using adjectives, like “mild,” “moderate,” and “severe.” In addition, the Wong-Baker FACES Pain Rating Scale uses faces, each representing a level of pain, where the child points to the face that depicts how they feel. 

During your assessment, remember that the most reliable indicator of pain is your patient’s own report of pain, but there may be times that you’ll need to base your pain assessment on observing your patient’s behaviors and nonverbal cues such as irritability, restlessness, grimacing, and moaning in situations where they are not able to verbalize their pain.  

For example, the Premature Infant Pain Profile, known as PIPP, is a scoring sys]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Rehabilitative_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v_JUi1VHRSSD0njizb3PToULRVWl8VTX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Rehabilitative care: Nursing]]></video:title><video:description><![CDATA[Rehabilitative care refers to the management of disabilities and chronic health conditions across the lifespan. It can take place in many settings like an acute care hospital, inpatient rehabilitation center, or at your patient’s home. As a nurse, you’ll collaborate with the interprofessional health care team, including nurses, social workers, case managers, physical therapists, dietitians, speech-language pathologists, and physicians, to support your patient’s functional abilities and prevent complications. 

When caring for your patient in rehabilitative care, your assessments will include physical, functional, psychosocial, vocational, and home safety assessments.  

Begin by completing a physical assessment of your patient’s major body systems with a focus on their current functional abilities. Assess their ability to complete activities of daily living, or ADLs, such as bathing, bowel and bladder elimination, and dressing.  

You’ll also assess their nutritional status, including the presence of chewing or swallowing problems, and their ability to prepare meals. Then, determine their level of mobility, their history of falls, and their need for any assistive devices, such as walkers or canes.  

Also be sure to assess their sensory function, and the use of glasses or hearing aids. During your assessment, note any signs or symptoms that may impact your patient’s ability to participate in rehabilitation, like shortness of breath or uncontrolled pain. 

Next, assess their psychosocial status by determining how they feel about their changes in health and loss of function, sources of stress, and their support system. Look for indications of anxiety or depression, such as loss of appetite or problems with sleep.  

Also, take note of any cultural, spiritual, or religious needs that may impact care. 

If your patient is employed, you’ll also perform a vocational assessment to examine the cognitive and physical demands of your patient’s job. Then, along with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Heparin:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IvVIXoddQQOUO3g5DpsRf9oBQs2WWd4B/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication administration - Heparin: Nursing pharmacology]]></video:title><video:description><![CDATA[Anticoagulants are medications that work by interfering with the clotting factors in the coagulation cascade. These medications are used to prevent the formation of thrombi, or blood clots, and prevent or treat thromboembolic events, which are conditions that occur when a blood clot obstructs a blood vessel like in deep vein thrombosis, pulmonary embolism, ischemic stroke, transient ischemic attack, coronary artery disease, or myocardial infarction.  

They&amp;#39;re also used to treat patients with coagulation disorders, like disseminated intravascular coagulation, and patients who underwent cardiac valve replacement or coronary angioplasty; and they are used during procedures like cardiopulmonary bypass, percutaneous coronary intervention, extracorporeal membrane oxygenation, and hemodialysis.  

Now, heparin is a commonly used anticoagulant, and it’s a high-alert medication, meaning there’s an increased risk of patient harm if administered in error. This is because heparin can cause unwanted and potentially dangerous bleeding. 

Okay now, when administering a heparin IV infusion, you’ll likely follow a weight-based protocol, meaning the dose is based on the patient’s weight, which helps to ensure safe dosing for each patient. Then, the infusion is adjusted, or titrated, based on their activated partial thromboplastin time, or aPTT, results, which measures both the intrinsic and common pathways of the coagulation cascade.  

Alright, since heparin is a high-alert medication due to the risk for bleeding, you will always infuse it using an electronic IV infusion pump. It is delivered in milliliters per hour, but because heparin is dosed in units, you need to calculate the heparin infusion rate in units per hour and convert that dosage into milliliters per hour, which is what you program into the infusion pump.  

So, to calculate an IV heparin dose, you first need to understand how to calculate a weight-based calculation. Let’s look at the following scen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Suicidal_ideation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JHMjB011QB6T7mzdoNEicOsJTUG2ZNf_/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Suicidal ideation: Nursing]]></video:title><video:description><![CDATA[Nurse Iris works on an inpatient psychiatric unit and is caring for Dee, a 30-year-old patient with a history of depression and previous suicide attempts, who was recently admitted for suicidal ideation. After settling Dee in his room, Nurse Iris goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Dee’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Iris recognizes important cues, including Dee’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 65 beats per minute, respirations 16 breaths per minute, and blood pressure 116/70 mmHg. She also notices Dee looks straight ahead during the assessment and has a flat affect. 

Nurse Iris: Hi Dee, I’ll be your nurse today. How are you feeling? 

Dee: I’m upset. I wanted to take all my pills at home, but my friend brought me to the hospital before I could. I don’t want to be here anymore. I wish I was dead. 

Nurse Iris: I’m sorry to hear that. I want you to know that I and the rest of your medical team care about you. We&amp;#39;re here to support you and keep you safe.  

Next, Nurse Iris analyzes these cues. She reviews the electronic health record, or EHR, and notes that Dee is prescribed fluoxetine for depression and has been hospitalized in the past year for suicidal ideation. She also notes that Dee scored a 19 out of 27 on his PHQ-9 assessment, which is a nine-question, self-reporting depression survey, indicating a moderately severe level of depression. Nurse Iris recognizes that Dee needs a safe environment while he receives treatment for his depression and suicidal ideation. 

Now, using the information she’s gathered, along with Dee’s medical history, Nurse Iris chooses a priority hypothesis of risk for suicide.  

Then, she generates solutions to address Dee’s suicidal ideation that will include pharmacologic and nonpharmacologic interventions; and]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_orders:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ud01peIAQfKoWa_S3sw1nbmcTMOgwQTB/_.png</video:thumbnail_loc><video:title><![CDATA[Medication orders: Nursing pharmacology]]></video:title><video:description><![CDATA[Medication orders are used to communicate which medications to administer to patients and are obtained from the health care provider in the form of written, electronic, or verbal orders. Written and electronic orders are entered directly by the health care provider, whereas verbal orders can be taken in-person or over the phone in certain situations, transcribed by the nurse, and then signed by the health care provider within a certain timeframe. All medication orders will include the date and time the order was made; the name of the medication; its dosage strength, route, and frequency; as well as the signature of the provider.  

As the nurse, you’ll provide safe medication administration by correctly interpreting medication orders. Start by ensuring all the elements of the order are provided. If the order is unclear or if there’s missing information, you’ll clarify it with the health care provider. If the order is handwritten, ensure that it’s legible. Importantly, be sure the order only uses approved abbreviations, since unapproved abbreviations can lead to medication errors. For example, the unapproved abbreviation QD is intended to mean “daily” but could be mistaken for the approved abbreviation QID, meaning “four times a day.” Instead, “daily” should be written out. Finally, be sure you know which medications and dosages are safe for your patient, so you can identify and clarify any concerns with the health care provider. 

Okay, let’s interpret a handwritten medication order to ensure all the elements are provided. You see the date and time the order was written, followed by the medication name, ondansetron. The dosage strength is 4 mg, the route   is IV, and the frequency is every 8 hours. Finally, it’s signed by the prescribing health care provider. Since all the required elements are present and clearly communicated in the medication order, you can begin the medication administration process. 

Let&amp;#39;s look at another handwritten medicati]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_labels:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KQpEbdTJROaRk-JKJFrZvayuSCmpdfLZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication labels: Nursing pharmacology]]></video:title><video:description><![CDATA[Medications come packaged with specific information about the medication on the label, which includes details such as the brand name, generic name, dosage strength, medication form, expiration date, lot number, manufacturer name, bar code, and additional information and directions for use. As a nurse, you’ll read the labels of all prescribed medications to ensure safe administration. 

Okay, so let’s identify the information on this label and what it means. Starting with the medication’s brand name, also known as the proprietary or trade name, which you’ll find in large, bold letters. This is the commercial name given to a medication by the manufacturer.   

The generic name is its nonproprietary name, which is an internationally recognized name based on the medication&amp;#39;s active ingredient or chemical structure. You’ll find the generic name in smaller, non-bolded letters, typically written below the brand name.  

Next, you&amp;#39;ll find the dosage strength and formulation. Dosage strength is the amount of medication contained in the medication form, like tablet, capsule, or suspension, and it’s indicated by a number with units of measurement.  

The formulation may follow the dosage strength or be noted after the generic name.  

Then, you’ll find the medication’s expiration date, or the date after which the medication shouldn’t be used anymore, since it may have lost potency. The expiration date is usually abbreviated as “exp” followed by a month and year.  

The lot number, which refers to the batch the medication came from during the manufacturing process, is usually found near the expiration date and is a string of numbers, letters, or both. You’ll use the lot number to determine if the medication is safe for use in the event a certain lot of medications are recalled due to a manufacturing error. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Oral:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o9LjkiZLRfCFSWTqecGHwvlhSdSmwY1m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication administration - Oral: Nursing pharmacology]]></video:title><video:description><![CDATA[Enteral medications are administered through the GI tract, either orally, rectally, or by a nasogastric or gastrostomy tube. Oral medications are available in tablets, capsules, and liquids, which can be either solutions or suspensions, and are the most commonly prescribed form of enteral medications for patients who are able to swallow.  

As the nurse, you’ll perform medication calculations to ensure the correct dose of an enteral medication is administered.  

To calculate a dosing using the Dimensional Analysis, or DA, method, the three components you need are D, for the Desired dose, or dose ordered by the health care provider; H, for Have, or the dosage you have available; and V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid. 
First, you’ll read the order, which is: acetaminophen 1 gram PO every 6 hours. 

Then, look at the medication label.   

Since the medication comes in 500 mg per tablet, you’ll calculate how many tablets you should administer to achieve the desired dose. To do this, first identify your components, Desired, Have, and Vehicle. 

In this case, D is 1 gram, which was obtained from the health care provider’s order. H is 500 mg, which was obtained from the medication label. And V, is 1 tablet, which was also obtained from the label.  

Next, you’ll determine if a conversion factor is required. To determine this, compare the units of D with the units of H, and see if they’re the same. Because D and H are in different units, a conversion factor is needed. In this case, you’ll use the following conversion factor from grams to milligrams:  

1 gram equals 1000 mg 

Now, set up your equation, where X is the dose you&amp;#39;ll administer in tablets, written like this:  

X number of tablets equals Vehicle over Have multiplied by Desired multiplied by the conversion factor for grams to milligrams. 

Remember, you should put the units you’re trying to convert to as the denominator so you can cance]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dosage_calculation_-_Dimensional_analysis_method:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n2SnqaZ4TVy4Z-gqF794ztX9TlixL1Bj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dosage calculation - Dimensional analysis method: Nursing pharmacology]]></video:title><video:description><![CDATA[As the nurse, you’ll perform medication calculations to ensure the correct dose of a prescribed medication is administered. The three methods for drug calculations are basic formula, also called Desired over Have; ratio and proportion; and dimensional analysis. Let’s take a deeper look into the dimensional analysis method.  

As with the other methods for drug calculation, the three components involved in dimensional analysis, or DA for short, are D, for the Desired dose, or dose ordered by the health care provider; H, for Have, or the dosage you have available; and V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid. 
The dimensional analysis method is set up like this: 

X = Vehicle   x   Desired / Have

Now, before the drug dosage can be calculated, all units of measurement must be converted into one system, so they’re all the same. For example, if the medication is ordered in grams and comes in mg, then grams are converted to mg or mg are converted to grams. So, to do this, you&amp;#39;ll use conversion factors, which are simply equivalents of measurements, like 1 gram equals 1000 mg or 1 L equals 1000  mL.  
Let’s look at some drug calculations using the DA method.  

First, you’ll read the order, which is: acetaminophen 1 gram PO one time.  

Now, let’s look at the following label: 

Since the medication comes in 500 mg per 1 tablet, you’ll calculate how many tablets to administer to achieve the desired dose. To do this, first identify your components, Desired, Have, and Vehicle.  

In this case, D is 1 gram, which was obtained from the health care provider’s order.  H is 500 mg, which was obtained from the medication label. And V, is 1 tablet, which was also obtained from the label.  

Next, you’ll determine if a conversion factor is required. To do this, compare the units of D with the units of H; and if they&amp;#39;re the same, no conversion factor is needed.  Because D is in grams and H is in mg, a conve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dosage_calculation_-_Ratio_and_proportion_method:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QWGP50LxT9KL8xVk4e3XFk5dQxaCv1ZF/_.png</video:thumbnail_loc><video:title><![CDATA[Dosage calculation - Ratio and proportion method: Nursing pharmacology]]></video:title><video:description><![CDATA[As the nurse, you’ll perform medication calculations to ensure the correct dose of a prescribed medication is administered. The three methods for medication calculations are the basic formula method; dimensional analysis; and the ratio and proportion method, or R&amp;amp;P for short.  

R&amp;amp;P is a method of dosage calculation using a ratio, which shows the relationship between two quantities, like 1:2; and a proportion, which shows the relationship between two ratios. 

Ratios and proportions can be set up two ways: vertically with fractions, or horizontally with colons.   

To solve an R&amp;amp;P problem set up as fractions, you&amp;#39;ll cross-multiply the numerator of the first fraction by the denominator of the second fraction, and then cross-multiply the denominator of the first fraction by the numerator of the second fraction. After that, division is needed as the final step to solve for the dose. 

To solve an R&amp;amp;P problem when it’s set up horizontally, the inside numbers, which are called means, are multiplied and then the outside numbers, which are called extremes, are multiplied. Then division is used to solve for the dose. 

Now, as with the other methods for medication calculation, the three components involved in Ratio and Proportion are D, for the Desired dose, which is the dose ordered by the health care provider; H, for Have, or amount you have available; and V, for Vehicle or the form in which the medication comes, like tablets or liquid. 
Now, before the drug dosage can be calculated, all units of measurement must be converted into one system of measurement, so they’re all the same. For example, if the medication is ordered in grams and comes in milligrams, then grams are converted to milligrams or milligrams are converted to grams. To do this, you&amp;#39;ll use conversion factors, which are simply equivalents of measurements, like 1 gram equals 1000 milligrams or 1 liter equals 1000 milliliters.  
Let’s lo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dosage_calculation_-_Formula_method:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/raUytfkFRKW1IOVlerOt09UgQ1Kdz5yV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dosage calculation - Formula method: Nursing pharmacology]]></video:title><video:description><![CDATA[As the nurse, you’ll perform medication calculations to ensure the correct dose of a prescribed medication is administered. The three methods for drug calculations are basic formula, also called Desired over Have; ratio and proportion; and dimensional analysis.  Let’s take a deeper look into the basic formula method.  

As with the other methods for drug calculation, the three components involved in the basic formula method are D for the Desired dose, or dose ordered by the health care provider; H for Have, or the dosage you have available; and V, for Vehicle or the form in which the medication comes, like tablets or liquid.  

The basic formula method is set up like this:  X = Desired x Vehicle / Have

Now, before the drug dosage can be calculated, all units of measurement must be converted into one system, so they’re all the same. For example, if the medication is ordered in grams and comes in milligrams, then grams are converted to milligrams or milligrams are converted to grams. To do this, you&amp;#39;ll use conversion factors, which are simply equivalents of measurements, like 1 gram equals 1000 mg or 1 liter equals 1000 mL.  
Let’s look at some drug calculations using the basic formula method. 

First, you’ll read the order, which is: diphenhydramine 25 mg IV one time.  

Now, let’s look at the medication label.  

Since the medication comes in 50 mg per 1 mL, you’ll calculate how many mL you should administer to achieve the desired dose. To do this, first identify your components, Desired, Have, and Vehicle. 

In this case, D is 25 mg, which was obtained from the health care provider’s order. H is 50 mg, which was obtained from the medication label. And V, is 1 mL, which was also obtained from the medication label.  

Next, you’ll determine if a conversion factor is required. To determine this, compare the units of D with the units of H, and see if they’re the same. Because both D and H are in milligrams, no conversion factor is needed.  

No]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Pediatric:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PxSkYTWTR3_6-QKkM8vJoGL8TOWQSyR4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Pediatric: Nursing]]></video:title><video:description><![CDATA[A comprehensive physical assessment allows the nurse to assess a child’s growth, development, and health status. As the nurse, you’ll assess the child’s general appearance, growth and physiologic measurements, and each body system.  

Now, unlike assessing an adult where a head-to-toe sequence is generally followed, with children, the sequence can be individualized to their developmental level. For instance, when examining infants, you’ll often need to auscultate lungs and heart when they are quiet and examine their oral cavity when they’re crying.  

You’ll also consider the child’s developmental stage when choosing techniques to prepare them for the examination. For infants you could examine the child on their caregiver’s lap. For toddlers, you could use a doll to demonstrate what to expect during the examination or tell a story like “I’m checking to see if your tummy is hungry.” Likewise, you can teach school-age children about body parts and their function as you examine them. 

As you begin your assessment, observe the child’s general appearance including facial expression, activity level, speech, posture, and interactions with you and their caregivers. Take note of certain observations that warrant further investigation, like if you notice the child is tilting their head to a specific side, it could mean they’re having trouble hearing or seeing; or if they have dirty clothes or an unusual body odor, this may indicate neglect or financial difficulties at home.  

Next, you’ll assess the child’s physical growth by measuring their length or height, weight, and head circumference. Until the child is around 2 years old, you’ll typically measure length using a length board with the child in a supine position. Once they’re older and can stand, height is measured in the upright position, usually against a wall chart. Once you’ve obtained the measurements, you’ll plot them on a growth curve, and compare them to the expected percentile for age and sex. Se]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Equipment:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gQcdGD4EQUCiPkTLkFtu_wEnSaqhx4Ve/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Equipment: Nursing]]></video:title><video:description><![CDATA[As the nurse, you’ll use examination equipment as you perform a physical assessment to collect information about your patient’s health status. Several commonly used items include a stethoscope, otoscope, ophthalmoscope, penlight, and tape measure.  

A stethoscope is used to auscultate, or listen to sounds made by your patient&amp;#39;s body, like lung, heart and bowel sounds. Your stethoscope should have both a diaphragm and a bell. The diaphragm is used to detect high-frequency sounds like bowel or lung sounds, while the bell is used to detect low-frequency sounds, like heart sounds. When you’re using the diaphragm, you’ll place it firmly against your patient’s skin. But when you’re using the bell, you’ll place it lightly on your patient’s skin, since too much pressure causes the bell to act like the diaphragm, and it won’t effectively transmit low-frequency sounds.  

Also remember to eliminate potential artifacts, which are extra sounds that can affect what you hear through the stethoscope. These can be caused by noises in the room, the patient’s body hair or clothing, or touching the tubing on the stethoscope. To eliminate artifacts, perform auscultation in a quiet setting, avoid bumping the tubing, and be sure to place the diaphragm or bell directly on your patient’s skin instead of auscultating through clothing. Lastly, when putting the earpieces into your ears, remember to keep them pointed in the same direction as your ear canals, which means they should be pointing toward your nose.  

Next is the otoscope, which is a device that shines light into the ear to visualize the ear canal and eardrum, also known as the tympanic membrane. The base of the otoscope serves as the handle, which also contains the batteries for the light source and the on-off switch. The handle attaches to the head, which contains the magnifying lens and light source. You’ll attach an appropriately sized, disposable, plastic speculum to the head, which funnels the light into ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gender-diverse_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3cc2C5iTQ3mgzI_NOl8O_PHOSBudIxwA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gender-diverse care: Nursing]]></video:title><video:description><![CDATA[Transgender and gender-diverse individuals experience health disparities such as reduced access to healthcare and high rates of mental health disorders, violence, and substance abuse. These disparities can be traced to cultural stressors like stigma, harassment, and discrimination. As a nurse, you’ll provide patient-centered and gender-inclusive care for members of the transgender and gender-diverse community. 

Okay, first let’s focus on some terminology. Sex assigned at birth is classified as male or female and is based on one’s reproductive anatomy at the time of birth, and occasionally genetics. Of note, intersex refers to a person with sex traits, such as genetics, hormones, or reproductive anatomy, that don’t fit the typical classification of male or female sexes. Gender refers to socially constructed characteristics, such as appearance, behaviors, and roles, and how those characteristics are named and expressed by a person. On the other hand, a person’s gender identity is their inner awareness and naming of their gender, which may be the same as or different from their sex assigned at birth.  

So, when a person’s gender identity is the same as their sex assigned at birth, that person is cisgender. For example, a cisgender female is a person who identifies as female and whose sex assigned at birth is female. In contrast, a person who is transgender has a gender identity that is different from their sex assigned at birth. For example, a transgender male is a person who identifies as male and whose sex assigned at birth is female.  

Now, sometimes, a person can experience significant psychological distress when there’s a mismatch between their gender identity and their sex assigned at birth; this is called gender dysphoria. Finally, it’s important to note that some people may identify as non-binary or gender diverse (e.g. genderqueer, genderfluid, agender, two-spirit, etc), meaning their gender identity is not exclusively male or female.  

Okay, now]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Intravenous_labor_and_delivery:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3dDGJ7x8SJSw215InJpwEy_tQN6EGdv5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication administration - Intravenous labor and delivery: Nursing pharmacology]]></video:title><video:description><![CDATA[The administration of IV medications used during labor and delivery requires the nurse to calculate medication concentrations, infusion rates, and titration factors, along with close monitoring of how both the pregnant patient and the fetus respond to the medication. Some medications used in this setting, like magnesium sulfate and oxytocin, are considered high-alert medications, meaning they can cause significant harm if administered incorrectly. These medications are always delivered through an IV pump to ensure accuracy. 

To calculate a dose using the Dimensional Analysis, or DA method, the three components you need are V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid, H, for Have, or the dosage you have available; and D, for the Desired dose, or dose ordered by the health care provider; and since there’s a time component, we also have T, for Time. 

Magnesium sulfate is a medication used as tocolytic to slow contractions in preterm labor or to reduce the risk of seizures in patients with preeclampsia. It&amp;#39;s typically administered starting with a loading dose, or a higher dose given over a shorter duration, so the desired therapeutic effect is achieved more quickly. After the loading dose is administered, a maintenance dose, or a slower rate of administration is administered to maintain a therapeutic level.  

Let’s look at how to calculate a loading dose of magnesium sulfate in mL/hr.  

First, you’ll read the order, which is: magnesium sulfate 6 g IV in Lactated Ringer’s solution over 30 minutes. 

Then, check the medication label: 

The medication is available in a concentration of 40 g in 1000 mL of Lactated Ringer’s solution. 

In this case, D is 6 g, which was obtained from the health care provider’s order; H is 40 g, which was obtained from the medication label; V is 1000 mL, which was also obtained from the label; and T is 30 minutes, which was obtained from the health care provider’s orde]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Intravenous:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hNF17Ax2SoKDFq665dc-_Y4GT4OnDu6g/_.png</video:thumbnail_loc><video:title><![CDATA[Medication administration - Intravenous: Nursing pharmacology]]></video:title><video:description><![CDATA[The intravenous, or IV, route is a common route for the administration of medications and solutions. Some common ones are antibiotics, electrolytes, and fat emulsions. 

IV medications can be administered through a peripheral intravenous catheter, or PIV, or a central venous catheter, or CVC. PIV catheters are typically inserted into veins on the hand or lower arms and are used for less than 1 week.  

On the other hand, CVCs are used for patients who need long-term infusions. They can be inserted at sites such as the internal jugular vein, subclavian vein, or femoral vein; and terminate at the junction of the superior or inferior vena cava and right atrium. If a central line is inserted peripherally, like in the basilic or brachial vein, it&amp;#39;s called a peripherally inserted central catheter, or PICC.  

Now, medications can be administered in 3 different ways: direct injection, continuous infusion, or intermittent infusion. 

First, medications given by direct injection are often referred to as IV push. This route uses the patient’s intravenous line to administer a small volume of medication directly into the bloodstream.  

When administering medications via direct injection, first, ensure the patency and status of the IV site by flushing with saline before use and assessing for redness, swelling, or pain at the site. Be sure to note the medication’s push rate, or the time spent administering the medication through the IV, since some medications should be pushed slowly, like furosemide, while other medications should be pushed quickly, like adenosine. Finally, if your patient is receiving multiple medications through their IV, ensure the medications and any fluids are compatible.  

As the nurse, you’ll perform calculations to ensure the correct dose of an IV medication is administered.  

To calculate a dose using the Dimensional Analysis, or DA, method, the three components you need are D, for the Desired dose, or dose ordered by the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Environmental_emergencies:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7u9EKxXWQq2FAioXbNWWHX4TSy2ls5sU/_.png</video:thumbnail_loc><video:title><![CDATA[Environmental emergencies: Nursing]]></video:title><video:description><![CDATA[An environmental emergency refers to an event or condition related to exposure to weather, which can include emergencies involving heat and cold. 

Alright, so heat-related emergencies happen when the body’s normal thermoregulatory mechanisms like sweating, vasodilation, and increased respirations, are less effective in situations where there’s prolonged exposure to heat, or if there’s brief exposure to intense heat.  

Heat exhaustion happens when heat exposure occurs over hours or days, like during a hike on a hot day, leading to a body temperature as high as 105.8° F or 41° C.  

Other assessment findings can include anxiety, fatigue, nausea, thirst, and pale skin. 

If left untreated, heat exhaustion can progress to heat stroke, which is a medical emergency. With heat stroke, the body’s thermoregulatory mechanisms fail, leading to a temperature above 105.8° F or 41° C. Other assessment findings can include weakness and hot, flushed, dry skin. 

Now, in both heat exhaustion and heat stroke, fluid and electrolytes are lost through perspiration, which can manifest as tachycardia, weak pulses, and decreased blood pressure. In heat stroke, an excessive loss of sodium can lead to cerebral edema, brain hemorrhage, and mental status changes ranging from confusion to coma.  

Alright, when caring for your patient with a heat-related emergency ensure they are in a cool environment. For heat exhaustion, provide fluid and electrolyte replacement orally, or intravenously, if needed. For heat stroke, provide high-flow oxygen and initiate continuous pulse oximetry; establish IV access to replace fluids and electrolytes; and initiate rapid cooling measures.  

These could include placing wet sheets over your patient and placing them in front of a fan to increase airflow over their body; placing ice packs on their groin and axillae; or immersing them in a tepid or cool water bath. Be sure to monitor their temperature closely to control shivering, which can lead to heat production.   ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Burn_injury:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QU7lhDnIRPWcwRuOE-WLMiAeQ0yBh8Mm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Burn injury: Nursing]]></video:title><video:description><![CDATA[Nurse Kamala works on an inpatient burn unit and is caring for Raul, a 42-year-old male who was recently admitted for a thermal burn following a house fire. After being stabilized in the emergency department through airway management and fluid therapy, Nurse Kamala settles Raul into his room on the inpatient burn unit. After introducing herself to Raul, Nurse Kamala goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Raul’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Kamala recognizes important cues, including Raul’s vital signs, which include blood pressure 128/88 mmHg, heart rate 105 beats per minute, and respirations 22 breaths per minute.  

From Nurse Kamala&amp;#39;s assessment of Raul’s skin, she notes Raul has partial- and full-thickness burns on his right lower extremity, extending up to his lower abdomen. The dressings over Raul’s burns are saturated with serosanguineous drainage and the surrounding skin is reddened and slightly swollen. She also notices that he appears uncomfortable and restless.  

Next, Nurse Kamala analyzes these cues.  She reviews Raul’s electronic health record, or EHR, and notes an order for sterile dressing changes with wound debridement and cleansing. She also sees that he’s prescribed medication for pain management and received his last dose in the emergency department 4 hours ago. She knows that dressing changes will facilitate healing and untreated pain can make dressing changes intolerable. Nurse Kamala realizes that Raul needs effective pain management so the prescribed wound care can be provided for his burns. 

Now, using the information she’s gathered, Nurse Kamala chooses a priority hypothesis of impaired skin integrity.  

Then, she generates solutions to address Raul’s impaired skin integrity using nonpharmacologic and pharmacologic interventions; and she establishes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Iron-deficiency_anemia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kIhzxENlRAm-tPNjjOfTEpQhRvCOj3zM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Iron-deficiency anemia: Nursing]]></video:title><video:description><![CDATA[Nurse Michael works on an inpatient Medical-Surgical unit and is caring for Hannah, a 26-year-old female with a history of Crohn disease who was admitted for iron deficiency anemia. After settling Hannah in her room, Nurse Michael goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Hannah’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Michael recognizes important cues, like Hannah&amp;#39;s laboratory results from the emergency department showing a hemoglobin of 6.5 g/dL and a hematocrit of 19 percent.  Further assessments reveal pallor and a heart rate of 110 per minute with a bounding pulse. Next, Nurse Michael asks Hannah about her prescribed medications. 

Nurse Michael: I see in your chart you’ve been taking infliximab for eight months. Has that helped your Crohn symptoms? 

Hannah: Well, I took it for a while, but I’ve had to skip my last two infusion appointments. I don&amp;#39;t have the money to keep going to the infusion clinic.   

Nurse Michael: I understand. How has that affected your symptoms? 

Hannah: The medicine really helped while I was getting it, especially since I didn’t feel as tired as I do now. I could also eat more foods that I like without pain.  

Nurse Michael: That makes sense. So, what types of food are you eating now? 

Hannah: Crackers and bananas, mostly. Sometimes an egg. That’s about it, because I feel like my symptoms are really flaring up. My belly really hurts after I eat. 

Nurse Michael: I&amp;#39;m sorry to hear that. I&amp;#39;m glad you are here so we can help you. 

Nurse Michael finishes his assessment and ensures Hannah is comfortable. He then places the call bell within her reach before leaving the room. 

Next, he analyzes these cues. Nurse Michael recognizes that stopping infliximab infusions puts Hannah at risk of experiencing a Crohn disease fla]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Acute_respiratory_distress_syndrome_(ARDS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8PeWrX0-Tb_p8v8YK8vUhPKOTNq7pjkH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Acute respiratory distress syndrome (ARDS): Nursing]]></video:title><video:description><![CDATA[Nurse Claire works in the Emergency Department and is caring for Joseph, a 65-year-old male with a history of smoking who was diagnosed with acute respiratory distress syndrome, or ARDS, secondary to pneumonia. As Nurse Claire stabilizes Joseph and prepares him for transfer to the ICU, she goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Joseph’s care.  She does this by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Claire recognizes important cues including Joseph’s vital signs, which are temperature of 102 F, or 38.9 C, heart rate 120 beats per minute, respirations 24 breaths per minute and shallow, blood pressure of 100/60 mmHg, and oxygen saturation 85 percent on 6 liters high flow nasal cannula. Joseph reports a pain level of 2 on a 0 to 10 scale. She also notices Joseph has clammy, flushed skin, and he’s short of breath. Upon auscultation, she notes fine crackles at his lung bases, bilaterally.  

Next, Nurse Claire analyzes these cues. She reviews the electronic health record, or EHR, and notes that Joseph’s arterial blood gas, or ABG, results show a low partial pressure of oxygen, or PaO2, an elevated partial pressure of carbon dioxide, or PCO2, and a decreased SaO2, or oxygen saturation of arterial blood. 

Nurse Claire recognizes that ARDS can happen in patients with pneumonia and, when paired with Joseph’s history of smoking, his risk of developing ARDS increases. She also recalls that with ARDS, there’s inflammation, injury to the alveolar-capillary membrane, and decreased lung compliance, leading to hypoxemia and retention of carbon dioxide. Nurse Claire realizes Joseph needs effective respiratory management to prevent respiratory failure.  

Now, using the information she has gathered, Nurse Claire chooses a priority hypothesis of impaired gas exchange. 

Then, she generates solutions to address Joseph’]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Acute_coronary_syndrome_(ACS):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h8FGHAQOQ_2BpMOxeoGOJ7GBSW60lzBo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Acute coronary syndrome (ACS): Nursing]]></video:title><video:description><![CDATA[Nurse Cameron works on a cardiovascular care unit, or CCU, and is caring for Kevin, a 55-year-old male with a history of coronary artery disease for which he’s prescribed aspirin at home. He was recently admitted to the CCU after undergoing a percutaneous coronary intervention, or PCI, with placement of one stent to treat an ST-segment elevation myocardial infarction, or STEMI for short. After settling Kevin in his room, Nurse Cameron goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Kevin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Cameron recognizes important cues including Kevin’s vital signs, which are temperature 98.8 F, or 37.1 C, heart rate 99 beats per minute, respirations 19 breaths per minute and regular, blood pressure 101/82 mmHg, and oxygen saturation 96 percent on 2 liters per nasal cannula.   

When asked about pain, Kevin reports a current pain level of 3 out of 10 in his groin incision. Upon assessment Nurse Cameron notes that Kevin has a moderate amount of dried blood on his groin dressing. 

Next, Nurse Cameron analyzes these cues.  He knows that the PCI procedure involves threading a catheter into a coronary artery and then opening a tiny balloon to compress the plaque against the artery wall, and that a stent can be placed to prevent the artery from closing again. He understands that this procedure can increase the risk of clot formation since the endothelial lining of the coronary artery can be injured, and because the stent can increase the risk of clot formation due to slowing of blood flow and turbulence at the stent site. Nurse Cameron also understands antithrombotic medications like aspirin and heparin are used before the procedure and antiplatelet medications like aspirin and clopidogrel are given after the procedure to reduce the risk of clot formation. Next, he reviews the e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pediatric_eczema:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uRd20qW4T66aYe7tkUSXxAewTS2uxxMW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pediatric eczema: Nursing]]></video:title><video:description><![CDATA[Nurse Lisa works in a primary care clinic and is caring for Jamie, a 2-and-a-half-year-old who was brought in for a rash, by her mother Claire. After settling Jamie in her room, Nurse Lisa goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Jamie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Lisa recognizes important cues, including Jamie’s skin assessment, which reveals several clusters of dry, red patches to her wrists and ankles. She also notes that Jamie is scratching her left wrist, which is eroded and excoriated. 

Nurse Lisa asks Claire about Jamie’s skin irritation. 

Nurse Lisa: I see that Jamie has some dry and reddened skin. When did these symptoms start? 

Claire: A few weeks ago, when the weather got colder. 

Nurse Lisa: Have you tried any treatments or therapies to help relieve the itching? 

Claire: Sometimes I put her in a hot bubble bath, but it doesn’t seem to help. I also put lotion on her every day, which helps a little. 

Next, Nurse Lisa analyzes these cues. Nurse Lisa understands that Jamie has an itchy inflammatory rash, and that Jamie’s scratching is causing excoriation. She also knows the breakdown of Jamie’s skin increases the risk for infection. Nurse Lisa recognizes that Jamie needs effective management of her rash.  

She reports her assessment findings to the health care provider, who diagnoses Jamie with eczema, or atopic dermatitis, and prescribes oral loratadine and a topical corticosteroid to reduce pruritis and inflammation.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Cerebral_palsy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fSawEOZ2QJeu8dhLd_5MmeM5R6_D_2rr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Cerebral palsy: Nursing]]></video:title><video:description><![CDATA[Nurse Jamie works as a nurse navigator at a pediatric neurology clinic and is caring for Lily, a 9-month-old with a history of cerebral palsy. Nurse Jamie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Lily&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jamie recognizes important cues including Lily’s vital signs, which are temperature of 99 F, or 37.2 C, heart rate 115 beats per minute, respirations 32 breaths per minute, and oxygen saturation 95% on room air. Lily’s weight is stable when compared to her last visit. Nurse Jamie also speaks with Lily’s caregiver, Linda, who reports that during feedings at home, Lily frequently gags and doesn&amp;#39;t swallow her food. When Nurse Jamie attempts to feed Lily a spoonful of baby food, he notices Lily produces a tongue thrust, which moves the food out of Lily’s mouth.   

Next, Nurse Jamie analyzes these cues. He reviews the electronic health record, or EHR, and sees that Lily has a history of delayed oral-motor skills and poor jaw control when feeding from a bottle. He remembers that children with cerebral palsy often have issues with oral-motor skills that can result in difficulty feeding, weight loss, and speech delays. He also notes that coughing and choking while eating can predispose children with cerebral palsy to aspiration and other respiratory problems.  

Nurse Jamie realizes that Lily needs effective management of care from a multidisciplinary team to support her activities of daily living, or ADLs, such as feeding.  

Now, using the information she&amp;#39;s gathered, along with Lily’s medical history, Nurse Jamie chooses a priority hypothesis of impaired oral intake.  
Then, he generates solutions to address Lily’s impaired oral intake that will include nonpharmacologic interventions; and he establishes the expected outcome that after inte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Atrial_fibrillation_(Afib):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bITQDY9lShCwHItR2QUYGnR-Q_esShQT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Atrial fibrillation (Afib): Nursing]]></video:title><video:description><![CDATA[Nurse Derek works on an inpatient cardiac unit and is caring for Mrs. Alvarez, a 76-year-old female with a history of hypertension, who was admitted with new-onset atrial fibrillation, or a-fib, with rapid ventricular rate, or RVR. She was given an IV bolus of diltiazem in the emergency department then started on a continuous diltiazem drip. After settling Mrs. Alvarez in the room, Nurse Derek goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about her care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Derek recognizes important cues, including Mrs. Alvarez’s vital signs, which are blood pressure 100/74 mmHg, heart rate 112 beats per minute, and respirations 22 breaths per minute. After placing Mrs. Alvarez on continuous cardiac monitoring, he evaluates her ECG, noting the QRS complexes are normal, but the rhythm is irregular and there are no P waves.  

She denies pain but reports mild shortness of breath, diaphoresis, and feeling dizzy and tired with movement. 

Next, Nurse Derek analyzes these cues. He determines that Mrs. Alvarez is still in a-fib. He then reviews the electronic health record, or EHR, and notes that her diltiazem drip is ordered to be titrated as needed to maintain a heart rate of less than 100 beats per minute; and the drip was last titrated in the emergency department one hour ago.  

Nurse Derek also realizes that rapid and irregular atrial contractions can lead to decreased cardiac output and tissue perfusion, causing Mrs. Alvarez’s symptoms, therefore, she needs more effective heart rate control.  

Now, using the information he&amp;#39;s gathered, Nurse Derek chooses a priority hypothesis of decreased cardiac output. 

Then, he generates solutions to promote heart rate control that will include pharmacologic interventions. He establishes the expected outcome that after intervening, Mrs. Alvarez w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Hypovolemic_shock:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T_yRrpkZSfK-sEIt06olhOPFQpGREO5d/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Hypovolemic shock: Nursing]]></video:title><video:description><![CDATA[Nurse Edwin works night shift at the emergency department and is caring for José, a 67-year-old male with a history of liver cirrhosis and hepatic encephalopathy. After settling José in his room, Nurse Edwin goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about José’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Edwin recognizes important cues, including José’s vital signs, which are blood pressure 88/46 mmHg, mean arterial pressure, or MAP of 60 mmHg, heart rate of 110 beats per minute and regular, peripheral pulses are weak and thready, and respirations 22 breaths per minute. Pulse oximetry is 88 percent on room air.  

He&amp;#39;s also confused and doesn’t know why he’s in the hospital. Nurse Edwin also notices that José appears pale, diaphoretic, and has a capillary refill of more than 3 seconds in his lower extremities. He also notes that José’s abdomen is round and distended. 

Next, Nurse Edwin analyzes these cues. He collaborates with the health care provider, who determines that José is in the early decompensated stage of hypovolemic shock, due to third spacing. Nurse Edwin realizes José needs effective tissue perfusion. 

Now, using the information he&amp;#39;s gathered, along with José’s medical history, Nurse Edwin chooses a priority hypothesis of fluid volume deficit.  

Then, he generates solutions to address José’s fluid and perfusion status with pharmacological and nonpharmacological interventions; and he establishes the expected outcome that after intervening, José’s MAP will be above 60 mmHg within one hour.  

Nurse Edwin then takes action to implement these solutions. He receives orders from the health care provider for IV fluids and albumin, oxygen at 10 liters per minute via non-rebreather mask, and insertion of an indwelling urinary catheter. Other orders include lactulose PO, and transfer t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malnutrition:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zFuSm-1cQeiGSK5_8er-ILmRQE_qac4E/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malnutrition: Nursing]]></video:title><video:description><![CDATA[Nutrition is the process by which nutrients are taken in and used by the body to support overall health and essential functions, such as metabolism, growth, and maintaining and repairing body tissues.  

When nutrition is imbalanced, it&amp;#39;s called malnutrition. Now, malnutrition can be overnutrition, or the ingestion of more nutrients and energy than the body needs; or undernutrition, where nutrient and energy intake is insufficient to meet the body’s daily needs. 

Okay, let’s review the different types and causes of malnutrition. First, starvation-related malnutrition, also called primary protein-calorie malnutrition, occurs when nutritional needs aren’t met due to starvation, like with anorexia nervosa.  

Then, there’s chronic disease–related malnutrition, also known as secondary protein-calorie malnutrition, where dietary intake is insufficient to meet the increased metabolic demands related to chronic inflammatory conditions, like rheumatoid arthritis.  

Lastly, there’s acute disease–related or injury-related malnutrition, where there is significant inflammation, like with major infections, burns, and trauma, and dietary intake is unable to supply enough calories for energy or protein for tissue repair. 

So, there are several risk factors for malnutrition, including socioeconomic factors, like food insecurity; health conditions, like prolonged physical illness, surgery, trauma, or prolonged immobility; incomplete diets, like with fad diets or poorly planned veganism; and malabsorption, like with vitamin B12 deficiency that occurs when intrinsic factor is lost after a gastrectomy.   

Now, as protein stores are depleted, synthesis of plasma proteins, like albumin, decreases.   This lowers oncotic pressure in the intravascular space, which causes a shift of fluids out into the interstitial tissues, leading to edema, as well as drying of the skin and mucous membranes. Protein deficits can also result in brittle nails and hair loss, as well as d]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obesity:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I3WQJZ-oTEG4octCnP4I7Fm7SemjWk4j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obesity: Nursing]]></video:title><video:description><![CDATA[Obesity refers to an increased number and size of fat cells, which are referred to as adipocytes. It is often classified using body mass index, or BMI, and is calculated by dividing weight in kilograms by the square of height in meters. A person is considered obese if their BMI is 30 kg/m2 or higher, and a BMI above 40 kg/m2 signifies extreme obesity, also known as morbid obesity. Obesity can seriously impact a person’s health, leading to chronic medical conditions, increased mortality, and reduced quality of life. 

Now, most people have primary obesity, meaning it’s the result of consuming more calories than the body requires for their metabolic needs. Causes of primary obesity include lifestyle factors such as dietary choices, like eating foods high in calories, drinking sweetened beverages, and consuming large portion sizes; eating outside the home or in front of television or computer; and being sedentary.  

Environmental factors also contribute to obesity, for example, patients with low income are at increased risk of obesity since inexpensive foods often have high calories and low nutritional value. Additionally, psychosocial factors can play a role in obesity, such as using food for comfort, reward, or eating more during times of stress, sadness, and anxiety.  

Lastly, certain genes can increase the risk of obesity by influencing appetite; satiety, or the feeling of fullness after eating; and how fat is stored or distributed in the body. 

On the other hand, secondary obesity is caused by medical conditions, such as certain congenital, endocrine, or central nervous system disorders. For instance, hypothyroidism slows metabolism, which can lead to excess weight gain. There are also certain medications that can contribute to obesity, including corticosteroids, estrogens, antipsychotics, antiepileptics, and oral antidiabetics.  

Okay, now let’s look at the health risks associated with obesity from head to toe. First, obesity can increase the risk f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Cholecystitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QBDaw0v9TQCVd4rCJOmlvVo7TPKrJmKk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Cholecystitis: Nursing]]></video:title><video:description><![CDATA[Nurse Sandy works in the emergency department and is caring for Natasha, a 40-year-old female with a history of obesity who&amp;#39;s been diagnosed with acute cholecystitis requiring surgical intervention. While Nurse Sandy prepares Natasha for surgery, she goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Natasha&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Sandy recognizes important cues, including Natasha’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 102 beats per minute, respirations 22 breaths per minute, blood pressure 159/97 mmHg, and pulse oximetry 99 percent on room air. Natasha rates her pain at 3 on a zero to 10 scale. She also notices that Natasha is holding an emesis bag, which contains a small amount of green emesis. 

Nurse Sandy performs a focused abdominal assessment, noting active bowel sounds in all quadrants. However, upon palpation, Natasha grimaces and puts her hand over her mouth. 

Natasha: Please don’t press down on my stomach, I feel like I’m going to throw up again. 

Nurse Sandy provides Natasha with a fresh emesis bag and rubs her back as she vomits.  

Afterwards, Nurse Sandy analyzes these cues. She reviews the electronic health record, or EHR, and notes that Natasha initially presented to the emergency department with right upper quadrant pain and vomiting that occurred hours after eating fried chicken for dinner. She also notes that Natasha is taking oral contraceptives, which Nurse Sandy recalls increases the risk for developing cholecystitis. Additionally, Nurse Sandy sees that, two hours ago, Natasha received 4 milligrams of ondansetron and 4 milligrams of morphine sulfate IV. 

Nurse Sandy then acknowledges the new preoperative orders for Nastasha, including NPO status, and a maintenance infusion of normal saline to run at 100 milliliters ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Chronic_kidney_disease_(CKD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V1gLsKqpRqSTIdLqlsRb3ZjUQTG_tLo2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Chronic kidney disease (CKD): Nursing]]></video:title><video:description><![CDATA[Nurse Marisol works in a family practice office and is caring for Robert, a 55-year-old male with a history of chronic kidney disease and type 2 diabetes, who&amp;#39;s arrived for a follow-up appointment. After settling Robert in the exam room, Nurse Marisol goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Robert’s care by recognizing cues, analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Marisol recognizes important cues including mild, pitting edema in Robert’s lower extremities, a blood glucose of 214 mg/dL, blood pressure of 145/85 mmHg, and a weight gain of 4.5 pounds since his last visit. 

Nurse Marisol asks about Robert’s insulin management at home. 

Nurse Marisol: I see that your blood sugar is higher than your last visit. Have you made any changes to your medications or the foods you eat? 

Robert: Yeah, my blood sugar’s been a little high. Sometimes I get tired and forget to take my insulin at night. 

Nurse Marisol: I also noticed that your ankles are swollen, too. Can you tell me how much water you’ve been drinking lately? 

Robert: Well, I’ve been really thirsty lately, so I’ve been drinking more than usual. Anyway, someone told me that drinking water helps to flush out my kidneys. 

Next, Nurse Marisol analyzes these cues. She reviews the electronic health record, or EHR, and notices that Robert is prescribed ten units of long-acting insulin nightly. She also notes that he’s recommended to follow a 1.5-liter fluid restriction daily. She knows that chronic kidney disease is a progressive and irreversible loss of kidney function, and that uncontrolled diabetes can worsen damage to nephrons over time. She also understands that nephron loss reduces the glomerular filtration rate, or GFR, leading to decreased fluid output, increased fluid retention, edema, and increased blood pressure.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_-_Culture:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eaQyrPYrT2a7fZctnSUrLUukRP_Wc6rE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment - Culture: Nursing]]></video:title><video:description><![CDATA[Culture is a complex phenomenon that includes the ever-changing attitudes, beliefs, self-definitions, norms, roles, values, and communication styles a person develops throughout life.   

When performing a cultural assessment, you’ll use a relational approach that accounts for the socio-environmental, geographical, historical, and other individual factors involved in your patient’s response to health and illness. 

Completing a cultural self-assessment will support a relational approach by clarifying your own background and values, and by building self-awareness and accountability for any biases or prejudices you may have.  

To perform a cultural self-assessment, consider how your own social and cultural heritage could impact your beliefs about health and illness and how you relate to your patients. You can also think about how your decision to become a nurse and your professional experiences can influence the assumptions you make and the care you provide for your patients.    

When assessing your patient’s culture, you’ll use clinical practice guidelines that support a relational approach, which include building trust, engaging through listening, conveying respect, and paying attention to context. During your initial interview, work on building trust by asking questions in a nonjudgmental way. For example, when gathering information about your patient’s presenting health concerns, you could ask them “What do you think might be causing you to feel this way?”  

You can build trust by conveying interest in their life context. So, if your patient has recently moved to your city, ask them about where they moved from or what language they are most comfortable speaking. Once trust is established, your patient will often be more willing to share more sensitive information.  

As you ask questions, engage with your patient through listening to their responses about their background, identity, and values, as well as their health beliefs and practices.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prenatal_screening:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nOdd44p8Rp_Kq2psKJnlnEx-S-mNjFB7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prenatal screening: Nursing]]></video:title><video:description><![CDATA[Prenatal screening can be done to identify the likelihood that a certain fetal disorder or condition is present. Screening is typically completed during the first and second trimesters and can be followed by diagnostic testing to confirm if the fetus is affected.   

Alright, so first trimester screenings are done between 11 to 14 weeks of gestation to look for evidence of chromosomal abnormalities, including aneuploidies, which means there’s an abnormal number of chromosomes. These tests include nuchal translucency, or NT, using ultrasound; as well as a measurement of maternal serum levels of pregnancy-associated plasma protein-A, or PAPP-A; human chorionic gonadotropin, or hCG; and cell-free fetal DNA, or cfDNA.  

Nuchal translucency measures the fluid-filled space behind the fetus&amp;#39; neck. An increased amount of fluid is associated with chromosomal abnormalities, including Trisomy 21, also known as Down syndrome, where there’s an extra copy of chromosome 21.  

Next, PAPP-A is a glycoprotein made by the placenta. Low levels of PAPP-A are also linked to Trisomy 21. Then, there’s hCG, which is a hormone made by the placenta. Increased levels of hCG are associated with Trisomy 21, whereas decreased levels are associated with both Trisomy 18, or Edward syndrome, where there’s an extra copy of chromosome 18; and Trisomy 13, known as Patau syndrome, where there’s an extra copy of chromosome 13.  

Lastly, cfDNA refers to fragments of DNA from the breakdown of maternal and fetal cells. cfDNA can be used to screen for trisomies, sex chromosome aneuploidies, and other chromosomal microdeletions or duplications.   ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_delayed_puberty:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xOqQjVRGSMyLck6jcKmvVu2dTmqwN26m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to delayed puberty: Clinical sciences]]></video:title><video:description><![CDATA[Puberty refers to the transition phase between childhood and adulthood, during which an individual develops secondary sexual characteristics and becomes capable of reproduction. In biological females, delayed puberty refers to the absence of breast development by age 13; while in biological males, it refers to the absence of testicular enlargement by age 14. The most common type of delayed puberty is the constitutional delay of growth and puberty, which is a normal developmental variant. However, delayed puberty can also be secondary to underlying causes, such as hypothyroidism, hyperprolactinemia, and hypo- or hypergonadotropic hypogonadism. 

Now, if your patient is presenting with chief concerns suggesting delayed puberty, first, perform a focused history and physical examination, including Tanner staging, and measure weight and height. 

Here’s a high-yield fact! Puberty begins with activation of the hypothalamic-pituitary-gonadal or HPG axis, which is when the hypothalamus releases gonadotropin-releasing hormone or GnRH that stimulates the anterior pituitary gland to secrete gonadotropin hormones called luteinizing hormone, or LH for short, and follicle-stimulating hormone, or FSH for short. These hormones then travel through the bloodstream to the gonads, where they stimulate the production of sex hormones like estradiol and testosterone! This process of gonadal activation, growth and maturation is also known as gonadarche. 

On the other hand, adrenarche is associated with adrenal gland maturation and increased adrenal hormone production, leading to the development of signs like axillary and pubic hair! In other words, adrenarche is independent of the HPG axis, so to determine the true onset of puberty, you should always look for signs of gonadarche, not adrenarche.

Alright, let’s look at some findings in delayed puberty. In biological females, the history will reveal the absence of breast development by age 13; while in biological males, it w]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_myelodysplastic_syndromes:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Oly2L_hVTdu-E52uYU7lvhtIT4yipZ6Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to myelodysplastic syndromes: Clinical sciences]]></video:title><video:description><![CDATA[Myelodysplastic syndromes or MDS, refers to a group of hematologic neoplasms associated with impaired hematopoiesis. Platelets, red blood cells, and neutrophils are the most common cell lines affected by MDS, which manifests with dysplasia, or abnormal blood cell morphology, along with cytopenia, which refers to a  decrease in blood cell count. Now, there are various types of MDS, which are classified based on the presence of defining genetic abnormalities, or morphologic characteristics of the bone marrow or peripheral blood.

Now, if your patient presents a chief concern suggesting MDS, first perform an ABCDE assessment to determine if they’re unstable or stable. If they’re unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen.

Now, here’s a clinical pearl! There are several ways that a patient with MDS can present as unstable. First, MDS can cause severe thrombocytopenia, which may result in intracranial or gastrointestinal bleeding. Second, MDS can cause neutropenia, leading to fungal and bacterial infections, such as pneumonia and sepsis. Lastly, MDS can transform into acute myeloid leukemia, which can cause tumor lysis syndrome, or acute disseminated intravascular coagulation. 

Now, let’s return to the ABCDE assessment and take a look at stable patients. In this case, obtain a focused history and physical exam, and order labs including a complete blood count with differential. Your patient will usually be over 60 years old, and symptoms will vary depending on the type of affected blood cells. If red blood cells are affected, they might report symptoms of anemia, like fatigue, shortness of breath on exertion, and palpitations. Interestingly, anemia is the most common cytopenia associated with MDS, and is generally associated with an inappropr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_fever_(over_2_months):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/f1NSaU_URFWgMPiP3Nh3ZJcvSwuC8FMj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a fever (over 2 months): Clinical sciences]]></video:title><video:description><![CDATA[Fever is defined as a temperature of 38 degrees Celsius or 100.4 degrees Fahrenheit, or higher. It’s crucial to determine the source of fever in children over 2 months of age in order to promptly identify the cause of the fever and initiate appropriate treatment. The most important underlying causes of fever include infection, malignancy, inflammatory conditions, and certain medications.

If a child over 2 months of age presents with a fever, you should first perform an ABCDE assessment. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, and consider starting IV fluids. Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation, and provide supplemental oxygen if needed. 

Okay, now let’s go back to the ABCDE assessment and look at stable patients. First, let’s start by obtaining a focused history and physical exam. The presence of a temperature of 38 degrees Celsius or higher confirms a fever, so your next step is to assess signs and symptoms of a clinical infection. 

First, let’s start with signs and symptoms that suggest a localized infection, such as a purulent middle ear effusion, tonsillar exudates, focal crackles on lung auscultation, or a history of dysuria with urinary urgency or frequency. If this is the case, consider ordering additional testing, like a urinalysis and urine culture, chest X-ray, rapid strep test, or throat culture. If the confirmatory testing identifies a focus of infection, or if you’re able to make a clinical diagnosis based on exam findings alone, you can diagnose a focal infection. Some common examples of focal bacterial infections in children include otitis media, urinary tract infection, pneumococcal pneumonia, and group A Strep pharyngitis.

On the other hand, in some individuals, you might identify signs and symptoms suggesting a systemic infection, such as malaise, fatigue, weakness, chills, muscle or join]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testicular_torsion_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UFue07TFTmSDV-c6s0v_jmbTScyyb-tD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Testicular torsion (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Testicular torsion occurs when the spermatic cord becomes twisted, which impairs blood flow to and from the ipsilateral testis. This condition is a surgical emergency that must be addressed quickly in order to prevent permanent ischemic damage to the testicle. Several factors can increase a patient’s susceptibility to testicular torsion, such as an abnormal fixation of the testicle within the scrotum, as well as rapid growth, increased vascularity, inflammation, and trauma. Based on history and physical examination findings, you can categorize testicular torsion as an acute or intermittent condition.

Now, if a pediatric patient presents with a chief concern suggesting testicular torsion, first perform an ABCDE assessment to determine if the patient is unstable or stable. If your patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and give IV fluids. Don’t forget to put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry.

Alright, let’s go back to the ABCDE assessment and look at stable patients. If your patient is stable, first obtain a focused history and physical examination.

Now, let’s look at patients who report a sudden onset of severe unilateral scrotal or testicular pain. This pain will often awaken the patient in the middle of the night or early morning. There might also be nausea and vomiting associated with the pain. The physical exam will reveal scrotal erythema, induration, or edema. Additionally, the affected testicle may appear to “ride higher” in the scrotum, or it could have a transverse orientation. 

You might also notice an absent cremasteric reflex on the affected side, which can be elicited by stroking your patient’s inner thigh. Usually, this stimulates the cremaster muscle to contract and pull the testicle upward, but the reflex is often absent on the affected side when torsion is present. These findings are highly suggestive of acute ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_penetrating_neck_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/H9zNOt1fQoiFTF30_jX0Btb9Sl6AY6UZ/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to penetrating neck injury: Clinical sciences]]></video:title><video:description><![CDATA[Penetrating neck injuries typically occur from stab or gunshot wounds and can be life-threatening depending on the location. Now, the neck is divided into three zones which contain vital structures.  

Zone I extends from the sternal notch,   to the cricoid cartilage.  

It contains the subclavian vessels, proximal carotid arteries, vertebral arteries, internal jugular veins, trachea, Thyroid gland, esophagus, apices of the lung, thoracic duct, spinal cord, and brachial plexus. 

Zone II extends from the cricoid cartilage,   to the angle of the mandible.  

It contains the common carotid arteries and their branches, vertebral arteries, jugular veins, larynx, pharynx, trachea, esophagus, spinal cord, vagus nerves, and recurrent laryngeal nerves.  

Finally, zone III extends from the angle of the mandible,   to the base of the skull.  

It contains the distal internal carotid arteries, vertebral arteries, jugular veins, pharynx, spinal cord, and cranial nerves IX through XII.  

Your first step when evaluating a patient with a penetrating neck injury is to perform a primary survey by assessing their ABCDE.  

Because any neck injuries can compromise the airway, it&amp;#39;s important to secure the airway as soon as possible. Make sure to stabilize the cervical spine with a C-collar and always have a low threshold for endotracheal intubation. Keep in mind that intubation should be performed carefully to avoid causing further damage. Now, if there is a laryngeal obstruction or exposed trachea, proceed with a surgical airway like a cricothyroidotomy.  

Once the airway is secured, ensure adequate ventilation by providing supplemental oxygen.  

Next, obtain two large bore IVs or an intraosseous line if intravenous access cannot be obtained.  

Continuously monitor vitals while starting appropriate resuscitative measures including blood transfusions.  

Then, assess for disability by performing a neurological assessment and calculating the Glasgow Coma Sca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_dysmenorrhea:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D-R2EbTST-_lg-jOMD1I8anfTGq9Yg0t/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to dysmenorrhea: Clinical sciences]]></video:title><video:description><![CDATA[Dysmenorrhea is pain with menstruation. It can be primary in nature, meaning pain without pelvic pathology; or secondary indicating pain from pelvic pathology or a recognized medical condition. Causes of secondary dysmenorrhea include endometriosis, adenomyosis, uterine leiomyomas, adnexal masses, pelvic inflammatory disease, vaginal obstructive anomalies, and cervical stenosis. Dysmenorrhea is one of the most common gynecologic conditions and can have a significant impact on your patients’ physical and mental well-being. 

Let’s begin with primary dysmenorrhea. When evaluating a patient your first step is to obtain a focused history. Pain typically begins with the onset of ovulatory cycles, which usually occurs within 6-12 months following menarche. The pain is typically located in the lower back, pelvis, and/or the upper thighs. It can be associated with other symptoms, like nausea, vomiting, diarrhea, headaches, muscle cramps, and poor sleep. If your patient’s history meets these criteria, you can diagnose primary dysmenorrhea, which is more common in adolescence. 

Here’s a clinical pearl! Keep secondary dysmenorrhea in mind for patients whose symptoms do not improve within 3 to 6 months of treatment; whose symptoms are progressively worsening; or if pelvic pathology is suspected. 

Okay, let&amp;#39;s move on to secondary dysmenorrhea. On history, common symptoms might include severe dysmenorrhea, which may have begun immediately after menarche or may have developed some time after menarche; progressively worsening dysmenorrhea; abnormal uterine bleeding; mid-cycle or acyclic pain; infertility; lack of response to empiric medical treatment…

Other symptoms can be dyspareunia or pain with intercourse, pelvic pain associated with vaginal discharge, and family history of pelvic pathology, such as endometriosis or congenital anomalies. Any of these symptoms should raise your suspicion for underlying pelvic pathology and secondary dysmenorrhea. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_mellitus_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QFjYFo58Tniay9Bubk6mxkXnTR2PbQV5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes mellitus (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Diabetes mellitus, or DM, is a condition characterized by reduced insulin secretion or resistance to insulin, which eventually results in various issues with carbohydrate, protein, and fat metabolism. 

Now, there are three main types of diabetes mellitus, including type 1 diabetes mellitus, type 2 diabetes mellitus, and monogenic diabetes, also called maturity-onset diabetes of the young. 

Now, if your pediatric patient is presenting with a chief concern suggesting Diabetes Mellitus, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, begin IV fluids, and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen.

Once you initiate acute management, obtain a focused history and physical examination, and obtain labs, including serum blood glucose, BMP, serum beta-hydroxybutyrate concentration, urinalysis, and arterial blood gas. Your patient or their caregiver often reports polyuria, polydipsia, and polyphagia, as well as vomiting, abdominal pain, or confusion. The physical examination may reveal somnolence often in combination with tachycardia, hypotension, and Kussmaul respirations, which refer to a consistently rapid, deep pattern of breathing. Other important findings include fruity breath and dry mucous membranes! 

At this point, suspect Diabetic Ketoacidosis or DKA and assess the criteria for biochemical diagnosis. These include a blood glucose level greater than 200 milligrams per deciliter; arterial pH less than 7.3 OR serum bicarbonate level less than 15 milliequivalents per liter; a beta-hydroxybutyrate concentration of 3 millimoles per liter or higher, and moderate to severe ketonuria. 

If your patient meets the criteria, diagnose DKA. Now, keep in mind that up to 25% of children with new-onset DM first present with DKA, and man]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypoglycemia_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OBQbGtNQTjSMzhi7ApLo0XanQvGEeTIW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypoglycemia (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Hypoglycemia refers to a plasma glucose concentration that’s less than the lower limit of normal for age. Because the brain primarily relies on glucose as an energy source, prolonged hypoglycemia can cause serious adverse effects, such as seizures and permanent brain injury.  

Infants less than 48 hours old frequently have transient physiologic hypoglycemia, while persistent hypoglycemia beyond 48 hours of life can be caused by medications or substances, as well as conditions unique to infancy and childhood, including inborn errors of carbohydrate metabolism, hypopituitarism, hyperinsulinism, fatty acid oxidation defects, disorders of gluconeogenesis, and ketotic hypoglycemic disorders.  

Now, if a pediatric patient presents with hypoglycemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain a fingerstick or heel stick glucose level, and obtain IV access to give IV dextrose. In addition, begin continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen. 

Here’s a clinical pearl! Be sure to consider sepsis in a newborn infant with hypoglycemia, especially if they are unstable or have temperature instability.  

Now, let’s go back to the ABCDE assessment and discuss stable patients. In this case, first, obtain a focused history and physical examination, as well as bedside glucose followed by a critical lab sample to confirm the plasma glucose level. Clinical manifestations of hypoglycemia differ based on age, with newborns and infants displaying symptoms like poor feeding, lethargy, or irritability; while an older child may report weakness, drowsiness, confusion, or hunger.  

Meanwhile, the physical exam in a newborn or infant might reveal pallor, jitteriness, and occasionally, seizures; while an older child may display confusion, diaphoresis, or weaknes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_shock_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K_YKZX2YSIelScvTMmxZPhnBQUqKg_w4/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to shock (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Shock is a condition characterized by circulatory failure that impairs the delivery of oxygen and nutrients to peripheral tissues. In the early stages, the human body activates compensatory mechanisms to maintain tissue perfusion and oxygen delivery. However, these mechanisms can fail. So, if not recognized and treated on time, shock can progress to organ failure and death.  

Now, based on the systemic vascular resistance and cardiac output, shock can be classified as warm or cold shock. Depending on the underlying cause, shock can also be subdivided into four main categories: distributive, hypovolemic, cardiogenic, and obstructive. 

Now, here’s a high-yield fact! Sometimes, you might hear of a fifth category of shock called dissociative shock, which occurs when oxygen is not appropriately bound to or released from hemoglobin, causing inadequate tissue oxygenation. Important examples of this type include carbon monoxide poisoning or methemoglobinemia. 

Now, if a pediatric patient presents with chief concerns suggesting shock, your first step is to perform an ABCDE assessment to determine if they are stable or unstable. Most patients in shock will be unstable, so be sure to initiate acute management by stabilizing the airway, breathing, and circulation. Sometimes, you might even need to intubate your patient and start mechanical ventilation. Next, obtain intravenous or intraosseous access and begin fluid resuscitation. Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, and if needed, don’t forget to provide supplemental oxygen.   

Once you’ve provided acute management, perform a focused history and physical examination. Patients usually report weakness, fatigue, lethargy, and dizziness, while their physical exam might reveal tachycardia, hypotension, tachypnea, and altered mental status.   

With these findings, consider shock, and assess the patient’s skin temperature, capillary refi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteomyelitis_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_c26grnDRzKrEGqolIjaGPP9QeGoCTak/_.png</video:thumbnail_loc><video:title><![CDATA[Osteomyelitis (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Osteomyelitis refers to bony inflammation caused by an underlying infection. In children, osteomyelitis is usually caused by Staphylococcus aureus, but it can also be caused by other bacterial pathogens, such as Group A Streptococcus.  

Children most commonly present with acute hematogenous osteomyelitis, meaning the infection spreads from the blood to the bone.  

Osteomyelitis often involves the metaphyseal region of tubular bones like the femur, due to the increased vascularity of the growth plate.  

In order to determine appropriate treatment, it’s important to distinguish stable patients from those with a rapidly progressive infection or worsening clinical status.   

Now, if a pediatric patient presents with a chief concern suggesting osteomyelitis, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation.  

Next, obtain IV access and start IV fluids. Begin continuous vital sign monitoring, including pulse oximetry, blood pressure, and heart rate. If needed, provide supplemental oxygen; and start antibiotics if your patient shows signs of sepsis. 

Alright, let’s go back to the ABCDE assessment and look at stable patients. First, obtain a focused history and physical examination.  

History may include fever, or a recent trauma or infection.  The patient or caregivers typically report pain in the affected bone and pseudoparalysis, meaning they are unable to bear weight or have reduced use of the affected extremity.  

Also keep in mind that nonverbal or pre-verbal children might only exhibit nonspecific symptoms, such as fussiness, decreased activity, or decreased appetite.  

Physical examination typically reveals  edema, warmth, and tenderness over the affected bone. At this point, you should suspect osteomyelitis. 

Here’s a clinical pearl! In neonates, osteomyelitis often causes septic arthritis of adjacent joints, due to the presence of vasc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_viral_exanthems_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AEJBeDHHQFOON513xAACJbfbTvyWYrIJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to viral exanthems (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[A viral exanthem is a widespread rash due to a viral infection. Most viral exanthems in children are associated with mild, self-limited illnesses, but some may indicate a serious or chronic disease. They can be categorized based on the rash morphology, which can be maculopapular, reticulated, papular, or vesicular. 

When a child presents with a chief concern suggesting a viral exanthem, obtain a focused history and physical exam.  Ask about known exposures to sick individuals, and review their immunization records. As patients or caregivers describe the rash, be sure to ask where the first lesions were seen; whether the rash is painful, pruritic, or asymptomatic; and determine the pattern in which it has spread. Finally, ask about other symptoms, like fever, malaise, rhinorrhea, or sore throat.  

On exam, assess the appearance and distribution of the skin lesions, and look for mucous membrane involvement, lymphadenopathy, or conjunctival injection. With this information, consider a viral exanthem and assess rash morphology.  

Let’s first look at maculopapular rash. Maculopapular rashes consist of flat red spots called macules, as well as small raised bumps, called papules. They should make you consider measles, rubella, roseola, HIV, and infectious mononucleosis.  

Let’s start with measles, also called rubeola. This highly contagious infection typically occurs in under-immunized individuals. It usually begins with the 3 C’s, which are cough, coryza, and conjunctivitis but some also report photophobia. Later on, there’s a high fever and a rash that starts behind the ears and spreads down toward the toes.  

The exam will reveal a morbilliform rash, which is a bright red maculopapular rash that becomes confluent as it spreads caudally, and it may involve the palms and soles. An early finding in measles is Koplik spots on the buccal mucosa, which consist of tiny bluish-gray spots with a white or pale center, on an erythematous base. You won’t always see t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_congenital_infections:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Ri2KC1qqRre_eo3YgmWSv7MbSAOhuPeO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to congenital infections: Clinical sciences]]></video:title><video:description><![CDATA[Congenital infections occur when a bacterial, viral, or parasitic pathogen crosses the placenta during pregnancy or is acquired by the newborn during labor and delivery.  

While some congenital infections are asymptomatic, many are associated with significant sequelae such as intrauterine growth restriction, microcephaly, hearing loss, and ocular abnormalities.  

Traditionally, congenital infections have been grouped under the mnemonic TORCH, which stands for Toxoplasma, Other, Rubella, Cytomegalovirus, and Herpes simplex virus. The category Other continues to evolve and includes pathogens such as Zika virus, Varicella-zoster virus, syphilis, and human immunodeficiency virus.  

When a patient presents with a chief concern suggesting a congenital infection, your first step is to obtain a focused history and physical examination.  

This includes measurement of weight, length, and head circumference; as well as a fundoscopic exam and a hearing screen.  

The antenatal history may reveal signs or symptoms of a maternal infection during the pregnancy;  immunosuppression, or there might be no prenatal care.  

The neonatal history may reveal that the infant was small for gestational age at birth; and the physical exam findings could include jaundice, hepatosplenomegaly or hsm, rash, or congenital malformations, depending on the type of infection.  With these findings, consider the possibility of a congenital infection. 

Now here’s a clinical pearl to keep in mind! Various congenital infections present with jaundice, hepatosplenomegaly, and rash, so consider ordering a CBC and CMP during your initial workup. The CBC commonly demonstrates anemia and thrombocytopenia, while the CMP may demonstrate elevated serum bilirubin levels. Remember, these findings aren’t specific, so correlate the results with clinical findings to focus your diagnostic evaluation! 

Once you’ve considered a congenital infection, begin your evaluation by assessing for a heart murmur.  

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kawasaki_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/74x9CUetTa2f_lvgg5RXIMmcQCOQ50zw/_.png</video:thumbnail_loc><video:title><![CDATA[Kawasaki disease: Clinical sciences]]></video:title><video:description><![CDATA[Kawasaki disease, or KD, previously known as mucocutaneous lymph node syndrome, is a vasculitis of unknown etiology that affects medium-sized arteries. Kawasaki disease is the leading cause of acquired heart disease in children in developed countries, and is primarily seen in children under the age of 5. This febrile illness can result in multi-organ dysfunction; however, the presence of coronary artery lesions determines its morbidity and mortality.  

Now, if your pediatric patient presents with a chief concern suggesting Kawasaki disease, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and consider starting IV fluids. Finally, begin continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry; and, if needed, don’t forget to provide supplemental oxygen.

Now, here’s a clinical pearl! Kawasaki disease shock syndrome, or KDSS, is a rare but potentially life-threatening complication of KD. It presents with hypotension, shock, and multi-organ failure. Because KDSS is associated with decreased peripheral resistance and reduced cardiac contractility, affected patients require fluid resuscitation and intravenous vasopressors such as epinephrine, along with IV immunoglobulins, which are essential to treat this type of shock.

Okay, let’s go back and take a look at stable patients. First, obtain a focused history and physical examination, and order labs, including a CMP, CBC, ESR, CRP, liver function tests, and a urinalysis. Patients or their caregivers typically describe an abrupt onset of a high, spiking fever lasting for at least 5 days with profound irritability. Some patients report joint pain, while others have abdominal pain, which is related to gallbladder hydrops. 

As far as the physical exam goes, you’ll usually notice a unilateral, enlarged, nontender cervical lymph node, as well as a bilateral nonexudat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Periorbital_and_orbital_cellulitis_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VBzLmbSfSJKIRwCVGy5nv5nFSTyYuLZ5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Periorbital and orbital cellulitis (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Periorbital and orbital cellulitis are bacterial infections of the soft tissues within or around the orbit. Based on the relation of the infection to the orbital septum and the presence or absence of increased intraorbital pressure, you can differentiate orbital from periorbital cellulitis. 

Orbital cellulitis occurs posterior to the orbital septum and is associated with increased intraorbital pressure, while periorbital cellulitis occurs in the soft tissues anterior to the orbital septum and is not associated with increased intraorbital pressure.

Now, if your patient presents with a chief concern suggesting orbital or periorbital cellulitis,  you should first perform an ABCDE assessment to determine whether the patient is unstable or stable. 

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, consider IV fluids, and put the patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen. Now, let’s go back and discuss stable patients. 

First, obtain a focused history and physical examination. History typically reveals unilateral eye pain and swelling. In some cases, the patient or their caregiver may report fever, a recent sinus or dental infection, or a recent trauma to the eye or surrounding skin, like an insect bite or even impetigo. The physical exam reveals unilateral erythema around the orbit, as well as warmth, tenderness to palpation, and swelling of the upper or lower eyelid. 

Now, here’s a clinical pearl to keep in mind! If your patient has severe pain or swelling, you might not be able to visualize the eye well enough to obtain a thorough exam. In this case, you should order a CT scan of the orbit to establish a diagnosis.

At this point, you should suspect orbital or periorbital cellulitis, so your next step is to assess your patient for signs of increased intraorbital pressure. 

These include blurr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_recreational_substance_exposure_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MSE2IAnRSqiLG_faRQCvexptQdisMW2G/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to recreational substance exposure (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Recreational substances are substances taken for enjoyment or psychoactive effects without medical justification. They often include alcohol, marijuana, over-the-counter medications, and inhalants. Substance use is common amongst the pediatric population, especially during the adolescent years. However, initial exposure can begin much earlier. Now, based on clinical manifestations, we can categorize recreational substance exposure into those associated with tachycardia and possibly hypertension, versus those associated with bradycardia and potentially hypotension.

Now, if a pediatric patient presents with recreational substance exposure, you should first perform an ABCDE assessment to determine if the patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation, and consider intubation if the patient is apneic or has shallow, ineffective respirations. Next, obtain IV access, give IV fluids, and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. If needed, provide supplemental oxygen, measure glucose, and obtain an ECG. Finally, don’t forget to consider administering naloxone if the possible offending agent is an opioid.

Now that we reviewed unstable patients, let’s go back to the ABCDE assessment and look at stable ones. In this case, obtain a focused history and physical examination, which can be difficult in a patient with recreational substance exposure, so you might want to ask accompanying friends or family to provide details. The history could reveal a known acute recreational substance exposure or a previous history of substance use; while the physical exam will show signs of altered mental status. 

At this point you should suspect substance exposure! Your next step is to obtain a urine drug screen, along with a serum ethanol concentration. Next, assess the patient’s cardiovascular status to narrow down what recreational substance exposure ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_congenital_heart_diseases_(acyanotic):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pMPUCkc9RmOBrRuLB8YRXeOMQMmMWkUu/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to congenital heart diseases (acyanotic): Clinical sciences]]></video:title><video:description><![CDATA[Acyanotic congenital heart disease refers to structural heart lesions that do not cause significant blood oxygen desaturation or cyanosis. It&amp;#39;s crucial to identify acyanotic congenital heart lesions promptly in order to treat any complications, like shock or heart failure.  

If a pediatric patient presents with chief concern suggesting acyanotic congenital heart disease, first perform an ABCDE assessment. If the patient is unstable, stabilize the airway, breathing, and circulation. You may even need to intubate and mechanically ventilate your patient. Next, obtain IV access, and consider starting IV fluids.  

Begin continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Finally, if needed, provide supplemental oxygen. Once you’ve initiated acute management, perform a focused history and physical examination. 

Then obtain pulse oximetry measurements in the right hand, which measures preductal saturation; and the feet, which measures post-ductal saturations. These measurements allow you to compare oxygenation of the systemic circulation before and after the ductus arteriosus inserts into the aorta.  

Unstable infants often present around 2 weeks of age, as the ductus arteriosus begins to close, with symptoms like poor feeding, lethargy, and respiratory distress. Additionally, there may have been a prenatal ultrasound showing a heart defect.  

Exam findings include signs of shock, like gray, cool, mottled skin. You might also find weak pulses in all 4 extremities, or the femoral pulses might be absent.  

On auscultation, many patients will have an audible S3, and some will have a murmur. On pulse oximetry, preductal saturations may be higher than postductal saturations.  

This suggests that deoxygenated blood is being shunted from the pulmonary artery to the aorta, through an open ductus arteriosus, and the lower extremities might appear cyanotic.  

This is called differential cyanosis and suggests ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_congenital_heart_diseases_(cyanotic):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gHQcy3ifRCS7a9HJ24iUtD8XQ5qLwtE4/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to congenital heart diseases (cyanotic): Clinical sciences]]></video:title><video:description><![CDATA[Cyanotic congenital heart disease refers to structural heart lesions that cause significant blood oxygen desaturation and cyanosis. Cyanotic congenital heart lesions can be categorized according to their characteristic circulatory patterns, which include increased or decreased pulmonary blood flow, decreased systemic blood flow, or inadequate pulmonary-systemic mixing. 

If a pediatric patient presents with a chief concern suggesting cyanotic congenital heart disease, perform an ABCDE assessment. Cyanosis indicates that your patient is unstable, so first stabilize the airway, breathing, and circulation. You may need to intubate and mechanically ventilate your patient. Next, obtain IV access, consider IV fluids, and begin continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Finally, provide supplemental oxygen, if needed. 

Next, obtain a focused history and physical exam, and measure pulse oximetry in the right hand, which measures pre-ductal saturation; and the feet, which measures post-ductal saturation. Pre- and postductal measurements allow you to compare oxygenation of the systemic circulation before and after the ductus arteriosus inserts into the aorta. If pre-ductal saturations are significantly higher than postductal saturations, it means that deoxygenated blood is being shunted from the pulmonary artery to the aorta, through an open ductus arteriosus. This is called differential cyanosis and suggests the presence of critical congenital heart disease. 

Okay, you might find a family history of congenital heart disease, or there may have been a prenatal ultrasound demonstrating a heart defect. Exam findings include central cyanosis in areas like the lips and chest. Some patients may display signs of respiratory distress, like dyspnea or tachypnea, as well as a heart murmur or hepatomegaly.  

Lastly, pulse oximetry measurements reveal an oxygen saturation below 90% in the right hand and feet,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_first_unprovoked_seizure_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LrdQ8aOQSJug8Izub3coKAoKSm6lJyJy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a first unprovoked seizure (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Seizures are paroxysmal events caused by abnormal neuronal activity in the brain, and they are considered unprovoked if no acute precipitant can be identified. Seizures present with a wide variety of manifestations, including focal or generalized motor activity and altered awareness. Unprovoked seizures can be categorized as either isolated unprovoked seizures or as epilepsy, which can be further classified as distinct syndromes with onset during infancy, childhood, or adolescence. 

If a pediatric patient presents with a chief concern suggesting a first unprovoked seizure, start with an ABCDE assessment. If the patient is unstable, first stabilize the airway, breathing, and circulation, and you may even need to intubate the patient. Next, obtain IV access, and consider starting IV fluids. Begin continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Provide supplemental oxygen if needed, and administer an anti-seizure medication if the seizure lasts longer than 5 minutes.  

Now here’s a clinical pearl! A convulsive seizure lasting longer than 5 minutes is considered status epilepticus. This neurologic emergency requires prompt administration of benzodiazepines, followed by anti-seizure medications like fosphenytoin or phenobarbital. Once stabilized, a patient with status epilepticus requires further diagnostic evaluation! 

Okay, let’s go back to the ABCDE and look at stable patients. First, obtain a focused history and physical exam, and consider ordering labs, such as a CMP and blood or urine toxicology screening. Caregivers typically report an episode of focal or generalized motor activity that could be described as tonic, which involves increased tone or rigidity; clonic, which consists of fast, rhythmic contractions; myoclonic, which is a shock-like muscle contraction; atonic, which is characterized by muscle flaccidity; or tonic-clonic, which starts with stiffening of the whole body followed by rhythmic jerks.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_skin_and_soft_tissue_infections:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N2bTLZgKQmKsg0-q3HXdXJ89R8Gmwi1m/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to skin and soft tissue infections: Clinical sciences]]></video:title><video:description><![CDATA[Skin and soft tissue infections, or SSTIs for short, are infections that affect the skin and the underlying soft tissues like the fat, fascia, muscles, ligaments, and tendons.  

They are typically caused by bacteria, but can also occur from viruses or fungi.  

In severe cases, these infections can cause life-threatening complications like necrotizing fasciitis and toxic shock syndrome that can quickly lead to septic shock; so, timely diagnosis is key to treat these infections promptly to prevent major complications. 

When a patient presents with a chief concern suggesting a skin and soft tissue infection, your first step is to perform an ABCDE assessment to determine if they are stable or unstable.  

If the patient is unstable, stabilize their airway, breathing, and circulation right away. Establish IV access and start IV fluids for resuscitation. You should also obtain blood and wound cultures, and then initiate broad spectrum IV antibiotics.  

Make sure to continuously monitor vitals like pulse oximetry, blood pressure, and heart rate as the patient’s condition can quickly deteriorate and require admission to the ICU. 

Once you’ve initiated acute management, your next step is to obtain a focused history and physical examination.  

Additionally, order labs like CBC, CMP, lactate, and check the previously obtained blood and wound cultures.  

Typically, unstable patients will have a history of fever and severe pain around the affected area.  

On exam, you might find signs of shock like altered mental status, tachycardia, or hypotension.  

Local examination will reveal erythema, edema and sometimes an associated rash.  

On palpation, the affected area will be tender with crepitus in severe cases. Crepitus feels like a crunching of small air pockets underneath the skin, and is a red flag for necrotizing soft tissue infection!  

In addition, you might see bullae, grayish or dark discoloration, and purulent drainage which is indicativ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_back_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X0kPCkLjTO6tPRxeUnlgg680RfalLHfd/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to back pain: Clinical sciences]]></video:title><video:description><![CDATA[Back pain is a very common and potentially challenging condition to diagnose. The vast majority of patients have musculoskeletal pain without a specific underlying condition, and improve within a few weeks. Although back pain is most often benign and self-limited, in some cases it could also be a sign of more severe disease, so these patients require prompt evaluation and treatment.  

Okay, if your patient presents with back pain, you should first perform an ABCDE assessment to determine whether your patient is unstable or stable. If they’re unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen!   

Here’s a clinical pearl! Unstable patients with back pain might present in a few ways. First, your patient might have sepsis due to underlying discitis, osteomyelitis or abscess. In this case, don’t delay starting IV fluids, obtain an MRI and cultures, and initiate empiric antibiotics! Another common cause of back pain in unstable patients is from a visceral source, such as bowel perforation leading to acute peritonitis. These patients might present with hypotension and abdominal pain that radiates to the back, so in this case, start IV fluids, empiric antibiotics, and consult the surgery team. And finally, your unstable patient might have back pain from a vascular source, such as a ruptured aortic aneurysm. So, if your patient presents with hypotension, sudden and severe back pain described as “ripping” or “tearing”, then immediately start IV fluids, obtain a CT angiogram, and consult the vascular surgery team!   

Now that we’ve addressed unstable patients, let’s go back and discuss stable ones. If your patient is stable, perform a focused history and physical examination. Your patient will report back pain, while the physical exam might reveal t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alcohol_use_disorder:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mfBYcmtYSkS5JRZU8gZ9BNj1TdKIu7l0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alcohol use disorder: Clinical sciences]]></video:title><video:description><![CDATA[Alcohol use disorder is a medical condition characterized by the inability to control the consumption of alcohol, despite adverse health and social consequences. The cause of alcohol use disorder is multifactorial and includes psychological, biological, social, and environmental factors. Based on criteria defined in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, or DSM-5, you can categorize alcohol use disorder as mild, moderate, and severe. 

Okay, if a patient presents with chief concerns suggesting alcohol use disorder, first perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize the airway, breathing, and circulation, which might require endotracheal intubation with mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring including blood pressure, heart rate, pulse oximetry, and cardiac telemetry.  

Now, here’s a clinical pearl! Patients with alcohol use disorder might present with a few potentially unstable conditions. The first to consider is alcohol intoxication, which can cause significant CNS depression, coma, and even death. Next, always look out for alcohol withdrawal, which typically begins 12 to 48 hours after the last drink and can result in fatal generalized tonic-clonic seizures. Finally, don’t forget about delirium tremens, which is a rare but severe form of alcohol withdrawal typically occurring 48 hours or more after the last drink.  

These patients will have fever, agitation, hallucinations, and extreme hypertension, with the potential for cardiovascular collapse. Treatment of acute intoxication is largely supportive with IV fluids and electrolyte replacement, while withdrawal symptoms are best managed with benzodiazepines. 

Now that we’ve addressed unstable patients, let’s return to the ABCDE assessment and take a look at stable patients. If the patient is stable, obtain a focused history and physical exam. Addition]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Opioid_use_disorder:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JuoQkYN1Q4OHrDVPoiGlwSGgS3q0PObp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Opioid use disorder: Clinical sciences]]></video:title><video:description><![CDATA[Opioid use disorder is a medical condition characterized by the inability to control the use of opioids, despite adverse health and social consequences. The cause of opioid use disorder is multifactorial, including psychological, biological, social, and environmental factors. Based on criteria defined in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, or DSM-5, you can categorize opioid use disorder as mild, moderate, or severe. 

Keep in mind that the terms opiates and opioids are sometimes used interchangeably, but they actually refer to different entities. Opiates refer to only naturally occurring compounds derived from the poppy plant like heroin, morphine, and codeine, all of which have agonistic effects on the opiate receptor.  

On the flip side, opioids refer to synthetic and semisynthetic compounds that resemble opiates in structure and their effects on the opioid receptor.  

Okay, if a patient presents with a chief concern suggesting opioid use disorder, first perform an ABCDE assessment to determine if the patient is unstable or stable. If your patient is unstable, stabilize the airway, breathing, and circulation, which might require endotracheal intubation with mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring including blood pressure, heart rate, pulse oximetry, and cardiac telemetry. In severe cases, opioid overdose can result in CNS depression, coma, and even death. In these patients, immediately administer the opioid antagonist naloxone to reverse the effects of an opioid overdose! 

Here’s a clinical pearl to keep in mind! Severe withdrawal can lead to unstable vital signs, and even lethal electrolyte abnormalities from vomiting. 

Now that we’ve addressed unstable patients, let’s return to the ABCDE assessment. If the patient is stable, first obtain a focused history and physical exam. Next, assess for substance use with a screening test, such as the Drug Abuse]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_myeloproliferative_neoplasms:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_R963VpbSnS0YaFjVEfTPVkFQlukXN9X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to myeloproliferative neoplasms: Clinical sciences]]></video:title><video:description><![CDATA[Myeloproliferative neoplasms are a group of neoplastic conditions characterized by the proliferation of bone marrow cells from the myeloid lineage. These include red blood cells and platelets, as well as granulocytes, which include neutrophils, eosinophils, basophils, and monocytes.  

The expanded cell lines are morphologically normal, meaning there’s no dysplasia, which distinguishes these conditions from myelodysplastic ones. The four classic myeloproliferative neoplasms include chronic myeloid leukemia, polycythemia vera, essential thrombocythemia, and primary myelofibrosis. 

Now, if your patient presents with a chief concern suggesting a myeloproliferative neoplasm, first, perform an ABCDE assessment to determine if they are unstable or stable.  If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen!   

Now, here’s a clinical pearl! Patients with myeloproliferative neoplasms may present as unstable due to several different reasons. The first one is thrombosis. In fact, some individuals have an increased risk of acquired hypercoagulability, which can result in life-threatening thrombotic events, such as myocardial infarction or pulmonary embolism! Next, there’s hemorrhage, which can occur due to platelet dysfunction and result in intracranial or gastrointestinal bleeding. Finally, some individuals can develop acute myeloid leukemia and present with tumor lysis syndrome or acute disseminated intravascular coagulation. 

Alright, now that we’ve addressed unstable patients, let’s go back to the ABCDE assessment and discuss stable ones. If your patient is stable, perform a focused history and physical examination and order labs, including a complete blood count with differential and a peripheral smear. Your patient will typically report a histor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertrophic_cardiomyopathy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UxLb0o2HSJSo8eByWUVxAX6HQWWu9Klt/_.png</video:thumbnail_loc><video:title><![CDATA[Hypertrophic cardiomyopathy: Clinical sciences]]></video:title><video:description><![CDATA[Hypertrophic cardiomyopathy, or HCM, is a genetic condition associated with left ventricular hypertrophy that cannot be attributed to another cardiac, systemic, or metabolic disease. In HCM, ventricular hypertrophy causes decreased compliance, which results in poor left ventricular filling.  

In some of these patients, ventricular septal hypertrophy combined with abnormal motion of the mitral valve causes left ventricular outflow obstruction, which can manifest as syncope or sudden cardiac death during intense physical activity.  

If a pediatric patient presents with a chief concern suggesting hypertrophic cardiomyopathy, you should first perform an ABCDE assessment to determine if your patient is stable or unstable.  

If the patient is unstable, stabilize the airway, breathing, and circulation. Unstable patients can present with life-threatening arrhythmias such as ventricular tachycardia, so attach a cardiac monitor, and be ready to perform defibrillation if needed! Next, obtain IV access, consider IV fluids, and begin continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Finally, if needed, provide supplemental oxygen. 

Here’s a high-yield fact! Hypertrophic cardiomyopathy is the most common cardiac condition associated with sudden cardiac death in young athletes. In these cases, sudden death can be the first presentation of HCM, since most affected individuals are asymptomatic. So, be sure to perform a careful cardiac examination in patients presenting for a sports pre-participation physical.  

Okay, now let’s go back to the ABCDE assessment and look at stable patients.  

Your next step here is to perform a focused history and physical examination. Patients might report symptoms like exertional dyspnea, atypical chest pain, palpitations, or syncope; but keep in mind that many patients with HCM are asymptomatic. Family history could reveal other family members with HCM or sudden cardiac death. Physical]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Short_bowel_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h2SsV9jgQ4Ofnsa1RXxcfd1mTAWt_vCG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Short bowel syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Short bowel syndrome is characterized by the insufficient length or function of the small intestines, resulting in malabsorption of water, electrolytes, as well as micro and macronutrients. It’s most commonly caused by extensive surgical resection of the small intestine due to trauma, inflammatory bowel disease, or congenital abnormality. Usually, patients with less than 200 cm of small bowel are at risk for developing short bowel syndrome as the decrease in absorptive surface area and shorter transit times through the gastrointestinal tract can impair the absorption of gastrointestinal contents. Consequently, patients can present acutely with volume depletion, or with metabolic abnormalities and weight loss from chronic intestinal failure. Management of short bowel syndrome requires multidisciplinary care, including nutritional support, medical management, and in some cases, surgery.

When a patient presents with a chief complaint suggestive of short bowel syndrome, the first step is to perform an ABCDE assessment to determine whether the patient is unstable or stable. If the patient is unstable, begin acute management by first stabilizing the airway, breathing and circulation. Then, establish IV access and administer fluids while monitoring vital signs like heart rate, blood pressure and oxygen saturation. 

Next, perform a focused history and physical examination, and obtain labs including a complete blood count, comprehensive metabolic panel, and serum lactate to assess for dehydration and electrolyte abnormalities.

Typically, patients will have a history of extensive bowel resection. In adults, the most common reasons for bowel resection are inflammatory bowel disease, mesenteric ischemia, radiation enteritis, or trauma. Patients might present with severe diarrhea or high stoma output, if they have one. Keep in mind, high stoma output is defined as more than 1.2 liters per day. Additionally, they might report significant weight loss, decreased or abs]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_unintentional_weight_loss:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5_ZD_ttFT7GZ23XHuqrBGF2bSVi7iLXK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to unintentional weight loss: Clinical sciences]]></video:title><video:description><![CDATA[Unintentional weight loss refers to a weight loss greater than 5 percent of body weight over 6 to 12 months in an individual who is not purposefully trying to lose weight. Unintentional weight loss can occur due to non-disease-related causes like medication side effects or socioeconomic factors. However, it could also occur due to disease-related causes, more specifically due to increased metabolic demands, impaired caloric intake, as well as gastrointestinal and neuropsychiatric conditions. 

Now, if your patient presents with unintentional weight loss, first, obtain a focused history and physical exam. Your patient will report weight loss over 6 to 12 months, despite not trying to lose weight. Additionally, they might report fatigue. Next, the physical exam will typically reveal muscle wasting, loss of subcutaneous fat, and, in severe cases, cachexia. With these findings, diagnose unintentional weight loss. 

Next, assess whether or not your patient is taking medications associated with adverse effects that might affect food intake! For example, anticholinergics are associated with dry mouth; chemotherapeutics and metformin can cause nausea; while antidepressants can suppress appetite. If your patient is taking any of the following medications, discontinue medication and check if the patient’s body weight is improving over time! If body weight improves, the underlying cause is the medication&amp;#39;s adverse effects. 

On the other hand, if your patient is not taking medications associated with weight loss, assess their socioeconomic factors. If your patient reports isolation, functional limitations, financial barriers, or poor access to transportation, diagnose unintentional weight loss due to socioeconomic factors!

However, if history reveals normal socioeconomic factors, assess for signs or symptoms suggesting an underlying medical condition. These include recurrent or chronic illness or infection and frequent vomiting or abnormal stooling. If any ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Herpes_simplex_virus_infection_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-LTjys0PRZuiCZBXoC2Gor8rQ06Hm9Rh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Herpes simplex virus infection in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Herpes simplex virus, or HSV infection is a common sexually transmitted infection or STI. There are two types of this virus: HSV1 and 2. Even though HSV1 is associated with cold sores, and HSV2 with genital ulcers, both can cause genital ulcers so presentation alone is not enough to differentiate between the two. Determining the HSV subtype is important as it can provide information on the risk of recurrence. 

Now, the infection itself carries some risks. A primary outbreak in the first trimester of pregnancy can result in neonatal chorioretinitis, microcephaly, and skin lesions, while a primary outbreak near the time of delivery significantly increases the risk for neonatal transmission. 

Recurrent infections can also be transmitted to the neonate during delivery through intrapartum exposure to the virus in the maternal genital tract and can result in disseminated disease or CNS disease, with the possibility for long-term neurologic impact.

When a patient presents with a chief concern suggesting HSV infection in pregnancy, start with a focused history and physical examination. 

History might reveal a prior HSV outbreak. Additionally, the patient might have a prior documented history of positive HSV antibodies. They might report single or multiple genital lesions, which are possibly painful. A primary outbreak typically involves multiple painful lesions, whereas a recurrent outbreak more commonly presents as a single ulcer that is mildly painful or non-painful. Be sure to ask about prodromal symptoms that occur with recurrent infections including burning or tingling in the area where the outbreak normally occurs. 

Lastly, patients might report vulvar pruritus, dysuria, or systemic symptoms such as fever, headache, or malaise. 

When it comes to the physical exam, the focus is on the genital area. You might find perineal erythema and genital ulcers. Ulcers could be single and unilateral or multiple and bilateral. Additionally, the exam might reveal ten]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Urinary_tract_infections_and_kidney_stones_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FQgLszPpT8ayHyUGma-Jw8JuR9qHl-y-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Urinary tract infections and kidney stones in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[During pregnancy, the urinary tract undergoes several physiologic changes that increase an individual&amp;#39;s risk of both urinary tract infections, or UTIs, and kidney stones, or nephrolithiasis. Specifically, ureteral compression from the gravid uterus and ureteral relaxation from elevated levels of progesterone lead to urinary stasis and vesicoureteral reflux, increasing the risk of bacterial colonization and ascending infection. 

Urinary tract infections in pregnancy exist on a spectrum with asymptomatic bacteriuria and acute cystitis affecting the lower urinary tract, while pyelonephritis affects the upper tract. Screening and treating the former helps prevent pyelonephritis, which is associated with maternal sepsis, disseminated intravascular coagulation, or DIC, acute respiratory distress syndrome, or ARDS, and preterm labor. Fetal complications like preterm birth and anemia may also occur. 

Now, kidney stones, which refer to hard deposits often made of insoluble calcium, occur as a result of the physiologic increased urine calcium excretion and elevated urine pH. In severe cases, they may lead to ureteral obstruction, causing damage to the affected kidney or even become infected and create a renal abscess. 

Your first step in evaluating a patient presenting with a chief concern suggesting a UTI or kidney stone is to perform an ABCDE assessment along with a primary obstetric survey to determine if they are stable or unstable. 

If the patient is unstable, first stabilize the airway, breathing, and circulation. Obtain IV access and monitor maternal vital signs. Additionally, assess the fetal status by monitoring the fetal heart rate.

A labor evaluation may then be performed by testing for rupture of membranes and checking cervical dilation. In this situation, you should be thinking about sepsis, urosepsis, or renal abscess.

Now, when it comes to stable patients, start your assessment with a focused history and physical examination and obtain ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_breast_pain_(mastalgia):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EKRP3puWRVaa52gPRVmTYGbEQHKMAHkt/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to breast pain (mastalgia): Clinical sciences]]></video:title><video:description><![CDATA[Breast pain, also called mastalgia or mastodynia, is a feeling of soreness, heaviness, or tenderness in one or both breasts. The causes of breast pain range widely, so the breast exam will help you narrow down your potential diagnoses.

When a patient presents with breast pain, the first step is to perform a focused history and physical examination, including a breast exam. First let’s talk about an abnormal breast exam, starting with mastitis. 

These patients usually have a history of fever, breast skin swelling and redness, and sometimes discharge from the nipple. If the patient is currently lactating, they may report incomplete emptying of breast milk. Non-lactating patients may have risk factors like smoking, diabetes, obesity, a prior history of radiation to the breast or chest, or a history of ductal ectasia or periductal mastitis. 

Physical exam will typically reveal erythema, induration, and tenderness of the breast. You may also see nipple retraction or purulent nipple drainage. In some cases, a fluctuant mass may be palpable. If these features are present, consider mastitis, with or without the presence of an abscess. 

Next order a CBC. If the patient is not lactating, consider imaging with a breast ultrasound and mammogram to look for an abscess or an underlying malignancy. Also, If there is drainage from the nipple, send it for gram stain and culture. 

CBC might reveal leukocytosis, while the ultrasound of the breast shows soft tissue inflammation, and possibly ductal dilation, or the presence of an abscess or fistula. The mammogram will show ill-defined, non-specific regions of increased density and skin thickening. Lastly, gram stain and culture may show bacterial growth. If these features are present, you can diagnose mastitis with or without an abscess. 

Here’s a clinical pearl. Inflammatory breast cancer is a form of locally advanced breast cancer that can sometimes mimic mastitis. Think about inflammatory breast cancer in patients wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_precocious_puberty:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VAuxe4muSRC6Qyze18KyjuJ_T-SfRkmQ/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to precocious puberty: Clinical sciences]]></video:title><video:description><![CDATA[Puberty refers to the transition phase between childhood and adulthood, during which an individual develops secondary sexual characteristics and becomes capable of reproduction. Precocious puberty is defined as pubertal development before age 8 in biological females and age 9 in biological males. Most isolated signs of early puberty are variants of normal, but an evaluation for precocious puberty is indicated when pubertal development and linear growth proceed rapidly. Precocious puberty can be divided into two main categories: central and peripheral precocious puberty. 

Now, let’s talk about what to do if your patient is presenting with chief concerns suggesting precocious puberty. First, perform a focused history and physical examination, including Tanner staging, and measure weight and height. 

Here’s a high-yield fact! Puberty begins with activation of the hypothalamic-pituitary-gonadal or HPG axis, which is when the hypothalamus releases gonadotropin-releasing hormone or GnRH that stimulates the anterior pituitary gland to secrete gonadotropin hormones called luteinizing and follicle-stimulating hormones, or LH and FSH for short. These hormones then travel through the bloodstream to the gonads, where they stimulate the production of sex hormones like estradiol and testosterone! This process of gonadal activation, growth and maturation is also known as gonadarche. On the other hand, adrenarche is associated with adrenal gland maturation and increased adrenal hormone production, leading to the development of signs like axillary and pubic hair! In other words, adrenarche is independent of the HPG axis, so to determine the true onset of puberty, you should always look for signs of gonadarche, not adrenarche.

Okay, first, let’s focus on benign variants of early puberty, starting with benign isolated premature adrenarche. These patients can be biological females under age 8 or biological males under age 9. The physical exam reveals normal linear growth v]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cervical_dysplasia_and_cervical_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BxljrOPSQQmfuaLPHWckYGcJSjStcvQ_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cervical dysplasia and cervical cancer: Clinical sciences]]></video:title><video:description><![CDATA[Cervical dysplasia refers to abnormal cells on the uterine cervix usually caused by persistent infection with high-risk types of the human papillomavirus, or HPV for short. Cervical abnormalities are classified as either low-grade dysplasia, also called cervical intraepithelial neoplasia 1, or CIN1; or high-grade dysplasia, which includes CIN2 and CIN3. High-grade dysplasia, especially CIN3, is a precursor to invasive cervical cancer, and its progression to cancer is usually gradual over several years.  

Cervical cancer screening is crucial for detecting dysplasia at an early stage when it’s more easily treatable. Most patients diagnosed with high-grade dysplasia are aged 25 years or older. However, individuals aged 21 to 24 can also develop high-grade dysplasia.

Your first step in evaluating a patient with a chief concern suggesting cervical dysplasia or cervical cancer is to obtain a focused history and physical exam. 

The most important information to look for is the patient’s current and previous cervical cancer screening results along with any history of treatment and the associated findings on pathology. 
Other important findings include the presence of abnormal vaginal bleeding that could implicate cervical cancer; a compromised immune system from an HIV infection or the use of immunosuppressive medications for a chronic illness, which can increase the patient’s risk for cervical cancer; and a history of vaccination against high-risk HPV types. 

Additionally, determine if your patient is pregnant. That’s important because endocervical curettage, endometrial biopsy, and expedited treatment without cervical biopsy are unacceptable for patients who are pregnant. Furthermore, a diagnostic excisional procedure or repeat cervical biopsy during pregnancy is recommended only if cancer is suspected. As for the physical exam, you’ll want to look for a visual cervical lesion. If one is present, biopsy it to evaluate for invasive cervical cancer. Okay, your]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Vulvar_dysplasia_and_vulvar_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Rtq3GbDDSXWO0k9FrzFix7kVRqyvkdU3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Vulvar dysplasia and vulvar cancer: Clinical sciences]]></video:title><video:description><![CDATA[Vulvar dysplasia and vulvar cancer are a group of conditions that include benign lesions associated with human papillomavirus, or HPV; premalignant lesions; and overt vulvar cancer. Vulvar cancers make up only a small percentage of gynecologic cancers, with squamous cell cancer as the most common type; and vulvar melanomas being less common. 

When evaluating a patient with a chief concern suggesting vulvar dysplasia or cancer, your first step is to obtain a focused history and physical examination. Patients typically report vulvar lesions, with possible pruritus or chronic irritation. Risk factors include tobacco use, immunocompromised status, and prior HPV exposure. 

Here’s a clinical pearl! HPV exposure and infection is generally thought of as a risk of cervical cancer; however, it also increases the risk of vaginal, vulvar, anal, penile, and oropharyngeal cancer. The HPV vaccine is recommended for all patients ages 9 to 26 and up to age 45 in certain populations after shared decision-making. 

On physical examination, you might see elevated or flat lesions with variable coloration from white to reddened, which should get you to suspect vulvar dysplasia.

Vulvar colposcopy with biopsies is the next step in management if: you are unable to make the diagnosis on clinical findings alone; malignancy is possible; the lesion is not responding to usual treatment; the lesion has an atypical vascular pattern; or a stable lesion has rapidly changed in color, border, or size. Biopsies are also indicated in any postmenopausal patient with grossly visual genital warts. 

Here’s another clinical pearl! The one exception where you can start management without colposcopy is if your exam findings are consistent with condyloma acuminate. In this case, you may first attempt treatment with topical medications. However, if the lesions do not respond, a biopsy is needed to confirm the diagnosis. 

Time for a high-yield fact! Bartholin gland cancer is a rare form of vul]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypernatremia_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-FThiuzVRumffNXZej8d3B57SzWqFdVO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypernatremia (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Hypernatremia is an electrolyte imbalance that occurs when the serum sodium concentration exceeds 145 milliequivalents per liter. It typically results from increased water loss or decreased water intake, but in rare cases, it can be caused by an excess salt load. 

Now, based on the volume status, hypernatremia can be classified as hypovolemic, euvolemic, and hypervolemic hypernatremia! Okay, if a pediatric patient presents with chief concerns suggesting hypernatremia, you should first perform an ABCDE assessment to determine if they are unstable or stable. 

If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and consider IV fluids. Next, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry; and don’t forget to monitor your patient’s urine output! 

Now, here’s a clinical pearl! Patients with an acute rise in serum sodium concentration can develop neurologic complications, such as seizures and coma. 

Moreover, increased serum osmolality causes water to rapidly shift out of cells, causing the brain to shrink, subsequently stretching intracranial blood vessels. In severe cases, blood vessels can rupture and result in intracranial hemorrhage. 

Also, be cautious when treating hypernatremia, since aggressive correction of serum sodium levels or giving aggressive fluid resuscitation can lead to rapid fluctuations in serum osmolality, resulting in cerebral edema. Now, let’s go back to the ABCDE assessment and take a look at stable patients. 

In this case, obtain a focused history and physical examination and order a basic metabolic panel, or BMP. Your patient or their caregiver will typically report neurologic symptoms, like irritability, restlessness, and sleepiness. Additionally, history often reveals a high-pitched cry in combination with increased thirst. 

Meanwhile, the physical exam may demonstrate increased muscle tone and brisk reflexes; while the BMP will reveal s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hematuria_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5Hhl_qPeTZOpQ9EapRP9sCMDQlu3rLD3/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to hematuria (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Hematuria is the presence of microscopic or macroscopic blood in the urine. Healthy kidneys filter blood by removing waste products while retaining important molecules and blood elements, while kidneys that have lost their filtering ability allow red blood cells, or RBCs, to pass into the urine. Hematuria can be benign and transient, while in other cases kidney damage causes persistent hematuria, which can be categorized as glomerular or non-glomerular in origin. 

When a pediatric patient presents with hematuria, your first step is to obtain a urine dipstick to confirm the presence of blood.  

Here’s a clinical pearl to keep in mind! At first glance, pink or red urine is suspicious for hematuria, but if a urine dipstick is negative for blood, be sure to consider other causes of discolored urine, such as beet ingestion; rifampin use; in porphyria due to oxidation of porphyrins; or build up of urate crystal precipitation in newborns. 

Okay, if the urine dipstick is positive for blood, obtain a focused history and physical examination, and order a urinalysis with microscopy to assess the quantity of RBCs. If microscopy reveals more than five RBCs per high-power field, you can confirm an abnormal amount of blood in the urine. 

Now, here’s a clinical pearl! If your patient presents with discolored urine that tests positive for blood on a urine dipstick, but no RBCs are seen on urine microscopy, evaluate for myoglobinuria and hemoglobinuria.  

Myoglobinuria can be seen in conditions like rhabdomyolysis, extreme exercise, or myopathies, in which myoglobin is excreted in the urine due to increased skeletal muscle breakdown. On the other hand, hemoglobinuria is caused by rapid hemolysis, which results in the excretion of hemoglobin in the urine; in this case, your patient may also be anemic or appear jaundiced. 

Once you confirm the presence of RBCs on urine microscopy, repeat the urinalysis twice more, one week apart. If the hematuria resolves, meaning ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_peripheral_lymphadenopathy_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kgL6EXdfSkaqtFHwckXjrZZST2Gr71xo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to peripheral lymphadenopathy (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Peripheral lymphadenopathy refers to subcutaneous lymph nodes that have an abnormal size or consistency. Lymph node size varies by age and normally increases from infancy to childhood, with a subsequent decrease in size during late childhood and adolescence. In general, enlarged lymph nodes are 1 centimeter or larger, but any degree of lymph node enlargement in atypical areas, such as the supraclavicular region, is considered abnormal. The most important underlying causes of peripheral lymphadenopathy include malignancy,  autoimmune conditions, and infections.

Now, if your patient presents with peripheral lymphadenopathy, obtain a focused history and physical examination. Patients or their caregivers typically describe a lump or mass, occasionally with symptoms like fever, fatigue, or poor appetite. Additionally, the physical exam findings will reveal one or more enlarged subcutaneous lymph nodes that could be tender to palpation. These findings confirm the presence of peripheral lymphadenopathy.

Now, the next step is to assess for malignancy. Physical exam findings include nontender nodes that are firm and immobile and fixed to the surrounding tissue as well as nodes that are matted, meaning that nodes are joined together so they feel connected when palpated. Palpable supraclavicular nodes are also concerning for malignancy, as well as persistently enlarged nodes. If your patient has any of these findings, consider the possibility of malignancy.

Next, assess for signs and symptoms of leukemia or lymphoma. Let’s start with leukemia. These patients often report abnormal bleeding or bone pain, while their physical exam typically reveals pallor, bruising, or petechiae. With these findings, consider leukemia and obtain a CBC with a peripheral smear and consider performing a bone marrow biopsy. If the CBC reveals leukocytosis and anemia; and if immature blasts are seen on the peripheral blood smear or bone marrow biopsy, diagnose leukemia.

Now, let’s move o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_proteinuria_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l2iwkfrxR3ymXLa3zAjyOYbLRySHj5_C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to proteinuria (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Proteinuria refers to the presence of protein in the urine, which occurs when the kidneys fail to filter blood properly. It can result from disruption of the glomerular basement membrane, allowing proteins to cross the filtration barrier; or from injury to the renal tubules, resulting in decreased protein reabsorption. Proteinuria can be benign, like with transient proteinuria or orthostatic proteinuria, or it can be pathologic and persistent, as the result of glomerular dysfunction or tubular dysfunction. 

Now, let’s discuss what to do when a pediatric patient presents with proteinuria. First obtain a urine dipstick as an initial assessment, preferably a first-morning void; and if the dipstick is positive for protein, consider proteinuria. Your next step is to obtain a focused history and physical examination and repeat the urine dipstick test twice. It’s generally recommended to repeat the urine dipstick on two separate occasions, again sampling the first-morning void if possible; because many factors can alter the results, such as a very high or low urine pH, or urine that’s very dilute or highly concentrated.  

Now, here’s a clinical pearl! A small amount of protein in urine can be normal. However, in the absence of hematuria or in an otherwise asymptomatic child, protein excretion is considered abnormal when it’s greater than 240 mg/m2/day for a child younger than 6 months of age; or greater than 150 mg/m2/day for children 6 months or older. 

Now, if both repeat urine dipsticks are negative for protein, diagnose transient proteinuria, which is a benign condition that doesn&amp;#39;t require further work-up. Although the cause may be unknown, your patient may have a history of fever or mild illness, stress, heavy exercise, significant heat or cold exposure, or dehydration. 

On the flip side, if repeat urine dipstick continues to be positive for protein, obtain a first-morning void spot urine collection and assess the urine protein to urine creatin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Autism_spectrum_disorder:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1mP5cWFPSfCFn0FIk9j9Je9JQMGi78tl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Autism spectrum disorder: Clinical sciences]]></video:title><video:description><![CDATA[Autism spectrum disorder, or ASD for short, is a neurodevelopmental condition characterized by deficits in social communication as well as patterns of restricted and repetitive behavior. Autism is considered a spectrum disorder due to the wide variability in the traits, behaviors, and degree of disability that individuals can experience. Autism is thought to be caused by a combination of genetic and environmental factors that result in altered neural connectivity and atypical brain development. Children with autism who are identified early and receive timely evaluation are more likely to benefit from intervention services, which ensure better developmental outcomes, including improvements in communication and functional skills.

Now, when a pediatric patient presents with a chief concern suggesting autism spectrum disorder, your first step is to obtain a focused history and physical exam. Caregivers commonly report that their child appears socially disengaged and does not communicate or interact with others in typical ways. For instance, many caregivers notice that their child has poor eye contact. The child may also perform repetitive movements, like hand flapping or body rocking, as a means of self-soothing. They may also lack flexibility and adaptability, so disrupted routines or unexpected changes often cause significant distress. 

Risk factors for ASD include prematurity, low birth weight, and certain genetic conditions, such as fragile X syndrome, which is the most common genetic cause, and Rett syndrome. It’s also important to note that autism is highly inheritable, so be sure to ask if there’s a family history of ASD. Although the physical exam is often unremarkable, some patients may have macrocephaly or low weight-for-age.

Now, here’s your first clinical pearl! ASD is frequently underdiagnosed or diagnosed late, especially in biologically female children, ethnic minorities, such as African American and Hispanic children, as well as in those wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preventative_care_for_women:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8LjGQmVFR92O_8lXJRP3yBNxQOuvmApT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preventative care for women: Nursing]]></video:title><video:description><![CDATA[Preventative health care refers to screenings that can identify diseases in the early stages, so they can be treated before they progress. Common preventative screenings for patients assigned female at birth include mammograms for breast cancer; Papanicolaou, or Pap, tests for cervical cancer; and bone density tests for osteopenia and osteoporosis.  

Mammograms screen for breast cancer and involve taking X-rays of the breasts. Patients typically start mammograms around age 45 but can be started earlier or later, depending on risk factors, like a positive family history of breast cancer or certain genetic mutations, like BRCA1 or BRCA2. 

When teaching your patient who&amp;#39;s having a mammogram, explain that the procedure involves the compression of the breast tissue between two plates while an X-ray is taken. Reassure them that the procedure uses a very low dose of radiation and that it causes brief discomfort. Be sure to recommend that they schedule their mammogram after their menstrual period when their breasts are less swollen and sensitive. Lastly, remind them to avoid wearing deodorant, lotions, or powder on the day of their mammogram, since these can cause white spots on the X-ray. 

Screening for cervical cancer involves the Papanicolaou, or Pap test, which screens for cervical cancer by swabbing the cervix during a pelvic examination and looking for abnormal cervical cells and testing for human papillomavirus, or HPV test, which detects strains of HPV, including the high-risk strains that may cause cervical cancer. When Pap and HPV tests are done together, it&amp;#39;s known as co-testing. Screening for cervical cancer should begin at age 21 and occur every three years until age 30. Then at age 30, testing can be done every five years.  

For patients with small-grade changes to cervical cells, testing should occur more frequently whereas those with high-grade cervical cell changes should have the cells removed through loop electrosurgical ex]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pediatric_diabetes_mellitus_type_1:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZMR56Z8HRa6ua0tK0NoMqYslTkyIpBRo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pediatric diabetes mellitus type 1: Nursing]]></video:title><video:description><![CDATA[Nurse Camden works on a pediatric Medical-Surgical unit and is caring for Tate, an 11-year-old who was recently admitted for new onset type 1 diabetes mellitus. After settling Tate in his room, Nurse Camden goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Tate’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Camden recognizes important cues including temperature 97.3 F or 36.2 C, pulse 101 beats per minute, respirations 19 breaths per minute, oxygen saturation 98% on room air, and blood pressure 105/70 mmHg. Tate’s mother is at the bedside and reports that lately, Tate’s been irritable, unusually hungry and thirsty, and he’s urinating frequently.   

Next, Nurse Camden analyzes these cues. He reviews the electronic health record, or EHR, and notes that Tate’s blood glucose level is 240 mg/dl and his hemoglobin A1C level is 7.8 percent. Nurse Camden also sees that Tate has lost four pounds in the past two months and that Tate’s urine is positive for glucose.  

Nurse Camden realizes that the glucose from the food Tate eats can’t move from his blood into his cells, due to a lack of insulin. Because of this, Tate isn’t able to convert the food he eats to energy, causing him to experience fatigue and increased hunger. He also realizes that Tate’s kidneys can’t reabsorb the excess glucose, so it ends up in the urine, where it pulls water out along with it as its eliminated, causing his other symptoms of frequent urination and increased thirst. Nurse Camden recognizes that Tate needs effective management of his blood glucose.  

Now, using the information he’s gathered, along with Tate’s medical history, Nurse Camden chooses a priority hypothesis of unstable blood glucose. 

Then, he generates solutions to address Tate’s unstable blood glucose using pharmacologic and nonpharmacologic solutions. Nurse Camden es]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pediatric_anaphylaxis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xwIUi1QgQGKRB5mCKrMlNO_ZSG6W_kVq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pediatric anaphylaxis: Nursing]]></video:title><video:description><![CDATA[Nurse Anya works in the emergency department and is caring for Pablo, a 10-year-old who’s having difficulty breathing following a bee sting. After settling Pablo in his room, Nurse Anya goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Pablo’s care, by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.     
First, Nurse Anya recognizes important cues, including Pablo’s vital signs which are temperature 98.2 F or 36.8 C, heart rate 128 beats per minute, respiratory rate 30 breaths per minute and labored, blood pressure 94/56 mmHg, and oxygen saturation 89 percent on room air.  

She notes angioedema to Pablo’s eyelids, lips, and tongue. She also notices that Pablo appears anxious.  

While auscultating Pablo’s lungs, Nurse Anya hears wheezing in the upper lobes. She asks Pablo’s father, Ramón, who’s at the bedside, about the onset of Pablo’s symptoms.   
Nurse Anya: Has Pablo had a reaction to a bee sting before? 

Ramon: Well, he’s been stung once before, but nothing like this happened. 

Nurse Anya: Did you give Pablo any medicine before coming to the hospital?   
Ramon: No, we came straight here.   
Nurse Anya then analyzes these cues. She understands that Pablo’s first exposure to a bee sting caused his body to produce antibodies against bee venom, sensitizing him.  

Then, on his second exposure, the antibodies triggered the release of chemical mediators, causing smooth muscle contraction and bronchoconstriction, leading to Pablo’s wheezing and difficulty breathing.  

The reaction also caused systemic vasodilation, leading to decreased blood pressure and tachycardia, as well as increased vascular permeability, resulting in angioedema. Nurse Anya recognizes that Pablo needs immediate airway management.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_health_care_settings:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vt415cJQTi_y0HMzHytca98nQ261wjrl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mental health care settings: Nursing]]></video:title><video:description><![CDATA[Patients with mental health disorders require treatment in settings specific to their condition and unique needs. These settings include outpatient settings, where treatment is conducted in the community; or inpatient settings, where treatment occurs in a hospital-like facility. 

Therapeutic activities provided in these settings include individual and group therapy; psychoeducation, which combines cognitive-behavior therapy, group therapy, and education; and nursing care for medication management and monitoring of existing medical conditions. 

Depending on the setting, patients may also partake in activities like rehabilitation services, such as occupational and physical therapy; gardening; yoga; or dance therapy. These services are provided by a multidisciplinary health care team, including providers, nurses, therapists, social workers, and case managers. 

Outpatient settings include group homes, partial hospitalization, and day treatment centers.  

Group homes are a structured, home-like living situation that provides 24-hour support for patients who are unable to function independently, such as adults with mental health conditions like schizophrenia or pediatric patients with behavioral or conduct disorders. In the group home setting, patients develop necessary life skills, like learning to adhere to house rules, including nighttime curfews and abstaining from illegal substances. Group homes can also serve as residential treatment centers for patients with substance use disorders.  

Next, partial hospitalization centers are short-term programs that provide ongoing treatment for patients who are transitioning from an inpatient facility. Patients typically spend four to six hours each day, five days per week in therapy, with the goal of decreasing the likelihood of being readmitted to inpatient treatment. After completing a partial hospitalization program, patients are often transferred to a lower level of care in a day treatment center, which are co]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Schizophrenia_with_paranoia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UMLMsWO1RKO1WOL7qVFeVC8ATWWwExea/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Schizophrenia with paranoia: Nursing]]></video:title><video:description><![CDATA[Nurse Kit works on an inpatient psychiatric unit and is caring for Albert, a 31-year-old with a history of schizophrenia, paranoid type, who was recently admitted for psychotic symptoms. After settling Albert in his room, Nurse Kit goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Albert’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Kit recognizes important cues, including Albert’s vital signs, which are temperature of 37 C, or 98.6 F, heart rate 98 beats per minute, respirations 22 breaths per minute, and blood pressure 136/82 mmHg. Nurse Kit notices that Albert appears disheveled, restless, and is looking back and forth suspiciously across the room.  

Nurse Kit: Hi Albert, how are you doing today? 

Albert: There’s a man coming after me, I’ve seen him watching me from inside the closet. 

Nurse Kit turns to look inside the closet, which is empty.  

Nurse Kit: That sounds scary. Although I don’t see anyone else here with us, I’m here to support you and keep you safe.  

Next, Nurse Kit analyzes these cues. They review the electronic health record, or EHR, and read that Albert has visited the emergency department three times in the past month for symptoms associated with his schizophrenia. Nurse Kit knows the development of schizophrenia is related to both genetic and environmental factors that disturb the brain’s structure and balance of neurotransmitters like dopamine and glutamate, leading to disabling alterations in behavior, emotions, thinking, and perception, like delusions and hallucinations. Nurse Kit realizes that Albert needs management of his acute episode of schizophrenia. 

Now, using the information they’ve gathered, along with Albert’s medical history, Nurse Kit chooses a priority hypothesis of altered perception.  

Then, Nurse Kit generates solutions to address Albert’s altered perception that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Ventricular_septal_defect_(VSD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3rGTWoZzRoi7pMqgeUQfyNvWSwSzn3NW/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Ventricular septal defect (VSD): Nursing]]></video:title><video:description><![CDATA[Nurse Antoinette works on a pediatric cardiac unit and is caring for Mabel, a 1-year-old female with a history of ventricular septal defect, or VSD, who was admitted for a surgical repair. After settling Mabel in her room, Nurse Antoinette goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Mabel’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Antoinette recognizes important cues, including Mabel&amp;#39;s vital signs, which are temperature 98.6 F or 37 C, heart rate 142 beats per minute, respirations 35 breaths per minute, and oxygen saturation 92 percent on room air. Upon assessment, Nurse Antoinette notes a systolic heart murmur and crackles in the bases of her lungs. She also notices that Mabel appears to be irritable.  

Next, Nurse Antoinette analyzes these cues. She reviews the electronic health record, or EHR, and sees that Mabel was diagnosed with a VSD as a newborn. The health care provider recommended close monitoring of the condition rather than immediate surgical correction because she was hemodynamically stable and asymptomatic.  

Nurse Antoinette knows that a VSD causes a left-to-right shunting of blood in the heart, causing a mixture of deoxygenated and oxygenated blood to go back to the right side of the heart and then into the lungs, creating fluid overload in the lungs and increased pulmonary vascular resistance.  
She also understands that the shunting of blood is causing Mabel’s systolic murmur, and that the pulmonary congestion is causing the crackles in her lungs. Additionally, Nurse Antoinette knows that less oxygen is being delivered to the tissues, so Mabel’s impaired perfusion is causing tachycardia and decreased oxygen saturation. Nurse Antoinette recognizes that Mabel needs effective perfusion management.  

Now, using the information she’s gathered, Nurse Antoinette chooses a priority]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Bipolar_I_disorder:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_I08e-xfR96sdZKv-eUn_zr8SaKjTiTE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Bipolar I disorder: Nursing]]></video:title><video:description><![CDATA[Nurse Nikil works on an inpatient psychiatric unit and is caring for Octavia, a 28-year-old with a history of bipolar I disorder, who was recently admitted for a manic episode. After settling Octavia in her room, Nurse Nikil goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Octavia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Nikil recognizes important cues, including Octavia’s vital signs, which are temperature 98.4 F or 36.9 C, heart rate 75 beats per minute, respirations 16 breaths per minute, and blood pressure 117/72 mmHg.  

Upon entering her room, Nurse Nikil notes Octavia is pacing back and forth, stopping intermittently to rearrange the items on her bedside table.  

Nurse Nikil: Hi Octavia, I see you’re cleaning your room. Could you pause for a moment and speak with me? 

Octavia: Oh sure, I totally have time for you. Don’t you see I’m doing something important? I really need to get my room cleaned so I can start writing. I have an amazing idea for a best-selling book about a forest like the one I grew up next to. My mom would know the name. I should call her. Do you have her number? Oh, look, what’s that on the floor? I’ll fix it!   

Next, Nurse Nikil analyzes these cues. They review the electronic health record, or EHR, and note Octavia is prescribed lithium but reports that she stopped taking it about two weeks ago. They note Octavia&amp;#39;s blood level of lithium is 0.5 mEq/L, but Nurse Nikil knows that the therapeutic index should be between 0.6 and 1.0 mEq/L.  

The nursing report from the night shift also stated that Octavia did not sleep.  

Nurse Nikil recognizes patients with bipolar I disorder experience extremes in emotions, moving from manic to depressive moods.  

Those in a manic state experience a persistent period of extreme emotions and may have symptoms, like racing thought]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Sickle_cell_anemia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L4jcFqgNQ7WbT58yHpy-3UneTlKj0EPy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Sickle cell anemia: Nursing]]></video:title><video:description><![CDATA[Nurse Maggie works in a pediatric hematology unit and is caring for Marcus, a 9-year-old with a history of sickle cell disease who was admitted for a vaso-occlusive crisis, or VOC. After settling Marcus in his room, Nurse Maggie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Marcus’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Maggie recognizes important cues, including Marcus’ vital signs which are temperature 99.0 F or 37.2 C, heart rate 104 beats per minute, respiratory rate 22 breaths per minute, blood pressure 122/72 mmHg, and oxygen saturation 97 percent on room air. She notices that Marcus’ hands and feet are edematous, and that he’s grimacing.  

Nurse Maggie: Marcus, you look uncomfortable. Can you rate your pain from zero to ten, zero being no pain and ten being the worst pain you’ve ever felt? 

Marcus: It’s about an eight in my hands and feet.  

Nurse Maggie: When did your pain start? 

Marcus: It started yesterday when I was playing in the snow, and it got worse this morning. 

Nurse Maggie then speaks with Marcus’ mother, who’s at the bedside. 

Nurse Maggie: Has Marcus taken any medications to help with the pain? 

Marcus’ mother: Not since we were in the emergency department a few hours ago.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pediatric_appendicitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JELMK7mZRkyQYP0kvDFFWIRATT2f8-Q1/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Pediatric appendicitis: Nursing]]></video:title><video:description><![CDATA[Nurse Cameron works in the emergency department and is caring for Trevor, a 14-year-old patient who was brought in by his father, Steve, because of abdominal pain and vomiting. After settling Trevor in his room, Nurse Cameron goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Trevor’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Cameron recognizes important cues such as Trevor’s vital signs, which are temperature 100.4 F, or 38 C, heart rate 112 beats per minute, blood pressure 140/90 mmHg, respiratory rate 22 breaths per minute, and pain 9 out of 10 in his abdomen. He also notices Cameron appears anxious, grimacing, and is holding on to his right lower abdomen.  

Nurse Cameron: Trevor, can you tell me more about your pain? 

Trevor: I don’t know, it just really hurts. 

Steve: He hasn’t been acting like himself all week. Yesterday, he missed soccer practice because he didn’t feel good and then he threw up and had diarrhea last night. He can’t really keep any food or liquids down. I thought it was a stomach bug, but his pain got much worse this morning, so I brought him here. 

Nurse Cameron: Did Trevor have any injuries to his abdomen?  

Steve: Not that I know of. 

Nurse Cameron then performs an abdominal assessment and notes tenderness in Trevor’s right lower quadrant. Then, in the area between Trevor’s navel and anterosuperior iliac spine, known as the McBurney point, he presses down and quickly releases, which reveals rebound tenderness.  

Next, Nurse Cameron analyzes these cues. He reviews the electronic health record, or EHR, and sees that Trevor’s blood work shows leukocytosis with a left shift, and an elevated C-reactive protein, or CRP. Nurse Cameron notifies the health care provider who comes to the bedside and performs abdominal ultrasound which is positive for appendicitis. Trevor will need to unde]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Supporting_Assessment:_Optimizing_evaluation_and_remediation_strategies_with_Elsevier</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9UTX6r1sSDO4uAmHnveddM8QSdyys0ci/_.png</video:thumbnail_loc><video:title><![CDATA[Supporting Assessment: Optimizing evaluation and remediation strategies with Elsevier]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Supporting Assessment: Optimizing evaluation and remediation strategies with Elsevier through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Intravenous_critical_care:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VS4YC4riRTGvDBsYnnCAu0dRTjmLioyO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication administration - Intravenous critical care: Nursing pharmacology]]></video:title><video:description><![CDATA[Medications used in critical care settings have significant physiologic effects; are typically administered intravenously, or IV; and they are usually administered by titrating, or adjusting, the infusion rate according to the health care provider’s order until the desired therapeutic effect is reached. Many of these medications are high alert medications, meaning they may cause significant harm to the patient if administered incorrectly, so these medications are always delivered through an IV pump to ensure accuracy. As the nurse, you’ll calculate volumes per unit of time, and dosages based on body weight. 

To calculate a dose using the Dimensional Analysis, or DA method, the three components you need are D, for the Desired dose, or dose ordered by the health care provider; H, for Have, or the dosage you have available; and V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid.   
Now let’s calculate an infusion rate using Dimensional Analysis.  

First, you’ll read the order, which is: heparin 1300 units/hr IV continuous infusion. 

Then, check the medication label. 

Since the available dose is 25,000 units per 500 mL, you will calculate how many milliliters per hour to administer to achieve the Desired dose. To do this, first identify your components, Desired, Have, and Vehicle. And since there’s a time component, we also have T, for Time. 

In this case, D is 1300 units, which was obtained from the health care provider’s order; H is 25000 units, which was obtained from the medication label; V is 500 mL, which was also obtained from the medication label; and T is 1 hour, which was also obtained from the health care provider’s order. 

Next, you’ll determine if a conversion factor is required. To determine this, compare the units of D with the units of H. They’re the same, so no conversion factor is needed. Likewise, since T is in hours and the infusion rate you’re calculating is in mL/hr, no conversion factor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Pediatric:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tlbF9hxqSIm7vGSuRkz3ZiAwQCeQY74r/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication administration - Pediatric: Nursing pharmacology]]></video:title><video:description><![CDATA[Physiological differences between children and adults alter the way medications are absorbed, distributed, metabolized, and eliminated, which means children require different dosages of medications and special techniques for administration. Most pediatric medications are dosed according to the patient’s current weight using either a prescribed dosage per kilogram of body weight or body surface area, known as BSA.   

Now, oral medications for pediatric patients are often formulated in a liquid or suspension. When measuring the quantity of a medication, be sure to use the measuring device supplied with the medication, like a dropper, oral syringe, spoon, or cup as these are calibrated to allow accurate measurement of a specific medication. 

As the nurse, you’ll perform medication calculations to ensure the correct dose of medication is administered.  

To calculate a dose using the Dimensional Analysis, or DA method, the three components you need are D, for the Desired dose, or dose ordered by the health care provider; H, for Have, or the dosage you have available; and V, for Vehicle or the form and amount in which the medication comes, like tablets or liquid.     
Let’s look at a pediatric oral dosage calculation where a weight-based calculation is required.  

First, you’ll read the order which is: amoxicillin 15 milligrams per kilogram PO every 8 hours. 

Then, check the medication label.

Since the medication comes in 125 milligrams per 5 milliliters, you’ll calculate how many milliliters you should administer to achieve the Desired dose. To do this, first identify your components, Desired, Have, and Vehicle.  
In this case, D is 15 milligrams per kilogram, which was obtained from the health care provider’s order. H is 125 milligrams, which was obtained from the medication label. And V is 5 milliliters, which was also obtained from the medication label. You also need to know the patient’s weight, which is 33 pounds. 

Next, you’ll determine if a conver]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pediatric_asthma:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PU_qIa_dREa6YQXqjWkj6AdcSqSQGdtu/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Pediatric asthma: Nursing]]></video:title><video:description><![CDATA[Nurse Lin works at a primary care clinic and is caring for Joey, an 8-year-old who’s had a cough for two months and recently developed chest tightness over the last two days. After settling Joey in the examination room, Nurse Lin goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Joey’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Lin recognizes important cues, including Joey’s vital signs which are temperature 98 F or 36.6 C, heart rate 94 beats per minute, respirations 26 breaths per minute, and oxygen saturation 93 percent on room air. Nurse Lin then completes a respiratory assessment and finds that Joey has expiratory wheezes in all lobes.  

She gathers additional information from Joey and his aunt, Angel, who’s at the bedside. 

Nurse Lin: Joey, I notice you’re having a hard time taking deep breaths, can you tell me more about that? 

Joey: My chest feels so tight. It’s hard to breathe.  

Nurse Lin: That must be very uncomfortable. When did you start feeling like this?  

Joey: I don’t know, I don’t feel good.  

Angel: He’s had a nagging cough for a while now. At first, I thought it was just the change in the weather making his allergies flare up, but his allergies don’t normally affect his breathing. That’s why I made the appointment.  

Nurse Lin: I’m glad you brought Joey in.  

Next, Nurse Lin analyzes these cues. She reviews the electronic health record, or EHR, and notes that Joey has no relevant medical history, other than seasonal allergies. She performs the ordered spirometry testing by having Joey breathe into a mouthpiece that’s connected to a device to measure the amount of air he’s able to breathe in and out. Nurse Lin notes that Joey can&amp;#39;t expel all the air after taking a deep breath.  
Then, she consults with the health care provider, who diagnoses Joey with asthma. 

Nurse L]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_from_Elsevier_Nursing:_UK_and_Ireland_Update</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gCTxvkYKSpeAH_dKq7fslcCNTpKzoMBL/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis from Elsevier Nursing: UK and Ireland Update]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis from Elsevier Nursing: UK and Ireland Update through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_-_Nutrition:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3GURqsHLScG7D33TQ8Jb1MkaSYCo1mXF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment - Nutrition: Nursing]]></video:title><video:description><![CDATA[Nutritional assessment involves the collection and analysis of subjective data, or the information your patient shares with you, and objective data, or the information you observe. As the nurse, you’ll use information about your patient’s nutritional status, which is the balance of nutrient requirements and intake, to provide insight into your patient’s overall health.

Start your collection of subjective data by gathering information about your patient’s eating patterns and access to food. You can use tools such as a 24-hour diet recall, where your patient lists everything they have had to eat or drink in the past 24 hours; a food frequency questionnaire, that estimates how often they eat certain foods; or a food diary, where they keep track of everything consumed over a certain period. Then, ask about religious or cultural diet traditions or restrictions, as well as food allergies or intolerances that could influence their eating patterns.

Lastly, be sure to gather information about their access to transportation to a grocery store, who shops for and prepares their food, and any difficulties obtaining or preparing food.

Next, determine if there are any physiological factors that can impair their nutritional status. Ask about changes in appetite, taste, smell, chewing, or swallowing; gastrointestinal issues such as nausea, vomiting, diarrhea, or constipation; and psychological symptoms like depression or anxiety.

Inquire about any chronic medical conditions such as diabetes or inflammatory bowel disease, as well as acute conditions such as a recent trauma or surgery.

Also gather information about any diet modifications, exercise regimens, medications, or surgery used to resolve weight-related problems; and ask them if they’ve recently experienced unintentional weight loss. Also, determine if they are taking any medications that can impact digestion, absorption, and metabolism of nutrients, including laxatives, steroids, or anticonvulsants; as well as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Child_maltreatment:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eVxiBlUwQ1yZgE6p2UJvRSWNR5G0rb8Q/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Child maltreatment: Nursing]]></video:title><video:description><![CDATA[Nurse Angelo works in a family practice clinic and is caring for Maya, a 2-and-a-half-year-old who&amp;#39;s brought in for a required wellness check before entering preschool. After settling Maya in the room, Nurse Angelo goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Maya’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Angelo recognizes cues, including Maya’s vital signs which are temperature 98.6 F or 37 C, heart rate 105 beats per minute, and respiratory rate 23 breaths per minute. Nurse Angelo notes that Maya has multiple circular bruises ranging in color from pale yellow to deep purple on her upper arms, as well as a rounded, punctate burn to the back of her left shoulder about one centimeter in diameter.  

Nurse Angelo also notes Maya grimaces occasionally and appears tense, so he determines Maya’s pain rating is two out of 10 according to the Face, Legs, Activity, Cry, and Consolability, or FLACC scale. Nurse Angelo also notes that when he asks Maya questions, she doesn’t respond or make eye contact with him.  

He gathers additional information from Maya’s mother, Josie, about her injuries. 

Nurse Angelo: I see that Maya has some bruising on her arms. Can you tell me what happened? 

Josie: Oh, those? She’s just clumsy. She’s always bruised easily. She probably fell down while she was playing or something. 

Nurse Angelo: I also noticed an injury to her left shoulder that looks like a burn. Do you know what happened there? 
  Josie: That doesn’t look like a burn to me. Like I said, I think she probably scraped herself when she was playing. 

Nurse Angelo then analyzes these cues. He reviews Maya’s electronic health record, or EHR, and notes that she has a history of a humerus fracture at age one year. When asked about the fracture, Josie says it was caused by a fall when Maya was learning to walk. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Parenteral:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6vAPrSg9T7yTiqfaG4SrQULRTuekjuJB/_.png</video:thumbnail_loc><video:title><![CDATA[Medication administration - Parenteral: Nursing pharmacology]]></video:title><video:description><![CDATA[Parenteral medications bypass the gastrointestinal system and can be administered through injection or the intravenous route. Four types of parenteral routes are intradermal, or ID; subcutaneous, or SubQ; intramuscular, or IM; and intravenous, or IV. 

Now, parenteral medications come in vials, ampules, or premixed IV bags. Vials are single- or multi-dose containers that are sealed with a rubber top through which a dose is drawn up with a needle and syringe. Another type of vial is the mix-o-vial, where a powdered medication and solvent are stored in separate compartments of the same vial and are mixed by pushing a plunger and releasing the stopper that separates them. Then, ampules are single-dose glass containers designed to break open by snapping along a scored line on the narrowed portion of the ampule’s neck. Be sure to open ampules using an alcohol wipe or sterile gauze to protect your fingers and use a filter needle to draw up the dose to prevent the medication from becoming contaminated with glass shards. 

As the nurse, you’ll choose an appropriate syringe and needle to administer medication, so let’s review the types and parts of a syringe first. The three syringe types are hypodermic, tuberculin, and insulin. Hypodermic syringes come in a variety of sizes, with the 3 mL and 5 mL syringes typically used for injectable medication volumes between 0.5 mL and 5 mL, whereas tuberculin syringes are 0.5 mL or 1 mL in size and used when the volume of medication administered is less than 1 mL, like tuberculin skin tests. Then, there are insulin syringes, which are marked in units instead of milliliters and should only be used to administer insulin. They typically can hold up to 100 units.  

So, all syringes have three main parts. The barrel, which is the outer shell that holds the medication, and the tip, which is also called a hub, is the end where the needle attaches. Lastly, the plunger is the inner part that fits inside the barrel and can move to wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Medication_administration_-_Insulin:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lPPfd2ckRWi5T6CyISUdXsttSOCiyk9a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Medication administration - Insulin: Nursing pharmacology]]></video:title><video:description><![CDATA[Insulin is a hormone secreted by beta cells in the pancreas that helps glucose enter the body’s cells, so it can be used for energy. In diabetes mellitus, insulin is either not produced at all, like in type I diabetes; or cells are resistant to insulin, like in type II diabetes. In either type, glucose can&amp;#39;t be utilized by the body’s cells, so it builds up in the bloodstream.   

Exogenous insulin, or synthetic insulin, can be administered to help regulate glucose levels, and is most often administered by subcutaneous, or SUBQ injection. It’s a commonly used, high-alert medication, meaning there’s an increased risk of patient harm if administered in error. This is because insulin can cause potentially dangerous hypoglycemia, or low blood glucose levels. 

Alright, so insulin typically comes in either a vial or a pen. Most insulin vials contain a concentration of 100 units of insulin per milliliter. It’s important to note that insulin doses are prescribed and measured in units, not milliliters so you’ll always use an insulin syringe, which measures increments of insulin in units. Insulin vials can include rapid-, short-, intermediate-, or long-acting insulins as well as pre-mixed solutions like 70/30 preparations, which contain 70 percent intermediate-acting insulin and 30 percent rapid-acting insulin. Most insulins are clear, but a type of insulin called NPH, which is short for neutral protamine Hagedorn is cloudy because a protein called protamine is added to prolong its action in the body over an extended period. 

There are also pre-filled insulin pens, which contain either 150 units of insulin per 1.5 milliliters or 300 units of insulin per 3 milliliters. These devices can be used for multiple injections for one patient. Before administering the insulin, a small disposable needle is placed on the end of the pen and the indicator dial is turned to the correct insulin dose. Following administration, the dose indicator returns to zero and the nee]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Attention-deficit_hyperactivity_disorder_(ADHD):_Nursing_process_(ADPIE)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fdg-PwQYQc2wJETGkTbA81XXTZCla90i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Attention-deficit hyperactivity disorder (ADHD): Nursing process (ADPIE)]]></video:title><video:description><![CDATA[Paul Truslow is a 11-year-old boy who is brought to the pediatrician by his mother, Ms. Truslow. Ms. Truslow is concerned because Paul hasn’t been performing well in school, stating that he doesn’t always turn in his homework assignments, and when he does, the assignments are often incomplete. At home, Ms. Truslow says that Paul forgets to do daily tasks like brush his teeth, make his bed, and take out the garbage. Ms. Truslow and his teachers are concerned about Paul, and are worried about his grades. The pediatrician is evaluating Paul for ADHD.

Attention-deficit hyperactivity disorder, or ADHD for short, refers to a range of behaviors characterized by inattention, as well as hyperactivity and impulsivity, and is the most common mental health disorder affecting pediatric clients in the US, with males being affected more frequently than females. However this may be due to bias in referral or diagnosis.

The exact cause of ADHD is still not well understood, but  it seems to be associated with the activity of dopaminergic and noradrenergic neurons within the brain. These neurons produce and store in small vesicles the neurotransmitters dopamine and norepinephrine, respectively. Dopamine binds to dopamine receptors and stimulates cognitive functions, motivation, and awakeness. On the other hand, norepinephrine binds to norepinephrine receptors, subsequently boosting alertness and focus. Now, in clients with ADHD, it’s thought that there are lower amounts of these two neurotransmitters in the brain, although the reason why is still unknown.

Some risk factors may reach back to a child’s development as a fetus during pregnancy and they include exposure to alcohol, tobacco, and cocaine; as well as premature birth, and a birth weight lower than 1,500 grams. On the other hand, early childhood risk factors include exposure to lead, iron deficiency, head trauma, obstructive sleep apnea, and certain infectious diseases, such as chickenpox and measles. Finally, psyc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Drug_reconstitution:_Nursing_pharmacology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zXNiya76SByTVynd1lda40GzSDWYKZT_/_.png</video:thumbnail_loc><video:title><![CDATA[Drug reconstitution: Nursing pharmacology]]></video:title><video:description><![CDATA[Reconstitution is the process of adding a liquid diluent, or solvent, to a powdered medication, or solute, and then dissolving the medication to form a solution. In some cases, reconstitution is necessary because a medication doesn&amp;#39;t remain stable long enough to be distributed in solution form, so it comes from the manufacturer in a powdered form and must be reconstituted with a liquid prior to administration.   

Now, if your patient is prescribed a medication that requires reconstitution, you’ll follow the steps of drug reconstitution to perform safe medication administration. First, read the directions on the medication label or medication insert; or you can consult the pharmacist at your facility. This information will tell you the type and amount of solvent to add to the powdered medication. Commonly used solvents include sterile water, bacteriostatic water, or sterile normal saline.  

Next, you’ll use a syringe and needle to draw up the desired volume of solvent from its vial and inject the solvent into the vial of powdered medication. After disposing of the syringe and needle according to your facility’s policy, you’ll typically roll the vial between your hands to mix it, unless the label specifies that you can shake it, making sure the medication dissolves completely, forming a solution. 

Some reconstituted medications are packaged in single-dose vials, meaning the vial and its contents should be disposed of following administration. Other reconstituted medications are packaged in multi-dose vials, meaning the contents can be stored and used later for additional doses. For multi-dose vials, be sure to label the vial with the date and time it was reconstituted, the expiration date and time, the dosage strength, and your initials. 

Okay, let’s look at some drug reconstitution examples. 

Let’s take a look at this label for methylprednisolone.

First, read the directions on the label, which instruct you to use 2 mL of bacteriostatic water ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Attention-deficit_hyperactivity_disorder_(ADHD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q4RbUROGRaONdw4BTtUXxc4XTauwq2ik/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Attention-deficit hyperactivity disorder (ADHD): Nursing]]></video:title><video:description><![CDATA[Nurse Sienna works in a family practice clinic and is caring for Paul, an 11-year-old who was brought in by his caregiver, Erin, for poor school performance over the past year. After settling Paul in his room, Nurse Sienna goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Paul’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Sienna recognizes important cues, including Paul’s vital signs which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respiratory rate 14 breaths per minute, and blood pressure 105/66 mmHg. She notices that Paul is restless and regularly stands up to look at and touch objects in the examination room.  

Nurse Sienna gathers more information from Erin and Paul.  

Nurse Sienna: Hi Paul, how are you doing today? 

Paul: Okay, I guess. I don’t know why I have to be here.  

Erin: Paul’s been having trouble in school. His grades have been getting worse over the past few months. He&amp;#39;s also been turning in his assignments late or not at all, and when he does turn them in, they’re incomplete.  

Paul: (shrugs) It&amp;#39;s hard to pay attention. 

Erin also reports that Paul’s teachers say he often disrupts class by standing up and blurting out answers to questions instead of raising his hand; and that he has difficulty following rules and waiting for his turn during group activities. When asked about the home environment, Erin reports that when Paul is asked to perform a household chore, he either forgets to do the chore or doesn&amp;#39;t finish it once he starts it.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_interventions_-_Overview:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YGE_TaK8TtGgSW4PNNA0VkZFS0eCJArd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric interventions - Overview: Nursing]]></video:title><video:description><![CDATA[Pediatric patients who are hospitalized require individualized care based on their developmental level. As the nurse caring for a hospitalized child, you’ll prepare them and their caregivers for procedures while promoting their comfort and safety.    

When providing care, begin by establishing rapport and trust with the child and their caregivers. You can do this by using therapeutic communication skills, like speaking in a calm tone, listening actively, and practicing therapeutic body language, like sitting down and leaning forward toward your patient.  

When explaining the plan of care, remember to avoid words that can cause confusion or fear. So, instead of using medical jargon like “edema,” you can describe a swollen body part as being “puffy.” Likewise, instead of “shot” when talking about an injection, you can use less threatening language like “medicine under the skin.”  

You can also ensure your patient and caregivers are familiar with other members of the health care team and their role in the child’s care. Lastly, be sure to collaborate with the child life specialist, who can provide therapeutic play activities that can decrease fear and anxiety in children and their families.   

Now, before your patient undergoes a procedure, you’ll need to ensure that informed consent is obtained from their caregiver, by verifying that the health care provider has explained the condition, proposed treatment plan, treatment alternatives, as well as potential risks and benefits of the procedure. As the nurse, you’ll witness the signatures on the consent form and reinforce the information provided by the health care provider. Also be sure to include the child in the discussion, and obtain their assent, as appropriate.  

During teaching, you may use a doll or stuffed animal to show a younger child where electrodes are placed or where their surgical dressing will be; whereas, with an adolescent, you can provide them with detailed information, since they’re typically eager to receive health teaching. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Delirium:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TzUVqb9QR8uHcAjoLVPNaTdxSxubdbpJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Delirium: Nursing]]></video:title><video:description><![CDATA[Nurse Melinda works on a medical surgical unit and is caring for Kadija, a 72-year-old with a history of heart failure who was admitted for pyelonephritis. After settling Kadija in her room, Nurse Melinda goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Kadija’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Melinda recognizes important cues, including Kadija’s vital signs, which are temperature of 102.2 F or 39 C, heart rate 102 beats per minute, respirations 19 breaths per minute, and blood pressure 140/80 mmHg.  

Nurse Melinda notices Kadija appears anxious, and her eyes are moving back and forth across the room. She gathers additional information from Kadija. 

Nurse Melinda: Hi Kadija, how are you feeling today? 

Kadija: Don’t you see that? There are a bunch of spiders on the wall behind you. 

Nurse Melinda turns around and notes there is nothing on the wall. 

Nurse Melinda: I don’t see any spiders, but I understand that must be very scary for you. You&amp;#39;re safe here with me. 

Nurse Melinda conducts a brief cognitive screening and determines that Kadija is oriented to self, but not time, place, or situation.  

Next, Nurse Melinda analyzes these cues. She reviews the electronic health record, or EHR, and notes that Kadija has no history of psychiatric illness.  

Nurse Melinda recognizes that underlying factors, such as infection, fever, pain, sleep deprivation, fluid and electrolyte imbalance, as well as certain medications, can lead to alterations in a patient’s mental status, causing problems like delirium, especially in patients with advanced age and preexisting medical conditions. 

She also recalls that delirium can develop over several hours or days and can result in a waxing and waning of mental function, including memory, thinking, language, behavior, mood, and personality. Hallucinations]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intimate_partner_violence_and_sexual_assault:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GMKns-YUSRuzubhskBExAwS3S1mJhfUm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intimate partner violence and sexual assault: Clinical sciences]]></video:title><video:description><![CDATA[Intimate partner violence and sexual assault, also known as IPV and SA, are significant public health problems that affect millions of individuals regardless of age, gender, socioeconomic status, or sexual orientation. 
IPV and SA encompass a continuum of aggressive, coercive, and potentially violent behaviors. Specifically, IPV consists of a pattern of behaviors that includes physical injury, psychological abuse, sexual assault, isolation, intimidation, and reproductive coercion. On the other hand, SA includes acts ranging from sexual coercion to contact abuse to acts of penetration. So remember that IPV may include SA but SA may or may not be from an intimate partner. 

Keep in mind that often patients do not disclose a history of IPV or SA, so it’s important to screen all patients for both. During obstetric care, screening should occur at the first prenatal visit, at least once per trimester, and at the postpartum checkup. 

When a patient presents with signs and symptoms of intimate partner violence or sexual assault, first perform a CABCDE assessment to determine if the patient is unstable. 

If the patient is unstable, control hemorrhage; stabilize airway, breathing, and circulation; obtain IV access, monitor vital signs, and manage severe injuries. 

Severe injuries specific to IPV and SA include head injuries, strangulation, fractures, and wounds related to guns or knives, as well as penetrative trauma. In pregnant patients, consider fetal well-being, particularly if there is abdominal trauma. If the patient is stable, perform a focused history and physical examination. 

A patient may report an incident of IPV or SA, but many actually won’t. 
However, they might reveal symptoms of anxiety or depression, disclose an inciting traumatic event, or report symptoms of chronic pain or illness such as chronic pelvic pain, dysmenorrhea, or sexual dysfunction. 

When interacting with patients who have experienced trauma, a trauma-informed approach to care i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sports_physical_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/10D8jwKFTH2ofv1mTqmOx6EuTkuNM4ye/_.png</video:thumbnail_loc><video:title><![CDATA[Sports physical (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[The goal of a pre-participation sports physical examination is to identify any underlying condition that may increase an athlete’s risk of injury, illness, or death. The sports physical can often be performed during a well-child visit, which provides the opportunity to offer immunizations, preventative care, and anticipatory guidance. 

When a pediatric patient presents for a sports physical, start with a comprehensive history and physical exam. First, review the medical history, and ask about any previous injuries or concussions. Then, screen for cardiovascular conditions by asking your patient if they had chest pain, syncope, difficulty breathing, or palpitations. Additionally, find out if there is a family history of cardiomyopathy; arrhythmias; or early, sudden, or unexplained cardiac death. If your patient has a chronic health condition, discuss their current management plan, and determine whether the condition is well-controlled. Ask about symptoms that suggest an underlying mental health condition, such as anxiety, depression, or disordered eating. Next, ask if they use any supplements or recreational substances such as tobacco, alcohol, drugs, or performance-enhancing substances, like anabolic steroids. Finally, if your patient is biologically female, obtain a menstrual history, including their age of menarche, and their cycle duration and frequency.

Next, measure your patient’s height, weight, and BMI; and take their blood pressure. Additionally, perform vision and hearing screening, if possible.

Then, perform a physical exam, starting with an assessment of your patient’s general appearance. Be sure to look for phenotypic features suggesting Marfan syndrome, such as arachnodactyly, tall stature, or pectus excavatum, since patients with this condition are at risk of aortic dissection and sudden death.

Also, perform a head-to-toe musculoskeletal exam to evaluate the range of motion, stability, and strength of each major joint and muscle group. Fi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Engage_your_audience_with_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8EnRDW6ZRAmkXlGX8NS_W8EoTX2Im_xG/_.png</video:thumbnail_loc><video:title><![CDATA[Engage your audience with Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Engage your audience with Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Celiac_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xng_8KA-QtabFnoJNgmlhH4YQIeBetU6/_.png</video:thumbnail_loc><video:title><![CDATA[Celiac disease: Clinical sciences]]></video:title><video:description><![CDATA[Celiac disease, also known as celiac sprue or gluten-sensitive enteropathy, is a genetic condition associated with an immune-mediated response to gluten, which is a protein found in wheat, barley, and rye. In genetically susceptible individuals, a component of gluten called gliadin, triggers an immune response within the small intestine, eventually causing local inflammation and production of antibodies against both gliadin and an enzyme called tissue transglutaminase. Over time, local inflammation results in malabsorption of various vitamins, minerals, and other nutrients. In children, celiac disease typically occurs after 6 months of life, because this is the period when caregivers introduce gluten-containing foods to their babies. 

Now, if your pediatric patient presents with a chief concern suggesting celiac disease, first perform a focused history and physical examination, and obtain labs, including CBC and CMP. Your patient will commonly present with typical gastrointestinal symptoms that are related to mucosal damage in the small intestines and subsequent malabsorption. These include bloating; abdominal pain; chronic diarrhea; and steatorrhea, which is a greasy, foul-smelling stool that’s difficult to flush; as well as poor weight gain in young children or weight loss in older children and adults. Other historical findings may include extraintestinal symptoms like irritability and changes in their child’s behavior. Additionally, there might be a history of pre-existing autoimmune conditions, such as Type 1 diabetes mellitus or rheumatoid arthritis; genetic conditions, like Down or Turner syndrome; or a positive family history of celiac disease. 

As far as the physical exam goes, you might notice abdominal distention; a pattern of short stature on growth charts; as well as signs of failure to thrive, or delayed puberty. Finally, some patients might present with dermatitis herpetiformis, which refers to an itchy, vesicular rash that typically appear]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cutaneous_squamous_cell_carcinoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tTKDbToORriaKw8Y_r5vmLhFTmayoypX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cutaneous squamous cell carcinoma: Clinical sciences]]></video:title><video:description><![CDATA[Cutaneous squamous cell carcinoma, or cSCC for short, is the second most common form of skin cancer, the first one being basal cell carcinoma. 

The most important risk factors for developing cSCC include ultraviolet light exposure, chronic immunosuppression, and a history of actinic keratosis. Timely diagnosis and treatment of these lesions are vital to ensure the best outcome for the patient.

When a patient presents with a chief concern suggesting cSCC, you should first obtain a focused history and physical exam. History typically reveals risk factors like fair skin and significant sun exposure or exposure to UV radiation. These patients might also report bleeding or rapid growth of the lesions as well as changes in the appearance of the lesion. 

When evaluating any lesions concerning for skin cancer, make sure to do a full body exam to look for any other suspicious lesions. The physical exam typically reveals an ulcerated non-healing nodule with irregular borders and possibly signs of active or recent bleeding. There is often erythema and induration surrounding the nodule as well as areas of actinic keratosis. The lesion might be painful or tender. Finally, you might find lymphadenopathy, often in the axilla, supraclavicular, cervical, or inguinal region depending on the location of the lesion. Based on these findings, suspect cSCC. 

Here’s a clinical pearl! Be sure to differentiate cSCC from basal cell carcinoma. Cutaneous basal cell carcinoma is often a non-healing, well-circumscribed pearly papule, nodule, or plaque with rolled borders. Even though both are found on sun-exposed areas of the skin, cSCC is more commonly found on the dorsal forearm and hands, and then the head and neck; while basal cell carcinoma is typically found on the face and neck.

Alright, once you suspect cSCC, your next step is to examine the lesion with dermatoscopy. Dermatoscopy is performed with a hand-held skin surface microscope that can allow you to better see the deta]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Flipping_your_classroom:_Strategies_and_tools_for_flipped-classroom_success_with_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SUQqzj_USIKONHv6c57OHcN7RJKY9nug/_.png</video:thumbnail_loc><video:title><![CDATA[Flipping your classroom: Strategies and tools for flipped-classroom success with Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Flipping your classroom: Strategies and tools for flipped-classroom success with Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_altered_mental_status:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cBdYTwkSSwmZf7R6RZaRDfh2TfWU3T4A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to altered mental status: Clinical sciences]]></video:title><video:description><![CDATA[Altered mental status refers to the abnormal change in consciousness, cognition, behavior, or mood, which can range from mild confusion to coma. It can occur suddenly, like following acute intoxication, or gradually, as in hepatic encephalopathy. Altered mental status can arise from various causes, including abnormal glucose levels, toxins and medications, central nervous system conditions, infections, and metabolic disorders. 

If your patient presents with altered mental status, perform an ABCDE assessment and start acute management. Stabilize the patient’s airway, breathing, and circulation. Next, assess their level of consciousness by checking the Glasgow Coma Scale or GCS, which measures eye-opening, verbal, and motor response to stimuli on a scale from 3 to 15. A GCS score of 3 represents a comatose state, while a score of 15 represents a normal level of consciousness. Moreover, individuals with a GCS of 8 or less might require intubation. After that, obtain IV access and check a fingerstick glucose. If it is low, give IV glucose. If you suspect opioid intoxication, administer naloxone. Lastly, don’t forget to start continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. 

Once you stabilize your patient, obtain a focused history and physical examination. Since these patients are often unable to provide a history, you may need to gather information from family members, caretakers, or witnesses. History usually reveals a change in the patient’s level of consciousness, behavior, or mood, which can be persistent or fluctuate in severity with time. Additionally, the physical exam reveals a decreased level of consciousness, as well as confusion and memory loss.  

As you are dealing with altered mental status, your next step is to assess the underlying cause. Start by obtaining serum glucose levels. If glucose levels are above 250 mg/dL, consider hyperglycemic hyperosmolar syndrome or HHS or diabetic ketoacidosis or DKA]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_stroke_(ischemic_or_hemorrhagic)_or_TIA:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q26OrXVESQGV9jP17Tpud62uRyuy6_vE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute stroke (ischemic or hemorrhagic) or TIA: Clinical sciences]]></video:title><video:description><![CDATA[Acute stroke can be hemorrhagic, which occurs due to vessel rupture and subsequent impaired blood flow, or ischemic, which occurs due to narrowing or blockage of an artery. On the flip side, a temporary interruption of blood flow that results in transient neurologic symptoms with no infarction on imaging is called transient ischemic attack, or TIA. 

Now, if your patient presents with chief concerns suggesting acute stroke or TIA, perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. At this point, you might even have to intubate the patient and start mechanical ventilation. Next, obtain IV access, consider starting IV fluids, and don’t forget to put your patient on continuous vital signs monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Finally, you might need to manage high intracranial pressure, especially in individuals with hemorrhagic stroke! 

Alright, now, let’s go back to the ABCDE assessment and take a look at stable patients.  First, obtain a focused history and physical exam, and fingerstick glucose because hypoglycemia can mimic stroke symptoms. Your patient will report a sudden onset of neurologic symptoms, such as weakness, numbness, incoordination, but also facial droop, slurred speech, and language difficulties. Some patients will also report changes in vision, including visual field defects, or they might report a “thunderclap” headache, which is suggestive of subarachnoid hemorrhage!  

Next, history might reveal risk factors, such as tobacco use, diabetes, hyperlipidemia, hypertension, and cardiovascular conditions, like carotid artery disease and atrial fibrillation. Keep in mind that risk factors like tobacco use, diabetes, hyperlipidemia, and hypertension are associated with both hemorrhagic and ischemic strokes!  

Some individuals could also present with hypercoagulable conditions, including antipho]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_increased_intracranial_pressure:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Gmg-K9EhR9i-O9Ic3566n4NfSkab31NU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to increased intracranial pressure: Clinical sciences]]></video:title><video:description><![CDATA[Increased intracranial pressure, or increased ICP for short, refers to intracranial pressure greater than 20 millimeters of mercury, which can occur due to an increase in the blood, brain, or cerebrospinal fluid compartment. According to the Monroe-Kellie doctrine, the total volume of these three compartments is constant, meaning a volume increase in one compartment should cause a decrease in the others.  

Common causes of increased ICP include intracranial hemorrhage, ischemic stroke, brain tumors or abscesses, or meningitis or encephalitis. 

Now, if your patient presents with a chief concern suggesting increased ICP, first, perform an ABCDE assessment. You should consider all patients with increased ICP as unstable, so be sure to stabilize their airway, breathing, and circulation. Sometimes, you might even need to intubate the patient and start mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. 

Once you have initiated the acute management, your next step is to obtain a focused history and physical exam and get a head CT. Your patient, or their family member or friend, will typically report symptoms, such as headache, and in some cases, nausea and vomiting.  On the exam, your patient will present with an altered mental status, more specifically a decrease or even loss of consciousness.  

Moreover, be sure to use the Glasgow Coma Scale, or GCS, to assess the patient’s level of consciousness by evaluating eye-opening, verbal, and motor responses to varying levels of stimulation. The scale goes from 3 to 15, with a lower number indicating a worse level of consciousness.  

A patient with a GCS score of 3 will have no eye-opening, verbal, or motor response to even the most noxious stimulation, such as sternal rub or nail bed pressure. On the other hand, a patient with a GCS score of 15 will have normal eye-opening,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Subarachnoid_hemorrhage:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5JGyg7NHR4ynRW1QnlGnDoBLTKys7lg0/_.png</video:thumbnail_loc><video:title><![CDATA[Subarachnoid hemorrhage: Clinical sciences]]></video:title><video:description><![CDATA[Subarachnoid hemorrhage refers to an intracranial bleed that occurs between the pia and arachnoid layers of the meninges, which are protective layers that cover the brain. If not promptly recognized and treated, blood pooling in the subarachnoid space can lead to a fatal increase in intracranial pressure. Now, based on the underlying cause, subarachnoid hemorrhage can occur as a result of traumatic head injuries, but it could also occur spontaneously, which is also known as non-traumatic subarachnoid hemorrhage.   

Now, if your patient presents with a chief concern suggesting subarachnoid hemorrhage, first, perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. At this point, you might even have to intubate the patient and start mechanical ventilation. Next, obtain IV access, consider starting IV fluids, and don’t forget to put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. Finally, you might need to manage high intracranial pressure, or ICP for short.  

Now, here’s a clinical pearl to keep in mind! In severe cases, subarachnoid hemorrhage can increase ICP, which triggers a physiological response known as the Cushing triad, which consists of bradycardia, hypertension, and irregular breathing. Moreover, important physical exam findings associated with dangerously high ICP and potential brain herniation include dilated pupils that are unresponsive to light!  

If you notice any of these signs, place an ICP monitor and start appropriate medical management, which includes elevating the head of the bed, hyperventilation, sedation, and hyperosmolar therapy.  

If high ICP is partly due to ventriculomegaly, your patient will require CSF diversion, such as placing an external ventricular drain. Finally, If high ICP persists despite medical management and CSF diversion, you should proceed to]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Substance_use_disorder:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NgowtYGyS8OxYNh_lDn1DXeoSneit8-a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Substance use disorder: Clinical sciences]]></video:title><video:description><![CDATA[Substance use disorder is a medical condition characterized by the inability to control the consumption of a substance despite adverse health and social consequences. The cause of substance use disorder is multifactorial and includes psychological, biological, social, and environmental factors. Based on criteria defined in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, or DSM-5, you can categorize a substance use disorder as mild, moderate, or severe. 

Okay, if a patient presents with a chief concern suggesting a substance use disorder, first perform an ABCDE assessment to determine if the patient is unstable or stable. If your patient is unstable, stabilize the airway, breathing, and circulation, which might require endotracheal intubation with mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, pulse oximetry, and cardiac telemetry.  

Here’s a clinical pearl to keep in mind! Patients with substance use disorder might present with a few potentially unstable conditions. For example, cocaine toxicity can cause cardiac ischemia and seizures, whereas heroin or other opioid toxicity can result in severe drowsiness, respiratory depression, and coma. Benzodiazepine toxicity can also cause CNS depression, whereas benzodiazepine or alcohol withdrawal can cause potentially fatal seizures!  

Now that we’ve addressed unstable patients, let’s return to the ABCDE assessment and take a look at stable patients. If the patient is stable, first obtain a focused history and physical exam. Next, assess for substance use with a screening test, such as the Drug Abuse Screening Test, or DAST-10. DAST-10 contains ten “yes” and “no” questions about substance use over the past 12 months and includes illicit drugs, prescription medication and over-the-counter medication. However, keep in mind that this screening test excludes alcohol use.   

Now, here’s a high-yie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Idiopathic_intracranial_hypertension:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/WxBRMZCmTFWsm351ApnuTwPtQpaKxkV2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Idiopathic intracranial hypertension: Clinical sciences]]></video:title><video:description><![CDATA[Idiopathic intracranial hypertension, or IIH, also known as pseudotumor cerebri, refers to an increased intracranial pressure of unknown precise etiology. Elevated intracranial pressure can cause debilitating headaches, but it can also lead to swelling of the optic disc, known as papilledema, which, if left untreated, can result in severe vision loss. Now, based on the immediate risk of vision loss, idiopathic intracranial hypertension can be classified as typical or fulminant.  

Now, if your patient presents with a chief concern suggestive of idiopathic intracranial hypertension, first, obtain a focused history and physical exam.  History will usually reveal an obese biological female of reproductive age with concerns, including headaches that may worsen with Valsalva maneuvers. Over time, elevated intracranial pressure can affect optic and abducens nerves and result in symptoms, such as blurred and double vision, or even vision loss. Vision loss may last only a few seconds, so it’s often referred to as transient visual obscurations. Additionally, your patient will report that vision loss typically occurs when changing positions, for example, when bending over to pick up a neurology textbook! 

Next, the patient might complain of pulsatile tinnitus, which is sound transmitted from turbulent blood flow in narrowed transverse and sigmoid venous sinuses. Finally, history might reveal medications associated with idiopathic intracranial hypertension, including tetracycline antibiotics and retinoids, such as vitamin A derivatives or all-trans retinoic acid. 

Now, here’s a clinical pearl to keep in mind! Idiopathic intracranial hypertension is usually seen in young, obese biological females. If your patient is not in this demographic group and presents with symptoms of elevated intracranial pressure, you should consider an alternative diagnosis, such as venous sinus thrombosis. 

On physical examination, these patients are normotensive with normal mental statu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_anxiety_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lNXat4dSSj6JBMO-dkQrewvJRRq0ejA1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to anxiety disorders: Clinical sciences]]></video:title><video:description><![CDATA[Anxiety disorders are conditions characterized by excessive fear and anxiety. Fear is an emotional reaction to a threat, either real or perceived, and is usually associated with autonomic arousal. Anxiety, on the other hand, is the anticipation of a future threat; it’s not usually associated with autonomic arousal; and it often causes maladaptive changes in thinking or behavior.  

Distinguishing between the various anxiety disorders requires identifying the triggers that set them off, any related changes in thinking or behavior, and assessing the Diagnostic and Statistical Manual, or the DSM-5 criteria. Common anxiety disorders include panic disorder with or without agoraphobia, obsessive-compulsive disorder or OCD, specific phobias, social anxiety disorder, and generalized anxiety disorder or GAD.  

When a patient presents with a chief concern suggesting an anxiety disorder, first perform a focused history and physical examination. 

Your patient will report excessive fear or anxiety, or sometimes both. In some cases, they might also report chest discomfort.  

The physical exam might show restlessness, a tense or constricted affect, tachycardia, or elevated blood pressure. With these findings, consider an anxiety disorder, and investigate further to determine the specific type.  

Let’s start by assessing for a history of panic attacks.  A panic attack is an abrupt period of intense fear, accompanied by an uncomfortable surge of autonomic arousal, where the heart beats faster, respirations increase, and muscles tense up.Patients might report trembling, sweating, chest discomfort, palpitations, shortness of breath, nausea, paresthesias, or lightheadedness. Additionally, there might be associated emotional symptoms, like crying, dissociation, feeling out of control, or fear of dying. Panic attacks can be triggered by stressful situations or can occur unexpectedly.Here’s an important clinical pearl! An acute panic attack can present like acute coronary sy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_dizziness_and_vertigo:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mgEXH7NRS0mwjxqkdSgfCQJjQJWoo-Cf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to dizziness and vertigo: Clinical sciences]]></video:title><video:description><![CDATA[Dizziness is a term used to describe symptoms such as loss of balance, lightheadedness, and altered spatial orientation, while vertigo refers to an abnormal sensation of self-motion or movement of the surrounding environment. Now, dizziness can occur because of metabolic, cardiac, and neurologic conditions, while vertigo typically occurs due to vestibular or focal brain conditions. 

Now, if your patient presents with dizziness or vertigo, the first step is to obtain a focused history and physical examination and establish which of these they are experiencing.  

First, let’s focus on dizziness! In this case, your patient will describe lightheadedness, altered orientation of space, or feeling faint. There will be no abnormal sensation of motion, but the patient might report feeling off-balance. In some cases, history might reveal nausea and vomiting, while the physical exam might demonstrate some degree of gait impairment and no nystagmus!  

With these findings, diagnose dizziness, so be sure to assess the timing of symptoms, which could be episodic or persistent.  Let’s first take a look at episodic dizziness.  

If the dizziness is episodic, further assess the underlying cause with additional history and exam evaluation. Some common causes include orthostatic hypotension and panic disorder. First, let&amp;#39;s discuss orthostatic hypotension... 

Orthostatic hypotension is typically associated with dizziness when moving to an upright position, such as with sitting or standing up. The patient may feel their heart racing, or that they are about to pass out with a darkening of their vision.  There might be a recent history of volume depletion, such as from vomiting, diarrhea, or blood loss. Additionally, history might reveal neurologic conditions causing autonomic dysfunction, such as Parkinson disease, multiple system atrophy, and neuropathy.  

The physical exam involves checking blood pressure in supine and standing positions. After standing up, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_convulsive_status_epilepticus:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QhCB0MPmTxShoxnXCsvV2FbCRuKDIH0K/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to convulsive status epilepticus: Clinical sciences]]></video:title><video:description><![CDATA[Convulsive status epilepticus is a neurologic emergency that refers to persistent tonic-clonic seizure activity lasting five or more minutes, or multiple seizures without return to baseline in between. This condition occurs when inhibitory mechanisms responsible for terminating seizures fail to work, or when pathways that lead to prolonged seizures are overactivated. Some common causes of status epilepticus are medication changes or noncompliance in patients with known epilepsy, substance use, metabolic derangements, and acute brain injury from infectious and non-infectious processes.  

Now, if your patient presents with chief concerns suggestive of convulsive status epilepticus, first, perform an ABCDE assessment. You should consider all patients with convulsive status epilepticus unstable, so be sure to stabilize their airway, breathing, and circulation. Sometimes, you might even need to intubate your patient and start mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. 

Once you are done with acute management, obtain a focused history and physical exam, and order labs, including fingerstick glucose, CBC, CMP, and a toxicology screen. Also, don’t forget to check anti-seizure medication levels. History will reveal a tonic-clonic seizure that started 5 or more minutes ago, or multiple seizures without return to baseline in between. Additionally, the physical exam will demonstrate altered mental status and alternating body stiffening and jerking movements consistent with a tonic-clonic seizure.  

At this point, you can diagnose convulsive status epilepticus, so your next step is to proceed with treatment! First, take a look at the fingerstick glucose because hypoglycemia can be an acute symptomatic cause of status epilepticus and seizures in general. If the patient’s glucose level is less than 60 milligrams per deci]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_trauma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9ulDJarJQDKiwuNe_PMzC387TMOQ0LhQ/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to trauma: Clinical sciences]]></video:title><video:description><![CDATA[Trauma is one of the major causes of mortality and morbidity worldwide. A standardized approach to trauma, known as the “trauma protocol” allows providers to systematically assess and quickly identify potentially life-threatening injuries, while simultaneously initiating resuscitation. The trauma protocol is composed of primary, secondary, and tertiary surveys, performed one after another. The goal is to first identify life-threatening injuries and stabilize the patient; then, perform a more thorough head-to-toe assessment to catch the not-so-obvious injuries; and finally, follow up 24 hours later to make sure no other injuries were missed. This protocol is performed on every trauma patient regardless of the mechanism of injury. 

So, when a patient presents with trauma, start with a primary survey. which can be summarized as A, B, C, D, and E. 

A stands for Airway. Ensure your patient has an open airway and the ability to maintain a patent airway. Start by asking them their name and what happened. If they can speak, they have an open airway. However, if they show any signs of airway compromise, such as altered mental status, gurgling noises, inability to speak clearly, or evidence of an expanding neck hematoma, secure the airway as soon as possible. In this case, intubate or consider obtaining a surgical airway via cricothyroidotomy. Also, stabilize the C-spine to maintain cervical spine restriction by placing a cervical collar and keeping it in place until a traumatic injury to this area has been ruled out. 

The next step in the primary survey is B for Breathing. This part focuses on identifying any injuries that affect ventilation and oxygenation. Key assessments include checking for tracheal deviation; evaluating for symmetrical chest rise; auscultating for lung sounds; and palpating the chest wall for evidence of trauma. Any injuries that can impair ventilation such as pneumothorax or hemothorax should be addressed immediate]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_blunt_and_penetrating_abdominal_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/boaMkcyrQmiUb3PAkfOT-Gf-SJWBdrLl/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to blunt and penetrating abdominal injury: Clinical sciences]]></video:title><video:description><![CDATA[Traumatic injuries to the abdomen can occur from blunt forces like shearing from rapid deceleration, or penetrating mechanisms like gunshot or stab wounds. The liver, spleen, and intestine are the most commonly injured organs, as well as major abdominal vasculature for penetrating injuries.  

Although the majority of blunt and penetrating abdominal injuries can be managed non-surgically, it is important to quickly identify life-threatening injuries like intraabdominal hemorrhage, retroperitoneal hemorrhage, intraabdominal visceral organ injury, unstable pelvic fracture, and diaphragmatic injury or rupture, to provide timely operative intervention.  

Alright, when evaluating a patient with a blunt or penetrating abdominal injury, start with the primary survey by assessing their ABCDE.First, secure the Airway with a low threshold for endotracheal intubation or surgical airway. Stabilize the cervical spine during intubation, and place a C-collar until c-spine injury has been ruled out.  

Next, ensure adequate Breathing or ventilation. Then, assess Circulation and obtain 2 large bore IVs or intraosseous access while continuously monitoring vitals. Consider starting resuscitative measures with IV fluids or transfusions if vitals are unstable.  

Next assess Disability by evaluating the patient’s Glasgow Coma Scale and perform a pupillary reflex exam. Make sure to immobilize the spine until spine injuries have been ruled out. Finally, expose the patient by removing all clothing and bandages to assess for additional injuries. Don’t forget to cover the patient with warm blankets to prevent hypothermia. 

Okay, now that you’ve finished your primary survey, lets begin by looking at unstable patients. If your patient is unstable with a penetrating abdominal injury, get them quickly to the OR because they need urgent surgical management. As for unstable patients with blunt abdominal injury, your next step is to perform the secondary survey including adjunctive test]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_blunt_cerebrovascular_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bOpaQ7AqS5u65ui7HN7ZZYNrRAuBLpqQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to blunt cerebrovascular injury: Clinical sciences]]></video:title><video:description><![CDATA[Blunt cerebrovascular injury, or BCVI for short, refers to the damage of the carotid or vertebral artery following blunt neck trauma. These injuries are often caused by motor vehicle collision, fall, strangulation, or even assault like a direct blow to the neck. BCVI is divided into 5 grades based on the luminal narrowing of the vessels. Regardless of the grade,  

BCVI has the potential for thrombus formation, vascular occlusion, or vascular wall hematomas which can lead to serious complications like a stroke.  

Alright, when evaluating a patient who presents with a chief concern suggestive of a blunt cerebrovascular injury, your first step is to perform a primary survey by assessing their ABCDE.Because BCVI can have associated neck injuries that can compromise the airway, it&amp;#39;s important to secure the airway as soon as possible. Always have a low threshold for endotracheal intubation, or even surgical airway like a cricothyroidotomy if you are unable to intubate. While securing the airway, make sure to stabilize the cervical spine to prevent further injury. Once the airway is secured, ensure adequate ventilation and provide supplemental oxygen, if needed.  

Next, obtain two large bore IVs or an intraosseous line if intravenous access cannot be obtained. Continuously monitor vitals and start appropriate resuscitative measures.  

Then, assess for disability by performing a neurological assessment and calculating the Glasgow Coma Scale. Also, perform a pupillary exam looking for unequal or delayed pupillary reflex. Make sure to lay the patient supine on a flat board for spine immobilization. Finally, expose the patient by removing all clothing and bandages to ensure no injuries are missed. Just like with any trauma patient, after the exam, place a warm blanket over them to avoid hypothermia.  

Now that the primary survey is complete, let’s talk about unstable patients that have obvious signs of neurologic deficits.  

In this case, proceed with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brain_death:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0wUtyd4bTtic8AiCSId22wwZQhSErnoQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brain death: Clinical sciences]]></video:title><video:description><![CDATA[Brain death is defined as the irreversible loss of all brain functions that results in permanent loss of consciousness, brainstem reflexes, and spontaneous respirations. Important causes of brain death include trauma, stroke, hypoxic-ischemic injury, mass lesions, infections, and toxic or metabolic disorders. As with death by cardiopulmonary criteria, declaring brain death means declaring the death of the patient.   

Now, if your patient presents with coma, which could be a sign of brain death, first, perform an ABCDE assessment. You should always consider these patients unstable, so begin acute management immediately! Stabilize the airway, breathing, and circulation. This means that you will need to intubate the patient and place them on mechanical ventilation. Next, obtain IV access, and begin continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry. 

Once you stabilize the patient, obtain a focused history and physical examination as well as labs, including a complete metabolic panel, toxicology screen, and alcohol level. Also, don’t forget to order an MRI or CT of the brain. 

History will reveal a recent loss of consciousness, often in combination with an event that led to a catastrophic brain injury, such as head trauma and stroke, as well as drowning, choking, or cardiac arrest which can result in hypoxia and anoxia.  

Additionally, there might be a recent brain infection or toxin ingestion. Brain death might also occur as a result of renal or hepatic failure, which can lead to severe metabolic derangements and subsequent cerebral edema.  

On physical examination, your patient will have an altered mental status, meaning they will be unconscious and unresponsive to visual, auditory, and tactile stimuli. They will not have cerebrally-mediated motor responses, like eye-opening or localizing to painful stimuli, such as nail bed pressure or sternal rub.  

Additionally, brainstem reflexe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spinal_fractures:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_kplQ0N0TmSPTHgcL2QIuu8dTYGPTw0z/_.png</video:thumbnail_loc><video:title><![CDATA[Spinal fractures: Clinical sciences]]></video:title><video:description><![CDATA[Spinal fractures refer to breakage of the spinal vertebrae in the cervical, thoracic, or lumbar spinal columns.  

These fractures can occur from traumatic injuries such as blunt trauma like falls or sports injury, or rapid deceleration from motor vehicle collisions. Sometimes, spinal fractures can be pathologic stemming from underlying conditions like osteoporosis or metastatic cancer.  

Regardless of the cause, these fractures can cause neurological impairment, so timely diagnosis and treatment are important in preventing spinal cord injuries. 

Alright, your first step when evaluating a patient with chief concern suggestive of a spinal fracture is to perform a primary survey by assessing their ABCDE.  

Start by securing the airway as soon as possible. The big concern here is the injury of the phrenic nerve, which originates at C3 through C5 spinal nerve roots. Any injury at this level or above prevents breathing due to diaphragm paralysis. For these reasons assume all trauma patients have a c-spine injury. Stabilize the cervical spine in a neutral position during intubation.  

This means you can&amp;#39;t do a head tilt to intubate like you normally would. Use a jaw thrust instead! Keep in mind that patients with phrenic nerve injury might need a surgical airway like tracheostomy and mechanical ventilation.  

Once the airway is secured and c-spine is stabilized, ensure adequate ventilation by providing supplemental oxygen.  

Next, obtain two large bore IVs or an intraosseous line if intravenous access cannot be obtained. Continuously monitor vitals while starting appropriate resuscitative measures including blood transfusions.  

Then, assess for disability by performing a neurological assessment and calculating the Glasgow Coma Scale. Ensure spine immobilization at all times by securing the patient in a supine position on the spine board.  

Make sure to assess for sensory or motor deficits in anyone with a suspected spine injury.  

Finally, exp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_extremity_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xPcrK-l3Q-GsDBZHcsFOzuF6QmCpojLu/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to extremity injury: Clinical sciences]]></video:title><video:description><![CDATA[Extremity injury is often caused by blunt trauma, including falls, crush injuries, and high-speed motor vehicle crashes. It can also result from penetrating trauma, such as gunshot or stab wounds.  

While many of these injuries are treated nonoperatively, some can be life- or limb-threatening and are considered surgical emergencies. 

When evaluating a patient with extremity injury, start with a primary survey by assessing their ABCDE.  

First, secure the Airway by endotracheal intubation if necessary and keep the cervical spine immobilized with a c-collar.  

Then comes Breathing, so ensure adequate ventilation and provide supplemental oxygen.  

Next is Circulation, so obtain two large bore IVs, making sure to avoid placing the IV on the injured limb. If you’re unable to obtain IV access, obtain intraosseous access instead.  

Continuously monitor patient’s vitals while starting appropriate resuscitative measures including crystalloid bolus and sometimes blood product transfusions.  

Then, assess for Disability by evaluating the patient’s neurologic status using the Glasgow Coma Scale. Also, quickly check for spinal cord injury by asking your patient if they can feel or move all four extremities.  

Finally, Expose the patient by removing all clothing and bandages to ensure no injuries are missed. After examining the patient, place a warm blanket over them to avoid hypothermia.  

Okay, if your patient is unstable, move on to a secondary survey.  

This includes history and a detailed head-to-toe physical exam to assess for life- or limb-threatening injuries.   

Keep in mind, limb-threatening injuries that are left untreated can quickly become life-threatening by hemorrhagic shock or sepsis. 

Here’s a clinical pearl! In trauma, the visible injury might not be the cause of instability, so always be sure to assess for internal injuries as well.  

Alright, let’s dive into our first case, traumatic amputation or mangled extremity. History typically rev]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_ankle_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lf4ebqPSRfWq7VJUVz_LC44bTQOH2Suo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to ankle pain: Clinical sciences]]></video:title><video:description><![CDATA[Ankle pain is a common symptom that can have many underlying causes, including conditions affecting the joints, bones, tendons, or skin. It’s important to first identify if your patient’s ankle pain is due to trauma or infection. Other possible types of ankle pain include neuropathic pain due to nerve damage, and nociceptive pain due to arthralgia, ostalgia, tendinopathy, and dermatologic ulcers. 

When a patient presents with ankle pain, first obtain a focused history and physical exam. History typically reveals ankle pain, while the exam might demonstrate ankle edema, erythema, or warmth. They may also have ankle tenderness, effusion, limited joint range of motion, crepitus, or even an obvious joint deformity.  

Your next step is to assess for trauma. This includes an obvious mechanism of injury, such as a motor vehicle collision or sports injury, or if there’s a joint deformity or ligamentous laxity.  

If trauma is present, assess the Ottawa ankle rules, which can tell you if imaging is needed or not.  

First, check to see if the patient has pain in either the malleolar or midfoot zones. Next, palpate for bony tenderness in the affected limb along the distal fibula, distal tibia, base of the 5th metatarsal, and the navicular bone. Third, determine if your patient was unable to bear weight on the affected foot immediately after their injury AND is unable to bear weight for at least four steps at the time of initial medical evaluation. 

If the patient has pain in either the malleolar or midfoot zones and at least one of the other two criteria, meaning bony tenderness or inability to bear weight they meet the Ottawa rules criteria. In this case, order an ankle x-ray. If it shows a fracture of one or more ankle bones, diagnose an ankle fracture.  

On the other hand, if the Ottowa rules criteria are not met, the likelihood of fracture is low, so an X-ray is not indicated. At this point, diagnose an ankle sprain or strain. 

Here’s a clinical pearl! Ankl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hip_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LJhULcJMRFqoNE5PWRCWKqT2R7KNViha/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to hip pain: Clinical sciences]]></video:title><video:description><![CDATA[Hip pain is a common presentation in the primary care setting. It’s important to first identify if your patient’s hip pain is due to trauma or infection. Other possible types of hip pain are assessed based on anatomic location and include either anterior, lateral, or posterior hip pain.  

If your patient presents with hip pain, start with a focused history and physical examination. Patients report pain in the hip, while the exam might reveal edema, erythema, warmth, hip tenderness, gait abnormalities, and limited joint range of motion. 

Your next step is to assess for trauma. This includes an obvious mechanism of injury, like a motor vehicle collision or sports injury, or if there’s a joint deformity or ligamentous laxity.  

If trauma is present, think fracture, dislocation, or labral tear. Patients with fractures or dislocations are likely older and may have osteoporosis. Physical exam reveals an inability to walk on the affected limb and a shortened externally rotated abducted leg. With these findings, consider fracture or dislocation and obtain a hip x-ray. If it shows a fracture or dislocation, that’s your diagnosis. 

Now, patients with labral tears are typically young athletic adults with abrupt onset of pain that might be from a sports injury or repetitive motion. They may also report a popping, catching, or clicking sound.  

Exam typically reveals a positive FADIR test which is when you reproduce pain in the groin when performing flexion, adduction, and internal rotation of the hip. They might also have a positive FABER test which is when you elicit hip pain with hip flexion, abduction, and external rotation. With these findings, consider a labral tear and obtain a hip MRI. If it shows a defect of the labrum, diagnose a labral tear. 

On the other hand, if trauma is not present, assess for signs of infection like fever, chills, myalgias, and localized tenderness. If signs of infections are present, your patient may report difficulty moving]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_acute_abdominal_pain_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GU8FFq2NQK6dP7hUKsoKCGtYSQeW6us1/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to acute abdominal pain (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Acute abdominal pain is a common presenting concern in pediatric patients. While severe abdominal pain combined with abdominal rigidity, rebound, or guarding suggests a condition requiring urgent surgical intervention, most underlying causes of acute abdominal pain in children are transient and non-life-threatening. Acute abdominal pain can be caused by gastrointestinal, urinary, pelvic, and neurologic or musculoskeletal conditions. 

When a pediatric patient presents with acute abdominal pain, you should first perform an ABCDE assessment to determine if they’re stable or unstable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, begin fluid resuscitation, and continuously monitor vital signs. Provide supplemental oxygen if needed, ensure that the patient does not take anything by mouth, and consider placing a nasogastric tube. Finally, obtain an emergency surgical consultation and administer broad spectrum IV antibiotics.   

Once you’ve initiated acute management, perform a focused history and physical examination. The history will reveal a sudden onset of severe abdominal pain, and the physical exam will often demonstrate abdominal tenderness, rebound, and guarding, possibly with abdominal distension and rigidity. These peritoneal signs indicate an acute “surgical” abdomen, which requires immediate surgical intervention.  

Here’s a high-yield fact! Appendicitis is the most common cause of a surgical abdomen in childhood, but other significant causes include intussusception, intestinal malrotation with volvulus, and incarcerated inguinal hernia. Remember that blunt abdominal injury and nonaccidental trauma can cause intraperitoneal bleeding and visceral damage, both of which can present with acute abdominal pain in the absence of obvious external signs. 

Now that we’ve discussed unstable patients, let’s move on to stable ones. First, perform a focused history and physical examination. The history will reveal a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_chronic_abdominal_pain_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Edi1-ZSvRXaOY6PTC8ojnwmtTLKmedHx/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to chronic abdominal pain (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Chronic abdominal pain is defined as constant, intermittent, or recurrent abdominal pain that’s present for at least two months. Associated symptoms to consider during an evaluation of chronic abdominal pain include growth and weight gain, changes in bowel habits, as well as the timing, pattern, and nature of the pain.  

Underlying causes of chronic abdominal pain can be categorized as organic disorders, which have an anatomic, histologic, or physiologic etiology; and functional disorders, which do not have a clear organic cause.  

When a pediatric patient presents with chronic abdominal pain, your first step is to perform an ABCDE assessment to determine if they’re stable or unstable. If unstable, stabilize their airway, breathing, and circulation; obtain IV or IO access; and administer intravenous fluids or packed red blood cells if indicated. Finally, implement continuous vital sign monitoring, including heart rate, respiratory rate, blood pressure, and pulse oximetry; and provide supplemental oxygen if needed.  

Okay, let’s return to the ABCDE assessment and discuss stable patients. First, perform a focused history and physical examination. Your patient will report constant, intermittent, or recurrent abdominal pain, occasionally with symptoms like nausea, vomiting, diarrhea, or fever. The physical examination might reveal abdominal tenderness or distension. To evaluate further, assess your patient’s growth curve. 

If your patient has had poor linear growth or suboptimal weight gain, your next step is to assess for bloody stools. The presence of blood in the stool should make you consider inflammatory bowel disease. These patients often report diffuse, crampy, periumbilical pain and fecal urgency. Some patients might have extraintestinal manifestations, like joint pain and swelling; eye redness or pain; and skin nodules or ulcers. There may also be a family history of inflammatory bowel disease.  

The physical exam usually demonstrates abdomi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_the_acute_abdomen_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sB0Fmr3DT6KWVtA_YZMltFSJRv2ZmMl3/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to the acute abdomen (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Acute abdomen refers to sudden, severe abdominal pain characterized by extreme abdominal tenderness, rebound, or guarding. These signs suggest the presence of peritoneal inflammation or peritonitis, and an underlying cause that requires urgent surgical intervention.  

Evaluation of a child with an acute abdomen depends on their age, the presence of an inguinal mass or bilious emesis, and the location of maximum abdominal tenderness.   

Here’s a high yield fact! The acute abdomen is often referred to as a “surgical abdomen,” but some non-surgical conditions can mimic peritoneal signs. Examples include acute bacterial peritonitis, diabetic ketoacidosis, pancreatitis, sickle cell crisis, familial Mediterranean fever, and lead poisoning.  

When a pediatric patient presents with a chief concern suggesting an acute abdomen, your first step is to perform an ABCDE assessment to determine if the patient is stable or unstable. Most patients with an acute abdomen are unstable, so be sure to stabilize their airway, breathing and circulation. Obtain IV access and start fluid resuscitation; continuous vital sign monitoring; and provide supplemental oxygen if needed.  Additionally, make your patient NPO in anticipation of surgical intervention, and consider placing a nasogastric tube. Finally, obtain an emergent surgical consultation and start broad spectrum IV antibiotics.  

Now that you’ve stabilized your patient, perform a focused history and physical examination. Patients typically describe severe, acute abdominal pain with a sudden onset. If the physical examination demonstrates abdominal tenderness with rebound and guarding; and possibly abdominal distension, or even a rigid abdomen; consider an acute abdomen.  

Here’s a clinical pearl! It can be tricky to interpret exam findings when a child is experiencing pain or anxiety, but certain techniques can help you obtain a more reliable exam.  

For instance, you might begin the exam by auscultating the heart and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_vomiting_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LtHDkoYmTtKAe7Nhm0COKaqIQKCJy0k0/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to vomiting (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Vomiting refers to the forceful expulsion of the stomach contents that is usually related to gastrointestinal illness, but it can also be a manifestation of other systemic conditions. Vomiting can be acute, occurring over hours to days; chronic, persisting for days to weeks; or episodic, which is characterized by a pattern of acute episodes separated by asymptomatic periods. 

When a pediatric patient presents with vomiting, first, perform an ABCDE assessment to determine if they are stable or unstable.  

If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and begin IV fluids. You might also need to keep your patient NPO and insert a nasogastric tube. Finally, if needed, put your patient on continuous vital sign monitoring and provide supplemental oxygen and antibiotics. 

Next, perform a focused history and physical examination and assess for signs and symptoms suggesting diabetic ketoacidosis, or DKA. These include polydipsia, polyuria, polyphagia; weight loss; fruity breath, dry mucous membranes, and Kussmaul respirations, or a rapid, deep pattern of breathing. 

If any of these signs and symptoms are present, consider DKA, and order labs,  

including a basic metabolic panel, venous blood gas, urine dipstick, and a serum beta-hydroxybutyrate.  

If the blood glucose is greater than 200 mg/dl, pH is less than 7.3 or bicarbonate levels are less than 15 mEq/L, the urine ketones are positive, and beta-hydroxybutyrate is 3 mmol/L or higher, diagnose DKA. 

On the other hand, if signs or symptoms of DKA are absent, consider acute “surgical” abdomen.  

These include a sudden onset of severe, acute abdominal pain with abdominal tenderness, rebound, and guarding. Also, you might notice a rigid abdomen. These findings suggest peritoneal inflammation and indicate an acute, or “surgical” abdomen. 

This commonly occurs as a result of appendicitis, but also intussusception and incarcerated hernia. 

Okay, now let’s return to the ABCDE]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_gastroenteritis_(acute)_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QOyvPU1yRgSJcrRFTTF3QG_dTo6-sTEP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious gastroenteritis (acute) (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Acute infectious gastroenteritis refers to an infection of the stomach and intestines that has a rapid onset and lasts 2 weeks or less. Gastrointestinal infections typically present with vomiting and diarrhea after fecal-oral contact or ingestion of contaminated food or water. Most cases of acute infectious gastroenteritis are caused by either viral or bacterial pathogens. 

Now, if a pediatric patient presents with a chief concern suggesting acute infectious gastroenteritis, first perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Obtain IV access, start IV fluids, and consider administering a fluid bolus. Next, begin continuous vital sign monitoring, including heart rate, respiratory rate, blood pressure, and pulse oximetry; provide supplemental oxygen if needed; and consider starting antibiotics. 

Now that we’ve discussed unstable patients, let’s return to the ABCDE assessment and take a look at stable patients.  

Start by obtaining a focused history and physical examination. 

History typically includes the acute onset of diarrhea, vomiting, anorexia, and abdominal cramps lasting 2 weeks or less. Some patients also report a fever or a sick contact.  

Physical exam may demonstrate abdominal tenderness and hyperactive bowel sounds, but in more severe cases, you might see signs of dehydration, like decreased skin turgor, sunken eyes, and dry mucous membranes.  

These findings are highly suggestive of acute infectious gastroenteritis. 

Next, assess whether there are indications for obtaining a stool culture. These include outbreaks in a childcare setting or school; exposure to animals or contaminated food; blood or mucus in the stool; or recent foreign travel. Additionally, any young or immunocompromised patient with a high fever should have stool sent for culture. 

Now, if there’s no indication for a stool culture, you should suspect viral gastroenteritis, whic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_gastroenteritis_(subacute)_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4NDtFaULTR6KsHTN3H86MeqjTziCHi6M/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious gastroenteritis (subacute) (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Subacute infectious gastroenteritis refers to an infection of the stomach and intestines that lasts longer than 2 weeks. Gastrointestinal infections typically present with diarrhea after fecal-oral contact or ingestion of contaminated food or water. Most cases of subacute infectious gastroenteritis are caused by either bacteria or parasites. 

Now, if a pediatric patient presents with a chief concern suggesting subacute infectious gastroenteritis, first perform an ABCDE assessment to determine if they’re unstable or stable. 

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, start IV fluids, and put your patient on continuous vital sign monitoring. Finally, provide supplemental oxygen if needed, and consider starting antibiotics. 

Now, let’s return to the ABCDE assessment and take a look at stable patients. Start by obtaining a focused history and physical examination. 

History will reveal more than 14 days of diarrhea, possibly in combination with fever, malaise, anorexia, vomiting, and abdominal cramps. The patient might also report a known sick contact or recent travel, and some patients may report weight loss. Finally, the exam may reveal abdominal tenderness. This clinical picture is highly suggestive of subacute infectious gastroenteritis. 

To look for the causative pathogen, collect a stool sample and order labs. Depending on the suspected pathogen, you may want to order a stool culture to identify bacterial pathogens; and a stool glutamate dehydrogenase, C. diff toxins A and B, and an nucleic acid amplification test, or NAAT, to look for Clostridioides difficile or C. diff. Additionally, send stool ova and parasites, Giardia and Cryptosporidium antigens, and a Cyclospora examination, to look for parasitic pathogens. First, let’s take a look at findings you’d expect to see in bacterial infection.  

In this case, the stool culture might be positive; or C. diff tests like the stool glutamate dehydrogenase ant]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_traumatic_brain_injury_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DYfVbiYZQiyGsDKcL84iEeFFRtaskoVm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to traumatic brain injury (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Traumatic brain injury, or TBI, refers to brain damage that results from an external mechanism, like a fall, motor vehicle accident, or non-accidental trauma. When a patient presents with traumatic brain injury, it is important to stabilize them urgently, assess the severity of the injury, and determine the need for imaging.  

Now, if a pediatric patient presents with a traumatic brain injury, perform a primary survey by assessing their ABCDE. Then, stabilize the airway, breathing, and circulation; and immobilize the neck and spine. Obtain IV or intraosseous access, start IV fluids, continuously monitor vital signs, and provide supplemental oxygen, if needed.  

It’s important to evaluate patients with TBI using the Glasgow Coma Scale, or GCS. This scale assesses the patient’s eye opening in addition to their motor and verbal responses, to determine their level of consciousness. The GCS provides an objective measurement to assess the degree of brain injury. For preverbal children, usually those under two years of age, a modified Pediatric GCS can be used instead. 

Here’s your first clinical pearl! Any patient with a TBI can develop increased intracranial pressure, or ICP, as a result of expanding intracranial hemorrhage or cerebral edema. If it’s not recognized and treated promptly, increasing ICP can lead to brain herniation, which can further cause long-term neurologic sequelae and death.  

Now, as ICP increases, it can lead to uncal herniation which can compress the oculomotor nerve. This impairs the parasympathetic function, leading to pupil dilation on the ipsilateral side. Other clinical signs of brain herniation include focal neurologic deficits and abnormal posturing. Finally, be on the lookout for Cushing triad, which consists of bradycardia; widened pulse pressure, which means there is a large difference between systolic and diastolic blood pressure; and irregular respirations known as Cheyne-Stokes breathing.  

Okay, let’s go back to GCS. If]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Brief,_resolved,_unexplained_event_(BRUE):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/njIdNN8lTVybvkBjy3Klb00KRve2Hixb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Brief, resolved, unexplained event (BRUE): Clinical sciences]]></video:title><video:description><![CDATA[Brief Resolved Unexplained Events, or BRUEs, are witnessed episodes during infancy, lasting less than one minute, that are characterized by cyanosis or pallor; absent, decreased, or irregular breathing; a marked change in muscle tone; or altered responsiveness; followed by a return to the infant’s baseline state of health.BRUE is diagnosed when no underlying cause for these symptoms can be identified after a thorough history and physical examination. Based on historical features and exam findings, infants who meet the criteria for BRUE can be classified into higher or lower-risk categories. 

When a pediatric patient presents with a chief concern suggesting BRUE you should start by obtaining a focused history and physical exam.  

These patients are under 1 year of age, and caregivers typically describe a witnessed episode lasting less than 1 minute, during which the infant’s skin appeared blue, dusky, or pale for no clear reason. They may also report that the infant had an irregular or shallow pattern of breathing during this episode, or that they stopped breathing altogether. Caregivers might also describe the infant’s tone as stiff or floppy, or report that the child was less responsive and excessively sleepy. Further history usually reveals no obvious symptoms suggesting an identifiable precipitant or an acute illness. As far as the exam goes, your patient will be well-appearing and afebrile, with normal vital signs. 

Keep in mind that, by definition, patients with BRUE present after the resolution of the episode and have returned to their baseline level of functioning, so an unstable child will not have the diagnosis of BRUE. 

Based on these findings, you should suspect a BRUE.  Next, you’ll need to assess the event criteria to determine if the event was really a BRUE. The criteria include one or more of the following: cyanosis or pallor; absent, decreased, or irregular breathing; a marked change in muscle tone; and altered responsiveness. Additiona]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_bacterial_causes_of_fever_and_rash_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uM44J7n7TZmEtZqfj2e-1UsMQLCIgY3_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to bacterial causes of fever and rash (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Fever and rash are common manifestations of bacterial infections in children. These infections are caused by a wide range of bacteria and can be either localized and mild or systemic and life-threatening. Underlying causes can be categorized on the basis of rash morphology. 

If a pediatric patient presents with a chief concern suggesting a bacterial cause of fever and rash, first perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, give IV fluids, and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. If needed, provide supplemental oxygen, and consider starting antibiotics.  

Now, here’s a clinical pearl to keep in mind! The combination of fever and palpable purpura in an unstable patient should raise concern for meningococcemia, which is caused by Neisseria meningitidis. On the other hand, fever with a generalized, sunburn-like rash can indicate toxic shock syndrome, which is typically caused by Staphylococcus aureus or Streptococcus pyogenes and is often associated with tampon use. In both cases, it’s important to respond quickly and initiate empiric antibiotics, because your patient can quickly progress to shock. 

Now that we’ve covered unstable patients, let’s go back to the ABCDE assessment and discuss stable patients. In this case, obtain a focused history and physical examination. History may reveal a sick contact or recent travel, while exam findings will include elevated temperature and a rash. To begin your evaluation, assess the rash morphology.  

Let’s start with maculopapular and macular rashes, which might appear as annular, ring-shaped lesions, or distinct spots. 

The presence of annular lesions should make you think of erythema multiforme major and Lyme disease.  

First let’s discuss erythema multiforme major, or EM major. Patients may report headache, malaise,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sepsis_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UNVC6lvZRUCrjBuNA33ns-RVSbeLmobN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sepsis (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Sepsis is a dysregulated immune response to infection, involving not only the initial location of the infection but other areas of the body not even near it. Sepsis is frequently associated with organ dysfunction, shock, and death. The infection can be bacterial, viral, or fungal, and may originate from any tissue, initiating a complex interplay between infectious virulence factors and host defense mechanisms. The main goals of management are to identify and treat the infection while maintaining hemodynamic stability to prevent or minimize organ damage.  

When evaluating a pediatric patient with a chief concern suggesting sepsis, your first step is to perform an ABCDE assessment.  These patients are generally unstable, so you’ll need to stabilize the patient’s airway, breathing, and circulation; and consider intubating your patient. Next, IV access should be established as soon as possible. Even though most patients require a central line, management should not be delayed for it. Alternatively, you might need to establish intraosseous  or IO access. Also, begin continuous vital sign monitoring, and provide supplemental oxygen, if needed. Finally, monitor your patient’s urine output. 

Next, obtain a focused history and physical exam, and order labs, including CBC, CMP, procalcitonin, or PCT, and a serum lactate level, as well as blood cultures. Keep in mind that obtaining labs should not delay care. 

Now, pediatric patients with sepsis often have vague symptoms, like irritability and poor feeding. On physical exam, they may have altered mental status or AMS and appear toxic or lethargic. They are often febrile or hypothermic. Patients commonly exhibit tachycardia, bradycardia, or hypotension; and occasionally, tachypnea and respiratory distress. With these findings, suspect sepsis, which is a clinical emergency.  

Urgently obtain additional labs and imaging to look for evidence of infection. The labs you choose will depend on clues from history and exam]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Staphylococcal_scalded_skin_syndrome_and_impetigo:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wXgrezneTQqyp9m9_w8mSs8USzqi5mAv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Staphylococcal scalded skin syndrome and impetigo: Clinical sciences]]></video:title><video:description><![CDATA[Staphylococcal scalded skin syndrome and impetigo are common pediatric skin infections that are most often caused by Staphylococcus aureus. While impetigo usually results from direct bacterial invasion of the skin or minor skin trauma, staphylococcal scalded skin syndrome is caused by hematogenous spread of Staphylococcal exotoxins from colonized areas to distal sites. Exam findings can be used to distinguish mild Staph infections such as impetigo from more severe infections like staphylococcal scalded skin syndrome. 

Now, if a pediatric patient presents with a chief concern suggesting staphylococcal scalded skin syndrome or impetigo, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and administer IV fluids. Put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. If needed, provide supplemental oxygen. Also remember to start antibiotics if you suspect your patient is septic! 

Now that we’ve discussed unstable patients, let’s go back to the ABCDE assessment and look at stable ones. First, obtain a focused history and physical examination. The history will reveal a rash, possibly in combination with fever. As far as the exam goes, you’ll notice skin lesions that  appear as vesicular or bullous. 

At this point, you should distinguish impetigo from staphylococcal scalded skin syndrome by assessing the presence of a Nikolsky sign, meaning that applying lateral pressure to the bullae or vesicle causes the upper skin layer to pull away from the underlying layers to reveal a raw, red base. 

If the Nikolsky sign is negative, suspect impetigo. This is a common, superficial bacterial infection that’s highly contagious. Impetigo can be either nonbullous or bullous, and history and exam findings can differentiate the two. 

Let’s start with nonbullous impetigo. The history usually reveals an in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Foreign_body_aspiration_and_ingestion_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ISPAwGmXRtO3XFoiNBiVf6ffRzOJjtOT/_.png</video:thumbnail_loc><video:title><![CDATA[Foreign body aspiration and ingestion (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Foreign body aspiration refers to the inhalation of an object, while foreign body ingestion refers to the swallowing of an object.  

Most cases require timely evaluation and treatment to prevent serious complications, like airway obstruction or gastrointestinal tract perforation.  

If a pediatric patient presents with a chief concern suggesting foreign body aspiration or ingestion, start with an ABCDE assessment to determine if they are stable or unstable. If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring. Finally, provide supplemental oxygen if needed. 

After starting acute management, obtain a focused history and physical examination to identify potential complications, like airway obstruction or gastrointestinal perforation. 

Patients may report a witnessed foreign body aspiration with acute onset of symptoms, like the inability to speak or cough, as well as gasping or blood in the sputum.  

The physical exam might demonstrate signs of respiratory distress, like tachypnea, nasal flaring, and retractions.  

These findings should immediately make you suspect an airway obstruction, so act quickly.  

Perform rapid sequence intubation and an emergent rigid bronchoscopy to remove the foreign body. In cases where a bronchoscopy is not immediately accessible, consider cricothyroidotomy. 

Here’s a clinical pearl! If a patient aspirates outside of a hospital setting, perform back blows and chest thrusts on an infant; or the Heimlich maneuver in an older child.  

However, if the patient is able to speak or cough, then do not perform these maneuvers since they may convert a partial obstruction to a complete one. 

Now let’s talk about different findings. Patients might report a known or suspected ingestion, typically of a sharp or magnetic object, or a button battery.  

They could also report symptoms like dysphagia; blood in the saliva; and neck, c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_common_musculoskeletal_injuries_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MIIgt4VHSYSM5r1MF8JvqBz1SS6Thzrg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to common musculoskeletal injuries (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Pediatric musculoskeletal injuries refer to various conditions affecting bones, joints, connective tissue, and muscles. While most childhood musculoskeletal injuries are related to low-energy trauma like falls or sports, severe injuries can result from high-energy trauma like motor vehicle accidents.  

Common pediatric musculoskeletal injuries include fractures, sprains, joint separation or subluxation, and overuse injuries. 

Now, if a pediatric patient presents with chief concerns suggesting a musculoskeletal injury, perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. 

Now, here’s a clinical pearl to keep in mind! Pelvic, hip, and proximal femur fractures can result in significant hemorrhage requiring urgent surgical intervention. Other orthopedic emergencies include open fractures and injuries associated with nerve or vascular damage. 

Now, let’s take a look at stable ones. First, perform a focused history and physical examination. Patients typically describe localized pain with a distinct mechanism of injury. During the exam, you can often locate a point of maximum tenderness, and you may notice deformity, swelling, ecchymosis, or decreased range of motion.  

With these findings, consider musculoskeletal injury, so be sure to assess the type and mechanism of the injury. 

Let’s first look at acute trauma. If your patient reports acute trauma with a clear mechanism of injury, assess for focal bony tenderness. If present, consider the possibility of a fracture. These patients will describe localized pain and may report a pop or snap at the time of injury. If the injury involves a lower extremity, your patient might be unable to bear weight.  

The physical exam will demonstrate maximum tenderness at the injury site, often in com]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Non-accidental_trauma_and_neglect_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/X73L0z5gTBizHr2lV6bZOww1SJuUGnEZ/_.png</video:thumbnail_loc><video:title><![CDATA[Non-accidental trauma and neglect (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Non-accidental trauma refers to any intentional act by a caregiver that causes physical or psychological harm, while neglect refers to inadequate provision of a child’s basic needs, which causes or could potentially cause harm. Non-accidental trauma, which is also called child maltreatment or child abuse, can be sub-categorized as neglect, physical abuse, sexual abuse, psychological abuse, or medical abuse.  

When a pediatric patient presents with a chief concern suggesting non-accidental trauma or neglect, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, consider IV fluids, and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, provide supplemental oxygen, if needed. 

Here’s a clinical pearl to keep in mind! Abusive head trauma, previously known as “shaken baby syndrome” occurs in children under the age of 2 through blunt force, trauma, shaking, or a combination of these. It can manifest with vomiting, seizures, or coma due to intracranial hemorrhage and brain swelling. This condition might be misdiagnosed or missed but early identification of this type of abuse can be life-saving. 

Okay, let’s go back to the ABCDE assessment and look at stable patients. First, obtain a focused history and physical exam, making sure to interview caregivers and children separately when possible. Children often don’t volunteer information about maltreatment, so look for behavioral changes, like social withdrawal or acting out. In the case of injury, there may have been a delay in seeking care; or the reported history might not explain the injury. Meanwhile, physical exam findings are often unremarkable, but some patients demonstrate poor growth or evidence of a physical injury. With these findings, suspect non-accidental trauma or neglect; and assess the subtype. 

Let’s start with phy]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hematochezia_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Gg8o-zviQq2gVcofP19F9TK9Q0_ExjiZ/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to hematochezia (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Hematochezia refers to the passage of bright red blood per rectum. The presence of hematochezia suggests a source of bleeding distal to the ligament of Treitz, in the small bowel or colon.  

Hematochezia can be an incidental finding and asymptomatic if blood loss is minor or occult; however, patients with brisk or heavy bleeding can develop anemia or even hemorrhagic shock.  

If a pediatric patient presents with hematochezia, you should first perform an ABCDE assessment to determine if they are stable or unstable.  

If unstable, stabilize the airway, breathing, and circulation. Next, obtain intravenous or intraosseous access, and consider administering IV fluids and a transfusion of packed red blood cells. Finally, remember to place your patient on continuous vital sign monitoring and provide supplemental oxygen if needed.  

Here’s a clinical pearl! Patients with brisk gastrointestinal bleeding can decompensate quickly, so monitor your patient closely for signs of hemorrhagic shock, like tachypnea, tachycardia, and hypotension.  

Remember to also consider the possibility of an upper gastrointestinal source of bleeding for any patient with hematochezia and rapid blood loss. 

Alright, let’s go back to the ABCDE assessment and look at stable patients.  First, perform a focused history and physical examination and obtain a fecal occult blood test.  

Here’s a high-yield fact! It’s important to perform fecal occult blood testing since many ingested substances can mimic hematochezia by making the stool appear red. Some common culprits include beets, blueberries, tomatoes, candy, or crayons. 

As far as the history goes, patients or their caregivers typically report seeing bright red blood in the stool. If the bleeding is chronic, the patient may report fatigue or shortness of breath. Additionally, some patients may have coexisting constipation or diarrhea.  

Physical exam might reveal abdominal distension and tenderness, as well as visible rectal ble]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_melena_and_hematemesis_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JiP8YJMmRZ6WAg74flqtwFs6QV_QzgKt/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to melena and hematemesis (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Melena refers to a dark, black, and tarry stool that contains partially digested blood, while hematemesis refers to the vomiting of blood. Patients with hematemesis might vomit bright red blood, but exposure to gastric acid can oxidize hemoglobin, causing the emesis to resemble coffee grounds.  

The presence of melena or hematemesis suggests a source of bleeding proximal to the ligament of Treitz,  in the esophagus, stomach, or duodenum.  

If a pediatric patient presents with melena or hematemesis, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV or IO access and consider administering IV fluids, as well as a transfusion of packed red blood cells.  

Patients with brisk gastrointestinal bleeding can decompensate quickly, so remember to monitor them closely for signs of hemorrhagic shock, such as tachypnea, tachycardia, and hypotension.  Place your patient on continuous vital sign monitoring, and provide supplemental oxygen if needed.  

Consider placing a nasogastric tube, with or without nasogastric lavage. Finally, consider an emergent endoscopy as a diagnostic or therapeutic intervention, as well as an infusion of a proton pump inhibitor or vasopressin. 

Alright, let’s go back to the ABCDE assessment and look at stable patients. First, perform a focused history and physical examination and obtain a fecal occult blood test.  

Patients or their caregivers usually report vomiting, with emesis containing bright red blood or debris that resembles coffee grounds. Some may describe black or tarry stools.  

Physical exam reveals no active bleeding from the oropharynx or nasal passages, but you might detect epigastric or abdominal tenderness, as well as abdominal distension. Finally, the fecal occult blood test is usually positive. 

With these findings, consider an upper gastrointestinal bleed, and perform an endoscopy within 24 to 48 hours. 

Here ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Respiratory_failure_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ewbixYp-SnC4ScPOIzjbFUG2Q9u4l200/_.jpg</video:thumbnail_loc><video:title><![CDATA[Respiratory failure (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Respiratory failure occurs when the respiratory system cannot adequately oxygenate the blood, remove carbon dioxide from the blood, or both.  

This life-threatening condition requires rapid recognition and management.  

Underlying causes of respiratory failure include pulmonary or airway disease, as well as conditions affecting the chest wall, muscles of respiration, and central or peripheral chemoreceptors.  

Respiratory failure can be categorized as hypoxemic, hypercapnic, or a combination of the two. 

Now, if a pediatric patient presents with a chief concern suggesting respiratory failure, you should first perform an ABCDE assessment.  

These patients are typically unstable, so you’ll need to immediately stabilize their airway, breathing, and circulation. Then, provide supplemental oxygen, and consider noninvasive positive pressure ventilation.  

If your patient has poor respiratory effort, you may need to perform endotracheal intubation and begin mechanical ventilation.  

Next, obtain IV access, and put your patient on continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring.  

Once you’ve provided acute management, obtain a focused history and physical exam, and order a chest X-ray and an arterial blood gas, or ABG for short.  

Verbal patients may describe shortness of breath, and their history may reveal cardiac or pulmonary disease, a neuromuscular disorder, recent illness, head trauma, or narcotic exposure.  

On exam, most patients are tachypneic, with signs indicating increased work of breathing, such as nasal flaring, head bobbing, grunting, tracheal tugging, retractions, and accessory muscle use.  

In other cases, patients may exhibit slow, shallow respirations, or even apnea. Your patient might appear somnolent or cyanotic, and pulse oximetry frequently reveals an oxygen saturation below 90 percent.  

Depending on the underlying cause, the chest X-ray might demonstrate abnormal findin]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Endometrial_intraepithelial_neoplasia_(hyperplasia)_and_carcinoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BpNh4qX2RD_B4Cvrhn_4z1QgTWSKtwf8/_.png</video:thumbnail_loc><video:title><![CDATA[Endometrial intraepithelial neoplasia (hyperplasia) and carcinoma: Clinical sciences]]></video:title><video:description><![CDATA[Endometrial intraepithelial neoplasia, or simply EIN, also known as complex atypical endometrial hyperplasia, is a precursor lesion to type I endometrial carcinoma.  

Endometrial carcinoma, or uterine cancer, is the most common genital tract malignancy with a lifetime prevalence of 2-3% in biological females. It is classified into two categories based on histology. Type I represents endometrial adenocarcinoma, while type II encompasses non-endometrioid carcinoma, including clear cell and papillary serous histologies. In general, type I accounts for the vast majority of all endometrial carcinoma cases, with most being low grade and confined to the uterus at the time of diagnosis. Type II carcinomas are considered high grade with an increased risk of extrauterine diseases and have a poorer prognosis compared to type I disease.  

When evaluating a patient with a chief concern suggesting EIN or endometrial carcinoma, your first step is to obtain a focused history and physical exam, as well as a pregnancy test with hCG if your patient is premenopausal.  

The hallmark symptom of a patient with EIN or endometrial carcinoma is abnormal uterine bleeding, or AUB, or postmenopausal bleeding. Your patient might also report less specific symptoms such as abdominal or pelvic pain and bloating. Risk factors include a history of unopposed estrogen exposure. This can be endogenous, such as from chronic anovulation in conditions like polycystic ovarian syndrome, or from conversion of androgens to estrone in adipose tissue, as seen in obesity. Unopposed estrogen exposure can also be exogenous, such as in patients using estrogen therapy without progesterone, which is not recommended in those with a uterus.  

Other risk factors include type 2 diabetes, age of 45 or greater, nulliparity, early age of menarche, late age of menopause, and a personal or family history of Lynch syndrome.  

On physical exam, you may find uterine bleeding and palpate an enlarged, globu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_acute_kidney_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1h0Ur1VBRq6rfJl6QvrwM6UDTu6JihEu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to acute kidney injury: Clinical sciences]]></video:title><video:description><![CDATA[Acute kidney injury, or AKI, refers to a sudden decline in kidney function that results in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste, such as ammonia and uric acid. 

If your patient presents with chief concerns suggesting AKI, perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, which might include dialysis access, and put your patient on continuous vital sign monitoring and cardiac telemetry!  

Finally, if you identify hyperkalemia, metabolic acidosis, volume overload, or symptomatic uremia, start emergent hemodialysis! 

Now, let’s go back to the ABCDE assessment and look at stable patients. In these individuals, obtain a focused history and physical exam, which is going to help you differentiate different types of AKI. 

First, let’s focus on prerenal AKI. 

Prerenal AKI is typically associated with reduced urine output, sometimes in combination with nonspecific symptoms, including malaise, fever, and vomiting.  

Additionally, your patient might have a history of congestive heart failure or cirrhosis, or they might report starting a new medication, such as NSAIDs.  

The physical exam might reveal signs of cardiovascular involvement, including blood pressure abnormalities, weak peripheral pulses, and tachycardia. Also, you might notice peripheral edema or signs of dehydration, like dry mucous membranes! With these findings, consider prerenal AKI.  

Next, order a basic metabolic panel or BMP and urinalysis with microscopy, measure the patient’s urine output or UOP over time, and check renal ultrasound! 

In all types of AKI, labs will reveal a rise in serum creatinine of 0.3 milligrams per deciliter or more over 48 hours; a rise of serum creatinine 1.5 times the baseline or more in the last 7 days, or urine output less than 0.5 milliliters per kilogram per hour for six hours.  

In prerenal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Benign_skin_lesions:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oBHAgw5XQe2CnqyMg7pWVqWbSMCY2RbR/_.png</video:thumbnail_loc><video:title><![CDATA[Benign skin lesions: Clinical sciences]]></video:title><video:description><![CDATA[Benign skin lesions are non-cancerous skin growths that are symmetrical in shape, color, and structure. They are typically stable with no change in appearance and no spontaneous bleeding. Benign skin lesions are classified by their cellular origin and include melanocytic, subcutaneous, keratinocytic, vascular, and fibrous. 

Here’s a clinical pearl! Benign skin lesions are often diagnosed clinically. However, dermatologists may use other methods to help diagnose skin lesions. One tool is dermoscopy, which is a skin surface microscope that helps differentiate benign lesions from dysplastic and malignant lesions. Another option is skin biopsy either with shave, scissor, curettage, punch, or scalpel excision. 

Now, if a patient presents with a chief concern suggesting a skin lesion, first obtain a focused history and physical examination. Your patient will report a growth on their skin, with no change in size, shape, or color.  Physical exam will reveal a dermatologic lesion, which is typically symmetric, with a well-defined border, consistent coloration, and a diameter less than 6 millimeters. With these findings, diagnose a benign skin lesion. 

Here’s a high-yield fact! When assessing a skin lesion, it&amp;#39;s also important to know the features of a malignant skin lesion, like melanoma. Use the acronym ABCDE to help in your assessment. This stands for asymmetry, irregular borders, varying colors, diameter usually greater than 6 millimeters, and evolving in size, shape, or color. If any of these features are present, suspect a malignant skin lesion! 

Your next step is to assess for a melanocytic lesion, most commonly a nevus!  Your patient will report a pink, tan, or brown mole that hasn’t changed in size, shape, or color. There will also be no report of bleeding. Physical exam will reveal a flesh-colored, pink, tan, or brown papule that’s dome-shaped or pedunculated with a stem. It is typically soft or rubbery in texture. With these findings, di]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_constipation_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zylbAM3_RlepbJormolnwlw-SwyRsvdw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to constipation (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Constipation refers to an abnormal stooling pattern that&amp;#39;s associated with hard stools and incomplete, infrequent, or painful defecation. The stooling pattern in healthy infants is highly variable, but when constipation occurs it suggests a pathologic condition. On the flip side, by 4 years of age, most healthy children pass one normally formed stool daily or every other day. Constipation in this age group is more likely to represent a functional gastrointestinal or GI disorder. 

Now, if a pediatric patient presents with constipation, you should first obtain a focused history and physical examination. These patients or their caregivers typically report infrequent bowel movements, straining during defecation, and hard stool consistency. Meanwhile, the physical exam may demonstrate mild abdominal distension, a palpable stool mass in the lower abdomen, or an anal fissure. These findings confirm a diagnosis of constipation. 

Now, here’s a clinical pearl! As part of your diagnostic workup, you can also perform a digital rectal exam to assess for impacted stool in the rectal vault. However, because it’s uncomfortable and invasive, many practitioners only perform this exam when alarm symptoms are present or when the diagnosis is unclear.  

Okay, now that you know your patient has constipation, your next step is to assess their age and proceed with your diagnostic workup. 

Let’s start by discussing constipation in newborns. In this age group, it’s essential to assess the timing of meconium passage. If your patient has not passed meconium within 48 hours of birth, examine your patient to assess anal patency. 

Let’s start with abnormal exam findings. If your patient has an imperforate anus, meaning you cannot identify an anal opening; or if the anal opening appears stenotic or anteriorly displaced, diagnose constipation due to an anorectal malformation. 

Time for a clinical pearl! Imperforate anus often occurs in combination with other congenital]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_cough_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MHhe7qaoTJ6-h6rGzBLbhe2pRzS_z9KB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a cough (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[A cough is a protective airway reflex that clears the airway of mucus or other irritants. This reflex is a common feature of conditions affecting the upper and lower airway, such as infection, inflammation, or airway obstruction. Depending on its duration, you can classify cough in pediatric patients as acute, chronic, or episodic.   

Now, if a pediatric patient presents with a cough, first perform an ABCDE assessment to determine if your patient is stable or unstable.  

If unstable, stabilize their airway, breathing, and circulation, and consider intubation for apnea or shallow, ineffective respirations. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, respiratory rate, and pulse oximetry. Finally, provide supplemental oxygen, if needed. 

Let’s move on to stable patients 

When it comes to stable patients, obtain a focused history and physical examination. History usually reveals a cough, possibly with wheezing and dyspnea. On physical exam, you might notice signs indicating increased work of breathing, like tachypnea, nasal flaring, or retractions. Additionally, you may hear wheezing, stertor, or stridor. Your next step is to assess the cough’s duration. 

First, let’s look at patients with an acute cough, meaning it started no more than 2 weeks ago.  

Here, assess the onset of the cough. If it began abruptly, consider foreign body aspiration. Caregivers may have witnessed a choking event, and physical exam could reveal localized wheezing, unilateral absence of breath sounds, and possibly stridor.  

Next, get a neck and chest X-ray, which might reveal a foreign body. However, since a lot of them are radiolucent, you should look for indirect signs like atelectasis or air trapping. If you see any of these, diagnose foreign body aspiration. 

Here’s a clinical pearl! The abrupt onset of cough, stridor, and wheezing can also be seen in anaphylaxis. You can differentiate anaphylaxis fr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Allergic_rhinitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s-pCLm_3TDekAvbn4TUgbe_iQgWCevsZ/_.png</video:thumbnail_loc><video:title><![CDATA[Allergic rhinitis: Clinical sciences]]></video:title><video:description><![CDATA[Allergic rhinitis is a hypersensitivity response of the upper respiratory tract to airborne allergens. When these allergens are inhaled, a process is initiated where immunoglobulin E causes mast cells to activate and release inflammatory mediators like histamine and leukotrienes. These inflammatory mediators then trigger an allergic response.  Based on the frequency and severity of the symptoms, allergic rhinitis is categorized as mild intermittent, severe intermittent, mild persistent, and severe persistent.  

When a patient presents with a chief concern suggesting allergic rhinitis, first perform a focused history and physical examination. Your patient will report symptoms which may include nasal congestion, runny nose, sneezing, and an itchy sensation in the nose. Patients may also have a history of atopic dermatitis or asthma.  

The physical exam will typically reveal swollen turbinates, clear nasal discharge, cobblestoning of the posterior pharynx, and postnasal drip. Your patient might also have conjunctival erythema with watery eyes. At this point, you can diagnose allergic rhinitis!  

Now, here’s a clinical pearl!  Allergic rhinitis generally presents with bilateral symptoms if you observe unilateral swelling of the nasal turbinates, nasal discharge, or ocular signs and symptoms, consider another underlying cause like a medication side effect. Some medications, such as beta-blockers and ACE inhibitors can induce nasal symptoms that mimic those of allergic rhinitis! 

Next, assess the frequency of your patient’s symptoms. If symptoms are present less than or equal to four days per week OR less than or equal to four weeks out of the year, diagnose intermittent allergic rhinitis! 

Now that you’ve diagnosed intermittent allergic rhinitis, your next step is to assess symptom severity.  If your patient reports that their symptoms do not interfere with their quality of life, like minimal work or school absences, diagnose mild intermittent allergic rhi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Perinatal_depression_and_anxiety:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N-sPfWSnTaaUKbX74NHyaspzRpaI7c_W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Perinatal depression and anxiety: Clinical sciences]]></video:title><video:description><![CDATA[Perinatal depression and anxiety are conditions that affect many pregnant and postpartum patients up to a year after childbirth. Depression can range from mild perinatal depression or “postpartum blues” to severe conditions with suicidal or infanticidal ideations, such as postpartum psychosis. Perinatal anxiety is often seen in combination with perinatal depression.  

Keep in mind that, prior to making the diagnosis of a perinatal mental health condition, it’s important to consider and evaluate other medical conditions that could cause similar symptoms. These include thyroid dysfunction, severe anemia, medication side effects, and substance use. Screening for, diagnosing, and treating perinatal anxiety and depression is essential, as they’re associated with adverse maternal and fetal outcomes.  

Your first step is to perform a safety assessment. Let’s first see what to do when there are safety concerns.  

Start by asking your patient about symptoms of depression and anxiety.You should also determine whether they have intrusive thoughts of harming themself or their baby, to the point where they’re comforted by those thoughts or feel as if acting on these thoughts will help the infant or society in general.  Additional safety concerns include a lack of insight into whether their intrusive thoughts are based on reality; and if they have auditory or visual hallucinations or other bizarre beliefs that aren’t based on reality. If you notice any of these findings, the patient is considered unsafe.This is an emergency and may indicate postpartum psychosis. 

Start with acute management right away. Be sure not to alarm your patient, but don’t leave them or their baby alone while seeking help. Admit them to the hospital and seek emergent psychiatric consultation. Continue one-on-one monitoring to reduce the risk of suicide or infanticide. 

Once you, your patient, and their baby are in a safe place, obtain a focused history and physical examination, which in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Premenstrual_syndrome_(PMS)_and_premenstrual_dysphoric_disorder_(PMDD):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hPuMgUO_TyaAxA7CtzqsP5F0QRKK9Xfl/_.png</video:thumbnail_loc><video:title><![CDATA[Premenstrual syndrome (PMS) and premenstrual dysphoric disorder (PMDD): Clinical sciences]]></video:title><video:description><![CDATA[Premenstrual syndrome, or PMS and premenstrual dysphoric disorder, or PMDD are disorders that are characterized by cyclically occurring physical and affective symptoms that impair daily functioning. PMS is associated with symptoms such as irritability, mood swings, lethargy, and bloating, that occur during the luteal phase of the menstrual cycle, and resolve during or shortly after menstruation. On the other hand, PMDD is a type of depressive disorder characterized by severe and sometimes disabling changes in affect, like mood lability, irritability, dysphoria, and anxiety, that also occurs during the luteal phase and resolves with onset of menses. While the pathophysiology is not entirely understood, it’s likely multifactorial, and could be explained by an increased sensitivity to normal fluctuations in estrogen and progesterone levels that occur during the menstrual cycle. 

Now, when a patient presents with a chief concern suggesting PMS or PMDD, your first step is to obtain a focused history and physical examination. Keep in mind that diagnosis of these premenstrual disorders is by exclusion, so before making your diagnosis, be sure to rule out other possible causes of your patient’s symptoms such as other mood disorders or medical conditions, such as thyroid disorders, anemia, depression, anxiety, and substance use. In addition, your patient should have experienced symptoms during most of their menstrual cycles over the past year, and ideally confirmed with at least two months of prospective monitoring with a symptom diary or calendar. 

Okay, let’s start with PMS. Your patient will typically report symptoms that are cyclic in nature, because they typically follow their monthly cycle that begins with the luteal phase and ends with the onset of menstruation. Symptoms are both physical and affective, and include bloating, breast tenderness, irritability, mood swings, lethargy, anxiety and tension, and feelings of rejection. With these findings, you can ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_diarrhea_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zj_krjJLRUaS0EqRh0p6KqxZT_qfmNLU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to diarrhea (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Diarrhea refers to stools that are unusually loose or frequent when compared to a patient’s normal stooling pattern. In pediatric patients, acute diarrhea is commonly caused by infection, whereas chronic diarrhea often represents a pathologic condition or a functional gastrointestinal disorder. The underlying cause of diarrhea can be determined after assessing its chronicity and associated symptoms.  

Now, if a pediatric patient presents with diarrhea, first perform an ABCDE assessment to determine if they are unstable or stable.  If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, administer IV fluids, and place your patient on continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac monitoring. Finally, if needed, don’t forget to provide supplemental oxygen. 

Alright, now let’s go back to the ABCDE assessment and look at stable patients.  First, obtain a focused history and physical examination. Patients or caregivers typically describe loose or frequent stools, while the physical exam might demonstrate abdominal tenderness, hyperactive bowel sounds, or dry mucous membranes. At this point, diagnose diarrhea and assess the duration of your patient’s symptoms. 

First, let’s focus on acute diarrhea, or diarrhea that lasts for less than two weeks.  In this case, your next step is to assess for red flag signs and symptoms, including high fever, blood or mucus in the stool, severe abdominal pain, and signs of dehydration. 

If your patient reports no red flag signs or symptoms, consider mild viral gastroenteritis, which is the most common cause of acute diarrhea in children. These patients often report a known sick contact, and symptoms including vomiting and watery stool, possibly in combination with a low-grade fever. Additionally, the exam may reveal mild abdominal tenderness and increased bowel sounds. These findings are highly suggestive of mild viral gastroenteritis, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_fever_in_the_returned_traveler:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LA-dHN5RS3aMoInM4nAmKhiWTOui5BTZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a fever in the returned traveler: Clinical sciences]]></video:title><video:description><![CDATA[Fever, defined as a body temperature of at least 100.4 degrees Fahrenheit or 38 degrees Celsius, is a common symptom that can indicate the presence of infection. When talking about patients returning from recent travel, a fever might point to an illness endemic to the area they visited or emigrated from. There are many conditions to think about here, but assessing for the presence and type of rash can help you narrow down the differential. 

When a patient presents with a fever after traveling, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, give IV fluids, and start continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. If needed, provide supplemental oxygen, and consider starting antibiotics.  

When it comes to stable patients, your next step is to obtain a focused history and physical examination. History typically reveals recent travel and fever with or without general malaise or headache. On exam, there is elevated temperature, but you might also find tachycardia and a rash. Assessing for the presence of rash is very important as it will help you narrow down potential diagnoses. If a rash is present, assess the rash morphology.  

Let’s start with macular rashes, which appear as flat discolorations on the skin. First up is African sleeping sickness, also known as African trypanosomiasis. This illness is caused by the protozoan parasite Trypanosoma brucei and transmitted via Tsetse fly. Patients report a history of recent travel from sub-Saharan Africa and getting bitten by Tsetse flies. Soon after, they develop headaches, and in some cases, mood changes, drowsiness, and even weight loss.  

As for the physical exam, it shows a painful chancre at the site of the fly bite and trypanid rash which is a transient rash on the trunk that appears as a predominantly macular rash with wheals. You might als]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mechanical_back_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3i9CZdlpSnOgS1BxRxQYbGCGQdGQ1fkc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mechanical back pain: Clinical sciences]]></video:title><video:description><![CDATA[Mechanical back pain refers to pain arising from the joints, intervertebral discs, nerves, and soft tissues of the spine. It accounts for the majority of back pain cases, with etiologies ranging from benign musculoskeletal causes to conditions associated with severe neurological deficits.  

Now, let’s take a moment to review the anatomy of the spine, starting with the vertebra itself. The anterior portion is known as the vertebral body, while the vertebral arch makes up the posterior and lateral aspects. Projections from the vertebral arch include the spinous and transverse processes as well as the articular processes that make up the facet joints. The pedicles are the bony elements connecting the body to the arch, while the lamina connects the transverse and spinous processes. This circle of bone creates the spinal foramen, and when joined together, adjacent vertebrae form the spinal canal. 

Laterally, the intervertebral neuroforamen is formed. The intervertebral disc lies between each set of adjacent vertebrae, creating the anterior intervertebral articulation, while the paired facet joints are located posteriorly. Now, several ligaments stabilize these articulations, including the ligamentum flavum, which attaches to the anterior surface of each vertebral arch. Finally, the spinal cord courses through the spinal canal and gives off spinal nerves at each intervertebral level, which exit through the neural foramen. 

Okay, if your patient presents with chief concern suggesting mechanical back pain, first perform a focused history and physical examination. Your patient will report back pain, while the physical exam might reveal tenderness to palpation of the spinal and paraspinal structures, as well as hypertonicity of surrounding musculature.  

At this point, you can diagnose mechanical back pain, so your next step is to assess your patient for red-flag signs and symptoms! These include age of onset before 20 or after 55 years of age; severe or progres]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_red_eye:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-rKknA5PSlSY5GK1HA8RtwIyQRGWgfFo/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to a red eye: Clinical sciences]]></video:title><video:description><![CDATA[A red eye is a key indication of ocular inflammation. Common causes of red eye include vision-threatening conditions such as angle-closure glaucoma, globe rupture, scleritis, uveitis, keratitis, corneal injury, and hyperacute bacterial conjunctivitis. On the other hand, benign causes of a red eye include subconjunctival hemorrhage, conjunctivitis, blepharitis, and keratoconjunctivitis sicca. 

Now, if your patient presents with a red eye, first perform a focused history and physical examination.  Your patient will report redness of one or both eyes, and the physical exam will reveal conjunctival hyperemia. At this point, diagnose ocular erythema and assess for red flags that indicate an immediate threat to vision. These include severe pain; decreased visual acuity; photophobia; pupillary changes; increased intraocular pressure, also known as IOP; anterior chamber inflammation; and corneal epithelial defects. If any of these red flags are present, assess for an emergent underlying cause.  

First up is angle-closure glaucoma!  These patients are generally 40 years of age or older and report severe eye pain, blurry vision, and headache with nausea. They may even see halos around lights or have a family history of angle-closure glaucoma! The physical exam will show a dilated unreactive pupil; a hazy cornea; and conjunctival injection, commonly referred to as blood shot eyes, which is redness due to dilation of the conjunctival blood vessels. At this point, consider angle-closure glaucoma and make an emergent referral to the ophthalmology team. A gonioscopy exam that reveals an angle between the iris and cornea of 20 degrees or less confirms the diagnosis of  angle-closure glaucoma!  

Here’s a clinical pearl! While not required for the diagnosis of angle-closure glaucoma, fundoscopy, slit lamp examination, and tonometry are also helpful tools. Both fundoscopy and slit lamp examination will show a shallow anterior chamber and an enlarged optic cup, which ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Conjunctival_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8tCybe6NR3CJgANrKDF25KcTRKW6xynA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Conjunctival disorders: Clinical sciences]]></video:title><video:description><![CDATA[Conjunctival disorders occur when the lubricating mucous membrane covering the eye becomes infected, damaged, or inflamed; and they’re the most common causes of a red eye encountered in the primary care setting. Emergent, vision-threatening conjunctival disorders include chemical injury and hyperacute bacterial conjunctivitis, while non-vision threatening conjunctival disorders include acute bacterial conjunctivitis, viral conjunctivitis, allergic conjunctivitis, and keratoconjunctivitis sicca.   

Now, if a patient presents with a chief concern suggesting a conjunctival disorder, first obtain a focused history and physical examination.  

Your patient will typically report redness of one or both eyes, while a physical exam will reveal conjunctival injection, commonly referred to as blood shot eyes, which is caused by dilation of the conjunctival blood vessels.  With these findings, diagnose a conjunctival disorder!  

Next, assess for red flags which indicate vision-threatening emergencies.  

Red flags include severe pain, decreased visual acuity, photophobia, anterior chamber inflammation, and corneal epithelial defects. If any of these red flags are present, assess for the emergent underlying cause.  

First up is chemical injury! Your patient will report a chemical or toxic exposure to something like household cleaners, for example bleach or ammonia. Other symptoms include pain and blurry vision. Your physical exam will reveal conjunctival injection, decreased visual acuity, and possibly eyelid edema. With these findings, diagnose chemical injury.  

Treat with supportive care by removing any offending agents and providing adequate ocular irrigation for at least 30 minutes to reach a neutral pH. Also be sure to use artificial tears throughout all stages of healing and combine with medical therapy such as topical antibiotics for infection prophylaxis and topical steroids to reduce inflammation. 

Here&amp;#39;s a clinical pearl! The main pitfall ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eyelid_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aMLKb22DQ1KDlkSOk0J3IoXTRI2ZaQ5V/_.png</video:thumbnail_loc><video:title><![CDATA[Eyelid disorders: Clinical sciences]]></video:title><video:description><![CDATA[Eyelid disorders can occur from inflammation, infections, or structural problems of the eyelids. While most eyelid disorders are non-emergent, you must quickly assess for orbital cellulitis which is a vision-threatening emergency. On the other hand, non-emergent eyelid disorders that do not threaten vision include preseptal cellulitis, blepharitis, hordeolum, chalazion, xanthelasma palpebrarum, blepharospasm, and ptosis. 

Now, if a patient presents with a chief concern suggesting an eyelid disorder, first obtain a focused history and physical exam. Your patient might report redness, swelling, and pain of the eyelid. On physical exam, you might find corresponding findings including erythema, edema, and tenderness to palpation.  If you see these, you’re dealing with an eyelid disorder.  

Your next step is to assess for orbital cellulitis, or postseptal orbital cellulitis. In this case, history reveals fever, a painful swollen eyelid, a bulging eye, and blurry vision. The patient might also report a preceding sinusitis or upper respiratory infection. Physical exam reveals an elevated temperature, tenderness of the periorbital region, eyelid edema, violaceous discoloration, decreased visual acuity, and possibly proptosis of the eye. 

With these findings, suspect orbital cellulitis and obtain labs, including a CBC, and cultures of both the blood and nasal passage or periorbital discharge cultures. Also, order imaging of the sinuses and orbits, either CT or MRI, to look for infection in the post septal region. Labs will reveal an elevated white blood cell count, while cultures might be positive. Imaging may show sinusitis, intracranial extension of the infection, or a retro-orbital abscess.  

With these findings, diagnose orbital cellulitis and start IV antibiotics to cover the most common causative pathogens including Streptococcus pneumoniae, Staphylococcus aureus, and Haemophilus influenzae b. You’ll need to consult the surgical team if there’s evide]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glaucoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6ZWjIHkRR4O6srMsfap9Z4-ES3izislj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glaucoma: Clinical sciences]]></video:title><video:description><![CDATA[Glaucoma is a group of ocular conditions characterized by optic neuropathy, which is usually associated with increased intraocular pressure, or IOP for short, due to impaired drainage of fluid, called the aqueous humor.  

Normally, most of the aqueous humor flows through a drainage pathway called the anterior chamber angle between the iris and the cornea. When this pathway becomes partially or completely blocked, the fluid can’t easily drain out, which increases IOP. The increased IOP causes damage to the optic nerve, resulting in progressive vision loss and potential blindness.  

Now, glaucoma is categorized as either angle-closure glaucoma, also known as closed-angle glaucoma, or open-angle glaucoma.  

If glaucoma is caused by an underlying identifiable medical condition, like injury to the eye or inflammation, it’s called secondary glaucoma; but the most common form is primary glaucoma, which can’t be attributed to any known medical condition.  

If a patient presents with a chief concern suggesting glaucoma, first obtain a focused history and physical examination. Your patient will typically report loss of peripheral vision and possibly blurred vision; while a physical exam will reveal peripheral visual field impairment, decreased visual acuity, and optic nerve edema on fundoscopy.  

If your patient presents with these findings, your next step is to assess for angle-closure glaucoma. Now, angle-closure glaucoma can be chronic, where the obstruction of aqueous humor outflow progresses slowly over time. Once the outflow is completely blocked, it’s called acute angle-closure glaucoma, which is a vision-threatening emergency! 

These patients are generally 40 years of age or older and report severe unilateral eye pain and headache with nausea. They may even see halos around lights or have a family history of angle-closure glaucoma. A physical exam will show a dilated unreactive pupil; a hazy cornea; and conjunctival injection, commonly referred to as b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_vomiting_(acute):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S1H_tPpSTfmBm1Jo2EO5DzzaQfmpLRdM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to vomiting (acute): Clinical sciences]]></video:title><video:description><![CDATA[Vomiting refers to the forceful expulsion of the stomach contents, which usually occurs after mechanical or chemical stimulation of emetic receptors in the brain. Life-threatening causes of acute vomiting lasting less than 4 weeks include surgical emergencies and medical conditions associated with an acute abdomen, severe gastrointestinal hemorrhage, or increased intracranial pressure, or ICP. Less critical causes include gastrointestinal and non-gastrointestinal intra-abdominal conditions as well as various extra-abdominal systemic and physiological conditions. 

Alright, if a patient presents with acute vomiting, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. Then, obtain IV access, start IV fluid resuscitation, and continuously monitor vital signs. If your patient is actively vomiting, keep them NPO, and consider NG tube placement to decompress the bowel and prevent aspiration. Finally, consider elevating the head of the bed. After initiating acute management, obtain a focused history and physical exam, and order labs, including a CBC, CMP, and serum lactate level.  

Let’s start by discussing surgical emergencies. Here, patients typically present with severe abdominal pain, and some may have bilious emesis or evidence of gastrointestinal bleeding, such as coffee-ground emesis, hematemesis, melena, or hematochezia. Physical exam might reveal altered mental status and signs of shock, such as tachycardia and hypotension. Patients with an acute surgical abdomen typically have severe generalized abdominal tenderness with distension, rebound, and guarding. Labs often show leukocytosis, electrolyte abnormalities, and elevated serum lactate levels. 

These findings should immediately make you consider an acute abdomen, abdominal sepsis, or gastrointestinal hemorrhage. These are surgical emergencies requiring urgent operative intervention, so promp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_vomiting_(chronic):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hx-Q13mtTdiPC9h7OEJ4DHA5Tue9vu_1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to vomiting (chronic): Clinical sciences]]></video:title><video:description><![CDATA[Vomiting refers to the forceful expulsion of the stomach contents caused by humoral stimulation of the chemoreceptor trigger zone or neural stimulation of the emetic center. If it persists for four weeks or more, that’s chronic vomiting. Based on the presence of abdominal symptoms, causes of chronic vomiting can be categorized into abdominal and non-abdominal ones. 

If a patient presents with chronic vomiting, first perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and administer IV fluids. Put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry, and if needed, provide supplemental oxygen.  

Also, keep in mind that unstable patients might have electrolyte abnormalities, acid-base disturbances, or signs of severe dehydration.  

Let’s move on to stable patients. Your first step is to obtain a focused history and physical examination and order labs, including a CMP.  

Your patient will report persistent vomiting for more than four weeks, usually associated with nausea and changes in bowel habits. Physical exam might reveal abdominal tenderness and distension, as well as poor skin turgor and dry mucous membranes. 

Labs might show electrolyte disturbances like hypokalemia or hyponatremia, elevated bicarbonate level, and renal insufficiency. With these findings, think about abdominal causes of chronic vomiting. 

Here’s a clinical pearl! Pregnancy is a can’t-miss cause of nausea and vomiting! If your patient is a biological female of child-bearing age, order a urine pregnancy test. Vomiting in pregnancy can range from mild to severe disease and hyperemesis gravidarum, which may even require hospitalization.  

Other causes of chronic vomiting include medications like opioids, antibiotics, chemotherapeutic agents; and substances like alcohol and cannabis, which can cause cannabinoid hyperemesis ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Generalized_anxiety_disorder,_agoraphobia,_and_panic_disorder:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MlPsMfR6QaC0tgh6zWD9HYQsRvGtGC4T/_.jpg</video:thumbnail_loc><video:title><![CDATA[Generalized anxiety disorder, agoraphobia, and panic disorder: Clinical sciences]]></video:title><video:description><![CDATA[Generalized anxiety disorder, agoraphobia, and panic disorder are common anxiety disorders seen in all types of practice settings. Generalized anxiety disorder is characterized by excessive anxiety and worry accompanied by physical symptoms. Agoraphobia is the fear of being in public places and is usually, but not always, associated with panic disorder. Finally, panic disorder is a condition of recurrent, unexpected panic attacks which are characterized by an abrupt surge of discomfort or fear. 

When your patient presents with a chief concern suggesting an anxiety disorder, your next step is to conduct a focused history and physical examination. 

Let’s start with generalized anxiety disorder, or GAD.  Your patient will report excessive anxiety and worry about routine situations, such as finances, relationships, work or school performance, or health. They might also report symptoms like muscle tension or fatigue. Physical exam might show a constricted or tense affect. 

Next, order labs to rule out physical conditions with symptoms like GAD. These include a CBC with differential to rule out anemia, TSH and free T4 levels to rule out thyroid disease, as well as a urine drug screen to rule out substance use. If these labs show abnormalities, consider an alternative diagnosis.  

On the other hand, if lab results are within normal limits, suspect generalized anxiety disorder or GAD and assess the DSM-5 criteria to confirm the diagnosis. 

To meet the criteria, your patient’s anxiety and worry must be present more days than not for at least 6 months and be associated with three or more of the following physical symptoms: restlessness, fatigue, poor concentration, irritability, muscle tension, or poor sleep.  

In addition, the anxiety and worry will be difficult to control; cause significant distress; or impair their ability to function.  

If these criteria are met, and there’s no medical condition, substance use, or other mental disorder that could cause th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obesity_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/afctE3mSQx_0mcK8qmxo3MbCSdGf3i6o/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obesity (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Obesity refers to excessive fat accumulation in the body that is strongly associated with dyslipidemia, diabetes mellitus type 2, nonalcoholic fatty liver disease, and cardiovascular conditions. Now, when assessing overweight and obesity, in children under two years of age, you should use weight-for-length classification, and in children above two years of age, you should use body mass index. 

If your patient is presenting with chief concerns suggestive of obesity, obtain a comprehensive history and physical examination, including measurements of weight and height. If the child is under 2 years of age, measure their length, not height. The patient’s prenatal and perinatal history may reveal risk factors, like gestational diabetes or fetal macrosomia, while family history might reveal parental obesity.  

Obesity is often associated with type 2 diabetes mellitus, so always ask about the presence of polydipsia, polyphagia, and polyuria! In some cases, history might reveal a limp and pain in the hip, groin, thigh, or knee, which is suggestive of slipped capital femoral epiphysis.  

Biological female adolescents could also report irregular menstrual cycles and heavy menstrual bleedings in combination with hair loss, which is suggestive of polycystic ovary syndrome.  

History might also reveal frequent snoring during sleep, which could be a sign of obstructive sleep apnea, as well as the use of medications associated with obesity, such as corticosteroids, anti-seizure medications, and antidepressants. 

Next, ask for symptoms of mental health and behavioral conditions that can increase the risk of obesity, such as depression, anxiety, and disordered eating.  

History could also reveal psychosocial stressors or adverse childhood experiences, like bullying, which can trigger physiologic changes that can result in weight gain. Finally, look for social determinants that can increase the risk of obesity. For example, in under-resourced communities, children ofte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immunizations_(adult):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dw3SsUVESa6vsGr8hqeU6zKWReWg2NsN/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immunizations (adult): Clinical sciences]]></video:title><video:description><![CDATA[Immunizations, also known as vaccines, stimulate the immune system to produce antibodies against specific microorganisms. These antibodies not only disable pathogens but also remain in the body to provide long-term immunity, decrease the likelihood of infection, and decrease the severity of infection.  

Adult vaccinations are commonly administered during annual wellness visits according to the patient’s age.  However, some special considerations such as international travel, pregnancy, and immunocompromised status may alter the usual sequence of immunization.  

Now, if your patient presents for routine vaccination, first assess their age. For patients 19 to 26 years old, offer the one- or two-dose COVID-19 series. This vaccine protects against variants of the SARS-CoV-2 virus, which can cause acute nose, lung, or throat infections, and sometimes respiratory distress, viral pneumonia, and even myocarditis. If previously vaccinated against COVID-19, give them a single dose as a booster. 

Next, patients should receive their influenza vaccine, also known as the flu shot. This annual vaccine helps to protect from influenza, an acute respiratory illness that can progress to viral pneumonia. 

Moving on, if your patient has not already received their completed Hepatitis B and HPV vaccinations, administer these as well. Hepatitis B immunizations are given in a multi-dose series and help protect against liver disease caused by acute or chronic hepatitis B infection.  

On the other hand, the two- or three-dose HPV vaccine series protects against the human papillomavirus. This virus can cause genital warts as well as various forms of genital and throat cancers.  

Next up is the Tdap vaccine, which stands for Tetanus, Diphtheria, and activated Pertussis. And you guessed it, it protects against the bacteria Clostridium tetani, Corynebacterium diphtheriae, and Bordetella pertussis.  As a reminder, Clostridium tetani produces the tetanus toxin that affects neuromusc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_cystic_kidney_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QdpnEgjkSu6YLOXLvKqTF0PFTFKJ-xPh/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to cystic kidney disease: Clinical sciences]]></video:title><video:description><![CDATA[Kidney cysts are fluid-filled sacs lined by a thin wall of cells that can be located either in the cortex, the medulla, or both. Kidney cysts can be associated with acquired or inherited renal conditions and might cause no symptoms or lead to progressive loss of renal function and end-stage renal disease. There are several different renal conditions associated with kidney cysts, including simple renal cysts, medullary sponge kidney disease, and acquired renal cystic disease, as well as autosomal dominant polycystic kidney disease and autosomal dominant tubulointerstitial kidney disease. 

If your patient presents with a chief concern suggesting cystic kidney disease, start by obtaining a focused history and physical exam.  

Your patient might report symptoms specific to kidney conditions, like flank pain and hematuria. Additionally, there might be a history of kidney stones or a family history of kidney disease.  

Next, the physical exam may reveal elevated blood pressure and palpable kidneys with costovertebral angle tenderness.  

With these findings, consider a kidney disorder. Your next step is to order labs, including BMP, serum uric acid, and urinalysis.  

Also, don’t forget a renal ultrasound. If the renal ultrasound reveals a single or multiple kidney cysts, diagnose cystic kidney disease and assess for a family history of kidney disease. 

Now, if there’s no family history of kidney disease, consider simple renal cysts, medullary sponge kidney disease, or acquired renal cystic disease.  

When it comes to simple renal cysts, they are typically incidentally found, as they are asymptomatic with no abnormalities on the physical exam and labs. The renal ultrasound reveals normal-sized kidneys with sharply demarcated cysts with smooth walls without septa, calcifications, or solid components. With these findings, diagnose simple renal cysts, which typically do not require treatment or follow-ups.  

Here’s a clinical pearl to keep in mind! ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hepatocellular_carcinoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jwXqe2BUS_i8KXP7XrzGPiGJRiS02CoU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hepatocellular carcinoma: Clinical sciences]]></video:title><video:description><![CDATA[Hepatocellular carcinoma, or HCC for short, is primary cancer of the liver parenchyma arising from hepatocytes. Most cases occur in patients with cirrhosis from chronic liver diseases like chronic alcohol consumption or viral hepatitis infection. Because patients can remain asymptomatic until the tumor grows substantially, screening patients with risk factors is important.  

Alright, the first step in evaluating a patient with a chief concern suggestive of hepatocellular carcinoma is to perform a focused history and physical examination. Let’s start with screening. These patients are asymptomatic but have risk factors for HCC like cirrhosis or non-cirrhotic chronic liver disease, which can include long-standing hepatitis B or C infections and non-alcoholic fatty liver disease. Exam will likely be normal, but some can have hepatomegaly and ascites. In this case, your next step is to obtain labs such as liver function tests, or LFTs, and alpha-fetoprotein, or AFP, as well as imaging like an ultrasound of the liver. 

Before we go on with the findings, let’s talk about symptomatic patients. If the patient is symptomatic, they might report jaundice, anorexia, weight loss, malaise, and vague upper abdominal pain. History might also reveal risk factors like cirrhosis or non-cirrhotic chronic liver disease.  

On exam, you might find hepatomegaly, ascites, as well as jaundice of the eyes or the skin. With these findings, your next step is to order labs including LFTs and AFP, in addition to an ultrasound of the liver. 

Now, if labs are normal and the liver ultrasound is normal with no nodules, the patient likely does not have HCC and can be followed up with routine surveillance every 6 months. If the patient was symptomatic, you will need to do additional workup to find out what is causing their symptoms. 

For patients with normal LFTs and negative AFP, but the liver ultrasound shows a nodule smaller than 10 millimeters, you should suspect high-risk liver]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypercoagulable_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZSEH5PacQEWBHwON7opN5M7FRemyZKqb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypercoagulable disorders: Clinical sciences]]></video:title><video:description><![CDATA[Hypercoagulable disorders, or thrombophilic disorders, include conditions associated with an increased tendency for blood clotting. Based on the underlying cause, hypercoagulable disorders can be classified as inherited, which are associated with genetic mutations; and acquired, which are characterized  by the presence of specific autoantibodies. Inheritable hypercoagulable disorders include factor V Leiden and prothrombin gene mutations, as well as protein C, S, and antithrombin deficiency. On the flip side, the most important example of an acquired hypercoagulable disorder is antiphospholipid syndrome. 

Now, if your patient presents with a chief concern suggesting a hypercoagulable disorder, obtain a focused history and physical examination. Your patient will typically report symptoms associated with venous thromboembolism, or VTE for short. For example, they might report pain and swelling in one or more limbs, or they might report shortness of breath, chest pain, and coughing up blood. On physical exam, you might notice edema, erythema, and warmth, as well as tenderness to palpation of the affected area, which are typical findings associated with deep vein thrombosis, or DVT for short. On the other hand, you could also observe tachycardia and decreased oxygen saturation, which are common findings associated with pulmonary embolism. 

With these findings, consider VTE. Your next step is to assess for VTE provoking risk factors. These include recent surgery, especially orthopedic and neurovascular procedures; immobilization, for example, if a limb is immobilized after a traumatic injury, or if your patient experiences prolonged immobility during an extended illness; malignancy; or a history of prior thromboembolism. Additionally, don’t forget pregnancy and estrogen therapy in biological females, especially if they are smoking. 

If provoking risk factors are present, you are likely dealing with provoked VTE. Because these patients usually have ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_vasculitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/g4_u9rL5RjWSEtG2qzdQBr0KTBSgXdTp/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to vasculitis: Clinical sciences]]></video:title><video:description><![CDATA[Vasculitis refers to inflammation of blood vessels, which can result in vessel wall damage, bleeding, and ischemia of affected organs. Based on the size of the affected blood vessels, large-vessel vasculitis affects vessels like the aorta and its branches; medium-vessel vasculitis primarily affects major visceral arteries like renal and mesenteric arteries; small-vessel vasculitis mostly affects arterioles and capillaries; and variable-vessel vasculitis can affect vessels of any size.  

Now, if your patient presents with a chief concern suggesting vasculitis, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Obtain IV access and put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry; as well as cardiac telemetry. If needed, provide supplemental oxygen. 

Now here’s a clinical pearl to keep in mind! Vasculitides that commonly present as unstable include ANCA-associated small-vessel vasculitis, which can cause diffuse alveolar hemorrhage; and anti-glomerular basement membrane or anti-GBM disease, which can cause damage to the glomerular basement membrane. Together, these conditions can result in pulmonary-renal syndrome, which can lead to respiratory and renal failure! 

Now, let’s go back to the ABCDE assessment and discuss stable patients. In this case, obtain a focused history and physical examination; and order labs, including CBC, CMP, ESR, CRP, and urinalysis. Your patient will typically report constitutional symptoms, including fever, fatigue, anorexia, and weight loss; as well as epistaxis, limb claudication, and Raynaud phenomenon.  

Ask about symptoms that could indicate involvement of specific organ systems. These patients may experience wheezing or hemoptysis; rash or skin discoloration; sensory disturbances like vision loss or limb weakness; or discolored urine or anuria. The physical exam may rev]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrinsic_acute_kidney_injury_(glomerular_causes):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hnNaMESNRJWXVJVYawKwa6WxSnyymZWH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intrinsic acute kidney injury (glomerular causes): Clinical sciences]]></video:title><video:description><![CDATA[Intrinsic acute kidney injury or AKI refers to a sudden decline in kidney function that results in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste, such as ammonia and uric acid. The underlying cause of intrinsic AKI can be glomerular, which involves damage to the glomerulus; and non-glomerular, which affects renal components like tubules or the interstitium. 

If your patient presents with chief concerns suggesting AKI, first, perform an ABCDE assessment to determine if they’re unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, which might include dialysis access, and put your patient on continuous vital sign monitoring and cardiac telemetry. Finally, if you identify hyperkalemia, metabolic acidosis, volume overload, or symptomatic uremia, start emergent hemodialysis! 

Now, let’s go back and take a look at stable patients. First, obtain a focused history and physical exam, which usually reveals nonspecific signs and symptoms. For example, history might reveal reduced urine output, bloody urine, or systemic symptoms, like fatigue, malaise, and fever. Additionally, patients might report taking nephrotoxic medications or having chronic conditions, like systemic lupus erythematosus or malignancy.  

Similarly, the physical exam is nonspecific and might reveal blood pressure abnormalities, rash, or periorbital and peripheral edema. In this case, suspect intrinsic AKI, so be sure to order a basic metabolic panel and urinalysis with microscopy, assess the patient’s urine output over time, and check renal ultrasound! 

In all types of AKI, labs will reveal a rise in serum creatinine of 0.3 milligrams per deciliter or more over 48 hours; a rise of serum creatinine 1.5 times the baseline or more in the last 7 days, or urine output less than 0.5 milliliters per kilogram per hour for six hours. However, with intrinsic AKI, the BUN-to-Cr ratio will be less than 20]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrinsic_acute_kidney_injury_(non-glomerular_causes):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/huH2_czMQZaEQ8WZ1z1yTQ-RSviRxz_L/_.png</video:thumbnail_loc><video:title><![CDATA[Intrinsic acute kidney injury (non-glomerular causes): Clinical sciences]]></video:title><video:description><![CDATA[Intrinsic acute kidney injury or AKI refers to a sudden decline in kidney function that results in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste, such as ammonia and uric acid.  

The underlying cause of intrinsic AKI can be glomerular, which involves damage to the glomerulus; and non-glomerular, which affects renal components like tubules or the interstitium. 

If your patient presents with chief concerns suggesting AKI, first, perform an ABCDE assessment to determine if they’re unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, which might include dialysis access, and put your patient on continuous vital sign monitoring and cardiac telemetry.  

Finally, if you identify hyperkalemia, metabolic acidosis, volume overload, or symptomatic uremia, start emergent hemodialysis! 

Now, let’s go back and take a look at stable patients.  

First, obtain a focused history and physical exam, which usually reveals nonspecific signs and symptoms. For example, history might reveal reduced urine output, bloody urine, or systemic symptoms, like fatigue, malaise, and fever. Additionally, patients might report taking nephrotoxic medications or having chronic conditions, like systemic lupus erythematosus or malignancy.  

Similarly, the physical exam is nonspecific and might reveal blood pressure abnormalities, rash, or periorbital and peripheral edema. In this case, suspect intrinsic AKI, so be sure to order a basic metabolic panel and urinalysis with microscopy, assess the patient’s urine output over time, and check renal ultrasound! 

In all types of AKI, labs will reveal a rise in serum creatinine of 0.3 milligrams per deciliter or more over 48 hours; a rise of serum creatinine 1.5 times the baseline or more in the last 7 days, or urine output less than 0.5 milliliters per kilogram per hour for six hours.  

However, with intrinsic AKI, the BUN-to-Cr ratio will ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postrenal_acute_kidney_injury:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vmvSLKniRnGFemWb300-q_1wRiWaYDn_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postrenal acute kidney injury: Clinical sciences]]></video:title><video:description><![CDATA[Acute kidney injury, or AKI, refers to a sudden decline in kidney function that results in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste, such as ammonia and uric acid.  

Based on the underlying cause, acute kidney injury can be subdivided into prerenal-, renal, and postrenal acute kidney injury. Postrenal acute kidney injury is further classified based on the location of the obstruction in the urinary tract as postrenal acute kidney injury due to upper and lower obstruction of the urinary tract.   

Now, if your patient presents with chief concerns suggesting postrenal AKI, perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, which might include dialysis access, and put your patient on continuous vital sign monitoring and cardiac telemetry!  

Finally, if you identify hyperkalemia, metabolic acidosis, volume overload, or symptomatic uremia, start emergent hemodialysis! 

Now, let’s go back to the ABCDE assessment and take a look at stable patients.  

In stable individuals, obtain a focused history and physical exam, which is going to help you differentiate different types of AKI. Patients with post-renal AKI typically report pelvic discomfort, often in combination with slow stream or dribbling. In acute cases, the patient could report sudden pelvic pain and urinary retention. Additionally, history might reveal sudden flank pain and bloody urine or conditions like prostate disease and nephrolithiasis.  

Next, the physical exam might show palpable bladder and flank tenderness. Finally, on the digital rectal exam, you might notice prostate enlargement or palpable mass! With these findings, you should suspect postrenal causes of AKI. Next, order a basic metabolic panel and urinalysis with microscopy, measure the patient’s urine output over time, and check renal ultrasound! 

In all types of AKI, labs]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_lymphoma:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XZhc2dQbQUKpSQbGn1XeLOE-RWi0kyHX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to lymphoma: Clinical sciences]]></video:title><video:description><![CDATA[Lymphoma refers to a group of hematologic malignancies characterized by the abnormal proliferation of clonal lymphocytes. These lymphocytes can infiltrate various lymph nodes, leading to lymph node enlargement or masses. They can also infiltrate extranodal sites, such as the skin and the gastrointestinal tract including the liver, and spleen, giving rise to extranodal signs and symptoms, like skin ulcers, hepatosplenomegaly, and gastrointestinal bleeding. Based on the clinical features and biopsy results, lymphomas can be divided into two major categories which include Hodgkin and non-Hodgkin lymphomas. 

Now, if your patient presents with a chief concern suggesting lymphoma, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. If needed, provide supplemental oxygen.  

Now, let’s go back to the ABCDE assessment and discuss stable patients. First, obtain a focused history and physical examination. Your patient will typically report painless swelling or a mass, possibly in combination with abdominal pain or discomfort. Additionally, they might report B symptoms, which include fever, night sweats, and unexplained weight loss. History could also reveal risk factors for lymphoma, such as autoimmune conditions, like systemic lupus erythematosus; HIV or EBV infections; use of immunosuppressive medications; or a prior history of chemotherapy or radiation therapy. Additionally, the physical exam often reveals nontender peripheral lymphadenopathy, and sometimes hepatosplenomegaly, as well as a palpable mass. 

With these findings, consider lymphoma, and order imaging depending on the location of the suspected mass or lymphadenopathy. These might include chest X-ray, ultrasound, or CT scan. If the imaging reveals a mass or enlarged lym]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_bleeding_disorders_(coagulopathy):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/10uJi7AFRLCM5wrMb3F0wT_aQdWBVMJ7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to bleeding disorders (coagulopathy): Clinical sciences]]></video:title><video:description><![CDATA[Coagulopathy refers to dysfunction in any step of the coagulation cascade, resulting in impaired blood clot formation. The most important coagulopathies include medication-induced coagulopathy, an acquired factor inhibitor, hemophilia A, hemophilia B, severe von Willebrand disease, chronic liver disease, and vitamin K deficiency. 

Now, if your patient presents with a chief concern suggesting a bleeding disorder, perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, give IV fluids, and consider transfusion of blood products, such as packed red blood cells, fresh frozen plasma, or cryoprecipitate. Finally, put your patient on continuous vital sign monitoring and, if needed, provide supplemental oxygen! 

Now, here’s a clinical pearl to keep in mind!  Unstable patients with bleeding disorders might present with hemorrhagic shock, so you must quickly locate the source of bleeding in order to stabilize the patient! They may have neurologic changes from intracranial bleeding; hematemesis or hematochezia from gastrointestinal bleeding; or vaginal bleeding from postpartum hemorrhage. If unclear, consider obtaining a CT angiography or endoscopy, and consulting the surgery team for interventions to stop the bleeding. 

Okay, let’s go back to the ABCDE assessment and look at stable patients, and start with a focused history and physical exam. Your patient is likely to report easy bruising possibly in combination with a history of deep soft tissue bleeding, such as muscle hematomas and joint hemarthrosis. They might also have a history of excessive bleeding after trauma or surgery, which is typically delayed hours to days after the event; as well as a family history of abnormal bleeding. Additionally, the physical exam typically reveals ecchymoses and hematomas; and you may even find evidence of current bleeding. With these history and physical findi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_bleeding_disorders_(platelet_dysfunction):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/49K4-HVHSAmDFo0s-BYSeUplRHOPQLNa/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to bleeding disorders (platelet dysfunction): Clinical sciences]]></video:title><video:description><![CDATA[Platelet dysfunction, also known as a platelet function disorder or thrombocytopathy, involves defects in the adhesion, aggregation, or activation of platelets. Based on the underlying cause, platelet dysfunction can be either acquired or inherited. Acquired platelet dysfunction includes medication-induced platelet dysfunction, uremic platelet dysfunction, platelet dysfunction due to liver disease and myeloid neoplasms, and acquired von Willebrand disease. On the flip side, inherited platelet dysfunction includes inherited von Willebrand disease, and conditions like Bernard-Soulier syndrome and Glanzmann thrombasthenia. 

Now, if your patient presents with a chief concerns suggesting a bleeding disorder, perform an ABCDE assessment to determine if the patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, start IV fluids, and consider transfusion of blood products, such as packed red blood cells. Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry; and if needed, don’t forget to provide supplemental oxygen! 

Now here’s a clinical pearl to keep in mind!  Unstable patients with bleeding disorders might present with hemorrhagic shock, so you must quickly locate the source of bleeding in order to stabilize the patient! They may have neurologic changes from intracranial bleeding; hematemesis or hematochezia from gastrointestinal bleeding; or vaginal bleeding from postpartum hemorrhage. If unclear, consider obtaining a CT angiography or endoscopy, and consulting the surgery team for interventions to stop the bleeding. 

Okay, let’s go back to the ABCDE assessment and take a look at stable patients and medication-induced cases. Start by obtaining a focused history and physical examination. Your patient will typically report easy bruising, and mucocutaneous bleeding, like epistaxis, gastrointestinal bleeding, or menorrhagia. They mi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_bleeding_disorders_(thrombocytopenia):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vcTfdDONTKm9qwqW-w4e5wxlQxarmsPo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to bleeding disorders (thrombocytopenia): Clinical sciences]]></video:title><video:description><![CDATA[Thrombocytopenia is defined as a platelet count of less than 150,000 cells/L. Mild thrombocytopenia is often asymptomatic, while platelet counts less than 50,000 are frequently associated with bleeding.  

Based on the underlying cause, thrombocytopenia can be associated with thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, disseminated intravascular coagulation, and bone marrow abnormalities; as well as liver disease, heparin-induced thrombocytopenia, and immune thrombocytopenia. 

Now, if your patient presents with a chief concern suggesting a bleeding disorder, perform an ABCDE assessment to determine if the patient is unstable or stable.  

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, give IV fluids, and consider transfusion of blood products, such as packed red blood cells and platelets. Finally, put your patient on continuous vital sign monitoring and, if needed, provide supplemental oxygen! 

Now here’s a clinical pearl to keep in mind!  Unstable patients with bleeding disorders might present with hemorrhagic shock, so you must quickly locate the source of bleeding in order to stabilize the patient! They may have neurologic changes from intracranial bleeding; hematemesis or hematochezia from gastrointestinal bleeding; or vaginal bleeding from postpartum hemorrhage. If unclear, consider obtaining a CT angiography or endoscopy, and consulting the surgery team for interventions to stop the bleeding. 

Okay, let’s go back to the ABCDE assessment and take a look at stable patients.  Start by obtaining a focused history and physical examination. Your patient will typically report easy bruising; as well as mucocutaneous bleeding, like epistaxis; gastrointestinal bleeding; or menorrhagia. They might also have a history of excessive bleeding after trauma or surgery, which typically occurs immediately following the event. The physical exam usually reveals petechiae, purpura, and ecchymoses. With these]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Thrombotic_microangiopathy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/REqfAK6FQaOyjaHGJSiz4ytLRVaqRjsD/_.png</video:thumbnail_loc><video:title><![CDATA[Thrombotic microangiopathy: Clinical sciences]]></video:title><video:description><![CDATA[Thrombotic microangiopathy, or TMA for short, is a rare but life-threatening blood condition characterized by uncontrolled formation of thrombi in the small blood vessels. These blood clots consume platelets, leading to thrombocytopenia. They also create turbulent shearing forces that destroy passing red blood cells, leading to microangiopathic hemolytic anemia, or MAHA. Now based on the underlying pathophysiology, there are several different types of TMA! The first one is thrombotic thrombocytopenic purpura, which is associated with von Willebrand factor-dependent coagulation and impaired function of a metalloprotease called ADAMTS13. Next, there’s atypical hemolytic uremic syndrome, which is characterized by uncontrolled complement activation. Finally, there’s classic hemolytic uremic syndrome, which is associated with E. Coli or Shigella infections! 

Now, if your patient presents with chief concern suggesting TMA, you should first perform an ABCDE assessment to determine they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and consider IV fluids. Finally, put your patient on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen.  

Okay, let’s go back to the ABCDE assessment and look at stable patients. In this case, start with a focused history and physical exam. Your patient is likely to report weakness and fatigue. They might also note non-specific symptoms, like fever and headache, often in combination with easy bruising or excessive bleeding. Additionally, some patients could report gastrointestinal symptoms, such as abdominal pain or diarrhea.  On physical exam, you might observe purpura, bruising, or mucosal bleeding.  

Based on these findings, you should suspect a disorder affecting platelets, such as TMA, so your next step is to order labs, including a CBC with peripheral blood sm]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mitral_stenosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kWWyaErzT0mx6CMTyAfDQJmUQQ2muI9b/_.png</video:thumbnail_loc><video:title><![CDATA[Mitral stenosis: Clinical sciences]]></video:title><video:description><![CDATA[Mitral stenosis is a condition in which mitral valve opening is narrowed, most commonly due to calcification of the leaflets, or rheumatic heart disease.  

This narrowing obstructs the inflow of blood into the left ventricle resulting in reduced diastolic filling, stroke volume, and, in turn, cardiac output.  

Additionally, the valvular narrowing can cause build-up of blood within the left atrium leading to elevated pressure within it as well as the pulmonary artery, which can lead to pulmonary edema.  

Now, as the right side of the heart has to pump harder to overcome the increased pressures, right ventricular hypertrophy develops.  

Over time, this can progress to right heart failure. Because the right heart can no longer pump enough blood to fill the left heart, there is an inadequate preload to the left ventricle, leading to reduced ejection fraction.  

Mitral stenosis is classified into 4 stages A through D, which represent the progressing severity of the disease.  

Alright, when a patient presents with a chief concern suggestive of mitral stenosis, your first step is to perform the ABCDE assessment to determine if they are stable or unstable. If unstable, initiate acute management by stabilizing the airway, breathing, and circulation. Make sure to  obtain IV access and provide supplemental oxygen, in addition to continuous vital sign monitoring. 

Next, obtain a focused history and physical exam. as well as labs including CBC, CMP, BNP, and cardiac enzymes. Be sure to get an ECG and a transthoracic echocardiogram, or TTE. 

Now, the history might reveal dyspnea at rest or on exertion, orthopnea, weakness, extremity swelling, abdominal bloating, rapid weight gain, and palpitations.  

Exam might reveal tachycardia with or without hypotension, respiratory distress, and pitting edema of the extremities.  

Since we are talking about cardiogenic shock, the patient will appear cool and clammy, cyanotic, with cold extremities, and cold sweat.  

On a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myocarditis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QDUMV2HSSMqlULVN4TA1ns5LRpyhL7SE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myocarditis: Clinical sciences]]></video:title><video:description><![CDATA[Myocarditis refers to the inflammation of the myocardium, which can occur due to various reasons, including viral infections, medications, as well as systemic conditions, like sarcoidosis. Based on severity, myocarditis can range from asymptomatic and mild to life-threatening fulminant myocarditis, which is associated with heart failure! 

Now, if your patient presents with chief concerns suggesting myocarditis, you should first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation, which may require endotracheal intubation and mechanical ventilation. Next, obtain IV access and start continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry.  

Myocardial inflammation can completely compromise myocardial function, so these patients could present with cardiogenic shock, requiring mechanical circulatory support and inotropes, like dobutamine! Finally, don’t forget to provide supplemental oxygen to maintain oxygen saturation above 90 percent. 

Once you stabilize the patient, obtain a focused history and physical examination. Next, order labs, including CRP, ESR, and cardiac troponin, and don’t forget to obtain an ECG and transthoracic echocardiography or TTE. History typically reveals a young adult with no risk factors for ischemic heart disease, such as tobacco use, hyperlipidemia, and hypertension. Some patients might also report recent flu-like symptoms, including fever, malaise, and headaches. Finally, myocardial inflammation results in chest pain, palpitations, as well as dyspnea, and fatigue. Additionally, in unstable patients, there is impaired heart function, which eventually leads to congestive heart failure and symptoms, such as orthopnea and leg swelling.  

Additionally, the physical exam will reveal signs of congestive heart failure, including jugular venous distention, S3 gallop, as well as lower extrem]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Valvular_insufficiency_(regurgitation):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OG8nDSSOSZiTwBJHOjHxfbPYRhiaOHua/_.png</video:thumbnail_loc><video:title><![CDATA[Valvular insufficiency (regurgitation): Clinical sciences]]></video:title><video:description><![CDATA[Valvular insufficiency refers to heart valves that are incompetent or leaky. Mild forms of valvular insufficiency can occur from natural aging, while moderate and severe forms can result from disease processes like long-standing hypertension, myocardial infarction, or infections such as rheumatic heart disease.  

Valvular insufficiency is divided into 4 types: aortic, mitral, pulmonic, and tricuspid regurgitation. If left untreated, these conditions can lead to arrhythmias, or heart chamber failure depending on the valve involved. 

If a patient presents with a chief concern suggestive of valvular insufficiency, first perform the ABCDE assessment to determine if they are stable or unstable. If unstable, immediately stabilize the airway, breathing, and circulation.  

Always have a low threshold for endotracheal intubation in these patients. Next, establish IV access with two large bore IVs and start appropriate fluid resuscitative measures. Be careful not to give too much fluids as it can lead to fluid overload and worsen the patient’s symptoms. Make sure to continuously monitor vitals as these patients can be at a high risk for sudden cardiovascular collapse.  

Once the acute management is initiated, your next step is to perform a quick focused history and physical exam. Unstable patients with valvular insufficiency might have a history of recent myocardial infarction, respiratory infection, or GI infection.  

Physical exam might reveal a murmur; and signs of acute heart failure like tachycardia, hypotension, diaphoresis, or peripheral edema. With these findings, suspect decompensated heart failure due to valvular insufficiency.  

Unstable patients should undergo emergent transthoracic echocardiogram, or transesophageal echocardiogram to confirm the diagnosis; often followed by surgical intervention to either repair or replace the valve. Keep in mind that diagnostic workup in unstable patients should not delay therapeutic intervention. 

Okay, now tha]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_differentiating_lesions_(neuromuscular_junction):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ca1XGYJkQkCm4iI0ZeO3LiEeTl2HtCS-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to differentiating lesions (neuromuscular junction): Clinical sciences]]></video:title><video:description><![CDATA[Neuromuscular junction disorders are characterized by muscle weakness due to abnormal synaptic neurotransmission of acetylcholine. The underlying pathology can be at the presynaptic membrane, such as impaired vesicular release of acetylcholine; within the synaptic cleft itself, such as decreased breakdown of acetylcholine; or at the postsynaptic membrane, such as a reduction in acetylcholine receptors.   

Some important conditions associated with abnormal synaptic neurotransmission of acetylcholine include myasthenia gravis, Lambert-Eaton myasthenic syndrome, botulism, and organophosphate toxicity.  

Now, if your patient presents with a chief concern suggestive of a neuromuscular junction disorder, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. At this point, you might need to provide noninvasive positive pressure ventilation or mechanical ventilation. Next, obtain IV access, and don’t forget to put your patient on continuous vital signs monitoring, including heart rate, blood pressure, and pulse oximetry. 

Now, here’s a clinical pearl to keep in mind! Patients with a neuromuscular junction disorder may have diaphragm weakness, which can lead to respiratory failure.  

In this case, be sure to perform bedside pulmonary function tests, which will reveal reduced vital capacity, which is the amount of air someone can exhale after a maximum inhalation. Also, you will notice reduced maximal inspiratory pressure, which is known as negative inspiratory force, and reduced maximal expiratory pressure. If vital capacity is less than 20 milliliters per kilogram, maximal inspiratory pressure is less than 30 centimeters of water, and maximal expiratory pressure is less than 40 centimeters of water, you should consider intubating the patient. This is known as the 20, 30, 40 rule to guide intubation timing in patients with neuromuscular weakness.  

Okay, let’s go back to ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_aphasia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HNAP57cDTG2HEPQ2Mp93f-2hSSKmt4DA/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to aphasia: Clinical sciences]]></video:title><video:description><![CDATA[Aphasia refers to an acquired communication disorder that can affect the patient’s ability to speak, understand speech, read, and write. Lesions anywhere along the language circuitry can result in this communication impairment. Now, based on the part of the brain that&amp;#39;s affected, we can further subdivide aphasia into several main types! Broca and transcortical motor aphasia are characterized by impairment in language production or expression, while Wernicke and transcortical sensory aphasia are associated with a loss of language comprehension or reception. Finally, conduction aphasia is characterized by a loss of repetition, and global aphasia is associated with a severe loss of language production and comprehension. 

Now, if your patient presents with a chief concern suggestive of aphasia, first, obtain a focused history and physical exam. Friends and family members will typically report that the patient has trouble communicating. Additionally, the physical exam will usually reveal limited verbal or written language output, nonsensical speech, impaired comprehension of verbal or written language, or impaired repetition. With any of these findings, you can diagnose aphasia, so your next step is to assess the type.  

First, let’s focus on expressive aphasia! These patients are speaking in short, poorly-formed sentences. Also, they will have difficulties coming up with words and they will have trouble with writing. The physical exam is notable for non-fluent speech, meaning speech that is not smooth, with word-finding difficulty, loss of grammar, and abnormal rate and cadence. The patient is sometimes described as having telegraphic speech, with improper grammar and using mainly nouns and verbs. Something similar to the early days when telegrams were a mode of long-distance communication, and the sender was charged by the word. You will also find impaired written language with mostly intact reading and hearing comprehension. In this case, dia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_diplopia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HAOsKNpPSJedomoBwvnbnAXZQbequEUu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to diplopia: Clinical sciences]]></video:title><video:description><![CDATA[Diplopia, or double vision, is the visualization of two images of a single object. Diplopia might be the result of impaired function of the structures within the eye itself, or due to impaired ocular motility that causes misalignment of the eyes. Diplopia can be classified as monocular, if it’s present when one eye remains closed, or binocular if it’s present only when both eyes are open. 

Now, if your patient presents with double vision, start with a focused history and physical exam.  They might describe double vision like seeing two images of the same object side by side or one above the other. If on physical exam, these symptoms persist with one eye closed, that’s monocular diplopia. This means that there’s pathology in the eye that perceives the visual abnormality, the open eye. Next, perform a pinhole exam, in which you ask the patient to read an eye chart through a pinhole. If their vision does not improve, the likely diagnosis is macular disease. Some common causes include macular edema from diabetic retinopathy, age-related macular degeneration, and uveitis.  

On the flip side, if the patient’s vision does improve with the pinhole exam, your next step is to assess for lens opacity on the fundoscopic exam. If lens opacity is present, you should diagnose a cataract. Risk factors for cataract development include advanced age, sunlight exposure, tobacco use, diabetes, and corticosteroid use.  

However, if lens opacity is absent, you can diagnose refractive error. The different types of refractive error are hyperopia, otherwise known as farsightedness; myopia, known as nearsightedness; and astigmatism, which is an irregular curvature of the cornea.  

Okay, let’s go back to the history and physical exam and look at some different findings. As before, patients report double vision. However, their symptoms improve with either eye closed on a physical exam, meaning that the double vision is due to misalignment of the eyes. In this case, we are talking ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myasthenia_gravis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gnk7WhvuSbC5mJ1N0pAKN4wwQNq5608s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myasthenia gravis: Clinical sciences]]></video:title><video:description><![CDATA[Myasthenia gravis is a progressive autoimmune neuromuscular junction disorder characterized by fatigable weakness in skeletal muscles. In myasthenia gravis, antibodies can bind to postsynaptic acetylcholine receptors, as well as to muscle-specific kinase and low-density lipoprotein receptor-related protein 4. Once bound, antibodies activate the classical complement pathway, which triggers local inflammation, eventually reducing the number of functioning acetylcholine receptors and flattening the postsynaptic folds.  

Ultimately, this impairs neuromuscular transmission and results in progressive weakness that worsens with repeated activity.  

Myasthenia gravis can be limited to the ocular muscles, or generalized, affecting the bulbar, axial, limb, and respiratory muscles as well. In severe cases, a person can present with respiratory failure, which is also known as a myasthenic crisis. 

Now, if your patient presents with chief concerns suggestive of myasthenia gravis, perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. At this point, you might need to provide noninvasive positive pressure ventilation or mechanical ventilation. Next, obtain IV access, and don’t forget to put your patient on continuous vital signs monitoring, including heart rate, blood pressure, and pulse oximetry. 

Next, obtain a focused history and physical exam, order arterial blood gas analysis, and assess your patient’s respiratory status by obtaining bedside pulmonary function tests, which include vital capacity, maximum inspiratory pressure, and maximum expiratory pressure.  

Your patient will report rapidly worsening painless weakness, shortness of breath, and difficulty swallowing or choking when eating. Most patients will have a known history of myasthenia gravis, but some individuals might present for the first time in a crisis.  Additionally, history might reveal conditions associated with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parkinson_disease_and_dementia_with_Lewy_bodies:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-sH1I-BeQVqAA8H9Vqbz8IupRT_M9CtP/_.png</video:thumbnail_loc><video:title><![CDATA[Parkinson disease and dementia with Lewy bodies: Clinical sciences]]></video:title><video:description><![CDATA[Parkinson disease and dementia with Lewy bodies are two related neurodegenerative conditions due to an abnormal accumulation of alpha-synuclein protein and neuronal loss. Both conditions are characterized by motor symptoms known as parkinsonism, and cognitive decline. Clinically, you can differentiate these conditions based on the timing of onset and severity of motor and cognitive symptoms. Keep in mind that Lewy body dementia is not the same thing, and is a broader term that includes Parkinson disease dementia and dementia with Lewy bodies. 

Now, if your patient presents with a chief concern suggesting Parkinson disease or dementia with Lewy bodies, you should first obtain a focused history and physical examination. History typically reveals a recent onset of slowness of movement, shakiness of the patient’s hands at rest, and in some cases, frequent falls. The physical exam reveals bradykinesia, which refers to slowness of movement as well as a decrease in amplitude or speed with continued movement. Additionally, you will notice a pill-rolling tremor, which is a hand tremor at rest with movements that look like the patient is rolling a pill between their thumb and index finger. Finally, the physical exam will reveal rigidity. Moreover, you may find cogwheeling or cog-wheel rigidity, which is shown if you passively move the patient’s limb and feel a series of stops or stalls. 

Now, based on findings of bradykinesia, tremor at rest, and rigidity, you can diagnose parkinsonism, so your next step is to assess the underlying cause. First, you should assess your patient for early-onset dementia, which can help you differentiate Parkinson disease from Parkinson-like syndromes, such as dementia with Lewy bodies.  

If you rule out early-onset dementia, suspect Parkinson disease. Next, initiate a trial of dopaminergic therapy, more specifically levodopa and carbidopa. Levodopa is a precursor of dopamine that can cross the blood-brain barrier. Once it reaches th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_tremor:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Su88bpY3SReYU68I8r_dymlZRYiZHx8Q/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to tremor: Clinical sciences]]></video:title><video:description><![CDATA[Tremor refers to an involuntary, rhythmic, oscillatory movement due to the actions of opposing muscles, which is most commonly observed in the upper extremities. It could also be present in other parts of the body, including the lower extremities, head, jaw, and trunk. The pathophysiology of tremor includes multiple neural pathways, such as those involving the basal ganglia, premotor and motor cortices, thalami, and cerebellum. The most common causes of tremor include Parkinson disease, cerebellar dysfunction, essential tremor, and enhanced physiologic tremor. 

Now, if a patient presents with chief concerns suggesting tremor, you should first obtain a focused history and physical examination. Patients typically report shaky hands, which can often cause difficulty performing tasks such as eating or writing. Sometimes, they might report shaking in other parts of the body, as well as a family history of a tremor. On examination, you might observe involuntary, rhythmic, oscillatory movements in the hands and possibly shaking of other parts of the body, for example, the head.  With these findings, you can diagnose a tremor. 

Your next step is to find the cause, so first assess for a medication-induced tremor. If your patient is taking a medication with a known side effect of tremor, such as lithium, valproic acid, amiodarone, β-adrenergic agonists like albuterol, or anti-psychotics with anti-dopaminergic activity like haloperidol, the likely diagnosis is a medication-induced tremor. 

Here’s your first clinical pearl! Patients with a medication-induced tremor can experience tremors at rest, known as a rest tremor, or with action, known as an action tremor. Sometimes, the tremors can be accompanied by parkinsonism with rigidity and bradykinesia. Finally, when the offending drug is discontinued the tremors will stop. 

On the flip side, if your patient does not report taking medications associated with tremor, the next step is to assess for a rest tremor. Alrig]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_medication-induced_movement_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JNLe_lQMRZ_w4TGoSoPC-u7WRnGjm95m/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to medication-induced movement disorders: Clinical sciences]]></video:title><video:description><![CDATA[Medication-induced movement disorders are a group of conditions characterized by abnormal movements resulting from exposure to certain medications. These medications often include serotonergic medications, dopamine antagonists, and anticonvulsants, which are all commonly prescribed in psychiatric treatment.  

Medication-induced movement disorders can range from mild to severe and from acute to chronic. Life-threatening ones requiring emergency intervention include serotonin syndrome and neuroleptic malignant syndrome. Less severe ones include acute dystonia, postural tremor, extrapyramidal symptoms, akathisia, and tardive dyskinesia. 

If a patient presents with a chief concern suggesting a medication-induced movement disorder, first, perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation, which may require supplemental oxygen and even endotracheal intubation. Next, obtain IV access, and consider starting IV fluids. Finally, begin continuous vital sign monitoring, including respiratory rate, pulse oximetry, and cardiac telemetry.   

Once you have initiated the acute management, your next step is to obtain a focused history and physical exam, and order labs, including a CPK or creatine phosphokinase, CBC, and CMP. In unstable patients, you should think about serotonin syndrome or neuroleptic malignant syndrome. 

Patients with serotonin syndrome typically report recent exposure to one or more serotonergic medications, such as serotonin reuptake inhibitors, tricyclic antidepressants, or monoamine oxidase inhibitors. Additionally, there might be exposure to synthetic opioid tramadol, the muscle relaxer cyclobenzaprine, and the antibiotic linezolid, all of which have serotonergic properties as well.  

As for the physical exam, look out for elevated temperature, hypertension, tachycardia, muscle rigidity, tremor or myoclonus, hyperreflexia, diaphoresis, and even confusion and s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_acute_vision_loss:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/28tC18WJS76XVXDK14bh0nkAQSeRVXgS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to acute vision loss: Clinical sciences]]></video:title><video:description><![CDATA[Acute vision loss is a relatively sudden worsening of visual perception. The underlying pathology could be anywhere along the visual pathway, including the eyes, optic nerves, optic chiasm, optic tracts, optic radiations, and the visual cortex.  

Now, vision loss associated with eye pain is common for conditions like infectious keratitis, glaucoma, and optic neuritis. However, painless vision loss is found with stroke, mass compression of the optic chiasm, retinal detachment, as well as central retinal artery or venous occlusion, or ischemic optic neuropathy.    

If your patient presents with acute vision loss, first obtain a focused history and physical exam, as well as a fundoscopic exam.  Patients typically report a sudden vision loss, while the physical exam demonstrates decreased visual acuity and possibly impaired visual fields. Don’t forget to perform the swinging flashlight test. This test is used to assess the pupillary reflex pathway, which involves the optic nerve as the sensory afferent limb, and the oculomotor nerve as the motor efferent limb.  

During the swinging flashlight test, you shine a light, such as with a penlight, back and forth between the two eyes. Normally, regardless of which eye the light is shining into, the sensory afferent limb of the optic nerve will send a signal to the Edinger-Westphal nucleus in the midbrain. From here, the signal will be sent back via the oculomotor nerves and the ciliary ganglia to the pupillary sphincter muscles in both eyes, causing both pupils to constrict.  

However, if there’s a lesion of the afferent pathway, when you swing the light from the normal eye to the affected eye, the stimulus will not reach the Edinger-Westphal nucleus. In other words, efferent signals will not reach pupillary sphincter muscles, so the patient’s pupils will not constrict, instead, they will dilate. This is known as a relative afferent pupillary defect or Marcus Gunn pupil. Finally, in some individuals with acute vi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_facial_palsy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HFujAvBsQ5_xtZqWkVOfExJSTAiqnuR9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to facial palsy: Clinical sciences]]></video:title><video:description><![CDATA[Facial palsy refers to weakness or paralysis of the muscles that control facial expression caused by injury anywhere along the motor pathway that innervates these muscles. One of the stops in this motor pathway is cranial nerve 7, also known as the facial nerve. Now, based on the location of the injury, facial palsy can be classified as central, which occurs due to an upper motor neuron lesion; or peripheral, which occurs as a result of a lower motor neuron lesion.  

Now, here’s a high-yield fact to keep in mind! The facial nerve motor nucleus is located in the pons and receives input from upper motor neurons in the primary motor cortex.  

It’s important to note that upper motor neuron innervation to the facial muscles is bilateral for the upper part of the face and contralateral for the lower part of the face.  

In addition to muscles, the facial nerve innervates other structures along its path, including taste receptors of the anterior two-thirds of the tongue, sensory receptors to the external auditory canal and pinna of the ear, as well as the stapedius muscle of the inner ear. Finally, don’t forget that the facial nerve carries parasympathetic fibers to lacrimal glands and all salivary glands except the parotid. 

Now, if your patient presents with facial droop, start with a focused history and physical exam. As a result of damage to the motor pathway, your patient will lose control of the muscles of facial expression, so they will typically report a relatively sudden onset of symptoms, such as drooling out of one side of the mouth and slurred speech. Sometimes, taste receptors of the anterior two-thirds of the tongue may lose function, causing impaired taste. Next, if sensory receptors to the external auditory canal and pinna of the ear are involved, signal dysfunction might cause pain behind the ear. Furthermore, the stapedius muscle might stop working, leading to discomfort when your patient is exposed to normal sound levels, which is also known]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrapartum_fetal_heart_rate_monitoring:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ub95trdpQgqPNaI8xJkWQyMnTQWEKVei/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intrapartum fetal heart rate monitoring: Clinical sciences]]></video:title><video:description><![CDATA[Intrapartum monitoring of the fetal heart rate, or FHR, is performed to evaluate FHR patterns, assess fetal well-being, and guide interventions during labor.  

The basis for monitoring is that the fetal brain modulates cardiac activity through sympathetic and parasympathetic effects which are influenced by oxygenation status and acid-base balance.  

The FHR demonstrates predictable patterns in response to intrapartum events, such as fetal sleep, maternal medications, compression of the umbilical cord, hypoxia, and acidemia.  

Two methods of FHR monitoring are electronic fetal monitoring, or EFM, and intermittent auscultation. EFM can be performed externally or internally, while intermittent auscultation involves periodic listening to the FHR using a Doppler device or fetal stethoscope on the maternal abdomen.  

Now, when a patient presents for evaluation and intrapartum fetal heart rate monitoring, your first step is to obtain a focused history and physical examination. Factors to consider in your patient’s history include gestational age; amniotic membrane status; and medications the patient is receiving such as oxytocin, IV opioids like butorphanol, or an epidural. On physical exam, note your patient’s vital signs, and keep in mind that abnormalities in maternal blood pressure, temperature, and oxygenation can cause significant FHR changes. Also, perform a sterile vaginal exam to check cervical dilation.  

Your next step is to assess for high-risk conditions, including hypertension or diabetes. If there are no high-risk conditions, you can monitor with either intermittent fetal auscultation or with continuous EFM. However, if a high-risk condition is present or if continuous monitoring is preferred by your patient, perform continuous EFM.  

Next, apply the monitors to the patient and assess the FHR and uterine contraction patterns. The fetal heart rate pattern is described by the baseline, variability, and presence of accelerations or decelera]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Venous_thromboembolism_in_pregnancy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jzuQqdjOQrKeNJap7Du4T3ucSIGJEWIE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Venous thromboembolism in pregnancy: Clinical sciences]]></video:title><video:description><![CDATA[Venous thromboembolism, or VTE for short, is when clots form within the venous system, leading to complications that include deep vein thrombosis, or DVT, and pulmonary embolism, or PE. While patients are at increased risk for VTE as early as the first trimester, their highest risk occurs in the first 1 to 2 weeks postpartum.  

If your patient presents with a chief concern suggesting venous thromboembolism in pregnancy, you should first perform an ABCDE assessment to determine if they are stable or unstable.  If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and place your patient on continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Don’t forget that you have two patients, so be sure to assess fetal heart rate, and depending on gestational age, consider continuous fetal monitoring as well. Finally, if needed, provide supplemental oxygen. 

Okay, let’s go back to the ABCDE assessment and talk about stable patients.  In this case, start by obtaining a focused history and physical examination. During pregnancy, most cases of VTE are caused by DVT, and unlike non-pregnant patients, the thrombus tends to be more proximal, typically in the iliac vein and iliofemoral veins, and occurs more frequently in the left lower extremity compared to the right. These patients will usually present with unilateral extremity pain and swelling.  

History might also reveal some risk factors for DVT, with the most important one being a personal history of thrombosis. Others include having a C-section; obesity; hypertension, preeclampsia, or eclampsia; and having an acquired or inherited thrombophilia. 

The most reliable physical exam finding is a difference in calf circumference measurements of at least 2 centimeters. You might also be able to palpate the thrombotic vein, which could be erythematous, warm, and tender. Labs are typically not necessary for diagnosis.  

Time for a clinical pearl! ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multifetal_gestation:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r4j4q2dNQYuDzjjKRVJOj0MLTO_x6auG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multifetal gestation: Clinical sciences]]></video:title><video:description><![CDATA[Multifetal gestation is any pregnancy in which more than one fetus is present. This includes twin, triplet, and other higher order pregnancies. Multifetal gestations carry increased maternal risks, including diabetes and preeclampsia, as well as increased fetal risks, such as preterm birth and intrauterine fetal demise, also known as IUFD. The amnionicity, meaning the number of amniotic sacs, and the chorionicity, meaning the number of placentas, influence the degree of risk for the pregnancy.  

When a patient presents with a suspected multifetal gestation, your first step is to obtain a focused history and physical examination. Patients may report significant nausea and vomiting, or hyperemesis; which is due to the increased beta human chorionic gonadotropin levels that occur with multifetal gestations. They may also have certain risk factors for a multifetal gestation such as assisted reproductive technology, like in vitro fertilization or ovulation induction; or increased maternal age or parity. On a physical exam, you may notice the uterine size is greater than expected based on your patient’s last menstrual period. 

Next, order an obstetric ultrasound, which will be most accurate when performed at the end of the first trimester or early second trimester. The ultrasound allows you to assess the number of fetuses, the chorionicity, and the amnionicity, which will guide the management of the pregnancy. This is also a good time to consult the maternal-fetal medicine team for their involvement in your patient’s care! 

If the obstetric ultrasound demonstrates two fetuses, then you know this is a twin pregnancy.  Next, look for the twin peak sign, also known as the lambda sign, which looks like a triangular wedge of placental tissue extending at the base of the intertwin membrane. If this is present, then you know there are two placentas and each fetus is separated by a thick membrane; so your diagnosis is a dichorionic diamniotic twin pregnancy! 

Now, s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_birth_injury_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LoIkGZq0Tt6joVR2xj140Hm2TOypvY_u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to birth injury (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Birth injury refers to any physical harm to a newborn that occurs during labor or delivery. Many birth injuries result from prolonged labor or a precipitous delivery; a difficult or instrumental delivery; macrosomia; or fetal malpresentation. Common birth-related injuries include head injuries, nerve damage, bone fractures, and soft tissue injury. 

When a pediatric patient presents with a chief concern suggesting a birth injury, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation, and consider intubation for ineffective respirations or apnea. Next, obtain intravenous access or perform an umbilical venous catheterization, and consider starting IV fluids or transfusing packed red blood cells. Then, place your patient on continuous vital sign monitoring, and provide supplemental oxygen if needed.  

Once you’ve initiated acute management, perform a focused history and physical examination. History might reveal risk factors such as preterm delivery, prolonged labor, or instrumental delivery. As far as the physical exam goes, you’ll often notice an altered level of consciousness and tachycardia. These findings should make you consider the possibility of a hemorrhage. Proceed with your evaluation by assessing the scalp for progressive edema. 

If progressive edema is present, consider a subgaleal hemorrhage. In this case, birth history often reveals that the delivery required vacuum assistance. The physical exam will reveal a boggy scalp with edema that crosses the suture lines, that manifests in the first few hours after birth, and moves posteriorly to the level of the ears, often pushing the ears outward and extending to the nape of the neck. The occipital-frontal head circumference will also be increased.  

Now, due to the potential for massive blood loss, in addition to tachycardia, these patients often develop tachypnea and hypotension, as well as pallor and eventua]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_postpartum_fever:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Nx9PWi_DSbSnkz-CfSgnzgy8RrW48AAe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to postpartum fever: Clinical sciences]]></video:title><video:description><![CDATA[Postpartum fever is a temperature of 38 degrees Celsius or 100.4 degrees Fahrenheit or more on two occasions at least four to six hours apart, excluding the first 24 hours after birth. Postpartum febrile episodes often resolve without intervention if occurring within the first 24 hours of delivery, and for this reason the threshold for a fever in the first day after delivery is typically set at 39 degrees Celsius or 102.2 degrees Fahrenheit. The source of a maternal postpartum fever varies based on how many days your patient presents after birth, particularly within the first 7 days postpartum. 

Now, if your patient presents with a postpartum fever, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and start fluid resuscitation, and consider starting broad-spectrum intravenous antibiotics. Place your patient on continuous vital sign monitoring, including blood pressure, heart rate, and oxygen saturation. Finally, if needed, provide supplemental oxygen! 

Okay, now let’s go back to the ABCDE assessment and take a look at stable patients. Start by obtaining a focused history and physical examination; then obtain labs including a CBC, urinalysis, and urine culture. Next, review the mode of delivery, and how many days away they are from delivery.  

Here’s a clinical pearl! It’s common for patients to have a transient low-grade fever within the first 24 hours postpartum, particularly in patients who delivered vaginally, or who have been treated for an intraamniotic infection. Other factors that might cause a transient postpartum fever include misoprostol use, dehydration, and epidural analgesia. However, if your patient has a temperature greater than 39 degrees Celsius or 102.2 degrees Fahrenheit on the first day after delivery, don’t delay looking for a cause! 

First let’s discuss conditions which can present within the firs]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Therapeutic_and_induced_abortions:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DevGd0k7Q5iXhzp2G-VxDJ1WQjii9xxO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Therapeutic and induced abortions: Clinical sciences]]></video:title><video:description><![CDATA[Therapeutic abortion refers to termination of pregnancy for medical indications; while an induced abortion, also known as an elective abortion, is performed because an individual chooses to end a pregnancy. Be sure to differentiate these two from pregnancy loss, which includes missed, threatened, inevitable, complete, incomplete, and septic abortion. 

Both therapeutic and induced abortions are extremely safe, especially in the first trimester when the vast majority of them occur. In fact, in the United States over 90% of induced abortions occur in the 1st trimester; fewer than 10% occur between 13 to 20 weeks, and fewer than 1%  occur after 20 weeks gestation.  

Before jumping into management, let’s review abortion care keeping reproductive rights in mind. These are focused on the understanding that all people have a fundamental right to decide whether to have children, the number and spacing of their children, and to have the information, education, and access to health services to make these choices.  

Across the United States, reproductive rights vary in legality and accessibility, particularly for adolescents, people of color, individuals living in rural areas, those with low incomes, and incarcerated individuals.  

Many factors influence the decision to obtain an abortion including contraceptive failure, barriers to contraceptive access and use, sexual assault, incest, intimate partner violence, fetal anomalies, and exposure to teratogenic medications.  

There are also scenarios where severe pregnancy complications can be life-threatening, in which case an abortion is safer than a continued pregnancy. These include hemorrhage from placental abruption, placenta previa, or inevitable abortions; preeclampsia and eclampsia; chorioamnionitis causing sepsis; and underlying cardiac or renal conditions in the pregnant patient.  

Here’s a clinical pearl! Strict abortion laws do not eliminate the occurrence of abortions; however, they creat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nephritic_syndromes_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/spQuK1xIQpybhush9mWU-0EdSpOe_W3U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nephritic syndromes (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Nephritic syndrome refers to a group of symptoms that result from glomerulonephritis, or inflammation and damage to the kidney’s glomeruli. This damage results in edema, hypertension, decreased urine output, and hematuria. Various underlying conditions can lead to nephritic syndrome, including infections, genetic conditions, and autoimmune diseases. 

When a pediatric patient presents with a chief concern suggesting nephritic syndrome, first perform an ABCDE assessment to determine if the patient is unstable.  

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, put your patient on continuous vital sign monitoring including heart rate, blood pressure, and pulse oximetry, and provide supplemental oxygen if needed. 

Here’s a clinical pearl to keep in mind! While you’re stabilizing your patient, also evaluate for and correct electrolyte abnormalities, like hyperkalemia, that can occur with nephritic syndrome. 

Now, let’s go back to the ABCDE assessment and look at stable patients.  

First, obtain a focused history and physical examination, which can help you distinguish nephritic syndrome from nephrotic syndrome. Keep in mind that these two conditions can have overlapping symptoms and even occur simultaneously.  

First, let’s discuss nephrotic syndrome.  

Patients with nephrotic syndrome usually report swelling, often in combination with malaise, headache, fatigue, or irritability. If the physical examination reveals edema, you should suspect nephrotic syndrome.  

To confirm the diagnosis, obtain a urinalysis; a urine protein-to-creatinine ratio; a serum albumin; and a lipid panel. If the urinalysis is positive for protein, the protein-to-creatinine ratio reveals nephrotic range proteinuria, the serum albumin is low, and serum lipids are elevated, diagnose nephrotic syndrome. 

Now, let’s discuss nephritic syndrome.  

These patients have frankly bloody urine, cola-colored, or tea-colored urine and decreased urine o]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_leukocoria_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7h2oT87MSkmRS9NVuYRQz594RYuU-n9o/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to leukocoria (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Leukocoria refers to a white or pale pupillary reflex, and its presence suggests a structural abnormality within the visual axis. It’s important to identify underlying causes of leukocoria promptly, since these conditions can either be lethal or lead to profound visual impairment if left untreated. A thorough ophthalmologic exam can distinguish intraocular masses from other abnormalities involving the lens, retina, or vitreous. 

When a pediatric patient presents with leukocoria, first perform a focused history and physical examination, including vision screening and direct ophthalmoscopy.  

Now here’s a clinical pearl to keep in mind! You can look for leukocoria by checking your patient’s red reflex. To do so, dim the lights to ensure the pupils are dilated. Then, look through an ophthalmoscope while standing approximately 2 feet away from your patient. View each eye separately and both eyes together. During this test, light from the ophthalmoscope normally reflects back from the illuminated retina, producing a reddish-orange glow. A bilateral red reflex suggests the absence of structural pathology within the visual axis, but a white, pale, or absent reflex requires further examination. 

Now back to our patient!  

History often reveals visual changes, and in some cases, there’s a family history of retinoblastoma. During vision screening, you may identify vision loss, and the exam will reveal a unilateral or bilateral white pupillary reflex. This confirms leukocoria, so to find out what&amp;#39;s causing it, refer your patient urgently for a complete ophthalmologic exam, including a dilated fundoscopic exam with indirect ophthalmoscopy and a slit lamp exam. Keep in mind that patients who cannot tolerate an office evaluation may require an exam under anesthesia. 

Here’s a clinical pearl! Although a white reflex raises concern for serious pathology, it can also represent a benign, transient finding called pseudoleukocoria, often seen in a flash photogra]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_jaundice_(newborn_and_infant):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y5cKekwfRzSnuBbYjQdsBTgVTjeYLxgR/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to jaundice (newborn and infant): Clinical sciences]]></video:title><video:description><![CDATA[Jaundice is a yellowish discoloration of the skin and sclerae caused by elevated serum bilirubin, or hyperbilirubinemia. While jaundice is a common and benign physiologic phenomenon in newborns, it&amp;#39;s considered pathologic if it progresses rapidly, begins within the first day of life, persists beyond 2 weeks of age, or if there is evidence of cholestasis. 

If a newborn or infant presents with jaundice, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, and begin IV fluids if needed. Put your patient on continuous vital sign monitoring and lastly, provide supplemental oxygen, if needed. 

Here’s a high-yield fact! Because unconjugated bilirubin is a lipid-soluble neurotoxic substance that crosses the blood-brain barrier, excessively high levels can lead to acute bilirubin encephalopathy. This life-threatening condition manifests with lethargy, hypotonia, and a high-pitched cry. If left untreated, it can lead to opisthotonos, seizures, death, or chronic bilirubin encephalopathy, known as kernicterus, due to permanent brain damage. Once you recognize severe jaundice, consider an urgent exchange transfusion. 

Okay, let’s return to the ABCDE assessment and discuss stable patients. In this case, obtain a focused history and physical examination. Caregivers usually notice jaundice in the face first, followed by the trunk and lower extremities. The exam may reveal scleral icterus and yellowish skin, suggesting unconjugated hyperbilirubinemia; or yellowish-green skin, suggesting conjugated hyperbilirubinemia. These findings confirm the presence of jaundice.  

Remember that a visual assessment of jaundice isn’t always reliable in newborns with deeply pigmented skin; so obtain a transcutaneous bilirubin level, which estimates the total serum bilirubin. Then, plot the result on a nomogram, using the patient’s age in hours. If it falls within ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hypotonia_(newborn_and_infant):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J9nzurG4Swen9BPgJWQmDj7KSz_fz4Sw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hypotonia (newborn and infant): Clinical sciences]]></video:title><video:description><![CDATA[Hypotonia, or decreased muscle tone, is characterized by poor movement and posture control or delayed motor skills. Newborns or infants with hypotonia are often described as “floppy”. You can categorize hypotonia as conditions affecting the central or peripheral nervous system. 

If a pediatric patient presents with hypotonia, perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation, and consider intubation if necessary. Obtain IV access, consider giving IV fluids, begin continuous vital sign monitoring, and provide supplemental oxygen if needed. Finally, consider a full sepsis workup and antibiotics for newborns, since hypotonia might be related to sepsis. 

When it comes to stable patients, your next step is to obtain a focused history and physical examination. There are a few things you should look out for. Generally, these patients present with motor delay. It is also important to determine if hypotonia was present at birth or developed progressively, as this will be a clue to the cause. Be sure to assess for clues of central nervous system (CNS) involvement like seizures, cognitive, vision, or hearing issues. Next, assess if there is upper or lower motor neuron involvement.  

As a reminder, upper motor neuron lesions will present with spasticity and hyperreflexia, while lower motor neuron lesions will present with hypotonia and reduced or absent reflexes. Finally, ask about family history.  

First, let’s discuss central nervous system etiologies of hypotonia. History might include developmental regression or seizures, while the exam reveals reduced alertness, normal strength, and hyperactive or normal reflexes, as well as the presence of primitive reflexes. Patients may have microcephaly or macrocephaly, and their eyes might not track. They might display hand fisting or scissoring on vertical suspension. With these findings, consider a central nervous system etiology. Obta]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_complications_of_prematurity_(early):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nflZcvGXS3ucVDpZuVswr35TQTynOmVF/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to complications of prematurity (early): Clinical sciences]]></video:title><video:description><![CDATA[Complications of prematurity, or birth before 37 weeks of gestation, can increase a newborn’s risk of morbidity and mortality. These complications are related to the newborn’s developmental and functional immaturity and tend to increase in frequency and severity with decreasing gestational age and birthweight. 

If a pediatric patient presents with a chief concern suggesting an early complication of prematurity, perform an ABCDE assessment to determine if they are stable or unstable. These patients are typically unstable, so stabilize their airway, breathing, and circulation; and consider intubation. Next, obtain intravenous or intraosseous access, or consider placing an umbilical venous catheter. Next, start IV fluids and begin continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry. Finally, if needed, don’t forget to provide supplemental oxygen. 

Once you’ve stabilized your patient, obtain a focused history and physical examination, which will often reveal nonspecific findings associated with various complications of prematurity. These may include a history of apneic episodes, lethargy, or poor feeding.  As far as the exam goes, some signs to look out for include temperature instability, tachycardia, or hypotension. 

A common complication to consider is sepsis, especially if there are risk factors such as chorioamnionitis, exposure to group B streptococcus during delivery, or prolonged rupture of membranes. Next, order blood cultures, possibly in combination with cerebrospinal fluid and urine cultures. Any bacterial growth of a pathogen confirms the diagnosis, which should be treated promptly with broad-spectrum IV antibiotics. 

Now, keep in mind that your patient’s cultures will be negative if there’s no underlying infection, or if not enough time has elapsed for an organism to grow. Regardless of culture results, you’ll need to continue your evaluation for other complications of prematurity.  

Start by assessing ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Neonatal_respiratory_distress_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cmeJw5QNRCuSaUIFZaIZ9VhDTm_Cuf-j/_.png</video:thumbnail_loc><video:title><![CDATA[Neonatal respiratory distress syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Neonatal respiratory distress syndrome, also called neonatal RDS or hyaline membrane disease, is a life-threatening condition characterized by lung immaturity and alveolar surfactant deficiency. Now, surfactant is a complex of phospholipids and proteins that reduces alveolar surface tension and prevents collapse of the alveoli. Alveolar cells called type 2 pneumocytes produce surfactant beginning around 24 to 26 weeks of gestation, and it doesn’t reach mature levels until 34 to 36 weeks of gestation, so the incidence of neonatal RDS is inversely related to gestational age at birth.  

Surfactant deficiency causes decreased lung compliance, atelectasis, low lung volumes, inflammation, pulmonary edema, and pulmonary arterial vasoconstriction; all of which result in hypoxia, hypercapnia, and acidemia. 

Now, if a pediatric patient presents with a chief concern suggesting neonatal RDS, perform an ABCDE assessment to determine if they are stable or unstable. These patients are typically unstable, so begin acute management immediately. First, stabilize their airway, breathing, and circulation; and then provide noninvasive respiratory support, such as nasal continuous positive airway pressure, or nasal CPAP. If your patient is apneic or has a poor respiratory effort, you may need to perform endotracheal intubation and begin mechanical ventilation. Next, obtain intravenous or intraosseous access, or consider placing an umbilical venous catheter.  

Then, start IV fluids; begin continuous vital sign monitoring, including heart rate, blood pressure, pulse oximetry, and respiratory rate; and provide supplemental oxygen to maintain oxygen saturations between 90 and 95 percent. 

Once you stabilize your patient, perform a focused history and physical examination and obtain pulse oximetry measurements. History will reveal the onset of respiratory distress within minutes or hours of birth. These patients are typically premature, with the majority being between 23 and 29 ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_cyanosis_(newborn):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MxiruqisR36hsVRaSqHtQKbbRjaz7XEq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to cyanosis (newborn): Clinical sciences]]></video:title><video:description><![CDATA[Newborn cyanosis refers to blue or purple skin discoloration that results from poor circulation or inadequate blood oxygenation and indicates a potentially life-threatening condition. Peripheral cyanosis involves the distal extremities only, while central cyanosis also involves the face, trunk, mucous membranes, and tongue. Possible causes of central cyanosis include cyanotic congenital heart disease, pulmonary hypertension, respiratory depression, upper airway obstruction, pulmonary disease, sepsis, and hemorrhagic shock.  

Here&amp;#39;s a high-yield fact! Acrocyanosis describes bluish-purple discoloration that is isolated to the hands and feet. Unlike central cyanosis, this is a common, transient, and benign finding in the immediate newborn period and is caused by immature vascular tone. 

When evaluating a newborn patient with cyanosis, first perform an ABCDE assessment to determine if they are stable or unstable.  Newborns with cyanosis are considered unstable, so stabilize their airway, breathing, and circulation; and intubate if needed. Next, obtain IV or IO access, place your patient on continuous vital sign monitoring, and provide supplemental oxygen.  

Once you’ve initiated acute management, obtain a focused history and physical exam.  The perinatal history might reveal maternal infection or opioid use, meconium-stained amniotic fluid, a complicated birth, or a cesarean or preterm delivery. On physical exam, you’ll notice a blue or purple discoloration of the skin of the extremities and trunk, as well as the mucous membranes and tongue. This finding confirms the presence of central cyanosis. Keep in mind that a visual assessment of cyanosis isn’t always reliable in newborns with deeply pigmented skin, so check areas where the skin is thinnest or has the least amount of pigment, like the oral mucosa, conjunctiva,  or nail beds, where cyanosis can sometimes present as grayish-blue!  

Now that you’ve identified cyanosis, you should consider the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_atypical_genitalia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZUDHxFn_S-O0ywX5T4EGnl-MS0OrXp8c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to atypical genitalia: Clinical sciences]]></video:title><video:description><![CDATA[Atypical genitalia refers to external genitalia that do not appear to be completely male or female and suggests a disorder of sexual development, which is also known as differences in sexual development, or DSD for short. These conditions occur due to complex interactions of genes, proteins, and hormones that regulate genital development and can be associated with gonadal malignancy, impaired fertility, as well as psychosocial issues, such as gender dysphoria and low self-esteem.  

Based on the underlying cause, atypical genitalia can result from chromosomal or genetic abnormalities, excess circulating androgens, gonadal dysfunction, and defects in steroid production or action.  

The first step in evaluating a patient who presents with atypical genitalia is to perform a focused history and physical examination. The history may reveal consanguinity or a family history of infertility, unexplained newborn deaths, as well as a history of steroid-based medications or some types of antiseizure medications.  

The physical exam reveals atypical genitalia with one or more atypical findings. In apparent male newborns, these include bilateral undescended testes; bifid scrotum; or hypospadias with coexisting micropenis or an undescended testicle. In apparent females, you might see clitoromegaly or posterior labial fusion; a single genitourinary opening; or an inguinal hernia or mass.  

Here are some important clinical pearls! At first glance, some normal findings can give the appearance of atypical genitalia. For instance, clitoral or labial swelling in newly born biological female infants might be mistaken for clitoromegaly, while an enlarged suprapubic fat pad can make a biological male infant’s penis appear smaller than it is. Some abnormal findings in biological males that require further evaluation but do not suggest DSD include isolated hypospadias or a unilateral undescended testicle. 

Now, the identification of atypical genitalia in a newborn can be distr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_feeding_and_eating_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ivO3NzyZTlWBP2mBRpXlaj3KRmypsQcZ/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to feeding and eating disorders: Clinical sciences]]></video:title><video:description><![CDATA[Feeding and eating disorders are conditions in which abnormal eating-related habits contribute to poor food consumption or absorption to such a degree that physical or mental health is impaired.  

Feeding disorders include conditions such as pica and avoidant restrictive food intake disorder while eating disorders include binge-eating disorder, bulimia nervosa, and anorexia nervosa.  

When a patient presents with a chief concern suggesting an eating disorder, first, perform an ABCDE assessment to determine if they are stable or unstable. If unstable, initiate acute management by stabilizing their airway, breathing, and circulation. Also, administer supplemental oxygen if needed, obtain IV access, and consider starting IV fluids. Then, continuously monitor vital signs including respiratory rate, pulse oximetry, and cardiac telemetry.  

Your next step is to obtain a focused history and physical exam and order labs, including CBC, CMP, serum magnesium, phosphate, and urinalysis, as well as a 12-lead ECG.  

History might reveal greater than 10 percent weight loss in the last 6 months, while the exam might show bradycardia, hypotension, or even hypothermia. Additionally, the body mass index, or BMI, might be less than 15.  

On labs, CBC could reveal low hemoglobin suggesting anemia. You might also find hypoglycemia, or electrolyte imbalances such as hyponatremia, hypomagnesemia, hypophosphatemia.   

In some cases there might be an acid-base disorder. For example, excessive vomiting can lead to metabolic alkalosis while laxative abuse causing excessive diarrhea can result in metabolic acidosis.  

Additionally, urinalysis might reveal the presence of ketones.  Finally, ECG findings can include QTc prolongation, arrhythmias, and other changes related to electrolyte disturbance. 

These findings should make you think of severe malnutrition from a feeding or eating disorder, most commonly anorexia nervosa or bulimia nervosa.When it comes to management,  patie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_growth_faltering:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0LOXhAg9TteK1xZgGwYhR3ZBSnmgInGf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to growth faltering: Clinical sciences]]></video:title><video:description><![CDATA[Growth faltering refers to the inability to gain or maintain adequate weight as a consequence of malnutrition. Growth faltering is most frequently caused by insufficient caloric intake, but it can also result from an underlying condition that’s associated with increased metabolic requirements or malabsorption. 

When a pediatric patient presents with growth faltering, you should first obtain measurements of weight and height or length; and plot the results on a standardized growth chart.  

Next, review the growth parameters. If your patient’s weight-for-age or BMI is more than 2 standard deviations below the mean for age and biological sex on multiple occasions; or if their weight-for-age has crossed 2 major percentile lines; your patient’s growth is faltering. 

Here’s a clinical pearl! In some circumstances, a low or decelerating weight-for-age represents a normal variant of growth. For example, preterm infants whose growth parameters haven’t been adjusted for gestational age may appear to have insufficient weight gain.  

Conversely, infants born large for gestational age experience catch-down growth in the first 6 months of life, and may appear to have faltering growth while their weight is regressing to their expected growth trajectory. Finally, a child with familial short stature may have a consistently low but appropriate weight-for-age. When in doubt, check your patient’s weight-for-length or weight velocity, to determine whether a low weight-for-age requires further evaluation. 

Now that you’ve identified growth faltering, your next step is to obtain a focused history and physical exam. Be sure to ask whether your patient has a chronic health condition, a history of frequent infections, or a significant developmental delay. Additionally, find out if your patient has had frequent vomiting or an abnormal stooling pattern.  

When it comes to the physical exam, some signs to look out for include characteristic facial features that suggest a genetic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_neurodevelopmental_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3fY8zI77QreybzYuizY5k5avTxa9S353/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to neurodevelopmental disorders: Clinical sciences]]></video:title><video:description><![CDATA[Neurodevelopmental disorders are conditions characterized by early childhood developmental delays and deficits, which can affect personal, social, academic, or occupational functioning.  

The severity of neurodevelopmental disorders varies widely. Some patients do well with the right support and can take part in family, school, and community life, while others have more severe challenges and need full-time assistance.  

It’s important to identify these disorders as early as possible because the sooner help begins, the better the outcome.  

Now, major types of neurodevelopmental disorders include autism spectrum disorder, attention deficit hyperactivity disorder or ADHD, Tourette syndrome, and intellectual disability. 

When a patient presents with a chief concern suggesting a neurodevelopmental disorder, your first step is to obtain a focused history and physical exam.  

Most patients present in early childhood, and caregivers commonly have concerns about the child’s development or behavior. Many of these children have already been diagnosed with one or more developmental delays, such as motor or language delays. They might also have been diagnosed with genetic conditions like fragile X or Rett syndrome.  

The physical exam is typically unremarkable unless the patient has distinct phenotypic features due to an underlying genetic syndrome. For example, with fragile X syndrome, the patient might have narrow long facies, with large ears; while those with Rett syndrome have a characteristic hand wringing. If you see these findings, consider a neurodevelopmental disorder. 

To identify the specific condition you are dealing with, you’ll need to investigate further. Start by assessing for social disengagement, a key feature of autism spectrum disorder, or ASD. If social disengagement is present as a primary concern for your patient, expand your history to ask specifically about signs and symptoms of autism.   

Caregivers commonly report that the child appe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Attention_deficit_hyperactivity_disorder_(ADHD):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nrmdc_eFTx_1LmM4YpiCrjVgR9eOQFg9/_.png</video:thumbnail_loc><video:title><![CDATA[Attention deficit hyperactivity disorder (ADHD): Clinical sciences]]></video:title><video:description><![CDATA[Attention-deficit hyperactivity disorder, or ADHD, is a common neurodevelopmental disorder characterized by excessive levels of inattention, hyperactivity, and impulsivity. As a result of these symptoms, children with ADHD experience impaired social, emotional, and academic functioning; and many exhibit poor impulse control. Timely diagnosis, and age-appropriate management of ADHD, improve long-term social, emotional, academic, and occupational outcomes. 

Now, if a pediatric patient presents with a chief concern suggesting ADHD, you should first obtain a focused history and physical exam. Most patients present after four years of age, and caregivers or teachers report excessive hyperactivity, impulsivity, or inattention. These children often demonstrate academic underachievement and poor emotional regulation, as well as delayed social and play skills.  

The history may also reveal risk factors for ADHD, such as prematurity, low birth weight, or adverse childhood experiences; while the family history often reveals one or more family members with ADHD. The physical exam is often unremarkable unless the patient has a coexisting condition with distinct phenotypic features, such as fetal alcohol syndrome or fragile X syndrome. 

Here’s a clinical pearl! Toddlers tend to have high energy levels and short attention spans, so it can be challenging to determine whether their behaviors are developmentally appropriate. For this reason, ADHD is not usually diagnosed before 4 years of age. However, any child with concerning behaviors should be referred for evaluation and early intervention services. 

Alright, with these findings, you should suspect ADHD and arrange for a comprehensive psychoeducational evaluation. This evaluation includes a developmental and behavioral history that focuses on early childhood development, troublesome behaviors, and academic performance.  

Parent- and teacher-reported behavioral rating scales can be used during the initial evaluation]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_child_with_Down_syndrome_(trisomy_21):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pxoIddw4TXqj6b0G7dELUmNZTIS_OEQ4/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to a child with Down syndrome (trisomy 21): Clinical sciences]]></video:title><video:description><![CDATA[Down syndrome, or trisomy 21, is a genetic condition most commonly associated with an extra copy of chromosome 21. The health and quality of life for children with Down syndrome can be optimized with medical surveillance, family and community support, and early intervention services.  

If a pediatric patient presents with a chief concern suggesting Down syndrome, first obtain a focused history and physical exam. These patients may have been identified with prenatal screening, and the biological mother might be of advanced maternal age, which is a risk factor for chromosomal nondisjunction. Physical exam reveals classic facial features, like upslanting palpebral fissures, epicanthal folds, a flat facial profile, and low-set small ears. Patients also have a short neck with excessive skin folds at the nape; a single palmar crease; and an unusually wide space between the first and second toes on their feet called a sandal toe gap. Finally, you’ll typically see generalized hypotonia, significant head lag, and a weak moro reflex.  

With these findings, consider Down syndrome and order a karyotype. If it reveals trisomy of chromosome 21, diagnose Down syndrome. 

Here’s a clinical pearl! In most cases, Down syndrome is caused by nondisjunction, which results in an extra copy of chromosome 21. However, it can also be caused by mosaicism, where some cells have 2 and others 3 copies of chromosome 21; or translocation, where part of chromosome 21 becomes attached to another chromosome. When a parent carries a balanced translocation, their children can acquire extra genetic material from chromosome 21, resulting in an unbalanced translocation. This form of Down syndrome carries a higher risk of recurrence compared to nondisjunction and mosaicism. Because all forms of Down syndrome can present with a similar phenotype, it&amp;#39;s important to perform genetic testing and offer genetic counseling, to determine the potential recurrence risk. 

After confirming the di]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_connective_tissue_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cxJ8847rRluUQeZZrQ3xjk2rSeiRIGkU/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to connective tissue disorders: Clinical sciences]]></video:title><video:description><![CDATA[Connective tissue disorders occur when a component of the extracellular matrix is deficient or defective, resulting in fragility of the bones, tendons, ligaments, blood vessels, and skin. While some connective tissue disorders cause mild manifestations, others result in chronic pain and disability due to progressive bone and joint deformity. Because some connective tissue disorders affect long bone growth, evaluation of these patients should include assessment of stature. 

Now, when a pediatric patient presents with a chief concern suggesting a connective tissue disorder, first obtain a focused history and physical examination. Children may present with chronic joint pain; recurrent joint dislocations or bone fractures; or fragile skin that heals poorly. These children also frequently have ophthalmological manifestations, such as severe myopia; and they might have a first or second degree relative with a connective tissue disorder.  

On physical exam, you’re likely to notice joint hypermobility, and you may detect changes in skeletal or facial morphology, such as excessively long or short limbs or unusual facial features. With any combination of these findings, consider connective tissue disorder. 

As a next step, assess your patient’s stature. To do this, look at their growth curve, and calculate a midparental height, to determine whether their linear growth rate correlates with their anticipated adult height. 

Now, if your patient is significantly taller than anticipated, consider connective tissue disorders that are associated with excessive growth of the long bones. These include Marfan syndrome and homocystinuria. 

Let’s start by discussing Marfan syndrome. These children usually experience chronic joint pain, and some have a history of ectopia lentis, which is dislocation of the optic lens that can result in ocular pain, myopia, and diplopia; pneumothorax; or aortic dissection. There may also be a family history of Marfan syndrome.  

Exam typic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Immediate_care_of_the_well_newborn:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pftwFdf5QCapaMNmwwF8BxvWSqW6Zx5U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Immediate care of the well newborn: Clinical sciences]]></video:title><video:description><![CDATA[Immediate care of the well newborn begins at birth and continues through hospital discharge. Routine newborn care includes identification of any abnormalities requiring further investigation, as well as support for newborn feeding; administration of immunizations and preventive medications; routine screenings; anticipatory guidance; and optional care such as circumcision. 

When a well newborn presents for immediate care, your first step is to obtain a comprehensive history and physical examination. Also be sure to review the prenatal and maternal history in addition to the birth history, along with the newborn’s gestational age and Apgar scores.  

Now, here’s a clinical pearl! The Apgar score provides a standardized assessment of a newborn’s general condition at 1 and 5 minutes after birth. This score consists of 5 categories: Appearance of the skin, which should be pink rather than pale or cyanotic; Pulse rate, which should be over 100 beats per minute; Grimace, or the newborn’s response to stimulation, also called reflex irritability; Activity, or muscle tone and spontaneous movement; and Respiration, or breathing effort. For each category, a newborn receives up to 2 points. A combined score of 7 to 10 is considered normal, whereas infants with scores lower than 7 require further monitoring.  

Remember to ask caregivers about any concerns, as well as social determinants of health, like tobacco exposure, intimate partner violence, and food insecurity. Next, perform a physical exam, starting with vital signs and general appearance. Also observe the caregiver-newborn interaction, including how they respond to their newborn’s cues by attempting to comfort or feed them when they cry. 

Then, proceed with a head-to-toe exam, starting with a skin assessment. A healthy newborn’s skin is pink, without cyanosis or jaundice. Keep in mind that a visual assessment of skin color isn’t always reliable in newborns with deeply pigmented skin, so check areas where the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_antisocial,_borderline,_histrionic,_and_narcissistic_(cluster_B)_personality_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t_zdIWTyRsakdl7ppiuOdwSZRwWd3lKk/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to antisocial, borderline, histrionic, and narcissistic (cluster B) personality disorders: Clinical sciences]]></video:title><video:description><![CDATA[Personality disorders represent an enduring and pervasive pattern of perceiving and relating to oneself, others, and the world in an atypical, and often detrimental, way.  

Unlike most psychiatric conditions, personality disorders are frequently ego-syntonic, meaning many people with personality disorders do not perceive their behaviors as problematic. Consequently, these disorders typically do not cause direct distress to the individual but can lead to significant interpersonal and occupational difficulties.  

There are ten personality disorders defined in the Diagnostic and Statistical Manual of Mental Disorders fifth edition, or DSM-5TR for short, and these are divided into clusters A, B, and C. Cluster B personality disorders include antisocial personality disorders, borderline personality disorders, narcissistic personality disorders, and histrionic personality disorders. 

Now, when a patient presents with a chief concern suggesting a personality disorder, first obtain a focused history and physical exam. Symptoms might include significant interpersonal or occupational difficulties, patterns of hyper-dependence or hyper-independence with others, and a tendency to blame others for their own feelings and behaviors. Additionally, you might find frequent or extreme mood swings, angry outbursts, and attention seeking behaviors.  

Keep in mind many of these traits might be reported by family, teachers, or friends.  The physical exam is often unremarkable, but you might notice extremes of affect, ranging from flat to exaggerated facial expressions during your interaction with the patient. With these findings, consider a personality disorder. 

Your next step is to assess your patient for a general personality disorder using the DSM-5 criteria. All personality disorders are characterized by an enduring pattern of thinking, feeling, and behaving in culturally atypical ways, and these traits are inflexible and maladaptive in multiple settings. The onset of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_avoidant,_dependent,_and_obsessive-compulsive_(cluster_C)_personality_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/btJoG4tvR4K8AjP_kpzUuVfnQau1FOfC/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to avoidant, dependent, and obsessive-compulsive (cluster C) personality disorders: Clinical sciences]]></video:title><video:description><![CDATA[Personality disorders are characterized by an enduring and pervasive pattern of perceiving and relating to oneself, others, and the world in atypical, and often detrimental, ways.  Unlike individuals with other psychiatric conditions, those with personality disorders have ego-syntonic thoughts and behaviors, meaning they do not perceive their condition as problematic. Consequently, personality disorders typically do not cause direct distress to the individual but can lead to significant interpersonal and occupational difficulties.  

There are ten personality disorders defined in the Diagnostic and Statistical Manual of Mental Disorders fifth edition, or DSM-5 for short; and these are divided into clusters A, B, and C. Cluster C personality disorders include avoidant personality disorder, obsessive-compulsive personality disorder, and dependent personality disorder. 

Now, when a patient presents with a chief concern suggesting a personality disorder, first obtain a focused history and physical exam. Symptoms might include significant interpersonal or occupational difficulties,  

And patterns of hyper-dependence on or hyper-independence from others. The patient could also have a tendency to blame others for their own feelings and behaviors.  Additionally, you might find frequent or extreme mood swings, angry outbursts, and attention seeking behaviors.  Keep in mind many of these traits might be reported by family, teachers, or friends.  

The physical exam is often unremarkable, but you might notice extremes of affect, ranging from flat to exaggerated facial expressions during your interaction with the patient.  With these findings, consider a personality disorder. Your next step is to assess your patient for a general personality disorder using the DSM-5 criteria.  

All personality disorders are characterized by an enduring pattern of thinking,  feeling,  and behaving in culturally atypical ways;  and these traits are inflexible and maladaptive in multi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_adrenal_masses:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YORt6VHDTVi2KYBeevIwncbuTsyRLtdU/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to adrenal masses: Clinical sciences]]></video:title><video:description><![CDATA[Adrenal masses are abnormal growths that develop in one or both adrenal glands, which are triangular-shaped glands located on top of each kidney.  

The majority of adrenal masses are benign adenomas, which can be either non-functional, meaning they don’t secrete hormones; or functional, meaning they secrete hormones like normal adrenal tissue would, which can cause specific symptoms depending on which hormone they secrete.  

When an adrenal mass is discovered, the two main questions that arise are if the mass is malignant or benign, and if it’s functional.  

Now, when a patient presents with a chief concern suggesting an adrenal mass, your first step is to obtain a focused history and physical examination. 

Next you must determine if the patient is asymptomatic or symptomatic.  

If your patient is asymptomatic, then you should ask about any recent imaging that has been done.  

Typically, these patients present after an incidental finding of an adrenal mass on CT or MRI; usually performed for an unrelated issue such as trauma or other intra-abdominal problem. They might also have a history of malignancy, so make sure to ask!  

The physical exam is often normal in these patients, leading you to consider an adrenal incidentaloma.  

Your next step is to obtain a CT scan or an MRI of the abdomen.  

If imaging reveals a mass less than 4 centimeters, with regular shape, smooth borders,  and a low density of less than 10 Hounsfield units on CT, it’s most likely a benign adrenal adenoma.  

These tumors have a very low malignant potential and usually remain stable in size. Small benign asymptomatic adenomas do not require any surgical intervention. 

Here’s a clinical pearl! Most adrenal incidentalomas are nonfunctional, but those that are at least one 1 centimeter should be investigated further with imaging and biochemical testing to identify adrenal hyperfunction.    

Now let&amp;#39;s go back and look at malignant masses.  

In this case, imaging will]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_Nursing_Platform_Tool</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ViAQIjANQV6_hLkWAoC0zIDPRYWbxutr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osmosis Nursing Platform Tool]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis Nursing Platform Tool through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_common_skin_rashes:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jGl3YsfJRwaW7ejggl4D0pQ6Ty2ruGao/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to common skin rashes: Clinical sciences]]></video:title><video:description><![CDATA[A skin rash is an area of irritated or inflamed skin that reflects the body’s reaction to a localized or systemic process. It can result from external contact exposure or an internal process causing immune dysregulation or infiltration of inflammatory cells. It’s important to first identify if an adverse medication reaction is the cause of your patient’s rash as this might be potentially life-threatening.  

Other possible diagnoses include infectious causes such as folliculitis, scabies, shingles, and tinea corporis; and inflammatory or autoimmune causes such as atopic dermatitis, contact dermatitis, seborrheic dermatitis, acne vulgaris, rosacea, and psoriasis.  

Now, if your patient presents with a skin rash, first perform a focused history and physical examination.  

Your patient will report a rash that might be red, itchy, scaly, or painful. The physical exam will reveal a rash that might be erythematous, macular, papular, vesicular, or comprised of discrete plaques. At this point, diagnose dermatitis, a nonspecific diagnosis that indicates inflammation of the skin.  

Next, assess for a cutaneous adverse medication reaction. These patients report a widespread rash that appeared in as little as one day and up to three weeks after starting a medication such as an antibiotic, NSAID, or antiepileptic.  

The physical exam will show an erythematous maculopapular eruption, and there might be dark red or purpuric macular lesions or urticaria.  

With these findings, diagnose cutaneous adverse drug reaction. 

Here’s a clinical pearl! Urticaria, better known as hives, is a common, usually self-limiting, skin reaction triggered by medications, certain foods, allergens, or stress. Symptoms include itchy, raised red wheals, also known as welts, on the skin’s surface. Acute urticaria may progress rapidly to life-threatening angioedema or anaphylactic shock. The mainstay of treatment is avoiding further exposure to the suspected trigger! 

Here&amp;#39;s a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_paranoid,_schizoid,_and_schizotypal_(cluster_A)_personality_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P_cwp2tkTHOt6xHLAcE6h7cESWaC44Ym/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to paranoid, schizoid, and schizotypal (cluster A) personality disorders: Clinical sciences]]></video:title><video:description><![CDATA[Personality disorders represent an enduring and pervasive pattern of perceiving and relating to oneself, others, and the world in atypical, and often detrimental, ways.  

Unlike most psychiatric conditions, personality disorders are frequently ego-syntonic, meaning many people with personality disorders don’t perceive their behaviors as problematic. Consequently, these disorders typically do not cause direct distress to the individual but can lead to significant interpersonal and occupational difficulties. 

There are ten personality disorders defined in the Diagnostic and Statistical Manual of Mental Disorders fifth edition, or DSM-5 for short, and these are divided into clusters A, B, and C. Cluster A personality disorders include paranoid personality disorders, schizoid personality disorders, and schizotypal personality disorders. 

Now, when a patient presents with a chief concern suggesting a personality disorder, first obtain a focused history and physical exam. Common symptoms can include significant interpersonal or occupational difficulties, patterns of hyper-dependence on or hyper-independence from others, and a tendency to blame others for their own feelings and behaviors. Additionally, frequent or extreme mood swings, angry outbursts, and attention seeking behaviors can be observed.  

The physical exam is often unremarkable, but can be characterized by extremes of affect, ranging from flat to exaggerated facial expressions. With this presentation, you should consider a personality disorder. 

Next, assess your patient using the DSM-5 criteria for personality disorder. All personality disorders are characterized by an enduring pattern of thinking, feeling, and behaving in culturally atypical ways, and these traits are inflexible and maladaptive in multiple settings. The onset of this pattern must be during adolescence or early adulthood, although traits can be recognized at much younger ages. Additionally, the patient’s symptoms must cause cli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Atrial_fibrillation_and_atrial_flutter:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EvXpaXwySMCdpzbVCMMpRiCmSFOpYE5s/_.jpg</video:thumbnail_loc><video:title><![CDATA[Atrial fibrillation and atrial flutter: Clinical sciences]]></video:title><video:description><![CDATA[Atrial fibrillation, also known as A-fib, is the most common atrial cardiac arrhythmia resulting from abnormal electrical impulse generation from multiple sites in the atria. This causes erratic and ineffective atrial contractions that can trigger clot formation and strokes, as well as an increased risk of developing heart failure due to ventricular dysfunction.  

Now, if a patient presents with a chief concern suggesting A-fib, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and consider starting your patient on IV fluids. Put your patient on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry, as well as cardiac rhythm monitoring. Finally, if needed, provide supplemental oxygen.  

Next, assess for signs and symptoms of unstable atrial fibrillation, which include hypotension, altered mental status, signs of shock, ischemic chest pain, and acute heart failure. If your patient has these signs and symptoms present, diagnose unstable atrial fibrillation.  

Then, you should proceed with immediate synchronized cardioversion. Finally, remember to treat any underlying causes or triggers including myocardial infarction, pulmonary embolism, thyrotoxicosis, or electrolyte abnormalities. 

Here’s a clinical pearl! Atrial flutter is another common atrial tachycardia, but unlike A-fib which occurs due to multiple ectopic foci and causes an irregular rhythm, A-flutter is from a single ectopic focus in the atria that causes a reentrant pathway leading to a regular rhythm. They both present with a rapid ventricular rate of greater than 120, however, the atrial rate of A-flutter is around 250-350 beats per minute, displaying a classic sawtooth pattern. While there is predictable and reproducible atrial activity in A-flutter, these waves are not true P waves and are instead called flutter waves.  

Okay, now that we’ve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_dysarthria_or_dysphagia:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8X9RpPy8Q4i5542Wmwqt9Rp-TtmKtPGV/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to dysarthria or dysphagia: Clinical sciences]]></video:title><video:description><![CDATA[Dysphagia, or impaired swallowing; and dysarthria, or impaired motor speech; are symptoms that can occur due to various neurologic- and non-neurologic conditions. Some important neurologic causes include cranial nerve dysfunction, neuromuscular junction disorders, neurodegenerative conditions, demyelination, and stroke.  

Now, if a patient presents with chief concerns suggestive of dysphagia or dysarthria, you should obtain a focused history and physical examination. First, let&amp;#39;s focus on dysphagia, which is  difficulty swallowing. In this case, history might also reveal choking, coughing, or pain during swallowing. On examination, you will also notice signs of impaired swallowing, such as difficulty clearing the mouth of food and water, and coughing with, or shortly after, swallowing.  

These findings are suggestive of dysphagia, so your next step is to determine the type of dysphagia, more specifically, whether the patient is presenting with oropharyngeal or esophageal dysphagia. 

But, before we proceed, let’s quickly review the mechanics of swallowing, which includes oral, pharyngeal, and esophageal phases. The oral phase is voluntary and includes mastication, bolus preparation and moving the bolus into the pharynx. The pharyngeal phase consists of propelling the bolus through the pharynx and the upper esophageal sphincter. During this phase, the epiglottis closes over the larynx to protect the airway. Finally, the esophageal phase includes peristalsis of the esophagus until the bolus passes through the lower esophageal sphincter into the stomach.  

The oral cavity, pharynx, upper esophageal sphincter, and upper part of the esophagus have striated muscles innervated by cranial nerves, while the lower esophagus and lower esophageal sphincter have smooth muscles innervated by the esophageal myenteric plexus.   

Now, first, let’s focus on oropharyngeal dysphagia, which is associated with difficulty initiating swallowing and clearing food and ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_neurocutaneous_syndromes:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V9Yipq6ARMStB4ljrRPl--R5Sj2TsN3f/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to neurocutaneous syndromes: Clinical sciences]]></video:title><video:description><![CDATA[Neurocutaneous syndromes are a heterogeneous group of genetic disorders that affect both the skin and the nervous system. Although several neurocutaneous syndromes present with manifestations during infancy and childhood, some are not usually diagnosed until adolescence or early adulthood. The most common neurocutaneous syndromes with childhood onset can be differentiated on the basis of skin lesion morphology. 

Now, if a pediatric patient presents with a chief concern suggesting a neurocutaneous syndrome, you should first obtain a focused history and physical examination.  

History commonly reveals delayed motor skills; cognitive deficits; and neurologic symptoms, such as weakness. Additionally, the family history might be positive for a neurocutaneous syndrome. The physical examination typically reveals focal neurologic findings and cutaneous lesions. 

With these findings, consider the possibility of a neurocutaneous syndrome, and then assess the morphology of your patient’s skin lesions. 

Lets take a look at our first skin lesion. If you identify multiple brown macules, known as café-au-lait spots, cafe-au-lait macules or CALMs; consider neurofibromatosis type 1, also known as NF1 or Von Recklinghausen disease. This autosomal dominant condition is caused by mutations of the NF1 gene on chromosome 17. 

These patients often have a family history of NF1 in a first-degree relative. Many present with symptoms of neurocognitive dysfunction, such as developmental delay, attention-deficit hyperactivity disorder, or a learning disability.  

Meanwhile, the exam typically reveals multiple café-au-lait macules; skin fold freckling, especially in the axillae or inguinal regions; and neurofibromas, which are benign peripheral nerve sheath tumors.  

During early childhood, you’ll typically see plexiform neurofibromas, which are irregular, diffuse, and poorly defined, and involve multiple nerve fascicles.  

In late childhood or adolescence, patients may develop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_splenic_masses:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K_GWC8PGTBic_9dew4p9Vc8VT5iibrvJ/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to splenic masses: Clinical sciences]]></video:title><video:description><![CDATA[Splenic masses are abnormal growths or tumors of the parenchyma or vasculature of the spleen. They are broadly categorized into solid and cystic lesions. Most splenic masses are benign and incidentally found. The patient’s history and the characteristics of the mass on ultrasound or CT scan are key factors in establishing the diagnosis.  

Your first step in evaluating a patient presenting with a chief concern suggestive of a splenic mass is to obtain a focused history and physical examination.  

The patient might report a history of night sweats, unintentional weight loss, or fevers. However, keep in mind that some patients might be asymptomatic, in which case their splenic mass was probably discovered incidentally on imaging due to some other concern.  

On the other hand, the exam might show left upper quadrant abdominal tenderness, a palpable left upper quadrant abdominal mass, petechiae, or ecchymoses. With these findings you should consider a splenic mass and order imaging like a left upper quadrant abdominal ultrasound or CT scan of the abdomen. These studies will determine if a splenic lesion is present and whether it is cystic or solid.  

First, let’s focus on cases where imaging shows cystic splenic masses. These are broadly divided into solitary lesions and multiple lesions.  

First up among solitary cystic splenic masses, are epithelial splenic cysts, also known as primary splenic cysts. They got their name because these cysts are lined with epithelial cells. These patients might report vague abdominal pain or fullness, or they may be asymptomatic.  

If the ultrasound or CT scan shows a thin-walled fluid-filled structure without internal debris or loculations you can make the diagnosis of epithelial splenic cyst.  

On the other hand, you might be dealing with a pseudocyst, also known as a secondary cyst, which are not lined with epithelial cells. These usually occur due to some damage to the spleen like trauma. Therefore, your patient migh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_stimulant_use,_intoxication,_and_overdose:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y8f5eZdNSO_YQZP3pJi7pOucQk_CjUyG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to stimulant use, intoxication, and overdose: Clinical sciences]]></video:title><video:description><![CDATA[Stimulants refers to a broad class of medications, supplements, and illicit substances that have sympathomimetic effects on the central nervous system. In general, they can cause increased alertness and wakefulness, elevated mood, enhance cognitive functions like focus and concentration, increase energy levels, and reduce the need for sleep.  

Common types of stimulants include amphetamines like dextroamphetamine, methamphetamine, and methylenedioxymethamphetamine, also known as MDMA or ecstasy; as well as cocaine, and caffeine. While pharmaceutical formulations of stimulants are commonly prescribed for the treatment of ADHD and narcolepsy, substances like methamphetamine and cocaine are manufactured and used illicitly for their similar sympathomimetic properties. Caffeine, on the other hand, is the most widely consumed stimulant in the form of coffee or tea for its desired effects of alertness and heightened focus. Regardless of the type and purpose of use, large amounts of these substances can lead to intoxication, overdose, and chronic dependance. 

Alright, when a patient presents with a chief concern suggesting stimulant use, your first step is to perform an ABCDE assessment to determine if they are stable or unstable.  

If the patient is unstable, stabilize the airway, breathing, and circulation right away. This may require supplemental oxygen or even endotracheal intubation and mechanical ventilation. Next, obtain IV access and consider starting IV fluids. Put your patient on continuous vital sign monitoring, including temperature, pulse, blood pressure, pulse oximetry, respiratory rate, and cardiac telemetry. Additionally, consider using cooling blankets for patients with hyperthermia, and sedation for those with severe agitation. 

Here’s a clinical pearl to keep in mind! When evaluating unstable patients with suspected ingestion of stimulants, always consider the possibility of overdose. Overdose is characterized by the ingestion of large amoun]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_trauma_and_stressor-related_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XXeC8eOPRqSNF0PPhz7OgZXlReayNcE3/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to trauma and stressor-related disorders: Clinical sciences]]></video:title><video:description><![CDATA[Trauma and stressor related disorders are psychiatric conditions, which develop following exposure to stressful or traumatic events. Stressors can include any experience that causes change, loss, or distress, while trauma is a specific type of stressful experience that involves significant danger or violence. For example, losing a job is a stressor, while a serious car crash is considered traumatic. Major disorders in this category include adjustment disorder, acute stress disorder, and post-traumatic stress disorder. 

When a patient presents with a chief concern suggesting a trauma or stressor related disorder, first obtain a focused history and physical examination. Your patient will report past exposure to stressful events, along with a change in mood or behavior. During the physical exam, you might notice that the patient has a constricted or labile affect.  

With these findings, consider trauma or related disorders, and then assess the DSM-5 criteria for trauma exposure. To qualify as a traumatic exposure, a patient must have been exposed to life-threatening danger, serious bodily injury, actual death, or sexual violence.  

There are a few ways the patient can be exposed to trauma. First, the patient may have experienced it firsthand as either the direct victim or a first-hand witness of someone else being threatened or harmed. It might also be through witnessing the direct aftermath of the danger or violence, such as with first responders. Finally, it is also considered traumatic if the person is a second-hand witness, in other words, learned about the danger second-hand, only if the victim was a very close family member or friend. In addition, if the trauma occurred second-hand, the danger must have been either violent or accidental. For example, learning that one’s parent died of complications of an illness would not meet criteria for trauma, but learning they died in a shooting would. Like other stressors, trauma can be a single event, such as ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Major_depressive_disorder_and_persistent_depressive_disorder_(dysthymia):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VHb_WzoXRqqrffQFtpulYr4UTaGiG9ZE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Major depressive disorder and persistent depressive disorder (dysthymia): Clinical sciences]]></video:title><video:description><![CDATA[Depression is a state of persistent sadness that affects how a person thinks, feels, and behaves. It can cause significant personal distress, strain relationships, and impair daily functioning. Additionally, depression significantly increases the risk of self-harm and suicidality. Depressive disorders include major depression and persistent depressive disorder, also known as dysthymia. 

When a patient presents with a chief concern suggesting a depressive disorder, first perform a safety assessment. Assess for features of psychosis like agitation, paranoia, aggression, hallucinations, and other forms of disorganized thoughts, speech, or behavior.  

Additionally, look for signs of catatonia, such as slow movements, holding odd poses, and minimal response to external stimuli, which can be accompanied by severe dehydration or malnutrition.  

Finally, assess specifically for homicidal and suicidal ideation, paying attention to the intensity and intention, as evidenced by plans and behaviors. If any of these features are present, the patient is at high risk of harm to self and others and requires acute management.  

Your management might include psychiatric hospitalization, medical and pharmacologic stabilization, and a one-to-one sitter, if appropriate. In severe, persistent treatment-resistant or life-threatening cases, electroconvulsive therapy might be necessary. 

On the other hand, if the patient is at low risk of harm to self and others, your next step is to obtain a focused history and physical exam. History usually reveals persistently sad, depressed, or hopeless mood, with decreased energy, and a lack interest and motivation that is significantly different from their baseline.  

On exam, the patient might exhibit poor posture, slow speech and movements, with a flat or tearful affect. Additionally, you might see signs of inattention and memory difficulties affecting focus, recalling information, and performing tasks that require mental effort.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_shoulder_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3cdXDvu1TXaJTphcdbMxtUNzSROxubeQ/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to shoulder pain: Clinical sciences]]></video:title><video:description><![CDATA[Shoulder pain is a common symptom with many underlying causes, including conditions affecting the joint, capsule, tendons, or bursa. It’s important to first identify if your patient’s shoulder pain is due to trauma or infection. Other possible types of shoulder pain include neuropathic pain from nerve damage and nociceptive pain from arthralgia, capsulitis, tendinopathy, and bursitis. 

When a patient presents with shoulder pain, first obtain a focused history and physical examination. History reveals shoulder pain, while the exam might demonstrate edema, erythema, or warmth over the joints. They may also have shoulder tenderness, effusion, limited joint range of motion, crepitus, or even an obvious joint deformity.  

Your next step is to assess for trauma. This includes an obvious mechanism of injury, such as a motor vehicle crash or sports injury; a joint deformity; or ligamentous laxity. If trauma is present, think fracture, dislocation or separation; or a tendon rupture or labral tear. 

Now, if your patient reports an inability to lift their arm above their head, and possibly a popping sensation; and if the physical exam reveals painful, limited range of motion; and possibly decreased sensation, decreased muscle strength, or diminished pulses, consider a fracture, dislocation, or AC joint separation and order a shoulder X-ray. If the X-ray results confirm a bone fracture, joint dislocation, or AC joint separation, diagnose a shoulder fracture, dislocation, or separation.   

Here’s a clinical pearl!  Shoulder separation is actually not an injury to the shoulder joint itself. Instead, it occurs in the setting of trauma to the ligaments of the acromioclavicular joint, known as the AC joint, which is where the clavicle and the scapula meet. The coracoclavicular, or CC joint, also connects the scapula to the clavicle. This type of injury can occur when a patient falls directly on their shoulder. Injuries range from partial tearing of the AC ligaments wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_unsteadiness,_gait_disturbance,_or_falls:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YFrQ3UTsSR_X5E3fHqWt5Hv-Tm_rpvYp/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to unsteadiness, gait disturbance, or falls: Clinical sciences]]></video:title><video:description><![CDATA[Unsteadiness, gait disturbance, or falls are common concerns, particularly in older individuals, which can significantly affect everyday activities and the patient’s overall quality of life. Now, these concerns can occur due to motor weakness, sensory loss, incoordination, or movement disorders. There are several different types of gait, including spastic, stomping, steppage, ataxic, and Parkinsonian gait. 

Alright, if the patient presents with unsteadiness, gait disturbance, or falls, your first step is to obtain a focused history and physical examination. These patients report difficulty walking, sometimes in combination with decreased balance and a history of near-falls or falls. Additionally, there might be a family history of difficulty walking. On physical exam, you will find an abnormal gait, so your next step is to assess the type of gait dysfunction. 

First, let’s focus on spastic gait. Spastic gait is associated with stiff legs and poor floor clearance. Often, you will see circumduction of the legs because they have trouble lifting the feet adequately off the floor. In other words, the patient will bring the leg outward and then inward in a half-circular motion to take a step. Also, their toes typically scrape the floor as they walk. You can confirm this by looking at the soles of their shoes. These findings are suggestive of spastic gait, so your next step is to assess the underlying cause.   

Let’s start with cervical myelopathy. These individuals usually report weakness and numbness of the arms and legs, as well as neck pain. Also, they might have a known history of disc herniation, spinal stenosis, or recent trauma to the neck and back. On the exam, you will find weakness and sensory loss in all extremities, as well as spasticity and hyperreflexia in all extremities. At this point, consider cervical myelopathy and obtain a cervical spine CT or MRI. If imaging shows compression of the cervical spinal cord, such as from a disc herniation, di]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_weakness_(focal_and_generalized):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/O8L80-neSQih2bymINPwFUqqTBOwHXn6/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to weakness (focal and generalized): Clinical sciences]]></video:title><video:description><![CDATA[Weakness, also known as impaired motor strength, can be subdivided into unilateral and bilateral weakness. Unilateral weakness can be seen in conditions like brain lesions and peripheral nervous system lesions, while bilateral weakness can be associated with neurologic conditions like acute and chronic polyneuropathy, but also brainstem and spinal cord lesions. Other important causes of bilateral weakness include neuromuscular junction disorder, motor neuron disease, and various myopathies. 

Now, if a patient presents with chief concerns suggestive of weakness, perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. In some cases, you might need to intubate the patient and provide mechanical ventilation. Next, obtain IV access and consider IV fluids. Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry. 

Okay, let’s go back to the ABCDE assessment and focus on stable patients. In this case, your next step is to obtain a focused history and physical exam. Let’s say your patient reports limb weakness on one side only, involving the arm, leg, or both, and the physical exam reveals unilateral weakness of the upper, or lower, or both extremities. These findings are suggestive of unilateral weakness, so be sure to assess for monoparesis. In other words, assess whether the weakness affects multiple body parts or one limb only. 

If the weakness involves more than one limb or if the weakness involves a limb and the face, you should think of a brain lesion contralateral to the side of the symptoms. Keep in mind that with a brain lesion, you might also notice a sensory loss ipsilateral to the side of weakness. 

Now, here&amp;#39;s a clinical pearl! Weakness on one side of the body involving the upper and lower extremities is known as hemiparesis. Less commonly, ipsilateral hemiparesis s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_differentiating_lesions_(brainstem):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pIKpoKP_RnatNfvN6ecdtRlvRF_ERcOW/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to differentiating lesions (brainstem): Clinical sciences]]></video:title><video:description><![CDATA[Brainstem lesions, or simply injuries to the midbrain, pons, or medulla, can result in various signs, because many important structures and pathways reside in the brainstem, including cranial nerves and nuclei, the reticular activating system, the respiratory centers, as well as the motor, somatosensory, cerebellar, and sympathetic pathways. 

Now, if your patient presents with a chief concern suggestive of a brainstem lesion, first, perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. In some cases, you might even have to use intubation and start mechanical ventilation.Next, obtain IV access, consider starting IV fluids, and don’t forget to put your patient on continuous vital sign monitoring and cardiac telemetry. Finally, if needed, be sure to manage high intracranial pressure. 

Now, let’s go back to the ABCDE assessment and take a look at stable individuals.  

In this case, your first step is to obtain a focused history and physical examination. Keep in mind that symptoms and physical exam findings will depend on the lesion location and the part of the brainstem that’s affected. In other words, symptoms could include confusion, changes in vision, facial droop and numbness, hearing loss, and trouble swallowing or speaking. Also, some individuals might report weakness or numbness in the arms or legs.  

Now, switching gears and moving on to physical exam findings. An injury to the reticular activating system will result in altered mental status and a decreased level of consciousness. Next, oculomotor nerve involvement in the midbrain will result in sluggish or nonreactive pupils and ptosis; while an injury to the midbrain or pons could also result in impaired extraocular movements. Additionally, injuries of the pons, where the trigeminal and facial nerve nuclei reside, can result in facial numbness and, or, weakness.  

Next, a lesion to the cochlear nerves ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_differentiating_lesions_(cerebellum):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xJ4mn7wiTjShzsKzDC_LpVFbRDqg_6Yd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to differentiating lesions (cerebellum): Clinical sciences]]></video:title><video:description><![CDATA[The cerebellum, which is the major control center for the coordination of voluntary movements and balance, is connected via multiple pathways to the cerebrum, brainstem, and the spinal cord. Conditions that can affect the cerebellum and these connecting pathways can be subdivided into acute, subacute, and chronic cerebellar lesions. 

Now, if your patient presents with chief concerns suggestive of a cerebellar lesion, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. In some cases, you might even have to intubate the patient and start mechanical ventilation. Next, obtain IV access and consider starting IV fluids. Finally, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. 

Alright, let’s go back to the ABCDE assessment and focus on stable patients. In this case, obtain a focused history and physical examination. These patients will report a loss of coordination, such as difficulty walking, keeping balance, sitting up straight, or using their arms to pick up objects. They might also report a room spinning dizziness with nausea and vomiting; difficulty focusing their vision; slurred speech; or difficulties with swallowing. 

On the exam, you will find limb-, truncal-, or gait ataxia, which refers to the loss of coordination of voluntary movement. Limb ataxia, which is predominantly seen with cerebellar hemispheric lesions, is associated with dysmetria on finger-to- nose or heel-to-shin testing. For example, on the finger-to-nose test, the patient might point past the target as they are unable to judge the distance properly, known as past-pointing. Another example of limb ataxia is dysdiadochokinesia on rapid alternating movements, which can be tested by asking the patient to alternate supinating and pronating their arms.  

On the flip side, truncal ataxia, which is most p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_differentiating_lesions_(cerebral_cortical_and_subcortical_structures):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MCXmdpdaQaChS7wElPTGDMeCR6mp9ksb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to differentiating lesions (cerebral cortical and subcortical structures): Clinical sciences]]></video:title><video:description><![CDATA[Cortical and subcortical lesions represent injury to the cerebral cortex and deeper structures of the cerebral hemispheres. Cortical lesions are associated with cortical signs and symptoms, such as aphasia, homonymous anopsia, agnosia, and neglect. On the other hand, subcortical lesions are associated with motor symptoms, like weakness and involuntary movements, and sensory loss, as well as cognitive and behavioral changes.  

Now, if your patient presents with chief concerns suggestive of a cortical or subcortical lesion, first, perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation. Sometimes, you might have to intubate the patient and start mechanical ventilation. Next, obtain IV access, consider starting IV fluids, and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry; as well as cardiac telemetry. Finally, if needed, be sure to manage high intracranial pressure. 

Now, let’s go back to the ABCDE assessment and discuss stable patients. First, obtain a focused history and physical examination. Depending on the lesion location, the patient may have cognitive and behavioral changes, difficulty identifying objects, and trouble speaking or understanding speech. Some individuals may report vision changes or motor symptoms like weakness or numbness.  

Next, the physical exam might demonstrate cognitive impairment and abnormal behavior, agnosia, aphasia, neglect, and visual field deficits. Also, you might identify weakness and sensory loss. Keep in mind that there will be no contralateral findings, such as weakness in the face and contralateral weakness in the limbs. With these findings, you should consider a cortical or subcortical lesion. 

At this point, your next step is to differentiate between the two by assessing for signs and symptoms that usually indicate a cortical lesion. These include aphasia, homonymous anop]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_differentiating_lesions_(muscle):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zGVXNmBNSQePVOt8vEZFdbQjQY_IiRtB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to differentiating lesions (muscle): Clinical sciences]]></video:title><video:description><![CDATA[Muscle lesions are conditions that affect the skeletal muscle system, eventually causing muscle weakness and atrophy. Based on the underlying cause, muscle lesions can be subdivided into hereditary conditions, which include periodic paralysis, muscular dystrophy, and myotonic dystrophy; and non-hereditary conditions, such as statin-induced myopathy, polymyositis, dermatomyositis, and inclusion-body myositis. Another type of acquired muscle lesion is called critical illness myopathy, which is seen in individuals requiring ICU management. 

Now, if your patient presents with chief concerns suggestive of a muscle lesion, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. At this point, you might have to intubate the patient and start mechanical ventilation. Next, obtain IV access, consider starting IV fluids, and place your patient on continuous vital signs monitoring, including heart rate, blood pressure, pulse oximetry, and cardiac telemetry. 

Alright, let’s go back to the ABCDE assessment and focus on stable patients. Your next step here is to obtain a focused history and physical exam. History typically reveals symptoms of muscle involvement, primarily limb weakness. However, if there is weakness in the bulbar and respiratory muscles, the patient might report difficulty swallowing and breathing. In some cases, muscle weakness might be associated with pain.  

On the exam, you will notice symmetric, bilateral limb weakness, sometimes in combination with weakness of neck and facial muscles. In advanced stages, you might even see muscle atrophy. Since these lesions only affect muscles and not sensory neurons or nerves, the sensory exam will be normal, while muscle tone and deep tendon reflexes could be normal or decreased. Finally, due to weakness of the hip and pelvic muscles, you might see a waddling gait. With these findings, consider a muscle lesion and assess the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_differentiating_lesions_(spinal_cord):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ByJduC4cRoyKXPM4JTAnFOOqS36W79Ly/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to differentiating lesions (spinal cord): Clinical sciences]]></video:title><video:description><![CDATA[Spinal cord lesions occur as a result of damage or injury to the spinal cord, which can eventually lead to various clinical manifestations below the lesion, including loss of function and sensation. The anterior spinal cord, which contains the corticospinal and spinothalamic tracts, is supplied by a singular anterior spinal artery; while the posterior spinal cord, which contains dorsal columns, is supplied by a pair of posterior spinal arteries.  

Now, there are several different spinal cord syndromes, including conus medullaris and cauda equina syndromes, as well as central cord-, anterior cord-, posterior cord-, hemicord-, and complete cord syndrome. 

Now, if your patient presents with chief concerns suggestive of a spinal cord lesion, first, perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation. At this point, you might even have to intubate the patient and start mechanical ventilation. Next, obtain IV access, consider starting IV fluids, and place your patient on continuous vital signs monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. 

Now, here’s a clinical pearl to keep in mind! Acute spinal cord injury above the T6 level can disrupt sympathetic innervation to the heart and peripheral vasculature and cause unopposed parasympathetic activity through the vagus nerve. Eventually, this can result in hypotension, bradycardia, and subsequent neurogenic shock. In addition, high cervical lesions can cause respiratory failure because C3 to C5 nerve roots innervate the diaphragm. 

Now, let’s go back to the ABCDE assessment and take a look at stable individuals. In this case, you should obtain a focused history and physical exam. The patient will describe numbness with or without weakness of the limbs and trunk, depending on lesion type and affected spinal tracts. Also, the patient might report bowel or bladder dysfunction, due ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_encephalopathy_(acute_and_subacute):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/qWa56hypTxqQOgIKmgDE4ajhSO2W7Pye/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to encephalopathy (acute and subacute): Clinical sciences]]></video:title><video:description><![CDATA[Encephalopathy refers to a change from baseline cognitive status, which can range from mild confusion to a comatose state.  

Now, acute or subacute encephalopathy refers to cognitive impairment that has occurred over the last three months.  

Based on the underlying cause, encephalopathy can occur as a result of primary neurologic conditions, but also due to non-neurologic causes, including toxins, metabolic derangements, nutritional deficiencies, and infections. 

Alright, when a patient presents with chief concerns suggestive of acute or subacute encephalopathy, first perform an ABCDE assessment to determine if they are stable or unstable.   

If unstable, stabilize the airway, breathing, and circulation. You might also need to intubate the patient and provide mechanical ventilation. Next, obtain IV access and consider IV fluids. Finally, put your patient on continuous vital signs monitoring, including heart rate, blood pressure, and pulse oximetry. Don’t forget to manage high intracranial pressure or ICP, if needed.  

Here’s a clinical pearl to keep in mind! Unstable patients with encephalopathy may have medical emergencies like status epilepticus or conditions associated with high intracranial pressure, such as intracranial hemorrhage. However, systemic conditions, like liver failure and sepsis, can also result in encephalopathy. 

Now, let’s go back to the ABCDE assessment and focus on stable patients.  

Your next step here is to obtain a focused history and physical examination. The patient or a loved one will report recent changes in cognition, level of consciousness, or behavior, typically over the last few days to weeks. Examples of such changes include drowsiness, memory loss, impaired attention, and paranoia. Additionally, the physical exam reveals altered mental status, sometimes in combination with focal neurologic deficits.  

These findings are highly suggestive of acute or subacute encephalopathy, so be sure to obtain labs, including a C]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_headache_or_facial_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KOeMRk9HQlWbCfQR5wRrlSmvTjuakWLX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to headache or facial pain: Clinical sciences]]></video:title><video:description><![CDATA[Headache and facial pain are common presentations that can occur due to various benign and concerning conditions. Primary headaches, which are not caused by other conditions, include tension-type headache, cluster headache, and migraine. On the flip side, secondary headaches are a presentation of an underlying condition, such as giant cell arteritis, infectious meningitis, and subarachnoid hemorrhage. 

Now, if your patient presents with headache or facial pain, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation. You might need to intubate your patient and provide mechanical ventilation. Next, obtain IV access, and put your patient on continuous vital signs monitoring and cardiac telemetry. Finally, you might need to manage increased intracranial pressure. 

Okay, let’s go back and talk about stable patients. In this case, obtain a focused history and physical examination, including a fundoscopic exam. First, let’s focus on facial pain, more specifically trigeminal neuralgia. These patients typically report recurrent, unilateral facial pain lasting a few seconds to minutes, often described as sharp pain or electric shock. The pain is usually precipitated by minor stimuli such as shaving, tooth brushing, or chewing.  

The physical exam is usually normal, but sometimes, you might find a sensory loss in the face. Finally, if the fundoscopic exam is normal, diagnose trigeminal neuralgia. 

Alright, now let’s focus on individuals presenting with headaches. Next to the headache, history might reveal visual disturbances, fever, nausea, and vomiting. On the exam, you might notice altered mental status or focal neurologic deficits. Finally, the fundoscopic exam could be normal, or it might show optic disc edema, also known as papilledema, which occurs due to increased intracranial pressure.  

These findings are suggestive of headaches, so your next step is to assess for re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_polyneuropathy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/im_Mi0qzQHCmYiPSKxgAxLZNSb6Onwht/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to polyneuropathy: Clinical sciences]]></video:title><video:description><![CDATA[Polyneuropathy is a condition associated with demyelination or axonal injury of multiple peripheral nerves, which can result in numbness, weakness, and pain. Now, hereditary polyneuropathies, which are caused by genetic mutations, include conditions like Friedreich ataxia, adrenomyeloneuropathy, and Charcot-Marie-Tooth disease. On the flip side, acquired polyneuropathies, which can be caused by autoimmune disease, infections, chronic conditions, or nutritional deficiencies, include conditions like Guillain-Barré syndrome, diabetic neuropathy, chronic alcohol use, and vitamin B12 deficiency.  

Now, if your patient presents with chief concerns suggestive of polyneuropathy, first, obtain a focused history and physical examination. History will typically reveal progressive bilateral symptoms, such as numbness and tingling of the extremities. Sometimes, the patient might report muscle weakness and trouble with walking. On the exam, assess the patient’s sensation, using different modalities, such as light touch, pinprick, and vibration. Also, be sure to check their muscle strength in extremities. The exam will reveal bilateral symmetric loss of sensation, sometimes in combination with muscle weakness. Additionally, you will notice hyporeflexia or areflexia.  

The physical exam might also reveal muscle atrophy and gait ataxia. Finally, be sure to perform Romberg testing. First, ask the patient to stand with their feet together and arms at their sides, and instruct them to close their eyes. By closing their eyes, you will remove visual cues that help maintain balance. If you notice any swaying or loss of balance, the test is positive, indicating impaired proprioception.    

These findings are suggestive of polyneuropathy, so be sure to assess for the family history of neuropathy. If present, consider hereditary polyneuropathies, such as Friedreich ataxia, adrenomyeloneuropathy, and Charcot-Marie-Tooth disease. 

First, let’s focus on Friedreich ataxia, whi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Meningitis_and_brain_abscess:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zSXfT5llR4mJForzbK1jq_99T0yrb8QG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Meningitis and brain abscess: Clinical sciences]]></video:title><video:description><![CDATA[Meningitis refers to inflammation of the meninges, the protective membranes covering the brain and spinal cord, most often due to an infection. On the flip side, brain abscess refers to an encapsulated area of purulent infection within the brain parenchyma. The underlying mechanism for both types of infections include contact with a specific pathogen via direct inoculation, such as from penetrating trauma; contiguous spread, for example, from the facial sinuses; or hematogenous spread of pathogens from distant focal infections. 

Now, if a patient presents with a chief concern suggestive of meningitis or brain abscess, perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. At this point, you might even have to intubate the patient and start mechanical ventilation. Next, obtain IV access, consider starting IV fluids, and put your patient on continuous vital sign monitoring and cardiac telemetry. Finally, start broad-spectrum antibiotics. If needed, manage increased intracranial pressure, which primarily relies on elevating the head of the bed, hyperventilation, sedation, and hyperosmolar therapy.  

Now, let’s take a look at stable patients, starting with brain abscesses. In this case, obtain a focused history and physical exam, which is typically associated with headache, sometimes in combination with fever, confusion, seizure, or focal neurological symptoms, such as language impairment, vision changes, and limb weakness.  

Patients may also have predisposing risk factors, including recent dental or neurosurgical procedures; penetrating head trauma; otitis media, mastoiditis, and sinusitis. Another important risk factor is IV substance use, which is associated with an increased risk of hematogenous spread of pathogens throughout the body.  

Lastly, patients might be immunocompromised, like from HIV infection, cancer, or organ transplantation; or they might have a congenital ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Benign_prostatic_hypertrophy_and_prostate_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4qPGWPWoSIWcFXSZ6STZstUiScGwlSjP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Benign prostatic hypertrophy and prostate cancer: Clinical sciences]]></video:title><video:description><![CDATA[Benign prostatic hyperplasia, or BPH, refers to non-malignant enlargement of the prostate gland  

caused by prostatic cell proliferation.  

BPH is the leading cause of lower urinary tract symptoms in biologically male adults, especially after the age of 30.  

On the other hand, prostate cancer is a common malignancy that usually affects biologically male patients between 64 and 75 years of age. While BPH and prostate cancer both present with urinary symptoms and are differentiated based on clinical and imaging findings, BPH does not increase the risk of prostate cancer.  

When a patient presents with a chief concern suggesting BPH or prostate cancer, first perform a focused history and physical examination.  

When it comes to BPH, affected individuals typically report difficulty urinating, a weak urine stream, and occasionally, nocturia or urinary incontinence. Digital rectal examination, or DRE, often reveals a firm, symmetrically enlarged prostate. With these findings, you should suspect BPH. 

Here’s your first clinical pearl! Keep in mind that DRE can only detect prostatic hypertrophy once the prostate volume reaches 50 milliliters or more.  

Whenever a patient presents with lower urinary tract symptoms, remember to perform a neurologic examination by assessing motor and sensory function of the pelvic region and lower extremities, to rule out other causes. 

Now, once you suspect BPH, order a urinalysis to rule out other urinary tract pathology such as infection, and consider ordering a prostate-specific antigen, or PSA, level.  

Here’s a clinical pearl! While PSA testing has a limited ability to accurately predict urinary retention or prostate size in patients with BPH, results might be useful when determining treatment. Using shared decision-making, be sure to discuss the risks and benefits of PSA testing with your patient. 

Okay, in addition to lab testing, consider ordering a post-void residual, or PVR, scan. This test measures the amo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Well-patient_care_(adult):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8AT3r_gfQ6iiojd8YPapikQKQfGG-pvk/_.png</video:thumbnail_loc><video:title><![CDATA[Well-patient care (adult): Clinical sciences]]></video:title><video:description><![CDATA[The well-patient care visit for adults ranging from 18 to 64 years old is a yearly check-up that promotes physical, mental, and social health while building trust between the healthcare provider and patient. For all patients, each visit includes a comprehensive history and physical exam, followed by screening and counseling about a variety of topics such as substance use, mental health, interpersonal and domestic violence, and optimizing diet and physical activity. Additional screening and counseling are provided based on the patient’s age, risk status, and biological sex. 

When an adult patient presents for well-patient care, begin with a comprehensive history and physical examination. First, review your patient’s age; past medical history and surgical history; their family history and social history; sexual activity; medications; and diet and exercise habits. Next, complete a physical examination including height, weight, body mass index, or BMI, and vital signs. 

Your next step is to provide screening and counseling for all adult patients, regardless of age or risk factors. First, ask about alcohol, tobacco, and substance use through direct conversation with your patient or by using validated questionnaires like the CAGE questionnaire for alcohol misuse, Fagerstrom questionnaire for nicotine dependence, and the Substance Use Brief Screen or SUBS for substance use. Because alcohol use, tobacco use, and substance use are significant preventable causes of disease, disability, and death, provide counseling and connect your patient to resources and referrals for further intervention and support, as needed. 

Next, use a validated questionnaire such as the Generalized Anxiety Disorder 7 scale or GAD-7 to check for anxiety, and the Patient Health Questionnaire-9 or PHQ-9 for depression, both of which are highly common in the adult population. A positive screening for either condition should prompt further evaluation. Along with medical management, your patie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_aneuploidies_and_microdeletions:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ffw_whWXSX6MczlW-JaS9Y60R7GzKY9W/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to aneuploidies and microdeletions: Clinical sciences]]></video:title><video:description><![CDATA[Aneuploidy refers to a missing or an extra chromosome, while microdeletions are small deletions of genetic material spanning multiple genes within a single chromosome. Aneuploidies and microdeletions are caused by errors in cell division, which often results in a characteristic phenotype and genetic syndrome. You can apply various genetic testing methods to categorize chromosomal abnormalities as aneuploidies or microdeletions. 

Now, if a pediatric patient presents with a chief concern suggesting aneuploidy or a microdeletion, you should first perform an ABCDE assessment to determine if they are stable or unstable.  

While most of these patients will be stable, some might have an associated anomaly that requires urgent intervention, such as a congenital heart defect. If the patient is unstable, stabilize the airway, breathing and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen. 

Now that we’ve discussed unstable patients, let’s go back to the ABCDE assessment and look at stable ones. In this case, obtain a focused history and physical examination.  

History might reveal abnormal findings on prenatal genetic and ultrasound testing, poor pre- and post-natal growth, or cardiac and renal anomalies. Affected patients may have intellectual or developmental delays, characteristic or unusual behaviors, and delayed puberty. The physical examination might demonstrate characteristic craniofacial features or limb abnormalities. With these findings, consider a chromosome abnormality and obtain further testing.  

This might include cytogenetic chromosomal analysis to identify aneuploidy using cell culture, chromosome staining, and microscopy to assess chromosome number and structure. Additionally, order a chromosomal microarray, also called CMA for short, or a fluorescence in situ hybridization, or FISH, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_gradual_cognitive_decline:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Iu6N53kbTH6TG7co111U9yL2SXWuRyI1/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to gradual cognitive decline: Clinical sciences]]></video:title><video:description><![CDATA[Gradual cognitive decline refers to the slow and progressive cognitive impairment that can affect memory, behavior, personality, organizational and decision-making skills, and visuospatial awareness. It can occur due to various neurologic conditions, including brain tumors, normal pressure hydrocephalus, Huntington disease, and different types of dementia. 

Now, if a patient presents with gradual cognitive decline, you should obtain a focused history and physical exam. You should also obtain cognitive screens, such as the Montreal Cognitive Assessment or Mini-Mental State Examination. Also, be sure to perform a depression screen because depression can sometimes present as cognitive impairment, which is also known as pseudodementia.  

History typically reveals memory difficulties, like forgetting important appointments; behavior or personality changes, such as aggressiveness or impulsivity; and difficulties with organization and completing tasks, known as loss of executive function. History might also reveal difficulty with visuospatial tasks, such as parking or using the stairs, resulting in accidents. In addition, there might be a family history of cognitive decline.  

Depending on the underlying cause and the stage of the disease, the physical exam may or may not be normal. On the flip side, the cognitive screen, which includes testing short-term memory, language, attention, and visuospatial skills, will be abnormal. Lastly, the depression screen will be negative, but keep in mind that many patients with cognitive impairment will also have a mood disorder. With these findings, diagnose cognitive impairment. 

Now, here’s a clinical pearl! Some metabolic conditions, including hypothyroidism and vitamin B12 deficiency, can cause cognitive impairment, so the initial evaluation should also include labs, like thyroid stimulating hormone and vitamin B12 levels. 

Time for a high-yield fact! If your patient has depressive symptoms prior to their cogniti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_sleep_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/AuOkVcpiRn2uPIDJni_L6ihgRF2Bk4xb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to sleep disorders: Clinical sciences]]></video:title><video:description><![CDATA[Sleep disorders are conditions that interfere with sleep or the transition between sleep-wake cycles. These disorders can affect different aspects of sleep, including sleep initiation, maintenance, or duration, and cause significant distress in daily activities.  

Some conditions are associated with abnormal motor or verbal activity during sleep, which include the REM parasomnias and non-REM parasomnias; while others are characterized by difficulties in sleep initiation or maintenance, or excessive sleepiness. These include restless legs syndrome, delayed sleep-wake disorders, and chronic insomnia, as well as narcolepsy with cataplexy and sleep apnea.  

Now, if a patient presents with chief concerns suggestive of a sleep disorder, you should first obtain a focused history and physical examination.  

Your patient will typically report poor sleep quality, meaning difficulty falling asleep, interrupted sleep, or waking up too early. Family or friends might also report that the patient has abnormal movements or vocalizations during sleep. The physical exam may or may not be normal. In this case, you should think of a sleep disorder, so be sure to assess for abnormal verbal or motor activity during sleep.   

Here’s a clinical pearl to keep in mind! Sleep disturbances can also be secondary to other medical conditions, such as hyperthyroidism and congestive heart failure, so be sure to keep a wide differential in mind! 

So, if abnormal verbal or motor activity is present during sleep. Assess if the patient has a detailed recall of recurrent dreams. If yes, diagnose REM-related parasomnia, which is typically seen in older adults and conditions like REM sleep behavior disorder and nightmare disorder. 

Here are some high-yield facts to keep in mind! Remember that there are different stages of sleep, with REM being the last stage. REM sleep is characterized by dreams, rapid eye movements, and muscle atonia. The longest periods of REM sleep occur during the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alzheimer_disease:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1T1fRtS9R3eaEWPe514RWdFfQbKuVmhJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alzheimer disease: Clinical sciences]]></video:title><video:description><![CDATA[Alzheimer disease, which is a neurodegenerative condition with slowly progressive cognitive and functional decline, is the most common cause of dementia in the developed world. Its pathology is characterized by extracellular deposits of amyloid plaques and abnormal intracellular accumulations of tau protein in neurofibrillary tangles.  

There’s also a degeneration of cholinergic neurons in the nucleus basalis of Meynert, with a decrease in acetylcholine levels throughout the cortex. Now, the four main stages of this condition include mild cognitive impairment and mild, moderate, and severe Alzheimer disease.  

Now, if your patient presents with a chief concern suggesting Alzheimer disease, several exams need to be done. First, obtain a focused history and physical exam. Be sure to perform a standardized screening cognitive exam, along with a depression screen, because many patients with Alzheimer disease or dementia have coexisting depression. Next, check vitamin B12 and TSH levels to rule out vitamin B12 deficiency and hypothyroidism, which are conditions that can cause cognitive impairment. Finally, order brain imaging with CT or MRI to ensure no structural processes are causing cognitive impairment. 

History typically reveals slowly progressive cognitive decline, such as memory loss and difficulty with visuospatial tasks and executing tasks. In particular, these patients tend to forget specific events, like appointments, important dates such as birthdays, or where they just placed an item, which is known as episodic memory loss.  

Also, they have difficulty with performing usual daily activities like self-care. Next, history will be negative for the use of medications or substances that can cause cognitive side effects, such as anticholinergics or excessive alcohol intake; and there will be no other medical conditions that could affect cognition, such as hepatic encephalopathy. Finally, your patient might be a known carrier of the apolipoprotein e4 ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Testicular_cancer:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NRuKvsIHRXuSilY38YH-z6R9Q7aFyMUE/_.png</video:thumbnail_loc><video:title><![CDATA[Testicular cancer: Clinical sciences]]></video:title><video:description><![CDATA[Testicular cancer is the most common solid tumor in young biological males aged 15 to 34. Since there are no standard recommendations to screen for this form of cancer, it is important to assess all testicular masses with a scrotal ultrasound. Testicular tumors can be categorized into germ cell tumors which include seminoma, non-seminoma, and mixed germ cell tumors; and sex cord, or stromal tumors.  

If your patient presents with a chief concern suggesting testicular cancer, first perform a focused history and physical examination, and obtain a scrotal ultrasound. These patients will report a scrotal lump, often associated with scrotal pain, and they may even have a history of cryptorchidism, infertility, or a positive family history of testicular cancer.  

The exam will reveal a palpable scrotal mass, and there might be scrotal tenderness and lymphadenopathy. Finally, scrotal ultrasound will show solid intratesticular mass. With these findings suspect testicular malignancy. 

Here’s a clinical pearl to keep in mind! Aside from testicular malignancies, scrotal masses and pain can have a wide differential diagnosis ranging from benign conditions to surgical emergencies. For example, hydroceles and varicoceles are benign conditions typically found incidentally by the patient or physician. A hydrocele is a buildup of fluid in the scrotum, whereas a varicocele refers to enlarged scrotal veins classically described as a &amp;quot;bag of worms.&amp;quot; Both can likely be managed conservatively.  

On the other hand, infectious causes of scrotal masses and pain include epididymitis and orchitis, with patients describing sudden pain at the epididymis, extending to the testicle. Most cases are caused by Chlamydia trachomatis and Neisseria gonorrhoeae and need immediate empiric antibiotic coverage. Finally, look out for sudden scrotal swelling caused by testicular torsion. In this case, the spermatic cord becomes twisted and strangulated, cutting off blood sup]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastroesophageal_reflux_disease_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0jfea6ZXSqOaMeDxtOAF19s9QLmIu0oS/_.png</video:thumbnail_loc><video:title><![CDATA[Gastroesophageal reflux disease (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Gastroesophageal reflux refers to the retrograde movement of gastric contents into the esophagus. When ongoing gastroesophageal reflux is severe enough to cause troublesome symptoms or complications like erosive esophagitis or Barrett esophagus, it’s called gastroesophageal reflux disease, or GERD. In the pediatric population, evaluation and treatment of GERD depends on the patient’s age and symptom severity. 

Now, if a pediatric patient presents with a chief concern suggesting GERD, first obtain a focused history and physical exam, and then assess your patient’s age. Let’s start by discussing GERD in infants. Caregivers typically report that their infant spits up frequently, and some may become irritable, refuse to feed, or arch their back during feedings. In this age group, exam findings are typically normal. With this clinical presentation, you should suspect GERD. 

Here’s a high-yield fact to keep in mind! Healthy infants commonly experience recurrent episodes of spitting up or regurgitation that peak around 6 months of age. These episodes of reflux are caused by relaxation of the lower esophageal sphincter, which allows gastric contents to enter the esophagus. When gastroesophageal reflux is not associated with troublesome symptoms or complications, it’s considered normal, and it usually resolves without intervention. 

Now, once you suspect GERD, you should assess for the presence of any warning signs that suggest a condition other than GERD. Some examples include an age of onset less than 1 week or over 6 months; weight loss or suboptimal weight gain; fever; or lethargy. Also look for signs suggesting intracranial pathology, such as seizures, microcephaly, macrocephaly, or a bulging fontanelle. 

Other red flags suggesting another disease include abdominal distention, hepatosplenomegaly, nocturnal or bilious emesis, hematemesis, chronic diarrhea, and rectal bleeding. If you identify one or more of these warning signs, consider an alternative diagn]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Peptic_ulcers,_gastritis,_and_duodenitis_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lLPZcsY2RtWHO2tLoc7FvlGvRL6l87oZ/_.png</video:thumbnail_loc><video:title><![CDATA[Peptic ulcers, gastritis, and duodenitis (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Peptic ulcers, gastritis, and duodenitis belong to a spectrum of conditions known as acid peptic disease. These conditions are characterized by excessive gastric acid production and weakened gastric or duodenal mucosa, which lead to superficial inflammation and erosions known as gastritis or duodenitis. When damage progresses deeper and invades the muscularis mucosa layer, a peptic ulcer forms. Treatment of acid peptic disease depends on the presence or absence of a coexisting Helicobacter pylori infection. 

Now, if a pediatric patient presents with a chief concern suggesting a peptic ulcer, gastritis, or duodenitis, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access and consider administering IV fluids or a transfusion of packed red blood cells. Put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry; and provide supplemental oxygen if needed. Consider placing a nasogastric tube, with or without nasogastric lavage. Also, if the patient has active bleeding or hypotension, obtain an emergent esophagogastroduodenoscopy, or EGD. Finally, consider an infusion of proton pump inhibitor or vasopressin. 

Here’s your first clinical pearl! Peptic ulcers, gastritis, and duodenitis can be complicated by bleeding, in the form of hematemesis or melena, as well as gastrointestinal perforation, stricture, and obstruction. Ulcers that cause heavy or brisk bleeding may require emergent intervention, such as coagulation therapy or vasopressor support.  

Now that we’ve discussed unstable patients, let’s return to the ABCDE assessment and take a look at stable ones. First, obtain a focused history and physical examination. Caregivers of younger children typically describe irritability, poor feeding, and regurgitation or vomiting; whereas older children report gas or bloating, nausea, and retrosternal chest]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_amblyopia_and_strabismus_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CSez4yaJQ32dLZOGl7kKzpeDQyafZoj0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to amblyopia and strabismus (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Amblyopia, sometimes called “lazy eye”, refers to decreased visual acuity in one or both eyes that prevents normal development of the visual cortex. It’s crucial to identify amblyopia at a young age before it becomes difficult or even impossible to treat. Common causes of amblyopia include strabismus, or misalignment of the eyes; as well as deprivation and refractive error. 

Now, if a pediatric patient presents with a chief concern suggesting amblyopia or strabismus, first perform a focused history and physical examination, including visual acuity and red reflex testing.  

Visual acuity testing techniques vary by age. For children under age 2, you can assess the pupillary response to light, as well as the ability to track, or fixate on and follow an object. After age 3, most children can recognize and match objects on cards; and when they are older, they can read an eye chart. For younger children or those who are unable to cooperate with standard testing, consider instrument-based screening with a photoscreener or autorefractor.  

Remember to perform vision screening monocularly, at a specified distance, and make sure your patient wears corrective lenses if they were prescribed. 

Now, to perform the red reflex test, view both eyes through an ophthalmoscope, and look for a symmetric red reflection from the retina. You’ll find it helpful to turn off or dim the lights to ensure the pupils are dilated. 

Alright, let’s look at some findings you might see in children with amblyopia or strabismus. Although young children are often asymptomatic, history might reveal blurred vision or vision loss, and caregivers might describe a “lazy” or deviated eye, as well as squinting, or head tilt, also called ocular torticollis. Infants may demonstrate a lack of eye contact. The physical examination typically reveals a unilateral or bilateral decrease in visual acuity. For verbal children, testing with a standard vision chart may reveal a two-line difference in vi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_head_and_neck_masses_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VkrQkc-oTnezcxsWbgp-mKimS_CaPZje/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to head and neck masses (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Head and neck masses are a relatively common presenting concern in children, which are usually benign. Most pediatric head and neck masses can be categorized as possible malignancies, infections, or developmental anomalies. 

If a pediatric patient presents with a head or neck mass, perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation, and intubate your patient if you need to secure the airway. Then, obtain IV access, and consider giving IV fluids. Finally, begin continuous vital sign monitoring, and provide supplemental oxygen if needed. 

When it comes to stable patients, obtain a focused history and physical examination, and then assess for characteristics suggesting malignancy. 

These include masses that are firm, have irregular borders, are immobile and matted, and grow rapidly. If any of these findings are present, consider malignancy, and obtain imaging, such as an ultrasound, CT scan, or MRI; as well as a tissue biopsy.    

Next, assess for systemic B symptoms. These include fever, night sweats, or weight loss. If your patient reports any B symptoms, consider lymphoma.  

Typical exam findings include a lateral neck mass with cervical lymphadenopathy, and you might detect a supraclavicular lymph node, which should raise your suspicion for malignancy. Imaging usually reveals enlarged lymph nodes, and in some cases a mediastinal mass. Finally, the presence of neoplastic lymphocytes on biopsy confirms lymphoma. 

On the flip side, if systemic B symptoms are absent, your next step is to assess the mass’s location. If it’s in the midline, consider a thyroid nodule, which carries a significant risk of malignancy in children.  

History may reveal previous head and neck radiation. On exam, you’ll detect a midline neck mass, and imaging may reveal a cystic or solid thyroid mass. Results of tissue biopsy could be benign, indeterminate, or consistent with thyroid cancer, but ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_complications_of_prematurity_(late):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NZlePfiLQLCruR7Y40VHrICHR_quFnxA/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to complications of prematurity (late): Clinical sciences]]></video:title><video:description><![CDATA[Preterm birth before 37 weeks of gestation can result in various complications that increase an infant’s morbidity and mortality. These complications are most common among patients who are born before 32 weeks of gestation or those with very low birth weight under 1500 grams. Late complications of prematurity can develop after the first month of life, and because they don’t typically cause acute or obvious signs and symptoms, many are identified through screening. 

Now, if a pediatric patient presents with a chief concern suggesting a late complication of prematurity, first obtain a focused history and physical examination. Then, review your findings to determine if your patient requires further evaluation.  

Let’s start by assessing your patient’s oxygen requirement. If your patient required supplemental oxygen for 28 days or more, consider bronchopulmonary dysplasia, or BPD. History will reveal an infant born before 32 weeks of gestation. They may have had a patent ductus arteriosus, required mechanical ventilation, or had prolonged exposure to hyperoxia. The exam might reveal chest retractions and audible pulmonary rales. And when attempting to wean your patient’s supplemental oxygen, they will usually become hypoxemic and tachypneic within 60 minutes. 

Even though BPD is a clinical diagnosis, you can consider ordering a chest X-ray to support the diagnosis, determine disease severity, and identify complications. Typically, the chest X-ray will reveal diffuse hazy opacifications and hyperinflation, with or without cystic lucencies. This combination of clinical and imaging findings confirms your diagnosis of bronchopulmonary dysplasia. 

Okay, here’s your first clinical pearl! In severe cases of BPD, disrupted pulmonary vascular development leads to increased pulmonary vascular resistance and ultimately pulmonary hypertension. Over time, the right ventricle hypertrophies in order to maintain cardiac output. These patients can experience pulmonary hype]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_delay_or_regression_in_developmental_milestones:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4AiL8FcOQYKFuSbEu6Kk0rFTSBWTsmGp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to delay or regression in developmental milestones: Clinical sciences]]></video:title><video:description><![CDATA[Developmental milestones are behaviors and functional skills that children typically achieve by a specific age, in a predictable sequence. Developmental delay occurs when a child doesn’t meet an expected milestone on time, while developmental regression refers to the loss of previously acquired skills. Any delay or regression can impair a child’s ability to learn, communicate, and interact with others. Developmental delay and regression may impact one or more domains, including motor, language, cognitive, and social-emotional development.  

Now, when a pediatric patient presents with a chief concern suggesting a developmental delay or regression... your first step is to obtain a focused history and physical exam and administer a validated developmental screening tool.  

Keep in mind that general developmental screening tools are used for surveillance purposes, but if a caregiver has a specific concern, you should use a specific screening tool. Developmental screening tools assess age-specific behaviors and skills across all developmental domains, which include gross and fine motor, cognitive, language, and social-emotional. Remember to also perform hearing and vision screening.  

Here’s a clinical pearl! Developmental screenings are routinely administered at the 9-, 18-, and 30-month well-child visits, and autism-specific screening is administered at the 18- and 24-month visits. However, screening can be administered at any point if a caregiver has a concern. Any child with a positive screen may benefit from a comprehensive developmental evaluation to assess developmental delay, even if caregivers report no specific concerns. 

Okay, most patients present during early childhood, typically before the age of 5, with missed, delayed, or lost developmental milestones. Caregivers are often the first to report concerns about the child&amp;#39;s development or behavior.  

History may reveal risk factors for developmental delay or regression, including premat]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_inborn_errors_of_metabolism_(acute):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pCef_uZyT6OBJjcbq0Ss7HnuR0C98wgb/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to inborn errors of metabolism (acute): Clinical sciences]]></video:title><video:description><![CDATA[Inborn errors of metabolism, or IEMs, are genetic conditions that result from alterations within a biochemical or metabolic pathway. IEMs that present with acute onset during infancy are typically caused by single gene defects that impair enzymes involved in the urea cycle, amino acid and carbohydrate metabolism, glycogen storage, or peroxisomal or mitochondrial activity. When you suspect an acute IEM, you can use results of an initial laboratory evaluation to guide confirmatory testing.  

Now, if a pediatric patient presents with a chief concern suggesting an IEM with acute onset, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation; and you may need to intubate your patient. Next, obtain intravenous access and consider starting IV fluids. Then, begin continuous vital sign monitoring, and if needed, provide supplemental oxygen. Finally, since patients with IEMs can present with signs and symptoms that mimic sepsis, consider starting IV antibiotics. 

Now, after you’ve stabilized your patient, obtain a focused history and physical examination and order an ABG, CBC, CMP, ammonia level, and urinalysis. Most patients present during infancy with poor feeding, vomiting, and irritability. Affected infants have no obvious infection; no history of trauma; and no known central nervous system or other anomalies. History may also reveal a positive newborn screen, a sibling with an unexplained death or similar symptoms, or a family history of a metabolic disorder.  

On exam, you’re likely to see an altered mental status; rapid, deep breathing or apnea; and hepatosplenomegaly. With these findings, consider an inborn error of metabolism, and assess the ABG for respiratory alkalosis.  

If the ABG shows a decreased partial pressure of arterial carbon dioxide, or PaCO2, which indicates respiratory alkalosis, this is the first clue that you should consider a urea cycle disorder.  

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_medication_exposure_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wupm2F80Tr6z5WoTvEeI8VlnSyC2r5w4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to medication exposure (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Medication exposure includes the ingestion, inhalation, or topical absorption of prescription or over-the-counter medications. Many medications pose a serious risk to the pediatric population, either through unintentional exposure often among infants and children, or intentional ingestion seen in adolescents. Using clinical manifestations, medication exposures can be roughly categorized into those that cause tachycardia and those that cause bradycardia.

Now, if a pediatric patient presents with a chief concern suggesting medication exposure, you should first perform an ABCDE assessment to determine if the patient is stable or unstable.

If unstable, stabilize the airway, breathing, and circulation. You may need to consider intubation if the patient is apneic or has shallow, ineffective respirations. This is especially important in children with altered mental status. Next, obtain IV access and give IV fluids. Don’t forget to put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. If needed, provide supplemental oxygen, measure glucose, and obtain an ECG. You should also consider administering naloxone if there is any concern for opioid ingestion.

Time for some clinical pearls! At this point you might find clues to the causative medication. For example, ECG might reveal a widened QRS complex or even life-threatening arrythmias, which points to tricyclic antidepressant toxicity.

Alternatively, you might find a prolonged corrected QT interval, in which case you should think of selective serotonin reuptake inhibitor or SSRI toxicity.

Now, depending on the substance and timing of ingestion, you can consider using a decontamination method to minimize absorption.

While ipecac syrup and gastric lavage are no longer recommended, activated charcoal can be effective if given within one hour of ingestion. Keep in mind that charcoal does not bind well to liquids or charged molecules like iron; and you should ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dehydration_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Jn-U-qPOSWeV_yxuT3kd12FhQvyRJBAC/_.png</video:thumbnail_loc><video:title><![CDATA[Dehydration (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Dehydration is a condition characterized by an excessive loss of body water. In children, dehydration most often results from acute gastrointestinal illnesses that cause vomiting, diarrhea, and decreased fluid intake. Less commonly, it can result from conditions associated with non-gastrointestinal fluid losses, such as polyuria, third spacing, or burns. Treatment of dehydration depends on its severity, which can be estimated from clinical findings. 

Now, if a pediatric patient presents with a chief concern suggesting dehydration, first perform an ABCDE assessment to determine if they’re unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV or intraosseous access, and administer a bolus of an isotonic crystalloid, such as normal saline. Finally, place your patient on continuous vital sign monitoring, and if needed, provide supplemental oxygen. Then, obtain a focused history and physical examination, and order a BMP and urine studies including urine osmolarity, specific gravity, and sodium.  

History usually reveals vomiting or diarrhea, which is often accompanied by decreased fluid intake. They also could have increased insensible losses from fever, excessive sweating, or sometimes extensive burns. Less commonly, your patient may have an underlying condition causing polyuria, such as diabetes mellitus or diabetes insipidus.  

Patients with severe dehydration are generally unstable and present with signs of shock. Pulses are typically weak, and perfusion is poor. These patients usually have skin tenting and very dry mucous membranes, with severely reduced or absent urine output. In children, late findings include drowsiness or lethargy, and vital signs will reveal tachycardia and hypotension in more severe cases.  

As for labs, the BMP may reveal hypo- or hypernatremia. You might also see hypokalemia, especially in patients with profuse diarrhea; or hyperkalemia, in the setting of acute kidney injury. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_a_suspected_brain_tumor_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hayACds_QPyi0NoHPlerbbrQSDO-Eoz8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to a suspected brain tumor (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Brain tumors are histologically diverse and can range from indolent, benign tumors to aggressive, infiltrating malignancies. Although both benign and malignant brain masses are associated with significant neurologic morbidity, they often present with nonspecific, vague, or intermittent symptoms. These symptoms are related to tumor location, disruption of neurologic function, and the onset of increased intracranial pressure, or ICP.  

When a pediatric patient presents with a chief concern suggesting a brain tumor, your first step is to perform an ABCDE assessment to determine if they are stable or unstable.  

If unstable, stabilize the airway, breathing, and circulation. Consider intubating your patient if they demonstrate shallow, ineffective, or absent respirations. Then, obtain IV access and consider administering IV fluids. Finally, continuously monitor vital signs and, if needed, administer supplemental oxygen 

Here’s a high-yield fact! An enlarging brain mass can obstruct cerebrospinal fluid drainage, causing elevated ICP. If not treated promptly, increased ICP can lead to brain herniation, which is associated with long term neurologic sequelae and death. Signs of increased ICP include bulging fontanelles; unilateral pupillary dilation, sometimes called a “blown pupil”; focal neurologic deficits; abnormal posturing; and the Cushing triad, which consists of bradycardia, a widened pulse pressure, and irregular respirations known as Cheyne-Stokes breathing.   

Now that we have discussed unstable patients, let’s return to the ABCDE assessment and look at stable ones.  

Your next step here is to obtain a focused history and physical examination. Presenting symptoms often include headaches, which usually start in the morning and are relieved by vomiting; nausea and vomiting; seizures; changes in school performance; or loss of developmental milestones.  

The physical exam might demonstrate altered mental status; cranial nerve p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_poor_feeding_(newborn_and_infant):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pIIcqfA1TSKaybMWAuYaYwwzRmmIgbEv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to poor feeding (newborn and infant): Clinical sciences]]></video:title><video:description><![CDATA[Any impairment in a newborn or infant&amp;#39;s latch, suck, and swallow-breathe mechanics can result in poor feeding. Although self-limited difficulties with latching and breastfeeding are common in otherwise healthy newborns and infants, persistent feeding problems might indicate a functional issue or an anatomic abnormality that impairs the ability to latch, suck, or swallow-breathe. 

When a newborn or infant presents with poor feeding, your first step is to perform a focused history and physical examination. Caregivers typically report that their infant is unable to effectively latch, suck, or swallow-breathe during feedings. As part of your workup, you’ll need to make sure your patient has no history of systemic conditions that might impact feeding, such as neurologic, cardiovascular, pulmonary, or gastrointestinal disorders, or infections; and no history of preterm delivery.  

Here&amp;#39;s a high-yield fact! The ability to suck and swallow develops in utero and is usually established by 34 weeks&amp;#39; gestation. Therefore, premature infants born before this age are often not able to effectively coordinate their latch, suck, and swallow-breathe mechanics. 

As for the physical exam, most patients will demonstrate normal muscle tone and reflexes, but you might notice atypical facial features, or you may even hear stertor or stridor with feedings. At this point, you should assess for any craniofacial abnormalities that might impact feeding mechanics.  

Let’s start with cleft lip or palate. Affected infants often have difficulty latching and sucking, and many experience nasal regurgitation or gasping with feedings. The exam might reveal a cleft lip, which can range in severity from a notch in the vermillion border to complete separation involving the skin, muscle, teeth, and bone.  

Patients with cleft palate can have a defect in the soft or hard palate. While a soft palate defect can occur in isolation, separation of the hard palate is ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nephrotic_syndromes_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I6CEI4SgSaKP-m7d0egXgk-2Q0OyviPz/_.png</video:thumbnail_loc><video:title><![CDATA[Nephrotic syndromes (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Nephrotic syndrome is characterized by the combination of proteinuria, hypoalbuminemia, edema, and hyperlipidemia, which result from glomerular damage. In pediatric patients, nephrotic syndrome is often idiopathic, but it can also be caused by infections and genetic or autoimmune conditions. 

If a pediatric patient presents with a chief concern suggesting nephrotic syndrome, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, put your patient on continuous vital sign monitoring, and if needed, provide supplemental oxygen. 

Let’s now look at stable patients. When it comes to stable patients, obtain a focused history and physical examination, which can help you distinguish nephrotic syndrome from nephritic syndrome. Keep in mind that these two conditions can have overlapping symptoms, and in some cases, they occur simultaneously. First, let’s discuss nephritic syndrome. 

Nephritic syndrome refers to the combination of hematuria, azotemia, hypertension, and edema caused by inflammation within the kidney’s glomeruli. Affected patients often report frankly bloody, cola- or tea-colored urine; and decreased urine output. Meanwhile, the physical examination often reveals elevated blood pressure and edema. These findings should make you suspect nephritic syndrome. To confirm the diagnosis, obtain a urinalysis with microscopy. If it’s positive for blood, with or without protein; and microscopy reveals RBCs, RBC casts, and possibly protein; diagnose nephritic syndrome. 

Now, let’s switch gears and discuss nephrotic syndrome. These patients usually report swelling, occasionally with non-specific symptoms, such as malaise, headache, fatigue, or irritability. Physical exam often reveals periorbital edema; but, in more severe cases, you might also notice edema of the scrotum, labia, or abdomen; as well as lower extremity edema that becomes more pronounc]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_trauma_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/N082n9qaSnaUqUm8yXoVcSm-Sv29f4Ud/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to trauma (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Trauma refers to any physical injury that is caused by an external force or impact, such as an accident or violence. When compared with adults, infants and children have unique anatomical and physiological differences that influence trauma evaluation and management. During a pediatric trauma evaluation, the goal of the primary survey is to recognize and treat life-threatening injuries, while the secondary survey serves to identify any additional injuries.  

When a pediatric patient presents with trauma, first perform a primary survey. This should be done using the ABCDE assessment to determine if your patient is stable or unstable.  

A stands for Airway. While maintaining cervical spine precautions, suction the oropharynx and assess for signs indicating airway obstruction, like stridor or a visible foreign body. Remember that patients who can speak clearly do not have airway obstruction. You may need to intubate your patient to secure their airway, so keep in mind that children&amp;#39;s airways are shorter and narrower than an adult’s; their tongues are relatively larger; and they have a more flexible and floppier epiglottis. For this reason, children often require differently sized laryngoscope blades. 

Here’s a high-yield fact! During the primary survey, you can use Broselow emergency tape to quickly estimate a child’s weight, endotracheal tube or laryngeal mask size, and medication dosing. 

Next up is B for Breathing. Now that the airway is secure, it’s time to assess your patient’s oxygenation and ventilation. Remember that infants are obligatory nose breathers, and nasal obstruction can interfere with an infant’s ventilation, so be careful not to obstruct the nares during your evaluation! Check oxygen saturation with pulse oximetry and provide supplemental oxygen if needed. Look for signs of respiratory distress, like accessory muscle use, tachypnea, or grunting. If your patient has poor respiratory effort or respiratory distress, they may requi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gastritis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HIL-1r7RTzyjWzvZpAJfaCWTR923X9W5/_.png</video:thumbnail_loc><video:title><![CDATA[Gastritis: Clinical sciences]]></video:title><video:description><![CDATA[Gastritis, or inflammation of the gastric mucosa, is typically associated with excessive acid production, which can eventually lead to erosions and ulcerations of the stomach lining, destruction of the glandular layer of the stomach, and fibrosis. Based on the duration of symptoms, gastritis can be classified as acute, persistent, and chronic. Acute and persistent gastritis last less than 30 days and include stress-, chemical-, and infectious gastritis. On the other hand, chronic gastritis persists for more than 30 days and includes autoimmune-, H. Pylori, and reactive gastritis. 

Now, if a patient presents with chief concerns suggesting gastritis, first obtain a focused history and physical exam as well as labs, including CBC and fecal occult blood test. These patients will report upper abdominal pain, indigestion, and, in some cases, symptoms like nausea, vomiting, and bloating. The physical exam may reveal epigastric tenderness and halitosis, as well as signs of pallor and tachycardia. Moreover, pallor and tachycardia are signs of anemia, which occurs when inflammation of gastric mucosa results in mucosal erosions, ulcers, and subsequent bleeding. So, keep in mind that, in some individuals, labs might reveal anemia or a positive fecal occult blood test. If your patient presents with these findings, suspect gastritis and assess the duration of symptoms.   

Symptoms that last 30 days or less are suggestive of acute- or persistent gastritis. Moreover, symptoms of acute gastritis last 14 days or less, while symptoms of persistent gastritis last from 15 to 30 days. Both types are associated with the same conditions, so your next step is to assess the underlying cause. First, review the patient’s history and physical exam findings and be sure to order esophagogastroduodenoscopy or EGD for short, to visualize gastric mucosa, and if needed, take biopsy samples. Additionally, if you suspect infectious gastritis, don’t forget to order relevant microbiology test]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_encephalitis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LIkVg8mBQXevEeHW0pkbge94S-CNmRAa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to encephalitis: Clinical sciences]]></video:title><video:description><![CDATA[Encephalitis refers to the inflammation of the brain parenchyma, which can occur due to infections, including herpes simplex virus-, varicella-zoster virus-, West Nile virus-, and Toxoplasma gondii infection; as well as autoimmune conditions, such as acute disseminated encephalomyelitis, anti-NMDA receptor encephalitis and anti-LGI1 encephalitis. 

Alright, if your patient presents with a chief concern suggestive of encephalitis, first, perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. At this point, you might need to intubate the patient and provide mechanical ventilation. Next, obtain IV access, consider intravenous fluids, and don’t forget to put your patient on continuous vital signs monitoring, including heart rate, blood pressure, and pulse oximetry. Finally, if needed, be sure to manage increased intracranial pressure. 

Now, let’s go back to the ABCDE assessment and take a look at stable individuals. In this case, you should obtain a focused history and physical examination. Your patient or their loved ones will report a new onset of progressive confusion, behavioral or personality changes, or a decreased level of consciousness. History might also reveal fever, headache, and seizures. 

Depending on the location of the injury, there might be additional neurologic symptoms like weakness, numbness, changes in vision, language impairment, or incoordination. On physical exam, you will notice altered mental status, sometimes in combination with focal neurologic deficits. With these findings, consider encephalitis and assess for current signs and symptoms of infection, such as fever, leukocytosis, or a viral exanthem.  

If present, consider infectious encephalitis. Next, obtain a brain MRI and perform a lumbar puncture for CSF analysis. First, let’s discuss herpes simplex virus, or HSV encephalitis for short. Both HSV type 1 and type 2 can cause encephalitis. In this c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_epilepsy:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cyPTDVJgTieGnTQ7LIjWHmXkTnyq2Uoi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to epilepsy: Clinical sciences]]></video:title><video:description><![CDATA[Epilepsy is a neurological condition characterized by recurrent, unprovoked seizures, which refer to sudden changes in the brain&amp;#39;s electrical activity that can result in various clinical manifestations, including convulsions and loss of consciousness. Now, there are several different types of seizures, including tonic-clonic, myoclonic, atonic, and absence seizures. All seizures can be classified as focal or generalized based on the affected brain area. 

Alright, if a patient presents with a chief concern suggestive of epilepsy, first perform an ABCDE assessment. If the patient is unstable, stabilize their airway, breathing, and circulation. You might need to intubate your patient and start mechanical ventilation. Next, obtain IV access and put your patient on continuous vital signs monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry. 

Most commonly, unstable individuals are presenting with convulsive status epilepticus. So, once you stabilize the patient, your next step is to obtain a focused history and physical examination. History will reveal a tonic-clonic seizure that started 5 or more minutes ago, OR multiple seizures without recovery to baseline mental status between attacks.  

On the physical exam, you will notice an altered mental status and alternating body stiffening and jerking movements. With these findings, diagnose convulsive status epilepticus.   

Here’s a clinical pearl to keep in mind! Immediate treatment for convulsive status epilepticus includes benzodiazepines, such as lorazepam, midazolam, or diazepam, followed by anti-seizure medications, like fosphenytoin, phenobarbital, valproic acid, or levetiracetam. Once you initiate the treatment, you can use EEG to monitor clinical response. Also, you can use EEG to assess for non-convulsive status epilepticus, which is a condition associated with abnormal brain activity with no or just a few physical manifestations. 

Now,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_mood_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qi_APDe1RjuYt_r-sfpDeZfVTLmepcRK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to mood disorders: Clinical sciences]]></video:title><video:description><![CDATA[Mood refers to a long-lasting emotional state that influences how a person views the world and behaves. So, mood disorders are characterized by persistent and excessive experience of emotions such as happiness, sadness, and irritation to a degree that affects an individual&amp;#39;s overall functioning. 

Now, if a patient presents with chief concerns suggesting a mood disorder, first, perform a safety assessment.  

Assess for features of psychosis, like agitation, paranoia, aggression, signs of auditory or visual hallucinations, and other forms of severely disorganized thoughts, speech, or behavior.  

Additionally, look for signs of mania, such as rapid speech, a decreased need for sleep, and an increase in goal-directed activity.  

Finally, ask specifically about homicidal and suicidal ideation. Patients experiencing psychosis, mania, and active homicidality or suicidality, are considered high risk to themselves and others, so proceed with acute management, which often requires psychiatric hospitalization, pharmacologic stabilization, and a one-to-one sitter, if appropriate. 

On the other hand, if the patient is not experiencing these features, they are considered low risk to themselves and others, so your next step is to obtain a focused history and physical exam.  

History will typically reveal a persistently euphoric, irritable, or depressed mood that is significantly different from their baseline. Next, on the exam, you will notice psychomotor changes, such as slowed or agitated movements; changes in the rate of speech, which can be increased or decreased; and extremes of affect, ranging from flat to exaggerated facial expressions. Finally, you might notice changes in appearance, such as being unusually unkempt. With these findings, you should consider mood disorder. 

Now, here’s a clinical pearl to keep in mind! When assessing patients with mood disorders, be sure to rule out other medical conditions as potential causes of mood changes. For e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_schizophrenia_spectrum_and_other_psychotic_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v8HIb9waR6O0izKDeM1sOV8KRw2rO_cu/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to schizophrenia spectrum and other psychotic disorders: Clinical sciences]]></video:title><video:description><![CDATA[Schizophrenia spectrum and other psychotic disorders are psychiatric conditions characterized by psychotic symptoms, such as delusions, hallucinations, disorganized speech, and disorganized behavior. These disorders are considered a spectrum because the severity and combination of symptoms can vary greatly among patients. Schizophrenia is the primary condition in this group, along with related disorders such as schizophreniform disorder and brief psychotic disorder, which present with similar but shorter and milder symptoms. Additionally, mood symptoms can occur alongside psychotic symptoms in conditions like schizoaffective disorder. Finally, psychotic symptoms can also be present in delusional disorders and certain cluster A personality disorders. 

Now, when a patient presents with a chief concern suggesting a schizophrenia spectrum or other psychotic disorder, start with a focused history and physical examination. Your patient may present with delusions, hallucinations, disorganized speech, or disorganized behavior.  

Now, to break it down really quick, delusions are fixed, false beliefs classified as bizarre or non-bizarre based on their plausibility. For example, a belief that aliens are controlling one&amp;#39;s mind is considered bizarre, while believing that the police are tracking a person is non-bizarre.  

On the other hand, hallucinations are false sensory experiences, most commonly auditory, like hearing familiar or unfamiliar voices, sounds, or commands. Other types of hallucinations are visual, tactile, olfactory, or gustatory.  

Next, disorganized speech may manifest as loosely connected topics or answers that are unrelated to the questions asked. In severe cases, speech can become a jumble of words, known as word salad, resembling aphasia. Some patients might present with echolalia, which is the meaningless repetition of words just spoken by another person; while others may speak in a sing-song or rhyming manner, known as clang. 

Fina]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Primary_headaches_(tension,_migraine,_and_cluster):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JQ2WDDdxT8ups-RqAnWw6qD-QHGvbfy9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Primary headaches (tension, migraine, and cluster): Clinical sciences]]></video:title><video:description><![CDATA[Primary headache is a type of headache that is not caused by another condition or injury. The underlying pathophysiology is not well understood, but it involves release of neurotransmitters, such as calcitonin gene-related peptide in migraines, and increased sensitization of pain pathways including sensory inputs from the trigeminal and upper cervical nerves. The most common types of primary headache are tension-type headache, cluster headache, and migraine. 

Now, if a patient presents with a headache, you should first obtain a focused history and physical examination, including a fundoscopic exam. History typically reveals a patient younger than 50 years of age who reports episodes of recurrent headaches that are similar in quality and progression and completely resolve between attacks. They also report that the intensity of headaches doesn’t require regular use of painkillers. Primary headaches are not positional, meaning that the quality of the headache does not change with positioning, such as when the patient is laying down versus standing up. Also, the headache is not worse with Valsalva maneuvers, such as sneezing, coughing, or straining for a bowel movement; or with jaw movement, such as chewing or talking.  

While obtaining history, be sure to rule out secondary causes of headaches. First, ask the patient if they have started any new medications recently because some headaches can be an adverse effect of medications.  

Also, the patient should report no history of head trauma, systemic symptoms such as fever, malignancy, or immunodeficiency. If any of these are present, think of secondary headaches.  

Finally, the physical exam reveals a normal neurologic exam in between episodes of headache; with normal appearance of the optic nerves on the fundoscopic exam. With these findings, diagnose a primary headache. 

The next step is to ask your patient about the laterality of their headaches. If their headaches are bilateral, suspect tension-type he]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_household_substance_exposure_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fKu9NB88Tg_D6pUVsPNKTizPS4_S223p/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to household substance exposure (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Inhalation or ingestion of various household substances can cause serious morbidity and mortality in the pediatric population.  

Increased mobility and frequent hand-to-mouth activity during the toddler and preschool years create the potential for unintentional or exploratory ingestions.  

While exposure to some substances like lead cause vague, subacute, or chronic symptoms; ingestion or inhalation of caustic substances, carbon monoxide, organophosphates, or toxic alcohols can cause acute, life-threatening symptoms. 

Now, if a pediatric patient presents with a chief concern suggesting a household substance exposure, you should first perform an ABCDE assessment to determine if the patient is unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation; and consider intubation if they demonstrate shallow, ineffective, or absent respirations. Next, obtain IV access and administer IV fluids. Then, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. If needed, provide supplemental oxygen, obtain a point-of-care blood glucose level, and order a 12-lead ECG. Finally, if indicated, consider a surgical consultation or endoscopy. 

Here’s your first clinical pearl! Depending on the substance and timing of ingestion, you can consider using a decontamination method to minimize absorption. While ipecac syrup and gastric lavage are no longer recommended, activated charcoal can be effective if given within one hour of ingestion. Keep in mind that charcoal does not bind well to liquids or charged molecules like iron; and you should avoid using it for caustic ingestions, since it can obscure visualization during endoscopy. Always make sure your patient can protect their airway before you give activated charcoal, since it can induce vomiting! 

Now that we have discussed unstable patients, let’s return to the ABCDE assessment and look at stable ones.  

First, obtain a focused history an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_altered_mental_status_(pediatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V2THvxA3TguU_d9rhqvneYAUTP_wRTGC/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to altered mental status (pediatrics): Clinical sciences]]></video:title><video:description><![CDATA[Altered mental status refers to any change in brain function that significantly impacts behavior, mood, or consciousness. Differential diagnosis for altered mental status includes metabolic disturbances, substance exposure, structural brain lesions, infection, hypoxemia, hypoventilation, shock, and seizures. 

If a pediatric patient presents with altered mental status, first perform an ABCDE assessment to determine if they are stable or unstable.  

Because altered mental status is a manifestation of many life-threatening conditions, you should consider your patient unstable and start acute management. First, stabilize the airway, breathing, and circulation. Then, assess their level of consciousness by checking the Glasgow Coma Scale or GCS, which measures eye-opening, verbal, and motor response to stimuli on a scale from 3 to 15. For children less than 5 years of age, use the Pediatric Glasgow Coma Scale instead. A GCS score of 3 represents a comatose state, while a score of 15 indicates a normal level of consciousness. In trauma patients, GCS of 8 or less might require intubation, however when dealing with a pediatric patient with altered mental status, you might want to intubate even with higher GCS to protect the airway! Next, obtain IV access, check a bedside glucose, and administer naloxone if you suspect opioid intoxication. Finally, begin continuous vital sign monitoring; and if needed, provide supplemental oxygen. 

Once you’ve stabilized your patient, obtain a focused history and physical exam.  

Since these patients are often unable to provide a history, you may need to gather information from family members or caregivers. They typically report a significant change in the patient’s level of consciousness, with decreased alertness; confusion; altered mood; or altered behavior, like inconsolable crying. These symptoms may fluctuate in severity. 

The exam reveals a decreased level of consciousness, with confusion, disorientation, or irritability.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_inborn_errors_of_metabolism_(progressive_or_chronic):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oHPjVH62SRymmbYsiSdLEEUYQp6-kaW7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to inborn errors of metabolism (progressive or chronic): Clinical sciences]]></video:title><video:description><![CDATA[Inborn errors of metabolism, or IEMs, are genetic conditions that result from alterations within a biochemical or metabolic pathway. IEMs with progressive or chronic onset are typically caused by single gene defects that impair enzymes involved in amino acid and carbohydrate metabolism or glycogen and lysosomal storage. Progressive or chronic IEMs can be broadly categorized according to the presence or absence of progressive neurologic deterioration and subcategorized further based on characteristic clinical findings. 

Now, if a pediatric patient presents with a chief concern suggesting a chronic or progressive IEM, first perform an ABCDE assessment to determine if they’re stable or unstable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain intravenous access and consider starting IV fluids. Finally, begin continuous vital sign monitoring, and if needed, provide supplemental oxygen. 

Now that we’ve discussed unstable patients, let’s return to the ABCDE assessment and look at stable patients. First, obtain a focused history and physical examination, including fundoscopy. History might reveal a positive newborn screen, and affected children often present with developmental delays, intellectual disability, behavioral changes, muscle weakness, or motor deficits. There might be a family history of a known metabolic disorder, a sibling with similar symptoms, or an unexplained death.  

The exam commonly reveals spasticity or hypotonia, occasionally in combination with organomegaly, ocular findings, and vision or hearing loss. With these findings, consider a chronic or progressive IEM, and assess for progressive neurological deterioration. 

Here’s a high-yield fact! Although newborn metabolic screening can detect many IEMs early, screening panels vary by state, and false negative results are possible. So, whenever you suspect a metabolic disorder, order confirmatory testing regardless of newborn screening results.  

Now, let’]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_mononucleosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hZSw0hJATGOLUTpnp6xPtsVHTHy60kRL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious mononucleosis: Clinical sciences]]></video:title><video:description><![CDATA[Infectious mononucleosis, or mono for short, is a viral illness primarily caused by human herpes virus-4, otherwise known as Ebstein Barr Virus, or EBV. The virus spreads through close personal contact, usually through saliva or respiratory secretions. Classically, this happens by sharing food or drinks, or by kissing, which is why mono is sometimes called the “kissing disease” and why it’s common in young adults. Once the virus reaches the new person’s mouth, it infects both epithelial cells and B cells in the oropharynx. It is then carried throughout the body, allowing it to infect other lymphoid tissues including the liver, spleen, and lymph nodes.  

Now, if a patient presents with a chief concern suggesting infectious mononucleosis, your first step is to obtain a focused history and physical exam. Your patient might report fever, fatigue, myalgia, sore throat, and in some cases, nausea, and vomiting. On the other hand, physical exam typically reveals posterior cervical lymphadenopathy, palatal petechia, tonsillar exudates, and possibly splenomegaly. 

Here’s a clinical pearl to keep in mind! Splenomegaly in infectious mononucleosis is a result of lymphocytic infiltration in the spleen. Some patients might note vague abdominal discomfort or referred pain of the left shoulder, while others might be completely asymptomatic. During physical examination, be sure to check for an enlarged spleen. Palpate below the left costal margin and feel for the splenic edge then percuss for dullness in the lowest intercostal space along the left axillary line.  

At this point, suspect infectious mononucleosis and obtain a heterophile antibody test, also known as a monospot test. If the heterophile antibody test is positive, diagnose infectious mononucleosis. Here’s the catch! A false negative heterophile antibody test is common in the early course of the illness. So, if the test is negative but you still clinically suspect infectious mononucleosis, order a CBC with dif]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_foot_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/avp_B6bQQuWftxgRWb1SKRK2TieTpIur/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to foot pain: Clinical sciences]]></video:title><video:description><![CDATA[Foot pain is a common symptom with many underlying causes, including conditions affecting the joints, bones, tendons, or skin. It’s important to first identify if your patient’s foot pain is due to trauma or infection. Other possible types of foot pain include neuropathic pain due to nerve damage; nociceptive pain due to arthralgia, ostalgia, or tendinopathy; and dermatologic ulcers or lesions. 

When a patient presents with foot pain, first obtain a focused history and physical exam. History typically reveals foot pain, while the exam might demonstrate foot edema, erythema, or warmth. They may also have foot tenderness, effusion, limited range of motion, or crepitus.  

Your next step is to assess for trauma. This includes an obvious mechanism of injury, such as a motor vehicle crash or sports injury, joint deformity, or ligamentous laxity. If trauma is present, think fracture or dislocation, and investigate further.  

Patients with a fracture or dislocation will report pain that may worsen with activity and improve with rest.  They might also report bruising. Physical exam will reveal tenderness to palpation and difficulty bearing weight. With these findings, consider a traumatic injury, such as a fracture or dislocation, and order a foot X-ray.  If the X-ray results confirm a bone fracture or joint dislocation, diagnose a foot fracture or dislocation!  

Now, here’s a clinical pearl to keep in mind! Stress fractures are caused by repetitive stress, such as frequent running, marching, or dancing. Patients with this condition may have a history of osteoporosis, tobacco use, vitamin D deficiency, or calcium deficiency. Their initial X-rays might be negative or show a faint fracture line, while an MRI typically shows fracture or osseous remodeling.   

Alright, if trauma is not present, assess for signs of infection like fever, chills, myalgias, and localized tenderness.  If there are signs of infection, think osteomyelitis. Patients with osteomyelitis oft]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_compressive_mononeuropathies:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BmdNY7y2R76NQyScP4OU-X9zRr_nDhCb/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to compressive mononeuropathies: Clinical sciences]]></video:title><video:description><![CDATA[Compressive mononeuropathies occur as a result of mechanical compression or entrapment of peripheral nerves, which can eventually lead to demyelination and axonal injury, causing symptoms like pain and loss of function. Now, based on a focused history and physical exam, you can identify the most common compressive neuropathies, including median, ulnar, radial, peroneal, and tibial mononeuropathies. 

Okay, if your patient presents with a chief concern suggestive of compressive mononeuropathy, your first step is to obtain a focused history and physical examination. First, let’s discuss a median neuropathy at the wrist, also known as carpal tunnel syndrome. Here, there’s a median nerve compression in the carpal tunnel, which is the area between the carpal bones and flexor retinaculum, also known as the transverse carpal ligament.  

History will reveal a weak grip and decreased dexterity, such as dropping small objects and having trouble with buttons. Additionally, the patient will report numbness, tingling, and pain in the first three fingers, from the thumb to the middle finger, usually worse at night. Next, they will likely report daily activities with repeated or sustained wrist flexion, such as typing or housekeeping. The patient might also report that shaking the affected hand in the air will improve the symptoms. Finally, history might reveal associated medical conditions and risk factors such as diabetes, hypothyroidism, obesity, pregnancy, or rheumatoid arthritis.  

These conditions can predispose a person to compressive neuropathy because they affect nerve health, causing nerves to be more susceptible to compression injury. However, in amyloidosis, the deposition of amyloid can directly compress the nerve and affect the conduction of signals. In some cases, this type of neuropathy might occur due to recent wrist trauma. In this case, direct force to the wrist can result in local edema and compression of the nerve within the carpal tunnel, eve]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obsessive_compulsive_disorder_(OCD):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hRc_OfihRi6-BP-MrH0AwT3FSD_T0J1j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obsessive compulsive disorder (OCD): Clinical sciences]]></video:title><video:description><![CDATA[Obsessive-compulsive disorder, or OCD, is a condition characterized by obsessions and compulsions. Obsessions are recurrent, intrusive thoughts that can manifest as images or urges that cause significant anxiety or distress.  

On the other hand, compulsions are ritualized attempts aimed at alleviating the anxiety caused by obsessions. The specific content of obsessions and compulsions varies widely among individuals, with common themes including contamination, concerns about symmetry, or danger. Depending on the severity of the condition and the extent of impairment it causes, OCD can be categorized as mild, moderate, or severe.  

When a patient presents with a chief concern suggesting OCD, you should first obtain a focused history and physical examination.   

Your patient may report excessive or persistent intrusive thoughts and urges to perform specific tasks, such as excessive hand washing or compulsive checking the locks on doors. On physical examination, you may observe repetitive actions like tapping or touching; skin lesions from repeated behaviors, such as excoriations on the hands; or the use of repetitive words and phrases. If your patient has these findings, suspect OCD.   

Your next step is to confirm the diagnosis by assessing the DSM-5 criteria for OCD. To meet the criteria, the patient must have obsessions or compulsions, or both. Obsessions or compulsions are distressing or time-consuming, to the level of interfering with their ability to function well in social or work settings. This interference can manifest as difficulty maintaining relationships, performing job duties, or engaging in daily activities.  

Additionally, ensure that their symptoms are not attributable to substances or another medical condition, such as hyperthyroidism. Also, confirm that their symptoms are not more appropriately explained by another mental disorder, such as an anxiety disorder. If these criteria are met, diagnose OCD. 

Here’s a high-yield fact! OCD is]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Specific_phobia_and_social_anxiety_disorder_(social_phobia):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2zZh02fASc2kawqhKcuclRY1T4yh0w6I/_.jpg</video:thumbnail_loc><video:title><![CDATA[Specific phobia and social anxiety disorder (social phobia): Clinical sciences]]></video:title><video:description><![CDATA[Specific phobia and social anxiety disorder are characterized by intense, irrational fear or anxiety triggered by a specific object, situation or activity that poses no inherent danger. This heightened sensation of fear or anxiety often causes significant distress impacting daily life and function.  

Often, individuals develop avoidance behaviors of a known trigger to deter these feelings. Common examples of specific phobias include arachnophobia, or fear of spiders; claustrophobia, or fear of confined spaces; and aerophobia, or fear of flying. On the other hand, social phobia, also known as social anxiety disorder or SAD, is the persistent fear of being in a social situation and being scrutinized by others.  

Alright, when a patient presents with a chief concern suggesting a phobia, your first step is to perform a focused history and physical examination including a mental status exam. On history, patients often report active avoidance of phobic stimulus, which can be an object, situation, or activity that provokes excessive fear and anxiety to a greater degree than in the general population.  

The physical exam might be grossly normal, but the mental status exam can reveal anxious behavior, abnormal speech patterns, and a change in affect by the phobic stimulus. The patient might also exhibit illogical thinking regarding the stimulus but have an insight into the exaggerated response.  

With these initial findings, your next step is to assess for social anxiety. When social anxiety is present, the patient will report fear of humiliation or embarrassment and anxiety in response to an anticipated social activity. They might experience physical symptoms of sweating, trembling, or a shaky voice when exposed to the trigger, and thereby avoid social situations.  

On mental status exam, the patient might display a depressed or anxious mood, soft speech with hesitancy, and normal thought content. In severe cases, they might even have suicidal ideation. In th]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_involuntary_movements:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DV3cY1HlREGjX2dffXcFercgSQSBVVIy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to involuntary movements: Clinical sciences]]></video:title><video:description><![CDATA[Involuntary movements are unintentional body movements that can occur due to various conditions, including metabolic derangements, medication effects, and neurodegenerative conditions. There are several distinct types of involuntary movements, such as tremors, dystonia, myoclonus, and chorea, and the underlying pathology is different for each condition.  

Important conditions associated with involuntary movements include those secondary to anti-dopaminergic medications, and neurologic conditions, such as Parkinson disease, Creutzfeldt-Jakob disease, Tourette syndrome, and Huntington disease.  

Now, if a patient presents with involuntary movements, first obtain a focused history and physical examination, and order a complete metabolic panel. History reveals body movements that the patient cannot control. The physical exam shows abnormal movements that persist even if you distract the patient, while the complete metabolic panel is normal. These findings are suggestive of movement disorder. 

Here’s a clinical pearl! Metabolic derangements can cause different abnormal movements.  For example, hypocalcemia can increase membrane excitability of peripheral nerves and cause muscle fasciculations and tetany. Less commonly, hypomagnesemia and hypokalemia can also cause fasciculations and tetany. Lastly, renal or hepatic failure might lead to asterixis, which is flapping of the hands when the arms are outstretched. 

Your next step is to assess the use of anti-dopaminergic medications, including antipsychotics, especially first-generation antipsychotics, and anti-emetics, such as metoclopramide. If your patient is taking an anti-dopaminergic medication, diagnose medication-induced movement disorder and determine the type of medication reaction the patient is having. 

Let’s start with medication-induced dystonia. These patients report sustained muscle tightening, twisting of the body that typically involves the face and neck, and recent use of an anti-dopaminergic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Well-patient_care_(geriatrics):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QEx24giCTCaVzw64fxlVBNAMTXWc46CE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Well-patient care (geriatrics): Clinical sciences]]></video:title><video:description><![CDATA[Well-patient geriatric care for adults aged 65 years and older, is an annual check-up that promotes physical, mental, and social health while building trust between the healthcare provider and patient.  

For all patients, each visit includes a comprehensive history and physical exam, followed by screening and counseling about a variety of topics such as substance use, mental health, functional status, and fall risk; and optimizing diet and physical activity. Additional screening and counseling are provided based on risk status and biological sex.  

When a geriatric patient presents for well-patient care, begin with a comprehensive history and physical examination.  

Review your patient’s age; past medical and surgical history; their family and social history; sexual activity; medications; and diet and exercise habits. Next, complete a physical examination including height, weight, body mass index, or BMI, and vital signs. 

Your next step is to provide screening and counseling for all geriatric patients, regardless of age or risk factors.  

First, review age-appropriate immunizations which includes COVID-19, influenza, RSV, and pneumococcal vaccines. Also, patients who have not completed their shingles vaccinations should do it now. Lastly, ensure your patient receives a Tdap or Td vaccine every 10 years. 

Next, ask about alcohol, tobacco, and substance use through direct conversation with your patient or by using validated questionnaires like the CAGE questionnaire for alcohol use; Fagerstrom questionnaire for nicotine dependence, and the Substance Use Brief Screen, or SUBS, for substance use. Because alcohol use, tobacco use, and substance use are significant preventable causes of disease, disability, and death, provide counseling and connect them to resources and referrals for further intervention and support. 

Let’s move onto cancer screenings for geriatric patients, including colorectal and lung cancer screening. For colorectal cancer, screen up]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexually_transmitted_infection_screening_(Family_medicine):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DsKM9lEIRf2aAMo2gdqzw3s2R3OF8Rdx/_.png</video:thumbnail_loc><video:title><![CDATA[Sexually transmitted infection screening (Family medicine): Clinical sciences]]></video:title><video:description><![CDATA[Sexually transmitted infections, also known as STIs, are infections acquired through sexual contact. While many STIs have symptoms, some patients present asymptomatically. For this reason, screening is important in diagnosing and treating STIs. Screening also provides an opportunity to educate patients on safe sexual practices and disease prevention. Specific screening recommendations for STIs vary according to biological sex, pregnancy status, sexual preference, and HIV status. 

For patients presenting for STI screening, first perform a focused history and physical examination.  

The patient might be asymptomatic, or they may report STI symptoms, such as dysuria, genital discharge, or rash. There also might be a history of known STI exposure. If so, ask about the timing of the sexual exposure and review previous screenings or treatment results. Physical examination may show cervical or penile discharge, or possibly genital, rectal, or pharyngeal lesions. 

Here’s a clinical pearl! Patients who are high-risk for STIs include those who have multiple sex partners, engage in transactional sex, use illicit substances, or have a history of incarceration.  

Here’s another clinical pearl! STI screening can be completed at a specific STI screening visit or as part of a preventative visit, like a well-patient care exam. STI screening can also be completed without a physical exam by patient-collected swabs, and lab tests such as blood and urine tests; however, this type of screening is only appropriate for asymptomatic patients. 

Okay, let’s start by talking about which infections are screened for and how that screening is completed.  

Chlamydia, caused by Chlamydia trachomatis, is the most frequently reported bacterial STI with the highest prevalence in patients who are under 25 years of age. Gonorrhea, caused by Neisseria gonorrhoeae, is the second most frequently reported bacterial STI. Testing for both is completed through a nucleic acid amplification ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_differentiating_lesions_(motor_neuron):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b8b92iEKTT2XweG7vLXFzRvOT2CMthHe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to differentiating lesions (motor neuron): Clinical sciences]]></video:title><video:description><![CDATA[Motor neuron lesions are conditions associated with a loss of strength and movement due to upper or lower motor neuron injuries. Upper motor neurons originate in the cerebral cortex, with axons that descend through the subcortical white matter and synapse with lower motor neurons in the brainstem and anterior horn cells in the spinal cord. These lower motor neurons then send axons out of the central nervous system via cranial nerves or spinal nerve roots to reach muscle cells.  

Now, some conditions affect only lower motor neurons, such as acute flaccid myelitis and adult-onset spinal muscular atrophy; while other conditions can affect both upper and lower motor neurons, such as amyotrophic lateral sclerosis. 

Now, if your patient presents with a chief concern suggesting motor neuron disease, first perform an ABCDE assessment to determine if they are unstable or stable.  

If unstable, stabilize the airway, breathing, and circulation. In some cases, you might even have to intubate the patient and start mechanical ventilation. Next, obtain IV access and consider starting IV fluids. Finally, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry; and if needed, provide supplemental oxygen. 

Now, let’s go back to the ABCDE assessment and focus on stable patients.  In this case, obtain a focused history and physical examination. The patient will describe progressive bilateral weakness, which could affect muscles of the face, neck, arms, or legs. Some patients might describe trouble standing up and walking, while others might report trouble speaking, swallowing, or breathing.  

On physical exam, you will notice weakness of the facial muscles, neck, trunk, or limbs, which may or may not be symmetric. Finally, the physical exam will reveal abnormal muscle tone and reflexes, and in some cases, cranial nerve dysfunction and an abnormal gait.   

Next, assess for sensory involv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_differentiating_lesions_(nerve_root,_plexus,_and_peripheral_nerve):_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kDnwWovuR-SSN0OR2CS19zLYSzuoMrJd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to differentiating lesions (nerve root, plexus, and peripheral nerve): Clinical sciences]]></video:title><video:description><![CDATA[Injuries involving different components of the peripheral nervous system, such as nerve roots, plexuses, and peripheral nerves, can result in symptoms such as muscle weakness and sensory deficits. Mechanisms of injury vary depending on the affected site and include trauma, compression, malignancy, and inflammatory disorders. Now, based on history and physical exam findings, you can differentiate between the most common causes of wrist drop, foot drop, and combined upper and lower extremity sensorimotor deficits. 

Now, if your patient presents with chief concerns suggesting a nerve root, plexus, or peripheral nerve lesion, first obtain a focused history and physical examination starting with wrist drop.   

Let’s start by discussing patients who present with wrist drop. History will reveal hand weakness and numbness; and on exam, you’ll notice weakness of wrist extension and loss of hand sensation. These findings are often referred to as wrist drop,  which could result from radial neuropathy, C7 radiculopathy, or brachial plexopathy; so your next step is to assess the underlying cause. 

Patients with radial neuropathy report numbness, tingling, and pain over the top of the hand, and sometimes, the back of the arm. In addition to wrist weakness, they may report weakness of the elbow. History might reveal prolonged positioning associated with radial nerve compression, or recent trauma to the humerus.  

As for the exam, you&amp;#39;ll typically notice weakness in wrist and finger extension, sensory loss in the dorsum of the hand, and decreased or absent brachioradialis reflexes. 

These findings are consistent with a radial nerve injury at the spiral groove of the humerus. However, if the radial nerve lesion is located higher in the axilla, you&amp;#39;ll also note weakness of elbow extension due to triceps weakness, sensory loss on the dorsal surface of the arm, and a decreased triceps reflex. With these findings, diagnose radial neuropathy. 

]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_sclerosis:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YvVjWqh-S-S2bB9v0S6N7Xy6Sx2h6N1h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple sclerosis: Clinical sciences]]></video:title><video:description><![CDATA[Multiple sclerosis, or MS for short, is an autoimmune condition characterized by demyelinating CNS lesions that are disseminated in space and time, resulting in neurologic symptoms and deficits. Based on the initial pattern of symptom progression, MS can be classified as relapsing-remitting, which is associated with stable neurologic disability between episodes of attacks; or primary progressive MS, which is characterized by progressive neurologic decline without relapses. 

Now, when a patient presents with chief concerns suggesting MS, first obtain a focused history and physical examination, and order a brain and spine MRI with contrast. You can also consider performing a lumbar puncture to analyze the cerebrospinal fluid, or CSF, for oligoclonal bands. If you do, remember to check serum oligoclonal bands for comparison, to see if the bands are only present in the CSF, which confirms intrathecal production of immunoglobulin G.     

History will reveal an episode of unexplained neurologic symptoms that develop over hours to days and last for at least 24 hours. Some common symptoms include vision loss, painful eye movements, double vision, slurred speech, facial or limb numbness or weakness, imbalance or incoordination, and vertigo.  

Your patient might also report symptoms of trigeminal neuralgia, such as intense, sharp facial pain provoked by touch.  

History typically does not reveal fever or other symptoms suggesting infection. Additionally, some patients might notice their symptoms temporarily worsen with heat or during a hot shower, which is known as the Uhthoff phenomenon;  while others might report an electric shock sensation down their back when they bend their neck forward, which is known as the Lhermitte sign.  

History might also reveal symptoms indicating autonomic dysfunction, like bladder, bowel, or erectile dysfunction;  and some patients may describe depression or fatigue.  

Although MS can affect anyone, most patients are biolog]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Guillain-Barré_syndrome:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eU2vnrcxR-CwIkfvVKVfT4KTQuKKTx-c/_.jpg</video:thumbnail_loc><video:title><![CDATA[Guillain-Barré syndrome: Clinical sciences]]></video:title><video:description><![CDATA[Guillain-Barré syndrome is an acute, monophasic, immune-mediated polyradiculoneuropathy that usually follows a respiratory or gastrointestinal infection. This condition occurs when immune cells inappropriately attack the peripheral nerves and nerve roots, eventually causing demyelination or axonal injury.  

Some common pathogens associated with Guillain-Barré syndrome include bacteria like Campylobacter jejuni and Mycoplasma pneumoniae, as well as viruses, such as cytomegalovirus, Epstein-Barr virus, and HIV.  Guillain-Barré syndrome is the most common cause of generalized paresis and can also result in sensory loss, autonomic dysfunction, and respiratory failure. 

If your patient presents with a chief concern suggesting Guillain-Barré syndrome, first perform  an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation.  In some cases, you might need to intubate your patient and provide mechanical ventilation. Next, obtain IV access and consider IV fluids. Finally, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry. 

Now, here’s a clinical pearl to keep in mind! Because individuals with Guillain-Barré syndrome may present with diaphragm weakness and can quickly progress to respiratory failure, be sure to perform bedside pulmonary function testing! Results will reveal reduced vital capacity, which is the amount of air a patient can exhale after a maximum inhalation. Additionally, you will notice reduced maximal inspiratory pressure, also known as negative inspiratory force; as well as reduced maximal expiratory pressure.  

To guide intubation timing in patients with neuromuscular weakness, you can apply the 20, 30, 40 rule. If vital capacity is less than 20 milliliters per kilogram, maximal inspiratory pressure is less than 30 centimeters of water, and maximal expiratory pressure is less than 40 c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_prenatal_teratogen_exposure:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Nq31clSqRRKy-u3YIfHrXCDhSHeUwH_B/_.png</video:thumbnail_loc><video:title><![CDATA[Approach to prenatal teratogen exposure: Clinical sciences]]></video:title><video:description><![CDATA[Prenatal teratogens are substances or conditions that disrupt normal fetal growth and development. Depending on the timing, dose, and duration of exposure, teratogens can increase the risk of early pregnancy loss, stillbirth, fetal growth restriction, congenital anomalies, and developmental delays. Potential teratogens include recreational substances, maternal conditions like diabetes, and prescription medications. 

Now, if a pediatric patient presents with a chief concern suggesting a prenatal teratogen exposure, you should first perform an ABCDE assessment to determine if the patient is stable or unstable.  

If unstable, stabilize their airway, breathing and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, if needed, provide supplemental oxygen. 

Now that we&amp;#39;ve discussed unstable patients, let’s return to the ABCDE assessment and look at stable ones.  

First, obtain a focused history and physical examination, and order a CBC and CMP.  

History usually reveals a known prenatal exposure to recreational substances or medications, or a maternal history of an underlying medical condition associated with teratogenicity. The patient also might have a history of fetal growth restriction, preterm birth, developmental delay, or congenital anomalies, like cardiac or neural tube defects.   

Additionally, the physical exam often demonstrates poor growth and certain characteristic facial features, occasionally with other anomalies such as cleft lip and palate or limb and digit abnormalities. 

At this point, consider prenatal teratogen exposure. Now, while some substances such as alcohol are directly teratogenic; other substances, such as opioids, most commonly cause complications due to withdrawal. So, as a next step, assess for a maternal history of substance use during pregnancy. 

If a history of substance use is present, assess your patie]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Schizophrenia_and_related_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NmXCUigIRMizNWkmXLNi3kYiQWqD-pJr/_.png</video:thumbnail_loc><video:title><![CDATA[Schizophrenia and related disorders: Clinical sciences]]></video:title><video:description><![CDATA[Schizophrenia and related disorders are psychiatric conditions characterized by psychotic symptoms, including delusions, hallucinations, disorganized thoughts and disorganized speech. Schizophrenia is the primary condition within this group of psychiatric conditions, along with related disorders such as schizophreniform disorder and brief psychotic disorder which share similar symptoms but are shorter in duration; schizoaffective disorder, where mood symptoms occur alongside psychotic symptoms; and mood disorders with psychotic features. 

When a patient presents a with concern suggesting schizophrenia or a related psychotic disorder, start with a focused history and physical examination. The patient may report psychotic symptoms such as delusions, which are fixed false beliefs; hallucinations, which are abnormal sensory experiences; disorganized speech, like loose associations or word salad; or disorganized behavior, such as agitation or possibly catatonia, which refers to a severe type of disorganized behavior, ranging from waxy flexibility to excessive movement.  

With these findings, suspect schizophrenia or a related disorder, and assess the key features to differentiate between the causes. 

Here’s your first clinical pearl! Psychotic symptoms are categorized as either positive or negative. Positive symptoms are experiences present in the affected patient but not in the general population. These include delusions, hallucinations, and disorganized speech or behavior. Negative symptoms, on the other hand, are experiences that are absent in the patient but present in the general population. So instead of social engagement, motivation, and goal-directed activity normally found in the general population, the patient will demonstrate social withdrawal, decreased motivation, and lack of affect. 

And here’s another clinical pearl! A first psychotic break requires a thorough medical workup to rule out possible underlying physical conditions that could bette]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_somatic_symptom_and_related_disorders:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tzsQ3Gb_RvSb0EJZ7GBR11LLTiG1F6Yb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to somatic symptom and related disorders: Clinical sciences]]></video:title><video:description><![CDATA[Somatic symptom and related disorders are a group of conditions that are characterized by excessive focus on physical symptoms the patient attributes to non-psychiatric illness, and related abnormal thoughts or behaviors that cause impairment or distress.  

These conditions include illness anxiety disorder, somatic symptom disorder, and functional neurologic symptom disorder, previously known as conversion disorder.  

Because these conditions present with physical symptoms it is very important to rule out underlying medical conditions first. Keep in mind, illness anxiety disorder and somatic symptom disorder can be diagnosed alongside a medical condition. 

Alright, when a patient presents with a chief concern suggesting a somatic symptom disorder, your first step is to obtain a focused history and physical exam. On history, the patient might describe specific somatic symptoms like focal weakness or gastrointestinal distress, or nonspecific ones like fatigue or pain.  

Additionally, they might report abnormal thoughts like excessive worry or obsession, or abnormal behaviors such as repeated self-examination or frequent emergency room visits.  

On physical exam, you might find the patient to be anxious. If you see these findings, assess the severity of the patient’s current symptoms.  

If the symptoms are mild or absent at the time of examination, you should consider illness anxiety disorder. These patients usually express excessive anxiety about the thought of possibly having a medical illness. To confirm your diagnosis, assess for the DSM-5 criteria of illness anxiety disorder.  

First, the patient must exhibit excessive preoccupation with the possibility of experiencing a physical illness or symptoms. These symptoms are typically absent or mild at the time of the encounter but may have been experienced by the patient in the past.  

The patient must also exhibit high levels of anxiety about health-related topics and worry about developing symptoms ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_hallucinogen,_inhalant,_and_cannabis_use,_intoxication,_and_overdose:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IwEwjbj0RE2m_StTujDI4qtYSR2koM7D/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to hallucinogen, inhalant, and cannabis use, intoxication, and overdose: Clinical sciences]]></video:title><video:description><![CDATA[Acute hallucinogen, inhalant, or cannabis intoxication causes a temporary state of altered consciousness as well as behavioral and psychological changes, impaired judgment, and physiological disturbances. These psychoactive recreational substances alter neurotransmitters and receptors within the central nervous system to produce various effects, including euphoria, distorted perceptions and thoughts, and sedation or psychomotor agitation.  

Okay, if a patient presents with a chief concern suggesting hallucinogen, inhalant, or cannabis use, intoxication, or overdose; first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize their airway, breathing, and circulation; and perform endotracheal intubation if your patient demonstrates shallow or ineffective respirations. Next, obtain IV access and consider starting IV fluids. Then, put your patient on continuous vital sign monitoring, pulse oximetry, and cardiac telemetry; and provide supplemental oxygen if needed. Additionally, if your patient is hyperthermic, provide cooling blankets; and if they are agitated, consider sedation. 

Here’s a clinical pearl to keep in mind! Patients with significant hallucinogen, inhalant, or cannabis exposure may present with overdose, which may cause hemodynamic instability, severe psychosis, seizures, or even coma. Additionally, individuals with acute inhalant intoxication can develop life-threatening cardiac dysrhythmias requiring resuscitative measures. 

Here’s a high-yield fact! 3,4-Methyl enedioxy methamphetamine, also known as MDMA, is a commonly abused recreational substance with serotonergic properties. Excessive ingestion can result in serotonin syndrome, characterized by elevated blood pressure; increased heart rate; myoclonus; hyperreflexia; diaphoresis; and seizures. If you suspect serotonin syndrome, immediately discontinue the offending substance and any serotonergic medications your patient might be taking.  

Now that]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osmosis_supports_Health_Education_Programs</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J33NTr6eS22HNQMwYSne4hlWTs2NhMeY/_.png</video:thumbnail_loc><video:title><![CDATA[Osmosis supports Health Education Programs]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Osmosis supports Health Education Programs through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obstructive_hypertrophic_cardiomyopathy_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-OCSOBWOQt_2pIu2o_4mbpB3STSMHW4i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obstructive hypertrophic cardiomyopathy (NORD)]]></video:title><video:description><![CDATA[Obstructive hypertrophic cardiomyopathy is a genetic disorder where the walls of the heart become thicker, or hypertrophied. While it might seem a thicker heart is a good thing, the larger muscles prevent the ventricles—the two lower chambers of heart—from fully relaxing between contractions. In addition, the walls of the heart are stiffer and less compliant, so they can’t stretch out as much.  This reduces the amount of blood that gets into the heart, lowering the cardiac output, or the amount of blood pumped out of the heart per minute.  

Usually, the left ventricle is more affected, and in most cases, muscle growth is asymmetrical, meaning that the wall between the two ventricles, called the septum, grows larger relative to the free wall. In some people, the thickened septum can obstruct the outflow of blood from the left ventricle, which is why hypertrophic cardiomyopathy is sometimes called obstructive hypertrophic cardiomyopathy. In these cases, the blood that comes out of the left ventricle is forced through a smaller opening, which creates a “pulling” effect on the nearby mitral valve that further obstructs the outflow of blood.  

Most cases of obstructive hypertrophic cardiomyopathy are familial. This means the condition is inherited from a parent. Inheritance is autosomal dominant, meaning only a single copy of a disease-causing gene variant is needed to cause the disease. Variants in many different genes that code for proteins found in heart muscle, such as myosin and troponin T. can cause obstructive hypertrophic cardiomyopathy.

Symptoms of obstructive hypertrophic cardiomyopathy can begin at any age, but they most often start in early adulthood. Over time, the heart becomes unable to do its job effectively, leading to signs of heart failure such as excessive tiredness and shortness of breath, especially during exercise.   

Because there is less blood coming out of the heart, the amount of blood transported to the brain can decrease. This m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Eosinophilic_granulomatosis_with_polyangiitis_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cKvVr-T5SXmUAYZWe_OmsUpbQd6zN1eG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Eosinophilic granulomatosis with polyangiitis (NORD)]]></video:title><video:description><![CDATA[Eosinophilic granulomatosis with polyangiitis, or EGPA, previously known as Churg-Strauss syndrome, is a rare immune disorder that causes systemic organ damage from eosinophilic involvement and inflammation of small blood vessels, called vasculitis. It is frequently associated with allergic manifestations like asthma, rhinitis, and sinusitis. 

EGPA is characterized by the presence of increased amounts of eosinophils in the blood. Eosinophils are a type of white blood cell that play a role in the body’s response to allergens and parasitic infections. It’s unclear how EGPA develops, but it’s thought that some kind of trigger— such as an infection, medication, or environmental allergen— sets off an exaggerated eosinophilic immune response that causes damage to tissues and organs. Some people may be more susceptible to developing EGPA. When not treated, EGPA leads to the development of granulomas, which are collections of immune cells that cluster together to wall off an area of inflammation.  

Signs and symptoms of EGPA can vary greatly from one individual to another, but there are typically three phases: prodromal, eosinophilic, and vasculitic, although they don’t always occur in that order. The prodromal phase is characterized by adult-onset asthma and rhinitis that are often attributed to allergies. Unlike asthma, EGPA often has progressive lung involvement, commonly with infiltrates. In addition, chronic inflammation of the nasal lining causes growth of tissue within the nasal cavity called polyps. These polyps contain large amounts of eosinophils, and can block the sinus tracts, preventing mucus from draining out of the sinuses and causing congestion or inability to smell. 

The eosinophilic phase results in infiltration of eosinophils into organs and can cause characteristic lesions called eosinophilic granulomas. When eosinophils infiltrate the lungs, pulmonary infiltrates can form that are seen on radiologic imaging. Eosinophils can also affect the ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fostering_Clinical_Reasoning_with_Osmosis_Clinical_Sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V4fBvgAiSuS9AKJpi7PwMQO1T2iyhDCb/_.png</video:thumbnail_loc><video:title><![CDATA[Fostering Clinical Reasoning with Osmosis Clinical Sciences]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Fostering Clinical Reasoning with Osmosis Clinical Sciences through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maximizing_Exam_Performance:_Osmosis_Tools_for_Student_Success</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LCgHzCjXSQGnSxW5SQOYwsoUTuCb_7uz/_.png</video:thumbnail_loc><video:title><![CDATA[Maximizing Exam Performance: Osmosis Tools for Student Success]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Maximizing Exam Performance: Osmosis Tools for Student Success through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Bipolar_I,_bipolar_II,_and_cyclothymic_disorder:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7As2Azl_QjCcMXqWfm6k1S6gSril7u2E/_.png</video:thumbnail_loc><video:title><![CDATA[Bipolar I, bipolar II, and cyclothymic disorder: Clinical sciences]]></video:title><video:description><![CDATA[Bipolar spectrum disorders refer to psychiatric conditions characterized by mood instability, which cause a sudden shift in how a person thinks, feels, and behaves. These disorders can lead to significant personal distress, strain relationships, and impair occupational functioning. Additionally, the depressive symptoms in bipolar spectrum disorders significantly increase the risk of self-harm and suicidality. Bipolar spectrum disorders include bipolar 1 disorder, bipolar 2 disorder, and cyclothymic disorder. 

Now, when a patient presents with a chief concern suggesting a bipolar spectrum disorder, first perform a safety assessment to determine the risk of self-harm or harm to others. Look for signs of psychosis such as agitation, paranoia, aggression, auditory or visual hallucinations, and disorganized thoughts, speech, or behavior. Also, watch for manic symptoms like fast talking, reduced need for sleep, and an increase in goal-directed activity. Be sure to ask about thoughts of harming oneself or others and assess their severity and intent including any plans or actions. 

Patients with psychosis, mania, active thoughts of harm, or suicidal tendencies are at high risk and need acute management involving psychiatric hospitalization, pharmacologic stabilization, and a one-to-one sitter, if appropriate. In severe or resistant cases, consider electroconvulsive therapy or ECT. 

On the other hand, if the patient is at low risk of harm to self and others, obtain a focused history and physical exam. They may describe a persistently euphoric, irritable, or depressed mood that is significantly different from their baseline and may report frequent mood changes. Also, be sure to ask about the family history of bipolar disorder among first-degree relatives because there is a strong genetic component.  

The physical exam may reveal changes in appearance, such as being unusually unkempt, or psychomotor changes, like slowed or agitated movements. Additionally, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Chronic_low_back_pain:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qkhj9JWeSwWLJilPFY90W8LLRNW-KdvK/_.png</video:thumbnail_loc><video:title><![CDATA[Chronic low back pain: Clinical sciences]]></video:title><video:description><![CDATA[Chronic low back pain is a common patient concern that can have many underlying causes, including conditions that affect the nerves, joints, bones, muscles, and other soft tissues. Common causes of chronic low back pain include neuropathic pain due to nerve damage, and nociceptive pain due to myalgia, arthralgia, ostalgia, and referred visceral pain. 

When a patient presents with chronic low back pain, first, obtain a focused history and physical exam. History typically reveals low back pain that has lasted three months or more, while physical exam might reveal limited range of motion of the spine, tenderness to palpation over the spine or paraspinal tissue, and in some cases, overlying edema or erythema. With these findings, you can diagnose chronic low back pain. To find the cause of low back pain, you should first assess for neuropathic pain. This type of pain is described as lancinating, electrical, radiating, burning, or cold in nature.  

Lets first look at If neuropathic pain is present.  In this case the patient might report a history of numbness and tingling, as well as radicular pain, which is pain radiating down one or both legs. Physical exam may reveal allodynia, which is when pain is elicited from a stimulus that doesn’t usually cause pain, like a feather. They may also have a positive straight leg raise test, decreased patellar or Achilles reflexes, dermatomal sensory deficits, and myotomal strength deficits. With these findings, diagnose neuropathic chronic low back pain.  

Here’s a clinical pearl! There are many possible causes of neuropathic chronic low back pain. For example, a herniated vertebral disc causing spinal nerve root impingement can lead to radicular pain.  

Alternatively, lumbar spinal stenosis, which occurs due to degenerative narrowing of the spinal canal, can cause nerve root impingement and subsequent back pain, numbness, and weakness of the lower extremities. Finally, postherpetic neuralgia can cause neuropathic chron]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_abdominal_wall_defects:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Uc4vFkZiQgy3xbXWixmmG-C-RZq72943/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to abdominal wall defects: Clinical sciences]]></video:title><video:description><![CDATA[An abdominal wall defect refers to when abdominal organs, such as the intestines, protrude through a weakness or opening in the abdomen. These are typically congenital and present with a wide variety of clinical findings. Patients may present as unstable with abdominal viscera outside of their abdominal cavity or stable with findings ranging from a generalized decrease of abdominal muscle tone to a localized inguinal or umbilical mass. 

Now, if a pediatric patient presents with an abdominal wall defect, perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and consider starting IV fluids and antibiotics. Then, place your patient on continuous vital sign monitoring, and provide supplemental oxygen if needed.  

Consider placing a nasogastric or orogastric tube to empty the stomach. Finally, cover any protruding abdominal viscera with a warm moist sterile gauze or bowel bag to decrease the risk of necrosis, infection, and evaporative fluid losses.  

Once you have initiated acute management, obtain a focused history and physical examination. History might include prenatal testing showing an elevated alpha-fetoprotein level and a prenatal ultrasound revealing an abdominal wall defect with viscera outside of the abdominal cavity. As far as the newborn physical exam goes, you’ll notice visceral herniation through a skin defect in the abdomen. These findings should make you consider gastroschisis and omphalocele. Proceed with your evaluation by assessing the viscera for a membrane covering. 

If a membrane is absent, consider gastroschisis.  In this case, history might include risk factors such as a teenage birthing parent or antenatal use of tobacco; drugs, like opioids and cocaine; or decongestants. The physical exam will reveal that the defect is to the right of the midline and umbilicus and that the herniation contains bowel, usually small intestine. Int]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_primary_immunodeficiencies:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tjTh-lnxTRi59WL4KLUAiP52R9iW06mj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to primary immunodeficiencies: Clinical sciences]]></video:title><video:description><![CDATA[Primary immunodeficiencies are inherited conditions that are characterized by defects in one or more components of the immune system. Patients with immunodeficiencies have increased susceptibility to infection and are at risk for autoimmune and inflammatory conditions, as well as malignancies. Primary immunodeficiencies can be categorized according to characteristic history and exam features as well as characteristic pathogens. 

Now, if a pediatric patient presents with a chief concern suggesting a primary immunodeficiency, first perform an ABCDE assessment to determine if they are stable or unstable. If unstable, stabilize the airway, breathing, and circulation. Then, obtain IV access, put your patient on continuous vital sign monitoring, and provide supplemental oxygen if needed. Finally, administer IV antibiotics and consider IV immunoglobulin. 

Next, obtain a focused history and physical examination and look for signs suggesting severe combined immunodeficiency, or SCID. SCID is a primary T cell deficiency associated with severe humoral and cellular immune deficits, which is considered a life-threatening medical emergency.  

Affected patients are typically 6 months or younger and experience frequent, atypical, or opportunistic infections caused by bacteria, fungi, viruses, or parasites. Caregivers commonly report chronic diarrhea, and if newborn screening is available, results may confirm SCID. 

The physical exam often reveals oral ulcers, decreased or absent lymphoid tissue, and possibly mucocutaneous candidiasis. You might also notice signs of Omenn syndrome, including scaly skin, alopecia, and edema.  

With these findings, consider SCID and obtain a CBC with differential, serum immunoglobulin levels, flow cytometry for T and B cells, and a chest X-ray. Labs typically reveal decreased lymphocytes and immunoglobulin levels, and decreased T and B cell counts or function; while the X-ray is likely to demonstrate a small or absent thymus. These comb]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Approach_to_benzodiazepine_and_barbiturate_use,_intoxication,_and_overdose:_Clinical_sciences</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4-kqrWrISGmHkYWaN8_FIVXXRBG8r4zP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Approach to benzodiazepine and barbiturate use, intoxication, and overdose: Clinical sciences]]></video:title><video:description><![CDATA[Benzodiazepines and barbiturates are two common types of sedatives and anxiolytics typically used to treat panic disorder, anxiety disorders, and insomnia. Both classes bind to gamma-aminobutyric acid, or GABA, receptors and increase the affinity of the receptor to bind to GABA, a primary inhibitory neurotransmitter. This results in an inhibitory effect within the central nervous system by reducing neuronal excitability. This process produces symptoms of sedation by preventing overstimulation of the brain.  

Both benzodiazepines and barbiturates have addictive properties, which can lead to chronic dependance, misuse and overuse. Of the two, benzodiazepines are more commonly used in clinical settings. Barbiturates, on the other hand, are no longer used as often due to their narrow therapeutic window and ease of overdose. Keep in mind that illicit use of these medications without a legitimate prescription is common.  

Alright, when a patient presents with a chief concern suggestive of benzodiazepine or barbiturate use, first perform an ABCDE assessment to determine if they are stable or unstable.  

Your goal here is to determine if the patient is actively experiencing an overdose which is a medical emergency. If the patient is unstable, stabilize their airway, breathing, and circulation right away. Provide supplemental oxygen and have a low threshold for endotracheal intubation. Make sure to assess for the Glasgow Coma Scale, or GCS. If the GCS score is less than 8, intubation is indicated.  

Additionally, obtain IV access and consider starting IV fluids. Then, continuously monitor vital signs including temperature, heart rate, blood pressure, respiratory rate, oxygen saturation, and cardiac telemetry. Lastly, consider using cooling blankets if the patient is hyperthermic.  

Next, perform a focused history and physical and order a urine and/or a serum toxicology screen. If the patient is unable to communicate, obtain history from a family member or a fr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Power_of_Quizzing_with_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lK0pp-GzQdWBrwqtLsf4aWBuSRudA2IJ/_.png</video:thumbnail_loc><video:title><![CDATA[The Power of Quizzing with Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of The Power of Quizzing with Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fluid_balance_-_Overview:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KNvltvFVQDC5YR3o8B8uqRDxRGecMT38/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fluid balance - Overview: Nursing]]></video:title><video:description><![CDATA[Fluid balance is the regulation of the body’s fluid compartments to maintain a stable internal environment. Fluid affects essential functions like cellular metabolism, temperature regulation, and the delivery of oxygen and nutrients to the cells. Any change in the volume or concentration of fluid can negatively affect these vital life processes. 

Okay, so let’s start by reviewing some basics about fluid balance. First, fluid is found in two major compartments in the body: inside the cells, called intracellular fluid, and outside the cells, called extracellular fluid. The extracellular fluid compartment is further divided into the intravascular space, which is inside the blood vessels; the interstitial space, which is found between cells; and the transcellular space, where fluid, like pericardial, cerebrospinal, and synovial fluid, is contained in epithelial-lined spaces. 

Now, the fluid in these compartments is mostly made up of water. In fact, over half of an adult&amp;#39;s body weight and volume is water, which is called total body water. In addition, fluid is also made up of small and large solutes. Small solutes can easily cross cell membranes and are found in both intracellular and extracellular spaces. They include gases like oxygen and carbon dioxide, glucose, and electrolytes. On the other hand, large solutes can&amp;#39;t easily cross cell membranes and are typically found in the extracellular space. These solutes include plasma proteins and blood components like red blood cells, platelets, and white blood cells.

Alright, fluid is in constant motion as it shifts in and out of cells and between fluid compartments through the processes of osmosis and filtration. First, osmosis is the diffusion of fluid across a semipermeable membrane from an area of low solute concentration, or osmolality, to an area of higher osmolality, until both sides are equalized. The force that pulls water from the area of low osmolality to high is called osmo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fanconi_anemia:_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uAFWhyNXS9imHk7bxCRTCsjKTbCkcWPo/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fanconi anemia: Year of the Zebra 2025]]></video:title><video:description><![CDATA[Fanconi anemia, or FA for short, is a rare genetic disorder that affects the body&amp;#39;s ability to repair damaged DNA.  

For cells to function properly, DNA needs to remain intact in order to pass on or express genetic information. Unfortunately, DNA damage is common, and it happens all the time due to toxic substances from cell metabolism and environmental factors, like cigarette smoke or radiation. Luckily, cells have specific DNA repair mechanisms that try to fix this damage and prevent too many DNA mutations from occurring. 

In FA, a network of proteins responsible for DNA repair and integrity don’t work properly, allowing damage to pile up. Affected cells either die or accumulate too many DNA mutations, increasing the risk of cancer, especially leukemia and tumors. 

Because FA affects cells during early development, most individuals have congenital birth defects, including a short stature, missing thumbs, kidney problems, and skin changes like café au lait spots. In cases where these signs aren’t apparent, diagnosis tends to be delayed until the development of bone marrow failure, which is one of the most common features of FA. 

Bone marrow failure usually occurs in childhood or early adulthood, when the bone marrow stops producing enough blood cells, leading to low levels of red blood cells, white blood cells, and platelets. This results in severe complications, including an increased risk of life-threatening anemia, infections, and bleeding problems.  

Individuals with FA also have a high risk of developing myelodysplastic syndrome, a bone marrow disorder that can progress to acute leukemia. They also have a higher risk of developing tumors at an earlier age than the general population, especially in the head, neck, and pelvic areas. 

 Diagnosis of Fanconi anemia is suspected in individuals with unexplained bone marrow failure and associated birth defects. Diagnosis can be confirmed with a chromosome breakage test, a blood test that asses]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hematohidrosis:_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s5OgbxFwQz2gY-d8LEQ7dIo1QyWnKA3v/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hematohidrosis: Year of the Zebra 2025]]></video:title><video:description><![CDATA[Hematohidrosis is an extremely rare condition that literally means “sweating blood”. Though it’s been described in historical texts for centuries, only a handful of cases have been documented in modern medicine. The exact cause isn’t fully understood, but the most widely accepted theory involves an extreme activation of the sympathetic nervous system, which is responsible for the body’s “fight or flight” response. 

Under severe physical or emotional stress, small blood vessels called capillaries surrounding the sweat glands may constrict and then suddenly dilate. It’s believed this abrupt change in pressure can cause the capillary walls to rupture. The leaked red blood cells then mix with sweat inside the gland ducts, oozing through the pores as bloody sweat. 

The hallmark of hematohidrosis is the sudden appearance of blood-tinged fluid on the skin. This most commonly occurs on the face, particularly the forehead, around the eyes, and the cheeks, but it can also affect other areas such as the trunk or limbs. The fluid may appear as droplets or as a thin film, resembling true sweat mixed with blood. 

Episodes are usually brief, lasting a few minutes to an hour, and can occur spontaneously or in relation to intense stress. They may be preceded by headache, abdominal pain, or anxiety. Although the visual effect can be alarming, the amount of blood lost is generally minimal, and the condition is not considered to be life-threatening. 

Diagnosing hematohidrosis can be challenging due to its rarity. The key finding is the presence of bloody fluid on intact skin, with no visible breaks or trauma. Testing the fluid under a microscope usually confirms the presence of sweat mixed with red blood cells. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_autoimmune_neuropsychiatric_disorders_associated_with_Streptococcus_infections_(PANDAS):_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8jpyRX5_QUq1qVjicaHfhfliRJ62iMXW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric autoimmune neuropsychiatric disorders associated with Streptococcus infections (PANDAS): Year of the Zebra 2025]]></video:title><video:description><![CDATA[PANDAS is short for pediatric autoimmune neuropsychiatric disorders associated with Streptococcal infections. It’s a rare condition where a simple strep infection, like strep throat, triggers a sudden onset of neuropsychiatric symptoms in children. 
The trigger is a common type of bacteria called Streptococcus pyogenes, the same one that causes strep throat or scarlet fever. When strep enters the body, the immune system responds by making antibodies, which are specialized proteins that recognize and attack the bacteria.  

Strep, however, has a clever way of deceiving the immune system: some of its surface proteins closely resemble molecules found in human tissues, a mechanism called “molecular mimicry”.  

On one hand, this defense mechanism helps the bacteria slip past detection, but in some cases, it can lead to cross-reactions, where the antibodies not only recognize strep antigens as foreign, but also mistakenly attack human tissues. In PANDAS, these antibodies target brain structures within the basal ganglia and thalamus, which are essential for regulating movement and behavior, leading to the abrupt onset of neuropsychiatric symptoms.  

Now, the hallmark manifestations of PANDAS are symptoms of obsessive-compulsive disorder, or OCD, and motor or vocal tics. OCD might look like constant handwashing, repeated checking, or intrusive fears that the child can’t dismiss, like a sudden, overwhelming worry that their family could get hurt if they don’t perform a specific routine. Tics can be as subtle as rapid blinking, or as obvious as repetitive jerking movements or sounds. 

Alongside these, many children experience mood swings, separation anxiety, irritability, depression, and even regression, where they might start behaving much younger than their actual age. As a result, school performance can drop unexpectedly, and handwriting may become messier. Also, and some children can develop joint pain; increased sensitivity to light, sound, or touch; urinary]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epitheloid_hemangioendothelioma:_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Xt9xjUNjTGabmRtUFDxedttIRwqPbfvb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epitheloid hemangioendothelioma: Year of the Zebra 2025]]></video:title><video:description><![CDATA[Epithelioid hemangioendothelioma, or EHE for short, is a very rare type of tumor that originates from endothelial cells in the inner lining of blood vessels. When these cells become abnormal, they change their shape under the microscope. Instead of staying thin and flat, they become rounder and fuller, almost resembling the epithelial cells that line organs, hence the name epithelioid.  

What makes EHE unique is that it doesn’t behave like a classic benign tumor, but it also doesn’t show the rapid growth or aggressive spread of high-grade cancers. Instead, it falls somewhere in between, meaning some people have slow, stable disease for years, while others can experience growth or metastases over time. 

Now, since endothelial cells can be found everywhere where there&amp;#39;s blood flow, EHE can develop in almost every organ, including the liver, lungs, bones, and soft tissues. Typically, it causes few symptoms, and when it does, they tend to be quite subtle. 

For example, in the liver, it can cause discomfort in the upper abdomen, fullness after meals, or mild nausea;whereas in the lungs, it can lead to persistent dry cough, slight shortness of breath, or chest tightness. Localized pain and vascular congestion are common, and generalized symptoms such as fever or weight loss can occur in association with tumor spread. 

Less commonly, EHE can develop in bones, especially weight-bearing bones like the femur, tibia, pelvis, or spine. People often notice persistent, localized pain, similar to the soreness you might feel after accidentally bumping into furniture. The bone may feel tender or swollen, and in rare situations, the affected bone might become weak enough that a minor fall or twist causes a fracture.  

Although not as common, EHE can also present as a slowly enlarging lump in muscle or soft tissues, which can be painless or cause a dull ache. 

As for diagnosis, EHE is often discovered incidentally on an ultrasound or a CT scan done for another]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nanophthalmos:_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lKl2V-DRTdSILWLMHigrndl-RG2M3oAc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nanophthalmos: Year of the Zebra 2025]]></video:title><video:description><![CDATA[Nanophthalmos is a rare birth condition where one or both eyes don’t grow to their full size during fetal development. Unlike microphthalmos, where there may be other structural anomalies, nanophthalmos refers specifically to the size of the eye, meaning despite being small, all eye structures are intact. 

The exact cause of nanophthalmos isn’t fully understood, though it appears to be linked to genetic changes that interfere with eye development. One of the most important measurements here is the axial length, which is the distance from the front to the back of the eye. Axial length plays a major role in how well the eye focuses light onto the retina, which is essential to see clearly. Imagine the retina as the screen in a movie theater, and the lens of the eye as the projector. If the projector is too close or too far from the screen, the image will end up looking blurry or out of focus.   

In nanophthalmos, the axial length of the eye is too short, which means light focuses behind the retina instead of on it. This leads to farsightedness, also called hyperopia, where nearby objects look blurry while distant ones may still be clear. 

Because the eye is smaller, the anterior chamber, or the space at the front of the eye where fluid normally drains, is shallow and tight. This poor drainage makes it easier for pressure to build up inside the eye, increasing the risk of glaucoma, particularly a type called angle-closure glaucoma. As pressure within the eye rises, it first damages the edges of the optic nerve, leading to loss of peripheral vision. Over time, if not treated, it can also affect central vision and lead to permanent vision loss. 

Another possible complication is serous retinal detachment, where fluid builds up between the retinal layers, causing them to peel away from the underlying layer of support tissue. This type of retinal detachment can cause blurry or distorted vision, like straight lines appearing wavy or a dark spot in the visual field. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Renal_coloboma_syndrome:_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Pjj2qzKMTJ6ZR7aYVQNBKvzRQ3eiJP3K/_.jpg</video:thumbnail_loc><video:title><![CDATA[Renal coloboma syndrome: Year of the Zebra 2025]]></video:title><video:description><![CDATA[Renal coloboma syndrome, also known as papillorenal syndrome, is a genetic condition that affects the development of the kidneys and eyes. Most cases are caused by changes in the PAX2 gene, which codes for a protein that acts as a transcription factor.

Transcription factors like PAX2 help regulate the activity of other genes by acting as &amp;quot;switches&amp;quot; that turn genes on or off, called gene expression, as needed. The timing and coordination of gene expression is crucial in the early weeks of fetal development, when all the organs begin to develop. Specifically, PAX2 orchestrates the development of the kidneys, urogenital system, eyes, and parts of the ear, turning them into functional structures.

Typically, inheritance of renal coloboma syndrome follows an autosomal dominant pattern, meaning only one copy of the mutated gene is needed to cause the condition. However, in about half of cases, there doesn’t seem to be any mutation in the PAX2 gene; meaning there are likely other mechanisms involved.

Clinically, individuals with renal coloboma syndrome tend to have small, underdeveloped kidneys that don’t function fully, often resulting in kidney failure by early adulthood.

The most common eye manifestation is a coloboma of the optic disc, a birth defect where the optic disc, or the point where the optic nerve exits the eye, appears larger and hollowed because it didn’t develop as usual. Depending on the extent of the coloboma, individuals may experience vision loss or blind spots. This is especially true when coloboma affects the macula, which is the part of the eye responsible for the sharp, central vision needed for activities like reading or driving.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aquagenic_urticaria:_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ALlw61cfQ16deDf0L_BGqYhGTLCIekqP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aquagenic urticaria: Year of the Zebra 2025]]></video:title><video:description><![CDATA[Aquagenic urticaria is a rare condition in which contact with water triggers the development of itchy, hive-like skin lesions. This reaction develops regardless of the water’s temperature and source, as it can occur after contact with tap water, salt water, rain, sweat, or even tears.

Even though urticaria is a common skin condition, aquagenic urticaria is exceptionally rare, with fewer than 100 cases documented in medical literature. Unlike typical allergic reactions, aquagenic urticaria isn’t due to any component in the water itself; rather, it’s the interaction between water and the person&amp;#39;s skin that triggers the immune response.  

Now, symptoms typically appear within 5 to 15 minutes of water exposure and include small, red, itchy wheals accompanied by a burning or stinging sensation. These lesions most often appear on areas like the neck, chest, arms, or back and usually fade within an hour.  

In people with aquagenic urticaria, everyday situations like showering, walking in the rain, sweating during exercise or in hot weather, or even crying may result in symptoms. Notably, drinking water does not trigger symptoms, as the condition is limited to skin contact. While most cases are mild, some people may experience more severe reactions like swelling or difficulty breathing after widespread water exposure.  

Because contact with water is difficult to avoid in daily life, aquagenic urticaria can lead to significant emotional distress and result in avoidance of social situations where water exposure is expected, like swimming, exercising, or being outdoors. In more severe cases, individuals may even avoid showering or washing their hands, which can further impact quality of life and self-esteem. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Andersen-Tawil_syndrome:_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i2XYQRKdQXS0i2-hQOZBy6U_RiCWdBZ9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Andersen-Tawil syndrome: Year of the Zebra 2025]]></video:title><video:description><![CDATA[Andersen-Tawil syndrome, or ATS for short, is a rare genetic disorder that affects the heart and skeletal muscles. It’s part of a group of conditions known as channelopathies, which are all caused by problems with ion channels—the proteins that control the flow of ions, like sodium or potassium, in and out of cells. These channels help reset the electrical state of muscle cells after a contraction by allowing potassium ions to flow out, enabling the cell to get ready for the next contraction. 

Specifically, most cases of ATS are caused by mutations in the KCNJ2 gene, which affects the function of potassium channels in muscle and heart cells. When potassium channels don’t work properly, muscle cells may become overly excitable or fail to reset properly after firing. In skeletal muscles, this may result in sudden episodes of muscle weakness, whereas in the heart, it may lead to abnormal heart rhythms, called arrhythmias.  

Signs and symptoms typically consist of the triad of weakness or paralysis; abnormal heart rhythms; and distinct facial features. Clinically, individuals with ATS have sudden episodes of muscle weakness or full paralysis, usually affecting the limbs. These episodes are often triggered by rest following exercise, emotional stress, prolonged fasting, or a high sugar intake, which can lead to a spike in insulin followed by potassium shifts in the blood. 

Individuals are also at increased risk of abnormal heart rhythms, specifically ventricular tachycardia, a rhythm that can cause the heart rate to rise above 250 beats per minute. If this happens, an individual can have symptoms of decreased blood supply to the brain and other organs, such as chest pain, fainting, dizziness, or shortness of breath. It can even cause sudden death. 

Finally, individuals with ATS often have distinctive facial features, including a broad forehead, wide-set eyes, low-set ears, short stature, scoliosis, or curved fingers and toes, although not all individuals sh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Alexander_disease:_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2CSGS2pqTs6ulhKoP0QqoU1-SXeY0FdR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Alexander disease: Year of the Zebra 2025]]></video:title><video:description><![CDATA[Alexander disease is a rare neurological disorder that primarily affects the white matter of the brain.  

If we look at a cross section of the brain, we can easily distinguish between two tissue types. 

First is white matter, which is the area responsible for transmitting signals between different brain regions, and gray matter. 

Gray matter contains nerve cell bodies.  White brain matter is made up of bundles of axons, which are projections of nerve cells that carry impulses.  

Axons are covered in myelin, a fatty insulating layer that helps speed up electrical signals.  

The production of myelin depends on glial cells called oligodendrocytes, with support from astrocytes—which are glial cells that have processes coming off their cell body, giving them a star-shaped appearance.  

Astrocytes influence when and where myelin is produced; they provide nutrients to sustain myelin production; and release signaling molecules that can either promote repair or contribute to myelin damage. 

In Alexander disease, mutations in the GFAP gene lead to the abnormal accumulation of proteins within astrocytes, disrupting their function. Astrocyte dysfunction triggers the breakdown of myelin and progressive white matter loss, resulting in neurological impairment. 

Alexander disease can typically be classified into three main types depending on the age of onset. The most common is the infantile-onset form, which typically manifests before age 2. Infants often present with macrocephaly, or an enlarged head circumference, and have seizures.  

They may also experience neurodevelopmental delays, including motor, language, and cognitive development. Affected infants typically face progressive deterioration, with death occurring before age 10 in most cases. 

The juvenile-onset form appears between ages 2 and 12 and generally progresses more slowly. Affected individuals often develop signs of cognitive decline, muscle spasticity, slurred speech, and loss of coordination, ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_system_atrophy_(MSA):_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FY4tINgFQbeWN92OHmliJFHlTrCjRKvk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple system atrophy (MSA): Year of the Zebra 2025]]></video:title><video:description><![CDATA[Multiple system atrophy, or MSA for short, is a neurodegenerative disorder that affects a person’s movement, sense of balance, and regulation of body functions like blood pressure, bowel and bladder control, and breathing. It’s part of a group of movement disorders called parkinson-plus syndromes, which cause parkinsonism, plus other clinical features. 

The exact mechanism why it happens isn’t completely understood, but it’s believed to result from the abnormal build-up of a protein called alpha-synuclein within glial cells, which are cells that support and protect the central nervous system. This build-up mainly affects the areas of the brain responsible for voluntary movement, balance, and coordination, as well as the autonomic nervous system, which is responsible for involuntary processes like blood pressure, breathing, and digestion. Ultimately, this build-up leads to widespread brain damage.  

Now, symptoms of MSA typically begin around the age of 50 and tend to progress rapidly over the course of 5 to 10 years. Clinically, MSA can present in two different ways. Most individuals experience symptoms that resemble those of Parkinson disease, including resting tremor, rigidity, slowness of movement, and postural instability, which often leads to a stooped posture and an increased frequency of falls.  

Other people experience symptoms related to the loss of cerebellar function. This can manifest as poor hand-eye coordination; difficulty with fine motor tasks, like buttoning a shirt; involuntary eye movements, known as nystagmus; and a wide-based gait due to poor balance.  

Both subtypes of MSA share signs of autonomic system failure, which may include fainting or dizziness when standing due to low blood pressure, known as orthostatic hypotension; impotence; and urinary incontinence or retention.  

In advanced stages, individuals may develop voice-tone changes, as well as difficulty speaking and swallowing due to weakness in the muscles in the mouth a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spastic_paraplegia_type_4_(SPG4):_Year_of_the_Zebra_2025</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5e4uotbjTiW3YZCkqDJ5kOREQqCCXVuR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spastic paraplegia type 4 (SPG4): Year of the Zebra 2025]]></video:title><video:description><![CDATA[Spastic paraplegia type 4, or SPG4 for short, is the most common form of hereditary spastic paraplegia, a group of genetic neurodegenerative disorders characterized by progressive weakness and spasticity of the lower limbs. There are over 80 known types of spastic paraplegia, each caused by mutations in a different gene, and each given a number in the order they were discovered.  

SPG4 is caused by changes in a gene called SPAST, which provides instructions for making a protein called spastin. Spastin’s job is to cut and reshape microtubules, which are tube-like structures used to transport molecules from one part of the cell to another. When transport along nerve fibers is disrupted, essential substances like nutrients, signaling molecules, and waste products can’t reach where they’re needed. Over time, this causes nerve cells, and particularly the long axons that carry movement signals from the brain to the legs, to become stressed or damaged. 

Mutations in the SPAST gene are usually inherited within families. However, the severity and age of onset can vary, even among family members with the same mutation. 

Now, the hallmark symptom of SPG4 is progressive lower limb spasticity or stiffness. As a result, the legs may feel tight or rigid, especially after sitting for a long time. Individuals have difficulties with balance and thus might walk with a stiff or scissoring gait. Additionally, they may notice it’s harder to keep up with others when walking long distances or going uphill, and they grow tired more easily. 

A physical exam may reveal overactive tendon reflexes, meaning when a clinician taps on a tendon—like the one just below the kneecap—the reflex is stronger and quicker than normal. This happens because the nerves controlling the reflexes are more excitable than usual.  

The same motor neuron damage that causes stiffness and reflex changes in the legs can also affect the nerve control of the bladder, resulting in urinary symptoms like increased urinary frequency and incontinence. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acid-base_balance_-_Overview:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/e4b6wWtGSvWUm5uWJho0-4G2TU6ISM40/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acid-base balance - Overview: Nursing]]></video:title><video:description><![CDATA[Acid-base balance refers to how the body maintains a balanced pH of body fluids within a narrow range. A balanced pH is essential for optimal cellular functioning; and any disruption in this balance can adversely affect important metabolic processes, such as the function of enzymes within cells, oxygen delivery to the tissues, and medication metabolism.

Alright, so, pH, which means potential of hydrogen, reflects the concentration of hydrogen ions, or H+, in the blood. An acid is a substance that releases H+, and there’s an inverse relationship between pH and H+, meaning that when there’s more H+, the pH decreases and the blood becomes more acidic; and, when there’s less H+, the pH increases, and the blood becomes less acidic. Now, hydrogen ions are continually produced by normal metabolic processes like ketone production from fat metabolism; phosphoric acid from the breakdown of proteins; and lactic acid resulting from aerobic respiration, which can be due to excess exercise or hypoxia.  

On the flip side, a base is a substance that accepts hydrogen ions, which neutralizes acid. Bicarbonate or HCO3-, is a base found in plasma, and it plays a crucial role in acid-base balance. When there’s more HCO3- the pH increases, and the solution becomes more basic; and when there’s less HCO3-, the pH decreases, and the solution becomes less basic.   

Okay, so pH is measured on a scale that ranges from 0 to 14, with a pH of 7 being neutral, less than 7 being acidic, and more than 7 being more alkaline. Optimal metabolic functioning occurs when the pH is maintained between a range of 7.35 and 7.45.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Communication_and_relational_practice:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wXpo9HsaQoWwkXbzjMZPB1R8S8qi5DON/_.jpg</video:thumbnail_loc><video:title><![CDATA[Communication and relational practice: Nursing]]></video:title><video:description><![CDATA[Communication is the exchange of information, thoughts, and feelings between individuals, groups, or organizations. Nurses use effective communication to create a therapeutic patient-nurse relationship that supports a high level of patient care, encourages interprofessional collaboration, and promotes quality health outcomes.

As a nurse, you can promote effective communication by using concepts of relational practice. This can involve skills like reaching out to your patients and listening to them to better understand their needs; being authentic in your communication by demonstrating respect for yourself and others; and creating a sense of mutuality by partnering with your patient to accomplish shared goals.

Now, when your patient needs assistance with communication, you can use the five steps of the nursing process, assessment, diagnosis, planning, implementation, and evaluation, to guide your communication while providing care.

Starting with assessment, you’ll gather data to determine all the contextual factors that can influence communication so you can understand your patient’s unique communication needs. During this step, you’ll assess the context in which the communication will occur between you and your patient. You can start by assessing physical and emotional factors, like visual or hearing impairments, as well as conditions like stroke, that can cause aphasia. Also be sure to look for emotional factors like anxiety, which can affect your patient’s ability to concentrate on what’s being said; or psychotic states which can cause distraction due to hallucinations.

Also be sure to include developmental factors in your assessment so you can adapt your communication techniques to meet your patient’s unique age-related needs, like infants and young children.

Next, you&amp;#39;ll establish a nursing diagnosis for your patient who needs assistance with communication, such as impaired verbal communication. You’ll also identify additional diagnoses t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hemorrhagic_conditions_of_pregnancy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/B6m4z0AkTDmjx7fXynprqJcURYm9cM1g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hemorrhagic conditions of pregnancy: Nursing]]></video:title><video:description><![CDATA[Hemorrhagic conditions during pregnancy are complications involving excessive blood loss that can jeopardize the health and well-being of the pregnant patient and fetus.  

In general, conditions that increase the risk of hemorrhage during pregnancy include multiparity, which refers to having two or more previous pregnancies; multiple gestation or being pregnant with more than one fetus at a time; and using assisted reproductive techniques, like in vitro fertilization or intrauterine device contraceptives. Other risk factors include a history of uterine surgery, sexually transmitted infections, or a hemorrhagic condition during a previous pregnancy; as well as alcohol use, excessive caffeine consumption, or cigarette smoking during pregnancy. 

First, let’s review early hemorrhagic conditions, which occur before 20 weeks of gestation, starting with spontaneous abortion. Spontaneous abortion, also known as miscarriage, is the involuntary loss of pregnancy during the first 20 weeks, or the loss of a fetus weighing 500 grams or less. Threatened abortion is when there’s only vaginal bleeding and the cervix remains closed. This can progress to cervical dilation, membrane rupture, and loss of the uterine contents, at which time it’s called a complete abortion. A missed abortion is when the fetus dies but remains in the uterus.   

Another early hemorrhagic condition is ectopic pregnancy, which is when the fertilized ovum doesn’t complete its journey to the uterus and implants elsewhere, like the abdominal cavity, ovaries, fallopian tube, or cervix. Depending on the implantation site, the embryo may receive enough blood supply to cause early pregnancy signs and symptoms, like a missed menstrual period. But eventually the implantation site can no longer support the embryo.  

And if the ectopic pregnancy happens in the fallopian tube, the growing embryo eventually runs out of space and damages the walls of the tube, potentially causing it to rupture, leading to ma]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_and_wellness_promotion:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/19Puif_lT1C5dSssRFP8b83xQd_2Vz99/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health and wellness promotion: Nursing]]></video:title><video:description><![CDATA[Health is more than just the absence of illness or disease and can be viewed as an objective state of functional stability, balance, and integrity. Illness is a subjective experience of poor health, and wellness can be thought of as a subjective experience of good health.  

Health, illness, and wellness are affected by multiple and interrelated dimensions of a person’s life, including physical, mental, social, environmental, and spiritual components.

Now, the health of people and communities is influenced by social determinants of health, which are conditions where people live, work, play, worship, and age.

Social determinants of health include genetic, social, and economic circumstances that promote health and wellness, such as having access to healthcare, healthy foods, education, a safe place to live, as well as one’s genetic inheritance.

Social determinants of health also include inequities like poverty, discrimination, and social inequities, and can limit access to the resources required to meet physical, mental, and emotional needs. This is especially true for specific groups, such as LGBTQ2, Black, and Indigenous peoples that have been disproportionately affected by health inequities.

The Ottawa Charter for Health Promotion, created by the World Health Organization in 1986, identifies prerequisites for health, such as peace, shelter, a stable ecosystem, sustainable resources, and social justice. 

It developed strategies for health for people and their communities to work towards. There are 5 strategies.  

Building healthy public policy shapes legislation, regulation and public policies that&amp;#39;ll determine how financial and material resources are allocated to people living in the community.

By creating supportive environments, the community acknowledges the interrelationship between health and the natural and built environments; and it’s focused on creating and sustaining healthy and safe spaces through programs like providing quality ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Abdominal_pain:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/fvQLQ5xsQq6l97Hp0dJYdlDoQXSUdNsR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Abdominal pain: Nursing]]></video:title><video:description><![CDATA[Abdominal pain is discomfort felt anywhere between the chest and groin that can occur because of tissue injury, which could be due to mechanical, inflammatory, and ischemic mechanisms.

Mechanical mechanisms of tissue injury include processes that can cut, tear, or crush abdominal contents, like penetrating injuries seen with knife wounds or blunt injuries that occur during a car crash. Next, inflammatory mechanisms involve swelling, stretching, and distention. This can occur due to infectious processes like appendicitis, diverticulitis, or gastroenteritis. Lastly, ischemic mechanisms can be caused by any condition that obstructs blood flow to abdominal contents, like with mesenteric artery occlusion, which is when a blood clot blocks the artery that supplies oxygenated blood to the intestines.

Abdominal pain can be acute, meaning it develops quickly and resolves over hours to days; or chronic, meaning it can come and go over months or even years. Pain can also be visceral, parietal, or referred.

Visceral pain is typically dull, crampy, or burning in nature and difficult to localize. It can be felt with conditions like appendicitis. 

Parietal pain tends to be sharp and easy to localize, like with the right upper quadrant pain felt in acute cholecystitis. 

Referred pain can be dull or sharp, difficult or easy to localize, but is typically noted outside the abdominal region, like when biliary tract disease causes pain in the right shoulder.

Other clinical manifestations that accompany acute abdominal pain may include fever, an elevated white blood cell count, nausea, and vomiting, as well as changes in bowel patterns, like constipation, diarrhea, or the presence of blood or mucus in stool.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Intrapartum_complications:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9kjFO0EVRh6JDnqhcURGUm1UTGi3Gp2i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Intrapartum complications: Nursing]]></video:title><video:description><![CDATA[The intrapartum period begins with the onset of labor and lasts until the delivery of the newborn and placenta. Complications during the intrapartum period can be related to premature rupture of membranes, or PROM, and preterm labor.  

PROM is when the amniotic membranes spontaneously rupture before the beginning of true labor. PROM can lead to complications such as oligohydramnios, meaning there isn’t enough amniotic fluid left to surround the fetus; and umbilical cord prolapse, which is when the umbilical cord moves ahead of the fetus and becomes compressed, which cuts off circulation to the fetus. PROM also makes it easy for microorganisms in the vagina to travel into the uterus, causing chorioamnionitis, which is an infection of the remaining amniotic tissue and fluid. 

PROM can present as either a gush of vaginal fluid or a slow leaking of fluid from the vagina.  Diagnosis of PROM is made by sterile speculum exam to look for a pool of fluid near the cervix. If fluid is present, PROM can be confirmed if pH testing shows alkalinity of the fluid. Other information can be gathered during the speculum exam, including an estimation of cervical dilation and effacement, as well as testing the fluid for the presence of phosphatidylglycerol, or PG, which is an indication of fetal pulmonary maturity. 

Nursing management of PROM primarily depends on the gestational age and involves weighing the risks of preterm birth versus expectant management, which consists of observation for infection, labor onset, and testing for fetal well-being. In all cases, you’ll administer antibiotics prophylactically, as ordered, even if infection isn’t suspected. If your patient is at 37 weeks of gestation and labor doesn&amp;#39;t start soon, labor will typically be induced with oxytocin after cervical softening agents like prostaglandin E2 have been administered, as needed. 

If gestation is between 34 to 36 weeks and there’s evidence of chorioamnionitis and fetal compromise, l]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_complications:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6v5ydmEcSTueGoptO4dAalJkQjCrNpDi/_.png</video:thumbnail_loc><video:title><![CDATA[Postpartum complications: Nursing]]></video:title><video:description><![CDATA[The postpartum period, also known as the fourth stage of labor, begins after delivery of the fetus and placenta, and it extends through the first six weeks after birth. Several complications can arise during the postpartum period, including postpartum hemorrhage, thromboembolic disorders, and infection. 

Now, postpartum hemorrhage is defined as cumulative blood loss of 1,000 mL or more, or blood loss that’s accompanied by signs or symptoms of hypovolemia within 24 hours after birth. Common causes can be remembered by the four Ts, including tone for uterine atony, or weak uterine muscle tone, which includes subinvolution, meaning the return of the uterus to its nonpregnant state is impaired; trauma to the birth canal, such as lacerations or hematomas; tissue, meaning retention of placental fragments; and thrombin, representing coagulation deficiencies, like von Willebrand disease. Other causes include placenta previa, or when the placenta is abnormally implanted over the cervix; and placenta accreta or abnormal placental adherence to the uterine wall.  

Signs and symptoms of hemorrhage may include a soft or displaced uterus and saturating one or more peri-pads per hour. If the hemorrhage is concealed within a hematoma, there could be severe perineal pain or rectal pain; a discolored bulging mass in the perineum; and abnormal vital signs like tachycardia.  

Treatment depends on the cause and may include fundal massage; bimanual compression of the uterus; uterotonic, antifibrinolytic, and analgesic medications; IV fluid and blood product administration; or surgery, like uterine artery ligation, hematoma repair, or hysterectomy.  

When caring for your patient with postpartum hemorrhage, closely monitor their vital signs, pain, skin color and temperature, and urine output. Assess their uterine tone and perform fundal massage to keep the uterus firmly contracted. Monitor the color and amount of lochia, or vaginal discharge, and weigh all blood-soaked pads an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain_Assessment_and_Management</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BdHI7y53QYStQpb74_QD5K_iR8WGGIFp/_.png</video:thumbnail_loc><video:title><![CDATA[Pain Assessment and Management]]></video:title><video:description><![CDATA[Pain is a feeling of discomfort that ranges from mild to severe, usually caused by an underlying condition, and can be acute or chronic. Acute pain is typically short-term and resolves once the underlying cause is addressed, while chronic pain lasts for six months or more. As the nurse, you’ll collaborate with the registered nurse, or RN, to obtain information about your patient’s pain by gathering subjective and objective data and performing a focused physical assessment.

Pain is a subjective experience, meaning that it’s based on a person’s perceptions and feelings, which can differ depending on their pain threshold, or the point when they start noticing pain; and pain tolerance, which is the amount of pain someone can endure. So, your patient’s report and description of pain is the most reliable source of information about their pain.

To obtain subjective data about your patient’s pain, ask them a series of questions. Begin by asking them to rate their pain using a standard tool, like a numeric scale that uses zero to ten to indicate pain level, with zero meaning no pain and ten meaning the worst pain possible. Sometimes older adults might prefer a pain scale that uses words like no pain, mild pain, or severe pain. For pediatric patients, it’s common to use the Faces Pain Scale where each face represents a different level of pain.

For a more detailed description of your patient&amp;#39;s pain, use the mnemonic OPQRST. First, O stands for onset, or when the pain started, which can be sudden, gradual, or progressive. Then, P stands for provocation and palliation, meaning whether certain factors make the pain worse, like pressure or movement; or better, like ice or medication. Q is for quality of pain, such as sharp, dull, burning, or achy; and if its intermittent or constant. R stands for region, which is the area of the body where the pain is felt; and radiation, or if the pain spreads to other areas of the body. Next, S is for severity, which y]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Down_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VY7JKUtoTrGnni94TeIgNuvhS1WE2xrb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Down syndrome: Nursing]]></video:title><video:description><![CDATA[Down syndrome is a chromosomal abnormality caused by a genetic mutation leading to an extra or partial copy of chromosome 21.

Now, chromosomes are molecules that carry packaged DNA information for a person, like a storage bin. Every cell in our body has 46 chromosomes, organized into 23 pairs. During human fertilization, each parent donates half of their chromosomes to create a zygote with a total of 46 chromosomes. But in some cases, like in Down syndrome, one parent donates an extra chromosome, leaving the zygote with 47 chromosomes. People with Down syndrome receive an extra copy of chromosome 21, which is why Down syndrome is also referred to as Trisomy 21, or “three chromosome 21s.&amp;quot;

The exact cause of Down syndrome is unknown. What we do know is that the likelihood of Down syndrome increases with the age of the mother. So, a 35-year-old mother is more likely to give birth to a baby with Down syndrome than a 25-year-old mother. Down syndrome also seems to arise more often from patients who have translocation of chromosomes 15, 21, or 22, where parts of one chromosome switch places with another chromosome, creating an atypical hybrid of the two original chromosomes. This is referred to as Robertsonian translocation.

Down syndrome has a number of clinical manifestations. Several changes to the face occur. Skin folds covering the inner corner of the eyes develop, called inner epicanthal folds, along with an upward slant in the palpebral fissure. A depressed nasal bridge or flattening of the top part of the nose may also develop along with a protruding tongue. Speckling of the iris, known as Brushfield spots, might also appear. People with Down syndrome may also have small ears with narrow canals.

Other clinical manifestations include a shortened rib cage, umbilical hernia, and protruding or loose abdominal muscles. People with Down syndrome typically have short stature, hyper-flexibility with muscle weakness, and atlantoaxial instability, or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_diseases_-_Pediatric:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7DbBKCKiSka2ajtieUfhYtrlRpWTfzbx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious diseases - Pediatric: Nursing]]></video:title><video:description><![CDATA[A communicable disease is an infection that spreads from person-to-person. These diseases can be transmitted through the air, respiratory droplets, or physical contact with a contaminated surface. Pediatric patients are more likely to contract communicable diseases because of their immature immune systems and lack of understanding of infection control.

Now, some communicable diseases, like measles, influenza, rotavirus, and varicella have vaccines available to help prevent their spread; while other diseases, like scarlet fever and fifth disease, do not. Vaccines, along with infection control measures, like hand washing and personal protective equipment, or PPE, can help limit the spread of common communicable diseases.

Okay, so, immunity can be acquired actively or passively. Active immunity happens when a person makes their own antibodies, like after recovering from a disease, like fifth disease, or is given a vaccination, like a flu shot for influenza. Now, vaccines use a weakened or inactivated version of a pathogen and the body’s natural defenses to strengthen the immune system against that pathogen. This can help prevent a disease, and may limit its spread, if a person encounters the pathogen in the future.

On the other hand, passive immunity occurs when a person receives the antibodies needed to fight the disease, like when a fetus receives IgG antibodies through the placenta, or when a newborn exposed to the hepatitis B virus is given immune globulin. 

Alright, now along with vaccines, infection control measures also limit the spread of communicable diseases.

Standard, or routine, precautions are broad protocols used to prevent infection when caring for all patients and involve hand hygiene by either washing with soap and water or alcohol-based disinfectants; and preventing contact with infectious agents using PPE, like gloves, gowns, masks, or face shields. 

On the other hand, transmission-based precautions are based on the specific method of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Newborn_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mqzNPXuQR926l7dCOYufq3rcTper_lI-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Newborn care: Nursing]]></video:title><video:description><![CDATA[Early care of newborns after birth involves supporting cardiorespiratory function and thermoregulation, monitoring for problems that need immediate intervention, and administering prophylactic medications. 

Okay so, you can quickly assess the newborn immediately after delivery by using the APGAR score to determine when cardiorespiratory support interventions are needed. The APGAR score is calculated 1- and 5-minutes following birth, and consists of these five parameters: Appearance, or skin color; Pulse; Grimace, or the newborn’s reaction to stimulation; Activity, or the amount of flexion and movement; and Respiration, or the strength of their respiratory effort. Each parameter is scored 0, 1, or 2 for a total of 10 possible points. Scores 7 and above are normal and require no special intervention. A score below 7 requires interventions    Interventions such as tactile stimulation, oxygen administration, and other resuscitation efforts, as well as repeat scoring every 5 minutes. If the newborn is having difficulty clearing secretions from their airway, you should position them on their back, with their head in a neutral position, and use a bulb syringe to suction their mouth first, and then their nose. 
 You’ll also support the newborn’s thermoregulation, which is the ability to maintain a steady core temperature by balancing heat loss with heat production. You can help prevent heat loss by establishing a neutral thermal environment, or NTE. Be sure the delivery room is warm and free of drafts; and immediately after birth, dry the newborn with warm linens to remove amniotic fluid. You’ll also perform your initial assessments under a radiant warmer; and then, you can either wrap them in a warm blanket and place a warm hat on their head, or initiate skin-to-skin contact with the mother.  

Now, a common problem in the newborn period is jaundice, also known as hyperbilirubinemia, which can cause yellowish pigmentation of the skin, sclera, and mucous membrane]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_-_Antepartum:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nS27G6U4R-a-pHXyLltaExzPTxup2cna/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment - Antepartum: Nursing]]></video:title><video:description><![CDATA[Assessment during pregnancy involves evaluating maternal and fetal health with the goal of a healthy pregnancy outcome. During the assessment, you’ll collect subjective data, or information your patient states, as well as objective data, or information you collect through observation.

Begin by collecting information about your patient’s reproductive and sexual health. Ask about their history of gynecological surgeries, especially those involving the cervix, since this could increase the risk of cervical insufficiency and early pregnancy loss; or the uterus, since this can increase the risk of obstetric complications like fetal malpresentation or uterine rupture. 

Also, review your patient’s obstetric history using the GTPAL notation, to document Gravidity or how many times your patient has been pregnant; the number of Term pregnancies and Preterm births; if they’ve had either a spontaneous or elective Abortion; and the number of Living children. 

Lastly, determine if they have a history of sexually transmitted infections, or STIs, which are risk factors for premature rupture of membranes, preterm labor, as well neonatal infections and birth defects.

Next, focus on their current pregnancy. Ask them about the first day of their last menstrual period and use this date to calculate the expected date of delivery, or EDD for short, using Naegele’s rule. Then, inquire about any new symptoms like pain, vaginal discharge, fatigue, or nausea and vomiting. Also be sure to ask them how they are feeling about their pregnancy, if the pregnancy was planned, and if they have any concerns that could adversely affect their pregnancy, such as intimate partner violence, lack of social support, or economic constraints.

Finally, review their medical history. Inquire about conditions that could complicate the pregnancy, like diabetes, hypertension, or asthma; current medications; known allergies; and immunizations. Also ask about their daily routine, including diet, physica]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_assessment_-_Examination_techniques:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/V6-MFjN3R1iaqesvCDig21GYScuzCkX6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical assessment - Examination techniques: Nursing]]></video:title><video:description><![CDATA[A physical assessment involves using examination techniques to collect data about a patient’s health, and includes inspection, palpation, percussion, and auscultation.

Inspection involves visually assessing your patient. It begins when you first see your patient and continues throughout the examination. These initial observations can include their general demeanor, facial expression, gait, and how they answer your questions. Your findings during your initial inspection can affect how you approach the rest of your exam; for example, if you notice your patient is guarding their stomach, you’ll likely start with an abdominal assessment. In addition to your visual assessment, use your sense of smell to alert you to issues such as a strong body odor or a foul-smelling discharge from a wound.

Palpation is where you’ll use touch to assess texture, temperature, moisture, pulsations, organ location and size, as well as the presence of swelling, lumps, and pain. You’ll use light palpation to detect superficial problems, like the presence of tenderness or changes in skin texture; followed by deeper palpation for determining the characteristics of organs and masses. Keep in mind that with deep palpation you should apply intermittent pressure and stop if your patient experiences pain.

Now, depending on what aspect you’re assessing, you’ll use different parts of your hands during palpation. For example, the pads of your fingers are best suited to feel skin texture, swelling, pulsation, and masses; the dorsal, or back side of your hand, is most sensitive to temperature, so it can be used to feel heat and cold; and the ulnar surface, or side of the hand closest to the pinky fingers, can be used to detect vibrations.

Percussion involves tapping on the surface of your patient’s skin with short, sharp strokes to produce sounds or vibrations, which can help determine the size, shape, and density of body tissue. Percussion can be direct, where you’ll percuss directly on yo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Postpartum_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jeI9u_NHRmOVyTX21pA6NIXsRBK5ueOJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Postpartum care: Nursing]]></video:title><video:description><![CDATA[The postpartum period, also known as the fourth stage of labor, begins after delivery of the fetus and placenta, and it extends through the first six weeks after birth. During this time, you’ll provide care for the newborn, the postpartum patient, and their family. 

When caring for the newborn, you’ll focus on maintaining cardiopulmonary function, supporting thermoregulation, and accurately identifying the newborn.  

Immediately after birth, you’ll assess cardiopulmonary function by calculating an Apgar score, which is a scoring system that assesses how the newborn is adapting to extrauterine life. The newborn&amp;#39;s heart rate, respiratory effort, muscle tone, reflexes, and skin color are scored 0, 1, or 2 for a total of 10 possible points. You’ll calculate the Apgar score at one minute and five minutes and then every 5 minutes, as needed until the score reaches 7 or more. During this time, if the newborn shows signs of distress, such as bradycardia or a weak respiratory effort, immediate intervention should be provided. 

Next, you’ll take steps to support thermoregulation. Remember that immediately after birth the newborn is covered in bodily fluids, putting them at risk for evaporative heat loss. If their temperature drops, the newborn will need to work hard to maintain their temperature, which will increase their need for oxygen and increases the risk of problems like hypoxemia and hypoglycemia. To prevent this, be sure to immediately dry them off with warm towels and provide warmth by either placing them on their parent’s chest to initiate skin-to-skin contact or by placing them on a radiant warmer. Once their temperature has stabilized, swaddle them in warm blankets, place a cap on their head, and continue to monitor their temperature. 

Lastly, you’ll attach identification bands on the newborn that will match the parents’ identification bands. To ensure the newborn is always returned to their family after separation, these bands won’t be remo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_and_acquired_conditions:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ORWwiEzMQYuKnB27-SCNUEyUTIuY2xfa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital and acquired conditions: Nursing]]></video:title><video:description><![CDATA[Congenital and acquired conditions are high-risk complications requiring prompt recognition and intervention. Congenital conditions refer to genetic disorders or physical anomalies that occur during fetal development, such as phenylketonuria, cleft palate, and cardiac defects.  

On the other hand, acquired conditions occur postnatally, meaning at or shortly after birth, and include pathologic jaundice, sepsis neonatorum, and meconium aspiration syndrome. 

Okay, so jaundice, also known as hyperbilirubinemia, is a condition caused by the build-up of a yellow pigment called bilirubin, that’s produced in the liver by breaking down hemoglobin from red blood cells. Most newborns develop mild hyperbilirubinemia, called physiologic jaundice, which is a self-limiting condition that requires no treatment.  

On the other hand, pathologic jaundice, sometimes called non-physiologic jaundice, is a more severe form of jaundice, that is most commonly caused by excessive hemolysis, or red blood cell destruction, leading to an excessive build-up of bilirubin in the blood.  

Risk factors for excessive hemolysis include incompatibility between the maternal and fetal ABO and Rh blood types; polycythemia, or an excessive amount of circulating red blood cells; or the presence of extravascular blood, like bruising or cephalohematoma from birth trauma. Other risk factors include sepsis and liver impairment.  

Without proper treatment, pathologic jaundice can lead to acute bilirubin encephalopathy, where bilirubin crosses the blood-brain barrier, deposits in the brain, and causes impaired neurologic function. This can progress to kernicterus, or chronic bilirubin encephalopathy, which is irreversible neurological damage, resulting in long-term effects like cerebral palsy and hearing loss. 

Clinical manifestations of pathologic jaundice include a rapid rise in bilirubin within the first 24 hours of life that persists at an elevated level longer than expected. The newborn may h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Assessment_-_Older_adult:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/p67hUu_bQjWQC63W3EBTOiuSSc2G0hBa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Assessment - Older adult: Nursing]]></video:title><video:description><![CDATA[The assessment of older adults is focused on identifying their self-care abilities and helping them achieve an optimal level of functioning. In addition to completing a comprehensive physical examination, you’ll assess their functional, cognitive, environmental, and social status.

Alright, a functional assessment evaluates your patient’s physical mobility and functional independence. Now, before assessing mobility, make sure your patient is wearing appropriate footwear, has their necessary assistive devices, and that you’re standing nearby to prevent falls.

Then, assess your patient’s physical mobility and gait by having them perform the “Timed Up and Go” test, or TUG for short, where you’ll ask them stand up from a seated position, walk ten feet, then return to the chair and sit down. During this time, note their ability to get up from the chair, their balance, gait, and speed, and balance.

Then to assess their functional independence, use your facility&amp;#39;s approved tool to evaluate their ability to perform basic activities of daily living, or ADLs like bathing, dressing, feeding, and toileting.

Next, ask them about how they perform more complex tasks, known as instrumental ADLs, or IADLs, like washing their clothes and shopping for groceries. You can also ask them to demonstrate how to use their phone and how they organize their medications.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Gestational_diabetes:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zk513USfTk2f_L2g2wEUz6WnSO_aXWYh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Gestational diabetes: Nursing]]></video:title><video:description><![CDATA[Gestational diabetes, also known as gestational diabetes mellitus, or GDM for short, is glucose intolerance that occurs during pregnancy, whereas pregestational diabetes is diabetes that is present prior to pregnancy. 

Alright, so, hormones produced during pregnancy cause changes in maternal glucose metabolism to support the pregnancy and to allow the fetus to receive a steady supply of glucose necessary for fetal growth and development.  

The early part of pregnancy can be described as an anabolic state, which increases fat stores, augments blood supply, and supports the growth of the fetus and maternal tissue like uterus, placenta, and breast tissue. During this time, insulin secretion increases, along with glucose utilization and storage in adipose and muscle cells.  

Later, as the pregnancy progresses, it begins to exert a diabetogenic effect on glucose metabolism, which means that there’s increasing maternal insulin resistance and decreased utilization of glucose. This results in higher levels of maternal blood glucose and increased transfer of glucose to the fetus. During this time GDM can develop when maternal insulin production is unable to compensate for the increased insulin resistance, resulting in hyperglycemia.  

GDM is more likely to affect those who have risk factors for diabetes mellitus, including obesity, a family history of diabetes, and advanced maternal age.   

Like all types of diabetes mellitus, clinical manifestations of GDM include polyuria, or increased urine production; polydipsia, or increased thirst; and polyphagia, or increased hunger.  

If left untreated, gestational diabetes can lead to complications. For example, excessive fetal nutrient intake can lead to macrosomia, or large birth weight, and result in the need for cesarean birth.  
Screening for GDM occurs between 24 and 28 weeks of gestation by measuring fasting blood glucose levels during an oral glucose tolerance test, or OGTT. The patient is given an oral gluco]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_care-associated_infection:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-i9C20VATouKsR4bsOMewRE3RDiyuWVR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health care-associated infection: Nursing]]></video:title><video:description><![CDATA[A health care-associated infection, or HAI, is when a pathogen is transmitted to a patient who’s been hospitalized for at least 48 hours.   
As the nurse, you can prevent health care-associated infections by breaking the chain of infection.  

The process of transmitting infection is known as the chain of infection and occurs in six continuous links: the causative agent, reservoir, portal of exit, mode of transfer, portal of entry and susceptible host.  

The first link is the presence of a causative agent, or pathogen, which is any disease-causing microorganism, like viruses, bacteria, yeast, fungi, or protozoa. Examples of common pathogens include the bacteria E. coli and the COVID-19 virus.  

The second link is the reservoir, or environment where the pathogen normally lives, multiplies, and grows. Reservoirs can be living, like humans, animals, or insects; waste products, like stool; food; water; or wounds.  

Common reservoirs in health care settings are unwashed hands, soiled linens, or medical equipment, like stethoscopes. 

Now, as the nurse you can reduce pathogens and reservoirs through asepsis, which is when pathogens are removed from the environment. There are two types of asepsis: medical asepsis and surgical asepsis. Medical asepsis, also known as clean technique, is when the number of pathogens or the risk of transmitting the pathogen, is reduced. This can be done through hand washing, wiping down equipment with a disinfectant, and preoperative skin cleansing. On the other hand, surgical asepsis, also known as sterile technique, is when equipment is sterilized eliminating all pathogens by using high heat or chemicals like when using surgical equipment that has been sterilized in an autoclave. 

Then, there’s the third link, portal of exit, where the pathogen leaves the reservoir. Common portals of exit in health care settings include the GI tract, where pathogens exit via feces or emesis; and the respiratory tract, where pathogens leave via ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mobility_-_Assistive_devices_for_ambulation:_Nursing_skills</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MchWLVeVSc2GIMS8Tt8Jb8LLTXqkavCU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mobility - Assistive devices for ambulation: Nursing skills]]></video:title><video:description><![CDATA[Assistive devices are tools to promote patient movement, including ambulation devices and mechanical lifts that move a patient from one location to another. Before using an assistive device, the registered nurse or physical therapist will assess the patient, determine which device is best for the patient, and provide them with initial teaching on the selected device. However, as the licensed practice nurse, or LPN, also known as a licensed vocational nurse, or LVN, you should know when these devices are appropriate and determine if they’re being correctly used by the patient, while reinforcing any previous teaching. 

Common ambulation devices include walkers, canes, and crutches. Let’s start by looking at walkers. 

These are lightweight devices that consist of a metal frame, two hand grips, and four legs. 

They provide stability due to their wide base, so they&amp;#39;re used for patients who can bear weight on their feet but have trouble walking due to weakness or balance issues. Before using a walker, make sure the hand grips are positioned at your patient’s waist level and that the ends of the legs have non-slip covers. 

To use a walker, assist your patient to stand straight while holding the hand grips. If the walker doesn’t have wheels, they’ll move it forward by lifting their walker and moving it six to ten inches in front of them, and then setting it down on the ground. Then, using the walker for support, they’ll move one leg forward, followed by the other. If the walker has 2 wheels on the front legs, your patient can push it to move forward. There are also walkers with 4 wheels, called rollator walkers. These walkers tend to roll forward, so brakes are built into the device. 

Next up, canes are lightweight devices typically made of wood or metal that consist of a handle, a shaft, and legs. There are single leg, triple leg, or quad leg canes. Canes with multiple legs typically provide more stability but can be heavy or inconvenient to transpo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Fluid_and_electrolyte_balance_-_Overview:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JElKjCVJSYupn8mOb6jjh2DCR0CVMxpv/_.jpg</video:thumbnail_loc><video:title><![CDATA[Fluid and electrolyte balance - Overview: Nursing]]></video:title><video:description><![CDATA[Fluid and electrolyte balance is the regulation of fluids and electrolytes, or charged molecules known as ions, to maintain a stable internal environment, known as homeostasis.  

Maintaining fluid and electrolyte homeostasis is essential for normal functioning of the body. 

Now, fluid is needed for essential functions like cellular metabolism and the delivery of oxygen and nutrients to the cells.  

It’s distributed in two major compartments: inside the cells, called intracellular fluid, and outside the cells, called extracellular fluid. The extracellular fluid compartment is further divided into the intravascular space, which is inside the blood vessels; the interstitial space, which is found between cells; and the transcellular space, where fluids, like pericardial, cerebrospinal, and synovial fluid, are contained in spaces lined with epithelial cells. 

Okay, so the fluid in these compartments is made up of water, as well as dissolved substances, called solutes. There are large solutes that can&amp;#39;t easily cross cell membranes, such as plasma proteins, like albumin; and small solutes that can easily cross cell membranes, such oxygen, glucose, and electrolytes. 

Now, electrolytes can be categorized as either cations, which are positively charged, like sodium; or anions, which are negatively charged, like phosphate. Electrolytes can be measured in the urine, cerebrospinal fluid, and blood, and they’re usually expressed as milliequivalents per liter of fluid, or mEq/L.  

Okay, so sodium, or Na+, is the most abundant cation in the extracellular fluid. Its major functions are maintaining fluid volume and  fluid osmolality, which is the concentration of particles dissolved in the fluid. Sodium’s normal range is between 135 to 145 mEq/L.  

Potassium, or K+, is the main cation in the intracellular fluid, and it’s responsible for maintaining the osmolality of the fluid within the cells.  
Potassium works closely with sodium to maintain the cell’s rest]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_health_theories_and_therapies:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wFjZJaSvTUiucuyrsq6RI3qCSNeABKFz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mental health theories and therapies: Nursing]]></video:title><video:description><![CDATA[Healthcare professionals can use theories to understand human development and behavior. Theories can also provide a framework for planning individualized care for patients and to guide the application of therapies to treat individuals with mental health disorders. 

Now, an early developmental theory about human behavior was developed by Sigmund Freud, called psychoanalytic theory. This theory is based on the idea that a person’s behaviors are influenced by their unconscious thoughts. Freud also developed the theory of psychosexual development, comprised of 5 stages from infancy to adulthood that explains how emotional disturbances are rooted in failure to progress through each stage.  

For example, a child aged 0 to 1 year is in the oral stage. During this stage, an infant finds pleasure and satisfaction through feeding and sucking. The child also begins to recognize their parent or caregiver as separate from themselves, and any disruption in the availability of the parent or caregiver could impair the child’s development, resulting in maladaptive behaviors later in life.  

Other developmental theories propose alternate ways to explain human development. Jean Piaget proposed a theory of cognitive development, which looks at how children develop 
their thinking and make sense of their world. According to Piaget, children&amp;#39;s development occurs in four distinct stages from birth to age 15. For example, during the concrete operations stage from age 8 to 11, children develop an understanding of the world in terms of words, numbers, and time. They also begin to use logic to understand principles like cause and effect, as well as size and difference; which allows the development of skills like arranging their toys according to their common or different characteristics, like color or shape. A learning disability or mental health disorder may be present if a child does not progress through the stages of cognitive development as expected.  

Another ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Growth_and_development_-_Hereditary_and_environmental_influences:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pwpSqaLAQwGSlueZCGB3jAZvTpmy82PU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Growth and development - Hereditary and environmental influences: Nursing]]></video:title><video:description><![CDATA[Hereditary and environmental factors influence a person’s development, even before conception. Hereditary factors refer to the genetic determination of traits, like eye color or the inheritance of disorders, like cystic fibrosis. On the other hand, environmental factors refer to external influences found where people live, work, and play that can impact how genes are expressed. Often, the impact on a person’s development is multifactorial, meaning it results from a combination of hereditary and environmental factors.

The hereditary material that determines a person’s development is contained in their chromosomes. Tightly packed into each chromosome is DNA, which is organized into genes that carry a person’s unique genetic code.

During fertilization, each parent donates half their chromosomes to create a fertilized ovum, called a zygote, which contains a total of 46 chromosomes organized into 23 pairs. These chromosome pairs are numbered from 1 to 22, with the 23rd pair, the sex chromosomes, labeled as X or Y.

Now, if chromosomes are altered, the person’s development can be negatively affected. These chromosomal alterations can involve changes in the structure of a chromosome, and can involve deletions, duplications, translocations, and inversions.  

A deletion is when part of the DNA is missing, like with cri-du-chat syndrome, where the short arm of chromosome 5 is missing.  

If there’s extra genetic material in a chromosome, it’s called duplication, like when there’s an extra copy of some of the genes found in the long arm of chromosome 7, resulting in developmental delay, behavioral problems, and other anomalies.  

Another structural alteration is translocation, where part of a chromosome moves to another chromosome. An example is the Philadelphia chromosome, which is chromosome 22 with a bit of chromosome 9 on it, resulting in a type of leukemia.  

Lastly, an inversion, which is where part of a chromosome is rearranged in reverse order. Inversion]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutrition_-_Pregnancy:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/S7C3U6qBTZeYzuGJrjqC6SiGS-aANaCl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutrition - Pregnancy: Nursing]]></video:title><video:description><![CDATA[During pregnancy, the patient and growing fetus require a variety of macro- and micronutrients and increased caloric intake to support sufficient weight gain and development.

Extra calories are needed during pregnancy to supply the energy needed to fuel the increased maternal basal metabolic rate and to support the production and maintenance of maternal tissues, placenta, and fetus. These calories should primarily come from nutrient-dense foods, like vegetables, meats, dairy products, legumes, and nuts; instead of empty calories, like fast food, cookies, cakes, and sweetened beverages.

Macronutrients are needed by the body in large amounts, and include carbohydrates, fats, and proteins. Carbohydrates are the primary source of calories used for energy. Carbohydrates can be simple, like the sucrose found in fruits; or complex which are found in sources of starch, like legumes, pasta, sweet potatoes, and whole grains. In addition to providing calories, complex carbohydrates contain additional nutrients like vitamins, minerals, and fiber. Fiber is the non-digestible part of carbohydrates that provide bulk to stool to help prevent constipation, which commonly occurs during pregnancy due to hormonal changes that slow the motility of the intestines.

Next, fats provide calories and fat-soluble vitamins. Good sources of fats include nuts, seeds, oils, meats, and dairy products. Fats also supply fatty acids that help with fetal neurological and visual development, such as alpha-linolenic acid, found in flax seeds; linoleic acid, found in vegetable or canola oils; and docosahexaenoic acid, found in cold-water fish like salmon.

Lastly, proteins are needed for essential processes like building and repairing tissue, making enzymes used in metabolic processes, and maintaining fluid balance. Proteins can also be used for energy when other sources aren’t available. Some sources of protein include eggs, legumes, tofu, nuts, meats, and fish.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Preterm_infant_complications:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rQrOvRmjTVSSd-0-LZo8spkTSG2s4PL7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Preterm infant complications: Nursing]]></video:title><video:description><![CDATA[A preterm infant is born before 37 completed weeks of gestation, which refers to the period between conception and birth, that typically lasts for 40 weeks.  

Now, the cause of preterm birth can be medically indicated, when there are maternal, fetal, and placental complications such as preeclampsia, fetal anomalies, or placenta previa.  
  Preterm birth can also be spontaneous, in which case the cause is often unknown, but there are certain factors that can lead to premature birth.  

These include maternal factors such as extremes of age, like teenage pregnancy or age over 40 years; history of prior preterm birth; being underweight or having a poor nutritional status; use of assisted reproductive technology, like with in vitro fertilization; cervical insufficiency; substance use, including tobacco, alcohol, or illicit drugs; infections, like bacterial vaginosis or an intrauterine infection; as well as factors like late or no prenatal care; high levels of stress; long working hours, especially when there’s long periods of standing; lack of social support; and intimate partner violence. 

Regardless of the cause, preterm infants are more likely to develop severe or life-threatening complications. Respiratory complications are common and are mostly related to insufficient surfactant production. This prevents the alveoli from expanding completely, resulting in hypoxia and respiratory distress syndrome. Other respiratory complications include transient tachypnea of the newborn, because of decreased absorption of fetal lung fluid and subsequent decreased gas exchange; pulmonary hemorrhage; apnea with accompanying bradycardia; as well as persistent pulmonary hypertension of the newborn, where pulmonary pressure remains high, resulting in continued shunting of blood away from the lungs through a patent ductus arteriosus.  

Given these complications, preterm infants may remain on prolonged mechanical ventilation. Unfortunately, mechanical ventilation can damage ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Spinal_cord_injuries:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RJ1zaUSrRp6ipk4OPkQ648peRZmPM27Y/_.jpg</video:thumbnail_loc><video:title><![CDATA[Spinal cord injuries: Nursing]]></video:title><video:description><![CDATA[A spinal cord injury refers to any damage to the spinal cord, which is a bundle of nerve fibers that serves as a highway that carries information between the brain and the body.

Now, a spinal cord injury can involve primary and secondary injury. Primary injury typically involves a sudden, traumatic impact on the spine that fractures or dislocates the protective vertebrae, damages the spinal cord, or interrupts its blood supply.

Then, after the primary injury, there’s usually additional damage, or secondary injury, that occurs due to the body’s natural response to trauma. Secondary injury begins immediately after the spinal injury, and includes bleeding, inflammation, and edema. This is followed by compression of the spinal cord, ischemia, and neuronal damage. As time goes by, additional neuronal cell death occurs.

Eventually, specialized glial cells begin to form scar tissue at the site of injury, which creates a barrier across the injured tissue, impairing cellular regeneration, which can result in permanent nerve damage and subsequent neurologic deficit.

Now, spinal cord injuries can have several different causes, including trauma, like with a motor vehicle crash or falls, such as falling from a ladder; penetrating trauma, like a stab wound in the back or a gunshot; or recreational injuries, like those caused by impact sports. They can also be caused by medical conditions, including spinal tumors, infections, or degenerative diseases of the spine, like a protruding intervertebral disk.

Risk factors for developing a spinal cord injury include engaging in high-risk behaviors, such as not wearing safety equipment when playing sports or speeding while driving. Lastly, a history of bone or joint disorders increases the risk, since even minor trauma could damage already weakened bones and injure the spinal cord.

Alright, now clinical manifestations of spinal cord injuries depend on the severity and location of the injury and may include partial or comple]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Head_injury_-_Pediatric:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bcztZ71lSCidvcoKJck5N1D3TyKCxxOC/_.png</video:thumbnail_loc><video:title><![CDATA[Head injury - Pediatric: Nursing]]></video:title><video:description><![CDATA[Head injuries involve trauma to the brain and its surrounding structures that are the result of an external force, and can include injuries like lacerations, skull fractures, and concussions.

Alright, so, lacerations are tears of the scalp typically caused by blunt trauma or penetration with a foreign object. Skull fractures are breaks in the skull bone, and include linear fractures, which cause a crack in the skull bone that does not cross suture lines; comminuted fractures, which consist of multiple linear fractures; depressed fractures, where pieces of skull bone push inward, causing hematomas, which is a pooling of blood outside a blood vessel, or lacerations of the brain tissue; and basilar fractures, which occur at the base of the skull.

Then, there are mild traumatic brain injuries, or concussions, which cause a transient disruption in normal neurologic function resulting in an alteration in mental status and sometimes a temporary loss of consciousness.

Now, head injuries can be caused by several mechanisms, like contact head injuries, acceleration-deceleration injuries, and penetrating injuries. Contact head injuries occur when a child hits their head on a hard surface, like when falling down the stairs; or when they receive a violent blow or jolt to the head, like when a child is tackled during a football game.

On the other hand, acceleration-deceleration injuries happen when the brain bounces around inside the skull, like in a car accident, or if a child is repeatedly shaken, like with shaken baby syndrome. The bouncing of the brain inside the skull causes a contusion, or bruising of the brain, at the site of impact, called coup injury.

Then, the recoil force directs the brain the other way to strike the opposite side of the skull, resulting in a contusion on the other side of the brain, called contrecoup injury. Lastly, head injuries can also be caused by penetrating injuries, like knife or gunshot wounds.

Risk factors for head injuri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Menstrual_and_breast_disorders:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/aj-zMRV7RyueHeEuzfArH8RFQDyDlmxh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Menstrual and breast disorders: Nursing]]></video:title><video:description><![CDATA[Women’s health focuses on strategies to promote the health and well-being of patients assigned female at birth. Common problems addressed in women’s health are menstrual and breast disorders.  

Okay, so two common menstrual disorders are amenorrhea and abnormal uterine bleeding. Amenorrhea is the absence of menses, or a menstrual period, which can be primary or secondary. Primary amenorrhea is when the first menses doesn&amp;#39;t occur by age 15 or within 3 years after developing breasts. It’s often caused by disorders in the hypothalamic-pituitary-ovarian axis; chromosomal abnormalities; or structural abnormalities of the uterus, vagina, or hymen that obstruct flow.  

Secondary amenorrhea is when a regular menstrual cycle stops for at least 3 months, or when an irregular menstrual cycle stops for at least 6 months. Secondary amenorrhea can be caused by natural processes, like pregnancy, lactation, and menopause; or by underlying conditions, like polycystic ovarian syndrome, thyroid disease, or an eating disorder.      

Diagnosis begins with a history and physical examination. Then, laboratory tests will be performed to identify potential causes, like human chorionic gonadotropin, or hCG to confirm pregnancy; thyroid stimulating hormone, or TSH to check for a thyroid disorder; and reproductive hormone levels, such as serum follicle-stimulating hormone, luteinizing hormone, and androgens to identify endocrine problems.  

Treatment will address the underlying condition and can include hormone replacement therapy or contraceptives to restart regular menstruation and promote normal ovarian function.  

Now, abnormal uterine bleeding, or AUB, refers to bleeding that’s heavy, extended, frequent, or irregular. AUB can be caused by an underlying condition, like uterine fibroids or polyps; cancerous lesions; coagulation problems, from medications like anticoagulants or clotting disorders, like von Willebrand disease; or complications of pregnancy, such a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Psychological_needs_of_patients_with_medical_conditions:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ykZksMs4SUmqGZ756JrUUlVXS3a4e0Mb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Psychological needs of patients with medical conditions: Nursing]]></video:title><video:description><![CDATA[Medical conditions can sometimes be accompanied by psychological symptoms that can cause negative health outcomes. Common psychological responses to medical conditions include stress, anxiety, depression, grief, and denial. 

Stress is a common physical and psychological response to a challenging experience. When diagnosed with a medical condition, patients may think about the amount of pain they could experience due to their illness; they may wonder if the condition will affect their quality of life and relationships with others; or they might worry about being able to continue to work. How the patient responds to questions like these will shape their perception of their illness, which will then impact the amount of stress they experience.  

Next is anxiety, which is apprehension about a stressful situation that causes feelings of fear, worry, and nervousness, as well as physical symptoms like breathlessness and palpitations. 

When a medical condition is diagnosed, it’s often accompanied by experiences like waiting for test results or surgical procedures, which can increase anxiety due to loss of control and feelings of helplessness. Overwhelming anxiety can negatively influence a patient’s ability to cope and adapt to their medical condition and can lead to the use of unhealthy defense mechanisms or compulsive behaviors.  

Now, depression is a persistent sadness or loss of interest in daily life. Depression can impact a patient’s course of illness by impairing their motivation or ability to adhere to the prescribed treatment regimen, and it can lead to unhealthy lifestyle choices, like not exercising, continuing to smoke, or indulging in an unhealthy diet. 

Grief is a psychological response to a medical condition that occurs when a patient deals with the loss of their physical well-being. When experiencing grief, patients may feel confused, frustrated, sad, and vulnerable as they work toward reaching a sense of acceptance and peace. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_to_use_Osmosis_in_the_classroom</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mjYyDQDkRBmTaZRu75dj5ewZRz2Y4O0d/_.png</video:thumbnail_loc><video:title><![CDATA[How to use Osmosis in the classroom]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How to use Osmosis in the classroom through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Glioblastoma_(NORD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/y8EQVWIdRZyYFnQQwV3CewWmTQ2cYqQa/_.jpg</video:thumbnail_loc><video:title><![CDATA[Glioblastoma (NORD)]]></video:title><video:description><![CDATA[Glioblastoma multiforme, or glioblastoma, is a rare cancerous brain tumor that grows from a helper nerve cell called an astrocyte. It is classified as a type IV astrocytoma, an aggressive type of tumor. Glioblastomas grow very quickly and usually affect the brain or spinal cord in adults impairing normal function.  

Glioblastoma is thought to be caused by a genetic change which leads an astrocyte to replicate uncontrollably, forming a tumor. As the tumor grows, it spreads quickly, invading and compressing nearby brain tissue. Although glioblastomas can affect any part of the brain, it most frequently affects the cerebral hemisphere, which controls movement, sensation, memory, cognition, or complex thinking, and language. 

Additional glioblastoma risk factors may include: previous radiation treatments to the brain; a history of working in synthetic rubber manufacturing or petroleum refining; or exposure to vinyl chloride or pesticides. Although most people who have had these experiences never develop this disease. 

Glioblastoma is more common in individuals between 45 and 70 years of age. Individuals often present with headaches, nausea, vomiting, and seizures. In addition, individuals may have neurologic abnormalities depending on the size and location of the tumor. For example, involvement of the motor cortex can lead to muscle weakness; involvement of the sensory cortex can cause numbness; involvement of the frontal lobe can cause personality changes; involvement of areas responsible for language can affect speech; and involvement of the areas responsible for vision can lead to blindness.  

Glioblastoma may also cause brain swelling or block the flow of cerebrospinal fluid, leading to increased pressure within the skull. These dangerous complications do not happen often but, if they do, may require emergency treatment.  

An MRI of the brain is usually one of the first tests performed when a brain tumor is suspected. Glioblastoma can be diagnosed whe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Health_Assessment_and_Screening_in_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UGcJSRkWSrSISNT3EK-3CmfjTy_G3L06/_.jpg</video:thumbnail_loc><video:title><![CDATA[Health Assessment and Screening in the Older Adult]]></video:title><video:description><![CDATA[Performing health assessments and health screenings provide information about a patient’s health status and identify those in need of further assessment and care. As the nurse caring for older adult patients, you’ll use this information to provide patient-centered care.  

Now, during a health assessment, you’ll collect comprehensive health information, which typically includes gathering a health history and conducting a physical examination. Health information can be categorized as either subjective or objective data. Subjective data refers to information the patient states or recounts, such as pain level or sleep quality, and tends to be obtained during a health history. On the other hand, objective data is collected during the physical assessment, and includes tangible information that’s observed or measured, like presence of a skin rash or blood pressure readings. 

Alright, starting with health history, this is where you’ll interview your patient to obtain subjective data about their perceived health and factors impacting their health. Begin by asking about basic identifying information, like name and date of birth.  

Next, move on to specific data like past medical and surgical history, such as previous hospitalizations and surgeries, current medications, and personal health habits like diet, physical activity, and sleep patterns.  

Then you’ll discuss the patient’s current health status and any pressing health concerns, as needed. Keep in mind that the patient is the preferred information source; however, a family member or caregiver can provide information if your patient has limited ability to recall or communicate, like those with dementia or aphasia.  

During the health history, remember to do your best to avoid the use of medical jargon. For example, instead of saying hypertension, say high blood pressure. Also, since word recall and response time can slow with age, be sure to speak slowly and clearly, and provide your patient with enough ti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acne</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TUCZ0_adRUSa6YeyMiknFGClSmSADUB5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acne]]></video:title><video:description><![CDATA[Acne vulgaris, often just called acne, is a skin condition that can be non-inflammatory or inflammatory. 

First, let’s look at the skin, which is the largest organ in the body. It provides important functions like protection, sensory perception, temperature regulation, and vitamin D production. Its two main layers, the dermis and epidermis, rest upon the hypodermis, or subcutaneous tissue.  

Starting with the most superficial layer of the skin, the epidermis is composed of layers of stratified squamous epithelial cells. There are various bacteria that live on the outer layer of the epidermis as part of its natural flora. Under normal circumstances, these bacteria don’t grow into numbers large enough to become pathogenic, meaning they typically don’t cause infection.  

Next is the dermis, which is made up of connective tissue that allows the skin to contract and stretch with body movements. It also contains hair follicles, oil and sweat glands, nerves, immune cells, and blood and lymphatic vessels.  

Now, each hair follicle in the dermis is part of a pilosebaceous unit, composed of a short, thin, non-pigmented hair, called a vellus hair, that extends to the epidermis through a pore called the follicular canal; an arrector pili muscle, which makes the hair stand up when it contracts; and one or more sebaceous glands, which produce and secrete oily sebum into the follicular canal and onto the skin’s surface. The sebum acts as a lubricant for the skin and protects from moisture loss. 

Finally, the hypodermis consists mainly of adipose, or fat, tissue that provides insulation and padding and loose connective tissue that helps anchor the skin to the underlying muscle.  

So, the main cause of acne is blockage of the follicular canals by dead skin cells, bacteria, and sebum. A primary risk factor is being an adolescent or young adult. This is because sebaceous glands are stimulated by the increased amounts of circulating androgens in puberty, causing the gla]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Patterns_of_Inheritance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/09X9wjEaSQK70PF7x0et_MCTRy6TA3lO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Patterns of Inheritance]]></video:title><video:description><![CDATA[Patterns of inheritance refer to the way certain traits are passed down genetically from parents to offspring. Mendelian patterns of inheritance typically follow four basic patterns and involve only one gene. 

First, let’s review the basics of genetics. Each gamete, also known as a sex or germ cell, such as sperm or ova, contains 23 chromosomes, which carry genetic information. When a sperm fertilizes an ovum, these chromosomes combine to form a zygote, or fertilized ovum, that now has 46 chromosomes, arranged into 23 pairs. These pairs of chromosomes are collectively called the genome. 

Now, the first 22 pairs of chromosomes are autosomes, whereas the 23rd pair are sex chromosomes. Sex chromosomes typically include an X chromosome from the mother and either an X or Y chromosome from the father, resulting in either a female offspring with XX chromosomes or a male offspring with XY chromosomes.  

Every chromosome contains multiple genes, which are regions of DNA that carry information for a specific trait. Different versions of a gene are called alleles. Alleles provide information for a phenotype, or the observable traits of an individual, such as eye color or height. Alleles can be dominant or recessive, with recessive alleles being masked by dominant alleles. Additionally, if an individual inherits two of the same alleles, they’re homozygous for that trait; whereas if the alleles are different, they’re heterozygous for that trait.  

For example, the allele for brown eyes is dominant and the allele for blue eyes is recessive. So, if an individual has one allele for brown eyes and one for blue eyes, the dominant allele masks the recessive allele, resulting in an individual with brown eyes, and they’re considered heterozygous for that trait. On the other hand, if an individual has two alleles for blue eyes, they’ll have blue eyes and be considered homozygous for that trait.  

Alright, let’s take a closer look at Mendelian patterns of inheritance. They’]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexually_Transmitted_Infections</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lmpu912hSzWfka8vR80IM47OQ3ucnV_O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sexually Transmitted Infections]]></video:title><video:description><![CDATA[Sexually transmitted infections, or STIs, are infections spread by sexual contact. These infections are sometimes also called sexually transmitted diseases, or STDs, and were formerly known as venereal diseases. 

Now, STIs can be bacterial, like chlamydia, gonorrhea, and syphilis; viral, such as herpes simplex virus, or HSV; human papillomavirus, or HPV; hepatitis; and human immunodeficiency virus, or HIV; or parasitic, such as in trichomoniasis.  

They’re spread through direct contact, including direct sexual contact like vaginal, oral, or anal intercourse; contact with infected blood or other bodily fluids; and even through close body contact.  

Additionally, some STIs, such as chlamydia, gonorrhea, syphilis, and HIV, can be spread through vertical transmission, meaning the infection passes from mother to fetus during pregnancy or to the infant during a vaginal birth. In other cases, infections can be transmitted by sharing personal items such as toothbrushes or razors or by sharing needles during IV drug use. 

Risk factors for STIs include having multiple sexual partners, especially without an effective barrier such as a condom; being an uncircumcised biological male; and being the receptive partner during intercourse. Also, biological females are at higher risk for infection, partly because the vaginal lining is relatively thin and more easily invaded by pathogens.  

Additionally, inadequate screening, lack of access to healthcare, or inadequate risk assessment by healthcare providers all increase the risk that an infected individual unknowingly transmits an STI to another individual. Lastly, STIs can occur at any age, but they’re most prevalent in young adults. 

Okay, so, the pathophysiology of STIs depends on the specific infectious agent and site.  

So, as an example, a common STI is Neisseria gonorrhoeae, a gram-negative bacterium that causes gonorrhea. The bacteria have hair-like extensions on their surfaces called pili which help the bacte]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Nutrition_and_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RPpLRK1-SY2Ewo-F8HIP9UIrRCCCuQgl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Nutrition and the Older Adult]]></video:title><video:description><![CDATA[Nutrition refers to the process in which nutrients are ingested and used by the body to support health and maintain essential functions, like metabolism and tissue repair. Nutritional needs fluctuate in response to age-related physiologic changes and the development of acute or chronic conditions.  As the nurse, you’ll consider how nutrition changes with aging and provide patient-centered care based on your patient’s nutritional needs. 

Now, the required number of calories, which reflect the available energy within food, decreases with age due to a reduction in lean muscle mass and an increase in adipose, or fat, tissue. In general, the minimal daily recommended caloric intake for an older adult is 1200 calories per day.  

However, caloric needs also vary depending on factors like age, biological sex, body size, activity levels, and the presence of illness. For instance, some older adults with conditions that restrict mobility or limit activity tolerance, such as arthritis or heart failure, may require fewer calories. In contrast, conditions that increase the metabolic rate, like cancer, may require consumption of more calories.   

Unlike caloric requirements, the amount of necessary nutrients remains stable as individuals age. Therefore, nutrient-dense foods, or foods with a high nutritional value, are ideal for older adults.   

First, carbohydrates include sugars and starches and are the main source of calories used for energy, so they should make up 45 to 65 percent of daily calories. Carbohydrates can be simple or complex. Simple carbohydrates, like honey or table sugar, are easily broken down and are less nutrient-dense; whereas complex carbohydrates, like whole grains and fruits, take longer to break down and are more nutrient-dense. Complex carbohydrates also contain soluble fiber, which is a non-digestible form of fiber that has numerous benefits, including increasing the bulk of stool which helps prevent constipation; lowering blood cholestero]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_Health_and_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mtyvph6SToajq57bfCWU0t5QSIqHSHU1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mental Health and the Older Adult]]></video:title><video:description><![CDATA[Stress is a normal response to internal and external threats to homeostasis, or the body’s stable equilibrium, caused by a real or perceived threat. The two types of stress are eustress and distress.  

Eustress, or positive stress, results from beneficial and motivational stressors, like starting a new job, whereas distress, or negative stress, occurs in response to a negative stressor, like the death of a loved one.  

Regardless of the source of stress, the body responds by undergoing a series of physiologic changes.  

In the short term, the body can adapt and return to homeostasis; but if sustained, stress can be detrimental to physical and even mental health, leading to problems with cognition, memory, depression, and anxiety, especially in those who aren’t able to cope, or effectively manage stress.  

As the nurse caring for an older adult patient, you’ll identify common stressors, recognize signs and symptoms of ineffective coping, and implement patient-centered care strategies to promote effective coping. 

Now, stress happens across the lifespan, but some stressors are more likely to impact older adults, such as major life changes involving loss and health conditions.  

Loss can be social, like losing independent driving privileges; emotional, such as the death of a partner; financial, like reduced income due to retirement; and physical, such as losing eyesight from a chronic condition like macular degeneration.  

Remember, older adults may use coping strategies that are both effective and ineffective to deal with stress. For example, an effective coping strategy is sublimination, when negative energy is channeled into a positive activity, like exercise; whereas an ineffective coping mechanism is suppression, when an individual avoids thinking about a stressor altogether. 

Alright, sustained stress over time can deplete the energy reserves required for effective coping, resulting in signs and symptoms of ineffective coping that can be categor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Arthritis_-_Osteoarthritis_and_Rheumatoid_Arthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bID-Knu6SCSIJ5_Pg6zNhJ6wS4eCC0Yd/_.png</video:thumbnail_loc><video:title><![CDATA[Arthritis - Osteoarthritis and Rheumatoid Arthritis]]></video:title><video:description><![CDATA[Osteoarthritis, or OA, and rheumatoid arthritis, or RA, are diseases that affect the synovial joints. OA is mostly a degenerative disease, while RA is a systemic autoimmune disease that can also impact other organs like the heart and lungs. 

Joints, or the places where bones meet, can be classified into three main groups based on their structure and range of movement. Fibrous joints, like those between the bones of the skull in young children, are composed of a thin layer of fibrous tissue that allows for some movement to accommodate a child’s growing brain; by adulthood, the fibrous tissue is replaced by bone. On the other hand, cartilaginous joints, like the joints of the spine, contain a pad of fibrocartilage, allowing for some movement. Lastly, synovial or diarthrodial joints, like those of the wrist, shoulders, hips, and knees, are freely movable. 

Okay, let’s take a closer look at synovial joints, which consist of two bones, each with its own layer of articular cartilage, a type of connective tissue that provides cushioning and allows the bones to glide against each other without friction. The cartilage has high tensile strength, which helps weight-bearing joints like the knees to distribute weight so the underlying bone absorbs the shock and weight. An important component of the articular cartilage are special cells called chondrocytes, which are essential for the maintenance and repair of the cartilage.  

Surrounding the joint is an outer fibrous joint capsule that forms an inner space called the joint cavity, which is filled with synovial fluid. The inner surface of the joint capsule is lined with a synovial membrane, or synovium, which is mostly composed of connective tissue, elastic fibers, blood, and lymphatic vessels. It also contains macrophages that remove bacteria and debris, and fibroblasts that produce a viscous substance called hyaluronate, which is the main component of the synovial fluid, that lubricates the articular surfaces.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epigenetics_Mechanisms_and_Human_Development</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/47c50-n7T8GYQVAB6zDfWZYrSX279-Sc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epigenetic Mechanisms and Human Development]]></video:title><video:description><![CDATA[Epigenetics is the study of how an individual’s environment and behavior can modify DNA without altering the DNA sequence. These modifications regulate genes by turning genes on, increasing gene expression, or off, decreasing gene expression. Epigenetic modifications can occur through three mechanisms: histone modifications, DNA methylation, and RNA-based mechanisms.  

As a quick review, the nucleus of each of the body’s cells contains DNA, the genetic material that holds the instructions, or code, for synthesizing specific proteins.  

These proteins direct the function of cells which give rise to an individual’s phenotype, or their observable characteristics and traits.  

The complete set of DNA instructions found in each cell is called the genome. 

Okay so, to make a protein, certain genes within the genome need to be activated, or expressed. Whether a gene is expressed or not is regulated through epigenetic modifications that shape the function of the genome. Consequently, epigenetics can help explain a lot of things, like how cells in the body, such as skin cells and brain cells,  

can differ from one another even though they all contain the same DNA.  

It can also help explain why identical twins with the same DNA often have subtle differences in their appearance, personality, and even diseases they might develop. 

Now, epigenetic modifications arise from fetal development and continue throughout an individual’s lifetime. These modifications can be the result of early experiences in life such as growing up in a nurturing environment, experiencing abuse or deprivation, and even through dietary choices, use of certain medications, or exposure to industrial pollutants.  

Whatever the cause, these modifications can impact physical and mental health outcomes through their influence on DNA activity. For example, since epigenetic mechanisms can switch on or off genes involved in cell growth, like tumor-suppressor genes, they can promote uncontrolled ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sickle_Cell_Anemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/QWjL-yy6TfyEpxN6v7XkHACuTUm_ID7J/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sickle Cell Anemia]]></video:title><video:description><![CDATA[Sickle cell anemia, one of the most common types of sickle cell disease, is a genetic condition resulting in red blood cells, or RBCs, that are sickle-shaped, inflexible, and easily destroyed.  

Alright, so, RBCs are produced through erythropoiesis, which occurs within the bone marrow. 

The bone marrow releases immature RBCs called reticulocytes into the circulation where they mature into erythrocytes. Erythrocytes contain hemoglobin, which allows them to deliver oxygen to the body’s tissues. 

Now, hemoglobin molecules are made up of four polypeptide chains of amino acids, which consist of two α-globin and two β-globin chains. Each of these polypeptide chains contains a heme group, which includes one iron atom where oxygen can bind. One oxygen molecule can bind to each polypeptide chain, allowing one hemoglobin molecule to carry up to four oxygen molecules.  

RBCs have some unique characteristics that make them well-suited for oxygen transport. Their unique biconcave shape increases surface area for oxygen diffusion, and their flexible membrane allows them to change their shape so they can squeeze through tiny capillaries and then return to their original shape while staying intact. This gives them a degree of durability as they travel throughout the body’s network of blood vessels. In fact, RBCs have a lifespan of up to 120 days.  

As RBCs age, become fragmented, or unhealthy, they’re ingested and destroyed by macrophages in the spleen and liver and replaced through erythropoiesis.   

Sickle cell anemia is caused by a mutation in the HBB gene that provides the instructions for making β-globin. It’s inherited in an autosomal recessive pattern, meaning that an individual must inherit two mutated copies of the HBB gene, one from each parent, to get the disease.  

On the other hand, if an individual has one mutated HBB gene and one normal HBB gene, then they have sickle trait, which doesn&amp;#39;t typically result in anemia.  

Risk factors include h]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leukemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jowz6deiSXuGzmjr0fuNQtOlQg6a4GVp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leukemia]]></video:title><video:description><![CDATA[Leukemia is a cancer of the blood-forming tissues, that disrupts the normal function of bone marrow. This disruption leads to the proliferation of immature white blood cells.  

Leukemias are classified as acute or chronic, and by the type of cells affected, either myeloid or lymphoid. The four primary types of leukemia include acute lymphoid leukemia, or ALL; chronic lymphoid leukemia, or CLL; acute myeloid leukemia, or AML; and chronic myeloid leukemia, or CML. 

Now, bone marrow is a spongy tissue found in the center of most bones. It contains stem cells, which are unspecialized cells that, through a process called hematopoiesis, differentiate into functional cells such as red blood cells, or RBCs; white blood cells, or WBCs, also called leukocytes; and platelets. Hematopoiesis is a continuous process that ensures there’s a steady supply of cells to replace old and damaged cells.  

As far as WBCs go, there are several types which come from two distinct stem cell lines: the lymphoid line, and the myeloid line. Immature cells, called blast cells, are formed from these stem cell lines and further differentiate into functional WBCs. In the lymphoid line, lymphoblasts produce lymphocytes, including B-cells, T-cells, and natural killer cells. In the myeloid line, myeloblasts produce neutrophils, eosinophils, basophils; and monoblasts produce monocytes. These cells function as part of the immune system, fighting infection and other diseases, and removing foreign substances from the body. 

While the exact cause of leukemia is not fully understood, genetic and environmental factors play a role. Inherited genetic conditions associated with an increased risk of leukemia include Down syndrome and neurofibromatosis. Other genetic changes such as chromosomal translocations, where pieces of two chromosomes split off and swap places, like with the Philadelphia chromosome, are also associated with an increased risk of leukemia.  

Environmental factors include exposur]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nc0UeINWRe6FL421cSU4uW4XSDCrGFB6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia]]></video:title><video:description><![CDATA[Anemia is a group of conditions that occurs when there&amp;#39;s a reduced number of healthy, functional red blood cells, or RBCs, in the blood.  

Now, RBCs are primarily responsible for carrying and delivering oxygen to the body’s tissues. They’re produced through erythropoiesis, which occurs within the bone marrow under the direction of erythropoietin, a hormone produced in the kidneys.  

Here, stem cells called proerythroblasts differentiate into erythroblasts, a type of immature RBC that synthesizes hemoglobin. Hemoglobin is a protein that binds and carries oxygen and is made up of four polypeptide chains called globins, which consist of two α and two β chains. Each chain contains a heme group, which includes an iron atom, where oxygen can bind. One oxygen molecule can bind to each protein chain, allowing one hemoglobin molecule to carry up to four oxygen molecules. And each RBC can contain hundreds of hemoglobin molecules!  

Eventually, erythroblasts differentiate into reticulocytes, another type of immature RBC. The bone marrow releases reticulocytes into the bloodstream where they ultimately become mature RBCs, which are called erythrocytes. Erythrocytes are especially effective in gas exchange, due to their flexible, biconcave shape, which makes them able to fit through narrow blood vessels, while increasing surface area to conduct gas exchange. 

Now, anemia can result from underproduction, increased destruction, or excessive loss of RBCs.  

First, underproduction can occur if the kidneys don’t produce enough erythropoietin, which can happen in chronic kidney disease. Without enough erythropoietin stimulating the bone marrow, not enough RBCs are produced. Also, if there’s not enough building blocks to support erythropoiesis, such as iron, vitamin B12, and folate, less fully functional RBCs can be produced. So, for example, lack of iron can lead to iron deficiency anemia.  

Additionally, if the bone marrow is damaged from conditions]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Aging_and_Cognition</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zbwupXZSR2iJ2qqOn147VT0QRmWC10iX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Aging and Cognition]]></video:title><video:description><![CDATA[Cognition describes the process of receiving, storing, sharing, and making sense of information, which include mental processes such as memory, language, concentration, and problem-solving. Cognition can be impacted by one’s environment, genetics, educational background, health status, and age-related brain changes.  

As the nurse, you’ll consider age-related changes to the brain, the physiologic processes that can compensate for these changes, and provide patient-centered care to promote brain health in your older adult patients. 

Now, as an individual ages, there&amp;#39;s typically a general slowing of function of the neuronal processes that doesn’t usually interfere with mental function or daily routines. This slowing in function is different for everyone and is related to changes in brain structure and neurotransmitter function.  

As far as structural changes go, there’s a decrease in the size and number of neurons, which are the nerve cells that receive and send messages throughout the body. Dendrites, which branch off from the neuron cell body and receive signals from other neurons, can experience shrinkage and decreased branching. Other age-related changes include a build-up of substances like plaque within the neurons, and a decrease in myelin, which is the substance that helps the neurons to quickly transmit electrical impulses.  

Additionally, there are changes that affect neurotransmitters, or chemical messengers, such as acetylcholine, glutamate, serotonin, and dopamine, that normally allow neurons to communicate with each other. These changes include alterations to enzymes that synthesize and break down neurotransmitters and changes to neurotransmitter receptor sites. 

Alright, so, the brain can compensate for age-related changes by developing cognitive reserve, which is the ability of the brain to maintain cognitive functioning, even when it experiences degeneration or damage. In other words, the stronger the cognitive reserve, the mor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Infectious_Process</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7eqCqRf5RQqsxuFvfnke33J0RyqjyarF/_.jpg</video:thumbnail_loc><video:title><![CDATA[The Infectious Process]]></video:title><video:description><![CDATA[The infectious process refers to the steps that occur when a pathogen, which is a disease-causing microorganism, enters the body, multiplies, spreads, and causes tissue damage.  

Okay, so, the body has lines of defense to protect itself against pathogens. The first line of defense includes physical and chemical barriers that prevent entry of pathogens into the body, like intact skin and mucous membranes, and molecules like lysozymes found in body fluids like tears and mucus, that can break down the cell walls of certain pathogens. Another key aspect of defense is the microbiome, or the collection of microorganisms that normally live in and on the body. These microorganisms don’t normally cause disease, and they help protect against invading pathogens by mechanisms like physically occupying space and even producing substances that inhibit the colonization of pathogens. 

If a pathogen gets past these barriers, it encounters the second line of defense, the inflammatory response, where immune cells like macrophages and neutrophils phagocytize, or ingest, bacteria and cellular debris. Other systems, like the complement system, also get activated, which assist in killing of pathogens. Both the first and second lines of defense are innate, meaning they’re natural, inborn defense mechanisms, and they’re non-specific, because they respond the same way to all pathogens. 

Now, if these mechanisms are not able to stop the invasion of the pathogen, the third line of defense, adaptive immunity, kicks in. It involves cellular immunity primarily with T lymphocytes and B lymphocytes, and the formation of antibodies, which is also called humoral immunity. Adaptive immunity mechanisms attack the current infection, and it even has a memory; so, the next time the body is exposed to this same pathogen, it can start attacking it faster.  

Alright, so, infections are caused by pathogens like bacteria, viruses, and fungi. Each of these organisms have their own characteristics ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malnourishment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MYnMd_iBSu2Xq0kK9QBU4xAwSlyFKYR1/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malnourishment]]></video:title><video:description><![CDATA[Malnourishment, also called malnutrition, is when there’s an imbalance of nutrients needed to support essential body functions. This imbalance can occur with overnutrition, where nutrient intake is more than the body requires, like with obesity; or with undernutrition, where nutrient intake is insufficient to meet the body’s needs, as seen in starvation. 

So, the three primary nutrients crucial for overall health are carbohydrates, proteins, and fats.  First, carbohydrates are the primary source of glucose used for energy and include monosaccharides, oligosaccharides, and polysaccharides. Monosaccharides are simple carbohydrates, like table sugar. They are easily broken down and less nutrient-dense. Oligosaccharides and polysaccharides are more complex carbohydrates, like soybeans and whole grains. These take longer to break down and are more nutrient-dense.  

Next, proteins are complex chains of amino acids and are the building blocks of the body. They construct tissues and important molecules, like enzymes and hormones, and they repair tissues. Proteins can also be used for energy, if needed. Amino acids are categorized as essential, meaning they must be ingested through the diet, and non-essential, because they are produced within the body. High protein foods include animal products, like meat and dairy, or plant-based foods like legumes and nuts.  

Lastly, fats, or lipids, are composed of glycerol and fatty acids. Fats are another source of energy, and they’re a critical component of cells and tissues. They also help absorb fat soluble vitamins and make up important molecules like steroids. Based on their chemical structure, fats are either saturated, like butter, or unsaturated, like the fats found in avocado.  

Once ingested, nutrients are broken down by the digestive system, absorbed, and used in various ways. Carbohydrates are broken down into glucose, which is transported throughout the body and used by cells for energy. Any excess glucos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Physical_Activity_and_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/85KkqLc9RUGD56Gy2UxTN7wWTEKkEq-S/_.jpg</video:thumbnail_loc><video:title><![CDATA[Physical Activity and the Older Adult]]></video:title><video:description><![CDATA[Staying active throughout one’s life can have a positive impact on health outcomes. Although physical capabilities vary from person to person, most individuals experience age-related changes to their mobility and activity levels over time.  

As the nurse, you’ll consider individual abilities and limitations and provide patient-centered care to promote physical activity in older adults.  

Alright, starting with the musculoskeletal system, over time there’s a gradual loss of muscle mass, which can decrease overall strength. Meanwhile the flexibility of the ligaments, tendons, and joints decreases, and the cartilaginous cushioning between the joints diminishes, potentially leading to impaired mobility and pain.  

In the nervous system, the speed of nerve transmission slows with age, so it takes longer to complete familiar activities, like getting dressed or cooking a meal. Also, decreasing agility, or the speed and smoothness of physical movements, can increase the difficulty of activities such as climbing stairs or avoiding hazards while walking. Similarly, fine motor skills, like sewing or playing an instrument, may become less precise.  

Lastly, there are also changes in the cardiovascular and respiratory systems with age. The heart’s muscle loses tone and becomes stiffer over time, making it a less effective pump. In the lungs, loss of alveolar elasticity, decreased alveolar surface area, and fewer pulmonary capillaries impairs the exchange of oxygen and carbon dioxide; and decreased lung capacity reduces the volume of air the lungs can hold. Together, these changes result in less oxygen-rich blood being pumped out to the body, which can result in reduced exercise tolerance and overall stamina.  

Now, being physically active can improve health and quality of life while providing an opportunity to safely maintain independence for longer. Exercising regularly preserves mobility and muscular function, improves cardiovascular health, and helps control we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stroke</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Gq8ptEfsThSPUqfY-vVufv1IR3WGrHmr/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stroke]]></video:title><video:description><![CDATA[A stroke, also known as a cerebrovascular accident, occurs when blood flow to the brain is disrupted, resulting in tissue ischemia and death. A stroke can be ischemic or hemorrhagic. An ischemic stroke is when there’s an occlusion in an artery in the brain; while a hemorrhagic stroke is when an artery in the brain ruptures and causes blood to leak into the brain tissue. 

Now, the brain is the communication and control center of the body, and to maintain neurologic function, all parts of the brain require a steady and consistent flow of oxygen- and nutrient-rich blood. The brain is supplied with blood through the internal carotid arteries and the vertebral arteries. The internal carotid arteries branch off into the middle cerebral arteries and the anterior cerebral arteries, while the vertebral arteries come together to form the basilar artery. The basilar artery then leads into the posterior cerebral arteries. The posterior cerebral arteries, along with the anterior cerebral arteries, internal carotids, and other smaller branched arteries form the circle of Willis. The circle of Willis is a group of arteries arranged in a circle that allows for collateral blood flow, meaning blood can circulate from one side of the brain to the other if a blockage occurs.  

Okay, so with ischemic strokes, blood flow is disrupted by obstruction from a thrombus or embolus. A thrombus is a clot that forms within a vessel, whereas an embolus is when a clot breaks off from one area and travels downstream, lodging in a smaller vessel.  

For example, a thrombus can occur from atherosclerotic plaque, where fats build up within a vessel supplying blood to the brain; and an embolus can occur from a blood clot in the atria of the heart due to atrial fibrillation that makes its way into cerebral circulation.  

Risk factors for ischemic strokes include hypertension, hyperlipidemia, increased age, heart disease, and sleep apnea. There is also an increased risk with smoking, oral con]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Age-related_Physiologic_Changes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-Thm5U9rSO6geFpP0Ghm72zESM6ceyeT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Age-related Physiologic Changes]]></video:title><video:description><![CDATA[Over time, the body gradually goes through normal age-related physiologic changes. As the nurse, you’ll recognize how these changes impact the body systems in older adults and consider conditions that can develop as a result.  

Starting with age-related changes of the cardiovascular system, the heart’s muscle loses tone and becomes stiffer. To compensate, muscle mass increases, but is a less effective pump. This decreases cardiac output and increases the risk of heart failure. The heart valves become thicker and calcified, which can lead to valve disease and murmurs. Additionally, the conduction system, including the sinoatrial node, known as the pacemaker of the heart, loses cells, decreasing heart rate and increasing risk for arrythmias.  

Also, blood vessels become stiffer, decreasing venous return from the periphery and contributing to dependent edema and varicosities; and the build-up of atherosclerotic plaque within the vessels can lead to coronary artery disease, peripheral artery disease, and hypertension.  

Lastly, an impaired baroreflex, which helps maintain blood pressure by adjusting heart rate, cardiac output, and peripheral vascular resistance during position changes, can result in orthostatic hypotension and an increased risk of falls.  

Okay, moving on to changes to the respiratory system. There are certain age-related changes that increase the risk of respiratory infections like pneumonia and influenza. These include fewer cilia, that trap and remove inhaled microbes and debris; fewer pulmonary macrophages, which are the first line of defense against inhaled pathogens; and a decreased cough reflex, which is needed to help expel inhaled pathogens and clear secretions.  

Other changes include thoracic muscle weakness and calcifications of rib cartilage, which can limit lung expansion, increase the work of breathing, and decrease the ability to take deep breaths. Lastly, loss of alveolar elasticity, decreased alveolar surface area, and f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Osteoarthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nAV4kOQTSMW-eyF8TnyJv3IKTbaFESD5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Osteoarthritis]]></video:title><video:description><![CDATA[Nurse Mary works at a family practice clinic and is caring for Ryker, a 70-year-old male with a history of osteoarthritis who presents to the office for worsening bilateral knee pain. In collaboration with the registered nurse, RN Ron, Nurse Mary goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ryker’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Mary recognizes important cues, including Ryker’s vital signs, which are temperature 97.2 F or 36.2 C, heart rate 98 beats per minute, respirations 22 breaths per minute, blood pressure 115/74 mmHg, and oxygen saturation 98 percent on room air. He currently rates his pain as 6 on a 0 to 10 numeric scale. 

Nurse Mary notes RN Ron’s assessment revealed Ryker has swelling, tenderness to palpation, and a decreased range of motion, or ROM, in both of his knees.  

Nurse Mary: I noticed you had quite a bit of pain when RN Ron touched your knees. Can you tell me more about your knee pain?  

Ryker: I used to really enjoy taking walks several times a day, but over the last few years my knees have felt so stiff when I wake up, and they hurt so much when I&amp;#39;m walking. So, I haven’t been walking much. It just keeps getting worse. I’ve been gaining a bit of weight too since I haven’t been walking as much as I used to. 

Nurse Mary: Is there anything that makes the pain feel better? 

Ryker: Usually sitting down and resting makes the pain go away. I try acetaminophen sometimes which helps a little, I guess. 

Next, Nurse Mary analyzes these cues. She reviews the electronic health record, or EHR, and notes Ryker’s BMI is calculated as 31 kg/m2 and that before retiring, he was a firefighter for many years.   

Nurse Mary knows that osteoarthritis is a degenerative disease that occurs when there’s a gradual destruction of the cartilage that covers the end of each bone found i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skeletal_Trauma</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r4lmX1dMRaGybh_tcgCvR-9CSDmCJnZ-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skeletal Trauma]]></video:title><video:description><![CDATA[Skeletal trauma occurs when there’s an injury to the bones or joints. Common conditions include fracture, which is a complete or incomplete break in the bone; subluxation, when there’s partial separation of a bone from a joint; and dislocation, when there’s a complete separation of a bone from the joint. 

Within the skeletal system, bones and joints work together with other tissues to provide structure, support, protection for internal organs, and to facilitate body movement. In addition to these functions, bones are metabolically active tissues that are involved in key functions in the body. First, long bones, such as the humerus or the tibia, contain marrow, the site where hematopoiesis occurs, which is the production of red blood cells, white blood cells, and platelets.  

Bones also serve as a reservoir for calcium and phosphate and play a key role in calcium homeostasis. Lastly, bones are continually involved in remodeling, which involves bone resorption, formation of new bone, and bone repair. This is accomplished through cells called osteoclasts, which break down old bone for reabsorption, and osteoblasts, which lay down new bone to replace the bone that was resorbed. This continual remodeling helps maintain the health and functionality of bones. 

The basic types of bone are cortical, or compact bone, which is found in the outer layer of bones; and cancellous, or spongy bone, which is found in the interior of bones. The structure of cortical bone helps it to tolerate compression and shearing forces, while cancellous bone is better equipped to absorb and distribute stress throughout the bone. 

Now, joints are the place where two or more bones come together, and they provide varying degrees of range of motion. For example, fibrous joints, like those between the bones of the skull, barely move at all; whereas, synovial joints, like those of the shoulders and hips, move more freely. Joints are supported by cartilage, ligaments, and tendons, which hel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acid-base_Imbalance</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3SsHd746Stye7llYAcjR_MQrSzy4uZfd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acid-base Imbalance]]></video:title><video:description><![CDATA[An acid-base imbalance occurs when the body fails to maintain the narrow balance between acids and bases. This imbalance can impair essential metabolic processes like functioning of enzymes, oxygen transport, and removal of waste products. 

Okay, so, the measurement of acids and bases is called the pH. On the pH scale, 7.0 is considered neutral; levels above 7.0 are alkalotic, or basic; and levels below 7.0 are acidotic. The normal range for pH in the blood  for adults is 7.35 to 7.45. 

The main molecules involved in acid-base balance are hydrogen bicarbonate, Partial pressure of carbon dioxide, and partial pressure of oxygen. hydrogen has an inverse relationship with the pH of body fluids. So, when there’s more hydrogen, the pH decreases and becomes more acidic; whereas when there’s less hydrogen, the pH increases.  

Next, bicarbonate is a basic substance; so, when there’s more bicarbonate the pH increases, and body fluids become more alkalotic. Likewise, when there’s less bicarbonate the pH decreases, and body fluids become more acidotic.  

Then there’s partial pressure of carbon dioxide which reflects the amount of acidic carbon dioxide dissolved in the arterial blood; and partial pressure of oxygen which reflects the amount of oxygen dissolved in the arterial blood.  

Now, acid-base balance is regulated by various mechanisms in the body.  

The cellular buffering system, located in the extra- and intracellular fluid compartments, is able to rapidly absorb excessive acidic and basic ions to minimize pH fluctuations.  

Also, the respiratory system controls pH through adjusting carbon dioxide amounts by changing the rate and depth of breathing; and the renal system manages the amount of excreted and reabsorbed bicarbonate by the kidneys.  

Alright, now, acid-base imbalances occur when the pH is outside the normal range.  

These imbalances are categorized as either acidotic or alkalotic, depending on the pH level, and metabolic or respiratory, depe]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/The_Inflammatory_Response</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r4mTGF3dRwCpZKr7vizuwvzLRJuiV6b4/_.jpg</video:thumbnail_loc><video:title><![CDATA[The Inflammatory Response]]></video:title><video:description><![CDATA[The inflammatory response, also just called inflammation, is the immune system’s non-specific, immediate response to tissue injury. Its effects are aimed at neutralizing the cause of tissue injury, removing debris, and creating an environment for healing and repair. 

Now, inflammation is a response to injury of vascularized tissue, which is any tissue that has a blood supply. Tissue injury can be related to pathogens such as bacteria, viruses, or fungi; physical injuries, like cuts, burns, and sprains; and environmental exposures, such as contact with allergens or toxins, or exposure to extremes of temperatures. Other factors can include tissue ischemia, like from a myocardial infarction or stroke.  

Inflammation begins when immune cells, like monocytes, macrophages, and dendritic cells, respond to tissue injury. The macrophages begin to phagocytize, or eat up, any invading pathogens, cellular debris, or foreign substances that are present.  

Meanwhile, molecules expressed by infectious agents, called pathogen-associated molecular patterns, or PAMPs, and molecules released by damaged and dying cells, called damage-associated molecular patterns, or DAMPs, are detected by special receptors on the immune cells, called pattern recognition receptors, or PRRs. When the PRRs bind to PAMPs or DAMPs, immune cells respond rapidly by releasing inflammatory mediators like histamine, prostaglandins, and leukotrienes. These chemical mediators initiate the inflammatory response that involves both a vascular response and a cellular response.  

The vascular response begins when nerve endings at the site of injury cause transient vasoconstriction, followed by the effects of inflammatory mediators as they act on the endothelial cells of the nearby capillaries, arterioles, and venules. These effects include local vasodilation and increased vascular permeability, which is where the endothelial cells separate from each other. Vasodilation brings additional blood flow to the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_Heart_Defects</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Z3sEy9QTTHeJcKW4WNNZ5iTRR4WuP91K/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital Heart Defects]]></video:title><video:description><![CDATA[Congenital heart defects, also sometimes called congenital heart disease, are a group of conditions involving structural abnormalities of the heart, great vessels, or both. They can be cyanotic or acyanotic based on the presence or absence of cyanosis, which is a blue discoloration of the skin and mucous membranes. 

As a quick review, during gestation, the fetal lungs are fluid-filled and have high vascular resistance, so they don’t participate in gas exchange. Instead, blood is shunted away from the lungs, and the fetus receives oxygenated blood from the placenta, where gas exchange occurs and metabolic wastes are removed.  

Now, the high vascular resistance in the lungs also causes the pressure in the right side of the heart to be much higher than the left side, so, as oxygenated blood enters the right atrium, most of the blood is shunted into the left atrium through the foramen ovale, an opening between the right and left atria. Blood then moves into the left ventricle where it’s pumped through the aortic valve, into the aorta, and out to the fetal body. Now, some blood from the right atrium passes into the right ventricle, through the pulmonary valve and into the pulmonary artery, heading for the lungs. But before it can get to the lungs, the blood is shunted through the ductus arteriosus, a vessel connecting the pulmonary artery to the aorta. The aorta then sends the blood out to the fetal body.  

Following birth, the foramen ovale and ductus arteriosus close. The pressure on the left side of the heart increases and pressure on the right side of the heart decreases as pulmonary vascular resistance lessens, and the lungs begin to participate in gas exchange. Deoxygenated blood now moves from the right side of the heart to the lungs for oxygenation and returns to the left side of the heart before being pumped to the rest of the body. 

Congenital heart defects don’t have a single cause, but there are several risk factors that can interfere with ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Strategies_for_Effective_Communication_with_Older_Adults</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wn7e0rkfT1Kcr-N6GwuivvhmRoa49pxR/_.jpg</video:thumbnail_loc><video:title><![CDATA[Strategies for Effective Communication with Older Adults]]></video:title><video:description><![CDATA[Using effective communication when caring for older adults can help inform assessments, plan care, develop the nurse-patient relationship, and even improve health outcomes. As the nurse, you’ll consider barriers to communication and implement strategies to promote effective communication for individuals and groups of older adults. 

Alright, now there are certain barriers to effective communication with older adults to keep in mind. One barrier is ageism, which involves stereotyping and discriminating against individuals based on their age. Ageism can lead to poor health outcomes, like cognitive and functional decline. Elderspeak is a type of ageism which refers to condescending speech patterns used when communicating with older adults. Common instances of elderspeak include using pet names such as “honey” or “sweetie”; substituting collective pronouns such as “we,” like saying, “We are going to eat dinner now”; and speaking to the patient’s family or caregiver rather than the patient.  

As the nurse, you can implement strategies to promote effective communication with your older adult patient. These include using open-ended questions, allowing for additional response time, and encouraging storytelling. 

Open-ended questions like, “What do you know about your family history?” can help you gather information but may cause some patients to verbalize what they assume you want to hear rather than how they truly want to answer. So, when asking open-ended questions, remember to seek validation of what you hear so you can clearly understand what your patient is telling you.  

Now, keep in mind that word retrieval can slow as individuals age. You can provide your patient with the opportunity to answer your questions fully by practicing patience, speaking slower to allow time for them to process what’s being said, and giving them additional time to respond.  

Lastly, storytelling can allow your patient the opportunity to share their memories and life experience]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pain_Management_and_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/33R1PQsBTVame_eWP9GOnEn0T-ODgJ9R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pain Management and the Older Adult]]></video:title><video:description><![CDATA[Pain is an unpleasant physical or emotional experience that occurs in response to actual or potential tissue damage, and is shaped by physical, emotional, and cultural components unique to everyone. Due to higher prevalence of acute and chronic health conditions, older adults are at increased risk of experiencing pain that’s often left underrecognized and undertreated.  

As the nurse, you’ll recognize age-related changes to pain perception and the consequences of untreated pain; identify barriers to effective pain management; and provide patient-centered care for older adults experiencing pain. 

Alright, so as one ages, a decreased density of nerve fibers can delay the transmission of pain signals from the origin site to the brain. This delayed transmission increases the risk of injury since it takes longer for the brain to perceive pain. For example, it might take an older adult more time to realize their hand is on a hot surface, increasing the risk of burns. Also, pain sensation resolves more slowly with age, meaning many older adults must tolerate pain for longer.  

Now, a common myth is that older adults feel less pain than younger adults, which is not only untrue, but it can lead to undertreatment of pain and poor health outcomes. Physical consequences of inadequately treated pain include impaired mobility, resulting in decreased muscle strength, increased fall risk, and poor sleep and appetite; and delayed healing and rehabilitation, leading to increased healthcare visits and costs.  

Other consequences include a significant impact on quality of life and mental health, contributing to new or worsening depression, anxiety, or social isolation, which can increase the risk of substance use and even impair cognition over time.  

Okay, so there are several barriers to effectively identifying and managing pain in older adults. Some of the most common barriers can stem from the patient or the healthcare team.  

Now, a patient’s personal beliefs, valu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congestive_Heart_Failure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DMvk0I53SdGVPlgTLQmuaZH5SyO9I7ME/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congestive Heart Failure]]></video:title><video:description><![CDATA[Heart failure, sometimes also called congestive heart failure, is a condition that occurs when the heart can’t pump enough blood to meet the body’s demands. Heart failure can be either systolic or diastolic, and it can affect the right, left, or both sides of the heart. In systolic heart failure, the heart is unable to effectively contract to push blood out of the ventricles; whereas with diastolic failure, the ventricles become stiff and unable to relax between beats, so they can’t fill with blood properly. 

Now, the heart acts as a pump to move deoxygenated blood through the right side of the heart, to the lungs for oxygenation, back to the left side of the heart, and then out to the body. Each beat of the heart has two phases: systole and diastole. Systole is when the heart is contracting and pumping blood, and diastole is when the heart is relaxed and filling with blood.  

The amount of blood pumped by the heart in one minute is called cardiac output, and it’s an important indicator of heart function. Cardiac output is determined by four factors: contractility, preload, afterload, and heart rate.  

Contractility is the heart’s ability to contract and eject blood during systole, which enhances the force of contraction during systole. Preload is the amount of stretch in the ventricles at the end of diastole as the ventricles fill with blood. In general, the more the preload, the stronger the contraction. On the other hand, afterload is the resistance the ventricles must push against during systole. Less afterload can decrease workload on the heart. Lastly, heart rate is the number of times the heart beats per minute. 

Okay so, cardiac output is calculated by multiplying the heart rate by stroke volume, which is the amount of blood pumped by the heart during systole. Now, the amount of blood within the ventricles at the end of diastole is called the end-diastolic volume; and the stroke volume is just a portion of the end-diastolic volume. Similarly, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cancer_of_the_Prostate</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XtPzxLksT8qO3WJ179WtVeOZTDCmHO7O/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cancer of the Prostate]]></video:title><video:description><![CDATA[Prostate cancer is a malignant growth that originates in the prostate gland.  

The prostate is a small walnut-shaped gland that sits under the bladder, in front of the rectum. It secretes an alkaline milky liquid, called prostatic fluid, which contains nutrients to nourish the sperm, support its movement, and help it survive in the acidic environment of the vagina.  

Now, the urethra travels through the prostate before reaching the penis. During ejaculation, smooth muscles in the prostate contract and push prostatic fluid into the urethra where it joins the sperm, along with the semen. 

The prostate can be divided into distinct zones based on their histological differences, including the peripheral, central, transitional, and fibromuscular zones. The peripheral zone is the outermost posterior section and is the largest of the zones, containing most of the prostate’s glandular tissue. It’s also the most common site for development of prostate cancers and is the part of the prostate that’s palpated during a prostate exam, called a digital rectal examination or DRE.  

Moving inward, there’s the central zone, followed by the transitional zone, the site that undergoes hyperplasia in a condition called benign prostatic hyperplasia, which is considered a normal part of aging. Part of the transitional zone that surrounds the urethra is sometimes called the periurethral gland region. Lastly, a fibromuscular zone covers the anterior portion of the prostate. 

Okay, so, the development and normal function of prostate cells depend on androgens, or sex hormones, like testosterone. Although most of the body’s testosterone is produced by the testes, a portion of testosterone is made in the prostate. In the prostate, testosterone is converted by the enzyme 5α-reductase into highly potent dihydrotestosterone, or DHT, which happens when dehydroepiandrosterone, or DHEA, produced by the adrenal glands enters the prostate and is converted into testosterone.  

Now, al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parkinson_Disease_(PD)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nD4LBm_pQLyXdn7UtKL30SDQRGmFLehg/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parkinson Disease (PD)]]></video:title><video:description><![CDATA[Parkinson disease, or PD, is a progressive neurodegenerative disorder that primarily impacts movement and results from loss of dopamine-producing neurons in the brain.  

Now, motor activity is regulated by complex neural circuits within the brain. One of the main structures responsible for motor activity is the basal ganglia, also called the basal nuclei, located deep within the cerebral hemispheres of the brain.  

The basal ganglia are a group of interconnected structures that are mainly involved in the planning, execution, and termination of motor activity through their connection with other parts of the brain. These include the thalamus, which serves as a major relay station in the brain, and cerebral cortex, which is responsible for many of the brain’s higher functions like reasoning and problem-solving and which also contains the motor cortex.  

One important part of the basal ganglia is called the substantia nigra. This structure contains dopaminergic neurons that produce dopamine, a neurotransmitter involved in motor function and the fine-tuning of movements. Dopamine also inhibits the excitatory effects of neurotransmitters produced in other parts of the basal ganglia, like acetylcholine. 

In addition to its key role in motor activity, the basal ganglia are also involved in coordinating cognitive, behavioral, and emotional functions through connections to the limbic system, which like the basal ganglia, is a group of interconnected structures. The limbic system is sometimes called the emotional brain due to its role in regulating emotions and behavior. 

Okay, so PD is classified as primary, or idiopathic, and secondary, or acquired. Although there’s no known cause for most cases of primary PD, the incidence increases with age.  

Other cases are related to familial or genetic factors, including those associated with the formation of Lewy bodies, which are aggregations of dysfunctional proteins in the brain, called alpha-synuclein, that play a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Overview_of_Childhood_Cancer_-_Etiology_and_Prognosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/KdjmPhnkSl_wOPoT0htc0lSGQNGjUWtK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Overview of Childhood Cancer - Etiology and Prognosis]]></video:title><video:description><![CDATA[Childhood cancer is a collection of conditions occurring in children and adolescents that are characterized by abnormal cells that divide and grow uncontrollably. 

Now, the cause of childhood cancer is multifactorial, meaning a child’s unique genetic factors and environmental factors interact to promote the development of cancer. Even so, these factors are often not known at the time of diagnosis, so in many cases the exact cause of cancer in children is unknown. 

Genetic factors involved in cancer can be mutations that are either inherited or acquired. These include mutations that typically occur in genes that regulate cell division, including proto-oncogenes, which promote cell division, or tumor suppressor genes, that inhibit uncontrolled cell division.  

For example, mutations to the MYCN proto-oncogene can predispose children to neuroblastoma and glioblastoma, both cancers of the nervous system. On the other hand, mutations to the RB1 tumor suppressor gene are associated with retinoblastoma, a type of cancer in the light-sensing layer of cells in the back of the eye called the retina. This mutation can be spontaneous, or it can be a familial cancer resulting from a germline mutation, meaning the mutation occurred in a reproductive cell, either the sperm or egg, so it becomes part of the DNA of each of the body’s cells.  

Other genetic changes such as chromosomal translocations, where pieces of two chromosomes split off and swap places, like with the Philadelphia chromosome, are also associated with an increased risk of leukemia, a cancer of blood-forming tissues that disrupts the normal function of bone marrow.  

Leukemia can also occur in children born with certain congenital conditions like Down syndrome, or trisomy 21, a condition where there’s an extra copy of chromosome 21. 

Environmental risk factors can include exposure to carcinogens, or substances that can promote the development of cancer, like tobacco smoke and certain chemicals and m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adaptive_Immunity</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lDJbit49R2S-0YUc3-Wf7QqMR02OysuF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adaptive Immunity]]></video:title><video:description><![CDATA[Adaptive immunity is part of the immune system that can provide long-lasting immunity. It’s sometimes called acquired immunity because it’s not present at birth and develops over time. 

Now, adaptive immunity has certain characteristics that sets it apart from the innate, or the general, immune defense an individual is born with, including that it’s inducible, specific, systemic, long-lived, and it has an immunologic memory.  

So, inducible and specific mean that adaptive immunity is not always actively present, but instead, it&amp;#39;s explicitly developed against a particular antigen, which are molecules found on the surfaces of microorganisms and abnormal cells that trigger an immune response.  

Next, systemic means that immune cells can mount an attack throughout the body.  

Finally, adaptive immunity is long-lived and has an immunologic memory, meaning certain immune cells called memory cells, linger in the body, so the next time the body is exposed to this same pathogen, it can mount a faster and stronger response.   

The main components of adaptive immunity include lymphocytes, or white blood cells, and antibodies. The most prominent lymphocytes in the adaptive immune system are T lymphocytes, or T cells, and B lymphocytes, or B cells. These cells interact with other components of the immune system, such as dendritic cells, natural killer cells, and macrophages. Antibodies, also called immunoglobulins, are glycoproteins that assist in fighting infections. 

Now, the main mechanisms of adaptive immunity are induction, cell-mediated immunity, humoral immunity, and immunologic memory. 

Induction involves the activation of the adaptive immune system in response to an antigen, and the process differs between B and T cells.  

The first step in T cell induction is when certain cells, most often macrophages and dendritic cells, serve as antigen-presenting cells, or APCs, because they identify, process, and present antigens to a T cell, which is cal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypersensitivity_Reactions</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/YO4D6YYXQxu-yLxf_ZjL4KmlQmSb9RG4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypersensitivity Reactions]]></video:title><video:description><![CDATA[Hypersensitivity reactions are immune responses that are excessive or have undesirable effects like disease or damage to the body. They are categorized as type I, II, III, or IV based on the immune response and its effect. 

Type I hypersensitivity reactions, also called immediate hypersensitivity reactions or IgE-mediated reactions, occur in response to normally harmless triggers, like pollen, bee stings, or medications.  

Type I hypersensitivity reactions occur in two steps which involve a primary exposure, called sensitization, and a subsequent exposure, when the inflammatory reaction occurs.  

First, the immune system is exposed to an antigen, or allergen.  

Next, antigen-presenting cells, called APCs, present the allergen to T cells which then become helper T-cells, or Th2 cells. The Th2 cells then release large amounts of cytokines that signal B cells to proliferate and turn into plasma cells that start producing IgE antibodies, which bind to mast cells, sensitizing them.  

Then, during subsequent exposure, the antigen forms crosslinks on the IgE antibodies on the mast cell membrane, causing mast cell degranulation and release of proinflammatory mediators like histamine, resulting in an acute inflammatory reaction.  

Because this is an immediate hypersensitivity reaction, clinical manifestations typically occur within 15 to 30 minutes of subsequent exposure to the antigen.  

Manifestations can include rhinitis, characterized by sneezing and nasal congestion; hives, along with rash, redness, and itching; angioedema, where swelling occurs in the deep layers of skin; bronchospasm, which is a tightening of the bronchial smooth muscle; and even systemic reactions like anaphylaxis, characterized by difficulty breathing, hypotension, and death if left untreated.   

Next, type II hypersensitivity reactions, also called tissue-specific or cytotoxic reactions, are mediated by IgG or IgM antibodies against target antigens on a specific tissue or cell.  
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Burn_Injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LUQPmq9QSMe7Zzf87wvBGom-RcuqGNs4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Burn Injury]]></video:title><video:description><![CDATA[Burns are injuries that occur when the skin and underlying tissues are damaged from exposure to heat, chemicals, electricity, or radiation. Burns can cause localized damage or have widespread effects that can impact multiple organs in the body.  

Okay, the skin is the largest organ in the body and provides important body functions like helping regulate body temperature, preventing loss of body fluids, and protecting against microorganisms, radiation, and mechanical stress.  

Now, the skin is comprised of two main layers, the epidermis and dermis, that rest upon the hypodermis, that’s sometimes considered a third layer of the skin. The epidermis, or the outermost layer, is composed of multiple layers of keratinocytes, that synthesize keratin, a protein that forms a tough, waterproof barrier to shield underlying structures from mechanical stress. The epidermis also contains melanocytes, which produce melanin, a pigment that helps protect the skin from ultraviolet radiation.  

The next layer is the dermis, which contains structures like hair follicles, nerves, sensory receptors, and sweat glands. This layer also contains macrophages and mast cells that aid in immune function. Lastly, the hypodermis is the subcutaneous layer, made up of fat and connective tissue that insulates deeper tissues and anchors the skin to the underlying muscle. 

Now, burn injuries can be classified as thermal or non-thermal. Thermal burns result from direct contact with a hot object, open flame, hot liquid, or steam. Other causes of thermal burns include electrical shock and friction. On the other hand, non-thermal burns come from a source other than heat. For example, chemical burns occur from exposure to strong acids, alkalis, or solvents, either by direct contact with the skin, inhalation into the respiratory tract, or ingestion into the GI tract. Non-thermal burns can also be caused by ultraviolet light and radioactive sources. 

Most burns occur in the home; and individuals ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Arthritis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SiLhwMj6Snad6wJak3oTyf8HTDGpFw_N/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Osteoarthritis: Nursing]]></video:title><video:description><![CDATA[Nurse Mary works at a family practice clinic and is caring for Ryker, a 70-year-old male with a history osteoarthritis who presents to the office for worsening bilateral knee pain. After settling Ryker in the room, Nurse Mary goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ryker’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Mary recognizes important cues, including Ryker’s vital signs, which are temperature 97.2 F or 36.2 C, heart rate 98 beats per minute, respirations 22 breaths per minute, blood pressure 115/74 mmHg, and oxygen saturation 98 percent on room air. He currently rates his pain as 6 on a 0 to 10 numeric scale. 

Upon physical assessment, Nurse Mary notes Ryker has swelling, tenderness to palpation, and a decreased range of motion, or ROM, in both of his knees.  

Nurse Mary: I noticed you had quite a bit of pain when I touched your knees. Can you tell me more about your knee pain?  

Ryker: I used to really enjoy taking walks several times a day,  

but over the last few years my knees feel so stiff when I wake up,  

and they hurt so much when I&amp;#39;m walking.  

So, I haven’t been walking much. It just keeps getting worse.  

I’ve been gaining a bit of weight too since I haven’t been walking as much as I used to. 

Nurse Mary: Does anything make the pain feel better? 

Ryker: Usually sitting down and resting makes the pain go away. I try acetaminophen sometimes which helps a little, I guess. 

Next, Nurse Mary analyzes these cues. She reviews the electronic health record, or EHR, and notes Ryker’s BMI is calculated as 31 kg/m2 and that before retiring, he was a firefighter for many years.   

Nurse Mary knows that osteoarthritis is a degenerative disease that occurs when there’s a gradual destruction of cartilage that covers the end of each bone found in most joints, like the knees.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Type_2_Diabetes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nYrLl1CuRJ6UYmhW_ksWTwi0S_OwhMeI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Type 2 Diabetes]]></video:title><video:description><![CDATA[Nurse Harvey works in a primary care office and is caring for Maru, a 69-year-old female who presents for a well-care visit. In collaboration with the registered nurse, RN Pam, Nurse Harvey goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Maru’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Harvey recognizes important cues, including Maru’s vital signs, which are temperature 98.9° F, or 37.2° C, heart rate 71 beats per minute, respirations 16 breaths per minute, blood pressure 108/62 mmHg, and oxygen saturation 99% on room air. She also rates her pain as 0 on a 0 to 10 numeric scale.  

Nurse Harvey also notices Maru has used the restroom twice while waiting and she reports she’s been thirstier lately.  

Next, Nurse Harvey analyzes these cues. He reviews the electronic health record, or EHR, and notes that Maru has been seen and treated for recurrent vaginal yeast infections three times in the past couple months. He also notes Maru’s routine lab work shows a fasting glucose of 155 mg/dL or 8.6 mmol/L and her hemoglobin A1C was 7%.  

Nurse Harvey suspects Maru is experiencing the effects of an elevated blood glucose level, which could be caused by diabetes mellitus. He knows that diabetes mellitus is a metabolic condition where there’s insufficient insulin to move glucose from the blood into cells for energy.  

He knows that as people age, insulin production decreases and insulin resistance increases, placing them at risk for diabetes. With insufficient insulin and increased insulin resistance, blood glucose levels increase, leading to a hyperosmolar state.  

This hyperosmolar state pulls water from cells into the blood vessels where it’s then removed through urination. This causes polyuria, or frequent urination.  

Lastly, Nurse Harvey knows that diabetes can increase the risk for certain infections because]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cancer_of_the_Breast</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/o0u-x5JlTxCtTKil2ZcgP3CDQT_oqSdi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cancer of the Breast]]></video:title><video:description><![CDATA[Breast cancer is the uncontrolled growth of abnormal cells in the breast tissue that can spread to other parts of the body.  

Okay, so, breasts, also called mammary glands, are milk-producing glands that sit on the chest wall on top of the ribs and the pectoral muscles, made up of glandular, adipose, and connective tissue.  

The glandular tissue makes the milk during lactation and is made up of 15 to 20 lobes that surround the nipple in a radial pattern, and each lobe contains many smaller lobules. Inside each of these lobes are grape-like structures called the alveoli containing secretory epithelial cells that produce milk during lactation and myoepithelial cells that contract to move milk from the alveoli.  

The alveoli, lobules, and lobes are connected through a network of ducts called the lactiferous ducts that drain the milk produced during lactation. Surrounding the glandular tissue is the stroma, which contains fibrous connective tissue and adipose tissue, which makes up the majority of the breast.  

Lastly, located throughout the breasts are blood vessels, as well as lymphatic vessels that drain into the lymph nodes. For examination purposes, the breasts are divided into quadrants which include the upper outer quadrant, upper inner quadrant, lower outer quadrant, and lower inner quadrant.  

Now, breast cancer is caused by mutations to DNA within breast tissue that results in uncontrolled cellular proliferation.  

There are modifiable and non-modifiable risk factors that increase the risk of breast cancer. Modifiable risk factors include exposure to ionizing radiation that can come from medical diagnostics and treatments; postmenopausal hormone replacement therapy; alcohol consumption; exposure to certain environmental chemicals like polychlorinated biphenyls, or PCBs; obesity; and physical inactivity.  

Non-modifiable risk factors include age over 65; early menarche or late menopause; being biologically female, though biological males can al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_Mellitus_(DM)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rd83WBb7RQKeG-bXR8jRD-65Tq2PAX4h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes Mellitus (DM)]]></video:title><video:description><![CDATA[Diabetes mellitus is a group of endocrine disorders characterized by hyperglycemia, or elevated blood glucose. The two main types are type 1 diabetes, which is caused by an absolute insulin deficiency; and type 2 diabetes which is caused by insulin resistance.  

Okay, so, the pancreas is an organ located in the abdomen that plays a role in glucose regulation and digestion. Scattered throughout the pancreas are small clusters of cells, called islets of Langerhans. Among these cells are α-cells and β-cells. The α-cells secrete glucagon in response to decreasing blood glucose. Glucagon increases blood glucose by stimulating the liver to breakdown glycogen, or stored glucose, by a process called glycogenolysis.  

Conversely, β-cells secrete insulin in response to increasing blood glucose. Insulin lowers blood glucose, which also suppresses α-cell secretion of glucagon. Along with insulin, β-cells co-secrete amylin, which prevents postprandial, or post-meal, spikes in blood glucose by inhibiting gastric emptying, increasing satiety, and suppressing glucagon release. 

Now, for cells to function, they need glucose as a source of energy. However, cell membranes are impermeable to glucose; so, for glucose to get inside the cell, insulin must first bind to insulin receptors on the cell membrane. This binding activates the cell’s glucose transporters that will then facilitate the movement of glucose into the cell. 

Type 1 diabetes is most commonly caused by an autoimmune destruction of β-cells, resulting in an inability to produce insulin. In other cases, the cause is idiopathic, meaning there’s no known cause. Risk factors include exposure to certain viruses and a family history of type 1 diabetes. 

As for type 2 diabetes, the main cause is insulin resistance in the tissues, which is when cells don’t respond as easily to insulin. Risk factors include obesity, physical inactivity, and a diet high in simple carbohydrates, saturated fats, and red meat. Additionall]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cancer_of_the_Skin</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G9F-f4s-SIK3DihGUclpjHRtTZiG4vpz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Cancer of the Skin]]></video:title><video:description><![CDATA[Skin cancer is a malignant proliferation of skin cells, and includes basal cell carcinoma, squamous cell carcinoma, and melanoma. 

Okay, let&amp;#39;s actually start with a quick review, the skin is the largest organ in the body and provides important functions like protection, sensory perception, temperature regulation, and vitamin D production.  

Its two main layers, the dermis and epidermis, rest upon the hypodermis, or subcutaneous tissue, which is sometimes considered a third layer of the skin.  

The hypodermis consists mainly of adipose, or fat, tissue that provides insulation and padding, and loose connective tissue that helps anchor the skin to the underlying muscle.  

Above the hypodermis is the dermis, which is made up of connective tissue that allows the skin to contract and stretch with body movements. It also contains hair follicle roots, nerves, oil and sweat glands, immune cells, and blood and lymphatic vessels.  

The most superficial layer of the skin is the epidermis. The epidermis is composed of stratified squamous epithelial cells called keratinocytes. The epidermis is divided into five layers, or strata, consisting of these cells. The basal layer, called stratum basale, is the deepest layer. Here, stem cells called basal cells continuously divide and produce new keratinocytes.  

As these new keratinocytes are formed, they move upward, pushing older cells toward the surface. In the process, the cells gradually flatten and become keratinized, meaning they fill with a protein called keratin, a strong, waterproof protein that gives skin, hair, and nails strength.  

The basal layer also contains melanocytes.  These cells synthesize and secrete melanin, the pigment that gives rise to skin color and helps protect against UV radiation. 

The next layer, the stratum spinosum, is composed of irregularly shaped skin cells. As they move upward, they begin to flatten and form the third layer, the stratum granulosum. Here, the cells continue ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Visual_Impairment_and_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n4180kgYTq6-bV25AbLJKjK5SjSAeHZW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Visual Impairment and the Older Adult]]></video:title><video:description><![CDATA[Visual impairment is a leading cause of disability in older adults, and it can have a negative impact on safety, social interactions, mobility, and activities of daily living such as grooming and eating. As the nurse, you’ll recognize age-related vision changes and provide patient-centered care for your patient with visual impairment. 

Alright, so eye structures commonly affected by age-related changes include the eyelids, cornea, iris, lens, vitreous humor, and retina.   

The eyelids, which protect the eyes and help with tear distribution, lose elasticity and tone as an individual ages. This can cause ptosis or drooping of the eyelids. If severe, ptosis can interfere with vision by obstructing the visual field. In addition, the muscles controlling the eyelids may spasm, which can cause the eyelids to turn inward, called entropion›. This can result in scratching of the cornea by the lower lashes. Other times, the muscles can weaken, which allows the eyelids to turn outward, called ectropion. This can lead to dry eyes due to a disruption of tear distribution and an inability to fully close the eye.  

Next, the cornea, which is responsible for protecting the eye and performing the initial refraction of light onto the lens, can thicken and become less curved, losing its ability to refract light efficiently. This leads to blurry or distorted vision called astigmatism.   

The iris is a circular set of muscles that sits in front of the lens. It controls the amount of light allowed into the eye through the pupil by constricting in bright lighting to allow less light in, and dilating in low lighting to allow more light in. With age, the iris becomes less reactive, resulting in difficultly transitioning between bright and low lighting.  

The lens, found behind the iris, changes its shape to focus light onto the retina. It tends to thicken and become rigid with age. In addition, the ciliary muscles, which are responsible for changing the shape of the lens, beco]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_Bowel_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hpcuTS_tTC_p6nPLLRTrU-yvTi26TexK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory Bowel Disease]]></video:title><video:description><![CDATA[Inflammatory bowel disease, or IBD for short, is a chronic condition that causes inflammation and ulceration in the intestinal tract. The two major types of IBD are Crohn disease, or CD, and ulcerative colitis, or UC. 

Okay, so, the gastrointestinal tract is a hollow tube that includes the oral cavity, pharynx, esophagus, stomach, small and large intestines, and anus. Now, zooming in on a cross section of the intestines, we can see that the walls are typically made up of the same four layers of tissue. From the inside out, there’s the mucosa, the inner lining that consists of mucosal epithelium, connective tissue, and smooth muscle that secretes mucus and digestive enzymes. It also serves as a highly selective barrier, that absorbs nutrients and water while preventing absorption of harmful substances and bacteria.  

Moving outward, the submucosa is a dense layer of tissue that provides support and contains blood vessels, lymphatics, and nerves. Next is the muscularis, which consists of a network of nerve fibers and layers of smooth muscle that contract to move intestinal contents forward in a process called peristalsis. And finally, the outermost layer is the serosa, composed of connective tissue. It anchors the intestines in place and secretes a lubricating fluid that promotes smooth movement of the intestines within the abdominal cavity.  

Now, the exact cause of IBD is unknown; however, it’s likely that a combination of genetic, environmental, and immune factors alters the protective barrier function of the mucosal epithelium, leading to a dysregulated immune response. On top of that, the normal gut microbiome may also be altered, resulting in an increasing population of potentially pathogenic bacteria. 

Risk factors include having a family history of IBD; dietary patterns such as a diet high in processed foods; and having another autoimmune disease. Interestingly, nicotine use increases the risk and disease severity of CD, while it’s associated wit]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Sedation_Assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0zAHQeBqR9a8ZCg6qOr2dXRcQjGKGPme/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Sedation assessment: Nursing]]></video:title><video:description><![CDATA[Sedation is a pharmacologically induced state of calm, relaxation, or sleepiness that alleviates the discomfort, anxiety, and agitation that’s often experienced by patients in critical care. It can be used to ensure patient safety during invasive procedures and to improve synchrony with mechanical ventilation. 

Now, the levels of sedation include light sedation, moderate sedation, deep sedation, and general anesthesia. Light sedation is a minimal level of sedation that provides relief of anxiety. The patient’s cognitive function and physical coordination is slightly impaired, but they can respond to verbal commands, and their ventilatory and cardiovascular functions are not impacted. Light sedation is used during procedures that can make patients feel anxious, like during an MRI.  

Next is moderate sedation, also known as conscious or procedural sedation. The patient’s level of conscious awareness is reduced, though they can respond purposely to verbal commands or to a tactile stimulus, like a gentle touch to the arm or hand. Patients can usually maintain their own airway but sometimes they may require supplemental oxygen. Cardiovascular function is also usually maintained. Moderate sedation can be used for procedures like certain tube or line insertions or endoscopic procedures. 

Then there&amp;#39;s deep sedation, where the patient’s consciousness is depressed to a point where they’re not easily aroused, but they can respond to repeated or painful stimuli. Patients can’t adequately maintain their own airway, so support is needed, like through intubation and ventilation. Cardiovascular function is usually maintained. This level of sedation is common in longer or more invasive procedures, like cardiac catheterization. 

Lastly, general anesthesia is where the patient is completely unarousable. Patients can’t maintain their airway or breathing so they require full ventilatory support through intubation and ventilation. This type of sedation is used duri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Myocardial_Infarction</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y-dZQZ0ITAyQlLuEnTlFfiyxQlGhuNPp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care case study - ST elevation myocardial infarction (STEMI): Nursing]]></video:title><video:description><![CDATA[Nurse Heidi works in the emergency department, or ED, and is caring for Fritz, a 65-year-old male with a history of hyperlipidemia, who was diagnosed with an ST-segment elevation myocardial infarction, or STEMI. Nurse Heidi goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Fritz’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Heidi recognizes important cues, including Fritz’s vital signs which are temperature 98.9 º F, or 37.1 º C, heart rate 116 beats per minute, respirations 26 breaths per minute, blood pressure 104/64 mmHg, and oxygen saturation 88% on 2 liters per nasal cannula.  

Upon assessment, Nurse Heidi notes Fritz has cool, clammy, and pale skin; weak peripheral pulses; and appears restless. He reports a squeezing pain in his chest that radiates to his left arm and rates his pain as a 9 on a 0 to 10 numeric pain scale.  

Next, Nurse Heidi analyzes these cues. She reviews the electronic health record, or EHR, and notes Fritz’s ECG shows ST-segment elevation in two contiguous leads, and his serum troponin and creatine kinase-MB, or CK-MB, levels are elevated. She also notes aspirin and nitroglycerin were administered by emergency medical services, or EMS, while transporting Fritz to the ED.  

Nurse Heidi knows that a myocardial infarction, or MI, occurs when a coronary artery is blocked, reducing blood flow to the myocardium, or heart muscle. She also knows that hyperlipidemia is a major risk factor for an MI because it contributes to atherosclerosis, where plaque builds up in the arteries causing a blockage.  

Nurse Heidi recognizes that a STEMI is a type of MI, where one of the coronary arteries is completely blocked, and the ECG shows there’s an elevation of the ST-segment in at least two contiguous leads. 

Nurse Heidi understands that as blood flow to the myocardium is reduced, the myocardial cells are]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kidney_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZROduqabRTKt7FJuRZMAZgfcTtyjrEY5/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kidney Disease]]></video:title><video:description><![CDATA[Kidney disease occurs when kidney function declines, disrupting the regulation of fluids, electrolytes, waste products, and acid-base balance. Acute kidney injury, or AKI, is a sudden decline in kidney function that’s typically reversible, whereas chronic kidney disease, or CKD, is kidney damage that is gradual and irreversible. 

Now, the kidneys are the body’s natural blood filter. They regulate what’s in the blood, clearing it of metabolic waste and toxins and excreting them through urine. They’re essential in regulating fluids and electrolytes; maintaining acid-base balance; secreting hormones essential for regulating blood pressure and stimulating the production of red blood cells; and activating vitamin D. 

Within each kidney, there are millions of tiny functional units called nephrons, which consist of a renal corpuscle and renal tubules. The renal corpuscle is where blood filtration occurs, and it includes a tiny bundle of capillaries called the glomerulus, and the glomerular capsule, or Bowman’s capsule, which is a cup-shaped structure that surrounds the glomerulus. 

As blood flows through the glomerulus, an ultrafiltrate of blood is created, which is then collected by Bowman’s capsule. Then, as it moves into the renal tubules, the filtrate is modified according to the body’s needs and urine is produced, in which waste is eliminated. The rate at which filtration takes place is called glomerular filtration rate, or GFR for short, and it’s one of the main measures of kidney function.  

Now, there are three different mechanisms that can cause kidney injury. First, prerenal kidney injury can occur when there’s decreased blood flow to the kidneys like from dehydration, hemorrhage, or shock. In certain individuals, medications like non-steroidal anti-inflammatory drugs, or NSAIDs; angiotensin-converting enzyme, or ACE, inhibitors; or angiotensin receptor blockers, or ARBs, can also cause prerenal kidney injury by altering the normal autoregulation of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obstructive_vs_Restrictive_Pulmonary_Disease</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ucIbE85yRcS7h8dSWCUaakSMRxyJkj6h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obstructive vs Restrictive Pulmonary Disease]]></video:title><video:description><![CDATA[Obstructive and restrictive lung diseases are groups of conditions affecting ventilation, which is the mechanical movement of inhalation and exhalation that moves air in and out of the lungs so gas exchange can occur. Obstructive lung diseases are characterized by obstruction of exhalation, causing air to be trapped within the lungs; whereas restrictive lung diseases restrict inhalation, preventing the lungs from filling with adequate amounts of oxygen-rich air. 

So, the primary role of the lungs is facilitating gas exchange between the external environment and the circulatory system, and a key step in this process is ventilation.  

During the inhalation phase of ventilation, the respiratory muscles, primarily the diaphragm and the external intercostal muscles, contract. The diaphragm moves downward and flattens, while external intercostal muscles cause the rib cage to expand, increasing the volume of the chest cavity. This creates pressure in the lungs that’s lower than atmospheric pressure, allowing oxygen-rich air to move in and fill the lungs.  

Then, during exhalation, the respiratory muscles relax, and the lungs return to their resting state. This creates pressure in the lungs that’s higher than the atmospheric pressure, allowing air to move out of the lungs. 

Now, there are some crucial factors that support the process of ventilation.  

First, there’s the ability of the lungs to expand and fill during inhalation, which is called compliance. Lung compliance is determined by other factors like the presence of elastin fibers within the lung tissue and the ability of the chest wall to expand and contract during ventilation.  

Compliance is also dependent on the surface tension within the alveoli, which are the tiny sacks where gas exchange happens. The alveoli are lined with a thin film of water which creates a force, called surface tension, that tends to collapse the alveoli.  

To counteract this, certain cells within the alveolar walls, called ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Falls_and_Fall_Risk_Prevention</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5LhYW1rETImEprc8Kv9_53htTKGEtJ4j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Falls and Fall Risk Prevention]]></video:title><video:description><![CDATA[A fall occurs when an individual unexpectedly drops from a higher surface to a lower surface, like from a standing position to the floor. Falls can occur in healthcare facilities, the community, or in an individual’s home and are one of the leading causes of injuries and death in older adults. As the nurse, you’ll identify factors impacting fall risk, consider the consequences of falling, and provide patient-centered care to prevent falls.  

Now, typically falls don’t occur for a single reason, but rather from a combination of risk factors which can be intrinsic or extrinsic. Intrinsic risk factors are specific to the individual, such as age-related changes. These include impaired sensory input from both vision and hearing, which can blunt the subtle visual and auditory cues that help an individual keep their balance and walk safely.  

Moreover, cardiovascular changes, like decreased arterial elasticity, can cause blood pressure instability during position changes. This can result in lightheadedness and neuromuscular changes, such as slowed reaction time and joint instability, which can make it more difficult to regain stability after losing balance. Other intrinsic risk factors include cognitive impairment, unsteady gait, chronic conditions like arthritis, and certain medications like beta blockers. 

On the other hand, extrinsic risk factors are associated with the individual’s environment, like poor lighting; presence of hazards such as throw rugs or standing water; and lack of safety devices like grab bars in the bathroom. In healthcare settings, factors like staff shortages or lack of a toileting schedule may increase the risk for falls since patients are more likely to attempt to get up without assistance. 

Okay so, once a fall occurs, the likelihood of falling again increases. Also, keep in mind that not all falls result in injuries; however, older adults who fall are at greater risk of sustaining injuries that can range from a bruise or a scrape]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caregivers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Zj02_sKgR52cQ1gcvv3O6aZ7RqyCAHLD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caregivers]]></video:title><video:description><![CDATA[Caregivers are individuals who assist others unable to fully care for themselves. Caregivers can be formal, meaning they’re hired and paid to provide care, like a home health nurse; or informal, where care is provided voluntarily by loved ones, such as spouses, grandparents, or friends. As the nurse, you’ll provide support and offer strategies to help reduce stress in informal caregivers. 

Caregiving can be a source of joy and fulfillment, while at the same time, it can be a source of physical, mental, and financial stress. Physical problems include poor sleep, physical strain, immunocompromise, and even higher mortality rates. Additionally, caregivers with existing chronic health problems may find their condition worsens; and some may even develop cognitive decline.  

Mental health conditions related to caregiver stress include depression, anxiety, increased alcohol use, and feelings of being overwhelmed, upset, or confined. If mental stress is left untreated, it can increase the risk for abuse or neglect by the caregiver.  

Financial issues faced by caregivers may include having to call out of work frequently, needing to take an extended leave, or paying for resources out-of-pocket. In fact, due to the unpaid nature of their caregiving, informal caregivers are more likely to live in poverty.  

Physical, mental, and financial stress can be exacerbated in certain situations, such as when caring for a spouse with dementia or a child with an intellectual or developmental disability. For example, individuals with dementia can require more time- and resource-intensive care due to impairments related to their activities of daily living, or ADLs, and instrumental activities of daily living, or IADLs. Caregivers may also have a difficult time communicating with their loved one due to their condition.  

Lastly, caregivers of a child with a disability may themselves be aging and worry about who will care for their child if they become too ill or die. They may ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/End-of-Life_Care_of_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K-qUJwwWTxy109wAQoHvP-9uTbaJAv1Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[End-of-Life Care of the Older Adult]]></video:title><video:description><![CDATA[End-of-life care involves the supportive care provided to an individual as they near death. As the nurse, you’ll provide end-of-life care for older adults by recognizing and managing the physiologic changes that occur at the end of life and providing emotional support for the patient and their family.  

Now, there are certain physiologic changes that occur during the dying process. Starting with the cardiovascular system, these changes are mostly related to diminishing cardiac output and blood pressure. As a result, heart sounds become faint, peripheral pulses weaken, and circulation slows. Subsequently, the skin becomes cool, pale, and mottled, with bluish coloring, known as cyanosis, especially in the extremities.  

Next, in the respiratory system, patients often report feelings of dyspnea, including a feeling of chest tightness or breathlessness, which is due to factors like respiratory congestion and weakened respiratory muscles. Keep in mind that patients experience dyspnea, even when typical signs like decreased oxygen saturation or rapid breathing are not observed.  

Other respiratory changes include slow and irregular respirations, often with Cheyne-Stokes respirations which are alternating episodes of apnea and hyperventilation. Patients may also develop distinctive wet, gurgled, noisy breathing, called the death rattle, which is caused by saliva and mucus building up in the back of the throat and upper airways.  

Okay, moving on to the neurologic system, decreased cerebral perfusion and metabolic disturbances can result in acute episodes of confusion, or delirium, which can alternate with moments of lucidity. Other symptoms include agitation, excessive sleepiness, or insomnia.  

They can also have sensory changes like diminished sight, visual hallucinations, and hypersensitivity to light and sound; although hearing typically remains intact up until the moment of death. As death nears, responsiveness decreases, and they eventually lose consci]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Portal_Hypertension_Pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J3xb9CVVR92sap068RrDQeVcQYqHIzkp/_.jpg</video:thumbnail_loc><video:title><![CDATA[Portal Hypertension Pathophysiology]]></video:title><video:description><![CDATA[Portal hypertension is a condition that occurs when there’s abnormally high pressure in the portal venous system, which is a network of vessels that drain blood from the abdomen into the liver.  

As a quick review, the portal vein is formed by the splenic vein merging with the superior and inferior mesenteric veins, so it receives blood from the spleen, stomach, pancreas, and small and large intestines.  

This blood contains all the nutrients absorbed in the GI tract, as well as ingested medications and potential toxins.  

The slow, low-pressure flow of blood provides adequate time for the liver to extract nutrients, metabolize medications, and remove toxins before they reach systemic circulation.  

Once the liver processes the blood it receives, it flows through the hepatic veins to the inferior vena cava, and to the right atrium of the heart. The blood then flows through the heart and lungs, and oxygenated blood is pumped out to the rest of the body.  

Now, portal hypertension is caused by any condition that obstructs blood flow in the portal venous system, and can be prehepatic, intrahepatic, or posthepatic.  

Prehepatic causes are those that result in obstruction of blood flow before reaching the liver such as splenic vein thrombosis, or a clot within the splenic vein.  

Intrahepatic causes are those which result in an obstruction within the liver. One of the most common causes is cirrhosis, a condition where healthy liver tissue is replaced by scar tissue resulting in increased resistance to blood flow through the liver. 

Other causes include certain infections like hepatitis or schistosomiasis, a parasitic infection that can affect multiple organs, including the liver.  

Lastly, posthepatic causes result in obstruction of blood flow from the liver, like right-sided heart failure where the right ventricle is not pumping effectively, causing blood to back up into the liver. 

Okay, so when an obstruction to blood flow develops, pressure builds]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Biology_of_Cancer</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cG4tSrbVTS_KwiaaLhlPl-8UTFu4qWy8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Biology of Cancer]]></video:title><video:description><![CDATA[Cancer is a collection of conditions that can affect any organ in the body and is characterized by abnormal cells that divide and grow uncontrollably. This can lead to the development of masses of tissue called tumors that can spread, or metastasize, throughout the body.  

Okay, as a brief review, there are some key attributes that characterize normal, functional cells. An important characteristic is differentiation, meaning normal cells become specialized in their structure, location, and specific function.  

For example, muscle cells have different shapes and functions than brain cells, and they’re found in different parts of the body. Normal cells also have a uniform shape; they tend to stick together; and have an orderly arrangement within their specific tissue.  

Another characteristic is that normal cells age naturally over time, and undergo apoptosis, or programmed cell death, when they become old or damaged.  

Lastly, normal cells grow and divide only when necessary. In fact, they can’t divide indefinitely because the process of growth and division is regulated by two types of genes, called proto-oncogenes and tumor suppressor genes.  

When needed, proto-oncogenes activate cell growth and division, a process known as proliferation; whereas tumor suppressor genes suppress uncontrolled cell proliferation. 

Alright, now cancer results from gene mutations, or changes to the DNA sequence, which can be inherited or develop spontaneously. Mutations are more likely to occur when risk factors are present, which can be either modifiable or non-modifiable.  

Modifiable risk factors include lifestyle choices that involve exposure to carcinogens, or substances that can initiate the development of cancer, like tobacco, alcohol, ultraviolet light, and high-fat foods. Additionally, exposure to certain hormones, chemicals, and viruses can heighten cancer risk. For example, estrogen is associated with endometrial cancer; harmful chemicals like asbestos can le]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Hyperosmolar_Hyperglycemic_Syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PpT5OenGSKar9dOd6OBbg_LVQViaGaI0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Hyperosmolar hyperglycemic syndrome (HHS): Nursing]]></video:title><video:description><![CDATA[Nurse Juana works on the medical unit and is caring for Ralph, a 76-year-old with a history of type 2 diabetes mellitus and osteoarthritis, who was transferred from the intensive care unit after being admitted for hyperosmolar hyperglycemic syndrome, or HHS, also known as hyperosmolar non-ketotic syndrome or hyperglycemic hyperosmolar non-ketotic coma.  

After settling Ralph in the room, Nurse Juana goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ralph’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Juana recognizes important cues, including Ralph’s vital signs, which are temperature 98.9 F, or 37.2 C, heart rate 92 beats per minute, respirations 22 breaths per minute, blood pressure 110/65 mmHg, and oxygen saturation 98% on room air. He also states he’s having pain in his hands and fingers and rates his pain as a 5 on a 0 to 10 numeric scale.  

Upon physical assessment, Nurse Juana notes Ralph has IV fluids infusing into a peripheral IV, and a moderate amount of light-yellow urine in his catheter bag. 

Nurse Juana: Tell me more about how this pain is affecting you, Ralph. 

Ralph: It’s my arthritis. It’s been okay if I take ibuprofen, but I ran out. My hands and fingers have been hurting so I haven&amp;#39;t wanted to cook. I’ve just been getting fast food. This past week, I was having trouble taking my insulin, too. It’s just too difficult to draw it up with the syringe and vial, even when my hands feel okay. 

Next, Nurse Juana analyzes these cues. She reviews the electronic health record, or EHR, and notes that before being stabilized in the ICU, Ralph was confused and his initial lab results were blood glucose 624 mg/dL or 34.7 mmol/L; serum osmolality 345 mOsm/kg, or 345 mmol/kg; hemoglobin A1C 8%; arterial blood gas, or ABG, revealed no acidosis; and his urine was free of ketones. She also notes]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Dehydration_and_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/T2TA-66BSyOFJMjfD5Z1bo6PS4_Gfwkm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Dehydration and the Older Adult]]></video:title><video:description><![CDATA[Dehydration is a condition that results in a reduction in total body water, which can be caused by insufficient fluid intake, increased fluid loss, or both. In older adults, dehydration can increase the risk of other problems, including constipation, delirium, venous thromboembolism, delayed wound healing, electrolyte imbalance, and even renal failure. As the nurse, you’ll identify risk factors, recognize signs and symptoms, and prevent dehydration in your older adult patient.  

Risk factors for dehydration can be categorized as can drink, can’t drink, won’t drink, and end-of-life.  

Can drink refers to individuals who don’t drink enough fluids even though they have access to fluids and are physically able to drink. This can be due to age-related changes such as decreased thirst sensation; lack of knowledge about fluid intake goals; or if they require prompts to remember to drink. For example, an individual with cognitive impairment, like dementia, may simply forget to drink fluids throughout the day.  

Additionally, some individuals may require an increased fluid intake if they’re prescribed diuretics or medications with anticholinergic effects, like psychotropics. Others experiencing an acute illness involving fever, vomiting, or diarrhea will need more fluid intake to address excess fluid loss. 

Next, can’t drink refers to individuals who are unable to drink. This can be related to factors like dysphagia, or difficulty swallowing; the need for physical aids to assist with drinking; or the need for assistance from others to consume fluids. Others can become dehydrated when they’re NPO, meaning they are restricted from taking anything by mouth. There are also certain comorbid conditions, like heart failure, which may require individuals to have a restricted fluid intake, potentially leading to dehydration. 

Then there’s won’t drink, which refers to individuals who have access to fluids and can drink, but don’t. This can include individuals who avoid ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Acute_Kidney_Injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/tr6-6jSFQtyRkg3iGyzv2fd5SXm1Q2V3/_.png</video:thumbnail_loc><video:title><![CDATA[Critical care case study - Acute kidney injury: Nursing]]></video:title><video:description><![CDATA[Nurse Greta works in the intensive care unit, or ICU, and is caring for Reggie, a 47-year-old diagnosed with acute kidney injury, or AKI. Nurse Greta goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Reggie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Greta recognizes important cues, including Reggie’s vital signs which are temperature 98.9 F, or 37.1 C, heart rate 100 beats per minute, respirations 26 breaths per minute, blood pressure 154/78 mmHg, and oxygen saturation 92 percent on 2 liters of oxygen per nasal cannula. Upon assessment, Nurse Greta notes Reggie’s urine output from his indwelling catheter was 25 milliliters in the last hour and has a dark amber color. He also has a 2+ pitting edema in his bilateral lower extremities and crackles upon auscultation to his lung bases.  

Next, Nurse Greta analyzes these cues. She reviews the electronic health record, or EHR, and notes Reggie’s admitting diagnosis was glomerulonephritis, and his most recent labs show a BUN of 31 mg/dL, creatinine of 2.6 mg/dL, and estimated glomerular filtration rate, or eGFR, of 65 milliliters per minute. Additionally, his potassium is 5.8 mEq/L; his urinalysis shows protein and blood; and his arterial blood gas results indicate metabolic acidosis.  

Nurse Greta knows AKI is a sudden decline in kidney function that occurs over hours or days and can be reversible if identified and treated promptly. She knows it can occur following glomerulonephritis, which is an inflammation of the network of capillaries in the kidneys that filter blood, called the glomeruli. This can cause intrarenal AKI, where part of the kidney itself, like the glomeruli, is damaged.  

When glomeruli are damaged, their permeability increases, allowing large molecules and cells, like protein and blood, to pass through into the urine, resulting in proteinuria a]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Safe_and_Secure_Environments</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DMojA4llQ2C5E61nH-nEPxbgQxCJuVrV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Safe and Secure Environments]]></video:title><video:description><![CDATA[Safe and secure environments can improve the health and well-being of older adults while providing an opportunity to age in place and live independently, safely, and comfortably.  

As the nurse, you&amp;#39;ll identify risks to safe and secure environments and promote safety for older adults by addressing risks associated with fires, firearms, transportation, and heat- and cold-related injuries. 

First let’s discuss fires, which can cause burns and smoke inhalation injuries.  

For older adults, there are several factors that can increase the risk of injury during a fire, including impaired mobility, sensory impairments, slower decision-making or response time, and certain preexisting health conditions.  

Now, fires can be caused by factors that include inadequate home repairs or maintenance, use of space heaters, and smoking materials, like cigarettes.  

For example, a fire can originate from a poorly maintained fireplace, a space heater placed next to flammable materials, or from falling asleep while smoking in bed.   

As the nurse, you’ll promote fire safety by ensuring your patient has well-maintained smoke alarms in every room. They should also have access to a fire extinguisher and know how to use it.  

If your patient smokes, instruct them to avoid smoking in bed or in a chair when there’s a possibility of falling asleep; to avoid smoking after taking medications that may cause drowsiness; and to dispose of all cigarette butts in a nonflammable container away from other items.  

Lastly, you can help your patient develop and practice a fire escape plan.  

Now, firearms are a significant cause of injury and death in older adults. Gun ownership is typically higher in older adults when compared to other populations. At the same time, older adults experience a higher rate of altered mood, memory, cognition, and function. These factors greatly increase the risk of unintentional firearm injuries which can occur from improper firearm care or handli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Elder_Abuse_and_Neglect</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/n1kugcAQR-uK0-6Sb9Wq0nTvS7ev2-rh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Elder Abuse and Neglect]]></video:title><video:description><![CDATA[Nurse Kyle works in a primary care office and is caring for Judy, a 78-year-old female with a history of Alzheimer disease, who was brought in for a medication refill by her son, Darrell. In collaboration with the registered nurse, RN Fatima, Nurse Kyle goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Judy’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Kyle recognizes important cues, including Judy’s vital signs, which are temperature 97.6 F or 36.4 C, heart rate 70 beats per minute, respirations 14 breaths per minute, and blood pressure 126/72 mmHg. Judy is oriented to person and place but not time. Nurse Kyle also notices Judy has a flat affect and avoids direct eye contact.   

Nurse Kyle: Alright, Judy, the healthcare provider ordered a urine sample to help monitor how your medication is working. Can I assist you to the bathroom?   

Nurse Kyle begins to assist Judy to the bathroom and notes she has a strong body odor. When helping Judy remove her incontinence underwear, he notices it’s saturated with urine, and her vulva is bright red with a surrounding rash. After collecting the sample, Nurse Kyle helps Judy clean up and put on a fresh pair of underwear. While Judy washes her hands, Nurse Kyle notes a circular bruise on her right arm.  

Nurse Kyle: Judy, I see you have a bruise on your arm. What happened?  

Judy: Oh, I don’t remember. It’s fine.  

He then helps Judy return to the exam room to wait for the healthcare provider.  

Nurse Kyle: Darrell, I noticed your mom has a bruise on her right arm. How did she get that? 

Darrell: Let me see it. Oh, yeah - that looks like the spot where she always hits on the doorknob. It’s nothing. Nurse Kyle: Okay, tell me more about what you mean. 

Darrell: Well, since mom gets confused, she started wandering into the street a lot. I’m trying to run my business fr]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Age-related_Changes</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LQcgSc9HSP_yLg8pfVZnfKvfQqq0OrwZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Age-related changes: Nursing]]></video:title><video:description><![CDATA[Normal, age-related physiologic changes occur gradually over time, resulting in a decrease in reserve capacity, which is the functional ability of the body’s organs to function beyond what’s needed for normal day-to-day activities. These changes can decrease the ability of the critically ill older adult to adapt to illness, which can increase the risk of complications. As the nurse, you’ll recognize these age-related changes and consider complications that can develop in your critically ill older adult patient as a result.  

Starting with the cardiovascular system, there’s an age-related tendency for a decrease in the number of contractile cells in the heart, called cardiomyocytes, along with an accumulation of collagen and fibrosis. The cardiomyocytes also tend to hypertrophy, or increase in size, resulting in a slight thickening of the left ventricular wall with no significant change in the size of the left ventricular cavity.  

There are also alterations with calcium signaling within the myocardium during contraction, leading to delayed relaxation during diastole and prolonged contraction during systole. Together, these changes can make the heart a less efficient pump, leading to reduced cardiac output.  

Additionally, a loss of cells in the sinoatrial node, which is responsible for generating impulses that stimulate a heartbeat, is associated with a reduced maximal heart rate, which is the highest number of times the heart can beat per minute during physical activity. These age-related changes reduce cardiac functional reserve, impairing the heart’s ability to meet increased demands that can occur during a critical illness. 

Other age-related vascular changes include dysfunction of the endothelial cells lining blood vessels. These cells become less effective in balancing substances that cause vasodilation and vasoconstriction. As a result, arteries tend to stiffen, blood flow decreases, and there’s an increased risk of atherosclerosis and thrombosi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hearing_Impairment_and_the_Older_Adult</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z3ebbEN0QQG0655WnIQ_yaZMQ_KJhNVk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hearing Impairment and the Older Adult]]></video:title><video:description><![CDATA[Hearing impairment is a common condition in older adults that can negatively impact their quality of life through communication difficulties, social isolation, decreased self-esteem, cognitive decline, and even depression. As the nurse, you’ll recognize age-related hearing changes and provide patient-centered care for your patient with a hearing impairment. 

Now, the ear is divided into three parts: the external, middle, and inner ear; and each part contains structures that can be affected by age-related changes.  

The external ear consists of the pinna, or the outer part of the ear, and the external auditory canal, which is a passageway connecting the outer ear to the tympanic membrane, commonly called the eardrum. The external auditory canal narrows with age due to decreased tissue elasticity. Additionally, ceruminous glands that produce cerumen, or ear wax, tend to atrophy over time, resulting in drier ear wax.  

These conditions put individuals at higher risk for cerumen impactions which can cause a type of hearing loss called conductive hearing loss, where cerumen blocks the external auditory canal, impairing the conduction of sound waves. 

Another type of conductive hearing loss can occur due to age-related changes in the middle ear, which is the air-filled space that consists of the tympanic membrane and the auditory ossicles. The auditory ossicles consist of three tiny bones that transmit sound waves collected by the tympanic membrane to the inner ear. Now, these ossicles are prone to otosclerosis, or stiffening. When this happens, they’re unable to transmit sound waves as effectively.  

Now, moving on to the inner ear. This includes the cochlea, which converts sound waves into electrical impulses for the brain to process, and a set of structures called the vestibular system, which helps maintain balance. Over time, the cochlear structures, including hair cells and conductive membrane, can deteriorate or become damaged, causing a type of heari]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Nutritional_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v2GWqV6hTOGHrpXuVmZGm3VvTci8OG4g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Nutritional therapy: Nursing]]></video:title><video:description><![CDATA[Nutritional therapy is an intervention used to meet nutrient requirements in critically ill patients who are unable to consume or tolerate oral nutrition or can’t digest or absorb food. The two main types of nutritional therapy are enteral nutrition and parenteral nutrition. As the nurse, you’ll provide patient-centered care while providing nutritional therapy to critically ill patients. 

Now, enteral nutrition, also known as tube feeding, involves the delivery of temporary or long-term nutrition through a tube directly into the GI tract. This is indicated for patients who have some digestive function but are unable to consume adequate nutrients by mouth, like intubated patients, patients with nervous system disorders that impact chewing or swallowing, or patients with increased caloric needs due to major surgery or burns.  

A common temporary route for enteral nutrition is through a nasogastric, or NG, tube which enters through the nose and goes into the stomach. For patients at increased risk of aspiration or with impaired gastric emptying, a small bowel feeding tube can be inserted directly into the small intestine.  

On the other hand, if long-term or permanent enteral feeding is needed, a tube can be placed through a surgical opening in the abdominal wall and into the stomach, known as a gastrostomy tube, or G-tube. One common type of gastrostomy tube is the percutaneous endoscopic gastrostomy tube, also called a PEG-tube. Tubes can also be inserted into a part of the small intestine called the jejunum, known as a jejunostomy tube, or J-tube for short.  

There are other conditions where a patient can’t digest and absorb any food via the GI tract, due to conditions like GI trauma or surgical procedures; as well as other illnesses, like intestinal cancer.  

In these cases, parenteral nutrition is prescribed, where liquid nutrition, formulated based on the nutritional needs of the patient, is infused intravenously. The most common type of parenteral]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertension_(HTN)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/UiS458wiRm6aCV7qTPAtVdyRQvSsZEnB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertension (HTN)]]></video:title><video:description><![CDATA[Hypertension occurs when the force of the blood pushing against the artery walls is too high, causing damage to organs. 

Okay, so, as the heart pumps blood throughout the body, it creates pressure against the walls of the arteries, which is referred to as blood pressure, or BP.  

Blood pressure is expressed as a fraction, where the top number, called the systolic pressure, represents the pressure in the arteries when the heart is contracting and pumping blood; and the bottom number, called the diastolic pressure, represents the pressure in the arteries when the heart is relaxed and filling with blood. Normal blood pressure is less than 120 mmHg systolic and less than 80 mmHg diastolic. 

Factors that impact blood pressure include cardiac output, or CO, and systemic vascular resistance, or SVR. First, cardiac output is the quantity of blood pumped by the heart and is measured in L/min. The two components of cardiac output are stroke volume, or SV, and heart rate, or HR. Stroke volume is the amount of blood leaving the heart with each contraction, and heart rate is the number of contractions in one minute.  

The higher the stroke volume and heart rate, the higher the cardiac output.  

Next, systemic vascular resistance is determined by the radius and elasticity of blood vessels. If blood vessels are narrow or stiff, systemic vascular resistance increases, which then increases blood pressure.   

Now, blood pressure is regulated by short-term and long-term mechanisms. Short-term regulation is mainly controlled by the autonomic nervous system, or ANS. For example, when changing from a lying to a standing position, blood pressure tends to drop.  

When this happens, baroreceptors, which are pressure-sensitive receptors located mostly in the aortic arch and carotid sinuses, respond by sending signals to the vasomotor center in the medulla. The medulla activates the sympathetic nervous branch of the autonomic nervous system, which increases heart rate, system]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Pacemakers</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/C0xThEofTQO1is-0uMeOzsf8RGi1lIq_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Pacemakers: Nursing]]></video:title><video:description><![CDATA[Pacemakers are electronic devices that deliver electrical impulses to help the heart maintain a cardiac rate or rhythm that can produce effective cardiac output. These electrical impulses initiate depolarization, the process where the impulse moves through the conduction system and causes cardiac contraction. Pacemakers can be used as a temporary supportive or preventive measure until the underlying cause of a conduction problem is resolved, or they can be implanted permanently. 

Common indications for a pacemaker include treatment of bradyarrhythmias, such as symptomatic bradycardia related to heart block or sick sinus syndrome; or tachyarrhythmias, like from supraventricular tachycardia. They’re also used for cardiac support during or after heart surgery; or during diagnostic studies and procedures, like atrial electrograms or catheter ablations.  

Temporary pacemakers can be categorized as transcutaneous, transvenous, or epicardial. Starting with transcutaneous pacing, this is where electrical stimulation is applied through the skin using two non-invasive electrode pads connected to an external pacemaker. Typically, one pad is attached anteriorly on the chest and the other pad is placed posteriorly on the back. This type of pacing is typically done in emergency situations; and sometimes they can also act as a defibrillator. 

Next is transvenous pacing, where a pacing electrode catheter is inserted through a large vein such as the subclavian, internal jugular, or femoral vein and into the right atrium or right ventricle. When there’s a lead in both chambers, then it’s called a dual-chamber pacemaker. From there, the external ends of the electrode wires are connected to a pulse generator. 

Then there’s epicardial pacing, which is established during cardiac surgery where ventricular, and sometimes atrial, pacing wires are loosely sewn onto the epicardium. They’re either removed before the chest wall is surgically closed, or they remain inside temporari]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Acute_Gastrointestinal_Bleeding</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Y0T0XgV6QLiaxsdMKMbqp7ZTR_SAmXNf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Acute gastrointestinal bleeding: Nursing]]></video:title><video:description><![CDATA[Acute gastrointestinal, or GI, bleeding occurs when there’s sudden loss of blood from the upper or lower GI tract.  Upper GI bleeds occur in structures above a suspensory ligament called the ligament of Treitz, including the esophagus, stomach, and duodenum. On the other hand, lower GI bleeds occur in structures below this ligament, including the colon, rectum, and anus. 

GI bleeds are caused by any condition that disrupts the integrity of the GI tract. Causes of upper GI bleeding include ulcers and varices, while causes of lower GI bleeds typically include cancer, hemorrhoids, and diverticulosis. As the nurse, you’ll provide patient-centered care for critically ill patients with acute GI bleeding.   

Okay, so the GI tract consists of multiple layers. The mucosa is the innermost layer which helps absorb nutrients; provides protection from harmful bacteria and substances, like excess stomach acid; and produces mucus to lubricate food and prevent excoriation. The submucosa layer is under the mucosa and contains connective tissue, blood vessels, and nerves. Then there’s the muscular layer, where the muscles of the GI tract reside, and the serosa layer, which is the outermost layer that helps reduce friction and protects the inner structures.  

Now, these mucosal layers can be disrupted, like when stomach acid auto-digests the layers or if a tumor within the GI tract, like colon cancer, directly invades the layers. Once the submucosal layer is disrupted, blood vessels can be damaged, leading to bleeding. Additionally, varices, which are dilated, fragile vessels commonly found in the esophagus, can easily rupture and bleed.  

If bleeding is severe, hypovolemic shock can occur due to a reduced circulating blood volume. When this happens, the body compensates by vasoconstricting blood vessels and increasing heart rate, which can help maintain cardiac output and mean arterial pressure, or MAP. If left untreated, acute GI bleeding can progress to multiple ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Intracranial_Hypertension</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A4WbcnHBRx_n018wdDzLRswlTPumifAq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care case study - Intracranial hypertension: Nursing]]></video:title><video:description><![CDATA[Nurse Kenji works in the neurological intensive care unit and is caring for Felix, a 22-year-old patient who was admitted after experiencing a blow to the head while playing ice hockey. Nurse Kenji goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Felix’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Kenji recognizes important cues, like Felix’s vital signs which are temperature 100.1 F, or 37.8 C, heart rate 84 beats per minute, respirations 18 breaths per minute, blood pressure 136/72 mmHg, and oxygen saturation 96% on 2 liters of oxygen per nasal cannula.  

He also has an intracranial pressure, or ICP, monitor in place that shows an ICP of 21 mmHg; and his cardiac monitor shows normal sinus rhythm.  

Nurse Kenji then performs a focused neurological assessment and calculates a Glasgow Coma Scale, or GCS, score of 11, with both pupils equal and reactive to light. 

Next, Nurse Kenji analyzes these cues. He reviews the electronic health record, or EHR, and notes that Felix had a computed tomography, or CT, scan that ruled out a skull fracture and intracranial bleeding but showed cerebral edema. 

Nurse Kenji knows the rigid skull contains fixed amounts of brain matter; cerebral spinal fluid, or CSF; and blood, and any increase in volume of one of these components must be compensated by a decrease in one of the other components.  For example, an increase in brain matter due to cerebral edema can be compensated by an adjustment to the volume of cerebral blood flow, increasing absorption of CSF, or shifting CSF from the intracranial space into the spinal column. However, in situations where these compensatory mechanisms fail, ICP can increase significantly. 

If left untreated, Nurse Kenji knows that a sustained increase in ICP above 20 mmHg, called intracranial hypertension, can compromise cerebral perfusion press]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_Management</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NddMiIvcQpCu4VZ8AQ0pGyoWTYyVkttE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case Management]]></video:title><video:description><![CDATA[Case management is a collaborative process that involves assessing, planning, and coordinating care to meet the evolving needs of patients and their families. The goals of case management vary depending on the health care setting and patient needs but generally aim to develop a patient-centered plan of care by helping patients manage their healthcare needs, navigate the healthcare system, and achieve positive health outcomes. As a nurse in case management, you&amp;#39;ll identify patient needs and use available resources to organize and coordinate patient-centered and cost-effective care. 

Nurses in case management, often called case managers, have traditionally worked in public health, mental health, and long-term care settings, but also provide services in places like ambulatory clinics, assisted living communities, primary care offices, and acute care settings.  

Case managers receive training and certification to perform specialized skills and functions involving care management, care coordination, and utilization review.  

Care management is a strategy used to improve the health of specific groups of people by organizing services, avoiding duplication of care, and encouraging self-management of disease to lower health risks and reduce healthcare costs.  

To do so, case managers identify patients and populations with modifiable health risks, tailor services and education to meet their needs, and ensure the right health professionals are able and available to provide care.  

For instance, a case manager in a cardiology clinic will review electronic health records and identify patients who have been hospitalized more than once in the past year for exacerbations of heart failure. Understanding that these patients are more likely to develop complications and be readmitted to the hospital, the case manager creates a protocol to reduce the likelihood of symptom exacerbation.  

On a regular basis, the case manager performs telephone check-ins with at-r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Diabetic_Ketoacidosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pNFyJzy3Qhmb8OHXW5TEpXvCSSOKhfqc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care case study - Diabetic ketoacidosis: Nursing]]></video:title><video:description><![CDATA[Nurse Ji Yun works in the emergency department and is caring for Osborn, a 47-year-old patient with a history of type 1 diabetes mellitus, who was diagnosed with diabetic ketoacidosis, or DKA. Nurse Ji Yun goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Osborn’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Ji Yun recognizes important cues, including Osborn’s vital signs which are temperature 99.4 F, or 37.5 C, heart rate 118 beats per minute, respirations 28 breaths per minute, blood pressure 90/56 mmHg, and oxygen saturation 91 percent on 2 liters of oxygen per nasal cannula. Upon assessment, Nurse Ji Yun notes Osborn’s breathing is deep and labored, and his breath has a sweet odor. He’s slightly lethargic and is oriented to person and place, but not time. Nurse Ji Yun notes that Osborn’s current blood glucose level is 400 mg/dL, or 22.2 mmol/L. 

Next, Nurse Ji Yun analyzes these cues. He reviews the electronic health record, or EHR, and sees that Osborn recently recovered from pneumonia and his urine is positive for ketones. Also, arterial blood gas results show a pH of 7.2 and a bicarbonate of 15 mEq/L, indicating metabolic acidosis.  

Nurse Ji Yun knows diabetic ketoacidosis is a life-threatening complication of type 1 diabetes mellitus caused by an insulin deficiency, where glucose can’t be taken up into cells and used for energy.  

He also knows that infections, like pneumonia, can precipitate diabetic ketoacidosis by increasing stress hormones that contribute to elevated glucose and reduced insulin utilization. As glucose levels rise, the kidneys reach the maximum amount of glucose they can reabsorb, so extra glucose spills into the urine, resulting in glycosuria. Additionally, since glucose is osmotically active, glycosuria is accompanied by a large amount of water in the urine, resulting in pol]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Homelessness</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GgszK_pNQTOC5J1EY-MCV72uRmObenwi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Homelessness]]></video:title><video:description><![CDATA[Nurse Margot works as a community health nurse in the health department and is assisting a local homeless shelter to address concerns among its residents. Nurse Margot goes through the steps of the Clinical Judgment Measurement Model to make decisions by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Margot recognizes cues. She distributes an anonymous questionnaire to residents at the shelter to gather demographic data, employment status, presence of medical conditions, and any other concerns they have. Nurse Margot then interviews willing residents to gather additional information on factors contributing to their need for the shelter and discusses with staff any concerns they have about residents.  

She also obtains data from the shelter on the number of residents it houses and services that’re offered.  

Next, Nurse Margot analyzes these cues. She reviews data from the questionnaire and her notes from the interviews to identify common themes. She notes many residents are unemployed and have indicated they’re unable to maintain employment due to mental health conditions. They cite lack of transportation and financial concerns as a barrier to accessing mental health care; and staff also report many residents have been struggling mentally due to lack of access to needed care. Nurse Margot reviews services provided by the shelter which include support groups, Wi-Fi, and assistance with housing applications. 

Nurse Margot knows homelessness is a complex socioeconomic issue that consists of a range of living situations. She knows there are many types of homelessness including rooflessness, sometimes called absolute homelessness, where individuals lack any shelter; houselessness, also called sheltered homelessness, such as those who don’t have a permanent residence but stay in temporary housing like shelters; insecure housing, where individuals face threat of eviction or ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Communicable_Disease_and_Public_Health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1Y8hRDwISjCqusyutXfhhBwdQNO_Pj90/_.jpg</video:thumbnail_loc><video:title><![CDATA[Communicable Disease and Public Health]]></video:title><video:description><![CDATA[Communicable diseases are contagious illnesses caused by infectious, or pathogenic, agents. As a public health nurse, you&amp;#39;ll prevent and control communicable diseases. 

Now, the ability of a communicable disease to spread and cause infection depends on the interaction between three main factors that form the epidemiological triangle. These factors include an infectious agent, which can be any disease-causing microorganism including bacteria, viruses, fungi, or parasites; a host, or any person or animal harboring the infectious agent; and the environment, which are the external factors that influence disease transmission, like sanitation, crowding, or the presence of disease-transmitting insects like ticks.  

The epidemiological triangle provides a foundation for understanding the sequence of events involved in the spread of infectious disease that are outlined in the chain of transmission. The first link in the chain is an infectious agent, which lives and multiplies in its reservoir. The reservoir can be another human, an animal, water, food, or contaminated surfaces. The pathway by which the infectious agent leaves the reservoir is the portal of exit, like bodily fluids or open wounds.  

After that, the mode of transmission is how the pathogen travels from the reservoir to a new host. This can involve direct transmission, such as through sexual intercourse, skin to skin contact, or respiratory droplets; or indirect transmission, like touching a contaminated object, such as a door handle. Next, the infectious agent needs a portal of entry, which is the pathway by which it enters a new host, like through the mouth, nose, eyes, mucous membranes, or breaks in the skin.  

Lastly, the susceptible host is anyone at risk for infection due to factors like age, health status, and immunity.  

Alright, so, controlling communicable diseases is a key means of protecting and supporting public health. Control involves reducing the incidence, or new ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Health_Education</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/INPAFAA2RjKmH1ClsvfqpmKRRNiqsKGQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community health case study - Health education: Nursing]]></video:title><video:description><![CDATA[Nurse Mitchell is a community health nurse who is preparing an educational workshop on physical activity for residents at a local independent living facility. He goes through the steps of the Clinical Judgment Measurement Model to make decisions about the workshop by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Mitchell recognizes important cues. He completes a needs assessment using a questionnaire distributed to the residents with questions about the type of physical activity they do and the amount of time they spend engaging in physical activity. He also includes questions about their learning preferences and demographic data such as age, education level, and any medical conditions they’re willing to disclose.  

Next, Nurse Mitchell analyzes these cues. He reviews the results of the questionnaire which indicate most of the residents are physically active for at least 60 minutes each week. Many said that their main source of activity is walking, although they’re interested in other forms of activity and learning how they can remain motivated. Regarding learning preferences, many note they prefer to learn in-person through multimedia, like animated videos or slideshows, but also appreciate having information written down to refer to later. Nurse Mitchell also reviews the demographic data, which reveals his learners are adults over the age of 55 with levels of education ranging from a high school diploma to undergraduate college degrees, and he notes there’s a high prevalence of diabetes and cardiovascular disease.   

Nurse Mitchell knows that health education involves learning experiences that are aimed at predisposing, enabling, and reinforcing healthy behaviors among individuals, groups, communities, and society at large. He recognizes that providing education about healthy behaviors can promote health; prevent disease; and maintain optimal wellness, especially wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Mechanical_Ventilation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/azpbTwaxQg6lwHikfQt3z8v5RNaAFnwM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Mechanical ventilation: Nursing]]></video:title><video:description><![CDATA[Mechanical ventilation is a process that partially or fully assumes breathing for patients who can’t independently maintain effective gas exchange. It can be used in the short-term, such as during surgery when a patient is sedated, or in the long-term, like in cases of respiratory failure, airway obstruction, or when a patient is comatose.  

Mechanical ventilation requires the placement of an artificial airway, such as an endotracheal tube, or ETT, which is a tube that’s inserted through the mouth and into the trachea through a procedure called intubation. Another artificial airway is a tracheostomy tube, which is inserted directly through a surgical opening made in the skin of the neck, that creates an opening into the trachea. Once inserted, the tube is connected to a ventilator, which is a mechanical device that pushes oxygen-rich air into the patient’s lungs. 

Now, mechanical ventilators have modifiable settings to meet the needs of each patient based on their health status, comorbidities, and goals of care. First, the respiratory rate or frequency determines the number of breaths the ventilator supplies and is typically set between 6 to 20 breaths per minute to mimic normal respiration. Next, tidal volume, or VT, is the volume of air delivered during each breath, which for most patients is between 4 to 8 mL/kg of body weight. So, let’s say your patient weighs 60 kilograms and is started on a VT of 6ml/kg. The ventilator will deliver a VT of 360 milliliters of air with each breath.  

Then there’s oxygen concentration, or the fraction of inspired oxygen, called FiO2 for short, which refers to the concentration of oxygen being delivered. FiO2 can be set anywhere from 21 to 100 percent to maintain a partial pressure of arterial oxygen, or PaO2, between 60 and 100 mmHg or oxygen saturation at 90 percent or more.  

Next, the inspiratory to expiratory ratio, or I:E ratio, is the length of inspiration compared to the length of expiration with a typical I:]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Transitions_of_Care</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZwRI0eK9TVq4a99b2sIHBNGwRpS2F5tf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Transitions of care: Nursing]]></video:title><video:description><![CDATA[Transitions of care refer to changing the healthcare setting or the level of care services provided. Care transitions depend on the acuity of the patient’s illness, the intensity of services required, and the need for advanced technologies to support care. Effective care transitions to and from critical care areas are essential for patient safety, continuity of care, and positive health outcomes. 

Alright, so there are various transitional locations and care levels which can be broadly categorized into acute care settings and post-acute care settings.  

Starting with acute care settings, these are generally located within hospitals where patients typically receive short-term care for urgent medical conditions.  

The highest level of care is critical care. Critical care includes emergency departments and intensive care units, or ICUs. This level of care may include advanced monitoring and technology, cardiopulmonary life support, and management of severe, acute injuries or illnesses.  

The next level down is called a step-down area which offers an intermediate level of care for patients who are unstable but don’t require intensive care, like patients recovering from surgery or acute illness who need additional monitoring for complications.  

Next, telemetry areas are used when continuous ECG monitoring or intensive interventions are needed for stable patients. There are also medical-surgical units which deliver comprehensive medical and pre- and post-surgical treatment for stable patients with diverse health conditions.  

And finally, long-term acute care hospitals provide care for stable patients with a need for complex care for an extended period, like patients with a traumatic brain injury or complicated wounds.  

Now, within these care areas, there are various types of care transitions that can be made. Patients are typically transferred from a higher level of care to a lower level of care as their condition stabilizes, like from a critical care ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Cardiogenic_Shock</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7UrpIGLSQ3qR7Qf5yTRznydwRhSa9TvZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care case study - Cardiogenic shock: Nursing]]></video:title><video:description><![CDATA[Nurse Raven works in the intensive care unit, or ICU, and is caring for Deirdre, a 72-year-old diagnosed with cardiogenic shock. Nurse Raven goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Deirdre’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Raven recognizes important cues, including Deirdre’s vital signs which are temperature 98.9 F, or 37.2 C; heart rate 111 beats per minute; respirations 24 breaths per minute; blood pressure 80/40 mmHg with a mean arterial pressure, or MAP, of 60 mmHg; and oxygen saturation 89 percent via mechanical ventilation.  

Upon assessment, Nurse Raven notes Deirdre’s peripheral pulses are weak; her skin is pale and cool; and dobutamine is infusing through a central line, along with a sedative and paralytic. She also notes Dierdre’s urinary output was 20 milliliters in the last hour. 

Next, Nurse Raven analyzes these cues. She reviews the electronic health record, or EHR, and notes Deirdre’s admitting diagnosis was myocardial infarction, or MI, and she underwent immediate percutaneous coronary intervention, or PCI.   

Nurse Raven knows that cardiogenic shock is a life-threatening condition where the heart is unable to effectively pump blood to supply the body’s needs that can occur following conditions that cause myocardial dysfunction, like an MI where ischemia results in death of the myocardium, or heart muscle. This impairs contractility, decreases stroke volume, and reduces cardiac output, leading to impaired tissue perfusion and decreased oxygen delivery.  

As cardiac output decreases, hypotension occurs, peripheral pulses weaken, and the skin becomes cool and pale as blood is diverted to critical organs.  

Also, blood begins to back up into the pulmonary circulation, resulting in pulmonary edema and impaired gas exchange, which further impairs oxygenation of tissues. To c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Burns</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/R_PqQtvvQaWamCS7xZmnsrGpRryXnqKW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Burns: Nursing]]></video:title><video:description><![CDATA[Burns are a type of injury where the skin and underlying tissues are damaged from exposure to heat, chemicals, electricity, or radiation. As the nurse, you’ll provide patient-centered care for critically-ill patients with burn injuries. 

Okay, the skin is the largest organ in the body and provides important functions like temperature regulation, protection, sensory perception, and vitamin D production.  

Its two main layers, the epidermis and dermis, rest upon the hypodermis, or subcutaneous tissue. Starting with the outermost layer, the epidermis is a waterproof barrier that shields underlying structures from mechanical stress and ultraviolet radiation. Next is the dermis which contains hair follicles, nerves, sensory receptors, sweat glands, and immune cells. Lastly is the hypodermis, made of fat and connective tissue that insulates the body and connects the dermis to the underlying muscle.  

Now, the type and severity of burn injury complications will depend on the depth and the size of the burn.  

Starting with burn depth, superficial burns, also known as first degree burns, involve only the epidermis.  

Partial thickness burns, or second-degree burns, can be either superficial or deep. Superficial partial thickness burns involve the epidermis and the top layer of the dermis, while deep partial thickness burns affect most of the dermis.  

Finally, full thickness burns are called third-degree burns when they extend through all layers of the skin and affect the subcutaneous tissue; and they&amp;#39;re called fourth-degree burns when they extend to the underlying muscle, tendons, or bones.  

Next, the size of the burn involves calculating the percentage of the total body surface area, or TBSA, impacted by the burn.  

One method of quickly estimating the TBSA uses the rule of nines, which involves dividing the body into sections that each represent approximately 9% of the TBSA. For burns that affect less than 20% of the TBSA, the effects are typic]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Disseminated_Intravascular_Coagulation</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/arwO03WeRxCB7TTNp1Yz1YlkQVSZOjb8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care case study - Disseminated intravascular coagulation (DIC): Nursing]]></video:title><video:description><![CDATA[Nurse Keisha works in the intensive care unit and is caring for Sharon, a 63-year-old patient who was diagnosed with disseminated intravascular coagulation, or DIC. Nurse Keisha goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Sharon’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Keisha recognizes important cues, including Sharon’s vital signs which are temperature 99.8° F, or 38.7° C, heart rate 112 beats per minute, respirations 18 breaths per minute, blood pressure 112/64 mmHg, and oxygen saturation 98 percent on 2 liters of oxygen by nasal cannula.  

Sharon is alert and oriented.  

In her fingertips, she reports chills and aching.  

Upon assessment, Nurse Keisha notices scattered areas of ecchymosis on Sharon’s arms bilaterally.  

As well, there’s a small amount of blood oozing from Sharon’s venipuncture site and her gums.  

Next, Nurse Keisha analyzes these cues. She reviews the electronic health record, or EHR, and notes that Sharon has been receiving treatment for bacterial pneumonia and has peripheral blood cultures pending for suspected sepsis.  

Her most recent laboratory results show a platelet count of 9,000/mm3; her activated partial thromboplastin time, or aPTT, and prothrombin time, or PT, are elevated, indicating coagulopathy, or impaired clotting.  

In addition, D-dimer and fibrin degradation products, which are protein fragments made when clots are dissolved, are elevated, and fibrinogen, a protein needed for clot formation, is decreased. 

Nurse Keisha knows DIC is a life-threatening complication that can be triggered by many different conditions, including sepsis.  

In this situation, the systemic inflammatory response to the infection causes an excessive activation of coagulation pathways and suppression of fibrinolysis, meaning there’s uncontrolled clotting along with an impaired cl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Acute_Respiratory_Distress_Syndrome_(ARDS)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PeftU83vSEKWch0ID55GlGdvTOGJw_C7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care case study - Acute respiratory distress syndrome: Nursing]]></video:title><video:description><![CDATA[Nurse Tamara works in the ICU and is caring for Matthew, a 67-year-old who was diagnosed with acute respiratory distress syndrome, or ARDS. Nurse Tamara goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Matthew’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tamara recognizes important cues, including Matthew’s vital signs which are temperature 101.2 F or 38.4 C, heart rate 110 beats per minute, respirations 24 breaths per minute, blood pressure 90/45 mmHg, and oxygen saturation 89 percent. Matthew is intubated and mechanically ventilated with an FiO2 of 50% and PEEP of 10 cm H2O; and he has a sedative and neuromuscular blocker infusing in a central line. Upon assessment, Nurse Tamara notes bilateral fine crackles in his lung bases. 

Next, Nurse Tamara analyzes these cues. She reviews the electronic health record, or EHR, and notes that Matthew was admitted for pneumonia and recently developed ARDS, after which he was intubated. His most recent chest X-ray shows diffuse alveolar infiltrates, bilaterally. She also reviews Matthew’s labs, including his most recent arterial blood gas, or ABG, which indicates respiratory acidosis; low partial pressure of oxygen, or PaO2; and an elevated partial pressure of carbon dioxide, or PaCO2.  

Nurse Tamara knows that ARDS is a severe condition characterized by lung inflammation and pulmonary edema that’s triggered by an underlying lung injury, like pneumonia. Inflammatory mediators are released at the site of injury, damaging the alveolar-capillary membrane where gas exchange occurs. This results in increased capillary permeability and edema, as protein-rich fluid leaks into the alveoli, impairing their ability to participate in gas exchange. Also, the damaged type II pneumocytes start producing less surfactant, so there’s more surface tension within the alveoli, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_Organ_Dysfunction_Syndrome_(MODS)</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ZziCPezyQ-eebaZRzzYUW3gURrGU4-yS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple Organ Dysfunction Syndrome (MODS)]]></video:title><video:description><![CDATA[Multiple organ dysfunction syndrome, or MODS, is the progressive dysfunction of two or more organ systems, where homeostasis can’t be maintained without intervention. It occurs when an insult or injury to the body, from conditions like severe infections, severe trauma, or a critical illness, initiates an uncontrolled inflammatory response. Depending on the severity and the number of organs involved, MODS can progress to organ failure and death. 

Now, a normal inflammatory response is protective and part of how the immune system reacts to an insult that causes injury to the body’s tissues.  

Within seconds of the injury, immune cells, such as macrophages and mast cells, release inflammatory mediators.  

These inflammatory mediators, including cytokines, chemokines, interleukins, and histamine, recruit more immune cells to the site of injury and act on the endothelial cells lining the blood vessels to cause vascular changes that support the inflammatory response.  

The endothelial cells release nitric oxide, causing vasodilation, which allows more blood to accumulate at the site of injury.  

Endothelial cells also express adhesion molecules, which allow immune cells, mostly neutrophils, to move along the endothelial surface so they can reach the injured site.  

Also, vascular permeability increases, which is when the endothelial cells begin to separate from each other. This allows fluid, proteins, and leukocytes to move from inside the vessels and out to the extravascular space, where the leukocytes begin to eat up any invading bacteria by phagocytosis.  

And finally, activation of plasma proteins initiates the formation of clots, which provides a foundation for healing.  

At the same time, the adrenal glands release stress hormones like epinephrine and cortisol to help regulate the inflammatory response. Regulation of the inflammatory response can promote the positive aspects of inflammation by helping to eliminate harmful infections, remove damaged]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pressure_injury_prevention:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kIbbmqOdRn6TElAo4JUU6R1UQAaKLkPS/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Pressure injury prevention: Nursing]]></video:title><video:description><![CDATA[Nurse Nathan works at a rehabilitation hospital and is caring for Larry, a 72-year-old with a left below-the-knee amputation related to complications from diabetes mellitus. In collaboration with the registered nurse, RN Ashmeet, Nurse Nathan goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Larry’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Nathan recognizes important cues, including Larry’s vital signs, which are  

temperature of 98.6 F or 37 C, heart rate 90 beats per minute, respirations 18 breaths per minute, blood pressure 130/80 mmHg, and oxygen saturation 95 percent on room air. Nurse Nathan notes that Larry has been incontinent of urine and is struggling to effectively reposition himself in bed. Nurse Nathan also notices that Larry has clinical signs of malnourishment such as dry, thin skin and brittle nails and hair.  

Next, Nurse Nathan analyzes these cues.  He reviews the electronic health record, or EHR, and notes that Larry developed a pressure injury on his sacrum during a past hospitalization that has since healed. He also sees that RN Ashmeet calculated Larry’s pressure injury risk using the Braden Scale which indicated that Larry is at high risk for developing another pressure injury.  

Nurse Nathan understands that pressure injuries involve damage to the skin or underlying tissue because of prolonged pressure, which causes reduced blood flow. This results in tissue hypoxia and ischemia, which ultimately leads to necrosis and ulceration. Nurse Nathan knows that most often, pressure injuries develop in patients who have difficulty moving around or are totally immobile. He also knows other factors increase the risk for pressure injury, like thinning of skin and subcutaneous tissue due to age and impaired nutrition and hydration; exposure to skin irritants, like urine; as well as diabetes mell]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_End-of-life_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/rbInFJe0SWmHQ50OsPsGgJFyRJWcy5RY/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - End-of-life care: Nursing]]></video:title><video:description><![CDATA[Nurse Leslie works in a hospice house and is caring for Esther, an 89-year-old with a history of end-stage chronic obstructive pulmonary disease, or COPD. In collaboration with the registered nurse, RN Zach, Nurse Leslie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Esther’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Leslie recognizes important cues, including Esther’s vital signs which are temperature 99 F or 37.2 C, heart rate 98 beats per minute, and blood pressure 88/42 mmHg. Her radial pulse is weak and thready. Esther’s breathing pattern is shallow, and there’s an audible gurgling sound as she breathes in and out. Nurse Leslie notices that Esther’s skin looks mottled and pale, and that it feels cool to the touch. She also notes that Esther appears restless and uncomfortable.  

Next, Nurse Leslie analyzes these cues. She reviews the electronic health record, or EHR, and sees that Esther has a current Do Not Resuscitate, or DNR, order and is on comfort care. She also notes that Esther’s urine output was 90 milliliters over the past 12 hours.  

Nurse Leslie knows that as death approaches, body functions begin to slow. Blood pressure and heart rate decrease, and pulses become weak. Then, as circulation slows, there’s less urine output due to decreased renal perfusion, and extremities can become edematous, mottled, dusky, and cool, since there’s less circulation to the periphery. Respirations become slow and irregular; and as death nears, a build-up of saliva and mucus in the throat and upper airways cause breathing to sound wet and gurgling. Episodes of apnea and hyperventilation, called Cheyne-Stokes respirations, may also occur. Nurse Leslie realizes that Esther needs supportive care at the end of her life. 

Now, using the information she has gathered, along with Esther’s medical history, Nurse Lesli]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Personal_hygiene:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0jsBD1BJQhqyFdb0_Y4w5ZEcTc_AuzGL/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Personal hygiene: Nursing]]></video:title><video:description><![CDATA[Nurse Melinda works on a medical-surgical floor and is caring for Beatrice, an 80-year-old with a history of iron-deficiency anemia. In collaboration with the registered nurse, RN Elijah, Nurse Melinda goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Beatrice’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Melinda recognizes important cues including Beatrice’s vital signs, which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 19 breaths per minute, and blood pressure 123/88 mmHg. During bedside report, Nurse Melinda learns that Beatrice tires easily, becomes short of breath with activity, and needs assistance to get up to the bathroom.  

Nurse Melinda then gathers information from Beatrice. 

Nurse Melinda: Hi Beatrice, how are you this morning? 

Beatrice: I’m tired. I want to get cleaned up, but it takes so much energy. 

Nurse Melinda: I can help you get cleaned up. How about you do as much as you can, and when you feel tired, I can take over? 

Beatrice: Okay. 

Nurse Melinda analyzes these cues.  She reviews the electronic health record, or EHR, and notes that prior to admission, Beatrice lived independently, but began having trouble performing activities of daily living, or ADLs, due to fatigue.  

Nurse Melinda understands that iron is essential to produce hemoglobin in red blood cells, or RBCs, which deliver oxygen to the tissues, and that iron-deficiency anemia develops when there’s not sufficient iron to sustain normal hemoglobin production. As a result, there’s not enough hemoglobin to fill a normal-sized RBC, so the bone marrow starts producing microcytic, or smaller, cells that contain less hemoglobin. She also knows that a lack of hemoglobin can cause decreased oxygenation, leading to symptoms like weakness, fatigue, and reduced exercise tolerance, making it difficult t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Supplemental_oxygen:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VaXmkP8URwKPKWsdnSkJ-SISSO_yia-j/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Supplemental oxygen: Nursing]]></video:title><video:description><![CDATA[Nurse Ahmad works on an inpatient medical-surgical unit and is caring for Marietta, a 72-year-old, who underwent a surgical procedure 3 days ago. In collaboration with the registered nurse, RN Laura, Nurse Ahmad goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Marietta’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Ahmad recognizes cues, including Marietta’s vital signs which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 24 breaths per minute, blood pressure 133/66 mmHg, and oxygen saturation 87 percent on room air. Nurse Ahmed notes that Marietta is taking short, shallow breaths and appears anxious. He also sees that Marietta is lying on her side, with the head of the bed flat.  

Nurse Ahmad raises the head of her bed and assists Marietta to reposition herself. 

Nurse Ahmad: Hi Marietta, it looks like you’re having trouble breathing. 

Marietta: It’s hard to take a deep breath. 

Nurse Ahmad: I’ve repositioned you, which should help your lungs expand. Focus on taking deep breaths in through your nose and out through your mouth.  

Then, Nurse Ahmad applies oxygen to Marietta via nasal cannula at two liters per minute, according to his unit’s protocol. 

Nurse Ahmad then analyzes these cues. He reviews the electronic health record, or EHR, and notes that despite seeing documentation that Marietta was taught how to use her incentive spirometer to help keep her lungs expanded, the device isn’t in her room. He also knows that anesthesia during surgery can reduce surfactant production in the lungs, which is needed to keep the little air sacs, called alveoli, open and full of air. He understands that when there’s less surfactant, the walls of the alveoli tend to collapse, leading to atelectasis, where portions of the lungs are not fully expanded.  

Nurse Ahmad realizes that thi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Urinary_retention:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6jDQ6kumRd2VZsvvIgCNJJfETP6NzEmW/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Urinary retention: Nursing]]></video:title><video:description><![CDATA[Nurse Tabitha works on an inpatient medical-surgical unit and is caring for Richard, a 61-year-old with a history of benign prostatic hyperplasia, or BPH, who underwent a cholecystectomy three days ago. In collaboration with the registered nurse, RN Jesse, Nurse Tabitha goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Richard’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Tabitha recognizes important cues, including Richard’s vital signs, which are temperature 98.6 F or 37 C, heart rate 100 beats per minute, respirations 20 breaths per minute, and blood pressure 130/80 mmHg. He also reports his pain as 4 out of 10 in his suprapubic region. Nurse Tabitha notices Richard appears restless, and he states that he has an urge to urinate but can’t.  

Next, Nurse Tabitha analyzes these cues. She reviews the electronic health record, or EHR, and sees that Richard received general anesthesia during his surgical procedure. She realizes that this can lead to urinary retention, due to disruption of the normal neuromuscular processes that control urination.  

Nurse Tabitha also realizes that Richard’s enlarged prostate is likely contributing to his urinary retention since it can block the outflow of urine from the lower part of the bladder and urethra. Nurse Tabitha realizes Richard is likely retaining urine due to a combination of the anesthesia from his surgery and history of BPH, and that he needs effective urinary elimination. 

Next, she notes that Richard has a PRN order for bladder scans. Nurse Tabitha then performs a bladder scan, which reveals 900 milliliters of urine in Richard’s bladder. 

Now, using the information she has gathered, along with Richard’s medical history, Nurse Tabitha reports her findings to RN Jesse, and they choose a priority hypothesis of altered urinary elimination.  

Then, they generate s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Chronic_constipation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LEyTnhAqTbaibX5_BC-J1elYTkKAMLhy/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Chronic constipation: Nursing]]></video:title><video:description><![CDATA[Nurse Kelly works at a primary care office and is caring for Francesca, an 83-year-old who is experiencing constipation. In collaboration with the registered nurse, RN Evan, Nurse Kelly goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Francesca’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Kelly recognizes important cues, including Francesca’s vital signs, which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 18 breaths per minute, and blood pressure 116/64 mmHg. Francesca denies pain, but states her abdomen feels full and distended. 

When asked about her last bowel movement, Francesca replies that she hasn’t had a bowel movement in 3 days, and normally has 2 to 3 hard, lumpy bowel movements each week. Nurse Kelly listens to Francesca’s bowel sounds, which are hypoactive in all four quadrants.  

Next, Nurse Kelly analyzes these cues. She reviews the electronic health record, or EHR, and sees that Francesca takes a diuretic which can increase her risk for constipation due to the elimination of excess body fluids.  

Then, she gathers information from Francesca about other risk factors for constipation.  

Nurse Kelly: Francesca, how would you describe your activity level?  

Francesca: I walk around my house, but that’s it. Sometimes, my knees bother me, and I can’t get around that well. So, I guess I sit around a lot.  

Nurse Kelly: Okay, and how would you describe your fluid intake and diet?  

Francesca: I try not to drink too much water because then I have to go to the bathroom all the time, especially with my water pill. As for my diet, I mostly have my meals delivered. I really like the frozen dinners they send me.  

Nurse Kelly realizes that Francesca has several risk factors for constipation. She has a mostly sedentary lifestyle, and because of Francesca’s age, her gast]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Burn:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Qnu7w61lT_2FJSeWKXhRYvvqRmqlEn6G/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Burn: Nursing]]></video:title><video:description><![CDATA[Nurse Kamala works in a rehabilitation center and is caring for Raul, a 42-year-old who was admitted following a thermal burn in a house fire. In collaboration with the registered nurse, RN Amy, Nurse Kamala goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Raul’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Kamala recognizes important cues, including Raul’s vital signs, which include temperature 98.4 F or 36.9 C, heart rate 100 beats per minute, respirations 21 breaths per minute, and blood pressure 128/88 mmHg.  

Nurse Kamala notes that Raul has partial- and full-thickness burns on his right lower extremity, extending up to his lower abdomen. The dressings over Raul’s burns have a small amount of serosanguineous drainage and the surrounding skin is reddened. She also notices that he appears uncomfortable and restless.  

Next, Nurse Kamala analyzes these cues. She reviews Raul’s electronic health record, or EHR, and notes an order for sterile dressing changes. She also sees that he’s prescribed medication for pain management, and he received his last dose 4 hours ago. She knows that dressing changes will facilitate healing and untreated pain can make dressing changes difficult to tolerate. Nurse Kamala realizes that Raul needs effective pain management so the prescribed wound care can be performed for his burns. 

Now, using the information she’s gathered, along with Raul’s medical history, Nurse Kamala reports her findings to RN Amy, and they choose a priority hypothesis of impaired skin integrity.  

Then, they generate solutions to address Raul’s impaired skin integrity using nonpharmacologic and pharmacologic interventions; and they establish the expected outcome that Raul’s pain will be at a tolerable level to undergo all scheduled dressing changes. 

Nurse Kamala then takes action to implement these solu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Traumatic_Brain_Injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xRIaYSFMSU2134KiPHAKOy2IRL_ZhgMZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Traumatic brain injury: Nursing]]></video:title><video:description><![CDATA[A traumatic brain injury, or TBI, is any damage to the brain caused by an external force. This can be from blunt trauma, such as from falls, motor vehicle crashes, or exposure to a blast wave from an explosion; or from penetrating trauma, like from a gunshot or knife wound, or if bone fragments enter the brain tissue when the skull is fractured. As the nurse, you’ll provide patient-centered care for critically ill patients with traumatic brain injuries. 

Now, TBIs involve primary and secondary injuries. Starting with primary injuries, these involve the initial, mechanical forces that cause direct damage to the brain tissue. Examples include concussions, contusions, hematomas, shearing injuries, and lacerations. A concussion occurs when there’s a bump or jolt to the head, causing the brain to shift within the skull. This leads to a temporary disruption to neural impulses that cause reversible and typically mild neurologic deficits.  

On the other hand, a contusion is bruising composed of small, scattered areas of bleeding in the brain tissue. Contusions often occur with acceleration-deceleration injuries, like a coup-contrecoup injury, where the coup injury occurs directly at the point of impact, and the contrecoup injury occurs on the opposite side of the brain where it collides with the inside of the skull.  

If the force of impact is strong enough, a hematoma can develop, which is a large collection of blood within the skull that can lead to significant pressure on the brain.  

On top of that, as the brain moves around inside the skull, a shearing injury, also known as a diffuse axonal injury, can occur as nerve fibers throughout the brain are stretched and torn. Finally, lacerations of the brain tissue can be caused by any type penetrating trauma.  

In contrast, secondary brain injuries are caused by the body’s response to the initial injury, which can cause further damage to the brain and complicate recovery. Inflammation causes cerebral edema, wh]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Occupational_Health_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/193imaPYQ6eEpv6OaJy4yX9WSQKdooaM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Occupational health nursing: Nursing]]></video:title><video:description><![CDATA[Occupational health is an area of nursing specializing in promoting health and safety of individual employees and groups of workers in employment settings.  

As the occupational health nurse, or OHN, you’ll identify occupational hazards, prevent illness and injury, and promote health by advocating for a safe and healthy work environment. 

Okay, so, occupational health nurses operate in various workplace environments. These include manufacturing companies, corporations, construction sites, utilities, and healthcare facilities.  

In many settings, occupational health nurses serve as the sole on-site healthcare professional. In other settings, like some larger companies, the occupational health nurse may work alongside other professionals like occupational physicians, compliance officers, toxicologists, and even ergonomists.  

The occupational health nurse will collaborate with these team members in addition to the workers, managers, and administrators to meet the needs of organizations as well as individuals and groups of employees.  

Now, in the United States, workplace regulations are guided by the Occupational Safety and Health Administration, or OSHA, which is a government agency responsible for protecting the health and safety of all workers.  

Occupational health nurses will also work closely with OSHA to enforce standards and provide the education and training necessary to ensure safe working conditions. 

As an occupational health nurse, your goals include identifying occupational hazards, preventing illness and injury, and promoting health by advocating for a safe and healthy work environment. 

Now, in order to identify potential hazards, you’ll assess the health and safety of individual workers and the workplace as a whole.  

On an individual level, start by gathering information about previous employment, past exposure to workplace hazards, and medical symptoms or ailments related to previous workplace illness or injuries.  

Next, ask abo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community_Health_Nurses_in_Canada</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/buVSZ1n0T__EAVhk1X2CfYEYQja2gceU/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community Health Nurses in Canada]]></video:title><video:description><![CDATA[Community health nursing is a branch of nursing focused on the health and well-being of communities. A community is a group of people who live in the same area or share certain experiences, values, or characteristics. Examples of communities include specific locations like a town or neighborhood; a family or group of neighbors; a sports team; or a religious group.  

Nurses can support communities by working in areas such as home health and hospice palliative care.  

Okay, so public health nurses are uniquely positioned to aid in community health through the development and implementation of public health interventions within provinces or across Canada. They use a population health approach to promote health and prevent disease while fostering collaboration among groups and community leaders to address health issues within the community.  

Public health nurses work under the direction of official agencies such as a public health department or regional health authority and work in a variety of settings, including homes, schools, community health centers, and clinical settings.  

The services provided by public health nurses depend on where they work and the needs of the community they serve. They engage in health promotion activities like cancer screenings or heart health clinics; and promote disease and injury prevention strategies, through screening and surveillance, or the act of collecting, analyzing, and interpreting health data on both infectious and noncommunicable diseases and then using the information to inform the public and community decision-makers.  

For example, a public health nurse might be responsible for tracking a rise in conditions like diabetes or hypertension in a particular community and then using that information to provide health education and counselling for members of the community.  

Other activities of public health nurses include supporting evidence-informed practice by engaging in research studies or synthesizing curren]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Acute_Pancreatitis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/CUPsKqADRtmU6kcr9z7FxGlbTe6GDSZT/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Acute pancreatitis: Nursing]]></video:title><video:description><![CDATA[Acute pancreatitis is an inflammation of the pancreas. Causes include damage to the pancreas from biliary conditions such as gallstones; chronic alcohol use; certain medications like sulfonamides and corticosteroids; certain endoscopic procedures like endoscopic retrograde cholangiopancreatography, or ERCP; and abdominal trauma. As the nurse, you’ll provide patient-centered care for critically ill patients with acute pancreatitis.  

So, the pancreas is a large gland located behind the stomach. Its endocrine function involves regulation of glucose by producing hormones like insulin and glucagon, while its exocrine function aids in digestion. As far as its digestive function goes, the acinar cells of the pancreas produce and release inactivated digestive enzymes into the small intestine. Here, they’re activated into amylase, lipase, and protease which break down carbohydrates, fats, and proteins. 

Now, in acute pancreatitis, the pancreatic acinar cells are injured, and the inactivated enzymes leak into surrounding pancreatic tissue where they become prematurely activated and begin the process of autodigestion of the tissue. As the pancreatic tissue is damaged by its own enzymes, edema, hemorrhage, fibrosis, and necrosis occurs, along with localized inflammation.  

As inflammation progresses, enzymes and inflammatory mediators are released into the systemic circulation, and travel to other organs, like the liver, kidneys, and lungs, causing widespread organ damage. Acute pancreatitis can progress to systemic inflammatory response syndrome, which leads to increased systemic vascular permeability, third-spacing of fluid, loss of circulatory volume and hypovolemic shock, as well as multiple organ failure, and potentially death. 

Alright, so, clinical manifestations will depend on the severity of the damage to the pancreas and the degree of systemic complications. Typically, there’s an acute onset of pain that’s often described as a knife-like or twisting sen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Depression</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/h1sOExHCTRSTWBw8Ao1kJnrzR-q01eHj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Depression]]></video:title><video:description><![CDATA[Nurse Betty works in a community health clinic and is caring for James, a 65-year-old male who presents for a 3-month follow-up after being diagnosed with depression. After settling James in the room, Nurse Betty goes through the steps of the Clinical Judgment Measurement Model to make decisions about James’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Betty recognizes important cues, including James’ vital signs, which are temperature 98.9 F, or 37.2 C, heart rate 70 beats per minute, respirations 14 breaths per minute, blood pressure 112/68 mmHg, and oxygen saturation 99% on room air. She also notices that James avoids making direct eye contact.   

Nurse Betty: Hi James, it’s good to see you back in the clinic. How are you doing? 

James: I’m fine, I guess.  

Nurse Betty: I remember from your last appointment you recently retired from your job. Tell me how you’re adjusting so far. 

James: It’s been pretty lonely. I haven’t been sleeping much. 

Nurse Betty: I’m sorry to hear that. Do you have any friends or family in this area? 

James: No, not since my wife passed away last year and my daughter moved away. 

Nurse Betty: That sounds very isolating. Have you ever thought about harming yourself or trying to take your own life? 

James: No. 

Next, Nurse Betty analyzes these cues. She reviews the electronic health record, or EHR, and notes that James is currently prescribed a low dose antidepressant to treat his depression. She also calculates that his score on the PHQ-9 scale today indicates a moderately severe level of depression. She also notes that he’s lost 7 pounds, or 3.2 kilograms, since his last clinic visit. 

Nurse Betty knows that depression is a mental disorder that causes loss of interest in activities that were previously enjoyable, and persistent feelings of sadness that interfere with daily life.  

In older adults, depression can be related]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Acute_Liver_Failure</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HMrrVRKJT2G6kTAkePKSdggASUKv85vi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Acute liver failure: Nursing]]></video:title><video:description><![CDATA[Acute liver, or hepatic, failure is a life-threatening condition characterized by severe damage to the liver that interferes with its ability to function. Causes include infections, like viral hepatitis; toxicity from medications, such as acetaminophen, or from substances like ethanol; hypoperfusion, like with portal vein thrombosis; and metabolic disorders such as Wilson disease. As the nurse, you’ll provide patient-centered care for critically ill patients with acute liver failure.  

Now, the liver is located in the upper right quadrant of the abdomen, just below the diaphragm. It performs numerous essential functions including supporting digestion through bile formation and secretion; and production of proteins such as clotting factors necessary for hemostasis, immunoglobulins that are needed to fight infection, and albumin, a protein essential to maintaining intravascular oncotic pressure.  

The liver conjugates bilirubin, a by-product of the breakdown of RBCs; regulates glucose metabolism through glycogenesis, or the storing glucose in the form of glycogen; glycogenolysis, or the breaking down of glycogen into glucose; and gluconeogenesis, or the production of glucose from non-carbohydrate sources. It also plays a crucial role in detoxification of medications, hormones, and other substances, and clearing bacteria from the bloodstream through phagocytic cells called Kupffer cells.  

In acute liver failure, the liver cells, called hepatocytes, are injured and begin to die. This results in the release of inflammatory mediators, loss of hepatocyte function, and an impaired ability to perform essential functions.  

Decreased hepatic bile production and subsequent reduction in bile flow, a condition called cholestasis, leads to a build-up of bile acids in the blood; and impaired glucose regulation results in hypoglycemia. Other problems include impaired hemostasis from lack of clotting factors; and hypoalbuminemia, or decreased albumin in the blood]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Decison_Making_at_End-of-Life</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nRyGI3PMSwuwU9TauVkBKqqqQveEarGh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - End-of-life decision making: Nursing]]></video:title><video:description><![CDATA[Providing support for decision making during end-of-life care is an important role for the critical care nurse. While guiding patients and their families through this unique time, you’ll consider several factors that affect end-of-life care decisions, including communication, the patient, the patient’s family, culture, and spirituality. 

Now, when discussing end-of-life decisions, communication between the patient, the healthcare team, and the patient’s family can take place at the bedside in an informal manner, and more formally during family meetings or conferences.  

Then, goals of care are identified using a shared decision-making approach, using the best available evidence about treatment options while respecting the values and preferences of the patient and family.  

As the nurse providing care during this process, you’ll use skills to facilitate effective communication, like reflection, empathy, and silence. For instance, you can ask the family to consider how they think their family member would proceed with decisions about their care if they were able to communicate their wishes and then pause to give them time to consider their response.  

Throughout this process be sure to use simple language to explain life-sustaining treatments such as cardiopulmonary resuscitation or CPR, and tube feedings. Also explain terms like do not resuscitate, or DNR, and explore what it means to transition to comfort care and remember to allow time for questions and provide comfort when talking about death. 

Decisions about end-of-life care should be made by the patient whenever they are able to communicate for themselves; however, many critically ill patients facing end-of-life care decisions have limited capacity for decision-making due to the cognitive effects of their illness or treatment. So, if the patient is unable to make their own decisions, advance directives like a living will or health care power of attorney should be obtained when available. These do]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Pain_Assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r4e89uj2T1qqVYRQ7SoWzqTWSAKEJkte/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Pain assessment: Nursing]]></video:title><video:description><![CDATA[Pain assessment helps to identify and manage a patient’s pain. Pain is commonly experienced by patients in the critical care unit, and it can act as a stressor that can worsen their condition. It can also have long-lasting effects on daily functioning, quality of life, and overall well-being. As the nurse caring for critically ill patients, you’ll provide patient-centered care by performing pain assessments to effectively address your patient’s pain.  

Now, pain is an unpleasant sensory and emotional experience that occurs in response to actual or potential tissue damage.  

So, you’ll start your assessment by obtaining your patient’s report of how they perceive and interpret their pain. If your patient is able to verbalize their response, you can begin by asking whether or not they have pain. If they answer yes, then you should gather more information to better understand their pain. To do this, you can use the PQRSTUV mnemonic.  

P stands for provocation, or what provokes or causes the pain, like moving or taking a deep breath. It also stands for palliation, or what relieves the pain, like resting or changing a position.  

Q refers to quality, or how your patient describes the pain, such as sharp, achy, burning, stabbing, or dull.  

R stands for region, or the location of the pain, like the arm, head, or abdomen. You can also ask if the pain radiates, or moves from one area to another, like chest pain that wraps around to the back. 

S refers to severity, or how your patient would quantify their pain. To determine severity, you can use a pain scale such as the numeric pain scale where your patient assigns their pain a number from 0 to 10, with 0 being no pain and 10 being the worst pain.  

Other pain scales include a visual analog scale where the patient places an “X” on a horizontal line, with one end representing no pain, and the other end representing the worst pain; and a face scale where the patient assigns a facial expression to their pain int]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Rural_Healthcare</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/86ZG8Y9JQIuTRZ9h4hvf9IASTG_h7pmb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Rural Healthcare]]></video:title><video:description><![CDATA[Nurse Mathias is a community health nurse who’s working on development of a mobile clinic in a rural community for residents to receive preventative and primary care. He goes through the steps of the Clinical Judgment Measurement Model to make decisions about the population’s needs by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Mathias recognizes important cues, including documentation from the regional community health office that indicates many area residents don’t have a primary health care provider. He also notes that two small, rural hospitals in the surrounding area have closed in the last year leaving residents to seek care at the nearest emergency department that’s over an hour drive away.  

Next, Nurse Mathias analyzes these cues. He reviews the most recent census data for the area and finds the population is approximately 5,000 people, which includes single older adults and families with small children and adolescents. He also notes that most of the employed residents work as farmers or at the power plant just outside of town.  

Nurse Mathias knows that barriers to healthcare in rural areas can include limited availability, accessibility, affordability, and acceptability of health care services and providers. He understands that because of the geographical isolation and population sparseness, rural areas tend to have fewer healthcare settings, services, and professionals available; and in cases when adequate healthcare is available, residents may find it inaccessible due to lack of transportation and cost.  

He also understands that acceptability of care can be impacted by cultural differences, stigma, language barriers, and low health literacy, and that these barriers can limit use of preventative services and lead to inadequate management of chronic conditions.  

In addition, Nurse Mathias knows that rural residents are at higher risk for chronic condi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Renal_Replacement_Therapy</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2O7fgK2WRm2PLoCHXnm57_KxRXyOX3RP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical Care - Renal Replacement Therapy]]></video:title><video:description><![CDATA[Renal replacement therapy, or RRT, is a treatment that replaces certain functions of the kidneys, such as fluid and electrolyte balance, acid-base regulation, and excretion of nitrogenous waste products and toxins.  

RRT is indicated in conditions where kidney function is impaired or absent, including acute kidney injury and end-stage renal disease, but it can also be used to treat other temporary serious conditions, like electrolyte imbalances, fluid overload, poisoning, or drug overdose.  

RRT can be done continuously over many hours or days like in continuous renal replacement therapy, or CRRT, or intermittently, like in hemodialysis or peritoneal dialysis, also known as PD. 

Okay, so to perform RENAL REPLACEMENT THERAPY, an access site is necessary to gain entry to the body. In hemodialysis, access to the bloodstream will vary depending on the type of therapy and whether RENAL REPLACEMENT THERAPY is needed temporarily or on a long-term basis. 

Starting with temporary RENAL REPLACEMENT THERAPY, vascular access can be obtained through a percutaneous catheter within a large central vein such as the internal jugular vein or the femoral vein. This temporary vascular access can be used immediately after placement, so it’s often used in conditions that require emergency RENAL REPLACEMENT THERAPY.  

For long-term hemodialysis access, an arteriovenous, or AV, fistula can be created. During this process, an artery and a vein are surgically connected, most commonly joining the radial artery and cephalic vein in the arm. This causes the vein to become “arterialized,” meaning it enlarges and develops thicker walls so it can withstand higher pressure and flow of blood; and it allows for the insertion of a large-bore needle to obtain arterial blood. This “maturing” process takes several weeks.  

Another type of access is an AV graft, which also involves connecting an artery and vein, but is done using a synthetic tube. The graft will also take weeks to mature b]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Spinal_Cord_Injury</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4qsmA0HZQ26LQAb_hTfCIJ_gQcaZv3EL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical Care - Spinal Cord Injury]]></video:title><video:description><![CDATA[A spinal cord injury, or SCI for short, refers to damage to the spinal cord, which is a collection of nerve fibers that transmit information between the brain and the body.  

Spinal cord injuries can result from a mechanical force that damages the neurological tissue, its blood supply, or both, which can result from traumatic events, such as motor vehicle crashes; falls; or injuries from recreational activities and sports. As the nurse, you’ll provide patient-centered care for critically ill patients with spinal cord injuries. 

Spinal cord injuries involve both primary and secondary mechanisms. The primary injury is the damage that occurs from a sudden trauma to the spine. It’s characterized by contusion, or bruising; compression, or crushing under pressure; laceration, or tearing; transection, or severing of the spinal cord; and distraction, where a stretching force causes two adjacent vertebrae to be pulled apart. 

Primary injuries involve several mechanisms, including hyperflexion, hyperextension, rotation, axial loading, and penetrating trauma. Hyperflexion injuries occur from a forward and downward head motion. In contrast, hyperextension injuries involve backward and downward head motion. Both of these injuries are common in the cervical area of the spine, which has the most mobility. 

Rotation injuries are a twisting motion of the spine. Axial loading, or compression injuries, occur when a force is applied vertically to the spinal cord, causing compression fractures and burst fractures of the vertebrae which send bony fragments into the spinal cord. Lastly, penetrating trauma, like a wound that comes from a stabbing, gunshot, or shrapnel from an explosion, can also cause spinal cord injuries.  

Now, after the primary injury occurs, the secondary injury begins and involves a series of events that result in further neurologic damage over weeks and months. The acute phase begins with depolarization of the neurons damaged by the trauma and an imbal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pain_(acute):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/TgAp9_j2Toubz0vf0w5NklyVR9GZlUML/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pain (acute): Nursing]]></video:title><video:description><![CDATA[Nurse Nadia works on an orthopedic unit and is caring for Brian, a 51-year-old with a history of degenerative joint disease, who was admitted for intractable back pain. In collaboration with the registered nurse, RN Katie, Nurse Nadia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Brian’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Nadia recognizes important cues, including Brian’s vital signs, which are temperature 98.8 F or 38.9 C, heart rate 99 beats per minute, respirations 21 breaths per minute, and blood pressure 152/82 mmHg. She also notices Brian is slightly diaphoretic and grimacing. When asked about his pain, he reports a current pain level of 6 out of 10, and that his tolerable level of pain is 3 out of 10.  

Next, Nurse Nadia analyzes these cues. She reviews the electronic health record, or EHR, and notes that Brian is prescribed IV ketorolac every six hours PRN, and he received his last dose two hours ago. Nurse Nadia compares her findings to Brian’s assessment conducted by RN Katie and realizes Brian needs effective pain management.  

Now, using the information she has gathered, along with Brian’s medical history, Nurse Nadia reports her findings to RN Katie who chooses a priority hypothesis of acute pain.  

Then, Nurse Nadia collaborates with RN Katie to generate solutions to address Brian’s pain that will include pharmacologic and nonpharmacologic interventions; and they establish the expected outcome that after intervening, Brian will report a pain level of 3 or less out of 10 within one hour.  

Nurse Nadia then takes action to implement these solutions. She knows that since Brian’s most recent dose of ketorolac was two hours ago, he can&amp;#39;t receive his next dose for four more hours. Since Brian is in moderate pain, she verifies that Brian isn’t allergic to any medications and the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/School_Nursing_in_Canada</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8t80BEW0R1_IrwiKtsfxrdfnTCaSrL9O/_.png</video:thumbnail_loc><video:title><![CDATA[School Nursing in Canada]]></video:title><video:description><![CDATA[School nursing is a branch of nursing dedicated to promoting and maintaining the health and well-being of school-age children through collaboration with families, school staff, and the community.    

Now, as the school nurse your role is multifaceted, meaning there are a variety of functions you’ll perform, and they can vary based on your location and specific institution.  

Functions can include promoting wellness, preventing illness, managing acute and chronic conditions, and providing emergency care.  

Let’s look at some examples. To promote wellness, you can provide health education for students by identifying their learning needs and delivering relevant information.  

For instance, you can provide information on ways to remain physically active or how to respond to peer pressure about substance use. Be sure to tailor the education to be age appropriate; so, when teaching about physical activity, younger children can benefit from education about playing on the playground, whereas teenagers are more likely to benefit from encouraging participation in team sports.  

Next, to prevent illness, you’ll aim to reduce the risk of disease. To do this, you can ensure students are up to date on required immunizations; conduct health screenings; and encourage frequent hand hygiene.  

You’ll also identify and address acute and chronic conditions in the student population. These might include acute conditions like lice or a sore throat; and chronic conditions such as asthma and diabetes. Caring for acute and chronic conditions can include developing a care plan, like an asthma action plan for a student with asthma; administering medications, like insulin for a student with diabetes; or administering paracetamol for a student with a fever.  

Be sure to collaborate closely with the student, their family, and their healthcare provider to ensure the student’s plan of care is comprehensive, clear, and up to date.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Poverty</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Eqju29oLS6GOzqRRoSAhRDjRReWf5gOf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Video Case Study - Poverty]]></video:title><video:description><![CDATA[Nurse Mozasu works as a community health nurse at the health department and is assisting a rural school to address dental care among its students. Nurse Mozasu goes through the steps of the Clinical Judgment Measurement Model to make decisions by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Mozasu recognizes important cues, including the results from a survey distributed to parents of students at the school. The survey included questions about access to dental products, such as toothbrushes, toothpaste, and floss; access to routine dental services, such as dental cleanings; financial ability to obtain products and access services; and other barriers to maintaining their child’s dental hygiene.  

Additionally, the survey gathered demographic data, including the number of individuals in each home; age of each family member; household income; and living situation, such as the type of dwelling or if they rent or own their home.  

Next, Nurse Mozasu analyzes these cues. He notes many parents, particularly those from low-income households, reported difficulty accessing dental products and services due to financial constraints and lack of reliable transportation. Several parents mentioned they can’t afford dental insurance and feel embarrassed that they were unable to provide their child with access to routine dental care and were reluctant to discuss their needs due to the stigma associated with poverty.  

Nurse Mozasu knows poverty occurs when there are insufficient financial resources to meet an individual or family’s basic living expenses, which includes medical services like dental care. He also knows that income level affects health, and that those living in poverty experience poorer health outcomes compared to those with higher incomes. Children are at particular risk, since poverty can negatively impact their growth, development, and overall health.  

Nurse Mozasu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Interpersonal_Violence</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/nwoqS8wfT0WdirsFV6rJzMczQUSoM20X/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community health case study - Interpersonal violence: Nursing]]></video:title><video:description><![CDATA[Nurse Alex is a school nurse who is caring for Charlie, a 6-year-old who came to the nurse’s office with a stomachache. Nurse Alex goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Charlie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Alex recognizes important cues, including Charlie’s vital signs, which are temperature 98.9 F, or 37.2 C, heart rate 102 beats per minute, respirations 20 breaths per minute, blood pressure 96/64 mmHg. They notice that Charlie doesn’t make eye contact with them and seems withdrawn.  

After obtaining her assent, Nurse Alex performs an assessment and notes Charlie’s abdomen is soft, non-distended, with active bowel sounds, and no guarding.  

Upon inspection, they observe a small, round burn mark on Charlie’s chest and a couple circular bruises on her upper arm in various stages of healing.  

Nurse Alex: Tell me how you’re feeling Charlie.  

Charlie: My belly hurts. It’s been hurting all morning. 

Nurse Alex: I’m sorry your belly hurts. I noticed you have some marks on your arm and chest, where did those come from? 

Charlie: I don’t know. Probably from playing outside. 

Next, Nurse Alex analyzes these cues. They review the electronic health record, or EHR, and note Charlie has been in the nurse’s office several times over the last year with complaints of stomachaches and headaches. They also note Charlie fractured her arm last year.  

Nurse Alex knows that child abuse... 

is a type of adverse childhood experience, or ACE, which is a traumatic event in a child’s life that has a lasting, negative impact on their growth and development.  

They also know there are different types of abuse including physical abuse, where there’s intentional physical force resulting in harm, like burns, bruising, and fractures; sexual abuse, which involves forcing a child into sexual acts; emotion]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Pulmonary_Embolism</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DRWCUQcxTM_DfC0WjwrX5YdSRF_PzfO7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care case study - Pulmonary embolism: Nursing]]></video:title><video:description><![CDATA[Nurse Joe works in the emergency department and is caring for Rachel, a 64-year-old who was diagnosed with a pulmonary embolism, or PE. Nurse Joe goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Rachel’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Joe recognizes important cues, including Rachel’s vital signs which are temperature 99.7° F, or 37.6° C, heart rate 110 beats per minute, respirations 26 breaths per minute, blood pressure 94/62 mmHg, and oxygen saturation 86 percent on 6 L/min nasal cannula. Upon assessment, Nurse Joe notes Rachel is apprehensive, short of breath, coughing, and has crackles in her bilateral lower lobes. She reports a sharp pain in her chest that worsens with inspiration that she rates as 4 on a 10-point numeric scale.  

Next, Nurse Joe analyzes these cues. He reviews the electronic health record, or EHR, and notes Rachel has a history of factor V Leiden, a genetic disorder that increases the risk of blood clots, and that she returned home from a long, overnight flight last night. He also reviews her ECG which shows sinus tachycardia and her CT that confirms a PE in her left lung.   

Nurse Joe knows a PE can occur when a clot or plug of material travels to the lungs and lodges in the small pulmonary vessels, obstructing blood flow. He realizes Rachel’s history of factor V Leiden and prolonged immobility during her flight place her at risk for venous thromboembolism, or VTE. VTE is when a deep vein thrombosis, or DVT, which is a blood clot that develops in a vein in an extremity, travels to the lungs, causing a PE.  

As the PE obstructs blood flow, it creates a ventilation-perfusion, or V/Q, mismatch where, in the affected area of the lung, there’s enough oxygen but not enough blood to pick it up. This results in ventilatory dead space, inadequate gas exchange, and hypoxemia, trigge]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Substance_Use</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kW-LerEZSFingdXYbXDsvDZ7Qg2-Tu9-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community health case study - Substance use: Nursing]]></video:title><video:description><![CDATA[Nurse Stevie is a community health nurse and is running a workshop about substance use for a group of parents and teachers of teenagers. She goes through the steps of the Clinical Judgment Measurement Model to make decisions about the group’s needs by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Stevie recognizes important cues, including the participants’ responses on a pre-workshop survey, where they submitted a variety of questions regarding concerns about the prevalence of substance use in teenagers and how to support their teenagers to make good choices.  

Next, Nurse Stevie analyzes these cues. She reviews the demographic data of the group, which includes a mix of parents and teachers with varying levels of experience and knowledge on substance use. She also reviews recent community data that indicates an increase in substance use among local teenagers.  

Nurse Stevie knows substance use includes any substance that threatens an individual’s health or impairs their social or economic functioning. Substances can include alcohol; tobacco, including e-cigarettes, or vapes; and drugs such as prescription, over-the-counter, and illicit drugs. She knows that teenagers are more likely to engage in binge-drinking, and that e-cigarettes are becoming popular and prevalent.  

Nurse Stevie recognizes that while risk-taking and experimentation is a normal part of adolescent development, younger individuals are at increased risk of dependence and poor health outcomes when using substances.  

She also understands that risks for substance use include family-related factors, such as genetics, family dynamics, and adverse childhood outcomes as well as social, financial, and cultural influences. Whereas protective factors against substance use include having a positive role model and a strong connection with family, friends, and the community; appropriate supervision; and engage]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Video_Case_Study_-_Septic_Shock</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/RwObLoKvSzOgCWn3-sB1hTapQXO97ajb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care case study - Septic shock: Nursing]]></video:title><video:description><![CDATA[Nurse Miguel works in the intensive care unit and is caring for Scott, a 64-year-old admitted for septic shock. Nurse Miguel goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Scott’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Miguel recognizes important cues, including Scott’s vital signs which are temperature 101.2 F, or 38.4 C; heart rate 105 beats per minute; respirations 28 breaths per minute; blood pressure 86/44 mmHg , with a mean arterial pressure, or MAP, of 58 mmHg; and oxygen saturation 89 percent on 4 liters of oxygen per nasal cannula. Upon assessment, Nurse Miguel notes Scott’s skin is warm and flushed; he&amp;#39;s oriented to person and place, but not time; and appears restless. Scott also has a 1 liter bolus of IV fluids that just finished infusing. 

Next, Nurse Miguel analyzes these cues. He reviews the electronic health record, or EHR, and notes Scott’s white blood cell, or WBC, count is elevated at 18,500 cells/ µL; his lactate is increased; and his arterial blood gas, or ABG, results indicate metabolic acidosis. 

Nurse Miguel knows septic shock is a condition in which there’s profound cellular, circulatory, and metabolic dysfunction, and that it’s a subset of sepsis, which involves life-threatening organ dysfunction caused by an extreme and dysregulated systemic response to an infection.  

He understands that the inflammatory mediators released by immune cells in response to the infection causes vasodilation of the endothelial cells lining the blood vessels, along with increased capillary permeability, where the endothelial cells begin to separate, allowing plasma proteins to move out into the tissues, pulling fluid with them.  

This results in circulatory alterations that include relative hypovolemia, reduced circulating volume, hypotension, decreased preload, and decreased cardia]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/School_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3LyWNFzGSueKu0l-I1gE8fLtRNWWswzY/_.png</video:thumbnail_loc><video:title><![CDATA[School Nursing]]></video:title><video:description><![CDATA[School nursing is a branch of nursing dedicated to promoting and maintaining the health and well-being of school-age children, through collaboration with families, school staff, and the community.  

Now, school nursing is meant to provide continuity of care between school, home, and the community healthcare system. While services vary among states, communities, and institutions, the services provided reflect the specific needs of students, availability of community resources, funding, and school preferences.  

Depending on the need, the school nurse may act in a variety ofassf roles including direct caregiver, educator, case manager, counselor, or community liaison.  

Regardless of the specific role, school nursing typically addresses health education, which aims to promote healthy behaviors and provide information on practices that can negatively impact health; physical education, which helps students develop skills and habits that promote physical fitness and health; and health services, consisting of preventative care; acute and chronic condition management; counseling; referrals; and emergency preparedness and response.  

Additionally, school nursing can expand to the school’s support staff, students’ families, and the community. Support staff can benefit from health promotion programs through the school, such as those that focus on maintaining a healthy blood pressure or encouraging physical activity. Students’ families and the surrounding community can benefit from community outreach programs based on local needs and available resources.  

So, as the school nurse you’ll provide education and offer health services based on the needs of the school and its students.  

Starting with health education, you can provide instruction on ways to prevent injuries such as sprains, fractures, and even traumatic brain injuries. Injury prevention education should begin early, so be sure to tailor your education to meet the needs of various age groups. For]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Culture_and_Population_Health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/41cMG5g1QvugsKQbFrgg0pG1SaWqxZ2u/_.jpg</video:thumbnail_loc><video:title><![CDATA[Culture and Population Health]]></video:title><video:description><![CDATA[Culture is an evolving and complex phenomenon that encompasses the beliefs, assumptions, and values that are widely shared by groups of people over time. As the community health nurse, or CHN, you’ll provide culturally competent care to promote positive population health outcomes for individuals, groups, and communities.  

Okay, so, there are some important concepts to keep in mind when caring for people from different backgrounds, to help you to be better equipped to practice cultural competence.  

First, race describes a person’s biological variations that have their origins in genetic ancestry, like skin color or hair texture.  

On the other hand, ethnicity refers to belonging to a group that shares cultural patterns, such as beliefs, values, and traditions, and is often influenced by factors, like geographic location, heritage, and education. Keep in mind that people of the same race can have different ethnic and cultural backgrounds.  

For instance, Black individuals are often wrongly viewed as sharing the same ethnicity and culture, even though they’re a culturally diverse group with ancestry and heritage that can be traced back through North America, Africa, and the Caribbean.  

Speaking of cultural diversity, this term encompasses the variations among populations based on factors like race and ethnicity, as well as sexual orientation, social class, and physical and mental abilities. 

Now, in order to provide effective and equitable care and promote positive population health outcomes for people of diverse cultural groups, you’ll work toward developing cultural competence. Although the process of developing cultural competence looks different for each person, it generally includes five key elements.  

First, cultural awareness involves examining one’s own cultural background to discover how attitudes, biases, and prejudices can impact the provision of care.  

Next, cultural knowledge is the process of gathering information about the wor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Anaphylactic_reaction:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l_YjX4bhR0yZhS1YI3HnZFNFSb2F-rBF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Anaphylactic reaction: Nursing]]></video:title><video:description><![CDATA[Nurse McKenzie works on an inpatient medical-surgical unit, and is caring for Demetrius, a 56-year-old, who was admitted for pyelonephritis. In collaboration with the registered nurse, RN Anita, Nurse McKenzie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Demetrius’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse McKenzie recognizes important cues, including Demetrius’ vital signs, which include temperature 100.4 F or 39 C, heart rate 110 beats per minute, respirations 23 breaths per minute, blood pressure 100/58 mmHg, and oxygen saturation of 91 percent on room air.  

She notices that Demetrius’ face is flushed, he has a has a worried expression, and that he’s short of breath. Nurse McKenzie auscultates his lung sounds and notes expiratory wheezes bilaterally. She also sees that ceftriaxone is currently infusing through Demetrius’ intravenous line along with normal saline.  

Next, Nurse McKenzie analyzes these cues. She reviews the electronic health record, or EHR, and notes that the infusion of ceftriaxone was started 10 minutes ago by RN Anita. She also sees that Demetrius has no documented allergy to ceftriaxone but understands that if Demetrius received the antibiotic in the past, that this first exposure may have caused his body to produce antibodies against it, sensitizing him, a process where certain immune cells, called T lymphocytes are activated and stimulate B lymphocytes to secrete IgE antibodies into the bloodstream.  

These IgE antibodies then bind to the surface of other cells, called mast cells and basophils, which are full of granules that contain proinflammatory molecules like histamine. Then, on his second exposure, the mast cells and basophils, which already have IgE antibodies on their surface, release their proinflammatory molecules, triggering an allergic reaction.  

Nurse McKenzie al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Chronic_obstructive_pulmonary_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/L1FXLHGBRpahMzrx-TVTF6ekRJiNb2c9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Chronic obstructive pulmonary disease: Nursing]]></video:title><video:description><![CDATA[Nurse Seema works on a medical-surgical unit and is caring for Richard, a 75-year-old male with a history of smoking, who was admitted for an acute exacerbation of chronic obstructive pulmonary disease, or COPD. Nurse Seema goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Richard’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Seema recognizes important cues including Richard’s vital signs, which are temperature 99.6 F or 37.5 C, heart rate 98 beats per minute, respirations 28 breaths per minute, blood pressure 142/90 mmHg, and oxygen saturation 85 percent on room air. When asked about pain, Richard reports a current pain level of 0 out of 10. Nurse Seema notes that Richard’s respirations are labored, he has expiratory wheezing, and he’s leaning over in a tripod position. 

Next, Nurse Seema analyzes these cues.  She reviews the electronic health record, or EHR, and notes Richard’s arterial blood gas, or ABG, shows a low PaO2, indicating hypoxemia. She also recognizes COPD causes airway inflammation, leading to obstructed airflow out of the lungs, causing CO2 retention, making gas exchange difficult. Nurse Seema knows that Richard’s hypoxemia, wheezing, and tripod positioning indicate he’s experiencing impaired respiratory function and needs effective respiratory management. 

Now, using the information she’s gathered, Nurse Seema chooses a priority hypothesis of impaired gas exchange. 

Then, she generates solutions to address Richard’s impaired gas exchange that will include pharmacologic and nonpharmacologic interventions. She establishes an expected outcome that after intervening, Richard will maintain an oxygenation saturation between 89 to 92 percent on 2 liters nasal cannula within one hour.   

Nurse Seema then takes action to implement these solutions. She places Richard on continuous pulse oximetry moni]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Anemia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/umRCpfQfTau6NKdJBoawpYWlQ_2oZJ-7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Anemia: Nursing]]></video:title><video:description><![CDATA[Nurse Lucia works in a medical-surgical unit and is caring for Ahmed, a 61-year-old with a history of peptic ulcer disease, who was admitted several days ago for gastrointestinal bleeding. In collaboration with the registered nurse, RN Jumei, Nurse Lucia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ahmed’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Lucia recognizes important cues, including Ahmed’s vital signs, which are temperature 98.6 F or 37 C, heart rate 102 beats per minute, respirations 22 breaths per minute, blood pressure 105/70 mmHg, and oxygen saturation 93 percent on room air. Ahmed appears pale and states that he has no energy. He also reports mild headache pain, which he rates as 3 out of 10.  

Next, Nurse Lucia analyzes these cues. She reviews the electronic health record, or EHR, and notes that Ahmed’s latest hemoglobin is 7.1 g/dL and his hematocrit is 21 percent. Nurse Lucia recognizes that Ahmed is exhibiting clinical manifestations of anemia, that can occur when a bleeding peptic ulcer causes gastrointestinal blood loss.  

She also knows that blood loss can result in loss of iron, which is needed to sustain normal hemoglobin production. This impairs the oxygen-carrying capacity of the blood, resulting in impaired tissue perfusion, and symptoms like weakness, fatigue, headaches, as well as signs like pallor and tachycardia. Nurse Lucia realizes that Ahmed needs management of his anemia to promote effective tissue perfusion and oxygenation. 

Now, using the information she has gathered, along with Ahmed’s medical history, Nurse Lucia works in collaboration with RN Jumei to choose a priority hypothesis of impaired peripheral tissue perfusion.  

Then, along with RN Jumei, she generates solutions to address Ahmed’s impaired perfusion that will include pharmacologic and nonpharmacologic me]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Chronic_lymphocytic_leukemia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dqhxj836TNSBDqClvqn-ZDCtSeiU_RBw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Chronic lymphocytic leukemia: Nursing]]></video:title><video:description><![CDATA[Nurse Tracy works on an inpatient oncology unit and is caring for Margie, a 60-year-old with a history of chronic lymphocytic leukemia, or CLL. In collaboration with the registered nurse, RN Lisa, Nurse Tracy goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Margie’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tracy recognizes important cues, including Margie’s vital signs which are temperature 98.8 F or 37.1 C, heart rate 90 beats per minute, respirations 18 per minute, blood pressure 122/84 mmHg, and oxygen saturation of 98 percent.  

Nurse Tracy notes Margie has various small bruises on her back and legs and generalized lymphadenopathy, or swollen lymph nodes.  

She notices Margie grimacing with movement, and when asked about pain, Margie reports a pain level of 5 out of 10 in her legs and a pain tolerance level of 3 out of 10.  

Nurse Tracy sees a sign on Margie’s door requesting no visitors, so she asks Margie about how she’s feeling. 

Nurse Tracy: Margie, I see you don&amp;#39;t want visitors today.  

Margie: No, I’m very tired. Besides, I’ve been such a burden to them; they probably want a break from me.  

Nurse Tracy: You don’t have to have visitors if you aren’t feeling up for it. Have your family or friends mentioned not wanting to visit? 

Margie: No, they haven’t, but I’d rather be alone. There’s so much I can’t control right now with my leukemia, and I’m feeling overwhelmed. Also, my pain is bothering me. I have extra doses of pain medicine to take between scheduled doses, but I forget to ask until my pain is too bad.  

Next, Nurse Tracy analyzes these cues. She reviews the electronic health record, or EHR, and notes that Margie has scheduled pain medication as well as doses to take as needed, or PRN, for breakthrough pain. The medication administration record shows that Margie hasn’t receiv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Primary_hypertension:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/-ddeAcrNQ1eJUUsNhOHYcCHbRwCfxPMz/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Primary hypertension: Nursing]]></video:title><video:description><![CDATA[Nurse Tom works at a primary care clinic and is caring for Mahlik, a 62-year-old who is being seen for a wellness check. In collaboration with the registered nurse, RN Jenny, Nurse Tom goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Mahlik’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tom recognizes important cues, including temperature 99.4 F or 37.5 C, pulse 75 beats per minute, respirations 16 breaths per minute, blood pressure of 156/89 mmHg, and oxygen saturation 97% on room air.  

Next, Nurse Tom asks Mahlik about his history.  

Nurse Tom: Do you usually have high blood pressure? Do any of your family members have high blood pressure? 

Mahlik: My dad and older brother do. My job is stressful, so maybe that’s contributing to it. I’ve checked my blood pressure at the drug store, and it’s been around 150/90, but with work, I haven’t had time to come in and have it checked. 

Nurse Tom: Stress can contribute to high blood pressure, and having family members with high blood pressure can increase your likelihood of having it too. What foods do you usually eat? 

Mahlik: I mostly eat fast food because I’m always on the go.  

Nurse Tom: Can you tell me about how often you smoke, drink alcohol, and exercise? 

Mahlik: I don’t smoke, never have. I drink maybe 1 to 2 beers a week on average, and honestly, I don’t exercise as much as I should. I’m just so busy with work.  

Nurse Tom analyzes these cues. He reviews the electronic health record, or EHR, and notes Mahlik’s body mass index, or BMI, is 28 kg/m2. Nurse Tom knows that blood pressure is determined by factors like peripheral vascular resistance, or the force the heart needs to overcome to pump blood into circulation, and the total volume of blood circulating in the body; and he knows if these increase, blood pressure can also increase. Nurse Tom also un]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Acute_coronary_syndrome:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/I-PF4cxkQgWx2SqRGl1kQvG6RkaV-Gzf/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Acute coronary syndrome: Nursing]]></video:title><video:description><![CDATA[Nurse Cameron works on a cardiovascular inpatient unit, and is caring for Kevin, a 55-year-old with a history of coronary artery disease for which he’s prescribed aspirin at home. He was admitted the previous day after undergoing percutaneous coronary intervention, or PCI, with placement of one stent to treat an ST-segment elevation myocardial infarction, or STEMI for short. In collaboration with the registered nurse, RN Rachael, Nurse Cameron goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Kevin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Cameron recognizes important cues including Kevin’s vital signs, which are blood pressure 101/80 mmHg, heart rate 99 beats per minute and regular, respirations 17 breaths per minute, oxygen saturation 96 percent on 2 liters per nasal cannula, and temperature 98.2 F or 36.8 C 

When asked about pain, Kevin reports a current pain level of 3 out of 10 in his groin incision. Nurse Cameron notes that Kevin has a small amount of dried blood on his groin dressing and the surrounding area is ecchymotic and tender to palpation. Nurse Cameron also notes Kevin is prescribed the antiplatelet medication clopidogrel.  

Next, Nurse Cameron analyzes these cues. He understands that PCI is a minimally invasive procedure that involves inserting a catheter through the radial or femoral artery to locate blockages in the coronary arteries. After the blockage is located, a tiny balloon is inserted in the obstructed coronary artery to compress plaque against the artery wall. If needed, a stent can be placed during PCI to keep the artery patent. After the procedure, patients are typically given antiplatelet medications, like clopidogrel, to prevent additional clot formation, especially around the new stent. Nurse Cameron realizes that Kevin’s history of aspirin therapy, combined with c]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Left-sided_heart_failure:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/G8SWoDQKRKeRaiSKFr6-Uo4GTyiYI9s9/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Left-sided heart failure: Nursing]]></video:title><video:description><![CDATA[Nurse Alex works on an inpatient cardiac unit and is caring for Manny, a 65-year-old with a history of hypertension, who was admitted for left-sided heart failure. In collaboration with the registered nurse, RN Donna, Nurse Alex goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Manny’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Alex recognizes important cues, including Manny’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 100 beats per minute, respirations 22 breaths per minute, blood pressure 100/60 mmHg, and pulse oximetry 89 percent on 2 liters nasal cannula. Upon auscultation, they note extra heart sounds, S3 and S4, as well as crackles throughout Manny’s lungs, which is consistent with RN Donna’s assessment. They also notice that Manny’s breathing is labored, and he reports increasing fatigue over the last week.  

Next, Nurse Alex analyzes these cues. They review the electronic health record, or EHR, and see that Manny’s most recent brain natriuretic peptide, or BNP, was 600 pg/mL and ejection fraction was 40 percent. Nurse Alex also notes that Manny is prescribed the loop diuretic, furosemide, and received his last PO dose yesterday. 

Nurse Alex understands that heart failure is a condition where the heart is unable to pump effectively enough to maintain cardiac output to meet the demands of the body. With left-sided heart failure, the left ventricle isn’t able to pump with enough force to push blood into the aorta and the rest of the body. When this happens, the blood remaining in the left side of the heart can back up into the lungs, causing pulmonary problems such as dyspnea, tachypnea, crackles, decreased oxygen saturation, and fatigue. Nurse Alex also knows that the heart’s extra workload and inability to pump out the excess fluid can cause extra heart sounds.  

Nurse Alex realiz]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Atrial_fibrillation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5iEEjNwySkKul7q9MEFpx05DSO6SW_m2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Atrial fibrillation: Nursing]]></video:title><video:description><![CDATA[Nurse Jamaal works on an inpatient cardiac unit and is caring for Laurie-Ann, a 64-year-old, with a history of hypertension, who was admitted two days ago after stabilization in the emergency department, or ED, for atrial fibrillation, commonly referred to as Afib, with rapid ventricular rate, or RVR. In collaboration with the registered nurse, RN Eden, Nurse Jamaal goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Laurie-Ann’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Jamaal recognizes important cues, including Laurie-Ann’s vital signs, which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respirations 16 breaths per minute, blood pressure 126/84 mmHg, and oxygen saturation of 95 percent on room air. Laurie-Ann is awake, alert, and appears comfortable. He also notes that the bedside cardiac monitor shows that she&amp;#39;s currently in an irregularly irregular heart rhythm.  

Next, Nurse Jamaal analyzes these cues. He reviews the electronic health record, or EHR, and notes that Laurie-Ann came to the ED for dizziness and shortness of breath and was diagnosed with Afib, which is a cardiac arrhythmia that occurs when the regular electrical impulses generated from the heart’s natural pacemaker, known as the SA node, are overridden by disorganized impulses from other areas of the heart. These areas have often been damaged from the effects of conditions like hypertension or coronary artery disease, and the impulses they generate result in many rapid mini contractions, usually between 350 and 600 per minute. 

So, instead of one efficient atrial contraction, the atria have a quivering, twitching movement, or fibrillation. The fibrillation causes inefficient emptying from the atria into the ventricles, which means that blood tends to stay in the atria for longer than usual, increasing the risk of ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Deep_vein_thrombosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Vk3nnwknRPW_H2N0_JYcFEz_Rvq1YDeD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Deep vein thrombosis: Nursing]]></video:title><video:description><![CDATA[Nurse Hakeem works on a medical-surgical unit and is caring for Lucille, a 72-year-old who was admitted for a deep vein thrombosis, or DVT in her left iliofemoral vein and is currently awaiting discharge. In collaboration with the registered nurse, RN Owen, Nurse Hakeem goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Lucille’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Hakeem recognizes important cues. He notes slight redness and swelling of Lucille’s left leg. Upon light palpation, Nurse Hakeem notes Lucille’s leg is tender, and she rates her pain as 2 out of 10 and describes it as aching, but tolerable. 

Next, Nurse Hakeem analyzes these cues. He reviews the electronic health record, or EHR, and sees that Lucille recently had surgery, and that an ultrasound identified the DVT. He also notes that Lucille has been receiving continuous IV heparin, which was discontinued yesterday, that she will be transitioned to oral anticoagulation therapy, and then discharged with a prescription for oral dabigatran.   

Nurse Hakeem recognizes that immobility after surgery increased Lucille’s risk for a DVT, and that the thrombus lodged in her vein caused inflammation and decreased venous return to her heart, resulting in swelling and pain in her leg. He understands that anticoagulants like heparin are often used initially to keep the clot from getting larger, to prevent the formation of new clots, and to decrease the risk of a venous thromboembolism, or VTE, which happens when the clot breaks free and travels to the heart and into the lungs.  

Nurse Hakeem also knows that oral anticoagulants, like dabigatran, can be used after a heparin infusion is discontinued to decrease the body’s ability to make clots, and that these treatments can also increase Lucille’s chances of bleeding.  

Now, using the information he&amp;#39]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Gastroesophageal_reflux_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oP4_bMUfREW_4WxMPi2jJdK8S6GhNGC7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Gastroesophageal reflux disease: Nursing]]></video:title><video:description><![CDATA[Nurse Max works in a primary care office and is caring for Anuja, a 54-year-old with a history of gastroesophageal reflux disease, or GERD, who&amp;#39;s being seen for a three-month follow-up appointment. In collaboration with registered nurse, RN Steve, Nurse Max goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Anuja’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Max recognizes important cues including vital signs which are temperature 98.2 F or 36.9 C, heart rate 76 beats per minute, respirations 14 breaths per minute and regular, blood pressure 128/84 mmHg, and oxygen saturation 98 percent on room air. Nurse Max asks Anuja if she’s having any pain, and she reports burning in her mid-upper abdomen after eating, despite taking her prescribed medication.   

Next, Nurse Max analyzes these cues. Nurse Max understands that a band of smooth muscle located between the esophagus and the stomach, called the lower esophageal sphincter, or LES, opens during swallowing to allow food to move from the esophagus into the stomach, and then closes, to keep food from backing up into esophagus. Nurse Max also knows that in patients with GERD, the LES may not close properly, or it may relax when it shouldn’t, so the acidic gastric contents can flow back, or reflux, into the esophagus. They recognize that when the esophageal lining is exposed to gastric contents, it causes symptoms like heartburn and pain in the chest and upper abdomen.  

Nurse Max then reviews the electronic health record, or EHR, and notes that Anuja has been on proton pump inhibitor, or PPI, therapy for three months to treat her GERD and should be experiencing symptom relief by now; so, they talk with Anuja about what she knows about GERD and her prescribed medication.  

Nurse Max: Anuja, I’m glad you’ve been taking your PPI every day and I’m sorry it hasn]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Liver_cirrhosis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5xFcBBN_RH6AS71X0g3zQiq8SAOR4jy4/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Liver cirrhosis: Nursing]]></video:title><video:description><![CDATA[Nurse Abigail works at a long-term care facility and is caring for Thomas, a 72-year-old male with a history of hyperlipidemia and obesity who was diagnosed with cirrhosis secondary to nonalcoholic fatty liver disease. In collaboration with the registered nurse, RN Raashida, Nurse Abigail goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Thomas’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Abigail recognizes important cues, including Thomas’ vital signs, which are temperature 98.8 F or 37 C, heart rate 98 beats per minute, respirations 20 breaths per minute, blood pressure 106/68 mmHg, and oxygen saturation 97 percent on room air.  

Nurse Abigail notes his sclera and skin are jaundiced, or yellow-tinged; he has scattered petechiae, which are small, reddish-purple spots that occur because of bleeding from tiny blood vessels underneath the skin; and his abdomen is round and distended with fluid from a condition called ascites. When asked to turn during his bed bath, Thomas becomes fatigued and short of breath. 

Next, Nurse Abigail analyzes these cues. She reviews the electronic health record, or EHR, and notes that Thomas has gained 9 pounds since his weight was last taken, approximately one week ago. She also sees that Thomas was seen by the physical therapist last week but refused treatment.  

Nurse Abigail knows that cirrhosis is a condition where chronic inflammation causes the liver to become irreversibly scarred. Over time, bands of scar tissue compress the network of blood supply in the liver, leading to increased venous pressure and portal hypertension, which occurs as blood backs up into the portal vein. Higher portal vein pressure means that fluid in blood vessels gets pushed out of the veins and into the peritoneal cavity, causing ascites. And she understands that, as pressure in the portal syst]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Pancreatitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Sps3jdq4Rya61q3hOgVHpAzyR_6gx30a/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Pancreatitis: Nursing]]></video:title><video:description><![CDATA[Nurse Gerdie works on a medical-surgical unit and is caring for Leo, a 47-year-old who was admitted for acute pancreatitis secondary to chronic alcohol use. In collaboration with the registered nurse, RN Don, Nurse Gerdie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Leo&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Gerdie recognizes important cues, including Leo’s vital signs, which include blood pressure 145/90 mmHg,  heart rate 88 beats per minute, temperature 99.2 °F, and respirations 18 breaths per minute. Nurse Gerdie notices Leo is diaphoretic, his gown is damp, and he’s holding an empty emesis bag. She also sees that he has IV fluids infusing in his right forearm.  

Nurse Gerdie: Hi Leo, it looks like you&amp;#39;re not feeling well. What&amp;#39;s your pain level right now on the 0 to 10 pain scale? 

Leo: My pain is a six. It feels like I can’t lie down on my back or get comfortable at all. And I’m nauseated.  

Nurse Gerdie: I understand, I’m going to help you feel more comfortable. 

Next, Nurse Gerdie analyzes these cues. She reviews the electronic health record, or EHR, and notes that Leo’s prescriptions include hydromorphone IV every 3 hours as needed, and his last dose was given two and a half hours ago; and she sees sublingual ondansetron is ordered PRN for nausea, but he hasn’t yet received a dose today.  

Nurse Gerdie understands that acute pancreatitis refers to the sudden inflammation and destruction of the pancreas, which is a long gland located in the upper abdomen, or the epigastric region, behind the stomach.  

She knows that the pancreas has acinar cells that produce pancreatic juice, which contains digestive enzymes like trypsin, amylase, and lipase, that’s released into the duodenum to help digest food. Nurse Gerdie recognizes that pancreatitis can be caused by ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Acute_cholecystitis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/gfyrXcgWTAavK3yMG2a0irAoQyCCG3sl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Acute cholecystitis: Nursing]]></video:title><video:description><![CDATA[Nurse Sandy works on a medical-surgical unit and is caring for Natasha, a 40-year-old female with a history of obesity who&amp;#39;s been diagnosed with acute cholecystitis and is awaiting surgical intervention. In collaboration with the registered nurse, RN Mark, Nurse Sandy goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Natasha&amp;#39;s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Sandy recognizes important cues, including Natasha’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 95 beats per minute, respirations 20 breaths per minute, blood pressure 109/83 mmHg, and pulse oximetry 99 percent on room air. Natasha rates her pain at 3 on the pain scale. She sees that Natasha is holding an emesis bag, which contains a small amount of emesis. Nurse Sandy also notices that Nastasha has IV fluids infusing into her peripheral IV. 

Nurse Sandy auscultates Natasha’s abdomen and notes active bowel sounds in all quadrants, which is consistent with RN Mark’s assessment. However, upon palpation, Natasha grimaces and puts her hand over her mouth. 

Natasha: Please don’t press down on my stomach, I feel like I’m going to throw up again. 

Nurse Sandy provides Natasha with a fresh emesis bag and rubs her back as she vomits.  

Afterwards, Nurse Sandy analyzes these cues. She understands that cholecystitis refers to inflammation of the gallbladder, which is a small, pear-shaped organ located beneath the liver. In patients with acute cholecystitis, bile or gallstones, which are made of bile that has hardened, build up inside the gallbladder, causing irritation of the mucosa lining its walls. This also causes pressure in the gallbladder to increase, leading to wall distension and inflammation.  

Nurse Sandy then reviews the electronic health record, or EHR, and notes that Natasha initially presented t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Urinary_tract_infection_(UTI):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/SrAr60ujTyyQEao404jJfjGdT1GskWcc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Urinary tract infection (UTI): Nursing]]></video:title><video:description><![CDATA[Nurse Steven is working in a long-term care facility and is caring for Louisa, a 79-year-old female with a history of diabetes mellitus. In collaboration with the registered nurse, RN Gene, Nurse Steven goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Louisa’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Steven recognizes important cues, including Louisa’s vital signs, which are temperature 99.0 F or 37.2 C, heart rate 86 beats per minute, respirations 16 breaths per minute, and blood pressure 108/52 mmHg. He also notices Louisa has asked to use the bedside commode to urinate four times in the past hour. Louisa also reports burning with urination and suprapubic discomfort that she rates as 6 out of 10 on the pain scale.  

Next, Nurse Steven analyzes these cues. He reviews the electronic health record, or EHR, and notes that Louisa&amp;#39;s biological sex, age, and medical history can increase the risk for developing urinary tract infections, or UTIs. He knows that patients assigned female at birth have shorter urethras, making it easier for bacteria to travel to the bladder; and that decreased estrogen following menopause results in atrophy of the urinary tract which can lead to decreased bladder emptying, urinary stasis, and more time for bacteria to grow in the urinary tract.  Urinary stasis can also occur in some patients with diabetes mellitus, where impaired smooth muscle contractility of the urinary tract leads to urinary retention.  

Nurse Steven also knows that as bacteria multiply within the urinary tract, they cause inflammation, which leads to suprapubic pain, feelings of bladder fullness, as well as urinary frequency and urgency. Nurse Steven realizes Louisa needs effective urinary elimination. 

Now, using the information he has gathered, along with Louisa’s medical history, Nurse Steven reports]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Chronic_kidney_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uuh1AQMpSSyFbSHIY_4zKAK1Qbar6tH7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Chronic kidney disease: Nursing]]></video:title><video:description><![CDATA[Nurse Marisol works in a family practice office and is caring for Robert, a 55-year-old with a history of chronic kidney disease and type 2 diabetes, who&amp;#39;s arrived for a follow-up appointment. In collaboration with the registered nurse, RN Rae, Nurse Marisol goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Robert’s care by recognizing cues, analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Marisol recognizes important cues including mild, pitting edema in Robert’s lower extremities, a blood glucose of 214 mg/dL, blood pressure of 145/85 mmHg, and a weight gain of 4.5 pounds since his last visit. 

Nurse Marisol asks about Robert’s insulin management at home. 

Nurse Marisol: I see that your blood sugar is higher than your last visit. Have you made any changes to your medications or the foods you eat? 

Robert: Yeah, my blood sugar’s been a little high. Sometimes I get tired and forget to take my insulin at night. 

Nurse Marisol: I also noticed that your ankles are swollen, too. Can you tell me how much water you’ve been drinking lately? 

Robert: Well, I’ve been really thirsty lately, so I’ve been drinking more than usual. Anyway, someone told me that drinking water helps to flush out my kidneys. 

Next, Nurse Marisol analyzes these cues. She reviews the electronic health record, or EHR, and notices that Robert is prescribed ten units of long-acting insulin nightly. She also notes that he’s recommended to follow a 1.5-liter fluid restriction daily. She knows that chronic kidney disease is a progressive and irreversible loss of kidney function, and that uncontrolled diabetes can worsen damage to nephrons over time. She also understands that nephron loss reduces the glomerular filtration rate, or GFR, leading to decreased fluid output, increased fluid retention, edema, and increased blood pressure.  

Nurse Marisol realizes that R]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Type_1_diabetes_mellitus:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/cD7R3pU6QPyCMQ_Bh_h7B-7OSiiZTlTi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Type 1 diabetes mellitus: Nursing]]></video:title><video:description><![CDATA[Nurse Charlotte works on a medical-surgical floor and is caring for José, a 53-year-old with a history of type 1 diabetes mellitus who was admitted for diverticulitis and just returned to the unit after a CT scan. In collaboration with the registered nurse, RN Luke, Nurse Charlotte goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about José’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking actions, and evaluating outcomes.  

First, Nurse Charlotte recognizes important cues, including José’s vital signs which are temperature 98 F or 36.6 C, heart rate 87 beats per minute, respirations 18 breaths per minute, and oxygen saturation 95 percent on room air. She also notices that José’s hands are trembling slightly, and he’s diaphoretic.  

Nurse Charlotte gathers more information from José. 

Nurse Charlotte: Hi José, welcome back from your scan. How are you feeling this morning? 

José: I’m okay I guess; I just feel a little weak and shaky. It started about ten minutes ago. 

Nurse Charlotte: Have you had anything to eat today?  

José: No, I haven’t eaten since last night because of that test I had this morning. 

Next, Nurse Charlotte analyzes these cues. She reviews the electronic health record, or EHR, and notes that José received five units of insulin, for a blood glucose level of 121 mg/dL last evening. She also sees that José was ordered to be NPO after midnight for an abdominal CT scan that he underwent this morning. 

Nurse Charlotte understands that type 1 diabetes mellitus is a condition caused by autoimmune destruction of the pancreatic beta cells, so they can’t produce and secrete insulin, and that treatment typically requires subcutaneous insulin administration. She also knows that hypoglycemia, or blood glucose below 70 mg/dL, is likely to occur if insulin is taken when a patient isn’t eating, like when a patient is NPO, leading to clinical findings such as]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Cancer_and_coping:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eRYgxAdFRoi1kro9Sy9T40CgTpeE0KAi/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Cancer and coping: Nursing]]></video:title><video:description><![CDATA[Nurse Rebecca works at an oncology clinic and is caring for Patricia, a 53-year-old female who had a breast biopsy confirming the diagnosis of breast cancer. Nurse Rebecca goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Patricia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Rebecca recognizes important cues, including Patricia’s vital signs, which include, temperature 98.6 F or 37 C, heart rate 105 beats per minute, respirations 21 breaths per minute, blood pressure 138/88 mmHg, and oxygen saturation 97% on room air. Nurse Rebecca also notes that Patricia is restless, crying, and shaking and states she just doesn’t know how to handle her diagnosis.  

Next, Nurse Rebecca analyzes these cues. She reviews the electronic health record, or EHR, and notes that Patricia has a family history of breast cancer. Nurse Rebecca also sees that previous nursing assessments document Patricia’s report of fatigue and difficulty sleeping. Nurse Rebecca recognizes that Patricia is experiencing emotional distress related to her breast cancer diagnosis.  

Now, using the information she&amp;#39;s gathered, along with Patricia&amp;#39;s medical history, Nurse Rebecca chooses a priority hypothesis of difficulty coping.  

Then, she generates solutions to address Patricia’s coping difficulties that will include nonpharmacologic interventions, and she establishes the expected outcome that Patricia will demonstrate effective coping skills regarding her breast cancer diagnosis by her next follow-up visit.  

Nurse Rebecca then takes action to implement these solutions. After the health care provider discusses the expected treatment plan with Patricia, the registered nurse provides Patricia with education on coping strategies. Later, Nurse Rebecca follows up to see how she’s feeling about the information she’s received and to reinforce]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Benign_prostatic_hyperplasia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vf-fyVFlQC2TGTXFlVPHmufERTGIv2Qw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Benign prostatic hyperplasia: Nursing]]></video:title><video:description><![CDATA[Nurse Suleena works on a Surgical Step-Down Unit and is caring for Pedro, a 55-year-old male with a history of benign prostatic hyperplasia, or BPH, who was admitted two days ago following a transurethral resection of the prostate, or TURP.  

Nurse Suleena goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Pedro’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Suleena recognizes important cues, including vital signs, which are temperature 98.0 F or 36.7 C, blood pressure 140/ 90 mmHg, heart rate 88 beats per minute, respirations 20 breaths per minute, and oxygen saturation 95 percent on room air. She also notices Pedro grimacing and shifting uncomfortably in bed. When examining the collection bag for Pedro’s continuous bladder irrigation, or CBI, Nurse Suleena notices large blood clots and amber-colored drainage.  

Next, Nurse Suleena analyzes these cues. She knows that the CBI output should be light pink, and that blood clots and amber-colored urine in the CBI drainage bag can indicate that the irrigation rate likely needs to be increased. Also, Pedro’s non-verbal cues and vital signs indicate he’s experiencing discomfort, which is also likely due to his ineffective urinary drainage. She also recognizes that bladder spasms resulting from his TURP procedure can cause additional pain. Then, she reviews the electronic health record, or EHR, and notes that Pedro’s last dose of pain medication was four hours ago. 

Nurse Suleena: Pedro, how are you feeling after your procedure? 

Pedro: I’m fine. Isn’t there a male nurse on this floor?  

Nurse Suleena: I understand that having a female nurse care for you after your TURP procedure can be unfamiliar. There are no male nurses available today, but I’m going to do my best to take care of you and make you comfortable. Is there anything I can do to help you? 

Pedro: I feel]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Concussion:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/J8zHonFtReWNCWbfscmVkBsoSJaCWEeM/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Concussion: Nursing]]></video:title><video:description><![CDATA[Nurse Kristin works at a university health clinic and is caring for Jay, a 20-year-old who is being seen after a mild concussion that occurred while playing football last week. In collaboration with the registered nurse, RN Sarika, Nurse Kristin goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Jay’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Kristin recognizes important cues, including Jay’s vital signs, which are temperature 98.0 F or 36.7 C, heart rate 66 beats per minute, respirations 14 breaths per minute, and blood pressure 110/60 mmHg. Jay reports that he has a headache, which he rates as a 2 out of 10 on the pain scale, and states he hasn’t needed medication to manage his pain. He also tells Nurse Kristin that he continues to be fatigued. 

Nurse Kristin then gathers additional information about Jay’s prescribed activity restrictions. 

Nurse Kristin: I know your health care provider explained that you’ll need to limit your activities for one more week. How has that been going so far?  

Jay: It’s been hard. Football is such a big part of my life. Without it, I don’t know what to do. And not being able to drive doesn’t help either. I’m getting stir crazy in my dorm. It got so bad that I drove to a friend’s house the other day even though I know I’m not supposed to yet.  

Then, Nurse Kristin analyzes these cues. She reviews the electronic health record, or EHR, and notes Jay’s concussion occurred following helmet-to-helmet contact during a football game. She notes his score on the Glasgow Coma Scale, or GCS was 13 at the time of the injury, and today RN Sarika scored the GCS at 15. Nurse Kristin knows a concussion is a type of traumatic brain injury that occurs when an event, like the head striking a hard object, causes the brain to hit the skull. This leads to a temporary disruption of neural acti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Community-acquired_pneumonia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/25L0qIDPS6K22rp1sSFqKETCS6KVOJDE/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Community-acquired pneumonia: Nursing]]></video:title><video:description><![CDATA[Nurse Jodie works on a medical-surgical unit and is caring for Ann, a 44-year-old with a history of smoking who was recently admitted for community-acquired pneumonia. In collaboration with the registered nurse, RN Seth, Nurse Jodie goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ann’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Jodie recognizes important cues including Ann’s vital signs, which are temperature 101.5 F or 38.6 C, heart rate 100 beats per minute, respirations 21 breaths per minute and regular, blood pressure 105/68 mmHg, and oxygen saturation 90 percent on room air. Upon auscultation, Nurse Jodie notes coarse crackles and slight wheezing. Nurse Jodie also observes that Ann can’t speak in full sentences without becoming short of breath.  

Next, Nurse Jodie analyzes these cues. Nurse Jodie reviews the electronic health record, or EHR, and notes Ann’s WBC count is elevated at 12,500 cells per mm3. Nurse Jodie knows that an infection is likely causing inflammation in Ann’s lungs. This can result in fluid entering Ann’s alveoli, which can impair gas exchange; as well as narrowing of her airways, which can interfere with her breathing. Nurse Jodie recognizes that Ann needs effective respiratory management.  

Next, using the information she has gathered along with Ann’s medical history, Nurse Jodie discusses her findings with RN Seth, and they choose a priority hypothesis of ineffective gas exchange. 

Then, they generate solutions to address Ann’s infection that will include pharmacologic and nonpharmacologic interventions. They establish the expected outcome that after intervening, Ann will maintain an oxygenation saturation above 92 percent during the shift.  

Nurse Jodie then takes action to implement these solutions.  

Nurse Jodie: I&amp;#39;m going to give you some oxygen to help you br]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Seizure:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bbNZkjjoTKWZviwOxhSB5pGBRyWrxrZ0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Seizure: Nursing]]></video:title><video:description><![CDATA[Nurse Cody works in a long-term care facility and is caring for Estelle, a 78-year-old with a history of epilepsy. In collaboration with the registered nurse, RN William, Nurse Cody goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Estelle’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Cody recognizes important cues, including Estelle’s vital signs, which are temperature 98.2 F or 36.8 C, heart rate 78 beats per minute, respirations 16 breaths per minute, and blood pressure 118/72 mmHg. They review the electronic health record, or EHR, and note Estelle takes lamotrigine twice daily for epilepsy and hasn’t had any seizures or associated auras recently. Nurse Cody also sees Estelle had a routine blood draw yesterday to monitor her lamotrigine serum level, and that Estelle’s lamotrigine level is below therapeutic level, meaning it’s too low to achieve the medication’s desired effect. 

Next, Nurse Cody analyzes these cues. They know that epilepsy is a chronic seizure disorder caused by abnormal, excessive, and synchronous firing from neurons in the brain. They also recognize that Estelle’s risk of having a seizure is greater when her antiepileptic medication is at a subtherapeutic level. Nurse Cody realizes that, until Estelle’s lamotrigine levels stabilize, she will need additional safety precautions to prevent injury related to a seizure.  

Now, using the information they’ve gathered, along with Estelle’s medical history, Nurse Cody reports their findings to RN William, and together they choose a priority hypothesis of risk for injury.   

Then, Nurse Cody collaborates with RN William to generate solutions to address Estelle’s increased risk for injury that include pharmacologic and nonpharmacologic interventions. Together, they establish the expected outcome that after intervening, Estelle will not sustain an in]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Alzheimer_disease:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/LlQa3ZqcT2OtRRUZC2ZWfyHJQOWDKdPl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Alzheimer disease: Nursing]]></video:title><video:description><![CDATA[Nurse Darian works in a long-term care facility and is caring for Rosemary, an 84-year-old female with a history of Alzheimer disease who was admitted following an open reduction and internal fixation, or ORIF, for a hip fracture a few weeks ago. In collaboration with the registered nurse, RN Piper, Nurse Darian goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Rosemary’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darian recognizes important cues, including Rosemary’s inability to recall her daughter’s name, her disorientation to date and time, and that she becomes agitated when asked several questions in a row. Nurse Darian also notes that as the evening progresses, Rosemary becomes more impulsive, and tries to get out of bed on her own. 

Next, Nurse Darian analyzes these cues. He understands that dementia is a neurological condition, caused by structural changes in the brain, and is characterized by a progressive decline in mental functions, including memory, thinking, language, behavior, mood, and personality. He knows that Rosemary’s dementia can be exacerbated by illness, such as the surgery for her hip fracture, and changes to her familiar environment.  

Nurse Darian re-enters Rosemary’s room to gather additional information.  

Nurse Darian: Hi Rosemary. How are you feeling? 

Rosemary: I&amp;#39;ve never met you. 

Nurse Darian: That’s okay, Rosemary. I’m your nurse, Darian. I met you earlier today. Are you having any pain right now? 

Rosemary: Why does everyone have so many questions all the time?  

Nurse Darian notes that Rosemary begins to sit up in bed and tries to swing her legs to the side of the bed to stand up. The two siderails by Rosemary’s head are up, as well as one siderail by her feet. She then moves towards the open space in the bed to exit, so Nurse Darian moves to prevent her from ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Left_hip_fracture:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9UPs5wQXRbap5lRwG6NvCCn2Q5WPmt7A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Left hip fracture: Nursing]]></video:title><video:description><![CDATA[Nurse Kenji works on a rehabilitation unit and is caring for Sharon, a 74-year-old female with a history of osteoporosis who was admitted post-surgery for a left hip fracture requiring an open reduction and internal fixation, or ORIF. In collaboration with the registered nurse, RN Betty, Nurse Kenji goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Sharon’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Kenji recognizes important cues, including Sharon’s vital signs, which are temperature 98.6 F or 37 C, heart rate 90 beats per minute, respirations 19 breaths per minute, and blood pressure 123/88 mmHg. During the bedside report, Nurse Kenji learned that Sharon declined repositioning during the night shift. Upon inspection, he notes that her hip appears mildly swollen and her surgical dressing is clean and dry. Nurse Kenji also notices that Sharon’s left foot is warm with intact sensation, 2+ palpable pulses, and she can wiggle her toes, which is consistent with RN Betty’s earlier assessment.  

Nurse Kenji asks Sharon about her comfort.  

Nurse Kenji: I see that you stayed in the same position throughout the night. Would you tell me your current pain level? 

Sharon: I don’t have pain right now, but I don’t want to move because I know it&amp;#39;ll hurt my hip. 

Nurse Kenji: I understand. Have you considered taking the prescribed medications to manage your pain? 

Sharon: I really don’t like pain medicine because I’m worried about becoming addicted. 

Next, Nurse Kenji analyzes these cues. He reviews the electronic health record, or EHR, and notes that Sharon is scheduled for physical therapy today. He also notes that Sharon is prescribed ice packs to reduce hip swelling, as well as oxycodone and acetaminophen every four hours as needed for pain management but hasn’t taken any medication since early yester]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Schizophrenia:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PCoDkDjRQMuRS9j_GDKcF-rTSlqzf4cw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Schizophrenia: Nursing]]></video:title><video:description><![CDATA[Nurse George works on an inpatient psychiatric unit and is caring for Kit, a 31-year-old with a history of schizophrenia, paranoid type, who was recently admitted for psychotic symptoms. In collaboration with the registered nurse, RN Juanita, Nurse George goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Kit’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse George recognizes important cues, including Kit’s vital signs, which are temperature of 37 C, or 98.6 F, heart rate 98 beats per minute, respirations 20 breaths per minute, and blood pressure 136/82 mmHg. Nurse George notices that Kit appears disheveled, restless, and is looking back and forth suspiciously across the room. 

Nurse George: Hi Kit, how are you doing today? 

Kit: There’s a man coming after me, I’ve seen him watching me from inside the closet.  

Nurse George turns to look inside the closet, which is empty.  

Nurse George: That sounds scary. Although I don’t see anyone else here with us, I’m here to support you and keep you safe.   

Next, Nurse George analyzes these cues. They review the electronic health record, or EHR, and note that Kit has visited the emergency department three times in the past month for symptoms associated with her schizophrenia.  

Nurse George knows the development of schizophrenia is related to both genetic and environmental factors that disturb the brain’s structure and balance of neurotransmitters, like dopamine and glutamate.  

This leads to disabling alterations in behavior, emotions, thinking, and perception, like delusions and hallucinations. Nurse George realizes that Kit needs management of her acute episode of schizophrenia. 

Now, using the information they’ve gathered, along with Kit’s medical history, Nurse George reports their findings to RN Juanita, and together they choose a priority hypothesis of altered p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Bipolar_disorder:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/sXqSzvnaSuiWucLfNfIe-dWPQcGxeMcj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Bipolar disorder: Nursing]]></video:title><video:description><![CDATA[Nurse Nikil works on an inpatient psychiatric unit and is caring for Octavia, a 28-year-old with a history of bipolar I disorder, who was recently admitted for a manic episode. In collaboration with the registered nurse, RN Andre, Nurse Nikil goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Octavia’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Nikil recognizes important cues, including Octavia’s vital signs, which are temperature 98.4 F or 36.9 C, heart rate 75 beats per minute, respirations 16 breaths per minute, and blood pressure 117/72 mmHg.  

Upon entering her room, Nurse Nikil notes Octavia is pacing back and forth, stopping intermittently to rearrange the items on her bedside table.  

Nurse Nikil: Hi Octavia, I see you’re cleaning your room. Could you pause for a moment and speak with me? 

Octavia: Oh sure, I totally have time for you. Don’t you see I’m doing something important? I really need to get my room cleaned so I can start writing. I have an amazing idea for a best-selling book about a forest like the one I grew up next to. My mom would know the name. I should call her. Do you have her number?   

Next, Nurse Nikil analyzes these cues. They review the electronic health record, or EHR, and note that prior to her hospitalization, Octavia had not been taking her lithium as prescribed. The nursing report from the night shift also indicated that Octavia hasn&amp;#39;t slept for the past two nights.  

Nurse Nikil recognizes patients with bipolar I disorder experience extremes in emotions, moving from manic to depressive moods.   

The patient may have symptoms, like racing thoughts, hyperactivity, distractibility, insomnia, and feeling an inflated sense of self.   

They understand that in patients experiencing mania, sleep disturbances can lead to exhaustion which can perpetuate manic or hyp]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Generalized_anxiety_disorder_(GAD):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DCp_5FpbT_CSQFsR7c6XtywaRjWzbs_Z/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Generalized anxiety disorder (GAD): Nursing]]></video:title><video:description><![CDATA[Nurse Aziza works in a primary care office and is caring for Clarence, a 25-year-old who presents with anxiety. Nurse Aziza, in collaboration with the registered nurse, RN Michael, go through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Clarence’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, nurse Aziza recognizes important cues, including Clarence’s vital signs which are temperature 98 F or 36.6 C, heart rate 88 beats per minute, respirations 18 breaths per minute, blood pressure 115/70 mmHg, and oxygen saturation 96 percent on room air. She notes that Clarence is biting his nails and appears restless. Nurse Aziza gathers more information from Clarence about his symptoms.    

Nurse Aziz: Hi Clarence, tell me how you’re feeling. 

Clarence: I&amp;#39;m having trouble sleeping lately. I’m worrying about everything, and I can’t seem to relax.   

Nurse Aziza: That sounds stressful. Have you had any major changes in your life recently?   

Clarence: Yeah, I lost my job two weeks ago.  

Nurse Aziz: I’m sorry to hear that, but you’re in the right place and we’re here to support you. 

Next Nurse Aziza analyzes these clues. She reviews the electronic health record, or EHR, and notes that RN Michael administered the Generalized Anxiety Disorder 7-item screening tool, known as GAD-7, and Clarence had a score of ten out of 21, indicating moderate anxiety. 

Nurse Aziza knows that one of the major findings associated with GAD is excessive worry. Although the exact cause of GAD isn’t known, it’s thought to be caused by an imbalance of the neurotransmitters, where serotonin system activity is low and noradrenergic system activity is elevated. This imbalance can cause symptoms of restlessness, difficulty concentrating, and impaired sleep. She also knows GAD can be brought on by stressful events or life changes, like losing a job. Nurse ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Personality_disorder:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2EF-GO8wQY6lbq9g3sdOO2cfTUyaCnpd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Personality disorder: Nursing]]></video:title><video:description><![CDATA[Nurse Amirah works on an inpatient psychiatric unit and is caring for Yang, a 42-year-old with a history of borderline personality disorder, who was admitted a week ago for self-harm ideation following a breakup with his partner. In collaboration with the registered nurse, RN Francie, Nurse Amirah goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Yang’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Amirah recognizes important cues, including Yang’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 70 beats per minute, respirations 16 breaths per minute, and blood pressure 132/82 mmHg. She notes that Yang’s breakfast tray is untouched on the bedside table.  

Nurse Amirah: Hi Yang, I noticed you haven’t eaten your breakfast. How are you doing today? 

Yang: Sorry, no offense, but that food is disgusting. I’m good, actually, and I’m happy I don’t have a sitter anymore. I’m ready to pack up my stuff and go home.  

Nurse Amirah: I’m glad you feel ready for discharge. To make sure you’re safe to leave, Nurse Francie and I need to gather some information and give you your medicine. 

Yang:  I know, I know. I’m still sad my boyfriend broke up with me, but I’m able to talk about it now. I have other people in my life that care about me, so I feel less alone. 

Nurse Amirah: That’s good to hear. 

Next, Nurse Amirah analyzes these cues. She reviews the electronic health record, or EHR, and notes Yang was diagnosed with borderline personality disorder, or BPD, five years ago, and has been hospitalized for self-harm ideation in the past.  

Nurse Amirah reviews the progress notes and sees that following the breakup between Yang and his partner, Yang called his sister and told her he wanted to commit suicide. His sister then called the emergency services, and he was taken to the hospital.  

Nuse Amirah re]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Attention-deficit_hyperactivity_disorder:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xkYewNv3TY_-ra3dNPeLYql6SS_ryv9t/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Attention-deficit hyperactivity disorder: Nursing]]></video:title><video:description><![CDATA[Nurse Sienna works in a family practice clinic and is caring for Paul, a 10-year-old who was brought in by his caregiver, Erin, for poor school performance over the past year.  In collaboration with the registered nurse, RN Joy, Nurse Sienna goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Paul’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Sienna recognizes important cues, including Paul’s vital signs which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respiratory rate 14 breaths per minute, and blood pressure 105/66 mmHg. She notices that Paul is restless and regularly stands up to look at and touch objects in the examination room.  

Nurse Sienna gathers more information from Erin and Paul.  

Nurse Sienna: Hi Paul, how are you doing today? 

Paul: Okay, I guess. I don’t know why I have to be here.  

Erin: Paul’s been having trouble in school. His grades have been getting worse over the past few months. He&amp;#39;s also been turning in his assignments late or not at all, and when he does turn them in, they’re incomplete.  

Paul: (shrugs) It&amp;#39;s hard to pay attention. 

Erin also reports that Paul’s teachers say he often disrupts class by standing up and blurting out answers to questions instead of raising his hand; and that he has difficulty following rules and waiting for his turn during group activities. When asked about the home environment, Erin reports that when Paul is asked to perform a household chore, he either forgets to do the chore or doesn&amp;#39;t finish it once he starts it.  

Nurse Sienna then analyzes these cues. She reviews Paul’s electronic health record, or EHR, and notes that he’s been to the clinic twice in the past year for similar behavioral difficulties and tested negative for underlying vision, hearing, or cognitive disorders. Nurse Sienna confers wi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Maltreatment_(pediatric):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/F9aGf40KQgOM-1pSAfgVkhUyS2y1FhRA/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Maltreatment (pediatric): Nursing]]></video:title><video:description><![CDATA[Nurse Angelo works in a family practice clinic and is caring for Maya, a 2-and-a-half-year-old who&amp;#39;s brought in for a required wellness check before entering preschool. In collaboration with the registered nurse, RN Rose, Nurse Angelo goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Maya’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Angelo recognizes important cues, including Maya’s vital signs which are temperature 98.6 F or 37 C, heart rate 105 beats per minute, and respiratory rate 23 breaths per minute. Nurse Angelo notes that Maya has multiple circular bruises ranging in color from pale yellow to deep purple on her upper arms, as well as a rounded, punctate burn to the back of her left shoulder about one centimeter in diameter.  

Nurse Angelo also notes Maya grimaces occasionally and appears tense, so he determines Maya’s pain rating is 2 out of 10 according to the Face, Legs, Activity, Cry, and Consolability, or FLACC scale. Nurse Angelo also notes that when he asks Maya questions, she doesn’t respond or make eye contact with him.  

Then, he gathers additional information from Maya’s mother, Josie, about her injuries. 

Nurse Angelo: I see that Maya has some bruising on her arms. Can you tell me what happened? 

Josie: Oh, those? She’s just clumsy. She’s always bruised easily. She probably fell down while she was playing or something. 

Nurse Angelo: I also noticed an injury to her left shoulder that looks like a burn. Do you know what happened there? 

Josie: That doesn’t look like a burn to me. Like I said, I think she probably scraped herself when she was playing. 

Nurse Angelo then analyzes these cues. He reviews Maya’s electronic health record, or EHR, and notes that she has a history of a humerus fracture at age one year. When asked about the fracture, Josie says it was caused by a fall]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Depression_and_suicidal_ideation:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vX8ejRmsT_qZ20FxoRQjygnFStKLsIIJ/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Depression and suicidal ideation: Nursing]]></video:title><video:description><![CDATA[Nurse Iris works on an inpatient psychiatric unit and is caring for Dee, a 30-year-old patient with a history of depression and previous suicide attempts, who was admitted for suicidal ideation. In collaboration with the registered nurse, RN Amrita, Nurse Iris goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Dee’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Iris recognizes important cues, including Dee’s vital signs, which are temperature 98.9 F or 37.1 C, heart rate 65 beats per minute, respirations 16 breaths per minute, and blood pressure 116/70 mmHg. She also notices Dee does not make eye contact and has a flat affect. 

Nurse Iris: Hi Dee, I’ll be your nurse today. How are you feeling? 

Dee: I’m upset.  My friend brought me to the hospital because I told him I wish I was dead.  I don’t want to be here anymore.  

Nurse Iris: I’m sorry to hear that. I want you to know that I and the rest of your medical team care about you. We&amp;#39;re here to support you and keep you safe.  

Next, Nurse Iris analyzes these cues. She reviews the electronic health record, or EHR, and notes that Dee is prescribed fluoxetine for depression and has been hospitalized in the past year for suicidal ideation. She also notes that Dee scored a 19 out of 27 on his PHQ-9 assessment, which is a nine-question, self-reporting depression survey, indicating a moderately severe level of depression. Nurse Iris recognizes that Dee needs a safe environment while he receives treatment for his depression and suicidal ideation. 

Now, using the information she’s gathered, along with Dee’s medical history, Nurse Iris reports her findings to RN Amrita, and together they choose a priority hypothesis of risk for suicide.  

Then, they generate solutions to address Dee’s suicidal ideation that will include pharmacologic and nonpharmacologic interv]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community_Assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JzqTqaoLTzOfKed56DZpqNL_SUe14q4C/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community assessment: Nursing]]></video:title><video:description><![CDATA[A community assessment is a systematic process used to detail the health needs within a community, which is a group of people who live in the same area or share certain experiences, values, or characteristics.  

As the community health nurse, you’ll conduct a community assessment to promote the health and well-being of people within it.  

Now, a community assessment can be performed to highlight a community’s strengths and assets, identify needs, or confirm the presence of a recognized problem.  

Priority problems can be brought to community leaders and partners to inform health policies and plans.  

A community assessment can also provide data on the progress of existing public health initiatives and ensure goals and standards are being met. 

Alright, so, before you begin your community assessment, you’ll first identify the community of interest, which includes the geographic area and the people within it.  

Keep in mind that, as a community health nurse, the community is your client; so, the goal of your nursing interventions is to improve the health and well-being of the community as a whole. This can often involve addressing environmental factors impacting the health of the entire community, like advocating for access to clean water, or taking steps to revise the speed limit near sensitive areas like parks.  

But it can also involve providing individual treatments for problems that can have far-ranging effects on the community, like addressing intimate partner violence or reducing the risk of a community epidemic by treating a patient with active tuberculosis. 

Start your assessment by gathering data about the community from primary and secondary sources.  

Primary data is collected directly through interactions with community members using interviews, focus groups, or surveys.  

At other times, primary data can be collected through participant observation. This is when you share in the life of the community by attending a local social event,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_Disease_Control_and_Prevention</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/r4XmAS86SKWOaMEPP-Yipwp-SB27sfae/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious Disease Control and Prevention]]></video:title><video:description><![CDATA[Infectious disease control and prevention involves stopping the occurrence and reducing the spread, or transmission, of infectious diseases, which are conditions caused by pathogenic organisms, like viruses, bacteria, fungi, and parasites.  

Now, infectious diseases are transmitted in a number of different ways. When an infection is transmitted from a parent to an offspring, via sperm, placenta, breast milk, or contact with the vaginal canal during delivery, that’s called vertical transmission. This is seen in syphilis, which is transmitted through the placenta; and HIV, that is transmitted through the placenta, during delivery, or through breastfeeding. 

Infectious diseases can also be transmitted from person-to-person, called horizontal transmission, through several routes.  

For example, diseases can spread through direct contact with an infected person, like with sexually transmitted infections, or STIs, that are spread during sexual intercourse; and diseases like ringworm and scabies, that spread through skin-to-skin contact.  

Other times, a disease can be spread through indirect contact, which involves a vehicle of transmission outside the infected person. This commonly occurs during contact with contaminated objects, called fomites, like doorknobs, countertops, or bedding. 

When contaminated medical equipment is involved, health care associated infections, or HAIs, can result, which is when a pathogen is transmitted to a patient within a health care setting while they’re receiving treatment for another condition.  

Patients can develop health care associated infections when infection control measures are inadequate, like during or after diagnostic or surgical procedures, or when pathogens are introduced through invasive devices like central lines, urinary catheters, and ventilators.  

Health care associated infections can also occur through the common vehicle route, which is when an infectious agent is spread to multiple people through a con]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Critical_Care_-_Multiple_Organ_Dysfunction_Syndrome</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/t3ZYOVdzSpeZ_dNTYkbFimGTS82VEsK_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Critical care - Multiple organ dysfunction syndrome (MODS): Nursing]]></video:title><video:description><![CDATA[Multiple organ dysfunction syndrome, or MODS, is the progressive dysfunction of two or more organ systems, where homeostasis can’t be maintained without intervention. It occurs when an insult or injury to the body, from conditions like sepsis, severe trauma, or a critical illness, initiates an uncontrolled inflammatory response. Depending on the severity and the number of organs involved, MODS can progress to organ failure and death. As the nurse, you’ll provide patient-centered care for critically ill patients with MODS.  

Now, MODS can be primary or secondary. First, primary MODS results from a direct, initial insult or injury to an organ that causes impaired perfusion and organ dysfunction. This initiates an inflammatory response, and the immune system, including immune cells, like neutrophils and macrophages, becomes primed, meaning it’s placed on high alert and prepared to respond if a secondary insult occurs.  

When this happens, these primed immune cells release an outpouring of chemical mediators, producing an exaggerated immune response called a cytokine storm.  

This uncontrolled inflammatory response affects organs distant from the site of initial insult, resulting in secondary MODS. 

During secondary MODS, there’s widespread endothelial cell damage. Extensive vasodilation occurs as endothelial cells release nitric oxide. This, along with massive capillary permeability, results in interstitial edema, maldistribution of circulating volume, and impaired tissue perfusion.  

The endothelial cells also release prothrombotic mediators, which can lead to the development of excessive microvascular clot formation that obstructs blood flow and impairs perfusion even more. Together, these events eventually result in profound tissue hypoxia. 

At the same time, the neuroendocrine system is activated, causing an extensive stress response, which involves the release of stress hormones that increase oxygen consumption and intensifies the metabolism of car]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Family_Assessment</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/OvpNNGz2SWuKCjeAoN-gNc-6SoGsOVf0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Family Assessment]]></video:title><video:description><![CDATA[A family assessment is a method of collecting and organizing information about a family’s structure and function. As a nurse, you’ll perform family assessments and initiate interventions to promote positive health outcomes and support the family’s well-being. 

A family can be defined as a group of people that depend on each other for physical, emotional, or economic support. They’re also bound together in relationships, either by blood, marriage, adoption, or by choice.  

Now, individual families can be better understood by considering their structure and function. Family structure refers to the family’s organization, which includes the individuals who make up the family, their relationships with each other, and how they interact with each other and other social systems.  

A family’s internal structure includes the individual members within the family. For example, a family may consist of a married couple, which may or may not have children or stepchildren; or, a family can be a multi-adult household, which could include a cohabiting couple and multiple generations of family members who share a home.  

Families also have an external structure, which refers to extended family members who are considered outside of the immediate family, like aunts, uncles, and cousins. The external structure also includes the family’s associations with their community, like with work, school, churches, and other institutions. Lastly, families have contextual structures which refer to their ethnicity, race, social class, and religion. 

Next, family function refers to the family’s activities that meet the needs of individual family members, the family as a whole, and family’s relationship with the community.  

There are five primary functions the family performs. First, there’s the economic function, which includes how the family makes decisions about managing expenses, such as housing, insurance, savings, and buying other goods and services for the family.  

Next is the]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epidemiology_in_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4Ex4NwUYT3uLtD6T88nSMP5rSKS1hzux/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epidemiology in Nursing]]></video:title><video:description><![CDATA[Epidemiology is the study of factors that determine health-related conditions in a population, including infectious and chronic diseases; accidents and injuries; and the effects of occupational and environmental exposures.  

As the nurse, you’ll use epidemiology to identify factors that affect health-related conditions in your community and use that information to reduce disease risk and promote health. 

Now, there are some common measures in epidemiology used to describe health-related conditions.  

Morbidity is the occurrence of a condition in a population, like the number of individuals who have asthma, influenza, or have experienced a hip fracture from a fall. You can measure morbidity using incidence rate and prevalence rate.  

An incidence rate refers to the occurrence of new cases of a certain condition within a population at risk during a specific time.  

To calculate an incidence rate, you’ll set up a ratio with the number of new cases as the numerator and the population at risk as the denominator.  

Keep in mind that the population at risk is comprised of individuals who are at risk for the condition; so known cases and individuals who are not susceptible to the condition, like those who are immunized against a certain disease, are subtracted from the total population.  

As an example, let’s say that in a community of 10,000 people there were 40 existing cases of asthma, and 10 new cases were diagnosed during one year. To find the incidence rate, subtract the 40 known cases from the total population of 10,000 to get the population at risk of 9,960. Then divide the 10 new cases by 9,960 to get an incidence rate of 0.001. You’ll then multiply this number by a factor, like 1,000, to avoid small fractions.  

This gives you an incidence of asthma cases per 1,000 individuals in the community, which is 1 per 1,000 during that year. 

On the other hand, a prevalence rate, which is also called prevalence proportion, is the number of existing ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Family_Health_Risks</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/s59IMm2qTDaLhUM6Jz0dsHWXQfmQ1bNd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Family Health Risks]]></video:title><video:description><![CDATA[Family health risks are factors that can contribute to illness within a family, which is a group of people that depend on each other for physical, emotional, or economic support, and are bound together in relationships, either by blood, marriage, adoption, or choice. As the nurse, you’ll work with families to identify and reduce their health risks. 

Alright, so, there are biological, behavioral, and environmental risk factors that can contribute to the development of unhealthy outcomes with families. Biological risk factors are related to genetics and life events. Starting with genetics, certain conditions can be inherited and passed down through families.  

For example, a mutation in certain genes, like BRCA1 or BRCA2, increases the risk of developing certain cancers, like ovarian and breast cancer.  

At other times, there’s a pattern of problems like high blood pressure, high cholesterol, or type 2 diabetes disease traced through several generations that can contribute to cardiovascular disease in family members.  

When assessing biological risk factors, keep in mind that these risks are influenced by both behavioral and environmental risk factors. 

Biological risks can also be related to life events, which happen as families enter new stages of life. Life events can be normative, or expected, like aging, or they can be non-normative, or unexpected, like the death of a spouse. Each transition between stages can affect family health due to fluctuations in familial demands, behaviors, and responsibilities.  

With normative events, the family has time to anticipate the required adaptations needed to cope with the change. For example, adopting a baby requires the family to learn about pediatric immunizations and normal developmental processes.  

On the other hand, unexpected events like a major illness or sudden loss of a family member can cause family stress and even dysfunction as the family works to adapt to their new reality.  

Now, behavioral ri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community_Health_Nurses</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oc9YKLLdTcCw6raBP4c1AR3RS9iA_NFi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community health nurses: Nursing]]></video:title><video:description><![CDATA[Community health nursing is a branch of nursing focused on the health and well-being of communities. A community is a group of people who live in the same area or share certain experiences, values, or characteristics.  

Examples of communities include specific locations like a town or neighborhood; a family or group of neighbors; a sports team; or a religious group.  

Nurses can support communities by providing home health, hospice, and palliative care.   

Okay so, nurses who work in public health departments, visiting nurse associations, home health agencies, hospice agencies, or schools may provide care for patients and families in their homes.  

Home health allows patients to retain as much independence as possible while receiving needed health care wherever they reside, which can be a family home, group facility, hotel, or temporary shelter. 

Now, the services home health care nurses provide will depend on the type of agency they work for, the community they serve, and the individual patient&amp;#39;s needs.  

Direct care services can include wound dressing changes, assisting with activities of daily living, administering medications or tube feedings, and assisting patients to transition from inpatient care to their home. 

Home health nurses can also assist with prevention strategies like administering vaccinations, screening for risk factors for certain health conditions, and monitoring patients for adverse effects of medications.  

They may also work with other members of the health care team to coordinate patient care to ensure medications are refilled, assist with scheduling screening tests, or confirm needed physical or occupational therapy sessions have been ordered.  

While providing direct care for the individual patient, the home health nurse will also assess the patient-family relationship, communication patterns, and methods of coping while providing education for the patient and their family.  

Other activities can include ensuri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Culture,_Diversity,_and_Relational_Practice</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3t1aBr_fSming3faNHLE3MsAT8iJpIp2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Culture, Diversity, and Relational Practice]]></video:title><video:description><![CDATA[Providing culturally responsive care requires adopting concepts of relational practice, which involves providing the best care for diverse populations while practicing self-awareness and recognizing differences without bias. As a community health nurse, or CHN, you’ll provide safe, competent, and ethical care. 

Okay, so there are some important concepts to keep in mind when providing care for your patients. Culture refers to behaviors and beliefs learned and shared within a group of people.  

Now, people aren’t born with culture, instead it’s learned from experiences, so it can adapt over time with new situations and contexts.  

Culture can be invisible in that it’s experienced through shared rituals and behaviors that can impact how people respond to situations and make decisions.   

In a cultural context, diversity looks at how traits (such as age, gender, race, religion, sexual orientation, and income level) shape similarities, differences, and power dynamics among people.  

Diversity can be visible or invisible. Visible diversity includes observable characteristics like age, physical appearance, race, and gender; ... 

... whereas invisible diversity involves traits that aren&amp;#39;t immediately obvious, such as religion, occupation, and sexual orientation.  

While those who are visibly diverse are at increased risk of experiencing stereotyping or discrimination, those with invisible diversity might feel overlooked. 

Race is a social classification where an imagined hierarchy of value is based on physical characteristics like skin color. On the other hand, ethnicity involves belonging to a social group that has certain cultural patterns in common, like beliefs, values, and customs, and is influenced by factors like geographic location, heritage, education, and income level.  

Keep in mind that people of the same race can have different ethnicities and cultures.  

For instance, Black individuals are often wrongly viewed as sharing the same e]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_New-onset_diabetes_mellitus:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8WSoo5I_RAOKsKGPKCcniud7RvGsA2uH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - New-onset diabetes mellitus: Nursing]]></video:title><video:description><![CDATA[Nurse Harvey works in a primary care office and is caring for Maru, a 69-year-old female who presents for a well-care visit. In collaboration with the registered nurse, RN Pam, Nurse Harvey goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Maru’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Harvey recognizes important cues, including Maru’s vital signs, which are temperature 98.9° F, or 37.2° C, heart rate 71 beats per minute, respirations 16 breaths per minute, blood pressure 108/62 mmHg, and oxygen saturation 99% on room air. She also rates her pain as 0 on a 0 to 10 numeric scale.  

Nurse Harvey also notices Maru has used the restroom twice while waiting and she reports she’s been thirstier lately.  

Next, Nurse Harvey analyzes these cues. He reviews the electronic health record, or EHR, and notes that Maru has been seen and treated for recurrent vaginal yeast infections three times in the past couple months. He also notes Maru’s routine lab work shows a fasting glucose of 155 mg/dL or 8.6 mmol/L and her hemoglobin A1C was 7%.  

Nurse Harvey suspects Maru is experiencing the effects of an elevated blood glucose level, which could be caused by diabetes mellitus. He knows that diabetes mellitus is a metabolic condition where there’s insufficient insulin to move glucose from the blood into cells for energy.  

He knows that as people age, insulin production decreases and insulin resistance increases, placing them at risk for diabetes. With insufficient insulin and increased insulin resistance, blood glucose levels increase, leading to a hyperosmolar state.  

This hyperosmolar state pulls water from cells into the blood vessels where it’s then removed through urination. This causes polyuria, or frequent urination.  

Lastly, Nurse Harvey knows that diabetes can increase the risk for certain infections because]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Elder_abuse_and_neglect:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/GzCRunGaR36kI4UrFykFz7LGRa_Yfnn2/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Elder abuse and neglect: Nursing]]></video:title><video:description><![CDATA[Nurse Kyle works in a primary care office and is caring for Judy, a 78-year-old female with a history of Alzheimer disease, who was brought in for a medication refill by her son, Darrell. In collaboration with the registered nurse, RN Fatima, Nurse Kyle goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Judy’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.   

First, Nurse Kyle recognizes important cues, including Judy’s vital signs, which are temperature 97.6 F or 36.4 C, heart rate 70 beats per minute, respirations 14 breaths per minute, and blood pressure 126/72 mmHg. Judy is oriented to person and place but not time. Nurse Kyle also notices Judy has a flat affect and avoids direct eye contact.   

Nurse Kyle: Alright, Judy, the healthcare provider ordered a urine sample to help monitor how your medication is working. Can I assist you to the bathroom?   

Nurse Kyle begins to assist Judy to the bathroom and notes she has a strong body odor. When helping Judy remove her incontinence underwear, he notices it’s saturated with urine, and her vulva is bright red with a surrounding rash. After collecting the sample, Nurse Kyle helps Judy clean up and put on a fresh pair of underwear. While Judy washes her hands, Nurse Kyle notes a circular bruise on her right arm.  

Nurse Kyle: Judy, I see you have a bruise on your arm. What happened?  

Judy: Oh, I don’t remember. It’s fine.  

He then helps Judy return to the exam room to wait for the healthcare provider.  

Nurse Kyle: Darrell, I noticed your mom has a bruise on her right arm. How did she get that? 

Darrell: Let me see it. Oh, yeah - that looks like the spot where she always hits on the doorknob. It’s nothing. 

Nurse Kyle: Okay, tell me more about what you mean. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Knee_osteoarthritis:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0Kvs2ECxRmi6lVTKMWF6DbQcTbms5Bud/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Knee osteoarthritis: Nursing]]></video:title><video:description><![CDATA[Nurse Mary works at a family practice clinic and is caring for Ryker, a 70-year-old male with a history of osteoarthritis who presents to the office for worsening bilateral knee pain. In collaboration with the registered nurse, RN Ron, Nurse Mary goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Ryker’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes.  

First, Nurse Mary recognizes important cues, including Ryker’s vital signs, which are temperature 97.2 F or 36.2 C, heart rate 98 beats per minute, respirations 22 breaths per minute, blood pressure 115/74 mmHg, and oxygen saturation 98 percent on room air. He currently rates his pain as 6 on a 0 to 10 numeric scale. 

Nurse Mary notes RN Ron’s assessment revealed Ryker has swelling, tenderness to palpation, and a decreased range of motion, or ROM, in both of his knees.  

Nurse Mary: I noticed you had quite a bit of pain when RN Ron touched your knees. Can you tell me more about your knee pain?  

Ryker: I used to really enjoy taking walks several times a day, but over the last few years my knees have felt so stiff when I wake up, and they hurt so much when I&amp;#39;m walking. So, I haven’t been walking much. It just keeps getting worse. I’ve been gaining a bit of weight too since I haven’t been walking as much as I used to. 

Nurse Mary: Is there anything that makes the pain feel better? 

Ryker: Usually sitting down and resting makes the pain go away. I try acetaminophen sometimes which helps a little, I guess. 

Next, Nurse Mary analyzes these cues. She reviews the electronic health record, or EHR, and notes Ryker’s BMI is calculated as 31 kg/m2 and that before retiring, he was a firefighter for many years.   

Nurse Mary knows that osteoarthritis is a degenerative disease that occurs when there’s a gradual destruction of the cartilage that covers the end of each bone found i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_management:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v-ppuo8WSgSYml-5_sUFsI4qR1a14tc-/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case management: Nursing]]></video:title><video:description><![CDATA[Case management is a collaborative process that involves assessing, planning, and coordinating care to meet the evolving needs of patients and their families. The goals of case management vary depending on the health care setting and patient needs but generally aim to develop a patient-centered plan of care by helping patients manage their healthcare needs, navigate the healthcare system, and achieve positive health outcomes. As a nurse in case management, you&amp;#39;ll identify patient needs and use available resources to organize and coordinate patient-centered and cost-effective care. 

Nurses in case management, often called case managers, have traditionally worked in public health, mental health, and long-term care settings, but also provide services in places like ambulatory clinics, assisted living communities, primary care offices, and acute care settings.  

Case managers receive training and certification to perform specialized skills and functions involving care management, care coordination, and utilization review.  

Care management is a strategy used to improve the health of specific groups of people by organizing services, avoiding duplication of care, and encouraging self-management of disease to lower health risks and reduce healthcare costs.  

To do so, case managers identify patients and populations with modifiable health risks, tailor services and education to meet their needs, and ensure the right health professionals are able and available to provide care.  

For instance, a case manager in a cardiology clinic will review electronic health records and identify patients who have been hospitalized more than once in the past year for exacerbations of heart failure. Understanding that these patients are more likely to develop complications and be readmitted to the hospital, the case manager creates a protocol to reduce the likelihood of symptom exacerbation.  

On a regular basis, the case manager performs telephone check-ins with at-r]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Communicable_disease_and_public_health:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/JhBfoAzGRr_sm5TN8EBWogK3SAaYOXue/_.jpg</video:thumbnail_loc><video:title><![CDATA[Communicable disease and public health: Nursing]]></video:title><video:description><![CDATA[Communicable diseases are contagious illnesses caused by infectious, or pathogenic, agents. As a public health nurse, you&amp;#39;ll prevent and control communicable diseases. 

Now, the ability of a communicable disease to spread and cause infection depends on the interaction between three main factors that form the epidemiological triangle. These factors include an infectious agent, which can be any disease-causing microorganism including bacteria, viruses, fungi, or parasites; a host, or any person or animal harboring the infectious agent; and the environment, which are the external factors that influence disease transmission, like sanitation, crowding, or the presence of disease-transmitting insects like ticks.  

The epidemiological triangle provides a foundation for understanding the sequence of events involved in the spread of infectious disease that are outlined in the chain of transmission. The first link in the chain is an infectious agent, which lives and multiplies in its reservoir. The reservoir can be another human, an animal, water, food, or contaminated surfaces. The pathway by which the infectious agent leaves the reservoir is the portal of exit, like bodily fluids or open wounds.  

After that, the mode of transmission is how the pathogen travels from the reservoir to a new host. This can involve direct transmission, such as through sexual intercourse, skin to skin contact, or respiratory droplets; or indirect transmission, like touching a contaminated object, such as a door handle. Next, the infectious agent needs a portal of entry, which is the pathway by which it enters a new host, like through the mouth, nose, eyes, mucous membranes, or breaks in the skin.  

Lastly, the susceptible host is anyone at risk for infection due to factors like age, health status, and immunity.  

Alright, so, controlling communicable diseases is a key means of protecting and supporting public health. Control involves reducing the incidence, or new ca]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epidemiology:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/76XMBYx9Q1GwGZ7irY2nTVdvSv2Ujj9z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epidemiology: Nursing]]></video:title><video:description><![CDATA[Epidemiology is the study of factors that determine health-related conditions in a population, including infectious and chronic diseases; accidents and injuries; and the effects of occupational and environmental exposures.  

As the nurse, you’ll use epidemiology to identify factors that affect health-related conditions in your community and use that information to reduce disease risk and promote health. 

Now, there are some common measures in epidemiology used to describe health-related conditions.  

Morbidity is the occurrence of a condition in a population, like the number of individuals who have asthma, influenza, or have experienced a hip fracture from a fall. You can measure morbidity using incidence rate and prevalence rate.  

An incidence rate refers to the occurrence of new cases of a certain condition within a population at risk during a specific time.  

To calculate an incidence rate, you’ll set up a ratio with the number of new cases as the numerator and the population at risk as the denominator.  

Keep in mind that the population at risk is comprised of individuals who are at risk for the condition; so known cases and individuals who are not susceptible to the condition, like those who are immunized against a certain disease, are subtracted from the total population.  

As an example, let’s say that in a community of 10,000 people there were 40 existing cases of asthma, and 10 new cases were diagnosed during one year. To find the incidence rate, subtract the 40 known cases from the total population of 10,000 to get the population at risk of 9,960. Then divide the 10 new cases by 9,960 to get an incidence rate of 0.001. You’ll then multiply this number by a factor, like 1,000, to avoid small fractions.  

This gives you an incidence of asthma cases per 1,000 individuals in the community, which is 1 per 1,000 during that year. 

On the other hand, a prevalence rate, which is also called prevalence proportion, is the number of existing ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Environmental_health:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zVrDUSueQeiadPt8MwF-tH9aS3CcQ7Th/_.jpg</video:thumbnail_loc><video:title><![CDATA[Environmental health: Nursing]]></video:title><video:description><![CDATA[Environmental health is focused on how human health and well-being is influenced by the environment in homes, schools, workplaces, and communities.  

Exposure to environmental hazards in the air, water, land, and food supply can negatively impact health.  

As the nurse, you’ll promote environmental health by assessing and managing environmental risk factors, providing education, and advocating for policies that support healthy environments.  

Okay, so hazards to environmental health can involve the air, water, land, and food supply. Starting with air, both outdoor and indoor air quality can be affected. Outdoor air quality is affected by natural events, like smoke from wildfires, and human activities, like emissions from driving motor vehicles. Also, industrial processes, such as emissions from chemical plants, power plants, and waste incineration that release heavy metals and other toxic chemicals into the atmosphere, leading to poor air quality.  

On the other hand, indoor air quality, like within homes, schools, and workplaces, can be impacted by factors like the use of certain appliances such as gas stoves that have the potential to produce carbon monoxide; building materials, such as those that contain formaldehyde; and tobacco smoke. Another cause of poor indoor air quality is the presence of pests like cockroaches, that release allergens in their feces, saliva, and shed skin, which can affect individuals with allergies or asthma.  

Poor air quality is also linked to other health problems, such as cardiovascular diseases, like hypertension, certain types of cancer, and even birth defects. Poor air quality can be especially harmful for older adults, small children, and those with preexisting respiratory conditions, like chronic obstructive pulmonary disease.  

Next up is water. The quality of surface water, like rivers, lakes, and streams, and groundwater can be contaminated through a variety of routes. These can include stormwater runoff from p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Family_health_risks:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NF4T7udGS1Sk4BfiloSDQ1GpS6uQjncB/_.jpg</video:thumbnail_loc><video:title><![CDATA[Family health risks: Nursing]]></video:title><video:description><![CDATA[Family health risks are factors that can contribute to illness within a family, which is a group of people that depend on each other for physical, emotional, or economic support, and are bound together in relationships, either by blood, marriage, adoption, or choice. As the nurse, you’ll work with families to identify and reduce their health risks. 

Alright, so, there are biological, behavioral, and environmental risk factors that can contribute to the development of unhealthy outcomes with families. Biological risk factors are related to genetics and life events. Starting with genetics, certain conditions can be inherited and passed down through families.  

For example, a mutation in certain genes, like BRCA1 or BRCA2, increases the risk of developing certain cancers, like ovarian and breast cancer.  

At other times, there’s a pattern of problems like high blood pressure, high cholesterol, or type 2 diabetes disease traced through several generations that can contribute to cardiovascular disease in family members.  

When assessing biological risk factors, keep in mind that these risks are influenced by both behavioral and environmental risk factors. 

Biological risks can also be related to life events, which happen as families enter new stages of life. Life events can be normative, or expected, like aging, or they can be non-normative, or unexpected, like the death of a spouse. Each transition between stages can affect family health due to fluctuations in familial demands, behaviors, and responsibilities.  

With normative events, the family has time to anticipate the required adaptations needed to cope with the change. For example, adopting a baby requires the family to learn about pediatric immunizations and normal developmental processes.  

On the other hand, unexpected events like a major illness or sudden loss of a family member can cause family stress and even dysfunction as the family works to adapt to their new reality.  

Now, behavioral ri]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Occupational_health_nursing_(OHN):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3Ag9wtH3Sae5HNrXA3bI-cAqSSWG4qnA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Occupational health nursing (OHN): Nursing]]></video:title><video:description><![CDATA[Occupational health nursing is a branch of nursing specializing in promoting health and safety of individual employees and groups of workers in employment settings. As the occupational health nurse, or OHN, you’ll identify occupational hazards, prevent illness and injury, and promote health by advocating for a safe and healthy work environment. 

Okay, so, occupational health nurses operate in various workplace environments. These include manufacturing companies, corporations, construction sites, utilities, and healthcare facilities.   

As an occupational health nurse, your goals include identifying occupational hazards, preventing illness and injury, and promoting health by advocating for a safe and healthy work environment. 

Now, in order to identify potential hazards, you’ll assess the health and safety of individual workers and the workplace as a whole.  

On an individual level, start by gathering information about previous employment, past exposure to workplace hazards, and medical symptoms or ailments related to previous workplace illness or injuries.  

Next, ask about present work conditions including specific responsibilities or tasks and current exposure to work-related hazards. These can include biological hazards, like a healthcare worker who is exposed to bloodborne pathogens that could lead to infections like hepatitis B and C; chemical hazards, like when a construction worker is exposed to toxic welding fumes; or physical hazards like heavy equipment operators who are exposed to vibrations, which over time can result in chronic musculoskeletal pain or even peripheral vascular and sensorineural problems.  

There are also enviro-mechanical hazards, where repetitive motions can cause musculoskeletal injuries, like an office worker at risk for carpal tunnel syndrome from repetitive hand and wrist movements that occur from typing and using a mouse.  

Finally, regardless of the profession, exposure to psychosocial agents like workplace stress]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community_health_case_study_-_Depression:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Be-hCUnmTP2Ed85y_46BxdLpSSarFC1Z/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community health case study - Depression: Nursing]]></video:title><video:description><![CDATA[Nurse Betty works in a community health clinic and is caring for James, a 65-year-old male who presents for a 3-month follow-up after being diagnosed with depression. After settling James in the room, Nurse Betty goes through the steps of the Clinical Judgment Measurement Model to make decisions about James’ care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Betty recognizes important cues, including James’ vital signs, which are temperature 98.9 F, or 37.2 C, heart rate 70 beats per minute, respirations 14 breaths per minute, blood pressure 112/68 mmHg, and oxygen saturation 99% on room air. She also notices that James avoids making direct eye contact.   

Nurse Betty: Hi James, it’s good to see you back in the clinic. How are you doing? 

James: I’m fine, I guess.  

Nurse Betty: I remember from your last appointment you recently retired from your job. Tell me how you’re adjusting so far. 

James: It’s been pretty lonely. I haven’t been sleeping much. 

Nurse Betty: I’m sorry to hear that. Do you have any friends or family in this area? 

James: No, not since my wife passed away last year and my daughter moved away. 

Nurse Betty: That sounds very isolating. Have you ever thought about harming yourself or trying to take your own life? 

James: No. 

Next, Nurse Betty analyzes these cues. She reviews the electronic health record, or EHR, and notes that James is currently prescribed a low dose antidepressant to treat his depression. She also calculates that his score on the PHQ-9 scale today indicates a moderately severe level of depression. She also notes that he’s lost 7 pounds, or 3.2 kilograms, since his last clinic visit. 

Nurse Betty knows that depression is a mental disorder that causes loss of interest in activities that were previously enjoyable, and persistent feelings of sadness that interfere with daily life.  

In older adults, depression can be related]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community_health_case_study_-_Homelessness:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hXna7bP8Qk6jcp0_KOZnkOgQReyyN5nx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community health case study - Homelessness: Nursing]]></video:title><video:description><![CDATA[Nurse Margot works as a community health nurse in the health department and is assisting a local homeless shelter to address concerns among its residents. Nurse Margot goes through the steps of the Clinical Judgment Measurement Model to make decisions by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Margot recognizes cues. She distributes an anonymous questionnaire to residents at the shelter to gather demographic data, employment status, presence of medical conditions, and any other concerns they have. Nurse Margot then interviews willing residents to gather additional information on factors contributing to their need for the shelter and discusses with staff any concerns they have about residents.  

She also obtains data from the shelter on the number of residents it houses and services that’re offered.  

Next, Nurse Margot analyzes these cues. She reviews data from the questionnaire and her notes from the interviews to identify common themes. She notes many residents are unemployed and have indicated they’re unable to maintain employment due to mental health conditions. They cite lack of transportation and financial concerns as a barrier to accessing mental health care; and staff also report many residents have been struggling mentally due to lack of access to needed care. Nurse Margot reviews services provided by the shelter which include support groups, WiFi, and assistance with housing applications. 

Nurse Margot knows homelessness is a complex socioeconomic issue that consists of a range of living situations. She knows there are many types of homelessness including rooflessness, sometimes called absolute homelessness, where individuals lack any shelter; houselessness, also called sheltered homelessness, such as those who don’t have a permanent residence but stay in temporary housing like shelters; insecure housing, where individuals face threat of eviction or i]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community_health_case_study_-_Poverty:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/1H-Z-ctiRv_rP4Hdz3aCX6JnS5ikkHjc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community health case study - Poverty: Nursing]]></video:title><video:description><![CDATA[Nurse Mozasu works as a community health nurse at the health department and is assisting a rural school to address dental care among its students. Nurse Mozasu goes through the steps of the Clinical Judgment Measurement Model to make decisions by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Mozasu recognizes important cues, including the results from a survey distributed to parents of students at the school. The survey included questions about access to dental products, such as toothbrushes, toothpaste, and floss; access to routine dental services, such as dental cleanings; financial ability to obtain products and access services; and other barriers to maintaining their child’s dental hygiene.  

Additionally, the survey gathered demographic data, including the number of individuals in each home; age of each family member; household income; and living situation, such as the type of dwelling or if they rent or own their home.  

Next, Nurse Mozasu analyzes these cues. He notes many parents, particularly those from low-income households, reported difficulty accessing dental products and services due to financial constraints and lack of reliable transportation. Several parents mentioned they can’t afford dental insurance and feel embarrassed that they were unable to provide their child with access to routine dental care and were reluctant to discuss their needs due to the stigma associated with poverty.  

Nurse Mozasu knows poverty occurs when there are insufficient financial resources to meet an individual or family’s basic living expenses, which includes medical services like dental care. He also knows that income level affects health, and that those living in poverty experience poorer health outcomes compared to those with higher incomes. Children are at particular risk, since poverty can negatively impact their growth, development, and overall health.  

Nurse Mozasu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Community_health_case_study_-_Rural_healthcare:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4m-A_kGlTKWsSFY3mAJZ_f48SbCKX7HD/_.jpg</video:thumbnail_loc><video:title><![CDATA[Community health case study - Rural healthcare: Nursing]]></video:title><video:description><![CDATA[Nurse Mathias is a community health nurse who’s working on development of a mobile clinic in a rural community for residents to receive preventative and primary care. He goes through the steps of the Clinical Judgment Measurement Model to make decisions about the population’s needs by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Mathias recognizes important cues, including documentation from the regional community health office that indicates many area residents don’t have a primary health care provider. He also notes that two small, rural hospitals in the surrounding area have closed in the last year leaving residents to seek care at the nearest emergency department that’s over an hour drive away.  

Next, Nurse Mathias analyzes these cues. He reviews the most recent census data for the area and finds the population is approximately 5,000 people, which includes single older adults and families with small children and adolescents. He also notes that most of the employed residents work as farmers or at the power plant just outside of town.  

Nurse Mathias knows that barriers to healthcare in rural areas can include limited availability, accessibility, affordability, and acceptability of health care services and providers. He understands that because of the geographical isolation and population sparseness, rural areas tend to have fewer healthcare settings, services, and professionals available; and in cases when adequate healthcare is available, residents may find it inaccessible due to lack of transportation and cost.  

He also understands that acceptability of care can be impacted by cultural differences, stigma, language barriers, and low health literacy, and that these barriers can limit use of preventative services and lead to inadequate management of chronic conditions.  

In addition, Nurse Mathias knows that rural residents are at higher risk for chronic condi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Culture_and_population_health:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_0MU9tyFTMu6Y1Lqkb3MsDaRRxK-KDwk/_.jpg</video:thumbnail_loc><video:title><![CDATA[Culture and population health: Nursing]]></video:title><video:description><![CDATA[Culture is an evolving and complex phenomenon that encompasses the beliefs, assumptions, and values that are widely shared by groups of people over time. As the community health nurse, or CHN, you’ll provide culturally competent care to promote positive population health outcomes for individuals, groups, and communities.  

Okay, so, there are some important concepts to keep in mind when caring for people from different backgrounds, to help you to be better equipped to practice cultural competence.  

First, race describes a person’s biological variations that have their origins in genetic ancestry, like skin color or hair texture.  

On the other hand, ethnicity refers to belonging to a group that shares cultural patterns, such as beliefs, values, and traditions, and is often influenced by factors, like geographic location, heritage, and education. Keep in mind that people of the same race can have different ethnic and cultural backgrounds.  

For instance, Black individuals are often wrongly viewed as sharing the same ethnicity and culture, even though they’re a culturally diverse group with ancestry and heritage that can be traced back through North America, Africa, and the Caribbean.  

Speaking of cultural diversity, this term encompasses the variations among populations based on factors like race and ethnicity, as well as sexual orientation, social class, and physical and mental abilities. 

Now, in order to provide effective and equitable care and promote positive population health outcomes for people of diverse cultural groups, you’ll work toward developing cultural competence. Although the process of developing cultural competence looks different for each person, it generally includes five key elements.  

First, cultural awareness involves examining one’s own cultural background to discover how attitudes, biases, and prejudices can impact the provision of care.  

Next, cultural knowledge is the process of gathering information about the wor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Health_assessment_and_screening:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3EUrbl2QTlevZ5VjJ4ZcfK1nTFmpIov4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Health assessment and screening: Nursing]]></video:title><video:description><![CDATA[Performing health assessments and health screenings provide information about a patient’s health status and identify those in need of further assessment and care. As the nurse caring for older adult patients, you’ll use this information to provide patient-centered care.  

Now, during a health assessment, you’ll collect comprehensive health information, which typically includes gathering a health history and conducting a physical examination. Health information can be categorized as either subjective or objective data. Subjective data refers to information the patient states or recounts, such as pain level or sleep quality, and tends to be obtained during a health history. On the other hand, objective data is collected during the physical assessment, and includes tangible information that’s observed or measured, like presence of a skin rash or blood pressure readings. 

Alright, starting with health history, this is where you’ll interview your patient to obtain subjective data about their perceived health and factors impacting their health. Begin by asking about basic identifying information, like name and date of birth.  

Next, move on to specific data like past medical and surgical history, such as previous hospitalizations and surgeries, current medications, and personal health habits like diet, physical activity, and sleep patterns.  

Then you’ll discuss the patient’s current health status and any pressing health concerns, as needed. Keep in mind that the patient is the preferred information source; however, a family member or caregiver can provide information if your patient has limited ability to recall or communicate, like those with dementia or aphasia.  

During the health history, remember to do your best to avoid the use of medical jargon. For example, instead of saying hypertension, say high blood pressure. Also, since word recall and response time can slow with age, be sure to speak slowly and clearly, and provide your patient with enough ti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Age-related_physiologic_changes:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/XfZkveKOST_juB5bwwfiT5UIRO2F4fmH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Age-related physiologic changes: Nursing]]></video:title><video:description><![CDATA[Over time, the body gradually goes through normal age-related physiologic changes. As the nurse, you’ll recognize how these changes impact the body systems in older adults and consider conditions that can develop as a result.  

Starting with age-related changes of the cardiovascular system, the heart’s muscle loses tone and becomes stiffer. To compensate, muscle mass increases, but is a less effective pump. This decreases cardiac output and increases the risk of heart failure. The heart valves become thicker and calcified, which can lead to valve disease and murmurs. Additionally, the conduction system, including the sinoatrial node, known as the pacemaker of the heart, loses cells, decreasing heart rate and increasing risk for arrythmias.  

Also, blood vessels become stiffer, decreasing venous return from the periphery and contributing to dependent edema and varicosities; and the build-up of atherosclerotic plaque within the vessels can lead to coronary artery disease, peripheral artery disease, and hypertension.  

Lastly, an impaired baroreflex, which helps maintain blood pressure by adjusting heart rate, cardiac output, and peripheral vascular resistance during position changes, can result in orthostatic hypotension and an increased risk of falls.  

Okay, moving on to changes to the respiratory system. There are certain age-related changes that increase the risk of respiratory infections like pneumonia and influenza. These include fewer cilia, that trap and remove inhaled microbes and debris; fewer pulmonary macrophages, which are the first line of defense against inhaled pathogens; and a decreased cough reflex, which is needed to help expel inhaled pathogens and clear secretions.  

Other changes include thoracic muscle weakness and calcifications of rib cartilage, which can limit lung expansion, increase the work of breathing, and decrease the ability to take deep breaths.  

Lastly, loss of alveolar elasticity, decreased alveolar surface area, an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Caregivers:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/i3GTGZtHRqiOOwTgaEhcw70NTsST6ZG0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Caregivers: Nursing]]></video:title><video:description><![CDATA[Caregivers are individuals who assist others unable to fully care for themselves. Caregivers can be formal, meaning they’re hired and paid to provide care, like a home health nurse; or informal, where care is provided voluntarily by loved ones, such as spouses, grandparents, or friends. As the nurse, you’ll provide support and offer strategies to help reduce stress in informal caregivers. 

Caregiving can be a source of joy and fulfillment, while at the same time, it can be a source of physical, mental, and financial stress. Physical problems include poor sleep, physical strain, immunocompromise, and even higher mortality rates. Additionally, caregivers with existing chronic health problems may find their condition worsens; and some may even develop cognitive decline.  

Mental health conditions related to caregiver stress include depression, anxiety, increased alcohol use, and feelings of being overwhelmed, upset, or confined. If mental stress is left untreated, it can increase the risk for abuse or neglect by the caregiver.  

Financial issues faced by caregivers may include having to call out of work frequently, needing to take an extended leave, or paying for resources out-of-pocket. In fact, due to the unpaid nature of their caregiving, informal caregivers are more likely to live in poverty.  

Physical, mental, and financial stress can be exacerbated in certain situations, such as when caring for a spouse with dementia or a child with an intellectual or developmental disability. For example, individuals with dementia can require more time- and resource-intensive care due to impairments related to their activities of daily living, or ADLs, and instrumental activities of daily living, or IADLs. Caregivers may also have a difficult time communicating with their loved one due to their condition.  

Lastly, caregivers of a child with a disability may themselves be aging and worry about who will care for their child if they become too ill or die. They may ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Aging_and_cognition:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/uy-uvnUrReu8nvNvs-GPXTlTSoG7SDfI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Aging and cognition: Nursing]]></video:title><video:description><![CDATA[Cognition describes the process of receiving, storing, sharing, and making sense of information, which include mental processes such as memory, language, concentration, and problem-solving. Cognition can be impacted by one’s environment, genetics, educational background, health status, and age-related brain changes.  

As the nurse, you’ll consider age-related changes to the brain, the physiologic processes that can compensate for these changes, and provide patient-centered care to promote brain health in your older adult patients. 

Now, as an individual ages, there&amp;#39;s typically a general slowing of function of the neuronal processes that doesn’t usually interfere with mental function or daily routines. This slowing in function is different for everyone and is related to changes in brain structure and neurotransmitter function.  

As far as structural changes go, there’s a decrease in the size and number of neurons, which are the nerve cells that receive and send messages throughout the body. Dendrites, which branch off from the neuron cell body and receive signals from other neurons, can experience shrinkage and decreased branching. Other age-related changes include a build-up of substances like plaque within the neurons, and a decrease in myelin, which is the substance that helps the neurons to quickly transmit electrical impulses.  

Additionally, there are changes that affect neurotransmitters, or chemical messengers, such as acetylcholine, glutamate, serotonin, and dopamine, that normally allow neurons to communicate with each other. These changes include alterations to enzymes that synthesize and break down neurotransmitters and changes to neurotransmitter receptor sites. 

Alright, so, the brain can compensate for age-related changes by developing cognitive reserve, which is the ability of the brain to maintain cognitive functioning, even when it experiences degeneration or damage. In other words, the stronger the cognitive reserve, the mor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Communication:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/bDM1p0jnTF_i-8hSXDKbdyLYQwCj4cx8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Communication: Nursing]]></video:title><video:description><![CDATA[Using effective communication when caring for older adults can help inform assessments, plan care, develop the nurse-patient relationship, and even improve health outcomes. As the nurse, you’ll consider barriers to communication and implement strategies to promote effective communication for individuals and groups of older adults. 

Alright, now there are certain barriers to effective communication with older adults to keep in mind. One barrier is ageism, which involves stereotyping and discriminating against individuals based on their age. Ageism can lead to poor health outcomes, like cognitive and functional decline. Elderspeak is a type of ageism which refers to condescending speech patterns used when communicating with older adults. Common instances of elderspeak include using pet names such as “honey” or “sweetie”; substituting collective pronouns such as “we,” like saying, “We are going to eat dinner now”; and speaking to the patient’s family or caregiver rather than the patient.  

As the nurse, you can implement strategies to promote effective communication with your older adult patient. These include using open-ended questions, allowing for additional response time, and encouraging storytelling. 

Open-ended questions like, “What do you know about your family history?” can help you gather information but may cause some patients to verbalize what they assume you want to hear rather than how they truly want to answer. So, when asking open-ended questions, remember to seek validation of what you hear so you can clearly understand what your patient is telling you.  

Now, keep in mind that word retrieval can slow as individuals age. You can provide your patient with the opportunity to answer your questions fully by practicing patience, speaking slower to allow time for them to process what’s being said, and giving them additional time to respond.  

Lastly, storytelling can allow your patient the opportunity to share their memories and life experience]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_End-of-life_care:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Wi-TTSUqR2uFXvAn5eK8pFJlQg2iuhMj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - End-of-life care: Nursing]]></video:title><video:description><![CDATA[End-of-life care involves the supportive care provided to an individual as they near death. As the nurse, you’ll provide end-of-life care for older adults by recognizing and managing the physiologic changes that occur at the end of life and providing emotional support for the patient and their family.  

Now, there are certain physiologic changes that occur during the dying process. Starting with the cardiovascular system, these changes are mostly related to diminishing cardiac output and blood pressure. As a result, heart sounds become faint, peripheral pulses weaken, and circulation slows. Subsequently, the skin becomes cool, pale, and mottled, with bluish coloring, known as cyanosis, especially in the extremities.  

Next, in the respiratory system, patients often report feelings of dyspnea, including a feeling of chest tightness or breathlessness, which is due to factors like respiratory congestion and weakened respiratory muscles. Keep in mind that patients experience dyspnea, even when typical signs like decreased oxygen saturation or rapid breathing are not observed.  

Other respiratory changes include slow and irregular respirations, often with Cheyne-Stokes respirations which are alternating episodes of apnea and hyperventilation. Patients may also develop distinctive wet, gurgled, noisy breathing, called the death rattle, which is caused by saliva and mucus building up in the back of the throat and upper airways.  

Okay, moving on to the neurologic system, decreased cerebral perfusion and metabolic disturbances can result in acute episodes of confusion, or delirium, which can alternate with moments of lucidity. Other symptoms include agitation, excessive sleepiness, or insomnia.  

They can also have sensory changes like diminished sight, visual hallucinations, and hypersensitivity to light and sound; although hearing typically remains intact up until the moment of death. As death nears, responsiveness decreases, and they eventually lose consci]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Nutrition:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/IiwvTcTvTESfepF-WNSfq0SARAypAsS6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Nutrition: Nursing]]></video:title><video:description><![CDATA[Nutrition refers to the process in which nutrients are ingested and used by the body to support health and maintain essential functions, like metabolism and tissue repair. Nutritional needs fluctuate in response to age-related physiologic changes and the development of acute or chronic conditions.  As the nurse, you’ll consider how nutrition changes with aging and provide patient-centered care based on your patient’s nutritional needs. 

Now, the required number of calories, which reflect the available energy within food, decreases with age due to a reduction in lean muscle mass and an increase in adipose, or fat, tissue. In general, the minimal daily recommended caloric intake for an older adult is 1200 calories per day.  

However, caloric needs also vary depending on factors like age, biological sex, body size, activity levels, and the presence of illness. For instance, some older adults with conditions that restrict mobility or limit activity tolerance, such as arthritis or heart failure, may require fewer calories. In contrast, conditions that increase the metabolic rate, like cancer, may require consumption of more calories.   

Unlike caloric requirements, the amount of necessary nutrients remains stable as individuals age. Therefore, nutrient-dense foods, or foods with a high nutritional value, are ideal for older adults.   

First, carbohydrates include sugars and starches and are the main source of calories used for energy, so they should make up 45 to 65 percent of daily calories. Carbohydrates can be simple or complex. Simple carbohydrates, like honey or table sugar, are easily broken down and are less nutrient-dense; whereas complex carbohydrates, like whole grains and fruits, take longer to break down and are more nutrient-dense.  

Complex carbohydrates also contain soluble fiber, which is a non-digestible form of fiber that has numerous benefits, including increasing the bulk of stool which helps prevent constipation; lowering blood cholest]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Pain_management:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/x4ZcdlgZTE6vX48kss0jRp66RDeuMJiG/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Pain management: Nursing]]></video:title><video:description><![CDATA[Pain is an unpleasant physical or emotional experience that occurs in response to actual or potential tissue damage, and is shaped by physical, emotional, and cultural components unique to everyone. Due to higher prevalence of acute and chronic health conditions, older adults are at increased risk of experiencing pain that’s often left underrecognized and undertreated.  

As the nurse, you’ll recognize age-related changes to pain perception and the consequences of untreated pain; identify barriers to effective pain management; and provide patient-centered care for older adults experiencing pain. 

Alright, so as one ages, a decreased density of nerve fibers can delay the transmission of pain signals from the origin site to the brain. This delayed transmission increases the risk of injury since it takes longer for the brain to perceive pain. For example, it might take an older adult more time to realize their hand is on a hot surface, increasing the risk of burns. Also, pain sensation resolves more slowly with age, meaning many older adults must tolerate pain for longer.  

Now, a common myth is that older adults feel less pain than younger adults, which is not only untrue, but it can lead to undertreatment of pain and poor health outcomes. Physical consequences of inadequately treated pain include impaired mobility, resulting in decreased muscle strength, increased fall risk, and poor sleep and appetite; and delayed healing and rehabilitation, leading to increased healthcare visits and costs.  

Other consequences include a significant impact on quality of life and mental health, contributing to new or worsening depression, anxiety, or social isolation, which can increase the risk of substance use and even impair cognition over time.  

Okay, so there are several barriers to effectively identifying and managing pain in older adults. Some of the most common barriers can stem from the patient or the healthcare team.  

Now, a patient’s personal beliefs, valu]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Physical_activity:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/oSHDTmhhTrquoU8VRIRl2RlNTZagaezH/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Physical activity: Nursing]]></video:title><video:description><![CDATA[Staying active throughout one’s life can have a positive impact on health outcomes. Although physical capabilities vary from person to person, most individuals experience age-related changes to their mobility and activity levels over time.  

As the nurse, you’ll consider individual abilities and limitations and provide patient-centered care to promote physical activity in older adults.  

Alright, starting with the musculoskeletal system, over time there’s a gradual loss of muscle mass, which can decrease overall strength. Meanwhile the flexibility of the ligaments, tendons, and joints decreases, and the cartilaginous cushioning between the joints diminishes, potentially leading to impaired mobility and pain.  

In the nervous system, the speed of nerve transmission slows with age, so it takes longer to complete familiar activities, like getting dressed or cooking a meal. Also, decreasing agility, or the speed and smoothness of physical movements, can increase the difficulty of activities such as climbing stairs or avoiding hazards while walking. Similarly, fine motor skills, like sewing or playing an instrument, may become less precise.  

Lastly, there are also changes in the cardiovascular and respiratory systems with age. The heart’s muscle loses tone and becomes stiffer over time, making it a less effective pump. In the lungs, loss of alveolar elasticity, decreased alveolar surface area, and fewer pulmonary capillaries impairs the exchange of oxygen and carbon dioxide; and decreased lung capacity reduces the volume of air the lungs can hold. Together, these changes result in less oxygen-rich blood being pumped out to the body, which can result in reduced exercise tolerance and overall stamina.  

Now, being physically active can improve health and quality of life while providing an opportunity to safely maintain independence for longer. Exercising regularly preserves mobility and muscular function, improves cardiovascular health, and helps control we]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Safe_and_secure_environments:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NIM2Al4FQfmQzgGxfITlK99eQxaISPgh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Safe and secure environments: Nursing]]></video:title><video:description><![CDATA[Safe and secure environments can improve the health and well-being of older adults while providing an opportunity to age in place and live independently, safely, and comfortably.  

As the nurse, you&amp;#39;ll identify risks to safe and secure environments and promote safety for older adults by addressing risks associated with fires, firearms, transportation, and heat- and cold-related injuries. 

First let’s discuss fires, which can cause burns and smoke inhalation injuries.  

For older adults, there are several factors that can increase the risk of injury during a fire, including impaired mobility, sensory impairments, slower decision-making or response time, and certain preexisting health conditions.  

Now, fires can be caused by factors that include inadequate home repairs or maintenance, use of space heaters, and smoking materials, like cigarettes.  

For example, a fire can originate from a poorly maintained fireplace, a space heater placed next to flammable materials, or from falling asleep while smoking in bed.   

As the nurse, you’ll promote fire safety by ensuring your patient has well-maintained smoke alarms in every room.  

They should also have access to a fire extinguisher and know how to use it.  

If your patient smokes, instruct them to avoid smoking in bed or in a chair when there’s a possibility of falling asleep; to avoid smoking after taking medications that may cause drowsiness; and to dispose of all cigarette butts in a nonflammable container away from other items.  

Lastly, you can help your patient develop and practice a fire escape plan.  

Now, firearms are a significant cause of injury and death in older adults. Gun ownership is typically higher in older adults when compared to other populations. At the same time, older adults experience a higher rate of altered mood, memory, cognition, and function. These factors greatly increase the risk of unintentional firearm injuries which can occur from improper firearm care or han]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Hearing_impairment:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/P36TWNpEQvWVBvCPKc9BzZYcQ5iUR0bc/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Hearing impairment: Nursing]]></video:title><video:description><![CDATA[Hearing impairment is a common condition in older adults that can negatively impact their quality of life through communication difficulties, social isolation, decreased self-esteem, cognitive decline, and even depression. As the nurse, you’ll recognize age-related hearing changes and provide patient-centered care for your patient with a hearing impairment. 

Now, the ear is divided into three parts: the external, middle, and inner ear; and each part contains structures that can be affected by age-related changes.  

The external ear consists of the pinna, or the outer part of the ear, and the external auditory canal, which is a passageway connecting the outer ear to the tympanic membrane, commonly called the eardrum. The external auditory canal narrows with age due to decreased tissue elasticity. Additionally, ceruminous glands that produce cerumen, or ear wax, tend to atrophy over time, resulting in drier ear wax.  

These conditions put individuals at higher risk for cerumen impactions which can cause a type of hearing loss called conductive hearing loss, where cerumen blocks the external auditory canal, impairing the conduction of sound waves. 

Another type of conductive hearing loss can occur due to age-related changes in the middle ear, which is the air-filled space that consists of the tympanic membrane and the auditory ossicles. The auditory ossicles consist of three tiny bones that transmit sound waves collected by the tympanic membrane to the inner ear. Now, these ossicles are prone to otosclerosis, or stiffening. When this happens, they’re unable to transmit sound waves as effectively.  

Now, moving on to the inner ear. This includes the cochlea, which converts sound waves into electrical impulses for the brain to process, and a set of structures called the vestibular system, which helps maintain balance. Over time, the cochlear structures, including hair cells and conductive membrane, can deteriorate or become damaged, causing a type of heari]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Visual_impairment:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5nOacY7wTfqyrQbwLIUQZloyTGeq9p0L/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Visual impairment: Nursing]]></video:title><video:description><![CDATA[Visual impairment is a leading cause of disability in older adults, and it can have a negative impact on safety, social interactions, mobility, and activities of daily living such as grooming and eating. As the nurse, you’ll recognize age-related vision changes and provide patient-centered care for your patient with visual impairment. 

Alright, so eye structures commonly affected by age-related changes include the eyelids, cornea, iris, lens, vitreous humor, and retina.   

The eyelids, which protect the eyes and help with tear distribution, lose elasticity and tone as an individual ages. This can cause ptosis or drooping of the eyelids. If severe, ptosis can interfere with vision by obstructing the visual field. In addition, the muscles controlling the eyelids may spasm, which can cause the eyelids to turn inward, called entropion›. This can result in scratching of the cornea by the lower lashes. Other times, the muscles can weaken, which allows the eyelids to turn outward, called ectropion. This can lead to dry eyes due to a disruption of tear distribution and an inability to fully close the eye.  

Next, the cornea, which is responsible for protecting the eye and performing the initial refraction of light onto the lens, can thicken and become less curved, losing its ability to refract light efficiently. This leads to blurry or distorted vision called astigmatism.   

The iris is a circular set of muscles that sits in front of the lens. It controls the amount of light allowed into the eye through the pupil by constricting in bright lighting to allow less light in, and dilating in low lighting to allow more light in. With age, the iris becomes less reactive, resulting in difficultly transitioning between bright and low lighting.  

The lens, found behind the iris, changes its shape to focus light onto the retina. It tends to thicken and become rigid with age. In addition, the ciliary muscles, which are responsible for changing the shape of the lens, beco]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Mental_health:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/khjNxqjJQKakXib3NaX4kW7jQBCQvTBu/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Mental health: Nursing]]></video:title><video:description><![CDATA[Stress is a normal response to internal and external threats to homeostasis, or the body’s stable equilibrium, caused by a real or perceived threat. The two types of stress are eustress and distress.  

Eustress, or positive stress, results from beneficial and motivational stressors, like starting a new job, whereas distress, or negative stress, occurs in response to a negative stressor, like the death of a loved one.  

Regardless of the source of stress, the body responds by undergoing a series of physiologic changes.  

In the short term, the body can adapt and return to homeostasis; but if sustained, stress can be detrimental to physical and even mental health, leading to problems with cognition, memory, depression, and anxiety, especially in those who aren’t able to cope, or effectively manage stress.  

As the nurse caring for an older adult patient, you’ll identify common stressors, recognize signs and symptoms of ineffective coping, and implement patient-centered care strategies to promote effective coping. 

Now, stress happens across the lifespan, but some stressors are more likely to impact older adults, such as major life changes involving loss and health conditions.  

Loss can be social, like losing independent driving privileges; emotional, such as the death of a partner; financial, like reduced income due to retirement; and physical, such as losing eyesight from a chronic condition like macular degeneration.  

Remember, older adults may use coping strategies that are both effective and ineffective to deal with stress. For example, an effective coping strategy is sublimination, when negative energy is channeled into a positive activity, like exercise; whereas an ineffective coping mechanism is suppression, when an individual avoids thinking about a stressor altogether. 

Alright, sustained stress over time can deplete the energy reserves required for effective coping, resulting in signs and symptoms of ineffective coping that can be categor]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Dehydration:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/5CXKabD0S2uSyG-6fw3JNsqkTWaZMSeA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Dehydration: Nursing]]></video:title><video:description><![CDATA[Dehydration is a condition that results in a reduction in total body water, which can be caused by insufficient fluid intake, increased fluid loss, or both. In older adults, dehydration can increase the risk of other problems, including constipation, delirium, venous thromboembolism, delayed wound healing, electrolyte imbalance, and even renal failure. As the nurse, you’ll identify risk factors, recognize signs and symptoms, and prevent dehydration in your older adult patient.  

Risk factors for dehydration can be categorized as can drink, can’t drink, won’t drink, and end-of-life.  

Can drink refers to individuals who don’t drink enough fluids even though they have access to fluids and are physically able to drink. This can be due to age-related changes such as decreased thirst sensation; lack of knowledge about fluid intake goals; or if they require prompts to remember to drink.For example, an individual with cognitive impairment, like dementia, may simply forget to drink fluids throughout the day.Additionally, some individuals may require an increased fluid intake if they’re prescribed diuretics or medications with anticholinergic effects, like psychotropics.Others experiencing an acute illness involving fever, vomiting, or diarrhea will need more fluid intake to address excess fluid loss. 

Next, can’t drink refers to individuals who are unable to drink. This can be related to factors like dysphagia, or difficulty swallowing; the need for physical aids to assist with drinking; or the need for assistance from others to consume fluids. Others can become dehydrated when they’re NPO, meaning they are restricted from taking anything by mouth. There are also certain comorbid conditions, like heart failure, which may require individuals to have a restricted fluid intake, potentially leading to dehydration. 

Then there’s won’t drink, which refers to individuals who have access to fluids and can drink, but don’t. This can include individuals who avoid drinki]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Geriatric_considerations_-_Falls_and_fall_risk_prevention:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zYe2_Vf1Q36-501mAn2QRFe6SvqUjwn6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Geriatric considerations - Falls and fall risk prevention: Nursing]]></video:title><video:description><![CDATA[A fall occurs when an individual unexpectedly drops from a higher surface to a lower surface, like from a standing position to the floor. Falls can occur in healthcare facilities, the community, or in an individual’s home and are one of the leading causes of injuries and death in older adults. As the nurse, you’ll identify factors impacting fall risk, consider the consequences of falling, and provide patient-centered care to prevent falls.  

Now, typically falls don’t occur for a single reason, but rather from a combination of risk factors which can be intrinsic or extrinsic. Intrinsic risk factors are specific to the individual, such as age-related changes. These include impaired sensory input from both vision and hearing, which can blunt the subtle visual and auditory cues that help an individual keep their balance and walk safely.  

Moreover, cardiovascular changes, like decreased arterial elasticity, can cause blood pressure instability during position changes. This can result in lightheadedness and neuromuscular changes, such as slowed reaction time and joint instability, which can make it more difficult to regain stability after losing balance. Other intrinsic risk factors include cognitive impairment, unsteady gait, chronic conditions like arthritis, and certain medications like beta blockers. 

On the other hand, extrinsic risk factors are associated with the individual’s environment, like poor lighting; presence of hazards such as throw rugs or standing water; and lack of safety devices like grab bars in the bathroom. In healthcare settings, factors like staff shortages or lack of a toileting schedule may increase the risk for falls since patients are more likely to attempt to get up without assistance. 

Okay so, once a fall occurs, the likelihood of falling again increases. Also, keep in mind that not all falls result in injuries; however, older adults who fall are at greater risk of sustaining injuries that can range from a bruise or a scrape]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Congenital_heart_defects:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/b6lV2EE9TBu4UPpulXt6NohkSiK7Jh-Q/_.jpg</video:thumbnail_loc><video:title><![CDATA[Congenital heart defects: Nursing pathophysiology]]></video:title><video:description><![CDATA[Congenital heart defects, also sometimes called congenital heart disease, are a group of conditions involving structural abnormalities of the heart, great vessels, or both. They can be cyanotic or acyanotic based on the presence or absence of cyanosis, which is a blue discoloration of the skin and mucous membranes. 

As a quick review, during gestation, the fetal lungs are fluid-filled and have high vascular resistance, so they don’t participate in gas exchange. Instead, blood is shunted away from the lungs, and the fetus receives oxygenated blood from the placenta, where gas exchange occurs and metabolic wastes are removed.  

Now, the high vascular resistance in the lungs also causes the pressure in the right side of the heart to be much higher than the left side, so, as oxygenated blood enters the right atrium, most of the blood is shunted into the left atrium through the foramen ovale, an opening between the right and left atria. Blood then moves into the left ventricle where it’s pumped through the aortic valve, into the aorta, and out to the fetal body.  

Now, some blood from the right atrium passes into the right ventricle, through the pulmonary valve and into the pulmonary artery, heading for the lungs. But before it can get to the lungs, the blood is shunted through the ductus arteriosus, a vessel connecting the pulmonary artery to the aorta. The aorta then sends the blood out to the fetal body.  

Following birth, the foramen ovale and ductus arteriosus close. The pressure on the left side of the heart increases and pressure on the right side of the heart decreases as pulmonary vascular resistance lessens, and the lungs begin to participate in gas exchange. Deoxygenated blood now moves from the right side of the heart to the lungs for oxygenation and returns to the left side of the heart before being pumped to the rest of the body. 

Congenital heart defects don’t have a single cause, but there are several risk factors that can interfere with de]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Heart_failure:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/eNVJMxEhS6_1tiDauFrkNmyaRCKFGSwJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Heart failure: Nursing pathophysiology]]></video:title><video:description><![CDATA[Heart failure, sometimes also called congestive heart failure, is a condition that occurs when the heart can’t pump enough blood to meet the body’s demands. Heart failure can be either systolic or diastolic, and it can affect the right, left, or both sides of the heart. In systolic heart failure, the heart is unable to effectively contract to push blood out of the ventricles; whereas with diastolic failure, the ventricles become stiff and unable to relax between beats, so they can’t fill with blood properly. 

Now, the heart acts as a pump to move deoxygenated blood through the right side of the heart, to the lungs for oxygenation, back to the left side of the heart, and then out to the body. Each beat of the heart has two phases: systole and diastole. Systole is when the heart is contracting and pumping blood, and diastole is when the heart is relaxed and filling with blood.  

The amount of blood pumped by the heart in one minute is called cardiac output, and it’s an important indicator of heart function. Cardiac output is determined by four factors: contractility, preload, afterload, and heart rate.  

Contractility is the heart’s ability to contract and eject blood during systole, which enhances the force of contraction during systole. Preload is the amount of stretch in the ventricles at the end of diastole as the ventricles fill with blood. In general, the more the preload, the stronger the contraction. On the other hand, afterload is the resistance the ventricles must push against during systole. Less afterload can decrease workload on the heart. Lastly, heart rate is the number of times the heart beats per minute. 

Okay so, cardiac output is calculated by multiplying the heart rate by stroke volume, which is the amount of blood pumped by the heart during systole. Now, the amount of blood within the ventricles at the end of diastole is called the end-diastolic volume; and the stroke volume is just a portion of the end-diastolic volume. Similarly, t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypertension:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/iRThKedeRrCb88laO-QeZWXORy_rDXOl/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypertension: Nursing pathophysiology]]></video:title><video:description><![CDATA[Hypertension occurs when the force of the blood pushing against the artery walls is too high, causing damage to organs. 

Okay, so, as the heart pumps blood throughout the body, it creates pressure against the walls of the arteries, which is referred to as blood pressure, or BP.  

Blood pressure is expressed as a fraction, where the top number, called the systolic pressure, represents the pressure in the arteries when the heart is contracting and pumping blood; and the bottom number, called the diastolic pressure, represents the pressure in the arteries when the heart is relaxed and filling with blood. Normal blood pressure is less than 120 mmHg systolic and less than 80 mmHg diastolic. 

Factors that impact blood pressure include cardiac output, or CO, and systemic vascular resistance, or SVR. First, cardiac output is the quantity of blood pumped by the heart and is measured in L/min. The two components of cardiac output are stroke volume, or SV, and heart rate, or HR. Stroke volume is the amount of blood leaving the heart with each contraction, and heart rate is the number of contractions in one minute.  

The higher the stroke volume and heart rate, the higher the cardiac output.  

Next, systemic vascular resistance is determined by the radius and elasticity of blood vessels. If blood vessels are narrow or stiff, systemic vascular resistance increases, which then increases blood pressure.   

Now, blood pressure is regulated by short-term and long-term mechanisms. Short-term regulation is mainly controlled by the autonomic nervous system, or ANS. For example, when changing from a lying to a standing position, blood pressure tends to drop.  

When this happens, baroreceptors, which are pressure-sensitive receptors located mostly in the aortic arch and carotid sinuses, respond by sending signals to the vasomotor center in the medulla. The medulla activates the sympathetic nervous branch of the autonomic nervous system, which increases heart rate, system]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Diabetes_mellitus:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/FvKz5Ly6RB62DKpZWzjYlXUcSpi3fjdS/_.jpg</video:thumbnail_loc><video:title><![CDATA[Diabetes mellitus: Nursing pathophysiology]]></video:title><video:description><![CDATA[Diabetes mellitus is a group of endocrine disorders characterized by hyperglycemia, or elevated blood glucose. The two main types are type 1 diabetes, which is caused by an absolute insulin deficiency; and type 2 diabetes which is caused by insulin resistance.  

Okay, so, the pancreas is an organ located in the abdomen that plays a role in glucose regulation and digestion. Scattered throughout the pancreas are small clusters of cells, called islets of Langerhans. Among these cells are α-cells and β-cells. The α-cells secrete glucagon in response to decreasing blood glucose. Glucagon increases blood glucose by stimulating the liver to breakdown glycogen, or stored glucose, by a process called glycogenolysis.  

Conversely, β-cells secrete insulin in response to increasing blood glucose. Insulin lowers blood glucose, which also suppresses α-cell secretion of glucagon. Along with insulin, β-cells co-secrete amylin, which prevents postprandial, or post-meal, spikes in blood glucose by inhibiting gastric emptying, increasing satiety, and suppressing glucagon release. 

Now, for cells to function, they need glucose as a source of energy. However, cell membranes are impermeable to glucose; so, for glucose to get inside the cell, insulin must first bind to insulin receptors on the cell membrane. This binding activates the cell’s glucose transporters that will then facilitate the movement of glucose into the cell. 

Type 1 diabetes is most commonly caused by an autoimmune destruction of β-cells, resulting in an inability to produce insulin. In other cases, the cause is idiopathic, meaning there’s no known cause. Risk factors include exposure to certain viruses and a family history of type 1 diabetes. 

As for type 2 diabetes, the main cause is insulin resistance in the tissues, which is when cells don’t respond as easily to insulin. Risk factors include obesity, physical inactivity, and a diet high in simple carbohydrates, saturated fats, and red meat. Additionall]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Inflammatory_bowel_disease:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7ad6pwShQUqyf3PXCuP710fkTVao9fOI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Inflammatory bowel disease: Nursing pathophysiology]]></video:title><video:description><![CDATA[Inflammatory bowel disease, or IBD for short, is a chronic condition that causes inflammation and ulceration in the intestinal tract. The two major types of IBD are Crohn disease, or CD, and ulcerative colitis, or UC. 

Okay, so, the gastrointestinal tract is a hollow tube that includes the oral cavity, pharynx, esophagus, stomach, small and large intestines, and anus. Now, zooming in on a cross section of the intestines, we can see that the walls are typically made up of the same four layers of tissue. From the inside out, there’s the mucosa, the inner lining that consists of mucosal epithelium, connective tissue, and smooth muscle that secretes mucus and digestive enzymes. It also serves as a highly selective barrier, that absorbs nutrients and water while preventing absorption of harmful substances and bacteria.  

Moving outward, the submucosa is a dense layer of tissue that provides support and contains blood vessels, lymphatics, and nerves. Next is the muscularis, which consists of a network of nerve fibers and layers of smooth muscle that contract to move intestinal contents forward in a process called peristalsis. And finally, the outermost layer is the serosa, composed of connective tissue. It anchors the intestines in place and secretes a lubricating fluid that promotes smooth movement of the intestines within the abdominal cavity.  

Now, the exact cause of IBD is unknown; however, it’s likely that a combination of genetic, environmental, and immune factors alters the protective barrier function of the mucosal epithelium, leading to a dysregulated immune response. On top of that, the normal gut microbiome may also be altered, resulting in an increasing population of potentially pathogenic bacteria. 

Risk factors include having a family history of IBD; dietary patterns such as a diet high in processed foods; and having another autoimmune disease. Interestingly, nicotine use increases the risk and disease severity of CD, while it’s associated with later onset and less disease severity of UC. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Portal_hypertension:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6dgJKvqTQ9OWVKgRStKYfo6KR4u9Y_73/_.jpg</video:thumbnail_loc><video:title><![CDATA[Portal hypertension: Nursing pathophysiology]]></video:title><video:description><![CDATA[Portal hypertension is a condition that occurs when there’s abnormally high pressure in the portal venous system, which is a network of vessels that drain blood from the abdomen into the liver.  

As a quick review, the portal vein is formed by the splenic vein merging with the superior and inferior mesenteric veins, so it receives blood from the spleen, stomach, pancreas, and small and large intestines.  

This blood contains all the nutrients absorbed in the GI tract, as well as ingested medications and potential toxins. The slow, low-pressure flow of blood provides adequate time for the liver to extract nutrients, metabolize medications, and remove toxins before they reach systemic circulation.  

Once the liver processes the blood it receives, it flows through the hepatic veins to the inferior vena cava, and to the right atrium of the heart. The blood then flows through the heart and lungs, and oxygenated blood is pumped out to the rest of the body.  

Now, portal hypertension is caused by any condition that obstructs blood flow in the portal venous system, and can be prehepatic, intrahepatic, or posthepatic.  

Prehepatic causes are those that result in obstruction of blood flow before reaching the liver such as splenic vein thrombosis, or a clot within the splenic vein.  

Intrahepatic causes are those which result in an obstruction within the liver. One of the most common causes is cirrhosis, a condition where healthy liver tissue is replaced by scar tissue resulting in increased resistance to blood flow through the liver. 

Other causes include certain infections like hepatitis or schistosomiasis, a parasitic infection that can affect multiple organs, including the liver.  

Lastly, posthepatic causes result in obstruction of blood flow from the liver, like right-sided heart failure where the right ventricle is not pumping effectively, causing blood to back up into the liver. 

Okay, so when an obstruction to blood flow develops, pressure builds an]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Anemia:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NEILY8mWSFye697IGpB-i2VPSR_4L-dn/_.jpg</video:thumbnail_loc><video:title><![CDATA[Anemia: Nursing pathophysiology]]></video:title><video:description><![CDATA[Anemia is a group of conditions that occurs when there&amp;#39;s a reduced number of healthy, functional red blood cells, or RBCs, in the blood.  

Now, RBCs are primarily responsible for carrying and delivering oxygen to the body’s tissues. They’re produced through erythropoiesis, which occurs within the bone marrow under the direction of erythropoietin, a hormone produced in the kidneys.  

Here, stem cells called proerythroblasts differentiate into erythroblasts, a type of immature RBC that synthesizes hemoglobin. Hemoglobin is a protein that binds and carries oxygen and is made up of four polypeptide chains called globins, which consist of two α and two β chains. Each chain contains a heme group, which includes an iron atom, where oxygen can bind. One oxygen molecule can bind to each protein chain, allowing one hemoglobin molecule to carry up to four oxygen molecules. And each RBC can contain hundreds of hemoglobin molecules!  

Eventually, erythroblasts differentiate into reticulocytes, another type of immature RBC. The bone marrow releases reticulocytes into the bloodstream where they ultimately become mature RBCs, which are called erythrocytes. Erythrocytes are especially effective in gas exchange, due to their flexible, biconcave shape, which makes them able to fit through narrow blood vessels, while increasing surface area to conduct gas exchange. 

Now, anemia can result from underproduction, increased destruction, or excessive loss of RBCs.  

First, underproduction can occur if the kidneys don’t produce enough erythropoietin, which can happen in chronic kidney disease. Without enough erythropoietin stimulating the bone marrow, not enough RBCs are produced. Also, if there’s not enough building blocks to support erythropoiesis, such as iron, vitamin B12, and folate, less fully functional RBCs can be produced. So, for example, lack of iron can lead to iron deficiency anemia.  

Additionally, if the bone marrow is damaged from conditions]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Leukemia:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2SoKnGnWQJ_isZ15aHN9_IkqSLOaFjiZ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Leukemia: Nursing pathophysiology]]></video:title><video:description><![CDATA[Leukemia is a cancer of the blood-forming tissues, that disrupts the normal function of bone marrow. This disruption leads to the proliferation of immature white blood cells.  

Leukemias are classified as acute or chronic, and by the type of cells affected, either myeloid or lymphoid. The four primary types of leukemia include acute lymphoid leukemia, or ALL; chronic lymphoid leukemia, or CLL; acute myeloid leukemia, or AML; and chronic myeloid leukemia, or CML. 

Now, bone marrow is a spongy tissue found in the center of most bones. It contains stem cells, which are unspecialized cells that, through a process called hematopoiesis, differentiate into functional cells such as red blood cells, or RBCs; white blood cells, or WBCs, also called leukocytes; and platelets. Hematopoiesis is a continuous process that ensures there’s a steady supply of cells to replace old and damaged cells.  

As far as WBCs go, there are several types which come from two distinct stem cell lines: the lymphoid line, and the myeloid line. Immature cells, called blast cells, are formed from these stem cell lines and further differentiate into functional WBCs. In the lymphoid line, lymphoblasts produce lymphocytes, including B-cells, T-cells, and natural killer cells. In the myeloid line, myeloblasts produce neutrophils, eosinophils, basophils; and monoblasts produce monocytes.  

These cells function as part of the immune system, fighting infection and other diseases, and removing foreign substances from the body. 

While the exact cause of leukemia is not fully understood, genetic and environmental factors play a role. Inherited genetic conditions associated with an increased risk of leukemia include Down syndrome and neurofibromatosis. Other genetic changes such as chromosomal translocations, where pieces of two chromosomes split off and swap places, like with the Philadelphia chromosome, are also associated with an increased risk of leukemia.  

Environmental factors include expo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sickle_cell_anemia:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MAluLoycSNiLdkM2E97Q_4lRQYuHt2ra/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sickle cell anemia: Nursing pathophysiology]]></video:title><video:description><![CDATA[Sickle cell anemia, one of the most common types of sickle cell disease, is a genetic condition resulting in red blood cells, or RBCs, that are sickle-shaped, inflexible, and easily destroyed.  

Alright, so, RBCs are produced through erythropoiesis, which occurs within the bone marrow. 

The bone marrow releases immature RBCs called reticulocytes into the circulation where they mature into erythrocytes. Erythrocytes contain hemoglobin, which allows them to deliver oxygen to the body’s tissues. 

Now, hemoglobin molecules are made up of four polypeptide chains of amino acids, which consist of two α-globin and two β-globin chains. Each of these polypeptide chains contains a heme group, which includes one iron atom where oxygen can bind. One oxygen molecule can bind to each polypeptide chain, allowing one hemoglobin molecule to carry up to four oxygen molecules.  

RBCs have some unique characteristics that make them well-suited for oxygen transport. Their unique biconcave shape increases surface area for oxygen diffusion, and their flexible membrane allows them to change their shape so they can squeeze through tiny capillaries and then return to their original shape while staying intact.  

This gives them a degree of durability as they travel throughout the body’s network of blood vessels. In fact, RBCs have a lifespan of up to 120 days.  

As RBCs age, become fragmented, or unhealthy, they’re ingested and destroyed by macrophages in the spleen and liver and replaced through erythropoiesis.   

Sickle cell anemia is caused by a mutation in the HBB gene that provides the instructions for making β-globin. It’s inherited in an autosomal recessive pattern, meaning that an individual must inherit two mutated copies of the HBB gene, one from each parent, to get the disease.  

On the other hand, if an individual has one mutated HBB gene and one normal HBB gene, then they have sickle trait, which doesn&amp;#39;t typically result in anemia.  

Risk factors includ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Adaptive_immunity_mechanisms:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/39bpl7eZTM_80TiREnvKvQiIRpe7KB-b/_.jpg</video:thumbnail_loc><video:title><![CDATA[Adaptive immunity mechanisms: Nursing pathophysiology]]></video:title><video:description><![CDATA[Adaptive immunity is part of the immune system that can provide long-lasting immunity. It’s sometimes called acquired immunity because it’s not present at birth and develops over time. 

Now, adaptive immunity has certain characteristics that sets it apart from the innate, or the general, immune defense an individual is born with, including that it’s inducible, specific, systemic, long-lived, and it has an immunologic memory.  

So, inducible and specific mean that adaptive immunity is not always actively present, but instead, it&amp;#39;s explicitly developed against a particular antigen, which are molecules found on the surfaces of microorganisms and abnormal cells that trigger an immune response.  

Next, systemic means that immune cells can mount an attack throughout the body.  

Finally, adaptive immunity is long-lived and has an immunologic memory, meaning certain immune cells called memory cells, linger in the body, so the next time the body is exposed to this same pathogen, it can mount a faster and stronger response.   

The main components of adaptive immunity include lymphocytes, or white blood cells, and antibodies. The most prominent lymphocytes in the adaptive immune system are T lymphocytes, or T cells, and B lymphocytes, or B cells. These cells interact with other components of the immune system, such as dendritic cells, natural killer cells, and macrophages. Antibodies, also called immunoglobulins, are glycoproteins that assist in fighting infections. 

Now, the main mechanisms of adaptive immunity are induction, cell-mediated immunity, humoral immunity, and immunologic memory. 

Induction involves the activation of the adaptive immune system in response to an antigen, and the process differs between B and T cells.  

The first step in T cell induction is when certain cells, most often macrophages and dendritic cells, serve as antigen-presenting cells, or APCs, because they identify, process, and present antigens to a T cell, which is cal]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Hypersensitivity_reactions_-_Overview:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/wVSHcZmRSQiZA5m3REbMxKi6QByWWp6i/_.jpg</video:thumbnail_loc><video:title><![CDATA[Hypersensitivity reactions - Overview: Nursing pathophysiology]]></video:title><video:description><![CDATA[Hypersensitivity reactions are immune responses that are excessive or have undesirable effects like disease or damage to the body. They are categorized as type I, II, III, or IV based on the immune response and its effect. 

Type I hypersensitivity reactions, also called immediate hypersensitivity reactions or IgE-mediated reactions, occur in response to normally harmless triggers, like pollen, bee stings, or medications.  

Type I hypersensitivity reactions occur in two steps which involve a primary exposure, called sensitization, and a subsequent exposure, when the inflammatory reaction occurs.  

First, the immune system is exposed to an antigen, or allergen.  

Next, antigen-presenting cells, called APCs, present the allergen to T cells which then become helper T-cells, or Th2 cells. The Th2 cells then release large amounts of cytokines that signal B cells to proliferate and turn into plasma cells that start producing IgE antibodies, which bind to mast cells, sensitizing them.  

Then, during subsequent exposure, the antigen forms crosslinks on the IgE antibodies on the mast cell membrane, causing mast cell degranulation and release of proinflammatory mediators like histamine, resulting in an acute inflammatory reaction.  

Because this is an immediate hypersensitivity reaction, clinical manifestations typically occur within 15 to 30 minutes of subsequent exposure to the antigen.  

Manifestations can include rhinitis, characterized by sneezing and nasal congestion; hives, along with rash, redness, and itching; angioedema, where swelling occurs in the deep layers of skin; bronchospasm, which is a tightening of the bronchial smooth muscle; and even systemic reactions like anaphylaxis, characterized by difficulty breathing, hypotension, and death if left untreated.   

Next, type II hypersensitivity reactions, also called tissue-specific or cytotoxic reactions, are mediated by IgG or IgM antibodies against target antigens on a specific tissue or cell.  
]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Infectious_process:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/MU_rrPcBSuOKQTCHeXmaGrP6SN2xBMqe/_.jpg</video:thumbnail_loc><video:title><![CDATA[Infectious process: Nursing pathophysiology]]></video:title><video:description><![CDATA[The infectious process refers to the steps that occur when a pathogen, which is a disease-causing microorganism, enters the body, multiplies, spreads, and causes tissue damage.  

Okay, so, the body has lines of defense to protect itself against pathogens. The first line of defense includes physical and chemical barriers that prevent entry of pathogens into the body, like intact skin and mucous membranes, and molecules like lysozymes found in body fluids like tears and mucus, that can break down the cell walls of certain pathogens.  

Another key aspect of defense is the microbiome, or the collection of microorganisms that normally live in and on the body. These microorganisms don’t normally cause disease, and they help protect against invading pathogens by mechanisms like physically occupying space and even producing substances that inhibit the colonization of pathogens. 

If a pathogen gets past these barriers, it encounters the second line of defense, the inflammatory response, where immune cells like macrophages and neutrophils phagocytize, or ingest, bacteria and cellular debris. Other systems, like the complement system, also get activated, which assist in killing of pathogens. Both the first and second lines of defense are innate, meaning they’re natural, inborn defense mechanisms, and they’re non-specific, because they respond the same way to all pathogens. 

Now, if these mechanisms are not able to stop the invasion of the pathogen, the third line of defense, adaptive immunity, kicks in. It involves cellular immunity primarily with T lymphocytes and B lymphocytes, and the formation of antibodies, which is also called humoral immunity. Adaptive immunity mechanisms attack the current infection, and it even has a memory; so, the next time the body is exposed to this same pathogen, it can start attacking it faster.  

Alright, so, infections are caused by pathogens like bacteria, viruses, and fungi. Each of these organisms have their own characteristi]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acne:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3WErQW05SOywPj_GKC4oieAtQBeSIZHh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acne: Nursing pathophysiology]]></video:title><video:description><![CDATA[Acne vulgaris, often just called acne, is a skin condition that can be non-inflammatory or inflammatory. 

First, let’s look at the skin, which is the largest organ in the body. It provides important functions like protection, sensory perception, temperature regulation, and vitamin D production. Its two main layers, the dermis and epidermis, rest upon the hypodermis, or subcutaneous tissue.  

Starting with the most superficial layer of the skin, the epidermis is composed of layers of stratified squamous epithelial cells. There are various bacteria that live on the outer layer of the epidermis as part of its natural flora. Under normal circumstances, these bacteria don’t grow into numbers large enough to become pathogenic, meaning they typically don’t cause infection.  

Next is the dermis, which is made up of connective tissue that allows the skin to contract and stretch with body movements. It also contains hair follicles, oil and sweat glands, nerves, immune cells, and blood and lymphatic vessels.  

Now, each hair follicle in the dermis is part of a pilosebaceous unit, composed of a short, thin, non-pigmented hair, called a vellus hair, that extends to the epidermis through a pore called the follicular canal; an arrector pili muscle, which makes the hair stand up when it contracts; and one or more sebaceous glands, which produce and secrete oily sebum into the follicular canal and onto the skin’s surface. The sebum acts as a lubricant for the skin and protects from moisture loss. 

Finally, the hypodermis consists mainly of adipose, or fat, tissue that provides insulation and padding and loose connective tissue that helps anchor the skin to the underlying muscle.  

So, the main cause of acne is blockage of the follicular canals by dead skin cells, bacteria, and sebum. A primary risk factor is being an adolescent or young adult. This is because sebaceous glands are stimulated by the increased amounts of circulating androgens in puberty, causing the gla]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Burns:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/8tTLBIIeSqSlWlg7IvAnj-8UQB2jcu7U/_.jpg</video:thumbnail_loc><video:title><![CDATA[Burns: Nursing pathophysiology]]></video:title><video:description><![CDATA[Burns are injuries that occur when the skin and underlying tissues are damaged from exposure to heat, chemicals, electricity, or radiation. Burns can cause localized damage or have widespread effects that can impact multiple organs in the body.  

Okay, the skin is the largest organ in the body and provides important body functions like helping regulate body temperature, preventing loss of body fluids, and protecting against microorganisms, radiation, and mechanical stress.Now, the skin is comprised of two main layers, the epidermis and dermis, that rest upon the hypodermis, that’s sometimes considered a third layer of the skin.The epidermis, or the outermost layer, is composed of multiple layers of keratinocytes, that synthesize keratin, a protein that forms a tough, waterproof barrier to shield underlying structures from mechanical stress. The epidermis also contains melanocytes, which produce melanin, a pigment that helps protect the skin from ultraviolet radiation.The next layer is the dermis, which contains structures like hair follicles, nerves, sensory receptors, and sweat glands. This layer also contains macrophages and mast cells that aid in immune function. Lastly, the hypodermis is the subcutaneous layer, made up of fat and connective tissue that insulates deeper tissues and anchors the skin to the underlying muscle. 

Now, burn injuries can be classified as thermal or non-thermal.Thermal burns result from direct contact with a hot object, open flame, hot liquid, or steam. Other causes of thermal burns include electrical shock and friction.On the other hand, non-thermal burns come from a source other than heat. For example, chemical burns occur from exposure to strong acids, alkalis, or solvents, either by direct contact with the skin, inhalation into the respiratory tract, or ingestion into the GI tract. Non-thermal burns can also be caused by ultraviolet light and radioactive sources. 

Most burns occur in the home; and individuals at highest ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skin_cancer:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/lE5a6kD3TJGgvm6ifO6QX6tZSFOtoAZj/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skin cancer: Nursing pathophysiology]]></video:title><video:description><![CDATA[Skin cancer is a malignant proliferation of skin cells, and includes basal cell carcinoma, squamous cell carcinoma, and melanoma. 

Okay, let&amp;#39;s actually start with a quick review, the skin is the largest organ in the body and provides important functions like protection, sensory perception, temperature regulation, and vitamin D production.  

Its two main layers, the dermis and epidermis, rest upon the hypodermis, or subcutaneous tissue, which is sometimes considered a third layer of the skin.  

The hypodermis consists mainly of adipose, or fat, tissue that provides insulation and padding, and loose connective tissue that helps anchor the skin to the underlying muscle.  

Above the hypodermis is the dermis, which is made up of connective tissue that allows the skin to contract and stretch with body movements. It also contains hair follicle roots, nerves, oil and sweat glands, immune cells, and blood and lymphatic vessels.  The most superficial layer of the skin is the epidermis.  

The epidermis is composed of stratified squamous epithelial cells called keratinocytes. The epidermis is divided into five layers, or strata, consisting of these cells. The basal layer, called stratum basale, is the deepest layer. Here, stem cells called basal cells continuously divide and produce new keratinocytes.  

As these new keratinocytes are formed, they move upward, pushing older cells toward the surface. In the process, the cells gradually flatten and become keratinized, meaning they fill with a protein called keratin, a strong, waterproof protein that gives skin, hair, and nails strength. The basal layer also contains melanocytes.   

These cells synthesize and secrete melanin, the pigment that gives rise to skin color and helps protect against UV radiation. 

The next layer, the stratum spinosum, is composed of irregularly shaped skin cells. As they move upward, they begin to flatten and form the third layer, the stratum granulosum.  

Here, the cells conti]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acid-base_imbalance:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Q6WNhvOmTBK0nHWFzQXXPFLtRgiirew_/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acid-base imbalance: Nursing pathophysiology]]></video:title><video:description><![CDATA[An acid-base imbalance occurs when the body fails to maintain the narrow balance between acids and bases. This imbalance can impair essential metabolic processes like functioning of enzymes, oxygen transport, and removal of waste products. 

Okay, so, the measurement of acids and bases is called the pH. On the pH scale, 7.0 is considered neutral; levels above 7.0 are alkalotic, or basic; and levels below 7.0 are acidotic. The normal range for pH in the blood for adults is 7.35 to 7.45. 

The main molecules involved in acid-base balance are hydrogen bicarbonate, partial pressure of carbon dioxide, and partial pressure of oxygen. Hydrogen has an inverse relationship with the pH of body fluids. So, when there’s more hydrogen, the pH decreases and becomes more acidic; whereas when there’s less hydrogen, the pH increases.  

Next, bicarbonate is a basic substance; so, when there’s more bicarbonate the pH increases, and body fluids become more alkalotic. Likewise, when there’s less bicarbonate the pH decreases, and body fluids become more acidotic.  

Then there’s partial pressure of carbon dioxide which reflects the amount of acidic carbon dioxide dissolved in the arterial blood; and partial pressure of oxygen which reflects the amount of oxygen dissolved in the arterial blood.  

Now, acid-base balance is regulated by various mechanisms in the body. The cellular buffering system, located in the extra- and intracellular fluid compartments, is able to rapidly absorb excessive acidic and basic ions to minimize pH fluctuations. Also, the respiratory system controls pH through adjusting carbon dioxide amounts by changing the rate and depth of breathing; and the renal system manages the amount of excreted and reabsorbed bicarbonate by the kidneys.  

Alright, now, acid-base imbalances occur when the pH is outside the normal range. These imbalances are categorized as either acidotic or alkalotic, depending on the pH level, and metabolic or respiratory, depending on t]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Epigenetics:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hgM_w6dfSQyZfV5WsOlk4oQ_SnSutRgm/_.jpg</video:thumbnail_loc><video:title><![CDATA[Epigenetics: Nursing pathophysiology]]></video:title><video:description><![CDATA[Epigenetics is the study of how an individual’s environment and behavior can modify DNA without altering the DNA sequence. These modifications regulate genes by turning genes on, increasing gene expression, or off, decreasing gene expression. Epigenetic modifications can occur through three mechanisms: histone modifications, DNA methylation, and RNA-based mechanisms.  

As a quick review, the nucleus of each of the body’s cells contains DNA, the genetic material that holds the instructions, or code, for synthesizing specific proteins. These proteins direct the function of cells which give rise to an individual’s phenotype, or their observable characteristics and traits. The complete set of DNA instructions found in each cell is called the genome. 

Okay so, to make a protein, certain genes within the genome need to be activated, or expressed. Whether a gene is expressed or not is regulated through epigenetic modifications that shape the function of the genome. Consequently, epigenetics can help explain a lot of things, like how cells in the body, such as skin cells and brain cells, can differ from one another even though they all contain the same DNA. It can also help explain why identical twins with the same DNA often have subtle differences in their appearance, personality, and even diseases they might develop. 

Now, epigenetic modifications arise from fetal development and continue throughout an individual’s lifetime. These modifications can be the result of early experiences in life such as growing up in a nurturing environment, experiencing abuse or deprivation, and even through dietary choices, use of certain medications, or exposure to industrial pollutants.  

Whatever the cause, these modifications can impact physical and mental health outcomes through their influence on DNA activity. For example, since epigenetic mechanisms can switch on or off genes involved in cell growth, like tumor-suppressor genes, they can promote uncontrolled cell growth,]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Malnourishment:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/2IpBsqBtTLq1J0F27w1NGB3NTtqL-uAJ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Malnourishment: Nursing pathophysiology]]></video:title><video:description><![CDATA[Malnourishment, also called malnutrition, is when there’s an imbalance of nutrients needed to support essential body functions. This imbalance can occur with overnutrition, where nutrient intake is more than the body requires, like with obesity; or with undernutrition, where nutrient intake is insufficient to meet the body’s needs, as seen in starvation. 

So, the three primary nutrients crucial for overall health are carbohydrates, proteins, and fats.  First, carbohydrates are the primary source of glucose used for energy and include monosaccharides, oligosaccharides, and polysaccharides. Monosaccharides are simple carbohydrates, like table sugar. They are easily broken down and less nutrient-dense. Oligosaccharides and polysaccharides are more complex carbohydrates, like soybeans and whole grains. These take longer to break down and are more nutrient-dense.  

Next, proteins are complex chains of amino acids and are the building blocks of the body. They construct tissues and important molecules, like enzymes and hormones, and they repair tissues. Proteins can also be used for energy, if needed. Amino acids are categorized as essential, meaning they must be ingested through the diet, and non-essential, because they are produced within the body. High protein foods include animal products, like meat and dairy, or plant-based foods like legumes and nuts.  

Lastly, fats, or lipids, are composed of glycerol and fatty acids. Fats are another source of energy, and they’re a critical component of cells and tissues. They also help absorb fat soluble vitamins and make up important molecules like steroids. Based on their chemical structure, fats are either saturated, like butter, or unsaturated, like the fats found in avocado.  

Once ingested, nutrients are broken down by the digestive system, absorbed, and used in various ways. Carbohydrates are broken down into glucose, which is transported throughout the body and used by cells for energy. Any excess glucos]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mendelian_patterns_of_inheritance:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/l_koqpAbRkaneF4JiOUnIMeoR8ahcV1R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mendelian patterns of inheritance: Nursing pathophysiology]]></video:title><video:description><![CDATA[Patterns of inheritance refer to the way certain traits are passed down genetically from parents to offspring. Mendelian patterns of inheritance typically follow four basic patterns and involve only one gene. 

First, let’s review the basics of genetics. Each gamete, also known as a sex or germ cell, such as sperm or ova, contains 23 chromosomes, which carry genetic information. When a sperm fertilizes an ovum, these chromosomes combine to form a zygote, or fertilized ovum, that now has 46 chromosomes, arranged into 23 pairs. These pairs of chromosomes are collectively called the genome. 

Now, the first 22 pairs of chromosomes are autosomes, whereas the 23rd pair are sex chromosomes. Sex chromosomes typically include an X chromosome from the mother and either an X or Y chromosome from the father, resulting in either a female offspring with XX chromosomes or a male offspring with XY chromosomes.  

Every chromosome contains multiple genes, which are regions of DNA that carry information for a specific trait. Different versions of a gene are called alleles. Alleles provide information for a phenotype, or the observable traits of an individual, such as eye color or height. Alleles can be dominant or recessive, with recessive alleles being masked by dominant alleles. Additionally, if an individual inherits two of the same alleles, they’re homozygous for that trait; whereas if the alleles are different, they’re heterozygous for that trait.  

For example, the allele for brown eyes is dominant and the allele for blue eyes is recessive. So, if an individual has one allele for brown eyes and one for blue eyes, the dominant allele masks the recessive allele, resulting in an individual with brown eyes, and they’re considered heterozygous for that trait. On the other hand, if an individual has two alleles for blue eyes, they’ll have blue eyes and be considered homozygous for that trait.  

Alright, let’s take a closer look at Mendelian patterns of inheritance. They’]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Multiple_organ_dysfunction_syndrome_(MODS):_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D9GVcPyHQ42icvJSDU2xCKBeRlSAgDY7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Multiple organ dysfunction syndrome (MODS): Nursing pathophysiology]]></video:title><video:description><![CDATA[Multiple organ dysfunction syndrome, or MODS, is the progressive dysfunction of two or more organ systems, where homeostasis can’t be maintained without intervention. It occurs when an insult or injury to the body, from conditions like severe infections, severe trauma, or a critical illness, initiates an uncontrolled inflammatory response. Depending on the severity and the number of organs involved, MODS can progress to organ failure and death. 

Now, a normal inflammatory response is protective and part of how the immune system reacts to an insult that causes injury to the body’s tissues.  

Within seconds of the injury, immune cells, such as macrophages and mast cells, release inflammatory mediators.  

These inflammatory mediators, including cytokines, chemokines, interleukins, and histamine, recruit more immune cells to the site of injury and act on the endothelial cells lining the blood vessels to cause vascular changes that support the inflammatory response.  

The endothelial cells release nitric oxide, causing vasodilation, which allows more blood to accumulate at the site of injury.  

Endothelial cells also express adhesion molecules, which allow immune cells, mostly neutrophils, to move along the endothelial surface so they can reach the injured site.  

Also, vascular permeability increases, which is when the endothelial cells begin to separate from each other. This allows fluid, proteins, and leukocytes to move from inside the vessels and out to the extravascular space, where the leukocytes begin to eat up any invading bacteria by phagocytosis.  

And finally, activation of plasma proteins initiates the formation of clots, which provides a foundation for healing.  

At the same time, the adrenal glands release stress hormones like epinephrine and cortisol to help regulate the inflammatory response. Regulation of the inflammatory response can promote the positive aspects of inflammation by helping to eliminate harmful infections, remove damaged]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Pediatric_cancer_-_Overview:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/mcOwXsadRSKtdn1dCxNHtLC4T-KrCSCq/_.jpg</video:thumbnail_loc><video:title><![CDATA[Pediatric cancer - Overview: Nursing pathophysiology]]></video:title><video:description><![CDATA[Childhood cancer is a collection of conditions occurring in children and adolescents that are characterized by abnormal cells that divide and grow uncontrollably. 

Now, the cause of childhood cancer is multifactorial, meaning a child’s unique genetic factors and environmental factors interact to promote the development of cancer. Even so, these factors are often not known at the time of diagnosis, so in many cases the exact cause of cancer in children is unknown. 

Genetic factors involved in cancer can be mutations that are either inherited or acquired. These include mutations that typically occur in genes that regulate cell division, including proto-oncogenes, which promote cell division, or tumor suppressor genes, that inhibit uncontrolled cell division.  

For example, mutations to the MYCN proto-oncogene can predispose children to neuroblastoma and glioblastoma, both cancers of the nervous system. On the other hand, mutations to the RB1 tumor suppressor gene are associated with retinoblastoma, a type of cancer in the light-sensing layer of cells in the back of the eye called the retina. This mutation can be spontaneous, or it can be a familial cancer resulting from a germline mutation, meaning the mutation occurred in a reproductive cell, either the sperm or egg, so it becomes part of the DNA of each of the body’s cells.  

Other genetic changes such as chromosomal translocations, where pieces of two chromosomes split off and swap places, like with the Philadelphia chromosome, are also associated with an increased risk of leukemia, a cancer of blood-forming tissues that disrupts the normal function of bone marrow.  

Leukemia can also occur in children born with certain congenital conditions like Down syndrome, or trisomy 21, a condition where there’s an extra copy of chromosome 21. 

Environmental risk factors can include exposure to carcinogens, or substances that can promote the development of cancer, like tobacco smoke and certain chemicals and m]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Osteoarthritis_and_rheumatoid_arthritis:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/v8hiW1e-RKSMVZZcF32d3anHRWGZfSBd/_.jpg</video:thumbnail_loc><video:title><![CDATA[Osteoarthritis and rheumatoid arthritis: Nursing pathophysiology]]></video:title><video:description><![CDATA[Osteoarthritis, or OA, and rheumatoid arthritis, or RA, are diseases that affect the synovial joints. OA is mostly a degenerative disease, while RA is a systemic autoimmune disease that can also impact other organs like the heart and lungs. 

Joints, or the places where bones meet, can be classified into three main groups based on their structure and range of movement. Fibrous joints, like those between the bones of the skull in young children, are composed of a thin layer of fibrous tissue that allows for some movement to accommodate a child’s growing brain; by adulthood, the fibrous tissue is replaced by bone. On the other hand, cartilaginous joints, like the joints of the spine, contain a pad of fibrocartilage, allowing for some movement. Lastly, synovial or diarthrodial joints, like those of the wrist, shoulders, hips, and knees, are freely movable. 

Okay, let’s take a closer look at synovial joints, which consist of two bones, each with its own layer of articular cartilage, a type of connective tissue that provides cushioning and allows the bones to glide against each other without friction. The cartilage has high tensile strength, which helps weight-bearing joints like the knees to distribute weight so the underlying bone absorbs the shock and weight. An important component of the articular cartilage are special cells called chondrocytes, which are essential for the maintenance and repair of the cartilage.  

Surrounding the joint is an outer fibrous joint capsule that forms an inner space called the joint cavity, which is filled with synovial fluid. The inner surface of the joint capsule is lined with a synovial membrane, or synovium, which is mostly composed of connective tissue, elastic fibers, blood, and lymphatic vessels. It also contains macrophages that remove bacteria and debris, and fibroblasts that produce a viscous substance called hyaluronate, which is the main component of the synovial fluid, that lubricates the articular surfaces.  

N]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Skeletal_trauma:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/D_gHtxTvRBeDLonxIU-4muYjS2CgsaXI/_.jpg</video:thumbnail_loc><video:title><![CDATA[Skeletal trauma: Nursing pathophysiology]]></video:title><video:description><![CDATA[Skeletal trauma occurs when there’s an injury to the bones or joints. Common conditions include fracture, which is a complete or incomplete break in the bone; subluxation, when there’s partial separation of a bone from a joint; and dislocation, when there’s a complete separation of a bone from the joint. 

Within the skeletal system, bones and joints work together with other tissues to provide structure, support, protection for internal organs, and to facilitate body movement. In addition to these functions, bones are metabolically active tissues that are involved in key functions in the body. First, long bones, such as the humerus or the tibia, contain marrow, the site where hematopoiesis occurs, which is the production of red blood cells, white blood cells, and platelets.  

Bones also serve as a reservoir for calcium and phosphate phosphorus and play a key role in calcium homeostasis. Lastly, bones are continually involved in remodeling, which involves bone resorption, formation of new bone, and bone repair. This is accomplished through cells called osteoclasts, which break down old bone for reabsorption, and osteoblasts, which lay down new bone to replace the bone that was resorbed. This continual remodeling helps maintain the health and functionality of bones. 

The basic types of bone are cortical, or compact bone, which is found in the outer layer of bones; and cancellous, or spongy bone, which is found in the interior of bones. The structure of cortical bone helps it to tolerate compression and shearing forces, while cancellous bone is better equipped to absorb and distribute stress throughout the bone. 

Now, joints are the place where two or more bones come together, and they provide varying degrees of range of motion. For example, fibrous joints, like those between the bones of the skull, barely move at all; whereas, synovial joints, like those of the shoulders and hips, move more freely. Joints are supported by cartilage, ligaments, and tendons]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Parkinson_disease:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/vpM-0mFIQGSQaEATVjXmJA_-TIqOX8KO/_.jpg</video:thumbnail_loc><video:title><![CDATA[Parkinson disease: Nursing pathophysiology]]></video:title><video:description><![CDATA[Parkinson disease, or PD, is a progressive neurodegenerative disorder that primarily impacts movement and results from loss of dopamine-producing neurons in the brain.  

Now, motor activity is regulated by complex neural circuits within the brain. One of the main structures responsible for motor activity is the basal ganglia, also called the basal nuclei, located deep within the cerebral hemispheres of the brain.  

The basal ganglia are a group of interconnected structures that are mainly involved in the planning, execution, and termination of motor activity through their connection with other parts of the brain. These include the thalamus, which serves as a major relay station in the brain, and cerebral cortex, which is responsible for many of the brain’s higher functions like reasoning and problem-solving and which also contains the motor cortex.  

One important part of the basal ganglia is called the substantia nigra. This structure contains dopaminergic neurons that produce dopamine, a neurotransmitter involved in motor function and the fine-tuning of movements. Dopamine also inhibits the excitatory effects of neurotransmitters produced in other parts of the basal ganglia, like acetylcholine. 

In addition to its key role in motor activity, the basal ganglia are also involved in coordinating cognitive, behavioral, and emotional functions through connections to the limbic system, which like the basal ganglia, is a group of interconnected structures. The limbic system is sometimes called the emotional brain due to its role in regulating emotions and behavior. 

Okay, so PD is classified as primary, or idiopathic, and secondary, or acquired. Although there’s no known cause for most cases of primary PD, the incidence increases with age.  

Other cases are related to familial or genetic factors, including those associated with the formation of Lewy bodies, which are aggregations of dysfunctional proteins in the brain, called alpha-synuclein, that play a ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Stroke:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/0lKA0UGCTCmwVssInacL_YZXTyKIv8Qx/_.jpg</video:thumbnail_loc><video:title><![CDATA[Stroke: Nursing pathophysiology]]></video:title><video:description><![CDATA[A stroke, also known as a cerebrovascular accident, occurs when blood flow to the brain is disrupted, resulting in tissue ischemia and death.  

A stroke can be ischemic or hemorrhagic. An ischemic stroke is when there’s an occlusion in an artery in the brain; while a hemorrhagic stroke is when an artery in the brain ruptures and causes blood to leak into the brain tissue. 

Now, the brain is the communication and control center of the body, and to maintain neurologic function, all parts of the brain require a steady and consistent flow of oxygen- and nutrient-rich blood. The brain is supplied with blood through the internal carotid arteries and the vertebral arteries. The internal carotid arteries branch off into the middle cerebral arteries and the anterior cerebral arteries, while the vertebral arteries come together to form the basilar artery. The basilar artery then leads into the posterior cerebral arteries. The posterior cerebral arteries, along with the anterior cerebral arteries, internal carotids, and other smaller branched arteries form the circle of Willis. 

The circle of Willis is a group of arteries arranged in a circle that allows for collateral blood flow, meaning blood can circulate from one side of the brain to the other if a blockage occurs.  

Okay, so with ischemic strokes, blood flow is disrupted by obstruction from a thrombus or embolus. A thrombus is a clot that forms within a vessel, whereas an embolus is when a clot breaks off from one area and travels downstream, lodging in a smaller vessel.  

For example, a thrombus can occur from atherosclerotic plaque, where fats build up within a vessel supplying blood to the brain; and an embolus can occur from a blood clot in the atria of the heart due to atrial fibrillation that makes its way into cerebral circulation.  

Risk factors for ischemic strokes include hypertension, hyperlipidemia, increased age, heart disease, and sleep apnea. There is also an increased risk with smoking, ora]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Breast_cancer:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6f1km3qCTmGDd5bwx_-s1YuPTSCBcMe7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Breast cancer: Nursing pathophysiology]]></video:title><video:description><![CDATA[Breast cancer is the uncontrolled growth of abnormal cells in the breast tissue that can spread to other parts of the body.  

Okay, so, breasts, also called mammary glands, are milk-producing glands that sit on the chest wall on top of the ribs and the pectoral muscles, made up of glandular, adipose, and connective tissue.  

The glandular tissue makes the milk during lactation and is made up of 15 to 20 lobes that surround the nipple in a radial pattern, and each lobe contains many smaller lobules. Inside each of these lobes are grape-like structures called the alveoli containing secretory epithelial cells that produce milk during lactation and myoepithelial cells that contract to move milk from the alveoli.  

The alveoli, lobules, and lobes are connected through a network of ducts called the lactiferous ducts that drain the milk produced during lactation.  

Surrounding the glandular tissue is the stroma, which contains fibrous connective tissue and adipose tissue, which makes up the majority of the breast.  

Lastly, located throughout the breasts are blood vessels, as well as lymphatic vessels that drain into the lymph nodes.  

For examination purposes, the breasts are divided into quadrants which include the upper outer quadrant, upper inner quadrant, lower outer quadrant, and lower inner quadrant.  

Now, breast cancer is caused by mutations to DNA within breast tissue that results in uncontrolled cellular proliferation.  

There are modifiable and non-modifiable risk factors that increase the risk of breast cancer. Modifiable risk factors include exposure to ionizing radiation that can come from medical diagnostics and treatments; postmenopausal hormone replacement therapy; alcohol consumption; exposure to certain environmental chemicals like polychlorinated biphenyls, or PCBs; obesity; and physical inactivity.  

Non-modifiable risk factors include age over 65; early menarche or late menopause; being biologically female, though biological males ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Prostate_cancer:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/3mtiMu1zQHGKUUDKn8uoMscHR1eia80f/_.jpg</video:thumbnail_loc><video:title><![CDATA[Prostate cancer: Nursing pathophysiology]]></video:title><video:description><![CDATA[Prostate cancer is a malignant growth that originates in the prostate gland.  

The prostate is a small walnut-shaped gland that sits under the bladder, in front of the rectum. It secretes an alkaline milky liquid, called prostatic fluid, which contains nutrients to nourish the sperm, support its movement, and help it survive in the acidic environment of the vagina.  

Now, the urethra travels through the prostate before reaching the penis. During ejaculation, smooth muscles in the prostate contract and push prostatic fluid into the urethra where it joins the sperm, along with the semen. 

The prostate can be divided into distinct zones based on their histological differences, including the peripheral, central, transitional, and fibromuscular zones. The peripheral zone is the outermost posterior section and is the largest of the zones, containing most of the prostate’s glandular tissue. It’s also the most common site for development of prostate cancers and is the part of the prostate that’s palpated during a prostate exam, called a digital rectal examination or DRE.  

Moving inward, there’s the central zone, followed by the transitional zone, the site that undergoes hyperplasia in a condition called benign prostatic hyperplasia, which is considered a normal part of aging. Part of the transitional zone that surrounds the urethra is sometimes called the periurethral gland region. Lastly, a fibromuscular zone covers the anterior portion of the prostate. 

Okay, so, the development and normal function of prostate cells depend on androgens, or sex hormones, like testosterone. Although most of the body’s testosterone is produced by the testes, a portion of testosterone is made in the prostate. In the prostate, testosterone is converted by the enzyme 5α-reductase into highly potent dihydrotestosterone, or DHT, which happens when dehydroepiandrosterone, or DHEA, produced by the adrenal glands enters the prostate and is converted into testosterone.  

Now, al]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Sexually_transmitted_infections:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/BSbvhjvpRKiuDVlMNhmzEb-tSEOR_12h/_.jpg</video:thumbnail_loc><video:title><![CDATA[Sexually transmitted infections: Nursing pathophysiology]]></video:title><video:description><![CDATA[Sexually transmitted infections, or STIs, are infections spread by sexual contact. These infections are sometimes also called sexually transmitted diseases, or STDs, and were formerly known as venereal diseases. 

Now, STIs can be bacterial, like chlamydia, gonorrhea, and syphilis;  

viral, such as herpes simplex virus, or HSV; human papillomavirus, or HPV; hepatitis; and human immunodeficiency virus, or HIV; or parasitic, such as in trichomoniasis.  

They’re spread through direct contact, including direct sexual contact like vaginal, oral, or anal intercourse; contact with infected blood or other bodily fluids; and even through close body contact.  

Additionally, some STIs, such as chlamydia, gonorrhea, syphilis, and HIV, can be spread through vertical transmission, meaning the infection passes from mother to fetus during pregnancy or to the infant during a vaginal birth. In other cases, infections can be transmitted by sharing personal items such as toothbrushes or razors or by sharing needles during IV drug use. 

Risk factors for STIs include having multiple sexual partners, especially without an effective barrier such as a condom; being an uncircumcised biological male; and being the receptive partner during intercourse. Also, biological females are at higher risk for infection, partly because the vaginal lining is relatively thin and more easily invaded by pathogens.  

Additionally, inadequate screening, lack of access to healthcare, or inadequate risk assessment by healthcare providers all increase the risk that an infected individual unknowingly transmits an STI to another individual. Lastly, STIs can occur at any age, but they’re most prevalent in young adults. 

Okay, so, the pathophysiology of STIs depends on the specific infectious agent and site.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Obstructive_and_restrictive_pulmonary_diseases:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/zjqeFeoxSGKfA0h1w4TUDDvsQLaEsqKK/_.jpg</video:thumbnail_loc><video:title><![CDATA[Obstructive and restrictive pulmonary diseases: Nursing pathophysiology]]></video:title><video:description><![CDATA[Obstructive and restrictive lung diseases are groups of conditions affecting ventilation, which is the mechanical movement of inhalation and exhalation that moves air in and out of the lungs so gas exchange can occur. Obstructive lung diseases are characterized by obstruction of exhalation, causing air to be trapped within the lungs; whereas restrictive lung diseases restrict inhalation, preventing the lungs from filling with adequate amounts of oxygen-rich air. 

So, the primary role of the lungs is facilitating gas exchange between the external environment and the circulatory system, and a key step in this process is ventilation.  

During the inhalation phase of ventilation, the respiratory muscles, primarily the diaphragm and the external intercostal muscles, contract. The diaphragm moves downward and flattens, while external intercostal muscles cause the rib cage to expand, increasing the volume of the chest cavity. This creates pressure in the lungs that’s lower than atmospheric pressure, allowing oxygen-rich air to move in and fill the lungs.  

Then, during exhalation, the respiratory muscles relax, and the lungs return to their resting state. This creates pressure in the lungs that’s higher than the atmospheric pressure, allowing air to move out of the lungs. 

Now, there are some crucial factors that support the process of ventilation. First, there’s the ability of the lungs to expand and fill during inhalation, which is called compliance. Lung compliance is determined by other factors like the presence of elastin fibers within the lung tissue and the ability of the chest wall to expand and contract during ventilation.  

Compliance is also dependent on the surface tension within the alveoli, which are the tiny sacks where gas exchange happens. The alveoli are lined with a thin film of water which creates a force, called surface tension, that tends to collapse the alveoli.  

To counteract this, certain cells within the alveolar walls, called typ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Kidney_disease:_Nursing_pathophysiology</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/4ygl-W44QTe2dVBrRElBgrzdRQKzj_mA/_.jpg</video:thumbnail_loc><video:title><![CDATA[Kidney disease: Nursing pathophysiology]]></video:title><video:description><![CDATA[Kidney disease occurs when kidney function declines, disrupting the regulation of fluids, electrolytes, waste products, and acid-base balance. Acute kidney injury, or AKI, is a sudden decline in kidney function that’s typically reversible, whereas chronic kidney disease, or CKD, is kidney damage that is gradual and irreversible. 

Now, the kidneys are the body’s natural blood filter. They regulate what’s in the blood, clearing it of metabolic waste and toxins and excreting them through urine. They’re essential in regulating fluids and electrolytes; maintaining acid-base balance; secreting hormones essential for regulating blood pressure and stimulating the production of red blood cells; and activating vitamin D. 

Within each kidney, there are millions of tiny functional units called nephrons, which consist of a renal corpuscle and renal tubules. The renal corpuscle is where blood filtration occurs, and it includes a tiny bundle of capillaries called the glomerulus, and the glomerular capsule, or Bowman’s capsule, which is a cup-shaped structure that surrounds the glomerulus. 

As blood flows through the glomerulus, an ultrafiltrate of blood is created, which is then collected by Bowman’s capsule. Then, as it moves into the renal tubules, the filtrate is modified according to the body’s needs and urine is produced, in which waste is eliminated. The rate at which filtration takes place is called glomerular filtration rate, or GFR for short, and it’s one of the main measures of kidney function.  

Now, there are three different mechanisms that can cause kidney injury. First, prerenal kidney injury can occur when there’s decreased blood flow to the kidneys like from dehydration, hemorrhage, or shock. In certain individuals, medications like non-steroidal anti-inflammatory drugs, or NSAIDs; angiotensin-converting enzyme, or ACE, inhibitors; or angiotensin receptor blockers, or ARBs, can also cause prerenal kidney injury by altering the normal autoregulation of]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Type_1_diabetes_mellitus_(pediatric):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/U0HO5pKnRD_32U15gtJCI5qBR6G2FGgb/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Type 1 diabetes mellitus (pediatric): Nursing]]></video:title><video:description><![CDATA[Nurse Camden works on a pediatric medical-surgical unit and is caring for Tate, an 11-year-old who was admitted several days ago for new onset type 1 diabetes mellitus. In collaboration with the registered nurse, RN Kande, Nurse Camden goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Tate’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Camden recognizes important cues including temperature 97.3 F or 36.2 C, pulse 96 beats per minute, respirations 18 breaths per minute, oxygen saturation 98 percent on room air, and blood pressure 105/70 mmHg. Tate’s mother is at the bedside and reports that over the last month, Tate’s been irritable, unusually hungry and thirsty, and he’s urinating frequently.   

Next, Nurse Camden analyzes these cues. He reviews the electronic health record, or EHR, and notes that Tate’s last blood glucose level was 135 mg/dL and his hemoglobin A1C level is 7.8 percent. Nurse Camden also sees that Tate has lost four pounds in the past two months and that Tate’s urine was positive for glucose upon admission. Nurse Camden also sees that Tate’s regular IV insulin infusion has been discontinued by RN Marge to transition him to subcutaneous insulin, per the healthcare provider’s order.  

Nurse Camden realizes that the glucose from the food Tate eats can’t move from his blood into his cells, due to a lack of insulin. Because of this, Tate isn’t able to convert the food he eats to energy, causing him to experience fatigue and hunger. He also realizes that Tate’s kidneys can’t reabsorb the excess glucose, so it ends up in the urine, where it pulls water out along with it as its eliminated, causing his other symptoms of frequent urination and increased thirst. Nurse Camden recognizes that Tate needs effective management of his blood glucose.  

Now, using the information he’s gathered, along with Tate’s]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Poisoning_(pediatric):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/__eve6nUSbqPUe3okO32fIAZTSGdiIzC/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Poisoning (pediatric): Nursing]]></video:title><video:description><![CDATA[Nurse Olivia works in a pediatric inpatient unit and is caring for Daisy, a 2-year-old who was admitted yesterday for observation after accidentally ingesting acetaminophen. In collaboration with the registered nurse, RN Tamika, Nurse Olivia goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Daisy’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Olivia recognizes important cues including Daisy’s vital signs which are temperature 98.6 F, or 37 C, heart rate 118 beats per minute, respiratory rate 27 breaths per minute, and blood pressure 92/52 mmHg. Nurse Olivia notes Daisy is pale and is restless at times, but easily consoled by Ellen, her caregiver. Nurse Olivia determines Daisy’s pain rating is 3 out of 10 according to the Face, Legs, Activity, Cry, and Consolability, or FLACC, scale.  Gentle abdominal palpation reveals no tenderness, which is consistent with RN Tamika’s previous assessment.  

Next, Nurse Olivia analyzes these cues. She reviews the electronic health record, or EHR, and learns that prior to admission, Daisy consumed an unknown quantity of acetaminophen pills while Ellen was busy preparing dinner. After counting the remaining pills in the bottle, Ellen realized Daisy ingested about 13 pills and immediately contacted Poison Control, who told her to bring Daisy to the emergency department.  

Nurse Olivia notes that Daisy’s weight is 12.7 kilograms, or 28 pounds. She also knows that the toxic dose of acetaminophen is 150 milligrams per kilogram in children, and since Daisy ingested 13, 160 milligram pills, she exceeded the toxicity level for her age and weight. Nurse Olivia recognizes that an overdose of acetaminophen can cause hepatotoxicity, and the clinical course progresses over time. 

Based on Daisy’s presentation and history of acetaminophen ingestion, Nurse Olivia determines that Dai]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Burn_(pediatric):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NC0H4jvJTOuaGVZs8ME7kHurQZKuzCRP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Burn (pediatric): Nursing]]></video:title><video:description><![CDATA[Nurse Lawrence works in a pediatric rehabilitation facility and is caring for Abigail, a 2-year-old who was admitted to the facility from a burn unit after being treated for an accidental scalding injury that resulted in partial- and full-thickness burns. In collaboration with the registered nurse, RN Miley, Nurse Lawrence goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Abigail’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Lawrence recognizes important cues, including Abigail’s vital signs, which are temperature 98.6 F or 37 C, heart rate 88 beats per minute, respirations 18 breaths per minute, blood pressure 96/52 mmHg, and oxygen saturation 100 percent on room air. Next, Nurse Lawrence uses the Face, Legs, Activity, Cry, and Consolability, or FLACC scale, and determines Abigail’s pain rating is 5 out of 10 according to her behavioral cues.  

Next, Nurse Lawrence analyzes these cues. He reviews the electronic health record, or EHR, with RN Miley, and they note an order for sterile dressing changes, and that Abigail is prescribed a topical antimicrobial to be applied to her burns. They also see that she’s been prescribed medication for pain management and that she received her last dose four hours ago.   

Nurse Lawrence recalls that a scald is a type of thermal burn caused by hot liquids or steam, and he knows that toddlers, like Abigail, are at high risk for these types of burns as they start to become more mobile and explore their environment.  

He recalls that partial-thickness burns involve the epidermis and part of the dermis layers of the skin, and that full-thickness burns involve both the epidermis and the entire dermis.  

This destroys the network of immune cells that reside in the epidermis and the physical barrier the skin provides against microorganisms. He further understands that the ris]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Head_injury_(pediatric):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Oexrth3ATainyrJqZ5Di6braTGCXQLqX/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Head injury (pediatric): Nursing]]></video:title><video:description><![CDATA[Nurse Tyisha works in a pediatric primary care clinic and is caring for Justin, a 10-year-old who is being evaluated following a concussion that occurred during a soccer game one week ago. In collaboration with the registered nurse, RN Christine, Nurse Tyisha goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Justin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Tyisha recognizes important cues, including Justin’s vital signs which are temperature 98.9 F or 37.1 C, heart rate 100 beats per minute, respirations 16 breaths per minute and blood pressure 104/70 mmHg. Justin reports a mild headache and rates it as a 2 out of 10 on a numeric pain scale. Justin is alert and oriented to person, place, and time.  There’s also a small, healing bruise above his left eyebrow.  

Nurse Tyisha gathers additional information from Justin and his caregiver, Mary, who’s at the bedside. 

Nurse Tyisha: Hi Justin. How are you feeling? 

Justin: Uhm, okay, my head feels kind of…  

Mary: (Interrupting Justin) He just hasn’t been acting like himself since the injury. He’s been irritable and forgetful, especially with his chores, which just isn’t like him. He’s especially tired after school, and I noticed he gets frustrated when working on his computer or even when he’s playing video games or watching television. 

Justin: I can answer for myself, Mom. I just feel tired. It’s making me grumpy, and my head is kind of fuzzy.  

Next, Nurse Tyisha analyzes these cues. She reviews the electronic health record, or EHR and notes that Justin’s concussion occurred following head-to-head contact during a soccer game one week ago. Although he didn’t lose consciousness, he had poor coordination following the event.  

Nurse Tyisha knows a concussion is a type of closed head injury that occurs when an event, like the head striking a hard objec]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Asthma_(pediatric):_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/6oAsPNLsTZyaa_00je8JzA4PT2uVRhJI/_.png</video:thumbnail_loc><video:title><![CDATA[Case study - Asthma (pediatric): Nursing]]></video:title><video:description><![CDATA[Nurse Lin works at a primary care clinic and is caring for Joey, an 8-year-old who’s had a cough for two months and mild chest tightness over the last week. In collaboration with the registered nurse, RN Marge, Nurse Lin goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Joey’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Lin recognizes important cues, including Joey’s vital signs which are temperature 98 F or 36.6 C, heart rate 94 beats per minute, respirations 20 breaths per minute, and oxygen saturation 95 percent on room air. Nurse Lin auscultates Joey’s lungs and hears mild wheezes in all lobes upon expiration, which is consistent with RN Marge’s previous assessment.  

She gathers additional information from Joey and his aunt, Angel, who’s at the bedside. 

Nurse Lin: Hi Joey, could you tell me about how your breathing has been? 

Joey: Sometimes my chest feels a little tight and it&amp;#39;s hard to take a deep breath. 

Nurse Lin: That must be uncomfortable. When did you start feeling like this?   

Joey: I don’t know. 

Angel: He’s had a nagging cough for a while now. At first, I thought it was just the change in the weather making his allergies flare up, but his allergies don’t normally affect his breathing. That’s why I made the appointment.   

Nurse Lin: It’s good you brought Joey in.   

Next, Nurse Lin analyzes these cues. She reviews the electronic health record, or EHR, and notes that Joey has no relevant medical history other than seasonal allergies. She assists Joey to a sitting position while RN Marge performs the ordered spirometry testing by having Joey breathe into a mouthpiece connected to a device that measures how much air he’s able to breathe in and out. They note that Joey can&amp;#39;t expel all the air after taking a deep breath. RN Marge then speaks to the healthcare provider, who ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Occupational_Health_Nursing_in_Canada</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/kvt6w2ohSimy8_jN3k2u6ss4Twi87-h6/_.jpg</video:thumbnail_loc><video:title><![CDATA[Occupational Health Nursing in Canada]]></video:title><video:description><![CDATA[Occupational health nursing is a branch of nursing specializing in promoting health and safety of individual employees and groups of workers in employment settings. As the occupational health nurse, or OHN, you’ll identify occupational hazards, prevent illness and injury, and promote health by advocating for a safe and healthy work environment. 

Okay, so, occupational health nurses operate in various workplace environments. These include manufacturing companies, corporations, construction sites, utilities, and healthcare facilities.   

As an occupational health nurse, your goals include identifying occupational hazards, preventing illness and injury, and promoting health by advocating for a safe and healthy work environment. 

Now, in order to identify potential hazards, you’ll assess the health and safety of individual workers and the workplace as a whole.  

On an individual level, start by gathering information about previous employment, past exposure to workplace hazards, and medical symptoms or ailments related to previous workplace illness or injuries.  

Next, ask about present work conditions including specific responsibilities or tasks and current exposure to work-related hazards. These can include biological hazards, like a healthcare worker who is exposed to bloodborne pathogens that could lead to infections like hepatitis B and C; chemical hazards, like when a construction worker is exposed to toxic welding fumes; or physical hazards like heavy equipment operators who are exposed to vibrations, which over time can result in chronic musculoskeletal pain or even peripheral vascular and sensorineural problems.  

There are also enviro-mechanical hazards, where repetitive motions can cause musculoskeletal injuries, like an office worker at risk for carpal tunnel syndrome from repetitive hand and wrist movements that occur from typing and using a mouse.  

Finally, regardless of the profession, exposure to psychosocial agents like workplace stress]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Environmental_Health</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/z_2SvhFKTx_L2QTxunSTaZNDTretfuNV/_.jpg</video:thumbnail_loc><video:title><![CDATA[Environmental Health]]></video:title><video:description><![CDATA[Environmental health is focused on how human health and well-being is influenced by the environment in homes, schools, workplaces, and communities.  

Exposure to environmental hazards in the air, water, land, and food supply can negatively impact health.  

As the nurse, you’ll promote environmental health by assessing and managing environmental risk factors, providing education, and advocating for policies that support healthy environments.  

Okay, so hazards to environmental health can involve the air, water, land, and food supply. Starting with air, both outdoor and indoor air quality can be affected. Outdoor air quality is affected by natural events, like smoke from wildfires, and human activities, like emissions from driving motor vehicles. Also, industrial processes, such as emissions from chemical plants, power plants, and waste incineration that release heavy metals and other toxic chemicals into the atmosphere, leading to poor air quality.  

On the other hand, indoor air quality, like within homes, schools, and workplaces, can be impacted by factors like the use of certain appliances such as gas stoves that have the potential to produce carbon monoxide; building materials, such as those that contain formaldehyde; and tobacco smoke. Another cause of poor indoor air quality is the presence of pests like cockroaches, that release allergens in their feces, saliva, and shed skin, which can affect individuals with allergies or asthma.  

Poor air quality is also linked to other health problems, such as cardiovascular diseases, like hypertension, certain types of cancer, and even birth defects. Poor air quality can be especially harmful for older adults, small children, and those with preexisting respiratory conditions, like chronic obstructive pulmonary disease.  

Next up is water. The quality of surface water, like rivers, lakes, and streams, and groundwater can be contaminated through a variety of routes. These can include stormwater runoff from p]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Active_Learning_with_Osmosis_from_Elsevier</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A753MkPATJKJ0Cmbln0-j7zaQbKIywVy/_.png</video:thumbnail_loc><video:title><![CDATA[Active Learning with Osmosis from Elsevier]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Active Learning with Osmosis from Elsevier through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Case_study_-_Ischemic_stroke:_Nursing</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/K639kvzTTzuwpdKDd3RRLjl1QfaXFYKw/_.jpg</video:thumbnail_loc><video:title><![CDATA[Case study - Ischemic stroke: Nursing]]></video:title><video:description><![CDATA[Nurse Darius works on a rehabilitation unit and is caring for Calvin, a 67-year-old with a history of hyperlipidemia who was admitted following a stroke. In collaboration with the registered nurse, RN Alli, Nurse Darius goes through the steps of the Clinical Judgment Measurement Model to make clinical decisions about Calvin’s care by recognizing and analyzing cues, prioritizing hypotheses, generating solutions, taking action, and evaluating outcomes. 

First, Nurse Darius recognizes important cues including Calvin’s vital signs which are temperature 98.8 F, or 37.1 C, heart rate 98 beats per minute, respirations 16 breaths per minute, blood pressure 146/92 mmHg, and oxygen saturation 96 percent on room air.  

Nurse Darius also notes that the left side of Calvin’s face is drooping and sees that he favors his right hand. Nurse Darius also overhears Calvin mixing up his words while trying to talk to the dietary staff about his lunch tray.  

Next, Nurse Darius analyzes these cues. He reviews the electronic health record, or EHR, and sees Calvin has undergone an MRI of his head. The results show that Calvin had an ischemic stroke, where an occlusion in an artery caused inadequate blood flow to his brain.  

Nurse Darius knows Calvin’s hyperlipidemia was likely a contributing factor to his stroke, since it can lead to atherosclerosis and blockage of arteries.  

He also knows the loss of oxygenated blood flow to the brain can cause damage to areas that control language and motor functions and lead to muscle weakness and aphasia.  

Nurse Darius recognizes that he needs to effectively communicate with Calvin to properly care for him. 

Now, using the information he’s gathered, Nurse Darius discusses his findings with RN Alli, and they choose a priority hypothesis of impaired communication.   

Then, they generate solutions to address Calvin’s impaired communication; and they establish the outcome that after intervening, Calvin will effectively communicate his n]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/How_Osmosis_Helps_Support_Clinical_Learners</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/DbIduFTRTdyzDaHw9jSXLVBjTMWPOLFc/_.png</video:thumbnail_loc><video:title><![CDATA[How Osmosis Helps Support Clinical Learners]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of How Osmosis Helps Support Clinical Learners through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Supporting_Clinical_Thinking_with_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HKzir2zsTley2ZohVcI9IzE5QKio5ZEc/_.png</video:thumbnail_loc><video:title><![CDATA[Supporting Clinical Thinking with Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Supporting Clinical Thinking with Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Identifying_and_Addressing_Learning_Gaps_with_Osmosis</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/We9ZpQbdTUS8an2eJTqIqRcfQkKGTCuL/_.jpg</video:thumbnail_loc><video:title><![CDATA[Identifying and Addressing Learning Gaps with Osmosis]]></video:title><video:description><![CDATA[Learn and reinforce your understanding of Identifying and Addressing Learning Gaps with Osmosis through video.]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amenorrhea:_Primary</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/pfHCpbMdTSq07Ino8djEJWpWR8mrhlS0/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amenorrhea: Primary]]></video:title><video:description><![CDATA[In amenorrhea, “menorrhea” refers to menstrual bleeding or simply menstruation, while “a” means the absence of something. So, amenorrhea is the absence of menstruation. Now, physiologic amenorrhea is normal and occurs before puberty, during pregnancy and lactation, and after menopause. However, there are also pathologic causes of amenorrhea. Primary amenorrhea refers to situations where a person has never had menstruation by 15 years of age, while secondary amenorrhea occurs when a person who used to have regular menstrual cycles stops having menstruation for a while. 

The menstrual cycle usually lasts about 28 days and starts on the first day of menstruation, when the lining of the uterus begins to shed. The entire process is controlled by the hypothalamic-pituitary-ovarian, or HPO axis, which is a connection between (you’re never gonna believe this) the hypothalamus, pituitary gland, and ovaries.  

First, the hypothalamus releases gonadotropin-releasing hormone, or GnRH, which travels through blood vessels of the pituitary stalk to reach the pituitary gland. Here, GnRH signals the pituitary gland to release follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH. Next, FSH and LH travel through the bloodstream to the ovaries where they regulate the release of estrogen and progesterone, which are crucial for maintaining normal menstrual cycles. 

Now, primary amenorrhea covers three scenarios. First, it refers to situations where a person hasn’t had their first menstruation by 15 years of age despite normal growth and the development of secondary sexual characteristics like breasts and pubic hair. Second, it refers to individuals who haven’t had their first menstruation by 13 years of age and haven’t developed secondary sexual characteristics. Third, it can mean no menstruation within five years after breast development begins. 

The most important causes of primary amenorrhea include Müllerian agenesis, Turner syndrome, androgen insen]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Amenorrhea:_Secondary</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/_7L24cagRi68xQQ24mhFu5i-QKixyI-g/_.jpg</video:thumbnail_loc><video:title><![CDATA[Amenorrhea: Secondary]]></video:title><video:description><![CDATA[In amenorrhea, “menorrhea” refers to menstrual bleeding or simply menstruation, while “a” means the absence of something. So, amenorrhea is the absence of menstruation. Now, physiologic amenorrhea is normal and occurs before puberty, during pregnancy and lactation, and after menopause. However, there are also pathologic causes of amenorrhea. Primary amenorrhea refers to situations where a person has never had menstruation by 15 years of age, while secondary amenorrhea occurs when a person who used to have regular menstrual cycles stops having menstruation for at least 3 months. 

The menstrual cycle usually lasts about 28 days and starts on the first day of menstruation, when the lining of the uterus begins to shed. The entire process is controlled by the hypothalamic-pituitary-ovarian axis, which is a connection between the hypothalamus, pituitary gland, and ovaries.  

First, the hypothalamus releases the gonadotropin-releasing hormone, or GnRH, which travels through blood vessels of the pituitary stalk to reach the pituitary gland. Here, GnRH signals the pituitary gland to release the follicle-stimulating hormone, or FSH, and luteinizing hormone, or LH. Next, FSH and LH travel through the bloodstream to the ovaries where they regulate the release of estrogen and progesterone, which are crucial for maintaining normal menstrual cycles. 

Now, secondary amenorrhea covers two scenarios. First, it refers to situations where a person who used to have regular menstruation stops having it for at least three months. Second, it can mean a person who used to have irregular menstruation stops having it for at least six months.  

Some of the most important causes of secondary amenorrhea include functional hypothalamic amenorrhea, polycystic ovarian syndrome, hyperprolactinemia, and primary ovarian insufficiency. 

First, let’s focus on functional hypothalamic amenorrhea, which occurs under extreme conditions of physical activity or emotional stress. 

In individual]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Acute_myeloid_leukemia_(AML):_Year_of_the_Zebra_2026</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/VoGzpkG6QUWb8IZlxEr2hTF2RN6ATNOh/_.jpg</video:thumbnail_loc><video:title><![CDATA[Acute myeloid leukemia (AML): Year of the Zebra 2026]]></video:title><video:description><![CDATA[Acute myeloid leukemia, or AML, is a type of blood cancer in which the bone marrow makes too many immature blood cells called myeloblasts. Even though it’s considered a rare disease, it’s the most common type of acute leukemia in adults, accounting for about 1% of all cancers in the United States. 

Now, every cell type in the blood starts out as a hematopoietic stem cell, which is a multipotent cell that can develop into multiple different cell types, depending on the signals it receives. As a stem cell divides, it doesn’t immediately become a mature blood cell. Instead, it first commits to one of two main pathways, or cell lineages, called myeloid or lymphoid.  

Cells that follow the myeloid lineage become red blood cells, which carry oxygen throughout the body; megakaryocytes that produce platelets, which help stop bleeding; and myeloblasts, which are large, immature white blood cells with a large central nucleus and very little surrounding cytoplasm. Under normal conditions, myeloblasts continue to mature into certain white blood cells, such as neutrophils and monocytes, which are especially important for fighting bacterial infections. 

In AML, myeloblasts get stuck partway through development, so instead of maturing into these different cell types, they begin to rapidly multiply and pile up in the bone marrow. This crowding of the bone marrow leaves less space for the development of healthy, mature blood cells, such as red blood cells or platelets. 

Affected cells usually have specific genetic mutations, such as pieces of DNA that are missing, duplicated, or rearranged. AML can be classified based on these genetic changes and how far those cells had progressed in their normal development before they got stuck. 

Alright, now acute leukemias tend to be aggressive and fast-growing, meaning symptoms can appear and worsen over weeks rather than years. Since the bone marrow becomes filled with immature cells that don’t work properly, there isn’t enough ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Isodicentric_chromosome_15_syndrome:_Year_of_the_Zebra_2026</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/HVBZmDkuTM_UJdV_8wxthiMFTHWlZ7f4/_.jpg</video:thumbnail_loc><video:title><![CDATA[Isodicentric chromosome 15 syndrome: Year of the Zebra 2026]]></video:title><video:description><![CDATA[Isodicentric chromosome 15 syndrome, also known as idic(15) or inverted duplication 15 syndrome, is a rare genetic condition where an individual has extra genetic material from chromosome 15.  

Chromosomes contain hundreds to thousands of genes that contain the genetic information needed to set up the normal structure and function of the human body. Each person has two sets of 23 chromosomes, for a total of 46. One full set of chromosomes is inherited from each parent.  

Idic(15) is a supernumerary marker chromosome, meaning it’s an additional chromosome beyond the usual 46. However, this chromosome doesn’t contain any new genetic information like the others. Instead, it comes from the long arm, or q arm, of chromosome 15. During cell division, this region is duplicated twice, like making two identical photocopies of a page in a book. These two copies then join together, but just before they fuse, one of the copies flips upside down, creating a mirror-like arrangement. 

Because there are two normal chromosome 15s, plus this extra marker chromosome, which itself contains two additional copies of the duplicated region, the cell ends up with four copies of those genes instead of the usual two.  

Naturally, you’d think this would lead to four active copies of the affected genes, but here’s the twist. Many of the genes in the 15q region are imprinted, meaning only the maternal copy is active, while the paternal copy is usually silenced. In symptomatic idic(15), the extra chromosome typically comes from the maternal parent, so each cell has three active copies of maternally expressed genes rather than one. This increases the expression of these genes, like turning up the volume on their expression, ultimately affecting development. ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Myelin_oligodendrocyte_glycoprotein_antibody-associated_disease_(MOGAD):_Year_of_the_Zebra_2026</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/Iwf6pMbJRiC6Jg6c6TDTVYXeTJ6L1l9A/_.jpg</video:thumbnail_loc><video:title><![CDATA[Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Year of the Zebra 2026]]></video:title><video:description><![CDATA[Myelin oligodendrocyte glycoprotein antibody-associated disease, or simply MOGAD, is a rare autoimmune condition that affects the brain, spinal cord, and optic nerves. It happens when the immune system mistakenly targets a protein that sits on the surface of myelin, the protective coating that wraps around nerve fibers and helps nerve signals travel more quickly and efficiently.  

Because this protein exists only in myelin-producing cells in the central nervous system, the immune system attack only targets the myelin in these areas, which explains why nerves elsewhere in the body are not affected. The exact reason why the attack develops in the first place is largely unknown, although it appears that viral illnesses might act to trigger an autoimmune response in some individuals, particularly children. 

Symptoms of MOGAD depend on which part of the nervous system is affected, and they usually develop over several days. These episodes are often called attacks or relapses, and they can be one-time events or recur over time. 

One of the most common manifestations is optic neuritis, which means inflammation of the nerve that connects the eye to the brain. This can cause eye pain that worsens with movement, blurred vision, partial or complete vision loss, and colors that appear washed out. Unlike other demyelinating diseases, MOGAD tends to affect both eyes simultaneously. 

Another common presentation is inflammation of the spinal cord, known as myelitis. This can cause weakness in the arms or legs, numbness or tingling, difficulty walking, or problems with bladder and bowel control.  

MOGAD can also cause inflammation in the brain, causing encephalitis. In children, brain inflammation typically appears as acute disseminated encephalomyelitis, or ADEM, which affects large areas of the brain at once. This can lead to symptoms that come on suddenly and are quite widespread, such as headaches, confusion, extreme fatigue, seizures, changes in consciousness, or]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Cockayne_syndrome:_Year_of_the_Zebra_2026</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/jEzpCQuNSQSSzWiPR3aYpTW3Qp_Mo4OJ/_.png</video:thumbnail_loc><video:title><![CDATA[Cockayne syndrome: Year of the Zebra 2026]]></video:title><video:description><![CDATA[Cockayne syndrome, or CS, is a rare genetic neurodegenerative condition resulting from defects in DNA repair and is characterized by distinct facial characteristics, disrupted growth, developmental delays, sunlight sensitivity, and premature aging.  

CS is caused by mutations, or pathogenic variants, in either the ERCC8 or ERCC6 gene, which code for the CSA and CSB proteins, respectively. This is an autosomal recessive condition, meaning that to be affected, a child must inherit two faulty copies of the gene, one from each parent. The CSA and CSB proteins from these genes are involved in the identification and repair of damaged DNA, the genetic code found in each cell. 

Everyone’s DNA is routinely damaged by normal wear and tear in the human body over time, as well as by harmful radiation found in the environment such as UV rays; x-rays; and gamma rays. Usually, damaged DNA is repaired during a process called nucleotide excision repair, or NER. In CS, faulty ERCC8 or CRCC6 genes produce proteins that cannot identify or remove damaged DNA. The damaged DNA then builds-up and leads to cell dysfunction or cell death. 

CSA and CSB proteins also do other jobs in cells, including the regulation of other proteins.  Whether the symptoms found in individuals with CS are due to the loss of DNA repair functionality, these other jobs, or both is the subject of ongoing research. 

Although CS affects overall growth and development, individuals with CS are happy and outgoing! They are very social and love to be around people! 

CS affects the eyes, ears, muscles, gastrointestinal system, and skin, and may reduce the ability to fight infection. Affected individuals develop distinct facial features, such as sunken eyes, a slender nose, and prominent ears. Physical growth is disrupted resulting in microcephaly, or a small head, and short stature. Neurologic symptoms include intellectual disabilities, tremors, speech difficulties, dementia, and sometimes seizures. Hearing]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Airway,_breathing,_circulation:_Clinical_decision_making</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/7Cvh7odNQ5mDcQcJrnMaF-M2Rj_7a7E7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Airway, breathing, circulation: Clinical decision making]]></video:title><video:description><![CDATA[The ABC acronym, which stands for airway, breathing, and circulation, helps nurses prioritize patient care. This approach can be used to make clinical decisions when caring for several patients and to guide the care of one patient with multiple concerns. Using the ABCs as a guide, nurses can rapidly make clinical decisions based on the severity of a patient&amp;#39;s condition, ensuring the most critical issues are addressed first. 

Okay, let&amp;#39;s start with A for airway, which involves evaluating whether the patient&amp;#39;s airway is open, patent, and clear. This has the highest priority because without an open airway, oxygen can’t reach the lungs, which can quickly lead to oxygen deprivation, brain injury, and eventually death. Cues that indicate a compromised airway include noisy breathing, like stridor, which is a high-pitched, whistling sound; gurgling or snoring respirations; choking; or being unable to speak. Injuries that could impair the airway may present as blood or secretions in the mouth or throat, as well as facial fractures or swelling. Additionally, if a patient is unconscious or obtunded, they may not be able to effectively maintain their own airway.  

If the patient’s airway is secure, the next priority is B for breathing, or the process of ventilation to support gas exchange. Even with a clear airway, other conditions like chest trauma, pulmonary disease, or lung infections can impair breathing. Cues that signal breathing impairment may include dyspnea, or shortness of breath; a rapid or slow rate of breathing; nasal flaring or use of accessory muscles like the sternocleidomastoid muscles in the neck; and color changes like pallor or cyanosis. Sometimes a patient might assume the orthopneic, or tripod, position, by leaning slightly forward with their arms propped up on an overbed table or their knees to help reduce the work of breathing.  

In addition, auscultation may reveal adventitious lung sounds like wheezing or rales; ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Maslow's_hierarchy_of_needs:_Clinical_decision_making</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/NJ5gLtowT2Oua4Cvc3HTP-YVTu_3hzkQ/_.jpg</video:thumbnail_loc><video:title><![CDATA[Maslow&apos;s hierarchy of needs: Clinical decision making]]></video:title><video:description><![CDATA[Maslow&amp;#39;s hierarchy of needs is a framework for understanding and prioritizing patient care based on ascending levels of human needs. Using Maslow’s hierarchy of needs allows nurses to successfully navigate patient needs within various clinical scenarios and is essential for providing safe, quality care and improving patient outcomes. 

Okay, so, Maslow&amp;#39;s hierarchy of needs organizes a patient’s needs by priority, typically illustrated as a five-tier pyramid. Fundamental needs must be met before higher-level needs can be pursued, so fundamental needs are at the pyramid base, while higher-level needs are at the top.   

So, at the base of the pyramid are physiological needs essential for human life, such as oxygen, fluids, nutrition, body temperature regulation, and elimination. Once these needs are satisfied, the focus shifts to safety and security needs, including physical and psychological safety. Physical safety includes the need for comfort and protection from harm, like violence or health threats, while psychological safety involves feeling emotionally secure and stable. Next up is the need for love and belonging, which refers to having social relationships, like friends, family, and other connections, which can include members of the health care team. Moving higher in the pyramid is the need for self-esteem, which encompasses a patient’s sense of self-worth and positive self-image, as well as feeling valued and respected by others. Finally, at the top of the pyramid is self-actualization, which involves reaching one&amp;#39;s full potential and achieving personal goals through continuous self-improvement. 

Maslow&amp;#39;s hierarchy of needs can guide nurses to prioritize interventions for patient care. For instance, when caring for a patient diagnosed with esophageal strictures, the nurse would first address nutrition and hydration needs. Once these basic needs are met, the nurse can go on to address the patient&amp;#39;s f]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Safety:_Clinical_decision_making</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/EAeWS3vaT2GAwjRbSAI7mCXtQWCy_X5R/_.jpg</video:thumbnail_loc><video:title><![CDATA[Safety: Clinical decision making]]></video:title><video:description><![CDATA[Patient safety involves the protection from psychological and physical injury by minimizing risk of harm to individuals seeking health care. Prioritizing patient safety allows nurses to successfully navigate patient needs within various clinical scenarios and is essential for providing safe, quality care and improving patient outcomes. 

Now, preventing patient harm is a top priority for healthcare organizations and requires a culture of safety, where every health care team member shares responsibility for keeping patients safe.  

Healthcare organizations adopt evidence-based practices that are recommended by organizations like the Joint Commission and the Agency for Healthcare Research and Quality to enhance patient safety.  

These practices involve implementing systems and processes that help nurses plan and prioritize safe care during activities such as patient identification, communication, medication administration, and the prevention of adverse events like falls and infections.  

Starting with patient identification, nurses use at least two methods to identify patients, such as their name and birthdate, to prevent misidentification.  

Similarly, communication tools, like SBAR, which stands for Situation, Background, Assessment, and Recommendation, allow the health care team members to organize and share the most essential information about a patient&amp;#39;s condition across teams and settings.    

As far as medication administration goes, safety can be enhanced by several methods. For instance, using medication reconciliation to compare the medications they are currently taking to the medications a patient has been prescribed can reduce errors by providing an up-to-date medication list.  

Additionally, medication errors can be reduced when systems are in place to properly label, store, prescribe, dispense, and administer Sound-Alike Look-Alike Drugs, or SALAD for short. For example, diazePAM and dilTIAZem; or metFORMIN and metroNIDAZOLE]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Classroom_readiness_and_engagement:_Nursing_student_success</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/PuYDJJUtTcGVW-gLIBEGtF6DRiyKmn47/_.jpg</video:thumbnail_loc><video:title><![CDATA[Classroom readiness and engagement: Nursing student success]]></video:title><video:description><![CDATA[Classroom readiness involves being prepared before class to maximize learning. Student engagement is the use of behavioral, cognitive, and emotional strategies to promote active participation during class.  

As a nursing student, being prepared for and engaging in class leads to better understanding of course concepts and a more positive learning experience, ultimately promoting your success.   

Now, as a student, you might be used to traditional passive teaching approaches where instructors deliver information to students, typically through lectures. After class, students then independently complete homework assignments, ideally designed to build upon the lecture or lesson.  

However, in nursing school, you&amp;#39;ll often encounter more active learning methods. Active learning involves engaging students with course material through activities or exercises, with the instructor acting as a facilitator rather than a lecturer. This method promotes critical thinking, development of clinical judgment, and allows nursing students to link theoretical knowledge with practical clinical applications.  

One example of active learning is the use of a flipped classroom. Instead of first having class lectures, and then reviewing at home, a flipped classroom is an approach where students independently review course material prior to class, such as readings and videos. Once in class, students work on their own or in groups to engage with course material and complete assignments, with instructor assistance. For active learning strategies like this, being prepared for class is essential so you can be successful in nursing school.  

Okay so, before a course begins, be sure you understand the course expectations. Start by reading the syllabus or course description to familiarize yourself with the expectations, learning outcomes, class schedule, and required readings and activities.  

If you&amp;#39;re taking multiple classes each term or semester]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Study_techniques:_Nursing_student_success</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/A7tTd-HrT4WB01U_6ccBt-zgQ-SxZOpP/_.jpg</video:thumbnail_loc><video:title><![CDATA[Study techniques: Nursing student success]]></video:title><video:description><![CDATA[Study techniques are strategies used to understand and retain information. They can help with comprehending complex material, enhancing critical thinking, developing clinical judgment, and making studying more efficient.  

As a nursing student, you’ll discover what study techniques work best for your learning style, personal preferences, and coursework. So, let’s explore a few study techniques!  

Starting with interleaving, this involves mixing up the order of the topics while you study. This differs from blocking, where you focus on one topic for a large amount of time.  

For instance, when using blocking while preparing for a pharmacology exam on cardiovascular medications, you may begin with a topic like diuretics, and once you feel comfortable with that topic, you move on to calcium channel blockers, and then on to anticoagulants, and so forth.  

In contrast, you can use interleaving by spending a bit of time reviewing diuretics, then calcium channel blockers, and then back to diuretics again. After that, you’ll go to anticoagulants, then back to calcium channel blockers, and finally, return to anticoagulants. 

Because interleaving forces you to switch between topics, it helps you practice retrieving information, which ultimately enhances your long-term memory. It can also help you improve decision making by showing how topics relate to each other, and this can help you apply the information to real world situations! 

Now, interleaving can be a challenging way to learn because it requires a lot of planning and organization in the short term, but if it works for you, you may find you have better long-term results!  

Next up is spaced repetition, where you space out your study of topics at increasingly spaced intervals. Typically, for information you’re familiar with, you’ll have more widely spaced intervals; whereas for information you’re less familiar with you’ll have shorter intervals. This sets you up to review information at the time you]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Taking_study_notes:_Nursing_student_success</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/ow6BoT7CSAmTRlh3frm6iPHORkmFheAF/_.jpg</video:thumbnail_loc><video:title><![CDATA[Taking study notes: Nursing student success]]></video:title><video:description><![CDATA[Note-taking involves writing down key information from different sources, such as lectures, textbooks, or recorded modules.  

Since class time is limited, instructors often focus on the most important concepts, leaving students to explore learning gaps independently.  

As a nursing student, taking good notes can help you understand and remember complex material and make studying more effective. Good note-taking can also enhance critical thinking and help develop clinical judgment by linking theoretical concepts with practical applications that support high-quality patient care. 

How you take notes can vary due to your own learning preference and the material you’re studying.  

You may choose to take notes by hand using paper and a pen or pencil; or you may choose to take digital notes using a computer, tablet, or smartphone.  

Taking handwritten notes can be time-intensive, but some research indicates that it enhances memory retention and recall due to the psychomotor act of writing.  

On the other hand, taking digital notes, like typing on a computer, can be fast and efficient, and they’re easily saved, stored, and edited. There are even digital programs and applications that can help you format your notes in different ways.  

Lastly, there’s a hybrid of these two note-taking forms which involves using a touchscreen device such as a tablet or smartphone to write notes using a special pen-like tool called a stylus. 

Now, there&amp;#39;s no single &amp;quot;best&amp;quot; way to take notes and there are several styles and formats to choose from. As a nursing student, you’ll find what works best for you which may evolve over time or depend on the material you’re learning. So, let’s explore a few note-taking formats you can try.  

Starting with the Cornell method, this involves formatting your notes into dedicated sections to help keep them organized. This method can be used during a class, while reading your textbook, or while watching a video.  ]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Combating_misinformation_and_disinformation:_Role_of_the_nurse</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/xNGfS6vlRvqDOE5yGvGq4rmaQAmTE9Y8/_.jpg</video:thumbnail_loc><video:title><![CDATA[Combating misinformation and disinformation: Role of the nurse]]></video:title><video:description><![CDATA[Combating misinformation and disinformation involves efforts to identify, challenge, and correct misleading or false information, especially when it can harm the understanding of health or safety.  

Let&amp;#39;s talk about information in the context of healthcare.  In this case, information refers to accurate, evidence-based data used to make informed decisions to ensure high-quality patient care. 

Misinformation is inaccurate and misleading information.   

Misinformation is spread without the intent to deceive – basically, it’s getting the facts wrong.  

On the other hand, disinformation involves deliberately misstating the facts by spreading false information.   

Disinformation is spread with the intent to deceive, manipulate, or cause harm; typically for financial, personal, or political gain.  

As the nurse, you&amp;#39;ll help patients combat misinformation and disinformation while guiding them to accurate sources to support informed healthcare decisions.  

Okay, so, both misinformation and disinformation can impact patient well-being and safety while undermining trust in clinicians, such as nurses, pharmacists, and physicians.  

When inaccurate health information leads to uninformed patient decision making, improper treatment, delays in care, or avoidance of necessary medical interventions, patient well-being and safety are at risk.  

For example, misinformation about vaccines and their proposed link to autism can contribute to vaccine hesitancy, leading to lower vaccination rates, and higher susceptibility to preventable diseases.  

Similarly, disinformation about dietary supplements that haven’t been approved for medical use can promote the use of quick fixes, and fear of medical-grade treatments.  

This can cause delays in seeking medical advice, reliance on unregulated products, and harmful side effects. 

Additionally, misinformation and disinformation can undermine trust in clinicians by distorting perceptions, obstructing cl]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Long-term_care:_Role_of_the_nurse</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/hf_gBmXhQaWMOCZE1RZ0f29IT-Wt5nL7/_.jpg</video:thumbnail_loc><video:title><![CDATA[Long-term care: Role of the nurse]]></video:title><video:description><![CDATA[Long-term care is a type of service where individuals can receive assistance with their care while living safely and as independently as possible. Long-term care includes nursing centers, formerly called nursing homes, and assisted living facilities. As the nurse, you’ll provide patient-centered care for your long-term care residents.  

Alright, so, nursing centers provide a high level of 24-hour care for residents with conditions that limit or completely impair their ability to safely perform activities of daily living, or ADLs, like dressing and toileting.  

Services usually include medical and nursing care, such as medication management; self-care assistance; tailored meal preparation and feeding assistance; and recreational activities, like music therapy.  

Additionally, residents may receive routine and emergency dental services, as well as rehabilitation services like physical and occupational therapy. Typically, residents reside permanently in nursing centers; however, some residents may reside in a nursing center temporarily as they regain function after a serious injury or illness. 

On the other hand, assisted living facilities offer a more independent, home-like environment for individuals who are relatively autonomous but are not able to live independently. Typical services include laundry, meal preparation, and housekeeping, as well as medication administration and personal care assistance like bathing and dressing, as needed.  

Residents usually have their own rooms and can keep their personal belongings, and they can attend group dining and participate in shared social activities, like exercise classes or book clubs. Lastly, memory care is a type of specialized assisted living where individuals with Alzheimer disease and other types of dementia can receive care in a more secure environment with a focus on individualized cognitive support and structured routines to support quality of life.   

When caring for your long-term care residents]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/Mental_health_care_settings:_Role_of_the_nurse</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/dFfq0i5dQ1CvsAkNPH_H7ak4T2KnfAxi/_.jpg</video:thumbnail_loc><video:title><![CDATA[Mental health care settings: Role of the nurse]]></video:title><video:description><![CDATA[Mental health care is delivered in a variety of settings, and the choice depends on the individual’s condition and level of need. Short-term or acute care settings include inpatient psychiatric hospitals or psychiatric units within general hospitals, and facilities that provide specialized psychiatric emergency services. Other settings include community mental health settings and home-based care. For some individuals with chronic and severe mental health conditions, long-term inpatient care may be necessary when outpatient treatment is not appropriate or safe. As the nurse in a mental health care setting, you’ll provide patient-centered care by ensuring safety and promoting recovery. 

Alright, so, each setting for mental health care provides a different level of support and services.  Inpatient psychiatric hospitals or hospital-based psychiatric units provide 24-hour care for patients experiencing severe symptoms or mental health emergencies, such as suicidal ideation, psychosis, or incapacitation from an acute behavioral crisis or psychiatric decompensation.  

On the other hand, settings that provide psychiatric emergency services initiate rapid stabilization procedures during a mental health crisis and prepare patients for transition to a less intense level of care. Admission to these settings can be voluntary when an individual seeks care and consents to treatment. It can also be involuntary when an individual poses danger to themselves or others or is unable to meet his or her own basic needs due to mental illness. 

Next, community mental health settings offer psychiatric therapy, medication management, and support services with the goal of maintaining stability and preventing relapse. These settings can include partial hospitalization programs, sometimes referred to as day treatment, where patients can receive structured care on weekdays and return home in the evenings and weekends; group homes where patients live in a shared therapeutic space with]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/video/School_health:_Role_of_the_nurse</loc><video:video><video:thumbnail_loc>https://d16qt3wv6xm098.cloudfront.net/9ogqFTa9RM64iT5jJI1x_GDqTFqarCwy/_.jpg</video:thumbnail_loc><video:title><![CDATA[School health: Role of the nurse]]></video:title><video:description><![CDATA[School health refers to the comprehensive approach to promoting and protecting the physical, mental, and emotional well-being of students in an educational setting. It ensures continuity of care from school to home to community and is present in all levels of education from early childhood through colleges and universities.  

As a school nurse, you’ll provide student-centered care within an educational setting. 

Alright, now, school nurses play a crucial role in developing and implementing school health programs, which can vary among states, communities, and school districts. These programs are designed to enhance health and academic outcomes by offering improved access to care, including preventative care and early intervention services. School health programs support healthy behaviors, like quality nutrition, regular physical activity, and adequate sleep, which can be linked to higher academic achievement. On top of that, school health programs can help reduce gaps in health disparities when designed with cultural humility and inclusivity in mind. 

Services offered by school nurses typically include health education, which uses information and motivation to promote health and prevent disease; physical education, which teaches the skills and behaviors needed to engage in lifelong physical activity; and a variety of direct health services, which includes the hands-on care provided by school nurses, such as medication administration, emergency care, and chronic condition management.  

Now, since school nurses care for students across a range of developmental stages, educational programs should be tailored to be age appropriate. For example, health education for elementary school students might incorporate visual aids and interactive games to teach about healthy food choices; whereas health education for high school students might focus on providing information about sexual health, substance use, and mental health. 

School nurses also provide support fo]]></video:description><video:content_loc>https://d16qt3wv6xm098.cloudfront.net/undefined</video:content_loc></video:video></url><url><loc>https://www.osmosis.org/learn-quiz/Abdominal_aortic_aneurysm:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Abdominal_aortic_aneurysm:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Abdominal_aortic_aneurysm:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Abdominal_hernias/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Abdominal_hernias/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Abdominal_hernias/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Abdominal_trauma_in_pregnancy:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Abdominal_trauma_in_pregnancy:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acetaminophen_(Paracetamol)_toxicity:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acetaminophen_(Paracetamol)_toxicity:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acetaminophen_(Paracetamol)_toxicity:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acid-base_disturbances:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acid-base_disturbances:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acid-base_disturbances:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acneiform_skin_disorders:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acneiform_skin_disorders:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acoustic_neuroma_(schwannoma)/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acoustic_neuroma_(schwannoma)/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acoustic_neuroma_(schwannoma)/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_cholecystitis/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_cholecystitis/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_cholecystitis/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_coronary_syndrome:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_coronary_syndrome:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_coronary_syndrome:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_group_A_streptococcal_infections_and_sequelae_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_group_A_streptococcal_infections_and_sequelae_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_leukemia/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_leukemia/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_leukemia/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_limb_ischemia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_limb_ischemia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_mesenteric_ischemia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_mesenteric_ischemia:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_mesenteric_ischemia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_pancreatitis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_pancreatitis:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_pancreatitis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_pyelonephritis/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_pyelonephritis/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_pyelonephritis/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_respiratory_distress_syndrome/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_respiratory_distress_syndrome/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_respiratory_distress_syndrome/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Acute_respiratory_distress_syndrom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oc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_feeding_and_eating_disorders:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_feeding_and_eating_disorders:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_first_trimester_bleeding:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_first_trimester_bleeding:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_foot_pain:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_foot_pain:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_gradual_cognitive_decline:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_gradual_cognitive_decline:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_growth_faltering:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_growth_faltering:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hallucinogen,_inhalant,_and_cannabis_use,_intoxication,_and_overdose:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hallucinogen,_inhalant,_and_cannabis_use,_intoxication,_and_overdose:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_head_and_neck_masses_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_head_and_neck_masses_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_headache_or_facial_pain:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_headache_or_facial_pain:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hematochezia_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hematochezia_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hematochezia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hematochezia:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hematochezia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hematuria_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hematuria_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hepatic_masses:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hepatic_masses:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hip_pain:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hip_pain:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_household_substance_exposure_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_household_substance_exposure_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hypercalcemia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hypercalcemia:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hypercalcemia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hypercoagulable_disorders:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hypercoagulable_disorders:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hyperkalemia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hyperkalemia:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hyperkalemia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hypernatremia_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hypernatremia_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_hypernatremia:_Clinical_scien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earn-quiz/Approach_to_interstitial_lung_disease_(diffuse_parenchymal_lung_disease):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_involuntary_movements:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_involuntary_movements:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_jaundice_(conjugated_hyperbilirubinemia):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_jaundice_(conjugated_hyperbilirubinemia):_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_jaundice_(conjugated_hyperbilirubinemia):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_jaundice_(newborn_and_infant):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_jaundice_(newborn_and_infant):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_jaundice_(unconjugated_hyperbilirubinemia):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_jaundice_(unconjugated_hyperbilirubinemia):_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_jaundice_(unconjugated_hyperbilirubinemia):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_joint_pain_and_swelling:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_joint_pain_and_swelling:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_knee_pain:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_knee_pain:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_knee_pain:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_leukemia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_leukemia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_leukocoria_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_leukocoria_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_lower_airway_obstruction_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_lower_airway_obstruction_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_lower_limb_edema:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_lower_limb_edema:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_lower_limb_edema:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_lymphoma:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_lymphoma:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_medication_exposure_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_medication_exposure_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_medication-induced_movement_disorders:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_medication-induced_movement_disorders:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_melena_and_hematemesis_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_melena_and_hematemesis_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_melena_and_hematemesis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_melena_and_hematemesis:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_melena_and_hematemesis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_metabolic_acidosis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_metabolic_acidosis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_metabolic_alkalosis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_metabolic_alkalosis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_mood_disorders:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_mood_disorders:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_myelodysplastic_syndromes:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_myelodysplastic_syndromes:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_myeloproliferative_neoplasms:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_myeloproliferative_neoplasms:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_neurocutaneous_syndromes:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_neurocutaneous_syndromes:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_neurodevelopmental_disorders:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_neurodevelopmental_disorders:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_nipple_discharge:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_nipple_discharge:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_nipple_discharge:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_non-healing_wounds:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_non-healing_wounds:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_non-healing_wounds:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_nosocomial_infections:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_nosocomial_infections:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_nosocomial_infections:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_pancreatic_masses:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_pancreatic_masses:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_paranoid,_schizoid,_and_schizotypal_(cluster_A)_personality_disorders:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_paranoid,_schizoid,_and_schizotypal_(cluster_A)_personality_disorders:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_penetrating_chest_injury:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_penetrating_chest_injury:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_penetrating_chest_injury:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_penetrating_neck_injury:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_penetrating_neck_injury:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_perianal_problems:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_perianal_problems:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_peripheral_lymphadenopathy_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_peripheral_lymphadenopathy_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_peripheral_lymphadenopathy:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_peripheral_lymphadenopathy:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_periumbilical_and_lower_abdominal_pain:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_periumbilical_and_lower_abdominal_pain:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_periumbilical_and_lower_abdominal_pain:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_pneumoconiosis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_pneumoconiosis:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_pneumoconiosis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_pneumoperitoneum_and_peritonitis_(perforated_viscus):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_pneumoperitoneum_and_peritonitis_(perforated_viscus):_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_pneumoperitoneum_and_peritonitis_(perforated_viscus):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_polyneuropathy:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_polyneuropathy:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_poor_feeding_(newborn_and_infant):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_poor_feeding_(newborn_and_infant):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postmenopausal_bleeding:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postmenopausal_bleeding:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_abdominal_pain:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_abdominal_pain:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_abdominal_pain:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_acute_kidney_injury:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_acute_kidney_injury:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_acute_kidney_injury:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_hypotension:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_hypotension:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_hypotension:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_respiratory_distress:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_respiratory_distress:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_respiratory_distress:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_wound_complications:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_wound_complications:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postoperative_wound_complications:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postpartum_fever:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postpartum_fever:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postpartum_hemorrhage:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postpartum_hemorrhage:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_postpartum_hemorrhage:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_precocious_puberty:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_precocious_puberty:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_prenatal_teratogen_exposure:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_prenatal_teratogen_exposure:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_primary_amenorrhea:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_primary_amenorrhea:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_primary_immunodeficiencies:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmos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Approach_to_syncope:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_syncope:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_syncope:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_tachycardia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_tachycardia:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_tachycardia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_the_acute_abdomen_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_the_acute_abdomen_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_third_trimester_bleeding:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_third_trimester_bleeding:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_trauma_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_trauma_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_trauma_and_stressor-related_disorders:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_trauma_and_stressor-related_disorders:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_trauma:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_trauma:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_traumatic_brain_injury_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_traumatic_brain_injury_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_traumatic_brain_injury:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_traumatic_brain_injury:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_traumatic_brain_injury:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_tremor:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_tremor:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_unintentional_weight_loss:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_unintentional_weight_loss:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_unsteadiness,_gait_disturbance,_or_falls:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_unsteadiness,_gait_disturbance,_or_falls:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_upper_abdominal_pain:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_upper_abdominal_pain:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_upper_abdominal_pain:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_upper_airway_obstruction_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_upper_airway_obstruction_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_urinary_incontinence_(GYN):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_urinary_incontinence_(GYN):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_vaginal_discharge:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_vaginal_discharge:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_vaginal_discharge:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_vasculitis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_vasculitis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_viral_exanthems_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Approach_to_viral_exanthe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eep_vein_thrombosis_and_pulmonary_embolism:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Deep_vein_thrombosis_and_pulmonary_embolism:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Deep_vein_thrombosis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Deep_vein_thrombosis:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Deep_vein_thrombosis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dehydration_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dehydration_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Delirium:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Delirium:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Delirium:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dementia_with_Lewy_bodies/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dementia_with_Lewy_bodies/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dementia:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dementia:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dementia:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Demyelinating_disorders:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Demyelinating_disorders:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Demyelinating_disorders:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dermatomyositis/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dermatomyositis/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_and_learning_disorders:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_and_learning_disorders:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_dysplasia_of_the_hip:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_dysplasia_of_the_hip:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_dysplasia_of_the_hip:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_milestones_(childhood):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_milestones_(childhood):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_milestones_(newborn_and_infant):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_milestones_(newborn_and_infant):_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_milestones_(newborn_and_infant):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_milestones_(toddler):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Developmental_milestones_(toddler):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_in_pregnancy_(GDM,_T1DM,_and_T2DM):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_in_pregnancy_(GDM,_T1DM,_and_T2DM):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_insipidus/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_insipidus_and_SIADH:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_insipidus_and_SIADH:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_insipidus_and_SIADH:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_insipidus:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_insipidus:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_mellitus/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_mellitus/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_mellitus/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabetes_mellitus_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Diabete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c>https://www.osmosis.org/learn-quiz/Down_syndrome_(Trisomy_21)/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Down_syndrome_(Trisomy_21)/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Alcohol:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Alcohol:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Hallucinogens:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Hallucinogens:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Hallucinogens:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Other_depressants:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Other_depressants:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Stimulants:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Stimulants:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Drug_misuse,_intoxication_and_withdrawal:_Stimulants:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dubin-Johnson_syndrome/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dubin-Johnson_syndrome/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ductal_carcinoma_in_situ:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ductal_carcinoma_in_situ:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ductal_carcinoma_in_situ:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dyslipidemia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dyslipidemia:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dyslipidemia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dyslipidemias:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dyslipidemias:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Dyslipidemias:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Early_pregnancy_loss:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Early_pregnancy_loss:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Eating_disorders:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Eating_disorders:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ectopic_pregnancy:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ectopic_pregnancy:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Electrolyte_disturbances:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Electrolyte_disturbances:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Electrolyte_disturbances:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Emergency_contraception:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Emergency_contraception:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Emphysema/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Emphysema/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Emphysema/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Empyema:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Empyema:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Empyema:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Encephalitis/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Encephalitis/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Encephalitis/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Endocarditis/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Endocarditis/pance/questions</loc></url><url><loc>https://www.osmosis.org/le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quiz/Intraamniotic_infection:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intraamniotic_infection:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intracerebral_hemorrhage/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intracerebral_hemorrhage/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intracerebral_hemorrhage/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrapartum_care_(1st,_2nd,_3rd,_and_4th_stages):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrapartum_care_(1st,_2nd,_3rd,_and_4th_stages):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrapartum_fetal_heart_rate_monitoring:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrapartum_fetal_heart_rate_monitoring:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrinsic_acute_kidney_injury_(glomerular_causes):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrinsic_acute_kidney_injury_(glomerular_causes):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrinsic_acute_kidney_injury_(non-glomerular_causes):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrinsic_acute_kidney_injury_(non-glomerular_causes):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrinsic_hemolytic_normocytic_anemia:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrinsic_hemolytic_normocytic_anemia:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intrinsic_hemolytic_normocytic_anemia:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intussusception:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Intussusception:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Invasive_ductal_carcinoma:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Invasive_ductal_carcinoma:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Invasive_lobular_carcinoma:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Invasive_lobular_carcinoma:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Invasive_lobular_carcinoma:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Iron_deficiency_and_iron_deficiency_anemia_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Iron_deficiency_and_iron_deficiency_anemia_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Iron_deficiency_anemia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Iron_deficiency_anemia:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Iron_deficiency_anemia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Irritable_bowel_syndrome:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Irritable_bowel_syndrome:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Irritable_bowel_syndrome:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ischemic_colitis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ischemic_colitis:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ischemic_colitis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ischemic_stroke/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ischemic_stroke/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ischemic_stroke/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Jaundice/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Jaundice/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Jaundice/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Jaundice:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Jaundice:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Jaundice:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Juvenile_idiopathic_arthritis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://ww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on-accidental_trauma_and_neglect_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Non-accidental_trauma_and_neglect_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Non-hemolytic_normocytic_anemia:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Non-Hodgkin_lymphoma/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Non-Hodgkin_lymphoma/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Non-Hodgkin_lymphoma/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obesity_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obesity_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obesity_and_metabolic_syndrome:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obesity_and_metabolic_syndrome:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obsessive_compulsive_disorder_(OCD):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obsessive_compulsive_disorder_(OCD):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obsessive-compulsive_disorder/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obsessive-compulsive_disorder/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obstructive_lung_diseases:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obstructive_lung_diseases:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Obstructive_lung_diseases:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_dependence/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_dependence/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_intoxication_and_overdose:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_intoxication_and_overdose:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_intoxication_and_overdose:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_use_disorder:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_use_disorder:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_withdrawal_syndrome:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Opioid_withdrawal_syndrome:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoarthritis/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoarthritis/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoarthritis/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoarthritis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoarthritis:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoarthritis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteogenesis_imperfecta/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteogenesis_imperfecta/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteogenesis_imperfecta/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteomalacia_and_rickets/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteomalacia_and_rickets/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteomalacia_and_rickets/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteomyelitis_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteomyelitis_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteomyelitis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteomyelitis:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteomyelitis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoporosis/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoporosis/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoporosis/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoporosis:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoporosis:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Osteoporosis:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Otitis_media_and_externa_(pediatrics):_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Otitis_media_and_externa_(pediatrics):_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Otitis_media_and_externa_(pediatrics):_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_cancer:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_cancer:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_cyst/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_cyst/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_cyst/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_cysts_and_tumors:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_cysts_and_tumors:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_cysts_and_tumors:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_germ_cell_tumors/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_germ_cell_tumors/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_germ_cell_tumors/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_sex-cord_stromal_tumors/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_sex-cord_stromal_tumors/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_sex-cord_stromal_tumors/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_surface_epithelial_tumors/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Ovarian_surface_epithelial_tumors/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pain_management_during_labor:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pain_management_during_labor:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pancreatic_cancer:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pancreatic_cancer:_Clinical_sciences/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pancreatic_cancer:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pancreatic_neuroendocrine_neoplasms/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pancreatic_neuroendocrine_neoplasms/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pancreatitis:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pancreatitis:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Pancreatitis:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Papulosquamous_and_inflammatory_skin_disorders:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Papulosquamous_and_inflammatory_skin_disorders:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Paraesophageal_and_hiatal_hernia:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Paraesophageal_and_hiatal_hernia:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parathyroid_disorders_and_calcium_imbalance:_Pathology_review/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parathyroid_disorders_and_calcium_imbalance:_Pathology_review/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parathyroid_disorders_and_calcium_imbalance:_Pathology_review/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parkinson_disease/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parkinson_disease/pance/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parkinson_disease/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parkinson_disease_and_dementia_with_Lewy_bodies:_Clinical_sciences/step2/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parkinson_disease_and_dementia_with_Lewy_bodies:_Clinical_sciences/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parvovirus_B19/step1/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Parvovirus_B19/cme/questions</loc></url><url><loc>https://www.osmosis.org/learn-quiz/Patent_ductus_arteriosus/step1/questions</loc></url><url><loc>https://www.osmosis.or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